Delee & Drez's Orthopaedic Sports Medicine: Principles and Practice (2 Volume Set)

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

By OkDoKeY

Frontmatter Title Page Copyright Page Dedication Contributors Preface 1 - Basic Science and Injury of Muscle, Tendon, and Ligaments Section A Muscle and Tendon

Section B Ligaments Section C Effects of Medications in Sports Injuries at the Tissue Level Section D Sports Medicine Terminology 2 - Basic Science and Injury of Articular Cartilage, Menisci, and Bone Section A Articular Cartilage Section B Meniscus Section C Bone 3 - The Effects of Medications in Sports Injuries Nonsteroidal Anti-inflammatory Drugs Corticosteroids Narcotics Nutritional Supplements Conclusion Acknowledgment References 4 - Biomechanics Basic Concepts Statics Dynamics Mechanics of Materials Conclusion References

References 5 - Research Design and Statistics in Sports Medicine The Research Process Research Design Assessing Accuracy and Precision Statistical Power Analysis Summary References Appendix One: Comparison of Pearson Product Moment Correlation and Intraclass Correlation Coefficient for Data with Systematic Error Appendix Two: Statistical Power Examples 6 - Surgical Principles Section A Suture Materials Section B Construction and Fixation of a Tendon Anterior Cruciate Ligament Graft Section C Suture Anchors Section D Biodegradable Materials Section E Allograft Tissues Section F Thermal Modification of Connective Tissue: Basic Science Considerations Section G Basic Arthroscopic Principles Section H Arthroscopic Knot Tying Section I Use and Abuse of the Pneumatic Tourniquet 7 - Risk Assessment and Management of Nonorthopaedic Conditions Section A Viral Disease Section B Paired Organ Loss Section C Hypertension and Other Cardiac Disease in Athletes Section D Athletes and Sudden Cardiac Death Section E Diabetes Mellitus Section F Exercise-Induced Asthma Section G Sports and Epilepsy 8 - Rehabilitation Section A The Language of Exercise and Rehabilitation Section B Open and Closed Chain Exercises (Non-Weight-Bearing and Weight-Bearing Exercises) Section C Therapeutic Modalities

Section C Therapeutic Modalities 9 - Complex Regional Pain Syndromes Including Reflex Sympathetic Dystrophy and Causalgia Introduction and Terminology Pertinent Anatomy and Physiology Review Theories of the Pathophysiologic Mechanism Clinical Presentation Diagnostic Procedures Patient Education and Information Treatment Principles and Methods Medications for Symptomatic Relief Surgical Sympathectomy Surgical Intervention Complex Regional Pain Syndromes in Children Authors' Preferred Method of Treatment Information for the Patient References 10 - Nutrition for Sports Goals of Sports Nutrition Energy Systems Energy Substrates Hydration Calorie Requirements Carbohydrate Requirements Example Protein Requirements Fat Requirements Micronutrient Requirements Weight Management Issues Supplement Use Summary References 11 - Sports Pharmacology Section A Ergogenic Drugs in Sports

Section A Ergogenic Drugs in Sports Section B Recreational Drug Use in Athletes 12 - Sport Psychology and Injured Athletes Prevalence of Athletic Injury The Injury Experience and the Rehabilitation Process Two-Factor Contextual Considerations of the Injury Experience and Precursors to the Rehabilitation Process The Injury Experience: A Closer Look Sport Psychology Conclusion References 13 - The Female Athlete Anatomic and Physiologic Differences between the Sexes That May Affect Performance The Preparticipation Physical Examination Pregnancy and Exercise Conditioning and Rehabilitation Musculoskeletal Injuries Arthritis, Exercise, and the Mature Female Athlete References 14 - The Orthopaedically Disabled Athlete History of Sports for the Disabled Individual Sports The Amputee Athlete Spinal Cord Injury Exercise Physiology Problems Encountered by Disabled Athletes Training Wheelchairs References 15 - Environmental Stress Section A Heat Intolerance Section B Cold Injury Section C Altitude Stress 16 - Imaging Techniques

Section A Imaging of Sports-Related Injuries Section B Differences between the Immature and Mature Skeleton 17 - Special Considerations in the Pediatric and Adolescent Athlete Section A Exercise Physiology Section B Sports and the Neurodevelopment of the Child and Adolescent Section C Preparticipation Evaluation of the Young Athlete Section D The Child Athlete with Chronic Disease Section E The Disabled Pediatric Athlete APPENDIX: Internet World Wide Web References Section F Psychological Aspects of Sports in Children and Adolescents Section G Overuse Injuries in the Skeletally Immature Athlete Section H Physeal Injuries in Young Athletes Section I Strength Training in Children and Adolescents 18 - The Team Physician: The Preparticipation Examination and On-Field Emergencies Philosophy Roles and Functions of the Team Physician Relationships Involving the Team Physician Team Physician Rewards References 19 - Head Injuries Section A Head Injuries in Adults Section B Pediatric Sports-Related Head Injuries 20 - Cervical Spine Section A Cervical Spine Injuries in the Adult Section B The Cervical Spine in the Child 21 - Shoulder

Section A Functional Anatomy and Biomechanics of the Shoulder Section B Imaging of the Glenohumeral Joint Section C Injuries to the Acromioclavicular Joint in Adults and Children Section D Injuries to the Sternoclavicular Joint in the Adult and Child Section E Clavicle Fractures Section F Glenoid and Scapula Fractures in Adults and Children Section G Fractures of the Coracoid in Adults and Children Section H Scapulothoracic Crepitus and Bursitis in Athletes Section I Sternum and Rib Fractures in Adults and Children Section J Glenohumeral Instabilities Section K Superior Labral Injuries Section L Rotator Cuff and Impingement Lesions in Adult and Adolescent Athletes Section M Injuries of the Proximal Humerus Section N Nerve Lesions of the Shoulder Section O Thoracic Outlet Syndrome 22 - Arm Section A Soft Tissue Injury and Fractures Section B Neurovascular Injury of the Arm 23 - Elbow and Forearm Section A Biomechanics of the Elbow and Forearm Section B Tendinopathies about the Elbow Section C Throwing Injuries Section D Olecranon Bursitis Section E Osteochondroses of the Elbow Section F Osteochondritis Dissecans Section G Fractures of the Elbow Section H Heterotopic Bone about the Elbow Section I Elbow Dislocation Section J Entrapment Neuropathies about the Elbow 24 - Wrist and Hand Section A Wrist Section B Hand

25 - Hip and Pelvis Section A Hip and Pelvis: Adult Section B Hip and Pelvic Injuries in the Young Athlete 26 - Thigh Section A Adult Thigh Section B Pediatric Thigh 27 - Thoracolumbar Spine Section A Thoracolumbar Spine in the Adult Section B Sports Injuries to the Thoracolumbar Spine in Children and Adolescents 28 - Knee Section A Relevant Biomechanics of the Knee Section B Imaging Sports-Related Injuries of the Knee Section C Factors Predisposing to Knee Injury Section D Meniscal Injuries Section E Patellofemoral Joint Section F Articular Cartilage Lesions and Osteochondritis Dissecans Section G High Tibial Osteotomy in the Anterior Cruciate Ligament-Deficient Knee with Varus Angulation Section H Medial Ligament Injuries Section I Lateral and Posterior Instabilities of the Knee Section J Anterior Cruciate Ligament Injuries APPENDIX A Patellar Tendon Autograft Reconstruction Minimum 2-Year Follow-up Studies APPENDIX B Hamstring Anterior Cruciate Ligament Reconstruction Minimum 2-Year Follow-up Studies Section K Posterior Cruciate Ligament Injuries Section L The Multiple Ligament-Injured Knee Section M The Use of Knee Braces in Sports Medicine Section N Knee Replacement in the Recreational Athlete 29 - The Leg

The Shin Splint Syndrome Stress Fractures of the Tibia and Fibula Compartment Syndromes Popliteal Artery Entrapment Effort-Induced Venous Thrombosis Tennis Leg Proximal Tibiofibular Joint Disorders Tibiofibular Synostosis Nerve Entrapment References 30 - Foot and Ankle Section A Biomechanics of the Foot and Ankle Linkage Section B Imaging of Sports Injuries of the Foot and Ankle Section C Etiology of Injury to the Foot and Ankle Section D Sports Shoes and Orthoses Section E Ligament Injuries of the Foot and Ankle in the Athlete Section F Stress Fractures of the Foot and Ankle Section G Tendon Injuries of the Foot and Ankle Section H Heel Pain Section I Entrapment Neuropathies of the Foot Section J Conditions of the Forefoot Section K Osteochondroses and Related Problems of the Foot and Ankle

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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DeLee & Drez's Orthopaedic Sports Medicine PRINCIPLES AND PRACTICE

2nd EDITION Jesse C. DeLee MD Clinical Professor of Orthopaedics Director, University of Texas Health Sciences Center at San Antonio Sports Medicine Fellowship Program San Antonio, Texas

David Drez Jr. MD Clinical Professor of Orthopaedics Head, Louisiana State University Knee and Sports Medicine Fellowship Program Lake Charles, Louisiana

Associate Editor: Mark D. Miller MD Associate Professor of Orthopaedic Surgery Co-Director, Division of Sports Medicine University of Virginia Charlottesville, Virginia

SAUNDERS An Imprint of Elsevier Science

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SAUNDERS An Imprint of Elsevier Science The Curtis Center Independence Square West Philadelphia, PA 19106

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

DELEE & DREZ'S ORTHOPAEDIC SPORTS MEDICINE: PRINCIPLES AND PRACTICE Copyright 2003, Elsevier Science (USA). All rights reserved. Volume 1: Part no. 9997635175 Volume 2: Part no. 9997635183 Set ISBN 0-7216-8845-4 No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior permission of the publisher (Saunders, The Curtis Center, Independence Square West, Philadelphia, PA 19106-3399).

Notice Orthopaedic sports medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. The Publisher

First Edition 1994. Mayo Foundation retains copyright of illustrations to the following chapters: 23A, 23B, 23F1, 23G1, 23H, 23I1, and 23J. Library of Congress Cataloging-in-Publication Data DeLee & Drez's orthopaedic sports medicine; principles and practice/[edited by] Jesse C. DeLee, David Drez, Jr. ; associate editor, Mark D. Miller.2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 0-7216-8845-4 (set) 1. Sports injuries. 2. Orthopedic emergencies. 3. Sports medicine. I. Title: Orthopaedic sports medicine. II. DeLee, Jesse. III. Drez, David. IV. Miller, Mark D. [DNLM: 1. Athletic Injuries. 2. Orthopedics. 3. Sports Medicine. QT 260 D346 2002] RD97 .D455 2002 617.1'027dc21 2001032001 Editor-in-Chief: Andrew Stevenson Acquisitions Editor: Richard Lampert Developmental Editors: Melissa Dudlick, Hilarie Surrena Project Manager: Linda Van Pelt Book Designer: Andrew Johnson MC/MVY Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

We dedicate these volumes to our wives, Anne and Judy, to our families who support us, and to all our teachers past and present. J.D., D.D.To my children, each an outstanding athlete in their own right, with a promise that I will become a better fan. M.M.

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Contributors

Karim Abdollahi MD Instructor of Orthopaedics, Department of Orthopaedic Surgery, Loma Linda University School of Medicine; Orthopaedic Surgeon, Loma Linda University Medical Center, Loma Linda, California Thoracic Outlet Syndrome P. David Adelson MD, FACS, FAAP Associate Professor of Neurosurgery, University of Pittsburgh School of Medicine; Director, Pediatric Neurotrauma, and Associate Director, Trauma and Trauma Research, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania Pediatric Sports-Related Head Injuries John P. Albright MD Professor,

Department of Orthopaedic Surgery, University of Iowa College of Medicine; Director, Sports Medicine Services, University of Iowa Hospitals & Clinics, Iowa City, Iowa The Use of Knee Braces in Sports Medicine David B. Allen MD Professor of Pediatrics, University of Wisconsin Medical School; Director of Endocrinology and Residency Training, University of Wisconsin Children's Hospital, Madison, Wisconsin Diabetes Mellitus Louis C. Almekinders MD Professor, Department of Orthopaedics, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina Muscle and Tendon John L. Andary MD, MBA Idaho Falls, Idaho; Formerly Sports Medicine Fellow, Department of Orthopaedics, Jacksonville Memorial Hospital, Miami, Florida Thermal Modification of Connective Tissue: Basic Science Considerations Robert Anderson BS President, Stretching Inc., Palmer Lake, Colorado Stretching James R. Andrews MD Clinical Professor of Orthopaedics and Sports Medicine, University of Virginia School of Medicine, Charlottesville, Virginia; Clinical Professor, Department of Surgery, Division of Orthopaedic Surgery, University of Alabama School of Medicine, Birmingham;

Medical Director, American Sports Medicine Institute; Orthopaedic Surgeon, Alabama Sports Medicine and Orthopaedic Center, Birmingham, Alabama Throwing Injuries in the Adult Jack T. Andrish MD Orthopaedic Surgeon, Cleveland Clinic Foundation, Cleveland, Ohio The Leg Christopher C. Annunziata MD Clinical Instructor, Department of Orthopaedics, Georgetown University School of Medicine, Washington, District of Columbia Posterior Cruciate Ligament Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Child John Antoniou MD, PhD, FRCSC Assistant Professor, Mc Gill University, Faculty of Medicine; Orthopaedic Surgeon, Jewish General Hospital, Montreal, Quebec, Canada Arthroscopic Knot Tying Robert A. Arciero Col. (ret.) MD Associate Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Sports Medicine Terminology; Patellar Fractures in the Adult; Knee Extensor Mechanism Injuries in Athletes Steven P. Arnoczky DVM Wade O. Brinker Professor of Veterinary Surgery, College of Veterinary Medicine,

Department of Small Animal Clinical Sciences, Michigan State University, East Lansing, Michigan Thermal Modification of Connective Tissue: Basic Science Considerations Bernard R. Bach Jr. MD Professor, Department of Orthopaedic Surgery, and Director, Sports Medicine Section, Rush Medical College of Rush University; Staff, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Anterior Cruciate Ligament Reconstruction in the Adult

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Marianne Backer MD Orthopaedic Surgeon and Senior Registrar, Bispebjeg Hospital and University Hospital of Copenhagen, Copenhagen, Denmark Glenohumeral Instability in Adults F. Alan Barber MD, FACS Plano Orthopedic and Sports Medicine Center, Plano, Texas Suture Anchors Sue D. Barber-Westin BS Director, Clinical Studies, Cincinnati Sportsmedicine Research and Education Foundation, Cincinnati, Ohio High Tibial Osteotomy in the Anterior Cruciate LigamentDeficient Knee with Varus Angulation Carl J. Basamania MD Assistant Professor, Division of Orthopaedic Surgery, Duke University Medical Center; Chief, Orthopaedic Surgery,

Durham Veterans Administration Hospital, Durham, North Carolina Clavicle Fracture in Adult Athletes; Clavicle Injuries in the Pediatric and Adolescent Athlete James B. Bennett MD Clinical Professor, Department of Orthopedic Surgery, University of TexasHouston Medical School; Chief of Staff, Texas Orthopedic Hospital, Houston, Texas Soft Tissue Injury and Fractures of the Arm in the Adult; Neurovascular Injury of the Arm Thomas M. Best MD, PhD Assistant Professor of Family Medicine and Orthopedic Surgery, University of Wisconsin Medical School, Madison, Wisconsin Muscle and Tendon Bruce D. Beynnon MS, PhD Professor of Orthopaedics and Rehabilitation, University of Vermont College of Medicine, Burlington, Vermont Biomechanics; Relevant Biomechanics of the Knee Tim Bollom MD Chief Resident, Department of Orthopaedics and Rehabilitation, University of Florida Health Science Center, Gainesville, Florida Biodegradable Materials Christine M. Bonci MS, ATC Co-Director, Division of Athletic Training/Sports Medicine, Intercollegiate Athletics, University of Texas at Austin, Austin, Texas Functional Training Progressions for the Prevention of Anterior Cruciate Ligament

Injuries in Female Athletes Leslie Bonci MPH, RD Adjunct Assistant Professor, Department of Orthopaedics, University of Pittsburgh School of Medicine; Director, Sports Nutrition, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Nutrition for Sports R. Luke Bordelon MD Clinical Professor, Louisiana State University School of Medicine in New Orleans; Attending, Children's Hospital, New Orleans; Director, Foot Clinic, Doctor's Hospital of Opelousis, Opelousis, Louisiana Heel Pain Andrew H. Borom MD Tallahassee Orthopedic Clinic, Tallahasse, Florida Sports Shoes and Orthoses Craig R. Bottoni LTC MD Clinical Instructor in Surgery, Department of Surgery, Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda, Maryland; Chief, Sports Medicine, Orthopaedic Surgery Service, Tripler Army Medical Center, Honolulu, Hawaii Patellar Fractures in the Adult; Knee Extensor Mechanism Injuries in Athletes James P. Bradley MD Clinical Associate Professor, Department of Orthopedic Surgery,

University of Pittsburgh School of Medicine; Staff Orthopedic Surgeon, UPMCSt. Margaret; Orthopedic Team Physician, Pittsburgh Steelers, Pittsburgh, Pennsylvania Elbow Injuries in Children and Adolescents; Osteochondritis Dissecans of the Humeral Capitellum, Pediatric Elbow Fractures and Dislocations, Pediatric Elbow Dislocations Brad E. Brautigan MD Team Physician, Muskingum College, Orthopaedic Associates of Zanesville, Zanesville, Ohio Allograft Tissues Mark R. Brinker MD Clinical Professor of Orthopaedic Surgery, Tulane University School of Medicine, New Orleans, Louisiana; Clinical Professor of Orthopaedic Surgery, Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas; Director of Acute and Reconstructive Trauma and C-Director, The Center for Problem Fractures and Limb Restoration, Texas Orthopedic Hospital; Fondren Orthopedic Group LLP, Houston, Texas Bone James W. Brodsky MD Clinical Professor of Orthopaedic Surgery, University of Texas Southwestern Medical Center at Dallas Southwestern Medical School; Director, Foot and Ankle Surgery Fellowship, Baylor University Medical Center Dallas, Texas Stress Fractures of the Foot and Ankle Andrew W. Brown MD Assistant Professor of Clinical Orthopaedic Surgery,

University of Arizona College of Medicine Tucson, Arizona The Use of Knee Braces in Sports Medicine

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Treg D. Brown MD Assistant Professor of Orthopaedics, Tulane University School of Medicine; Division of Sports Medicine & Shoulder Reconstruction, Tulane Institute of Sports Medicine; Active Staff, Tulane University Hospital & Clinics, New Orleans, Louisiana Adult thigh; Pediatric thigh James F. Bruce Jr. MD, FAAOS Orthopedic Clinic of West Georgia, LaGrange, Georgia The Wrist in the Adult Michael E. Brunet MD Professor of Orthopaedic Surgery, Tulane University School of Medicine; Section Chief, Division of Sports Medicine, Tulane Institute of Sports Medicine; Active Staff, Tulane University Hospital & Clinics, New Orleans, Louisiana Adult Thigh; Pediatric Thigh Joseph A. Buckwalter MD Professor and Head, Department of Orthopaedics, University of Iowa College of Medicine; Department of Orthopaedic Surgery, University of Iowa Hospitals and Clinics, Iowa City, Iowa Ligaments; Effects of Medications in Sports Injuries at the Tissue Level; Anticular Cartilage;

Meniscus Edmund R. Burke PhD Professor, Biology Department, University of Colorado at Colorado Springs, Colorado Springs, Colorado Stretching Kenneth P. Butters MD Clinical Senior Instructor Department of Orthopaedics and Rehabilitation, Oregon Health Sciences University School of Medicine, Portland; Upper Extremity Orthopedist, Sacred Heart Hospital, Eugene, Oregon Nerve Lesions of the Shoulder; Olecranon Bursitis; Osteochondroses of the Elbow David M. Caborn MD Professor of Orthopaedic Surgery, University of Louisville, Louisville, Kentucky Allograft Tissues S. Terry Canale MD Professor and Chairman, Department of Orthopaedic Surgery, University of Tennessee, Memphis, College of Medicine; Chief-of-Staff Emeritus, Campbell Clinic, Memphis, Tennessee Osteochondroses and Related Problems of the Foot and Ankle Robert C. Cantu MA, MD, FACS, FACSM Clinical Instructor, Neurosurgery/Pediatrics, Boston University School of Medicine, Boston; Chief, Neurosurgery Service,

and Director, Service Sports Medicine, Emerson Hospital, Concord, Massachusetts; Medical Director, National Center for Catastrophic Sports Injury Research, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Head Injuries in Adults Mark M. Casillas MD Clinical Assistant Professor, Department of Orthopaedics, University of Texas Medical School at San Antonio, San Antonio, Texas Ligament Injuries of the Foot and Ankle in Adult Athletes Frank M. Chang MD Associate Professor, Department of Orthopaedic Surgery and Department of Pediatrics, University of Colorado School of Medicine; Director, Orthopaedic Surgery, and Co-Medical Director, Center for Gait and Motion Analysis, The Children's Hospital, Denver, Colorado The Disabled Pediatric Athlete John D. Childs MPT, MBA, OCS, CSCS Doctoral Student, Department of Physical Therapy, University of Pittsburgh School of Health and Rehabilitation Sciences, Pittsburgh, Pennsylvania The Language of Exercise and Rehabilitation Chang-Hyuk Choi MD Assistant Professor, Department of Orthopaedic Surgery, Hanyang University Medical School, Hanyang University Hospital, Seoul, Korea Injuries of the Proximal Humerus in Adults

Thomas O. Clanton MD Professor and Chairman, Department of Orthopaedics, University of TexasHouston Medical School, Houston, Texas Etiology of Injury to the Foot and Ankle; Sports Shoes and Orthoses Henry D. Clarke MD Attending Orthopaedic Surgeon, Insall-Scott Kelly Institute for Orthopaedics and Sports Medicine, Beth Israel Medical Center, New York, New York Knee Replacement in the Recreational Athlete Robert O. Cone III MD Radiologist, South Texas Radiology, San Antonio, Texas Imaging Sports-Related Injuries of the Knee Kathryn M. Coughlin MS Biomedical Engineer, University of Vermont, Burlington Vermont Relevant Biomechanics of the Knee Michael J. Coughlin MD Clinical Professor, Division of Orthopaedic Surgery and Rehabilitation, Oregon Health Sciences University, Portland, Oregon Conditions of the Forefoot Frances Cuomo MD Assistant Professor, Department of Orthopaedic Surgery, New York University School of Medicine; Chief, Shoulder and Elbow Service, New York University Hospital for Joint Diseases,

New York, New York Injuries of the Proximal Humerus in Adults

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Ralph J. Curtis Jr. MD Clinical Assistant Professor, Department of Orthopedics, University of Texas Medical School at San Antonio, San Antonio, Texas Anatomy, Biomechanics, and Kinesiology of the Child's Shoulder; Glenohumeral Instabilities in the Child Samuel D. D'Agata MD Team Orthopedic Surgeon, Gettysburg College, Gettysburg; Director of Sports Medicine, Rehabilitation Center, and Chairman, Department of Surgery, Hanover Hospital, Hanover, Private Practice, Hanover, Pennsylvania Factors Predisposing to Knee Injury Michael J. D'Amato MD Sports Medicine Fellow, Rush Medical College of Rush University; Staff, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Anterior Cruciate Ligament Reconstruction in the Adult Allen Deutsch MD Clinical Assistant Professor, Department of Orthopaedic Surgery, Baylor University College of Medicine; Kelsey Seybold Clinic, Houston, Texas Glenoid and Scapula Fractures in Adults and Children; Fractures of the Coracoid in Adults and Children Lee H. Diehl MD

Fellow, Sports Medicine, Section of Orthopaedic Surgery and Rehabilitation Medicine, University of Chicago, Chicago, Illinois Acute Dislocation of the Patella in the Adult Keith Duerler MS, PT Physical Therapist, Lexington Sports Medicine Center, Lexington, Kentucky Electrical Stimulation; Application of Heat Jeffrey R. Dugas MD Clinical Instructor and Attending Orthopaedic Surgeon, American Sports Medicine Institute, Birmingham, Alabama Throwing Injuries in the Adult James S. Dunnick MD, FACC Department of Medicine, Division of Cardiology, Louisiana State University School of MedicineLake Charles Campus; Medical Director, Nuclear Cardiology, CHF Clinic, and Cardiac Rehabilitation, Lake Charles Memorial Heart and Vascular Center, Lake Charles, Louisiana Athletes and Sudden Cardiac Death Craig J. Edson MS, PT/ATC Physical Therapist, Geisinger Medical Center, Danville, Pennsylvania The Multiple Ligamentinjured Knee William P. Elsass MD Chief, Pediatric Behavioral Medicine, Ramstein AFB, Germany

Psychological Aspects of Sports in Children and Adolescents Frank J. Eismont MD Professor and Vice Chairman, Department of Orthopedics, University of Miami, Jackson Memorial Hospital, Miami, Florida Thoracolumbar Spine in the Adult Mark A. Erickson MD Assistant Professor, Department of Orthopaedics, University of Colorado Children's Hospital, Denver, Colorado Medial Ligament Injuries in Children; Lateral and Posterior Injuries of the Knee in Children Gregory C. Fanelli MD Chief, Arthroscopic Surgery and Orthopaedic Sports Medicine, Geisinger Clinic Medical Center, Danville, Pennsylvania The Multiple Ligamentinjured Knee Daniel D. Feldmann MD Resident in Orthopaedic Surgery, Geisinger Medical Center, Danville, Pennsylvania The Multiple Ligamentinjured Knee Gerald A. M. Finerman MD Professor and Chairman, Department of Orthopaedic Surgery, University of California Los Angeles, UCLA School of Medicine, Los Angeles, California Physeal Injuries in Young Athletes; Hip and Pelvis: Adult Peter J. Fowler MD, FRCSC

Professor, Orthopaedic Surgery, University of Western Ontario Faculty of Medicine; Medical Director, Fowler Kennedy Sports Medicine Clinic, London, Ontario, Canada Anterior Cruciate Ligament Injuries in the Child Freddie H. Fu MD, DSc Chairman, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Meniscal Injuries in the Adult John P. Fulkerson MD Clinical Professor of Orthopaedic Surgery, University of Connecticut School of Medicine; Orthopaedic Surgeon, Orthopaedic Associates of Hartford, Farmington, Connecticut Anterior Knee Pain and Patellar Subluxation in the Adult Chris Fults-Ganey MD, PhD Radiologist, Wilford Hall Medical Center, San Antonio, Texas Imaging of Sports-Related Injuries Dina H. Galvin MD Orthopedic Hand Surgeon, Jordan Hospital, Plymouth, Massachusetts Hand Injuries in Children

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Ralph Garretson MD Staff, Rush-Presbyterian-St. Luke's Medical Center,

Chicago, Illinois Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children William E. Garrett Jr. MD, PhD Frank C. Wilson Professor and Chair, Department of Orthopaedics, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina Muscle and Tendon; Acute Dislocation of the Patella in the Adult Christian Gerber MD Professor and Chairman, Department of Orthopaedic Surgery, University of Zurich Faculty of Medicine, Zurich, Switzerland Suture Materials J. Robert Giffin MD, FRCSC Assistant Professor, Orthopaedic Surgery, University of Western Ontario Faculty of Medicine; Fowler Kennedy Sports Medicine Clinic, London, Ontario, Canada Meniscal Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Child Martin J. Gillespie MD Assistant Professor, Department of Orthopaedics, University of Texas Medical School at San Antonio, Chief, Sports Medicine and Arthroscopy, University Hospital, and Veterans Affairs Hospital, and Audie Murphy Memorial Hospital, San Antonio, Texas The Effects of Medications in Sports Injuries James S. Gilley MD Assistant Professor of Radiology,

University of Texas Medical School at San Antonio; Medical Director, South Texas Radiology Imaging Centers, San Antonio, Texas Imaging of Sports Injuries of the Foot and Ankle John E. Glorioso Jr. MD Director, Primary Care Sports Medicine, Department of Family Practice, and Emergency Medical Services, Tripler Army Medical Center, Honolulu, Hawaii Viral Disease David M. Gloystein BS Medical Student, University of Texas Medical School at San Antonio, San Antonio, Texas The Effects of Medications in Sports Injuries Jorge E. Gómez MS, MD Associate Professor and Director, Program in Pediatric Sports Medicine and Fitness, Department of Pediatrics, University of Texas Medical School at San Antonio; Medical Team Physician, University of Texas at San Antonio, San Antonio, Texas Paired Organ Loss Frank A. Gottschalk MD, FRCSEd, FCS(SA)Orth Professor, Department of Orthopaedic Surgery, University of Texas Southwestern Medical Center at Dallas Southwestern Medical School; Attending, Zale Lipshy University Hospital and Parkland Memorial Hospital, Dallas, Texas The Orthopaedically Disabled Athlete Thomas J. Graham MD Chief, Curtis National Hand Center, Union Memorial Hospital,

Baltimore, Maryland Athletic Injuries of the Adult Hand William A. Grana MD, MPH Professor and Head, Department of Orthopaedic Surgery, University of Arizona College of Medicine, Tucson, Arizona Application of Cold Gary A. Green MD Clinical Associate Professor, Department of Family Medicine, Division of Sports Medicine, University of California, Los Angeles, UCLA School of Medicine, Los Angeles; Team Physician, Pepperdine University, Malibu, California; Team Physician, U.S. Soccer Recreational Drug Use in Athletes Donald E. Greydanus MD FAAP, FSAM Professor, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine, Kalamazoo, Michigan Sports and the Neurodevelopment of the Child and Adolescent Letha Y. Griffin MD, PhD Adjunct Professor, Department of Kinesiology and Health, and Team Physician, Georgia State University, Atlanta, Georgia The Female Athlete George W. Gross MD Professor of Radiology, University of Maryland School of Medicine; Director of Pediatric Radiology, University of Maryland Medical Center,

Baltimore, Maryland Differences between the Immature and the Mature Skeleton Dan Guttmann MD Clinical Instructor, Department of Orthopaedic Surgery, University of New Mexico School of Medicine, Albuquerque; Director, Upper Extremity Surgery, Taos Orthopaedic Institute, Taos, New Mexico Injuries of the Proximal Humerus in Adults Bettina M. Gyr MD Fellow, Pediatric Orthopaedic Surgery, Primary Children's Medical Center and Shriner's Hospital for Children, Salt Lake City, Utah Strength Training in Children and Adolescents

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Christopher D. Harner MD Blue Cross of Western Pennsylvania Professor, University of Pittsburgh School of Medicine Medical Director, UPMCSCenter for Sports Medicine, Pittsburgh, Pennsylvania Posterior Cruciate Ligament Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Child Douglas T. Harryman II MD * *Deceased Associate Professor, Department of Orthopaedics, University of Washington School of Medicine, Seattle, Washington Arthroscopic Knot Tying Richard J. Hawkins MD, FRCSC(c)

Clinical Professor, Department of Orthopaedic Surgery, University of Colorado School of Medicine, Denver; Orthopaedic Consultant, Steadman Hawkins Clinic, Vail, Colorado Rotator Cuff and Impringement Lesions in Adult and Adolescent Athletes Morley A. Herbert PhD Manager, Biomedical and Surgical Research, Medical City Dallas Hospital, Dallas, Texas Suture Anchors M. Alan Hinton MD Clinical Assistant Professor and Assistant Director for Sports Medicine, Department of Orthopaedics, Louisiana State University School of Medicine, Louisiana State University at New Orleans; Lake Charles Memorial Hospital and Christus St. Patrick Hospital, Lake Charles, Louisiana Heat Intolerance Edward G. Hixson MD Adirondack Surgical Group, Saranac Lake, New York Cold Injury; Altitude Stress Stephen M. Howell MD Adjunct Associate Professor of Mechanical Engineering and Adjunct Associate Professor of Biomedical Engineering, University of California, Davis, California Construction and Fixation of a Tendon Anterior Cruciate Ligament Graft L. M. Hull MS, PhD Professor of Mechanical Engineering and Professor of Biomedical Engineering,

University of California, Davis; Scientific Staff, Shriners Hospital, Sacramento, California Construction and Fixation of a Tendon Anterior Cruciate Ligament Graft David M. Hunter MD Assistant Professor, Department of Orthopaedic Surgery, University of California, Los Angeles, UCLA School of Medicine, Los Angeles, California Hip and Pelvis: Adult Jon Hyman MD Peachtree Orthopaedic Clinic, Atlanta, Georgia Patellofemoral Tendinopathy Peter A. Indelicato MD Professor and Chief, Orthopaedics and Rehabilitation, University of Florida, Gainesville, Florida Medial Ligament Injuries in the Adult James J. Irrgang PhD, PF, ATC Assistant Professor and Vice Chairman for Clinical Services, Department of Physical Therapy, University of Pittsburgh School of Health and Rehabilitation Sciences; Vice President of QI and Outcomes and Director of Sports and Orthopaedic Physical Therapy, Centers for Rehab Services, Pittsburgh, Pennsylvania The Language of Exercise and Rehabilitation Nizar N. Jarjour MD Associate Professor of Medicine, Section of Pulmonary and Critical Care, Department of Medicine, University of Wisconsin Medical School, Madison, Wisconsin

Exercise-Induced Asthma Darren L. Johnson MD Associate Professor and Chairman, Department of Surgery, University of Kentucky School of Medicine; Lexington, Kentucky Research Design and Statistics in Sports Medicine; Allograft Tissues Robert J. Johnson MD Professor, Department of Orthopaedics and Rehabilitation, University of Vermont College of Medicine, Director, Sports Medicine Center, Fletcher Allen Health Care, Burlington, Vermont Relevant Biomechanics of the Knee Ron M. Johnson PT, MPT, ATC, CSCS Physical Therapist and HealthSouth National Clinical Education Instructor, HealthSouth Sports Medicine, Houston, Texas Open and Closed Chain Exercises (Non-Weight-Bearing and Weight-Bearing Exercises); Exercise Modalities: Cycle Ergometry, StairMaster, Elliptical Fitness Trainer, Slideboard, Elastic Resistance James S. Keene MD Professor of Orthopedic Surgery, Department of Orthopedic Surgery and Rehabilitation Medicine, University of Wisconsin Medical School, Madison, Wisconsin Tendon Injuries of the Foot and Ankle W. Ben Kibler MD Associate Clinical Professor, University of Kentucky College of Medicine; Medical Director, Lexington Sports Medicine Center, Lexington, Kentucky Electrical Stimulation;

Application of Heat

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Donald T. Kirkendall PhD Department of Orthopaedics, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina Muscle and Tendon Scott H. Kitchel MD Athletic Medicine Staff, University of Oregon, Eugene, Oregon Thoracolumbar Spine in the Adult John J. Klimkiewicz MD Assistant Professor of Orthopaedic Surgery and Sports Medicine, Georgetown University School of Medicine; Georgetown University HospitalMEDSTAR Health; Head Team Physician, Georgetown University Hoyas, Washington, District of Columbia Pediatric Elbow Fractures and Dislocations; Pediatric Elbow Dislocations Mininder Kocher MD, MPH Instructor of Orthopaedic Surgery, Harvard Medical School; Program in Clinical Effectiveness, Harvard School of Public Health; Attending Orthopaedic Surgeon, Department of Orthopaedic Surgery, Children's Hospital, Boston, Massachusetts Hip and Pelvic Injuries in the Young Athlete DeAnn M. Koehler MS, ATC, CSCS, CFT Assistant Athletic Trainer, Intercollegiate Athletics,

University of Texas at Austin, Austin, Texas Functional Training Progressions for the Prevention of Anterior Cruciate Ligament Injuries in Female Athletes Jon D. Koman MD Orthopaedic Specialty Center, Baltimore, Maryland The Wrist in the Adult John O. Krause MD Clinical Assistant Professor of Surgery, University of Texas Medical School at San Antonio, San Antonio, Texas; Assistant Professor of Surgery, Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda, Maryland; Chief, Orthopedic Foot and Ankle Service, Wilford Hall Medical Center, Lackland AFB, Texas Stress Fractures of the Foot and Ankle Sumant G. Krishnan MD Assistant Clinical Professor, Department of Orthopaedic Surgery, University of Texas Southwestern Medical Center at Dallas Southwestern Medical School; Staff, Shoulder Service, W.B. Carrell Memorial Clinic, Dallas, Texas Rotator Cuff and Impingement Lesions in Adult and Adolescent Athletes John E. Kuhn MD Associate Professor, Department of Orthopaedic Surgery, Division of Sports Medicine and Shoulder Surgery, University of Michigan Medical School; Team Physician, University of Michigan, and Team Physician, USA Hockey National Team Development Program, Ann Arbor, Michigan

Scapulothoracic Crepitus and Bursitis in Athletes Frank A. Kulling EdD Associate Professor, School of Applied Health and Educational Psychology, Oklahoma State University, Stillwater, Oklahoma Exercise Physiology Roger V. Larson MD Associate Professor, Department of Orthopaedics and Sports Medicine, University of Washington School of Medicine, Seattle, Washington Lateral and Posterolateral Instability of the Knee in Adults William C. Lauerman MD Associate Professor of Orthopaedic Surgery, Georgetown University School of Medicine; Chief, Division of Spine Surgery, Department of Orthopaedic Surgery, Georgetown University Hospital, Washington, District of Columbia Sports Injuries to the Thoracolumbar Spine in Children and Adolescents Kenneth M. Leclerc MD, FACC Director, Cardiac Rehabilitation Unit and Staff Cardiologist, Brooke Army Medical Center, San Antonio, Texas Hypertension and Other Cardiac Disease in Athletes Robert F. Lemanske Jr. MD Professor of Pediatrics and Medicine, University of Wisconsin School of Medicine; Head, Division of Pediatric Allergy, Immunology, and Rheumatology, University of Wisconsin Medical School, Madison, Wisconsin Exercise-Induced Asthma Scott M. Lephart PhD ATC

Associate Professor of Orthopaedic Surgery and Associate Professor of Health and Rehabilitation Sciences, University of Pittsburgh School of Medicine; Director, Neuromuscular Research Laboratory, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Role of Proprioception in Functional Joint Stability Thomas N. Lindenfeld MD Volunteer Instructor, Department of Orthopaedic Surgery, University of Cincinnati College of Medicine; Associate Director, Cincinnati Sportsmedicine and Orthopaedic Center, Cincinnati, Ohio Complex Regional Pain Syndromes Including Reflex Sympathetic Dystrophy and Causalgia

XIV

Russell C. Linton MD Attending, Baptist Memorial HospitalGolden Triangle, Columbus, Mississippi Medial Ligament Injuries in the Adult Jeffrey L. Lovallo MD Assistant Clinical Professor, Department of Orthopaedics, Georgetown University School of Medicine, Washington, District of Columbia; Staff, Anderson Orthopedic Clinic, Arlington, Virginia Wrist Injuries in the Child; Hand Injuries in Children Lisa D. Lowe MEd ATC, CSCS, USAW, CFT Strength and Conditioning Specialist, Intercollegiate Athletics, University of Texas at Austin,

Austin, TX Functional Training Progressions for the Prevention of Anterior Cruciate Ligament Injuries in Female Athletes Walter R. Lowe MD Clinical Associate Professor, Department of Orthopaedics, Baylor University College of Medicine; Baylor Sports Medicine Institute; Team Physician, Houston Rockets, Houston, Texas Superior Labral Injuries Christopher C. Madden MD Private Practice, Longs Peak Sports and Family Medicine and Longs Peak Family Practice, Longmont; Team Physician, Niwut High School, Niwut, Colorado The Team Physician: The Preparticipation Examination and On-Field Emergencies Mark W. Maffet MD Clinical Assistant Professor, Department of Orthopedics, Baylor University College of Medicine; Baylor Sports Medicine Institute; Team Physician, Houston Comets, Houston Texas Superior Labral Injuries David Maish MD Resident in Orthopaedic Surgery, Geisinger Medical Center, Danville, Pennsylvania The Multiple Ligamentinjured Knee Roger A. Mann MD Associate Clinical Professor, Department of Orthopaedic Surgery, University of California at San Francisco School of Medicine, San Francisco; Director, Foot Fellowship Program, Oakland, California

Biomechanics of the Foot and Ankle Linkage; Entrapment Neuropathies of the Foot Carl G. Mattacola PhD, ATC Assistant Professor and Director, Division of Athletic Training, College of Allied Health Professions, University of Kentucky, Lexington, Kentucky Research Design and Statistics in Sports Medicine Augustus D. Mazzocca MD Assistant Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children Frank C. McCue III MD Professor of Orthopaedic Surgery and Plastic Surgery of the Hand, Department of Orthopaedic Surgery; Division Head, Division of Sports Medicine, University of Virginia Medical Center, Charlottesville, Virginia The Wrist in the Adult Edward R. McDevitt MD Assistant Clinical Professor of Surgery, Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda; Orthopaedic Staff, Anne Arundel Medical Center, Annapolis, and North Arundel Medical Center, Glen Burnie, Maryland Ergogenic Drugs in Sports Patrick J. McMahon MD Assistant Professor, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine;

Assistant Team Physician, Football, Shoulder and Elbow Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania Functional Anatomy and Biomechanics of the Adult Shoulder Thomas L. Mehlhoff MD Team Physician, Houston Astros; Staff, Texas Orthopedic Hospital, Houston, Texas Soft Tissue Injuries and Fractures of the Arm in the Adult; Neurovascular Injury of the Arm Sacheen H. Mehta MD Sportsmedicine Fellow, Cincinnati Sportsmedicine and Orthopaedic Center, Cincinnati, Ohio Complex Regional Pain Syndromes Including Reflex Sympathetic Dystrophy and Causalgia Keith Meister MD Associate Professor and Team Physician, Department of Orthopedics, University of Florida, College of Medicine, Orthopaedic Surgeon, Shands Hospital, Gainesville, Florida Biodegradable Materials Morris B. Mellion MD Adjunct Associate Professor, Department of Family Practice and Orthopaedic Surgery, University of Nebraska College of Medicine, Adjunct Professor, School of Health, Physical Education, and Recreation, University of Nebraska at Omaha; Team Physician Emeritus, University of Nebraska at Omaha, Omaha, Nebraska The Team Physician: The Preparticipation Examination and On-Field Emergencies Mark D. Miller MD

Associate Professor of Orthopaedic Surgery and Co-Director, Division of Sports Medicine, University of Virginia School of Medicine, Charlottesville, Virginia; Associate Professor, Department of Surgery, Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda, Maryland Basic Arthroscopic Principles

XV

Michael B. Millis MD Associate Professor of Orthopaedic Surgery, Harvard Medical School; Director, Adolescent and Young Adult Hip Unit, Children's Hospital, Boston, Massachusetts Hip and Pelvic Injuries in the Young Athlete Bernard F. Morrey MD Professor of Orthopedics, Mayo Medical School; Emeritus Chairman, Department of Orthopedics, Mayo Clinic, Mayo Foundation, Rochester, Minnesota Biomechanics of the Elbow and Forearm; Tendinopathies about the Elbow; Osteochondritis Dissecans of the Elbow and Forearm in the Adult; Fractures of the Elbow in Adults; Heterotopic Bone about the Elbow; Elbow Dislocation in the Adult Athlete; Entrapment Neuropathies about the Elbow Charles T. Morton Col. MD, USAF, MC Clinical Assistant Professor, University of Texas Medical School at San Antonio, San Antonio, Texas; Clinical Assistant Professor, Uniformed Services University of the Health Sciences

F. Edward He(c)bert School of Medicine, Bethesda, Maryland; Chief, Developmental Pediatrics Service, San Antonio Military Pediatric Center, Lackland AFB, Texas The Child Athlete with Chronic Disease Van C. Mow PhD Chairman, Department of Biomedical Engineering, Columbia University, New York; Director, Orthopaedic Research Laboratory, New York Presbyterian Hospital, New York, New York Articular Cartilage; Meniscus Kenneth J. Mroczek MD Assistant Professor of Orthopaedic Surgery, New York University School of Medicine; Attending Surgeon, Department of Orthopaedic Surgery, Hospital for Joint Diseases Orthopaedic Institute, New York, New York Factors Predisposing to Knee Injury Daniel J. Mullen MD Curtis National Hand Center, Union Memorial Hospital, Baltimore, Maryland Athletic Injuries of the Adult Hand Joseph B. Myers PhD, ATC Assistant Professor of Kinesiology, Louisiana State University, Baton Rouge, Louisiana Role of Proprioception in Functional Joint Stability Blaise A. Nemeth MD Chief Resident,

Department of Pediatrics, University of Wisconsin Hospital and Clinics, Madison, Wisconsin Diabetes Mellitus David C. Neuschwander MD Clinical Instructor, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh; Orthopedic Associates of Pittsburgh, Monroeville, Pennsylvania Peripatellar Pathology John E. Novotny MS, PhD Professor of Mechanical Engineering, University of Delaware, Newark, Delaware Biomechanics Frank R. Noyes MD Volunteer Professor, Department of Orthopaedic Surgery, University of Cincinnati College of Medicine; Chairman, Cincinnati Sportsmedicine and Orthopaedic Center, Cincinnati Sportsmedicine Research and Education Foundation, Cincinnati, Ohio High Tibial Osteotomy in the Anterior Cruciate LigamentDeficient Knee with Varus Angulation Stephen L. Nuccion MD Resident, Department of Orthopaedic Surgery, UCLA Medical Center, Los Angeles, California Hip and Pelvis: Adult James P. O'Leary MD Sports Medicine Consultant, University of South Carolina, Columbia, South Carolina

Meniscal Injuries in the Adult Russell M. Paine PT Rehab. Consultant Houston Rockets, Houston Astros, and NASA; Clinical Director, HealthSouth Sports Medicine, Houston, Texas Open and Closed Chain Exercises (NonWeight-Bearing and Weight-Bearing Exercises); Exercise Modalities: Cycle Ergometry, StairMaster, Elliptical Fitness Trainer, Slideboard, Elastic Resistance William D. Parham PhD, ABPP Associate Director of Clinical Services, Student Psychological Services, and Consultant, Department of Intercollegiate Athletics, University of California, Los Angeles; Consulting Psychologist, Department of Health Psychology, Children's Hospital of Orange County, Orange, California Sports Psychology and Injured Athletes Dilip R. Patel MD, FAAP, FAACPDM Professor, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine, East Lansing, Michigan; Kalamazoo Center for Medical Studies, Kalamazoo, Michigan Sports and the Neurodevelopment of the Child and Adolescent Robert A. Pedowitz MD, PhD Associate Professor and Chief, Sports Medicine, Department of Orthopaedics, University of California, San Diego, School of Medicine, San Diego, California Use and Abuse of the Pneumatic Tourniquet Russell S. Petrie MD Team Physician, Vanguard University, Costa Mesa; Staff Orthopedic Surgeon,

Hoag Memorial Hospital, Newport Beach, California. Elbow Injuries in Children and Adolescents; Osteochondritis Dissecans of the Humeral Capitellum

XVI

Marilyn M. Pink PhD, PT Director of Biomechanics Laboratory, Centinela Hospital Medical Center, Inglewood, California Functional Anatomy and Biomechanics of the Adult Shoulder Peter D. Pizzutillo MD Professor, Department of Orthopaedic Surgery and Department of Pediatrics, MCP Hahnemann School of Medicine; Director, Orthopedic Surgery, St. Christopher's Hospital for Children, Philadelphia, Pennsylvania The Cervical Spine in the Child Helen D. Pratt PhD, DABPS Professor, Department of Pediatrics and Human Development Michigan State University College of Human Medicine, Kalamazoo, Michigan Sports and the Neurodevelopment of the Child and Adolescent William D. Regan MD Assistant Professor of Orthopaedic Surgery, University of British Columbia Faculty of Medicine, Vancouver, British Columbia, Canada Tendinopathies about the Elbow; Entrapment Neuropathies about the Elbow Bruce Reider MD Professor, Department of Surgery,

Section of Orthopaedic Surgery and Rehabilitation Medicine, University of Chicago Division of the Biological Sciences Pritzker School of Medicine; Director of Sports Medicine, University of Chicago Hospitals, Chicago, Illinois; Editor, American Journal of Sports Medicine Factors Predisposing to Knee Injury Bryan L. Riemann PhD, ATC Assistant Professor of Athletic Training, Graduate Athletic Training Program, Georgia Southern University, Statesboro, Georgia Role of Proprioception in Functional Joint Stability Rudy Robbe MD Resident, University Hospital, Lexington, Kentucky Allograft Tissues Charles A. Rockwood Jr. MD Professor and Chairman Emeritus, Department of Orthopaedics, University of Texas Medical School at San Antonio; Chief, Shoulder Service, University Hospital of University of Texas HSC, San Antonio, Texas Injuries to the Sternoclavicular Joint in the Adult and Child Scott A. Rodeo MD Instructor of Orthopaedic Surgery, Weill Medical College of Cornell University; Assistant Scientist, Department of Research, The Hospital for Special Surgery, New York, New York Patellofemoral Tendinopathy Anthony A. Romeo MD Associate Professor,

Department of Orthopaedic Surgery, Rush Medical College; Director, Shoulder Service, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children Richard Rozencwaig MD Clinical Instructor of Surgery, Nova Southeastern University, Fort Louderdale; Orthopaedic Surgeon, Orthopaedic Care and Sports Medicine Center, Aventura, Florida Arthroscopic Knot Tying Timothy G. Sanders MD Assistant Clinical Professor, Department of Radiology, University of Texas Medical School at San Antonio; Chairman, Department of Radiology, Wilford Hall Medical Center, San Antonio, Texas Imaging of Sports-Related Injuries, Imaging of the Glenohumeral Joint Jeffrey R. Sawyer MD Associate Professor of Orthopaedics, Rush Medical College of Rush University; Pediatric Orthopedic, and Spinal Deformity, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Pediatric Elbow Fractures and Dislocations; Pediatric Elbow Dislocations Robert C. Schenck Jr. MD Professor and Division Chief, Sports Medicine Section, Department of Orthopaedics and Rehabilitation, University of New Mexico School of Medicine; Staff, University Hospital, Albuquerque; New Mexico The Effects of Medications in Sports Injuries

Gregory A. Schmale MD Assistant Professor, Department of Orthopaedic Surgery, Children's Hospital and Regional Medical Center of Washington, Seattle, Washington Medial Ligament Injuries in Children; Lateral and Posterior Injuries of the Knee in Children Alberto G. Schneeberger MD Assistant Professor, Department of Orthopaedic Surgery, University of Zurich Faculty of Medicine, Zurich, Switzerland Suture Materials W. Norman Scott MD Clinical Professor of Orthopaedics Surgery Albert Einstein Medical College of Yeshiva University, Bronx; Chairman, Department of Orthopaedic Surgery, and Director, Insall-Scott Kelly Institute for Orthopaedics and Sports Medicine, Beth Israel Medical Center, New York, New York Knee Replacement in the Recreational Athlete

XVII

Robert Sellards MD Assistant Professor, Department of Orthopaedic Surgery, Louisiana State University School of Medicine, Baton Rouge, Louisiana Injuries to the Acromioclavicular Joint in Adults and Children Benjamin S. Shaffer MD Clinical Assistant Professor of Orthopaedic Surgery, Georgetown University School of Medicine; Team Physician, Washington Capitals, Washington, District of Columbia Sports Injuries to the Thoracolumbar Spine in Children and Adolescents

Matthew S. Shapiro MD Orthopaedic Surgeon, Orthopedic Healthcare Northwest, Inc., Eugene, Oregon Olecranon Bursitis; Osteochondroses of the Elbow Barry P. Simmons MD Associate Professor of Orthopedic Surgery, Harvard Medical School; Chief, Hand and Upper Extremity Service, and Senior Orthopedic Surgeon, Brigham and Women's Hospital, Boston, Massachusetts Wrist Injuries in the Child; Hand Injuries in Children Richard Simon MD Orthopaedic Surgeon, Orthopaedic Center of South Florida, Plantation, Florida High Tibial Osteotomy in the Anterior Cruciate LigamentDeficient Knee with Varus Angulation Kenneth M. Singer MD Clinical Associate Professor in Orthopaedic Surgery, Oregon Health Sciences University School of Medicine, Portland; Adjunct Assistant Professor, Department of Health and Movement Science, University of OregonEugene, Eugene, Oregon Nerve Lesions of the Shoulder; Olecranon Bursitis; Osteochondroses of the Elbow Douglas K. Smith MD Musculoskeletal Radiologist, South Texas Radiology Group, Southwest Texas Methodist Hospital, San Antonio, Texas Imaging of Sports Injuries of the Foot and Ankle

Carl L. Stanitski MD Professor of Orthopaedic Surgery, Medical University of South Carolina, Charleston, South Carolina Overuse Injuries in the Skeletally Immature Athlete; Meniscal Injuries in the Skeletally Immature Patient; Patellar Instability in the Skeletally Immature Patient; Acute Tibial Tubercle Avulsion Fractures in the Skeletally Immature Patient; Patellofemoral Mechanism; Articular Cartilage Lesions and Osteochondritis Dissecans of the Knee in the Adult; Articular Cartilage Lesions and Osteochondritis Dissecans of the Knee in the Skeletally Immature Patient Keith L. Stanley MD East Oklahoma Orthopaedic Center, Tulsa, Oklahoma Preparticipation Evaluation of the Young Athlete Enrico J. Stazzone MD Assistant Professor, Division of Pediatric Orthopaedics, Carrie Tingley Hospital, Albuquerque, New Mexico Physeal Injuries in Young Athletes Kevin L. Stevenson MD Chief Resident, Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Pediatric Sports-Related Head Injuries J. Andy Sullivan MD Professor and Don H. O'Donoghue Chair, Department of Orthopaedics, University of Oklahoma College of Medicine, Children's Hospital of Oklahoma, Oklahoma City, Oklahoma Ligament Injuries of the Foot/Ankle in the Pediatric Athlete Dean C. Taylor MD

Clinical Assistant Professor of Surgery, Uniformed Services University of the Health Sciences F. Edward He(c)bert School of Medicine, Bethesda, Maryland; Director, U.S. Army Joint and Soft Tissue Trauma Fellowship, Keller Army Hospital, West Point, New York Sports Medicine Terminology; Patellar Fractures in the Adult; Knee Extensor Mechanism Injuries in Athletes Peter C. Theut MD Orthopaedic Surgeon, Orthopaedic Associates of Grand Rapids, Grand Rapids, Michigan Anterior Knee Pain and Patellar Subluxation in the Adult James E. Tibone MD Professor, Department of Orthopaedics, University of Southern California School of Medicine; Associate, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, California Functional Anatomy and Biomechanics of the Adult Shoulder Edwin M. Tingstad MD Clinical Instructor, Department of Orthopaedics and Sports Medicine, University of Washington School of Medicine, Seattle, Washington Lateral and Posterolateral Instability of the Knee in Adults Joseph S. Torg MD Professor of Orthopaedics, Temple University School of Medicine, Philadelphia, Pennsylvania Cervical Spine Injuries in the Adult Thomas C. Turturro PT, OCS Department of Physical Therapy,

University of Texas Health Sciences Center, San Antonio, Texas Continuous Passive Motion

XVIII

Marc W. Urquhart MD Clinical Faculty, Liberty Orthopaedics, Springfield, New Jersey; St. Barnabas Sports Medicine Institute, Livingston, New Jersey Meniscal Injuries in the Adult C. Thomas Vangsness Jr. MD Professor of Orthopaedic Surgery, Department of Orthopaedic Surgery, University of Southern California, Los Angeles, California Articular Cartilage Lesions and Osteochondritis Dissecans of the Knee in the Adult W. Michael Walsh MD Clinical Associate Professor of Orthopaedic Surgery, Department of Orthopaedic Surgery and Rehabilitation, University of Nebraska, College of Medicine; Adjunct Graduate Associate Professor, School of Health, Physical Education, and Recreation, and Team Orthopaedic Surgeon, University of Nebraska at Omaha, Omaha, Nebraska The Team Physician: The Preparticipation Examination and On-Field Emergencies; Recurrent Dislocation of the Knee in the Adult Keith L. Wapner MD Clinical Professor of Orthopaedic Surgery, University of Pennsylvania School of Medicine; Professor of Orthopaedic Surgery, MCP Hahnemann School of Medicine, Director, Foot and Ankle Orthopaedic Fellowship Program, Pennsylvania Hospital, Philadelphia, Pennsylvania

Heel Pain Russell F. Warren MD Professor of Surgery (Orthopaedics) and Chairman, Division of Orthopaedic Surgery, Weill Medical College of Cornell University; Surgeon-in-Chief, Department of Orthopaedic Surgery, The Hospital for Special Surgery, New York, New York Glenohumeral Instability in Adults Daniel C. Wascher MD Associate Professor and Chief, Division of Sports Medicine, Department of Orthopaedics and Rehabilitation, University of New Mexico Health Science Center, Albuquerque, New Mexico Physeal Injuries in Young Athletes Thomas Wickiewicz MD Professor of Clinical Orthopaedic Surgery, Weill Medical College of Cornell University; Attending Orthopaedic Surgeon, The Hospital for Special Surgery, New York, New York Patellofemoral Tendinopathy John H. Wilckens MD Clinical Assistant Professor of Surgery, Uniformed Services University of Health Sciences F. Edward He(c)bert School of Medicine, Bethesda; Orthopaedic Surgeon and Head Team Physician, U.S. Naval Academy, Annapolis, Maryland Viral Disease Kaye E. Wilkins DVM, MD Professor, Department of Orthopedics and Department of Pediatrics, University of Texas Medical School at San Antonio, San Antonio, Texas

Fractures of the Proximal Humerus in the Child; Fractures and Soft Tissue Injuries of the Arm in the Child Gerald R. Williams Jr. MD Associate Professor, University of Pennsylvania School of Medicine; Chief, Shoulder and Elbow Surgery, University of Pennsylvania Health System, and Chairman, Orthopaedic Surgery, Presbyterian Medical Center, Philadelphia, Pennsylvania Glenoid and Scapula Fractures in Adults and Children; Fractures of the Coracoid in Adults and Children Ilaina M. Wingler MA Staff Psychologist and Chief, Substance Abuse, MacDill AFB, Florida Psychological Aspects of Sports in Children and Adolescents Michael A. Wirth MD Associate Professor, Department of Orthopaedics, University of Texas Medical School at San Antonio; Chief, Orthopaedic Shoulder Service, Audie Murphy Veterans Hospital, San Antonio, Texas Injuries to the Sternoclavicular Joint in the Adult and Child Edmund G. Witkowski MD Private Practice, Suncoast Orthopaedic Surgery and Sports Medicine, Venice, Florida Clavicle Injuries in the Pediatric and Adolescent Athlete Savio L.-Y. Woo PhD, DSc A. B. Ferguson Professor, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Professor of Bioengineering, Professor of Mechanical Engineering, and Professor of Rehabilitation Science and Technology, University of Pittsburgh;

Vice Chairman for Research, Department of Orthopaedic Surgery, and Director, Musculoskeletal Research Center, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Ligaments; Effects of Medications in Sports Injuries at the Tissue Level Robert M. Wood MD, FRCS Orthopedic Surgeon, Sports Medicine North, Lynnfield, and North Shore Medical Center, Salem, Massachusetts Etiology of Injury to the Foot and Ankle Virchel E. Wood MD Professor, Department of Orthopaedic Surgery, Loma Linda University School of Medicine; Consulting Chief, Hand Surgery Service, Loma Linda University Medical Center, Loma Linda, California Thoracic Outlet Syndrome Richard J. Wyzykowski MD John Muir Medical Center, Walnut Creek, California Wrist Injuries in the Child

XIX

Kazunori Yasuda MD, PhD Professor and Chairman, Department of Medical Bioengineering and Sports Medicine, Hokkaido University School of Medicine, Sapporo, Japan Construction and Fixation of a Tendon Anterior Cruciate Ligament Graft Mary L. Zupanc MD

Associate Professor, Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York; Director, Pediatric Epilepsy Program, Children's Hospital of New York City, New York, New York Sports and Epilepsy

XX

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MD Consult L.L.C. http://www.mdconsult.com /das/book/view/29433162/1103/4.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Preface

One might ask, Why publish a book on sports medicine when the subspecialty simply treats athletes with or thopaedic injuries? There is no question the orthopaedic sports medicine specialist must be soundly schooled in orthopaedic knowledge; however, the athletes often present special considerations that are not part of the everyday practice of orthopaedics. The intense desire and determination of the athlete to return to sports are not commonly encountered in the day-to-day practice of orthopaedics. The various stress syndromes of the musculoskeletal system that occur secondary to training and athletic competition and the specialized rehabilitation techniques also present special problems not seen in other orthopaedic patients. The contributors to this two-volume treatise on orthopaedic sports medicine are leaders in their subspecialty. They have shared with us their experience and perspectives by addressing specific problems of the athlete in their areas of expertise. Each contributor gives an excellent review of the particular topic and completes the contribution with preferred treatment. The early chapters address certain nonorthopaedic conditions that the orthopaedic sports medicine specialist must address when caring for the athlete. Nutrition, heat illness, biomechanics, and sports psychology are areas that must be part of the orthopaedic sports medicine physician's data base. In the later chapters, contributors discuss diagnosis and various methods of treatment

and present their chosen method of treatment of specific athletic injuries. When to return an athlete to activity is an important responsibility the orthopaedic sports medicine specialist must assume. Each contributor has addressed this issue for his or her particular anatomic area. It is our hope that this work will prove useful to our fellow orthopaedic surgeons. If so, it will be a tribute to the contributors who have shared with us their expertise. We are indebted to them for their time and effort. We also offer our sincere appreciation to Marti Daigle and to the staff at Elsevier Science for their patience and untiring efforts in bringing these volumes to publication. JESSE C. DELEE M.D. DAVID DREZ JR. M.D. MARK D. MILLER M.D.

MD Consult L.L.C. http://www.mdconsult.com /das/book/view/29433162/1103/5.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

1

Chapter 1 - Basic Science and Injury of Muscle, Tendon, and Ligaments Section A Muscle and Tendon Thomas M. Best MD, PhD Donald T. Kirkendall PhD Louis C. Almekinders MD William E. Garrett Jr. MD, PhD Skeletal Muscle Structure

Skeletal muscle is the single largest tissue in the body, comprising 40% to 45% of the total body weight in the average individual. The primary function of skeletal muscle is to generate force producing joint and limb locomotion and movement. Consequently, the muscle moment arm is an important parameter because it affects the ability to generate joint torques. To resist a given externally applied moment, the larger the moment arm, the less the muscle force that is required. Muscle maintains posture, stabilizes joints, and generates heat through the functional characteristics of excitability, contractility, elasticity, and extensibility. The gross structure of skeletal muscle is highly variable, as is apparent from a study of surface anatomy and deep dissection. In general, muscle originates from bone or dense connective tissue, either directly or from a tendon of origin. The muscle fibers themselves pass distally, usually to a tendon of insertion, which connects with bone. This structural framework is necessary to support the musculotendinous unit against injury and to organize the individual units into tissues and

organs ( Fig. 1A-1 ). The muscle-tendon unit can cross one or more joints. Generally, muscles that cross one joint are located close to bone and frequently are involved more in postural or tonic activity (e.g., soleus). Morphologically, one-joint muscles are broad and flat, possessing a decreased speed of contraction but increased strength (force output) compared with two-joint muscles. Two-joint or phasic muscles lie more superficially. Examples include the gastrocnemius, which is more superficial than the soleus, and the rectus femoris, which is the most superficial of the quadriceps group. Compared with one-joint muscles, two-joint muscles have a greater speed of shortening and capacity for length change; however, they are less effective in producing tension over the full range of motion. Architecture

Fiber architecture plays a major role in muscle function. The muscle fiber is the basic structural unit of skeletal muscle, and the sarcomere is the smallest contractile unit of the fiber. These fibers are grouped into small bundles known as fascicles, which most often are oriented obliquely to the longitudinal axis. Fiber arrangement within the muscle is variable, and a large number of configurations can be seen ( Fig. 1A-2 ), including fusiform, parallel, unipennate, bipennate, and multipennate. In general, fusiform muscles permit greater range of motion. Pennate muscles usually are more powerful (force of contraction) than parallel-fibered muscles of the same weight because their organization allows a larger number of fibers to work in parallel. Because pennate muscles contain short fibers, the maximal velocity of shortening is lower, and the work performed by the muscle can be considerably less.[166] Because of their orientation angle to the tendon, muscle fibers seldom extend the entire length of the muscle, and there is no location within the muscle belly that is crossed by all fibers. This geometry makes cross-sectional area of muscle a difficult property to define. Force production is proportional to muscle cross-sectional area and the fiber orientation. It has been shown that force production is independent of fiber type when cross-sectional area differences are taken into consideration ( Fig. 1A-3 ). In addition to the arrangement of muscle fibers, the fibrous connective tissue network within the muscle is important. Tendons often are spread out on the surface or within the muscle substance, providing a wide area for attachment of muscle fibers. Connective tissue surrounds the whole muscle (epimysium), each bundle of fibers (peri mysium), and the individual fibers themselves (endomysium). This connective tissue framework is continuous within the muscle and attaches to the tendon of insertion to produce an efficient means for movement. Myofibrillar Proteins

Muscle fibers are composed of four major proteins: myosin, actin, tropomyosin, and troponin. Together with the remaining structural proteins ( Table 1A-1 ), they comprise about 12% of the total weight of vertebrate striated muscle.

Myosin is a hexameric molecule composed of two high-molecular-weight (200,000) heavy chains and four low-molecular-weight light chain subunits termed A-1, A-2, and DTNB (two units). Figure 1A-4 shows a typical myosin molecule. This molecule can be cleaved by trypsin to yield

2

Figure 1-A-1 Schematic drawing of the structure of striated muscle, showing the organizational framework necessary for effective function. (See text for further explanation of structures.)

two fragments, heavy meromyosin and light meromyosin. Papain cleaves the light meromyosin fragment into a globular protein, S-1, and a helical protein, S-2. The adenosine triphosphatase (ATPase) activity and the actin-combining property of myosin are associated completely with the heavy meromyosin component, whereas the solubility properties of the molecule are associated with the light meromyosin fraction. Functionally, it is the heavy-chain component that possesses ATPase activity, whereas the light-chain component appears to regulate this action and is not essential for ATPase activity. The other three major structural proteins are incorporated into the thin filaments. Of these, actin is present in the largest amount. Actin molecules are small, roughly spherical structures arranged in the thin filaments as if to form a twisted strand of beads. Actin and myosin molecules have a recognizable polarity that is essential to muscular contraction. The remaining two major structural proteins, tropomyosin and troponin, constitute a protein complex that enables calcium to regulate the contraction-relaxation cycle of actomyosin. Tropomyosin molecules (molecular weight, approximately 65,000 d) are long, thin proteins that attach

Figure 1-A-2 Muscle fiber architecture. A, Parallel; B, unipennate; C, bipennate; D, fusiform.

end to end, forming a thin filament on the surface of an actin strand. Each strand carries its own filament, which lies near the groove between the paired strands. Together with the troponin myofibrillar protein, they collectively form native tropomyosin. The two main subunits are termed the and polypeptide chains with molecular weights of 34,000 and 35,000 d. These two chains differ mainly in their cysteine content and electrophoretic mobility;

Figure 1-A-3 The role of muscle architecture in force development and length change. Length of A is twice that of B; cross-sectional area of A equals that of B. Maximum force of A is one half that of B, whereas maximum length change of A is twice that of B. In C, the force is diminished by only a small factor when fibers are arranged in pennate fashion.

3

TABLE 1-A-1 -- Relative Proportions of Myofibrillar Proteins in Rabbit Skeletal Muscle Protein Percentage of Total Structural Protein Myosin

55

Actin

20

Tropomyosin

7

Troponin

2

C protein

2

M proteins

1-cm diameter area

Grade IV

Erosion of cartilage to bone

62

TABLE 1-D-7 -- General Grading of Translation/Joint Opening for Ligament Testing 1-5 mm 1+ or grade I >5 mm and 4 cm cm

Suspected disorder

Stretch to ligaments involved without macroscopic disruption

Partial tear/partial macroscopic disruption to ligaments involved

Complete tear of ligaments involved

Weight-bearing capability

Full or partial without significant pain

Difficult or impossible without supportive device (i.e., brace, tape, cane)

Impossible

Edema/ecchymosis

Well-localized

± localized

Diffuse

Significant

Significant

Localization of tenderness

Syndesmosis sprains Slight

Special tests

Positive squeeze or external rotation stress tests Radiographno mortise widening Minimal edema superior and anterior to lateral malleolus

Positive squeeze and external rotation stress tests Radiographno mortise widening Moderate edema superior and anterior to lateral malleolus

Signs and symptoms of grade II sprain but will have mortise widening radiographically

ATaFL, anterior talofibular ligament; CFL, calcaneal fibular ligament; PTaFL, posterior talofibular ligament. Modified from Gerber JP, Williams GN, Scoville CR, et al: Persistent disability associated with ankle sprains: A prospective examination of an athletic population. Foot Ankle Int 19:655, 1998. opening of the medial joint space consistent with a partial tear (1+ or 2+ opening). As Hughston[13] demonstrated, our understanding of the best way to treat MCL injuries is impaired by the use of various classifications. We recommend the use of the AMA system owing to its simplicity and the overall awareness of the classification. Based on physical examination findings, grade I (interstitial) injuries have no increased medial opening to valgus stress, grade II (partial injuries) have 1+ or 2+ opening, and grade III (complete tears) have 3+ opening. We recommend that authors clearly define their classifications and readers understand that many classifications exist so that the data are properly presented and interpreted. Fibular Collateral Ligament

The grading of fibular collateral ligament injuries usually follows the standard I, II, and III scheme for ligament injuries. Instability is usually graded based on amount of lateral joint-line opening to varus stress with the knee in 30 degrees of flexion. Again, some authors use the instability grading as injury grading, which results in confusion and inability to compare studies. We recommend the use of the AMA guidelines for ligament injury, as described for MCL injuries. Anterior and Posterior Cruciate Ligaments

It is unusual to classify ACL or posterior cruciate ligament injuries using the AMA's nomenclature because it is difficult to identify grade I injuries. ACL and posterior cruciate ligament injuries therefore are usually considered to be either partial or complete. Additionally, the method of treatment of cruciate ligament injuries is dependent on the presence or the absence of injuries to other knee ligaments. ACL and posterior cruciate ligament injuries therefore are usually classified as isolated injuries, with no other ligamentous injury evident on examination, or as combined injuries, if there is evidence of injury to the ACL and one of the collateral ligaments.

Ankle Sprains

Ankle sprains are usually separated into medial, lateral, and syndesmosis types. Grading of ankle sprains using the AMA classification can be difficult because many times, more than one ligament is involved. As a result, a mild, moderate, or severe grading scheme is usually employed to document the severity of injury. The West Point Ankle Grading System[11] ( Table 1D-13 ) provides guidelines for grade I, II, and III injuries.

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References American Medical Association: Standard Nomenclature of Athletic Injuries. Chicago, American Medical Association, 1968. 1.

Bach BR, Warren RJ, Wickiewicz TL: The pivot shift phenomenon: Results and description of a modified clinical test for anterior cruciate ligament insufficiency. Am J Sports Med 16:571-576, 1988. 2.

Bauer M, Jackson RW: Chondral lesions of the femoral condyles: A system of arthroscopic classification. Arthroscopy 4:97-102, 1988. 3.

Bigliani LU, Ticker JB, Flatow EL, et al: The relationship of acromial architecture to rotator cuff disease. Clin Sports Med 10:823-838, 1991. 4.

Curl WW, Krome J, Gordon ES, et al: Cartilage injuries: A review of 31,516 knee arthroscopies. Arthroscopy 13:456-460, 1997. 5.

6.

Daniel DM: Assessing the limits of knee motion. Am J Sports Med 19:139-147, 1991.

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7.

Dorland's Illustrated Medical Dictionary, 27th ed. Philadelphia, WB Saunders, 1988.

Dougados M, Aayral X, Listrat V, et al: The SFA system for assessing articular cartilage lesions at arthroscopy of the knee. Arthroscopy 10:69-77, 1994. 8.

9.

Fairbank TJ: Knee joint changes after meniscectomy. J Bone Joint Surg Br 30:664-670, 1948.

Fetto JF, Marshall JL: Medial collateral ligament injuries of the knee: A rationale for treatment. Clin Orthop 132:206-218, 1978. 10.

Gerber JP, Williams GN, Scoville CR, et al: Persistent disability associated with ankle sprains: A prospective examination of an athletic population. Foot Ankle Int 19:653-660, 1998. 11.

Hawkins RJ, Boker DJ: Clinical evaluation of shoulder problems. In Rockwood CA, Matsen FA III (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 164-197. 12.

Hughston JC: The importance of the posterior oblique ligament in repairs of acute tears of the medial ligaments in knees with and without an associated rupture of the anterior cruciate ligament. J Bone Joint Surg Am 76:1328-1344, 1994. 13.

Maffulli N, Khan KM, Puddu G: Overuse tendon conditions: Time to change a confusing terminology. Arthroscopy 14:840-843, 1998. 14.

Noyes FR, Cummings JF, Grood ES, et al: The diagnosis of knee motion limits, subluxations, and ligament injury. Am J Sports Med 19:163-171, 1991. 15.

Noyes FR, Grood ES, Cummings JF, et al: An analysis of the pivot shift phenomenon. The knee motions and subluxations induced by different examiners. Am J Sports Med 19:148-155, 1991. 16.

Noyes FR, Grood ES, Torzilli PA: Current concepts review: The definitions of terms for motion and position of the knee and injuries of the ligaments. J Bone Joint Surg Am 71:465-471, 1989. 17.

Noyes FR, Stabler CL: A system for grading articular cartilage lesions at arthroscopy. Am J Sports Med 17:505-513, 1989. 18.

19.

Outerbridge RE: The etiology of chondromalacia patellae. J Bone Joint Surg Br 43:752-757, 1961.

Rockwood CA: Fractures and dislocations of the shoulder: Part II, Subluxations and dislocations about the shoulder. In Rockwood CA, Green DP (eds): Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984, pp 722-985. 20.

Rosenberg TD, Paulos LE, Parker RD, et al: The forty-five degree posteroanterior flexion weight-bearing radiograph of the knee. J Bone Joint Surg Am 70:1479-1483, 1988. 21.

Rowe CR: Recurrent transient anterior subluxation of the shoulder. The dead arm syndrome. Clin Orthop 223:11-19, 1987. 22.

Seddon HJ: Surgical Disorders of the Peripheral Nerves, 2nd ed. Edinburgh, Churchill Livingstone, 1975. 23.

24.

Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990.

Sunderland S: Nerve Injuries and Their Repair: A Critical Appraisal. Edinburgh, Churchill Livingstone, 1991. 25.

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Chapter 2 - Basic Science and Injury of Articular Cartilage, Menisci, and Bone Section A Articular Cartilage Joseph A. Buckwalter MD Van C. Mow PhD Synovial joints make possible the rapid controlled movements necessary for sports. Normal function of these complex diarthrodial structures depends on the structural integrity and the macromolecular composition of articular cartilage. Sports-related traumatic disruptions of cartilage structure or alterations in cartilage macromolecular composition or organization change the biomechanical properties of the tissue and compromise joint function. Even more important, they can lead to progressive lifelong pain and disability. Sports injuries to articular cartilage present far more difficult diagnostic and treatment problems than injuries to ligament, tendon, or bone, partly because less is known about these injuries and partly because of the unique structure and function of articular cartilage. The specialized composition and organization of articular cartilage [34] [35] make the diagnosis of many injuries difficult, but these are also the qualities that provide the unique biomechanical properties that make possible normal synovial joint function. Articular cartilage is very soft and yields its interstitial water easily when compressed, [6] [106] [140] [143] yet it is very stiff in tension along planes parallel to the articular surface. Intact cartilage provides a smooth, lubricated gliding surface with a coefficient of friction better than most man-made bearing materials.[56] [84] [142] [144] In the joint, cartilage distributes the loads of articulation, thereby minimizing peak stresses acting on the

subchondral bone while the tensile strength of the tissue maintains its structural integrity under loading. These biomechanical properties make the tissue remarkably durable and wear resistant, enabling it to last many decades, even under high and repetitive stresses. Alterations in the mechanical properties of cartilage due to injury, disease, or increasing age have not been well defined, but the available information shows that these properties change with age and loss of structural integrity. Cartilage from skeletally immature joints (bones with open growth plates) is much stiffer than cartilage from skeletally mature joints (those with closed growth plates).[173] Older cartilage and fibrillated cartilage have much lower tensile stiffness and strength. [1] [99] Declines in stiffness and strength may increase the probability of injury to cartilage. Participation in sports often subjects the articular cartilage to intense repetitive compressive forces that can cause injury and deterioration of the tissue. Falls or other high-energy impacts can damage the articular cartilage without disrupting the articular surface. These abnormally large forces generate high shear stresses at the cartilage-subchondral bone junction, causing matrix lesions [7] [55] that may lead to clinically significant cartilage deterioration and joint dysfunction.[39] [55] [132] [168] Furthermore, repetitive trauma that leaves the articular surface intact can cause other injuries, including subtle damage to the matrix macromolecular framework and cartilage cells (chondrocytes).[55] [59] [168] [171] These injuries disrupt the well-organized macromolecular fabric of the matrix, alter cell function, and disturb normal cell-matrix interactions, thereby adversely altering the cell activities required to maintain cartilage mechanical properties.[30] [36] [85] [120] [121] [122] [123] [148] Because cartilage lacks nerves and blood vessels, damage limited to cartilage is not likely to be detected at the time of injury, but cartilage with this type of damage may become fatigued and fail more easily when subjected to acute or repetitive trauma. Less frequent but more severe sports injuries can acutely disrupt the articular surface by fracturing both cartilage and the underlying bone.[24] [86] Therefore, both acute traumatic injuries and repetitive excessive loading resulting from participation in sports can lead to cartilage deterioration and loss of synovial joint function. Despite their importance, sports injuries to articular cartilage remain poorly understood. Because injuries limited to cartilage do not cause pain or inflammation, patients and physicians rarely suspect cartilage damage following excessive acute or repetitive joint loading. Even when the physician suspects that cartilage injury exists, making a precise diagnosis of many types of cartilage injuries is difficult or impossible at present. Partly because of the difficulty in making a diagnosis, the natural history of many types of cartilage injury remains unknown, and it seems likely that some of the deterioration of articular surfaces now attributed to sports-related ligamentous or meniscal injuries is due to undetected cartilage damage. This chapter first reviews the important aspects of articular cartilage composition, organization, and biomechanical properties that make possible normal synovial joint function. The next sections summarize the response of cartilage to different types of injury and the results of cartilage repair, cartilage shaving, and abrasion of subchondral bone. The last section describes the use of cartilage grafts to replace lost or damaged

articular surfaces. Composition of Articular Cartilage

Like the dense fibrous tissues and meniscus, articular cartilage consists of cells, matrix water, and a matrix macromolecular

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Figure 2-A-1 (Figure Not Available) Normal articular cartilage structure. Histologic (A) and schematic (B) views of a section of normal articular cartilage. The tissue consists of four zones: the superficial tangential zone (STZ), the middle zone, the deep zone, and the calcified zone. Notice the differences in cell alignment among zones. The cells of the superficial zone have an ellipsoidal shape and lie with their long axes parallel to the articular surface. The cells of the other zones have a more spheroidal shape. In the deep zone, they tend to align themselves in columns perpendicular to the joint surface. (From Nordin M, Frankel VH: Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989, pp 31-57. Used with permission.)

framework.[8] [9] [27] [28] [34] [35] [66] [146] [148] [151] Unlike the most dense fibrous tissues, however, cartilage lacks nerves, blood vessels, and a lymphatic system. These conditions are responsible for its unusual physiologic requirements, cell behavior, and responses to injury. Chondrocytes

Only one type of cell exists within normal cartilagethe highly specialized chondrocyte. Chondrocytes contribute relatively little to the total volume of mature human articular cartilage, usually 5% or less. Like other mesenchymal cells,[27] [191] chondrocytes surround themselves with their extracellular matrix and rarely form cell-to-cell contacts. In normal cartilage, they are isolated in the extracellular matrix, and, because the tissue lacks blood vessels, the cells depend on diffusion through the matrix for their nutrition and rely primarily on anaerobic metabolism. Figure 2A-1 (Figure Not Available) shows a histologic section of normal adult articular cartilage with the chondrocytes embedded in the matrix (A) and a schematic representation of chondrocyte morphology (B). Three distinct zones of chondrocytes are seen: the superficial tangential zone, with ellipsoidal cells with their long axes aligned parallel to the surface; the middle zone, with spherical cells randomly distributed throughout the region; and the deep zone, with similar spherical cells forming columns aligned perpendicular to the tidemark and the calcified zone. More details on this arrangement are presented later in the chapter. Articular cartilage chondrocytes contain the organelles necessary for matrix synthesis, including endoplasmic reticulum and Golgi membranes. Also, they frequently contain intracytoplasmic filaments and glycogen, and at least some chondrocytes have a cilium that extends from the cell into the extracellular collagen-proteoglycan matrix. These structures may play a role in sensing mechanical changes in the matrix. After

completion of skeletal growth, chondrocytes rarely divide, but throughout life they synthesize and maintain the extracellular matrix that gives cartilage its essential material properties. Synthesis and turnover of proteoglycans are relatively fast, whereas collagen synthesis and turnover are very slow.[11] [151] [154] (For more details concerning turnover of cartilage matrix macromolecules, see the excellent review by Lohmander.[117] ) Extracellular Matrix

Tissue Fluid

Water contributes up to 80% of the wet weight of articular cartilage, and the interaction of water with the matrix macromolecules significantly influences the material properties of the tissue.[57] [92] [113] [114] [122] [125] [127] [140] [151] [197] This tissue fluid contains gases, small proteins, metabolites, and a high concentration of cations to balance the negatively charged proteoglycans.[125] [127] [152] [198] The volume, the concentration, and the behavior of the tissue water depend on its interaction with the structural macromolecules. In particular, large aggregating proteoglycans organize the tissue water and impede its flow through the matrix. The large proteoglycans also help maintain the fluid within the matrix and the fluid electrolyte concentrations. These matrix macromolecules have large numbers of negative charges, which attract positively charged ions and repel negatively charged ions. This increases the concentration of positive ions (e.g., sodium) and decreases the concentration of negative ions (e.g., chloride). The increase in the total inorganic ion concentration increases the tissue osmolarity (i.e., it creates a Donnan effect). The collagen network resists the Donnan osmotic pressure caused by the

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inorganic ions associated with proteoglycans.[125] [126] [127] This interaction between proteoglycans and tissue fluid significantly influences the compressive stiffness and resilience of articular cartilage.[109] [110] [127] [140] [153] Structural Macromolecules

The structural macromolecules that provide 20% to 40% of the wet weight of cartilage include collagens, proteoglycans, and noncollagenous proteins.[28] [117] [151] Chondrocytes synthesize all three types of molecules from amino acids and sugars, but differences in the types and the organization of amino acids and sugars give each type of molecule a different form and function. [27] [28] [117] [151] Abnormalities in these molecules or in their organization can adversely affect the durability and the mechanical properties of the cartilage and may lead to deterioration of the articular surface. [1] [31] [78] [84] [127] [140] [141] [142] [147] [151]

The three classes of macromolecules differ in their concentrations within the tissue and in their contributions to tissue properties. Collagens contribute about 60% of the dry

weight of cartilage, proteoglycans contribute 25% to 35%, and the noncollagenous proteins and glycoproteins contribute 15% to 20%. Collagens are distributed relatively uniformly throughout the depth of the cartilage except in a collagen-rich region near the surface.[114] The collagen fibrillar meshwork and the cross-linking among collagen fibers give cartilage its form and its tensile strength.[99] [173] [183] [205] Figure 2A-2 (Figure Not Available) shows a schematic representation of the fibrillar collagen ultrastructure throughout the depth of the tissue (A), along with three scanning electron micrographs that show the appearance of the fibrillar collagen network in the three zones of uncalcified cartilage (B).[145] Figure 2-A-2 (Figure Not Available) Schematic representation (A) and scanning electron micrographs (B) of the interterritorial matrix collagen fibril orientation and organization in normal articular cartilage. In the superficial tangential zone (STZ), the fibrils lie roughly parallel to the articular surface. In the middle zone, they assume a more random alignment, and in the deep zone, they lie roughly perpendicular to the articular surface. (From Nordin M, Frankel VH: Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989, pp 31-57. Used with permission.)

Proteoglycans and noncollagenous proteins bind to the collagenous meshwork or become mechanically entrapped within it, and water fills this molecular framework. Proteoglycans give cartilage its stiffness in compression and its resilience. Figure 2A-3 shows a proteoglycan monomer attached to a hyaluronate chain and a linking protein (A), a proteoglycan aggregate (B), and an electron micrograph of a proteoglycan aggregate (C). Some noncollagenous proteins help organize and stabilize the matrix macromolecular framework, whereas others help chondrocytes bind to the macromolecules of the matrix. The reader is referred to the references section for more detailed reviews of cartilage molecular organization.[28] [29] [34] [35] [117] [151] Collagens

Collagens, a family of 13 or more protein molecules produced by more than 20 distinct genes, form a critical part of every tissue.[65] [154] They have a region consisting of three amino acid chains wound into a triple helix. This triple-helical region makes up a major part of all collagen molecules and provides some of the distinctive structural and mechanical properties of collagens. By virtue of their tensile stiffness and strength, collagens contribute to the structure of the articular cartilage matrix, and articular cartilage, like most other tissues, contains multiple genetically distinct collagen types (specifically, types II, VI, IX, X, and XI). Collagen types II, IX, and XI form the cross-banded fibrils seen on electron microscopy. The organization of these fibrils into a tight meshwork that extends throughout the tissue provides the tensile stiffness and strength of articular cartilage.[1] [98] [99] [173] [205] This meshwork also contributes to the cohesiveness of the tissue by mechanically entrapping the large proteoglycans. The principal articular

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Figure 2-A-3 Proteoglycan structure. A, Details of proteoglycan monomer structure, showing chondroitin sulfate and keratan sulfate chains and the interaction of the monomer with hyaluronate chain and link protein. B, Molecular conformation of a typical proteoglycan aggregate, showing size of the molecule. C, An electron micrograph of a proteoglycan aggregate.

cartilage collagen, type II, accounts for 90% to 95% of the cartilage collagen and forms the primary component of the cross-banded fibrils. Type IX collagen contains both collagenous and noncollagenous regions and has one or possibly two chondroitin sulfate chains.[25] [99] Type IX collagen molecules bind covalently to the superficial layers of the cross-banded fibrils and project into the matrix. Type XI collagen molecules also bind covalently to type II collagen molecules and probably form part of the interior structure of the cross-banded fibrils. The functions of types IX and XI collagens remain uncertain, but presumably, by acting together, they help form and stabilize the collagen fibrils assembled primarily from type II collagen. The position of type IX collagen molecules on the surface of the fibrils suggests that they may influence the diameter and the stability of fibrils and may interact with other matrix macromolecules. The position of type XI collagen mole cules within the fibrils suggests that they may contribute to the formation and may influence the diameter of fibrils. The functions of types VI and X collagen remain unknown. Type VI collagen is often described as an adhesion protein and in some regions reaches its highest concentration in the immediate vicinity of the chondrocytes. Type X collagen appears near the cells of the calcified cartilage zone of articular cartilage and the hypertrophic zone of the growth plate, where the longitudinal cartilage septa begin to mineralize. This pattern of distribution suggests that it contributes to mineralization of cartilage. Proteoglycans

Proteoglycans consist of a protein core and one or more glycosaminoglycan chains (long, unbranched polysaccharide chains consisting of repeating disaccharides that contain an amino sugar). Each disaccharide unit has at least one negatively charged carboxylate or sulfate group, so that the glycosaminoglycans form long strings of negative charges that repel other negatively charged molecules and attract cations. The sugars included in the polysaccharide chains of these molecules vary, but all the molecules consist of repeating disaccharide units containing a derivative

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of either glucosamine or galactosamine.[117] [172] Glycosaminoglycans found in cartilage include hyaluronic acid, chondroitin sulfate, keratan sulfate, and dermatan sulfate. Articular cartilage contains at least three types of proteoglycans: a large aggregating proteoglycan called aggrecan, which contains large numbers of chondroitin sulfate and keratan sulfate chains, and two small dermatan sulfate-containing, nonaggregating proteoglycans called biglycan and decorin. Other matrix molecules that have glycosaminoglycan chains and therefore could be classified as proteoglycans include

type IX collagen (discussed in the section on collagens) and fibromodulin (discussed in the section on noncollagenous proteins and glycoproteins). The tissue probably also contains other small proteoglycans and some large nonaggregating proteoglycans. The aggrecan molecules fill most of the interfibrillar space of the cartilage matrix.[28] [34] [35] [80] [117] [151] They contribute about 90% of the total cartilage matrix proteoglycan, whereas large nonaggregating proteoglycans contribute 10% or less and small nonaggregating proteoglycans contribute about 3%. The large nonaggregating proteoglycans resemble the large aggregating proteoglycans in structure and composition[117] and may represent degraded aggregating proteoglycans. The large aggregating proteoglycans consist of protein core filaments with many covalently bound chondroitin sulfate and keratan sulfate chains ( see Fig. 2A-3 ). [29] [117] [151] [172] Chondroitin sulfate and keratan sulfate form about 95% of the molecule, and protein forms about 5%. The protein cores consist of five domains: three globular domains and two extended domains ( see Fig. 2A-3 ). A short extended region of the protein core separates the G1 (first globular domain) region from the G2 (second globular domain) region. A longer extended region of the protein core contains covalently bound keratan sulfate and chondroitin sulfate chains and separates the G2 and the G3 (third globular domain) regions. Keratan sulfate chains cluster together in a region near the G2 domain (the keratan sulfaterich region), and the chondroitin sulfate chains cluster together in a region between the keratan sulfaterich regions and the G3 domain (the chondroitin sulfaterich region). The G1 domain binds noncovalently to hyaluronic acid filaments and small proteins called link proteins. The functions of the G2 and G3 domains remain unknown. Because each keratan sulfate and chondroitin sulfate chain contains many negative charges, adjacent chains repel each other and tend to maintain aggrecan molecules in an expanded form. This conformation promotes the trapping of proteoglycans within the fine collagen meshwork.[80] [151] In the articular cartilage matrix, most aggregating proteoglycan monomers noncovalently associate with hyaluronic acid filaments and link proteins to form proteoglycan aggregates ( see Fig. 2A-3 ). These large molecules have a central hyaluronic acid backbone that can vary in length from several hundred nanometers to more than 10,000 nm.[29] [31] [117] [151] Large aggregates may have more than 300 associated monomers. Link proteins and other small noncollagenous proteins stabilize the association between monomers and hyaluronic acid. They appear to play a role in directing the assembly of aggregates and help maintain the stability of the matrix and provide added mechanical strength.[29] [147] Aggregate formation helps anchor proteoglycans within the matrix, preventing their displacement during deformation of the tissue, and also helps organize and stabilize the relationship between proteoglycans and collagen fibrils. Recently, it has been found that proteoglycans at physiologic concentrations form elastic networks capable of storing energy.[78] [141] Link protein greatly increases the stiffness and the strength of these proteoglycan networks.[147] The interaction between the collagen and the proteoglycan networks provides the strength and the cohesiveness of the articular cartilage extracellular matrix.[140] [148] The interaction between large proteoglycans and the tissue fluid contributes significantly

to the compressive stiffness and the resilience of cartilage. These proteoglycans have a structure that fills a large volume with negatively charged glycosaminoglycan chains ( see Fig. 2A-3 ) that interact with water and cations. By repelling each other, these charged chains hold the monomers stiffly extended, thereby inflating the collagen fibril meshwork with water. Compression of the intact matrix drives the glycosaminoglycan chains closer together, increasing resistance to further compression and forcing water out of the molecular domain. Release of compression allows the molecules to re-expand and imbibe the lost fluid. Comparison of the maximum volume that can be occupied by proteoglycans in solution with their concentration in articular cartilage matrix shows that if the cartilage matrix proteoglycans expanded fully, they would fill a volume many times larger than the tissue that contains them.[29] In the matrix, their domains must overlap or be collapsed; the repulsive forces from charges on these molecules and the osmotic pressure generated by counter-ions associated with these charges exert a constant pressure to expand. Only the collagen fibril meshwork restrains the expansion of the proteoglycans.[58] [109] [110] [125] [126] [127] [152] [153] Disruption of this collagen meshwork releases the matrix proteoglycans to extend their protein cores and glycosaminoglycan chains, thereby increasing the concentration of water and decreasing the proteoglycan concentration within the extracellular matrix. These molecular changes increase the permeability and decrease the stiffness of the matrix. Thus, loss of proteoglycans, or collagen network disruption due to acute or repetitive trauma, will have significant effects on the mechanical properties of articular cartilage.[1] [6] [99] [127] [140] [148] Small nonaggregating proteoglycans have shorter protein cores than aggrecan molecules, and two of thembiglycan and decorincontain a different type of glycosaminoglycan (dermatan sulfate) as well as other glycosaminoglycans. [172] They also have far fewer glycosaminoglycan chains than aggrecan molecules; biglycan has two glycosaminoglycan chains, and decorin has one. In adult articular cartilage, at least some of these smaller proteoglycans form close associations with collagen fibrils. Unlike the large aggregating molecules, they do not fill a large volume of the tissue or contribute directly to the mechanical behavior of the tissue. Instead, they bind to other macromolecules and probably influence cell function. For example, the dermatan sulfate proteoglycans appear to inhibit cartilage repair. Noncollagenous Proteins and Glycoproteins

The noncollagenous proteins and glycoproteins are not as well understood as collagens and proteoglycans. They

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consist primarily of protein and have a few attached monosaccharides and oligosaccharides. At least some of these molecules appear to help organize and maintain the macromolecular structure of the matrix, whereas others may help stabilize the relationship between chondrocytes and other matrix macromolecules.

Link proteins help organize and stabilize the matrix through their effects on proteoglycan aggregation.[117] [147] [151] Other noncollagenous proteins found in articular cartilage may help mediate the adhesion of chondrocytes to the matrix and possibly may stabilize the relationship between the chondrocytes and the matrix.[117] Fibromodulin, a glycoprotein that contains keratan sulfate, also has been found within cartilage. Because of its keratan sulfate content, fibromodulin may be considered a form of proteoglycan as well as a glycoprotein. It appears to be associated with cartilage collagen fibrils and may influence collagen turnover. Cell-Matrix Interactions

Maintenance of cartilage depends on continual complex interactions between chondrocytes and the matrix they synthesize. Normal degradation of matrix macromolecules, especially proteoglycans, requires that the cells continually synthesize new molecules.[117] [151] [172] The cells can sense the content of the matrix and respond appropriately. If they did not, the tissue would lose its biomechanical properties. For example, experimental depletion of matrix proteoglycan with papain stimulates proteoglycan synthesis.[117] If the cells did not replace the lost proteoglycans, the tissue would deteriorate. Mechanical loading also affects cartilage homeostasis.[97] [103] [160] [161] [194] These interactions between the cells and their matrix have considerable importance for sports injuries to articular cartilage because mechanical injury that interferes with the ability of chondrocytes to replace matrix macromolecules or lack of appropriate mechanical stimulation will lead to deterioration of the tissue. At present, the mechanism or mechanisms through which chondrocyte synthetic function is stimulated or suppressed remain unknown. Although the details of the mechanisms of chondrocyte control and modulation are unknown, it is known that in general, chondrocytes sense and respond to changes in patterns of matrix deformation owing to persistent changes in joint use. It is likely that both mechanical and physicochemical events occurring during matrix deformation play significant roles in stimulating chondrocytes. When cartilage is loaded, it is deformed. Figure 2A-4 shows a chondrocyte embedded in the charged extracellular matrix in an undeformed state and in a deformed state. Deformation alters the charge density around the cells and induces a streaming potential throughout the tissue during compression. These physicochemical effects vary in the different zones of the charged collagen-proteoglycan extracellular matrix owing to varying proteoglycan concentrations, according to depth from the surface.[28] [117] [127] [151] [172] Results from recent compression studies have suggested that these physicochemical events are important in modulating chondrocyte proteoglycan biosynthesis. [74] [177] Additionally,

Figure 2-A-4 Confocal laser microscopic view of a chondrocyte from the middle zone of articular cartilage embedded in the extracellular matrix in the unloaded state (t = 0) and the compressed state at

equilibrium (Equil.).

the increase in charge density within the extracellular matrix increases the interstitial Donnan osmotic pressure and the osmotic pressure gradients and produces streaming polarization and electro-osmosis effects around the chondrocytes.[110] [125] These electrical events may also be important in stimulating chondrocyte biosynthetic activities. The stress-strain environment and the strain-energy density around the cell may also play important roles in stimulating chondrocytes.[76] [77] In addition to these mechanical, electrical, and physicochemical events, biochemical agents such as growth factors, cytokines, and enzymes have been shown to be potent stimulators of chondrocytes. Indeed, each of these stimulators may play a role in modulating chondrocyte activities, and their effect may be synergistic. At present, how mechanical, electrical, and physicochemical forces work is unknown. How each of the chemical agents modulates cartilage homeostasis and how they influence each other are also unknown. Studies addressing these important questions offer great challenges for the future.

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Organization of Articular Cartilage

To form articular cartilage, chondrocytes organize collagens, proteoglycans, and noncollagenous proteins into a unique, highly ordered structure (see Figs. 2A-1 (Figure Not Available) and 2A-2 (Figure Not Available) ). The composition, the organization, and the mechanical properties of the matrix as well as cell morphology and probably cell function vary according to the depth of these elements from the articular surface. [28] [34] [117] [127] [151] [172] Matrix composition, organization, and function also vary with distance from the cell.[34] [35] [181]

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Zones of Articular Cartilage

Morphologic changes in articular cartilage cells and matrix from the articular surface to the subchondral bone make it possible to identify four zones or layers of articular cartilage: the superficial tangential zone, the middle or transitional zone, the deep or radial zone, and the zone of calcified cartilage (see Figs. 2A-1 (Figure Not Available) and 2A-2 (Figure Not Available) ). Although each zone has distinct morphologic features, the boundaries between zones cannot be sharply defined. Recent biologic and mechanical studies have shown that this morphologic zonal organization has functional significance. Cells in each zone differ in shape, size, and orientation relative to the articular surface and appear to differ in synthetic activity. They may also respond differently to mechanical loading, suggesting that development and maintenance of normal articular cartilage depend in part on differentiation of phenotypically distinct populations of chondrocytes. The heterogeneity of chondrocytes presumably is responsible for the differences in matrix composition and organization that result in different mechanical properties in each zone.

Superficial Zone

The thinnest zone, the superficial tangential zone, has two layers. A sheet of fine fibrils with little polysaccharide and no cells covers the joint surface (see Fig. 2A-1 (Figure Not Available) ). This layer presumably corresponds to the clear film that can be stripped from the articular surface in some regions. On phase-contrast microscopy, it appears as a narrow bright line, the lamina splendens. In the next layer of the superficial zone, flattened ellipsoid chondrocytes are arranged so that their major axes are parallel to the articular surface (see Fig. 2A-1 (Figure Not Available) ). They synthesize a matrix that has a high collagen concentration and a low proteoglycan concentration relative to the other cartilage zones. Water content is the highest in this zone, averaging 80%.[114] [127] [151]

Transitional Zone

The transitional, or middle, zone has several times the volume of the superficial zone (see Fig. 2A-1 (Figure Not Available) ). The cells of this zone have a higher concentration of synthetic organelles, endoplasmic reticulum, and Golgi membranes than do the cells of the superficial zone. They assume a spheroidal shape and synthesize a matrix with collagen fibrils of a larger diameter and a higher concentration of proteoglycans than is found in the superficial zone. In this zone, the proteoglycan concentration is higher than in the superficial zone, but the water and the collagen concentrations are lower. [114] [127] [197] Deep Zone

The chondrocytes in the deep zone resemble those of the middle zone, but they tend to align in columns perpendicular to the joint surface (see Fig. 2A-1 (Figure Not Available) ). This zone contains the collagen fibrils with the largest diameter, the highest concentration of proteoglycans, and the lowest concentration of water. The collagen fibers of this zone pass through the tidemark (a thin basophilic line seen on light microscopic sections of decalcified articular cartilage that marks the boundary between calcified and uncalcified cartilage)[39] [170] into the calcified zone, anchoring adult articular cartilage to the subchondral bone.[170] Zone of Calcified Cartilage

A zone of calcified cartilage lies between the deep zone of uncalcified cartilage and the subchondral bone (see Fig. 2A-2 (Figure Not Available) ). The cells of the calcified cartilage zone have a smaller volume per cell than the cells of the deep zone and contain only small amounts of endoplasmic reticulum and Golgi membranes. During aging, the tidemark advances, causing thinning of the uncalcified cartilage.[38] [39] This remodeling process may be due to repetitive microtrauma in the deep zone of cartilage.[7] [55] [168] Results of stress-strain analysis suggest that cartilage thinning is detrimental to the tissue.[10] [168]

Matrix Regions

Variations in the matrix within zones have been described by dividing the matrix into regions or compartments called the pericellular region, the territorial region, and the interterritorial region (Figs. 2A-5 (Figure Not Available) and 2A-6 (Figure Not Available) ). [28] [34] [164] [181] The pericellular and the territorial regions appear to serve the needs of chondrocytes (i.e., they bind the cell membranes to the matrix macromolecules and protect the cells from damage during loading and deformation of the tissue).[77] They may also help transmit mechanical signals to the chondrocytes. The primary function of the interterritorial matrix is to provide the mechanical properties of the tissue.[127] [140] [148] Pericellular Matrix

Chondrocyte cell membranes appear to attach to the thin rim of the pericellular matrix that covers the cell surface (see Figs. 2A-5 (Figure Not Available) and 2A-6 (Figure Not Available) ). This matrix region probably contains noncollagenous proteins and possibly nonfibrillar collagens and is rich in proteoglycans.[28] [181] It contains little or no fibrillar collagen. Territorial Matrix

An envelope of territorial matrix surrounds the pericellular matrix of individual chondrocytes and, in some locations, pairs or clusters of chondrocytes and their pericellular matrices (see Figs. 2A-5 (Figure Not Available) and 2A-6 (Figure Not Available) ). In the deep zone, a territorial matrix surrounds each chondrocyte column. The thin collagen fibrils of the territorial matrix nearest the cell appear to adhere to the pericellular matrix. At a distance from the cell, they decussate and intersect at various angles, forming a fibrillar basket around the cells.[164] This collagenous basket may provide mechanical protection for the chondrocytes during loading and deformation of the tissue. The results of a recent stress-strain analysis support this concept; the analysis showed that the matrix regions

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Figure 2-A-5 (Figure Not Available) A and B, Electron micrographs showing chondrocytes and the regions of articular cartilage matrix. In both electron micrographs, short cell processes protrude from the chondrocytes through the pericellular matrix (arrowheads) to the border between the pericellular matrix and the territorial matrix (*). The interterritorial matrix (**) contains larger collagen fibrils and surrounds the territorial matrices, the pericellular matrices, and the cells. (From Buckwalter JA, Hunziker EB, Rosenberg RC, et al: Articular cartilage: Composition and structure. In Woo SL, Buckwalter JA [eds]: Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1988, pp 405-426.) Figure 2-A-6 (Figure Not Available) Electron micrographs showing the matrix compartments of articular cartilage. A, The pericellular matrix (arrowheads) consists of a narrow, dense coat of proteoglycans and possibly glycoproteins as well as other nonfibrillar molecules. The territorial matrix (*) sur rounds the

pericellular matrix. Notice the intimate contact between the pericellular matrix and the cell membrane. B, The territorial matrix consists of a dense network of fine collagen that may extend around one cell or a group of cells (a territorium or a chondron). Notice the absence of a sharp border between the pericellular and the territorial matrices. C, The interterritorial matrix consists of parallel large-diameter collagen fibrils and fibers with matrix granules (arrows) interspersed between fibrils. These granules consist of proteoglycans precipitated with ruthenium hexamine trichloride. (From Buckwalter JA, Hunziker EB, Rosenberg RC, et al: Articular cartilage: Composition and structure. In Woo SL, Buckwalter JA [eds]: Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill, American Academy of Orthopae dic Surgeons, 1988, pp 405-426.)

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surrounding the cells function as a protective buffer against the development of high stresses and strains in the chondrocyte when the tissue is loaded.[77] An abrupt increase in collagen fibril diameter and a transition from the basket-like orientation of the collagen fibrils to a more parallel arrangement mark the boundary between the territorial and the interterritorial matrices. Many collagen fibrils connect the two regions, making it difficult to identify the precise division between these two regions.[18] [28] Interterritorial Matrix

The interterritorial matrix (see Figs. 2A-5 (Figure Not Available) and 2A-6 (Figure Not Available) ) makes up most of the volume of mature articular cartilage. It contains the largest-diameter collagen fibrils. Unlike the collagen fibrils of the territorial matrix, these fibrils are not organized to surround the chondrocytes, and they change their orientation relative to the joint surface by 90 degrees from the superficial zone to the deep zone (see Fig. 2A-2 (Figure Not Available) ).[46] [111] [150] [171] In the superficial zone, the fibril diameters are relatively small, and the fibrils generally lie parallel to the articular surface. Creation of pinhole defects in some articular surfaces produces split lines that show a tendency to extend parallel to the plane of joint motion,[17] [88] suggesting that collagen fibrils in the interterritorial matrix of the superficial zone may also be oriented relative to the motion of the joint. In the middle zone, interterritorial matrix collagen fibrils assume more oblique angles relative to the articular surface, and in the deep zone, they generally lie perpendicular to the joint surface. Because the interterritorial matrix forms most of the volume of cartilage, and because collagen provides the tensile stiffness and strength of articular cartilage, these biomechanical properties should vary with changes in collagen fibril orientation and organization in the interterritorial matrix (see Fig. 2A-2 (Figure Not Available) ). Experimental studies show that cartilage tensile stiffness and strength do vary among cartilage zones.[99] [173] [205]

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Mechanical Properties of Cartilage

The behavior of cartilage when subjected to compression, tension, or shear depends on the concentration, the properties, and the organization of the matrix macromolecules, the water content, and the physical and electrical interactions between the water and the macromolecular framework.[98] [144] [148] Because cartilage has a solid phase (the macromolecular framework of collagens, proteoglycans, and noncollagenous proteins) and a fluid phase (the tissue water), it behaves as a biphasic (two-phase) viscoelastic material; that is, its response to loading combines viscosity, a characteristic of fluids, with elasticity, a characteristic of solids. When a viscoelastic material is subjected to a constant load or a constant deformation, its response varies with time. A viscoelastic material subjected to a constant load responds with rapid initial deformation followed by further slow, progressive deformations until it reaches an equilibrium state, a behavior called creep. A viscoelastic material subjected to constant deformation responds with high initial stress followed by a slowly progressive decrease in the stress required to maintain the deformation, a behavior called stress relaxation. In articular cartilage, because it is a porous-permeable hydrated soft tissue, creep and stress relaxation in compression are predominantly caused by fluid flow through the matrix.[106] [140] [148] In shear, when no interstitial fluid flow occurs, creep and stress relaxation occur because the macromolecular framework is altered.[82] [83] [140] [185] [188] An important characteristic of articular cartilage is its ability to undergo deformation and then revert to its original form by reversing fluid flow. This feature is important in joint lubrication and tissue fluid circulation, particularly because of the load-bearing function of cartilage and because of its lack of a vascular supply and lymphatic system. [142] [144] Changes in the composition or the organization of the matrix macromolecular framework can cause deterioration of these essential mechanical properties. Collagen fibrils provide tensile strength but little resistance to compression. Interaction of the

proteoglycans with water provides resistance to compression, swelling pressure, and resilience but little tensile strength. For these reasons, disruption of the collagen fibril meshwork allows the proteoglycans to expand, increasing the water concentration and decreasing the proteoglycan concentration.[110] [126] [148] [152] [153] This results in a decrease in cartilage stiffness and an increase in matrix permeability.[6] [140] [148] These changes make the tissue less capable of supporting the loads of articulation and more vulnerable to further injury from loading, which may cause progressive mechanical failure of the matrix and clinical osteoarthritis.[36] [37] [148]

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Cartilage Injury and Repair

The response of cartilage to trauma and the potential for repair of cartilage depend to a large extent on the type of injury sustained and whether the injury involves the subchondral bone. Sports-related synovial joint trauma can fracture or rupture the cartilage matrix, causing visible splits in the articular surface, or it can damage the macromolecular framework and alter cell function without disrupting the surface of the tissue.[7] [23] [34] [51] [55] [96] [100] [128] [148] [171] [210] Because cartilage lacks blood vessels, damage to the cartilage alone does not cause inflammation. If an injury disrupts both the cartilage and the subchondral bone, the blood vessels in the bone participate in the inflammation that initiates the fracture healing.[36] The clot and the repair tissue from bone can then fill the articular cartilage defect and follow the sequence of inflammation, repair, and remodeling, as in the repair of other tissues such as ligament.[36] Unlike repair tissue in ligaments, however, the repair tissue that fills cartilage defects differentiates initially toward articular cartilage rather than toward dense fibrous tissue.[33] [34] [36] [37] Differences in the potential for cartilage repair separate acute injuries of articular cartilage into three general types[30] [34] [36] [37] : (1) loss of matrix macromolecules or disruption of the macromolecular framework without visible tissue disruption; (2) mechanical disruption of articular cartilage alone; and (3) mechanical disruption of articular

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TABLE 2-A-1 -- Acute Sports Injuries to Articular Cartilage

Injury Type

Clinical Presentation

Tissue Response

Potential for Healing

Damage to matrix or cells without visible disruption of articular surface

No known symptoms Direct inspection of the articular surface and current clinical imaging methods cannot detect this type of injury

Synthesis of new matrix macromolecules Cell proliferation?

If basic matrix structure remains intact and a sufficient number of viable cells remain, the cells can restore the normal tissue composition If the matrix or the cell population sustains significant damage, or if the tissue sustains further damage, the lesion may progress

Cartilage disruption (cartilage fractures or ruptures)

May cause mechanical symptoms, synovitis, and joint effusions

No fibrin clot formation or inflammation Synthesis of new matrix macromolecules and cell proliferation, but new tissue does not fill cartilage defect

Depending on the location and the size of the lesion and the structural integrity, stability, and alignment of the joint, the lesion may or may not progress

Cartilage and bone disruption (osteochondral fractures)

May cause mechanical symptoms, synovitis, and joint effusions

Formation of a fibrin clot, inflammation, invasion of new cells, and production of new tissue

Depending on the location and the size of the lesion and the structural integrity, stability, and alignment of the joint, the lesion may or may not progress

cartilage and subchondral bone. Each of these types of cartilage damage presents a different problem for repair, although the categories overlap. Progressive loss of matrix macromolecules or disruption of the organization of the matrix macromolecular framework eventually results in mechanical disruption of the tissue; mechanical disruption of the cartilage may release tissue factors that stimulate matrix degradation and loss of matrix macromolecules. Table 2A-1 lists the types of acute sports-related injuries to cartilage caused by direct blunt trauma, high-energy joint loading, and forceful joint twisting. This table summarizes the current understanding of the clinical presentation, the tissue response, and the potential for healing of these injuries. The exact mechanisms of injury and the natural history of these injuries remain poorly understood. Injuries limited to the articular

cartilage do not cause pain or inflammation, but these injuries commonly occur in association with injuries to other tissues that have nerves and blood vessels, including synovium, ligament, joint capsule, meniscus, and bone. Therefore, people with injuries of the articular cartilage may have symptoms and signs that result from damage to innervated vascularized tissues. Matrix Damage without Visible Tissue Disruption

Acute or repetitive direct blunt trauma and acute or repetitive high-energy joint loading can cause cartilage damage without visible tissue disruption ( see Table 2A-1 ). Because of the demands of competitive or recreational sports, these injuries probably occur frequently in athletes. Presumably, they are often associated with other joint injuries such as ligament and meniscal tears, but lack of a tissue inflammatory response, lack of nerves in cartilage, or lack of visible disruption of the articular surface prevents detection of these injuries even on direct examination of the articular surface or on magnetic resonance imaging. The intensity and the type of cartilage loading that can cause matrix damage without gross tissue disruption have not been well defined.[7] [148] [170] Physiologic levels of joint loading do not appear to cause cartilage injury, but impact loading above that associated with normal activities and less than that necessary to produce cartilage disruption can cause tissue alterations. Other causes of this type of cartilage injury include traumatic or surgical disruption of the synovial membrane, prolonged joint immobilization, some medications, joint irrigation, and synovial inflammation. [7] [30] [34] [36] [37] [55] The effects of decreased loading and motion on articular cartilage and the effects of medications on articular cartilage are discussed elsewhere in this text. Cartilage damage without tissue disruption has not been studied as extensively as other types of cartilage injury, but the available evidence shows that loss of proteoglycans or disruption of their organization occurs before other signs of tissue injury.[3] [129] [192] The loss of proteoglycans and the alteration of their molecular structure may be due to either increased degradation or altered synthesis of the molecules.[30] [34] [36] [44] Loss of matrix proteoglycans decreases cartilage stiffness and increases its hydraulic permeability.[6] [140] [148] These alterations may cause greater loading of the remaining macromolecular framework, including the collagen fibrils, increasing the vulnerability of the tissue to damage from further impact loading. These injuries may cause matrix abnormalities other than loss of proteoglycans (e.g., rupture or distortion of the collagen fibril meshwork or disruption of the collagen fibrilproteoglycan relationships), and they may alter chondrocyte function or even damage the chondrocytes. For example, impact loading of dog articular cartilage caused cartilage swelling, collagen fibril swelling, and disturbances in the relationships between collagen fibrils and proteoglycans.[55] Mildly fibrillated cartilage from human femoral condyles shows a significant decrease in tensile stiffness and an increase in swelling, whereas cartilage specimens obtained adjacent to focal lesions show a dramatic loss of tensile properties and an even greater increase in swelling.[1] [2] Lack of a reliable method of detecting cartilage injuries that do not cause visible

disruption of the matrix in humans has made it impossible to define the natural history of this type of damage. Probing the intact articular surface may show soft regions, but the significance of softening remains

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uncertain. Methods that may eventually help identify these injuries in humans include imaging techniques that show the state of water within the cartilage and devices that measure cartilage stiffness. The ability of chondrocytes to sense changes in matrix composition and to synthesize new molecules makes it possible for them to repair damage to the macromolecular framework. The available evidence indicates that following a loss of proteoglycans, the cells increase synthesis of these macromolecules and begin to restore the matrix concentration of proteoglycans toward normal. As a result, the material properties of the matrix return toward normal. Following significant depletion of proteoglycans, the process of repairing the matrix may require many weeks or possibly months to complete.[36] If the cells do not repair significant matrix macromolecular abnormalities, or if the loss of matrix molecules progresses, the tissue will deteriorate.[37] It is not clear at what point this type of injury becomes irreversible and leads to progressive loss of articular cartilage. Presumably, if the basic collagen meshwork remains intact, and if enough chondrocytes remain viable, the chondrocytes can restore the matrix as long as the loss of matrix proteoglycan does not exceed the amount that can be produced rapidly by the cells.[30] [34] [37] When these conditions are not met, the cells will not succeed in their attempt to restore the matrix, the chondrocytes will be exposed to excessive loads, and the tissue will degenerate.[37] For these reasons, insults that cause this type of articular cartilage injuryincluding immobilization, exposure of articular cartilage, and inflammationshould be minimized. Because this type of matrix macromolecular injury may temporarily increase the vulnerability of cartilage to mechanical injury, it appears advisable to minimize the intensity of impact loading of cartilage following severe blunt trauma, prolonged immobilization, or inflammation. Articular Cartilage Injuries That Disrupt the Tissue

Severe blunt trauma, penetrating injuries, and fractures can cause visible disruption of the articular cartilage matrix. These injuries rupture, lacerate, or fracture the matrix macromolecular framework and kill chondrocytes at the site of injury without directly damaging the subchondral bone. Penetrating joint injuries that lacerate cartilage rarely occur as a result of sports, but study of experimental lacerations has provided most of our current understanding of the potential for healing of injuries limited to cartilage. The lack of blood vessels and cells that can repair significant tissue defects limits the response of cartilage to injury.[30] [34] [36] [37] [55] [120] [121] [123] Because cartilage lacks blood vessels, these injuries do not cause hemorrhage, fibrin clot formation, or inflammation,

and the local response to injury depends entirely on chondrocytes. Undifferentiated mesenchymal cells cannot migrate from blood vessels to the site of injury, proliferate, differentiate, and synthesize a new matrix. Chondrocytes are tightly encased in the collagenproteoglycan matrix, and therefore they cannot migrate through the matrix to the site of injury. They do respond to tissue injury by proliferating and increasing the synthesis of matrix macromolecules near the injury site[30] [34] [36] [37] [120] [121] [123] ; however, the newly synthesized matrix and the proliferating cells do not fill the tissue defect, and soon after injury, the increased proliferative and synthetic activity ceases. When cartilage injury is associated with damage to the synovial membrane, blood may fill the joint. Even when this happens, fibrin clots do not form in the cartilage injury, and cells from the synovium and blood vessels do not migrate into the cartilage defect. The failure of clot formation and of cell migration and adhesion may be due to proteoglycans, specifically dermatan sulfate proteoglycans, which inhibit cell adhesion to the cartilage matrix. Cartilage Lacerations

Both penetrating injuries of synovial joints and surgical instruments passed across an articular surface can cut or abrade articular cartilage without damaging subchondral bone. Because this type of injury has been studied more extensively than blunt trauma to cartilage, more is known about the response of the tissue in such injuries.[30] [34] [36] [120] [121] [123] Lacerations perpendicular to the articular surface kill chondrocytes at the site of injury and create matrix defects.[30] [34] [130] Because these lesions cannot cause hemorrhage or initiate an inflammatory response, and because fibrin clots rarely form on exposed damaged articular cartilage, platelets do not bind to the damaged cartilage, and a fibrin clot does not appear. Inflammatory cells, capillaries, and undifferentiated mesenchymal cells do not migrate to the site of injury. Chondrocytes near the site of injury proliferate and form clusters, or clones, and synthesize new matrix. They do not migrate to the site of the lesion, perhaps because the matrix restrains their movement or perhaps because of their limited ability to respond to injury. The new matrix they produce remains near the cells and therefore does not repair the damage. Shortly after the injury, these cells proliferate, and synthetic activities cease. Unlike similar osteoarthritic lesions, experimental lacerations of articular cartilage do not show evidence of progression. Superficial lacerations or abrasions of cartilage that are tangential or parallel to the articular surface also do not stimulate a successful repair response. Some cells next to the site of injury may die, whereas others show evidence of increased proliferation and matrix synthesis. A thin layer of new, acellular matrix may form over the surface. The available evidence shows that as in cartilage defects perpendicular to the surface, the remaining normal tissue does not deteriorate. Blunt Trauma That Disrupts

Cartilage Alone

During sports activities, impact loading, twisting, and direct blows to synovial joints

occur frequently. The resulting compression of an articular surface can rupture the cartilage matrix, producing chondral fissures, flaps, or fractures without bone injury. If the compressive force is sufficiently high, the uncalcified cartilage may shear off the calcified cartilage.[7] The mechanisms of these injuries

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have not been studied extensively, but the available evidence shows that impact loading of the articular surface can rupture the matrix.[170] Disruption of normal articular cartilage via a single impact requires substantial force. A study[170] of the response of human articular cartilage to blunt trauma showed that articular cartilage could withstand impact loads of up to 25 newtons per square millimeter (25 MPa) without apparent damage. Impact loads exceeding this level caused chondrocyte death and cartilage fissures. The authors suggested that a stress level that could cause acute cartilage disruption required a force greater than that necessary to fracture the femur. Another study [81] measured the pressure on human patellofemoral articular cartilage during impact loading and found that impact loads less than those necessary to fracture bone caused stresses greater than 25 MPa in some regions of the articular surface. With the knee flexed 90 degrees, 50% of the load necessary to cause a bone fracture produced joint pressures greater than 25 MPa for nearly 20% of the patellofemoral joint. At 70% of the bone fracture load, nearly 35% of the contact area of the patellofemoral joint pressures exceeded 25 MPa; at 100% of the bone fracture load, 60% of the patellofemoral joint pressures exceeded 25 MPa. These results suggest that impact loads can disrupt cartilage without fracturing bone. Other experimental investigations show that repetitive impact loads can split the articular cartilage matrix and can initiate progressive cartilage degeneration.[51] [202] Cyclic loading of human cartilage samples in vitro caused surface fibrillation,[202] and periodic impact loading of bovine metacarpal phalangeal joints in vitro combined with joint motion caused rapid degeneration of articular cartilage.[166] Repeated overuse of rabbit joints in vivo combined with peak overloading caused articular cartilage damage, including formation of chondrocyte clusters, fibrillation of the matrix, thickening of subchondral bone, and penetration of subchondral capillaries into the calcified zone of the articular cartilage.[51] [167] The extent of cartilage damage appeared to increase with longer periods of repetitive overloading, and deterioration of the cartilage continued following cessation of excessive loading. An investigation of the effects of repetitive loading of cartilage plugs also showed that repetitive loading disrupts the tissue and that the severity of the damage increases as the load and the number of loading cycles increase.[210] Two hundred and fifty cycles of a compression load of 1000 pounds per square inch caused surface abrasions. Five hundred cycles produced primary fissures penetrating to calcified cartilage, and 1000 cycles produced secondary fissures extending from the primary fissures. After 8000 cycles, the fissures coalesced and undermined the cartilage fragments. Higher loads caused similar changes with fewer cycles. The experiments suggested that repetitive loading can cause propagation of vertical cartilage fissures from the joint surface to

calcified cartilage and extension of oblique fissures into areas of intact cartilage, extending the damage and creating cartilage flaps and free fragments. Clinical studies have identified articular cartilage fissures, flaps, and free fragments similar to those produced experimentally by single and repetitive impact loads.[23] [96] [100] [128] In at least some patients, acute impact loading of the articular surface or twisting movements of the joint apparently caused these injuries. In other patients, cartilage damage may have resulted from repetitive loading. Frequently, other joint injuries, including rupture of the anterior cruciate ligament and meniscal tears, occur in association with cartilage damage. Taken together, the clinical and the experimental studies suggest that closed injuries to synovial joints, including direct blows and loading combined with torsion, can split articular cartilage matrix without causing bone fractures. These injuries disrupt the cartilage matrix macromolecular framework and kill chondrocytes near the injury. Because chondrocytes cannot repair these matrix injuries, either the fissures remain unchanged or they progress. The experimental studies suggest that excessive repetitive loading weakens the cartilage macromolecular framework before visible matrix disruption occurs. Presumably, the chondrocytes could repair at least some of this molecular damage before cartilage fissures developed if the tissue were protected from further injury. Osteochondral Fractures and Osteochondral Defects

Sports injuries can cause fractures that extend through cartilage into the subchondral bone. Severe osteochondral fractures may result in loss of part of the articular surface. Unlike injuries limited to cartilage, fractures that extend into subchondral bone cause pain, hemorrhage, and fibrin clot formation and activate the inflammatory response ( see Table 2A-1 ).[16] [30] [33] [34] [37] [41] [43] [49] [53] [69] [120] [121] [123] [131] [135] Because undifferentiated mesenchymal cells migrate into the region of the fibrin clot, proliferate, and synthesize a new matrix, most osteochondral defects fill with new cells and matrix. Soon after an osteochondral injury, blood escaping from the blood vessels in damaged bone forms a hematoma that temporarily fills the injury site. Fibrin forms within the hematoma, and platelets bind to fibrillar collagen and establish hemostasis. A continuous fibrin clot fills the bone defect and extends for a variable distance into the cartilage defect. Platelets within the clot release potent vasoactive mediators (including serotonin, histamine, and thromboxane A2 ) and growth factors or cytokines (small proteins that influence multiple cell functions including migration, proliferation, differentiation, and matrix synthesis), including transforming growth factor-beta and platelet-derived growth factor.[36] Bone matrix also contains growth factors, including transforming growth factor-beta, bone morphogenic protein, platelet-derived growth factor, insulin-like growth factor I, insulin-like growth factor II, and possibly others. Release of these growth factors may play an important role in the repair of osteochondral defects. In particular, they probably stimulate vascular invasion and migration of undifferentiated cells into the clot and influence the proliferative and synthetic activities of the cells.

Shortly after entering the tissue defect, the undifferentiated mesenchymal cells proliferate and synthesize a new matrix. Within 2 weeks of injury, some of the mesenchymal cells assume the rounded form of chondrocytes and begin to synthesize a matrix that contains type II collagen and a relatively high concentration of proteoglycans.[30] [34] [36] [37] These cells produce regions of hyaline-like cartilage in the chondral and bone portions of the defect. In many

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osteochondral defects, the regions of hyaline-like cartilage first appear next to the exposed bone matrix, leaving the central region of the defect filled with more fibrous tissue.[33] Six to eight weeks following injury, the repair tissue within the chondral region of most defects contains many chondrocyte-like cells in a matrix consisting of type II collagen, proteoglycans, some type I collagen, and noncollagenous proteins.[33] Unlike the cells in the chondral portion of the defect, the repair cells in the bone portion of the defect produce immature bone, fibrous tissue, and hyaline-like cartilage.[30] [33] [37] They soon restore the original level of subchondral bone. Capillaries that approached or entered the chondral portion of the defect recede. Six months after injury, the mesenchymal cells have repaired the bone defect with a tissue consisting primarily of bone but also containing some regions of fibrous tissue, small blood vessels, and hyaline cartilage.[33] In contrast, the chondral portions of large osteochondral defects rarely fill completely with repair tissue.[30] [33] [37] In animal experiments, repair tissue filled about two thirds of the total volume of the chondral portion of large osteochondral defects and more than 95% of the total volume of the bone portion of the defects, [34] [36] and the tissue in the chondral portion of the defect differed significantly in composition from that in the bone portion of the same defect.[33] The chondral repair tissue did not contain bone or blood vessels and had a significantly higher proportion of hyaline-like cartilage. In most regions of the chondral defects, it had a composition and a structure intermediate between hyaline cartilage and fibrocartilage, and it rarely replicated the elaborate structure of normal articular cartilage. The differences in the differentiation of the repair tissue in the chondral and the bony parts of the same defect show that the environment in the two regions causes the same repair cells to produce different types of tissue. It is not clear whether the important differences in environment are mechanical, biologic, electrical, or caused by unknown factors. Occasionally, the cartilage repair tissue persists unchanged or progressively remodels to form a functional joint surface, but in most large osteochondral injuries, the chondral repair tissue begins to show evidence of depletion of matrix proteoglycans, fragmentation, and fibrillation; increasing collagen content; and loss of cells with the appearance of chondrocytes within 1 year or less.[30] [34] [36] [37] [69] [135] The remaining cells often assume the appearance of fibroblasts as the surrounding matrix comes to consist primarily of densely packed collagen fibrils. This fibrous tissue usually fragments and

often disintegrates, leaving areas of exposed bone.[30] [34] [37] [135] The inferior mechanical properties of cartilage repair tissue may be responsible for its frequent deterioration.[37] Several experimental studies show that even repair tissue that successfully fills osteochondral defects lacks the stiffness of normal articular cartilage. [12] [48] [203] Cartilage repair tissue formed in rabbit metatarsophalangeal joint arthroplasty sites deformed more easily and took longer to recover from deformation than did normal articular cartilage.[48] Repair cartilage formed in pig joints swelled in Ringer's solution more than normal cartilage and had greater permeability and less stiffness on compression.[203] Detailed study of chondral repair cartilage in primate osteochondral defects also showed that the repair tissue was more permeable and less stiff on compression than normal articular cartilage.[12] [13] [14] Differences in matrix composition and organization may explain the differences between the mechanical properties of repair cartilage and the mechanical properties of normal cartilage.[37] The increased swelling of repair cartilage indicates a lack of organization or a weakness of the collagen fibril meshwork. Microscopic studies of repair cartilage support this suggestion. They show that the orientation of the collagen fibrils in even the most hyaline-like cartilage repair tissue does not follow the pattern seen in normal articular cartilage. [33] In addition, the repair tissue cells may fail to establish the normal relationships between matrix macromolecules (in particular, the relationship between cartilage proteoglycans and the collagen fibril network). This may occur because of lack of organization of the macromolecules, insufficient concentrations of some macromolecules, or the presence of molecules that interfere with the assembly of a normal cartilage matrix. For example, the presence of type I collagen or high concentrations of dermatan sulfate proteoglycans might interfere with the establishment of normal collagen proteoglycan relation ships. The decreased stiffness and the increased permeability of repair cartilage matrix subjects the macromolecular framework to increased strain fields during joint use, resulting in progressive structural damage to the matrix collagen and proteoglycans.[37] Mechanical failure of the matrix may expose the repair chondrocytes to excessive loads, further compromising their ability to restore the matrix. Thus, cartilage repair tissue may initially have a composition and a structure that closely resemble normal articular cartilage, but defects in organization of the matrix macromolecular framework could compromise the function and the durability of the repair tissue. Clinical experience and experimental studies suggest that the success of chondral repair in osteochondral injuries may depend to some extent on the severity of the injury, as measured by the volume of tissue or surface area of cartilage injured, the stability of the injury site, and the age of the individual. [36] Experimental studies suggest that smaller osteochondral defects heal more predictably and more successfully than larger defects.[33] [34] [36] [49] [179] A study of intra-articular fractures of the distal femur in rabbits showed that anatomically reduced cartilage fractures that were stabilized by compression fixation healed with apparently normal articular cartilage. [136] Inadequately and adequately reduced fractures that were not stabilized by compression fixation healed with fibrocartilage.

The age of the individual may also influence the success of osteochondral repair. Potential age-related differences in repair have not been thoroughly investigated, [37] but bone heals more rapidly in children than in adults, and the articular cartilage chondrocytes in skeletally immature animals show a better proliferative response to injury and synthesize larger proteoglycan molecules than do those from mature animals.[26] [29] [31] [195]

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Surgical Treatment of Articular Cartilage Damage

Because localized cartilage disruption can compromise joint function and may lead to progressive cartilage deterioration,

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surgeons have sought methods of treating localized cartilage damage. Currently, shaving damaged cartilage and abrading exposed subchondral bone are the most common surgical treatments for damaged cartilage. Shaving Fibrillated Articular Cartilage

Many surgeons shave fibrillated cartilage to decrease joint symptoms and leave a smoother articular surface. Shaving degenerating articular surfaces can remove frayed and fibrillated superficial cartilage, but the efficacy of this procedure in decreasing pain, improving joint function, or stimulating restoration of a damaged articular surface has not been established.[32] [37] Several reports describe a decrease in symptoms following arthroscopic débridement of loose cartilage fragments and flaps, torn menisci, osteophytes, and proliferative synovium in osteoarthritic knee joints,[15] [187] but experimental and clinical studies have not shown that there is a clear benefit to shaving fibrillated cartilage. Shaving normal rabbit patellar cartilage did not stimulate significant repair but also did not cause progressive deterioration.[137] In one series of patients, shaving fibrillated patellar cartilage produced unpredictable results.[18] [19] [20] Only 25% of patients had satisfactory results, and the investigators concluded that the procedure is disappointing and ineffective.[18] [19] [20] Another group studied regions of human femoral articular cartilage after arthroscopic shaving for treatment of cartilage damage. They did not find evidence

of restoration of a smooth articular surface and suggested that shaving may have increased fibrillation and chondrocyte necrosis in and adjacent to the region of the original defect.[182] Despite these observations, removal of fragments of degenerating cartilage and joint irrigation may decrease symptoms of mechanical catching and pain in some patients. Experimental injection of cartilage fragments into rabbit knees produced inflammatory arthritis, which included joint effusions, increased levels of synovial enzymes, and articular cartilage friability, pitting, and discoloration. [64] This report suggests that cartilage fragments can contribute to synovitis. Presumably, débridement of fibrillated cartilage and the associated joint irrigation would temporarily decrease this synovial inflammation by removing cartilage particles, degradative enzymes, and inflammatory mediators. Abrasion of Subchondral Bone

Arthroscopic abrasion offers a potentially attractive treatment for articular surfaces that have small regions of full-thickness cartilage loss. [32] The surgeon removes the most superficial layers of subchondral bone, usually 1 to 3 mm, to disrupt intraosseous vessels.[93] [94] [95] The resulting hemorrhagic exudate forms a fibrin clot, and undifferentiated cells invade the clot, forming repair tissue over the abraded bone. Protection of the joint from excessive loading allows the repair tissue to remodel and to form a new articular surface. Controlled trials of arthroscopic abrasive treatment of full-thickness cartilage loss have not been published, but several authors have reported that arthroscopic abrasion of the knee can decrease pain in 60% or more of patients.[68] [93] [94] [95] Abrasion of regions of exposed subchondral bone has resulted in formation of a fibrocartilaginous repair tissue that in at least some patients persists for years.[93] [94] [95] Examination of the repair tissue shows that like the repair tissue formed in the chondral regions of experimental osteochondral defects,[30] [33] [34] it has a fibrocartilaginous appearance and contains variable concentrations of type II collagen.[94] [95] No studies of the tissue formed following abrasion have shown regeneration of normal articular cartilage. Despite the ability of arthroscopic abrasion to stimulate formation of cartilage repair tissue and the encouraging reports of symptomatic improvement, it is difficult to assess the value of this procedure. The available evidence suggests that it can provide temporary symptomatic improvement in selected patients.[32] [37]

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Cartilage Grafts

Because of the inferior mechanical properties of most cartilage repair tissue that forms following osteochondral injury or surgical treatment of cartilage defects, investigators and surgeons have explored the use of a variety of cartilage grafts, including osteochondral autografts and allografts and periosteal and perichondrial grafts, to replace regions of damaged or lost articular surface. More recently, several groups of investigators have developed methods of isolating chondrocytes or undifferentiated mesenchymal cells, growing them in culture and then implanting them in a gel or other artificial matrix to replace articular cartilage. Cartilage Autografts

Lack of donor sites limits the use of cartilage autografts. Animal experiments show that articular cartilage autografts transplanted with a thin shell of bone heal to the recipient site tissue.[42] [54] [112] [162] [165] The chondrocytes in most adequately stabilized autografts remain viable, and the matrix remains intact for 1 year or more. Because of the limited sources of cartilage for grafting, surgeons rarely use cartilage autografts in humans. Sources of possible cartilage autografts include the proximal tibiofibular joint, the sternum, and the patella. Animal experiments show that sternal osteochondral autografts can replace segments of articular cartilage, [193] and surgeons have used osteochondral patellar grafts to replace severely damaged portions of the tibial articular surface in humans.[204] Radiographs show that the bone of the graft heals with the recipient site bone, and clinical evaluation shows that grafts can provide satisfactory joint function without knee effusions or evidence of degeneration for 18 years or more. Periosteal and Perichondrial Autografts

Periosteum and perichondrium provide other sources of tissue for repair of articular cartilage defects. Cells from

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both tissues can synthesize the necessary matrix macromolecules to form hyaline cartilage and to survive transplantation without a vascular pedicle.[4] [5] [40] [47] [60] [155] [156] [175] [176] [209] In experimental and clinical studies, most grafts have been harvested from the recipient, but allografts also can restore a joint surface.[139] Experimental work shows that periosteal grafts will fill large defects in rabbit articular surfaces with hyaline-like cartilage and that this tissue remains intact for as long as 1 year after transplantation.[155] [156] [157] [159] [175] [176] Perichondrial grafts have produced similar results in rabbits and dogs.[4] [5] [60] [61] [62] [63] [104] [105] [186] [206] The graft cells produce a matrix that contains type II collagen,[4] [104] [156] and the concentration of type II collagen may increase with time.[5] The mechanical properties of these grafts have not been thoroughly examined, but one study showed that the viscoelastic properties of perichondrial grafts improved following surgery and approached the properties of normal cartilage 26 weeks after surgery.[206] These observations suggest that the grafts remodel so that their composition and mechanical properties more closely resemble those of articular cartilage. Although these experimental studies show that periosteal and perichondrial cells can survive transplantation and form a new articular surface, the results vary among animals and possibly among regions of the joints. An investigation of rabbit perichondrial grafts found that 50% produced unacceptable results owing to fractures, failures of graft attachment, or infection.[4] A subsequent examination of rabbit perichondrial grafts showed that 38% of the grafts produced unacceptable results.[5] A study of periosteal grafts in rabbits showed that these grafts frequently succeeded in rabbit femoral condyles and patellar grooves but usually failed in the patella. [158] Despite the evidence that the composition and the mechanical properties of grafts can improve after transplantation,[5] [206] other studies show that at least some of the grafts deteriorate. In one set of experiments, dog perichondrial grafts had formed new cartilage with smooth articular surfaces by 2 to 8 months after surgery; by 12 to 17 months, however, the grafts had degenerated, leaving exposed bone in some regions and fragments of graft tissue in others.[61] [62] A study of periosteal grafts in sheep also found that the grafts deteriorated with use of the joint. One year following placement of periosteal grafts, moderately well-differentiated fibrocartilage covered the previously exposed bone, but 2 years after transplantation, the graft tissue had degenerated. The age of the graft may influence the results. Periosteum and perichondrium become thinner and less cellular with age, and the potential of the cells to proliferate and to synthesize new matrix decreases.[36] The possible differences in results with grafts of different ages have not been thoroughly studied experimentally, but cryopreserved periosteal allografts from young rabbits produced better results than grafts from older animals.[139] Early motion of the joint following grafting may influence the results. Although it is not

clear how motion affects cell function in cartilage repair tissue, motion stimulates fibrocartilage formation following joint resection,[138] and treatment with passive motion may promote cartilage formation by periosteal grafts. [52] [155] [156] [157] [159] [209] Grafts placed in immobilized joints also form cartilage, but they form less than grafts treated with passive motion.[52] Despite these encouraging results, the long-term benefits of passive motion treatment remain uncertain.[36] One group of investigators found that the apparent beneficial effect of early motion treatment of rabbit perichondrial grafts did not persist.[104] [108] [206] Passive joint movement appeared to improve the quality of the grafts initially, but 1 year after transplantation, there were no apparent benefits. Thus, it appears that passive joint motion soon after graft transplantation may affect the initial behavior of the graft cells, but the mechanism of the effect, the optimal timing and the duration of motion, and the long-term benefits have not yet been established. In addition to these experimental studies, surgeons have replaced damaged or lost articular cartilage in human osteoarthritic and rheumatoid joints with perichondrial grafts. After removing degenerated or damaged cartilage, the surgeon places a rib perichondrial autograft in the defect.[63] [87] [163] [186] [207] Most reports of this procedure have described results for joints of the upper extremity. Some patients have experienced improved range of motion and decreased pain, but the results have not been predictable.[63] One clinical series showed that the results of rib perichondrial allograft arthroplasty in metacarpophalangeal and proximal interphalangeal joints depended to a large extent on the age of the patient.[184] One hundred percent of patients in their 20s had good results with metacarpophalangeal joint arthroplasty. Only 75% of the patients in their 30s treated with similar procedures had good results. Seventyfive percent of patients in their teens had good results with proximal interphalangeal joint arthroplasty, compared with 66% of patients in their 20s and none of the patients older than 40 years of age. These results agree with the concept that the ability of perichondrium or periosteum to produce new cells and matrix declines with age and that the best clinical results with these procedures may be expected in skeletally immature patients or those who have recently reached skeletal maturity. Cartilage Allografts

Cartilage allografts have the advantage of providing osteochondral segments of any size or shape without donor site morbidity. Surgeons have used allografts to replace segments of articular surfaces, entire articular surfaces, and entire synovial joints. Biopsies of the allograft cartilage show that many chondrocytes remain viable years after transplantation.[50] Large grafts have been used for joint reconstruction following tumor resection or major trauma.[70] [124] Smaller grafts, usually consisting of articular cartilage and a thin shell of subchondral bone, have been used to replace damaged regions of articular cartilage in young, physically active patients. Generally, the larger grafts have caused more frequent and more severe surgical and postoperative complications, including infection and mechanical failure.[118] [124] [134] Fresh and cryopreserved grafts have been used experimentally and clinically. Fresh grafts presumably have the advantage of maintaining the maximum viability of the

chondrocytes[50] ; a study of osteochondral allografts from

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large dogs showed that fresh grafts produced better results than frozen grafts. [190] Use of preserved grafts makes it possible to accumulate a bank of grafts of different sizes and shapes, and freezing has the advantage of decreasing graft immunogenicity. [67] [190] Recent studies report that cryopreservation and storage for up to 28 days do not alter the mechanical properties or the structure of cartilage.[101] [107] Chondrocytes can survive freezing and thawing, [180] [196] but in one study, only a few chondrocytes survived freezing. Frozen grafts had more evidence of structural deterioration and lower concentrations of glycosaminoglycans than did fresh grafts.[190] Cartilage allografts can survive transplantation and heal to the recipient-site tissue.[80] [162] A study of articular allografts used to replace the tibial articular surface in skeletally mature rabbits showed that articular cartilage, growth plate, and cultured chondrocyte allografts resulted in significantly better repair than did the natural repair response. [11] The authors concluded that correctly positioned and secured cartilage allografts could repair limited articular defects in mature rabbits. Other studies have shown that at least some allograft cartilage degenerates when subjected to loading,[42] [178] [190] and one recent study of dog osteochondral allografts showed that allograft cartilage became thin, dull, and roughened.[190] The host response to osteochondral allografts may depend to some extent on the size of the graft (including the amount of bone transplanted with the cartilage), freezing of the graft, and antigen matching. Small cartilage allografts do not cause an apparent inflammatory reaction,[80] [162] but large osteochondral allografts can cause synovial inflammation.[189] [190] To some extent, this difference may depend on the amount of bone in the graft. Large antigen-mismatched osteochondral allografts stimulate systemic humoral, cell-mediated, and antibody-dependent cell-mediated and local immune responses,[189] [190] but even large antigen-matched osteochondral grafts can cause synovitis.[190] A study of large osteochondral allografts in dogs suggests that host immune responses adversely affect cartilage grafts.[190] The authors compared the results of leukocyte antigenmismatched frozen allografts, leukocyte antigenmismatched fresh allografts, leukocyte antigenmatched fresh allografts, and leukocyte antigenmatched frozen allografts. Leukocyte antigenmismatched fresh allografts stimulated the most severe inflammatory response. Invasive pannus appeared more frequently in joints with fresh grafts, especially those joints with leukocyte antigenmismatched grafts. In some of these joints, the pannus eroded the cartilage to the subchondral bone. Antigen mismatching increased cartilage deterioration and exacerbated the damage due to freezing. Fresh antigen-matched grafts produced results similar to those seen with autogenous grafts. The results of this study showed that at least for large segmental osteochondral allografts, fresh tissue-matched grafts produced the best results.

Clinical studies show that fresh osteochondral allografts can replace localized regions of damaged articular cartilage in humans.[116] [133] [134] Fresh osteochondral grafts used to replace portions of damaged tibial plateaus decreased pain and improved function in 10 of 12 patients followed for more than 2 years.[116] Evaluation of 40 knees 2 to 10 years after transplantation of fresh osteochondral allografts for localized degeneration of the articular surface showed that 31 of the grafts had healed and 9 had failed. [134] Of the 31 successful transplants, 13 had an excellent result, 14 had a good result, and 4 had a fair result. The authors recommended use of fresh osteochondral shell allografts for treatment of post-traumatic degenerative arthritis of the patella, for post-traumatic arthritis and traumatic defects of the tibial plateau, and for traumatic defects, osteochondritis dissecans, and avascular necrosis of the femoral condyle. They advised against use of grafts for unicompartmental degenerative arthritis of the knee involving both the femur and the tibia. Only 3 of 10 of these procedures succeeded. These studies suggest that fresh allografts can provide at least temporary improvement for selected patients with disabling symptoms due to isolated regions of degenerated or damaged cartilage. Chondrocyte and Artificial Matrix Grafts

Use of synthetic matrix grafts, with or without cells and growth factors that stimulate cartilage formation, is another method of replacing regions of damaged or lost articular cartilage.[21] [22] [30] [34] [37] [45] [72] [73] [75] [89] [90] [200] [201] The creation of synthetic matrices that vary in size and shape makes it possible to fill any chondral defect precisely. A synthetic matrix provides a framework for cell migration and attachment and may give the cells some protection from excessive loading. The cells included in these grafts may be autografts or allografts. Chondrocytes or mesenchymal cells harvested from the intended recipient or from another individual can be grown and maintained in culture and then reimplanted. Most synthetic matrices used to replace articular cartilage and to implant growth factors or cells consist of reconstituted collagen, but one group of investigators has reported improved cartilage repair with carbon fiber pads.[149] The matrix composition and organization can influence cell migration, proliferation, and differentiation.[102] [119] For example, an in vitro study showed that a collagenous matrix promoted formation of cartilage by mesenchymal cells.[119] Several experimental studies have shown the feasibility of implanting chondrocytes or mesenchymal cells in cartilage defects.[34] [37] The implanted cells survive and synthesize a collagenous matrix that often resembles that of normal articular cartilage.[89] [90] [200] [201] This tissue appears to resemble hyaline cartilage more closely than the tissue that forms in defects not treated with chondrocyte artificial matrix and synthetic matrix transplants. In one series of experiments, the investigators created 4-mm (in diameter) osteochondral defects in rabbit articular surfaces and then placed collagen gels containing allograft chondrocytes in the defects.[200] [201] Eighty percent of the treated defects showed successful healing 24 weeks later. Other groups have also reported improved cartilage healing using similar methods.[72] [73] [89] [90] Thus far, investigators have not identified the optimal type of synthetic matrix, defined

the benefits of implanting various cell types and growth factors, or shown that implantation

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of synthetic matrices containing chondrocytes or undifferentiated mesenchymal cells or growth factors can predictably restore a durable articular surface in large cartilage defects. Yet these studies show that this approach has the potential to improve repair of limited osteochondral defects.

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Conclusions

The specialized composition and organization of articular cartilage provide its unique biomechanical properties, which make possible normal synovial joint function. Blunt trauma, high-energy joint loading, and forceful joint loading and twisting can damage cartilage without causing visible disruption of the matrix, can fracture cartilage without damaging the subchondral bone, or can fracture both cartilage and subchondral bone. Injuries that alter the biomechanical properties of cartilage compromise the smooth pain-free joint motion necessary for participation in sports and may lead to progressive deterioration of the articular surface. Damage to cartilage that does not cause visible matrix disruption has been studied in animals, but this type of injury is difficult to detect in humans. Improved imaging methods or devices that measure in vivo cartilage mechanical properties may solve this problem. Currently, the natural history of these injuries remains unknown, but the experimental evidence shows that if the basic structure of matrix remains intact and the cartilage is spared further injury, the chondrocytes can repair damage. Chondrocytes do not heal injuries that disrupt cartilage, but injuries that disrupt cartilage and bone stimulate an inflammatory response and migration of undifferentiated cells into the injury site. These cells proliferate, differentiate into chondrocyte-like cells, and synthesize a new matrix, but the tissue they produce usually fails to restore the normal volume of articular cartilage, and the repair tissue lacks the biomechanical properties of articular cartilage. Because cartilage has a limited capacity for restoring normal tissue after significant injury, surgeons and other investigators have sought reliable methods of repairing or replacing damaged articular surfaces. Many diverse approaches have been taken with varying success both in animal studies and in limited clinical use. Thus far, all these approaches have important limitations, but the knowledge gained from these studies provides a basis for developing better methods of treating injuries of articular cartilage and preventing progression of cartilage damage.

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Guilak F, Meyer BC, Ratcliffe A, Mow VC: The effect of static loading on proteoglycan biosynthesis and turnover in articular cartilage explants [abstract]. Trans Orthop Res Soc 16:50, 1991. 76.

Guilak F, Ratcliffe A, Hunziker EB, Mow VC: Finite element modeling of articular cartilage chondrocytes under physiological loading [abstract]. Trans Orthop Res Soc 16:366, 1991. 77.

Hardingham TE, Muir H, Kwan MK, et al: Viscoelastic properties of proteoglycan solutions with varying proportions present as aggregates. J Orthop Res 5:36-46, 1987. 78.

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Moran ME, Kreder HJ, Salter RB, Keeley FW: Biological resurfacing of major full thickness defects in joint surfaces by neochondrogenesis with cryopreserved allogenic periosteum stimulated by continuous passive motion [abstract]. Trans Orthop Res Soc 14:542, 1989. 139.

Mow VC, Holmes MH, Lai WM: Fluid transport and mechanical properties of articular cartilage. J Biomech 17:377-394, 1984. 140.

Mow VC, Mak AF, Lai WM, et al: Viscoelastic properties of proteoglycan subunits and aggregates in varying solution concentrations. J Biomech 17:325-338, 1984. 141.

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Mow VC, Kwan MK, Lai WM, Holmes MH: A finite deformation theory for nonlinearly permeable soft hydrated biological tissues. In Woo SL, Schmid-Schonbein G, Zweifach B (eds): Frontiers in Biomechanics. New York, Springer-Verlag, 1986, pp 153-179. 143.

Mow VC, Rosenwasser MP: Articular cartilage: Biomechanics. In Woo SL, Buckwalter JA (eds): Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1988, pp 427-464. 144.

Mow VC, Proctor CS, Kelly MA: Biomechanics of articular cartilage. In Nordin M, Frankel VH (eds): Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989, pp 31-57. 145.

Mow VC, Fithian DC, Kelly MA: Fundamentals of articular cartilage and meniscus biomechanics. In Ewing JW (ed): Articular Cartilage and Knee Joint Function. New York, Raven Press, 1989, pp 1-18. 146.

Mow VC, Zhu W, Lai WM, et al: The influence of link protein stabilization on the viscometric properties of proteoglycan aggregate solutions. Biochim Biophys Acta 112:201-208, 1989. 147.

Mow VC, Setton LA, Ratcliff A, et al: Structure-function relationships of articular cartilage and the effects of joint instability and trauma on cartilage. In Brandt KD (ed): Cartilage Changes in Osteoarthritis. Indianapolis, University of Indiana Press, 1990, pp 22-42. 148.

Muckle DS, Minns RJ: Biological response to woven carbon fiber pads in the knee: A clinical and experimental study. J Bone Joint Surg Br 72:60-62, 1990. 149.

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Section B Meniscus Joseph A. Buckwalter MD Van C. Mow PhD As recently as the 1970s, some surgeons assumed that knee menisci were vestigial structures that had little effect on joint function, and they treated small meniscal tears with total meniscectomy. Since then, understanding of meniscal function and common treatments of meniscal injuries have changed considerably. Advances in our understanding of meniscal function have been derived from comparisons of meniscal structure and function among species; investigations of the relationships between the biomechanical function and the composition and organization of menisci; and studies showing that total meniscectomy adversely affects joint function and increases the probability of joint degeneration. Appreciation of the adverse effects of loss of menisci on joint function has encouraged surgeons and other investigators to seek methods of promoting meniscal healing and replacing menisci. The study of menisci in other species illustrates their importance in the specialized synovial joints. They exist in many animals other than humans. [6] [61] Monkeys, some types of bats, and amphibians such as crocodiles and bullfrogs have menisci, although in the latter two, the menisci are discoid. In birds and chickens, the menisci are C-shaped, similar to the knee joints of humans and the larger bovine species. Bovine knee menisci are closer to discoid in shape than are menisci of human knees, which are often described as semilunar.[6] [55] [56] [90] There is also a disk-shaped fibrocartilaginous disk in the temporomandibular joint of humans and rodents, and a meniscus is present in the ankle joint of kangaroos, which is subjected to large forces when the animal jumps.[26] [61] (The temporomandibular joint disk is very similar to knee meniscus in terms of composition and structure.) From these and other comparative anatomic studies, investigators have recognized that a firm intra-articular fibrocartilaginous structure with great tensile strength is necessary in joints in which rotation and translation occur (because these joints require excellent lubrication and probably additional mechanical

stability) as well as in joints across which high forces are transmitted. [44] [61] [84] [98] Recent investigations using microscopy, biochemistry, and bioengineering have significantly advanced the understanding of the relationships between meniscal function

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and meniscal composition and organization. Like articular cartilage, knee meniscal tissue performs important mechanical functions,[6] [16] [17] [19] including load bearing,* shock absorption,[57] [90] [106] joint stabilization,[50] [57] [60] [96] [108] and possibly joint lubrication.[27] [61] [75] [78] [90] These functions depend on a highly organized extracellular matrix consisting of fluid and a macromolecular framework formed of collagen (types I, II, III, V, and VI), proteoglycans, elastin, and noncollagenous proteins. Unlike articular cartilage, some regions of meniscus have a blood supply (the peripheral 25% to 30% of the lateral meniscus and the peripheral 30% of the medial meniscus[6] [10] [11] [24] [55] [66] ) and a nerve supply (the peripheral regions of the meniscus, especially the meniscal horns [6] [83] [114] [118] ). Because loss of menisci alters the loading of articular cartilage in ways that may increase the probability and the severity of degenerative joint disease, (Figure Not Available) surgeons and investigators have studied the response of menisci to injury and have sought methods of preserving, repairing, and replacing menisci.[31] [41] [42] [43] [77] [89] [103] [104] Experimental and clinical studies show that tears through the vascular regions of the meniscus can heal, but tears through the avascular regions do not undergo a repair process that can heal a significant tissue defect.[6] [8] [11] [55] A number of reports suggest that methods of stimulating healing of tears in avascular meniscal tissue and of replacing meniscal tissue exist and may help to maintain or restore meniscal function.[6] [7] [8] [9] [12] [49] [74] [103] [104] [109] [110] [111]

This chapter first summarizes the current understanding of meniscal composition, structure, mechanical properties, blood supply, and nerve supply. Subsequent sections review the response of menisci to injury and methods of stimulating meniscal healing. The final section discusses meniscal grafts. Composition

Like bone, cartilage, and ligament, meniscus consists of scattered cells surrounded by an abundant extracellular matrix.[6] [17] [19] [41] [66] [74] [92] Continued structural integrity and function of the tissue depend on interactions between the cells and their surrounding matrix. The material properties of the tissue result from the composition and the organization of the matrix macromolecules and the interactions between these solid components of the matrix and the tissue fluid. Cells

Based on morphologic characteristics, there are two major types of meniscal cells.[40] [66]

Near the surface, the cells have flattened ellipsoid or fusiform shapes; in the deep zone, the cells are spherical or polygonal. These differences in cell shape and size between the superficial and the deep regions of the tissue resemble the changes in cell morphology seen between the superficial and the deep regions of articular cartilage. Like the cells from the superficial and the deep zones of articular cartilage, the superficial and the deep meniscal cells appear to have different synthetic functions or perhaps different responses to loading.[109] Within the meniscus, these cells produce and maintain the macromolecular framework of the tissue. They contain the synthetic organelles, the endoplasmic reticulum, and the Golgi membranes, which are necessary to accomplish their primary function of synthesizing matrix macromolecules. In addition, like most other mesenchymal cells, they lack cell-to-cell contacts.[6] [17] Because most of them lie at a distance from blood vessels, they rely on diffusion through the matrix for transport of nutrients and metabolites. The membranes of meniscal cells attach to matrix macromolecules via adhesion proteins (fibronectin, thrombospondin, type VI collagen[39] [65] [66] [87] ), and the matrix, particularly the pericellular region, protects the cells from damage due to physiologic loading of the tissue.[46] [47] Deformation of the macromolecular framework of the matrix causes fluid flow through the matrix[35] [75] [80] [90] and influences meniscal cell function.[46] [47] In all these features, the meniscal cells resemble articular cartilage, chondrocytes. Because meniscal tissue is much more fibrous than hyaline cartilage, however, some authors have proposed that meniscal cells be called fibrochondrocytes.[66] [110] Extracellular Matrix

Water

Water contributes 65% to 75% of the total weight of meniscus.[3] [35] [88] [90] Table 2B-1 (Table Not Available) summarizes the water, sulfated glycosaminoglycan, and hydroxyproline content of meniscus.[35] Although some portion of the water may reside within the intrafibrillar space of the collagen fibers,[51] [64] [105] most of the water is retained within the tissue in the solvent domains of the proteoglycans by means of both their strong hydrophilic tendencies and Donnan osmotic pressure exerted by the counter-ions associated with the negative charge groups on the proteoglycans. [28] [52] [59] [63] [76] [90] Because the pore size of the tissue is extremely small ( .91

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Chapter 6 - Surgical Principles Section A Suture Materials Alberto G. Schneeberger MD Christian Gerber MD Essentially no orthopaedic procedure is carried out without the use of sutures. The selection of the type and the size of the suture material is, however, often related to what a surgeon has learned empirically during training rather than to logical conclusions based on material properties and imposed demands. The role of the type and the size of suture material and the surgical suturing technique in the development of fixation failure is not well established. The technique of tying knots is not given particular attention because most knots are thought to be safe for tissues that are not under tension. It is established, however, that the success of orthopaedic operations (e.g., tendon or ligament repairs) depends on the type of suture material used and the technique.[8] [23] [24] [25] [26] [28] [29] [42] Thus, a more precise analysis of the role of sutures and suturing techniques is needed to allow a more scientifically based selection of material and of suturing and knotting technique. Imposed Demands on Suture Materials

Different demands are imposed on suture materials. Their importance or priority may change with the specific application of the suture material considered. A variety of mechanical, biomechanical, and biologic properties should be considered when a specific suture material is selected. Such properties include the following:

1. Biologic characteristics a. Biocompatibility 2. Mechanical characteristics a. Ultimate tensile strength b. Elasticity and deformation under load (gap formation under tensile load) c. Adequate maintenance of mechanical properties during healing (absorbable sutures) d. Knotting properties (ease of knotting, loss of strength after tying knots, number of knots necessary for stability) 3. Handling characteristics a. Ease in practical use This chapter summarizes the current knowledge about suture materials and compares potential advantages and disadvantages of sutures used in daily practice. Table 6A-1 , a compilation of the most important data from the literature and from our own studies, is intended to be an easily accessible reference for the rational selection of the optimal suture for a specific application.

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Biologic Characteristics and Biocompatibility

A number of studies have assessed the compatibility of different suture materials, either by means of semiquantitative analysis of the histologic foreign body reaction to the implanted material or by means of experimental or clinical testing of the healing properties of the sutured tissues.[2] [3] [17] [19] [22] [28] [32] [33] [34] [35] [36] [40] [47] Biocompatibility depends on the type of suture material, its structure (braided versus monofilament), the amount of material implanted, and the site of implantation.[1] In general, the implantation of suture material causes an initial inflammatory reaction characterized by the presence of polymorphonuclear cells, lymphocytes, and monocytes. This acute inflammatory foreign body reaction peaks between days 2 and 7. By day 4, mononuclear cells start to predominate, and fibroblasts appear. By day 7, mature fibroblasts are present; the foreign material becomes encapsulated in a fibrous mantle by day 10.[1] At that point, no further tissue reaction is expected if the implanted material is nonabsorbable. Most currently used nonabsorbable materials are inert and are therefore extremely well tolerated. Absorbable materials elicit a second boost of inflammatory reaction at the time of their resorption. The intensity of this reaction depends on the specific chemical process that leads to resorption and on the amount of material to be resorbed. Suture materials such as polyglactin (Vicryl), polyglycolic acid (Dexon Plus), polyglyconate (Maxon), poliglecaprone 25 (Monocryl), polydioxanone (PDS), and poly(L-lactide/glycolide) (Panacryl) are absorbed by simple hydrolysis, whereas catgut requires enzymatic degradation, which tends to provoke a much more intense soft tissue reaction. Of the commonly used materials, monofilament stainless steel provokes the least amount of foreign body reaction in skin and other musculoskeletal tissues. Almost no foreign body reaction is seen after implantation of nylon, polypropylene (Prolene), polyester (Ethibond, Tevdek, Ti-Cron), polybutester (Novafil), or absorbable materials (Maxon and PDS). Polyglycolic acid (Dexon Plus) and polyglactin (Vicryl), which are dissolved via simple hydrolysis, also elicit a minimal foreign body response ( see Table 6A-1 ) but are probably tolerated somewhat less well than polydioxanone (PDS) and

polyglyconate (Maxon).[21] [32] [33] [35] The tissue response may be more pronounced if these materials are used in the skin. Catgut and, at the time of its resorption, chromic catgut cause a moderate-to-intense inflammatory

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Suture Materials

TABLE 6-A-1 -- Characteristics of Commonly Used Suture Materials* Maximum Elongation Knots Required Tensile Location of Tensile Under Strength Implant Strength 40-N Load After n Knotted (%) Weeks (N) (%/n)

Ethibond 5

131 ± 10[5]

Ethibond 3

106 ± 9

4.5 ± 0.3

Surgilon 3

88 ± 6

12.8 ± 0.5

Monofilament 134[39] steel 2 PDS II 2

109 ± 15

57%/2[5] ; 0%/4[5]

Horse, pony: subcutaneous fat[5]

1=1=1=1/2=1=1

14.7 ± 2.2 1=1/2=1/1=2 [39] 6.1 ± 0.6

123 ± 13[5] Vicryl 2

90 ± 7

7.5 ± 0.4

Tevdek II 2

84 ± 7

5.5 ± 0.4

Mersilene 2

83 ± 7; 71[39]

5.4 ± 0.5

Ethibond 2

82 ± 3

5.6 ± 0.4

Surgilon 2

82 ± 5

13.9 ± 0.5

Novafil 2

77 ± 14

20.9 ± 2.0

Dacron 2

73 ± 8

6.2 ± 0.5

Dermalon 2

69 ± 9;

12.3 ± 2.0

62 ± 4[46]

Horse, pony: subcutaneous fat[5]

1=1/2=1/1=2 [39]

Multifilament 102[39] steel 2 Dexon Plus 2 101 ± 7;

100%/4[5]

Ethilon 2

51 ± 8[5]

100%/4[5]

Horse, pony: subcutaneous fat[5]

80%/13[12]

Panacryl 2

60%/26[12] PDS II 1

85 ± 8

20.2 ± 2.5

1=1=1=1=1 [36]

Maxon 1

85 ± 19;

14.8 ± 3.0

2=1=1/(1=1=1); 2=2/2=1=1/1=1=1[4]

Dexon Plus 1 71 ± 7

8.5 ± 0.5

2=1=1=1[37]

Tevdek II 1

69 ± 5

5.9 ± 0.6

1=1=1=1/2=1=1

Ti-Cron 1

68 ± 4

9.3 ± 0.7

Vicryl 1

66 ± 6;

8.3 ± 1.0

2=1=1=1[37] ; 2=2/2=1=1/1=1=1[4] 1=1=1=1/2=1=1

82 ± 3[4] ; 77[43]

54 ± 3[4] Ethibond 1

65 ± 4

7.0 ± 0.5

Surgilon 1

65 ± 9

16.0 ± 1.3

Novafil 1

57 ± 8; 48[43]

25.7 ± 2.5

Prolene 1

55[43] ; 54 ± 4 [4]

Suturamid 1

52 ± 7

Dermalon 1

1=1=1=1[36] ; 2=2/2=1=1/1=1=1[4] 15.5 ± 1.5

[4]

1=1=1=1/2=1=1/2=2 [4]

46 ± 4 ; 43 ± 5[46]

Ethilon 1

47 ± 4; 40[43]

2=2=1/2=1=1=1/1=1=1=1 [4]

Monofilament 83[39] steel 0 Maxon 0

67 ± 15; 68[43]

Multifilament steel 0

65[39]

PDS II 0

59 ± 6

1=1/2=1/1=2 [39] 20.4 ± 3.8

50%/3[3]

Rabbit: subcutaneous fat[3]

50%/6[3] ; 50%/5[36] ; 0%/8[36]

Rabbit: under trapezius[36] ; fat[3]

1=1/2=1/1=2 [39] 26.7 ± 2.6

1=1=1=1[36]

Ethibond 0

54 ± 7

7.8 ± 0.7

Dexon Plus 0 53 ± 6

12.1 ± 2.7

Tevdek II 0

48 ± 3

8.3 ± 0.8

Ti-Cron 0

46 ± 5

11.5 ± 2.5

Surgilon 0

44 ± 3

25.5 ± 3.6

Prolene 0

42 ± 2; 36[39] [43]

32.6 ± 4.2

Novafil 0

41 ± 6; 33[43]

28.8 ± 1.9

Ethilon 0

41 ± 3; 29[43]

34.6 ± 4.7

Mersilene 0

39[39]

Dermalon 0

32 ± 5[46]

50%/2[3] [37]

Rabbit: under trapezius[3] ; fat[37]

14%/6[16]

Rat: subcutaneous fat[16]

14%/6[16]

Rat: subcutaneous fat[16]

60%/2[9] ; 2%/4[9]

Rat: subcutaneous fat[9]

1=1=1=1=1 [32] ; 2=1=1=1[37]

60%/2[9] ; 4%/4[9]

Rat: subcutaneous fat[9]

1=1=1=1[36]

74%/6[16]

Rat: subcutaneous fat[16]

1=1=1=1[36] ; 1=1=1/1=2[39]

1=1[20]

Monofilament steel 2-0 Maxon 2-0

1=1=1=1[32] ; 2=1=1=1[37]

43[43]

PDS 2-0

1=1=1=1[36]

Multifilament steel 2-0

1=1[20]

Dexon Plus 2-0

1=1=1=1[32] ; 2=1=1=1[37]

Dexon 2-0

Vicryl 2-0

Dermalon 2-0

28 ± 3[46]

Prolene 2-0

27[43]

Novafil 2-0

25[43]

Ethilon 2-0

20[43]

56%/6[16]

Monofilament 33[38] steel 3-0

1=1/2=1[22] [37] /1=2[38]

Maxon 3-0

31 ± 3[41] ; 32[43]

1=1=1[41]

PDS II 3-0

25 ± 1[41]

1=1=1[41]

Multifilament steel 3-0

24[38]

1=1[21] [22] [38] /2=1 [22] [38] /1=2 [38]

Dexon Plus 3-0

24 ± 2[41]

1=1=1[41] ; 1=1=1=1[32] ; 2=1=1=1 [37]

Vicryl 3-0

23 ± 2[41]

1=1=1[41] ; 1=1=1=1=1[32] ; 2=1=1=1[37]

Prolene 3-0

14[38] ; 17[43]

1=1=1/1=2 [22] [37] ; 1=1=1=1[36]

Mersilene 3-0

16[38]

1=1/1=2/2=1 [22]

Tevdek 3-0

1=1=1=1[22]

Dacron 3-0

1=1=1/1=2 [22] ; 1=1=1=1[20]

Dermalon 3-0

14 ± 1[46]

1=1=1=1/1=2 [22]

Ethilon 3-0

14[43]

1=1=1=1/1=2 [22]

Novafil 3-0

13[43]

Monocryl 3-0

23 ± 2[41]

1=1=1[41]

Monofilament 19 ± 2[40] steel 4-0

1=1[20] [40]

Maxon 4-0

Multifilament steel 4-0

1=1=1[40] 65.8 ± 16[40]

16 ± 4[40]

60-70%/1[12] ; 30-40%/2[12] ; 0%/3[12]

28.7 ± 20[40]

17 ± 2[40] ; 21[43]

PDS 4-0

Rat: subcutaneous fat[16]

1=1[40]

50%/3[33]

Rat: peritoneum[33]

50%/4[33]

Rat: peritoneum[33]

1=1=1=1[32]

Dexon Plus 4-0 Dexon 4-0

13 ± 2[40]

30.5 ± 6[40] 1=1=1[40]

1=1=1=1[32]

Vicryl 4-0

Prolene 4-0

11[43]

Ti-Cron 4-0

10 ± 2[40]

50%/2[9] ; 5%/4[9]

Rat: subcutaneous fat[9]

55-65%/2[33] Rat: ; 0-8%/4[33] subcutaneous fat,[9] peritoneum[33]

1=1=1 to 1=1=1=1=1[40] 27.6 ± 9[40]

Dermalon 4-0 Novafil 4-0

9 ± 1[40] ; 10 ± 1[46]

1=1=1 to 1=1=1=1[40] 78.9 ± 22[40]

8 ± 1[40] ; 130.9 ± 6[40] 1=1=1=1[40] 9[43]

Ethilon 4-0 Chromic catgut 4-0

8[43] 50%/1[33] ; 25%/2[33]

Rat: peritoneum[33]

Monofilament steel 5-0

Dog: tendon[35]

Multifilament steel 5-0

Dog: tendon[35]

Dexon 5-0

Dog: tendon[35]

Ti-Cron 5-0

Dog: tendon[35]

Chromic catgut 5-0

Dog: tendon[35]

Silk 5-0

Dog: tendon[35]

Tissue reaction: (+) very mild, + mild, ++ moderate, +++ intense, ++++ very intense. *The data in the table without reference have been previously published by Gerber and associates. [ 15]

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response.[19] [33] Silk, which used to be the standard material for skin closure, is probably the least well tolerated of all materials still in use, and its application experimentally has been proved to compromise the results of intra-articular ligament repairs.[28] [35] Optimal selection of materials for skin closure has also been shown clinically to reduce the incidence of wound infection (polydioxanone plus polypropylene versus chromic catgut plus silk).[47] A monofilament structure has a variety of biologic advantages. There is less surface area exposed to the body, so that the foreign body reaction is less intense than that seen with use of multifilament sutures.[1] Because less suture material is exposed to hydrolysis, monofilament sutures retain their mechanical properties longer.[3] There is increasing concern that braided capillary materials may favor the propagation of infection, whereas noncapillary materials or monofilament sutures do not.[1] [2] It appears that bacteria can colonize these materials, not so much on the surface of the suture as within it, where immunocompetent cells have insufficient access. This accounts for the lack of support for the use of multifilament sutures in situations with potential contamination.[17] Because the implantation of braided suture material very close to the skin incites a much more intense and lasting reaction than burying the suture material in well-vascularized tissue, and because contamination very close under the epidermis is always possible, we feel that the use of braided suture materials immediately under the epidermis should be avoided. Clearly, the presence of large amounts of suture material incites more intense foreign body reactions. Therefore, sutures with optimal strength and knotting characteristics are needed so that small sutures requiring few throws for a stable knot can be used.

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Mechanical Characteristics Ultimate Tensile Strength

From an engineering standpoint, ultimate tensile strength should be measured in relation to the cross section of the material tested. Material properties become system properties when the suture material is knotted. For practical purposes, however, the orthopaedic surgeon selects the suture size exclusively according to the United States Pharmacopeia (USP) size, which is designed in numbers ranging from 12-0 to 6. When comparing data from different suture materials of different sizes, it should be understood that the cross section (or the diameter) of one material with a specific USP number may be different from the cross section of another material with the same USP number.[46] In addition, we never use unknotted sutures in daily practice. The mechanical properties of suture materials presented in Table 6A-1 refer, therefore, to knotted sutures (unless indicated otherwise) of commercially available sizes expressed in USP numbers. This appears reasonable because the surgeon is not interested in verifying the diameter of a certain suture and because essentially all sutures invariably fail at the site of the knot.[15] [39] Until recently, only thin suture materials had been widely tested, and the mechanical properties of heavier materials (e.g., sizes 0 to 6) were only sparsely documented. [3] [20] [21] [31] [36] [37] [43] [44] Repairs of large musculotendinous units are performed with the use of thick sutures, which have so far not been proved to be adequate, let alone optimal, for their respective applications. We recently tested the mechanical in vitro properties of the heavier sutures (gauges 0 to 3).[15] Not all suture materials were available in all sizes. The known mechanical in vitro properties of the commonly used suture materials are summarized in Table 6A-1 . Maximum tensile in vitro strength of comparable-sized sutures was found for monofilament stainless steel sutures and for absorbable monofilament materials (polyglyconate [Maxon] and polydioxanone [PDS]). Braided absorbable polyglactin (Vicryl) and polyglycolic acid (Dexon Plus) as well as braided polyester (Mersilene, Ethibond, Tevdek) showed excellent ultimate tensile strength, whereas nylon

(Dermalon, Prolene) was somewhat weaker. Our own data are in rough agreement with those found in the literature. In contrast to the study of Bourne and colleagues, we did not find a decrease in the ultimate tensile strength of wet sutures compared with dry material.[3] Deformation under Tensile Load

Although monofilament sutures tend to be more compliant, they are favored for certain arthroscopic techniques because they can be passed more easily through arthro-scopic instruments.[6] Both suture elongation under load and thread or knot failure, however, may lead to gap formation and may impair successful healing and functional recovery.[24] [26]

Table 6A-1 shows that the very strong, absorbable monofilament polyglyconate (Maxon) and polydioxanone (PDS II) sutures are very compliant under tensile loadsas opposed to the also very strong and absorbable but braided polyglycolic acid (Dexon) and polyglactin 910 (Vicryl) sutures, which are very stiff. Among the commonly used nonabsorbable sutures, only monofilament stainless steel sutures are stiff; the other monofilament sutures (polypropylene and nylon) are very compliant. The most commonly used nonabsorbable braided suture material is polyester; it is characterized by high tensile strength and low compliance. Clinically, it may be advantageous to employ a very compliant suture, especially a running type, because it may yield rather than break. [30] For tendons, suture repair techniques that prevent gapping are considered optimal because scar and adhesion formation is reduced and early functional treatment, which promotes remodeling, can be undertaken.[24] [47] An optimal tendon-to-bone repair should not allow gap formation under tensile load, but moderate extensibility may be beneficial for healing. If a rotator cuff tendon is sutured to a trough in the greater tuberosity, transosseous suture loops of roughly 7 cm are tied over the proximal humeral cortex. If such repairs are brought under a tension of, for example, 200 N, which is possible when the arm is lowered, the elasticity of the suture material alone may allow gapping of the repair. Under a load of 200 N, the suture material properties alone would allow the following gaps: 2.2 mm for Ethibond No. 3, 3.2 mm

171

for Ethibond No. 1, 6.7 mm for Surgilon No. 1, and 9.1 mm for PDS II No. 1.[15] Therefore, suture material alone may prevent stable anchoring of a tendon in bone if the repair is subjected to load; the selection of appropriate suture material is critical. Also, it is extremely important to know the loads to which a repair will be subjected to determine the optimal suture material. Maintenance of Mechanical Properties in Vivo

It is widely believed that nonabsorbable suture materials maintain their strength during

healing. This is true for braided polyester (Ethibond), which remains stable after implantation.[16] It is surprising, however, that Ethilon and Prolene, which both are nonabsorbable, lose 56% and 74%, respectively, of their initial ultimate tensile strength 6 weeks after subcutaneous implantation.[16] Even greater changes in the mechanical properties of absorbable suture materials are demonstrated after implantation.[16] Catgut loses its strength essentially within 1 week. Polyglactin 910 (Vicryl) loses about 50% of its initial ultimate tensile strength after 2 weeks, loses 75% by 3 weeks, and loses 100% by 4 weeks.[3] The material is absorbed after 56 to 90 days.[9] [19] Polyglycolic acid (Dexon Plus) has similar mechanical properties in vivo; 20% of its initial strength is lost within the first week, 50% is lost by 2 weeks, and essentially 100% is lost by 4 weeks.[40] Dexon Plus remains in the wound longer than Vicryl and is resorbed only after about 120 days.[9] Polyglyconate (Maxon) loses its strength distinctly less rapidly; its very high initial strength is reduced by roughly 50% after 3 weeks and is almost completely lost by 6 weeks.[3] [16] Polydioxanone (PDS) is initially somewhat less strong. Because it seems to be hydrolyzed more slowly than Maxon, it is already distinctly stronger at 3 weeks after implantation and maintains about 14% to 50% of its initial breaking strength for 6 weeks.[3] [16] Its resorption requires roughly half a year.[19] Of particular interest is a new absorbable suture material, poly(L-lactide/glycolide) (Panacryl). According to the manufacturer, Panacryl maintains 80% of its ultimate tensile strength for 3 months after in vivo implantation and maintains 60% of its strength for half a year. Full absorption occurs after 1.5 to 2.5 years. For absorbable sutures, Panacryl preserves its mechanical properties longer than any other suture material; it almost behaves as a nonabsorbable suture. The selection of the appropriate suture material depends on the expected type and rate of wound healing. For simple adaptation of subcutaneous tissue that is not under tension, the rapid resorption of polyglycolic acid or of polyglactin 910 may be desirable. Because the fibroblastic response dictates that a healing wound will rapidly regain strength between days 5 and 14, and because collagen content increases until day 42 with subsequent remodeling of the wound, a suture material such as polyglyconate (Maxon) may have optimal resorption characteristics for a wound that is under slight tension.[1] If a tendon or fascia is repaired under moderate tension and a longer period of protection is desired, a material such as polydioxanone (PDS) may be optimal. If, however, prolonged holding power is required and gapping is to be prevented, braided polyester (Ethibond, Tevdek, Mersilene) may be the best choice. Poly(L-lactide/glycolide) (Panacryl) may be an alternative to braided polyester, though this has not yet been proved by objective in vivo studies. Knotting Properties

Tera and Åberg have introduced an internationally accepted terminology for knotting techniques.[38] They distinguished between parallel and crossed knots and established that in general, parallel knots ( Fig. 6A-1 ) are more stable than crossed knots. Knotting properties appear to be similar for different sizes of the same material.[21] [39] Knots are indeed of great importance because suture material almost invariably fails at the site of

the knot.[15] [22] [38] Whereas stainless steel loses little strength when knotted, catgut and silk lose a large part of their strength when knotted. [38] [39] Indeed, the failure strength of suture material may be reduced by 10% to 70% by tying a knot.[22] Slipping of the knot depends on the number of throws and on the material.

Figure 6-A-1 Parallel knots and the nomenclature of Tera and Åberg. [ 39]

172

In general, any knot with six throws should not slip.[3] We were, however, able to show that the 2=1=1 configuration leads to stable knots for all tested sutures, and this is our preferred technique, although some sutures may require even fewer throws.[15] Zechner and colleagues have shown that the reduction in tensile strength can be partly prevented if knots are tied in the horizontal branch of the suture rather than in the region where linear stress is applied.[48] Although one may believe that knots of monofilament sutures slide easily, therefore necessitating multiple knots, this is not true; polyglyconate has excellent knotting properties, as have other monofilament sutures.[3] [15] [33] [40] The braided absorbable sutures tend to slip less when wet.[3] Knotting is more delicate in coated materials such as Ti-Cron (braided polyester) because coating reduces friction and therefore favors slipping of the knot. Coated and particularly stiff sutures are better knotted with double throws.[22] [40] In our hands, the sliding knot is the most convenient surgically; it corresponds to a parallel square knot and has the same properties.[27] It should be noted, however, that a double throw for the first knot increases tensile strength in a statistically significant manner.[15] If such a double throw is pinched with a ribbed needle holder, the tensile strength of sutures sized 0 to 3 is not significantly impaired. Pinching a smaller-sized thread reduces the tensile strength by up to 30%, however. [3] [15] Handling Properties

Modern suture materials are available with atraumatic precision needles, which are adapted to the intended use of the suture and thus essentially solve needle problems. Among suture materials, stainless steel has little popularity despite its superb soft tissue tolerance because of its stiffness and its potential for breaking if the suture is kinked. [8] Handling of the other sutures is mostly a matter of personal preference, and there are no clear-cut advantages of one suture over another in regard to handling properties.

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Personal Approach to the Selection of Sutures

To fix large tendons to bone or to secure a bone block of a patellar ligamentbone complex to the bone, we prefer heavy (No. 3), nonabsorbable, braided polyester (Ethibond) sutures. They are inert, have a very high tensile strength, and are extremely stiff, which prevents gapping.[13] [14] For tendon sutures, we use fine polypropylene (Prolene) or polydioxanone (PDS). They are somewhat elastic but have extremely high tensile strength, and polydioxanone maintains its mechanical properties sufficiently long to allow tendon healing.[3] If strength needs to be maintained, as in closures of aponeuroses (fascia lata), we prefer to use heavier elastic running sutures with polydioxanone. In subcuticular tissue, the breaking strength of the suture can be lost rapidly, so 4-0 polyglyconate (Maxon) appears optimal. For sutures placed very close to the skin, as well as in situations with questionable contamination, we try to avoid the use of braided suture materials. For closure of the skin, we prefer polypropylene (Prolene), 4-0 or 3-0. We do not use very rapidly absorbed polyglactin (Vicryl Rapid) or polyglycolic acid (Dexon), which have been recommended for skin closure, but these can be used for approximation of subcuticular tissues.[7] [10] [11] Within the skin, these materials tend to cause irritation and may serve as a wick, promoting contamination. Although it is still recommended, we have no use for any form of catgut. [45] The selection of suture remains personal in every field of surgery but should be done on a rational basis.[18]

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Meniscal Grafts

To prevent the degeneration of the articular cartilage that may result from loss of a meniscus,[14] [34] [57] [69] [72] [73] [95] many surgeons currently attempt to preserve or repair menisci whenever possible. Because of the limitations of intrinsic meniscal repair in the avascular portions of the meniscus, and because some meniscal injuries or degenerative diseases prevent successful repair, even in the vascularized regions of the meniscus, surgeons cannot always preserve or repair damaged menisci. In these circumstances, partial or total meniscectomy may be necessary. To protect knee joint cartilage from degeneration after these procedures, investigators and surgeons have been exploring several approaches to meniscal tissue replacement. Meniscal Allografts

Experimental studies have shown that allograft menisci will heal to host tissues. Studies of dog meniscal allografts[7] [9] showed that cryopreservation and short-term storage did not alter the shape or the mechanical properties of the menisci, but only about 10% of the meniscal cells remained metabolically active, meniscal cell synthetic activity decreased to less than 50% of normal, and total metabolic activity of the tissue declined with increasing storage time. Transplanted cryopreserved dog allograft menisci did not cause apparent rejection reactions, healed to the host tissues, and appeared to function normally after transplantation.[9] [12] Transplantation of lyophilized and deep-frozen menisci in sheep also showed that grafts can heal to the recipient site tissues. [111] Experimental studies have shown that meniscal grafts remodel and may help decrease the probability of degenerative joint disease following removal of the original meniscus. With time, the cell density of dog meniscal grafts increased; 3 months after transplantation, they had a cell numerical density and level of cell metabolic activity similar to those of normal menisci. Six months following transplantation, small blood vessels penetrated the grafts to about one third of their width from the periphery. The articular cartilage underlying the menisci remained intact 6 months following

transplantation, but the exposed tibial cartilage had fissures and degenerative changes. These changes appeared less severe than those found in dog knees subjected to total meniscectomy,[25] suggesting that the allografts provide some protection for the articular cartilage. The long-term results of the use of experimental meniscal allografts have not been reported, so the efficacy of allografts in decreasing the probability or the severity of degenerative joint disease remains uncertain.[74] Limited clinical studies confirm that meniscal allografts heal with host tissues.[111] [119] One group of investigators used fresh meniscal allografts.[119] They found that most of the grafts appeared structurally sound and functional at followup evaluation and reported survival of grafts for as long as 8½ years, although no biomechanical tests were performed to assess their mechanical properties. Another group used lyophilized and deep-frozen allografts.[111] They reported that operative complications and rejection reactions did not occur, but the grafts decreased in size. Although these clinical results show the potential for allograft meniscal replacement, other studies are needed to determine whether meniscal allografts decrease the frequency and the severity of degenerative joint disease after loss of menisci.

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Synthetic Matrix Meniscal Grafts

Synthetic matrices, created from reconstituted collagen, fibrin, or other materials and shaped to fit specific meniscal defects, can replace lost or damaged meniscal tissue.[74] [103] Recipient-site cells and blood vessels might grow into these synthetic matrices and remodel them to resemble meniscal tissue. Initial experimental investigations suggest that synthetic collagen matrices may have the potential to replace menisci.[74] [103] These synthetic matrices could also serve as vehicles for implantation of growth factors that promote host cell migration, proliferation, and differentiation in the graft or for implantation of cultured mesenchymal cells that could synthesize a new matrix.

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Section B Construction and Fixation of a Tendon Anterior Cruciate Ligament Graft Stephen M. Howell MD L. M. Hull PhD Kazunori Yasuda MD, PhD Overview

There is renewed interest in the use of tendons (e.g., semitendinosus, gracilis, posterior tibialis, anterior tibialis) instead of bonepatellar tendonbone (BPTB) as a graft for a torn anterior cruciate ligament (ACL).[18] [21] [28] [53] [54] The interest stems from studies that show that an ACL graft made from tendons has better strength and stiffness[21] [22] [62] and less harvest morbidity[21] [70] than a BPTB graft. Another advantage of a hamstring ACL graft is that the graft may survive in the synovial environment because the original cells are retained after implantation,[18] and the graft does not require revascularization for viability.[26] In contrast, a BPTB graft does not survive in the synovial environment, becomes acellular after implantation, and requires repopulation by cells of external origin.[33] Despite the advantages noted here, tendons as an ACL graft have not been adopted universally because of two concerns. The first is that the fixation characteristics of a tendon ACL graft, which include strength, stiffness, and slippage, have not been perceived as equivalent to those of a BPTB graft. The second is that because the fixation characteristics may be lacking, aggressive rehabilitation is not safe with a tendon ACL graft. A clear definition of terms is required to discuss the fixation characteristics of a tendon ACL graft. Strength is defined as the load that causes a permanent and nonrecoverable displacement of a tendon ACL graftfixation methodbone complex. Stiffness is defined as the displacement produced by a given force. Slippage is defined as the change in

elongation at a specified number of load cycles.[17] [35] [36] The purpose of this chapter is to review the current state of knowledge regarding tendon ACL grafts and their fixation. The first section explains two principles for constructing and tensioning a tendon ACL graft. The second introduces three principles for designing an effective fixation method for a tendon ACL graft. The third discusses the expected loads in an ACL graft and three issues pertaining to in vitro biomechanical testing that should be considered when determining fixation characteristics. The fourth discusses the strength, the stiffness, and the slippage of three categories of fixation, including suture fixation and cancellous and cortical fixation methods. The fifth section

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discusses ways to improve the fixation characteristics of the complex after implantation and the phenomenon of tunnel enlargement. The final section justifies that aggressive rehabilitation is safe with a tendon ACL graft when fixation methods are used that provide high strength and stiffness and resist slippage under cyclic load.

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Principles for Constructing and Tensioning a Tendon ACL Graft

An effective tendon ACL graft has to be strong and stiff to stabilize the knee and avoid reinjury. This section explains two principles for constructing a tendon ACL graft and discusses how tensioning determines whether the strength and the stiffness of the graft are optimized at implantation. Constructing a Tendon ACL Graft

The first principle is that a tendon ACL graft requires multiple strands.[21] Multiple strands are needed because a single tendon has a cross-sectional area less than the normal ACL and is neither strong enough nor stiff enough at implantation to function as a graft. For example, the cross-sectional area of a one-strand semitendinosus tendon (11 mm 2 ) is only 22% and a one-strand gracilis tendon (7.4 mm2 )[21] is only 15% of the cross-sectional area of the normal ACL (50 mm 2 ). [47] Because the strength of a tendon ACL graft increases linearly as the cross-sectional area increases, combining multiple strands is necessary to provide an ACL graft with sufficient strength and stiffness.[21] The semitendinosus, gracilis, anterior tibialis, and posterior tibialis tendons can be combined to construct a tendon ACL graft with a cross-sectional area that approximates the normal ACL and functions well clinically ( Fig. 6B-1 and 6B-2 ). [28] [53] [54] An equally tensioned two-strand allograft formed from a single loop of posterior tibialis tendon has an average cross-sectional area of 42 mm2 , a strength of 3594 N, and a stiffness of 948 N/mm when normalized to a 30-mm length.[22] A two-strand allograft formed from a single loop of posterior tibialis tendon has an average cross-sectional area of 48 mm2 , a strength of 4122 N, and a stiffness of 1150 N/mm when normalized to a 30-mm length.[22] A 30-mm-long four-strand graft formed from a double-loop of semitendinosus and gracilis (DLSTG) hamstring tendons has an average cross-sectional area of 50 mm2 , a strength of 4590 N, and a stiffness of 861 N/mm.[21] These three tendon ACL grafts are as strong as, or stronger and substantially stiffer than, a femur-ACL-tibia complex [46]

[68]

and a 10-mm-wide BPTB graft[12] [46] at implantation.

The second principle for constructing a tendon ACL graft is that the strands should be aligned in parallel fashion and neither braided nor weaved. [21] [45] Although braiding or weaving strands was recommended as a way to increase strength and stiffness of a multistrand tendon ACL graft, this concept was not supported by biomechanical studies.[61] A recent biomechanical study determined the properties of two braiding techniques compared to a nonbraided four-stranded tendon graft using an in vitro sheep tendon model. The braided samples had 58% less strength and up to 85% less stiffness than the nonbraided grafts. These results indicate that braiding of strands is not advisable because it significantly reduces both strength and stiffness of a tendon ACL graft at implantation.[45] Tensioning a Tendon ACL Graft

The second principle for optimizing the strength and the stiffness of a tendon ACL graft at implantation is that each strand must be tensioned equally. Applying tension to each strand of a four-strand DLSTG graft by hand produces

Figure 6-B-1 Comparison of strength of femur-ACL-tibia (F-ACL-T) complex, bonepatellar tendonbone (BPTB), and equally tensioned multistrand tendon ACL grafts including the double-strand posterior tibialis (DSPT), double-strand anterior tibialis (DSAT), and double-loop of semitendinosus and gracilis (DLSTG) grafts from several studies. The average cross-sectional area of each graft (mm 2 ) is noted at the base of each column. In general, the strength increases with the cross-sectional area of the graft. The tendon ACL grafts are as strong as or stronger than the F-ACL-T complex and the BPTB graft. ACL, anterior cruciate ligament.

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Figure 6-B-2 Comparison of stiffness of femur-ACL-tibia (F-ACL-T) complex, bonepatellar tendonbone (BPTB), and equally tensioned multistrand tendon ACL grafts including the double-strand posterior tibialis (DSPT), double-strand anterior tibialis (DSAT), and double-loop of semitendinosus and gracilis (DLSTG) grafts from several studies. The stiffness of each tendon ACL graft is normalized to a length of 30 mm to allow a comparison between the F-ACL-T and the BPTB graft. The tendon ACL grafts are two to three times stiffer than the F-ACL-T and the BPTB graft. ACL, anterior cruciate ligament.

enough unequal tension that the strength and stiffness of the tendon ACL graft is like two semitendinosus strands alone without the two gracilis strands ( Fig. 6B-3 ). Applying tension to each strand of a four-strand DLSTG graft with a weight produces equal tension so that the tensile properties of the individual strands are additive. Therefore, a multistrand tendon ACL graft must be tensioned equally to maximize the strength and stiffness at implantation.[21]

Tensioning each strand of a tendon ACL graft equally may not be possible with some methods of graft preparation and fixation. For example, a requirement of the quadruple hamstring all-inside technique and the bone-hamstring-bone construct is that the strands are either sewn together or sewn to bone plugs ( Fig. 6B-4 ).[4] [35] [40] [59] No method has been proved to ensure equal tension between strands after they are sewn together or to bone. Interference screw fixation of a tendon ACL graft may cause unequal tension because the strands of the graft can twist during insertion of the screw,[6] and this movement may change the tension between strands. Surgeons should understand that sewing strands either together or to bone and fixing the graft with interference screws may compromise the strength and the stiffness of a tendon ACL graft at implantation. One method of applying equal tension to each strand of a four-strand DLSTG graft by hand is to turn the graft into a continuous loop by leaving the insertion of each tendon attached to the tibia ( Fig. 6B-5 ). A continuous loop can be formed by passing the tendons through the knee around a fixation post in the femoral tunnel and tying the sutures attached to the free strand of each tendon together to close the loop. Tension applied by hand to a metal rod placed in the loop of suture produces equal tension in all four strands because the fixation post functions like a pulley,[63] which maximizes the strength and stiffness of the multistrand graft at implantation.

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Designing a Fixation Method for a Tendon ACL Graft

This section introduces three principles for designing an effective fixation method for a tendon ACL graft to allow aggressive rehabilitation. The rationales for fixing the graft distal to the joint line in cortical bone, conserving graft length, and countersinking and stabilizing the fixation device

Figure 6-B-3 Tensioning each strand of a four-strand double-loop of semitendinosus and gracilis graft by hand produces enough unequal tension between strands that the strength and the stiffness of the construct are comparable to two semitendinosus strands alone without the two gracilis strands. [ 21] Unequal tension between strands may occur with insertion of an interference screw because the strands of the graft twist. [ 6]

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Figure 6-B-4 Unequal tension occurs between strands with techniques that sew strands together, [ 4] sew strands to bone plugs, [ 35] [ 40] [ 59] and either weave or braid strands of tendon. Unequal tension between strands compromises the strength and the stiffness of a multistrand tendon graft at implantation. [ 21]

to reduce the incidence of device removal and migration are discussed. Fixing the Graft Distal to the Joint Line in Cortical Bone

A fixation device should be placed distal to the joint line in cortical bone if possible to avoid poor-quality cancellous bone.[2] [36] The quality of bone, specifically the thickness of the cortical bone, determines the strength of a fixation method ( Fig. 6B-6 ). The

strength of screws, bollards, toggles, and staples increases as the local thickness of cortical bone increases. Cancellous bone does not determine the strength of a fixation method because it is much weaker and more variable in quality than cortical bone.[2] In humans, the bone mineral density decreases permanently in both the femur and the tibia after knee ligament injury.[3] [30] These studies explain why the incidence of restoring stability is poor with interference screw fixation of a tendon ACL graft in cancellous bone,[5] especially in women.[13] [32] Fixing a tendon ACL graft in cortical bone requires that the fixation device be inserted distal to the joint line rather than proximal just below the joint line (aperture fixation) because the thickness of cortical bone increases as the distance from the joint line increases. It has recently been shown for a bone-tendon-bone graft that aperture fixation is preferred over distal fixation to increase anterior knee stability.[29] The principle behind aperture fixation of a BPTB graft is that the stiffness of the graftfixation devicebone complex is increased because fixing the graft at the joint line shortens and improves the stiffness of the graft.[29] [40] This principle has been extrapolated to the fixation of a tendon ACL graft to justify aperture fixation with a soft tissue interference screw.[4] [13] [66] This principle does not apply to fixation of a tendon ACL graft,[36] [56] [57] [62] however, and is an unjustified misinterpretation of the Ishabashi study by other authors.[4] [13] [48] [66] Understanding why aperture fixation of a tendon ACL graft does not provide better stiffness than distal fixation at implantation requires an explanation of how the stiffness of a tendon ACL graftfixation methodbone complex is determined. The stiffness of the complex at implantation is determined by two factorsthe stiffness of the fixation method and the length of the graft.[62] In tests performed in human tissue, the stiffness of the complex is similar with interference screw (248 N/mm), WasherLoc (273 N/mm), and two spiked washers and screws (259 N/mm), even

Figure 6-B-5 One method of tensioning each strand of a four-strand double-loop of semitendinosus and gracilis graft equally by hand is to turn the graft into a continuous loop by leaving the semitendinosus and gracilis graft attached to the tibia. A continuous loop is formed by passing the tendons through the knee around a fixation post in the femoral tunnel, and tying the sutures attached to the free strand of each tendon together to close the loop. Tension applied by hand to a metal rod placed in the loop of suture produces equal tension in all four strands because the fixation post functions like a pulley. [ 63]

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Figure 6-B-6 Comparison of the results of strength test for eight fixation methods showing the importance of placing the fixation device in thicker cortical bone. For each method, the strength of the fixation increases as the thickness of the cortical bone increases. [ 2] (From Amis AA: The strength of artificial ligament anchorages. A comparative experimental study. J Bone Joint Surg Br 70:397-403, 1988.)

though the site of fixation is 15 and 20 mm more distal for the WasherLoc and the two spiked washers and screws, respectively, than for the interference screw. The reason that the stiffness is similar for these three fixation complexes in spite of three different graft lengths is that the fixation with the WasherLoc (506 N/mm) and the two spiked washers and screws (414 N/mm) is stiffer than with the interference screw (340 N/mm).[36] Therefore, the stiffness of the fixation method is a more important consideration for increasing the stiffness of a tendon ACL graftfixation methodbone complex at implantation than where the graft is fixed relative to the joint line ( Fig. 6B-7 ). Conserving Graft Length

Aggressive rehabilitation of a multistrand DLSTG graft requires firm fixation of both ends of the graft to bone.[25] [28] Fifteen percent to 20% of gracilis tendons are too short to be fixed directly to bone and require a bridge of suture to connect the strand of tendon to a fixation device.[28] [36] A suture bridge should not be used because the suture is elastic and slips under cyclic load, resulting in permanent elongation of the tendon ACL graftfixation methodbone complex.[24] [36] [69] Looping the graft around a fixation post inside either the tibial or the femoral tunnel is a strong and stiff fixation technique that conserves graft length and shortens the point of fixation 4 to 5 cm ( Figs. 6B-3 and 6B-8 ). [25] [28] [62] Studies have shown that aggressive rehabilitation is safe and effective with post fixation of a DLSTG graft because enough graft length is conserved so that the free end can be fixed directly to bone without a weak, elastic suture.[25] [28] Countersinking and Stabilizing the Fixation Device

Removal of hardware, because of prominence and migration, is the most common reason for reoperation using a tendon ACL graft ( Fig. 6B-9 ). [10] [25] [55] In one study, prominent washers and staples were removed from the tibia in 26% of subjects (21 of 82), but low-profile endobuttons were not removed from the femoral cortex. [55] In another study, prominent washers and staples were removed from the tibia in 21% of subjects (14 of 67), but countersunk bone mulch screws were not removed from the femur. [25] In a third study, prominent hardware was removed from the tibia in 11% of subjects (2 of 18), and small-in-diameter cross-pins that migrated because of poor fixation were

Figure 6-B-7 Comparison of the stiffness of different tibial fixation methods (value within column) with a high-stiffness femoral fixation method (bone mulch screw, 575 N/mm) on the combined stiffness using both fixations (value above column) calculated using a spring-in-series analysis. The combined stiffness increases as the stiffness of the tibial fixation method increases and is greater with the distal tibial fixation method (i.e., two spiked washers and screws, WasherLoc) than with aperture fixation with an interference screw.[ 36]

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Figure 6-B-8 An effective method for conserving graft length in the tibia is to loop the multistrand double-loop semitendinosus and gracilis graft around a post inside the tibial tunnel (two solid lines).[ 28] Enough length of the gracilis tendon is conserved with this fixation method so that the two free ends, along with the semitendinosus tendon, are fixed under a screw and washer proximal to the femoral tunnel. The dotted line represents the slope of the intercondylar roof.

removed from the femur in 11% of subjects (2 of 18).[10] Clearly, the most effective way to improve stability and to reduce the 21% to 26% reoperation rate and associated costs is to design tibial and femoral fixation methods that are countersunk and cancellous femoral fixation methods that are strong and stiff and do not migrate ( Fig. 6B-10 ).

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Evaluation of Fixation Methods in Vitro

The primary reason that strength, stiffness, and slippage of a tendon ACL graftfixation methodbone complex are studied in vitro is to support their use in humans.[36] [60] [62] [66] [67] To speculate whether a fixation device has the potential to perform well in humans requires estimation of the maximum tensile force in an ACL graft during various activities and exercise as well as a model that simulates the bone quality of the young human knee at the time of implantation. This section discusses several studies that have estimated the tensile force in the ACL and an ACL graft and three issues that should be considered when designing in vitro studies to determine the strength, the stiffness, and the slippage of a fixation method. These issues include the species of bone used to test the fixation method, the use of an extensometer to determine stiffness, and cyclic tests to predict slippage, the strength of fixation after repetitive movement, and the initial tension required in an ACL tendon graft. Estimating the Maximum Tensile Force in an ACL Graft

Interpreting the results of in vitro studies requires an understanding of the maximum tensile forces in an ACL graft imposed by activities of daily living and exercise. The tensile forces in an ACL graft have not been measured in vivo in humans, but estimates are available. The maximum tensile force in an ACL is estimated to be 150 N during walking,[41] 450 N during jogging, [42] and 500 N during activities of daily living. [16] The maximum tensile force in an ACL graft may be greater than in the ACL because an initial tension is applied to the graft at the time of implantation to restore anterior laxity.[38] The maximum tensile force is greater with a low-stiffness graftfixation methodbone complex than with a high-stiffness complex because a low-stiffness complex requires more initial tension to restore anterior laxity.[9] [15] [37] Based on these studies, it is reasonable to assume that with optimal tunnel placement, the maximum tensile force in an ACL graft may reach 500 N during exercise, especially with a low-stiffness complex. Therefore, for daily activities and rehabilitation exercises to be performed safely without slackening of the graft, the fixation characteristics of the

fixation methods must be effective at tensile forces in the graft of up to 500 N.[36] Species of Bone

The species of bone in which fixation methods are tested determines whether the results for strength, stiffness, and

Figure 6-B-9 Removal of symptomatic hardware is the most common cause of a second surgery in patients with a tendon ACL (anterior cruciate ligament) graft. Femoral cross-pins, which are small in diameter with only a few shallow threads, can migrate in soft cancellous bone after implantation and can irritate the iliotibial band.[ 10] Prominent tibial hardware such as staples can irritate overlying tissue, causing pain.

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Figure 6-B-10 The most effective way to reduce the 21% to 26% reoperation rate and associated costs is to use fixation methods that are countersunk in both anteroposterior and lateral views and femoral fixation methods that do not migrate.[ 25]

slippage can be applied to humans.[36] Cancellous bone from canine, porcine, bovine, and ovine donors has greater bone mineral content, density, and fracture stress than human bone.[1] It is not surprising that the strength, the stiffness, and the slippage of cancellous fixation methods such as interference screws are a best case when tested in animal bone compared to young human bone.[8] [17] [36] [58] [66] For example, the strength, the stiffness, and the slippage of fixation in cancellous bone with an interference screw are significantly worse in young human tibia than when tested in porcine tibia.[36] Conversely, the strength of fixation in cancellous bone with an interference screw is worse in cadaver knees obtained from elderly specimens than in young specimens because of the inevitable reduction in bone density associated with advanced age.[8] For the fixation characteristics of cancellous fixations such as the interference screw to be applied to humans, the testing must be performed in young human bone and not in either animal bones or cadaver bones obtained from elderly specimens. [36] In contrast to cancellous fixation methods, cortical fixation methods have similar strength, stiffness, and slippage when tested in either animal or human bone. For example, a tendon ACL graft fixed with either two spiked washers and screws or the WasherLoc has similar fixation characteristics in both porcine and human tibia.[36] Although not proved, the most likely explanations for this finding are that the structural properties of cortical bone are sufficiently higher than the structural properties of the fixation methods, or there is little interspecies variation in the structural properties of cortical bone.

Use of an Extensometer to Determine Stiffness

Achieving normal knee kinematics at the time of reconstruction may be more dependent on matching the stiffness of a tendon ACL graftfixation methodbone complex to that of the native ACL than on matching its ultimate strength.[29] [62] Therefore, an in vitro study must accurately determine the stiffness of a tendon ACL graftfixation methodbone complex. An accurate determination of stiffness requires an extensometer. One type of extensometer is a linear variable differential transformer attached at the two points of fixation. The extensometer measures only the elongation between the two points of fixation, thereby ignoring any deflections in the testing setup. [36] [62] Any deflection in the testing setup introduces an error in the determination of stiffness of a tendon ACL graftfixation methodbone complex, which can be excluded only if an extensometer is used. For example, a 20% error occurs when the elongation of the complex is 5 mm and the deflection from the testing setup is 1 mm. The extensometer measures elongation more accurately than a displacement transducer that registers the movement of the actuator on a material testing system because movement of the actuator includes any deflections in the fixtures, the mounts, the femur, and the tibia.[36] [62] The large variability in reported stiffnesses of fixation methods is explained by the inconsistent use of an extensometer

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and differences in the rigidity of the testing setup. Without an extensometer, the stiffness is similar between different fixation methods.[51] [60] [66] With an extensometer, the stiffness varies greatly between different fixation methods. [36] [62] For the stiffness of a fixation method determined from an in vitro study to be applicable to a human, the stiffness should be calculated from elongation measurements made with an extensometer. Cyclic Tests to Determine Slippage, Strength, and Initial Tension

Cyclic tests should always be part of the evaluation of the fixation characteristics of a tendon ACL graft fixation method because a one-shot test to failure is of limited value.[17] [36] [49] The forces imposed on the reconstruction during rehabilitation exercises and normal activities such as walking are not likely to cause graft rupture; however, progressive slippage of the graft at the point of fixation due to repetitive loading that occurs in daily life remains a possibility. Cyclic tests apply a repetitive submaximal load in an attempt to represent or simulate the tensile loads in an ACL graft expected during postoperative activities and rehabilitation. [17] Cyclic tests allow slippage to be measured. Slippage is a measure of the permanent

elongation of a tendon ACL graftfixation methodbone complex that results from movement of the graft relative to the initial point of fixation at a subfailure load.[17] [35] [36] [58] Quantifying slippage is important because it indicates whether a fixation method might allow an insidious return of excessive knee laxity.[17] A fixation method should limit slippage to less than 3 mm because a reconstructed knee with an increase in anterior tibial translation of 3 mm is considered unstable. [25] [28] The goal of a cyclic test is to simulate the repetitive tensile forces in an ACL graft imposed by activities of daily living and exercises. Unfortunately, there are no well-founded guidelines for creating an accurate simulation. Simulating the tensile forces in a tendon ACL graftfixation methodbone complex during these activities requires estimation of the submaximal forces in an ACL graft and estimation of the number of cycles that occur before the graft heals in the tunnel. Because there is no consensus for either of these parameters, investigators have not agreed on a standard method for performing cyclic tests, which limits comparisons between studies. Three different methods have been used to perform cyclic tests, and each has advantages and disadvantages. These methods include a cyclic test that applies a cycle of a constant amplitude under displacement control,[43] [69] a cyclic test that applies a cycle of a constant amplitude under load control,[17] [52] and a cyclic test that applies a cycle at progressively higher loads under load control until failure.[35] [36] [58] The advantage of using a cyclic test that applies a cycle of constant amplitude under displacement control is that the magnitude of the resulting load does not need justification.[69] The disadvantage of this method is that the load required to produce a displacement of constant amplitude is different, depending on the stiffness of the fixation method. A low-stiffness fixation method requires a lower load than a higher-stiffness fixation method. Therefore, a cyclic test that applies constant amplitude under displacement control overestimates the performance of a low-stiffness fixation method because a lower load is used, and it underestimates the performance of high-stiffness fixation methods because a higher load is used. The advantage of using a cyclic test that applies a cycle of constant amplitude under load control is that the same load is applied to every fixation method.[17] The disadvantage of this method is that the magnitude of the load is difficult to justify without knowing the submaximal load during different daily activities and exercises. One compromise is to use 150 N of tension, which is the estimated load in the ACL during walking.[17] [41] The graft tension of other daily activities such as active knee extension with a 1500-N quadriceps load is 250 N[19] and jogging is 450 N,[42] however, which are both greater than walking. Some fixation methods (stirrup) perform well at both low and higher loads, yet other fixation methods (a single washer and interference screw) only perform well at low loads.[17] Therefore, a study that uses a cyclic test that applies a cycle of constant amplitude to a lower peak load under load control overestimates the performance of fixation methods that do not resist slippage well at higher loads. There are several advantages of a cyclic test that applies a cycle at progressively higher load under load control until failure. One is that the magnitude of the load does not need to be justified, and another is that the same load is applied to both low- and

high-stiffness fixation methods.[35] [36] A third advantage of this method is that the strength with this type of cyclic test is more conservative than the strength obtained with a one-shot failure test, which eliminates the need for a separate load-to-failure test.[36] The main disadvantage of a cyclic test that applies a cycle at progressively higher loads under load control until failure is that activities of daily living and exercise are not stimulated because the fixations fail after relatively few cycles, especially with greater incremental increases in the applied load. Even though there are limitations to each type of cyclic test, recent studies have shown that cyclic testing can reveal fixation methods that may not function well with aggressive rehabilitation.[17] [24] [36] [43] Fixation of a hamstring tendon graft with a tape tied to an endobutton and sutures has significantly more permanent elongation (3.8 mm) than fixation over a cross-pin proximally and two soft tissue washers distally (0.3 mm) after cyclic loading at low load levels (20 to 150 N). The large permanent elongation following repetitive loading of a graft construct with tape and suture material during the early postoperative period is of concern.[24] Similarly, the failure load of a flexor tendon graft fixed with interference screw (302 N) is significantly less than the failure load of a BPTB graft with interference screws (809 N) after cyclic testing to an elongation of 2 mm.[43] This study, as well as others, concluded that vigorous activities should not be avoided with interference screw fixation of a tendon ACL graft because of its low ultimate failure load.[17] [36] [43] Cyclic testing is also important for detecting changes in the biomechanical behavior of tendon grafts after implantation, which affects the level of initial graft tension required

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to restore anterior stability to the knee. For example, relatively high initial tension is needed for tendon grafts fixed with suture, tape, or interference screws because the tension decreases soon after implantation owing to slippage.[43] [71] Sustained high tension should be avoided because it may result in focal degeneration or deterioration of biomechanical properties of the graft by biologic responses[71] [72] and posterior subluxation of the tibia.[15] [39] On the other hand, high initial tension is not recommended for fixation methods that are stiff and slip minimally under cyclic load.[71] It may be possible to minimize the initial tension of a tendon ACL graft, restore the anterior limit of motion, and prevent posterior subluxation of the tibia by using high-stiffness fixation techniques that slip minimally under cyclic loading.[14]

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Fixation Characteristics of Suture, Cancellous, and Cortical Fixation Methods

The two previous sections emphasized the importance of fixing the graft distal to the joint line in cortical bone, determining fixation characteristics from tests performed in young human bone, calculating stiffness using an extensometer, and using cyclic tests to measure slippage. The purpose of this section is to interpret the strength, the stiffness, and the slippage results of a variety of fixation methods for use in human ACL reconstructions. Fixation characteristics are discussed for all reported fixation methods that have been evaluated in young human bone using a tendon ACL graft and an extensometer. The results are ordered according to whether the fixation method requires sutures or is implanted in either cancellous or cortical bone. These interpretations are based on the assumptions that the strength exceeds a tensile force of 500 N, the stiffness is similar to the intact ACL (300 N/mm), and the slippage is less than the 3 mm at 500 N of load to restore stability. [27] The fixation characteristics of several other fixation methods in use at the time of this writing are not discussed because results from testing in young human bone using an extensometer were not available. These fixation methods include the closed loop endobutton (Smith and Nephew), cross-pins (Arthrex, Innovasive, Mitek), and intratunnel fixations such as the bioabsorbable interference screw and Intrafix (Innovasive). Suture Fixation Methods

Suture fixation is a class of fixation separate from cancellous and cortical fixation methods because the suture determines the fixation characteristics of the complex as a consequence of its being weaker and more elastic than the fixation device (button, screw) and bone.[36] [62] In the femur, the most common suture fixation method is to suspend the tendon ACL graft from a fixation device (endobutton, Mitek anchor) placed either on or in the cortical

surface of the femur using a loop of suture ( Fig. 6B-11 ). The average strength of this suture fixation method

Figure 6-B-11 Suture fixation of a tendon ACL (anterior cruciate ligament) graft in the femur. The graft is suspended from a loop of tape threaded through a button drawn against the femoral cortex. Whether the loop is closed with a knot or is a continuous loop, the length of the loop and the material properties of the tape determine the fixation characteristics. (From To JT, Howell SM, Hull ML: Contributions of femoral fixation methods to the stiffness of anterior cruciate ligament replacements at implantation. Arthroscopy 15:539-545, 1997.)

is only 430 N, which is less than the estimated tensile load in an ACL graft of 500 N. The knot used to close the suture into a loop and the material properties of the suture determine the stiffness of this suture fixation method. The average stiffness is 24 N/mm, which is only 8% of the stiffness of the intact ACL.[62] The results from these in vitro tests suggest that aggressive rehabilitation is not safe with this suture fixation method in the femur. This lack of safety has been confirmed in a clinical study that showed that even with a nonaggressive rehabilitation program, only 70% of knees had less than a 3-mm increase in anterior translation compared with the normal knee, at 134 N of anterior load.[55] In the tibia, the most common suture fixation method is sewing 4 to 5 cm of the end of each strand of tendon with a No. 5 suture and tying the sutures to a bicortical screw placed on the tibial cortex distal to the tibial tunnel.[36] The average strength of this suture fixation is only 442 N, which is less than the estimated tensile load in an ACL graft of 500 N. Cinching of the suture in the tendon and tightening of the knot under cyclic load determine the stiffness and the slippage of this suture fixation method.[36] [49] The average stiffness is 70 N/mm, which is only 23% of the stiffness of the intact ACL. The average slippage is 5 mm, which is greater than the 3-mm limit required for restoring stability.[36] The results from these in vitro tests suggest that aggressive rehabilitation should not be used with this suture fixation method in the tibia. To our knowledge, there are no clinical studies reporting that aggressive rehabilitation is safe with this suture fixation method. Cancellous Fixation Methods

Cancellous fixation is a class of fixation separate from cortical fixation because the quality of the cancellous bone determines the fixation characteristics of the complex as a consequence of cancellous bone being weaker than cortical bone. [2] [36]

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In the femur, the most common cancellous fixation methods are the cross-pins (bone mulch screw [Arthrotek], transfix [Arthrex, Innovasive]) and the interference screw. The only cancellous fixation method tested in young human bone with an extensometer is the bone mulch screw ( Figs. 6B-5 and 6B-10 ). The large dimensions of the bone mulch

screw (the screw body is 20 to 35 mm long and 10.5 mm in diameter) prevent angulation under load[25] and determine the strength and the stiffness of this fixation method. The average strength of the bone mulch screw is 1126 N, which is 2.3 times greater than the estimated tensile load in an ACL graft. Compaction of bone into the femoral tunnel through the body of the bone mulch screw improves stiffness 41 N/mm[62] and produces reciprocal tensile behavior between the anterior and the posterior strands in a single femoral tunnel.[64] With bone compaction, the average stiffness of the bone mulch screw is 575 N/mm, which is 1.9 times stiffer than the intact ACL.[62] The results from these in vitro tests suggest that aggressive rehabilitation should be safe with the bone mulch screw in the femur. This safety has been confirmed in a clinical study, which reported that 91% of knees had less than a 3-mm increase in anterior translation compared with the normal knee at a maximum manual anterior load.[25] In the tibia, the most common cancellous fixation method is the interference screw. A 9-mm diameter and 25-mm long interference screw inserted in a tibial tunnel drilled to within 0.5 mm of the diameter of the DLSTG graft has been tested in young human bone with an extensometer. The average strength of the interference screw is 350 N, which is less than the estimated tensile load in an ACL graft of 500 N. The average stiffness is 350 N/mm, which is 1.2 times stiffer than the intact ACL. The average slippage of the few fixations (43%) that did not fail before 500 N of load is 4 mm, which is greater than the 3-mm limit required for restoring stability.[36] The results from these in vitro tests suggest that aggressive rehabilitation is not safe with interference screw fixation in the tibia. This lack of safety has been confirmed in two clinical studies. One study reported that even with a nonaggressive rehabilitation program, only 35% of knees had less than a 3-mm increase in anterior translation compared with the normal knee (134 N anterior load).[5] The other showed poor stability in females,[32] which the authors associated with weaker interference screw fixation due to diminished bone quality in the cancellous metaphysis of the tibia.[13] Cortical Fixation Methods

The thickness of the cortical bone determines the strength of cortical fixation methods.[2] In contrast to cancellous fixation methods, cortical fixation methods have similar strength, stiffness, and slippage when tested in either human or porcine bone.[36] For this reason, the fixation characteristics of fixation methods tested in animal bone are included in this section. In the femur, the most common cortical fixation devices are the spilked washer and the clawed washer. Two 14-mm diameter spiked washers with bicortical screws were tested to failure in bovine femur. The average strength of the spiked washer fixation was 724 N, which is more than the estimated tensile load in an ACL graft of 500 N. The stiffness and the slippage for this method of fixation were not determined. [7] The clawed washer with a cancellous screw was tested in bovine femur using both a load-to-failure test and a cyclic test under load control to 450 N to stimulate jogging. The average strength of the clawed washer was 502 N, but the device failed rapidly during cyclic testing, which prompted the authors to conclude that the complex will slacken if rehabilitation is too aggressive with this cortical fixation method.[17] The results from these in vitro studies suggest that the fixation characteristics of cortical fixation with spiked and clawed

washers in bovine femur are less effective than cancellous fixation with the bone mulch screw in human femur. In the tibia, the most common cortical fixation devices are double staples, a single spiked washer, two spiked washers and screws, and WasherLoc. Of these four fixation devices, the two spiked washers and screws and the WasherLoc have the best fixation characteristics when tested in young human bone with an extensometer. The average strength of the two spiked washers and screws is 768 N, which is greater than the estimated tensile load in an ACL graft of 500 N. The average stiffness is 318 N/mm, which is nearly as stiff as the intact ACL. The average slippage is 1 mm, which is less than the 3-mm limit required for restoring stability. For comparison, the average strength of the WasherLoc is 905 N, which is greater than the estimated tensile load in an ACL graft of 500 N. The average stiffness is 506 N/mm, which is 1.7 times stiffer than the intact ACL. The average slippage is 2 mm, which is less than the 3-mm limit required for restoring stability.[36] The results from these in vitro tests suggest that aggressive rehabilitation should be safe with either two spiked washers and screws or the WasherLoc in the tibia ( Fig. 6B-10 ).

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Improving the Fixation Characteristics after Implantation and the Phenomenon of Tunnel Enlargement

Improving the healing of a tendon ACL graft in the bone tunnel may allow earlier and more aggressive rehabilitation and earlier return to sport or work.[50] This section discusses several factors that affect the fixation characteristics of a tendon in a bone tunnel after implantation. These factors include maximizing tendon length and tendon fit in the bone tunnel, using distal fixation rather than aperture fixation to improve the strength and the stiffness of the complex and the biologic interface, and using growth factors to enhance healing. Finally, the phenomenon of tunnel enlargement is discussed. Maximizing Tendon Length and Tendon Fit in the Bone Tunnel

The surgical technique and the method of fixation influence the tendon length and the tendon fit within a bone tunnel.

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The influence of tendon length and tendon fit on the strength of a tendonbone tunnel complex was studied in a canine model. The long digital extensor was transplanted into a metaphyseal bone tunnel and was held with suture in both hind limbs of 14 mongrel dogs, which were killed after 6 weeks. To test the effect of tendon length on fixation strength, the tendonbone tunnel complex in six animals was frozen and cut to leave only 1 cm (right limb) or 2 cm (left limb) of tendon within the bone tunnel. To test the effect of tendon fit on fixation strength, the tunnel in eight animals was drilled to a 4.2-mm diameter in the right hind limb and to 6 mm in the left hind limb. The strength of the biologic interface with 1 cm of tendon length (154 ± 79 N) was only 57% of the strength with 2 cm of tendon length (266 ± 93 N) (P = .004). The strength of the tendon that fit

snugly in the 4.2-mm diameter tunnel (301 ± 61 N) was 32% greater than the strength of the tendon that fit loosely in the 6-mm diameter tunnel (228 ± 65 N) (P = .03). These data suggest that the strength of the biologic interface can be improved by increasing the length of the tendon in the tunnel and by producing a snug fit between the tendon and tunnel wall.[20] Using Distal Fixation Rather than Aperture Fixation to Improve the Fixation Characteristics of the Complex after Implantation

Because surgeons can use either distal or aperture fixation, it is important to determine whether the site of fixation compromises either the strength or the stiffness of a tendon ACL graftfixation methodbone complex after implantation. If the site of fixation compromises the fixation characteristics of the complex after implantation when the loads in the graft increase as a result of resuming activities, then the pace of rehabilitation may need to be adjusted.[56] In the laboratory, the authors determined the effect that distal and aperture fixation methods have on the strength and the stiffness of a tendonfixation methodbone complex 4 weeks after implantation in an ovine model ( Fig. 6B-12 ). The long digital extensor tendon was transplanted into a drill hole in the proximal tibia in 16 ovine models. The strength of distal fixation with a WasherLoc (448 N) was 283% greater than the strength of aperture fixation with an interference screw (157 N) (P = .011). Similarly, the stiffness of distal fixation with a WasherLoc (701 N/mm) was 302% greater than the stiffness of aperture fixation with an interference screw (232 N/mm). These results indicate that the site of fixation compromises the fixation characteristics of a tendon ACL graftfixation methodbone complex after implantation. If these findings are applicable to humans, then the strength and the stiffness of a tendon ACL graft after implantation will be better with distal fixation than with interference screw fixation. These findings can help clinicians decide whether to use distal fixation or aperture fixation with interference screw fixation and whether to adjust the pace of rehabilitation when an interference screw is used.[56]

Figure 6-B-12 Aperture fixation of the tendon in the tunnel was performed using a 7.0-mm diameter, 28-mm long, cannulated, bioabsorbable, interference screw. A 30-mm long, 6-mm diameter tunnel was drilled obliquely across the metaphysis of the ovine tibia. The tunnel was further dilated to 7.0 mm in 0.5-mm increments. The screw was inserted over a guidewire until the tip reached the aperture of the tibial tunnel (arrow). Distal fixation of the tendon in the tunnel was performed using a Wash-erLoc countersunk in the end of the tibial tunnel. A 30-mm long, 7-mm diameter tunnel was drilled. Four weeks after implantation, the animals were killed. The specimens were divided into two groups, and the strength and the stiffness were determined with and without the implants. Using Distal Fixation Rather than Aperture Fixation to Improve the Fixation Characteristics of the Biologic Interface after Implantation

Pinczewski and coworkers claim that direct contact between the graft and the bone by

interference screw fixation is important for formation of the biologic interface. [48] The interference screw may compromise the formation of the biologic interface, however, if the screw blocks contact between the tendon and the bone tunnel and reduces the surface area of the tunnel.[57] Pinczewski's claim was investigated in the author's laboratory in an ovine model in which the strength and the stiffness of the biologic interface of a tendon in a bone tunnel were studied 4 weeks after implantation after removing the distal (WasherLoc) and aperture (interference screw) fixation device ( Fig. 6B-12 ). The strength of the biologic interface of distal fixation with a WasherLoc (277 N) was greater by 208% than the strength of aperture fixation with an interference screw fixation (131 N) (P = .03). Similarly, the stiffness of the biologic interface of distal fixation with a WasherLoc (424 N/mm) was greater by 307% than the stiffness of the biologic interface of aperture fixation with interference screw fixation (138 N/ mm). Aperture fixation with a bioabsorbable interference screw compromised both the strength and stiffness of the biologic interface of a tendon in a bone tunnel after implantation. These results do not support the claim that an interference screw is important for formation of the biologic interface. In fact, the interference screw interferes or severely retards the formation of the biologic interface. The cause

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of the interference of the biologic interface may be a reduction in the surface area of the tunnel available for healing, as a result of the screw preventing contact between the tendon and the tunnel wall.[57] Growth Factors

The weakest region in the early postoperative period after an ACL reconstruction is the site of fixation. Methods to augment tendon-to-bone healing using biologic factors may allow earlier and more aggressive rehabilitation and earlier return to sport and work. One factor that has been tested in a canine model and has promise as an enhancer of the healing of tendon ACL grafts in humans is recombinant human bone morphogenic protein-2 (BMP).[50] Rodeo and associates examined the hypothesis that recombinant human bone BMP enhances bone ingrowth into a tendon graft placed into a bone tunnel as well as the fixation characteristics of the biologic interface.[50] The long digital extensor tendon was transplanted into a drill hole in the proximal tibia in 65 adult mongrel dogs. Two different doses of the BMP were applied to the tendon-bone interface in one limb using an absorbable type I collagen sponge carrier and only the collagen sponge to the contralateral (control) limb. The healed tendon-bone attachment was evaluated at serial times between 3 days and 8 weeks using radiography, histologic examination, and biochemical testing. At all time points, histologic and radiographic examination demonstrated more extensive bone formation around the tendon with closer apposition

of new bone to the tendon in the protein-treated limb than in the paired control limb. Biomechanical testing demonstrated higher tendon strength in the protein-treated side at all time points, with a statistically significant difference between the low-dose-treated side and the control side at 2 weeks. These histologic and biomechanical data suggest superior healing at the lower protein dose. These results indicate that bone morphogenetic protein can accelerate the healing process when a tendon graft is transplanted into a bone tunnel.[50] Phenomenon of Tunnel Enlargement

Tunnel enlargement occurs with tendon ACL grafts; however, the cause of this phenomenon has not been clarified.[23] One theory is that low-stiffness fixation (suture) allows high shear forces acting on the tunnel wall, which could delay osseous incorporation and lead to tunnel enlargement. [23] [34] Based on this mechanism, several authors have proposed that aperture fixation with a bioabsorbable or metal interference screw may overcome these forces and limit tunnel enlargement. [34] [65] A multicenter study examined the hypothesis that tunnel enlargement is less with interference screw fixation than with extra-articular fixation using other methods.[11] Four different combinations of fixation methods were evaluated in 259 subjects from four centers: 87 subjects were reconstructed with bioabsorbable interference screws (Bioscrew), 55 subjects were reconstructed with metal interference screws (RCI), 48 subjects were reconstructed with a bone much screw and staples, and 69 subjects were reconstructed using an endobutton and staples. Tunnel enlargement was calculated as a percentage increase in cross-sectional area based on the initial cross-sectional area of the tunnel, which was calculated from the diameter of the drill bit, and the follow-up cross-sectional area. The follow-up cross-sectional area was determined 1 year postoperatively by measuring the diameter of the widest section of each tunnel from the anteroposterior (AP) and lateral roentgenograms, adjusting for magnification, adding the two diameters, dividing by four, and calculating the area. The tunnel enlargement for a combination of fixation methods was the average of the percentage increase in cross-sectional area of the femoral and tibial tunnels. Contrary to expectation, tunnel enlargement was greatest with bioabsorbable interference screw fixation (122%) and least for elastic fixation with the endobutton and staples (36%) (ANOVA P < .0001, Tukey's P < 0.05). These results do not support the claim that tunnel enlargement is caused by low-stiffness fixation (suture) because the subjects with endobutton and staple fixation had the least amount of tunnel enlargement. In fact, tunnel enlargement is worst with the bioabsorbable interference screw, which is contrary to the predictions of proponents of this fixation method.[13] [48] [59] [67] If the goal is to limit tunnel enlargement, then bioabsorbable interference screw fixation should be avoided.[11]

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Aggressive Rehabilitation with a Tendon ACL Graft

The use of aggressive rehabilitation following ACL reconstruction should be decided based on strength, stiffness, and resistance to slippage under cyclic load of the fixation method used to secure the graft. Because all grafts are stronger and stiffer than the fixation methods, the fixation methods determine whether aggressive rehabilitation can be used safely.[17] [27] [28] Aggressive rehabilitation has been shown to be safe with a tendon ACL graft only with fixation methods that provide high strength and stiffness and resist slippage under cyclic load ( Fig. 6B-13 ). Patients with a DLSTG graft fixed with fixation methods with these characteristics have been safely rehabilitated without a brace and returned to sport at 3 to 4 months with no deterioration in stability at 2 years after the reconstruction. [25] [27] [28] On the other hand, slowing the rehabilitation and using an immobilizer or a brace with low-strength, low-stiffness, and high-slippage fixation techniques such as the endobutton and interference screw do not prevent a higher incidence of instability at 2 years.[5] [44] [55]

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Summary It is important to understand that a tendon ACL graft requires multistrands, which must be tensioned equally and neither braided nor weaved to optimize structural properties. The fixation characteristics of strength, stiffness, and

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Figure 6-B-13 Comparison of the stability of knees reconstructed with a tendon anterior cruciate ligament graft using different fixation methods (MMT = manual maximum anterior load, approximately 200 to 300 N; 134 N = anterior load).[ 5] [ 25] [ 44] [ 55] The incidence of a stable knee (65°C), will also destroy these adjacent afferent receptors. Temperatures at 70°C are known to kill nerves in rat skin, which start to regenerate around 14 days after insult.[83] The destruction of the capsular nerves and mechanoreceptors will disrupt the nociceptive and proprioceptive feedback, decreasing painful stimuli and the sensation of instability, respectively. It is unknown whether the nerve endings or specialized mechanoreceptors will regenerate in the human after thermal insult. If regeneration occurs, in what quantity

Figure 6-F-6 Magnetic resonance images demonstrating the thickness of the axillary pouch (arrow) in a normal shoulder (A) and a shoulder 3 months after thermal capsular shrinkage (B). Note the increase in thickness of the thermally modified tissue.

and to what quality will nociception and proprioception return? The subsequent local anesthesia postulated to occur after thermal insult might result in the reported symptomatic relief experienced by patients. This theory has yet to be proven. In contrast to a loss in afferent stimulation, authors have postulated that capsular shrinkage may create improved proprioception, producing the favorable clinical results. Although the role of capsular mechanoreceptors on shoulder proprioception is controversial, many will agree that they play a role at least complementary to that of muscle receptors. Blasier and colleagues found decreased proprioception in patients with joint laxity.[6] Proprioceptive ability improved with increasing external rotation and diminished with internal rotation, suggesting that capsular tension provides important afferent information involved in proprioception.[6] Levy and coworkers reported improved proprioception in patients with atraumatic instability 9 weeks after capsular shrinkage.[45] The authors believe that the shrinkage creates re-tensioning of the proprioceptors of the shoulder capsule. [45] This recovery in proprioception has previously been reported after open or arthroscopic Bankart's repairs in patients with traumatic anterior instability.[82]

The same authors reported similar restoration of proprioception

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after thermal capsulorrhaphy.[42] It is felt that the re-tensioning of the capsule allows for greater dynamic shoulder control and less sensation of instability, thus producing the therapeutic result.[45] The mechanism of efficacy is likely multifactorial and may include various aspects of these explanations and others not discussed. Wound contraction and growth factors moderating this contraction have been proposed as possible mechanisms, but this research is very preliminary.[82] Whatever the reason for the efficacy, these early successes may turn sour with time, and the results should be approached with cautious optimism and long-term scrutiny.

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Conclusion

Wound healing is a natural and well-orchestrated biologic event. Indeed, the ability of wounds to heal is the foundation on which the practice of surgery is predicated. The successful surgeon maintains a delicate alliance with Mother Nature, balancing the magnitude of the surgical insult against the capacity of the tissue for repair. [3] Thermal injury is one of the most traumatic insults a tissue can sustain, and the high degree of cell death and matrix alteration associated with thermal burns has been shown to result in a protracted healing time. Thus, the use of thermal energy as a stimulant for tissue shrinkage must be tempered with an appreciation of the biologic events that accompany this phenomenon. Furthermore, it must be realized that the initial degree of capsular shrinkage observed after the application of thermal energy may have little bearing on the long-term biologic and biomechanical status of the joint capsule. [3] Therefore, the desire to see a redundant capsule shrink and become taut at surgery should be weighed very carefully against the level of damage imparted to the tissue to achieve this result. In the words of Dr. Hackett, the simple initiation of the healing response may be in itself sufficient to rehabilitate an incompetent structure through the generation of new cellular tissue. [25] Although the ultimate applications of thermal modification of connective tissues have yet to be completely defined, its ultimate role may be that of a low-level stimulant for inducing a biologic repair response rather than a highly aggressive mechanism for primary tissue shrinkage.[3]

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Section G Basic Arthroscopic Principles Mark D. Miller MD Arthroscopy has its roots in Japan, when in 1918 Takagi used a cystoscope to look inside a knee.[29] Watanabe, another Japanese surgeon, is credited with further refinements of the arthroscope and development of the concept of triangulation.[29] North American arthroscopic pioneers include Jackson, Joyce, McGinty, Cassceles, Dandy, O'Connor, and Johnson. Arthroscopy has grown rapidly and is the standard of care for the treatment of many orthopaedic injuries. Textbooks, journals, societies, and subspecialization have expanded the scope of arthroscopic surgery further. Arthroscopy often can be done more quickly, with increased accuracy, lower complication rates, decreased hospitalization time, and shorter recovery periods than many operative techniques.[12] The effective use of arthroscopy is based on the understanding of benefits and use of arthroscopy as well as its limitations. In the first issue of Arthroscopy, the Journal of Arthroscopic and Related Surgery, guidelines were elucidated for the practice of arthroscopic surgery[16] : 1. The arthroscopist should perform an adequate history and physical examination as well as obtaining radiographs or other pertinent laboratory evaluations for each patient or determine that these already have been performed. 2. The risks, benefits, alternatives of treatment, and potential complications should be outlined carefully to each patient before an arthroscopic evaluation. 3. The arthroscopist should select carefully the correct arthroscopic procedure for a particular condition. 4. A detailed report of the procedure should be prepared, including the arthroscopic findings and description of the operation.

Operative Suite

Arthroscopy is performed most commonly in a standard surgical suite in either a hospital or an ambulatory surgical facility. Office arthroscopy, although advocated by some, may have significant limitations and is used primarily for diagnosis in selected patients. Newer flexible fiberoptic catheter systems resulted in underrecognition and underestimation of the severity of intra-articular knee disease in one study. [36] A relatively large room that can accommodate the bulky arthroscopic equipment is preferred. Storage space for video equipment, shaver blades, instruments, and other equipment should be available in the room or nearby. Dedicated, well-trained operating room personnel are required. Adequate electrical support, lighting, suction, and other logistic concerns should be considered. Equipment sterilization is important. Standard autoclaving is not appropriate for arthroscopes, cables, and many of the instruments used in arthroscopy. Gas sterilization with ethylene oxide is effective, but because of the long turnover times associated with this method, instruments cannot be reused during the same operative day.[31] Because of the these concerns, most centers have elected to accept high-level disinfection in lieu of sterilization. A newer system that uses peracetic acid (Steris, Menor, Ohio) is convenient and efficacious, and it largely has replaced other methods of sterilization.[13]

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Arthroscopic Equipment

Arthroscopy requires an arthroscope, a camera, a light source and fiberoptic cable, an irrigation system, cannulas, and various hand and motorized instruments. An arthroscope is a small-diameter fiberoptic instrument that allows direct visualization of joints (Fig. 6G-1 (Figure Not Available) ).[12] It is designed to fit into a sleeve, or cannula. The cannula first is inserted into the joint with a sharp or blunt rod called a trocar, then the trocar is exchanged for the arthroscope. A fiberoptic cable and camera are attached to the arthroscope, and irrigation fluid is attached to one or more cannulas. A specially adapted video camera usually is attached to the eyepiece of the arthroscope, and images can be recorded directly onto video or onto an accompanying printer (Fig. 6G-2 (Figure Not Available) ). Arthroscopes are classified according to their diameter and viewing angle. The most commonly used arthroscope is 4 mm with a 25- to 30-degree angle. Smaller arthroscopes (2.5 and 1.9 mm) can be used for smaller joints (e.g., wrist). Different angles (70 or 90 degrees) sometimes are useful when visualization can be difficult (e.g., posterior knee). Instruments used during arthroscopy include hand-operated instruments (e.g., probes, baskets, grabbers) and motorized

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Figure 6-G-1 (Figure Not Available) Top to bottom: 30-degree arthroscope with attached cable, 70-degree detached arthroscope, detachable camera cable (left) and sleeve (cannula) (right), trocar for introduction of sleeve, and 30-degree detached arthroscope. (From DiGiovine NM, Bradley JP: Arthroscopic equipment and setup. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 543-556.)

instruments (e.g., shavers) (Fig. 6G-3 (Figure Not Available) ). Commercially available shavers of various sizes, shapes, angles, and blades are useful in a variety of situations (Fig. 6G-4 (Figure Not Available) ). Intra-articular cautery can be useful, and specially adapted Figure 6-G-2 (Figure Not Available) Top to bottom: Arthroscopic cart showing camera, light source with cable, video equipment, and printer. A monitor (not shown) can be placed on top of the cart. (From DiGiovine NM, Bradley JP: Arthroscopic equipment and setup. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 543-556.) Figure 6-G-3 (Figure Not Available) Probes (top two instruments) and baskets (bottom three instruments) come in a variety of sizes and angles. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

tips that can be used with normal irrigating systems are available. Other available systems include special heat probes and lasers. Irrigation is used during arthroscopy for joint distention, improved visualization, and removal of debris. Lactated Ringer's solution usually is used because it is more physiologic than normal saline.[45] A study suggested, however, that 5% mannitol may prevent excessive loss of proteoglycan from hyaline cartilage.[26] Cannulas are used for fluid egress or ingress. Hydrostatic pressure is necessary to maintain joint distention. This pressure can be attained by gravity or through commercially available pumps (Fig. 6G-5 (Figure Not Available) ).

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Arthroscopic Visualization

One must understand several fundamental concepts to interpret arthroscopic images accurately. First, the typical Figure 6-G-4 (Figure Not Available) Arthroscopic shavers come in a variety of sizes, angles, and blades. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

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Figure 6-G-5 (Figure Not Available) Commercially available arthroscopy pump allows precise control of flow rate and hydrostatic pressure. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

arthroscope does not look straight ahead but instead is directed at a 25- to 30-degree angle off the axis.[42] This angle allows greater visual control and improves the field. The arthroscopist can keep the arthroscope stationary and rotate the viewing angle, allowing a 60-degree view from a 30-degree scope (Fig. 6G-6 (Figure Not Available) ). Another consideration is that an object's size as seen on the monitor is magnified. The degree of magnification varies with the distance of the object from the lens of the arthroscope. Judging distances and size requires practice. Knowing the dimensions of an instrument, such as an arthroscopic probe, helps in determining the relative size of the object being visualized. It is helpful to know about normal versus abnormal findings in each joint.

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Arthroscopic Technique

Extreme care should be taken in positioning the extremity for arthroscopy to avoid any compression that can result in neurapraxia. The nonoperative side is padded and protected, and excessive traction or unnecessary motion of the operative extremity is avoided. Numerous positioning and traction devices are commercially available and are Figure 6-G-6 (Figure Not Available) Rotation of a 30-degree arthroscope allows a 60-degree view. ( From Crane L, Sullivan DJ: Instrumentation. In McGinty JB [ed]: Operative Arthroscopy. New York, Raven Press, 1991, p 6.)

often helpful. Tourniquets, when used, should be as wide as possible, and tourniquet time should be minimized. Surgical preparation and draping should be performed carefully to seal the operative field and to create a sterile environment. A joint-specific systematic diagnostic examination should be done before any therapeutic procedures are performed. A complete arthroscopic examination usually can be performed in a few minutes, then a complete operative plan can be confirmed or modified according to these findings.

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Arthroscopic Complications

Any operation carries a risk of complications, and arthroscopy is no exception.[47] Perhaps the most common complication is inadvertent damage to the intra-articular structures.[15] This risk is inversely proportional to the surgeon's experience and the care with which the surgeon performs the procedure. Proper portal placement, gentle technique, and attention to detail are crucial. Instruments can break, especially when older, unserviced instruments are used.[34] Nerve or vessel injury can result from improper portal placement. A thorough knowledge of local anatomy is needed before performing arthroscopy. In joints at particular risk (e.g., the elbow), the nick and spread method is preferred. The skin only is cut with a blade, and a small hemostat is used to clear the way before inserting instruments with this method. Tourniquet paresis can be reduced with a wide cuff and by limiting tourniquet time to less than 90 minutes whenever possible.[46] Positioning devices (e.g., leg holders) can have a tourniquet effect, even when the tourniquet is not inflated. Fluid extravasation has been reported,[37] although the incidence of this complication can be reduced with careful placement of inflow cannulas and proper use of inflow pumps. Synovial fistula formation is a rare complication of arthroscopy and usually is remedied by 7 to 10 days of immobilization and, occasionally, delayed closure. Infection is an extremely rare complication of arthroscopy, usually the result of a break in sterile technique.[14] High-dose antibiotics and arthroscopic irrigation and débridement may be indicated in severe cases.[28]

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Arthroscopic Applications

Arthroscopy can be used for a variety of diagnostic and therapeutic purposes. Arthroscopy is useful in almost all major joints for irrigation and débridement, loose or foreign body removal, synovectomy, débridement of loose soft tissue, addressing osteoarticular lesions or fractures, and diverse other procedures. The use of arthroscopy in the knee and shoulder has increased steadily. Arthroscopy has become the standard for treatment of meniscal tears. Applications continue to expand, and the future scope of arthroscopic applications is limited only by the imagination of the arthroscopist. A brief introduction of arthroscopy for each joint follows.

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Knee Arthroscopy

Indications

Arthroscopy has diverse application to various forms of knee disease. Diagnostic arthroscopy helps to confirm suspected knee injuries. Arthroscopic synovectomy can be useful for synovial biopsies to aid the diagnosis of rheumatologic disorders, to remove diseased synovium, and to resect synovial folds or plicae. A six-portal technique is favored for complete synovectomy. Treatment of meniscal disease is perhaps the most common application of arthroscopy. Meniscal tears account for approximately 50% of knee injuries that require surgery.[30] Osteochondral lesions commonly are addressed arthroscopically. Injuries to the cruciate ligaments can be diagnosed easily with arthroscopy; endoscopic reconstruction of these ligaments is one of the most common orthopaedic procedures. Other procedures that sometimes are aided with arthroscopy include tibial plateau

fracture reduction, reduction and fixation of tibial eminence fractures, loose body removal, anterior fat pad débridement, lateral release for patellar malalignment, and irrigation and débridement of septic arthritis. Positioning and Portal Placement

Two different forms of positioning are used commonly for knee arthroscopy. The patient can be placed supine on the operating table, and a lateral post can be used for countertraction. Alternatively, the operative leg can be positioned in a commercially available leg holder ( Fig. 6G-7 ). The operative leg is allowed to hang freely over the end of the operating table, and the opposite leg is positioned in a well-padded leg holder with care taken not to compress the peroneal nerve. Standard arthroscopic portals for knee arthroscopy include a superomedial or superolateral portal for fluid inflow and outflow and inferomedial and inferolateral portals positioned just above the joint line on both sides of the patellar tendon for arthroscopy and instrumentation ( Fig. 6G-8 ). The inferolateral portal usually is used during diagnostic arthroscopy. Accessory portals for the knee include the posterome dial, posterolateral, far medial and lateral, and proximal superomedial portals. The posteromedial portal is often helpful for visualizing the posterior cruciate ligament[19] and the posterior horn of the medial meniscus.[25] The posterolateral portal, located between the iliotibial band and the biceps tendon, sometimes is helpful, but extreme care should be taken to ensure that the portal is anterior to the biceps tendon to avoid injury to the peroneal nerve. Other portals include the midpatellar portal; far medial and lateral portals (sometimes helpful for instrument placement in hard-to-reach areas); and the proximal superomedial portal, located 4 cm proximal to and in line with the medial edge of the patella (for assessment of patellar tracking). Arthroscopic Anatomy

As with any joint, systematic examination of the knee is appropriate. Before positioning the patient, a complete

Figure 6-G-7 Arthroscopic positioning with a commercially available leg holder for the operative leg and a well-padded gynecologic leg holder for the nonoperative extremity. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 50. )

Figure 6-G-8 Arthroscopic portals for knee arthroscopy. FL, far lateral; FM, far medial; IL, inferolateral; IM, inferomedial; MP, midpatellar; PL, posterolateral; PM, posteromedial; PSM, proximal superomedial; SL, superolateral; SM, superomedial. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 50.)

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Figure 6-G-9 Normal arthroscopic anatomy of the knee. (Inset shows posteromedial aspect of the knee as seen through the notch.) ACL, anterior cruciate ligament; PCL, posterior cruciate ligament. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 51.)

examination under anesthesia is conducted to assess instability in all planes. An arthroscopic cannula is placed in the superomedial or superolateral portal for inflow and outflow, and the arthroscope is introduced into the inferolateral portal. Although many examination sequences are possible, it is important to visualize the suprapatellar pouch, patellofemoral joint, medial and lateral gutters, medial and lateral compartments (meniscus and articular cartilage), and intercondylar notch (cruciate ligaments) in all patients. Accessory viewing portals are established as necessary if other areas need to be evaluated. After a complete evaluation of the joint ( Fig. 6G-9 ), all surgical pathology is addressed. Hip Arthroscopy

Indications

The indications for hip arthroscopy are more limited than for other joints. Because of its anatomy, the hip joint is difficult to access via arthroscopy, and maneuverability is difficult. Arthroscopy may be indicated for cases of loose bodies, torn labral tissue, articular cartilage lesions, synovial or ligamentum teres impingement, and refractory pain of undetermined cause. Arthroscopy can be used in young arthritic patients to delay the need for total joint arthroplasty.[23] Positioning and Portal Placement

Two positions are popular for hip arthroscopy, the supine and the lateral decubitus position. The latter, developed by Glick and colleagues[24] after their initial dissatisfaction with the supine position, is performed with the patient on his or her side with the involved hip on top. The patient is placed in the lateral decubitus position on a fracture table with a peroneal post, and traction is applied through the footplate, skeletal traction, or a commercially available external traction device. The leg is abducted 45 degrees and forward flexed 10 degrees. [24] Approximately 50 pounds of traction is necessary to distract the hip 8 to 10 mm

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Figure 6-G-10 Portals for hip arthroscopy include the anterior portal and two portals adjacent to the superior edge of the greater trochanter. (From Miller MD, Cooper DE, Warner JJP: Review of Sports Medicine and Arthroscopy. Philadelphia, WB Saunders, 1995.)

for arthroscopic visualization.[23] The supine position was reintroduced by Byrd,[6] who also used a fracture table. A padded peroneal post is lateralized to the operative side, the hip is positioned in extension and 25 degrees of abduction, and traction is applied. Fluoroscopy is recommended for either position to confirm entry into the joint. Portals are similar for both positions and include the anterior, anterolateral (anterior trochanteric), and posterolateral (posterior trochanteric) portals ( Fig. 6G-10 ). The anterior portal is established at the intersection of a sagittal line drawn distally from the anterior superior iliac spine and a transverse line across the superior margin of the greater trochanter. The arthroscope can be inserted in this portal in a direction 45 degrees cephalad and 30 degrees toward the midline. Although this portal places the lateral femoral cutaneous nerve at risk, studies show that the nerve, which arborizes before this point, lies lateral to this portal.[7] The other two portals are established at the anterior and posterior margins of the superior edge of the greater trochanter. These portals lie approximately 4 cm below the superior gluteal nerve, and the posterolateral portal is approximately 3 cm superior to the sciatic nerve.[7] Special extra-long cannulas and sheaths (5.25 inches) have been developed for hip arthroscopy. Surgical instruments and the arthroscope can be exchanged easily with these cannulas. Cannulated trocars are commercially available to allow insertion over a guidewire that can be introduced through a large-diameter spinal needle, which facilitates portal placement. Arthroscopic Anatomy

Most of the hip joint can be visualized with the arthroscope ( Fig. 6G-11 ).[33] Of the femoral head, 80% or more can be seen, and the insertion of the ligamentum teres into the anteromedial portion of the femoral head is a readily identifiable landmark. The acetabulum is well visualized with the horseshoe-shaped, lunate surface of the acetabulum that extends to the peripheral labrum and central acetabular fossa. The acetabular fossa extends inferiorly and is filled with vascular adipose tissue extending to the transverse ligament. Viewing the joint through different portals helps evaluate all forms of hip disease. Ankle Arthroscopy

Indications

The most accepted indication for ankle arthroscopy is removal of loose bodies. This situation is uncommon but may be a result of osteochondritis dissecans of traumatic osteochondral injuries. These lesions can be débrided or repaired with arthroscopic techniques. Synovial or osteophytic impingement is perhaps the most common indication for ankle arthroscopy.[17] [20] [50] Another procedure that is gaining acceptance is

arthroscopically assisted tibiotalar arthrodesis. [39] Other relative indications for ankle arthroscopy include adjunctive treatment of fractures, stabilization procedures, and synovectomy for rheumatologic conditions. Positioning and Portal Placement

Most surgeons perform ankle arthroscopy with the patient supine. Several commercially available ankle distracters are available and provide enough distraction for adequate visualization. Alternatively, the patient's knee and leg can be positioned over the end of the operating table, and a gauze-bandage loop can be fashioned as the surgeon's foot provides a distraction force.[53] The standard 4.0-mm arthroscope can be used for most procedures, although small arthroscopes (2.7 mm) may be helpful for areas that are more difficult to visualize (e.g., the posterior ankle). A 3.5-mm diameter shaver is often helpful for ankle arthroscopy. The most commonly used portals are the anteromedial and anterolateral portals.[18] The anteromedial portal is placed just medial to the tibialis anterior tendon at the level of the ankle joint. A spinal needle helps to localize this site and instill saline into the joint. The anterolateral portal is established just lateral to the peroneus tertius tendon at the joint line level ( Fig. 6G-12 ). The nick and spread technique helps to establish these portals to ensure that superficial nerves and veins are avoided. A posterolateral portal, placed just lateral to the Achilles tendon, can be used for outflow or occasionally to visualize the posterior ankle. A 70-degree arthroscope placed through an anterior portal usually provides adequate visualization of the posterior ankle, however. Because of the significant neurovascular risk, the anterocentral (dorsalis pedis artery and deep peroneal nerve) and posteromedial (posterior tibial artery and tibial nerve) portals usually are not recommended.

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Figure 6-G-11 Arthroscopic anatomy of the hip. AL, anterior labrum; AW, wall of acetabulum; FH, femoral head; L, labrum; LT, ligamentum teres; PL, posterior labrum; PW, posterior wall. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 101.)

Figure 6-G-12 Portals for ankle arthroscopy are anteromedial, anterolateral, and posterolateral. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 134.)

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Figure 6-G-13 Arthroscopic anatomy of the ankle. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 134. ) Arthroscopic Anatomy

The anterolateral portal is used most commonly for visualization. The joint should be evaluated systematically ( Fig. 6G-13 ). The lateral sulcus and tip of the fibula usually can be visualized. The medial sulcus and tip of the medial malleolus is seen best with the arthroscope placed in the anteromedial portal. Pathology is addressed as necessary. Shoulder Arthroscopy

Indications

Indications for shoulder arthroscopy are evolving, but there are proponents and opponents for each proposed application, and the controversy continues. Shoulder arthroscopy has been applied to the diagnosis and treatment of shoulder instability, impingement syndrome, distal clavicle problems, rotator cuff disease, inflammatory and degenerative diseases of the shoulder, adhesive capsulitis, sepsis, and other diagnoses. Arthroscopy has been advocated for débridement of loose tissue and washout of degenerative arthritis,[9] treatment of adhesive capsulitis,[1] [27] irrigation and débridement of septic joints,[41] removal of foreign bodies, and a variety of other procedures. Positioning and Portal Placement

Two methods of positioning are popular, the lateral decubitus position and the beach-chair position. The lateral decubitus position involves placement of the patient with the affected arm up; traction is used to suspend the arm. Transient neurapraxia can be a common problem with this positioning.[35] Other disadvantages of this position are that regional anesthesia is tolerated poorly, conversion to an open procedure is difficult, the capsular anatomy is distorted, and arm positioning can be more difficult. [2] Because of these problems, the beach-chair position was developed by Warren in 1986.[52] This positioning allows easy access for arthroscopy without the disadvantages of other positions. The most commonly used arthroscopic shoulder portals are the posterior, anterosuperior, anteroinferior, and lateral portals. The superior, or Neviaser, portal and the posterolateral

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Figure 6-G-14 Arthroscopic portals for shoulder arthroscopy. 1, Posterior; 2, anterosuperior; 3, anteroinferior; 4, lateral; 5, superior or Neviaser portal. (From Miller MD, Cooper DE, Warner JJP: Review of Sports Medicine and Arthroscopy. Philadelphia, WB Saunders, 1995.)

portal (of Wilmington) are used by some surgeons as accessory portals ( Fig. 6G-14 ). The posterior portal, placed 2 cm medial and 2 to 3 cm inferior to the posterolateral corner of the acromion, is used primarily for arthroscopic visualization. The anterosuperior portal, located lateral to the coracoid and just distal to the anterior edge of the acromion, is used most commonly for instrumentation. The anteroinferior portal, located approximately 2 cm below the anterosuperior portal just above the subscapularis tendon (visualized arthroscopically), is used primarily for arthroscopic Bankart repair. The lateral portal is used for instrumentation during bursoscopy. The superior (or supraspinatus or Neviaser) portal is located at the corner of the supraspinatus fossa and is oriented slightly anteriorly and laterally. This portal is used for visualization of the anterior glenoid and may be helpful in addressing superior labral and biceps injuries. The posterolateral portal (port of Wilmington) is used most commonly for superior labral repairs. Arthroscopic Anatomy

Although many sequences are recommended for arthroscopic evaluation of the shoulder, it is important to visualize and palpate the biceps tendon, labrum, glenohumeral articular surfaces, glenohumeral ligaments, and rotator cuff as a minimum ( Fig. 6G-15 ). During bursoscopy, the superior surface of the rotator cuff, the inferior acromion, and the acromioclavicular joint should be evaluated. The interface of the biceps tendon and superior labrum most commonly is visualized first to allow the surgeon to become oriented, then the surgeon can address the possibility of a superior labral anterior-to-posterior lesion. The labrum is inspected and probed to detect any labral injury (Bankart's tear), especially in a patient with anterior instability. Separation of the superior labrum from the glenoid may be normal.[11] The articular surfaces of the glenoid and humerus are examined for any articular injuries or degenerative joint disease. By rotating the arm, one can visualize most of the proximal humerus. With the arthroscope positioned posterior and inferior to the superior surface of the glenoid, internal rotation of the humerus allows visualization of a Hill-Sachs defect, or impression fracture, associated with anterior instability. Then the glenohumeral ligaments can be evaluated. The superior glenohumeral ligament is located in the biceps tendon and subscapularis. The middle glenohumeral ligament drapes over the subscapularis tendon. The inferior glenohumeral ligament complex is composed of two bands, anterior and posterior, and attaches to the inferior labrum. Arthroscopy of the inferior axillary pouch, the rotator cuff insertion (superiorly), and the sub-acromial bursa completes the examination.

Elbow Arthroscopy

Indications

Although the indications for elbow arthroscopy are evolving, it is a well-accepted technique for removal of loose bodies, irrigation of an infected joint, synovectomy, and osteophyte excision. Loose or foreign bodies can be removed easily from the joint using the contralateral portal.[8] [38] [40] A septic joint can be irrigated with only two portals (proximal-medial and posterolateral). [43] Osteophytes can be removed using arthroscopic burs and generous irrigation.[51] Synovectomy can be accomplished via anterior and posterior portals and can provide considerable pain relief in patients with chronic synovitis.[4] Other proposed procedures include arthroscopic capsular[32] and radial head excision.[43] Positioning and Portal Placement

Elbow arthroscopy can be done with the patient supine[3] or prone.[44] The prone position, which is more popular, allows improved arthroscopic manipulation and better visualization without the use of an overhead suspension device.[43] The soft spot, or anconeus triangle (defined by the lateral epicondyle, tip of the olecranon, and radial head) should be palpated, and 30 to 50 mL of fluid should be injected to distend the capsule before establishing arthroscopic portals. Three portals commonly are used for elbow arthroscopy: the proximal-medial, posterolateral, and anterolateral portals. A fourth portal, the direct posterior portal, can be established when posterior instrumentation is necessary. A final portal, the proximal lateral portal, has been advocated for improved safety ( Fig. 6G-16 ).[21] [48] [49] The nick and spread method should be used when establishing all arthroscopic portals about the elbow because of the attendant neurovascular risk. The proximal-medial portal is the primary diagnostic arthroscopic portal with the patient in the prone position.[43] This portal is located 2 cm proximal to the medial epicondyle, just anterior to the intermuscular septum. The arthroscopic

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Figure 6-G-15 Arthroscopic anatomy of the shoulder. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 160. )

sheath should contact the anterior surface of the humerus and is directed toward the radial head. The posterolateral portal is made in the anconeus triangle and can be used for inflow and outflow. The arthroscope can be introduced into this portal to allow

visualization of the posterior joint. Some authors favor establishing this portal proximal and posterior to this location, 2 cm proximal to the tip of the olecranon and adjacent to the lateral edge of the triceps tendon. The anterolateral portal is established 3 cm distal and 2 cm anterior to the lateral epicondyle with the elbow flexed 90 degrees. The portal can be established with an inside-out technique using a blunt rod. The radial nerve is at risk with this portal and is immediately adjacent to the portal in 50% of cases.[49] The direct posterior portal is made 2 cm proximal to the tip of the olecranon, through the triceps tendon, and is used primarily for instrumentation in the posterior joint. The proximal-lateral portal was developed to reduce the risk associated with other portals.[48] It is located 1 to 2 cm proximal to the lateral epicondyle, directly on the anterior surface of the humerus. As with the proximal-medial portal, the trocar is kept in direct contact with the anterior humerus during insertion. The proximal-lateral portal has been advocated in lieu of the more hazardous anterolateral portal.[10] The radial head and capitellum can be well visualized

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Figure 6-G-16 Arthroscopic portals for elbow arthroscopy. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 197.)

through this portal. The anteromedial portal, located 2 cm distal and 2 cm anterior to the medial epicondyle, can jeopardize the anterior branch of the medial antebrachial cutaneous nerve and the median nerve and usually is not recommended. The standard anterior portals used in elbow arthroscopy should be proximal-medial and proximal-lateral portals. The anteromedial and anterolateral portals, if necessary, should be established proximal to the radial head. Arthroscopic Anatomy

With the arthroscope placed in the proximal medial portal, the humeroulnar and radiocapitellar joints, the coronoid fossa, and the medial and lateral gutters can be well visualized ( Fig. 6G-17 ). The posterior joint (olecranon and olecranon fossa) can be well visualized through the posterolateral portal. Wrist Arthroscopy

Indications

Wrist arthroscopy is becoming increasingly useful in the diagnosis and treatment of wrist disorders. Treatment of injuries to the triangular fibrocartilage complex (TFCC),

treatment of ligament injuries, fracture management, and treatment of wrist disease are enhanced with arthroscopy. Type 1C volar rim tears of the TFCC that involve the origins of the ulnotriquetral and ulnolunate ligaments are managed with an open procedure after arthroscopic identification. The treatment of these injuries is controversial, but two good choices currently exist. Bednar and Osterman[5] advocated direct repair augmented with a strip of the flexor carpi ulnaris tendon. The other option is to advance the origin of the ulnotriquetral and ulnolunate ligaments into the triquetrum with a bone anchor. Type 1D tears of the radial attachment of the TFCC by definition involve the dorsal radioulnar ligament or the volar radioulnar ligament or both. Tears close to the radial attachment of the TFCC, which spare the dorsal radioulnar ligament and volar radioulnar ligament, are best considered type 1A tears and are treated with débridement. Arthroscopic reduction and fixation of intra-articular distal radius fracture is being employed more frequently. In the search for the most appropriate and beneficial treatment for this difficult injury, the arthroscope has some important potential advantages.[10] [32] Positioning and Portal Placement

Wrist arthroscopy is performed with the patient supine. Wrist distraction (10 to 12 pounds) usually is achieved

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Figure 6-G-17 Arthroscopic anatomy of the elbow. (Inset, posterior view.) (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 198.)

Figure 6-G-18 Arthroscopic wrist portals. Numbers indicate wrist extensor compartments and associated portals. MCR, midcarpal radial; MCU, midcarpal ulnar; R, radial; STT, scaphotrapeziotrapezoid; U, ulnar. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 220.)

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with a commercially available traction device. A small 1.9-to 2.7-mm arthroscope and small joint instruments with a maximum diameter of 3.0 mm are used.

Arthroscopic portals about the wrist are designated based on their location in reference to the dorsal extensor compartments ( Fig. 6G-18 ). The standard portals for any diagnostic wrist arthroscopy are the 3-4, the 4-5, and the radial midcarpal portal. Accessory radiocarpal portals include the 1-2, 6R, and 6U. The 3-4 is the primary portal for arthroscopic visualization. Inflow usually is established through the scope. Outflow can be done with an 18-gauge catheter through either the 1-2 or 6U portal. Alternatively, a pressure-sensitive inflow-outflow pump device can be used. The 4-5 and 6R portals are primarily for instrumentation. The optimal configuration for working on the TFCC is to place the arthroscope in the 4-5 portal and to introduce instruments through the 6R portal. The midcarpal portals include the midcarpal radial, midcarpal ulnar, and scaphotrapeziotrapezoid (STT) portals. The midcarpal radial portal is 1 cm distal to the 3-4 portal, and the midcarpal ulnar portal is 1 cm distal to the 4-5 portal. Generally, visualization is accomplished through the midcarpal radial portal. Instruments are introduced through the midcarpal ulnar portal, although the steps can be reversed. The STT portal is located just ulnar to the extensor pollicis longus tendon over the STT joint. When débriding the STT joint, visualization is accomplished through the midcarpal radial portal. Instruments are introduced through the STT portal. Arthroscopic Anatomy

A thorough and complete wrist arthroscopy details the anatomy of the articular surfaces, intrinsic carpal ligaments, extrinsic carpal ligaments, and TFCC ( Fig. 6G-19 ). Proceeding from radial to ulnar in the radiocarpal joint, the following structures are observed: radial styloid, radioscaphocapitate ligament, long radioulnate ligament, scaphoid proximal pole, radius scaphoid facet, scapholunate interosseous ligament, radioscapholunate ligament (ligament of

Figure 6-G-19 Arthroscopic wrist anatomy. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 221.)

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Testut), lunate proximal pole, radius lunate facet, short radiolunate ligament, TFCC (including the dorsal and volar radioulnar ligaments), ulnolunate ligament, ulnotriquetral ligament, lunatotriquetral interosseous ligament, and triquetrum proximal pole. Proceeding from radial to ulnar in the midcarpal joint, examination of the following structures is accomplished: STT, capitate proximal pole, scaphoid distal pole, scapholunate interval stability, lunate distal pole, lunatotriquetral interval stability, triquetrum distal pole, capitohamate interval, hamate proximal pole. The ligaments that cross the midcarpal joint often are difficult to visualize because of

overlying synovium. If a midcarpal instability is suspected, visualization can be accomplished by débriding the synovium carefully. The ligaments in question include the radioscaphocapitate, ulnocapitate, triquetrocapitate, and triquetrohamate.

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Conclusion

Arthroscopy is a useful tool in the orthopaedic surgeon's operative approach. Arthroscopy is not the only tool, however, and well-founded open techniques should be available and understood. New applications of arthroscopy in the future may include cartilage regeneration, ligament reconstruction and repair, and genetic engineering.

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Byrd JWT, Pappas JN, Pedley MJ: Hip arthroscopy: An anatomic study of portal placement and relationship to the extra-articular structures. Arthroscopy 11:418-423, 1995. 7.

Cameron SE, Travis MT, Kruse RW: Foreign body arthroscopically retrieved from the elbow. Arthroscopy 9:220-221, 1993. 8.

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Cooney WP, Berger RA: Treatment of complex fractures of the distal radius: Combined use of internal and external fixation and arthroscopic reduction. Hand Clin 9:603-612, 1993. 10.

Cooper DE, Arnoczky SP, O'Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum. J Bone Joint Surg Am 74:46-52, 1992. 11.

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Coward DB: General principles and instrumentation of arthroscopic surgery. In Chapman MW (ed):

Operative Orthopaedics. Philadelphia, JB Lippincott, 1988, pp 1549-1559. Crow S: Peracetic acid sterilization: A timely development for a busy healthcare industry. Infect Control Hosp Epidemiol 13:111-113, 1992. 13.

DeLee JC: Complications of arthroscopy and arthroscopic surgery: Results of a national survey. Arthroscopy 4:214-220, 1988. 14.

DiGiovine NM, Bradley JP: Arthroscopy equipment and setup. In Fu FH, Harner CD, Vince KG (eds): Knee Surgery. Baltimore, Williams & Wilkins, 1994. 15.

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Ewing JW: Arthroscopic management of transchondral talar dome fractures (osteochondritis dissecans) and anterior impingement lesions of the ankle joint. Clin Sports Med 10:677-687, 1991. 17.

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Fanelli GC, Giannetti BF, Edson CJ: The posterior cruciate ligament: Evaluation and treatment. Curr Concepts Rev Arthrosc 10:673-688, 1994. 19.

Ferkel RD, Karzel RP, Del Pizzo W, et al: Arthroscopic treatment of anterolateral impingement of the ankle. Am J Sports Med 19:440-446, 1991. 20.

Field LD, Altchek DW, Warren RF, et al: Arthroscopy anatomy of the lateral elbow: A comparison of three portals. Arthroscopy 10:602-607, 1994. 21.

Geissler WE: Arthroscopically assisted reduction of intra-articular fractures of the distal radius. Hand Clin 11:19-29, 1995. 22.

Glick JM: Hip arthroscopy. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, pp 663-676. 23.

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Gold DL, Schaner PJ, Sapega AA: The posteromedial portal in knee arthroscopy: An analysis of diagnostic and surgical utility. Arthroscopy 11:139-145, 1995. 25.

Gradiner R, Trager J, Klauser RJ: Influence of various irrigation fluids on articular cartilage. Arthroscopy 11:263-269, 1995. 26.

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Jackson RW: Quovenis quovadis: Evolution of arthroscopy. Arthroscopy 15:680-685, 1999.

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Jones GS, Savoie FH III: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277-283, 1993. 32.

Keene GS, Villar RN: Arthroscopic anatomy of the hip: An in vivo study. Arthroscopy 10:392-399, 1994. 33.

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Kieser C: A review of the complications of arthroscopic knee surgery. Arthroscopy 8:79-83, 1992.

Klein AH, France JC, Mutschler TA, Fu FH: Measurement of the brachial plexus strain in arthroscopy of the shoulder. Arthroscopy 3:45-52, 1987. 35.

Meister K, Harris L, Indelicato PA, Miller G: A comparison of an optical catheter office arthroscope with a standard rigid rod-lens arthroscope in the evaluation of intra-articular pathology of the knee. In Book of Abstracts and Outlines, American Academy of Sports Medicine 21st Annual Meeting, July 16-19, 1995, Toronto. 36.

Noyes FR, Spievack ES: Extraarticular fluid dissection in tissues during arthroscopy: A report of clinical cases and a study of intraarticular and thigh pressures in cadavers. Am J Sports Med 10:346-351, 1982. 37.

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Ogilvie-Harris DJ, Lieverman I, Fitsalos D: Arthroscopically assisted arthrodesis for osteoarthritic ankles. J Bone Joint Surg Am 75:1167-1174, 1993. 39.

Ogilvie-Harris DJ, Schemitwch E: Arthroscopy of the elbow for removal of loose bodies. Arthroscopy 9:5-8, 1993. 40.

Olgilvie-Harris DJ, Wiley AM: Arthroscopic surgery of the shoulder: A general appraisal. J Bone Joint Surg Br 68:201-207, 1986. 41.

Olsen EJ, King NA: Arthroscopic anatomy. In Fu FH, Harner CD, Vince KG (eds): Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 77-99. 42.

43.

Poehling GG, Ekman EF: Arthroscopy of the elbow. Instr Course Lect 44:217-223, 1995.

Poehling GG, Whipple TL, Sisco I, et al: Elbow arthroscopy: A new technique. Arthroscopy 5:222-224, 1989. 44.

Reagan BF, McInery VK, Treadwell BV, et al: Irrigating solutions for arthroscopy: A metabolic study. J Bone Joint Surg Am 65:629-631, 1983. 45.

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47.

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Stothers K, Day B, Regan W: Arthroscopic anatomy of the elbow: An anatomical study and description of a new portal. Arthroscopy 9:362-263, 1993. 48.

Stothers K, Day B, Regan WR: Arthroscopy of the elbow: Anatomy, portal sites, and a description of the proximal lateral portal. Arthroscopy 11:449-457, 1995. 49.

Thein R, Eichenblat M: Arthroscopic treatment of sports-related synovitis of the ankle. Am J Sports Med 20:496-499, 1992. 50.

Ward WG, Anderson TE: Elbow arthroscopy in a mostly athletic population. J Hand Surg Am 18:220-224, 1993. 51.

Warner JJP: Shoulder arthroscopy in the beach-chair position: Basic setup. Oper Tech Orthop 1:147-154, 1991. 52.

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Section H Arthroscopic Knot Tying John Antoniou MD, PhD, FRCSC Richard Rozencwaig MD Douglas T. Harryman II MD Arthroscopic advances now allow the orthopaedic surgeon to repair and reconstruct a vast array of disorders. Although new devices have been introduced that may obviate the need for arthroscopic knots in selected procedures, the ability to tie strong and reproducible knots is essential for the arthroscopic surgeon who wishes to achieve results comparable with those associated with open repairs. A secure arthroscopic knot provides optimal tissue apposition for healing. Because postoperative rehabilitation protocols include immediate loading of a repair, improved knot security will ultimately maximize functional outcome. Arthroscopic knot tying is technically demanding and requires considerable practice. Therefore, the authors suggest that the arthroscopic knot-tying instruments be used initially in the laboratory to practice the knot-tying technique. [1] [4] [8] [16] [18] [31] [32] Many courses are available for those who benefit from a combination of didactic and hands-on workshops. Suture Limbs

Once the suture is passed through the tissue to be repaired, two limbs (i.e., the suture limbs) are available to be tied. The post is the suture that is typically under tension, whereas the loop is the suture that is thrown around the post. To position the knot farthest from the joint, the suture limb farther from the joint center is selected as the post. The suture limb can be passed either over or under the post to create a loop. As the loops are thrown, the suture limb that serves as post can be changed. Different sequences of throw and post selection can create different knot configurations. [18]

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Knot-Tying Instruments

Arthroscopic instruments manufactured by Linvatec, Arthrex, Arthrotek, and Mitek to aid the surgeon with knot tying abound. Therefore, the knot-tying instrument chosen should be the one that provides the surgeon with the most reliable and consistent ability to tie arthroscopic knots. Commonly, knot pushers are used to push a half-hitch loop down the post limb to the knot. Tightening is achieved by applying tension alternately to the two suture limbs. An alternative to this is to use the knot pusher to push past the half-hitch loop and then to tighten the knot by simultaneous and symmetric pulling on both suture limbs.[9] [18] [25] The surgeon should keep only one set of suture limbs in a cannula when knot tying is being performed. Other suture limbs may be passed through accessory cannulas while the knot is being tied and can afterward be returned to the original cannula for definitive fixation. Once the suture is passed through the tissue to be repaired, the suture limbs should be assessed for twists and tangles before the knot-tying sequence is initiated. The arthroscopist should slide the knot pusher down one of the suture limbs before passing any suture loops.[18] [25] Tissue tension should be minimized before beginning the knot-tying sequence. If limb rotation cannot eliminate the tension, a traction suture can be used. If the knots must be tied with the tissue under tension, consideration should be given to using a sliding knot, as described later.[18] [25]

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Suture Selection

The choice of suture for arthroscopic repair or reconstruction is dependent on the surgeon's preference. The choice of suture carries implications in terms of which knot is chosen to secure the suture. Absorbable monofilament suture material is often selected for arthroscopic interventions because it can be easily advanced through arthroscopic suturing devices, facilitates the tying of slipknots, and maintains reasonable strength during suture resorption and tissue healing.[14] Absorbable monofilament suture slips more easily than braided suture and can expand by up to 30% of its length before breaking.[19] Therefore, braided nonabsorbable suture is often chosen to avoid knot slippage and suture stretch. It is widely accepted that braiding suture strands have increased pliability, ductility, and strength of the final knot construct as compared with similarly sized monofilament sutures. In braided sutures, knot security is

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increased by roughening the surface. Surface coating partly reduces this effect by decreasing friction between strands, however.[12] [14] [26] Coating a braided suture reduces tissue drag and improves knot rundown; however, the lowered coefficient of friction can increase knot slippage.[12] [14] [26] [29] Nonetheless, a comparison of knot displacement in polydioxanone monofilament versus Ethibond braided sutures demonstrated a more than 50% greater displacement in the monofilament group after cyclic loading. [15] Because the cyclic loads were of low magnitude, the authors attributed the displacement to cinching and slippage, as opposed to elongation of the monofilament fibers. Although braided absorbable suture has become available, knot-tying studies using this material have not been conducted. Mishra and colleagues compared five different knot configurations tied with equal-sized Maxon and Ti-Cron.[17] They noted that all the knots tied with the monofilament Maxon

had a significantly decreased ultimate failure load when compared with Ti-Cron. Whichever suture is chosen, the surgeon needs to be aware of the different properties of sutures, which may impart different knot strengths. In Loutzenheiser's study,[15] the Duncan loop with switched-post, reversed-direction half hitches had the greatest holding capacity of the monofilament sutures. Of the braided sutures, the Revo knot had the strongest configuration. Regardless of type of suture, it seems that switching the post is the most important factor influencing knot security. [2] [15] [28] [30] No single suture material is optimal for all suturing conditions. Characteristics to consider are tensile strength, knot security, and tissue reaction. Ideally, one elects to use sutures of finer sizes and with fewer knots to reduce tissue reaction, granuloma formation, and other complications of suture use. [12] To this end, one should attempt to use sutures of superior tensile strength and knot security, minimizing the risk of suture line disruption and reducing the amount of foreign material left in the wound.

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Knot Security

Although suture breaking strength and anchor pullout strength are defined variables, knot security is less predictable. Knot security refers to the ability of a knot configuration to resist slippage under load.[11] Several authors[1] [3] [14] [17] have suggested that knot failure occurs at 3 mm of slippage, whereas others[27] [30] [33] have set 2 mm of slippage as the criteria for failure. Considerable variation has been noted among knots tied by different individuals as well as by the same individual on different occasions.[12] [14] [30] Knot security increased with the number of throws on the knot, but the increment of additional security gained with each throw decreased.[12] Some authors have suggested that three half hitches incorporating post switching should be thrown subsequent to creation of the initial knot.[14] [17] Despite the variability in knot configurations reported by many authors, Mishra and coworkers suggest that suture material is a more important consideration. [17] These authors analyzed the ultimate strength of Ti-Cron using several knot configurations (Duncan loop, Roeder knot, Snyder knot, and square knot) and noted that most of the knots failed as a result of suture breakage rather than knot slippage.

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Nonsliding Knots

Nonsliding knots are used when suture limbs cannot slide freely through the anchor or the soft tissue.[18] Nonsliding knot configurations include the square knot, the granny knot, the half hitch (varying post and throw combinations), and the Revo knot. Square Knots

Hand-tied square knots are generally regarded as the standard for open surgical procedures ( Fig. 6H-1 ).[10] [14] [17] [30] Some studies have shown that switched-post, reversed-direction half hitches may have a holding capacity that approaches that of square knots.[10] [14] [17] [30] Square knots are the most difficult to tie correctly during arthroscopy, however, and will easily flip into two nonidentical half hitches if tension is applied asymmetrically. If this occurs,

Figure 6-H-1 A square knot. (From Nottage WM, Lieurance RK: Arthroscopic knot tying techniques. Arthroscopy 15:515-521, 1999.)

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the knot will slide freely over the post.[10] [18] [20] This is particularly true with monofilament sutures. The square knot begins with an overhand loop thrown around the post. The knot pusher is placed on the loop limb of the suture instead of the post. The square knot is the only knot that requires placement of the knot pusher on the loop limb. The loop is pulled into the joint by placing tension on the free end of the loop suture. The knot pusher is passed beyond the point where the loop will appose, and tension is applied (pushing past the knot). The knot pusher can be wound 180 or 360 degrees around the

post to ensure that the loop is overhand and not a half hitch. The knot pusher is removed from the joint, and an underhand loop is thrown around the post. This second loop is pulled into the joint, as performed previously with the knot pusher. This loop is gently secured on top of the initial loop to prevent slipping. The knot pusher is removed and is placed on the post. After ensuring that the loop lies correctly as an underhand loop, the arthroscopist advances the knot pusher past the knot. Symmetric tension is applied to both suture limbs to tighten the square knot. Finally, alternating loops are created to reinforce the knot.[14] [18] [25] [28] [29] [30] A granny knot is a less desirable relative of the square knot. Surprisingly, a properly tied granny knot will have the same ultimate strength as a square knot; however, a surgeon is typically less able to tie granny knots in a reproducible manner.[33] The granny knot differs from the square knot in that the second loop is thrown overhand. This knot configuration is more prone to slippage.[1] Half-Hitch Knots

In half hitches, the post is the suture limb around which one makes a loop. Different knot configurations are determined by the loop patterns ( Fig. 6H-2 ). An overhand throw indicates that the loop limb is passed over the post to make the knot, whereas an underhand throw indicates that the loop limb is passed under the post to make the knot. Although the half hitch is the simplest of knots, it is

Figure 6-H-2 Half-hitch knots can be passed down the post by one of two techniques: pulling (A) or pushing (B). (From Chan KC, Burkhart SS: How to switch posts without rethreading when tying half-hitches. Arthroscopy 15:444-452, 1999. )

difficult to maintain the tension of the first half hitch on the underlying tissue while attempting to slide the second hitch down the cannula. To maintain the integrity of the first throw, braided suture with nonsliding anchors is primarily used with half-hitch knots. Monofilament sutures are not ideal for use with these knots owing to the slipperiness of the suture material. With monofilament sutures, half-hitch knots are used to fix a slipknot into place.[18] [25] Loutzenheiser and colleagues described the method of reversing throws and alternating posts to optimize knot strength with monofilament suture. [14] The half-hitch loop is passed over the post and is pushed down to the knot that is securing the tissue. The knot pusher is removed and is placed on the other limb as the new post. The half-hitch loop is passed under the new post and is pushed down to the knot. The procedure of reversing the half hitches and alternating the posts is continued until the knot is completed. A later study suggests that reversing the direction of the half hitches does not enhance knot security for a braided suture. [15] Burkart and coworkers compared the security of four simple knot configurations with four throws each (same post with same loop, same post with alternating loop, alternating post with same loop, and alternating post with alternating loop). [3] They

found that the knot configuration of the same post with the same loop failed at low loads. The remaining three configurations had similar security for polydioxanone sutures, however. For Ethibond sutures, the authors suggest that reversing posts enhances knot security. Revo Knot

Snyder developed the nonsliding Revo knot, in which the throws are reversed for each half-hitch loop, as recommended by Harryman ( Fig. 6H-3 ).[22] In addition, the posts are alternated with every second loop. To anchor the knot, the half-hitch loop is passed over the post and is pushed down to the knot that is securing the tissue. Subsequently, the knot pusher is withdrawn but is kept on the same post, and an underhand loop is created around the post and is pushed down the knot. At this point, the knot pusher is removed and is placed on the other limb, which will serve as the new post. The half-hitch loop is passed over the new post and is pushed down to the knot. It is important to continue reversing the half hitches and alternating the posts on every other throw. Regardless of the initial knot configuration, at least three locking loops should be thrown over the knot, because more loops increase knot security. [14] [25] Loutzenheiser indicated that regardless of whether a braided or a monofilament suture is used, one should make certain to alternate posts.[14] Failure to do so will result in a knot that will slip and fail at significantly lower stresses ( Fig. 6H-4 ). Chan and Burkhart published a technical note describing how to switch posts when tying half hitches without rethreading the knot pusher ( Fig. 6H-5 ).[5]

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Sliding Knots

Sliding knots or slipknots are principally used with a monofilament suture to crimp the suture as the knot is slid

241

Figure 6-H-3 A Revo knot. (From Nottage WM, Lieurance RK: Arthroscopic knot tying techniques. Arthroscopy 15:515-521, 1999.)

and tightens on the tissue. Nonetheless, the sliding knot may be used with braided suture. Regardless of which suture is used, it must be able to slide freely through the tissue and the anchor. This knot must hold long enough to be secured with subsequent half hitches created on top of it. The half hitches are vital to the ultimate security of the knot.[18] [25] Although there are many different types of sliding knots, the most commonly used are the overhand loop,[14] the Duncan loop, the Tennessee slider, and the Roeder knot.[23] The modified taut-line hitch is another sliding knot, which is also known as the Tarbuck knot or Nicky's knot. Other less commonly used sliding knots include the following: Tayside knot,[21] Melzer knot[21] (modified Roeder knot), cross-square knot[21] (modified square knot), blood knot,[21] Tim's knot, [24] half-blood knot,[20] Delimar knot,[7] and Khatri

Figure 6-H-4 The configuration found to be strongest with braided suture.[ 15] Loutzenheiser and associates also found that the Duncan loop (DL) configuration had the best strength in monofilament sutures. [ 14] S, Reverse half hitch; TLH, taut-line hitch; //, switch post. (From Loutzenheiser TD, Harryman DT II, Ziegler DW, Yung SW: Optimizing arthroscopic knots using braided or monofilament suture.

Arthroscopy 14:57-65, 1998.)

Figure 6-H-5 One can switch posts without rethreading the suture in the fashion described by Chan and Burkhart. [ 5] A, The half hitch is pulled forward with a single-lumen knot tier. B, The tension on the post limb is released, and the tip of the knot tier is repositioned. C, The half hitch is transformed into a flat knot. D, The captured knot is pulled back to flip the knot completely. (A-D from Chan KC, Burkhart SS: How to switch posts without rethreading when tying half-hitches. Arthroscopy 15:444-450, 1999. )

242

Figure 6-H-6 A Duncan loop. (From Nottage WM, Lieurance RK: Arthroscopic knot tying techniques. Arthroscopy 15:515-521, 1999.)

knot.[13] The Duncan loop, the Tayside loop, and the blood knot have been referred to as fisherman's knots. The overhand loop is the simplest of the sliding knots: An overhand throw is made around the post and is brought into the joint. Duncan Loop

The Duncan loop is also referred to as the hangman's knot ( Fig. 6H-6 ). To begin this slipknot, the suture is held so that one limb is short and the other is markedly longer. The suture limb closest to the joint center is pulled, leaving the shorter one farther from the joint center to serve as the post. The sutures are grasped between the thumb and the index finger. One then creates a small loop by passing the loop strand over the post. A succession of four loops is then passed around both the post and the loop strands. The tail of the loop strand is passed through the original loop and is pulled to tighten the knot configuration. Once the Duncan loop is advanced, the sliding loop may be advanced with a knot pusher on the post strand while tension is applied to the post limb of the suture. The Duncan loop is slid under direct visualization until the tissue and the loop are tight. Tension is maintained on the post while a half-hitch loop is placed on top of it. This locks the knot into place. Three additional reversing half hitches are placed on alternating posts to secure the knot.[18] [25] Tennessee Slider

The Tennessee slider consists of a buntline hitch followed by two half hitches thrown in alternate directions on opposite posts ( Fig. 6H-7 ). To create this knot, the suture limbs need to be uneven in length. The loop limb should be approximately twice the length of the post limb.[18] The loop strand is passed one time around both the post and the loop strands. A second pass is created around only the post limb. The end of the loop strand is then

brought up through the parallel limbs between the first and the second loops. This is then pushed into the joint until the tissue and the loop are tight. The knot is locked by a series of three or four alternating half hitches with post switching.[18] Roeder Knot

The Roeder knot is named after the surgeon who recommended a special loop for tonsillectomy in children, but it was popularized for laparoscopic use by Semm ( Fig. 6H-8 ). [23] [24] This sliding knot is a variation of the Duncan loop. It also begins with the creation of two uneven parallel limbs. The loop limb should be twice the length of the post limb as it protrudes from the cannula. [18]

Figure 6-H-7 A Tennessee slider. (From Nottage WM, Lieurance RK: Arthroscopic knot tying techniques. Arthroscopy 15:515-521, 1999.)

243

Figure 6-H-8 A Roeder knot. (From Nottage WM, Lieurance RK: Arthroscopic knot tying techniques. Arthroscopy 15:515-521, 1999.)

The first loop is created around the post limb, the second around both limbs, and the third around only the post limb. The tail of the loop strand is passed between the second and the third loops. Slack is removed from the knot, and the knot is pushed into the joint with the knot pusher on the post limb. The knot and the underlying tissue are tightened with the help of the knot pusher. Tension is maintained on the post while the locking half-hitch loop is placed on top of it. Three additional reversing half-hitch knots are passed by alternating posts to secure the knot.[18] Modified Taut-line Hitch

To create the modified taut-line knot, one must slide the suture so that one limb is quite short and the other is quite long. The suture limb closest to the joint center is pulled, leaving the other limb short to serve as the post. Two overhand throws are made with the loop strand over the post. The loop strand is passed behind the two loops and then over and under the post strand. After the slack in the knot is removed, the knot is slid forward by pulling on the post strand. To facilitate this sliding, the knot pusher is placed on the post and is used to push the sliding loop down the post while tension is applied to the post limb of the suture. Tension is maintained on the post while the first locking half-hitch loop is placed on top of the knot. Additional reversing half hitches are placed on alternating posts to secure the knot.[6] [14]

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Conclusion

An arthroscopic suture repair can fail by one of the following mechanisms: (1) suture pullout from the tissue to be repaired, (2) suture failure, or (3) knot failure. Suture pullout from the soft tissues can be minimized by appropriate selection of patients for surgical repair or reconstruction. The high pullout strength of soft tissue anchors as well as the high tensile strength of suture material in comparison to the ultimate loads to knot failure suggests that the arthroscopic surgeon should focus concern primarily on knot security. Although a multitude of arthroscopic knots have been described, the surgeon needs to be familiar with only two basic knot configurations: nonsliding and sliding.

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References Batra EK, Taylor PT, Franz DA, et al: A portable tensiometer for assessing surgeon's knot tying technique. Gynecol Oncol 48:114-118, 1993. 1.

Brouwers JE, Oosting H, de Haas D, Klopper PJ: Dynamic loading of surgical knots. Surg Gynecol Obstet 173:443-448, 1991. 2.

Burkart A, Imhoff AB, Roscher E: Foreign-body reaction to the bioabsorbable suretac device. Arthroscopy 16:91-95, 2000. 3.

Champion JK, Hunter J, Trus T, Laycock W: Teaching basic video skills as an aid in laparoscopic suturing. Surg Endosc 10:23-25, 1996. 4.

Chan KC, Burkhart SS: How to switch posts without rethreading when tying half-hitches. Arthroscopy 15:444-450, 1999. 5.

De Beer JF, van Rooyen K, Boezaart AP: Nicky's knota new slip knot for arthroscopic surgery. Arthroscopy 14:109-110, 1998. 6.

7.

Delimar D: A secure arthroscopic knot. Arthroscopy 12:345-347, 1996.

Franz DA, Batra EK, Morgan RF, Edlich RF: A portable tensiometer for assessing knot-tying technique. Orthopedics 18:555-558, 1995. 8.

9.

Grace PA, Burke P, Bouchier-Hayes D: Tying a laparoscopic knot. Br J Surg 79:512, 1992.

Gunderson PE: The half-hitch knot: a rational alternative to the square knot. Am J Surg 154:538-540, 1987. 10.

Hanna GB, Frank TG, Cuschieri A: Objective assessment of endoscopic knot quality. Am J Surg 174:410-413, 1997. 11.

Herrmann JB: Tensile strength and knot security of surgical suture materials. Am Surg 37:209-217, 1971. 12.

13.

Khatri VP, Balshi JD: Slip knot for tying monofilament nylon sutures. Am Surg 61:735-737, 1995.

Loutzenheiser TD, Harryman DT II, Yung SW, et al: Optimizing arthroscopic knots. Arthroscopy 11:199-206, 1995. 14.

Loutzenheiser TD, Harryman DT II, Ziegler DW, Yung SW: Optimizing arthroscopic knots using braided or monofilament suture. Arthroscopy 14:57-65, 1998. 15.

16.

Melvin WS, Johnson JA, Ellison EC: Laparoscopic skills enhancement. Am J Surg 172:377-379, 1996.

Mishra DK, Cannon WD Jr., Lucas DJ, Belzer JP: Elongation of arthroscopically tied knots. Am J Sports Med 25:113-117, 1997. 17.

18.

Nottage WM, Lieurance RK: Arthroscopic knot typing techniques. Arthroscopy 15:515-521, 1999.

Ray JA, Doddi N, Regula D, et al: Polydioxanone (PDS), a novel monofilament synthetic absorbable suture. Surg Gynecol Obstet 153:497-507, 1981. 19.

Shaw AD, Duthie GS: A simple assessment of surgical sutures and knots. J R Coll Surg Edinb 40:388-391, 1995. 20.

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Shimi SM, Lirici M, Vander Velpen G, Cuschieri A: Comparative study of the holding strength of slipknots using absorbable and nonabsorbable ligature materials. Surg Endosc 8:1285-1291, 1994. 21.

22.

Snyder SJ: Technical manual for the Revo screw and knot. Largo, Fla., Linvatec Corporation, 1994.

Soper NJ, Hunter JG: Suturing and knot tying in laparoscopy. Surg Clin North Am 72:1139-1152, 1992. 23.

Swain CP, Kadirkamanathan SS, Gong F, et al: Knot tying at flexible endoscopy. Gastrointest Endosc 40:722-729, 1994. 24.

25.

Sweeney HJ: Knot Tying. Chicago, Arthroscopy Association of North America, 1996.

26.

Taylor FW: Surgical knots. Ann Surg 107:458, 1938.

Tera H, Åberg C: Tensile strengths of twelve types of knot employed in surgery, using different suture materials. Acta Chir Scand 142:1-7, 1976. 27.

28.

Trimbos JB: Security of various knots commonly used in surgical practice. Obstet Gynecol

64:274-280, 1984. Trimbos JB, Niggebrugge A, Trimbos R, Van Rijssel EJ: Knotting abilities of a new absorbable monofilament suture: Poliglecaprone 25 (Monocryl). Eur J Surg 161:319-322, 1995. 29.

Trimbos JB, Van Rijssel EJ, Klopper PJ: Performance of sliding knots in monofilament and multifilament suture material. Obstet Gynecol 68:425-430, 1986. 30.

Vossen C, Van Ballaer P, Shaw RW, Koninckx PR: Effect of training on endoscopic intracorporeal knot tying. Hum Reprod 12:2658-2663, 1997. 31.

32.

Young WW: Teaching surgical knot-tying skills. Acad Med 67:64, 1992.

Zimmer CA, Thacker JG, Powell DM, et al: Influence of knot configuration and tying technique on the mechanical performance of sutures. J Emerg Med 9:107-113, 1991. 33.

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Section I Use and Abuse of the Pneumatic Tourniquet Robert A. Pedowitz MD, PhD History

Pneumatic tourniquets are used commonly to provide a bloodless field for modern extremity surgery. Temporary occlusion of blood flow to control bleeding is not a new idea, however. Limb amputations probably were performed during the Neolithic ages, and control of bleeding by pressure over a main artery with a pebble was described in 600 B.C. The Romans used various constricting devices to control hemorrhage associated with amputation. During the 16th and 17th centuries, compression devices were fashioned from cloth or rope and tensioned by twisting with a stick. In the 18th century, Petit described a screw device that compressed the limb externally to induce ischemia, and his tourniquet (from the French tourner, to turn) is the namesake for the current instrument.[33] Lister emphasized the importance of extremity elevation for several minutes before application of the tourniquet, to decrease blood in the venous pool of the distal extremity. von Esmarch described a more efficient method of venous exsanguination by application of a tight circumferential bandage. Clinicians still use the Esmarch bandage, but the current device is based on refinement by Von Langenbeck and by Martin, who recommended use of softer and more elastic latex wraps.[33] Cushing[5] is credited with initial development of the pneumatic tourniquet. His inflatable rubber device was attached to a bicycle pump and a Riva-Rocci blood pressure apparatus. This device allowed for rapid cuff inflation, which minimized venous congestion caused by slower inflation. It is remarkable that Cushing originally described the pneumatic tourniquet for application around the head as a method to minimize blood

loss and improve visualization during craniotomy. Earlier pneumatic inflation devices were controlled by simple screw valves and monitored by needle pressure gauges. These devices were particularly risky because excessive pressure could cause the needle to rotate full circle around the face of the gauge, with erroneous indication of a safe pressure. Recognition of associated severe nerve palsies led to introduction of a needle stop device on the pressure gauge. These devices largely have been replaced by electronically controlled systems with digital pressure and time displays. The modern devices still must be calibrated regularly, however, against standard manometers to avoid inadvertent overpressurization of the limb.

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Tourniquet Morbidity

Despite the many technical improvements in tourniquet design and inflation control technology, tourniquet complications continue to be a significant problem for extremity surgeons. The advantages of a bloodless field are obvious, particularly for delicate microsurgical procedures. Tissue ischemia is a profoundly pathologic condition, however, and viability is incompatible with prolonged tissue ischemia. Inflation of a pneumatic device adds further to the ischemic injury by direct mechanical deformation in the zone of tissue compression. It is essential that the surgeon (and preferably the entire surgical team) understand the pathophysiologic sequelae of iatrogenic circulatory arrest, to manage appropriately the risks and benefits of the pneumatic tourniquet ( Fig. 6I-1 ). Major (i.e., permanent) neurologic injuries are relatively rare with modern tourniquets and current clinical paradigms. The incidence of permanent nerve palsy after tourniquet application was 0.13% and 0.01% in retrospective studies by Flatt[10] and Middleton and Varian. [20] Severe neurologic injury, myonecrosis, and compartment syndrome occur with tourniquet use, misuse, or abuse and continue to be a source of major litigation. More subtle forms of neuromuscular injury are associated commonly with routine tourniquet application. Randomized, prospective studies showed electromyography (EMG) abnormalities in 70% of lower extremity surgeries[7]

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Figure 6-I-1 Tourniquet-induced neuromuscular injury is a multifactorial process with an interaction of

factors related to tissue compression and ischemia.

and in 77% of upper extremity surgeries[29] performed with a tourniquet compared with 0.0% and 3.4% after similar cases performed without a tourniquet. These types of EMG abnormalities are associated with decreased postoperative function and longer clinical recovery time[17] [44] [46] and probably reflect subtle evidence of denervation and reinnervation as a result of tissue compression and ischemia. The EMG changes may take 6 months to recover after surgery. Daniels and coworkers[6] noted greater functional deficit 6 months after anterior cruciate ligament reconstruction performed with a tourniquet compared with reconstruction without a tourniquet, with similar functional status at 1 year after surgery. This observation correlates well with earlier electrophysiologic studies.

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Tourniquet Ischemia

Skeletal muscle is particularly sensitive to ischemia, and considerable basic research has attempted to define the safe duration of tourniquet ischemia. These thresholds must be defined by objective measurement parameters, and it is important to understand the specific assessment techniques used in the literature to define ischemic thresholds. Ultra-structural changes and microvascular flow abnormalities are noted after just 30 minutes of skeletal muscle ischemia, whereas overt fiber necrosis occurs after 4 to 6 hours of warm ischemia in animal experiments.[33] Basic experimental studies in various animal models indicated a time threshold between 1 and 2 hours of warm muscle ischemia for significant metabolic derangement, postischemic microvascular disturbance, histologic abnormality, and functional deficit. There is little rational expectation that ischemic thresholds would be markedly different for human skeletal muscle. This literature forms the basis for common clinical use of a 2-hour time limit for continuous tourniquet inflation in otherwise healthy tissue. Microvascular disturbance, edema formation, and structural fiber abnormalities appear to increase significantly between 1 and 2 hours of ischemia, however. This fact has important implications for clinical reperfusion paradigms during extended tourniquet application (see later). It is important for the surgeon to recognize that short intervals of ischemia are expected to cause some degree of tissue injury, and the cost-to-benefit ratio of this exposure must be considered individually. Many surgeries are accomplished safely and efficiently without a tourniquet, and such opportunities should be exploited if possible. Anterior cruciate ligament reconstruction can be performed easily without tourniquet inflation, given appropriate attention to surgical hemostasis, arthroscopic fluid management, and control of systemic blood pressure.[6] This approach may decrease postoperative hemarthrosis owing to control of bleeders intraoperatively.

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Tourniquet Compression

Although skeletal muscle is particularly vulnerable to short periods of warm ischemia, nerve and muscle are sensitive to the combined effects of compression and ischemia beneath the inflated tourniquet cuff. Compression, in and of itself, may not be pathogenic. Deep-sea divers tolerate enormous uniform compressive loads without apparent adverse sequelae. This principle was described by Grundfest[13] when he noted that excised sciatic nerve continued to conduct at 760,000 mm Hg (1000 atm) in a high-pressure container. It is likely that local pressure gradients, from the compressed to the noncompressed tissue segments, are specifically pathogenic and that injury is maximal at the edges of tissue deformation (the edge effect[42] ). This concept is relevant because cuff design (shape, width, material) and underpadding can affect distribution of pressure to the affected tissues. Although pressure gradients are maximal beneath the edges of the tourniquet, absolute pressures are greatest under the midposition of the cuff. Tissue pressure decreases from the subcutaneous tissues to the deeper tissues of the limb. [14] [19] [39] [45] Pressure distribution and tissue deformation are not uniform in the transverse plane, however. A stellate deformation pattern probably is most common,[33] which explains the longitudinal lines of skin erythema sometimes seen in patients on cuff deflation and removal. The pathophysiologic sequelae of nonuniform deformation are not known.

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Pressure Thresholds

Multiple animal studies showed that tissue injury is greater beneath than distal to the tourniquet, owing to the combined effects of compression and ischemia. [11] [16] [18] [21] [23] [30] [33] [34] [36] [37] [38] [39] Although muscle is exquisitely sensitive to ischemia, nerve may be particularly vulnerable to local deformation. There is a growing body of evidence that tissue injury under the cuff may exacerbate distal tissue injury and induce systemic microvascular changes. It is not known whether remote injury is caused by metabolic effects (e.g., generation of proinflammatory mediators), by microvascular perturbation (e.g., systemic leukocyte activation

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leading to adhesion and flow obstruction), or by other mechanisms. Most of the literature has focused on ischemic time limits, with relatively little attention to tissue compression thresholds. Thresholds must be relevant to the specific clinical situation of concern. Proximal nerve injury might be crucial after distal repair with replantation surgery, whereas thigh muscle injury could be the crucial factor for rehabilitation of an athlete after anterior cruciate ligament reconstruction. Some investigators examined muscle injury caused by a given cuff pressure for various time periods,[31] [32] and others evaluated muscle injury after a specific time interval with various tourniquet pressures.[12] To address multiple variables experimentally, a controlled animal model was developed for evaluation of pressure and time variables in muscle and nerve beneath and distal to the cuff. [39] A series of studies showed that the magnitude of tissue compression injury is related to complex interaction of cuff pressure and duration.[11] [16] [18] [21] [30] [34] [37] [38] Four hours of

tourniquet inflation consistently caused severe muscle injury beneath the cuff, with less severe injury in the distal ischemic zone. Muscle compression injury beneath the cuff increased markedly between 1 and 2 hours of continuous compression (this effect depended partially on the applied cuff pressure[37] ). These findings suggest careful clinical consideration because there appears to be a pressure/time threshold for significant exacerbation of tissue injury before 2 hours of cuff inflation. Experimental studies in small animals are not directly applicable to humans. There is no rational expectation, however, that tourniquet compression and ischemia would not produce some degree of tissue injury. All of the available animal and human data suggest that tissue injury may be minimized by application of the lowest possible cuff pressure for the shortest necessary duration. If prolonged ischemia times are required clinically, other protocols may be employed to minimize iatrogenic tissue injury (see later).

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Controllable Parameters

Given the appreciation of potential tourniquet-induced morbidity, the surgical team should strive to minimize tissue injury caused by this appliance. Many of the important variables are within the surgical team's control, including tourniquet time (discussed previously), cuff pressure, cuff width and shape, underpadding, reperfusion intervals, and tissue preconditioning. Cuff Pressure

It is still common in clinical practice for surgeons to select arbitrary cuff pressures of 250 to 300 mm Hg for upper extremity surgery and 350 to 400 mm Hg for lower extremity procedures. These pressure settings usually surpass the lowest possible cuff pressure that can be used to achieve reliable surgical hemostasis. It is desirable to exceed the minimal cuff pressure by a bit to provide a buffer against fluctuation of systolic blood pressure. Blood pressure elevation can cause loss of a bloodless field, which may interfere with the surgical procedure. With this exception, there is no rational reason to apply excessive tourniquet pressure to the limb. Several studies showed that pneumatic tourniquet pressures do not reflect the tissue pressure beneath the inflated cuff.[14] [39] [45] In the transverse plane, tissue pressure decreases from superficial to deep. In the longitudinal plane, maximal pressures occur under the center of the cuff, with maximal pressure gradients (see earlier) under the edges of the cuff. Wide cuffs occlude flow at lower inflation pressures than narrow cuffs, probably as a result of more efficient transmission of pressure to the deep tissues (in the region of the major arteries). Larger limbs (e.g., with obesity or in muscular individuals) require higher inflation pressures to induce hemostasis than smaller limbs (e.g., in children). In rare cases, high cuff pressures are needed to compress vessels that are inelastic because of atherosclerosis. To accommodate these multiple variables, some authors have used direct determination

of the lowest possible cuff inflation pressure for a given patient with a given tourniquet before the start of surgery.[35] [40] After direct measurement of the arterial occlusion pressure using a distal Doppler or other appropriate device, cuff pressure for the case can be set by adding a buffer (generally 50 to 75 mm Hg). Using this approach, Reid and colleagues[40] used average cuff pressures of 189 mm Hg for the upper extremity and 231 mm Hg for the lower extremity. Pedowitz and coworkers[35] used average pressures of 184 mm Hg and 208 mm Hg for upper and lower extremity surgeries ( Fig. 6I-2 ). Measurement of the arterial occlusion pressure is time-consuming and cumbersome for general clinical application. These studies show, however, that relatively low pressures can be used in most patients to induce effective surgical hemostasis. Some authors[41] recommended cuff pressures 100 to 150 mm Hg above systolic pressure. Egkher and colleagues[9] showed that the cuff pressure only had to be slightly higher than systolic blood pressure. Moore and coworkers[24] offered a more complex formula based on blood pressure, limb circumference, and cuff width. In a normotensive patient with normal limb anatomy, I select 200 to 225 mm Hg cuff pressure for upper extremity procedures and 225 to 250 mm Hg for lower extremity surgeries. I adjust cuff pressure downward for patients with small limbs and upward for large limbs or if hypertension is anticipated. If bleeding is encountered, cuff pressure may be increased in increments of 25 mm Hg as needed, but inflation pressures should not exceed 350 mm Hg. Cuff Width and Shape

Wider cuffs induce a broader zone of deep tissue compression than narrow cuffs.[4] Lower cuff inflation pressures may be used with wider tourniquets to achieve a bloodless field.[4] [24] [25] [35] Hemostasis can be induced effectively by wide tourniquets at subsystolic cuff pressures. Pedowitz and coworkers[35] noted that slightly lower cuff pressure could be used with curved cuffs on conically

247

Figure 6-I-2 The lowest possible cuff pressure should be used to achieve surgical hemostasis. In this study, tourniquet pressure was set by direct determination of the arterial occlusion pressure in the operated extremity. Cuff pressure was less than 250 mm Hg in virtually all cases and averaged approximately 200 mm Hg in upper and lower extremity cases. (Adapted from Pedowitz RA, Gershuni DH, Botte MJ, et al: The use of lower tourniquet inflation pressures in extremity surgery facilitated by curved and wide tourniquets and an integrated cuff inflation system. Clin Orthop 287:237-244, 1993. )

shaped limbs compared with straight cuffs of equal width. Curved cuffs are particularly convenient for muscular or obese thighs. They are less useful for upper extremity

procedures. Long Tourniquet Times

Careful planning is appropriate when long ischemia times are anticipated. Clinical situations arise that require extended periods of hemostasis; these situations are particularly problematic and may pose a dilemma for the surgeon. In general, if tourniquet ischemia is needed, it is probably best to keep the tourniquet time less than 1 to 2 hours. If longer periods are required, several strategies may be considered. In 1951, Bruner[1] recommended a 10-minute breathing period after each hour of ischemia to allow tissue recovery before an additional period of ischemia. Other authors suggest 5- to 15-minute reperfusion intervals after 1 hour, 1.5 hours, or 2 hours of tourniquet compression.[2] [3] [15] [26] [28] [43] 47 Early studies focused on histologic and systemic metabolic parameters, with more recent investigations using nuclear magnetic resonance spectroscopy to evaluate local tissue metabolism. All of these studies focused on skeletal muscle distal to the tourniquet, without consideration of tissue injury beneath the tourniquet. Pedowitz and coworkers[36] examined effects of reperfusion intervals on muscle injury beneath and distal to the tourniquet in rabbits. Muscle injury under the cuff was minimized by 10 minutes of reperfusion after each hour of cuff inflation, with a total 4-hour tourniquet time. Tissue reperfusion after 2 hours tended to increase muscle injury under the cuff when the inflation pressure was 350 mm Hg. This observation correlates well with earlier studies that showed a marked increase of tissue injury with a 2-hour, 350-mm Hg tourniquet. The same experimental model was used to examine nerve injury beneath and distal to the cuff after 4 hours of ischemia with and without reperfusion intervals.[22] Nerve injury was worse beneath than distal to the cuff; however, reperfusion intervals did not have a significant effect on the magnitude of neurologic dysfunction or histologic abnormality. Taken together, current data suggest that 10 minutes of reperfusion at hourly intervals should be employed to minimize skeletal muscle injury (back to Bruner's recommendations of a half-century ago). This approach probably does not ameliorate nerve compression injury, however. A reperfusion interval after 2 hours of compression may be detrimental, owing to recompression of tissue that has exceeded a crucial pressure/time threshold. It may be better to go a little while longer, rather than deflate and reinflate the cuff after 2 hours. It is best to anticipate the potential for a long tourniquet time and reperfuse every hour to avoid this difficult situation. Temporary tourniquet deflation may interfere with the surgical procedure when tissues become swollen and blood-stained, with obscuration of structural detail.[33] Other approaches have been described to increase the safe period of tourniquet hemostasis. Precooling of the extremity may decrease metabolic demand and preserve function, though icing the extremity before surgery is an impractical solution. Neimkin and Smith[27] recommended a double-cuff technique to transfer the compression zone, while maintaining hemostasis. The narrow bladders in a double cuff

require

248

higher inflation pressure, however, than a single wide tourniquet.[8] In the future, it may be possible to extend the ischemic interval by attenuation of the reperfusion injury using pharmacologic methods (e.g., systemic pretreatment designed to limit postischemic microvascular dysfunction).

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Author's Preferred Method

Many surgical procedures can be done safely and effectively without a tourniquet. If required, a wide cuff is used to facilitate lower inflation pressure. A smooth layer of cotton underpadding is applied under the cuff, and the distal edge of the cuff is sealed away from the preparation solutions with adhesive plastic drapes. Tourniquet pressure usually is set at 200 to 225 mm Hg in the upper extremity and at 225 to 250 mm Hg in the lower extremity for a normal size, normotensive patient. Cuff pressure is adjusted downward or upward if appropriate. Higher cuff pressures are used for obese or extremely muscular individuals. In most cases, tourniquet time should be less than 1 to 1.5 hours, with every effort not to exceed 2 hours of continuous compression. If long tourniquet times are required, 10 minutes of reperfusion are allowed at hourly intervals.

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References Bruner JM: Safety factors in the use of the pneumatic tourniquet for hemostasis in surgery of the hand. J Bone Joint Surg Am 33:221-224, 1951. 1.

2.

Bunnell S: Surgery of the Hand, 3rd ed. Philadelphia, JB Lippin cott, 1956.

Chiu D, Wang H, Blumenthal MR: Creatine phosphokinase release as a measure of tourniquet effect on skeletal muscle. Arch Surg 111:71-74, 1976. 3.

Crenshaw AG, Hargens AR, Gershuni DH, Rydevik BL: Wide tourniquet cuffs more effective at lower inflation pressures. Acta Orthop Scand 59:447-451, 1988. 4.

Cushing H: Pneumatic tourniquets: With especial reference to their use in craniotomies. Med News 84:577-580, 1904. 5.

Daniel D, Lumkong G, Stone M, Pedowitz RA: Effects of tourniquet use in anterior cruciate ligament reconstruction. Arthroscopy 11:307-311, 1995. 6.

Dobner J, Nitz AJ: Post-meniscectomy tourniquet palsy and functional sequelae. Am J Sports Med 10:211-214, 1982. 7.

Dreyfuss UY, Smith RJ: Sensory changes with prolonged double-cuff tourniquet time in hand surgery. J Hand Surg Am 13:736-740, 1988. 8.

Egkher E, et al: Blutdruckabhängige, prozessgesteuerte Blutsperre zur Minimierung des Tourniquet-Syndroms. Unfallchirurgie 12:200-203, 1986. 9.

10.

Flatt AE: Tourniquet time in hand surgery. Arch Surg 104:190-192, 1972.

Fridén J, Pedowitz RA, Thornell L-E: Sensitivity of different types of fibres in rabbit skeletal muscle to pneumatic compression by tourniquet and to ischemia. Scand J Plast Reconstr Surg Hand Surg 11.

28:87-94, 1994. Gersoff WK, Ruwe P, Jokl P, Panjabi M: The effect of tourniquet pressure on muscle function. Am J Sports Med 17:123-127, 1989. 12.

Grundfest H: Effects of hydrostatic pressure upon the excitability, the recovery, and the potential sequence of frog nerve. Cold Spring Harbor Symp Quant Biol 4:179-187, 1936. 13.

Hargens AR, McClure G, Skyhar MJ, et al: Local compression patterns beneath pneumatic tourniquets applied to arms and thighs of human cadavera. J Orthop Res 5:247-252, 1987. 14.

Heppenstall RB, Balderston R, Goodwin C: Pathophysiologic effects distal to a tourniquet in the dog. J Trauma 19:234-238, 1979. 15.

Jacobsen MD, Pedowitz RA, Oyama BS, et al: Muscle functional deficits after tourniquet ischemia. Am J Sports Med 22:372-377, 1994. 16.

Krebs DE: Isokinetic, electrophysiologic, and clinical function relationships following tourniquet-aided knee arthrotomy. Phys Ther 69:803-815, 1989. 17.

Lieber RL, Pedowitz RA, Fridén J, Gershuni DH: Decreased muscle speed, strength and fatigability following two hours of ischemia. Scand J Plast Reconstr Surg Hand Surg 26:127-132, 1992. 18.

McLaren AC, et al: The pressure distribution under tourniquets. J Bone Joint Surg Am 67:433-438, 1985. 19.

20.

Middleton RWD, Varian JP: Tourniquet paralysis. Aust N Z J Surg 44:124-128, 1974.

Mohler LR, Pedowitz RA, Lopez MA, Gershuni DH: Effects of tourniquet compression on neuromuscular function. Clin Orthop 359:213-220, 1999. 21.

Mohler LR, Pedowitz RA, Myers RR, et al: Intermittent reperfusion fails to prevent post-tourniquet neurapraxia. J Hand Surg Am 24:687, 1999. 22.

Mohler LR, Pedowitz RA, Ohara WM, et al: Effects of an antioxidant in a rabbit model of tourniquet induced skeletal muscle ischemia-reperfusion injury. J Surg Res 60:23-28, 1996. 23.

Moore MR, Garfin SR, Hargens AR: Wide tourniquets eliminate blood flow at low inflation pressures. J Hand Surg Am 12:1006-1011, 1987. 24.

25.

Muirhead A, Newman RJ: A low-pressure tourniquet for lower limb surgery. Injury 17:53-54, 1986.

Nakahara M: Tourniquet effects on muscle oxygen tension in dog limbs. Acta Orthop Scand 55:576-578, 1984. 26.

Neimkin RJ, Smith RJ: Double tourniquet with linked mercury manometers for hand surgery. J Hand Surg Am 9:938-941, 1983. 27.

Newman RJ: Metabolic effects of tourniquet ischaemia studied by nuclear magnetic resonance spectroscopy. J Bone Joint Surg Br 66:434-440, 1984. 28.

29.

Nitz AJ, Dobner J: Upper extremity tourniquet effects in carpal tunnel release. J Hand Surg Am

14:499-504, 1989. Ohara WM, Pedowitz RA, Oyama B, Gershuni DH: Comparison of functional deficits in the rabbit tibialis anterior following tourniquet ischemia and tourniquet compression. J Orthop Res 14:626-632, 1996. 30.

Patterson S, Klenerman L: The effect of pneumatic tourniquets on the ultrastructure of skeletal muscle. J Bone Joint Surg Br 61:178-183, 1979. 31.

Patterson S, Klenerman L, Biswas M, Rhodes A: The effect of pneumatic tourniquets on skeletal muscle physiology. Acta Orthop Scand 52:171-175, 1981. 32.

Pedowitz RA: Tourniquet-induced neuromuscular injury: A recent review of rabbit and clinical experiments. Acta Orthop Scand 62(suppl 245):1-33, 1991. 33.

Pedowitz RA, Fridén J, Thornell L-E: Skeletal muscle injury induced by a pneumatic tourniquet: An enzyme- and immuno-histochemical study in rabbits. J Surg Res 52:243-250, 1992. 34.

Pedowitz RA, Gershuni DH, Botte MJ, et al: The use of lower tourniquet inflation pressures in extremity surgery facilitated by curved and wide tourniquets and an integrated cuff inflation system. Clin Orthop 287:237-244, 1993. 35.

Pedowitz RA, Gershuni DH, Friden J, et al: Effects of ten minute reperfusion intervals upon muscle injury beneath and distal to a pneumatic tourniquet. J Hand Surg Am 17:245-255, 1992. 36.

Pedowitz RA, Gershuni DH, Schmidt AH, et al: Muscle injury induced beneath and distal to a pneumatic tourniquet: A quantitative study of effects of tourniquet pressure and duration. J Hand Surg Am 16:610-621, 1991. 37.

Pedowitz RA, Nordborg C, Rosenqvist A-L, Rydevik BL: Nerve function and structure beneath and distal to a pneumatic tourniquet applied to rabbit hindlimbs. Scand J Plast Reconstr Surg Hand Surg 25:109-120, 1991. 38.

Pedowitz RA, Rydevik BL, Gershuni DH, Hargens AR: An animal model for the study of neuromuscular injury induced beneath and distal to a pneumatic tourniquet. J Orthop Res 8:899-908, 1990. 39.

Reid HS, Camp RA, Jacob WH. Tourniquet hemostasis: A clinical study. Clin Orthop 177:230-234, 1983. 40.

Rorabeck CH: Tourniquet-induced nerve ischemia: An experimental investigation. J Trauma 20:280-286, 1980. 41.

Rydevik B, Lundborg G, Skalak R: Biomechanics of peripheral nerves. In Nordin M, Frankel VH (eds): Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989. 42.

249

Sapega AA, Heppenstall B, Chance B, et al: Optimizing tourniquet application and release times in extremity surgery. J Bone Joint Surg Am 67:303-314, 1985. 43.

Saunders KC, Louis DL, Weingarden SI, Waylonis GW: Effect of tourniquet time on post-operative quadriceps function. Clin Orthop 143:194-199, 1979. 44.

Shaw JA, Murray DG: The relationship between tourniquet pressure and underlying soft-tissue pressure in the thigh. J Bone Joint Surg Am 64:1148-1152, 1982. 45.

Weingarden SI, Louis DL, Waylonis GW: Electromyographic changes in postmeniscectomy patients: Role of the pneumatic tourniquet. JAMA 241:1248-1250, 1979. 46.

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Chapter 7 - Risk Assessment and Management of Nonorthopaedic Conditions Section A Viral Disease John H. Wilckens MD John E. Glorioso Jr. MD The importance of optimal health in the competitive athlete is obvious. Viruses are a ubiquitous health challenge to the athlete. Of all the pathogens, viruses are the most common, the least understood, and the most evasive to treat. Viruses encompass the spectrum from the common cold and the plantar wart to herpes to the universally fatal human immunodeficiency virus (HIV). All these viruses affect athletes, and, equally important, sport and fitness affect viral disease. Exercise and Immunology

The best defense to viral disease transmission is the athlete's own natural immune system. Exercise and fitness have measurable effects on the immune status. Elite athletes anecdotally complain of frequent viral infections, in particular while they are attempting to peak for an upcoming contest. Meanwhile, other athletes preach the wellness they have enjoyed with few viral infections because of their fitness program.[30] In exercise, participants experience a rise in white blood cell count, mostly polymorphonuclear neutrophils (PMNs). Lymphocytes and monocytes also rise. The more intense the exercise or less fit the athlete, the greater the effect. Much of this rise can be attributed to the hormonal effect of epinephrine and the increased cardiac

output. Demargination of cells from the vessel walls and surge from the spleen, liver, and lungs prepare the body to address any insult that it may soon encounter. There may be a second rise in PMNs with prolonged or strenuous exercise. This rise seems to result from the release of cortisol. Cortisol limits the release of PMNs from the blood vessels and stimulates additional release from the bone marrow. When exercise stops, the release of short-acting epinephrine ceases, and the effects of slower acting cortisol go unopposed. The PMN count returns to normal shortly after the cessation of exercise. With prolonged workouts, this return to normal could take 24 hours. Lymphocyte count returns to normal in minutes and for a few hours may be below normal. Lymphocyte count returns to baseline in the next 6 to 24 hours when lymphocytes return to lymph organs.[18] [20] [43] The lymphocytosis induced by exercise is predominantly natural killer (NK) cells with some T-suppressor lymphocytes. Epinephrine released during exercise can activate the NK cells, representing a ready line of defense against common viruses. Basal NK activity can be enhanced with a fitness training program. This activity may be lessened by age, with less response seen in elderly who exercise. As higher levels of fitness are achieved, NK activity may taper. When compared with sedentary controls, however, athletes have higher basal NK activity.[18] [20] Immunoglobulins, in particular salivary and nasal im munoglobulin A (IgA), have been measured in athletes. IgA has been observed to fall after strenuous exercise and to return to normal with 24 hours of rest. This effect on the ability of nasopharyngeal mucosa to defend against viral illness has not been proved, however. [18] Although exercise seems to have a positive effect on the immune system, there is a suppression in the recovery period. As the duration and intensity of exercise increase, this period of blunted immune response becomes prolonged, creating an open window for viral disease transmission. In prolonged strenuous exercise, the following deleterious effects have been observed: cortisol-induced low lymphocyte blood counts; decrease in nasal neutrophil phagocytosis and mucociliary clearance; decrease in granulocyte and NK cell killing activity; increase in plasma concentrations of proinflammatory and anti-inflammatory cytokines; decreased macrophage recognition of the major histocompatibility complex; decrease in the delayed-type hypersensitivity reaction; decrease in T-cell function; and, in response to muscle damage, increase in blood granulocyte and monocyte phagocytosis. The effects of complement activation and interleukin, interferon, and tumor necrosis factor release during prolonged exertion are not clear in the native immune system. [18] [43] Many of these observed changes in the immune system from exercise may represent the effects of stress. Stress can affect the immune system adversely, making an individual more susceptible to illness. This effect is displayed by increased incidence of disease in individuals undergoing life stresses, such as final examinations, divorce, death in the family, and exaggerated weight loss. Equally noted is that exercise may represent a release of stress. Some of the positive effects of modest exercise on the immune system could be related to exercise use in stress management. Weight loss commonly is encountered in exercise programs, and many exercise programs are undertaken to lose weight. Rapid weight loss is a stress that can affect the immune

system adversely. At higher levels of athletic activity, participants maximize lean body mass and minimize

252

percent body fat. There appears to be a threshold of percent body fat needed to maintain an active immune system. Male athletes with less than 8% body fat and female athletes with less than 12% body fat have a higher incidence of viral infections. [20] [43] Although good nutrition is intuitively essential to optimal physical performance, the effect of nutritional supplements on the immune system has not been shown uniformly. Several studies offer contradictory conclusions to the effects of vitamin C in runners in reducing upper respiratory tract infections. Although reduced glutamine levels and the effect on lymphocytes have been observed in strenuous activity, the importance of glutamine in protecting athletes against viral disease transmission has not been proved. Much of the stress induced by prolonged exercise is motivated nutritionally. As glucose levels drop, a complex hormonal response is triggered in the hypothalamic-pituitary-adrenal axis. There is an increased release of adrenocorticotropic hormone (ACTH) and cortisol, increased growth hormone, a variable response in epinephrine, and a drop in insulin. A study revealed that a carbohydrate beverage before, during, and after prolonged exercise results in higher glucose levels with concomitant smaller rises in cortisol and growth hormone. The observed immunologic effects included fewer changes in white blood cell counts, lower granulocyte and monocyte phagocytosis, and diminished cytokine concentrations. Although carbohydrate beverages appear to attenuate the physiologic stress of prolonged exercise, the clinical significance needs to be studied further.[43]

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Section E Diabetes Mellitus Blaise A. Nemeth MD David B. Allen MD Diabetes mellitus is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin; it affects almost 1 in 500 children younger than 18 years old. Worldwide incidence rates vary from 1 in 100,000 in Japan to 30 in 100,000 in Scandinavia, and the disorder is approximately four times more common in whites than in blacks. The predominant form of diabetes affecting children is type 1 diabetes mellitus, a disorder in which the insulin-producing islet cells of the pancreas selectively are destroyed by the body's immune system. The resulting insulin deficiency invariably requires treatment with exogenous insulin and is the hallmark of type 1 insulin-dependent diabetes mellitus (IDDM). Type 2 diabetes mellitus (non-insulin-dependent diabetes mellitus [NIDDM]) occurs predominantly during adulthood, but the incidence of type 2 diabetes mellitus is increasing in adolescence and childhood as a result of obesity-associated insulin resistance. Children and adolescents may manifest either type 1 or type 2 diabetes mellitus in association with genetic syndromes (e.g., Down's syndrome), drug treatment (e.g., glucocorticoids), or other systemic diseases (e.g., cystic fibrosis). Other features differentiating IDDM from the more common adult-onset NIDDM are listed in Table 7E-1 . Physical exercise traditionally is considered beneficial in the treatment of IDDM,[28] and it is one of the mainstays of treatment of NIDDM. Attainment and maintenance of ideal body weight, improvement in self-image, and decreases in hypertension and lipid-related cardiovascular risk factors[12] [18] all can be achieved by the diabetic patient who exercises. Observations of exercise-associated reductions

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TABLE 7-E-1 -- Distinguishing Characteristics of the Two Major Types of Diabetes Mellitus Characteristic Type 1 Type 2 Synonym

Juvenile onset, insulin-dependent diabetes mellitus (IDDM)

Adult-onset, noninsulin-dependent diabetes mellitus (NIDDM)

Age of onset

Most often during growing years, occasionally during adulthood

Adulthood; increasing incidence in adolescence/childhood

Contributing causative factors

Immunologic destruction of Age, obesity, pregnancy insulin-producing cells of the pancreas

Predominant insulin abnormality

Insulin deficiency

Insulin resistance

Response to stress, illness, failure to administer insulin

Hyperglycemia and ketoacidosis

Hyperglycemia without ketoacidosis

Treatment with diet and Negligible efficacy weight reduction alone

Improvement expected

in blood glucose[14] have been substantiated by in vivo and in vitro[27] findings of increased insulin sensitivity as a result of enhanced insulin receptor binding after physical training; these effects can be seen after a single exercise session in an inactive individual,[9] albeit probably not to the same degree as in a trained individual. Although the value of exercise in improving long-term metabolic control is controversial[20] in IDDM (the effects in NIDDM are well established), athletic participation by young individuals with IDDM is encouraged to achieve the same health and cardiovascular[34] benefits enjoyed by exercising nondiabetic individuals. Management of these athletes requires knowledge of the metabolic responses to exercise in diabetic individuals. Careful monitoring and adjustment of insulin doses and nutrition plans can make possible the safe and successful participation of patients with IDDM in virtually any athletic activity. The presence of endogenous insulin production simplifies glycemic regulation during exercise in patients with NIDDM. Relevant Physiology and Pathophysiology Glucose Metabolism during Exercise

Maintenance of a normal plasma glucose level during exercise depends on a precise balance between mobilization of fuel sources and glucose use by tissues. The exercising muscle fiber can increase its metabolic rate and production of adenosine triphosphate (ATP) tremendously, with oxidative processes 50 times higher than resting levels and glucose uptake 35 times higher than resting levels.[30] Primary sources of

energy include fat and carbohydrate present in muscle and glucose released from the liver as a result of breakdown and mobilization of stored glycogen (glycogenolysis). The relative contributions of these sources vary with the duration and intensity of exercise. At the onset of muscular activity, energy is derived predominantly from anaerobic breakdown of muscle glycogen to form lactate. Aerobic metabolism of a combination of hepatic-derived glucose and free fatty acids from adipose tissue contributes the most energy after 20 to 30 minutes of activity. With prolonged exercise (60 to 90 minutes), free fatty acids constitute the principal energy source, although glycogen remains an important fuel, and depletion of muscle glycogen has been shown to coincide with the time of exhaustion.[10] Intensity of exercise is measured by the percentage of the individual's maximum oxygen consumption (VO2max ) required for fuel usage. During exercise at high intensity, oxidation of glucose for energy predominates; with less intense exercise, fat usage is preferred. Physical training enables the athlete to perform the same work at a lower percentage of VO2max and to conserve glucose and improve endurance by using a greater proportion of free fatty acids. Insulin is an anabolic hormone that has important effects on carbohydrate, protein, and fat metabolism. A commonly held misconception is that insulin exerts its major effect on blood glucose by increasing the uptake of glucose into tissue such as muscle. The major means by which insulin decreases blood glucose is by suppressing the production of glucose by the liver. Insulin inhibits protein degradation, encouraging growth and preventing weight loss and tissue breakdown. Use of fat for energy (lipolysis) is highly sensitive to the inhibitory effects of insulin, and the appearance of fat-derived ketones in blood or urine signifies marked insulin deficiency in the diabetic patient. Fuel supply during exercise is orchestrated by a variety of hormonal responses. In exercising nondiabetic individuals ( Fig. 7E-1 ), insulin secretion is inhibited by increased sympathetic (-adrenergic) nervous system activity. This suppression of endogenous insulin release and increased secretion of hormones that oppose the actions of insulin (counterregulatory hormones), such as glucagon, epinephrine, and norepinephrine, allows hepatic glucose production to increase, satisfying the demands of exercising muscle ( Table 7E-2 ). Lowered serum insulin concentrations facilitate lipolysis and the liberation of free fatty acids and glycerol (used with lactate, pyruvate, and alanine as precursors for gluconeogenesis). Stimulation of insulin-independent glucose uptake by skeletal muscle through exercise compensates for declining insulin concentrations and facilitates delivery of substrate to exercising tissues. The exact mechanism by which exercise independently stimulates glucose transport into muscle appears to be related to an increase in plasma membrane glucose transporter number, although the precise stimulus for this increase is unknown.[24] Physical training increases the athlete's sensitivity to insulin,[17] an effect that predominates in skeletal muscle rather than liver. An increase in insulin binding[26] resulting from augmentation of insulin receptor number and affinity

299

Figure 7-E-1 The response to exercise in healthy individuals and in insulin-dependent diabetics. When plasma insulin is normal or slightly diminished, hepatic glucose production increases markedly, as does skeletal muscle usage of glucose, whereas blood glucose remains unchanged. FFA, free fatty acids. (From Ekoe JM: Overview of diabetes mellitus and exercise. Med Sci Sports Exerc 21:353-368, 1989. © The American College of Sports Medicine.)

has been shown after short periods of physical training. Reductions in body adipose tissue contribute to a greater insulin effect after prolonged training. Changes in insulin sensitivity correlate directly with improvements in VO2max ,[17] although this may reflect primarily frequency of exercise rather than fitness per se. Glucose Regulation during Exercise in Athletes with Insulin-Dependent Diabetes Mellitus

Soon after the implementation of insulin therapy, it was observed that physical activity could reduce the insulin requirements of patients with IDDM and that the decrease in blood glucose after an insulin injection was magnified by subsequent exercise.[16] In contrast to the effect of insulin suppression observed in nondiabetic athletes, absorption of exogenously administered insulin is enhanced by exercise in the patient with IDDM ( Fig. 7E-2 ).[6] This effect is TABLE 7-E-2 -- Actions of Major Counterregulatory Hormones Hormone Mechanism of Hyperglycemic Effect Glucagon*

Activates hepatic glycogenolysis and gluconeogenesis

Epinephrine*

Stimulates hepatic glucose production, limits peripheral glucose use, suppresses insulin secretion

Growth hormone

After initial glucose-lowering effect, limits glucose transport into cells, mobilizes fat, and provides gluconeogenic substrate (glycerol)

Cortisol

Initially inhibits glucose use; with time, mobilizes substrate (amino acids and glycerol) for gluconeogenesis

*Hormones important in recovery from acute hypoglycemia.

Figure 7-E-2 The response to exercise in hyperinsulinemic insulin-dependent diabetics. When plasma insulin is increased, skeletal muscle usage of glucose during exercise increases markedly, but the increase in hepatic glucose production is smaller than normal: Blood glucose levels fall. FFA, free fatty acids. (From Ekoe JM: Overview of diabetes mellitus and exercise. Med Sci Sports Exerc 21:353-368, 1989. © The American College of Sports Medicine.)

pronounced when insulin is administered less than 60 minutes before exercise and, for most activities, is augmented when a leg (versus an arm) injection site is used.[29] Increased serum insulin levels would inhibit hepatic glucose production and peripheral lipolysis. At the same time, continued insulin-independent glucose uptake by exercising muscles depletes energy stores. Deficiencies of counterregulatory hormones such as glucagon (common) and epinephrine (less common) develop in many patients with IDDM and further limit fuel availability during exertion. The balance between energy supply and usage may be disrupted in the exercising diabetic athlete by an unregulated (either excessive or insufficient) insulin effect and a variable antagonism of insulin by counterregulatory hormones. Consequences of Excessive Insulin Effect during Exercise

Suppression of glycogenolysis by excessive insulin action combined with insulin-independent glucose uptake by working muscles can result in hypoglycemia during, immediately after, or several hours after exercise. Failure to anticipate the occurrence or intensity of exercise and to make appropriate adjustments in insulin dosage and caloric intake accounts for most instances of hypoglycemia during activity. Most diabetic patients are aware of the effect of exercise on blood glucose and alter their daily insulin and nutrition plan accordingly. This caution, combined with some immediate hyperglycemic effects of strenuous exercise,[29] explains the relative rarity of hypoglycemia during exercise or 1 to 2 hours after exercise. A more common but perhaps less widely recognized occurrence is the development of hypoglycemia 6 to 15 hours after strenuous activity. [2] A 2-year prospective case

300

TABLE 7-E-3 -- Clinical Characteristics of Postexercise Late-Onset Hypoglycemia Occurs 6-15 hours after unusually strenuous or prolonged activity (frequently nocturnal) Frequently severe (stupor, coma, and/or seizure) with few warning signs Unrelated to age of patient or duration of diabetes Unrelated to strict metabolic control or excessive evening insulin administration study of 300 children and adolescents with IDDM revealed that 48 (16%) experienced such postexercise late-onset hypoglycemia.[19] Distinctive characteristics of this phenomenon are summarized in Table 7E-3 . In addition to its delayed occurrence, postexercise late-onset hypoglycemia is distinguished by its severity. Stupor, coma, and seizures during the episode are relatively common, and warnings of impending hypoglycemia often are absent. Patient age, duration of IDDM, and tightness of metabolic control are unrelated to the likelihood of experiencing postexercise late-onset hypoglycemia. A predisposing factor is the associated intensity or duration of exercise,

considered to be exceptional for essentially all patients affected. Diabetic athletes making the transition from an untrained to a trained state are more likely to experience delayed hypoglycemia. Intuitively, one would expect the hypoglycemic effect of exercise to disappear within a few hours after the activity. In fact, the occurrence of nocturnal hypoglycemia after an intervening meal and bedtime snack and occasionally in the absence of nocturnal exogenous insulin indicates that the effects of acute exercise on glucose metabolism persist for several hours. Enhanced glucose uptake and glycogen synthesis by muscle,[7] increased sensitivity of muscle to insulin,[23] and increased binding of insulin to monocytes[15] combine to improve glucose tolerance in untrained subjects for at least 18 hours after exercise.[9] This increased sensitivity to insulin, combined with the avid extraction of glucose from the circulation for the repletion of muscle and liver glycogen stores depleted during exercise, explains the occurrence of nocturnal postexercise late-onset hypoglycemia in most cases. Diabetic patients with diminished glucagon, epinephrine, and cortisol responses to hypoglycemia have an additional risk of experiencing delayed hypoglycemia. Deficient counterregulation contributes to the lack of warning signs and increased severity of postexercise late-onset hypoglycemia and may explain its occurrence in patients not using insulin with peak activity in the night or early morning. Consequences of Insufficient Insulin Effect during Exercise

High-intensity, short-term exercise normally is associated with transient rises in plasma glucose levels, which peak 5 to 15 minutes after exercise is stopped and return to baseline within 40 to 60 minutes.[21] Suppression of insulin secretion, stimulation of the sympathetic nervous system and release of counterregulatory hormones, and stimulation of hepatic glucose production in excess of peripheral

Figure 7-E-3 The response to exercise in insulin-deficient insulin-dependent diabetics. When plasma insulin is diminished markedly, hepatic glucose production is increased markedly during exercise, but the increase in skeletal muscle usage of glucose is smaller than under normal circumstances: Blood glucose levels rise. FFA, free fatty acids. (From Ekoe JM: Overview of diabetes mellitus and exercise. Med Sci Sports Exerc 21:353-368, 1989. © The American College of Sports Medicine.)

glucose uptake combine to produce this glycemic response. After the termination of exercise, insulin secretion is stimulated promptly in the presence of elevated plasma glucose levels and declining epinephrine concentrations. Consequently, transiently elevated plasma glucose levels return rapidly to normal. [4] In the athlete with IDDM, the postexercise rise in plasma insulin levels does not occur, and hyperglycemia after intense exertion may be sustained and of greater magnitude.[3] This effect is exaggerated when a pre-exercise insulin deficiency is present and the plasma glucose concentration is elevated ( Fig. 7E-3 ). Severe insulin deficiency results in accelerated lipolysis and ketogenesis and is heralded (in the nonfasting state) by ketonuria. Exercise in this setting leads to further impairment of glucose usage,

enhancement of lipolysis, and stimulation of hepatic glucose production and ketogenesis. In addition to prompt elevation in blood glucose concentrations, defective peripheral clearance of ketones leads to a rapid worsening of an already compromised metabolic state.[8]

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Viral Blood-Borne Pathogens Human Immunodeficiency Virus

The other end of the spectrum of viral diseases is represented by blood-borne pathogens. Blood-borne pathogens include hepatitis B virus (HBV) and HIV, which at this writing continues to be a chronic progressive disease that ultimately leads to death. As the pool of infected persons has increased worldwide and in the United States, the risk of disease transmission during athletic competition has increased. HIV is a viral disease that directly involves the immune system and is responsible for acquired immunodeficiency syndrome (AIDS). Specifically, the human retrovirus HIV-1 affects CD4 T-helper cells, which causes a progressive decrease in immune function. It is a chronic disease, with infected patients living an average of 10 years. Individuals with HIV ultimately succumb to malignancies and opportunistic infections because of their progressive immunosuppression. Many individuals with HIV live long enough to transmit the disease. Worldwide, HIV has been reported in more than 150 countries with an estimated 20 million persons infected with HIV. In the United States, it is estimated that there are more than 1 million HIV-infected individuals. Overall, this represents an incidence of 1 in 250. Among U.S. men, 18 to 24 years old, the incidence of HIV in whites is 1 in 400, in Hispanics is 1 in 150, and in African Americans is 1 in 50.[14] There are five recognized stages of HIV, which are based on signs and symptoms, CD4 count, and timing. The first stage is the acute retroviral stage, and in the second stage the HIV-positive individual is asymptomatic. In these first two stages, the viral proliferation is taking place in the lymph system, and the patient is relatively healthy and commonly can participate in athletic competition. In the third stage, the HIV-positive individual begins to manifest signs that include low-grade fevers, weight loss, lymphadenopathy, diarrhea, and symptoms of lethargy and fatigue, also known as AIDS-related complex. The fourth and fifth stages, the late symptomatic stage and the advanced stage, are marked with malignancies and opportunistic infections. Individuals

with the AIDS diagnosis at this point have a 75% death rate by 3 years. [14] Although much research is being done and advances in medications have been introduced, to date, AIDS has no cure. Long-term survivors of HIV have noted, however, that exercise and lifestyle changes have improved the quality and longevity of their lives. Research has shown that exercise can increase the number of CD4 cells in HIV-positive individuals. Exercise is psychologically beneficial for the HIV-positive individual as a stress reducer. Mild-to-moderate exercise has been shown to limit or decelerate the body wasting seen in AIDS patients. Exhaustive physical training and the stress of competition represent at least a theoretical concern in elite athletes with HIV, however, and safety of continued competition is unknown.[18] [20] Limited experience has led to the following preliminary guidelines for exercise in HIV-infected athletes: 1. Exercise is a safe and beneficial activity for the HIV-infected person. 2. HIV-infected individuals should begin exercising while healthy and adopt strategies to help them maintain an exercise program throughout the course of their illness. 3. HIV-infected persons, through the use of exercise, can play an important role in the management of their illness, while improving quality of life. 4. Exercise has the potential of other subtle and effective behavioral therapeutic benefits regardless of ethnicity, exposure category, or gender and is particularly promising in areas in which pharmacologic treatments are not readily available (e.g., underdeveloped countries).[20] Because there exists a symptom-free period while HIV infected, and because exercise is encouraged for the HIV-positive individual, it is at least a theoretical concern that HIV can be transmitted during athletic competition. In addition, as a group, athletes by nature are risk takers. Although this attribute may be successful in athletic competition, this attribute can be particularly detrimental in social situations. Risk taking off the athletic fields can result in high-risk behavior for HIV transmission. Risk taking includes shared needles used for illicit drugs, including androgenic steroids, and care-free sexual habits, which includes multiple partners and unprotected sexual intercourse.[3] Although there may be a growing cohort of HIV-infected athletes, the risk for transmission during athletic competition continues to be remote. For the most part, the HIV particle is a fastidious organism that requires a significant environment to remain infectious. It is found in concentrations of only a few hundred to a few thousand particles per milliliter of blood (compared with HBV, which exists in concentrations of 100 million particles/mL). As a result, only 1 in 300 needle-stick injuries with infected blood have resulted in disease transmission. In most of these cases, the transmission usually involved a hollow-bore needle with a deep intramuscular injection.[24] Transmission of HIV has been documented in semen, vaginal and cervical secretions, breast milk, and amnionic

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fluid in addition to blood and blood products.[1] [14] No evidence of transmission of HIV has been documented through sputum, urine, tears, saliva, and perspiration, all of which athletes are exposed to during and surrounding an athletic competition. HIV has not been cultured in sweat. HIV has not been transmitted through casual contact. [1] [14] There have been no documented cases of HIV transmission during athletic competition. The one alleged case of HIV transmission during competition reported in 1990 between two Italian soccer players was discounted. One player was HIV negative 1 year before the game involving the contact with the HIV-positive opponent. Two months later, the previously HIV-negative player became HIV positive. The virus was not typed, and the identity of the strain transmitted was not known. Behavior off the athletic field accounted for a more logical transmission scenario.[34] A razor was implicated in the transmission of HIV from a hemophiliac twin to his brother. Another case of sibling transmission has been documented presumably through an unrecognized blood exposure.[26] In 1995, a study estimated the theoretical risk of HIV transmission from bleeding injuries in the National Football League (NFL) during the 1992 season, which was calculated from observing professional football players from 11 NFL teams through 155 regular season games. The risk of transmission was calculated as equal to the prevalence of persons infected with HIV (seropositive college men, 1 in 200), risk of percutaneous HIV transmission in the health care environment (1 in 300), risk for laceration in an opponent (0.41 lacerated players per game/45 players per game), and risk for any bleeding injury per game for each player (3.46 bleeding players per game/45 players per game). These calculations suggest the mathematical probability of HIV transmission during an NFL football game to be 1 HIV transmission per 85 million game contacts. The mechanics of the study may have overestimated this transmission rate. The real risk of transmission in the NFL as in other athletic communities is off-the-field, high-risk behaviors of intravenous drug use including anabolic steroids, multiple sexual contacts, and unprotected sex.[17] Because the risk of HIV transmission is still possible, a strategy needs to be used to reduce further the risk of HIV transmission during athletics. The individuals most at risk to contact HIV-infected blood during competition are the attending medical staff, in particular, the athletic trainers. Common sense, basic hygiene principles, and the Centers for Disease Control and Prevention universal guidelines provide a simple and effective method of reducing further the risk of HIV and other blood-borne pathogens, such as HBV, during athletic competition. The American Medical Society for Sports Medicine (AMSSM) and the American Orthopaedic Society for Sports Medicine (AOSSM) offer the following specific guidelines: 1. Pre-event preparation includes proper care for existing wounds. Abrasions, cuts, or oozing wounds that may serve as a source of bleeding or as a portal of entry for blood-borne pathogens should be covered with an occlusive dressing that will withstand the demands of competition. Likewise, care providers with healing wounds or dermatitis should have these areas covered adequately to prevent transmission to or from a

patient. 2. Necessary equipment and supplies important for compliance with universal precautions should be available to caregivers, including vinyl gloves; disinfectant; bleach (freshly prepared in a 1:10 dilution with tap water); antiseptic; designated receptacles for soiled uniforms (with separate waterproof bags or receptacles appropriately marked for uniforms and equipment contaminated with blood), bandages, and dressings; and a container for appropriate disposal of needles, syringes, and scalpels. 3. During the sports event, early recognition of uncontrolled bleeding is the responsibility of officials, athletes, and medical personnel. Participants with active bleeding should be removed from the event as soon as this is practical. Bleeding must be controlled and the wound cleansed with soap and water or an antiseptic. The wound should be covered with an occlusive dressing that will withstand the demands of the activity. When bleeding is controlled and the wound covered properly, the player may return to competition. Any participant whose uniform is saturated with blood, regardless of the source, must have the uniform changed before returning to competition. 4. Athletes should be advised that it is their responsibility to report all wounds and injuries in a timely manner, including those recognized before the sporting activity. It is the athlete's responsibility to wear appropriate protective equipment at all times, including mouth protectors, in contact sports. 5. The care provider managing an acute blood exposure must follow the guidelines of universal precautions. Appropriate gloves should be worn when direct contact with blood, body fluids, and other fluids containing blood can be anticipated. Gloves should be changed after treating each individual participant, and as soon as practical after glove removal, hands should be washed with soap and water or antiseptic. 6. Minor cuts, abrasions, or both commonly occur during sports. These types of wounds do not require interruption of play or removal of the participant from competition. Minor cuts and abrasions that are not bleeding should be cleaned and covered during scheduled breaks in play. Likewise, small amounts of bloodstain on a uniform do not require removal of the participant or a uniform change. 7. Lack of protective equipment should not delay emergency care for life-threatening injuries. Although HIV is not transmitted by saliva, medical personnel may prefer using protective airway devices. These devices should be made available whenever possible. 8. Any equipment or area (e.g., wrestling mat) soiled with blood should be wiped immediately with paper towels or disposable cloths. The contaminated areas should be disinfected with a solution prepared with 1 part household bleach to 10 parts water, which should be prepared fresh daily. The cleaned area should dry before reuse. Persons cleaning equipment or collecting soiled linen should wear gloves. 9. Postevent considerations should include reevaluation of any wound sustained during the sporting event. Further cleaning and dressing of the wound may be necessary.

Bloodstained uniforms or towels should be collected for eventual washing in hot water and detergent. 10. Procedures performed in the training room are governed by adherence to universal precautions. Gloves should

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be worn by care providers. Any blood, body fluids, or other fluids containing blood should be cleaned in a manner as described previously. Equipment handlers, laundry personnel, and janitorial staff should be advised to wear gloves whenever contact with bloody equipment, clothing, or other items is anticipated. Appropriate containers for disposal of needles, syringes, or scalpels should be available. 11. Some of the members of the athletic health care team may be considered to be covered under Occupational Safety and Health Administration (OSHA) guidelines. Assessment of the application of these guidelines must be made on an individual basis. This application may include consideration for HBV immunization for some personnel who are involved with the athletic health care team. No recommendation has been made specifically for the immunizations against HBV for athletes in particular. Several groups now recommend, however, universal immunization against HBV of newborns and college-aged individuals.[1] The issue of HIV mandatory testing for athletic competition is complex. If implemented, could it reduce the extremely remote possibility of HIV transmission during sport? Who should be tested? If professional or Olympic athletes are tested, what is the implication for college, school, and community athletic programs? How often should athletes be tested? With a negative test result, the athlete could be in the 3-month window between infection and HIV-positive seroconversion. With any screening, especially on a large-scale basis, the problem of false-positive test results arises and its attendant issues. As a result, the AMSSM and AOSSM believe that mandatory HIV testing is not supported by medical reasons to allow athletic participation. Such testing would not effectively prevent infection, promote health, or easily be implemented.[1] Voluntary testing of athletes who exhibit high-risk behaviormultiple sexual partners, injectable drug use, acquired sexually transmitted disease, sexual contact with a high-risk personor who have had a blood transfusion before 1985 should be encouraged to be tested. Knowledge of HIV status can provide an opportunity for individual education and counseling. In addition to counseling about athletic competition, the individual should be counseled to modify behavior that may prevent further transmission of HIV and participate in newly available therapy for asymptomatic patients. All testing should be done with counseling and informed consent.[1] The AOSSM and AMSSM suggest that the team physician or athletic trainer be aware of the following legal considerations: 1. The HIV-positive individual (or parent in the case of a minor) dictates the

confidentiality of his or her status. In contrast to other blood-borne pathogens or infectious diseases, HIV infections reporting is not mandatory in all states. The clinician should consult the local or state health department for reporting guidance. 2. Because confidentiality rests with the infected athlete, health care providers are not free to inform coaches, teammates, opponents, or other physicians of the HIV-positive athlete. The physician is not liable for failure to warn an uninfected opponent. That responsibility lies with the HIV-infected athlete. Inherent to sports and athletic competition is the risk of injury, and the noninfected athlete should be informed of the remote risk of HIV transmission because the HIV status of competitors is unknown. 3. To date, the courts continue to find the responsibility for sexual transmission of HIV to be with the HIV-positive person. There has been no legal precedent with HIV transmission in sports. 4. Health care providers should be familiar with state and federal statutes governing confidentiality. Equally important, physicians should be familiar with government regulations, in particular OSHA, in blood-borne pathogens.[1] The risk for HIV transmission in the athletic arena is highest among sports medicine personnel. Even with strict adherence to the universal precautions, accidents or emergency situations may occur that expose an individual to not only HIV, but also HBV. After the immediate cleaning of the exposure or wound, the exposed person should contact the local health care facility because many medical centers have a comprehensive procedure for body fluid exposure. The exposed individual should have a laboratory evaluation that includes the following: Complete blood count, corrected sedimentation rate, urinalysis, and a Chemscreen if antiviral therapy is to be given Hepatitis A antibody, hepatitis B surface and core antibody, hepatitis B surface and core antigen, and hepatitis C antibody HIV serology after counseling and signed consent Serologic test for syphilis Obtain 5.0 mL of serum to save in blood bank for 6 months

The donor individual, if identifiable, should have the following tests: Hepatitis A antibody Hepatitis B antibody and surface antigen Hepatitis C antibody Serology for syphilis HIV serology, after counseling and signed consent

Laboratory testing should be done as soon as possible, but not necessarily before treatment is begun.

The following treatment is recommended: All individuals at risk should receive tetanus-diphtheria toxoid, 0.5 mL intramuscularly (if skin-penetrating injury); human immune globulin, 2.0 mL intramuscularly; hepatitis B globulin, 0.06 mg/kg body weight if source unknown or is HBsAg positive; and hepatitis B immunization series if not already immunized. The individual at risk for HIV should be staged for HIV risk according to the current Centers for Disease Control guidelines. These guidelines are updated and appended as revised. The individual should be counseled regarding risks and recommendations of HIV treatment. Therapy should begin within 1 or 2 hours of injury. Follow-up of the body fluid-exposed individual requires regular complete blood count, urinalysis, erythrocyte sedimentation rate, and Chemscreen every 2 weeks while on anti-HIV therapy and serial serology for HIV, HBV, hepatitis A virus, hepatitis C virus, and syphilis.[2]

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Hepatitis B

Hepatitis B virus and, to a lesser extent, hepatitis C virus, although not universally fatal like HIV, represent a larger health care issue in sports medicine. There are greater than 300,000 acute infections reported annually in the United States. It is reported that 1 in 3 infections result in severe hepatitis; 1% of affected individuals die of fulminant hepatitis, and 5% to 10% become chronic carriers of HBV. There are an estimated 1 million HBV carriers in the United States, with 25% of these individuals developing chronic active hepatitis. Although hepatitis C virus is less common, 50% of individuals that become infected with hepatitis C virus become chronic carriers, and 25% develop cirrhosis.[1] [14] Transmission is similar to HIV, by way of direct contact with infected blood and body fluids. Exposure should be considered whenever HIV is suspected. Transmission from household contacts has been reported, not only with shared needle use and sexual intercourse, but also rarely from shared razors and toothbrushes as well as through unrecognized wound or mucous membrane injury. In the health care literature, HBV transmission from a needle stick is approximately 33%, compared with HIV transmission, which is 0.35%.[1] In the sporting arena, a case of HBV transmission has been documented involving an outbreak of hepatitis B in 1982 in high school-aged sumo wrestlers in Japan.[28] It appears that the chronic HBV carrier who is e-antigen positive presents the greatest concern for transmission.[1] [34] Because of the large chronic HBV pool and greater infectivity, individuals at risk for HBV exposure should be immunized against hepatitis B; this includes all sports medicine staff. Some have advocated hepatitis B immunization for all college-bound individuals.[36] [47] [52] Similar to HIV, the greatest risk to HBV transmission is in individuals engaged in the high-risk behaviors identified earlier. When infected with HBV, the athlete has an incubation period of 60 to 90 days. Symptoms include loss of appetite, fatigue, and low-grade fever. The illness may be

mild or result in fulminant hepatitis and death. The infectious state begins before the athlete is symptomatic and continues for several months after subjective recovery. Chronic carriers may have few symptoms and yet are infectious for prolonged periods. Hepatitis B virus transmission is a reportable disease. The patient is given hepatitis B immune globulin and Heptovax. In addition to a complete blood count, erythrocyte sedimentation rate, urinalysis, and Chemscreen, hepatitis B surface and core antigen should be tested.[2] Depending on exposure, HIV serology should be considered after counseling and informed consent. [14] The athlete with HBV is managed similarly to the athlete with IM. Patients should be examined serially for hepatosplenomegaly. It is prudent to limit the athlete's exposure to high contact and bleeding sports, such as wrestling, until the athlete's status in regards to infectivity is known. HBV antigen probably is the best marker for infectivity. The athlete who is a chronic HBV carrier with the e-antigen presents a special problem. Individuals should be counseled regarding their infectivity and advised against competition involving bleeding and close contact. There is no evidence that intense, highly competitive training is a problem for the asymptomatic HBV carrier (acute or chronic).[1] [41]

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Immunizations

Keeping track of athletes' immunizations and ensuring that they are up to date is important in preventing and reducing the transmission of many infectious diseases. Measles outbreak can affect entire teams. Indoor sporting arenas are a prime environment for the spread and transmission of measles, with airborne outbreaks occurring in gymnasts, wrestlers, and basketball players.[18] [54] If the athlete was born after 1957 and received the vaccine before 15 months of age, he or she should receive the live attenuated measles vaccine. All young adults who have not received a booster since 1980 should be revaccinated. A booster is recommended before entering college. The influenza vaccine may be beneficial for athletes competing in fall and winter sports. Athletes who should not receive this vaccine include those who are allergic to eggs or who have a current febrile illness. With this vaccine, high levels of antibodies can be present for 1 year. A strategic plan on immunizing winter athletes who are at the greatest risk is to immunize early in the preseason (in September). In this way, athletes still have adequate antibody levels for the peak influenza season. With this strategy, unwanted side effects, such as muscle soreness at the injection site, fever, or generalized myalgias, do not affect the athlete during the competitive season.[47] The hepatitis B vaccine should be considered in all contact or collision sport athletes or any athlete that may be exposed to infectious body fluids. For athletes, the risk of disease transmission exists in any form of competition in which people are in close contact.[36]

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Becker TM, Kodsi R, Bailey P, et al: Grappling with herpes: Herpes gladiatorum. Am J Sports Med 16:665, 1988. 6.

Behan PO, Behan WM, Bell EJ: The post viral fatigue syndromean analysis of the findings in 50 cases. J Infect 10:211, 1985. 7.

Belongia EA, Goodman JL, Holland EJ, et al: An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med 325:906, 1991. 8.

Brown LS, Drotman DP, Chu A, et al: Bleeding injuries in professional football: Estimating the risk for HIV transmission. Ann Intern Med 122:271-274, 1995. 9.

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Coyle PK: Overview of acute and chronic meningitis. Neurol Clin 17:691, 1999.

Dienst WL, Dightman L, Dworkin MS, et al: Pinning down skin infections: Diagnosis, treatment, and prevention in wrestlers. Physician Sports Med 25:45, 1997. 13.

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Dimmed RJ: HIV and blood borne pathogens in sports. Instr Course Lect 361:35-47, 1997.

Dommerby H, Stangerup SE, Stangerup M, et al: Hepatosplenomegaly in infectious mononucleosis, assessed by ultrasonic scanning. J Laryngol Otol 100:573, 1986. 15.

Doolittle R: Pharyngitis and mononucleosis. In Fields KB, Fricker PA, Delaney MJ (eds): Medical Problems in Athletes. Malden, MA, Blackwell Science, 1997, p 11. 16.

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Eichner ER: Neck check. Runners World 27:16, 1992.

Eichner ER: Contagious infections in competitive sports. Gatorade Sports Science Institute Sports Science Exchange 8:56, 1995. 18.

Eichner ER: Infectious mononucleosis: Recognizing the condition, reactivating the patient. Physician Sports Med 24:49, 1996. 19.

Eichner ER, Calabreese LH: Immunology and exercise: Physiology, pathophysiology, and implications for HIV infection. Med Clin North Am 78:377-388, 1994. 20.

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Freeman MJ, Bergfeld WF: Skin diseases of football and wrestling participants. Cutis 20:333, 1977.

Goodman RA, Thacker SB, Solomon SL, et al: Infectious disease in competitive sports. JAMA 271:862, 1994. 23.

Henderson DK, Fahey B, Wiley M, et al: Risk for occupational transmission of human immunodeficiency virus type I (HIV-1) associated with clinical exposure. Ann Intern Med 113:740-746, 1990. 24.

Hirsch MS: Cytomegalovirus and human herpesvirus types 6, 7, and 8. In Fauci AS, Braunwald E, Isselbacher KS, et al (eds): Harrison's Principles of Internal Medicine, 14th ed. New York, McGraw-Hill, 1998, p 1092. 25.

HIV transmission between two adolescent brothers with hemophilia. MMWR Morb Mortal Wkly Rep 42:948-951, 1993. 26.

Horwitz CA, Henle W, Henle G, et al: Clinical and laboratory evaluation of cytomegalovirus-induced mononucleosis in previously healthy individuals: Report of 82 cases. Medicine 65:124, 1986. 27.

Kashiwagi S: Outbreak of hepatitis B in members of a high school wrestling club. JAMA 248:213-214, 1982. 28.

Kramer JS: Pericarditis and myocarditis. In Fields KB, Fricker PA, Delaney MJ (eds): Medical Problems in Athletes. Malden, MA, Blackwell Science, 1997, p 59. 29.

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Madeley CR: Viruses and athletes. Br J Sports Med 32:281-286, 1998.

Maffulli N, Vittorino T, Capasso G: Post-viral fatigue syndrome: A longitudinal assessment in varsity athletes. J Sports Med Phys Fitness 33:392, 1993. 31.

Maki DG, Reich RM: Infectious mononucleosis in the athlete: Diagnosis, complications, and management. Am J Sports Med 10:162, 1982. 32.

Maron BJ, Isner JM,. McKenna WJ: 26th Bethesda Conference: Recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 3: Hypertrophic cardiomyopathy, myocarditis, and other myopericardial diseases and mitral valve prolapse. Med Sci Sports Exerc 26(suppl):S261, 1994. 33.

Mast EE, Goodman WW, Bond MS, et al: Transmission of blood borne pathogens during sports: Risk and prevention. Ann Intern Med 122:283-285, 1995. 34.

McDonald W: Upper respiratory tract infections. In Fields KB, Fricker PA, Delaney MJ (eds): Medical Problems in Athletes. Malden, MA, Blackwell Science, 1997, p 8. 35.

Mellman MF, Schelkun PH: Immunization strategies for active adults. Physician Sports Med 22:91, 1994. 36.

Miser WF: Acute minor illnesses in the athlete. In Lillegard WA, Butcher JD (eds): Handbook of Sports Medicine: A Symptom Oriented Approach, 2nd ed. Boston, Butterworth-Heinemann, 1999, p 353. 37.

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Moeller JL: Aseptic meningitis: A seasonal concern. Physician Sports Med 25:35, 1997.

Moeller JL: Contraindications to athletic participation: Spinal, systemic, dermatologic, paired-organ, and other issues. Physician Sports Med 24:57, 1996. 39.

Moore M, Baron RC, Filstein MR, et al: Aseptic meningitis and high school football players. JAMA 249:2039, 1983. 40.

National Collegiate Athletic Association: Guideline 2h. Blood-borne pathogens and intercollegiate athletics. In Potts KA (ed): NCAA Sports Medicine Handbook, 13th ed. Indianapolis, National Collegiate Athletic Association, 2000, pp 35-39. 41.

Nelsen S, Sealy DP, Schneider EF: The aseptic meningitis syndrome. Am Fam Physician 48:809, 1993. 42.

Nieman DC: Immunity in athletes: Current issues. Gatorade Sports Science Institute Sports Science Exchange 69:1-10, 1998. 43.

Noffsinger J: Physical activity considerations in children and adolescents with viral infections. Pediatr Ann 25:585, 1996. 44.

Rogues AM, Dupon M, Cales V, et al: Spontaneous splenic rupture: An uncommon complication of cytomegalovirus infection. J Infect 29:83, 1994. 45.

Rutkow IM: Rupture of the spleen in infectious mononucleosis: A critical review. Arch Surg 113:718, 1978. 46.

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Sevier TL: Infectious disease in athletes. Med Clin North Am 78:389, 1994.

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Sharp JCM: Viruses and the athlete. Br J Sports Med 23:47, 1989.

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Shute P, Jeffries DJ, Maddocks AC: Scrum-pox caused by herpes simplex virus. BMJ 2:1629, 1979.

Strauss RH, Lanese RR, Leizman DJ: Illness and absence among wrestlers, swimmers, and gymnasts at a large university. Am J Sports Med 16:653, 1988. 50.

Swain RA, Kaplan B: Upper respiratory infections: Treatment selection for active patients. Physician Sports Med 26:85, 1998. 51.

Task Force on Vaccine Preventable Disease (American College Health Association) Institutional Statement on Hepatitis B Vaccination. Baltimore, MD, 1993. 52.

Viral diseases. In Beers MH, Berkow R, Burs M (eds): The Merck Manual of Diagnosis and Therapy, 17th ed. Whitehouse Station, NJ, Merck Research Laboratories, 1999, p 1276. 53.

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White J: Measles: A hazard of indoor sports. Physician Sports Med 19:21, 1991.

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Section B Paired Organ Loss Jorge E. Gómez MS, MD The purpose of this chapter is to provide information on the epidemiology of paired organ loss due to sports trauma, means by which the sports medicine physician might prevent organ loss, and recommendations for participation in sports for athletes with a single functioning eye, kidney, or testicle. Risk of Paired Organ Loss in Sports The Eye

Sports-related eye injuries are common. In 1997, an estimated 32,789 sports- and recreation-related eye injuries were treated in emergency departments in the United States.[51] The true rate of sports-related eye injuries, including injuries cared for in private offices and clinics, is probably closer to 100,000 injuries per year. Anywhere from 4% to 50% of sports-related eye injuries result in legal blindness, with higher rates of blinding injuries associated with rugby and hockey.[6] [16] [34] [35] [44] [47] It must be remembered that loss of vision need not necessarily involve anatomic loss of the eye. In many applications, legal blindness is defined as a best corrected vision of worse than 20/40. Conditions such as retinal detachment and corneal abrasion may result in significant vision loss. Sports associated with the highest number of eye injuries are basketball, baseball, and softball.[51] The sports-related risk varies somewhat with age. From ages 5 to 14, baseball and softball report the highest rates of eye injuries, and between ages 15 and 24, basketball documents the highest rates.[51] As a percentage of total injuries, boxing, soccer, swimming, and racquet sports account for the highest incidence of eye injuries.[43] Basketball, baseball, softball, and racquetball should be considered to carry a high risk of eye injury, as should boxing, karate, tae kwon do, and other martial arts.

Sports with moderately high risk of eye injury include badminton, football, golf, handball, hockey, lacrosse, squash, tennis, and wrestling. Cycling, cross-country, and track and field present low risks of eye injury. The Kidney

Sports activity is a common cause of renal injury. In a study of significant renal injuries in all age groups, Glenn found that 19% occurred during sports activities.[17] Among children, 9% to 28% of significant renal injuries from blunt trauma occurred during sports. [1] [33] [37] The kidney is the abdominal organ injured most commonly during sports participation. [10] However, the loss of a kidney as a result of a sporting injury is rare, even in contact/collision sports. In 1959, Vermooten published the results of an extensive survey of genitourinary tract injuries occurring among intercollegiate athletics.[53] After compiling reports from six universities cumulatively spanning 73 years of reporting, Vermooten found 3 renal lacerations/ruptures (1 of which required nephrectomy), 2 other renal injuries requiring nephrectomy, and 25 renal contusions. Nearly all of these injuries occurred during football. Significant renal injuries have also been reported in winter sports such as downhill skiing, sledding, and tobogganing.[9] [24] Most of these have been penetrating injuries caused by a ski blade or wood shard. Scharplatz and associates[45] reported 5 renal contusions and 6 additional serious injuries requiring nephrectomy from downhill skiing. Hildreth and colleagues[25] reported 10 renal contusions from skiing, 4 requiring surgery. It is not possible to accurately estimate the risk of losing a kidney in sports, but it must be very low. On the other hand, there may be more of a risk of kidney loss or significant renal injury if there is a preexisting renal abnormality. Kuzmarov and coworkers[33] reported that 5 of 9 pediatric patients who required nephrectomy after blunt abdominal trauma had preexisting renal malformations. I am aware of a case of a 17-year-old high school football player who received a blow to the abdomen during a tackling drill and subsequently developed left flank pain. He eventually developed significant flank tenderness, rigidity of the abdominal wall, and gross hematuria. Computed tomography (CT) scan revealed a significantly enlarged left polycystic kidney with a small subcapsular hematoma. Renal scan showed the polycystic kidney to be nonfunctioning. The patient was disqualified from further participation in contact/collision sports. The Testicle

Significant testicular injury, including rupture of the tunica albuginea ( Fig. 7B-1 ), crush injury, intratesticular hematoma, and testicular dislocation, resulting from participation in sports is sufficiently rare to continue to warrant the publishing of case reports. The most common traumatic mechanisms that result in loss of a testicle are a kick to the groin during a brawl, and straddle injuries. Significant testicular injuries occurring during sports that either required surgery or resulted in orchiectomy are summarized in Table 7B-1 . Even in sports, the majority of significant testicular injuries occur because of a kick. This is true in American football, rugby, soccer, rules football, and martial arts.

Loss of Other Organs

The loss of a lung or ovary as a result of sports trauma has not been reported.

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Figure 7-B-1 Rupture of the tunica albuginea with hematocele.

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Prevention of Organ Loss The Eye

An important step in preventing vision loss from sports is performing vision screening during the sports preparticipation examination, which includes a medical history (e.g., documenting previous eye surgery, use of corrective lenses). Occasionally, an athlete is encountered during preparticipation screening whose best correctable vision is less than 20/40 (legally blind). Such an athlete should be re ferred to an ophthalmologist. Another important step in preventing vision loss is the initial evaluation and treatment of eye injuries. An outline of sideline eye injury evaluation is shown in Table 7B-2 . A decision tree for the initial management of sports-related eye trauma is shown in Figure 7B-2 . All team and sideline physicians should be aware of the signs and symptoms of TABLE 7-B-1 -- Case Report of Serious Testicular Injury in Sports* Sport Rupture Torsion Other or Unspecified Rugby

13

Total 13

Baseball

9

1

10

Soccer

5

2

7

Football

4

Cycling

1

Golf

2

2

Softball

2

2

Karate Hockey

1

5 2

2 1

3

2 1

Wrestling

1

1

Shooting

1

1

Other

4

4

Total

42

2

7

[ 3] [ 8] [ 18] [ 20] [ 26] [ 32] [ 35] [ 36] [ 39] [ 40] [ 42] [ 46] [ 48] [ 49] [ 52] [ 53] [ 54] [ 56]

* References Injury resulted from rifle recoil.

51 and

[ 57]

.

TABLE 7-B-2 -- Sideline Eye Injury Evaluation History Mechanism of injury, complete or partial vision loss, decreased visual acuity, a bright flash of light associated with the blow, a sudden increase in floaters, pain, tearing, foreign body sensation, photophobia, or double vision Examination General inspectionfor obvious deformity (rupture, penetrating injury), foreign body Inspection of the anterior segmentirregularity of the pupil, absent or abnormal pupillary response, clouding of the cornea or anterior chamber, hyphema Inversion of the eyelidsfor foreign body Ocular motility Fundoscopic examinationopacity or dislocation of the lens, retinal detachment, floaters Visual fieldstested by confrontation Visual acuityusing a pocket vision card Palpationfacial bone survey for associated fractures Inspection under cobalt light with fluoresceinfor corneal abrasion when foreign body sensation is present significant eye injury. Symptoms include complete or partial vision loss, decreased visual acuity, a bright flash of light associated with the blow, a sudden increase in floaters, pain, tearing, foreign body sensation, photophobia, and double vision. The sideline physician should have in his or her medical bag the following ophthalmologic equipment: penlight, ophthalmoscope with cobalt light, vision card, sterile eyewash, fluorescein strips, antibiotic ointment (e.g., erythromycin ophthalmic), sterile cotton-tipped applicators, and eyeshields. Immediate treatment for significant eye injuries is crucial for preventing vision loss.[21] In cases of penetrating foreign body, corneal laceration, or ruptured globe, no eye medicines should be given. A foreign body should not be removed in the field. A rigid

eyeshield is taped in place that places no direct pressure on the globe. Such a patient should be instructed not to take anything further by mouth. The patient should be immobilized on a stretcher and taken immediately to an emergency center with an ophthalmologist on call. The patient with a corneal abrasion ( Fig. 7B-3 ), suspected orbital fracture, or traumatic hyphema ( see Fig. 7B-3 ) should have the eye covered with an eyeshield and should be sent immediately to the ophthalmologist. The patient with a hyphema should be transported with the head elevated 30 to 40 degrees to enhance settling of the blood clot.[21] Eye protection is mandatory for athletes with significant vision loss in one or both eyes, who are allowed to participate in high-risk sports.[5] A detailed list of recommended protective eyewear for high-risk sports is available. [5] In general, protective eyewear for these sports should be made of polycarbonate. Ready-to-wear, nonprescription polycarbonate sports goggles are currently available from optometrists and opticians, starting at less than $90. Sports eyewear custom-made to prescription should be fitted properly by an ophthalmologist, optometrist, or optician. Protective eyewear that does not fit properly will not provide maximum eye protection. For low-risk sports such as cycling, cross-country, or track and field, protective eyewear may be made of CR-39 plastic, which is not as strong as polycarbonate.

266

Figure 7-B-2 Initial management of sports-related eye trauma. The Kidney

The diagnosis of significant renal injury may be difficult to make clinically. Hematuria is common in sports; it appears to be more frequent in endurance-type activities such as running and swimming than it is in contact/collision sports.[12] Hematuria by itself is not indicative of structural injury to the kidney. Furthermore, the degree of hematuria corresponds poorly with the degree of renal injury.[56] The importance of a high index of suspicion in patients with possible renal injury cannot be overemphasized. Kidney damage must be suspected when an athlete has sustained a blow to the flank, abdomen, or lower chest.

Figure 7-B-3 A, Corneal abrasion. B, Traumatic hyphema. (Courtesy of Dr. Tomy Stark, Department of Ophthalmology, University of Texas Health Science Center at San Antonio, San Antonio, Tex.)

267

A decision tree for the initial evaluation and management of blunt flank and abdominal sports trauma is shown in Figure 7B-4 . The most common type of renal injury in sports is the contusion. Although there is a history of trauma, signs and symptoms may or may not be present. Flank pain and hematuria are the most common complaints. Fortunately, the tight fascia of Gerota, which invests the kidney, usually contains parenchymal bleeding by tamponade. In this case, the hematoma slowly resolves and the parenchyma scars uneventfully. [12] Caliceal lacerations may present in similar fashion, although the pain and hematuria may be more pronounced. Currently, CT scanning with intravenous contrast has replaced peritoneal lavage for assessment of intraperitoneal hemorrhage and injury, especially in the evaluation of youngsters.[29] When CT scan is unavailable, an intravenous pyelogram may used to confirm the diagnosis of renal injury. Both renal contusions and caliceal lacerations are treated with bed rest, with close monitoring of perfusion status, hematocrit, and hematuria. Occasionally, when a caliceal laceration results in considerable blood loss, surgery is required. [12] Patients with renal fracture or vascular pedicle injuries bleed extensively and do require surgery. It must be remembered that up to 20% of patients with blood in the peritoneal cavity from blunt trauma will have a benign abdominal examination initially.[14] When symptomatic, these patients may present with exquisite flank tenderness, unwillingness to move or use the flank muscles, abdominal rigidity, and an abdominal mass.[12] [37] In a review of 66 cases of renal parenchymal injury in children, abdominal pain, generalized abdominal signs (as opposed to localized abdominal signs), ileus, and shock were much more common among patients with renal laceration or transection than in patients with renal contusion.[1] Symptoms and signs of volume loss include pallor, diaphoresis, complaints of extreme thirst, and a thready pulse.[14] In the worst cases, the patient presents in hypovolemic shock. In the field, athletes presenting with a history or physical findings suspicious for significant

Figure 7-B-4 Initial evaluation and management of blunt flank/abdominal sports trauma.

268

intra-abdominal injury should be placed in the recumbent position with the legs elevated. [14] Nothing should be given by mouth. Emergency medical transport should be summoned and the athlete taken to an emergency department with a trauma surgeon available. The athlete should have his or her circulatory status followed closely with frequent checks of blood pressure, peripheral pulses, heart rate, peripheral perfusion, and mental status. The Testicle

The most important aspects of preventing testicle loss from sports injury are awareness

of testicular abnormality, recognition of significant injury, early treatment, and protection. Examination of the scrotum for two healthy testicles should be a part of the preparticipation evaluation. The undescended or retractile testicle may be more prone to trauma because it often lies directly between the skin and the pubic bone.[56] Athletes with apparently one testicle should be referred for ultrasonographic or urologic evaluation to determine if the testis is absent, undescended, or retractile. [56] A decision tree for the initial evaluation and management of testicular sports trauma is shown in Figure 7B-5 . Because symptoms of testicular rupture may not be severe at presentation, it is important to consider the possibility of rupture, especially when a post-traumatic hematocele is present. The presence of a painful, firm scrotal mass that fails to transilluminate, associated with ecchymosis of varying degrees of the scrotal skin and the base of the penis, is indicative of hematocele within the tunica vaginalis, and represents rupture of the testicle in up to 50% of cases.[7] [42] Ultrasound examination of the testicle has been shown to be highly sensitive in diagnosing rupture and distinguishing it from other causes of acute scrotum.[50] Surgical exploration is indicated when ultrasound examination reveals testicular rupture, or when clinical suspicion is high for testicular rupture or torsion because of expanding post-traumatic swelling or acute worsening of symptoms after trauma. In many cases, the injured testicle can be repaired and saved. Early surgical exploration in these cases is critical.[22] Cass and associates[11] reported that 5 of 11 (45%) patients with significant testicular injury in whom surgical exploration was delayed for longer than 3 days needed orchiectomy, whereas 4 of 43 (9%) patients surgically explored within 3 days required orchiectomy. Between 6% and 30% of cases of traumatic rupture of the testicle will require orchiectomy.[36] Testicular torsion may also result in loss of a testicle. Torsion is known to result occasionally from trauma, and has been reported to occur after sports-related trauma. Elsaharty and colleagues[15] identified a history of blunt trauma in 5% of cases of testicular torsion and 10% of cases of torsion of a testicular appendage. Williamson [55] found 7% of cases of torsion associated with trauma. Cases of trauma-associated testicular torsion have been reported in football, soccer, hockey, wrestling, cycling, and swimming.[13] [15] [27] [31] [32] [38] Testicular torsion has a decided predilection for the adolescent; the mean age of patients diagnosed with torsion is approximately 15 years, and the vast

Figure 7-B-5 Initial evaluation and management of testicular sports trauma.

269

majority of cases occur during the second decade of life. [2] [30] Acute onset of scrotal pain, with or without trauma, scrotal swelling, and associated nausea in a teenager should be considered torsion until proven otherwise. Physical examination often reveals

tender scrotal swelling, with the affected testis slightly higher than the other, and absence of the cremasteric reflex on that side. Elevation of the involved testicle may in some cases relieve the pain, but the absence of this sign does not rule out torsion. As with rupture of the testicle, early surgical exploration is the key to salvaging the torsed testicle. Salvage rates approaching 100% have been seen when surgical exploration was performed within 12 hours of the onset of pain.[30] [31] Salvage rates are much lower when surgical exploration is performed 12 hours or longer after the onset of symptoms.[30] [31] [32] The patient with signs and symptoms suggestive of torsion should be taken immediately to a hospital for testicular ultrasound or radionuclide scanning and evaluation by a urologic surgeon. Both ultrasound and scrotal scanning are highly effective in confirming torsion. [19] Radiologic studies to confirm the diagnosis should be abandoned, however, and the patient taken to the operating room directly if such studies would unduly delay surgical exploration.

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Legal Considerations

Athletes missing an eye, kidney, or testicle cannot be excluded from sports solely on the basis of their organ loss. Athletes with these conditions have both legal and constitutional rights to participate in sports under the Rehabilitation Act of 1973, and the Americans With Disabilities Act (ADA) of 1990.[28] Athletes missing an eye, kidney, or testicle are not considered to have diminished athletic abilities solely on the basis of their organ loss. Neither are such athletes viewed as jeopardizing their lives by choosing to participate in sports. Even the loss of a kidney is not felt to be associated with imminent loss of life because of the availability of dialysis and kidney transplantation. Athletes must otherwise be able, however, to meet all other physical requirements of a given sport. This is the basis on which athletes with serious heart conditions may be disqualified without violating the ADA; such heart ailments may significantly limit their ability to perform. It is legally defensible to require an athlete to undergo a medical evaluation as a precondition for participation in a sport. Courts in the United States generally have found it unlawful for public schools to require an athlete to sign a release from injury liability before participating in intramural or interscholastic sports. This is based primarily on the grounds that public schools are federally subsidized and are therefore governed by the ADA. Furthermore, the courts view interscholastic sports as a public service that is deemed a practical necessity for students, even though participation in interscholastic sports is voluntary.[23] Waivers signed by adult athletes or athletes' parents releasing physicians from liability in cases in which athletes had preexisting conditions that created considerable risk of injury from sports participation generally have not alone prevented courts from finding against physicians. In most such rulings, it was successfully argued that despite signing the waiver, the athlete or the athlete's parents were not fully and satisfactorily informed by the physician of the risks of participating with the given medical condition. The rules governing informed consent apply to clearing an athlete to participate with a single paired organ. The current judicial trend is to require physicians to disclose all information to the athlete, and to his or her parents if the athlete is a minor, regarding

the risks of sports participation with his or her medical condition.[41] This disclosure should take the form of a verbal discussion. Physicians should make every reasonable effort to ensure that the transmission of information regarding risk results in adequate comprehension of the information necessary for the athlete or parent to make an informed decision. The discussion of risk by the physician should be provided in clear terms that are easy for the layperson to understand. Certain techniques have been used for enhancing communication of risk information.[28] These include providing written information about risks, meeting with the athlete and his or her parents on more than one occasion, and having the athlete bring a third party to the meeting, such as a teacher or coach, who might assist the athlete or parent in framing appropriate questions. The physician may also test the athlete's and parents' comprehension of the conveyed information by asking them questions, or having the athlete or parent write in his or her own words their understanding of the conveyed information. Most importantly, all details of these discussions should be completely and clearly documented in the medical record. In order for physicians to provide accurate and complete information regarding risks of sports participation with a single paired organ, it is important that they be familiar with current recommendations for participation in sports by athletes with specific medical conditions.[4]

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Allowing Participation in Sports

Physicians have historically been strongly paternalistic regarding decisions about allowing athletes with single paired organs to participate in high-risk sports.[37] Although the Rehabilitation Act and the ADA have provided the athlete with a legal basis for disputing a team physician's advice not to play, the team physician should not be pressured into allowing an athlete to participate in a sport against his or her professional judgment and ethical obligation to protect the athlete's health.[41] Both the American Academy of Pediatrics (AAP) and the American Medical Association (AMA) emphasize the importance of assessing each individual case of an athlete with a single paired organ on its own merits.[4] It is left to the physician's judgment whether to defer to a qualified ophthalmologist or urologist decisions about allowing an athlete with a single functioning eye, kidney, or testicle to participate in sports. The AAP recommends that functionally one-eyed athletes be allowed to participate in all sports if, in the opinion of the physician, the benefits of playing a given sport outweigh the risks.[4] The physician must inform the athlete, and the athlete's parent if he or she is a minor, that

270

participation in high-risk sports, even with adequate protection, may result in loss of the functioning eye and blindness. The physician prescribing protective eyewear must also inform the patient and/or parent that use of protective lenses made with any material other than polycarbonate (e.g., CR-39 plastic, glass) will not afford maximum protection. Also, patients who have previously undergone eye surgery or who have had a significant eye injury may be at increased risk of vision loss because of weakened eye structures. Prescription protective eyewear must be approved by the American Society for Testing Materials (ASTM). It should be made clear that even the best protective eyewear cannot protect against all sports-related eye injuries.

The AAP recommends that athletes with a single normal kidney be allowed to participate in all sports if, in the opinion of the physician, the benefits of playing a given sport outweigh the risks.[4] The physician must inform the athlete and the athlete's parents that although loss of a kidney due to sports participation is very rare, contact/collision sports and winter sports carry a higher risk of serious kidney damage, with potential for loss of the kidney. Athletes and their parents must be informed that loss of the remaining functioning kidney may result in death, may result in lifelong dependence on dialysis, or may lead to kidney transplantation, which carries with it significant risk of graft-versus-host disease, sepsis, thromboembolism, and shortened life span. If a decision is made to allow play, protective padding made specifically for the flank area should be ordered and procured before the athlete participates in high-risk sports. It must be made clear, however, that protective padding does not entirely eliminate risk. Athletes with an abnormal kidney should not be discouraged from participating in contact/collision sports, or in winter sports such as skiing, snowboarding, or sledding. Anatomically abnormal kidneys and kidneys that are abnormally placed (ectopic) appear to be at greater risk of laceration or rupture from sports trauma, with the potential for massive internal bleeding and death. The AAP recommends that athletes with a single functioning testicle be allowed to participate in all sports with protection. Patients with a single functioning testicle and their parents should be informed that loss of a testicle as a result of sports is rare, but that certain sports, such as rugby, baseball/softball, soccer, and football, are associated with a higher risk than others. The athlete and his parent should be told that loss of the remaining normal testicle would not be a threat to life, but would result in both inability to father a child and lifelong dependence on hormone replacement. If such an athlete is allowed to play sports, he must be instructed always to wear an athletic supporter and a cup to minimize risk. Even the use of a cup, however, does not totally eliminate risk. Acknowledgment

I would like to thank Gilberto Aguirre, MD, ophthalmol ogist, for his helpful comments.

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2.

Allan WR: The testis: Torsion and trauma. Practitioner 226:1837-1844, 1982.

Altarac S, Marekovic Z, Kalauz N, et al: Testicular trauma sustained during football. Acta Med Croatica 47:141-143, 1993. 3.

American Academy of Pediatrics Committee on Sports Medicine & Fitness: Medical conditions affecting sports participation. Pediatrics 94:757-760, 1994. 4.

American Academy of Pediatrics Committee on Sports Medicine & Fitness and American Academy of Ophthalmology Committee on Eye Safety & Sports Ophthalmology: Protective eyewear for young athletes. Pediatrics 98:311-313, 1996. 5.

Antaki S, Labelle P, Dumas J: Retinal detachment following ice hockey injury. Can Med Assoc J 117:245-246, 1977. 6.

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Bergqvist D, Hedelin H, Karrlson G: Abdominal trauma during 30 years: Analysis of a large case series. Injury 13:93-99, 1981. 9.

Bergqvist D, Hedelin H, Karlsson G, et al: Abdominal injury from sporting activities. Br J Sports Med 16:76-79, 1982. 10.

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Cianflocco AJ: Renal complications in exercise. Clin Sports Med 11:437-451, 1992.

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Diamond DL: Sports-related abdominal trauma. Clin Sports Med 8:91-99, 1989.

Elsaharty S, Pranikoff K, Magoss IV, Surfin G: Traumatic torsion of the testis. J Urol 132:1155-1156, 1984. 15.

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Goldman MS: Repair of shattered solitary testicle. Urology 24:229-231, 1984.

Golimbu M, Florio FE, Al-Askari S, et al: Value of scrotal scanning. Report of 62 cases. Urology 25:89-92, 1985. 19.

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Golji H, Jaffar DJ: Traumatic rupture of the testicle. Am J Surg 93:127-130, 1957.

Grewal RK, Dhaliwal DK, Hersh PS, Zagelbaum BM: Anterior segment injuries. In Zagelbaum BM (ed): Sports Ophthalmology. Cambridge, Mass, Blackwell Science, 1996, pp 184-209. 21.

Gross M: Rupture of the testicle: The importance of early surgical exploration. J Urol 101:196-197, 1969. 22.

Hander DG: Negligence. Shifting risks: Washington blocks student athlete releases. Gonzaga Law Rev 25:359-372, 1989. 23.

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Hildreth JA, Cass AS, Khan AV: Winter sports-related urological trauma. J Urol 121:62-65, 1979.

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Hildreth TA, Cass As, Khan AV: Skiing injuries to the urinary tract. Minn Med 62:155-158, 1979.

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Hirata I: Traumatic rupture of the testicle in tackle football. J Am Coll Health Assoc 21:165, 1972.

27.

Jackson RH, Craft AW: Bicycle saddles and torsion of the testis. Lancet 1:983-984, 1978.

Jones CJ: College athletes: Illness or injury and the decision to return to play. Buffalo Law Rev 40:113-215, 1992. 28.

Kane NM, Cronan JJ, Dorfman GS, Deluca F: Pediatric abdominal trauma: Evaluation by computed tomography. Pediatrics 82:11-15, 1988. 29.

King LM, Sekaran SK, Sauer D, Schwentker FN: Untwisting in delayed treatment of torsion of the spermatic cord. J Urol 112:217-221, 1974. 30.

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Korbel EI: Torsion of the testis. J Urol 111:521-522, 1974.

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Kursh ED: Traumatic torsion of testicle. Urology 17:441-442, 1981.

Kuzmarov IW, Morehouse DD, Gibson S: Blunt renal trauma in the pediatric population. A retrospective study. J Urol 126:648-649, 1981. 33.

Larrison WI, Hersh PS, Kunzweiler T, et al: Sports-related ocular trauma. Ophthalmology 97:1265-1269, 1990. 34.

Lawson JS, Rotem T, Wilson SF: Catastrophic injuries to the eyes and testicles in footballers. Med J Aust 163:242-244, 1995. 35.

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36.

MacDermott JP, Gray BK, Stewart PAH: Traumatic rupture of the testis. Br J Urol 62:179-181, 1988.

Mandell J, Cromie WJ, Caldamone AA, et al: Sports-related genitourinary injuries in children. Clin Sports Med 1:483-493, 1982. 37.

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McCormack JL, Kretz AW, Tocantins R: Traumatic rupture of the testicle. J Urol 96:80-82, 1966.

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Mitten MJ: Team physicians and competitive athletes: Allocating legal responsibilities for athletic injuries. Univ Pittsburgh Law Rev 55:129-169, 1993. 41.

Munter DW, Faleski EJ: Blunt scrotal trauma: Emergency department evaluation and management. Am J Emerg Med 7:227-234, 1989. 42.

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44.

Pashby TJ: Eye injuries in Canadian amateur hockey. Am J Sports Med 7:254-257, 1979.

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Schneiderman C: Traumatic rupture of the testicle. J Urol 78:54-57, 1957.

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12:115-130, 1991. Turriff T: Product Summary ReportEye Injuries OnlyCalendar Year 1997. Chicago, Prevent Blindness America, 1998. 51.

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Section C Hypertension and Other Cardiac Disease in Athletes Kenneth M. Leclerc MD, FACC Athletes, whose skills and accomplishments are revered and often handsomely rewarded, are considered the healthiest and most vigorous individuals in society. Through self-selection and a generally healthy lifestyle, athletes often avoid serious illness. Athletes are not immune from cardiovascular disease, however. Numerous cardiovascular conditions may manifest in athletes as a matter of natural occurrence or as a consequence of the extreme stresses of their sport. The demands of their sport may expose athletes to extremes of environmental and emotional conditions that may affect their health adversely as well as any overt or covert disease. Examples of such effects include alteration in blood volume and viscosity, electrolyte balance, and temperature. Although only a few clinicians are involved with elite amateur or professional athletes, many clinicians encounter individuals of various ages and levels within youth, interscholastic, collegiate, and masters competition who take their endeavors seriously, regardless of ability. Congenital or acquired cardiovascular disease may manifest in any of these groups with potentially significant consequences. Preparticipation Screening

The role of the physician in preparticipation screening is an important one and yet one that has not been defined clearly. The athlete's best interests should be paramount, but there may be conflicting pressures for or against continued participation by the athlete, the institution the athlete plays for, family members, coaches, and legal professionals. The scope and success of preparticipation screening are affected by factors such as cost-efficiency, practical limitations of screening large populations, and the realization that it is not possible to prevent every athletics-related death or injury. It is estimated that the cumulative prevalence of congenital cardiovascular malformations (e.g., hypertrophic cardiomyopathy, anomalous coronaries, prolonged QT syndrome, arrhythmogenic right ventricular dysplasia, or Marfan syndrome) among athletic

populations is only about 0.2%.[3] It is beyond the scope of this chapter to cover comprehensively the aspects of preparticipation screening, but a few points are worth emphasizing. The impetus behind the perceived need for preparticipation screening has been the high-profile sudden deaths among professional and collegiate athletes. Preparticipation screening goes beyond the detection of cardiovascular abnormalities and includes detection of all predispositions and conditions that might interfere with safe sports participation.[9] [40] Currently in the United States and other countries, there is no universally accepted standard for preparticipation screening. In Italy, junior and senior national team members have been subject to mandatory screening since 1963, whereas in the United Kingdom, systematic widespread population screening is not deemed appropriate.[28] [35] To guide clinicians, the American Heart Association (AHA) scientific statement on cardiovascular preparticipation screening of competitive athletes makes the following recommendations:[3]

272

...[S]creening (a history and physical examination) is recommended before participation in organized high school and collegiate sports, and should be repeated every 2 years, with the goal of identifying (or raising suspicion of) those cardiovascular lesions known to cause sudden death or disease progression in young athletes.... Specifically, athletic screening ... should include a complete medical history and physical examination, including brachial artery blood pressure measurement .... The cardiovascular examination should emphasize precordial auscultation ... to identify heart murmurs consistent with dynamic left ventricular outflow obstruction; assessment of femoral pulses to exclude coarctation of the aorta; recognition of the physical stigmata of Marfan syndrome; and brachial blood pressure measurement.... Clinicians should refer athletes for additional cardiovascular evaluation if their history indicates a family history of sudden death, premature myocardial infarction, Marfan syndrome, or hypertrophic cardiomyopathy or a personal history of presyncope, syncope or palpitations, chest pain or tightness, or high blood pressure. All athleteswith diastolic heart murmurs and any systolic murmurs that cannot be characterized confidently as benign (see the section on physical examination subsequently) should be referred. Interested readers are referred to the AHA's statement for a more thorough discussion of this subject.

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26th Bethesda Conference

In 1994, the American College of Sports Medicine (ACSM) and the American College of Cardiology (ACC) jointly published the report of the 26th Bethesda Conference addressing the issue of eligibility for competition in athletes with cardiovascular abnormalities.[32] This is an excellent comprehensive report that is referenced several times in this chapter. Clinicians interested in sports medicine would find this report to be an invaluable resource in guiding athletes with cardiovascular disease toward safe activity and competition. This report classifies sports by type (dynamic or static) and intensity (low, medium, or high) so that appropriate sports can be recommended based on the presumed physiologic demands of a cardiovascular disorder ( Table 7C-1 ). Although these recommendations were developed to guide clinicians working with competitive athletes, they may serve as a guide for recreational athletes who pursue vigorous exercise as well. Although this publication is not a definitive legal medical authority, it has been considered a meaningful consensus statement in legal courts.[31]

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Physical Examination and the Athlete's Heart

For each of the individual cardiac abnormalities discussed later in this chapter, the hallmark historical and TABLE 7-C-1 -- Classification of Sports Low Dynamic Moderate High Dynamic Dynamic Low static

Billiards

Baseball

Badminton

Bowling

Softball

Cross-country skiing (classic technique)

Cricket

Table tennis

Field hockey*

Curling

Tennis (doubles)

Orienteering

Golf

Volleyball

Race walking

Riflery

Racquetball Running (long distance) Soccer* Squash Tennis (singles)

Moderate static

Archery

Fencing

Basketball*

Auto racing*

Field events (jumping)

Ice hockey*

Diving*

Figure skating*

Cross-country skiing (skating technique)

Equestrian*

Football (American)*

Football (Australian rules)*

Motorcycling*

Rodeoing*

Lacrosse*

Rugby*

Running (middle distance)

Running (sprint) *

Surfing

Swimming Team handball

Synchronized swimming High static

Bobsledding*

Bodybuilding*

Boxing*

Field events (throwing)

Downhill skiing*

Canoeing/kayaking

Gymnastics*

Wrestling*

Cycling*

Karate/judo*

Decathlon

Luge*

Rowing

Sailing

Speed skating

Rock climbing* Waterskiing* Weightlifting* Windsurfing* Reprinted with permission from the American College of Cardiology (Journal of the American College of Cardiology, 1994, 24, 845-899.) *Danger of bodily collision. Increased risk if syncope occurs.

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physical examination findings are mentioned. This chapter does not provide an exhaustive review of cardiac examination. This section addresses findings that examiners involved with the evaluation of athletes may encounter commonly. Despite the fact that athletes exhibit the epitome of physical health, the cardiac examination may show some findings that otherwise would be considered abnormal. The athlete's heart is a nonstandardized reference to a variety of findings attributable to athletic training that otherwise might be considered abnormal.

Palpation

Palpation of the chest wall may detect a displaced or prominent point of maximal impulse of an enlarged heart. This point of maximal impulse may be supported further by imaging studies, such as a chest radiograph or echocardiography. As discussed, this point of maximal impulse could be a reflection of normal physiologic hypertrophy. Palpation of the pulse may suggest abnormalities in heart rhythm. The electrocardiogram (ECG) is not a required part of the examination, but if obtained routinely or prompted by concerning historical or examination findings, the ECG could reveal one of a variety of rhythm and morphologic abnormalities (Table 7C-2 (Table Not Available) ).[27] The most common are benign bradyarrhythmias that arise because of the high degree of vagal tone exhibited by highly trained athletes. Frequent examples include sinus bradycardia, first-degree atrioventricular block (a prolonged PR interval), second-degree type I atrioventricular block (Wenckebach's block, a sequential prolongation of PR interval with eventual dropped beat), and junctional rhythms (narrow QRS rhythms originating in the His bundle and not preceded by P waves). Auscultation

Cardiac auscultation of athletes may reveal several abnormal findings as listed in Table 7C-3 (Table Not Available) . Clinicians who are inexperienced in auscultation skills and detect what they believe are abnormal findings of uncertain significance may choose to refer the athlete to a more experienced TABLE 7-C-2 -- Common Normal Electrocardiographic Findings in Highly Trained Athletes (Not Available) From Chizner MA (ed): Classic Teachings in Clinical Cardiology: A Tribute to Proctor Harvey. Cedar Grove, NJ, Laennec Publishing, 1996, p 1455.

TABLE 7-C-3 -- Common Normal Auscultatory Findings in Highly Trained Athletes (Not Available) From Chizner MA (ed): Classic Teachings in Clinical Cardiology: A Tribute to Proctor Harvey. Cedar Grove, NJ, Laennec Publishing, 1996, p 1454. examiner. The finding of a murmur need not mandate immediately a referral for echocardiography. There are published criteria for the characteristics of murmurs and extra sounds that are likely to be benign versus those that are pathologic (e.g., the outflow murmur of hypertrophic cardiomyopathy or the murmurs of aortic stenosis, mitral valve prolapse, or atrial septal defect).[1] [13] In general, a benign systolic murmur has the following characteristics: grade 1 or 2 out of 6 intensity, of short duration, present at the left sternal border, with a normal S2 and absence of other abnormal sounds or a thrill,

and failure to increase in intensity with the Valsalva maneuver.[1] Other Measures

As mentioned in the section on preparticipation screening, a few other simple measures should be included in the directed examination of an athlete. A greater than 10 mm Hg difference in bilateral brachial artery blood pressure measurement may indicate subclavian stenosis. Diminished lower extremity pulses can suggest aortic coarctation. Of all the diagnostic criteria, the skeletal manifestations of Marfan syndrome may be most apparent to sports physicians, such as an arm span 5 cm greater than the subject's height, arachnodactyly (long, narrow spider fingers), and pectus excavatum. Interested readers are referred to additional references for a more detailed discussion on Marfan syndrome and exercise.[7]

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Exercise Recommendations for Specific Types of Cardiac Disease

It is beyond the scope of this chapter to review all possible cardiac abnormalities that affect exercise. Some of the more common conditions that sports medicine clinicians may see are addressed. Unless otherwise specified, the exercise recommendations noted follow the ACSM/ACC consensus guidelines.[32] Hypertension

Hypertension affects greater than 50 million Americans, of which at least 90% are classified as having essential

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hypertension.[8] Epidemiologic studies have shown the increased risk of cardiovascular events and deaths in people with hypertension.[22] [35] Hypertension is likely to be the most prevalent cardiovascular disorder affecting athletes that all clinicians encounter. The propensity for hypertension is due to a yet undefined genetic predisposition. In the setting of this underlying substrate, there are other contributing causes of hypertension, including sodium and chloride excess, insulin resistance, obesity, autonomic nervous system imbalance, central and peripheral cardiac factors, renin-aldosterone axis aberrations, and catecholamine responsiveness.[22] [34] This section briefly outlines various issues dealing with hypertension, including responses to exercise testing, the varying mechanisms of hypertension that may be unique to various athletes, and nonpharmacologic and pharmacologic treatment options. The normal exercise blood pressure response is for the systolic pressure to increase linearly, the diastolic blood pressure to remain relatively stable (±10 mm Hg), with the

mean arterial pressure moderately increasing. [4] [12] Abnormal exercise responses generally are considered to be a systolic pressure greater than 250 mm Hg, a decrease or increase of diastolic pressure by greater than 10 mm Hg, or an absolute diastolic pressure greater than 110 mm Hg. [4] Transient arterial pressures of 480/350 mm Hg have been documented in athletes involved in extremes of weightlifting.[29] The effect of regular endurance exercise in individuals with existing hypertension has been well examined. Meta-analyses of available studies revealed that reductions in systolic pressure of 5 to 25 mm Hg and in diastolic pressure of 3 to 15 mm Hg could be expected from a regular exercise program.[18] [44] Such reductions may either prevent the initiation of drug therapy or reduce the medication requirements for control. Although not studied as extensively, there is some evidence that a moderate resistance training program (such as in a circuit weight training program) may be an effective option.[44] No sustained benefit has been shown in normotensive individuals. The mechanisms of hypertension can be viewed as an increase in either cardiac output or peripheral resistance, as illustrated in the derivation of Ohm's law: BP = CO × TPR, where BP is blood pressure, CO is cardiac output, and TPR is total peripheral resistance. The specific factors that influence all of these variables are numerous and diverse. The interplay among some of these factors and how they influence blood pressure are shown in Figure 7C-1 (Figure Not Available) . As stated earlier, most cases of hypertension are classified as essential or primary hypertension: No single identifiable cause exists. For older adults, hypertension is not simply an increase in systemic blood pressure and may represent a syndrome of risk factors (syndrome X) for cardiovascular disease, including high blood pressure, lipid abnormalities, insulin resistance (diabetes), obesity, altered left ventricular structure or function, and decreased vascular compliance.[23] Some of the specific factors that underlie the above-mentioned variables include a genetic predisposition that is polygenic and multifactorial, fetal environment (fetal status affecting nephron formation), renal sodium and fluid retention, vascular hypertrophy, endothelial cell dysfunction, sympathetic nervous activity, the renin-angiotensin system, and insulin resistance. Dietary factors influence or promote hypertension as well, including high sodium intake, with evidence for sodium restriction (35 years) trained athletes. Top, Causes of sudden cardiac death in young competitive athletes (median age, 17 years), based on systematic tracking of 158 athletes in the United States, primarily from 1985 to 1995. In an additional 2% of the series, no evidence of cardiovascular disease sufficient to explain death was evident at autopsy. Possible HCM denotes hearts with some morphologic features consistent with (but not diagnostic of) hypertrophic cardiomyopathy. (Adapted from Maron BJ, Shirani J, Paliac LC: Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles. JAMA 276:199-204, 1996. Copyright 1996, American Medical Association.) Bottom, Causes of sudden cardiac death in older trained athletes. Data were assembled by collating findings from available published studies. Ao, aorta; ARVD, arrhythmogenic right ventricular dysplasia; AS, aortic stenosis; CAD, coronary artery disease; LAD, left anterior descending; MVP, mitral valve prolapse. (From Maron BJ, Epstein SE, Roberts WC: Causes of sudden death in competitive athletes. J Am Coll Cardiol 7:204-214, 1986. Reprinted with permission from the American College of Cardiology.)

a more localized hypertrophy. Average values have been reported to be 21 or 22 mm in wall thickness.[37]

The most severe case to date was recorded by Maron to have a wall thickness measured at 60 mm.[47] Some hypertrophic cardiomyopathy phenotypes show only very mild increases in wall thickness, perhaps never reaching as much as 15 mm. There may be a smaller number of individuals with the genetic abnormality but normal wall thickness, with numbers measuring less than 12 mm.[7] [52] Finally, to add to the complexity of the problem, it has been reported that during autopsy, some hearts with increased wall thickness and normal left ventricular cavity size (all consistent with a hypertrophic cardiomyopathy) have failed to reveal the objective morphologic findings that would lead to a diagnosis of hypertrophic cardiomyopathy.[52] Several reasons have been proposed for this. It may represent yet another form of hypertrophic myopathy, for which a separate nomenclature of idiopathic left ventricular hypertrophy has been used. It may also be the result of the normal physiologic changes noted in athletes who undergo high-intensity training, and thus not a disease state at all. A fatal sudden death event may have occurred in such an individual for unknown reasons.[52] The ability to predict which athlete with hypertrophic cardiomyopathy is at risk for sudden cardiac death is limited by the variability and heterogeneity of the pathophysiology. Further information may ultimately be gleaned from noted racial differences. Blacks have a higher percentage of sudden cardiac death syndromes than whites, with one third (30% to 40%) of sudden cardiac deaths occurring among blacks. Of those events, one third to one half (30% to 46%) are secondary to hypertrophic cardiomyopathies.[42] Blacks represent 12% of the U.S. population but are responsible for 33% of sudden cardiac deaths. The reason for this disproportionate percentage is unclear. Is this a function of the greater percentage of blacks who participate in sports? Do members of the black race participate in a particular type of sport more frequently such that the sport itself is associated with an increased risk of sudden death? Are there additional athletic training and competition stresses such as dehydration and electrolyte disturbances that for some reason affect black athletes to a greater degree than those who are nonblack? Does this reflect a difference in access to health care from one group to another? Because of tremendous genetic variations, is there a predilection for a specifically malignant form to occur with greater frequency in one race than another? Gender differences have been noted as well. Sudden cardiac death is less common in women and accounts for approximately 10% of all deaths. Again, is this secondary to a lower total number of sports participants, less severe training demands, fewer physically demanding sports in many women's athletic programs (such as fewer women football or wrestling teams)? Is there an increased frequency of a less severe form of hypertrophic cardiomyopathy that has a greater tendency to express itself in women than men? [8] Sudden death events among patients with hypertrophic cardiomyopathy have a tendency to occur during or immediately

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Figure 7-D-2 Age distribution of 78 patients who died from hypertrophic cardiomyopathy. (From Maron BJ, Fananapazir L: Sudden cardiac death in hypertrophic cardiomyopathy. Circulation 85:1[suppl 1], 1992.)

after exertion. A bar graph ( Fig. 7D-2 )[47] in an article from Dr. Barry Maron, showing the age distribution for 78 patients who died, shows again the increased incidence of death from hypertrophic cardiomyopathy that occurred in this younger-than-35 age group. A pie graph ( Fig. 7D-3 ) [47] shows the functional state before, and the activity level noted at ( Fig. 7D-4 ), [47] the time of sudden death. Note that 22% of sudden deaths were totally asymptomatic, and that 11% of these patients were believed to have rare transient symptoms to the extent that a full one third were either completely symptom-free or at least very nearly so. Only 15% were believed to have severe symptoms. In regard to activity level at the time of death, only 39% died during exercise that was believed to be greater than moderate, leaving 24% that died during only mild exertion and 37% that died during minimal or even sedentary activity. Sixty-one percent were not significantly exerting themselves at the time of death. Among athletes, 90% of sudden deaths appear to occur during exercise, predominantly during late afternoon and early evening hours. This may reflect a matter as simple as timing. The increase in frequency of sudden death events during late afternoon and early evening hours seems to correlate well with the increased frequency of practices and games during these hours, but that is not known to be causative. It has been noted that in the nonathlete, hypertrophic cardiomyopathy causes sudden death most often in midmorning. Coronary Artery Anomalies

Coronary artery anomalies[24] [46] [75] (Figs. 7D-5 (Figure Not Available) and 7D-6 ) account for approximately one fifth of the total number of sudden deaths in the younger-than-35 age group. There are

Figure 7-D-3 Functional state before the time of sudden death.[ 23] SVT, supraventricular tachycardia.

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Figure 7-D-4 Activity level at the time of sudden death. [ 23] *Includes four patients who died during sleep.

multiple types of coronary artery anomalies. It may be that the most famous person to have suffered sudden death from a coronary anomaly was Pete Maravich (1947-1988), a national collegiate and ultimately professional level basketball player. He died at an age when death from coronary artery disease rather than as the result of a coronary artery anomaly would have been the more expected cause. Again, this helps us to understand that we are talking about this subject in terms of probabilities and possibilities rather than absolutes. One of the most important of these anomalies is the origin of the left main coronary artery from the right sinus of Valsalva, which then courses between the aorta and pulmonary artery. During exercise, dilation of the aorta and pulmonary arteries may occur. With abnormal left coronary artery placement, the aorta and pulmonary arteries dilate as they impinge on the left coronary artery and compromise its blood flow. These circumstances can be very difficult to identify ante mortem; many sources have suggested that coronary arteriography is the only way to make this diagnosis. This approach is not optimal, however, in terms of its invasiveness and expense.[75] In one third of anomalous left main coronary arteries originating from the right sinus of Valsalva, patients have sudden death as the first manifestation of their congenital abnormality. Some may have symptoms such as angina, syncope, or a myocardial infarction. The majority of these are related to exertion.[9] [59] The right coronary artery may arise from the left main sinus and may course between the aorta and the pulmonary arteries. With the increased stroke volume and myocardial oxygen demands associated with exertion, the ascending aorta enlarges and can compromise flow down the right coronary artery in a very similar fashion to the anomaly of the left main coronary artery coming from the right sinus of Valsalva. Figure 7-D-5 (Figure Not Available) Coronary artery anomalies associated with sudden cardiac death in athletes. The two most frequent congenital coronary artery anomalies associated with exercise-related sudden death involve the origins of both the left and right coronary arteries from the right and left sinuses of Valsalva. The coronary ostium of the anomalous vessel is slitlike compared with the normal oval shape. LAD, left anterior descending coronary artery; LC, left circumflex coronary artery; LM, left main coronary artery; R, right coronary artery. (From Waller BF, Hawley DA, Clark MA, et al: Incidence of sudden athletic deaths between 1985 and 1990 in Marion County, Indiana. Clin Cardiol 15:851-885, 1992.)

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Figure 7-D-6 Hypoplastic coronary arteries. Note the area enclosed by the internal elastic lamina in the left anterior descending (LAD) and the left circumflex (LCX) coronary arteries from a normal, age-matched heart (A and B), as compared with the arterial size of the LAD and LCX coronary arteries from a patient with hypoplastic coronary artery (C and D). The right artery was similar to the left circumflex, and neither extended to the lateral wall of the left ventricle. E, Diagram illustrating the

differences between normal coronary arteries and hypoplastic coronary arteries. Note that neither the right nor the left circumflex arteries supplied the posterior wall of the heart. Ao, aorta; LC, left circumflex; LD, left diagonal; LM, left main; LOM, left obtuse marginal; PT, pulmonary trunk; R, right. (A, B, C, and D from Virmani R, Burke AP, Farb A, et al: Causes of sudden death in young and middle-aged competitive athletes. Cardiol Clin 15:457, 1997. E from Virmani R, Rabinowitz M, McAllister HA Jr: Exercise and the heart. In Sommers SC, Rosen PP, Fechner RE [eds]: Pathology Annual, Part 2. Norwalk, Conn, Appleton-Century-Crofts, 1985, p 451.)

There are other types of coronary artery anomalies as well. Hypoplasia of any of the three major coronary arteries may occur. The left coronary or right coronary artery may originate from the pulmonary trunk.[59] The absence of a coronary artery (Pete Maravich had a single coronary artery arising from the right, and this single artery provided the blood flow to the normal distribution of the right coronary artery, the left circumflex artery, and the left anterior descending artery) is a known anomaly. Lumen occlusion can be caused by coronary artery intussusception. Any of these anomalies can result in symptoms of cardiovascular disease or sudden death events. Marfan's Syndrome

In the 18th century, Antoine-Bernard Marfan, who was at the time medical director of the Asala Hospital, described the musculoskeletal features of a 5-year-old girl that we now find consistent with the syndrome of Marfan. Over time, ocular and cardiovascular features also were identified. At present, the clinical diagnosis depends on observation of three of the following four criteria: (1) A positive family history of a connective tissue disorder inherited as autosomal dominant; (2) ocular disorders that can include myopia, retinal detachment, flat cornea, and ectopic lentalis; (3) musculoskeletal abnormalities, including pectus excavatum, pectus carinatum, flatfoot, extreme joint mobility, and a tall slender body habitus* ; and (4) cardiovascular features, including aortic aneurysms, dilatations, and dissections, as well as diseases of the aortic and mitral valves. It is the cardiovascular features on which I focus here. The estimated prevalence of Marfan's syndrome is 1 in 10,000. [8] Its contribution to sudden cardiac death syndrome has been noted. It has been described globally with no known increase in frequency for nationality, race, or gender. Molecular genetics has shown abnormalities in the fibrillin-1 gene. Elastic components of the aorta, as well as the chordal and valvular structures of the heart, have significant amounts of fibrillin. Fibrillin is also significantly present in the ligaments that hold the lens of the eye in place, which accounts for the ocular findings. The abnormalities of fibrillin and elastin begin in utero. The flaws and structure of the aortic root and aortic valve can be noted in neonates and may *In the tall slender body habitus, a wing span of greater than two thirds the height has been discussed as a marker for Marfan's syndrome. It has also been argued that this simply represents a mechanical and functional advantage for an individual and may be the reason for attainment of this level of athletic success, rather than a marker of specific disease.

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worsen over time. The mechanical forces generated by the left ventricular contraction of each heartbeat increase and accelerate damage to already defective structures at baseline. As the decrease in aortic tissue elasticity worsens, vascular injury leads to medial cell death, which is one of the hallmarks of Marfan's syndromethat is, cystic medial necrosis. Approximately 20% to 30% of patients have a negative family history, which is the result of spontaneous mutations. As aortic dilatation progresses, the risks of an event seem to increase. As is seen in many genetic disorders, a spectrum of severity in clinical course exists in any given individual. The natural history of Marfan's syndrome results in a shortened life span. Ninety percent of the causes of death are related to cardiovascular complications. New diagnostic and treatment techniques have improved outcomes. Mitral valve prolapse is present in one half to two thirds of Marfan's syndrome patients and appears to be a particularly virulent form, with an associated increase in the frequency of atrial and ventricular dysrhythmias, as well as endocarditis. Arrhythmogenic Right Ventricular Dysplasia

Arrhythmogenic right ventricular dysplasia (ARVD) has had various names by which to refer to this predominantly right ventricular problem. These have included Uhl's anomaly, parchment heart syndrome, right ventricular dysfunction, and right heart syndrome, among others. Osler may have described this condition first. [55] Morphologically, it is characterized by myocyte death. Fibrosis or adipose tissue replaces the myocytes. It can involve the right ventricle either segmentally or diffusely and occasionally involves the left ventricle. It has been thought to be an unusual cause of sudden cardiac death syndrome. Reports from Italy[71] indicate that this is a more frequent cause of sudden death in Italy compared with other countries, in particular, the United States. It has been believed to represent fewer than 5% of sudden cardiac death syndromes in countries outside of Italy.[46] [74] In Italy, and specifically certain regions of Italy, it has been shown to occur with a much higher frequency. ARVD is a familial disease that is autosomal dominant and occurs with a variable penetrance. This disorder has been localized to the specific chromosomes 14q23-q24,[58] 14q12-q22,[57] and 1q42-q43.[12] Sudden death with ARVD results from the increased predisposition for significant dysrhythmias from the diseased right ventricle. Syncope or sudden death can be the first symptom. Extent of disease duration increases the chances for malignant dysrhythmias. Prolapse of the Mitral Valve

A variety of other causes can predispose athletes to sudden cardiac death, but prolapse

of the mitral valve, because of its frequent diagnosis and discussion among the lay population, deserves specific mention. Mitral valve prolapse can, on occasion, be an overused term. Many times, patients, especially those who are younger, can have symptoms that do not readily have an explanation. In the physician's efforts to place some type of name on the constellation of symptoms from shortness of breath to chest discomfort to the sensation of palpitations, often mitral valve prolapse is used. I suspect that many of these patients do not truly have mitral valve prolapse. This is further compounded by the fact that in the earlier days of echocardiography, mitral valve prolapse was initially overdiagnosed. This tendency has been reduced with more structured criteria for the diagnosis of abnormalities of the mitral valve as they appear on two-dimensional and M-mode echocardiography. Mitral valve prolapse is probably best diagnosed by auscultation rather than echocardiography. Auscultation requires not just a degree of training of health care professionals (it is a skill that many published articles have suggested is being lost) but also an optimal listening environment such as a quiet office and the time to perform dynamic auscultation. In general, most cardiologists believe that the overwhelming majority of patients who carry the diagnosis of mitral valve prolapse will go on to have a benign clinical course. There may, however, be some markers for any given patient who is at increased risk. If a patient with mitral valve prolapse has a family history of sudden death, this may increase risk. A history of unexplained syncope or near-syncope may also indicate increased risk. The degree of abnormality of the mitral valve and the severity of the accompanying murmur can also increase the risk of a sudden death event. Significant ventricular ectopy is also a reason for concern. Any of these additions to the diagnosis of prolapse of the mitral valve indicates that a patient should undergo further evaluation, which may reveal that this particular athlete is at increased risk for a sudden cardiac death event.

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The Athlete's Heart

In 1899, using only a history and physical examination as tools, Henschen described the athlete's heart as follows: ...skiing causes an enlargement of the heart....This enlarged heart can perform more work... therefore, a physiologic enlargement due to athletic difficulty.[30] Universal agreement on this subject, however, could not be reached. In 1908, Dietlen worried that excessive and continued strain could lead to collapse of the cardiovascular system.[16] Others[15] [38] [39] have expressed similar cautions and beliefs. As late as 1972, Friedberg[23] still had concerns. He believed that these cardiovascular changes noted among athletes were more a function of disease (acquired or congenital, but nonetheless, disease) than a physiologic response to the adaptations caused by the athlete's training. Athletes participate in sports that involve dynamic exercise (for example, marathon running or soccer), static exercise

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(weightlifting or shot putting), or a combination of both (rowing or boxing). Sports classifications as listed by the 16th Bethesda Conference are listed in Table 7D-1 .[50] Oxygen consumption (VO2 ) is equal to the cardiac output (CO) times the arteriovenous oxygen difference (A-VO2 ), which is represented by the equation, VO 2 = CO × A-VO2 . In dynamic exercise, cardiac output or an increased arterial venous oxygen difference is noted (or both). Cardiac output equals heart rate times stroke volume. Cardiac output initially increases because of an increase in heart rate but then subsequently increases because of an increase in stroke volume. The maximum heart rates of trained and

untrained athletes are similar, and the improved cardiac output to increasing demands is a function of improved systolic abilities (stroke volume) gained from training. As one goes from the supine to the upright position, heart rate increasesa response to decreased venous return and subsequent increased sympathetic reflex activation. Upright posture decreases volume in the chest and reduces stroke volume. Baroreceptor reflexes are activated, which may cause a slight shift in sympathetic tone. With the start of exercise, central nervous system mechanisms cause withdrawal of vagal tone and an initial rapid increase in heart rate. As continued effort is demanded, increases in heart rate are mediated by increases in sympathetic nervous system activity and increases in the circulation of catecholamines. The maximum heart rates of trained and untrained athletes are similar, as was described earlier, and continued increases in cardiac output must result from an increase in stroke volume. With exercise, venous return secondary to skeletal muscle activity is increased. Left ventricular pressure is increased, as is left ventricular diastolic volume. At this point of exercise, with heart rate maximized and thus a shortened diastolic filling time, stroke volume can only be further maximized by sympathetic nervous system stimulation and an increase in the circulation of catecholamines. This leads to increased contractility.[7] At rest, cardiac muscle extracts approximately 75% of the available oxygen.[36] Metabolically active organs increase oxygen extraction. For cardiac delivery of oxygen to be increased, there must be an increase in coronary blood flow. This happens via an increase in vasodilatation and a decrease in coronary vascular resistance.[2] Static exercise does not improve maximum oxygen consumption in a fashion similar to dynamic exercise. In static exercise, the energy used comes from anaerobic mechanisms. An increase in cardiac output is not needed to accomplish this physical task. Static exercise is a function of the training or adaptation of a specific muscle or muscle groups. With dynamic exercise, gender differences are noted, with women showing 20% to 30% less maximum oxygen consumption than their male counterparts. This is multifactorial, with the reasons including that women are TABLE 7-D-1 -- Classification of Sports Based on Peak Dynamic and Static Components during Competition Low Dynamic Moderate High Dynamic Dynamic Low static

Billiards

Baseball

Badminton

Bowling

Softball

Cross-country skiing (classical technique)

Cricket

Table tennis

Field hockey*

Curling

Tennis (doubles)

Orienteering

Golf

Volleyball

Race walking

Riflery

Racquetball

Running (long-distance) Soccer* Squash Tennis (singles) Moderate static

High static

Archery

Fencing

Auto racing*

Field events (jumping)

Basketball*

Diving*

Figure skating*

Ice hockey*

Equestrian*

Football (American)

Cross-country skiing (skating technique)

Motorcycling*

Rodeoing*

Football (Australian rules)*

Rugby*

Lacrosse*

Running (sprint)

Running (middle-distance)

Surfing*

Swimming

Synchronized swimming

Team handball

Bobsledding*

Body building*

Boxing*

Field events (throwing)

Downhill skiing

Canoeing/kayaking

Gymnastics*

Wrestling*

Cycling*

Karate/judo*

Decathlon

Luge*

Rowing

Sailing

Speed skating

Rock climbing* Water skiing* Weightlifting* Wind surfing* From reference [4] with permission. *Danger of bodily collision. Increased risk if syncope occurs.

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slightly smaller in size than men, have a lower lean body mass and lower levels of hemoglobin, and tend to participate in less intensive training programs. With advancing age, maximum oxygen consumption decreases. Training can improve the skills of an individual in any age range, and continuous training has benefits that can decrease the rate of decline. Ultimately, however, advancing time will win out. Frequency, duration, and intensity of training influence the response to training.[11] Dynamic exercise of 30 to 60 minutes three to four times per week and training that occurs at 60% to 70% of the maximum oxygen consumption are needed for any anatomic or physiologic training effects to be noted. Physiologic and anatomic responses to dynamic training include a lower resting heart rate and a lower heart rate at any given level of activity. [3] These occur secondary to increased parasympathetic tone. At rest, lower blood pressure is noted among trained persons. With any given level of activity, the blood pressure of these individuals augments less. Therefore, the double product (the product of the systolic blood pressure times the heart rate) is lower for any given level of activity in a trained person than in an untrained person. The left ventricular end-diastolic dimension is increased. When corrected for body surface area, it still is larger than that of sedentary age-matched controls. Maron[43] has suggested that this increase usually remains within normal limits; however, greater values do occur. Pelliccia [56] suggested that approximately 4% of athletes had left ventricular end-diastolic dimensions greater than 6 cm (3.0 to 5.4 for a normal range), and Rost[61] in 1982 suggested that cyclists as a group may have the greatest overall values. One might wonder what training effect is conferred if the average increase in left ventricular end-diastolic dimension is only 10%. With evaluation of the physics of the relationship of dimension to volume, the 10% average increase in left ventricular end-diastolic dimension correlates with a 30% increase in left ventricular volume.[56] Left ventricular wall thickness does not seem strikingly increased. In the Pelliccia[56] study, with 4% of athletes showing an increased left ventricular end-diastolic dimension, only 1.7% were noted to have an increase in the posterior wall or septal thickness of greater than 1.3 cm (normally in the 0.7- to 1.1-cm range). Allen[1] reported 83% of childhood swimmers with septal hypertrophy, and Roeske[60] reported 60% of professional basketball players with septal hypertrophy. Therefore, the subsequent ratio of ventricular septum-to-left ventricular posterior wall thickness increased. This, however, most often remained in a normal range of lower than a 1.2:1.0 cm ratio.

If left ventricular mass is represented by left ventricular end-diastolic diameter and left ventricular wall thickness, the previously discussed increases result in an increase in total left ventricular mass. The left ventricular mass remains increased in trained athletes when corrected for body surface area. Again, the increase in left ventricular end-diastolic dimension and the increase in wall thickness are modest, and perhaps in general, still remain within normal limits. As we calculate mass using end-diastolic dimension and wall thickness, however, we can achieve a mass increase of 45%.[19] [65] These wall thickness and chamber size changes are consistent over multiple studies in various sports. Some have argued that they simply represent the preordained physical abilities of any given individual. The serial increase with training and subsequent decrease with discontinuation of training, however, suggest that these changes are indeed related to the effects of training. [11] [13] [22] [31] [32] [62] Other cardiac chambers may be influenced. The right ventricle may be increased by up to 24%.[35] The left atrium may increase, and in cyclists older than 35 years of age, the changes in left atrial dimensions may be greater than those found in other groups.[35]

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Evaluation of the Athlete

After looking at various causes and percentages of those causes, we try to use these statistical data along with our diagnostic tools. Cost, affordability, and availabilitythese are factors that are simply part of our society, and they influence not just health care distribution but also such matters as academic learning access, leisure activities, and dietary intake. If we have financial, geographic, and technical limitations, we need to apply tests judiciously based on the knowledge that we have acquired. History and Physical Examination

The first step is simply the cornerstone not just of the evaluation of sudden cardiac death syndromes, but of every doctor/patient relationshipthe history and physical examination. Let's begin with comments regarding the history, because often a breakdown occurs at this very first fundamental step. An adult in a householdcommonly, the motheroften will carpool three or four of the neighborhood children to the doctor's office for the pre-sports examination and signing of the typical school sports waiver. In doing so, she believes she is performing a service by providing transportation and allowing the other children's parents to continue with their daily activities of working, caring for other children, and so forth. At the conclusion of the doctor's office visit, the mother will return the children to their respective homes. Unfortunately, however, this well-meaning plan does great damage to the start of the evaluation process. One of our most cost-effective and widely available techniques is the history and physical examination, and the history here is severely damaged. The junior high school, high school, or even college student is often unaware of personal family history. Such students may not be aware of problems with a relative of their

mother or father who could have had some type of congenital cardiac difficulty or unexplained sudden cardiac death. Often, this death occurred when the athlete being examined was at such a young age that he or she has no memory of the event or of missing the relative. Because of the sadness associated with the event, the remaining adult relatives frequently do not openly discuss that history with their children.

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The solution, at least in part, is educationeducation of the parents to understand the reason we are asking them to accompany their own children to the doctor's office, and education of the performing physicians, who must realize the risk markers of siblings with known heart disease, unexplained sudden death in family members, and so forth. With a more thorough history, we increase our chances of trying to hone in on that higher-risk individual. After improved history taking has been done, we can move to the physical examination. In efforts to be of help (both convenience help and cost help), physicians may organize a physical sports examination session in which all athletes trying out for a given team are examined at the same time. On some occasions, all athletes trying out for any team playing that given school year can receive examinations at the same time. The athletes all present to the school gymnasium over the course of a Saturday or Sunday, and all are evaluated. The physician believes that he or she is helping by having one smaller group of peoplethe doctor and staffcome to the larger group of people, that is, the patients receiving the examination. This certainly is a convenience for the patients who would otherwise have to make the trip to the doctor's office. Often there is minimal or no cost to the athlete or the athlete's family, which is an economic benefit to them as well. Again, though certainly physicians mean well, this situation is not optimal. The acoustics of the gym, the background noise generated by the volume of people present, and an insufficient amount of time spent with each athlete do not allow the subtleties of auscultation, specifically dynamic auscultation, to be accomplished. Many have suggested that we are losing auscultation skills in younger physicians; if that is the case, additional difficulties will be created. It may be ultimately possible to have primary care physicians who are especially interested in sports medicine and screening for sudden death acquire extra training in auscultatory techniques and extra training in physical examination findings or history taking that may enhance the likelihood of identifying an athlete who is at risk. Specific Diagnostic Tools

Electrocardiography

The electrocardiogram (ECG) as a diagnostic tool has multiple strengths. First, it is widely available and simple to perform. Interpretation can be accomplished by an

on-site physician who is trained in electrocardiographic analysis, or an off-site physician can participate via simple fax. The test is noninvasive and, with the exception of possible skin allergies to the tape of the electrode patches (uncommon), it has no real adverse effects. Finally, it is a relatively inexpensive test. The ECG does, however, have limitations. The accuracy of it for predicting left ventricular hypertrophy is poor. Various sources have recorded sensitivities that at a maximum are in the 50% to 55% range, with a significant number of false positives. ( Table 7D-2 [10] demonstrates this.) Echocardiography is a strong tool for determining the presence or absence of left ventricular hypertrophy.

TABLE 7-D-2 -- Sensitivity and Specificity of Other Criteria for the Diagnosis of Left Ventricular Hypertrophy Criterion Sensitivity (%) Specificity (%) (false positives) SV1 or SV2 + RV5 35

56

13

SV1 + RV5 or V6 > 30

56

11

SV1 or V2 + RV5 or V6 > 35

56

12

SV2 + RV4 or RV5 > 35

56

15

R + S > 40

55

14

SV1 + RV5 > 30

51

11

SV2 + RV5 > 35

50

11

RS > 35

41

9

39

7

RV5 20

38

9

SV1 or SV2 + RV6 > 40

38

3

SV2 + RV5 or RV6 > 45

34

3

LAD = 30° or greater

24

13

RaVL > 7.5

23

4

RV6 > RV5

23

11

RV6 > 20

22

2

SV1 24

19

0

Lewis index* = + 17 or greater

18

2

RaVL 11

13

1

RI > 13

11

0

RaVL > 12

9

0

RI > 15

8

0

RaVL > 13

8

0

RaVF > 19

1

1

Adapted from Romhilt and associates. *Lewis index = (R1 R3 ) + (S 3 S1 ).

Body build plays a significant role in the risk for sudden death. Underdiagnosis of left ventricular hypertrophy in obese people and overdiagnosis in slender people are noted to contribute. Men have greater QRS amplitudes than women, especially in the precordial leads, and especially if the anterior V4 lead is placed on rather than under a large breast. Certain disease states such as pericardial effusion, pleural effusion, or pneumothorax may cause reduced amplitude of the QRS complex, thereby leading to a false-negative electrocardiogram. Age is a factor. Younger populations have larger QRS complex amplitudes. During the third and fourth decades of life (20 to 39 years of age), if the left ventricular hypertrophy diagnostic voltage criteria of the amplitude of the S wave in V2 added to the amplitude of the R wave in V5 are used, more than one third of normal males meet the voltage requirement of greater than 35 mm.[10] [40] The ECG of trained athletes may be entirely within normal limits, but it may show changes now understood to be physiologic responses to training rather than pathologic responses to a disease state. P waves are broader and taller and may be bifid. QRS complexes may be delayed in duration, and incomplete right bundle branch block patterns are seen. ST segments may be elevated (more common) or depressed (less common). T waves can have an increased amplitude and may be notched or inverted. A resting bradycardia is common. Sixty-five percent of athletes had rates lower than 50 beats per minute while awake, and lower than 40 beats per

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minute during sleep.[18] First- and second-degree levels of atrioventricular (AV) block, including Mobitz I and Mobitz II, as well as potentially complete heart block, have been seen.[28] [29] [33] [34] [73] [76] Sinoatrial block, junctional escape rhythms, and wandering atrial pacemakers have all also been reported.[40A] Left ventricular hypertrophy is often noted.[21] [69] [76] This reflects a combination of increased cardiac mass (caused by the challenges that training brings to the cardiovascular system) and the previously mentioned potentially slimmer, leaner body build of the typical athlete. These changes appear to reverse with cessation of training.[17] [73] Echocardiography

It is not the least expensive test, but two very important features make echocardiography an excellent diagnostic tool. First, it is noninvasive. (I am not aware of any significant risks associated with the examination.) Second, when we refer back to Maron's figure of the incidence of disease ( see Fig. 7D-1 ),[46] the echocardiogram again shows itself as an extremely helpful diagnostic tool. Hypertrophic cardiomyopathy (36%), concentric left ventricular hypertrophy (10%), aortic stenosis (4%), dilated cardiomyopathy (3%), mitral valve prolapse (2%), and arrhythmogenic right ventricular dysplasia (3%) all can be identified by echocardiography. These account for approximately 58% of all causes of sudden cardiac death in the younger-than-35 age range. We can also visualize at least some of the proximal aorta and, with visualization of the mitral and aortic valves, we can try to begin to eliminate the potential for Marfan's syndrome among our athletes (5%). In some patients, we see the take-off of the right coronary artery from the right sinus of Valsalva. We can visualize the left main coronary artery coming from the left sinus of Valsalva and can see it bifurcate into the left circumflex and left anterior descending arteries. With congenital anomalies accounting for 19% of cases, we have the potential to identify an additional 24% (to the previously described 58%) of cases. This brings us to the approximately 80% range with which one test can safely and effectively screen for the potential causes of sudden cardiac death. The echocardiogram can be, in general, an examination lasting up to 30 minutes, depending on the experience of the echocardiographic technician. Not all views of a standard echocardiogram need to be obtained, however, for the specific heart disease information to be acquired that is needed for screening. Parasternal long-axis and short-axis views should suffice for this evaluation. In an Indiana trial by Weidenbener,[78] an abbreviated study was specifically aimed at certain disease states. Supplies were donated to try to further decrease the cost and make this type of examination available to local schools. A great deal of the success of an effort such as this is a function of the ability of any given locality to have a company donate the use of a machine or supplies, to obtain a technician who would volunteer his or her time, and to find a physician who would donate his interpretation skills. The Indiana article did not address the liability

issues. Treadmill Testing with and without Additional Imaging of Echocardiography or Nuclear Medicine

Although it is commonly thought of as a tool to help diagnose obstructive coronary artery disease, treadmill testing has a variety of other uses as well, including the evaluation of functional capacity, claudication, heart rhythm disturbances, and treatment responses to medications. Treadmill testing is associated with greater morbidity and mortality than an electrocardiogram or echocardiogram, but it is stillwhen performed by technicians and physicians trained in the procedure and who do a sufficient volume to maintain these skillsa relatively safe procedure. Resuscitative equipment should be available. During the treadmill evaluation, an electrocardiogram is performed at rest and during successive stages of exercise. The test is terminated based on patient symptoms, ECG changes, blood pressure responses, rhythm responses, or attainment of a predetermined target heart rate. With the recovery phase, ECGs continue to be recorded at various time intervals. Continuous telemetry is used throughout the stress and rest phases, and periodic blood pressure recordings are obtained. The patient is monitored for any symptoms that may occur; at the conclusion of the test, the data that have been recorded are analyzed. The most significant purpose of treadmill tests as a screen for sudden cardiac death syndrome is in identifying coronary artery disease. Certain coronary artery anomalies or even dysrhythmias may be uncovered. In terms of coronary artery disease alone, the test is most helpful in the older-than-35 athlete, for whom approximately 80% of all sudden cardiac death syndromes are related to coronary artery disease. The treadmill test, with or without the addition of echocardiography or nuclear imaging, does not have 100% sensitivity and specificity. Therefore, not all of the potential 80% of sudden deaths related to coronary artery disease can be diagnosed, but again, it remains the best single test for athletes older than 35 years of age. The treadmill test would be less helpful in athletes younger than 35 years of age, for whom only 2% of sudden cardiac death syndromes are related to coronary artery obstructive disease. Cardiac Catheterization

Cardiac catheterization has become a very common and relatively safe procedure. Again, this procedure is best accomplished in centers where the physicians and the technicians have been well trained and are able to use satisfactory equipment. Sufficient volumes of patients must be present for continued maintenance of skills. A catheter is advanced through an artery using the percutaneous approach. The brachial, radial, and femoral arteries have all been used, although the right femoral artery currently is most frequently used. A catheter is advanced into the femoral artery

and then retrogradely through the iliac, abdominal aorta, and thoracic aorta, and into the descending and (ultimately) the ascending aorta. There, the left main coronary artery is cannulated, and

295

injections of contrast media enable visualization of the left main coronary artery and its bifurcation arteries, the left anterior descending and circumflex arteries. Diagonal and septal branches of the left anterior descending artery, as well as marginal branches of the circumflex artery, are also visualized. The catheter is then removed, and a subsequent catheter is placed into the right coronary artery where the right coronary artery and its branches are visualized. Removing the catheter from the right coronary artery and replacing this with a ventricular catheter allows the performing physician and his or her team to assess the pressure of the left ventricle. This information is of significant help in the evaluation of left ventricular diastolic function. With left ventriculography, the left ventricular size and shape are determined, as well as systolic function. At the conclusion of the procedure, catheters are withdrawn and the initial needle-point entry site develops hemostasis with manual compression. Cardiac catheterization is done as an outpatient procedure and after a short period of bed rest, the patient is discharged home. Right heart catheterization is accomplished using a similar technique. The right femoral vein, rather than the right femoral artery, is entered, and the catheter is placed retrogradely up the venous system into the right atrium, right ventricle, main pulmonary artery, and ultimately, the pulmonary capillary wedge position. Pressures are taken with the catheter in each position and, when this information is combined with the pressures obtained from the left heart catheters, valvular disease, constrictive pericarditis, restrictive pericarditis, and other conditions can be evaluated. Again, at the conclusion of the test, the catheter is removed; the patient is monitored with bed rest and is ultimately discharged, in general, following an outpatient procedure. In the younger-than-35 age group, patients with a significant potential for sudden cardiac death that could be evaluated by this technique would include those with coronary artery anomalies (19%), aortic stenosis (4%), dilated cardiomyopathy (3%), mitral valve prolapse (2%), and cor onary artery disease (2%). Thus, a total of approximately 30% can be identified. It may be possible to evaluate and diagnose hypertrophic cardiomyopathy with the use of this technique, but that disease can be assessed far more noninvasively with echocardiography. The risk of cardiac catheterization is believed to be lowless than 1% for elective procedures. In the older-than-35 age group with coronary artery disease that accounts for 80% of sudden cardiac death syndromes, left heart catheterization can be a very effective technique for diagnosis. As was described earlier, treadmill testing with or without an additional imaging modality may also help with the diagnosis of obstructive coronary

artery disease. These treadmill-type tests are less invasive and therefore are associated with less risk. Cardiac catheterization remains the best anatomic evaluation. The treadmill is of tremendous importance in terms of a physiologic evaluation and, on many occasions, both cardiac catheterization and treadmill testing are required for the significance of an obstructive coronary lesion to be determined.

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Classification of Sports

Different parameters can be used to classify sports into various categories. These include duration or intensity of exercise, as well as the potential for collision (i.e., body-to-body, or impact of a projectile such as a puck or baseball). Commonly, dynamic (isotonic) sports and static (isometric) sports are divided into classification schemes. Dynamic sports include long-distance running, swimming, and tri-athletic events. Static-type sports include weightlifting and shot putting. Dynamic exercises include a rhythmic contraction, and the increased demand for oxygen by the active muscle group is met by a decrease in total peripheral vascular resistance and redistribution of the increased cardiac output. This occurs through sympathetically induced vasoconstriction of organs and nonexercising muscles. Heart rates range from 60 to 100 beats per minute at rest and increase with exercise to a maximum of 190 to 200 beats per minute. The maximum heart rate achieved is not altered by or based on the degree of training. It is a function of age. In general, the maximum heart rate for any individual is 220 minus age. Blood pressure may range from 90/60 to the upper limits of normal (140/90)[33] at rest. With exercise, systolic blood pressures may augment into the 200 to 250 range and diastolic blood pressure may decrease. The calculated mean arterial pressure will slightly increase. As was discussed earlier, cardiac output is a product of heart rate and stroke volume. At rest, cardiac output is approximately 5 liters per minute; it increases during exercise. Maximum cardiac output is in the 20- to 25 L-per-minute range, although this rate may double in highly trained endurance athletes. In static exercise, the sustained contractions of muscle groups cause an increase in

intramuscular pressure and an increase in total peripheral resistance. During exercise, perfusion is maintained by increased sympathetic tone and cardiac output. Cardiac output is increased by an increase in heart rate. In contrast to dynamic exercise, static exercise leads to a large increase in mean arterial pressure. The risk for sudden cardiac death in any given individual may be a function of the specific sport for which he or she is seeking approval to play. It may be that a given disease state, for example, congenital aortic stenosis, precludes an athlete from playing basketball but does not preclude him or her from golf. This is so because of the different physiologic demands of different sports. This situation can become complicated further. The athlete in our current example who has congenital aortic stenosis treated with aortic valve replacement may now have a hemodynamic event that does not increase the risk for a sudden death event. With the anticoagulation that is required for the prosthetic heart valve, however, there may be a greater risk of a bleeding complication in a sport in which a body collision (football) or the impact from a projectile used in that sport (baseball, hockey) could be expected to cause significant morbidity or mortality. All of this must be taken into account when efforts are made to give advice to the athlete.

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Conclusions

In the preceding pages, I have tried to outline some knowledge regarding the athletic heart's response to exercise,

296

and to determine some differentiations between normal and abnormal responses. I have discussed the incidence of sudden death, the potential screening tools, and the more detailed diagnostic testing techniques available. The end result of all of this becomes not a specific answer but a rough framework for discussion. Many questions are raised. If an athlete is believed to be at increased risk, but his or her decision is to accept this increased risk and continue with the sport, does the physician, school, or professional organization have the authority to deny him or her the opportunity to pursue the selected sport? If the school is aware of an athlete at risk, does it have the right to prohibit the athlete from obtaining access to education that the athlete might not be able to afford? Does the school have the right to deny the athlete access to a setting in which an individual's skills could be developed and showcased to increase opportunities for future employment? These questions will be debated as long as there are people with a vested interest in the debate, but there does not appear to be any simple solution. I believe that the best answer is for medical personnel to assess the risk in terms of ranges and then apply that knowledge to the specific sport the athlete has chosen. Then, in group discussion with the athlete and the athlete's family, as well as the coaching staff, support personnel of the team, and the administration of the school or the professional sports team, a mutual agreement can be reached. If it is believed that the pluses of the potential gains outweigh the minuses of the potential risks, then the athlete continues. It is of the utmost importance for clinicians to recognize that making

the decision not to participate does not mean that the athlete will not go on to suffer a sudden death event, and making the decision to participate does not mean that the sudden death event will indeed occur. When discussing athletes and sudden death events, we continue to talk in ranges and possibilities. The goals are to risk-stratify, educate, and reach a mutually agreed-on conclusion and recommendation.

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Cardiol 7:204-214, 1986. Maron BJ, Fananapazir L: Sudden cardiac death in hypertrophic cardiomyopathy. Circulation 85(suppl 1):I-57-I-63, 1992. 47.

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Mitchell JH, Maron BJ, Epstein SE: 16th Bethesda conference: Cardiovascular abnormalities in the athlete. J Am Coll Cardiol 6:1198-1199, 1985. 51.

Nimura H, Bachinski LL, Sangwatanaroj S: Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy. N Engl J Med 338:1248-1257, 1998. 52.

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Rampazzo A, Nava A, Danieli GA, et al: The gene for arrhythmogenic right ventricular cardiomyopathy maps to chromosome. Hum Mol Genet 3:959-962, 1994. 58.

Roberts WC: Cardiac valvular residua and sequelae after operation for congenital heart disease. Am Heart J 106:1181-1187, 1983. 59.

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Sargin O, Alp C, Tansi C: Electrocardiogram of the month. Wenckebach phenomenon with nodal and ventricular escape in marathon runner. Chest 57:102-105, 1970. 63.

Severini GM, Krajinovic M, Pinamonti B: A new locus for arrhythmogenic right ventricular dysplasia on the long arm of chromosome 14. Genomics 31:193-200, 1996. 64.

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Siscovick DS, Weiss NS, Fletcher RH: The incidence of primary cardiac arrest during vigorous exercise. N Engl J Med 311:874-877, 1984. 68.

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Thiene G, Nava A, Corrado D: Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 318:129-133, 1988. 71.

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Common Viral Infections in the Athlete Upper Respiratory Tract Infections

The viral upper respiratory tract infection is one of the most frequently encountered infections among athletes.[50] Upper respiratory tract infection also is known as acute coryza or the common cold. This is an acute, usually afebrile, benign and self-limited viral infection that can be due to multiple viral strains. The hallmark is inflammation in the respiratory tract, which can include the nose, paranasal sinuses, throat, larynx, trachea, and bronchi. The most common causes are the rhinoviruses, coronaviruses, respiratory syncytial virus, parainfluenza virus, and adenoviruses.[35] Infection often can prevent the athlete from competition or lead to suboptimal performance. Review of reported illnesses among winter and summer Olympic athletes consistently revealed URIs to be the most treated condition by the medical staff.[47] In addition to the stress of conditioning and competition, other factors in the athlete's world may contribute to frequent or untimely upper respiratory infections. Because the viral strains responsible for upper respiratory infections are so many and varied, immunity is difficult to achieve. Athletes who travel and compete with other athletes who travel are exposed to a greater number of strains of viral diseases. Competition typically involves close physical contact in which transmission of viral particles takes place through direct and indirect contact, including sharing water bottles, towels, and athletic equipment.[47] Actual transmission takes place when an aerosolized viral particle makes contact with a susceptible hostthe athlete's mucous membranes, most commonly the nose, but also the mouth and eyes. The close contact of athletes in competing gyms, crowded living spaces, and group transportation, particularly in the winter months, may account for an increased incidence of upper respiratory infection. Upper respiratory symptoms usually begin 1 to 2 days after exposure and generally last 1 to 2 weeks.[47]

The diagnosis of an upper respiratory infection is clinical. Signs and symptoms include malaise, sneezing, chills, nonproductive cough, myalgias, nasal congestion with clear rhinorrhea, sore throat and possibly a low-grade fever. An increased resting heart rate may be noted. Acute symptoms last 2 to 7 days. Complete resolution is expected by 7 to 14 days. Rhinoviruses cause most cold illnesses in adults. Although they may occur year-round, a demonstrated rise is prevalent and noted in the fall and spring months. Other viral strains also can cause upper respiratory infection symptoms. The coronaviruses are responsible for many winter colds, in particular in the adolescent age group. Enteroviruses occur in late summer and early autumn. Included in the enteroviruses is the coxsackievirus. Although an uncommon cause of upper respiratory infection, animal studies have shown an increased occurrence and severity in extensively exercised subjects. Coxsackievirus strains can cause myocarditis. Sudden death in exercising athletes has been attributed to fatal arrhythmias during a subclinical case of myocarditis. Viral cardiomyopathy may result in athletes that exercise through a coxsackievirus infection.[47] Just as exercise can influence immune function and susceptibility to viral infection, so too can viral infection affect exercise performance. Viral disease may affect athletic performance via several parameters. In the pulmonary system, respiratory muscle strength as measured by maximal respiratory and expiratory mouth pressures is decreased during a viral illness. Decreased maximal inspiratory and expiratory flow rates have been detected in patients with upper respiratory infections. Changes have been noted in the peripheral airways as well as impaired pulmonary gas exchange. Systemic viral illness may decrease cardiac output and cardiac stroke volume. Many sudden deaths have occurred during exercise in association with a recent upper respiratory infection to suggest a direct effect of viral disease on the cardiac system. In the musculoskeletal system, athletes frequently complain of myalgias and weakness. A 5% to 15% decrease in isometric strength has been documented in patients with an upper respiratory infection. Muscle biopsy specimens from infected patients have shown reduced oxidative and glycolytic skeletal muscle enzyme activity. Performance also can be affected by the effect of fever on the athlete's motivation to compete or train. Overall, measured performance may take 14 days to recover in the athlete. [47] The fluid status of the athlete is affected by viral infection. Fever, diarrhea, and vomiting can decrease volume status by fluid losses or decrease fluid intake. Alterations

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in fluid status in turn can affect temperature regulation and increase the athlete's risk of heat injury. Many infections in athletes may be subclinical. Additionally the prodromal and early acute phase of a viral illness may not have a subjective effect on performance.

Exercising during these periods, particularly exhaustive exercise, puts the athlete at risk, however, for a prolonged clinical course, more severe clinical course, increased complication rate, and slower return to preinfection performance levels.[47] Treatment of the athlete with a viral upper respiratory infection is supportive and symptomatic. Rest and adequate intake of clear fluids are the mainstays of therapy. Nonsteroidal anti-inflammatory drugs may be used for myalgias and headaches. Antibiotics should not be prescribed routinely for athletes if a viral cause is suspected. Antibiotics should be reserved for patients who may have bacterial complications of upper respiratory infections. Medications may be prescribed for symptomatic relief and include antipyretics, antihistamines, nasal decongestants, and cough suppressants. There are multiple concerns with the athlete taking medications for upper respiratory illnesses.[51] Sport governing bodies may disqualify athletes for taking substances found in medications or cold preparations. Medications may impair athletic performance or predispose to injury. Alcohol-based cold preparations may cause drowsiness and impair coordination. Decongestants usually are sympathomimetic agents that decrease rhinorrhea by inducing a vasoconstriction of the nasal mucosa. Pseudoephedrine, phenylpropanolamine, and ephedrine are banned by many sport organizations and can cause tachycardia, dizziness, and blood pressure elevations. Anticholinergic compounds taken to dry mucous membranes can induce an orthostasis and interrupt heat regulation. Antihistamines are used for their drying action on the mucous membranes. These agents can cause orthostasis and drowsiness and disrupt sweating and temperature regulation, predisposing the athlete to heat injury. When medicating the athlete, care should be taken to ensure that prescription or over-the-counter medications would not disqualify the athlete and should be based on regulations of the sport governing body. Medications that may be approved may cause side effects such as drowsiness and impair performance or predispose to heat illness. As a result, athletes need to devise a strategy to avoid or minimize viral disease transmission. In general, athletes need to maintain adequate rest and relaxation and minimize life stresses, especially while preparing for an upcoming season or competition. Psychological or physical stress affects the athlete's susceptibility to viral disease transmission. Weight loss should be gradual over the competitive season. As much as practical, competition should be scheduled so as not to coincide with other significant life stresses, such as examinations, work deadlines, and social demands. The athlete should avoid overtraining and chronic fatigue. Athletes engaged in exhaustive training should allow for adequate rest and repair. Frequent use of a carbohydrate drink during exhaustive exercise reduces the physiologic stress. During periods of outbreaks of viral upper respiratory infections, the athlete should avoid any unnecessary contact with people, particularly those who are ill. Increased hand washing reduces this likelihood of indirect transmission of viral diseases. Yearly influenza vaccination is recommended.[18] [43] [47] When infected with an upper respiratory infection, it is unlikely that any suboptimal exercise routine would improve an athlete's fitness or skill level. Exercising through a viral illness can prolong and increase the severity of the illness. As a general rule, 1 to 2 days of relative rest (if not absolute rest, then reduced training intensity) is

recommended. Exhaustive training can be begun safely when symptoms are resolved. For elite or in-season athletes who believe they must exercise through a viral illness, the neck check offers a safe and practical guideline to monitor their training. If an athlete has upper respiratory infection symptoms limited to above the neck (scratchy throat, head congestion, runny nose), a half-speed workout can be initiated. If symptoms improve, the intensity of the practice can be increased gradually. If symptoms occur below the neck (body aches, diarrhea, vomiting), a workout should not be initiated because these symptoms suggest a more systemic infection and greater likelihood of prolonged illness, increased illness, and increased potential complications.[17] Athletes are at increased risk of viral infection as a result of several variables, including frequent travel, close contact with other athletes, long periods of training in enclosed spaces, exposure to contaminated equipment, and sharing contaminated objects such as towels and water bottles. Regularly scheduled exercise of moderate intensity seems to enhance immunologic integrity and to serve a protective function. Intense activity and training may impair the immunologic response, however, and increase the susceptibility to viral infection. If infection does occur, recovery is quickest for the athlete who allows for adequate rest. Influenza

Influenza is an acute, febrile viral infection of the respiratory tract common in the winter sporting season. Similar to upper respiratory infection, the virus is spread via airborne droplets, person-to-person contact, or contact with contaminated objects. Fever and more severe constitutional symptoms differentiate influenza from upper respiratory infection or common cold. Symptoms often begin after a 48-hour incubation period. Chills and fever of 102°F to 103°F (39°C to 39.5°C) present suddenly. Malaise and generalized myalgias occur as early symptoms. Headache is common and can cause photophobia. Although respiratory tract symptoms may be mild at first (scratchy sore throat and nonproductive cough), more severe lower respiratory symptoms predominate later in the course of the illness. Such lower respiratory symptoms include a productive and persistent cough. Fever and most acute symptoms abate after 2 to 3 days. Persistent symptoms such as weakness and fatigue may persist for several days or weeks. Complications of influenza include secondary bacterial infections of the bronchi and lungs, which are suggested by persistent fever and cough with purulent sputum into

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the second week. Other less common complications include encephalitis, myocarditis, and pericarditis. When these complications are present, exercise potentially can induce fatal arrhythmias. Pulmonary function may be affected adversely by a viral upper respiratory infection even if there is no clinical evidence of lung involvement. [47] This deterioration is manifest by dyspnea or breathlessness noted on exertion.

Treatment is supportive, with rest and hydration as the mainstays of therapy. Antipyretics, decongestants, and analgesics can be used for symptomatic care. Amantadine and rimantadine, if given early in uncomplicated influenza A, are beneficial for fever and respiratory symptoms.[53] Interest has been focused on the use of amantadine and rimantadine as prophylactic medications. These drugs are effective prophylactically against influenza A, but not influenza B. The influenza virus vaccine is recommended for winter athletes, especially athletes who train and compete indoors. This is an annual vaccine. It is the predicted influenza strains that have been killed and do not themselves cause influenza. Athletes with an allergic reaction to eggs should not have the vaccine. No well-controlled studies have determined specific return-to-play guidelines after a viral illness. Certain viruses, such as adenovirus, influenza, and coxsackievirus, have been linked to myocarditis and sudden death during exertion. Febrile illness and medications taken for symptomatic relief, such as antihistamines, can predispose the athlete to heat injuries. Alterations in sensorium that accompany viral illnesses can lead to poor performance and injury. The return-to-play recommendations should be individualized and based on the demands of the sport and severity of illness. In the prodrome or early phase of infection, the athlete should be advised to rest because exertion at this time may worsen or prolong the effects of the illness. In general, the athlete who has only minor symptoms, who has no fever or myalgias, and who does not suffer any impairment of alertness or coordination that may be due primarily to the illness or the medications being taken can return a few days after symptoms have resolved. Athletes with more severe illness and in whom displayed signs and symptoms of systemic involvement, such as fever, increased resting heart rate, and myalgias, or who are suspected of having a coxsackievirus or influenza infection can return 2 to 4 weeks after symptoms have resolved.[37] [47] A slow, gradual return to activity should occur. Proper conditioning should be ensured before full return and participation. Pharyngitis

Pharyngitis is encountered commonly in the training room. Most causes of pharyngitis are viral. Common viruses that produce pharyngitis as the main symptom include adenovirus, coxsackievirus A and B, Epstein-Barr virus (EBV), and herpes simplex. Viruses that cause pharyngitis as a secondary symptom include rhinovirus, coronavirus, influenza, respiratory syncytial virus, and measles. [16] Symptoms include painful swallowing and scratchiness of the throat. On physical examination, a mildly edematous and erythematous pharynx may be noted. Tonsillar exudates may or may not be present. Treatment is symptomatic and supportive. Common therapeutic regimens include nonsteroidal anti-inflammatory drugs, throat lozenges, and warm saltwater gargles. A common dilemma is whether or not to treat with an antibiotic. If a bacteriologic cause is suspected, the throat may be cultured or a streptococcal rapid antigen test performed. Primary infection with herpes simplex virus types 1 and 2 can cause a sore throat. The

pharynx in these patients displays the classic vesicles and ulcers on an erythematous base. Patients often have a fever and tender cervical lymphadenopathy. Herpangia may cause a sore throat and is caused by coxsackievirus A and B and echovirus. These patients present with fever, malaise, and anorexia in addition to pharyngitis. Vesicles measuring 1 to 2 mm are noted on the soft palate, tonsillar pillars, and uvula. It is important to recognize this condition because coxsackievirus has been noted to be a cause of myocarditis in athletes. Meningitis

Viral meningitis, the most common form of aseptic meningitis, can be a cause of concern in athletes and in team sports. Enteroviruses cause most cases of viral meningitis. Outbreaks of viral meningitis have been reported during the football season.[4] [40] This association has been attributed to the season of the sport (peak enteroviral activity occurs in late summer and early fall), close contact of players, sharing of hydration receptacles, and strenuous physical activity.[40] The mode of viral transmission is fecal-oral with the infection occurring across the mucous membranes. When the virus has gained access into the gastrointestinal tract, it replicates and induces a viremia. When in the bloodstream, the virus can cross the blood-brain barrier, altering the permeability to white blood cells and other inflammatory components.[42] The athlete may present with an acute (1 hour before exercise Decrease insulin that has peak activity coinciding with exercise period Assess metabolic control If blood glucose 250 mg/dL, delay exercise and measure urine ketones If urine ketones are positive, take insulin and delay exercise until negative During Exercise Supplement calories with carbohydrate feedings (30-40 g for adults, 15-25 g for children) every 30 minutes during extended, strenuous activity Replace fluid losses adequately Monitor blood glucose hourly during exercise of long duration After Exercise Monitor blood glucose, including overnight if amount of exercise is not habitual Increase calorie intake for 12-24 hours after activity, according to intensity and duration of exercise Reduce insulin dosage that reaches peak effect in evening and night, according to intensity and duration of exercise

Adapted from Horton ES: Role and management of exercise in diabetes mellitus. Diabetes Care 11:201-211, 1988. Copyright © 1988 by American Diabetes Association, Inc. of carbohydrate (15 to 25 g for school-aged children) aid in preventing hypoglycemia. (The failure of exercising IDDM patients to lose weight and gain improved metabolic control is due largely to this need for supplemental caloric intake).[32] Monitoring of blood glucose should occur at hourly intervals during prolonged exercise. Because fluid losses are increased by glycosuria, and an awareness of and response to dehydration can be impaired by autonomic dysfunction, adequate fluid replacement is crucial for the athlete with IDDM. Awareness of the possibility of postexercise late-onset hypoglycemia is the most important step in preventing it. Education of diabetic athletes about the need to distinguish between extraordinary and ordinary physical activity is paramount. The lack of warning signs of impending postexercise late-onset hypoglycemia emphasizes the need to implement preventive measures in the hours after unusually strenuous or prolonged activity. Reductions in short-acting and long-acting insulin dosages as well as increases in caloric intake are appropriate in proportion to the degree to which exertion has exceeded the daily routine. The frequency of blood glucose monitoring should be increased so that appropriate readjustments can be made to avoid worsening of metabolic control. In general, athletes with IDDM who experience a significant increase in appetite or who feel weaker and more exhausted than usual in the evening after exercise can minimize or avoid hypoglycemia by increasing caloric intake, taking less insulin that peaks in the evening and overnight, and checking blood glucose levels more frequently during the night. Increasing numbers of motivated diabetic athletes are

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receiving continuous subcutaneous insulin through an insulin pump. These devices use only short-acting (regular or insulin lispro) insulin delivered through exposed tubing and a needle temporarily implanted most often in the skin of the abdomen. Continuous low-dose, short-acting insulin (basal rate insulin) is supplemented by additional premeal (bolus) insulin also delivered through the pump setup. The pump can be detached temporarily if not waterproof, allowing for participation in water sports. Although the insulin pump does not improve diabetes control invariably, studies of adolescents with diabetes (not all of whom are athletes) suggest that better long-term blood glucose control can be achieved with less risk of nocturnal hypoglycemia. The pump also allows greater flexibility in timing of meals and activity. When appropriate adjustments in insulin dosage (especially during the evening and night after intense exercise) and caloric intake as detailed previously are made, the insulin pump can be used safely by the athlete. For short-to-moderate periods of exercise (e.g., 10 mg prednisone/day) therapy. Patients who require corticosteroids for adequate control of airway obstruction should be informed about the side effects associated with their use and be monitored carefully to ensure early detection and appropriate management of any side effects should they develop over time. Inhaled corticosteroids (ICS), when used in recommended doses, have the advantage of delivering the drug directly to the target organ, while producing minimal systemic side effects compared with oral forms. Although ICS are not first-line drugs for EIA treatment, regular use can decrease the severity of EIA[20] and enhance the protective effect of -agonists when they are administered routinely for at least 4 weeks.[21] ICS may be associated with oralthrush (candidiasis), dysphonia (hoarseness), and cough. The occurrence of oral thrush can be prevented completely by rinsing the mouth after each use of the inhaler. When thrush occurs, it is treated easily with oral nystatin (or other anticandidal therapies) and temporary discontinuation of the ICS. Hoarseness appears to be a local form of steroid myopathy affecting the muscles of the vocal cords and improves after the withdrawal or lowering of the dose of an ICS. Coughing while inhaling the medicine occasionally is reported and is thought to be related to the propellant in the inhaled steroid. It often responds to use of a spacer device for inhalation. Although systemic side effects are seen occasionally with ICS, they are infrequent and are seen mainly when ICS are given in doses higher than recommended. Patients whose EIA is not controlled with bronchodilator medications should be evaluated more carefully for their overall level of symptom control and pulmonary function because such situations suggest suboptimal treatment of asthma in general. Commonly used ICS in the United States include beclomethasone dipropionate, flunisolide, and triamcinolone acetate. High-potency ICS are available, including budesonide and fluticasone. Many of the ICS can be dispensed using a variety of delivery systems, including metered-dose inhalers (chlorofluorocarbon and hydrofluoroalkane propellants) dry powder inhalers, and nebulizer solutions. ICS are not beneficial in the prophylaxis of EIA when administered immediately before exercise; however, long-term use can modify EIA and reduce the required -agonist inhaler dose needed to block it.

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Effects of Physical Training on the Severity of Exercise-Induced Asthma

Exercise is a common stimulus for asthma, and asthmatic patients may tend to avoid physical activities that frequently provoke an attack. This situation may have a significant influence on a patient's lifestyle and sense of well-being, especially among children. The effects of physical training on EIA have been studied with encouraging but occasionally conflicting results. Most of the discrepancies can be explained by differences in study design, method of analysis, or interpretation of results. In most studies, patients experience improvement in self-confidence and the ability to cope with asthma after training; however, objective evidence of improvement in EIA has been shown by some but not all investigators.[2] [13] [17] [22] [48] Because well-structured physical training programs may help to decrease the severity of EIA in addition to improving work capacity and self-confidence, they should be encouraged. Patients should be advised to use prophylactic medications properly to maximize their participation and enjoyment in a full range of activities.

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Treatment of Exercise-Induced Asthma in Athletes Participating in National and International Competitions

A substance that is banned by a national or international official sports organization remains a banned substance, even when prescribed by a physician for a clinically justifiable purpose. Approved antiasthma medications include theophylline, nedocromil, cromolyn, leukotriene modifiers, anticholinergics, corticosteroids, and selective 2 -agonists. The National Collegiate Athletic Association (NCAA) publishes a list of banned drugs on its website (www.ncaa.org). The U.S. Olympic Committee and U.S. antidoping agency have a website (www.usantidoping.org) and a drug reference hotline (1-800-233-0393) for questions relating to these issues. Because of possible changes in the policies of various athletic organizations, it is important always to obtain the most recent guidelines of the organization involved at least 1 month before any scheduled competition to allow time to adjust therapeutic strategies well in advance of the actual sporting event.

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Authors' Recommended Method of Treatment

EIA can be controlled in most asthmatic patients and athletes by proper use of physical training, a pre-exercise

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warm-up, correct choice of exercise, antiasthma medications, and minimizing airway heat and water loss during exercise. Physical training improves cardiopulmonary fitness, a sense of well-being, and self-confidence. Because improved fitness permits the athlete to perform the same exercise with less minute ventilation (i.e., less heat and water loss), the frequency and severity of EIA may decrease. The choice of exercise is most important in the amateur athlete. Certain types of exercise, such as biking, jogging, and skiing, are more likely to cause EIA than swimming or less aerobic exercises. A pre-exercise warm-up can help to decrease the severity of EIA by inducing a refractory period. Because half of asthmatics may develop a refractory state, athletes should be encouraged to perform a routine warm-up before exercise to determine whether such an activity may attenuate their asthmatic response. The use of antiasthma medications helps to control EIA in most asthmatics. For individuals with asthmatic symptoms associated only with exercise, the prophylactic use of a 2 -agonist inhaler before exercise prevents EIA in most cases. Short-acting -agonists (e.g., albuterol) have the advantage of providing prevention and rescue therapy for EIA. Although long-acting -agonists (e.g., salmeterol) provide a longer duration of EIA prophylaxis, they should not be used as a first-line treatment for EIA because of their slow onset of action. In a small group of asthmatic patients, the protection provided by a 2 -agonist may be incomplete, and in these athletes the addition of inhaled cromolyn sodium (or nedocromil) can provide a second level of prophylaxis. In patients who have difficulty mastering the technique of using a metered-dose inhaler

or who prefer using pills, a leukotriene-modifying agent can be tried. These drugs are effective in attenuating EIA in at least 50% of patients with asthma. In asthmatic patients in whom symptoms are provoked by exercise as well as other stimuli (persistent asthma), overall control should be optimized with the use of various controller medications, including ICS, long-acting -agonists, leukotriene-modifying drugs, and theophylline. Because the pivotal stimuli for EIA appear to be airway heat and water loss, any measures taken to minimize these losses can help to decrease the incidence and severity of EIA. Measures include avoiding outdoor exercise during cold, dry winter days and using a scarf over the nose and mouth when exposure to these conditions is unavoidable.

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Summary EIA is a common problem in asthmatic children and adults. It is characterized by airway obstruction that occurs shortly after vigorous physical activity; symptoms improve gradually and usually are reversed completely within 30 to 60 minutes after exercise. Half of patients with EIA may experience a refractory period for at least 1 hour after their initial exercise-induced asthmatic response. The pathogenesis of EIA is not established clearly but may be related to heat and water loss across the airway wall during exercise, mast cell mediator release, or the rate of airway rewarming after termination of exercise. Despite the lack of precise knowledge about the pathogenesis of EIA, its occurrence can be prevented (or treated if it occurs) in most cases. Proper choice of a suitable exercise type and exercise conditions and the use of a prophylactic 2 -agonist should help to achieve optimal prevention of EIA in most asthmatic athletes and should allow them to engage in a full range of sports activities. The outstanding record of asthmatic athletes on U.S. Olympic teams should be an encouragement to patients with asthma to pursue excellence in physical fitness and sports unrestricted by their illness.

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Svenonius E, Arborelius M Jr, Wieberg R, Ekberg P: Prevention of exercise induced asthma by drugs inhaled from metered dose aerosols. Allergy 43:252-257, 1988. 47.

Svenonius E, Kautto R, Arborelius M Jr: Improvement after training of children with exercise-induced asthma. Acta Paediatr Scand 72:23-30, 1983. 48.

Tsankas JN, Milner RDG, Bannister OM, Boon AW: Free running asthma screening test. Arch Dis Childh 63:261-265, 1988. 49.

Tullett WM, Tan KM, Wall RT, Patel KR: Dose-response effect of sodium cromoglycate pressurized aerosol in exercise-induced asthma. Thorax 40:41-44, 1985. 50.

Yang XX, Powell WS, Hojo M, Martin JG: Hyperpnea-induced bronchoconstriction is dependent on tachykinin-induced cysteinyl leukotriene synthesis. J Appl Physiol 82:538-544, 1997. 51.

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Section G Sports and Epilepsy Mary L. Zupanc MD In the United States and elsewhere, millions of children and adults participate in organized and unorganized sports. Because 0.5% to 1.0% of the general population has epilepsy, individuals with seizures often are sports participants.[3] [9] [12] [16] The diagnosis of epilepsy does not preclude this participation. Most children with epilepsy are seizure-free with the use of one antiepileptic drug (AED) without side effects. Children with epilepsy who are seizure-free can participate in sports events, unless the activity itself precipitates their seizures, which is a rare occurrence. Children who have breakthrough seizures can participate in some sports activities, depending on the nature of the sports activity, the severity of the seizure, and the treatment. It is the responsibility of the health care provider who treats patients with epilepsy to ensure that the patient with epilepsy can participate within safe guidelines. Terminology

Epilepsy refers to unprovoked, recurrent seizures. An epileptic seizure is the clinical manifestation of an abnormal synchronous discharge of a group of neurons in the cerebral cortex. The features of a clinical epileptic seizure differ according to the anatomic location of the neurons in the cortex. In this way, an epileptic seizure can cause an altered state of consciousness, tonic-clonic movements, stereotypic or repetitive movements, loss of muscle tone, sensory or psychic experiences, or autonomic dysfunction. These disturbances usually, but not always, are accompanied by electrographic epileptogenic activity during scalp electroencephalography (EEG). There are many different types of epileptic seizures. In the past, the classification of epileptic seizures was confusing, and many redundant terms were used. The International League Against Epilepsy

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has published an international classification of epileptic seizures.[5] According to this classification, epileptic seizures are divided into two categoriesgeneralized and partial. Generalized seizures are characterized by bilaterally synchronous discharges involving the entire cortex of the brain. They can be subdivided further into nonconvulsive and convulsive seizures. Nonconvulsive generalized seizures include absence seizures (petit mal) and myoclonic seizures. Convulsive generalized seizures are the more familiar tonic-clonic seizures (grand mal). Partial seizures are seizures that begin in one part of the brain. Partial seizures can be either simple partial seizures (without impairment of consciousness) or complex partial seizures (with impairment of consciousness). Simple partial seizures are what used to be called the aura before the more recognizable complex partial seizures. Simple partial seizures can encompass a range of symptoms, including motor, sensory, autonomic, and psychic phenomena. As the epileptogenic discharges spread across the neocortex, these simple partial seizures typically transform to complex partial seizures. A typical complex partial seizure emanating from the temporal lobe is characterized by staring, diminished responsiveness, and stereotypic automatisms, such as repetitive swallowing or lip smacking. If a partial seizure evolves into a generalized tonic-clonic seizure, it is called a secondarily generalized seizure.[25] Epileptic seizures, if recurrent and unprovoked, are termed epilepsy. Epileptic syndromes also have been identified and classified.[6] The three big subdivisions are localization-related epilepsies, generalized epilepsies, and unclassified epilepsies. Simplistically, generalized epileptic syndromes often are idiopathic, contain a genetic predisposition, are associated with bilateral synchronous discharges on EEG, and often have a good prognosis. Localization-related epileptic syndromes are divided into idiopathic, age-related onset, and symptomatic. The idiopathic category implies a probable hereditary predisposition, and all diagnostic studies are negative. In the age-related category, the most common localization-related epilepsy is benign rolandic epilepsy. This epilepsy is a self-limited condition with a hereditary predisposition and is outgrown by the time the child reaches puberty. Benign rolandic epilepsy is associated with temporal-central spikes seen during drowsiness and light sleep on the EEG; the seizures can be either partial or secondarily generalized tonic-clonic seizures. The seizure semiology typically is characterized by sensorimotor symptoms and clonic activity of the face, arm, and leg, usually associated with hypersalivation and speech arrest. Seizure frequency varies, but they usually are rare, occur nocturnally, and are precipitated by sleep deprivation. Treatment with AEDs is optional, depending on seizure frequency and the psychosocial impact of the seizure disorder itself. The symptomatic category comprises epileptic syndromes caused by focal brain abnormalities, such as malformations of cortical development, trauma, and tumor. Central nervous system infections, toxic or metabolic abnormalities, and neurodegenerative disorders are categorized under this heading; these causes usually result in unifocal or multifocal damage to the brain. Symptomatic localization-related epilepsies tend to have a poorer prognosis for complete seizure control or cure. In some of the symptomatic localization-related epilepsies, resective epilepsy surgery can be

curative or reduce the seizure burden considerably.

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Treatment

It is not necessary to treat the first unprovoked seizure. The chance of a recurrent seizure after a first seizure is approximately 30% to 40%. If the EEG shows temporal epileptiform discharges or generalized spike and slow wave discharges, the chance of recurrence is much higher, bordering on 90%. If a child has a second seizure, the risk for continued seizures is much higher. Antiepileptic medication generally is recommended after a second seizure. There are exceptions to this, particularly if a benign epileptic syndrome is identified (discussed previously). There also are epileptic syndromes that are malignant. When identified, treatment should begin without delay, regardless of seizure frequency. When discussing AED therapy, it is important to recognize the seizure type as well as the epileptic syndrome. The categorization of the seizuretype and epileptic syndromeis the most important criterion in making a decision about antiepileptic medication. There are basic principles to remember in choosing AED therapy, as follows: 1. AED monotherapy is effective in most patients and avoids undesirable drug interactions. 2. AEDs should be titrated slowly and only to the point of seizure control, if possible. 3. Seizure control should not be achieved at the expense of side effects. 4. Drug compliance is enhanced when medication is given once or twice daily. Sustained-release medication should always be considered. 5. Therapeutic blood levels are not absolute. They are formulated on the basis of trough levels and represent a statistical range of efficacy.

Various medications commonly are used to treat epilepsy. Older medications include phenobarbital, carbamazepine, phenytoin, valproate/valproic acid, ethosuximide, clonazepam, and primidone. Since 1993, seven new AEDs have been approved by the Food and Drug Administration (FDA): felbamate, gabapentin, lamotrigine, topiramate, tiagabine, zonisamide, and levetiracetam. Phenobarbital, phenytoin, and primidone are among the oldest AEDs. Most child neurologists do not use these medications nearly as frequently as they did previously. There are newer, better AEDs that have fewer side effects. Phenobarbital, phenytoin, and primidone all have been reported to produce significant cognitive and behavioral side effects. In one study, phenobarbital reduced IQ scores in children, an effect that outlasted administration of the drug.[10] Phenobarbital and primidone have also been noted to produce sedation in adults; irritability, poor attention and concentration in children; depression in adolescents; mood lability; and sleeping disorders. Phenytoin has been reported to depress cognitive function, slow overall performance, and produce sedation.[24] Phenytoin is also difficult

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to dose because of its pharmacokinetics. The advantages of these older medications, however, are that they are relatively inexpensive and can be given once or twice daily, increasing patient compliance. Carbamazepine is the most widely used AED in the treatment of partial seizures. Carbamazepine is generally well tolerated but should be introduced slowly. Gradual introduction reduces the risk of toxicity and enhances compliance. Autoinduction of carbamazepine metabolism through the P-450 enzyme system occurs within the first month of therapy, often necessitating an increase in the total dosage of carbamazepine. If possible, when the dosage has been adjusted, attempts should be made to change to a sustained-release preparation (i.e., Tegretol-XR or Carbatrol). The toxic side effects of carbamazepine include dizziness, diplopia, sedation, ataxia, and nausea. Rare idiosyncratic reactions include aplastic anemia and hepatic dysfunction. Transient leukopenia occurs in 10% of children, usually during the first month of therapy. Allergic rash occurs in about 8% to 10% of patients; cases of Stevens-Johnson syndrome have been reported. Other rare side effects include irritability and dystonia. The antibiotic erythromycin alters the kinetics of carbamazepine, resulting in significant increases in carbamazepine levels.[25] [26] Valproate is a broad-spectrum AED with demonstrated efficacy for partial and generalized seizures. Valproate comes in several formulations, including the liquid valproic acid, sodium valproex tablets, and sodium valproex sprinkle capsules. The most common side effects of valproate include an increase in appetite with concomitant weight gain and tremor. The weight gain may be troublesome for athletes.

Rarely, valproate causes an encephalopathy with sedation and cognitive impairment. With high doses, tremor, transient alopecia, and thrombocytopenia (with easy bruising and bleeding) can occur. The most publicized and serious side effect of valproate is hepatotoxicity. This is a rare, idiosyncratic reaction that occurs in the first few months of therapy. The highest risk group is infants and toddlers less than 2 years old who have an abnormal neurologic examination and are on multiple AEDs. The risk in a school-aged child is less than 1 in 30,000. Another rare side effect of valproate is pancreatitis.[25] Literature has implicated valproate in the development of polycystic ovary syndrome. This syndrome is associated with infertility, dyslipidemia, and insulin-resistant diabetes mellitus. The exact mechanism by which this syndrome occurs is still being investigated. Further research needs to be done to confirm these preliminary findings and their extent in pediatric and adolescent patients. Initial studies suggest a specific predilection for adolescent girls. Gabapentin (Neurontin) is one of the newer AEDs that is used commonly in the treatment of partial seizures. One of the biggest advantages of gabapentin is the lack of drug interactions. In contrast to other AEDs, gabapentin is not metabolized by the liver, does not induce the P-450 enzyme system, and is not highly protein bound. It is excreted through the kidney. Gabapentin is generally safe and well tolerated. There are no known fatal side effects. In pediatric patients, particularly in children with an underlying encephalopathy, irritability, aggressiveness, agitation, and other behavioral side effects have been reported.[26] Lamotrigine (Lamictal) was released in 1994. It has been approved as adjunctive therapy for the treatment of partial seizures and for the treatment of generalized tonic-clonic seizures. Lamotrigine is probably another broad-spectrum AED, effective in the treatment of partial and generalized seizures. Clinical research is ongoing to determine its efficacy in generalized epilepsies. Lamotrigine comes in several formulations, including tablets and sprinkle capsules. Lamotrigine carries a risk for an allergic rash, especially when combined with valproate. Valproate inhibits the metabolism of lamotrigine, resulting in an increase in the half-life from 12 hours to 72 hours. When initiating lamotrigine, the dosage must be increased slowly. If the appropriate titration schedule is used, the risk of an allergic rash is no greater than for other AEDs. If a rash is reported, the patient should be seen immediately because the rash can progress rapidly. Patients who have reported skin allergies to other drugs, especially to carbamazepine, are at a higher risk for an allergic rash from lamotrigine.[26] Other less common side effects of lamotrigine include dizziness, headaches, diplopia, sedation, and movement disorders, including choreoathetosis and dystonia. Positive behavioral side effects, including antidepressant effects, have been reported with lamotrigine. Topiramate (Topamax) is another broad-spectrum AED. Drug interactions are minimal. Topiramate comes in several formulations, including tablets and sprinkle capsules. The

major side effect of topiramate is cognitive dysfunction. A slow titration process can minimize these side effects. Topiramate can cause renal stones, owing to its weak action as a carbonic anhydrase inhibitor. Athletes should be kept well hydrated if they are taking topiramate.[26] Tiagabine (Gabitril) has been approved by the FDA for the treatment of partial seizures, as adjunctive therapy. There are no known drug interactions. The major side effects of tiagabine include lethargy, irritability, aggressive behaviors, dizziness, headache, and tremor. It is 96% protein bound and is metabolized by the liver.[26] Alternatives to Antiepileptic Drugs

The ketogenic diet as a treatment of epilepsy has been known since Biblical times. It became repopularized in the modern era by Dr. Keith from the Mayo Clinic and more recently by Johns Hopkins Medical Center. Patients with a particularly intractable form of epilepsy, called Lennox-Gastaut syndrome, have the best chance of responding to this diet. The diet can be difficult for children who already have dietary preferences because most of the calories are obtained from fat. Carbohydrates are extremely limited in this diet. Typically, there also is a fluid restriction. The diet would be difficult to maintain for a high-performance athlete but could be used in patients who are competing in intramural and neighborhood sports. The vagal nerve stimulator was approved by the FDA for use as adjunctive therapy in the treatment of medically refractory localization-related epilepsy in adults and children

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older than age 12. The vagal nerve stimulator is a pacemaker implanted in the chest pocket below the clavicle and delivers pulses from a bipolar electrode connected to the vagus nerve. The exact mechanisms of action by which the vagal nerve stimulator works remain an enigma. Most likely, the vagal nerve stimulator influence over the EEG is mediated by brainstem pathways with concomitant cortical projections. Stimulation of the vagus nerve appears to result in EEG desynchronization and eventual attenuation of seizure frequency. Side effects include bleeding, infection, voice alteration or hoarseness when the vagal nerve stimulator cycles on, cough, throat pain, dyspepsia, and nausea. There are no reports of cardiac arrhythmias with this device. Immunotherapy and steroids have been used in the treatment of a variety of rare and unusual epileptic syndromes, such as Rasmussen's syndrome and Landau-Kleffner syndrome. Epilepsy surgery is another therapeutic option for children who have intractable epilepsy and who have an identifiable, easily resectable epileptogenic focus or lesion on neuroimaging. Most individuals who undergo epilepsy surgery have a significant reduction in seizure frequency, and many are completely cured of their epilepsy. If a patient has mesial temporal sclerosis and seizures emanating from this temporal lobe,

the chance of surgery producing a seizure-free outcome is 85% to 90%. Athletic participation can be resumed within months after surgery in most cases.

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Management of Seizures

Although epilepsy generally is controlled easily, children and adolescents with epilepsy occasionally have a seizure while participating in athletic events. This situation can be embarrassing for the individual, frightening to those who observe it, and at times dangerous, particularly if it occurs during a swimming event. For the team physician, coach, and other supervisors of the event, the main tenet to remember is to stay calm and keep others calm. A seizure almost always is a self-limited event that requires minimal intervention. The next recommendation is to prevent the individual with epilepsy from self-injury. This goal can be accomplished by removing objects close to the individual, particularly during a generalized tonic-clonic seizure. If the individual has been swimming, a skilled lifeguard should remove the individual from the water as quickly as possible. A tongue blade or other object never should be inserted between the teeth of an individual who is having a seizure; the individual will not swallow his or her tongue, and chances are that the individual will bite the object in two or injure the person who is attempting to insert the object. If a mouthpiece is present, it should be removed only if this can be accomplished easily. When a seizure is over, usually within minutes, the individual often is tired. The individual should be allowed to lie down. If the episode has been a convulsive (i.e., tonic-clonic) seizure, the individual should be turned onto his or her side to prevent aspiration of vomitus. If the episode has been a nonconvulsive seizure (e.g., partial complex seizure consisting of stereotypic movements or bizarre behaviors), this usually is not necessary, although the individual often is lethargic and semiresponsive after the seizure. If a seizure occurs during a sporting event, the individual should not participate further that day. The one exception to this rule may be the child who has absence epilepsy (petit mal) and experiences occasional breakthrough seizures. When the physical needs of the individual who has experienced a seizure have been met, attention should be turned to the emotional needs of this individual and others. The embarrassment that many people feel after a seizure should be acknowledged and addressed; this implies listening to the individual and his or her feelings. A simple How are you feeling? may be enough to elicit a conversation. Alternatively, the person who

had the seizure may not want to discuss it at all. The significant adults in the individual's life may want to let him or her know that they are willing to listen and talk at any time in the future. The same thing applies to other people who witnessed the event. These people need to know that seizures are not harmful, that the person will recover, and that most individuals with epilepsy lead normal lives with only rare or no breakthrough seizures. The lay public still has many misconceptions about epilepsy.

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Clinical Evaluation of the Sports Participant

Evaluation of an individual with epilepsy who wishes to participate in sports is relatively easy. There are only a few questions that need to be answered in assessing the ability of an individual with epilepsy to participate in sports: (1) How well controlled are the individual's seizures? (2) Is the individual experiencing significant side effects from the anticonvulsant medication? (3) In what sport activity does the individual wish to participate? (4) How great is the individual's desire to participate?

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Treatment Options and Criteria for Sports Participation

Individuals with epilepsy, even those whose seizures are not under complete control, should be allowed to participate in a variety of sports. Severely limiting sports participation may impose unduly harsh restrictions on the individual with epilepsy, resulting in a feeling of being stigmatized as an outsider. As stated by the American Academy of Pediatrics in their Committee Report on this subject, in today's culture, sports and athletics are extremely important, and unnecessarily strict interpretations of medical conditions may do more harm than good.[12] Most authors agree that individuals with epilepsy can participate in most sports even if incomplete control of seizures exists.[3] [11] [14] [16] There is widespread agreement that some sports by their nature pose situations that could be dangerous even if only one breakthrough seizure were to occur. These sports include rock-climbing, rope-climbing, activity on parallel bars, high diving, and prolonged underwater swimming.[12] If it is known that hyperventilation

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would increase one's propensity to have a seizure, other sports activities may have to be modified, such as track, swimming, and basketball. If fatigue is a major precipitant of an individual's seizures, reevaluation of the appropriateness of a particular sports activity may be necessary. In most circumstances, the sport can be allowed but with certain restrictions. There are two areas of controversy among various authors: body contact sports and swimming. Individuals with epilepsy used to be universally denied participation in body contact sports such as football. It was hypothesized that repeated head trauma would result in further brain injury with eventual aggravation of the epileptic condition. There are no studies in the medical literature that prove that chronic head trauma increases

the frequency of epileptic seizures.[1] [7] [14] Authors have argued against restriction, stating that it does not happen in reality. Their conclusion is that the decision to participate in body contact sports must be made on an individual basis. Frequent seizures (occurring daily or weekly) are considered a relative contrain dication by these authors because of the possibility that a seizure would incapacitate the patient at an inopportune moment, for example, a football lineman experiencing a seizure right after the beginning of a play. Swimming represents a special case. Fatalities of individuals with epilepsy in swimming pools, the ocean, and bathtubs are well-documented but relatively rare events. An individual with epilepsy is four times more likely to drown than an individual without epilepsy.[16] [19] [20] [21] Various contraindications for swimming have been proposed by different authors,[2] [4] [15] [19] [20] [21] [23] and include the following: 1. 2. 3. 4. 5. 6. 7. 8.

Frequent seizures, more than once a month A seizure-free status that has lasted for less than 3 months A patient who is going through a period of adjustment to AED therapy Noncompliance with drug regimen Unstable blood levels of AED Lack of one-to-one supervision Murky water in oceans and lakes Mental retardation

Frequent seizures pose a danger to the individual with epilepsy who swims. Oceans and lakes with murky water are particularly dangerous because it may be impossible to find a drowning individual before the onset of disastrous consequences. Most authors concur that participation in swimming can be allowed if an individual with epilepsy has been seizure-free for 6 months, is mentally normal, has stable and therapeutic AED levels, and is supervised closely by a lifeguard who is aware of the individual's condition and knows cardiopulmonary resuscitation (CPR).[11] [16] [19] The buddy system should be used. If these requirements are met, swimming poses little risk. Bathing is a much bigger risk. [16] [17] [18] Several studies have shown that taking a bath presents a more serious risk of drowning than swimming.[13] [22] Older adolescents and adults run the highest risk. They tend to bathe alone, whereas younger children are supervised closely during bath time by parents.

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Author's Preferred Method of Treatment

Most children and adolescents with epilepsy should be encouraged to participate in athletics and sports. The opportunities to participate are much greater than they used to be. Individuals who are physically or cognitively impaired can become active in sports. Special Olympics provides opportunities for these children and adolescents, often with positive results in self-esteem. Children and adolescents can participate in contact sports such as football. One must always strike a balance between the patient's medical condition and his or her perceived need to participate in contact sports. Contact sports can result in head trauma. Mild head trauma can result in attention or concentration problems, memory problems, headache, and other somatic complaints. Moderate-to-severe head trauma can result in further brain injury and a decreased seizure threshold. Individuals with epilepsy, similar to the general population, should be outfitted with the proper protective equipment for the particular contact sport involved, including a mouthpiece. An individual with epilepsy will not choke on the mouthpiece in the event of a seizure. Recommendations for swimming must be conservative because of the risks of drowning. If an individual with epilepsy can be supervised closely (one-on-one) by a competent lifeguard who is trained in CPR and who is aware of the individual's condition, swimming can be allowed. Swimming can be unrestricted if the individual has been seizure-free for more than 3 months or if the individual's usual seizure is brief and results in no or only brief alteration of consciousness. If an individual with epilepsy has chosen a sport that is thought to be unsafe (based on the criteria outlined previously), attempts should be made to steer the individual into an alternative sport or to set limitations or modifications on the sport chosen.

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Summary Children and adolescents with epilepsy should be allowed and encouraged to participate in sports and athletic events. These individuals can participate in most sports activities with no or only a few restrictions or modifications. The sense of satisfaction and the growth in self-esteem that result from participation usually far outweigh the risks.

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References 1.

Aisenson MR: Accidental injuries in epileptic children. Pediatrics 2:85, 1948.

Berggreen SM: Accidents and surgical emergencies in a population of mentally retarded children. Acta Paediatr Scand 62:289-296, 1972. 2.

3.

Berman W: Sports and the child with epilepsy. Pediatrics 74:320, 1984.

Bowerman DL, Levisky JA, Urich RW: Premature deaths in persons with seizure disorders: Subtherapeutic levels of anticonvulsant drugs in postmortem blood specimens. J Forensic Sci 23:522-526, 1978. 4.

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Commission on Classification and Terminology of the International League Against Epilepsy: Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia 22:489-501, 1981. 5.

Commission on Classification and Terminology of the International League Against Epilepsy: Proposal for classification of epilepsies and epileptic syndromes. Epilepsia 26:268-278, 1985. 6.

Corbitt RW: Epileptics and contact sports. AMA Committee on the Medical Aspects of Sports. JAMA 229:820-821, 1974. 7.

Dreifuss FE, Santilli N, Langer DH: Valproic acid hepatic fatalities: A retrospective review. Neurology 37:379-385, 1987. 8.

9.

Engel J Jr: Seizures and Epilepsy. Contemporary Neurology Series. Philadelphia, FA Davis, 1989.

Farwell JR, Young JL, Hirtz DG: Phenobarbital for febrile seizureseffects on intelligence and on seizure recurrence. N Engl J Med 322:364-369, 1990. 10.

11.

Freeman JM: Epilepsy and swimming. Pediatrics 76:139, 1985.

Fremont AC, et al: Sports and the child with epilepsy. Committee on Children with Handicaps and Committee on Sports Medicine. Pediatrics 72:884-885, 1983. 12.

13.

Krohn W: Causes of death among epileptics. Epilepsia 4:315, 1963.

Livingston S, Berman W: Participation of the epileptic child in contact sports. J Sports Med 2:170-174, 1974. 14.

15.

Livingston S, Pauli LL, Pruce I: Epilepsy and drowning in childhood. BMJ 3:515-516, 1977.

O'Donahoe NV: What should the child with epilepsy be allowed to do? Arch Dis Child 58:934-937, 1983. 16.

Orlowski JP: Prognostic factors in drowning and the post-submersion syndrome. Crit Care Med 6:94, 1978. 17.

Orlowski JP: Prognostic factors in pediatric cases of drowning and near-drowning. Ann Emerg Med 8:176-179, 1979. 18.

Orlowski JP, Rothner D, Lueders H: Submersion accidents in children with epilepsy. Am J Dis Child 136:777-780, 1982. 19.

20.

Pearn JH: Epilepsy and drowning in childhood. BMJ 1:1510-1511, 1977.

Pearn J, Part R, Yamaoka R: Drowning risks to epileptic children: A study from Hawaii. BMJ 2:1284-1285, 1978. 21.

22.

Sonnen AEH: Epilepsy and swimming. Monogr Neurol Sci 5:265-270, 1980.

23.

Williams CE: Accidents in mentally retarded children. Dev Med Child Neurol 15:660-662, 1973.

Woodbury DM, Penry JK, Pippenger CE (eds): Antiepileptic Drugs, 2nd ed. New York, Raven Press, 1982. 24.

25.

Zupanc ML: Update on epilepsy in pediatric patients. Mayo Clin Proc 71:899-916, 1996.

Zupanc ML: Epilepsy in infants and children. In Rakel R, Bope E (eds): Conn's Current Therapy. Philadelphia, WB Saunders, 2002. 26.

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Chapter 8 - Rehabilitation Section A The Language of Exercise and Rehabilitation John D. Childs MPT, MBA, OCS, CSCS James J. Irrgang PhD, PT, ATC Rehabilitation involves procedures designed to minimize impairments, functional limitations, and disability after injury or illness. In sports medicine, rehabilitation includes procedures designed to restore athletes to their previous level of function within the shortest time possible. Rehabilitation begins immediately after injury and culminates in return to sport or return to the highest functional level possible based on the nature and severity of the injury. For the athlete, rehabilitation frequently consists of a combination of various physical agents and therapeutic exercise techniques aimed at minimizing the impairments, functional limitations, and disability associated with the injury. Knowledge of the theoretical principles, indications and contraindications, and proper application of each technique is necessary to maximize the potential for return to sport and to minimize the risk for reinjury. Disablement

In rehabilitation of the athlete, it is useful to consider the model of disablement proposed by Nagi.[45] In this model, an active pathologic process is the interruption of or interference with normal processes in the body. Impairment is the loss of or abnormality in structure or function at the organ or system level. Impairments are consequences of the pathologic process and may be manifested as signs or symptoms. Signs are those findings perceived by the clinician during examination (e.g., decreased knee range of

motion, knee joint laxity). Symptoms are manifestations of the pathologic process that are perceived by the athlete and reported to the clinician during the examination (e.g., giving way of the knee during physical activity). Functional limitations are those limitations that are imposed on performance at the level of the whole organism or person. In essence, they are the functional consequences of the pathologic process and subsequent impairments. Disability is a limitation in performance of socially defined roles and tasks within a sociocultural and physical environment that is a consequence of the athlete's functional limitations. To illustrate the disablement process, consider the athlete who suffers a knee injury resulting in a torn anterior cruciate ligament. The active pathologic process in this case is disruption of the anterior cruciate ligament. The physical impairments associated with this injury may include pain, swelling, loss of motion and strength, and laxity. The resulting functional limitations from this injury may be the inability to run and perform cutting and pivoting maneuvers. The resulting disability experienced by the athlete may be the inability to perform in sports that require cutting and pivoting. Rehabilitation of this athlete should ultimately address the disability or inability to participate in sporting activities. To accomplish this, the rehabilitation program may initially need to address the physical impairments (pain, swelling, instability, limited range of motion, weakness, laxity, and loss of proprioception) resulting from the injury. As the physical impairments improve, rehabilitation then focuses on reducing the functional limitations experienced by the athlete. This includes activities to improve the athlete's ability to run, cut, and pivot without symptoms. The final phase of rehabilitation addresses the disability experienced by the athlete. This includes functional training activities that allow the athlete to resume participation in sports that require running, cutting, and pivoting. In rehabilitation of an athlete, it is useful to consider this model of disablement. Rehabilitation should not only focus on the physical impairments experienced by the athlete but also address the functional limitations and disability the athlete experiences. Goal of Rehabilitation

The ultimate goal of rehabilitation after athletic injury is to eliminate or to minimize the disability experienced by the athlete. For this goal to be accomplished, the physical therapist or athletic trainer will focus on eliminating or minimizing the athlete's physical impairments and functional limitations. This requires restoration of symptom-free motion and function to allow individuals to return to their previous level of activity in the shortest time possible. Specific goals in the rehabilitation program depend on the phase of rehabilitation. They include limiting inflammation; decreasing pain and swelling; improving joint mobility and flexibility; improving muscle strength, endurance, and power; improving cardiovascular endurance; and promoting coordination. The rehabilitation program must be appropriately designed to meet each of these goals. Furthermore, the athlete's program must be progressed as successive goals are accomplished. Development and progression of the athlete's rehabilitation program depend on the physical therapist's and athletic trainer's clinical decision-making and problem-solving skills. The physical therapist and athletic trainer must closely evaluate and

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monitor the impairments and functional limitations demonstrated by the athlete.

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Interventions

Rehabilitation requires athletic trainers and physical therapists to have basic knowledge of the effects of therapeutic exercise and physical agents. The purpose, indications, contraindications, and precautions for the use of these procedures must be known. Athletic trainers and physical therapists must be able to relate the effects of physical agents and therapeutic exercise to the rehabilitation goals for the athlete. Establishment of appropriate goals during rehabilitation depends on the ability to assess the extent of injury and functional status of the injured athlete. An understanding of disease and the healing process is necessary to ensure appropriate rehabilitation. Anatomy, kinesiology, and biomechanics must also be considered in the development of a rehabilitation program. Assuming a thorough clinical examination has been performed, physical therapists and athletic trainers can choose from a number of potential interventions in their armamentarium to address an athlete's impairments and functional limitations. These include various physical agents, therapeutic exercise (e.g., range of motion and stretching, resistance exercise, functional training), and education of the patient. The choice of intervention and the specific parameters associated with the intervention should be based on the best available evidence in peer-reviewed literature. The remainder of this chapter is limited to the use of therapeutic exercise to eliminate or to minimize impairments, functional limitations, and disability in athletes. In addition, we review basic principles and considerations for the use of each intervention.

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Therapeutic Exercise

Therapeutic exercise is defined as those movements that are designed to eliminate or to minimize the athlete's physical impairments, functional limitations, and disability. Therapeutic exercise can be used to maintain or to improve range of motion, muscle function, and proprioception. A therapeutic exercise program should be individually designed to address physical impairments, functional limitations, and disability experienced by the athlete. A therapeutic exercise program must consider the nature and severity of the injury or illness, the purpose of the exercise, the sequence and progression of the exercise, and the contraindications and precautions. In addition, the intensity, frequency, and duration of the exercise must be appropriate for the stage of inflammation, healing, and conditioning. Therapeutic exercise may take one of several forms, including range of motion and stretching exercise, resistance exercise, neuromuscular training, and functional training. Range of Motion

The range of motion available at a particular joint is determined by the configuration of the joint surfaces as well as surrounding soft tissue structures, such as the capsule, ligament, muscle, tendon, fascia, and skin. The range of motion available at a particular joint is termed joint range. [32] Joint range is measured in degrees with a goniometer. Muscle range is related to the functional excursion produced by muscles that cross the joint.[32] The functional excursion of a muscle is the distance that it is capable of lengthening and shortening. For a one-joint muscle, the functional excursion is directly influenced by the joint that the muscle crosses. A one-joint muscle is expected to shorten and lengthen sufficiently to permit full active range of motion at the joint that it crosses. The functional excursion of a multijoint muscle exceeds the joint range of any one of the joints that it crosses. A multijoint muscle cannot lengthen or shorten sufficiently to permit the simultaneous extreme range of motion at all the joints that it crosses, however. For example, the hamstrings cannot lengthen sufficiently to permit simultaneous full hip flexion and full knee extension. In this position, the hamstrings are

said to be passively insufficient. In the passive insufficient position, further motion is limited by tension in the musculotendinous unit. Similarly, the hamstrings cannot shorten sufficiently to permit simultaneous full active knee flexion and hip extension. In this position, the hamstrings are said to be actively insufficient. In the active insufficient position, the muscle fibers cannot shorten any further and are ineffective in generating additional tension. Assessment of active range of motion indicates the individual's ability and willingness to perform the movement requested, the range of motion available, and the muscle function. Limited active range of motion may be due to pain, limited muscle function, or limited passive movement. If there are contraindications or restrictions to assessment of active motion, one should assess passive motion. Passive motion is assessed as long as there are no contraindications or restrictions to assessment of passive motion. If there are contraindications or restrictions to assessment of passive motion, the physical therapist or athletic trainer should wait for tissue healing to occur before either active or passive motion is assessed. Assessment of passive motion should include assessment of joint mobility. Causes of limited passive motion include limited joint play, musculotendinous shortening, limited scar mobility, capsuloligamentous adhesions and tightness, internal derangement of the joint, and bony block to motion. The cause of the limited passive motion must be determined so that appropriate treatment can be rendered to improve passive motion. Although the specifics of assessment of motion are beyond the scope of this discussion, some basic principles need to be understood. Mechanical Characteristics of Connective Tissue and Muscle.

To increase motion, the properties of the tissue that limits the motion must be considered. These tissues are traditionally divided into noncontractile and contractile tissues. Noncontractile tissues are the ligaments, capsule, fascia, and connective tissue components of muscle and skin. Contractile tissues are the muscle, tendon, and tendinous insertion to bone. The material strength of tissue is its ability to resist load or stress. Stress is defined as force per unit of cross-sectional area and can be tensile, compressive, or shearing. Strain is defined as the deformation that occurs in response

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to stress. It is typically expressed as the percentage of elongation (i.e., change in length divided by original length). The mechanical properties of tissue are often plotted in a stress-strain curve that relates strain as a function of stress for a given tissue ( Fig. 8A-1 ). The toe region occurs at the beginning of the stress-strain curve. This is the region where little force is required to elongate the tissue. This probably represents straightening of the wavy pattern of connective tissue fibers. The elastic range consists of that area of the stress-strain curve in which the tissue returns to its original size and

shape when the stress is removed. The upper end of the elastic range is termed the elastic limit. This is the point beyond which the tissue will not return to its original size or shape when the stress is removed. The plastic range of the stress-strain curve represents the range beyond the elastic limit that results in permanent elongation when the stress is removed. The upper end of the plastic range is associated with failure of the tissue. Sequential failure of collagen fibers in tendon occurs between 4% and 8% strain. Frank failure of the tissue occurs beyond 8% to 10% strain of the collagen fibers.[8] This corresponds to 20% to 40% strain of the entire tendon. [48] Connective tissues are viscoelastic, that is, they exhibit the properties of viscosity and elasticity. Elasticity refers to the tissue's ability to return to its original length when stress is removed. Viscosity refers to a tissue's ability to resist elongation. Because of the viscoelastic nature of connective tissue, it exhibits the properties of creep, relaxation, and stiffness. Creep is the elongation of tissue that results from constant loading over time ( Fig. 8A-2 ). Creep can be increased by increasing tissue temperature.[37] Relaxation is the progressive decrease in internal stress over time as a result of lengthening to a constant strain. Stiffness is the ability of the tissue to resist elongation and is indicated by the slope of the stress-strain curve shown in Figure 8A-1 . Because connective tissue is viscoelastic, stiffness

Figure 8-A-1 Typical stress-strain curve for connective tissue. Toe region represents the region where little stress is required to lengthen the tissue; it probably represents straightening of wavy pattern of collagen fibers. Elastic region is that portion of the curve in which tissue returns to its original length when the stress is removed. Plastic region is that portion of the curve that results in permanent elongation when the stress is removed. (Modified from Kisner C, Colby, LA: Therapeutic Exercise: Foundations and Techniques, 3rd ed. Philadelphia, FA Davis, 1996.)

Figure 8-A-2 Graphic representation of phenomenon of creep. Tissue undergoes gradual elongation over time when subjected to constant stress. (From Irrgang JJ: Rehabilitation. In Fu FH, Stone DA [eds]: Sports Injuries. Baltimore, Williams & Wilkins, 1995, pp 81-95.)

is dependent on the rate of loading. Increased rate of loading is associated with greater stiffness. Lengthening of connective tissue requires plastic deformation that results in gradual rearrangement of the connective tissue. Adequate time must be provided for remodeling to prevent fatigue or rupture of the tissue, or both. Plastic deformation of connective tissue can be maximized by use of the principles of creep, relaxation, and stiffness. To maximize permanent lengthening, low-magnitude forces are applied for prolonged periods. This process can be facilitated by the use of heating modalities and by maintaining the lengthened position during the period of cooling.[37] Brand[6] suggested that if a joint is held at its end range for a significant time, then it will grow. The amount of time the joint is positioned at its end range is referred to as the total end-range time. Flowers and La-Stayo[16] provided evidence to support this hypothesis when they demonstrated that passive range of motion at the distal interphalangeal joint was almost

doubled in patients with contractures of the distal interphalangeal joint who were casted for 6 days compared with subjects who were casted for only 3 days. The mechanical characteristics of contractile tissue must be considered in attempting to increase the functional excursion of muscles. Muscle consists of both contractile and noncontractile components.[55] The noncontractile components include the series elastic and the parallel elastic components. The series elastic component is the connective tissue that connects the muscle fiber to bone; the parallel elastic component consists of the connective tissue that surrounds each muscle fiber. Lengthening of the musculotendinous unit lengthens both the series and the parallel elastic components, producing a sharp rise in tension. As lengthening of the musculotendinous unit continues, mechanical disruption of the cross-bridges begins, as the actin and myosin filaments slide apart and an abrupt lengthening of sarcomere occurs. This is termed sarcomere give.[15] Sarcomeres are elastic, and when short-term stretch is removed, they return to their original length. This implies that short-term stretching is not effective in increasing the length of the contractile components of a muscle.

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Plastic deformation of contractile tissue can be achieved with prolonged immobilization. Prolonged immobilization in the lengthened position results in the addition of sarcomeres and permanent lengthening of the contractile tissues. This occurs to maintain the greatest functional overlap of the actin and myosin filaments. Prolonged immobilization in the shortened position results in a decreased number of sarcomeres.[58] [62] Techniques to Increase Motion.

Various strategies exist to improve motion. These include active and passive range of motion exercises, stretching and flexibility exercises, joint mobilization and manipulation, and neurophysiologic techniques to stretch muscle. To decide which strategy may be most appropriate, the physical therapist or athletic trainer must assess both active and passive motion. If joint play is limited, treatment to restore passive motion includes joint mobilization followed by range of motion and stretching exercises for the joint. If passive motion is limited and mobility testing reveals normal joint play, the functional excursion of the musculotendinous unit is assessed. If functional excursion of the musculotendinous unit is limited, neurophysiologic stretching techniques can be incorporated to relax the muscles before elongation. This allows the contractile component to be lengthened more easily. Range of Motion Exercise

Range of motion exercises are exercises that are performed within the unrestricted range of motion to maintain joint mobility and functional excursion of muscles. Range of

motion exercises can be passive, active assistive, or active. Passive range of motion exercises are movements that are produced by an external force without voluntary muscle effort on the part of the athlete. The external force may be applied by an athletic trainer or therapist, another part of the athlete's body, a machine, or gravity. Passive range of motion exercises are indicated when the athlete is not able to move the body segment voluntarily or when voluntary muscle activity would be detrimental to the healing process. Passive range of motion can be used to limit the adverse effects of immobility and to demonstrate motion when teaching other forms of exercise. In addition, passive range of motion techniques may be applied before stretching. Passive range of motion will not prevent muscle atrophy or affect muscle strength or endurance, nor will it improve circulation to the same extent that voluntary, active use of the muscles does. True passive movement may be difficult to obtain when muscles are innervated. Active range of motion exercises are exercises within an unrestricted range of motion that are produced by active voluntary muscle contraction. Active-assistive exercises combine active voluntary contraction with an outside force to complete motion within the unrestricted range. Both active and active-assistive range of motion exercises are used when the athlete is able to contract the muscles actively to move the segment and when there are no contraindications to active voluntary muscle contraction. Active and active-assistive range of motion exercises can be used (1) to limit the adverse effects of immobility and maintain contractility of muscles, (2) to provide sensory feedback, (3) to provide a stimulus for maintaining integrity of bone, (4) to increase circulation, (5) to improve coordination and motor skills necessary for functional activities, and (6) to improve strength of weak muscles. Sustained active exercises involving large muscle groups can be used to improve cardiorespiratory function. Active-assistive and active exercises cannot be used to strengthen muscles or to maintain strength of muscles that are already strong, however. Active exercises develop skill and coordination only in the movement patterns used. Range of motion exercises may be performed in anatomic planes or in combined patterns incorporating movement in several planes simultaneously. Range of motion exercises can also be performed in sport-specific functional patterns. They should be performed within the pain-free range of motion. Motion beyond the available range of motion should not be forced. In general, 5 to 10 repetitions several times per day are adequate to limit the adverse effects of immobility. The athlete's response to range of motion exercises should be closely monitored and documented. Range of motion exercises are contraindicated when motion is disruptive to the healing process. It is important to recognize signs of excessive exercise if range of motion exercises are performed acutely after injury. These signs are increased pain, swelling, warmth, redness, and loss of motion that persists for more than 1 to 2 hours after the exercise is completed. Range of motion exercises should not be confused with stretching exercises when the treatment goal is to increase range of motion. Stretching and Flexibility Exercise

Stretching exercises are designed to increase range of motion and lengthen pathologically shortened soft tissue structures. Flexibility is defined as the ability of the muscle to relax and yield to a stretching force[32] ; as such, flexibility exercises are used to increase length of the musculotendinous unit. The term flexibility exercise is often used synonymously with stretching exercise, as is done here unless it is otherwise necessary to make the distinction. Several general guidelines should be followed to enhance the effectiveness of stretching exercises and to minimize the risk for injury. Before stretching, local application of heat or engagement in light active exercise to elevate body temperature may be beneficial because it increases soft tissue extensibility. Massage and biofeedback may be employed to promote relaxation and to decrease muscle spasm, making it easier to stretch tight muscles. If mobility of a joint surface is limited, mobilization techniques are used before stretching exercises. Athletes should stretch until tightness is first perceived. Stretching exercises should avoid forcing the joint beyond the normal range of motion required for athletic activity. Stretching exercises should not be performed in the acute stages of healing. Stretching during this period may jeopardize the healing tissue and aggravate inflammation. During this time, range of motion exercises rather than stretching exercises should be used. Stretching exercises should not cause a persistent increase in pain that lasts longer than 1 to 2 hours. Caution must be used in stretching across the fracture site of a newly united fracture. Stretching exercises should not be used in an attempt to increase motion that is limited by a bony block.

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Stretching exercises may be performed actively or passively. During passive stretching, the stretch is produced by forces external to the body. The external force can be applied manually or mechanically. Manual passive stretching exercises are performed by the physical therapist or athletic trainer. Passive mechanical stretching is performed by use of a mechanical device to apply a low (5- to 10-pound) external load to the shortened tissues. Passive mechanical stretching may be performed with the use of ankle weights or other mechanical equipment. In active stretching, the stretching force is created by active voluntary contraction of the athlete's muscles. Active stretching allows incorporation of the neurophysiologic principles of stretching, which are discussed later. Stretching exercises may be cyclic or prolonged. Cyclic stretching refers to a stretch that is maintained for a short time (i.e., less than 10 seconds) but performed for many repetitions. Prolonged stretching, on the other hand, consists of low-load stretches that are maintained for longer times for a fewer number of repetitions. The length of a prolonged stretch is variable and may range from 30 seconds or more to several hours, depending on the patient's level of tolerance. The total end-range times for repeated cyclic and prolonged stretches may be similar. Prolonged stretching may result in greater permanent lengthening of contractile and noncontractile tissues; however, cyclic

stretching may be better tolerated by the athlete. Stretching exercises can also be performed statically or ballistically. A slow static stretch is less likely to elicit a stretch reflex response. Ballistic stretching refers to a high-intensity, short-duration stretch that results in rapid lengthening of the muscle, which in turn stimulates the muscle spindle and facilitates a stretch reflex. The musculotendinous unit is susceptible to microtrauma with ballistic stretching. Ballistic stretching may be beneficial immediately before engaging in exercise, but it should be performed only after a warm-up that includes slow static stretching. When the athlete demonstrates limited range of motion in the subacute or chronic phases of healing, stretching exercises are indicated to regain the motion that is necessary for athletic activity. Stretching exercises can also be used to correct muscle imbalances that result when a muscle group is tight and its opposing muscle group is weak. In general, the tight muscle group should be stretched before strengthening exercises are performed to improve strength of the opposite muscle group. Stretching exercises may also be indicated before activity as a warm-up and after activity as a cool-down. Proper warm-up and cool-down minimize the risk for musculotendinous injuries associated with physical activity and sports. Physiologic Motion and Accessory Motion

To understand the principles related to joint mobilization, it is necessary to understand the distinction between physiologic motion and accessory motion. Physiologic motion is the angular displacement of a bone about its axis of rotation, referred to as swing. Physiologic motion is also referred to as osteokinematics. These are movements that the patient can perform under voluntary muscle control (i.e., flexion-extension, abduction-adduction, and internal-external rotation). Accessory motions are the component movements necessary for physiologic motion. These are not under voluntary control. These movements consist of rolling, gliding, compression, distraction, and spin. Accessory motion is also referred to as arthrokinematics. [63] Rolling occurs when new points on one surface meet new points on an opposing surface, much like a tire rolling along the road (Fig. 8A-3B (Figure Not Available) ). Rolling of the joint surface always occurs in the same direction as the swing of the bone. During normal movement of a joint, rolling does not occur in isolation. Rolling is accompanied by gliding of the joint surfaces to prevent the convex joint surface from rolling off the concave surface. Gliding of the joint surface involves contact of the same point on one surface with new points on the opposing surface, much like a locked tire sliding over a road (Fig. 8A-3A (Figure Not Available) ). The direction of gliding depends on the shape of the articular surface. Convex joint surfaces glide in the direction opposite the swing of the bone, whereas concave joint surfaces glide in the same direction as the swing of the bone. Normal joint motion combines both rolling and gliding of the joint surfaces. Joint mobilization techniques are designed to restore the normal gliding of joint surfaces that is necessary for physiologic motion.

Joint Mobilization

Joint mobilization is a manual therapy technique comprising a continuum of skilled passive movements to the joints and related soft tissues that are applied at varying speeds and amplitudes, including a small-amplitude, high-velocity therapeutic movement.[24] Joint mobilization is used to reduce pain and to restore accessory joint motion (joint play) of a hypomobile joint. Restoring normal joint play is necessary to restore full physiologic motion of the joint. Joint mobilization by use of sustained movements increases the extensibility of tight capsules and ligaments that limit mobility of the joint surfaces. Joint mobilization can also be used to reduce pain and spasm. These techniques are typically small-amplitude, oscillatory motions that stimulate joint mechanoreceptors to inhibit the perception of pain. Joint mobilization techniques may also reduce pain by stimulating movement of synovial fluid and preventing fluid stasis. Proper application of joint mobilization techniques requires grading of the forces that are used. The Maitland or Australian system[41] uses oscillatory techniques. Techniques are graded I through V. Grade I oscillations are small-amplitude movements at the beginning of the available range of motion. Grade II oscillations are large-amplitude motions performed within the available range but not up to the motion barrier. Grade III oscillations are large-amplitude motions performed up to and beyond the motion barrier. Grade IV oscillatory movements are small movements performed at and beyond the motion barrier. Grade V mobilization is a high-velocity small-amplitude motion that is used to restore the final few degrees of motion of the joint, to alter positional relationships, to break adhesions, or to stimulate joint receptors, which in turn reduces pain. Grade V mobilization is synonymous with manipulation of a joint ( Fig. 8A-4 ). The Kaltenborn or Norwegian system uses sustained

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Figure 8-A-3 (Figure Not Available) A, Representation of gliding. The same point on one surface comes into contact with new points on the opposing surface. B, Representation of rolling. New points on one surface contact the new points on opposing surface. (Modified from Kisner C, Colby LA: Therapeutic Exercise: Foundations and Techniques, 3rd ed. Philadelphia, FA Davis, 1996.)

mobilization techniques.[29] This system has three grades of motion. Grade I motion, also called piccolo motion, separates the joint surfaces just enough to equalize intra-articular and atmospheric pressure and is typically used to decrease pain. Grade II motion, or slack technique, removes the slack from the capsule and surrounding ligaments and can be used as a trial treatment to increase range of motion in the subacute stage of inflammation. Grade III motion, or stretch technique, uses sufficient force to stretch joint structures to improve mobility. Proper application of joint mobilization techniques requires a thorough examination of the involved joint to determine what tissues are limiting motion as well as the stage of

inflammation. The mobilizing force should be correlated with the sequence of pain to resistance of motion. Pain that occurs before resistance to motion is reached indicates an acute condition. Mobilization for acute conditions consists of grade I or grade II oscillating techniques to decrease pain and maintain joint play. Pain synchronous with resistance to motion indicates a subacute condition. A trial of gentle stretching is used for subacute conditions. Maitland or Kaltenborn grade II mobilization techniques are appropriate for subacute conditions. Pain engaged after resistance to motion has been encountered is indicative of a chronic condition. Vigorous stretching is indicated for chronic conditions. Joint mobilization techniques for chronic conditions include primarily Maitland grade III or grade IV or Kaltenborn grade III techniques. When joint mobilization is performed, the athlete should be positioned to promote relaxation and stabilization of the part to be mobilized. Mobilization is initially performed with the joint in the position in which the capsule has the greatest amount of laxity. This position generally occurs in the middle of the available range of motion. As range of motion improves, joint mobilization techniques can be performed in the restricted position. Forces should be applied as close to the opposing joint surfaces as possible. The area of contact with the hand should be as large as possible to improve the patient's comfort. The force of the mobilization technique is graded according to the stage of the condition and the intended goals of treatment as described before. The direction of movement is dictated by the direction of the restricted motion and the shape of the joint surface. The treatment plane is a plane perpendicular to a line from the axis of rotation to the center of the concave joint surface (Fig. 8A-5 (Figure Not Available) ). When joint surfaces are distracted, the force should be applied perpendicular to the treatment plane. With gliding joint surfaces, the forces should be applied parallel to the treatment plane, using the convex-concave rule. According to the convex-concave rule, concave joint surfaces should be glided in the direction of the limited swing of the bone, whereas convex surfaces should be glided in the direction opposite the limited swing of the bone. In performing joint mobilization techniques, angular motion of the bone should be minimized. Angular motion during gliding of joint surfaces may result in compression of the joint surfaces, which may damage the articular surface. Oscillatory joint mobilization techniques are performed at a rate of 1 or 2 cycles/second for 1 to 2 minutes. Sustained joint mobilization techniques are sustained for 5 to 15 seconds and repeated 10 times. Joint mobility and range of motion are assessed at the completion of joint mobilization. The athlete should also perform range of motion and stretching exercises as a follow-up treatment to joint mobilization. The athlete should be warned that it

Figure 8-A-4 Grading system for joint mobilization/manipulation. A, Normal range of motion (ROM) available for a given joint. B, ROM available for a joint with restricted motion. The motion barrier represents resistance to motion engaged near the end of the motion. Motion beyond the motion barrier is achieved with overpressure. C, Grade I motionsmall-amplitude movement at the beginning of the range. D, Grade II motionlarge-amplitude motion within the available range but not up to the motion barrier. E, Grade III motionlarge-amplitude movement up to and beyond the motion barrier. F, Grade IV

motionsmall-amplitude motion at and beyond the motion barrier. G, Grade V motionhigh-velocity, small-amplitude motion performed beyond the motion barrier. (From Irrgang JJ: Rehabilitation. In Fu FH, Stone DA [eds] Sports Injuries. Baltimore, Williams & Wilkins, 1995, pp 81-95.)

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Figure 8-A-5 (Figure Not Available) Treatment plane (T.P.) is a line perpendicular to the line drawn from the axis of rotation for a joint to the center of a concave joint surface. Forces to distract the joint are applied perpendicular to the treatment plane. Forces to glide the joint are applied parallel to the treatment plane. (Modified from Kisner C, Colby LA: Therapeutic Exercise: Foundations and Techniques, 3rd ed. Philadelphia, FA Davis, 1996.)

is common to experience some increase in soreness; however, this should subside within several hours. Joint mobilization techniques should be used only when mobility testing reveals decreased joint play. Joint mobilization is contraindicated with hypermobile joints. Joint mobilization techniques that stretch the joint capsule are contraindicated during the period of active inflammation. During this period, joint mobilization will aggravate inflammation. Joint mobilization is also contraindicated in the presence of a large joint effusion in which the capsule is already stretched because of distention of the joint. Use of mobilization techniques after fractures should be delayed until there is radiographic evidence of union. Neurophysiologic Stretching

The neurophysiologic properties of contractile tissue must also be considered in attempting to increase range of motion limited by musculotendinous structures. The muscle spindle is a sensory organ sensitive to muscle lengthening. Quick stretching of the muscle results in lengthening of the muscle spindle and initiation of the monosynaptic stretch reflex. Consequently, sudden or ballistic stretching of musculotendinous units may cause the muscle to contract while it is being lengthened, thus resulting in increased soreness after ballistic stretching. Another sensory organ, the Golgi tendon organ, is found in the musculotendinous junction; it is sensitive to tension caused by passive stretching or active contraction of the musculotendinous unit. Excessive musculotendinous tension causes the Golgi tendon organ to discharge, inhibiting contraction. Reciprocal inhibition occurs when the opposing muscle is inhibited as a muscle contracts. These neurophysiologic principles can be incorporated to relax muscles before elongation, allowing the contractile component to be lengthened more easily; however, they generally do not result in a permanent increase in length. Examples of neurophysiologic stretching are contract-relax and contract-relax-contract techniques. Contract-relax stretching techniques involve isometric contraction of the tight muscle followed by lengthening of the muscle. The prestretch contraction of the short muscle

results in autogenic inhibition of the muscle as the Golgi tendon organ is stimulated, allowing the shortened muscle to lengthen. As an example, a contract-relax stretching technique for the hamstrings incorporates contraction of the hamstrings by simultaneous hip extension and knee flexion followed by passive lengthening of the hamstrings after the contraction. Contract-relax-contract stretching techniques incorporate an isometric contraction of the tight muscle followed by relaxation and contraction of the opposing muscle while the tight muscle is lengthened. Contract-relax-contract stretching techniques combine autogenic inhibition with the principle of reciprocal inhibition. Reciprocal inhibition results in inhibition of the antagonist muscle when the agonist is contracted. As an example, a contract-relax-contract technique to lengthen the hamstrings incorporates contraction of the hamstrings by simultaneous hip extension and knee flexion followed by relaxation of the muscle and contraction of the quadriceps and hip flexors while the hamstrings are lengthened. Muscle Function

Rehabilitation of athletes frequently incorporates resisted exercises to address impairments of muscle performance, such as strength, work, power, and endurance. These terms are often misused when they are applied to exercise and muscle performance. Strength is defined as the maximal amount of force a muscle can generate for a given type and speed of contraction.[32] [34] Force is an action that tends to change the state of rest or motion of matter.[34] [44] It is a linear quantity measure that is measured in newtons. When a muscle exerts force on the skeleton, it produces rotation about an axis.[34] [44] Torque is a rotational measure and is equal to the product of the force multiplied by the perpendicular distance from the line of action of the force to the axis of rotation. In assessing strength or force generated by a muscle acting on the bony skeleton, one is measuring torque. Work, power, and endurance are often included in the discussion of strength. Work is force expressed through a distance with no limitation on time. [34] For linear motion, work is the product of force multiplied by distance; for rotational movements, work is equal to the product of torque multiplied by distance. Power is the rate of doing work or work per unit of time.[34] It can also be expressed as a product of force times velocity. Power should not be confused with torque generated at a high-contractile velocity. Maximal power is generated at intermediate contractile velocities.[34] Endurance is the ability of a muscle or muscle group to generate force or work over time without fatigue. Muscle endurance can be quantified as the length of time that a contraction can be maintained or as the number of repetitions that can be performed at particular force or power level through a specified range of motion.[32] As endurance improves, the muscle is capable of performing a greater number of contractions or holding against a load for a longer time. Strength versus Endurance Exercises

Strength training exercises are designed to increase the maximal force that a muscle

can generate. Traditionally,

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strength training involves heavy-resistance, low-repetition exercise. The definition of heavy resistance varies for individuals and from muscle group to muscle group. In general, heavy resistance is considered to mean the amount of weight that can be lifted for 6 to 12 repetitions before fatigue develops. Strength training exercises using heavy resistance are typically performed for 6 to 12 repetitions. Response to strength training includes hypertrophy of muscle fibers. The increased cross-sectional area of muscle fibers is related to increased contractile protein and the number of fibrils within the muscle fiber as well as to increased density of the capillary bed surrounding individual muscle fibers. Hypertrophy may also be related to an increase in the connective tissue component of muscle. Heavy-resistance training appears to hypertrophy fast-twitch (type II) muscle fibers selectively. Hyperplasia is an increase in the number of muscle fibers that results from longitudinal splitting of muscle fibers. Hyperplasia has been observed in laboratory animals exposed to heavy-resistance exercise[21] [22] [23] ; however, hyperplasia is controversial in humans. In response to strength training, individuals are able to recruit an increased number of motor units. Improved generation of muscle force may also be related to improved recruitment and synchronization of motor units. This may explain increases in strength early in the training program in the absence of hypertrophy. Biochemical changes associated with strengthening are small and inconsistent. Endurance training makes use of low- to moderate-resistance high-repetition exercises. Endurance training results in peripheral and central adaptations that improve an individual's ability to sustain work. The peripheral adaptations are localized to the muscle or muscles involved in the endurance training exercises. The peripheral responses generally improve oxidative capacity of the muscle fiber. This is a result of an increased concentration of myoglobin within the muscle fibers. Increased myoglobin concentration aids in the delivery of oxygen from the cell membrane to mitochondria. Endurance training also improves oxidation of carbohydrates and fats within the muscle fiber. This is the result of an increase in the size, number, and membrane surface area of mitochondria as well as of an increase in the concentration and activity of oxidative enzymes. The intramuscular stores of adenosine triphosphate and creatine phosphate also increase with endurance training. There appears to be selective hypertrophy of slow-twitch (type I) muscle fibers; however, this may be modified by the intensity of the endurance exercise. High-intensity endurance training (>90%) results in improved endurance capabilities in type II fibers. [20] [25] Anaerobic glycolysis is not appreciably affected by endurance training. Cardiovascular responses to endurance training occur if the training stimulus is sufficient. In general, the cardiovascular response to endurance training is increased cardiac output related to increased stroke volume. Resting heart rate and heart rate at a

given workload decrease in response to endurance training. Factors That Influence Muscle Strength

Strength of normal muscle is influenced by several factors. The amount of force that a muscle can generate is related to its cross-sectional size. Length of the muscle also influences force generation. According to the length-tension relationship, muscle can generate maximal force at its resting length. This is the position at which there is a maximal number of cross-bridges between the actin and myosin filaments. As the muscle shortens, greater overlap of the actin-myosin filaments results in a decreased number of cross-bridges. Because of this, the force that a muscle can generate in a shortened position is decreased. The contractile force generated by a muscle also decreases as the muscle is lengthened beyond its resting position. There is increased force, however, because of passive lengthening of the connective tissue. Therefore, the total force produced by the musculotendinous unit (including both contractile and noncontractile forces) increases as the muscle lengthens ( Fig. 8A-6 ). The number of motor units recruited also influences the level of force generated. The level of force increases as the number of motor units recruited increases. According to Henneman's size principle, small motoneurons are recruited before large motoneurons. Small motoneurons innervate slow-twitch (type I) muscle fibers. These fibers produce low levels of force and are resistant to fatigue. Large motoneurons innervate fast-twitch (type II) muscle fibers. Fast-twitch muscle fibers produce high levels of force, but they fatigue rapidly. Because small motoneurons are recruited before large motoneurons, activities involving low levels of muscle tension are produced primarily by slow-twitch muscle fibers. As force requirements increase, progressively more fast-twitch fibers are recruited. The speed and type of muscle contraction also influence the amount of force that a muscle can generate. During a concentric contraction, the muscle shortens as it contracts, whereas during an eccentric contraction, the muscle lengthens as it contracts. Concentric contractions occur when the internal force created by the muscle is greater than the external resistance that is applied. Conversely, eccentric

Figure 8-A-6 Relationship of contractile and noncontractile tension to total tension of a muscle. Contractile tension is greatest at the resting length for a muscle. As the muscle is shortened or lengthened, contractile tension decreases. Noncontractile tension increases as the muscle is lengthened. Total tension produced by a muscle is the sum of contractile and noncontractile tension. (From Irrgang JJ: Rehabilitation. In Fu FH, Stone DA [eds]: Sports Injuries. Baltimore, Williams & Wilkins, 1995, pp 81-95.)

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contractions occur when external resistance overcomes the internal resistance created by the muscle. Concentric contractions are necessary to accelerate the body, and eccentric contractions are necessary for deceleration. For concentric contractions, the

torque created by the muscle decreases as the speed of contraction increases. During an eccentric contraction, however, the torque created by the muscle increases as the speed of lengthening increases up to some maximal value ( Fig. 8A-7 ). This is believed to result from facilitation of the stretch reflex and stretching of the connective tissue component within the musculotendinous unit, both of which give rise to increased muscle tension with increased speed of lengthening. A maximal eccentric contraction produces greater force than a maximal isometric contraction, and a maximal isometric contraction produces greater force than a concentric contraction. If performed inappropriately, eccentric exercise is associated with increased muscle soreness and increased injury. Stanish and colleagues[57] suggested in 1986 that eccentric exercise should be incorporated into the treatment of tendinitis. Alfredson and coworkers[1] demonstrated that a greater number of individuals with chronic Achilles tendinitis who completed a 12-week eccentric training program were able to return to their preinjury levels of function compared with control subjects who did not receive eccentric training. The mechanism for the positive effects of eccentric training in the rehabilitation of tendinitis is unclear. It is thought that eccentric training may serve to lengthen the musculotendinous unit, thus decreasing the imposed load during physical activity. Another hypothesis is that eccentric training leads to greater hypertrophy and increased tensile strength of the tendon, thus facilitating the tissue remodeling process after injury.[57] The ability of eccentric training to prevent these types of injuries is not known. A final factor that can influence the ability of a muscle to generate force is motivation. The individual must be willing and motivated to put forth maximal effort to generate maximal forces.

Figure 8-A-7 Force-velocity relationship for muscle. For concentric contraction, force decreases as the speed of shortening increases. For eccentric contraction, force increases up to some maximum value as the speed of lengthening increases. (Modified from Curwin S, Stanish WD: Tendinitis: Its Etiology and Treatment. Lexington, Mass, DC Heath and Co, 1984.) Techniques to Improve Muscle Function

Exercise to improve muscle function can take one of several forms. These exercises can be classified as static or dynamic exercise. Static exercise is isometric exercise in which no observable joint movement occurs. The length of the muscle appears to be constant; however, there is shortening at the sarcomere level. An isometric contraction occurs when torque produced by the muscle is equal to the external resistance. Dynamic resisted exercise results from voluntary contraction of muscles. Active resistance exercises are those exercises in which the individual uses voluntary muscle contraction to move against an applied external resistance. Active resistance exercises include isotonic and isokinetic exercises. Specificity of the exercise must be considered in designing a resistance exercise program. This means that the exercise program must be designed to strengthen the

muscle or muscle groups in a manner that is specific to the way the muscle functions during activity. The speed of the exercise should match the speed of the functional movement. The resistance exercise program should also reproduce the type of contraction required during function. Isometric exercises are used to develop muscles that stabilize the body or a body segment. Concentric exercises are used to develop muscles that are responsible for acceleration, whereas eccentric exercises are used to develop muscles that are responsible for deceleration of the body. Specificity of the exercise program should also consider the intensity of force required by the muscles during activity. The exercises should be performed through the entire range of motion in which strength is required. Isometric Exercises

Isometric exercises are a form of resisted exercise in which the muscle contracts without an appreciable change in the length of the muscle or visible joint motion. Because isometrics occur in the absence of joint motion, isometric exercises can be used when motion is contraindicated. They are also easy to perform and require little equipment. Until recently, it was thought that isometric exercises develop strength only at the position at which the exercise is performed, and the exercises had to be performed in 15- to 30-degree increments to develop strength throughout the full range of motion. Bandy and Hanten[2] demonstrated that isometric quadriceps exercises result in improvements in strength at angles other than those at which the exercise is performed. Isometric exercises with the muscle in the lengthened position resulted in greater carryover of strength to other angles than did isometric exercises performed with the muscle in the shortened position. Isometric exercises do not significantly improve endurance. When performing isometric exercises, the athlete is instructed to contract the muscle maximally, holding it for 5 to 10 seconds to allow time for development of peak tension. The isometric exercises should be performed at multiple angles to improve strength throughout the range of motion. Submaximal isometrics can also be used to maintain mobility between muscle fibers during the healing phase and to improve circulation through a muscle pumping effect.

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Isotonic Exercises

Isotonic exercises make use of movement against a constant external resistance. They can be performed manually or mechanically to improve strength, power, and endurance. For improvement of strength, the overload principle must be applied, and the muscle must be progressively loaded by increasing resistance or repetitions to make continued improvements in function. Isotonic exercises include both concentric and eccentric exercises. In developing an isotonic exercise program, one must consider the load, repetitions,

sets, and frequency. Load is the amount of resistance used during the exercise. For improvement of strength, the load must be progressively increased. Repetitions are the number of times an exercise is performed in a given bout. The number of repetitions must be progressively increased to improve endurance. Sets are the number of bouts of repetitions that are performed. Many combinations of sets and repetitions can be used to improve strength and endurance. Strength is generally improved by lifting heavy amounts of weight for 3 to 5 sets of 6 to 12 repetitions. For exercises designed to improve strength, heavy resistance is defined as the amount of weight that can be lifted for 6 to 12 repetitions. As strength improves, the amount of resistance must be progressively increased. For endurance to be increased, multiple high-repetition sets should be performed with light to moderate resistance. Frequency is the number of times the exercises are performed per day or week. Early in rehabilitation, isotonic exercises are usually submaximal and can be performed several times daily. As rehabilitation progresses to reconditioning, the isotonic exercises should become more vigorous, but it should be performed less frequently to allow adequate time for recovery to prevent fatigue. Most heavy resisted exercise programs designed to improve strength are done every other day. Six weeks may be required for improved strength to be seen. Variable-resistance exercise machines have been developed in an attempt to provide a variable resistance pattern that matches the torque curves produced by a particular muscle or muscle group. For variable-resistance exercise, the resistance is not accommodating and the speed is not controlled. Isokinetic Exercises

Another type of resisted exercise that has increased in popularity during the past 20 years is isokinetic exercise. Isokinetic exercise involves movement at a constant speed. During isokinetic exercise, the speed of exercise is typically controlled by an isokinetic dynamometer. Most dynamometers allow concentric and eccentric exercise from 0 to 450 degrees/second. During isokinetic exercise, the resistance is accommodating and proportional to the effort put forth by the athlete. Research indicates that there may be some carryover of training from one speed to another. To ensure improvement in muscle performance across the spectrum of speeds, however, isokinetic training should be performed at a variety of contractile velocities.[9] Ideally, the speed of exercise selected for isokinetic training is comparable to the speed of movement required during function. The angular velocity during function typically exceeds the speed of movement permitted by the isokinetic dynamometer, however. Caution must be used in performing isokinetic exercise to ensure that further inflammation or injury does not occur. Inappropriate use of isokinetic exercise can be detrimental. During the earlier phases of rehabilitation, isokinetic exercise should be submaximal. Maximal isokinetic exercise should be reserved for the final stages of rehabilitation. Isokinetic testing has been used to measure muscle performance and to determine when an athlete is ready to return to full activity. There is little scientific evidence to validate the use of isokinetic testing for predicting the ability to return to athletic function, however. Intensity of Resistance Exercise

The intensity of exercise depends on the stage of inflammation and healing as well as

on the goals of the exercise program. In general, submaximal exercises are used to increase muscle endurance. They are emphasized during the early stages of rehabilitation to protect healing tissues and to avoid pain and further aggravation of the injury. Exercises with maximal resistance are used in the later stage of rehabilitation when the goal is to recondition the athlete to improve strength and power. Several specific exercise regimens to improve strength have been proposed. DeLorme and Watkins[11] proposed a technique of progressive resistance exercises that begins by establishing a 10-repetition maximal weight. This is defined as the amount of weight that can be lifted precisely 10 times; it is usually established by trial and error. In the scheme proposed by DeLorme, 3 sets of 10 repetitions are performed. The first set is against half of the 10-repetition maximal weight. The second set is against three quarters of the 10-repetition maximal weight, and the third set is against the full 10-repetition maximal weight. A new 10-repetition maximal weight is determined each week. The method proposed by DeLorme builds in a gradual warm-up. The Oxford technique[67] is the opposite of the DeLorme method. The first set is performed against the full 10-repetition maximal weight and the third set is performed against half of the 10-repetition maximal weight. This method attempts to accommodate the effects of fatigue; however, warm-up is required before beginning. Knight[33] proposed a program of daily adjustable progressive resistance exercises. The daily adjustable progressive resistance exercise program attempts to determine objectively when and by how much to increase resistance. Knight originally proposed use of a 6-repetition maximal weight, which is the amount of resistance that can be lifted precisely 6 times. Four sets of exercises are performed. The first set of six repetitions is performed with half of the 6-repetition maximal weight. The second set of 6 repetitions is performed with three quarters of the 6-repetition maximal weight. The third set consists of as many repetitions as possible against the full 6-repetition maximal weight. The number of repetitions performed during the third set is used to determine the resistance for the fourth set. If more than 6 repetitions are performed during the third set, the weight for the fourth set is increased; if 4 or fewer repetitions are performed for the third set, the weight

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for the fourth set is decreased. The weight is kept the same if 5 or 6 repetitions are performed. The number of repetitions performed during the fourth set determines the amount of weight used for the next session. If 5 or more repetitions are performed during the fourth set, the weight for the next session is increased; if 2 or fewer repetitions are performed for the fourth set, the weight for the next session is decreased. The weight is kept the same if 3 or 4 repetitions are performed. The methods proposed by DeLorme and Knight and the Oxford technique make use of heavy-resistance, low-repetition exercise in an attempt to increase strength. In this case, heavy resistance is operationally defined as the amount of resistance that can be

lifted 6 to 10 times. Heavy-resistance exercise may be inappropriate for the early stages of healing. Heavy resistance may not be tolerated by the joint and the healing structures during this time. Therefore, during the early phases of healing, exercises using submaximal resistance for a greater number of repetitions may be performed. We commonly use resistance that can be performed for 30 to 50 repetitions during the early phase of healing. Heavy-resistance exercises are delayed until the athlete enters the reconditioning phase of rehabilitation. Isotonic exercises can be performed mechanically or manually. Mechanical resisted exercises have several advantages. The amount of resistance and the number of repetitions performed can be used to quantify the patient's baseline level of muscle performance and progression. In addition, athletes can see their progress when they are performing mechanically resisted exercise. This visible progress provides motivation. Resistance applied during mechanically resisted exercises is not limited by the strength of the athletic trainer or therapist. A variety of equipment provides mechanically resisted exercises. During manually resisted exercises, resistance is applied by the therapist or athletic trainer. Manually resisted exercise can make use of dynamic or static muscle contractions and can be performed in the cardinal planes or in more functional diagonal patterns. Proprioceptive neuromuscular facilitation is a technique of manually resisted exercise that emphasizes movement in diagonal patterns. Other Issues Related to Strength Training

Open versus Closed Chain Resistance Exercise.

When possible, functional exercise patterns should be used to develop strength. This implies the use of closed chain activities for the lower extremity and open chain activities for the upper extremity. During open chain activities, the distal extent of the extremity is free to move. Movement is produced by contraction of the agonist muscle. During closed chain activities, the distal aspect of the extremity is fixed, and motion occurs simultaneously at all joints that compose the kinetic chain. Movement is produced by co-contraction of muscles. Closed chain exercise simulates functional demands placed on the extremity during a variety of activities. Stability is enhanced as a result of increased joint compression and muscle co-contraction during closed chain activities. Although closed chain exercise may be attractive because of its ability to simulate functional activities, it may not provide an optimal stimulus for strength gains. For example, Ninos and colleagues[47] found that electromyographic activity of the quadriceps is only 25% to 30% of the electromyographic activity produced during a maximal voluntary isometric contraction when a squat is performed with 25% of body weight applied to the shoulders. Thus, high resistance must be used to increase strength of the quadriceps when performing closed chain exercises for the lower extremity. As noted before, the joint may not tolerate this high level of resistance during the early phases of healing. Strengthening of the quadriceps should therefore make use of a combination of open and closed chain exercises.

Safety.

Several precautions must be observed with respect to the use of resisted exercise in rehabilitation programs for athletes to minimize the risk for injury. Contraindications to resisted exercise include active inflammation and pain. Use of resisted exercise in the presence of active inflammation can lead to further tissue trauma and aggravate pain and swelling. Resisted exercises should be eliminated or reduced if they produce an increase in pain that persists more than several hours after exercise. One significant precaution in performing resisted exercises is avoidance of a Valsalva maneuver, which may cause a transient but marked increase in blood pressure that places abnormal stress on the cardiovascular system. Exercise-induced arterial hypertension from the Valsalva maneuver during heavy-resistance exercise may be a risk factor for an acute stroke in healthy young adults.[46] During resisted exercise, systolic blood pressure is often in excess of 200 mm Hg, depending on the force and length of the Valsalva maneuver. Narloch and Brandstater [46] found lower mean blood pressures during execution of the double-leg press at both 85% and 100% of the 1-repetition maximal weight when subjects slowly exhaled during the concentric contraction than when they had a closed glottis. Athletes should thus be warned to avoid use of the Valsalva maneuver. They should specifically be instructed to exhale during the forced phase of the movement, regardless of the movement's direction or anatomic position. In other words, they should exhale during the sticking phase, or the most difficult part of the lift. This is known as the principle of biomechanical matching of breathing phases.[66] Prolonged resisted exercises result in local muscle fatigue and total body fatigue. Local muscle fatigue is a diminished response of a muscle to sustain work. The fatigue may be due to disturbances in the contractile mechanism of the muscle, including decreased energy stores, insufficient oxygen, and lactic acid accumulation. Local muscle fatigue may also result from inhibitory influences from the central nervous system, pain, and discomfort. Total body fatigue occurs in response to prolonged resisted exercises and may result from decreased blood glucose concentration or depletion of muscle or liver glycogen. No biologic marker of overtraining exists. Adequate time in the training program must be included for recovery from vigorous exercise to avoid fatigue. Recovery is associated with a removal of lactic acid and with replenishment of energy and oxygen stores. Light exercise may facilitate recovery, and recovery after each exercise session is required to improve performance. This requirement has implications for rehabilitation, particularly in the later stages,

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when the intensity of exercise is increased and more time for recovery is required from session to session. Resisted exercises may also cause muscle soreness. Immediate muscle soreness

develops during or directly after strenuous exercise. It may be related to muscle ischemia or the buildup of metabolites. Muscle soreness of immediate onset generally subsides quickly with rest after exercise. By contrast, delayed-onset muscle soreness develops 24 to 48 hours after vigorous exercise. Numerous causes have been postulated, none satisfactory. Accumulation of lactic acid in the muscle was one of the postulated causes; however, lactic acid is cleared approximately 1 hour after exercise. The reflex pain-spasm theory as proposed by DeVries[12] held that ischemia produces pain that in turn produces a reflex muscle spasm. A positive feedback loop develops as spasm creates further pain and ischemia. The original evidence for this theory included increased electromyographic activity from muscles with delayed muscle soreness; however, this evidence has not been duplicated by others. Currently, the most plausible explanation for delayed-onset muscle soreness is microscopic tearing of muscle or connective tissue during vigorous exercise. Disruption of tissue results in inflammation and pain. This theory is supported by the observation that delayed-onset muscle soreness is more common after eccentric exercise. Micro-tearing of muscle and connective tissue may be more pronounced as the muscle lengthens against resistance. Prevention of delayed-onset muscle soreness includes an appropriate period of warm-up and cool-down before and after the resisted exercise. In addition, delayed-onset muscle soreness may be prevented by a gradual progression of the resisted exercise program and the avoidance of the eccentric component of exercise. The athlete performing resisted exercises must be observed carefully for detection of substitute motions, that is, alternative motions or muscles complete the motion when the prime movers are weak or fatigued. Use of substitute motion allows muscle weakness to persist. Substitute motions can be avoided by using appropriate amounts of resistance and instructing the athletes to perform the exercise precisely. Proprioception and Neuromuscular Control

Once adequate strength and endurance of the musculature have been established, it is necessary to incorporate activities to improve proprioception and neuromuscular control for improvement of dynamic stability. There has been interest in the role that these factors play in the rehabilitation and prevention of injuries. It has been hypothesized that proprioception is important for providing smooth, coordinated movement as well as protection and dynamic stabilization of joints. Neuromuscular training after injury requires the individual to learn how to recruit muscles with the proper force, timing, and sequence to prevent abnormal joint motion. To understand the role that proprioception and neuromuscular control play in the maintenance of joint integrity, a brief anatomic review is provided. Anatomic Basis of Neuromuscular Control

Proprioception has been characterized as a specialized variation of touch, including the ability to detect both joint motion and joint position.[40] It is important to distinguish this term from kinesthesia, which traditionally refers only to the ability to sense joint motion.[38] Proprioception occurs by a complex integration of somatosensory input (both

conscious and subconscious) from a variety of mechanoreceptors. It contributes to an athlete's neuromuscular control, which can be defined as the coordination and timing of muscle firing in response to an applied load. There are basically three classes of peripheral mechanoreceptors that have been delineated in the literature, including muscle receptors, articular (joint) receptors, and cutaneous (skin) receptors.[40] These mechanoreceptors, which respond to mechanical deformation, signal information about the tissues in which they lie to the central nervous system, modulating the overall state of the neuromuscular system. Afferent signals synapse in the dorsal horn of the spinal cord and then directly, or through interneurons, synapse on alpha motoneuron pools, which relay control information back to the periphery. Afferent information is also processed and modulated at other control centers in the central nervous system (e.g., brain stem, cerebellum, cortex). All three types of mechanoreceptors have an interactive role in the maintenance of joint stability. Mechanoreceptors have been identified in the ankle,[65] in the knee,[10] [30] [35] [49] [52] and in the shoulder.[59] [60] Joint receptors are commonly located in the connective tissue of the joint capsule and ligaments. Specifically, they have been identified in the joint capsules, ligaments, menisci, labrum, and fat pads. Four types of joint mechanoreceptors have been described. [28] [65] Type I mechanoreceptors are Ruffini-like receptors that have a low mechanical threshold for activation yet a slow adaptation to the deformation. These characteristics make them uniquely qualified to detect static joint position, amplitude, and velocity of movement. Type II mechanoreceptors are pacinian corpusclelike receptors that have a low threshold for excitation and adapt rapidly. They are responsible for signaling acceleration and deceleration of the joint. Type III mechanoreceptors are similar to Golgi tendon organs that lie in the musculotendinous unit. They have a high threshold for excitation and are nonadapting. They respond at the extremes of motion and may be responsible for mediating protective reflex arcs. Type IV mechanoreceptors are free nerve endings that convey pain. Muscle receptors primarily consist of muscle spindles and Golgi tendon organs. The muscle spindle helps regulate the smooth, precise control of muscle activity. Muscle length and velocity of movement are detected by primary and secondary afferent fibers that are intimately entwined in specialized intrafusal muscle fibers (as opposed to the predominant extrafusal fiber type). Primary afferent (type I) fibers sense the degree and rate of stretch in the muscle, whereas secondary afferent (type II) fibers detect primarily the degree of stretch. This information is relayed to the central nervous system, where it is processed, integrated, and modulated in the spinal cord, brain stem, cerebellum, cortex, and other control centers. Once the information is processed, the appropriate regulatory response is transmitted back to the muscle through efferent alpha and gamma

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motoneurons that stimulate extrafusal and intrafusal muscle fibers, respectively, helping to maintain precise control of movement. The muscle stretch reflex at the knee is a classic representation of this mechanism occurring at the spinal cord level.

The Golgi tendon organ, on the other hand, responds to increases and decreases in muscle tension by allowing the muscle to stretch and shorten, respectively. Together, the muscle spindle and Golgi tendon organ assist with the precise regulation of movement. Some investigators have hypothesized that the muscle spindle system may be the most significant component of the neuromuscular system during normal activities of daily living.[17] [18] [42] [43] This is because joint receptors contribute sensory information primarily at the end of the available joint motion, positions that do not typically occur during normal activities. The muscle spindle system is persistently active during ambulation, for example, to facilitate smooth limb progression during the gait cycle. Joint receptors are likely to play a much more significant role in athletic performance, however, in which the extremes of joint excursion are more likely to occur. Function of the Neuromuscular Control Mechanism

Research has demonstrated that mechanoreceptors play an important role in joint stabilization through both feedback and feedforward control paradigms. The feedback mechanisms are mediated by numerous protective reflexes that continuously update muscle activity. For example, slight deformation in the knee ligaments has been demonstrated to evoke a marked increase in activity of muscle spindle afferents, which set the joint in its functional context.[28] Kim and associates[31] demonstrated that stimulation of the knee collateral ligaments results in a contraction of muscles about the knee. Furthermore, Solomonow and colleagues[56] and Buchanan and coworkers[7] elicited a muscle response with stimulation of the anterior cruciate ligament (ACL) and with an applied varus and valgus load at the knee, respectively. Solomonow and colleagues[56] described an ACL-hamstring arc in anesthetized cats. High loading of the ACL resulted in increased electromyographic activity in the hamstrings with electrical silence in the quadriceps. The increase in hamstring electromyographic activity was not evident when light to moderate loads were applied to the ACL. It was proposed that this ACL-hamstring reflex arc serves to protect the ACL during high loading conditions. It is unknown whether this reflex arc can protect the joint from injury if high loads are applied rapidly, however. Under rapid loading conditions, the ligament may be loaded and ruptured before sufficient muscle tension can be generated to protect the ligament. It is likely that similar reflex arcs exist in other joints. Other proprioceptive reflexes originating from the joint capsule or musculotendinous unit probably exist. This was demonstrated by Solomonow and colleagues, [56] who reported increased hamstring electromyographic activity in a patient with an ACL-deficient knee during maximal slow-speed isokinetic testing of the quadriceps. The increased electromyographic activity occurred simultaneously with anterior subluxation of the tibia at approximately 40 degrees of knee flexion and was associated with a sharp decrease in quadriceps torque and electromyographic activity. Because the ACL was ruptured, reflex contraction of the hamstrings could not have been mediated by receptors originating in the ACL. It was proposed that this reflex contraction was mediated by receptors in the joint capsule or hamstring muscles. It is likely that similar reflex arcs exist in other areas of the body. Although feedback mechanisms have traditionally been considered the primary

mechanism of neuromuscular control, feedforward mechanisms also play an important role in the maintenance of joint stability. The feedforward mechanism of neuromuscular control is characterized by the use of proprioceptive information in preparation for anticipated loads or activities that will be encountered. This mechanism suggests that an internal construct for joint stability is developed that undergoes continuous updates on the basis of previous experience under known conditions. This preparatory information is then coupled with real-time proprioceptive input to generate preprogrammed motor commands to achieve a desired outcome.[13] [19] [36] Several clinical studies have evaluated proprioception in terms of the threshold to detection of passive motion and reproduction of joint position. Barrack and coworkers [3] demonstrated deficits in the threshold to detection of passive motion in subjects with a unilateral ACL-deficient knee. Lephart and associates[39] studied the threshold to detection of passive motion in patients who had undergone ACL reconstruction. Testing was performed at 15 degrees and 45 degrees of flexion. Three trials were performed moving into flexion and extension. The results indicated that threshold to detection of passive motion was less sensitive in the reconstructed knee than in the noninvolved knee. In addition, threshold to detection of passive motion was more sensitive in the reconstructed and normal knee at 15 degrees of flexion compared with 45 degrees of flexion. The enhanced sensitivity to passive motion near full extension may be due to increased stress on the ligament, making it more sensitive to detect motion. Kinesthetic deficits in the shoulder in patients after anterior glenohumeral dislocation were demonstrated by Smith and Brunolli.[54] They found deficits in angular reproduction, threshold to detection of motion, and end-range reproduction of joint angle in the shoulder that had been dislocated. Injury to a joint may result in abnormal sensory feedback and altered neuromuscular control. With a traumatic injury to the knee, for example, it is hypothesized the mechanoreceptors are anatomically disrupted. This causes the joint receptors to aberrantly fire, which leads to impaired neuromuscular control. [40] Others suggest that injuries alter joint motion characteristics; thus, the normal coordination of joint receptor firing is interrupted. [26] Evidence for Neuromuscular Training

Fortunately, there is significant redundancy in the relay of afferent information to the central nervous system. Therefore, after acute injury, individuals should theoretically be able to train their neuromuscular control system, with the hope of restoring the system to a more normal state. The terms proprioceptive training and neuromuscular

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training are often used interchangeably. We use the term neuromuscular training. Neuromuscular training contributes to the improvement of both proprioception and neuromuscular control.

There is some evidence that neuromuscular training can improve neuromuscular control of abnormal joint motion.[4] [27] [64] Ihara and Nakayama[27] studied the effects of a dynamic joint control training program, in which subjects were instructed to resist randomly applied perturbations of support surfaces with their lower extremities, on hamstring muscle reaction times. Four subjects with chronic knee instability received 3 months of training at a frequency of four times per week and were compared with a control group consisting of five subjects without knee injury who did not receive training. Hamstring muscle reaction times were measured indirectly by recording knee flexion movement reaction times and the time to generate peak knee flexion torque in response to passive knee extension motion, provided by a dynamometer. Subjects in the training group exhibited reduced knee flexion movement reaction times and reduced time to generate peak knee flexion torque after training. There were no significant changes in these variables for the control group. In addition, three of the four subjects in the training group were able to return to competitive sports activities after training. The fourth subject was able to return to recreational sports activity. Beard and colleagues[4] conducted a double-blind randomized clinical trial to compare the efficacy of two rehabilitative programs for individuals with ACL deficiency. One group received a neuromuscular training program designed to enhance proprioception and to improve hamstring contraction reflexes. This program consisted of perturbation training techniques, cyclical repetitive lower extremity motions emphasizing speed of movement, mini-trampoline activities, and skipping activities. The second group received a standard program of resisted lower extremity strengthening exercises, step-up exercises, and stationary cycling. An indirect measurement of proprioception represented by reflex hamstring contraction latency was recorded before and after the 12-week course of rehabilitation. The Lysholm Knee Function Scale was used as a self-report measure of knee function. After the training, there was improvement in the reflex hamstring contraction latency and self-reported knee functional score in both groups; however, the improvement in the group that received the neuromuscular training was significantly more than the improvement in the group that received the standard training program. Changes in the reflex hamstring contraction latency were also correlated with the self-reported knee function scores. Wojtys and colleagues[64] compared changes in lower extremity muscle function in 32 healthy volunteer subjects who were assigned to an isokinetic training group, an isotonic training group, an agility training group, or a control group. The agility training program consisted of sliding board activities, box jumping, carioca drills (a lateral running drill that incorporates combined crossover steps and side-steps), figure-of-eight running, and backward running. Muscle reaction times of the quadriceps, hamstrings, and gastrocnemius muscles in response to an externally applied anterior tibial translation load as well as the time to generate peak torque for these muscle groups were used as measures of neuromuscular function. The agility-trained group demonstrated significantly improved reaction times of the quadriceps, hamstrings, and gastrocnemius in response to anterior tibial translation. Perhaps just as important, they found that the reaction time of the medial hamstring and the medial quadriceps muscles in the isokinetic group significantly slowed by 39.1 and 32.4 msec, respectively, after 6 weeks of training. They concluded that isotonic and isokinetic strength training of the lower extremities was not adequate to improve muscle reaction time to anterior tibial

translation, but agility exercises did improve this parameter. More research needs to be conducted to substantiate these findings. There is evidence to suggest that neuromuscular training is a useful adjunct in rehabilitative programs to return athletes to high levels of physical activity. Fitzgerald and colleagues[14] conducted a randomized controlled trial to compare a standard agility training program with an agility training program that was supplemented with a perturbation training program in patients with an ACL-deficient knee that was treated nonoperatively. These individuals were screened on the basis of criteria established by the investigator that could more accurately determine which patients might be candidates for a nonoperative course of treatment. Most of these patients were young, active individuals who tore the ACL during a competitive sport season and wanted to return to play as soon as possible, postponing surgery, if necessary, until after the season was complete. One group of patients was randomized to a standard nonoperative ACL rehabilitation program consisting of open and closed kinetic chain exercises and agility training. The other group was randomized to receive the standard training plus a perturbation training program designed to improve neuromuscular control. Both groups received 12 weeks of rehabilitation. Successful outcome was defined as being able to return to a high level of activity without any episodes of giving way. Subjects in both groups were able to return to premorbid levels of sports activity after training. During a 6-month follow-up period, however, a significantly greater number of subjects who received the perturbation training (11 of 12) were able to complete their athletic seasons without experiencing episodes of giving way compared with subjects receiving only the standard training program (7 of 14). In addition, subjects receiving perturbation training maintained higher scores on self-reported and physical performance measures of knee function than did the standard exercise group at 6 months of follow-up. More patients were successful in the group that received the perturbation training than in the group that received the standard training program alone. Fitzgerald and colleagues [14] hypothesized that the continued ability of the perturbation-trained group to maintain high levels of physical function without experiencing episodes of knee instability may be attributed to the development of adequate lower extremity neuromuscular control mechanisms to maintain dynamic knee stability. Techniques to Improve Proprioception and Neuromuscular Control

Athletes who have sustained an injury to the stabilizing structures of a joint may need to rely on compensatory

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neuromuscular mechanisms to maintain dynamic stability. Therefore, rehabilitation should, in part, promote development of these compensatory muscle activity patterns. Although studies seem to be consistent with regard to the muscles involved in the compensatory patterns used after injury to the knee (i.e., quadriceps, hamstrings, and gastrocnemius muscles), there seem to be differences in the way individuals alter the activity of these muscles to maintain joint stability.[53] Thus, treatment techniques should

be designed to develop individualized compensatory neuromuscular responses to potentially destabilizing loads that may be encountered during functional activities. Several factors need to be considered in planning interventions that are designed to promote compensatory lower extremity neuromuscular responses. Because individuals will encounter a variety of potentially destabilizing forces on the knee during functional activities, it is logical that they be provided with experiences in dealing with these forces during rehabilitation. Treatment techniques should therefore be designed to allow the application of potentially destabilizing loads to the lower extremity in a controlled manner. Another factor to be considered is that destabilizing loads encountered during functional activities usually occur rapidly and without warning, making voluntary neuromuscular responses inadequate for protecting the knee. Treatment techniques should therefore also be designed to promote quick, automatic, protective neuromuscular responses to potentially destabilizing loads by, for example, the application of potentially destabilizing loads to the lower extremity in a quick, random manner during treatment. Finally, it is important to ensure that treatment techniques designed to enhance the development of protective neuromuscular responses to destabilizing loads provide the carryover of learned responses to functional activities. Techniques may be more successful if they are practiced in the context of functional and sport-specific tasks. Several treatment options are available that have the potential for promoting protective neuromuscular responses in the lower extremity to maintain dynamic stability during physical activity. Balance and agility training techniques, such as shuttle runs, cut and spin drills, cariocas, lateral sliding, and balance boards, can provide the patient with experience in dealing with potentially destabilizing loads on the knee during rehabilitation. Wojtys and colleagues[64] reported that subjects who underwent 6 weeks of agility training exhibited improved reaction times in the quadriceps, hamstrings, and gastrocnemius muscle in response to unexpected anterior tibial translation. It seems that agility training techniques may enhance protective neuromuscular responses to potentially destabilizing loads on the knee. Another treatment option for improving neuromuscular control of the lower extremity involves perturbational support surfaces, such as roller boards and tilt boards ( Fig. 8A-8 ). In these techniques, the patient stands on the support surface, on the involved limb, and potentially destabilizing loads are applied to the lower extremity by the therapist through multidirectional perturbations of the roller board or tilt board. The therapist is able to apply the load in a random manner, without warning to the patient, in an attempt to encourage quick, automatic responses to the destabilizing loads. These techniques can also be modified so that patients can experience the perturbations during performance of activity-related tasks, which may also enhance carryover of learned protective responses to functional performance situations. Ihara and Nakayama [27] and Beard and coworkers[4] have shown that hamstring reaction time and functional ability were improved after training with these techniques. Fitzgerald and colleagues[14] reported that ACL-deficient subjects who received perturbation training demonstrated a greater likelihood of success in returning to preinjury-level sports activities than did those subjects who did not receive this type of training as part of the rehabilitation program. These activities generally progress from slow to fast speed, from low to high force, and from controlled to uncontrolled activities. The performance of these activities

initially requires the individual's conscious effort. With practice and repetition, however, control of abnormal joint motion should become automatic and occur subconsciously. Activities in a neuromuscular training program should also be randomly ordered during

Figure 8-A-8 Roller boards (A) and tilt boards (B) can be used to provide a destabilizing force to which the individual must respond.

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training sessions to improve motor learning, thus enhancing long-term carryover. [51] Neuromuscular control is also important for dynamic joint stability in the upper extremity of the athlete. Reactive neuromuscular training that incorporates principles of proprioceptive neuromuscular facilitation may be used to improve neuromuscular control in the overhead-throwing athlete, for example, who is at risk for shoulder instability. Proprioceptive neuromuscular facilitation patterns include techniques such as rhythmic stabilization, which is the application of skilled input from the clinician to facilitate a desired movement pattern. At the shoulder, this may initially consist of slow, regular perturbations with the joint in the resting position, such as in the plane of the scapula with the shoulder in 30 to 45 degrees of external rotation. These techniques can be progressed by employing fast, random perturbations with the joint in the provocative position. At the shoulder of the throwing athlete, this might be conducted with the shoulder in 90 degrees of abduction at the end range of external rotation. The athlete's sport should determine specific activities for the upper extremity. Return to throwing for throwing athletes after injury has been described by Pappas and coworkers,[50] Blackburn and colleagues,[5] and Wilk and associates.[61] Return to throwing should progress from a short-toss program to a long-toss program. Velocity should be increased gradually as tolerated. The functional progression for return to activity must provide the athlete with adequate time to ensure a safe return to sport with minimal risk for reinjury. Further research is required to determine the effectiveness of neuromuscular training for dynamic protection of the injured area.

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Summary We have presented basic guidelines and considerations for rehabilitation of the injured athlete. These principles can be applied to rehabilitation of the common musculo skeletal injuries that occur in athletics. The use of various physical agents and therapeutic exercise in the rehabilitation of the injured athlete has been discussed. Development of a rehabilitation program is a problem-solving process. This requires thorough evaluation of the athlete for development of goals and a plan of care that addresses the impairments, functional limitations, and disability experienced by the athlete. Rehabilitation of the injured athlete at any point in time may focus on any one area or a combination of these areas. The ultimate goal of rehabilitation of injured athletes is to minimize or to eliminate the disability associated with the injury and to return them to their previous level of sports activity.

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biomechanics of the joint. Crit Rev Biomed Eng 18:341-368, 1991. Kaltenborn FM: Mobilization of the Extremity Joints: Examination and Basic Treatment Techniques, 3rd ed. Oslo, Norway, Olaf Norlis, 1985. 29.

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Lephart SM, Giraldo JL, Borsa PA, Fu FH: Knee joint proprioception: A comparison between female intercollegiate gymnasts and controls. Knee Surg Sports Traumatol Arthrosc 4:121-124, 1996. 38.

Lephart SM, Kocher MS, Fu FH: Proprioception following anterior cruciate ligament reconstruction. J Sports Rehabil 1:188-196, 1992. 39.

Lephart SM, Pincivero DM, Giraldo JL, Fu FH: The role of proprioception in the management and rehabilitation of athletic injuries. Am J Sports Med 25:130-137, 1997. 40.

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(ed): Clinics in Physical Therapy: Measurement in Physical Therapy. New York, Churchill Livingstone, 1985, pp 57-102. Nagi SZ: Disability concepts revisited: Implication for prevention. In Pope AM, Tarlov AR (eds): Disability in America: Toward a National Agenda for Prevention. Washington, DC, National Academy Press, 1991, pp 309-327. 45.

Narloch J, Brandstater M: Influence of breathing technique on arterial blood pressure during heavy weight lifting. Arch Phys Med Rehabil 76:457-462, 1995. 46.

Ninos JC, Irrgang JJ, Burdett R, Weiss JR: Electromyographic analysis of the squat performed in self-selected lower extremity neutral rotation and 30 degrees of lower extremity turn-out from the self-selected neutral position. J Orthop Sports Phys Ther 25:307-315, 1997. 47.

Noyes FR, Keller CS, Grood ES, Butler DL: Advances in the understanding of knee ligament injury, repair, and rehabilitation. Med Sci Sports Exerc 16:427-443, 1984. 48.

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Pappas AM, Zawacki RM, McCarthy CF: Rehabilitation of the pitching shoulder. Am J Sports Med 13:223-235, 1985. 50.

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Schultz RA, Miller DC, Kerr CS, Micheli L: Mechanoreceptors in human cruciate ligaments. A histological study. J Bone Joint Surg Am 66:1072-1076, 1984. 52.

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Tabary JC, Tabary C, Tardieu C, et al: Physiological and structural changes in the cat's soleus muscle due to immobilization at different lengths by plaster casts. J Physiol 224:231-244, 1972. 58.

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Washington, DC. Wilk KE, Arrigo C, Andrews JR: Rehabilitation of the elbow in the throwing athlete. J Orthop Sports Phys Ther 17:305-317, 1993. 61.

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Wojtys EM, Huston LJ, Taylor PD, Bastian SD: Neuromuscular adaptations in isokinetic, isotonic, and agility training programs. Am J Sports Med 24:187-192, 1996. 64.

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Section B Open and Closed Chain Exercises (Non-Weight-Bearing and Weight-Bearing Exercises) Russell M. Paine PT Ron M. Johnson PT, MPT, ATC, CSCS With the advent of intra-articular anterior cruciate ligament (ACL) reconstructions using graft materials that require protection during the maturation process, many attempts have been made to describe the effect various exercise conditions have on the healing graft. Old mechanical engineering terminology was used to describe new common rehabilitation exercisesopen kinetic chain and closed kinetic chain exercises. Closed kinetic chain exercises were believed to be safer to the healing graft and to be more functional in nature, but this belief has been challenged. Using mechanical engineering concepts, the kinetic chain concept was described first by Steindler in 1955.[62] Steindler sought to describe various types of exercise conditions with this new concept. The mechanical engineering definition of the kinetic chain describes a series of interconnected

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joints, fixed proximally and distally. In this system, movement of one joint has an effect on all joints above and below. Steindler[62] separated the mechanical engineering definition into two statesopen and closed kinetic chain. He described the open chain state as a peripheral extremity able to move freely, such as waving the hand or the swing phase of the gait pattern. The closed kinetic chain state was described as the distal segment meets considerable resistance,

as it does with a pull-up or squat. Considerable ambiguity exists when describing various exercises by open and closed chain definitions. Confusion sometimes exists when determining what is a true closed kinetic chain state. A more simple and precise description may be weight-bearing (WB) and non-weight-bearing (NWB) exercises and the relationship to the anatomic structureis the ligament loaded or unloaded during the WB exercise? How do these two conditions relate to other anatomic structures, such as the muscles and the patellofemoral joint? Because of the ambiguity of closed and open chain states, this chapter describes more specifically what is occurring to pertinent anatomic structures. Ligament Loading Exercises

Ligament loading exercises are exercises that produce considerable strain and may be harmful to a healing graft after ACL or posterior cruciate ligament (PCL) reconstruction. A strain that causes a disruption of the collagen cross-linking could cause harm to the healing graft. A strain that is so severe that it causes a ligament to pass its yield point leads to collagen elongation and ligament failure. It is difficult to define what level of strain is significant because a low level of strain during collagen cross-linking has been shown to be helpful.[67] Noyes and colleagues[51] determined through observation that the ACL elongates 10% to 15% of its length before failure. Separate investigators determined the ultimate tensile strength of the ACL to handle forces of 1725N and 2160N before failure.[10] [50] The ultimate tensile strength of the PCL has been estimated at 4000N.[55] Tables 8B-1 and 8B-2 list peak loads and strains to the ACL and PCL as TABLE 8-B-1 -- Peak Loads on the Anterior Cruciate Ligament with Common Rehabilitation Exercises Activity Author Mean Peak Loads Weight-bearing Squat Stationary bicycle

Nisell and Ekholm[46]

500N (20 degrees)

Beynnon et al[3]

136N (10 degrees)

Erickson and Nisell[19]

37N (65 degrees)

McCoy and Gregor[42]

125N (70 degrees)

Grood et al[24]

350N (0 degrees)

Lutz et al[39]

285N (30 degrees)

Wilk et al[75]

248N (14 degrees)

Nisell et al (30 degrees/sec) [47]

700N (25 degrees)

Non-weight-bearing Knee extension

Isokinetic knee extension

TABLE 8-B-2 -- Peak Loads on the Posterior Cruciate Ligament with Common Rehabilitation Exercises Activity Author Mean Peak Loads Weight-bearing Squat

Beynnon et al[3]

136N (0 degrees)

[21]

Escamilla et al

1868N (63 degrees)

Lutz et al[39]

538N (90 degrees) [46]

Nisell and Ekholm [65]

Leg press

1800N (130 degrees)

Stuart et al

295N (93 degrees)

Wilk et al[75]

1783N (90 degrees)

[75]

1667N (94 degrees)

Wilk et al

Non-weight-bearing Knee extension Knee flexion

Lutz et al[39]

387N (90 degrees)

Wilk et al

[75]

1178N (91 degrees)

Lutz et al

[39]

1780N (90 degrees)

seen in common rehabilitation exercises. From the biomechanical studies given, the clinician can surmise which exercises may be deleterious to the healing graft. Many authors have reported ACL and PCL load values during NWB resisted knee extension.* It has been concluded that strain on the ACL substantially increases in the last 60 degrees of knee extension.[16] [39] [41] [57] [75] [80] Knee extension exercises performed in ranges of 110 to 60 degrees place dramatically higher loading on the PCL.[16] [39] [75] [80] As seen in Tables 8B-1 and 8B-2 , the peak loads donot approach the ultimate tensile strengths of these ligaments (when healthy). These loads may be deleterious in the early phases of rehabilitation, when the strength of the reconstructed graft is a concern. Studies have been performed on the magnitudes of tibial translation during NWB knee extension. Using varying methods, each of these investigators documented that NWB knee extension elicits significant anterior tibial translation during the terminal degrees of the movement and imposes excessive stress and strain on the ACL. Similarly, many of these studies documented significant posterior tibial displacements when extending the knee from full flexion to approximately 60 degrees against resistance.[2] [3] [29] [34] [35] [48] Resultant posterior tibial translation provides evidence for the stresses placed on the PCL. Researchers have documented the effects of performing NWB isokinetic knee extension exercises. As with NWB isometric or isotonic knee extension activities, increases in anterior tibial translation were seen in the terminal degrees of extension. [34] [35] [47] [71] Nisell and coworkers[47] and Wilk and Andrews[71] reported significantly higher anterior-directed shear forces with a more distal pad placement (versus a single,

proximally placed pad). Wilk and Andrews[71] documented significantly higher anterior tibial displacement at lower isokinetic speeds (60 degrees/second compared with 180 and 300 degrees/second). Numerous authors have documented resultant shear forces during NWB knee flexion. Each investigator reported posterior shear forces throughout the entire range of NWB knee flexion.[2] [3] [16] [35] [39] [80] Kaufman and associates[35] *See references [ 2] [ 16] [ 24] [ 27] [ 29] [ 33] [ 35] [ 39] [ 41] [ 47] [ 48] [ 57] [ 71] [ 75] [ 78] and [ 80] . See references [ 2] [ 3] [ 24] [ 27] [ 29] [ 33] [ 34] [ 41] [ 48] [ 54] [ 57] [ 59] and [ 78] .

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reported that posterior shear forces increased linearly with increased knee flexion while performing isokinetic knee flexion at 60 degrees/second and 180 degrees/second. Resisted knee flexion places possible deleterious stresses on a healing PCL graft and should be avoided in the early and intermediate phases of PCL reconstruction rehabilitation. Paine[53] showed there to be no anterior tibial displacement while performing a straight-leg raise. If the leg raising was performed with a flexed knee (extensor lag), however, there was a significant increase in anterior tibial translation. Adding a 5-pound ankle weight increased the anterior tibial displacement further. When considering PCL loading, the resultant posterior shear forces seen in some WB exercises should be taken into account. Several authors concluded that as the flexion angle increases during a WB exercise, posterior shear forces increase, with maximal loads occurring around 90 degrees.[11] [26] [46] [52] [65] [75] WB exercises such as the squat, leg press, lunge, and front squat are considered detrimental to a healing PCL when performed in ranges greater than 60 to 70 degrees of flexion in the early phases of rehabilitation. According to the literature, the therapeutic exercises that produce the greatest amount of load to the ACL are (1) NWB resisted terminal knee extension, (2) slow-speed isokinetic terminal knee extension, and (3) resisted straight-leg raises with a flexed knee. When considering loads on the PCL, the following exercises appear to apply the most stress: (1) NWB resisted knee flexion, (2) NWB knee extension from full flexion to approximately 70 degrees, and (3) WB exercises with depths greater than 70 degrees of knee flexion. These exercises should be avoided in the early stages of a respective ACL or PCL reconstruction rehabilitation program.

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Ligament Unloading Exercises

Ligament unloading exercises are exercises that transmit minimum or no strain to the ACL, PCL, or healing graft. Ligament unloading exercises can be used during the initial phases of rehabilitation when early protection to the graft is desired. These exercises should not be harmful to different graft fixation techniques, which is considered a crucial factor during the first 6 weeks. Realistically, exercises fall somewhere on a continuum of ligamentous loading. On one end lie the most offending exercises, and on the other are exercises that minimally stress the ligamentous structures. The exercises should be added to the rehabilitation protocol in a manner that begins with the least loading and advances to greater loading exercises as the graft healing allows. Tables 8B-3 and 8B-4 outline a continuum of common therapeutic exercises, categorizing them from relative low to high ligamentous loading on the ACL or PCL. In accordance with the findings of Butler and colleagues,[9] our interpretation of the research literature is that anterior shear forces primarily strain the ACL and posterior shear forces strain the PCL. Two studies reported anterior shear forces during the squat exercise, [3] [46] whereas several other investigations found posterior shear forces and resultant PCL loading throughout the squat.[21] [52] [65] [75] [80] Similarly, posterior shear forces were seen in the leg press[75] as well as the front squat and lunge exercises.[65] Several authors concluded that as the flexion angle increases, shear and compressive forces also increase.[11] [26] [46] [52] [65] [75] As seen in Tables 8B-1 and 8B-2 , however, these shear forces do not approach the ultimate tensile strengths of the cruciate ligaments. This situation may be due in part to the increased stability gained by the increasing tibiofemoral compressive forces during WB exercises.[24] [30] [39] [40] [59] [68] [75] [79] In 1997, Beynnon and coworkers[3] published an article that described ACL strain during WB exercises. Before this publication, it was the general consensus that because of the compression forces present during WB exercises, the amount of anterior tibial

translation and calculated shear forces was reduced.[24] [40] [79] Beynnon's strain gauge study showed similar strain in the ACL during WB and NWB exercises such as the squat (with body weight) and active knee extension. Strain did not increase during the squat when resistance was added. Strain did increase, however, during the active NWB knee extension as resistance was increased.[2] Increasing external loads to the squat exercises could be considered safe when strengthening patients after ACL reconstruction surgery. Likewise, adding resistance to NWB knee extensions may cause excessive strain on a healing ACL graft. Several investigators studied squat mechanics further and noted how variables in squat performance affect shear forces in the knee joint. Escamilla and colleagues[20] studied the effects of stance width (narrow, wide, normal) and foot angle (parallel, turned out 45 degrees) on tibiofemoral shear and compressive forces during the squat and leg press. These investigators analyzed the effects of foot placement on the footplate during the leg press (high, low, natural). No significant differences in shear forces were found with these varied parameters. Escamilla and colleagues[20] did document higher compressive forces with the wider stance, which may be beneficial in limiting shear forces. Results of a study by Ariel[1] determined that when the knees move forward during the squat, and when the individual bounces at the end of the descent, higher shear forces occur. Stationary cycling has been studied for its effects on the cruciate ligaments. Henning and coworkers[27] and Fleming and associates[22] determined that ACL strain was evident during cycle ergometry. These values were given as low, however, in comparison with other commonly prescribed exercises. It has been determined that ACL forces can be decreased further with stationary cycling by lowering the workload,[19] using an anterior foot position,[19] and using a high seat height.[42] To lower posteriorly directed shear forces, seat heights should be lowered.[42] The strain produced in the normal ACL has been measured during stair climbing.[22] Strain values were shown to increase as the knee moved from flexion to extension. Although ACL strains increased with the stair-climbing motion, the forces were considered moderate in comparison with other previously tested rehabilitation activities, including squatting. The authors of this study were unable to make clinical recommendations for stair climbing because

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TABLE 8-B-3 -- Continuum of Stress Placed on the Anterior Cruciate Ligament in Relation to Various Parameters of Common Rehabilitation Exercises Lower StressHigh Stress Activity

Ligament Unloading

Ligament Unloading

NWB resisted knee extension[2] [16] [24] [27] [29] [33]

90-60 degrees

30-0 degrees*

[35] [39] [41] [47] [48] [57] [71] [75] [78] [80]

NWB resisted knee extensionexternal load placement[34] [47] [71]

Proximal

Distal*

Straight leg raise[53]

Knee extended

Knee flexed with resistance*

Isokinetic knee extensionspeed [35] [71]

>180 degrees/sec

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Pertinent Anatomy and Physiology Review

The human nervous system consists of somatic and autonomic branches. The somatic system includes the central nervous system (brain and spinal cord) and the peripheral nervous system. Motor nerve fibers exit the spinal cord through ventral rootlets; sensory nerves enter through dorsal rootlets. Sensory nerve endings in the periphery have cell bodies at the level of the neuroforamen of each vertebra. This collection of sensory nerve cell bodies is called the dorsal root ganglion. The ventral and dorsal rootlets join together to form the root of a peripheral nerve. [36] Specialized somatic sensory nerve endings known as nociceptors, mechanoreceptors, and thermoreceptors perceive pain stimuli, pressure stimuli, and temperature stimuli, respectively.[115] The autonomic nervous system is composed of the sympathetic and parasympathetic divisions. Anatomically, the parasympathetic nerve cell bodies are located in ganglia that are primarily cranial or sacral. In contrast, sympathetic nerve cell bodies are mainly located in paravertebral chains TABLE 9-3 -- Diagnostic Criteria of the International Association for the Study of Pain for CRPS Type I and Type II CRPS Type I (Reflex Sympathetic Dystrophy) An initiating noxious event is present. Spontaneous pain or allodynia/hyperalgesia occurs beyond the territory of a single peripheral nerve and is disproportionate to the inciting event. There is or has been evidence at some time of edema, skin blood flow abnormality, or abnormal sudomotor activity in the region of the pain since the inciting event. This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction. CRPS Type II (Causalgia)

This syndrome follows nerve injury. It is similar in all other respects to type I. A more regionally confined presentation about a joint (e.g., ankle, knee, or wrist) or area (e.g., face, eye) is associated with a noxious event. Spontaneous pain or allodynia/hyperalgesia is usually limited to the area involved but may spread variably distal or proximal to the area, not in the territory of a dermatomal or peripheral nerve distribution. Intermittent and variable edema, skin blood flow changes, temperature change, abnormal sudomotor activity, and motor dysfunction, disproportionate to the inciting event, are present about the area involved. CRPS, Complex regional pain syndrome. *See references and [ 127] .

[ 3] [ 4] [ 7] [ 13] [ 18] [ 31] [ 34] [ 38] [ 58] [ 73] [ 79] [ 81] [ 82] [ 83] [ 87] [ 89] [ 91] [ 92] [ 102] [ 103] [ 113] [ 117] [ 118] [ 120] [ 121] [ 123] [ 125]

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at the thoracolumbar levels. There are three sympathetic chain ganglia located at the cervical level, and they are known as the superior, middle, and inferior cervical ganglia. The inferior cervical ganglion is also known as the stellate ganglion and is commonly thought to supply the majority of sympathetic innervation to the upper extremity. The sympathetic nervous system is responsible for the classic fight-or-flight response needed in crisis situations.[36] A nerve carrying impulses from the periphery to the center of the body is defined as afferent or sensory; nerves carrying impulses from the center to the periphery are defined as efferent or motor. Preganglionic sympathetic neurons are nerves with cell bodies located in the gray matter of the spinal cord that send axonal endings into the paravertebral chain. The preganglionic neuron then synapses with postganglionic neurons in the sympathetic chain ganglion. The postganglionic nerve then carries the impulse to the end organ in the periphery. Communication between the sympathetic chain ganglia and the spinal cord or peripheral nerve occurs through gray and white rami communicantes. These rami allow the sympathetic chain to send and receive nerve fibers to and from the spinal cord and the periphery.[69] The catecholamines are a class of biologic chemicals including epinephrine and norepinephrine. These chemicals function as neurotransmitters that carry messages across synaptic clefts in the sympathetic nervous system. The terms adrenergic and noradrenergic refer to those synapses in which epinephrine and norepinephrine are used. The receptors for these two catecholamines are known as alpha and beta receptors. Subtypes of these receptors are known as alpha 1 , alpha2 , beta1 , and beta2 . Alpha receptor stimulation produces skin vasoconstriction, pilomotor contraction, cardiac acceleration, and intestinal relaxation. Excitation of beta receptors causes muscle vasodilation, bronchial relaxation, and cardiac acceleration. [69] The catecholamines also have roles as sympathetic hormones released from the adrenal

glands into the systemic circulation. In contrast to the primarily adrenergic sympathetic nervous system, the somatic nervous system is cholinergic. The term cholinergic refers to the use of the neurotransmitter acetylcholine to carry an impulse across a synapse. One notable exception to these general rules is that the sweating mechanism, which is sympathetically controlled, is a cholinergic system.[11]

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Theories of the Pathophysiologic Mechanism

Much of what is known about the pathophysiologic mechanisms of CRPS is based on a multitude of animal and human studies. These studies have been compiled in an attempt to support a unifying theory. [11] Whereas great strides in our understanding of this complex disorder have been made since Mitchell's time, many of our current hypotheses are still unproven and highly controversial.[14] [18] [85] [86] [102] [105] The following summary of the proposed mechanisms of disease is intended to provide the reader with an overview of the most plausible current theories in the literature based on the experimental evidence to date. Current leading theories are based on the supposition that a pathologic interaction occurs between the somatic (central and peripheral) nervous system and the sympathetic branch of the autonomic nervous system. This interaction is believed to occur between somatic sensory nerves and sympathetic efferent nerves, when an abnormal synapse is formed.[11] [65] The abnormal synapse is termed an ephapse.[51] The location of the ephapse may be peripheral, central, or both. A short circuit produced by an ephapse allows sympathetic discharge to directly stimulate sensory nerves. [47] [48] This pathologic sensory nerve stimulation is believed to produce symptoms associated with CRPS, including SMP.[11] It has been hypothesized that the most symptomatic regions of an extremity with CRPS correlate with those regions where sympathetic innervation density is greatest.[19] Sympathetically Maintained Pain

It is known that under normal conditions, somatic pain receptors (nociceptors) are unaffected by sympathetic outflow. Although somatic sensory neurons do contain the messenger ribonucleic acid necessary to produce alpha receptors, sensory nerves normally do not express adrenergic receptors and, therefore, have no interaction with circulating or local catecholamines.[11] In CRPS type II, a known traumatic nerve injury is, by definition, the inciting event that leads to a pathologic interaction between the two

nervous systems. In this scenario, the pathologic interaction occurs both in the periphery and centrally in the dorsal root ganglion.[11] [65] Peripheral pathologic interaction occurs when there is complete nerve transection and subsequent development of a neuroma. The transected sensory nerve endings then develop catecholamine sensitivity through the expression of alpha2 receptors.[97] These newly expressed receptors can be stimulated by circulating catecholamines as well as by sympathetic efferent nerves that grow into the neuroma. Central pathologic interaction in the dorsal root ganglion also follows complete nerve injury. Sensory nerve cell bodies in the dorsal root ganglion begin to express alpha2 receptors, while sympathetic efferent nerves that normally innervate blood vessels in the dorsal root ganglion begin to sprout and surround the injured nerve cell bodies (Fig. 9-2A (Figure Not Available) ). It is through these peripheral and central mechanisms that an abnormal coupling between the sensory (pain) nerves and the sympathetic nervous system occurs.[11] In CRPS type II, the nerve injury may be partial, as would occur with a nerve contusion or incomplete transection. In this scenario, a slightly different mechanism produces the abnormal interaction. One must consider the possibility that sympathetic nerve fibers may be injured. This leads to a decrease in the sympathetic innervation density in the periphery and may incite the production of alpha receptors by intact sensory nerve endings. This alpha receptor expression constitutes an abnormal synapse between sympathetic and somatic nerves and results in pain (Fig. 9-2B (Figure Not Available) ).[11] The clinical findings of light touch pain (allodynia) and cold hypersensitivity (hyperalgesia) are postulated to occur

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Figure 9-9-2 (Figure Not Available) Influence of sympathetic activity and catecholamines on primary afferent neurons (PAN). A, Nerve transection. The sympathetic-afferent interaction is located in the neuroma and in the dorsal root ganglion. It is mediated by norepinephrine (NA) released from sympathetic postganglionic neurons (SPGN) and 2 -adrenoreceptors expressed at the plasma membrane of afferent neurons. PGN, preganglionic neuron. B, Partial nerve lesion. Partial nerve injury is followed by a decrease of the sympathetic innervation density (stippled sympathetic postganglionic neuron). This induces an upregulation of functional 2 -adrenoreceptors at the membrane of intact afferent fibers. C, After tissue inflammation, intact but sensitized primary afferents acquire norepinephrine sensitivity. Norepinephrine is not acting directly on afferents; rather, it induces the release of prostaglandins (PG) from sympathetic terminals that sensitize the afferents. Accordingly, bradykinin- and nerve growth factor (NGF)-induced nociceptor sensitization is also mediated by the release of prostaglandins from sympathetic postganglionic neurons. (From Baron R, Levine JD, Fields HL: Causalgia and reflex sympathetic dystrophy: Does the sympathetic nervous system contribute to the generation of pain? Muscle Nerve 22:678-695, 1999. © 1999, John Wiley & Sons. Reprinted by permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

by a central sensitization mechanism known as the Raja model.[96] Nociceptors upregulate their production of alpha receptors in response to injury through the pathway

described before. These alpha receptors are persistently stimulated by sympathetic efferent nerve endings, which results in reduced threshold of central pain neurons (wide dynamic range neurons in the dorsal horn of the spinal cord). [28] [100] Light touchsensing mechanoreceptors or cold-sensing thermoreceptors produce the abnormal painful response by stimulating the sensitized central pain neurons. In the Raja model, sympathetic blockade produces a temporary inhibition of norepinephrine release, thereby preventing nociceptor activation. This leads to desensitization of the central pain neurons, thereby reducing the painful response to light touch. Continuous or repeated sympathetic blockade may ultimately lead to downregulation of the alpha receptors and elimination of the SMP.[11] One must also consider the situation in which SMP occurs without known nerve injury, as in CRPS type I. There is evidence that inflammation plays a role in the early stages of CRPS. An initiating noxious event produces a peripheral inflammatory tissue reaction that sensitizes the sensory nerve ending. Sensitization of the sensory nerve endings occurs through an indirect mechanism. In this inflammatory induction model, norepinephrine and inflammatory mediators such as bradykinin and nerve growth factor lead to the release of prostaglandins from the sympathetic terminals. The prostaglandins then stimulate the nociceptor, producing the pain response. Thus, an indirect action of norepinephrine on sensory nerve endings is postulated (Fig. 9-2C (Figure Not Available) ).[11] The inflammatory induction theory is supported by experimental evidence of nociceptor sensitivity to catecholamines after thermal or chemical stimulus application in animals. In addition, it is known that if norepinephrine is experimentally injected into animals, surgical postganglionic sympathectomy can prevent sensitization of the nociceptor. This occurs because norepinephrine can no longer stimulate the release of prostaglandins from the transected sympathetic nerve. Because of these and other experimental observations, it is thought that norepinephrine-induced afferent sensitization is accomplished through an indirect mechanism.[11] Sympathetic Vasomotor and Sudomotor Abnormalities

Both peripheral and central mechanisms have been postulated to explain symptoms of CRPS that are classically thought to be under sympathetic control. These symptoms include swelling, skin color, and local temperature changes that are under vasomotor control and sweating abnormalities, a sudomotor function. The peripheral mechanism by which these abnormalities may occur is called denervation supersensitivity. After a peripheral nerve injury (CRPS type II), some of the sympathetic fibers that normally innervate blood vessels to control vasoconstriction are injured. This local blood vessel denervation leads to acute vasodilation. Over time, the chronic loss of sympathetic tone leads to increased alpha receptor concentration (upregulation). The alpha receptor upregulation increases blood vessel sensitivity to sympathetic innervation, which induces late vasoconstriction. Consistent with this theory is the clinical finding that some patients initially display warm, swollen, red skin that is followed later by a cold and mottled appearance with less or no swelling. [11] Some evidence exists for a central mechanism of vasomotor dysfunction as well. This

mechanism may also more readily explain the development of sympathetic dysfunction without known nerve injury (CRPS type I). The central control theory is known as decentralization supersensitivity. Although the peripheral and central theories agree that supersensitivity of the end organ does occur, they differ in their respective explanations of how this occurs. The central theory contends that a central nervous system inhibition of sympathetic vasoconstrictor activity is the initiating event. This inhibition leads to vasodilation and subsequent skin redness, warmth, and swelling. Continuous central inhibition can lead to upregulation of blood vessel alpha

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receptors. Increased alpha receptor concentration induces a supersensitive state causing late vasoconstriction. The central theory thus accounts for clinical signs of sympathetic overactivity despite experimental evidence of reduced sympathetic output. Indeed, measurements of norepinephrine in venous drainage taken proximal to areas with sympathetic dysfunction have shown an overall lower than normal level. [39] Further support for the upregulation of adrenergic receptors comes from the finding of increased levels of alpha receptors in skin biopsy specimens from involved areas. Whereas the peripheral and central mechanisms differ in their explanations, there is also some evidence that these both play a role in modulating the abnormalities of sympathetic vasoconstrictor function.[11] Sweat glands, in contrast to blood vessels, do not exhibit denervation or decentralization supersensitivity; therefore, a direct central mechanism of increased sudomotor function is believed to play a role here as well. A centrally triggered increase in sympathetic outflow to sweat glands may occur, causing the clinical finding of increased sweating.[13] That vasomotor dysfunction and sudomotor dysfunction occur by separate mechanisms is confirmed by lack of correlation between these two clinical findings.[11]

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Clinical Presentation

The clinical presentation of CRPS is highly variable and difficult to characterize.[93] Classic findings are described, but these are not necessarily the most common clinical findings. Delayed or failed diagnosis is common, partially because of the syndrome's wide variability and nonspecific set of signs and symptoms. Epidemiologic factors are not particularly helpful in diagnosis because there is no sex predilection, all ages may be affected, and side-to-side differences are not seen. In addition, there is no particular predilection for involvement of the dominant limb over the nondominant limb.[18] The defining criteria of CRPS dictate that a noxious event or peripheral nerve injury initiates the symptoms. The common noxious conditions include blunt trauma, surgical intervention, inflammatory reactions, fractures, arthritis, and others. [69] The clinical history and physical examination findings of CRPS can be classified into several overlapping categories including sensory disturbances, sympathetic dysfunction, motor abnormalities, trophic changes, and psychological issues. Sensory Disturbances

Perhaps the hallmark sensory finding of CRPS is pain that is disproportionate to the expected response for the inciting condition. The disproportionality applies to the duration of pain response, the severity of the response, and the distribution of the painful area. Within hours or days after the initial injury, the pain becomes more diffuse and unrelated to the site of the injury. As the syndrome progresses, the painful area takes on an even more nondermatomal distribution, with a preference for distal limb involvement (i.e., stocking or glove distribution). The character of pain is also an important diagnostic clue. Patients commonly describe a burning, shooting, or deep, constant aching. A classic finding is pain with light pressure (allodynia). Patients commonly report an inability to tolerate the faint touch of bed sheets, clothing, or air currents. Night pain is an occasional complaint. The symptoms of hyperalgesia,

hyperpathia, hyperesthesia, and dysesthesia may also be present ( Table 9-4 ). The pain of CRPS may also fluctuate and recur, depending on several common factors. These aggravating factors include overaggressive physical therapy (active and passive motion), environmental and local temperature changes (particularly cold intolerance), dependent limb position, and emotional excitement.[127] Sympathetic Dysfunction

Sympathetic dysfunction is commonly manifested through skin color and temperature abnormalities, swelling, abnormal sweating, and local cold intolerance. The classic skin pattern changes from acutely red, warm, and dry skin to the chronic appearance of bluish or mottled, cold, and moist skin ( Fig. 9-3 ). One author reports that approximately 80% of patients will have side-to-side differences in limb temperature averaging 3.5°C.[127] Swelling is a common finding, although objective evidence of swelling occurs less frequently than subjective reports.[103] The swelling of CRPS is generally painful, and usually extra-articular, although joint effusions are also reported.[35] Swelling is most pronounced acutely in the course of the disease and usually becomes less pronounced with chronicity. The soft, puffy edema seen acutely is eventually replaced with tight, shiny skin that lacks normal creases.[28] The character and severity of limb swelling vary with recurrent acute flares of sympathetic dysfunction. Acutely decreased and chronically increased sweating with a predilection for the palmar hand or plantar foot occurs.[127]

Pain

TABLE 9-4 -- Definition of Pain-Related Terminology An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

Allodynia

Pain due to a stimulus that does not normally provoke pain (e.g., light touch)

Hyperalgesia

An increased response to a stimulus that is normally painful

Hyperesthesia Increased sensitivity to stimulation, excluding the special senses. Hyperesthesia may refer to various modes of cutaneous sensibility, including touch and thermal sensation without pain, as well as to pain (e.g., cold hypersensitivity). Hyperpathia

A painful syndrome characterized by a delayed reaction and reaction that outlasts the stimulus and spreads beyond the site of the stimulus (commonly a repetitive stimulus)

Dysesthesia

An unpleasant abnormal sensation, whether spontaneous or evoked

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Figure 9-9-3 In the early stages of complex regional pain syndrome (CRPS), the color of the extremities often changes to blue or dusky red. This 14-year-old girl presented to the emergency department 2 weeks after sustaining an inversion ankle sprain. Her pain, swelling, and dysfunction had increased despite a treatment program of wraps, ice, elevation, and home-based range of motion exercises. A venogram was obtained in the emergency department to rule out deep venous thrombosis, and CRPS was diagnosed soon after. Because an initial course of oral corticosteroids relieved symptoms only partially, the patient had a series of five paravertebral blocks, each of which alleviated pain for a progressively longer time. The patient also participated in a program of physical therapy that included massage to control swelling, active and active-assisted range of motion and strengthening exercises, and weight-bearing as tolerated. After about 4 months, she was able to resume normal activities.

A final manifestation of sympathetic dysfunction is cold intolerance. [61] This finding is nonspecific but particularly sensitive with regard to diagnosis of SMP. Cold intolerance is commonly first discovered when cryotherapy is employed by the physical therapist to control swelling and a significant painful reaction is exhibited by the patient.[69] We recommend office use of the ice test, in which ice is applied to the involved area and the patient is questioned about the sensation. The common response to the ice test is that the ice produces an intolerable burning sensation, whereas the application of ice to the normal limb is described as cold. Cold weather also commonly precipitates recurrent flares of sympathetic dysfunction in CRPS patients.[69] Patients often report the need to wear socks to bed because of cold feet. The natural history of sympathetic dysfunction has classically been divided into three sequential but overlapping stages.[119] The acute stage is characterized by sympathetic hyperfunction manifested by disproportionate pain; red, warm, and dry skin; and extra-articular swelling. The classic presentation of the acute stage lasts less than 6 months. The dystrophic stage begins when the increased sympathetic output succumbs to a period of reduced sympathetic activity, typically 3 to 9 months after onset. This stage is characterized by cyanotic or mottled, cold, moist skin; muscle wasting; thick nails and coarse hair; and other early trophic changes. After a period of chronic sympathetic dysfunction, the atrophic stage begins. This stage is characterized by thin, tight, glossy skin; osteoporosis; and joint contractures. The clinical usefulness of this classic staging system has been called into question because of the profoundly variable appearance of symptoms from patient to patient as well as the variable time course of any particular patient's disease.[13] The usefulness of the staging system is best realized when the clinician understands that the disease does not progress systematically through stages. Instead, the common scenario is the frequent toggling back and forth between stages in almost random order. The staging system does improve our understanding of the classic presentation as long as the clinician recognizes that exceptions not only exist but are common. For example, many patients with CRPS may present with disproportionate pain as the only symptom. The astute clinician will correctly consider the diagnosis of CRPS even in the absence of other signs of sympathetic dysfunction. One specific exception to the classic presentation, termed cold reflex sympathetic dystrophy, may have implications for prognosis. Van der Laan and colleagues[122] found that CRPS type I patients with cold initial skin temperature were much more likely to

develop a severe complication, such as infection, ulceration, chronic edema, dystonia, and myoclonus. Motor Abnormalities

Motor impairment is a more recently appreciated phenomenon associated with CRPS.[106] Although not essential for diagnosis, motor dysfunction does occur. The spectrum of motor abnormality ranges from weakness and disuse to increased tone and hyperfunction.[103] In the absence of traumatic nerve injury (CRPS type I), findings of electromyography/nerve conduction velocity studies are usually normal, suggesting that motor abnormalities are centrally mediated, presumably at the spinal cord level.[127] Weakness of the affected limb occurs for several reasons, including disuse and muscle wasting. The finding of pseudoparalysis in patients with CRPS suggests that some motor abnormalities may be psychogenic or pain related. Paresis and limb neglect are also seen. Motor abnormalities characterized by hyperfunction include action tremor, myoclonus, hyper-reflexia, muscle spasm, and voluntary guarding.[125] Dystonia, apraxia, and lack of coordination are findings typically associated with long-standing disease.[127] Trophic Changes

Persistent or recurrent CRPS symptoms may result in trophic changes. [125] Atrophy of the tissues probably occurs from disuse and as a direct result of sympathetic dysfunction. Tissues known to undergo atrophy in response to chronic CRPS include skin, subcutaneous fat, muscle, tendon, and bone. Thin, shiny, smooth, tight skin is the typical end result of chronic CRPS. Atrophy of subcutaneous fat

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is particularly evident in the digits and results in a pencil-like appearance. Tendon atrophy is known to occur. The classic finding of patchy periarticular osteoporosis is known as Sudeck's atrophy, but it is relatively uncommon and nonspecific. [116] Chronically increased blood flow to the limb leads to local hypertrichosis, coarsening of the hair, and thickening of the nails. Chronic joint stiffness ultimately leads to fixed contractures. Psychological Issues

In the face of such severe and debilitating symptoms, it is no surprise that psychological disturbances are observed. Great debate rages about whether psychological issues are a cause or a result of CRPS. Ochoa and Verdugo[86] have gone so far as to suggest that this disease is a pseudoneuropathy of psychogenic origin. One must take care to exclude from the diagnosis of CRPS those patients with factitious disorders, malingering, somatization disorders, and conversion reactions, however ( see Table 9-2 ).[18] [102] These psychiatric disorders represent examples without an organic pathologic

basis and therefore must be considered separate diagnostic entities. The presence of secondary gain issues, such as worker's compensation claims, disability cases,[34] and pending litigation, also complicates matters. When secondary gain represents a patient's sole motivation, the individual is considered a malingerer by definition. A patient's motivation, however, may be difficult or impossible to discern. Patients with apparent secondary gain potential may also have true CRPS organic disease; therefore, they must not be dismissed even when alternative motivations are suspected to play a role. Whereas some authors have suggested that a particular personality or psychological profile puts some patients at risk for the development of CRPS, [34] most authors currently reject this notion. [21] [74] It is more likely that the emotional and behavioral disturbances are the result of chronic pain and loss of function.[81] Psychological disturbances have been shown to resolve when the patient is relieved of the physical symptoms of CRPS. Moreover, Ciccone and associates[21] found no evidence to suggest that CRPS type I patients were psychologically unique compared with CRPS patients with other chronic pain disorders. Few would dispute the existence of psychological symptoms in conjunction with many chronic pains and illnesses including CRPS.[21] Symptoms such as depression and anxiety are often observed. It has also been documented that certain subscales of the MMPI evaluation are commonly elevated in chronic pain states.[117]

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Diagnostic Procedures

Objective methods used to aid diagnosis of CRPS are aimed primarily at assessing the degree of sympathetic dysfunction. These methods are fraught with high levels of inaccuracy and poor sensitivity or specificity. Because of these factors, the diagnosis of CRPS is made primarily on clinical grounds and then secondarily confirmed with objective tests. Establishing and confirming the presence of sympathetic dysfunction (pain and vasomotor and sudomotor abnormalities) are useful because of the implications for treatment. Hematologic Evaluation

Blood studies, such as white blood cell count, erythrocyte sedimentation rate, and C-reactive peptide determination, are indicative of inflammatory processes but are neither sensitive nor specific in the diagnosis of CRPS. These and other studies, including rheumatoid factor and antinuclear antibody titers, are more useful in ruling out other inflammatory conditions. Radiography

Objective assessment of virtually any extremity pain begins with plain radiographs. Standard radiographic series of the affected area typically reveal soft tissue swelling and osteoporosis. Sudeck's atrophy is classically described as patchy periarticular osteoporosis of the long bones, whereas the osteoporosis seen in the small bones of the hand and foot is more diffuse. Subchondral bone margins are usually retained. These radiographic findings are non-specific; they may be subtle and generally indicate chronicity of disease.[116] Comparison films of the contralateral extremity are recommended.

Bone Scanning

Use of the triple-phase bone scan is highly controversial.[44] [45] [60] [75] [132] The scan consists of images obtained seconds (arterial phase), minutes (soft tissue phase), and hours (bone phase) after the intravenous injection of the radionuclide tracer.[125] Increased periarticular uptake of the tracer in the soft tissue phase and bone phase images is the classic bone scan finding in early CRPS. This occurs because of both increased blood flow and increased bone turnover in early CRPS. The increased tracer uptake seen acutely eventually gives way to normal or reduced uptake that is characteristic of the dystrophic and atrophic stages. Whereas the sensitivity and specificity of the bone scan have been reported to be as high as 96% and 97%, respectively, [45] these numbers drop significantly 6 months after onset of disease. In addition, a small percentage of patients have bone scans early in the course of disease that show an abnormally decreased tracer uptake. This may account for the wide variability in the literature with regard to reported sensitivity rates (60% to 100%) and specificity rates (80% to 98%). [44] [45] [60] [132] Use of bone scans to track the success of treatment or spontaneous resolution of disease is not recommended.[44] There is a natural tendency for the bone scan findings to return to normal over time despite persistence of disease. The clinician must understand that a normal bone scan finding does not rule out CRPS.[125] In addition, bone scans

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taken after successful sympatholysis procedures show a paradoxical intensification of the tracer uptake. A normal scan finding, therefore, may indicate progression of disease beyond the acute phase, and a hyperintense scan finding may be the result of successful sympatholysis.[44] [75] For these reasons, bone scans should not be used to monitor treatment. Like the finding of osteoporosis on radiographs, a hypointense or normal bone scan finding in a patient with CRPS may be indicative of chronicity of disease and a poorer prognosis. The real usefulness of the triple-phase bone scan, however, is to confirm clinical suspicion of the diagnosis of CRPS early in the course of disease and to help localize symptoms. Some authors have observed that the bone scan can show abnormal findings even before symptoms appear.[44] Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is generally not used to confirm the diagnosis of CRPS. Typically, MRI is used to rule out other pathologic processes and narrow the differential diagnoses or to discover the inciting event that triggered CRPS. Several nonspecific findings of CRPS have been described on MRI. The characteristic findings acutely include thickening of the skin, soft tissue swelling that enhances with contrast, and intra-articular effusions. Over time, these findings abate, and chronic changes including muscle atrophy and skin thinning are observed. Bone marrow edema (once

thought to be characteristic) is usually not seen as part of CRPS. [35] [109] [116] Paravertebral Sympathetic Ganglion Blockade

The diagnosis of SMP as a component of CRPS is made by the degree of the patient's response to sympatholytic procedures. Several methods of achieving diagnostic sympathetic blockade are available. The most effective method and the gold standard in diagnosis of SMP is the paravertebral sympathetic ganglion block.[69] [108] [118] [127] [129] Under fluoroscopic control, the lumbar paravertebral sympathetic ganglion for lower extremity CRPS or the stellate ganglion for upper extremity CRPS is injected with local anesthetic. The accuracy of the injection is assessed by evaluating vasomotor and sudomotor functions (skin color, skin temperature, and sweating) in the affected limb. Skin temperature changes, therefore, must be monitored and recorded. One cannot be sure a technically adequate block has been accomplished unless local skin temperature approaches core body temperature. In addition, the induction of Horner's syndrome (ipsilateral ptosis, miosis, and anhidrosis) is required to confirm adequate stellate ganglion blockade. Inadvertent spread of local anesthetic to sensory nerve roots is screened by a carefully documented sensory examination. Partial or complete pain relief with intact sensation indicates the presence of SMP.[125] Several limitations of this technique exist and must be recognized. First, the technique is dependent on the accuracy of the injection's location, and the result can be influenced by the anesthetic agent selected. The systemic uptake of the anesthetic may also adversely bias results. Last, placebo responses may be as high as 33% because of the high expectations of the patient and physician.[86] Despite these limitations, the paravertebral block remains the diagnostic procedure of choice to quantify the degree of SMP objectively. Pain that remains after successful paravertebral sympathetic block is by definition SIP. In cases of chronic CRPS, the majority of the patient's pain may be SIP; therefore, the diagnosis of CRPS cannot be excluded solely on the basis of the paravertebral block. Differential Spinal and Epidural Blockade

Physicians not skilled in the technique of paravertebral block may substitute a more common interventional method for the diagnosis of SMP, that is, spinal or epidural blockade. In this common technique, a spinal or epidural puncture is performed, and variable concentrations of an anesthetic agent are injected over time. At first, a saline placebo may be injected. The patient is then questioned about symptoms. Increasingly concentrated solutions of the agent are then injected, and after each injection, the patient's symptoms are again recorded. Low concentrations should penetrate the least myelinated sympathetic nerve fibers and relieve SMP. A moderate concentration of anesthetic agent will additionally block moderately myelinated sensory fibers, and a high concentration adds motor blockade. The weakness of this method is that there is a variable amount of sensory blockade even at low anesthetic concentrations. As a result, it may be inaccurate to attribute the pain relief solely to sympathetic blockade. Therefore, the more sympathetic-specific paravertebral ganglion block is preferred.[69] Phentolamine Testing

Phentolamine (Regitine) is a nonspecific alpha antagonist with a short (17 minutes)

serum half-life. By blocking alpha receptors (mediators of sympathetic pain), the drug provides temporary relief to the patient and valuable diagnostic information for the clinician. The results of the phentolamine test may correlate with the patient's responses to paravertebral ganglion block, and therefore some use the test to predict outcomes for patients after paravertebral blocks.[8] [97] The phentolamine test for the diagnosis of SMP was described independently by two different groups in 1991.[8] [97] Several advantages of phentolamine testing support the use of this test to confirm diagnosis. The test is safe for the patient and simple to administer in the office because adverse reactions are rare, fluoroscopy is not required, and injection into the painful affected area and the use of a tourniquet are not required. Patients routinely prefer less invasive diagnostic options. The medication can be given in a single-blinded, placebo-controlled manner to increase its diagnostic accuracy. The protocol states that injections are given behind a screen, and patients are not told whether they are receiving saline or phentolamine. Their responses

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are recorded after the injections and compared to eliminate the placebo effect.[97] The phentolamine test is also most practical when more than one limb is affected by disease. Critics of the phentolamine test argue that as for many of the diagnostic and therapeutic modalities used in CRPS, few controlled studies have clearly demonstrated its efficacy.[8] [97] Because of the short duration of phentolamine's results, the test is useful for diagnosis but is not an effective form of treatment. We do not routinely use the phentolamine test, but we do recommend the test in selected cases in which additional diagnostic information is needed or more than one limb is involved. Regional Intravenous Sympathetic Blockade

Regional intravenous sympathetic blockade is another means of confirming one's clinical diagnosis, and the blocking effect is sometimes used for treatment as well. The most common agent used in this technique is guanethidine; however, reserpine and bretylium blocks have also been described.[125] The common denominator of these medications is their mechanism of action. The drugs are taken into sympathetic terminals where they deplete norepinephrine for up to 2 days by stimulating its release and inhibiting its reuptake.[19] This explains the initial burning pain on injection experienced by many patients, indicating the presence of SMP. Significant pain relief lasting 2 weeks to 6 months may occur and constitutes a positive test result. Little or no pain relief for less than 5 days favors the diagnosis of SIP. Central ephapses (in the dorsal root ganglion) as a source of SMP cannot be excluded on the basis of tourniquet-controlled regional alpha blockade. Intravenous administration of guanethidine is not currently approved for this use in the United States, but it has been used extensively in other countries for more than 25 years. Conflicting studies exist in the literature, and the usefulness of regional intravenous sympathetic blockade is highly debated.[29] [50] [58] [98] We currently do not recommend

intravenous regional sympathetic blockade for several reasons. First, the specificity of these medications for sympathetic functions is undetermined. Second, local anesthetics are commonly injected in conjunction with these medications and may confuse results. Third, injection of these medications is often painful for patients and often poorly tolerated. Fourth, the use of a tourniquet on a limb with profound sympathetic dysfunction is generally unfavorable.[124] [125] Paravertebral ganglion injection is our preferred method of achieving prolonged sympathetic blockade and has the added advantage of blocking central ephapses for a more complete sympatholytic effect. Vasomotor and Sudomotor Measurements

Accurate quantitative assessment of sympathetic functions has proved difficult but remains important. A concept that is not necessarily obvious is that sympathetic dysfunction may exist without the presence of pain (SMP or SIP) and may ultimately lead to dystrophic and atrophic changes. This phenomenon has specifically been observed in the contralateral extremity of patients with CRPS.[13] As a result of this observation, studies of autonomic function using side-to-side comparisons may be inherently flawed. Accurate quantification of skin temperature, sweat output, blood flow, and edema volume compared with normative values from control groups is a better way to evaluate for autonomic dysfunction. Such normative values have not been clearly established; therefore, side-to-side comparison remains the current standard by which autonomic dysfunction is quantified. The most commonly used method of sympathetic dysfunction measurement is thermography.[13] [17] [41] [54] [103] [111] Infrared cameras that sense heat are connected to a computer and produce colorized images of affected and unaffected limbs compared with those of control groups. These images provide valuable area-specific information about extremity surface temperature variations. Surface temperature is thought to correlate with surface blood flow, a sympathetically controlled parameter. Some authors have reported on the ability of thermography to provide earlier detection of CRPS. [17] [41] [54] Although early diagnostic information may be obtained with this method, several drawbacks have prevented its widespread implementation. First, video thermography requires a carefully controlled environment consisting of a draft-free, temperature- and humidity-controlled room. It also requires a period of acclimatization before testing that can range from 20 minutes to 2 hours. Another difficulty in thermography is that the amount of side-to-side temperature difference that constitutes dysfunction is unknown. It is known that when this temperature difference threshold is set at 0.4°C, the test is sensitive but nonspecific. If, on the other hand, the threshold is set at 1.2°C, the test is specific but not sensitive. Most authors currently use 1.0°C as the cutoff value.[17] Sympathetic dysfunction exists when the affected extremity is either warmer or cooler than the opposite extremity. When patients are evaluated at all stages of disease, however, the majority of patients demonstrate cooler affected limbs, reflecting the frequency with which patients with subacute and chronic CRPS are encountered. A somewhat more specific but less sensitive method of sympathetic function analysis is the measurement of sweat output. [13] [71] [103] Dysfunctional sweating is thought to occur independently of dysfunctional vasomotor activity even though both are under sympathetic control.[13] This independence of vasomotor and sudomotor control may

reflect the different pathophysiologic mechanisms by which each occurs. The most common method of sweat output measurement is the quantitative sudomotor axon reflex test (QSART).[13] [71] [103] In this test, the sweat response to topical application of acetylcholine or other sweat-inducing agent is measured and compared with resting sweat output levels. The QSART response is mediated entirely by the postganglionic sympathetic neuron. A criticism of this test is that the increased sudomotor activity in CRPS is thought to be centrally mediated. Therefore, the QSART response may not be an accurate reflection of CRPS sympathetic overactivity. As a result, the thermoregulatory sweat test, which stimulates sudomotor function by activation of thermal

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neurons in the ventral hypothalamus, has been advocated.[13] Neither sweat test is widely available, and they are currently used primarily for research purposes. Some authors have advocated measurement of other sympathetic functions, including regional blood flow and edema volume.[49] [71] Blood flow measurements are made by transcutaneous oxygen pressure measurements, and edema is quantified with volume displacement methods. [125] These tests are not widely used, and their sensitivity and specificity for sympathetic dysfunction are unknown.

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Patient Education and Information

Many patients report that the establishment of a definitive diagnosis provides significant emotional relief from the torment of not knowing what is wrong. Once the diagnosis is made, it is the job of the clinician to help educate the patient about the disease through careful explanation and question answering. This can be reinforced in several ways, including the distribution of printed information booklets on CRPS. In addition, the patient can be provided with the names of support organizations, which are now easily and widely accessible through the Internet.

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Treatment Principles and Methods Physical Therapy

Physical therapy with or without occupational therapy is generally regarded as the mainstay of CRPS treatment.[89] On occasion, physical therapy alone can reverse CRPS. Many of the medical, interventional, and surgical treatment options are intended to improve patients' symptoms with the purpose of facilitating an active physical therapy program. Controlled trials demonstrating efficacy of physical therapy are scant, [87] [88] [89] [110] but several guiding principles must be followed in designing therapy programs for patients with CRPS. These principles are based on science, experience, and the recommendations of consensus panels. Confrontations between aggressive therapists and resistant patients are to be avoided. The physical therapy program must never induce intolerable pain because this is always counterproductive. The program must work within the limits of a patient's pain tolerance, supplemented by medications and blocks. The goals of any therapy program in the treatment of CRPS are prevention and treatment of pain, swelling, stiffness, weakness, and disuse and restoration of function. A four-step program emphasizing gradual progressive return to function has been outlined.[117] The first step involves the development of a patient-therapist treatment alliance. By remaining a strong advocate for the patient in all matters, the therapist will gain the confidence and trust of the patient, lending credibility to the treatment program.[117] The second step involves motivation of the patient and desensitization and mobilization of the affected limb. Desensitization is accomplished through high- and low-frequency vibration,[40] gentle textured massage,[12] contrast baths using temperatures within the pain-free range,[40] and transcutaneous electrical nerve stimulation.[12] Movement

phobias must be overcome. Motion exercises in CRPS are best accomplished through active and active-assisted exercises. Passive motion takes control of the limb away from the patient and is often poorly tolerated. Passive stretching exercise is thought to increase sympathetic output and can thereby aggravate pain, swelling, and sympathetic dysfunction.[40] Techniques of immobilization (splints and casts) are generally counterproductive and are avoided when possible. Active motion, elevation, massage, and compression, if tolerated, will also help with edema control.[12] The third step involves strengthening and stress loading. Muscle strengthening is best done in an isometric fashion to minimize unnecessary motion. The patient is gradually progressed to isotonic methods. Stress loading is encouraged to prevent disuse and restore functionality. Upper and lower extremity load-bearing activities are implemented gradually through the use of weight-carrying or water exercises. Postural training and balanced use of bilateral extremities are then undertaken with use of BAPS boards. General aerobic conditioning helps maintain range of motion, strength, and balance.[117] The last step emphasizes return to normal function. Patients are enrolled in vocational rehabilitation with work hardening. Eventually, a functional capacity evaluation is performed, and job modifications are implemented as needed. Patients are encouraged to return to work, school, sports, or other daily activity. This program is supplemented by sympathetic blocks and medications whenever appropriate to allow the patient to make steady progress without intolerable pain.[117] A conspicuous deficiency of blinded, randomized, placebo-controlled clinical trials evaluating the efficacy of specific treatments exists in the CRPS literature.[58] Therefore, many of the current recommendations are based on the art of medicine more than on the science of medicine. Significant placebo effects have been observed in up to 33% of patients with CRPS, emphasizing the need for placebo control. Uncontrolled trials must be interpreted with extreme caution for this reason. Furthermore, because the diagnostic criteria of CRPS have only recently become standardized, comparison between studies is virtually impossible. In spite of these limitations, several general statements about treatment principles and specific treatment methods can be made with confidence. Perhaps the most important principle is that of early recognition and treatment. * Ideally, treatment should begin within 2 to 3 weeks of onset. Many authors have emphasized that the long-term prognosis is critically dependent on the amount of time from disease onset to the beginning of treatment. Delay of longer than 6 months is associated with a poor long-term prognosis.[24] [126] [131] The diagnosis of CRPS mandates a full and thorough investigation in search of a persistent painful focus. Any such painful focus will aggravate and perpetuate SMP. *See references

[ 23] [ 24] [ 33] [ 66] [ 68] [ 70] [ 82] [ 107] [ 114]

and [ 125] .

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Elimination of this painful focus is a critical step in treatment of CRPS. Whereas correction of a painful focus alone will not always eliminate CRPS, SMP will generally not resolve without elimination of the painful lesion. When the patient is scheduled to undergo sympathetic blockade, ask the patient to think about the character and location of the pain that remains while the block is working. When the burning, nonspecific pain is gone, an underlying pain may be unmasked. The patient can often describe a specific location and may now point to the medial joint line, for example, rather than the entire medial knee. The clinician should remember that MRI and other diagnostic tests may miss small or large lesions. Correctable lesions, such as meniscal tears, chondral lesions, infections, painful neuromas, and many others, that were not previously revealed by MRI are often discovered by arthroscopy.[69] Surgery is generally not recommended for patients with active CRPS because of the risk of worsening the pain syndrome. In the senior author's experience (T.N.L.), however, patients with chronic refractory CRPS with complaints that suggest a painful non-neurologic condition frequently require diagnostic arthroscopy to correct a painful condition that exacerbates CRPS. Treatment often requires a multidisciplinary team approach. Patients must often seek the cooperative advice of an orthopaedic surgeon, anesthesiologist or pain management specialist, physical or occupational therapist, psychologist or psychiatrist, neurologist or physiatrist, and primary care physician. An open line of communication between health care providers is essential to provide the most effective and efficient care. The primary care physician, orthopaedic surgeon, or pain management specialist will often serve as the team manager to help coordinate the treatment program. Nevertheless, for patients with recurrent exacerbations or flares of CRPS, the patient's direct access to the pain management specialist improves efficiency and reduces the patient's frustration. It is imperative always to remain the patient's advocate. Personality conflicts between patients and health care providers must be set aside, and confrontations are almost always counterproductive. Patients must believe that their physicians, nurses, and therapists are on their side to lend credibility to the prescribed treatment programs. Therefore, the development of rapport and the establishment of a therapeutic alliance between physician and patient are critical to success.[117] A sound physician-patient relationship can also help to eliminate the doctor shopping tendency that many patients display.[4] [32] Because specific treatment protocols have not been validated, good clinical judgment must be used to individualize treatment on the basis of the patient's signs and symptoms.[127] The decision to use medications, injections, interventional techniques, therapy, psychiatric treatments, or surgery must be made individually on the basis of all of the available medical information. The myriad available treatment options reported in the literature stand as testimony to the fact that few are backed by conclusive scientific support. The widely ranging treatment techniques are generally separable into categories of patient education, physical therapy, medications, psychiatric management, moderately invasive

techniques, and surgical procedures.

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Medications for Symptomatic Relief

Many different medications are used in the treatment of CRPS, but few have more than anecdotal support. The perfect combination of medications for each patient is still based on a trial-and-error approach.[117] The correct dosages must be titrated to allow maximal benefit with minimal side effects [127] ( Table 9-5 ). Symptom-relieving medications are intended to increase the patient's comfort and to facilitate the implementation of a physical therapy program. The following medications are thought to provide some benefit to patients with CRPS,[117] although their use must be individualized.[127] Corticosteroids

Corticosteroids are particularly beneficial in the early stages of the disease. Their anti-inflammatory effect is most pronounced when the clinical signs of redness, warmth, and swelling are present.[20] [37] [58] We have found that trial of a corticosteroid, such as methylprednisolone (Medrol Dosepak), early after onset sometimes results in complete resolution of the syndrome. Antidepressants

The use of antidepressants for neuropathic pain is well established. [58] The nonspecific serotonin and norepinephrine reuptake inhibitors, such as amitriptyline (Elavil) and desipramine (Norpramin), often provide relief of burning pain. In addition, these drugs can help patients with sleep difficulties and mood and anxiety disturbances. In general, the dose required for neuropathic pain control is much lower than the dose necessary for antidepressant effect. The onset of action of these medications occurs within 2 to 3 weeks, and the peak effect is not felt for 4 to 6 weeks. In our experience, amitriptyline used at bedtime provides effective symptom relief in many patients with burning pain or sleep disturbances. If the side effects (including sedation, dry mouth and eyes, urinary retention, and constipation) are tolerable, the dose can be titrated for maximal benefit.[57]

Selective serotonin reuptake inhibitors are not effective for neuropathic pain relief.[117] Membrane Stabilizers

Membrane stabilizers include medications from several therapeutic categories, including anticonvulsants, antiarrhythmics, and local anesthetics. The use of many different membrane-stabilizing medications is reported in the literature with mixed results. Controlled trials, however, are rarely found. The anesthetic agent lidocaine (Xylocaine) has been administered locally through several different routes, including intravenous, subcutaneous, and topical, and as the oral analogue mexiletine (Mexitil).[67] [83] [118] Results have been favorable in some articles, [58] but only short-term follow-up is commonly reported. [67] [83] Perhaps the most

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Drug

TABLE 9-5 -- Medications Mechanism of Use Action

Side Effects

Alpha Blockade Phenoxybenzamine Blocks peripheral (Dibenzyline) 100 to 300 alpha1 receptors mg (100 mg qhs or tid) Decreases sympathetic tone Prazosin (Minipress) 1 mg bid to tid

Causalgias

Hypotension

Hypotension Tachycardia Decreased sexual function Nasal congestion

Terazosin (Hytrin) Clonidine (Catapres)

May have fewer side effects Alpha2 agonist Blocks alpha1 transmission peripherally and centrally

Beta Blockade*

Pain relief can Hypotension be obtained with clonidine patches

Propranolol (Inderal) up to 320 mg/day

Beta-adrenergic response presynaptically (centrally)

Central RSD

Hypotension

Migraine

Bradycardia

Facial pain

Depression Aggravation of asthma and cardiac arrhythmias Decreased libido Decreased memory Sudden withdrawal

Timolol (Blocadren) Atenolol (Tenormin)

Sensitivity to catecholamines Resultant cardiac arrhythmias and myocardial infarction

Antidepressants Trazodone (Desyrel) 50 mg tid

Blocks serotonin receptors

Most chronic pain syndromes

Multiple

Activates descending pain-inhibitory fibers Tricyclic antidepressants: Desipramine (Norpramin) 100-200 mg/day

Myocardial ischemia Urinary retention

Doxepin (Sinequan) 10-25 mg tid Amitriptyline (Elavil) 25 mg tid Calcium Channel Blockers

Orthostatic hypotension

Nifedipine (Procardia) 10-30 mg tid

Relaxes smooth muscle

Peripheral nerve Headaches injury, especially in decreased Increases peripheral blood flow states Hypotension blood flow Decreases discharges from ephaptic scars

Diltiazem (Cardizem) 30 mg qid, increase to 60-90 qid Verapamil (Calan) Nicardipine (Cardene) Anticonvulsants Carbamazepine Suppresses (Tegretol) 100 mg po bid pathologic electrical up to 800 mg/day discharges in CNS and PNS

Ephapses

CNS depression

Burning pain

Drowsiness

Sharp discharges

Multiple

SMP

Nasal irritation

Clonazepam (Klonopin) tricyclic 0.5 mg bid to tid, may increase Gabapentin (Neurontin) Valproic acid (Depakene) Other Medications Salmon calcitonin Inhibits bone (Miacalcin) nasal spray 1 resorption puff daily Direction of action on SMP unknown Narcotics and Benzodiazepines Exogenous sources of narcotics and benzodiazepines cause decreases in endorphins and endobenzodiazepines. In brain stem and limbic systems, this may lead to drug dependence, depression, and increased pain. NSAIDs Cyclooxygenase inhibitorthree actions: 1. Decreased peripheral inflammation mediated by prostanoids. 2. Spinalprostanoids facilitate substance P and glutamate pain fiber transmission.

3. Central (supraspinal effects)present mechanism is unclear. CNS, central nervous system; NSAIDs, nonsteroidal anti-inflammatory drugs; PNS, peripheral nervous system; RSD, reflex sympathetic dystrophy; SMP, sympathetically maintained pain. *Not currently accepted for treatment of reflex sympathetic dystrophy. Question of usefulness of Paxil, Prozac, and othersthere are some proponents of these selective serotonin reuptake inhibitors, but they are probably no better than other antidepressants, except for migraine headache.

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promising drug in the membrane stabilizer category is the anticonvulsant agent gabapentin (Neurontin). This drug has recently shown promise in the relief of burning neurogenic pain and improvement in sleep patterns. The mechanism of action of gabapentin is unknown, but it is believed to act centrally. It is administered orally in doses up to 1200 mg/day in divided doses. Major advantages of gabapentin are the absence of significant drug interactions and the more tolerated side effect profile compared with the antidepressants.[78] We have seen encouraging results in our patients treated with gabapentin but admit that solid evidence supporting its use is lacking. Calcium Channel Blockers

The calcium channel-blocking agent nifedipine (Procardia), in doses of 10 to 20 mg three times daily, has been associated with pain reduction and improvement in signs of sympathetic dysfunction in uncontrolled trials. Care must be taken to warn patients of the possibility of adverse effects, including orthostatic hypotension and headaches.[82] In general, nifedipine is safe and effective in our experience, particularly when it is used early in the course of the disease. Nonsteroidal Anti-inflammatory Drugs

Nonsteroidal anti-inflammatory medications may be useful in mild cases of CRPS that display typical inflammatory signs of rubor, swelling, and warmth. These medications irreversibly inhibit the enzyme cyclooxygenase, thereby reducing production of a prostaglandin. Their use as analgesic agents is generally reported to be ineffective for SMP,[58] but they may be helpful when arthritis, tendinitis, or other inflammatory disease is a painful focus. Side effects include gastrointestinal ulceration and renal or hepatic failure.[117] Capsaicin

Topical capsaicin cream (Zostrix) in concentrations of 0.025% and 0.075% may be

useful for localized areas of hyperalgesia from neurogenic causes.[58] [117] Capsaicin is a protein derived from a common hot pepper plant and acts by depleting stores of substance P from sensory neurons. Because of the initial release of substance P, the cream produces an initial burning sensation. Repeated application results in desensitization and inactivation of depleted sensory neurons. Early reports indicate that the desensitizing effect may be reversed within 2 to 4 weeks after discontinuation of the cream.[43] Opioids and Benzodiazepines

Opioid use in CRPS is highly controversial. No controlled trial demonstrating long-term efficacy and safety has been undertaken.[117] Few would dispute the efficacy of narcotic agents in temporarily reducing pain. Chronic use, however, leads to the development of drug tolerance, rendering opioids ineffective for pain control. Tolerance to opioids also creates problems of perioperative pain management when surgical intervention is necessary. The potential for drug abuse and the development of physical drug dependency are also strong arguments against the use of opioids and benzodiazepines in any nonterminal chronic pain state. In rare cases, chronic opioid administration is necessary. To minimize the potential for abuse, it is recommended that one physician dispense all narcotics.[69] We recommend avoidance of the routine use of opioid analgesics and benzodiazepines by patients with CRPS. When narcotic use is unavoidable, such as in patients already addicted, pain management consultation is appropriate. Other Medications

Calcitonin has recently gained attention for a possible mild effect on spontaneous pain. Its efficacy in the subcutaneous or intranasal form has yet to be established. When it is effective, however, the result is usually observed soon after the initiation of treatment.[117] Bisphosphonate therapy improved some patients' pain and swelling in several open trials.[2] [76] [104] Bisphosphonates are powerful inhibitors of bone resorption through the inhibition of osteoclasts. Relief of pain and swelling may be caused by an effect on prostaglandins.[104] No trial has reported results with follow-up longer than 1 year; therefore, interpretation of results must be made with caution.[104] A randomized, double-blind, placebo-controlled trial of vitamin C to prevent CRPS after wrist fractures has been published.[130] The authors showed a statistically significant difference (P = .03)[5] in the rate of development of CRPS in the vitamin C group versus the placebo group. Patients in the vitamin C group received a single 500-mg vitamin C capsule daily for 50 days after wrist fractures. The authors speculate that the protective effect of vitamin C may be exerted through its antioxidant properties, although they concede that the role of toxic oxygen radicals in CRPS is not known.[130] The limited evidence substantiating the toxic oxygen radical theory and the relatively small number of patients in this study are causes for cautious interpretation of the results.[5]

Psychotherapy

Early in the course of disease (0 to 2 months), psychological changes are not present because patients expect to be cured. Only mild abnormalities are seen on MMPI evaluations. At 2 to 6 months, patients become anxious about their disease, and this is accompanied by a progression of the MMPI abnormalities. Education of the patient is critical in this phase to lessen anxiety. Psychological counseling and stress management training are appropriate,[33] and low-dose antidepressants may be necessary. After 6 months, nearly all patients demonstrate a degree of

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depression because of sleep deprivation, chronic pain, and anxiety. If the response to suicide risk testing is abnormal, a 10-fold increase in the risk of suicide is present and psychiatric hospitalization is required. Antidepressants in higher doses may be required. Group therapy with patients with chronic pain can be beneficial. After 8 months, depression wanes as patients begin to accept the chronic disease state and adapt to it. Attendance of family members at group therapy sessions can be helpful.[117] Sympatholysis

Sympatholytic measures may be used for diagnosis as described previously, but they are more often used in treatment of CRPS. Sympatholytic procedures for diagnosis must have specificity for the sympathetic nervous system, but sympatholysis in treatment need not be specific. In general, continuous sympatholysis is probably more effective than pulsed sympatholysis, but this has not been verified in the literature. Continuous or repetitively pulsed sympathetic blockade may lead to complete resolution of the syndrome in many cases, particularly when it is used early.[69] As a result, sympatholytic techniques are commonly implemented soon after diagnosis when a short trial of conservative measures fails. Sympatholysis can be accomplished through topical patches, oral medications, interventional techniques, and surgical procedures. Topical Clonidine

Topical clonidine (Catapres) patches may have efficacy in reducing localized hyperalgesia.[25] [59] Clonidine is an alpha2 receptor agonist that inhibits presynaptic release of norepinephrine.[125] Clonidine has also been administered orally and by epidural injection in patients with CRPS, but further research is needed to evaluate efficacy and safety.[58] Oral Sympatholytics

Clinical usefulness of oral alpha blockers such as prazosin (Minipress), terazosin (Hytrin), and phenoxybenzamine (Dibenzyline) is suspect. By blocking alpha receptors,

the drugs interrupt sympathetic outflow. [82] These medications have significant cardiovascular side effects because their alpha receptorblocking effects are systemic, and their long-term efficacy is unknown. [117] Interventional Sympatholysis

Paravertebral sympathetic chain ganglion blockade techniques are described earlier. Controlled trials demonstrating significantly better results than placebo injections have not been done. Upper extremity CRPS requires stellate ganglion blockade, and lower extremity CRPS is addressed through lumbar ganglion blockade. Continuous blockade can be achieved through the use of a constant catheter infusion. More commonly, however, sympatholysis is achieved by repetitive injections of the ganglion.[62] [126] Administration of the blocks within 6 months of onset of disease is associated with a much better long-term success rate. [126] Duration of relief obtained from each injection is recorded.[95] Progressively increasing duration of relief with each subsequent block is an indication that repeating the blocks as many as 10 to 15 times may be beneficial.[129] Ultimately, the longer the pain relief after sympathetic blockade, the better the prognosis.[69] We advocate early use of multiple paravertebral ganglion blocks when a short course of medications and physical therapy fail to demonstrate significant improvements. Continuous cervical or lumbar epidural infusion can be used to treat SMP, and it is the anesthetic method of choice when surgical intervention is necessary.[66] Bupivacaine 0.25% (Marcaine) or an opioid such as fentanyl (Sublimaze) or a combination is administered through an indwelling catheter in the epidural space. Optimal dosage allows sensory and sympathetic blockade while allowing motor function so that an active physical therapy program can be performed.[24] The infusion is continued for a period of 2 to 5 days postoperatively to minimize the risk of a perioperative exacerbation of disease.[66] Continuous epidural infusion requires meticulous nursing care to prevent complications. Sacral and heel sores are prevented by log-rolling the patient every 2 hours, using heel pads and an egg crate or air mattress, and requiring patients to get out of bed at least three times daily. Physical therapy should start on the first postoperative day. Patients must be protected against deep venous thrombosis with mechanical means such as sequential compression devices and compression stockings because anticoagulant medication is contraindicated. Urinary retention may require insertion of a Foley catheter, and bladder voiding must be carefully monitored after removal of the catheter. Our procedure is to stop the infusion the night before planned discharge. The patient's pain is evaluated on the morning of discharge. If symptoms are quiescent, the catheter is removed and the patient is discharged. This protocol generally prevents iatrogenic recurrence of SMP when surgical intervention is necessary. Other methods of regional neural blockade are also possible, including brachial or lumbar plexus blocks, axillary blocks, and isolated peripheral nerve block (e.g., saphenous nerve block).[125] The efficacy of these techniques is unknown in the treatment of CRPS.

Implantable pumps and intrathecal catheters are being investigated for long-term administration of a variety of medications including bupivacaine and opioid analgesics. These techniques are currently used in severe or refractory cases. [73] [125]

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Surgical Sympathectomy

Surgical sympathectomy has been used in chronic unrelenting cases of SMP with mixed results. Surgical sympathectomy is considered only when regional sympathetic blockade provides relief, but the effect is short-lived. As with many of the treatments of CRPS, results are best when it is performed early after onset of disease.[1] [107] Relief after sympathectomy may initially be dramatic. The effect

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may be short because the symptoms tend to recur within 2 to 5 years. Multiple explanations for this recurrence have been postulated. Incomplete surgical removal of all sympathetic innervation to an extremity may be a common cause of failure. [90] Upper extremity sympathectomy must include not only the stellate ganglion but also the T2 and T3 ganglia for complete sympathetic denervation.[90] [107] Lower extremity complete sympathectomy should include removal of L2, L3, and L4 ganglia and also extend above the diaphragm, possibly as high as T10.[69] Failures have also occurred because of collateral reinnervation from the contralateral ganglion.[27] Therefore, contralateral sympathectomy is sometimes required. Bilateral interruption of sympathetic outflow carries risk of bowel, bladder, or sexual dysfunction. Another cause for concern from sympathectomy is the sudden development of deep muscle ache that has a character different from CRPS pain. Postsympathectomy neuralgia is usually self-limited and typically resolves in 2 to 3 months. In addition to open surgical disruption, ablation of the sympathetic chain ganglia may be accomplished in a number of ways. Percutaneous chemical ablation of sympathetic ganglia with phenol or alcohol is possible but risks damage to adjacent structures.[117] Radiofrequency percutaneous sympathectomy is reported as a safe means of sympathetic interruption, but efficacy is unknown. [101] Endoscopic sympathectomy is also advocated because of reduced morbidity compared with open sympathectomy and

equal efficacy. [52] [77] We do not recommend surgical sympathectomy except as a last resort in chronic refractory cases only. Neuromodulation Techniques

Neuromodulation techniques, including peripheral nerve stimulation and spinal cord stimulation, are hypothesized to work by one of two theories. In the gate control theory, stimulation of large myelinated nerve fibers blocks transmission in the smaller pain nerve fibers. An alternative theory postulates that nerve stimulation causes the release of endogenous opioids.[125] Peripheral implanted nerve stimulation may provide relief in patients with symptoms relatively confined to the distribution of one major peripheral nerve. Stimulating electrodes are surgically placed directly on the involved nerve.[22] Hassenbusch and colleagues[42] documented pain relief in 63% of patients with 2- to 4-year follow-up after peripheral nerve stimulator implantation. Spinal cord stimulation has been used for a variety of chronic pain conditions for several years.[10] [46] [64] Its efficacy in CRPS is unproven but promising nonetheless. Electrodes are implanted through laminotomy or percutaneously in the epidural space at C4 or C5 for upper extremity treatment and at T9 to T11 for lower extremity treatment. A trial period allows confirmation of symptom relief before surgical implantation of the stimulator.[56] In one published report, 12 of 12 patients achieved pain relief with average 41-month follow-up.[63] Stanton-Hicks and coworkers[117] stated that 70% of patients with CRPS will respond to peripheral nerve or spinal cord stimulation. Complications include infection, nerve damage, and electrode displacement or breakage.[56] Further study of spinal cord stimulation is needed before definitive recommendations can be made.

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Surgical Intervention

Surgical intervention in patients with CRPS should be avoided whenever possible. In patients with chronic refractory CRPS with complaints that suggest a painful non-neurologic condition, however, diagnostic arthroscopy is frequently necessary to correct a painful condition that exacerbates CRPS. In those cases, surgical intervention becomes unavoidable and should be performed as soon as CRPS symptoms are quiescent.[23] [55] Optimal control of CRPS symptoms is desirable at the time of surgical intervention. Continuous postoperative epidural infusions for 2 to 5 days will help prevent exacerbations of CRPS.[24] [66] In general, tourniquet hemostasis is to be avoided.[124] Exacerbation of CRPS after surgical procedures is reported to occur in 13% to 47%.[55] [124] CRPS of the knee commonly requires surgical intervention to correct intra-articular disease or to rule out intra-articular derangement definitively. Patellofemoral surgery is associated with a high rate of exacerbation of CRPS symptoms. [30] Injury to the saphenous nerve or its branches can produce a saphenous neuritis, which is a form of CRPS type II.[72] [93] [94] Operative resection of painful neuroma or release of nerve entrapment has been shown to be effective in selected cases of CRPS type II.[53] [131] To avoid injury to the infrapatellar branch, a medial portal incision can be made horizontally and above the joint line. In addition, the concomitant vein can be transilluminated with the arthroscope in the lateral portal to avoid the nerve. [99] Chronic CRPS of the knee is associated with the development of patella infera and arthrofibrosis.[9] Although frustrated patients with chronic unrelenting CRPS may demand amputation, results of this treatment are alarming. Dielissen and associates [26] reviewed the results of 34 amputations in patients with CRPS with intractable pain. Only two patients obtained complete pain relief after amputation. Twenty-eight patients experienced CRPS symptoms in the stump, and phantom pain and phantom sensations occurred in 24 and 29 patients, respectively. [26] Because of these appalling statistics and poor

outcomes, amputation for treatment of CRPS should be avoided.

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Complex Regional Pain Syndromes in Children

Complex regional pain syndrome is a commonly missed diagnosis in children.[84] Wilder and colleagues[128] found that the average time between disease onset and diagnosis in children was 12 months. CRPS affects children in a ratio of girls-to-boys of 3:1.[84] The most common age group affected is the 9- to 15-year-old cohort.[112] [125] In contrast to CRPS in adults, lower extremity involvement is more common than upper extremity disease in children.[84] [125] Bone scan findings in children with CRPS are typically normal, and therefore bone scans are used primarily to rule out other causes of extremity pain, such as infection, tumor, osteoid osteoma, and stress fracture. [125] In addition, this disease in children is typically triggered by emotional or psychological stress or a minor trauma.[84] The treatment program typically centers on stress management, psychological counseling, and behavioral modification techniques.

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Psychiatric referral is recommended early as a matter of routine.[84] Children with CRPS commonly have dysfunctional family situations; therefore, family therapy is often needed as well.[117] Children with CRPS typically respond to conservative forms of treatment better than adults do.[112] [117] [125] Aggressive physical therapy employing exercise programs that build up to 5 hours per day are the mainstay of treatment.[112] Parents should not be allowed to be present during exercise sessions because parental presence may hinder the child's progress.[112] The judicious use of medications, such as nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, or anticonvulsants, is sometimes helpful.[117] [128] Sympathetic blocks become necessary only when physical therapy is intolerable or unsuccessful at resolving symptoms.[125] When sympathetic blockade techniques are necessary, a single block is generally sufficient. Repeating sympathetic blocks multiple times, as is commonly done in adults, is usually not required in

children.[117] In general, the prognosis of the disease in children is somewhat more favorable than that for the adult form. [112] [117] [125] Murray and coworkers[84] reported that the median time from diagnosis to recovery was 7 weeks in the majority of their patients, although late recurrences were common. In rare cases in children, however, a severe and debilitating form of the syndrome may occur that may be refractory to traditional conservative treatment methods.[84] These patients commonly require more aggressive forms of treatment and typically will experience a chronic or recurring form of the disease. As an alternative to repeated injections, a continuous infusion catheter technique for sympathetic blockade is preferable. Only in the most severe and refractory cases is spinal cord stimulation or sympathectomy required.[117] In dealing with athletic children who develop CRPS, the clinician must be sensitive to the possibility that a child's disease may offer an escape from intense competition and parental expectations. Therefore, return to athletic participation must not be the primary goal; rather, treatment should focus on pain relief, functional rehabilitation, and improvement in school attendance.[125] Overall, Wilder and colleagues[128] reported a 50% rate of return to sports in children with CRPS who were involved with athletics before the onset of disease. Many of those who did not return to athletic participation required long-term management plans.[128]

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Authors' Preferred Method of Treatment

Orthopaedic surgeons are frequently the first to see the signs and symptoms of patients with CRPS. This places the surgeon in the best position for early diagnosis and successful treatment of patients with CRPS ( Fig. 9-4 ). Some of the simpler interventions, when used early, have the highest chance of success; therefore, the orthopaedic surgeon should be comfortable using some of these techniques. When patients present with chronic CRPS, the

Figure 9-9-4 An algorithm showing the decision-making process in the diagnosis and treatment of sympathetically maintained pain (SMP). MRI, magnetic resonance imaging; PT, physical therapy; TENS, transcutaneous electrical nerve stimulation.

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orthopaedist's role may be limited to finding and correcting a painful non-neurologic cause that perpetuates the CRPS. Long-term management of patients with chronic CRPS is often best undertaken in a specialized pain clinic. Patients may often present in the office with early signs of CRPS, such as stiffness of the hand and upper extremity, burning pain, or changes in sweating. In patients with symptoms of short duration, massage and gentle active range of motion will occasionally cause these symptoms to resolve. If physical measures alone are not enough to resolve symptoms, our preference is to provide the patient with a steroid burst and taper (Medrol Dosepak). Once the 3- to 5-day course of steroid is completed, the patient should return and report symptoms to the physician. When taken early enough in the course, this treatment will often prevent

progression and actually reverse the effects of CRPS. If this provides partial but incomplete relief, a second steroid burst and taper will sometimes be prescribed. For those patients not responding to steroids who are in a later stage of CRPS, we recommend a quick referral to a skilled anesthesiologist for cervical or lumbar sympathetic blockade. Skin temperature should always be monitored, and repeated blocks should automatically be scheduled if the patient obtains good but temporary relief. Patients who do not respond to these methods need specialized care and should be referred to a pain center experienced with the treatment of CRPS. Orthopaedists who are familiar with the use of several drugs may continue their use in patients with persistent symptoms of CRPS after treatment. Salmon calcitonin (Miacalcin) can be used with few side effects and may help prevent bone loss in the female patient as well. Nifedipine (Procardia) has relatively few and easily controllable side effects and seems to help patients, particularly when they have flares of symptoms during cold weather. Most orthopaedists are not comfortable using multiple drug combinations; therefore, these patients would be better served by referral to a neurologist or other physician experienced in multiple-drug therapy. The exact cause and nature of CRPS are still not completely understood. Its many manifestations, however, are well described. Orthopaedic surgeons can perform a tremendous service to the patient by recognizing the symptoms and initiating treatment as early as possible. Orthopaedists can also play a major role in the treatment of CRPS by finding underlying painful organic causes and correcting these through methods that are as painless as possible. The orthopaedist is both the primary care physician and the specialist in dealing with patients with CRPS. Appropriate medical and surgical treatment works best to bring about recovery in these patients.

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Information for the Patient

Several support groups currently exist on the World Wide Web, which provides information and support to patients with CRPS. These sites are the Reflex Sympathetic Dystrophy Syndrome Association of America (www.rsds.org), the International Reflex Sympathetic Dystrophy Foundation (www.rsdinfo.com), the Reflex Sympathetic Dystrophy Coalition (www.rsdcoalition.com), and the International Association for the Study of Pain (www.halcyon.com/iasp).

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van der Laan L, Veldman P, Goris RJA: Severe complications of reflex sympathetic dystrophy: Infection, ulcers, chronic edema, dystonia, and myoclonus. Arch Phys Med Rehabil 79:424-429, 1998. 122.

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Veldman PHJM, Goris RJA: Surgery on extremities with reflex sympathetic dystrophy. Unfallchirurg 98:45-48, 1995. 124.

Walker SM, Cousins MJ: Complex regional pain syndromes: Including reflex sympathetic dystrophy and causalgia. Anaesth Intensive Care 25:113-125, 1997. 125.

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Wu CT, Ho ST, Tsai CS, et al: Repeated lumbar sympathetic blockade for complex regional pain syndromes type Ia case report. Acta Anaesthesiol Sin 36:155-158, 1998. 129.

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Chapter 10 - Nutrition for Sports Leslie Bonci MPH, RD

For an athlete to perform to his or her best ability, the body must be optimally fueled. Not only is nutrition important on the playing field, but also it promotes muscle growth, enhances recovery, prevents injury, and supports rehabilitation. The science of nutrition is constantly expanding, as are consumer confusion and misinformation. Confounding the issue further is the increasing availability and variety of so-called sports supplements aimed at helping an athlete become faster, stronger, and leaner. Any health professional involved in the care of athletes needs to understand the basics of sports nutrition from macronutrient and micronutrient requirements to weight management and supplements. Sports nutrition is a part of the athlete's training, and those who fuel optimally improve performance and health. The collection of baseline data for athletes with a basic nutrition screening form can be invaluable in troubleshooting, making referrals, and enhancing performance. Figure 10-1 details a nutrition screening form for athletes. The few minutes it might take for an athlete to complete this form can help to identify the individual who may be at risk for disordered eating, injury, and overtraining. Goals of Sports Nutrition

The goals of sports nutrition are: To achieve and maintain ideal body mass To maintain proper hydration and electrolyte balance To provide adequate carbohydrates to optimize respiratory metabolism To preserve lean body mass with essential amino acids To maximize oxygen delivery systems and oxidative phosphorylation with trace elements To develop high-density skeletal structure To promote recovery from training To improve performance by increasing the speed of muscle fiber contraction and the number of muscle fibers that contract Qualitative similarities exist across the spectrum of athletes, but there may be quantitative differences based on type of sport, gender, body composition, and age. In discussing the science of sports nutrition, it is important to understand the energy systems and the energy substrates that fuel activity.

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Energy Systems

For any muscle to do physical work, adenosine triphosphate (ATP) is required. ATP is the energy catalyst derived from the storage forms of carbohydrate and fat (i.e., glycogen and fatty acids) and must be continuously formed, used, and reformed during physical activity. The other storage form of energy that can be used to fuel activity is creatine phosphate, or phosphocreatine. Creatine is manufactured in the liver, the kidneys, and the pancreas and is stored in muscle. When energy demand increases during exercise, the body relies on different types of energy systems to transfer stored energy to ATP to enable physical work to continue. Three energy systems are used, depending on the duration and the intensity of exercise. The phosphagen system is the initial system used when energy demand increases. This is an anaerobic energy system dependent on ATP and creatine phosphate for high-intensity, maximal outburst activity lasting less than 1 minutethe energy required for a powerlift, a 6-second sprint, or a slam dunk. As the duration of activity increases and the availability of ATP and creatine phosphate diminishes, the anaerobic glycolysis system allows ATP to be produced under anaerobic conditions for an additional 1 to 3 minutes. This energy system is used at the beginning of a road race; for a short-duration, high-intensity event such as a 400-meter sprint; in sports that are a combination of endurance and maximal outbursts, such as soccer, football, hockey, and basketball; and at the end of a road race. The aerobic system uses the three fuel substratescarbohydrate, fat, and proteinin the form of glucose, fatty acids, and amino acids. Carbohydrate stores are not unlimited, and the aerobic system allows the use of fatty acids as a fuel, thereby sparing glycogen. Protein is used as an energy source when glycogen stores are limited, but it is not the preferred fuel source for the body.

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Energy Substrates

To be fueled optimally during activity, the body must have adequate stores of the macronutrients used as energy substrates. Glycogen, the storage form of carbohydrate, is stored in the muscle and liver. The majority of exercise is fueled by carbohydrate and fat; protein provides a fuel source if carbohydrate stores are inadequate. Fuel use is determined by the intensity and the duration of activity as well as by the level of training. Muscle glycogen is the major source of carbohydrate, followed by liver glycogen and then blood glucose. Aerobic training and diet manipulation can significantly increase muscle glycogen stores.[36] Muscle glycogen is used for intense, short-duration activity as well as for endurance exercise. The rate of muscle glycogen use is most rapid during the early part of exercise and is related to exercise intensity. Muscle glycogen declines with continued exercise and is selectively depleted from the muscles that are involved in physical work. As muscle glycogen stores decline, blood glucose and liver glycogen become important fuel sources. Plasma free fatty

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Figure 10-10-1 Nutrition screening form for athletes. HMB, beta-hydroxy-beta-methylbutyrate; DHEA, dehydroepiandrosterone.

acids are used as a fuel source during endurance-type activities through the process of adipose tissue lipolysis. As mentioned earlier, amino acids can be broken down to glucose to provide energy during activity, but only when carbohydrate stores are low. One of the main concerns of athletes is to prevent fatigue. When inadequate rest is ruled out as a causal factor, suboptimal nutrition can be a significant cause of fatigue

through one or more of the following mechanisms: Inadequate fluid intake Inadequate calorie intake Inadequate carbohydrate intake Inadequate protein intake Iron deficiency Vitamin and mineral deficiency

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Hydration

Fluid balance is essential to cardiovascular function, thermoregulation, injury prevention, optimal performance,

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and recovery from exercise. Fluid loss can be significant during exercise (up to 3 L/hr).[25] Fluid loss increases heart rate by 8 beats per minute and impairs performance when it is more than 1.8% of total body water; mental functioning is impaired through a decrease in sustained attention, response time, and task accuracy, and error rate is increased.[20] Heat-related injuries increase with increased body water loss. In addition, an athlete can become dehydrated because of changes in altitude, increases in training intensity and frequency, sudden climate changes, and long plane flights. The body cannot tolerate even slight dehydration, but unfortunately, thirst sensation is dulled by exercise, and voluntary fluid consumption is insufficient to meet fluid needs. Dehydration also reduces the gastric emptying rate, complicating the rehydration process.[23] Curtailing fluid intake is a common practice in certain sports. The chronic dehydration that often accompanies weight-class sports can impair the athlete's ability to train and compete optimally. The goal of fluid intake is to prevent dehydration. The American College of Sports Medicine published a position stand on fluid replacement in 1996 providing the rationale and the guidelines for hydration.[1] Athletes require a minimum of 20 to 48 ounces of fluid per hour of exercise, but most athletes consume only 8 ounces per hour.[1] A larger fluid intake during exercise leads to greater cardiac output, greater skin blood flow, lower core temperature, and reduced perceived effort of exertion.[24] The overall goal is clear and copious urine as a sign that the body is well hydrated. Athletes may ask for a recommendation about the types of fluid to consume. It is important to consider the sport, the duration, the calorie needs, and the taste preferences. Water is a noncalorie fluid that works well for short-duration activities, but it

not as beneficial for exercise lasting longer than 60 minutes. Juices can provide calories and carbohydrate, but they contain fructose, which has a decreased absorption rate and may cause gastrointestinal distress; juices are generally not advised before exercise. Carbonated beverages before activity may cause gastrointestinal distress and often confer a feeling of fullness before fluid needs have been met. Caffeine-containing and alcoholic beverages have a diuretic effect, causing the body to lose valuable fluids before activity begins. The sports drinks can be an appropriate option for longer-duration sports and are certainly extremely popular with young athletes. The sports drinks contain a dilute glucose solution that stimulates water and sodium absorption so that more fluid is absorbed than from plain water. [17] [18] Because sports drinks have a fairly low carbohydrate content, they empty more rapidly from the stomach than a more concentrated beverage does. For optimal gastric emptying to be achieved, fluids should be cold or cool. A large volume of fluid empties more rapidly than smaller amounts do. One liter of fluid empties from the stomach and will be absorbed by the intestine within 1 hour.[1] Athletes need to practice drinking during training to determine a comfort level and to learn to drink proactively, instead of reactively. The recommended fluid intake is 2 to 3 quarts of fluid per day for basic needs plus 1 liter of fluid for every 1000 calories expended.[1] Fluid guidelines for specific sports are listed in

Sport

TABLE 10-1 -- Fluid Guidelines for Specific Sports Cups of Fluid per Hour

Hockey

3-6

Football

3-6

Volleyball

2.5-4

Soccer Males Females

3-5 2.5-4

Basketball Males Females

3-6 2.5-4

Table 10-1 .[24] Strategies for fluid replacement before, during, and after exercise are as follows[1] : Before exercise 500 mL (17 ounces) of fluid 2 hours before exercise 16 ounces of fluid 30 minutes before exercise 8 to 16 ounces of fluid 15 minutes before exercise During exercise 4 to 8 ounces of fluid every 15 to 20 minutes during exercise with sports drink for sports lasting longer than 1 hour

After exercise 24 ounces of fluid for every pound lost during exercise to achieve normal hydration within 6 hours after activity For children younger than 10 years, the goal is to drink to satisfy thirst plus an additional 3 to 4 ounces of fluid. Older children and adolescents should also drink to satisfy thirst plus an additional 8 ounces of fluid.[2] Some athletes may inquire about the use of glycerol for hyperhydration. Glycerol is a three-carbon molecule that is the structural core of triglycerides and phospholipids. Glycerol ingestion increases blood osmolarity, decreasing urine production and increasing fluid retention. Even though glycerol is easily absorbed, the increased weight may be a disadvantage, and glycerol loading can cause headaches, dizziness, bloating, and nausea.[19] If an athlete wants to try glycerol, the best option may be to try a premixed solution, such as Pro Hydrator, or to purchase glycerate and mix it with water in the proportion of 0.45 g of glycerate per pound of body weight mixed in 48 ounces of water and consumed 1 to 1½ hours before exercise.[33] This should be tried only in a practice situation, when the athlete can assess his or her tolerance to glycerol, without the stress of a competition situation. To encourage optimal hydration, coaches, athletic trainers, parents, and other health care professionals can assist the athlete in the following ways: Recommend that the athlete carry fluid with him or her. Dry mixes of lemonade, fruit punch, or sports drinks are lightweight and easy to carry, and they can be added to drinking water to provide fluid and carbohydrate. Reinforce the need to drink on schedule, not sporadically. Advise the athlete to drink beyond thirst. Advise the athlete to drink enough before exercise to have a full stomach. Gastric emptying is more rapid and efficient when the stomach is somewhat full rather than empty. 464

Instruct the athlete that fluid is useful to the body only if it is swallowed, not poured over one's head. Gently encourage beverages other than alcoholic and caffeine-containing ones. These are not optimal rehydration beverages because of their diuretic potential.

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Calorie Requirements

Working muscles require fuel; if calorie needs are suboptimal, the body will fatigue earlier and performance will be curtailed. Some athletes regularly undercut their energy needs, increasing the likelihood of early fatigue and risk of injury. Others eat in excess of need, resulting in excess stores of adipose tissue, which can adversely affect performance. Calorie needs are higher for an athlete than for a nonexercising person and need to be individualized according to gender and weight. An athlete who has been injured may require additional calories early in the recovery process to aid tissue repair, but fewer calories are often required as the frequency and intensity of activity decline. Athletes who retire from their sport need to learn how to eat less than in their playing days or suffer the consequences of carrying around excess weight. In general, the calorie requirements for active adults, children, and adolescents are as follows: Men: weight (pounds) × 23 = minimum number of calories per day[33] Women: weight (pounds) × 20 = minimum number of calories per day[33] Children and adolescents: Boys and girls aged 7 to 10 years: 2000 calories per day[14] High-school boys: 3000 to 6000 calories per day[14] High-school girls: 2200 to 4000 calories per day[13] The composition of these calories influences performance. The primary fuel substrates for activity are carbohydrate and fat; protein plays more of a supporting role. The goal is to achieve a balance in the diet through a mix of carbohydrate, protein, and fat. This has become especially challenging in light of the popular eating plans recommending that entire categories of foods be limited or avoided. Endurance athletes have traditionally relied heavily on carbohydrate as the mainstay of diet, whereas in strength-type sports (e.g., football), athletes have been told that a high-protein diet should be the focus. Although the overall amount of food consumed may vary, every athlete should aim to include protein, carbohydrate, and fat at every

meal and snack.

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Carbohydrate Requirements

Achieving optimal carbohydrate nutriture is important to maintain the usual training intensity, to prevent hypoglycemia during exercise, to serve as fuel substrate for working muscles, and to assist in postexercise recovery. Carbohydrate use increases with increased exercise intensity but decreases with increased exercise duration. The higher the initial glycogen stores, the longer an athlete can exercise TABLE 10-2 -- Carbohydrate Needs per Hour of Training Hours of Daily Training Grams of Carbohydrate per Pound of Body Weight 1

2.7-3

2

3.6

3

4.5

4+

5.4-5.9

at a given intensity level. The goal of carbohydrate feeding is to fill carbohydrate stores in the muscles and liver. Eating increases glycogen stores, whereas exercise depletes glycogen stores. Glycogen depletion can occur in sports requiring nearly maximal bursts of effort. Athletes who do not optimally refuel may experience gradual and chronic glycogen depletion that can decrease endurance and performance. Training glycogen depletion is often accompanied by a sudden weight loss. For optimal glycogen stores to be maintained, carbohydrate needs must be estimated on the basis of the number of hours the athlete trains daily. Carbohydrate requirements are always higher for training than for competition. Athletes may consume inadequate amounts of carbohydrate because of calorie restriction, avoidance of certain foods (e.g., sugar), fad diets, sporadic or infrequent meals, and poor nutrition knowledge of good carbohydrate sources versus marginal choices. Needs can be estimated as in Table 10-2 .[9] [34] There has been much discussion about which type of carbohydrate is better for sports,

simple or complex. The distinction is not that clear, and what matters most is the total amount of carbohydrate consumed on a daily basis. Athletes can use the nutrition facts panel on a food label to quantify the amount of carbohydrate ingested. Some athletes are more comfortable ingesting carbohydrates in a liquid form, such as Gatorade Energy Drink, UltraFuel, and the like. Table 10-3 lists some of the most frequently consumed carbohydrate-containing foods. Athletes have recently begun experimenting with manipulating the type of carbohydrate consumed at various points

Food

TABLE 10-3 -- Carbohydrate Content of Certain Foods Amount Carbohydrates (g)

Bagel

2 ounces

38

Bagel

4 ounces

76

Cheerios

1 cup

23

Corn Pops

1 cup

28

Granola, low-fat

1 cup

82

Swedish fish

1 handful

39

Orange juice

8 ounces

27

Coke

8 ounces

27

Gatorade

8 ounces

14

Sports gel

1 ounce

28

Gatorade Energy Drink

12 ounces

79

Yogurt, fruit

8 ounces

42

Raisins

¼ cup

31

Pretzels

1 handful

22

465

during exercise according to the glycemic index of the food.[7] The glycemic index indicates the actual effects of carbohydrate-rich foods and fluids on blood glucose and insulin levels. The glycemic index ranks foods by measuring the blood glucose response after ingestion of a test food that provides 50 g of carbohydrate compared with the blood glucose response to a reference food. The response reflects the rate of digestion and absorption of a carbohydrate-rich food. Foods are classified into the three categories of high, moderate, and low glycemic index as outlined in Table 10-4 . Manipulating the meal choices on the basis of the glycemic index may enhance

carbohydrate availability and improve athletic performance. Carbohydrate-rich foods of low glycemic index may help to promote sustained availability of carbohydrates when they are consumed before exercise. Carbohydrate-rich foods of moderate to high glycemic index may promote carbohydrate oxidation when they are ingested during exercise and may promote glycogen repletion when they are consumed after exercise. Athletes will need to experiment to find out which foods work well and, more important, do not cause gastrointestinal distress. Consuming dried beans or lentils before exercise may be fine for a cyclist, but it may not be desirable for a runner. Athletes have also experimented with the concept of carbohydrate loading or muscle glycogen supercompensation, which combines tapering of exercise with a high-carbohydrate intake to top off muscle glycogen stores. The original method called for a depleting exercise protocol coupled with a low-carbohydrate diet, followed by 3 days of rest with an extremely high carbohydrate diet. This often made the athlete feel exhausted during the low-carbohydrate intake phase and heavy during the carbohydrate-loading phase. Current guidelines recommend 3 to 5 days of carbohydrate loading to attain maximal glycogen levels, and the exercise done to lower glycogen stores must be the same as the athlete's competitive event.[26] Carbohydrate loading is advantageous only for endurance athletes whose event lasts longer than 90 minutes. Carbohydrate loading before a 10K event is not helpful and may actually make the athlete feel heavier and stiff. Carbohydrate needs for activity are divided into three distinct time periods: before, during, and after exercise. The goal of pre-exercise carbohydrate is to provide energy for the athlete who exercises heavily in excess of 1 hour. Pre-exercise carbohydrate also helps prevent the feelings of hunger, which can be distracting, especially in a competition. The pre-exercise carbohydrate also elevates blood TABLE 10-4 -- Glycemic Index of Various Foods High Glycemic Index Moderate Glycemic Index Low Glycemic Index Glucose

Sucrose

Fructose

White bread

Soft drinks

Milk

Potatoes

Oats

Yogurt

Breakfast cereals

Tropical fruits

Lentils, dried beans

Sports drinks

Bagels, wheat bread

Pasta, rice

Carrots

Cookies, cake

Cold climate fruits

glucose levels to provide energy for the exercising muscles. Current guidelines recommend 1.8 g of carbohydrate per pound of body weight within 3 to 4 hours before exercise and 0.5 g per pound 1 hour before exercise.[27] [28]

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Example

1.8 g carbohydrate 3 to 4 hours before exercise 120-pound athlete requires 216 g carbohydrate 12-ounce glass of cranberry juice = 54 g carbohydrate 8 ounces of yogurt flavored with 1/2 cup granola = 96 g carbohydrate English muffin with 1 tbsp peanut butter and 1 tbsp jelly = 46 g carbohydrate Total: 196 g carbohydrate 0.5 g carbohydrate 1 hour before exercise 120-pound athlete: 60 g carbohydrate 12 ounces of Gatorade Energy Drink = 79 g carbohydrate Carbohydrate consumption during exercise maintains the availability and oxidation of blood glucose late in exercise and improves endurance. During exercise, the ingestion of carbohydrate exerts a liver glycogen-sparing effect, resulting in delayed hypoglycemia. Ingesting carbohydrates may also be advantageous in stop-and-go sports and should be encouraged during breaks in play. Guidelines[10] recommend 30 to 60 g of carbohydrate per hour during exercise in the form of 5 to 10 ounces of sports drink every 15 to 20 minutes 2 gels per hour + water (average, 20 to 28 g carbohydrate per packet) A handful of gummy-type candy + water The goal of postexercise carbohydrate ingestion is to elevate glucose as quickly as possible. Waiting too long to refuel will reduce muscle glycogen storage and impair recovery. The recommendation is 0.7 g of carbohydrate per pound within 30 minutes after exercise and again 2 hours later for those training longer than 90 minutes at a time.[15] Postexercise carbohydrate repletion can be from solid or liquid sources. The body can store twice as much muscle glycogen with sucrose or glucose sources than with fructose sources.[3] The following foods can be used for repletion: Lemonade

Fruit punch A concentrated carbohydrate beverage Granola Cereal bars Sweetened cereal Gummy-type candy For the 120-pound athlete, 84 g of carbohydrate: 4-ounce bagel with 1 tbsp jelly = 89 g carbohydrate 16 ounces of UltraFuel = 100 g carbohydrate

466

16 ounces of fruit punch and a cereal bar = 87 g carbohydrate Some studies have suggested that consuming protein and carbohydrate together after exercise can enhance muscle glycogen resynthesis by stimulating insulin. The recommended guidelines call for a protein-to-carbohydrate ratio of 1:3.[6] [29] [30] Examples of this are the following: Gatorade Nutrition Shake (carbohydrate-protein sports supplement beverage) Sports bars Trail mix of three parts cereal to one part nuts Yogurt and granola

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Protein Requirements

Although most athletes are aware of the need for carbohydrate as part of a good training diet, protein intake tends to run the gamut from minimal to excessive; the athletes who need the most consume the least, and those who need the least consume the most. Protein is important for muscle growth and aids in recovery and repair after muscle damage. As a fuel source, protein provides up to 15% of the fuel during activity, when muscle glycogen stores are low, and only 5% when muscle glycogen stores are adequate.[16] As exercise increases in intensity and duration, so does the use of protein as a fuel source. Exercise promotes muscle protein loss because of reduced protein synthesis and increased protein catabolism during and immediately after exercise.[16] With training, the breakdown and loss of muscle protein diminish, which is why protein needs are often higher in the initial phases of training than in an athlete who is well trained. As a result of training, protein anabolism is enhanced in the recovery period after exercise, and regular training increases the effectiveness of protein synthesis during recovery.[16] If training sessions are too frequent or protein intake is insufficient to meet needs, protein catabolism will exceed anabolism, resulting in reduced gains or loss of body protein.[16] Achieving optimal protein nutriture can be challenging. Athletes who do not meet their needs are more likely to have decreased muscle mass, suppressed immune system, increased risk of injury, and chronic fatigue. Conversely, athletes who routinely exceed protein needs may have increased risk of dehydration, increased body fat stores, calcium loss, and an unbalanced diet that is often deficient in carbohydrate. Protein requirements are outlined in Table 10-5 .[8] Strength-training athletes have traditionally emphasized protein, sometimes to the exclusion of other essential nutrients, and more protein is initially required to support an increase in muscle mass, but not in excess of 1 g of protein per pound of body weight. Surprisingly, endurance athletes also require more protein in the early stages of training to increase aerobic enzymes in the muscle, to form red blood cells and myoglobin, and to replace protein stores that are oxidized during exercise. Food sources of protein will ideally compose the majority of the protein in the diet, rather than protein powders or

amino acid supplements. Table 10-6 lists various food sources of protein. Many athletes are drawn to protein powders or amino TABLE 10-5 -- Protein Requirements for Various Types of Athletes Type of Athlete

Protein Requirements (g/pound body weight/day)

Recreational athlete

0.5-0.75

Competitive athlete

0.6-0.9

Athlete building mass

0.7-0.9

Teenage athlete

0.9-1.0

Athlete restricting intake

0.7-1.0

Maximal usable amount by athletes in weight-class sports (e.g., crew, wrestling)

1.0

acid supplements as a means to increase protein intake. No studies have shown benefits of amino acid supplements as an ergogenic aid, and gastrointestinal distress can be a problem. [16] Protein powders can be fairly costly; they require mixing, and palatability can be a problem. If an athlete wants to use a protein powder, nonfat dry milk powder is inexpensive, shelf stable, and tasteless, and it is an excellent source of calcium as well. As of August 2000, the National Collegiate Athletic Association will permit institutions to provide only non-muscle-building supplements to student athletes, so meeting protein needs through food will be extremely important.[22]

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Fat Requirements

Fat is an energy substrate for low-intensity, longer duration exercise. Fat supplies a concentrated calorie source to provide energy for the athlete. A diet that is too low in fat may limit performance by inhibiting intramuscular triglyceride storage, therefore resulting in earlier fatigue during exercise.[35] Excess fat intake can increase fat stores and cause gastrointestinal discomfort before exercise. Conversely, inadequate fat intake can decrease serum testosterone

Food

TABLE 10-6 -- Protein Content of Select Foods Amount Protein (g)

Chicken breast

3 ounces

21

Chicken thigh

3 ounces

21

Cod

3 ounces

21

Hamburger

3 ounces

21

Steak

3 ounces

21

Pork chop

3 ounces

21

Egg

1

7

Soy burger

1

15-18

Nuts

¼ cup

10

Peanut butter

2 tbsp

8

Cheese

1 slice

7

Refried beans

½ cup

7

Milk

8 ounces

8

Yogurt

8 ounces

9-11

Protein powders

per scoop

32-45

Nonfat dry milk powder

¼ cup

8

Amino acid pills

1 serving

10

467

TABLE 10-7 -- Fat Content of Select Foods Amount Fat Content (g)

Food Item Olive oil*

1 tbsp

14

1 tbsp

11

1 tbsp

11

Italian*

1 tbsp

7

Ranch

1 tbsp

10

Blue cheese

1 tbsp

8

¼ cup

32

Peanut butter

2 tbsp

16

Cream cheese

2 tbsp

11

Bacon

2 slices

6

Chips

1 ounce

10

French fries

small

12

Ice cream

1 scoop

20

Prime rib

3 ounces

23

Burger

1 regular

10

Big Mac

1

32

Drumstick, fried

1

11

Wing, fried

1

15

Soft margarine

*

Mayonnaise Salad dressings

Nuts

* *

*Heart healthier choice.

concentration, therefore decreasing muscle mass.[5] The recommendation for fat intake

is weight (pounds) × 0.45 = number of grams of fat per day. [21] Sources of fat are listed in Table 10-7 .

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Micronutrient Requirements

Athletes often inquire about the need for vitamin and mineral supplementation. The needs of an athlete may be slightly higher than those of someone who does not exercise regularly, but these requirements can be met through a multivitamin and mineral supplement, not a megadose tablet. In 1998, the Food and Nutrition Board of the National Academy of Sciences established Dietary Reference Intakes for select vitamins and minerals.[12] These recommendations are listed in Table 10-8 . For athletes who need to boost iron stores through food or supplemental iron, TABLE 10-8 -- Dietary Reference Intakes Zinc: 15 mg Vitamin C Women: 75 mg Men: 90 mg Tolerable upper limit: 2000 mg Iron Women: 15 mg Men: 10 mg Calcium, men and women 9-13 yr: 1300 mg 19-50 yr: 1000 mg >51 yr: 1200 mg

Tolerable upper limit: 2500 mg it is important to note that some foods and nutrients interfere with iron absorption: Phytates (bran, whole grains) Oxalates (spinach, beer, nuts) Polyphenols (coffee, tea) Excess intake of calcium and magnesium The following factors help to enhance iron absorption: Heme iron (animal source) Low body stores of iron Consuming a food high in vitamin C with meals Waiting 1 hour before or after meals to drink coffee or tea

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Weight Management Issues

Every athlete has to face issues surrounding weight at some point in his or her career. The question is whether body fat or weight is the most important variable, and the answer depends on the type of sport. Weight standards are used more in certain sports than in others, such as Sports based on skill (archery, bowling)weight is generally not an issue Sports with weight division (crew, wrestling, jockeys) Sports with low body fat for optimal performance (distance runners) Sports with appearance and aesthetic criteria (gymnastics, figure skating) Many athletes strive to attain the lowest body fat possible, jeopardizing health and performance in the process. Disordered eating behavior to make weight can decrease the metabolic rate, making the body less efficient at burning fat. Rapid weight loss reduces the plasma volume and blood distribution to active tissues and may adversely affect thermoregulation, which can impair performance. Because athletes will do whatever it takes to make weight, guidelines are presented here for making weight, for weight loss, and for weight gain. An athlete who is interested in losing or gaining weight should seek the expertise of a sports nutritionist who can customize a program to allow the athlete to meet his or her goals. Table 10-9 provides guidelines for making weight in weight-class sports. Because athletes often try fad diets for weight loss that are often restricted in energy intake, the end result can be a tired, poorly nourished athlete who is overly hungry and does not exercise or recover efficiently. Table 10-10 offers some commonsense guidelines for weight loss that can help the athlete to achieve his or her goals without sacrificing energy. Achieving success with weight management requires a minimal investment of 3 months to change the underlying habits that determine food choices.

Some athletes, try as they can, seem unable to gain TABLE 10-9 -- Techniques for Making Weight Maintain weight within 2-5 pounds of weight class during training 7-10 days before a competition, the athlete can try the following: Decrease sodium intake through added salt and salty snacks Decrease high-fiber foods, which can cause the body to retain fluid 1 day before: Liquid meals instead of solid meals

468

TABLE 10-10 -- Weight Loss Guidelines Healthy weight loss is 1-2 pounds per week Smaller, more frequent meals are preferred to larger, sporadic meals Decrease empty calories from beverages, high-calorie snacks, condiments, and dressings Make eating purposefulknow what is being consumed, and pay attention to the portion Eat foods with fiber to promote a feeling of fullness. They also take longer to eat Eat foods that promote satiety (foods with some fat enable the body to feel fuller for longer) Eat to satisfy taste and appeal to all of the senses weight. The problem is often an erratic eating pattern and the assumption that eating as much as one can at one time will rectify the problem. Consistency with number of meals per day is the most important variable for weight gain. Table 10-11 outlines techniques for weight gain.

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Supplement Use

Athletes have always been in quest of products that will make them stronger, leaner, and faster. Genetics, talent, training, and optimal fuel are certainly the most important variables, but that will not stop athletes from looking for the edge. The major issues of the moment are the wide-spread availability of supplements, the lack of purity, and the belief that more must be better. Health care providers must be aware of the products athletes take and why they are taken. These are some important facts about supplements: Supplements are not one size fits all. The terms natural and safe are not synonymous. Supplements may interfere with prescribed medications. Athletes may not willingly disclose information about supplements being used. Supplement use is not necessarily according to package instructions. Supplements may be sports specific. Supplements do not confer the same effects in everyone who takes them. The efficacy of any supplement depends on the underlying diet, hydration status, and training level. The issue of stacking has become a problem with over-the-counter supplements. The Internet has increased the availability and accessibility of supplements. The Dietary Supplement and Health Education Act of TABLE 10-11 -- Techniques for Weight Gain Aim for 500-1000 additional calories daily Eat on a schedule, more frequent meals and snacks The goal is ½ pound of weight gain per week

Foods and beverages need to contain calories (juice instead of water) Choose higher-calorie items (nuts instead of pretzels) Eating needs to be a priority

TABLE 10-12 -- Nutrition Resources Books Sarubin A: The Health Professional's Guide to Popular Dietary Supplements. Chicago, American Dietetic Association, 2000. Williams MH: The Ergogenics Edge: Pushing the Limits of Human Performance. Champaign, Ill, Human Kinetics, 1998. PDR for Herbal Medicines. Montvale, NJ, Medical Economics, 2000. PDR for Nutritional Supplements. Montvale, NJ, Medical Economics, 2001. Web Sites Dietary Supplements: An Advertising Guide for Industry: http://www.ftc.gov/bcp/guides/guides.htm Dietary Supplements Quality Initiative: http://www.dsqi.org Product Evaluation: Consumer Labs: www.consumerlabs.com Office of Dietary Supplements (National Institutes of Health): http://dietary-supplements.info.nih.gov Gatorade Sports Science Institute: www.gssiweb.com International Bibliographic Information on Dietary Supplements (IBIDS): http://odp.od.nih.gov/ods/databases/ibids.html National Center for Drug Free Sport: (816) 474-8655 or http://[email protected] 1994 details labeling guidelines that were put into effect in March 1999. Labels must have a supplement facts panel, detailing contents and amount, and an ingredient list. This act also allows companies to make claims about their products that can cause consumer confusion. Table 10-12 lists helpful resources for the health professional and the athlete. Whether at the recreational, high-school, collegiate, professional, or Olympic games level, athletes have turned to nutritional supplements as ergogenic aids or performance enhancers. Supplements are advertised to do anything from alter body composition to boost energy, improve memory, and eradicate pain. Many products are innocuous, but some can be harmful and ergolytic, or performance detracting. The most commonly used supplements are listed in Table 10-13 . With all of these products, the major issues are the

TABLE 10-13 -- Most Commonly Used Supplements Muscle-building supplements Creatine Protein powders Amino acid supplements Prohormones: DHEA, androstenedione, norandrostenediol, Tribulus terrestris (Tribestan), yohimbe Thermogenic products or fat burners Ephedra Caffeine Chitosan L-Carnitine Pyruvate Hydroxycitrate Energy boosters Ginseng Carbohydrate supplements Vitamin-mineral supplements Products for pain management Glucosamine, chondroitin DHEA, dehydroepiandrosterone.

469

safety, purity, efficacy, cost, and in certain cases legality of the supplement. The results with creatine have not been consistent, and the added weight with a loading regimen may be a performance detractor more than an enhancer. Ephedra is a potent central nervous system stimulant that can cause elevated heart, blood pressure, and respiration rates in addition to insomnia, jitteriness, chest pain, and stroke. The safe level is 24 mg in a 24-hour period, and many of the products exceed this dosage. [11] Ephedra is a banned substance in the National Collegiate Athletic Association, the International Olympic Committee, and, most recently, the National Football League. Protein powders are costly and in many cases provide more protein to the body than can be used efficiently. An athlete who is adamant about taking a protein product would be well advised to try nonfat dry milk powder or an Instant Breakfast product as an excellent source of protein and calcium at a low cost. Amino acid supplements are an inefficient, costly fuel source for the body that can cause gastrointestinal distress. Prohormones

such as dehydroepiandrosterone (DHEA), androstenedione, norandrostenediol, and Tribulus terrestris are substances banned by the National Collegiate Athletic Association, the National Football League, and the United States Olympic Committee. Yohimbe may cause kidney damage, and chromium does not confer an anabolic effect. Some products have a laxative or diuretic effect, such as Dieter's Tea, hydroxycitrate, and caffeine (as Taroxotone, guarana, mate, or kola nut). Products for weight loss, such as pyruvate and hydroxycitrate, have been used clinically in doses far exceeding those of products sold over the counter. Chitosan and quercetin are ineffective weight loss agents. Although glucosamine and chondroitin may help with the pain, swelling, and tenderness associated with osteoarthritis, there may be a 2-month trial period before results are seen. Glucosamine may cause indigestion and nausea and may worsen insulin resistance in persons with diabetes.[4] [32] Chondroitin sulfate may also cause indigestion and nausea and is contraindicated for hemophiliacs or individuals receiving blood-thinning medications or aspirin therapy because it is similar in molecular structure to heparin. [31] Gamma-hydroxybutyrate and gamma-butyrolactone are extremely dangerous; they induce coma, seizures, and death and should never be used. Health care providers need to realize that athletes will experiment with products and should follow these recommendations: Inquire as to what supplements are used. Inquire as to the dose and frequency. Ask to see the product label. Document the information in the chart.

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Summary Being optimally nourished is an essential part of training and conditioning. The goals of sports nutrition should be reinforced at any opportunity, from the playing field to the physician's office. The role of nutrition in maximizing performance, enhancing recovery, preventing injury, and supporting rehabilitation can only help the athlete perform at his or her peak as well as improve the quality of life.

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Bar-Or O: Children's responses to exercise in hot climates: Implications for performance and health. Sports Sci Exchange 7:49, 1994. 2.

Blom PCS, Hostmark AT, Vaage O, et al: Effects of different post exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc 19:471-496, 1987. 3.

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Bradley TS, Tsourounis C, McCart GM: Glucosamine. Ann Pharmacother 32:574-579, 1998.

Brownell KD, Nelson-Steen S, Wilmore JH: Weight regulation in athletes: Analysis of metabolic and health effects. Med Sci Sports Exerc 18:546-556, 1987. 5.

Burke LM, Collier GR, Beasley SK, et al: Effect of co-ingestion of fat and protein with carbohydrate feedings on muscle glycogen storage. J Appl Physiol 78:2187-2192, 1995. 6.

Burke LM, Collier GR, Hargreaves M: The glycemic index: A new tool in sports nutrition? Int J Sports Nutr 8:401-415, 1998. 7.

8.

Clark N: Nancy Clark's Sports Nutrition Guidebook, 2nd ed. Champaign, Ill, Human Kinetics, 1997.

Coleman E: Carbohydrate and exercise. In Rosenbloom C (ed): Sports Nutrition: A Guide for the Health Professional Working with Active People. Chicago, The American Dietetic Association, 2000, pp 13-31. 9.

Coyle EF, Montain SJ: Benefits of fluid replacement with carbohydrate during exercise. Med Sci Sports Exerc 24(Suppl):S324-S330, 1992. 10.

Dietary supplements containing ephedrine alkaloids; proposed rule (21 CFR 111). Federal Register 62(pt 2):30678-30724, June 2, 1997. 11.

Food and Nutrition Board: Dietary Reference Intakes. Washington, DC, National Academy Press, 1998. 12.

Food and Nutrition Board: Recommended Dietary Allowances, 10th ed. Washington, DC, National Academy Press, 1989. 13.

Hickson JF, Duke MA, Risser WL, et al: Nutritional intake from food sources of high school football athletes. J Am Diet Assoc 87:1656-1659, 1987. 14.

Ivy JL, Lee MC, Broznick JT, Reed MJ: Muscle glycogen storage after different amounts of carbohydrate ingestion. J Appl Physiol 65:2018-2023, 1988. 15.

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Lemon PWR: Effects of exercise on dietary protein requirements. Int J Sports Nutr 8:426-447, 1998.

Maughan RJ, Shirreffs SM, Galloway DR, Leiper JB: Dehydration and fluid replacement in sports and exercise. Sports Exerc Inj 1:148-153, 1995. 17.

Montain SJ, Coyle EF: The influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. J Appl Physiol 73:1340-1350, 1992. 18.

Murray R: Nutrition for the marathon and other endurance sports: Environmental stress and dehydration. Med Sci Sports Exerc 24(Suppl):S319-S323, 1992. 19.

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Murray R: Fluid needs in hot and cold environments. Int J Sports Nutr 5:S62-S73, 1995.

Murray R, Horswill CA: Nutrient requirements for competitive sports. In Wolinsky I (ed): Nutrition in Exercise and Sport, 3rd ed. Boca Raton, Fla, CRC Press, 1998, pp 521-558. 21.

22.

NCAA Proposal 99-72.

Neufer PD, Young AJ, Sawka MN: Gastric emptying during exercise: Effects of heat stress and dehydration. Eur J Appl Physiol 58:433-439, 1989. 23.

Rosenbloom C (ed): Sports Nutrition: A Guide for the Professional Working with Active People. Chicago, The American Dietetic Association, 2000. 24.

Sawka MN, Pandolf KB: Effects of body water loss on physiological function and exercise performance. In Gisolfi CV, Lamb DR (eds): Perspectives in Exercise Science and Sports Medicine: Fluid Homeostasis During Exercise. Indianapolis, Ind, Benchmark Press, 1990, pp 1-38. 25.

Sherman WM, Costill DL, Fink WJ, Miller JM: The effect of exercise and diet manipulation on muscle glycogen and its subsequent use during performance. Int J Sports Med 2:114-118, 1981. 26.

Sherman WM, Brodowicz G, Wright DA, et al: Effects of 4h preexercise carbohydrate feedings on cycling performance. Med Sci Sports Exerc 12:598-604, 1989. 27.

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Sherman WM, Peden MC, Wright DA: Carbohydrate feeding 1 h before exercise improves cycling performance. Am J Clin Nutr 54:866-870, 1991. 28.

Tarnopolsky MA: Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol 84:890-896, 1998. 29.

Tarnopolsky MA, Bowman M, MacDonald JR, et al: Post exercise protein-carbohydrate supplementation increases muscle glycogen in men and women. J Appl Physiol 83:1877-1883, 1997. 30.

The Arthritis Foundation: Glucosamine sulfate and chondroitin sulfate. Available at http://www.arthritis.org/resource/statements/glucosamine.asp.html. 31.

Virkamaki A, Daniels MC, Hamalainen S, et al: Activation of the hexosamine pathway by glucosamine in vivo induces insulin resistance in multiple insulin sensitive tissues. Endocrinology 138:2501-2507, 1997. 32.

Wagner DR: Hyperhydrating with glycerol: Implications for athletic performance. J Am Diet Assoc 99:207-212, 1999. 33.

Walberg-Rankin J: Dietary carbohydrate as an ergogenic aid for prolonged and brief competition in sport. Int J Sports Nutr 5(Suppl):S13-S28, 1995. 34.

William C: Dietary macro and micronutrient requirements of endurance athletes. Proc Nutr Soc 57:1-8, 1998. 35.

36.

William MH: Nutrition for Health, Fitness and Sport, 5th ed. Boston, McGraw-Hill, 1999.

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Chapter 11 - Sports Pharmacology Section A Ergogenic Drugs in Sports Edward R. McDevitt MD There is no room for second place. There is only one place in my game, and that's first place. Vince Lombardi[60] The word ergogenic is derived from the Greek érgon, to work, and gennan, to produce, and means increasing the ability to do work. Athletes use ergogenic drugs to help them perform at a higher level. Athletes always have looked for ways to improve their performance in sports. Almost 3000 years ago, Greek Olympians ate substances that they thought would give them an advantage in competition, including dried figs, mushrooms, large amounts of meat, and strychnine.[40] Strychnine, known from ancient times as a poison, is extracted from the seeds of the plant nux vomica and in small amounts is a central nervous system stimulant and potentially an ergogenic substance. In slightly larger amounts, however, strychnine is deadly. The ancient Greek athletes were willing to risk taking a substance that might kill them because they thought it would help them win in competition. Although it was centuries ago that athletes used the poison strychnine for the first time, athletes in the 1904 Olympics as well as the 1992 Barcelona Olympics also used strychnine. The desire to win is so strong that athletes continue to use potentially harmful ergogenic drugs in their quest for success in competition.

Mirkin[75A] conducted a poll of Olympic athletes in the 1980s that asked the question: If you could take a pill that would guarantee you the Olympic gold medal, but would kill you within a year, would you take it? The poll revealed that more than 50% of the athletes would take the pill. Goldman conducted a modified poll in the 1990s and asked 198 aspiring Olympians, all elite athletes, two questions[7] : 1. If you were offered a banned performance-enhancing substance that guaranteed that you would win an Olympic medal, and you could not be caught, would you take it? Of 198 athletes, 195 answered yes. 2. Would you take a banned performance-enhancing drug with a guarantee that you will not be caught, you will win every competition for the next 5 years, but then die from the side effects of the substance? Greater than 50% of the athletes said they would take the substance. The results of these two polls reveal that athletes, in surprisingly high percentages, may be willing to use substances that are potentially fatal if they think those substances will help them win. Athletes want to win now and may not worry about the consequences of substance use in the future. Individuals entrusted with the care of athletes, including coaches, athletic trainers, therapists, physicians, parents, and spouses, have a difficult dilemma: How do they help their athletes compete safely at an elite level, when so many athletes are willing to take substances that are potentially dangerous to their health? One of the first physicians to approach this problem was Ziegler, an American Olympic team physician in the 1950s. Concerned about the tremendous gains made by the Soviet Bloc nations in Olympic weightlifting, Ziegler was determined to discover the secret of the Soviets' athletic success.[45] Ziegler allegedly learned from a Soviet physician over drinks that the impressive gains made by the Soviets were not due to changes in training or diet but were due to a powerful new drug being injected into the Soviet athletes' bodies, the male hormone testosterone. Ziegler was impressed with the strength-building effects of testosterone, but he was wary of potential problems with testosterone injections. There were rumors that the Soviet weightlifters used catheters to urinate because the injectable testosterone, although responsible for increases in their strength, had caused such enlargement of the prostate that normal urinary flow was possible only by catheter. Ziegler, as a dedicated team physician, was inspired to do something to help his American athletes compete.[27] He wanted to manufacture a better, safer drug to give the American athletes an advantage in sport without the worrisome side effects of testosterone. Working with the CIBA Company, Ziegler helped develop a drug that was designed to have anabolic (muscle building) properties without the androgenic (malelike) side effects. The drug developed, methandrostenolone (Dianabol), was a great improvement over testosterone and is used widely by athletes today. As the developer of methandrostenolone, Ziegler was an ardent advocate for its use. He later regretted the important role he had played in the history of ergogenic drugs.[45] Initially, Ziegler thought he was doing what was best for his American athletes, and methandrostenolone was a superior ergogenic drug when compared with testosterone. Methandrostenolone was responsible for gains in strength, but it was realized later that methandrostenolone had adverse side effects related to its potent androgenic

properties. Ziegler realized that he was responsible for encouraging his American athletes to use drugs that had many unintended side effects. Ziegler was just the first of many well-meaning scientists who have attempted to develop a pure anabolic agent, without androgenic features. This perfect anabolic drug has not yet been found. With androgenic properties come potentially deadly side effects. This situation emphasizes the importance of thorough, long-term testing of

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drugs before their use by athletes. In their quest for improvement, today's athletes continue to use drugs that have not yet been proved to be efficacious and safe. To underscore the important point that derivatives of testosterone have anabolic and androgenic properties, we describe all ergogenic derivatives of testosterone in this chapter as anabolic-androgenic steroids (AAS). There are more than 100 ergogenic variants of testosterone now being used by athletes. History of Testosterone

One of the first scientists to promote the ergogenic properties of testosterone was the prominent French physiologist, Brown-Séquard.[53] Although remembered in the medical world today for his description of a spinal cord syndrome, Brown-Séquard played an important role in the history of AAS. In June 1889, at the Societe de Biologie meeting in Paris, the 72-year-old Brown-Séquard announced he had found a rejuvenating compound that had reversed many of his physical and mental ailments related to aging. He reported that he had injected himself with a liquid extract made from the testicles of dogs and guinea pigs and that these injections had increased dramatically his strength, improved his mental acumen, relieved his constipation, and increased the arc of his urinary stream. Although most of his colleagues greeted Brown-Séquard's findings with disdain, he had made an important discovery with protean implications for the medical and athletic worlds. Brown-Séquard's discovery of the positive properties of the testicular extract was based on the earlier work of Berthold. Berthold proposed in 1849 that the implantation of testicles in the abdomen of roosters reversed the effects of castration.[12] There appeared to be some ingredient in testicular tissue that made male animals male. Brown-Séquard realized through the experiments he performed on himself that internal secretions of organs could act as physiologic regulators. His postulation of physiologic regulators predated the discovery of hormones in 1905. Scientists continued the work of Berthold and Brown-Séquard in an attempt to isolate the active ingredient in testicular function. Several other scientists made important discoveries contributing to a better understanding of the properties of the testicular hormone. In the 1920s, Zoth and Pregl performed experiments to determine whether testicular extracts could increase muscle strength. They injected themselves with extracts of bull testicles and found that they had increased their finger strength.[53] In an attempt to identify the strength-building compound in testicular tissue, in 1931 the German scientist Butenandt isolated 15 mg of

a pure substance, androsterone, from the extract of 15,000 L of urine obtained from policemen.[22] Studies with androsterone did not reproduce fully all of the anabolic-androgenic properties of testicular tissue. David, a Dutch scientist, and colleagues first isolated testosterone in 1935.[29] German scientists soon published an article describing the synthesis of testosterone from cholesterol.[21] Physicians as well as veterinarians soon started using testosterone and its intermediaries clinically. Testosterone first was used medically in humans to help chronically ill patients recover muscle mass.[75] Testosterone was found to have positive effects on almost every organ of the body. Sixty years after Brown-Séquard, testosterone was promoted again as a rejuvenation compound. Boje, in 1939, suggested that male sex hormones might improve athletic performance.[16] In 1941, a racehorse dramatically improved his performance after receiving injections of testosterone. [69] Human competitors started experimenting with testosterone looking for an advantage in competition.[30] The first systematic use of testosterone in the sporting world took place in the 1950s by the Soviet Olympic athletes. The use of testosterone and derivatives such as methandrostenolone spread rapidly to athletes on both sides of the Iron Curtain. In the 1960s, use of AAS became prevalent.[110] During that time, there were no sanctions against the use of ergogenic drugs. Many athletes believed that they had to use ergogenic drugs to keep up with their competitors. In the 1960s, there was extensive use of AAS by athletes in the strength sports (shot put, hammer throw, and javelin) in track and field.[102] By the 1968 Olympics, the use of AAS was ubiquitous. New drugs claiming to be more anabolic were being marketed openly.[110] Male athletes from other sports soon began taking AAS. American professional football players were among the first groups to try the new muscle-building drugs in large numbers. Many of the early professional football players were given AAS without their knowledge.[42] Similar so-called vitamins, which were later identified as AAS, were given to college football players in the 1970s. Even if some athletes were duped into taking drugs, however, many athletes would have taken the AAS willingly. The use of AAS escalated in the 1970s and 1980s. It was estimated that 40% to 90% of professional football players were using AAS.[110] College football players soon followed the lead of the professionals.[61] When Steve Huffman, a Notre Dame football player, claimed that the use of AAS was commonplace among his teammates, however, his claim was denied vehemently by Notre Dame coaches, players, and officials. The use of AAS was not something that could or would be admitted openly. The positive effects experienced by the male track athletes were noted not only by male athletes in other sports, but also by female athletes. Women taking AAS experience anabolic effects that can increase muscular strength as well as androgenic or masculinization effects, such as a deepening of the voice, increase in body hair, loss of breast tissue, and enlargement of the clitoris. Masculinization of female athletes from the Soviet Bloc nations was so dramatic that sex tests, or chromosomal analyses, were initiated at the 1967 European championships. There was concern that male athletes were masquerading as female athletes; these athletes were not males but female athletes taking male hormones. In the trial of former East German team physician Kipke, his testimony revealed a systematic prescription of supporting means to young East German female athletes. The supporting means turned out to be Oral-Turinabol

(dehydrochloromethyltestosterone), an AAS manufactured in East Germany. [72] Kipke contended that he was just following orders, and he stated he was unaware of any potential side effects of the AAS on the young women other than a deepening of their voices. He admitted administering

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the drugs for decades to the East German swim team. Convicted by a German court and sentenced to 15 months in jail, Kipke was the 26th East German sports official to be convicted on charges of giving AAS to East German athletes in a wide variety of sports. Many female athletes from the former East Germany have complained that they suffer from a variety of medical maladies that they believe were secondary to their being given AAS without their knowledge. Women in Western nations have been suspected of using ergogenic drugs. Florence Griffith Joyner became one of the most famous athletes in the world when she came out of semiretirement to become a tremendous success at the 1988 Olympic Games. Joyner had progressed from a good runner to a world champion whose record in the 100-m run was unsurpassed for 10 years. Her muscular physique, combined with her newfound athletic success, led to speculation that her gains were due to performance-enhancing drugsa charge she vehemently denied.[63] Joyner claimed her changes were due to relentless training supervised by her husband, Olympic athlete Al Joyner, and not to ergogenic drugs. When Joyner died in her sleep at age 38, speculation was raised that her death may have been related to side effects from taking ergogenic drugs. No proof exists that Joyner used ergogenic drugs or that her death was related to use of drugs. Doubts similarly were raised about the tremendous gains made by Irish swimmer, Michelle Smith. In 1993, Smith had not been ranked among the top 25 female swimmers in any stroke.[8] At the 1996 Olympic games, at age 26 (considered old in women's swimming), Smith won four Olympic medals. Smith claimed her amazing progression from a second-tier swimmer to Olympic champion was a result of intensive training and proper nutrition and not to ergogenic drugs. Her husband, Erik de Bruin, monitored her training. A two-time Olympian from the Netherlands, de Bruin competed in the shot put and discus, failed a drug test in 1993, and was suspended for 4 years. No evidence exists, however, that Smith used performance-enhancing drugs. Smith was banned in 1998 from swimming for 4 years after being found guilty of tampering with a urine sample. The International Swimming Federation ruled that Smith manipulated an out-of-competition drug test by spiking her sample with a lethal concentration of alcohol. The presence of alcohol, which the doping laboratory found is in no way compatible with human consumption, suggested a possible attempt to mask the presence of any banned drugs.[55] Competitors were quick to assume that Smith was trying to hide an illegal ergogenic drug use that would have been detected on her drug test.

Many young athletes apparently think that use of ergogenic drugs is a risk worth taking. Buckley's study published in 1988 revealed that 6.6% of 12th graders had used anabolic steroids.[19A] Another disturbing finding was that 30% of users were nonathletes. These nonathletes were using ergogenic drugs to improve their appearance rather than their athletic performance.[84] Evidence reveals that ergogenic drug use is starting as early as middle school age. The National Institute of Drug Abuse funded the 1999 Monitoring the Future study, which surveyed drug abuse among adolescents in middle school and high school. The study found evidence that 2.7% of 8th and 10th graders had taken AAS at least once in their lives.[56] Ergogenic drug use is not limited to young men. Yesalis found that the percentage of 14- to 18-year-old girls using anabolic steroids has almost doubled in 7 years. [47] Many women consider ergogenic drugs an effective means to obtain athletic scholarships to college.[47] [112] When a Danish cyclist died at the 1960 Olympics after ingesting a combination of nicotinic acid and amphetamines, there was concern that drug use by athletes was not only unfair, but also dangerous. The authorities decided to do something about the problem with ergogenic drugs. One of the first steps in the process was to define the problem. In 1963, the Council of Europe established a definition of doping as the administration or use of substances in any form alien to the body or of physiological substances in abnormal amounts and with abnormal methods by healthy persons with the exclusive aim of attaining an artificial and unfair increase in performance in competition.[18] The origin of the word doping was attributed to the Dutch word dop. Dop was a narcotic mixture of opium used to stimulate racing horses.[45] The Council of Europe decided that it was imperative to ban these drugs and developed a list of doping drugs used by athletes. In 1967, the International Olympic Committee published a list of banned drugs and a medical code to protect the health of athletes and to ensure respect for the ethical concepts implicit in Fair Play, the Olympic Spirit, and medical practice.[89] Sports governing bodies worldwide adopted rules regarding the use of ergogenic drugs. Developing tests to determine who was using banned drugs was problematic. Few laboratories were able to perform the necessary testing. The cost of each test was more than $100, which made the testing of large number of athletes prohibitive. The fact that new AAS were being developed and used by athletes required that laboratories develop new specific screening tests. Effective laboratory testing to detect ergogenic drugs was not readily available until the 1976 Olympics. Nineteen athletes were banned for using illegal drugs at the 1983 Pan-American games, and many athletes left voluntarily when faced with mandatory testing. When athletes knew ahead of time that there was to be testing at the conclusion of an event, the numbers of athletes detected using banned ergogenic drugs was small, usually less than 2%.[110] In 1984 and 1985, the U.S. Olympic committee conducted unannounced testing of Olympic-level athletes, however, and 50% of athletes tested positive for banned ergogenic drugs. [105] Apparently athletes had learned to taper off AAS before major events at which announced drug testing was going to be done or they masked their drug use. Athletes taking ergogenic drugs put themselves at risk not only for serious sports

sanctions, but also for potential jail terms. The Anti-Drug Abuse Act of 1988 prohibited the distribution of AAS for any use other than the treatment of a disease. It is illegal for physicians to prescribe AAS to enhance athletes' performance. The Anabolic Steroids Control Act of 1990 placed all AAS in Schedule III of the Code of Federal Regulations Schedules of Controlled Substances. This law places AAS in the same legal class as amphetamines, methamphetamines, opium, and morphine.

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Simple possession of any Schedule III substance is a federal offense punishable by 1 year in prison or a minimum fine of $1000 or both. Possession by a person with a previous conviction for certain offenses, including any drug or narcotic crimes, requires imprisonment of 15 days to 2 years and a minimum fine of $2500. Individuals with two or more such previous convictions face imprisonment of 90 days to 3 years and a minimum fine of $5000. Selling AAS or possessing them with intent to sell is a federal felony. This crime is punishable by 5 years in prison or a $250,000 fine or both.[59] Athletes take risks to obtain and use banned drugs such as AAS because they believe the drugs will help them compete, and the athletes do not think they will be caught. Ziegler's crucial role in the development of methandrostenolone was a result of his desire as team physician to help his team compete against the Soviet athletes. If the competition was using drugs, some athletes, coaches, administrators, and team physicians thought that they had to use drugs as well or fall behind. When mainstream medical opinion was sought in the midst of the controversy, the opinion rendered help divide athletes from their physicians. The official medical response was that AAS did not work and that the apparent benefits were due largely to a placebo effect. The potential for side effects was great. Physicians were concerned that athletes using AAS would be destined for a life of steroid-related complications, which might threaten or end the athletes' life. Athletes were skeptical of this advice. They could see that other athletes using AAS were making gains and did not appear to have serious physical problems. The official medical world lost credibility with athletes, and athletes turned to other sources, not only to get their drugs, but also to get information regarding performance-enhancing drugs. Magazines such as Muscle and Fitness and Muscle Media became valuable sources of information concerning performance-enhancing medicine. The Underground Steroid Users Handbook [36] became a trusted source of information concerning ergogenic drugs. This book promised to tell the truth about AAS and belittled the negative views of physicians regarding AAS. The author stated that steroids do work. He stated that although there are definite side effects associated with their use, the dangers of AAS are exaggerated by physicians. The author made a valid point that most of the studies regarding AAS were poorly done. The studies did not use elite athletes as subjects and did not test the supraphysiologic doses used by athletes. The author's view was that athletes should be allowed to use AAS in the same way that women are allowed to use female hormones in birth control pills. In defense of physicians, there was little scientific proof to enable them to make recommendations concerning the efficacy and safety of AAS. The early testing of ergogenic drugs was not done scientifically. Prospective randomized studies, with

placebo controls, had not been performed. Side effects were not studied adequately to prove that AAS were safe. Many physicians believed that AAS could not be recommended because AAS had not been tested scientifically. In addition, the side effects seen in athletes taking AAS were worrisome. Another consideration was that no one had studied the long-term effects of AAS in animal or human studies. Many medical authorities considered it unconscionable to recommend any therapy that had not been studied sufficiently.

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Mechanism of Action and Efficacy of Anabolic-Androgenic Steroids

The three main steroids in the body are the androgens, which are responsible for the development of male characteristics; the estrogens, which are responsible for the development of female characteristics; and the corticosteroids, which are compounds manufactured in the adrenal glands, such as cortisol. Females produce small amounts of androgens in the ovary and adrenal gland, and males produce small amounts of estrogen, but it is the production of androgens that make males masculine and the production of estrogen that makes females feminine. The most abundant androgen in males is testosterone, produced primarily in the testes. In many target cells in the body, testosterone is reduced at the 5 position to dihydrotestosterone, which serves as the intracellular mediator of the actions of testosterone.[107] Dihydrotestosterone binds to androgen receptors more tightly than testosterone and is a more stable and more potent androgen. Precursors in the metabolic pathway to testosterone, dehydroepiandrosterone (DHEA) and androstenedione, bind weakly to the androgen receptors and are known as weak androgens. Etiocholanolone and androsterone, metabolites of testosterone, also bind weakly to the receptors and are weak androgens. Weak androgens still can have definite anabolic effects, however. In the male, testosterone production peaks at three distinct phases. The first peak is in the fetal period, during the second trimester, and is responsible for the development of the fetus as a male. There is a smaller surge during the first year of life. The largest surge of testosterone production is during puberty. At puberty, androgens cause laryngeal enlargement, which deepens the voice. The penis and scrotum grow. Spermatogenesis is stimulated in the testicles. Testosterone stimulates growth of bone and muscle tissue. As muscular tissue increases, body fat decreases. The skin becomes thicker and oilier. Body hair in the face, axilla, and groin grows to adult levels. Testosterone, or its more active metabolite, dihydrotestosterone, works by binding to an intracellular androgen receptor in the cytoplasm. The steroid-androgen receptor complex is transported to the nucleus, where it is attached to a specific hormone regulatory complex on nuclear chromosomes. Here the complex stimulates the

synthesis of specific RNAs and proteins. The RNA compounds are transported through the bloodstream to act on target organs to stimulate spermatogenesis, effect sexual differentiation, and increase protein synthesis in muscle tissues.[14] The androgenic message is received in all organs that have androgenic receptors, which includes the hair follicles and the sebaceous glands. With androgens, in addition to muscle development, one gets oily skin, which can lead to acne; increased body hair; and male pattern baldness, with hairline recession and thinning and loss of central scalp hair. Testosterone and its metabolites are metabolized quickly in the liver. Testosterone given by mouth is absorbed

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quickly and metabolized and is ineffective. Scientists have developed methods of altering the basic structure of the testosterone molecule to delay its metabolism and increase its half-life in the plasma. There are more than 100 testosterone variants. Testosterone esters, such as cypionate and enanthate esters, are more potent than testosterone. These compounds must be injected intramuscularly, usually at 1- to 3-week intervals.[107] The ultralong active testosterone bucuclate is administered intramuscularly every 3 months. Manipulation of the testosterone molecule by alkalization delays its metabolism in the liver and allows the drugs to be administered orally. Newer preparations of testosterone can be administered transdermally.[4] Initially, these preparations were applied to the scrotum, but new transdermal patches and creams can be applied to other parts of the body.

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Androgens and Athletic Performance

Despite the perceptions of athletes, the scientific data regarding the effects of anabolic steroids on athletic performance are mixed. When used at therapeutic doses, neither strength nor performance would be expected to be improved. Hormonal levels are maintained closely in the body in a homeostatic fashion. If a therapeutic dose of a hormone is given, the body halts endogenous production of the hormone to maintain homeostasis. Athletes have taken doses that may be 50 to 100 times the therapeutic dose. This supratherapeutic dosing shuts down endogenous production of AAS, but will it improve performance? Steroid users believe that in combination with training, AAS increase lean body mass and decrease body fat. Early studies looking at these effects were equivocal.[10] Athletes believe that AAS increase their muscle strength. The early studies, mostly using low-dose AAS, were not conclusive. [1] [70] In 1996, Bhasin and colleagues studied the effect of supraphysiologic doses of testosterone on normal men.[10] This was the first prospective randomized study that looked at the effect of superdosing of AAS. In this study of 43 healthy men, the steroid group had definite increases of strength and muscle size compared with the placebo group. No significant side effects were seen in the steroid group. This study was criticized, however, because it was a short-term (6-week) study, with limited follow-up. This study was significant because it was the first study to provide scientific evidence for a theory that athletes have believed for decades: Steroids work, especially at athletic doses. AAS work not only because they stimulate protein synthesis, but also because they stimulate the production of growth hormone, a potent ergogenic agent. AAS have anticatabolic effects. Cortisol is released in response to physical and psychologic stress and cause protein degradation and muscle atrophy.[52] Testosterone acts by displacing the corticosteroids from receptor sites, reversing the effects.[6] AAS may increase oxygen uptake, increase cardiac output, and increase stroke volume.[103] AAS may improve athletic performance by increasing aggressive behavior. One unsubstantiated rumor in the history of AAS was that AAS were given to German troops in World War II

to increase their aggressiveness to make them more fierce warriors.[40] Although some studies show an association between testosterone levels and aggressive behavior,[98] others do not.[8] Several problems exist with most of the scientific studies regarding AAS. The studies were not tested on athletes. The subjects tested had various levels of fitness. The doses were not supratherapeutic. The studies are largely short-term. Athletes take large doses for long periods of time. Athletes often stack, or take more than one drug at a time. They also cycle drugs, taking various amounts for certain periods of time, then going on a drug holiday. It is easy to see why there are difficulties making a clear medical judgment concerning the efficacy and safety of AAS. There are ethical questions for scientists seeking to study AAS. It is illegal to use AAS for sports performance. AAS are being used at doses that have received only limited scientific study at the supratherapeutic doses being used by athletes. AAS have potential adverse side effects that have not been studied adequately.

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Adverse Effects of Anabolic-Androgenic Steroids

A wide variety of transient and permanent adverse effects can be seen with the use of AAS. Most side effects are temporary and are reversible when the drugs are stopped. Many athletes think that the medical community overstates the potential problems with anabolic steroids, trying to scare athletes from using the drugs. Physicians have legitimate concerns that long-term studies regarding the benefits and potential adverse effects have not been done on athletes. Athletes who have adverse reactions to ergogenic drugs often do not tell physicians that they are taking the illegal drugs. Many potential problems with AAS are underreported because athletes do not tell physicians that they are using illegal ergogenic drugs. A physician may not make the connection between a possible adverse reaction and ergogenic drugs. Athletes are reassured when they see that although many athletes are using ergogenic drugs illegally, they know few that have serious problems. A variety of side effects have been seen, and there are myriad other problems that might be seen with prolonged use of AAS. There are reports that many of the illegal drugs being used are manufactured in overseas laboratories, where quality control is not a priority.[88] More information is needed from long-term scientific studies and from athletes communicating honestly with their physicians. Most male athletes understand that using AAS causes oily skin, acne, small testicles, gynecomastia, and changes in their hair patterns often leading to baldness. Small doses of androgens increase sebaceous gland secretions leading to the changes in the skin and acne.[96] Gynecomastia is enlargement of the male breast characterized by the presence of firm glandular tissue, usually associated with increased production of estrogens or decreased levels of androgens.[19] The reason men on AAS develop breast tissue is not known. One theory is that when men elevate their androgen levels through drug use, the body homeostatically shuts down production of endogenous androgens. When

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the user stops the drugs, there is an increase in the relative level of estrogens, which leads to the development of gynecomastia. Gynecomastia is not reversible when the normal levels of androgens return. Men using AAS also often develop small testicles. The testicles atrophy, responding to homeostasis. With high exogenous AAS, the body ceases the production of endogenous AAS, and the testicles shrink in size. Often the testicles remain smaller in size after stopping the drug. There are other adverse effects on the male reproductive system. Oligospermia (decreased number of sperm) or azoospermia (absence of sperm) are possibilities.[86] Taking exogenous AAS not only decreases levels of endogenous testosterone, but also decreases circulation of follicle-stimulating hormone and luteinizing hormone, which can lead to male infertility. As the Soviet weightlifting team in the 1950s discovered, use of AAS also causes prostatic enlargement. AAS also cause prostatic cancer to grow. Patients with prostatic cancer are given antitestosterone preparations or are castrated to lower testosterone levels. An athlete with an undiscovered prostatic cancer could cause his cancer to grow by taking AAS. Women who take AAS experience adverse virulization effects, including deepening of the voice, increased body hair, loss of breast tissue, and enlargement of the clitoris. Irregularities in the menstrual cycle as well as infertility or early menopause may develop. Many of these adverse effects in women are not reversible. [110] The musculoskeletal system may be affected adversely, especially in the prepubertal athlete who takes AAS. Although bone growth is stimulated immediately, there may be premature closure of the growth plates of the long bones. The resultant short stature is permanent.[14] Changes in the muscle-tendon unit increase muscle strength to a greater extent than the tendon strength, and tendon ruptures may occur.[74] The heart, the most important muscle in the body, may be affected adversely by AAS. Androgens are modulators of serum lipoproteins. Androgens increase the plasma levels of low-density lipoproteins (the bad lipoproteins) and decrease the levels of high-density lipoproteins (the good lipids). Oral AAS and synthetic AAS have more pronounced negative effects on lipid metabolism than injectable AAS or natural AAS.[14] The altered lipid pattern may lead to atherosclerotic heart disease. Male and female AAS users show similar adverse changes in lipid metabolism.[73] Animal studies have suggested that AAS might cause myocardial damage.[2] A study investigated the relationship between resistance training, anabolic steroid use, and left ventricular function in elite bodybuilders. Concentric left ventricular hypertrophy was seen, but there was no effect on cardiac function. This study suggests that the heart might enlarge as a physiologic adaptation to intensive training potentiated by AAS.[34] In a set of bodybuilding twins, one of the twins used AAS for more than 15 years, and the other twin did not use AAS. No significant difference in cardiac function was found between the twins.[99] Significant changes in cardiac function with AAS use have been reported in other cases, however. Cases of myocardial infarction and death of young athletes taking AAS have been documented. [35] [71] These case reports are worrisome

but are not scientific proof that AAS use directly led to myocardial infarction and death of the athlete. Steve Courson is a former all-pro football player for the Pittsburgh Steelers who admitted to heavy use of AAS. He presently is awaiting heart transplantation for severe cardiomyopathy. Although there is no direct proof of a causal relationship between his use of AAS and his severe heart disease, Courson believes that there is a direct correlation and is a strong opponent of AAS use by athletes. Some athletes hear Courson's message and listen to only part of the story. They are attracted to AAS when they hear that Courson used AAS and intensive training to become a highly successful collegiate and professional football player. They ignore the consequences of a damaged heart. Many rationalize that what happened to Courson was just bad luck and could never happen to them. The liver is the organ responsible for most of AAS metabolism. Potential damage to the liver by use of AAS is a major concern. Athletes with preexisting liver dysfunction may be at greatest risk for serious liver abnormalities with AAS use. The oral AAS (the 17-alkylated androgens) are absorbed rapidly after ingestion and transported quickly to the liver. Oral AAS are more potentially damaging to the liver than injectable AAS. Temporary liver disturbances are common in athletes who use oral androgens.[78] AAS have a multiplicity of effects in the liver, which have multiple AAS receptor sites. These disturbances in liver function usually are transient, and function returns to normal after stopping the use of drugs.[106] Some investigators believe that AAS-induced hepatotoxicity is overstated, noting that elevations in transaminase levels seen in users might be due to skeletal rather than liver damage. [33] A study of the effect of AAS on rats showed definite cellular damage to hepatocytes, however.[15] Long-term studies on the effect of AAS on the liver in human subjects have not been conducted. Until these long-term studies are performed, hepatotoxicity must remain a major concern with use of AAS. One of the most serious adverse effects of AAS use occurring in the liver is peliosis hepatis. This condition results in the development of blood-filled cysts in the liver. If the cysts rupture, peliosis hepatis can be life-threatening. The first association between AAS use and peliosis hepatis was described in 1952. [20] In contrast to most adverse effects of AAS, peliosis hepatis does not appear to be dose related and can occur at any time after starting AAS use.[94] The proposed mechanism of action of AAS-induced liver toxicity, including peliosis hepatis, is through AAS-mediated hepatocyte hyperplasia.[79] Enlarged liver cells block venous and lymphatic flow, producing cholestasis and peliosis cysts. A relationship between androgens and hepatic tumors first was suggested in 1971.[11] Hepatocellular carcinoma is more common in men than women, and the link between AAS and hepatocellular carcinoma has been studied. No definite proof exists, although there are multiple reports of hepatocellular carcinoma developing after AAS use. [44] These tumors are pernicious in that they present silently with few symptoms until the late stages of tumor growth. The most commonly associated psychiatric effect of AAS is an increase in aggressiveness. Defendants accused of violent crimes have claimed that their crimes were committed under the influence of AAS. They have claimed that the AAS made

them more aggressive and violent. There are few good prospective, randomized studies of AAS on behavior. Most studies using therapeutic doses of

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exogenous testosterone show no adverse effects. The short-term study of supratherapeutic dosing of AAS in athletes revealed no significant psychiatric effects.[10] Many of the studies reported only a positive effect on mood. [14] In Brown-Séquard's 19th century study of self-administration of testicular substrates, one of the reported positive effects was improvement in mood that accompanied improvement in his physical stature. Synthetic testosterone derivatives became available in the 1930s. One of the first uses of AAS was by physicians exploring the effects of AAS on mood as well as psychiatric maladies.[88] [104] AAS were used to treat a variety of conditions ranging from depression to psychoses, but the results were disappointing. Studies in animals and humans have linked high levels of endogenous AAS with aggressive behavior.[9] A study of 41 athletes using supratherapeutic doses of AAS for an average of 45 weeks revealed that 34% experienced psychiatric symptoms based on criteria in the Diagnostic and Statistical Manual of Psychiatric Disorders, third edition.[82] This study linked major mood disorders, such as severe depression or mania, with AAS use. AAS users are more likely to use alcohol, tobacco, and illicit drugs.[14] AAS users have been reported abusing the opioid agonist-antagonist nalbuphine.[109] In a study of 227 men admitted to a private inpatient facility for substance-dependence treatment, 9.3% had a history of AAS abuse.[109] None of the men had any form of substance abuse or dependence before their use of AAS; 86% of the men using opioids said they had started using them to counteract the side effects of the AAS; 81% had purchased the opioids from the same drug dealer who had sold them the AAS. This study suggested that AAS might be the gateway to opioid dependence. The subjects using opioids were suburbanites with an average income of $69,800. Disorders of body image have been reported with use of AAS. Many weightlifters who may appear muscular when compared with the average athlete consider themselves small or weak. This disorder is similar to women with anorexia nervosa who despite being very thin when compared with the average woman think that they are fat. The Adonis Complex: The Secret Crisis of Male Body Obsession addresses what the authors describe as an obsession by men to achieve physical perfection.[83] The authors claim that men are struggling with the same pressures to achieve physical beauty that women have dealt with for centuries. The authors see the tremendous interest in AAS by the general population as a reflection of the glorification in the media of athletes and movie actors who are using AAS to achieve their muscular bodies. Although concerned about the medical hazards of AAS, the authors state that what is far more dangerous are the psychiatric effects of irritability and aggression seen with AAS use and the depression present on AAS withdrawal. The authors also are concerned that billions are being spent not only on illegal AAS, but also on muscle-building supplements legally available on the Internet or at health food stores.

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Steroid Supplements

One of the most important laws passed by the U.S. Congress that has protean implications for individuals involved in the care of athletes is the Dietary Supplement Health and Education Act of 1994 (DSHEA). This law allows a tremendous variety of substances to be sold without approval from the U.S. Food and Drug Administration (FDA) as long as they are sold as dietary supplements and not as drugs. The DSHEA established a formal definition of dietary supplement using several criteria. A dietary supplement is a product (other than tobacco) that is intended to supplement the diet. It bears or contains one or more of the following dietary ingredients: a vitamin; a mineral; an herb or other botanical; an amino acid; a dietary substance to supplement the diet by increasing the total daily intake; or a concentrate, metabolite, constituent, extract, or combinations of these ingredients. The product is intended for ingestion in pill, capsule, tablet, or liquid form. The product is not recommended for use as a conventional food or as the sole item of a meal or diet, and it is labeled as a dietary supplement. Products have included approved new drugs, certified antibiotics, or licensed biologics that were marketed as dietary supplements or food before approval, verification, or license.[57] Since this bill passed, many synthetic AAS have become commercially available as dietary supplements. As such, these products do not have to pass the efficacy and safety requirements of the FDA. They do not have to meet quality control standards. [80] Claims made concerning their effectiveness do not have to be substantiated by scientific proof as long as a disclaimer is listed on the product. If scientifically unproven claims are made, the federal government is responsible for establishing that the claim is false or misleading. Two dietary supplements that are used widely and purchased legally by athletes are DHEA and androstenedione. DHEA is a weak androgen but is one of the main precursors of testosterone. DHEA is made in large quantities by the adrenal cortex. DHEA is the most abundant steroid in the body and is a precursor not only of testosterone, but also of estrogen, progesterone, and corticosterone. DHEA is available as a nutritional supplement because it is found naturally in wild yams. [24] DHEA levels

are high in the prenatal period and in puberty and gradually and progressively decrease as individuals age. Studies done in patients older than age 50, when DHEA levels are decreasing significantly, showed beneficial results when DHEA supplements were taken.[14] DHEA has been described as a wonder drug, and it has been marketed especially to middle-aged and older individuals as an antiaging drug. Although few scientific studies have been done with DHEA, it has been marketed as a fat-burning, muscle-building, sexual stimulant.[14] One study found that high doses of DHEA decreased low-density lipoproteins.[77] Many athletes use it for its androgenic and anticatabolic effects.[14] One of the problems with athletes taking DHEA in an attempt to increase their testosterone levels is that the DHEA may be converted to estrogen, which does not have the anabolic effects desired by the athletes. Feminization may occur in the male athlete. There is little evidence to support the claims for DHEA either as a potent anabolic agent or as an antiaging drug. There are no published studies of the long-term effects of taking DHEA, particularly in the large doses used by athletes. [26] Androstenedione is a potent AAS produced endogenously in the adrenal glands and gonads. In the liver,

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androstenedione is metabolized to testosterone. Similar to DHEA, androstenedione is purchased easily as a dietary supplement. Originally touted as the secret weapon of the East Germans, androstenedione first was used in the 1970s. Its reputation as an effective anabolic agent resulted in worldwide use. The International Olympic Committee, the National Collegiate Athletic Association, and the National Football League ban the use of androstenedione as a testosterone precursor. Baseball players are not banned from using this supplement. Androstenedione received tremendous exposure in the media during the 1998 baseball season when St. Louis Cardinals slugger Mark McGuire was discovered to be using androstenedione, legally, as a nutritional supplement. Although McGuire stopped using the supplement after the discovery, sales of androstenedione rose dramatically.[111] Studies indicate that androstenedione does not enhance muscle building and has some adverse effects.[67] Similar to DHEA, as androstenedione is metabolized, it can be converted to testosterone or to estrogen. A male athlete taking androstenedione theoretically can elevate estrogen levels. The adverse effects seen with androstenedione in this study were associated with androstenedione's conversion to estrogens. Male subjects taking androstenedione developed elevated estradiol levels. These estradiol levels are equal to the estradiol levels seen in women at the follicular phase, when estradiol levels are highest. This study was criticized as being a small study, with only 20 subjects. It also was a short-term study; the subjects were given androstenedione for only 6 weeks. The two groups might not have been truly comparable because they had significant differences in free testosterone levels of almost 50%. As a testosterone precursor, the possibility of adverse reactions as are seen with testosterone must be considered. Priapism, or persistent painful erection, was seen in a healthy young man using androstenedione. [66] No precipitating factors of priapism were found in the patient. Other studies, done in monkeys, found hyperplastic changes in the prostate after androstenedione administration.[50] Good scientific prospective, randomized studies of

athletes are needed to determine the efficacy and safety of androstenedione and other ergogenic drugs.

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Creatine

One of the most popular supplements currently embraced by athletes is creatine. Creatine is a nitrogenous compound synthesized in the body by the liver, pancreas, and kidneys. Creatine also is absorbed through the diet. Fish and meat are good sources of exogenous creatine. Chevreul, who named creatine after the Greek word for flesh, discovered the compound in 1832. In the 1920s, it was discovered that creatine played a crucial part in the structure and function of adenosine triphosphate (ATP), the body's prime energy source.[6A] Creatine is found principally in skeletal muscle. In its free and phosphorylated form, creatine plays a crucial role in the regulation of skeletal muscle metabolism. Creatine is synthesized, largely in the liver, from the amino acids arginine, glycine, and methionine. The creatine is transported to the skeletal muscles, where it is absorbed into the muscle cells by a sodium-dependent transporter system. When in the muscle cell, creatine becomes phosphorylated by the activity of creatine kinase, and creatine is synthesized into creatine phosphate. Creatine phosphate serves as an energy substrate contributing to the resynthesis of ATP during strenuous exercise. Phosphocreatine is stored in the muscle cell until it is needed as an anaerobic energy source. When motion is initiated, the creatine phosphate bond is broken, and the phosphate is donated to adenosine diphosphate (ADP) to make ATP and provide instant energy.[93] Later, with sufficient oxygen, creatine is reconverted to phosphocreatine in an aerobic reaction. In 1992, it was discovered that creatine supplementation increases the ability of skeletal muscles to accumulate creatine and phosphocreatine.[51] More substrate is available for energy-sapping anaerobic activities. Creatine is vital for the heart, brain, kidneys, and retinae.[91] Creatine acts as a lactic acid buffer during exercise. Lactic acid is generated during intense exercise. Hydrogen ions are consumed when phosphocreatine is used to generate ATP: PCr + ADP + H+ Creatine kinase Cr + p

Not only does creatine provide energy for anaerobic activities, but also it helps buffer lactic acid, which prevents prolonged anaerobic exercise. With increased phosphocreatine available, there is more ability to buffer lactate. The athlete can exercise anaerobically for a longer period with delayed fatigue. A third way that creatine may help athletic performance is through stimulation of protein synthesis and increasing muscle mass.[64] Although creatine was believed to have bodybuilding effects in the 1920s, it was not until the 1970s that seminal research on rats indicated potential benefits for athletes.[64] Creatine supplementation soon was seen to provide performance-enhancing and fatigue-delaying effects in athletes. [49] Creatine supplementation increased the synthesis of the myosin heavy chain in skeletal muscles. These studies indicated that creatine not only might have benefits in energy production and lactate buffering, but also might increase muscle cell mass. A study using creatine supplementation in patients with the ophthalmologic condition of gyrate atrophy showed a significant increase in type II (fast-twitch) muscle fibers. [92] All these findings suggested that creatine might be used optimally in athletes who engage in sports that emphasize short bursts of intense anaerobic activity, such as football, soccer, lacrosse, hockey, basketball, and powerlifting. Short-term creatine supplementation enhanced the ability to maintain muscular forces during jumping,[17] intense cycling,[13] and weightlifting.[49] Creatine use became widespread among athletes as the benefits of its use were spread by word of mouth. Not all athletes benefited from creatine supplementation, however. Athletes involved in aerobic sports did not seem to benefit from creatine supplementation.[39] In studies in cyclists, creatine did not improve performance in repeated 700-m sprints or in longer cycling. Creatine did not increase maximal isometric strength or the rate of maximal force production. There appears to be athletes who are responders to creatine supplementation as well as athletes who are nonresponders, no matter what the sport. [97] It is estimated that approximately 30% of athletes

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are nonresponders. There also appears to be a maximum amount of creatine that can be stored by the body. Early studies emphasized the importance of loading creatine. Athletes would use large doses (20 g of creatine a day for 5 days) before reaching a maintenance dose (2 g/day).[62] More recent evidence revealed that loading is not necessary. A low-dose regimen of 3 g/day is just as effective.[95] The low dose of 3 g of creatine could be obtained through the diet by eating 5 pounds of meat or fish. Athletes most commonly use creatine monohydrate as the mode of taking creatine supplementation. Studies by Greenhaff and colleagues indicated that creatine intake could be facilitated by combining creatine with insulin-releasing carbohydrates. [49] Many athletes mix their creatine with a fruit drink to facilitate uptake. Commercial carriers have combined creatine with dextrose and a variety of amino acids and minerals to maximize creatine

absorption.[81] Accompanying creatine supplementation is an increase in body mass up to 2 kg.[48] This gain is believed to be secondary to an increase in body water. The effect of creatine on body fluid balance requires further investigation. When college football teams first used creatine, there were reports of severe cramping occurring in the athletes. It was recommended that creatine be taken with large volumes of water. It also was recommended that creatine not be taken before or during exercise.[101] Other case reports of gastrointestinal problems, including diarrhea, were common, but no definite evidence points to creatine as the definitive cause. There has been a lot of excitement about the ergogenic potential for creatine in athletes because creatine supplementation is a legal means of improving performance during short-duration, repetitive bursts of intense exercise. There are potential problems with creatine, however. Creatine does not work for all athletes; 30% may be nonresponders. Athletes in anaerobic sports seem to benefit much more than athletes participating in aerobic sports. Creatine may be detrimental to aerobic performance.[31] The ability of creatine to increase the intake of water into the muscle cells may affect the body's fluid balance. Recommendations for the use of creatine have been developed. Drinking high amounts of water when taking creatine is crucial. Creatine should not be used during periods of intense exercise. Creatine should be avoided during periods of high heat and humidity. No studies have been done on the effects of creatine on young athletes, and creatine is not recommended for athletes younger than 18 years old. [101] Further research regarding creatine is warranted. Long-term studies on the effect of creatine on athletes have not been done. The effect of creatine on prepubertal athletes needs to be studied.

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Growth Hormone

One of the most fascinating ergogenic drugs used by athletes is human growth hormone (GH). Human GH is a polypeptide produced and stored in the anterior pituitary gland. Pituitary cells called somatotropes make human GH. Greater than 50% of the anterior pituitary gland consists of somatotropes. Although it is well known that human GH secretion is high during puberty, human GH is secreted throughout a person's lifetime. GH secretion occurs daily in a pulsatile fashion, with the highest levels seen immediately after going to sleep. [5] GH was discovered in the 1920s when researchers found that after an injection of ox pituitary glands, normal rats reached abnormally large size. Not only were their skeletal muscles enlarged, but also all organs and viscera were enlarged. Animal breeders soon used GH extracts to increase the size of animals. It was discovered that animals treated with GH developed increased muscle mass and decreased body fat.[69] In the 1950s, GH was injected into children whose growth was stunted by absence of GH.[84] The GH was extracted from the brains of cadavers, many of whom came from Africa and Asia. Thousands of short stature children were being treated with human GH successfully until Creutzfeldt-Jakob disease, a disease causing progressive dementia and loss of muscle control leading to death, was transmitted via the cadaver extracts to the children. Transmitted through prions, proteins that contain neither RNA nor DNA, Creutzfeldt-Jakob disease is related to bovine spongiform encephalopathy.[100] By the early 1990s, seven children had developed Creutzfeldt-Jakob disease after injection of human GH. [68] The FDA stopped distribution of the drug. There was a need to develop a safe drug to treat children of short stature caused by low levels of human GH. The Genentech Company used recombinant DNA technology to manufacture a biosynthetic GH, somatrem (Protropin). Protropin had the identical sequence of 191 amino acids as human GH with an additional amino acid, methionine, on the N-terminus of the molecule. [58] Human GH now could be safely given to children with low GH levels, and studies of its effects were undertaken. GH affects almost every cell in the body. Because human GH levels drop to low levels as one ages, human GH has been promoted as an antiaging agent. Long-term studies of the effectiveness of

human GH have not been done. In the liver, human GH is converted into insulin-like growth factor (IGF-1). IGF-1 is responsible for most of the actions of human GH in the body. Athletes have used human GH and IGF-1 as ergogenic supplements. Human GH has many actions that would be attractive to athletes. Human GH stimulates protein metabolism. Nitrogen is retained, and urinary nitrogen excretion is decreased. Human GH stimulates amino acid uptake and protein synthesis. GH is a potent regulator of carbohydrate metabolism. Human GH decreases insulin sensitivity and decreases cellular uptake of glucose. Human GH stimulates the catabolism of lipids, making free fatty acids available for quick energy use and sparing muscle glycogen.[41] Human GH stimulates bone growth, which is crucial in a prepubertal youth but may cause problems in an adult with fused growth plates. In adults, some bones enlarge with human GH, and acromegalic changes develop, with facial bone, hand, and foot enlargement. Other problems can occur with human GH. With decreased insulin sensitivity comes a predisposition to developing diabetes. Heart disease, including cardiomyopathy and congestive heart failure, has been seen with human GH administration.[41] Lyle Alzado, an all-pro football player and self-admitted heavy user of

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human GH, died of a brain tumor. Alzado became an opponent of illegal ergogenic drugs for athletes, and he was sure his brain tumor was a direct result of his use of human GH. No proof for his contention exists. Human GH can cause enlargement of intracranial lesions.[58] Intracranial hypertension with papilledema has been seen in patients taking human GH. Leukemia has been seen in patients with low human GH levels treated with recombinant human GH. There are no good scientific studies that show improved athletic performance with human GH. Nevertheless, human GH has been used widely by athletes. In patients with acromegaly, muscles become larger in size but are weaker as a result of a human GH-induced myopathy. Because much of human GH is obtained clandestinely from overseas sources, quality control of the product is not ensured. Human GH is not available orally and must be administered by injection, which can cause problems for the athlete. Using injectable drugs subjects the athlete to a risk of infection. If athletes are sharing needles, they put themselves at a risk of exposure to the human immunodeficiency virus (HIV) and hepatitis viruses. Human GH is expensive, costing approximately $1000 per month of use. One reason that human GH is so appealing to athletes, despite the costs and plethora of adverse effects, is that there is no test to prove its use. Athletes can take human GH without fears of detection. The International Olympic Committee and the National Collegiate Athletic Association ban human GH.

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Erythropoietin

The sporting world was alerted to the importance of high-altitude training by the results of the 1969 Summer Olympics in Mexico City. Athletes who had trained at high altitudes had an apparently significant advantage in the endurance sports. Because aerobic endurance athletic activities are limited by the ability of the blood to deliver oxygen to the working muscle, activities to increase red cell mass theoretically should improve aerobic performance.[90] It has been known for centuries that people who reside at high altitudes adapt to the altitude and are able to do more work than people from lower altitudes. In 1893, Miesher discovered that lower oxygen saturation, which occurs in high altitudes, produced changes in the bone marrow to cause increased number of red blood cells. In 1906, Carnot and DeFlandre discovered that injecting serum from anemic rabbits into normal rabbits caused an increased number of red blood cells in the normal rabbit. Carnot and DeFlandre named this red blood stimulating factor hemopoietine. Further work by Bonsdorff and Jalavisto in 1943 led to a discovery of the blood-stimulating hormone they named erythropoietin (EPO). Miyake purified erythropoietin in 1977, and Lai discovered the molecular structure in 1986. Recombinant human EPO was synthesized in 1986.[108] Red blood cells have an average life span of 120 days, and a percentage of the cells are replaced by the bone marrow. The production of red blood cells is regulated mainly by EPO, which is manufactured in the kidney. If a person develops anemia, EPO can stimulate the bone marrow to increase red blood cell production by 3 to 10 times.[41] Berglund and Ekblom found a 17% increase of time to exhaustion in male athletes after 6 weeks of EPO administration.[10A] When EPO became safely available with the manufacture of recombinant EPO, athletes were quick to see the implications of EPO as an ergogenic drug. Many athletes had become interested in blood boosting, or increasing one's blood cell mass by transfusion, after the 1968 Mexico City Olympics.[37] EPO allowed increased red cell volume without the dangers associated with blood transfusions. Although the Olympic Committee banned recombinant EPO in 1990, there are no laboratory tests that can detect EPO use. Recombinant EPO has a short half-life of 20 hours, and its effects last for 2 weeks

after its use.[97] Athletes can use EPO without fear of being caught. Increasing the red blood cell mass in the blood can lead to increases in blood viscosity, which can harm the athlete. Increased red blood cells can lead to hypertension, stroke, headache, congestive heart failure, venous thromboses, and pulmonary emboli.[41] Studies have not been done in a controlled, scientific fashion to determine the efficacy and safety of EPO. Because it is accepted that a high blood volume is important to cardiac function in aerobic athletes, it would seem intuitive that EPO should benefit endurance athletes in whom aerobic performance is crucial. It appears, however, that many highly trained endurance athletes have a blood volume that places the heart near or at its ability to fill during diastole.[43] A well-conditioned athlete attempting to increase blood flow to a heart that is at its maximum ability to hold blood may put himself or herself in danger.

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Conclusion

For centuries, athletes have been willing to risk death in an attempt to improve their ability to compete in sports. What can individuals entrusted with the health of athletes do to protect athletes from themselves? First, it is essential to become educated regarding ergogenic drugs. It is helpful to read not only the scientific literature regarding these agents, but also the lay literature that is being read by the athletes. The health care professional should be able to communicate openly with athletes in the area of ergogenic drugs as well as nutrition, vitamin supplementation, and training for sport. Second, the medical community should conduct scientific controlled studies on athletes using ergogenic drugs. Such studies would be difficult to conduct because many of these drugs are illegal. Many ergogenic drugs have significant side effects. Research oversight committees often are reluctant to approve studies using drugs with known or suspected adverse effects, but such studies need to be conducted. Third, if athletes are using banned ergogenic drugs, and society and the athletic community agrees that drug use should be precluded, effective drug testing and appropriate punishments of athletes, coaches, teams, and nations ignoring these bans should be implemented. This is a difficult task because many drugs cannot be detected presently. Athletes have competed in a variety of sports for centuries. Their quest for improved performance has brought

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many developments in training practices as well as the use of ergogenic drugs. Significant questions remain regarding the safety and advisability of the use of

ergogenic drugs available today. Careful scientific studies are needed to enable athletes and their health care providers to make wise decisions regarding use of ergogenic drugs and to understand the risks involved in their use.

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Section B Recreational Drug Use in Athletes Gary A. Green MD Although sports organizations typically focus on the problems associated with ergogenic or performance-enhancing drugs, recreational drug use by athletes results in tragic consequences. The cocaine-related deaths of Don Rogers and Len Bias in 1986 and the alcohol-influenced traffic fatalities of Bobby Phils and Derrick Thomas in 2000 illustrate that athletes are no more immune to the dangers of these drugs than nonathletes. Some studies have suggested that athletes engage in high-risk behavior, including recreational drug use, more so than the general population. Rather than define a substance purely by its pharmacologic action, sports pharmacology classifies drugs according to reasons for use (i.e., ergogenic, recreational, and therapeutic). This classification can lead to confusion because some drugs can be taken for a variety of reasons. Caffeine can be a recreational drug when ingested in a single cup of coffee, an ergogenic drug in when ingested in high doses by long-distance cyclists to increase free fatty acid mobilization, or a therapeutic drug when ingested as a component of analgesic compounds for migraine headaches. For the purposes of this chapter, a recreational drug is a substance that athletes consume primarily for social reasons or to alter their mood. A recreational drug is not used to enhance athletic performance (ergogenic) or to treat an underlying medical condition (therapeutic). This chapter discusses the prevalence and patterns of recreational drug use in athletes, some of the common drugs of abuse, and strategies for prevention and treatment of substance abuse problems in athletes. A discussion of every potential recreational drug used by athletes is beyond the scope of this chapter. Four common drugsalcohol, marijuana, tobacco, and cocaine and crack cocaineare discussed as examples because of their high prevalence of use. These drugs are the quintessential recreational drugs, as represented in the 1997 National Collegiate Athletic Association (NCAA) survey,[35]

which asked athletes: What is the one main reason you use these drugs? ( Table 11B-1 ). Prevalence in Athletes

A great deal of research has been devoted to determining the prevalence of drug use in athletes and whether participation in sports leads to higher or lower levels of usage. Many problems are associated with this type of study, including defining who is an athlete, what is the appropriate control group, and any type of a gold standard for accurate reporting of drug use. The last-mentioned issue has been most problematic. If one relies on drug-testing information, the rate of drug use is low. The NCAA conducts drug testing at championship events and screens for a full drug panel, including recreational drugs. In 1998, of the 1883 tests conducted at these championships (including Division I football bowl games), 34 athletes were ruled ineligible as a result of a positive test (1.8%). Only 23 of the 34 positive test results were for recreational drugs (marijuana or cocaine metabolites), however, leaving a low recreational drug rate of 1.2%.[32] [35] The difficulty with relying on drug-testing information is that these tests generally are of the announced variety in that athletes are aware of when they will be tested. Another confounder is that except for marijuana use, which may cause a positive test for metabolites for 1 month after discontinuing its use, most substances are cleared fairly rapidly by the system. Unless testing is conducted frequently and without prior announcement, positive results are unlikely. A summary of the NCAA drug-testing program is given in Figure 11B-1 .[33] TABLE 11-B-1 -- What Is the One Main Reason You Use the Following Drugs? Response Choice Alcohol Cocaine/Crack Marijuana/Hashish Spit Tobacco To improve my athletic performance

0.20%

3.90%

0.60%

0.80%

It makes me feel good

13.70%

44.70%

34.70%

29.30%

For recreational or social reasons

83.40%

42.10%

61.20%

54.40%

To help me deal with stresses of college life

2.10%

3.90%

3.10%

13.20%

To help me deal with stresses of college athletics

0.60%

5.30%

0.40%

2.30%

From 1997 NCAA Study of Substance Use and Abuse Habits of College Student-Athletes. Presented to NCAA Committee on Competitive Safeguards and Medical Aspects of Sports, September 1997, Kansas City, Missouri.

484

Figure 11-B-1 Summary of National Collegiate Athletic Association positive tests, 1986-1998. Comp, competition. (From National Collegiate Athletic Association 2000 Drug Testing Program Web page. http://www.ncaa.org/sports_sciences/drugtesting. )

Another strategy for determining prevalence of use is by conducting surveys. The advantages of surveys are that they are cheap, can be given to large numbers of athletes, and can inquire about drug use over a much greater time period than a substance would appear in the urine. If given anonymously and conducted properly to ensure confidentiality, surveys can elicit relatively honest answers and provide a more realistic profile of drug use. The disadvantage of surveys is that there is no way to validate the results and be certain that the questions were answered correctly and honestly. Subjects who are aware that there are penalties for drug use may not be honest in their answers. In general, even with these limitations, surveys have provided the best indication of substance abuse prevalence in athletes. The NCAA conducts a survey every 4 years of the substance use and abuse habits of NCAA student-athletes. The survey performed in 1997 included 13,914 male and female student-athletes competing in 30 sports at 991 institutions. [35] The overall response rate was 64.3% with 637 of the 991 institutions reporting information on drug use within the past year. Although ergogenic drugs also were surveyed, this chapter focuses only on the responses regarding recreational drug use. The results for the six categories of recreational drugs are listed in Table 11B-2 . Alcohol is the most widely used recreational drug, with 80.5% admitting to use in the past 12 months. The NCAA asked student-athletes about their perceptions on their teammates' use of these substances. The question was asked, How many of your teammates would you estimate have used any of these substances in the last 12 months? ( Table 11B-3 ). Another contentious issue is whether athletes are more or less likely to use recreational drugs. Of NCAA athletes, 94.2% either disagreed or strongly disagreed with the statement, College athletes use drugs more than other college students.[35] Among researchers, the question is more controversial, however, and depends on which drugs are being investigated. There is one theory that participation in sports is a deterrent to recreational drug use because athletes are less likely to use a substance that has a negative effect on performance. Another difficulty in studying recreational drug use in athletes is defining who is an athlete and who can serve as an appropriate control group. Defining who is an athlete presupposes that participation in sports is an independent variable. In reality, athletes generally are not separated from their nonathletic peers and are influenced by many factors in addition to their athletic team. Regarding control groups, attention must be paid to the composition of the control groups in evaluating studies between athletes and nonathletes. Because of these difficulties, there must be large clinical as well as statistical differences between groups to establish that athletes use substances more or

TABLE 11-B-2 -- Prevalence of Drug Use in the Past 12 Months Among NCAA Student Athletes Alcohol Marijuana/Hashish Spit Cocaine/Crack Psychedelics Amphetamines Tobacco 80.50%

28.40%

22.50%

1.50%

5.60%

3.10%

From 1997 NCAA Study of Substance Use and Abuse Habits of College Student-Athletes. Presented to NCAA Committee on Competitive Safeguards and Medical Aspects of Sports, September 1997, Kansas City, Missouri.

485

TABLE 11-B-3 -- How Many of Your Teammates Would You Estimate Have Used Any of These Substances in the Past 12 Months? Substance None Almost Less than Half More than Almost None Half Half All Spit tobacco

29.10%

19.90%

21.90%

13.80%

11.20%

4.00%

3.10%

3.90%

6.80%

11.90%

26.20%

48.10%

Marijuana/hashish 23.30%

30.70%

27.90%

10.70%

5.60%

1.80%

Cocaine/crack

84.60%

13.40%

1.50%

0.30%

0.10%

0.20%

Amphetamines

73.10%

20.60%

4.70%

1.10%

0.30%

0.20%

Psychedelics

71.50%

21.70%

5.20%

1.00%

0.30%

0.20%

Alcohol

From 1997 NCAA Study of Substance Use and Abuse Habits of College Student-Athletes. Presented to NCAA Committee on Competitive Safeguards and Medical Aspects of Sports, September 1997, Kansas City, Missouri. less than the general population. Experimentation with substances as well as risk-taking behavior is normative for young adults in these studies. Two studies have compared college student athletes and nonathletes. [25] [34] Nattiv and colleagues studied 2298 college athletes and showed that the athletes appeared to be at a higher risk for maladaptive lifestyle behaviors, including consuming a greater quantity of alcohol with greater frequency and use of spit tobacco.[34] The athletes were less likely to use seat belts and rode more often as a passenger with a driver under the influence of alcohol. These findings may explain the number of athletes involved in serious traffic accidents, especially with alcohol. Nattiv and colleagues noted that not all athletes had the same risk profile, and male athletes and athletes participating in contact sports were at higher risk. [34] Kokotailo and associates further stratified the risk by examining 1210 male and female

athletes and nonathletes.[25] Table 11B-4 shows that female athletes had a much lower use of recreational drugs. Among male athletes, the differences were not as dramatic, and except for spit and smoked tobacco, the male athletes and nonathletes appeared clinically similar. The distinction in this case is that although the difference between female athletes and nonathletes for alcohol use in the past 30 days may be statistically significant at the P < .05 level, the intervention for a group with 70.6% of use and one with 84.2% would be similar.[25] The conclusion of these studies is that although athletes may have an incentive not to use drugs that have negative effects on performance, with few exceptions, they are relatively similar to their nonathlete peers. It seems likely that the reason not to use recreational drugs is balanced by an athlete's feeling of invulnerability and the degree of risk taking that often causes athletes to succeed on the playing field. Where the differences are more relevant is the treatment and prevention aspect of substance abuse, in which the participation in athletics can be used as a motivational tool.

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Alcohol

Although there may be debate about patterns of use between athletes and nonathletes, studies have shown consistently that alcohol is the number one recreational drug of abuse. Alcohol also is the most abused drug in the United States and is responsible for at least 200,000 deaths per year.[34] Ethanol is considered pharmacologically to be a depressant and is responsible for many social, personal, and legal problems. There is evidence that the brewing and consumption of alcohol has been occurring since the dawn of time. Throughout history, various qualities have been assigned to ethanol, including ergogenic properties.[17] In the early 1900s, marathoners were provided with brandy during a race.[11] That attitude seems to have vanished in that less than 2% of NCAA athletes believed that alcohol was slightly helpful or helpful to their athletic performance.[35] Today, alcohol is regarded as an ergolytic (performance reducing), rather than an ergogenic substance. As stated previously, alcohol consumption has been shown to be prevalent among athletes. The survey by Leichliter and coworkers of 51,000 college students revealed TABLE 11-B-4 -- Prevalence of Substance Abuse in Athletes and Nonathletes by Gender Substance Used

Male Male Female Female Athletes (n = Nonathletes (n = Athletes (n = Nonathletes (n = 162) 313) 109) 462)

Cigarette smoking (past 30 days)

16.1%

26.5%

11%

27.1%

Spit tobacco (past 30 days)

22.4%

9.6%

2.8%

0.2%

Alcohol use (past 30 days)

79%

85.6%

70.6%

84.2%

Binge drinking (past 30 days)

65.4%

68.4%

46.8%

51.7%

Marijuana use (past 30 days)

11.7%

18.9%

4.6%

14.9%

3.1%

4.5%

0.9%

5.4%

Cocaine use (lifetime)

From Kokotailo PK, Henry BC, Koscik RE, et al: Substance use and other health risk behaviors in collegiate athletes. Clin J Sports Med 6:183-189, 1996.

486

that athletes consumed significantly more alcohol per week, engaged in binge drinking more often, and suffered more adverse consequences from alcohol use than the self-identified nonathletes.[27] The self-identified team leaders of the male sports appeared to be significantly more at risk, eroding the notion that team leaders are more responsible. Older male and female distance runners with an average age of 39.7 and 35.2 were compared with a sedentary control group with respect to drinking patterns. It was found that except in subjects who previously had reported a drinking problem, running was associated with increased alcohol consumption. [20] Compared with the control groups, the male runners (there was no difference in females) were more likely to report not knowing the effect of alcohol on their running performance. One predominant theme among all college students, including athletes, is that binge drinkingdefined as drinking 5 or more drinks at a sittingis common.[44] This behavior leads to a high risk in that the lack of judgment associated with large quantities of alcohol can have serious costs, including unintended sexual behavior and potential pregnancy, sexually transmitted diseases, and rape; motor vehicle incidents; violent behavior; and alcohol intoxication. One study has suggested that participation in athletics in college is a risk factor for binge-drinking behavior.[45] In addition to the acute effects of alcohol bingeing and related behavior, there is the potential for long-term consequences. Two studies have shown an increase in all-cause mortality in men who drink more than six drinks per session.[23] [24] Although the overall detrimental effects of alcohol on health are beyond the scope of this chapter, the effects of alcohol in relation to sports performance are discussed. The 1982 position paper of the American College of Sports Medicine (ACSM) on the use of alcohol in sports outlined the many negative ergogenic aspects of alcohol, including a deleterious effect on a wide variety of psychomotor skills, such as reaction time, hand-eye coordination, accuracy, balance, and complex coordination.[1] The ACSM stated that alcohol has little influence on metabolic or physiologic functions, such as maximal oxygen consumption or respiratory dynamics. According to the ACSM, alcohol

may decrease strength, power, and local muscular and cardiovascular endurance. Further evidence of the negative effects of alcohol on performance was provided by two studies that examined the influence of short-term alcohol use on running. These placebo-controlled studies showed decreased running times as the blood alcohol level increased.[21] [30] With chronic ingestion of alcohol, it has been shown that alcohol is toxic to striated muscle in a dose-dependent manner.[41] The presence of alcoholic myopathy suggests an accompanying cardiomyopathy.[14] Injury to skeletal and heart muscle can be damaging to athletic performance. Overall, the negative effects of alcohol on athletic performance are well documented. The position of most major sports organizations is that the use of alcohol is not banned, and it is not tested with urine drug testing. The only exceptions are the NCAA and International Olympic Committee, which have a provision for testing for alcohol only in shooting (e.g., rifle, pistol, archery) events. In cases in which there is the suspicion of acute intoxication, international federations reserve the right to perform blood alcohol or Breathalyzer testing. In practice, these situations rarely arise. Traditional urine testing for alcohol is fraught with difficulties and has minimal practical utility. The major difficulty with alcohol use is identifying the 10% of the population that is at risk for alcoholism. The definition of alcoholism is problematic; I define an alcoholic as someone who continues to drink despite repeated negative experiences. The appearance of repeated negative occurrences usually makes the diagnosis of alcoholism obvious. The challenge is to develop a method to identify an alcoholic before he or she has encountered these problems. Many tools have been developed for early identification with the goal of being able to intervene and prevent further damage, including the Perceived Benefit of Drinking Scale (PBDS), the CAGE questionnaire, and the Michigan Alcoholism Screening Test (MAST).[39] None of these tools is a gold standard in the diagnosis of alcoholism. These tools merely provide the clinician with standard questions for a basis of further investigation. One study of college freshmen found that a composite screening measure had improved sensitivity and specificity over either the CAGE or PBDS alone.[47] Sports and alcohol are connected intimately, and this association comes with a cost. Athletes frequently have advertised for alcoholic beverages; in contrast, Mickey Mantle died prematurely from the effects of alcohol. His battle with alcohol is testimony to the consequences that alcohol can have even on a gifted athlete.[28] Alcohol is likely to continue to be the number one drug of abuse among athletes, and it is incumbent on the team physician to educate, prevent, and recognize its effects.

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Marijuana

Marijuana is not classified easily, but in terms of its pharmacologic effects, it is considered a euphoriant. Marijuana is an illegal drug, and users are subject to criminal penalties in the United States. Marijuana occurs naturally and contains varying amounts of the active ingredient -9-tetrahydrocannabinol (THC); it can be absorbed easily through the oral route or by combustion and inhalation. The actual amount that is ingested depends to a large degree on the route, smoking technique, and amount altered by pyrolysis.[19] The use of marijuana is centuries old, and marijuana has been employed by many cultures for its ability to alter mood. [40] There are at least 17 million regular users of marijuana, and more than 43 million people in the United States have tried it.[36] Athletes are not immune to trying marijuana, as reflected in the 1997 NCAA study that revealed marijuana to be the second highest recreational drug after alcohol (25%),[35] and other studies have found marijuana use to be common among athletes.[25] [35] Among high school students, one study found that male athletes who participate in sports had a higher incidence of marijuana use than nonathletes, although female athletes had a lower incidence compared with nonathletes.[13] According to the NCAA study, 53% of student-athletes who report using marijuana do so at least once a month, with 24% admitting to greater than 40 times per year.[35]

487

Marijuana is absorbed readily, and THC has effects on many sites throughout the body, most prominently the central nervous system, cardiovascular system, and respiratory tree. Although the effects of marijuana vary depending on the route of entry, actual dose of THC, and previous experience of the user, some general statements are applicable. The central nervous system is the area that is affected most obviously by THC because

this is the target organ for most users. In addition to acute intoxication and the psychotropic effects, the action of THC crossing the blood-brain barrier can lead to impaired motor coordination, decreased short-term memory, and difficulty concentrating. A decline in work performance has been noted with an attendant attenuation in the ability to carry out multistep tasking.[17] Of all the systems affected, the changes to the central nervous system are extremely variable and depend on the individual and the dose received. Perhaps the most consistently observed phenomena associated with the ingestion of THC relate to the cardiovascular system. The effects most commonly observed include tachycardia, increased supine systolic blood pressure, decreased upright blood pressure, and conjunctival reddening. Tachycardia is a dose-dependent occurrence mediated through the sympathetic nervous system and can be prevented by the administration of -blocking agents. All of these are acute effects. The chronic use of THC can give rise to an increase in plasma volume, although the mechanism responsible is unclear.[17] Although chronic inhalation of marijuana smoke can have detrimental effects on the pulmonary system in the form of bronchitis and asthma, the acute response is different. Acutely, THC causes bronchodilation in normal and asthmatic subjects and is independent of the route of administration, although the mechanism currently is unknown.[40] Acute ingestion of smoked marijuana can result in an increased resting oxygen consumption. The tar that is produced by ignition is much more carcinogenic on a per-weight basis than that of tobacco smoke.[17] Long-term use of smoked marijuana produces air flow obstruction and nonspecific airway hyperreactivity, which most likely is due to chronic irritants in the smoke. In the immune system, THC has been shown to suppress cellular and humoral immunity in animals and in vivo. The hypothalamic-pituitary-gonadal axis has been investigated, and some data suggest that THC lowers the concentration of testosterone, reversibly inhibits spermatogenesis, and causes anovulatory cycles. The clinical significance of these effects is undetermined.[17] Although the overall effects of marijuana have been studied fairly extensively, few studies using small numbers of subjects have examined specifically the effect of THC on exercise. In one study of men cycling against resistance, 10 subjects showed diminished peak exercise performance under the influence of marijuana. [11] Renaud and Cormier performed an extensive study of the acute effects of marijuana on several physiologic parameters associated with maximal exercise performance.[37] The study of subjects at rest found that marijuana smoking resulted in tachycardia, bronchodilation, and a decreased maximum work capacity. The last finding was most likely the result of premature attainment of maximal oxygen consumption. Renaud and Cormier found an increased metabolic rate associated with marijuana smoking, although it was unclear whether this was secondary to marijuana alone or in combination with exercise.[37] Another study of 161 men and women given oral THC showed a reduction in standing steadiness, simple and complex reaction times, and various psychomotor skills.[11] Although these subjects were not athletes performing specific athletic skills, it is easy to

extrapolate that coordinated athletic performance would be expected to decline. A study examining the combined effects of marijuana and alcohol in terms of general performance showed attenuation greater than when either drug was used alone. This finding is clinically relevant in that the two drugs often are used together. [11] Marijuana currently is classified as a Schedule I drug, indicating that it is potentially addictive and has no medical uses. Many have argued that marijuana is misclassified because it does have approved medical uses. THC has been approved for use as an antiemetic, an analgesic for refractory pain, and as an antiglaucoma drug in the United States. THC has been touted as an appetite stimulant for wasting states associated with human immunodeficiency virus (HIV) infection, metastatic cancer, and cancer chemotherapy. There has been an increased call to change marijuana to a Schedule II drug (potentially addictive but with some acceptable medical use). [22] Several states have passed referendums making it easier for physicians to recommend THC for specific conditions. The Drug Enforcement Agency has opposed these efforts by the states. The dosage of marijuana used at a particular sitting can vary tremendously and can be difficult to quantify because of the variability in potency of marijuana and the experience of the user. According to the 1997 NCAA survey, 91% of student-athletes who admitted to using marijuana stated that they smoke fewer than three marijuana cigarettes when they use, and 72% stated that they smoke fewer than 2 marijuana cigarettes when they use.[35] Two to three puffs of high-potency marijuana can provide enough THC to intoxicate a 70-kg adult.[38] Although the standard marijuana cigarette has been thought to contain about 20 mg of THC, the exact dosage that an individual consumes is variable.[15] Despite the difficulty in predicting marijuana dosage, THC has an extremely long half-life and can be detected for several weeks by urine testing. THC is lipophilic, and gas chromatography/mass spectroscopy can identify its presence easily. To avoid the possibility of a positive test resulting from passive inhalation, sports organizations generally have considered 12 to 15 ng/mL as a threshold for a positive test result. Sports organizations' policies vary with respect to sanctions for marijuana use. The NCAA considers marijuana an illegal drug and tests at a level of 15 ng/mL. A survey of NCAA member institutions reveals that almost every school tests for marijuana. The International Olympic Committee has changed its interpretation and now bans THC, although the rationale for not prohibiting its use was that it is not a performance-enhancing drug. Because athletes usually reflect the drug habits of their peers, sports medicine practitioners need to be knowledgeable about marijuana use by athletes. In addition to educating athletes about the negative effects of THC on performance, physicians should be aware of the possibility of

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THC dependency. Although dependency is not common in comparison with the absolute numbers of marijuana users, it does occur and should be recognized and treated. Frequently the sports medicine practitioner encounters a marijuana user on the basis of a positive drug test. In this situation, it is incumbent on the physician to assess the relative depth of the problem with respect to marijuana and to do a thorough assessment of the athlete's total substance use. It is common in that situation to find that marijuana is not the major problem, but that another substance (usually alcohol) is having a significant effect on the athlete and impairing his or her judgment.

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Tobacco

The discussion of athletes and tobacco necessarily focuses on the practice of chewed tobacco products, rather than cigarettes. Although it is rare in most sports to see an athlete smoking a cigarette, it is not unusual to see an athlete competing with a mouthful of tobacco. There has been some confusion as to the nomenclature regarding these products, being called chewing, smokeless, or spit tobacco. The trend has been to use the term spit tobacco because the term smokeless tobacco implies a nonoffensive, safe product, whereas spit tobacco is a more accurate representation of the way it is used. For this chapter, all products such as loose leaf, snuff, or plug tobacco are referred to as spit tobacco. The active ingredient in spit tobacco is nicotine, a volatile alkaloid that is classified as a tertiary amine and is responsible for the many effects of tobacco. [5] Tobacco in its many forms has been present for at least 500 years and was introduced to Christopher Columbus by the native inhabitants of the New World. The native peoples used tobacco for ceremonial rituals, as medicine, and as a gift. [18] When introduced to Europe, tobacco rapidly gained in popularity and was used for a variety of purposes, including medicinal remedies. It eventually became popular in the United States as well in the 1800s, and compressed (plug) and powdered (snuff) tobacco became widely used. The association between sports and spit tobacco dates back to the mid-1800s. In 1845, during a time of spit tobacco popularity, the rules of baseball first were written in the United States.[7] Historians have supposed that the early ballplayers used spit tobacco to keep their mouths moist while playing in dusty ballparks or to produce saliva to soften their gloves or create a spitball.[7] The tuberculosis epidemic of the early 1900s created an awareness of the public health dangers of expectoration, and chewing and spitting became socially unacceptable and illegal in some places. This situation coupled with the availability of machine-rolled cigarettes led to the rapid increase of cigarettes and the relative decline of spit tobacco. Although baseball continued to hold on to the tradition of spit tobacco through the 1940s (the spitball was banned in 1920), by the 1950s cigarette smoking was common in the major leagues, and many star players appeared in

television and print advertisements.[8] In the 1970s and 1980s, health concerns caused a change in tobacco habits, and the increasing reports of the dangers of smoking led to a revival of spit tobacco. As a result of aggressive advertising, star-athlete spokesmen, and free sampling, the use of spit tobacco increased rapidly. National cigarette sales declined from 1978 through 1985, but the sales of moist snuff increased 55%. [7] Despite the ban on television advertising of tobacco products, companies often circumvent this through the use of sponsorships. During the 93-minute telecast of the 1989 Marlboro Grand Prix car race, the Marlboro logo was visible for 46 minutes (49% of the televised time).[3] A further example of the success of the advertising program is that in 1970, the heaviest users of snuff were men older than age 55. By 1985, the heaviest users had become young men less than 19 years old.[3] Young male athletes have a high prevalence of spit tobacco use. The prevalence of spit tobacco use among athletes seems to be concentrated among certain sports, most heavily on male teams. According to the 1997 NCAA survey, 22.5% of all athletes had used spit tobacco in the preceding 12 months.[35] The range for male teams was 6% to 47% versus a range for female teams of 1% to 12%. Some sports, such as baseball (46%) and wrestling (47%), are at high risk.[35] A 1997 study of two major league baseball teams and minor league affiliates revealed 31% current users and 7% former users among the 304 players. Spit tobacco is one of the few drugs that has a significantly higher prevalence among athletes. A study showed a 17% usage rate among athletes compared with 5% in the nonathlete population.[34] Participation in athletics is a risk factor for spit tobacco use. Although tobacco use has been known for centuries, nicotine is a complex chemical that is active throughout the body through several mechanisms. Regardless of the route of administration, nicotine can cross cell membranes easily and binds to acetylcholine and nicotine receptors.[5] After ingestion, nicotine crosses the blood-brain barrier rapidly and affects a variety of sites, although its direct effects are on brain receptors. Through these receptors, nicotine acts as a short-term stimulant by effecting the release of catecholamines and neurotransmitters from vascular sympathetic nerves.[5] A complex dose-response effect develops during exposure to nicotine. Low doses result in ganglionic stimulation, whereas high doses cause ganglionic blockade; this can be seen clinically whereby low-dose nicotine causes a sympathetic discharge and increases in blood pressure and tachycardia.[5] Paradoxically, high doses of nicotine result in hypotension and bradycardia that likely are mediated by ganglionic blockade, vagal nerve stimulation, or direct central depressor effects.[5] In addition to this biphasic response, pharmacodynamic tolerance to nicotine develops rapidly, perhaps in 1 day. [5] These factors must be taken into account when studying the effects of nicotine on athletes. Although nicotine is well absorbed by several routes, there are a few differences between cigarette smoking and spit tobacco. A well-done study revealed that although all forms of tobacco cause an increase in urinary catecholamines, urinary sodium excretion was much higher for spit tobacco.[4] This finding likely is the result of the large amount of sodium (average 1.75% by weight) that is added to spit tobacco for flavoring

and to improve absorption. [4] One of the myths of baseball is that spit tobacco improves

489

performance. This myth has been refuted by players and research. A 1988 study of professional baseball players who used spit tobacco revealed that only 10% used spit tobacco for concentration, and none used it to improve their game or to sharpen reflexes.[7] The 1997 NCAA study revealed that of athletes who had used spit tobacco in the past year, only 0.8% stated that the main reason was to improve athletic performance. [35] Controlled, scientific studies have concluded that spit tobacco does not have any effect on reaction time and may affect detrimentally maximum voluntary force and the maximum rate of force generation.[10] [12] Spit tobacco users and researchers agree that nicotine is not an ergogenic aid. The amount of nicotine that a user of spit tobacco consumes varies depending on the nicotine content of the various forms of spit tobacco: loose leaf, snuff, or plug. About 10% of the available nicotine is absorbed across the oral mucosa, and spit tobacco users have blood nicotine levels similar to those of nicotine-dependent smokers.[7] [19] Spit tobacco users consuming 8 to 10 dips or chews per day receive a nicotine dose equivalent to 30 to 40 cigarettes per day.[7] Of the spit tobacco users in the NCAA survey, 50% reported using it one to five times per day, and an additional 13% used it more than five times per day. [35] It is an incongruity that health-conscious athletes, who never would dream of smoking a pack of cigarettes per day, regularly expose themselves to an equivalent amount of nicotine. The adverse effects of nicotine are well known. Spit tobacco products have specific effects that deserve mention. The most concerning is the association with cancers of the oral cavity and pharynx, the prevalence of which is at least double the rate among snuff dippers. Among chronic users, the risk of developing cancers of the gum and buccal mucosa was almost 50 times higher.[18] This risk is in addition to the development of leukoplakia, whitish, soft tissue lesions ( Fig. 11B-2 ) that become squamous cell cancers in 3% to 6% of cases. One study of professional baseball players revealed that 56% of the spit tobacco users had associated oral mucosal lesions.[42] The overall 5-year survival rate of patients with oropharyngeal cancers is only 40%.[18] In addition to the carcinogenic nitrosamines derived

Figure 11-B-2 Leukoplakia secondary to spit tobacco use.

from nicotine, spit tobacco contains a significant amount of sugar, which helps account for the 2.4 times increase in dental caries. Spit tobacco users have a high incidence of gingival recession and periodontal disease.[18] The long-term use of spit tobacco has

been found to reduce taste sensitivity and perhaps alter taste preferences, although the mechanism is unclear.[31] The nicotine absorbed from spit tobacco potentially can cause the same systemic effects as cigarettes, including increased myocardial workload and increased sympathetic tone leading to vascular disease.[4] As mentioned, spit tobacco contains large amounts of sodium that are added for flavoring and to increase absorption; this can lead to hypertension as well as fluid retention. Increases in urine mutagenicity after using spit tobacco have been reported and may contribute to the development of cancers of the kidneys and bladder.[4] Currently, no sports organizations conduct drug testing for nicotine. The NCAA bans the practice of spit tobacco use by players, coaches, and officials during NCAA-sanctioned events, and spit tobacco is banned in many minor baseball leagues. Although nicotine is not listed as a banned substance, sports organizations increasingly are concerned about the use of spit tobacco and have taken steps to curb its use and help users quit. Researchers have attempted to develop methods to promote spit tobacco cessation using dental screenings, nicotine replacement, and buproprion.[42] Although studies have shown that athletes who use spit tobacco are aware of the health risks, dental screening showing tobacco associated lesions can be a powerful motivation. All users should be encouraged to seek a thorough dental screening. The preparticipation physical examination is an excellent venue to make this referral. Several sports organizations, including major league baseball and the NCAA, have joined the National Cancer Institute and other health organizations in developing written materials to assist spit tobacco users in quitting. These brochures are written for athletes and provide a template for quitting the spit tobacco habit. Tolerance and addiction are a major problem with any form of nicotine use, and cessation can be difficult. It is imperative that the team physician be aware of spit tobacco use and continue positive attempts to encourage quitting.

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Cocaine

The use of cocaine in the general population has followed a cyclical rise and fall for more than 100 years, and its use by athletes has reflected these variations. At its most basic level, cocaine is derived from the leaves of the Erythroxylon coca plant, which is grown abundantly in South America.[6] Although thought of as a relatively modern phenomenon, there is historical evidence of definitive use of cocaine back to at least 3000 BC. [43] Despite the fact that cocaine is a potent vasoconstrictor, it is absorbed easily from almost any route, including nasally, intravenously, or igniting the base and smoking in the form of crack cocaine. The first use of cocaine in sport was apparently by the ancient Incas of Peru, who used cocaine as a stimulant for

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the runners who took messages between villages. The Incas also recognized cocaine for its recreational properties and gave it as a reward and used it ceremonially. [26] In general, today's athletes who use cocaine usually partake for its recreational properties. The 1997 NCAA study revealed that 87% used cocaine for recreational purposes or to feel good, and only 3.9% took it to improve athletic performance.[35] Drug use by athletes generally reflects overall societal patterns, and cocaine is no exception. During the 1980s, when cocaine enjoyed widespread popularity, use by athletes also increased. A study by Anderson and colleagues of NCAA athletes in 1985 revealed that 17% had used cocaine during the previous year.[2] By 1997, that number had dropped to 1.5%, reflecting an overall decline on college campuses.[35] Although the overall prevalence apparently has declined, there are still reports of high-profile athletes succumbing to cocaine addiction. Professional baseball players Tony Phillips, Dwight

Gooden, and Darryl Strawberry are examples. Coincident with the declining prevalence, there are data to support the view that college athletes do not see cocaine as socially acceptable within their team. Of NCAA athletes who had used cocaine, 73% stated that they either seldom or never engaged in cocaine use with their teammates. This group of college athletes also sees cocaine use as secretive. For all of the eight classes of drugs surveyed in 1997, athletes were asked if the coaching staff knew of their use. Of cocaine users, 64% stated that they were certain that the coaching staff did not know of their use. This was the highest percentage of any of the drugs surveyed and compares with 8% of alcohol users and 49% of marijuana users.[35] The mechanism of action for cocaine is increase in the release and blocking of the reuptake of norepinephrine at the neuronal level. The result is an abundance of norepinephrine and epinephrine flooding the neurons with the consequence being the typical sympathetic actions of these drugs, including a feeling of euphoria, increased blood pressure, tachycardia, ventricular arrhythmias, and an attenuated seizure threshold. This overwhelming outflow of sympathetic response also results in hyperthermia, hyperglycemia, and hyperreflexia.[8] In addition to the general effects of cocaine, there are some specific consequences for athletic participation. Despite the experience of the ancient Incas, it seems clear that cocaine can have negative effects on performance through a variety of mechanisms. Cocaine has been shown to damage muscles and impair athletic activity.[11] Animal data showed that cocaine reduced significantly and dramatically endurance during exercise.[11] Cocaine increases temperature, probably via central thermoregulation, and one of the limiting factors in long-distance running is thought to be overall temperature control. In this regard, cocaine would be ergolytic. Cocaine use has been associated with increased mortality when the ambient temperature rises so that there may be further risks of using cocaine when the body temperature increases, as with exercise. [29] Some researchers have postulated that an athlete with a high percentage of glycolytic muscle fibers, such as a sprinter, would be at an increased risk for severe lactic acidosis and cocaine-induced seizures.[18] One study reported that there was a higher incidence of myocardial events associated with the combined use of anabolic-androgenic steroids and cocaine.[46] The 1930 edition of the Merck Index listed 17 different cocaine formulations for a variety of ailments, but now the therapeutic uses of cocaine are extremely limited. [26] Cocaine is listed as a Schedule II pharmaceutical, and its use is limited to topical anesthesia, mostly in otolaryngeal procedures. Its high abuse potential, coupled with alternative treatments, has restricted its therapeutic uses severely. As stated, cocaine is absorbed in many ways, and the dosage varies according to method. Although a recreational, intranasal user may consume about 1 to 3 g per week, a dose of crack cocaine may be 60 to 70 mg.[26] The effect of this small dose is intense and rapid, usually lasting 5 to 10 minutes. This type of effect can lead to drug-seeking behavior and a rapidly progressive addiction.

As mentioned, cocaine can be ingested by a variety of routes, and each method has its own attendant risks. Smoking crack cocaine has been reported to cause bronchiolitis obliterans and severe pulmonary damage.[43] Intravenous use of cocaine is well known to be associated with the spread of infections, such as hepatitis B, hepatitis C, and HIV. The use of crack in association with unsafe sexual practices provides a high risk for HIV infection. A study of inner-city young adults found that crack cocaine users were three times more likely to be HIV positive than the control group.[9] Because of the relatively short half-life of cocaine, drug testing is ineffective in detecting cocaine use. With an estimated half-life of 2 to 6 hours, cocaine probably can be detected in the urine only for 3 days after use. Because most athletes are only occasional users, random drug testing would be unlikely to detect cocaine use. Many of the athletes who are caught using cocaine are discovered because of legal violations, rather than drug testing by sport. An exception is Cuban high jumper Javier Sotomayor, who failed a drug test in 1999 because of cocaine and was suspended from competition.

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Conclusion

All of the drugs discussed in this chapter are used by athletes and nonathletes, and a sports medicine practitioner will encounter athletes using these substances. To determine the best approach for the problem, the first step is deciding on the level of intervention needed. Primary prevention refers to when the athlete has never tried a particular drug. The 1997 NCAA survey asked at what age an athlete had tried each drug, and the results are summarized in Table 11B-5 .[35] For most drugs, effective primary prevention must be done at a young age (i.e., before high school and college). When an athlete has used a particular drug, the appropriate intervention must shift to determining the actual or potential problems associated with use. The difficulty is to establish the extent of use to determine the appropriate intervention. To some extent, experimentation with recreational drugs is normative behavior for teenagers and young adults. It can be challenging to decide between

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TABLE 11-B-5 -- Initial Use of Recreational Drugs Response Choice Alcohol Marijuana Spit Tobacco Cocaine/Crack Junior high or before

14.2%

8.6%

17.8%

10.7%

High school

63.2%

62.7%

58.7%

34.7%

Freshman year of college

18.2%

17.4%

15%

10.7%

4.3%

11.4%

8.4%

44%

After freshman year of college

From 1997 NCAA Study of Substance Use and Abuse Habits of College Student-Athletes. Presented to NCAA Committee on Competitive Safeguards and Medical Aspects of Sports, September 1997, Kansas City, Missouri. experimentation and problem usage, and the decision depends on the drug involved. Of NCAA athletes, 80% drink alcohol, yet the rate of problem drinking is much lower. With cocaine use, the risk of addiction is much higher. Although many tests have been developed to try to identify the addict, there is no absolute answer. The best definition of problem use is an individual who uses despite repeated negative consequences (e.g., medical, social, financial, or athletic). This information can be obtained only by a thorough history and physical examination in a private setting by a qualified physician. The team physician frequently is in an excellent position to perform this function by virtue of a trust that has been established between the athlete and physician. Although most nonathlete adolescents rarely have regular access to a physician, athletes are unique in that they see physicians at least once a year for a preparticipation physical examination. Confronting an athlete with concerns about a recreational drug problem can be difficult. Denial usually is present, and athletes often have the feeling of invincibility that reinforces the sense of denial; this can be especially true of an elite athlete used to performing high-level athletic feats despite substance use.[28] To overcome the denial, the physician should listen to the athlete and attempt to discover what problems have arisen secondary to substance abuse. The physician should use this information to help bridge the gap between perception and reality and steer the athlete toward appropriate counseling. All athletic programs should have substance abuse counselors available. Helping any individual to change a behavior such as substance use requires that the clinician discover a particular motivating factor for that person. In this regard, athletes are a special group, and participation in sports can be used as positive motivation. Most athletes are motivated to train and perform at the highest athletic level. All of the recreational drugs mentioned in this chapter have negative effects on performance, and this can be a powerful tool ineducating athletes. Most recreational drugs result in a positive drug test, which translates into loss of athletic eligibility. A first-time positive test by the NCAA for cocaine or marijuana results in a 1-year suspension from play. Given that an athlete has only 4 years of intercollegiate eligibility, this is a significant penalty and can serve as a major deterrence to use. The team physician frequently may be in a position to raise the subject of substance abuse and should not miss these opportunities. It would be appropriate to discuss substance use with the athlete who suffers a fifth metacarpal fracture on a weekend. The team physician may have more obvious occasions, such as receiving a positive drug test result. In any event, the team physician may have to break confidentiality if a crisis ensues and consult with athletic department personnel and counselors if there is imminent danger and arrange for an intervention. Communication is the key, and an athlete's teammates and coaches often employ collusion as long as performance is maintained.

Given that athletes generally are motivated to perform at their best, the team can be used as a positive peer group to deter use of recreational drugs. In my experience, team meetings to establish normative behavior and setting limits can be effective. The sports team can act as a positive peer group to motivate athletes not to use substances. Placing the responsibility on the team to set rules regarding recreational drug use can be a helpful exercise, when combined with appropriate guidance from professionals. Although drug testing is necessary for ergogenic substances, I believe that interactive, educational programs are the foundation for dealing with the problem of recreational drug use. Too often educational programs focus on the athletes, but neglect personnel such as trainers and coaches, who have more direct access to athletes. The team physician can play an active role not only with the athletes, but also in raising awareness with coaches and all athletic support personnel. Drug use is a multidisciplinary problem, and it is imperative to involve other professionals in the community, such as psychologists, drug counselors, and educators, in developing an education and treatment program. Although patterns of drug use may change, athletes always use recreational drugs, and the sports medicine practitioner needs to be aware of these issues.

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Acknowledgments

The author thanks Mark DeMars, for his help in the preparation and editing of the manuscript, and Dr. Nicholas Cassisi, for the use of a photograph.

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Edlin BR, Irwin KI, Faruque S, et al: Intersecting epidemicscrack cocaine use and HIV infection among

inner-city young adults. Multicenter Crack Cocaine and HIV Infection Study Team. N Engl J Med 331:1422-1427, 1994. Edwards SW, Glover ED, Schoeder KL: The effects of smokeless tobacco on heart rate and neuromuscular reactivity in athletes and nonathletes. Physician Sports Med 15:141-146, 1987. 10.

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Eichner ER: Ergolytic drugs. Intern Med 11:74-80, 1990.

Escher SA, Tucker AM, Lundin TM, Grabiner MD: Smokeless tobacco, reaction time, and strength in athletes. Med Sci Sports Exerc 30:1548-1551, 1998. 12.

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Ewing BT: High school athletes and marijuana use. J Drug Educ 28:147-157, 1998.

Fernandez-Sola J, Estruch R, Grau JM, et al: The relation of alcoholic myopathy to cardiomyopathy. Ann Intern Med 120:529-536, 1994. 14.

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Fuentes RJ, Rosenberg JM (eds): Athletic Drug Reference '99. Durham, NC, Clean Data, 1999.

Giammarco RA: The athlete, cocaine, and lactic acidosis: A hypothesis. Am J Med Sci 294:412-414, 1987. 16.

Gilman AG, Goodman LS, Rall TW, Murad F (eds): Goodman and Gilman's the Pharmacologic Basis of Therapeutics, 7th ed. New York, Macmillan, 1985, pp 559-561. 17.

Glover ED, Edmundson EW, Edwards SW, Schroeder KL: Implications of smokeless tobacco use among athletes. Physician Sportsmed 14:95-105, 1986. 18.

Gritz ER, Baer-Weiss V, Benowitz N, et al: Plasma nicotine and cotinine concentrations in habitual smokeless tobacco users. Clin Pharmacol Ther 30:201-209, 1981. 19.

Gutgesell ME, Timmerman M, Keller A: Reported alcohol use and behavior in long-distance runners. Med Sci Sports Exerc 28:1063-1070, 1996. 20.

Houmard JA, Langenfeld ME, Wiley RL, Siefert J: Effects of 5-mile run times. J Sports Med Phys Fitness 27:253-257, 1987. 21.

22.

Kassirer JP: Federal foolishness and marijuana. N Engl J Med 336:366, 1997.

Kauhanen J, Kaplan GA, Goldberg DE, Salonen JT: Beer bingeing and mortality. BMJ 4:846-851, 1997. 23.

24.

Klatsky AL, Armstrong MA, Friedman GA: Alcohol and mortality. Ann Intern Med 117:646-654, 1992.

Kokotailo PK, Henry BC, Koscik RE, et al: Substance use and other health risk behaviors in collegiate athletes. Clin J Sports Med 6:183-189, 1996. 25.

26.

Kunkel DB: Cocaine then and now: Part I. Emerg Med June 15:125-138, 1986.

Leichliter JS, Meilman PW, Presley CA, Cashin JR: Alcohol use and related consequences among students with varying levels of involvement in college athletics. College Health 46:257-262, 1998. 27.

28.

Mantle M, Lieber J: Time in a bottle. Sports Illustrated April 18, 1994, pp 66-77.

Marzuk PM, Tardiff K, Leon AC, et al: Ambient temperature and mortality from unintentional cocaine overdose. JAMA 279:1795-1800, 1998. 29.

McNaughton L, Preece D: Alcohol and its effects on sprint and middle distance running. Br J Sports Med 20:56-59, 1986. 30.

31.

Mela DJ: Smokeless tobacco and taste sensitivity [letter]. N Engl J Med 316:1165-1166, 1987.

32.

Milhorn HT: The diagnosis of alcoholism. Am Fam Physician 37:175-813, 1988.

National Collegiate Athletic Association: 2000 Drug Testing Program. Available at http://www.ncaa.org/sports_sciences/drugtesting 33.

Nattiv A, Puffer JC, Green GA: Lifestyles and health risks of collegiate athletes: A multi-center study. Clin J Sports Med 7:262-272, 1997. 34.

1997 NCAA Study of Substance Use and Abuse Habits of College Student-Athletes. Presented to NCAA Committee on Competitive Safeguards and Medical Aspects of Sports, September 1997, Kansas City, Missouri. 35.

36.

Powell DR: Does marijuana smoke cause lung cancer? Prim Care Cancer 10:15, 1987.

Renaud AM, Cormier Y: Acute effects of marijuana smoking on maximal exercise performance. Med Sci Sports Exerc 18:685-689, 1986. 37.

38.

Schwartz RH: Identifying and helping patients who use marijuana. Postgrad Med 86:91-95, 1989.

Secretary of Health and Human Services: Ninth Special Report to the U.S. Congress on Alcohol and Health. NIH publication no. 97-4017. Washington, DC, Government Printing Office, 1997. 39.

Tashkin DP, Gong H, Fligiel SEG: How the lungs are affected by marijuana smoke. J Respir Dis 8:87-107, 1987. 40.

Urbano-Marquez A, Estruch R, Navarro-Lopez F, et al: The effects of alcoholism on skeletal and cardiac muscle. N Engl J Med 320:409-415, 1989. 41.

Walsh MM, Greene JC, Ellison JA, et al: A dental-based, athletic trainer-mediated spit tobacco cessation program for professional baseball players. Calif Dent Assoc J 26:365-372, 1998. 42.

43.

Warner EA: Cocaine abuse. Ann Intern Med 119:226-235, 1993.

Wechsler H, Davenport A, Dowdall G, et al: Health and behavioral consequences of binge drinking in college: A national survey of students at 140 campuses. JAMA 272:1672-1677, 1994. 44.

Wechsler H, Davenport AE, Dowdall GW, et al: Binge drinking, tobacco and illicit drug use and involvement in college athletics. J Am Coll Health 45:195-200, 1997. 45.

Welder AA, Melchert RB: Cardiotoxic effects of cocaine and anabolic-androgenic steroids on the athlete. J Pharmacol Toxicol Methods 29:61-68, 1993. 46.

Werner MJ, Walker LS, Greene JW: Screening for problem drinking among college freshmen. J Adolesc Health 15:303-310, 1994. 47.

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Chapter 12 - Sport Psychology and Injured Athletes William D. Parham PhD, ABPP

The injury experience that befalls some athletes and its subsequent rehabilitation process can trigger an interactively complex set of emotions that can make an unfortunate circumstance feel arduous and burdensome. At the same time, the injury-recovery process can also turn into an experience ripe with tremendous opportunity. Research efforts that address sport injury and the rehabilitation process are numerous. Yet, a clear picture of the nature, course, and resolution of the injury experience has not emerged. When current data on the psychology of athletic injury are distilled into commonly accepted assumptions, however, two sets of factors that best describe the salient features of the injury experience draw the most agreement. Understanding the injury experience involves knowing (1) the kind, type, and degree of impairment imposed by the injury and (2) the way in which the athlete views the recently sustained injury. The kind, type, and degree of actual impairment provide some indication of what will be required physiologically for maximal healing to take place. The physiologic prognosis for an anterior cruciate ligament injury with respect to time needed for healing, for example, is different from that for an ankle sprain. The cognitive appraisal of the injury event represents the second and most salient

factor. The meaning that an athlete assigns to the injury event determines the type of emotional response to the injury that the athlete will exhibit. The injury event also stimulates focus on the degree to which an athlete's identity is connected to his or her involvement in athletics. For some athletes, involvement in athletics represents an all-consuming endeavor from which they receive abundant emotional nourishment. It is often not until an athlete receives an injury that the degree of attachment to the sport becomes evident.* This attachment realization is one of the more surprising features of the injury experience and one that can feed its emotional intensity. An injury can be experienced suddenly and unexpectedly, or it can have a gradual onset. Both kinds of injury experiences often stimulate a floodgate of competing emotions that can be dramatic and overwhelming. Injury is not an experience athletes plan for, despite knowing that injury is a reality that could be an experience at some point in their career. Athletes also have a tendency to believe themselves to be invincible and that injury will not happen to them; rather, it will happen to the proverbial other. Circumstances that influence the way in which an athlete thinks about a current injury include (1) the emotional reliance on the sport versus other life domains, (2) the degree of perceived disruption in athletics (and perhaps in other areas of the athlete's life), (3) the way in which the athlete has coped with past injuries with similar disruptive outcomes, and (4) the ability of the athlete to access assistance resources. When the two-factor characteristics of the injury and rehabilitation experience are viewed within the context of an athlete's current personal and environmental realities, the exponential complexity of the injury and rehabilitation experience can be more fully appreciated. Specifics of the two-factor contextual model describing the injury and rehabilitation process are discussed later in this chapter. Finally, the injury-recovery process is also ripe with opportunities. From the onset of injury and through the completion of the rehabilitation process, the athletes will be afforded time to think critically about self in relation to the sport that heretofore has played such a pivotal role in their lives. Athletes are also afforded an opportunity for self-assessment and stocktaking of goals achieved versus goals unmet in other areas of their life, including academic, occupational, personal, familial, relational, and spiritual. This chapter offers for consideration a more detailed account of the injury and rehabilitation experience of athletes. The hope is to foster in the reader a conceptual appreciation of an athlete's responses to injury juxtaposed to the physiologic healing that is also taking place. A second goal is to introduce the reader to the role of sport psychologists vis-à-vis their participation as members of the athlete's injury management team. Expanded roles for sport psychologists in helping athletes manage the injury experience are also identified. Prevalence of Athletic Injury

Discussion of the athletic injury experience and concomitant rehabilitation process would be incomplete without an understanding of the frequency with which injury

occurs. Despite considerable improvement in the quality of athletic equipment and of sports and recreational facilities and in the way in which today's athletes are conditioned and trained, sports participation and injury prevalence data across age and across sports yield some noteworthy findings. Competitive or recreational sports pursuits by children outside of their school experiences number almost 20 million. An additional 6 million students participate in high-school sports. Annually, in excess of 3.5 million children aged 5 to 14 years present at hospital emergency departments, clinics, ambulatory surgery centers, and physicians' offices for injuries related to their participation in sports.[2] Participation of young children in football, basketball, baseball, soccer, hockey, gymnastics, and volleyball produces overuse injuries (small injuries to immature bodies) and acute injuries (caused by sudden trauma), including contusions, sprains, strains, and fractures.[2] *See references

[ 6A] [ 9A] [ 9B] [ 14] [ 31A] [ 32] [ 40] [ 47A] [ 47B] [ 50]

and [ 50B] .

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Approximately 354,000 student-athletes participate annually in National Collegiate Athletic Association (NCAA) sporting events. The NCAA Injury Surveillance System provides current data on injury trends in intercollegiate athletics across 16 sports. In the fall of 1999, for example, rates for practice-related (4.7 injuries per 1000 athlete-exposures) and game-related (44.9 injuries per 1000 athlete-exposures) sports injuries in football were significantly higher than the 14-year NCAA Injury Surveillance System football game (35.9 injuries per 1000 athlete-exposures) and practice (4.1 injuries per 1000 athlete-exposures) averages. The practice and game concussion rates continue the rise seen during the last 4 years. Men's practice (4.2 injuries per 1000 athlete-exposures) and game (20.8 injuries per athlete-exposure) rates for soccer held constant during the last 14 years, and women's soccer showed practice (5.1 injuries per 1000 athlete-exposures) injury rates slightly lower than the 14-year average of 5.8 injuries per 1000 athlete-exposures. Game (18.5 injuries per 1000 athlete-exposures) injury rates for women's soccer showed a slight increase from the average of 17.7 injuries per 1000 athlete-exposures. Women's volleyball and field hockey showed slightly lower practice (4.2 and 3.4 injuries per 1000 athlete-exposures, respectively) and game (4.3 and 5.9 injuries per 1000 athlete-exposures, respectively) injury rates compared with the 14-year averages of 4.5 (women's volleyball) and 4.1 (women's field hockey) injuries per 1000 athlete-exposures. In all of these cases, 30% to 40% of the injuries required restricted or missed participation for 7 days or longer. The most prevalent body parts injured across these referenced sports included knee, ankle, and upper leg.[43] Spring sports (e.g., softball, baseball, men's and women's lacrosse, and spring football) showed a similar practice and game injury rate pattern of slightly more or less than their respective 14-year averages. Sports that required restricted or missed participation for 7 days or more included softball (32%), baseball (43%), women's lacrosse (33%), men's lacrosse (30%), and spring football (48%). In addition to the knee, ankle, and upper leg injuries, spring sports recorded shoulder, head, and face injuries among the most

prevalent. [44] Data that profile sports-related injuries to persons 65 years of age and older yield several interesting observations.[61] In a 6-year span from 1990 to 1996, sports-related injuries to persons in this age category increased significantly (54%) from 34,000 to approximately 53,000. In the same 6-year period, the increase in the population aged 65 years and older was just above 8%. Thus, increased injury to this age group cannot be attributable solely to the increase in the number of people. Persons 75 years of age and older saw a 29% increase in sport-related injuries. The increases in the numbers of persons in both age categories (65 years and older, 75 years and older) are in contrast to the 18% increase in sport-related injuries to persons 25 to 64 years of age. Interestingly, the highest number of injuries to the age group 65 years and older was associated with bicycles. Equally interesting is the fact that injuries resulting from exercise activity increased 173% from 1990 to 1996. Finally, there is clear indication that some of the injuries to the population aged 65 years and older resulted from their participation in sports such as snowboarding and in-line skating. These injury data correspond to the increased number of persons in their 70s, 80s, and 90s maintaining physically active lifestyles, including increased participation in organized and recreational sports.

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The Injury Experience and the Rehabilitation Process

Efforts to document the injury experience as well as the process of psychological adjustment to the athletic injury have resulted in descriptions of the injury-recovery process that are impressionistic at best. Research has targeted injury prediction and injury response as foci for study.[80] Injury prediction research aims to identify variables that contribute to injury vulnerability. Included in this category are studies that took a look at injury proneness as it relates to personality, * psychosocial risk factors,[4] [27] [28] [36] [47] [67] [68] [79A] [83] and psychological states.[30] [38] [39] [60] [69] Injury response research attempts to identify an athlete's psychological reaction to athletic injury. Included in this category are studies that took a look at injury recovery and its relationship to a sequence of emotional stages through which injured athletes pass on the road to healing,[6] [19] [34A] [37] [57A] [69B] [72A] [75A] psychological states not necessarily tied to stage or phase sequencing, and compliance with the rehabilitation regimen. Results in both injury prediction and injury response research are predictably and reliably mixed. Within the injury prediction category, for example, some studies conclude that factors such as personality,[33A] [58] [74A] [81] psychosocial risk factors,§ and various psychological states [4A] [32A] correlate highly with injury occurrence. In this vein, perhaps the most promising work within the psychosocial risk factors category is the Andersen and Williams model,[4] which offers us a way of understanding the relationship between stress and athletic injury. The authors suggest a framework for predicting, and thus preventing, stress-related injuries, using cognitive, behavioral, physiologic, attentional, and interpersonal correlates as anchors to their model. Several other studies, however, using personality, [1] [6B] [8A] [27] [48A] [59] psychosocial risk factors,[50A] [79B] [81] and various psychological states,[29A] strongly suggest that injury occurrence has little to do with these factors or is questionable, at best. Likewise, research efforts that purport to address injury response [34A] [50C] [57A] [67A] [69B] [72A] suggest, for example, that the various stage models aid in understanding the process of psychological adjustment to injury.[37] [53] [77] [78] Several other studies suggest that stage models do a disservice because they do not accurately reflect universal psychological

adjustment experiences.[7] [37] [67] Caution needs to be exercised in asserting that either of these research domains merits favor over the other. Perusal of the collective works in the injury prediction and injury *See references [ 4A] [ 8B] [ 12A] [ 29B] [ 33A] [ 48A] [ 58] [ 59] [ 74A] and [ 82] . See references [ 1] [ 7] [ 8] [ 10] [ 11] [ 18] [ 24] [ 29] [ 34] [ 41] [ 47] [ 51] [ 53] [ 56] [ 63] [ 64] [ 66] [ 67] [ 67A] [ 71] See references [ 12] [ 13] [ 17] [ 20] [ 21] [ 22] [ 23] [ 24] [ 25] [ 26] [ 29] [ 37] [ 52] [ 70] [ 76] [ 78] and [ 79] . §See references [ 1A] [ 4] [ 6C] [ 6D] [ 11A] [ 27] [ 28] [ 35] [ 36A] [ 50A] [ 69A] [ 79A] and [ 81] .

[ 72] [ 72B]

and [ 75] .

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response categories reveals significant methodologic confounds along several dimensions, the sum of which leads to questions of generalizability. These confounds might also explain the tremendous variations in outcomes in the research. First, there is not a uniformly agreed on definition of injury. Injury is conceptualized partly as forced time away from athletic participation. The challenge presented in both domains with use of this criterion is that time away from athletic participation varies from 1 day to more than 7 days. Variations in the number of days off make comparisons regarding physical and emotional adaptation difficult. Research using injury severity as the topical focus (e.g., wherein injury is defined as catastrophic and traumatic [5] ) alternates between stage models to explain the journey of the injured athlete and cognitive appraisal models.[7] Although both models acknowledge physiologic as well as psychological adjustment correlates,[77] they offer different ways of conceptualizing the emotional aftermath that the athlete experiences.[29] This difference in conceptualization of the emotional aftermath comes irrespective of the way in which the injury or illness occurred (e.g., injury from competition, injury from physical illness, injury received outside of sport, or injury from a traumatic event). The net result, however, is a lack of agreement on how best to describe the injury-recovery process. A second confound has to do with the populations (e.g., college students, high-school students, young children, and senior citizens) chosen for study. The challenges in this area stimulate the question of how representative the smaller sample is of the respective larger groups of athletes purportedly represented. Related to the population confound is the concern about the limited number of sport teams that have been studied. Collegiate football players have been the most frequently studied athlete population,[80] but athletes representing other sports, such as gymnastics, swimming, alpine skiing, soccer, wrestling, baseball, volleyball, basketball, cross-country, and track and field, to name a few, have been studied as well. The research challenge from the standpoint of being able to generalize the results centers around addressing the degree to which athletic teams studied and those not studied share similar experiences. Careful review of the research in the injury prediction and injury response domains reveals concerns about the instruments used to test hypotheses, to measure injury-related and rehabilitation-related phenomena, and to evaluate outcomes.* Each of the instruments used to test, measure, and evaluate the various populations is

challenged psychometrically and is limited by its ability to assess usually only a single phenomenon. When multiple phenomenaare likely to be contributing to the resultant observations of a given investigation, the limitations of the chosen instruments become even more salient. Finally, individual sport-related variables, such as size, strength, level of conditioning, and demands of the sport at the time the injury occurred, have not been factored into studies of athletic injury and rehabilitation. Individual personal variables, such as age, ethnicity, race, sexual-affectional orientation, and disability status, have also been conspicuously absent as factors that contribute to research-based observations of injury and rehabilitation. The net result of the confounding elements associated with individual sport-related and individual personal variables points, again, to the compromised ability of sport psychology research to generalize to populations of athletes beyond the immediate teams under investigation. Despite these limitations in sport psychology research, cautious interpretation of the available empirically based data and of consistently cited anecdotal reports from sport psychology practitioners generates two factors that seem to best characterize the driving force behind the injury-rehabilitation process.

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Two-Factor Contextual Considerations of the Injury Experience and Precursors to the Rehabilitation Process

The kind, type, and degree of impairment constitute the first set of factors that most sport psychology researchers and practitioners agree come into play in understanding the injury-recovery process. Actual physiologic compromise or damage provides sort of a diagnostic barometer of the injury-recovery process that the athlete must now experience. An injury in which the degree of impairment is slight, and for which the prognosis is relatively quick return to active participation in practice and game situations, might be experienced by the athlete as inconvenient, at best. On the other hand, an injury of significant magnitude, such as an anterior cruciate ligament or back injury, which would require dismissal from active participation in the sport for 6 to 18 months, will generate a different, perhaps more intense emotional response. Personal factors (e.g., body build, level of conditioning, preexisting injuries) and structural factors (e.g., equipment failures, compromised playing fields or surfaces) influence injury predisposition. Intrapersonal factors (e.g., self-confidence, sense of control, confidence in the treatment team and treatment approach, commitment to comply with the treatment regimen) and resource access factors (access to nutritionist or nutrition information, availability of rehabilitation equipment, access to professionals trained to assist with a rehabilitation) coupled with an innately healing body contribute to injury rehabilitation. The actual degree of compromise sustained by the body and the kind of intervention and course of treatment needed to rehabilitate the injury are best determined by the orthopaedic surgeon or other physician. Trainers and physical therapists can assist in the administration of rehabilitation activities. The cognitive appraisal of an injury situation is the second factor that most sport psychology researchers and practitioners agree contributes to the driving force behind the injury-rehabilitation process.[3] [10] [17A] An injury event in and of itself is just an injury event. The way in which an athlete views the injury event determines the emotional valence of the situation as well as the degree of urgency with which the challenges imposed by the injury will be

*For a detailed account of research issues in sport psychology, the reader is referred to Petrie and Falkstein,[ 54] Duda, [ 16] Ostrow,[ 48] and Singer, Murphey, and Tennant.[ 65]

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met. In essence, the cognitive appraisal of the injury event sets in motion all subsequent affective, behavioral, and cognitive responses. Furthermore, it is the key to understanding the complexity of the injury experience. For example, the cognitive appraisal of an injury event may result in an athlete's believing that the event will have a traumatic, devastating, long-term, and adverse impact on his or her athletic career. If there had been no history of injury, and thus never a need to access rehabilitative services, what lies ahead with respect to the current rehabilitation challenges would be uncertain. In this instance, an injured athlete might also feel overwhelmed, helpless, even despairing. Subsequent feelings and behaviors might be seen in an athlete's strict compliance with the established rehabilitation regimen. Compliance, in this case, might spring from the intent to ensure the quickest possible recovery to preinjury condition and form. The factors that influence the way an athlete views an injury event include (1) the degree to which the athlete relies on athletics as a source of emotional nourishment; (2) the degree of concurrent reliance on other life domains (e.g., academic, personal, familial, spiritual) for emotional nourishment; (3) the degree of perceived interference or disruption in the athlete's current and future sport and other life domain-related activities; (4) the way in which the athlete has coped affectively, behaviorally, and cognitively with past injuries of similar emotional magnitude; and (5) the ability to access available resources in the management of the current injury challenges. Emotional Nourishment

With respect to the degree of emotional nourishment, some athletes receive applause and accolades abundantly beginning from a young age when they are mastering basic athletic skills. Successful mastery coupled with fine execution of the sport-related skills results in praise and recognition from the family, peers, community, school, and media, which after a while begins to feel satisfying. Acknowledgment of fans and support from around the world via Internet communications add to the impact. Thus, as success in the sport increases, and as attention and recognition for athletic success also increase, the felt connection to the sport into which a lot of time and energy have been devoted strengthens and an athlete's identity with the sport becomes solidified. Not only does the athlete begin to identify emotionally with the sport, but family, peers, the immediate community, and the greater local, state, national, and international communities all find themselves attracted to a person over whose image they both marvel and fantasize. In time, athletes become accustomed to this rich source of emotional nourishment, and the slightest hint suggesting that this emotional nourishment will cease triggers anxiety, depression, and a host of other emotional responses. Athletic injury, therefore, represents a situation that can feel threatening to many athletes. For athletes whose

emotional investment in the sport is considerable, injury often results in the perception that the emotional nourishment on which they have come to rely will now be withdrawn because of their decreased ability to perform and, thus, earn it. Reliance on Other Sources of Emotional Nourishment

Reliance almost exclusively on athletics as a source of emotional nourishment carries a cost, namely, that other potential sources of praise, recognition, and favor for achieved success are overlooked and ignored. Family, friends, academic environments, work settings, and spiritual life activities represent other sources from which emotional nourishment and self-esteem energies are derived. Rarely, however, does the significance of these other sources of emotional support become evident until an athlete has an injury experience. Disruption and Interference

Success in athletics, particularly for athletes for whom athletics has become a sole source of life satisfaction, breeds dreams and ambitions. These dreams and ambitions are fed by the lure of huge salaries and other perks that today's professional sports careers seem to promise.[33] The path on which these athletes choose to travel to achieve their athletic desires becomes clear and straightforward, that is, until injury occurs and the disruption in an athlete's athletic life proves to be significant. Injury can introduce considerable interference in the life of an athlete, particularly one whose focus is almost exclusively on achieving fortune and fame according to a prescribed timetable. A dream deferred can be disheartening. Disruption is a relative experience, however, in that the degree of disruption is determined by the way the athlete thinks about the impact of the injury. An injury that is actually minor can seem to be just as devastating as one that is more significant. On the other hand, a major injury can seem not as disruptive when it is viewed from a perspective of considering injury, for example, an opportunity for stocktaking. In that same vein, an athlete who has experienced success in a sport yet finds extreme difficulty responding assertively to parents, family, and coaches regarding continued participation beyond the current season would conceivably experience the injury event as a sort of relief. In this instance, temptation to thwart ongoing compliance with the rehabilitation process might be high, as might an athlete's anxiety, as return to practice and competition becomes more of a reality. Thus, teasing out the disruptive feature of the injury experience is important in understanding its emotional magnitude. Assessing the degree of disruption that an injury has imposed on an athlete's life often provides the starting point for determining what needs to be worked out to achieve some measure of resolve about the injury. Past Coping

Athletes, like all people, are creatures of habit and pattern. Thus, how an athlete responded cognitively, affectively, and behaviorally to past injuries provides a clue to how the athlete will respond to a current injury situation

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of at least similar emotional magnitude. Let us assume, for example, that past injuries resulted in an athlete's approaching the injury-rehabilitation challenge with a belief that injury is simply an unfortunate experience. Let us assume further that the athlete believed that a return to preinjury shape and conditioning is possible as long as there is compliance with prescribed treatment. Given these conditions, it seems reasonable to predict that the current injury and rehabilitation challenges will be approached in a similar mindset. Alternatively, let us assume that a cognitive, affective, and behavioral approach to past injuries resulted in the athlete's feeling overwhelmed emotionally, including feeling angry and combative. Let it also be suggested that the athlete complied sporadically with rehabilitation. In this scenario, it seems reasonable to expect that the current injury-rehabilitation challenge will be approached similarly. Accessing Services

Injury creates an opportunity to access medical and other help resources. The kind, type, and degree of impairment initially influence where the athlete will turn for help. Factors such as perceived talents of the service providers and confidence in the proposed treatment plan contribute to athletes' choosing a person or persons with whom they will work. Readiness to commit to the rehabilitation regimen and belief that the rehabilitation process will result in the desired outcome contribute to an athlete's willingness to surrender to the rehabilitation process. Physicians are consulted most often about general medical conditions, and other allied health persons (e.g., nutritionists, trainers, and psychologists) enter the picture at various junctures of the rehabilitation process. The quality of various help resources varies considerably, as does access to the resources most desired and preferred. For example, financial status may contribute to an athlete's feeling stymied by the ability to access resources of a desired caliber. A young male Latino high-school gymnast from an economically challenged background whose gymnastics talents and abilities could result in a full scholarship to college might experience considerable emotional distress with a recently received anterior cruciate ligament injury. The athlete's distress might be especially overwhelming when he acknowledges that the expert medical intervention and subsequent rehabilitation service that are available will be rendered from the county hospital where the family traditionally receives medical attention.

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The Injury Experience: A Closer Look

The injury experience is additionally characterized by an immediate attentional shift in time perspective. The often pivotal nature of the injury event forces an athlete to address concerns about time played versus time not played and to reconcile any differences, especially when these differences draw consideration of having to defer sport-related dreams and ambitions. An injury can be a sudden and unexpected minor setback (e.g., strains, sprains) or a traumatic and catastrophic event (e.g., spinal cord injury). It can also be gradual in its onset (e.g., when the athlete has lived with injury pain and discomfort until the discomfort can no longer be tolerated). Irrespective of the way in which injury becomes manifest, the importance of the injury event usually triggers an immediate need to reassess time investments. Injury is not an experience that athletes plan for; thus, most are not prepared for the considerable self-involvement as well as the involvement of others that seems part and parcel of the injury experience. In addition, most athletes are not prepared to handle the unnatural feel of an injury. Walking with the assistance of crutches or with the support of a knee brace is not a natural experience or an innate movement. Holding an arm in a sling is not natural. Yet, ready or not, injury stimulates a quick need for resolute action regarding participation in future sport activity. When the type, kind, and degree of injury impairment and the athlete's cognitive appraisal of an injury experience are viewed within the context of personal (e.g., age, race, ethnicity, sexual orientation, disability status, life circumstances, personal baggage) and environmental (e.g., community, fans, media, physical equipment, unsafe playing surfaces) realities, the focus on intrapersonal distress and other external consequential realities of an athlete's injury and recovery becomes more acute. The contextual parameters also highlight more clearly the gaps in empirically and anecdotally based sport psychology information about the injury-recovery process. For example, the data are not clear on how the cognitive appraisal of an injury event varies by age, race, ethnicity, gender, sexual orientation, and disability challenge. The data are also not clear on how these contextual parameters influence the degree to

which an athlete relies almost exclusively on sport or other sources for emotional nourishment. How do the contextual parameters affect how an athlete coped with past injuries? How do the contextual parameters influence the differential expression of feelings and emotions from injury onset through injury recovery? What impact do the contextual parameters have on the ability of an athlete to access resources in the management of the current injury's challenges? What about the collegiate female cross-country Olympics aspirant who was recently declared athletically ineligible because of the severely compromised condition of her body owing to a never before treated eating disorder? Empirically and anecdotally based sport psychology data suggest that the emotional response to feeling so powerless and to feeling that an eating disorder treatment program would be an arduous undertaking could reach dramatic proportions; but could the declaration of athletic ineligibility also be a blessing in disguise? A female athlete expecting to receive positive results from a well-trained and seasoned sport psychologist who is treating her performance anxiety (after successful rehabilitation of a foot injury) with a straightforward, commonly implemented set of relaxation and visualization exercises is disappointed. After several weeks, the therapist concedes that the interventions did not work, and cessation of sessions or referral to another psychologist is suggested. The new therapist conducts a thorough investigation and

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discovers a past riddled by childhood molestation. What becomes clear is that nothing was wrong with the female athlete's ability to implement the performance enhancement program in the presence of her male therapist. Her rigidity and tension proved to be a self-protective response to the memory of an emotionally painful time in her life. What mental or psychological cost was incurred when the first therapist chose not to do a thorough initial evaluation? Worse yet, what if the treating therapist did not even know to inquire about childhood abuse? Why did the belief in her status as a gifted athlete take precedence over her emotional well-being and psychological safety? What about the 68-year-old widower of 12 months, whose only passion now is golf, who learns that he will need hip surgery, a process that will keep him out of golf for several months, even a year? With what additional challenges, concerns, and issues might he be struggling? A female softball athlete just returning to practice after having completed a several-month rehabilitation program for her surgically repaired shoulder pushes herself mentally and emotionally to regain her position on the team. Although it is not an unheard of strategy, her hour-long before-and-after practice work habits did seem a bit unusual, especially given that she was just released by the team physician only 3 days ago to return to practice. When confronted by the psychologist she began seeing during rehabilitation, the athlete finally confesses her discomfort with homosexuality. She

further shares that several lesbian teammates had in the past approached her sexually. What comes to light is that the athlete had been dealing with her discomfort with her teammates' advances. To avoid future encounters, the athlete showed up to practice early, ahead of the team, and remained 1 hour after practice hoping that all of her teammates would have showered and left the premises. Thus, what appeared to be dedication to returning to top form and to reclaiming her position on the team was, in reality, the athlete's method of coping with a difficult and sensitive situation. The foregoing scenarios suggest that actual injury and physiologic compromise to the body as well as the subsequent rehabilitation can be the least of the athlete's challenges. Quality surgical intervention, active use of expert rehabilitation services, and an innately healing body position the athlete for maximal physiologic healing. The more critical feature of the injury experience, namely, the interactively complex set of emotions that are stimulated by the injury, is where the injury recovery work comes into play. The emotional aftermath of an injury can trigger a host of intrapersonal (e.g., confidence, self-esteem) and interpersonal (relationships with parents, peers, intimate others) issues and concerns. Because of the restrictive and in some cases immobilizing features of some injuries, athletes report feeling forced to come to terms with, versus run away from, important aspects of their life. Without an adequate support system, forced confrontation of personal baggage can feel jarring, especially when solutions to the challenges that have arisen do not appear to be immediately obvious. The emotional aftermath of an athletic injury is also characterized in part by an attentional shift in time perspective from time played to time not played. Furthermore, the injury experience can feel significant and urgent. Questions that begin to surface include Why me? Will I ever be as good as I once was? What are my coaches and teammates saying about me? Emotions, including anger, depression, anxiety, grief, loss, and sorrow, flood the athlete's senses. Issues, concerns, and challenges in other areas of an athlete's life, such as academic, social, familial, occupational, and spiritual, are also stimulated by the injury experience. These scenarios represent just a sample of the cases that might present to a team of athletic injury rehabilitation professionals, including the orthopaedic surgeon, trainers, physical therapist, and sport psychologist. The scenarios are by no means inclusive. Rather, they are offered as examples of injury situations in which the surface presentation might appear different from the truer picture that emerges after further examination and learning directly from the athlete how the injury has affected his or her life.

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Sport Psychology

Simply stated, sport psychology is the science of human behavior applied to athletics. A sport psychologist possesses the education, background, and training in psychology and in the sport sciences and applies professional skills and competencies to the areas of teaching, research, and clinical practice. This final section addresses the role and function of the sport psychologist in athletic injury and the benefits of working with a sport psychology practitioner. A sport psychology practitioner moves flexibly in and out of at least three roles with the injured athleteas the clinician, educator, and facilitatorand has a consulting role with the sports medicine team. Each of the roles is outlined. Sport Psychologist as Clinician

A sport psychologist as clinician plays a pivotal role in assisting the injured athlete to navigate the emotional twists and turns of the injury and rehabilitation process. Because the myriad concerns and issues that surface with injury can be complex, referral to a well-trained psychologist is of utmost importance. Ways of identifying a sport psychologist who possesses the skills, knowledge, and abilities to work with injured athletes, their trainers, and the orthopaedic physicians are presented in the closing sections of this chapter. On referral to a sport psychologist, the referring parties as well as the injured athlete accepting the referral can expect the following responses from the sport psychologist-clinician who is now part of the athletic injury-rehabilitation treatment team. The injured athlete can expect to participate in an extensive assessment process. It is a process that invites the athlete to talk about at least three substantive areas. The first area involves obtaining a better understanding of the injury event and the athlete's experience of that event. A detailed description of the experience including the concerns, issues, and realities that frame the injury experience for that particular athlete will be solicited. Equally important to solicit is the degree to which the injury has interrupted or detracted from the athlete's goals, dreams, and aspirations. Thus, this first

core set of questions

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will result in both the practitioner's and the injured athlete's being able to construct a big-picture perspective of the injury and of its role in the athlete's current and future activities. The second set of core questions targets the clinical or psychological profile of the athletes with whom the psychologists are working. A standard clinical interview, which allows a comprehensive and systematic evaluation of the athlete's current mental health, is conducted during this juncture. Framed within a context of a biopsychosocial model, questions are designed to determine clinical disorders, personality disorders, general medical conditions, psychosocial and environmental problems, and level of functioning (DSM-IV, 1994).[2A] The third set of core questions is designed to gather data that help the psychologist construct as clear a picture as possible of the athlete as a person. The picture that will emerge will be one born out of a context of race, ethnicity, gender, sexual orientation, disability status, and religious affiliation. To claim to understand the athlete without appreciating the contextual parameters that shape the athlete's reality is to fall short in your knowledge about and respect for the individual with whom you purport to be working. The gathered information generates a snapshot of the challenges the athlete in now confronting. On the basis of the resultant diagnostic impressions and in collaboration with the athlete, the sport psychologist-clinician suggests interventions that are aimed at addressing the surfaced problems. Mechanisms for evaluating the effectiveness of the interventions are also set in place.* Sport Psychologist as Educator

Acquiring accurate information about the injury and the rehabilitation process (e.g., factors that predisposed injury to occur, specific features of the current injury, goals for injury treatment, detailed information about the medical and rehabilitation procedures that will be used, and prognosis for complete recovery) is an important and paramount concern for the athlete. Factual information about the injury and rehabilitation process contributes to decreased worry and anxiety, decreased cognitive distortions about injury severity and treatment course, expectations that are increasingly aligned with realistic outcomes, and increased compliance with suggested treatment interventions. The sport psychologist can be instrumental in gathering information about the injury and the rehabilitation process and in disseminating information in such a way that the athlete not only hears the information but makes plans to use it. The sport psychologist, with an athlete's permission, can also serve to educate the injury-rehabilitation team of physicians, trainers, and nutritionists about the treatment and treatment responses of

the athlete to the services the sport psychologist is rendering. Finally, the sport psychologist as educator can conduct in-service training for other professionals working with athletes who desire to learn more psychology and its application to athletics. Sport Psychologist as Facilitator

The injury and rehabilitation process generates multiple needs for the injured athlete. The injured athlete may need to access multiple resources to meet the surfaced needs. It may be determined, for example, that an injured athlete struggles with alcohol and substance problems; thus, the athlete would benefit from involvement with groups like Alcoholics Anonymous or other outpatient substance use and abuse services. An athlete's history of sexual assault may result in the need for a referral to a therapist or agency that offers specialized services for these concerns. Specialized services in the form of therapy or support groups are also suggested for the athlete struggling with disordered eating. Family or marital concerns may contribute to the ongoing stress that an injured athlete experiences. In these instances, referral to a therapist with expertise in family therapy or couples counseling might prove to be a useful adjunct to the services already prescribed for the physical rehabilitation. Access to vocational counseling services, referral to services for senior citizens, consultation regarding legal concerns, or guidance regarding spiritual matters may also be needed adjunctively. A sport psychologist working collaboratively with a sports medicine team of professionals could prove to be instrumental in helping the injured athlete to alleviate some of the stresses that may very well help to exacerbate the injury. Use of these additional services may contribute positively to the injured athlete's physical and psychological healing. Sport Psychologist as Consultant

Sport psychologists play a pivotal role serving as consultants to the team of sports medicine professionals, including orthopaedic surgeons, family practice physicians, athletic trainers, physical therapists, nutritionists, and strength and conditioning coaches. Practitioners in each of these disciplines are expert in their respective areas, yet they may not have mastered core learning material in the disciplines of their collaborative colleagues. Of the group of sports medicine professionals, athletic trainers[42] and family practice physicians[58] may have received an introduction to basic principles of psychology during their formal academic training. Most of the other disciplines have little or no formal education in psychology fundamentals. Given the person-focused nature of each professional domain, it seems reasonable to expect that each would have had at least a formal introduction to the field of psychology. Enter the sport psychologist, a professional who not only can provide mental health services to the injured athlete but who can also communicate an opinion about the psychological well-being of an injured athlete to the team of sport medicine professionals. Input from the sport psychologist regarding an athlete's psychological well-being could help the injury-rehabilitation team in their overall formulation, coordination, and implementation of an agreed-on intervention plan. A sport psychologist is also in a position to provide education by in-service training of

the sports medicine staff in a variety of mental health topics. Athletes, like all *Readers are referred to references [ 14] [ 22B] [ 31] psychological interventions for athletic injury.

[ 37A] [ 46] [ 58A] [ 59] [ 62] [ 75A]

and [ 77] for details of specific

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people, struggle with the array of mental health challenges, so acquiring substantive information about mental health and mental illness sensitizes the sports medicine staff to be on the lookout for athletes who might feel challenged psychologically but whose struggle with their challenges might otherwise go undetected. Caveat Emptor: Let the Buyer Beware

Sport psychologists play an important role as members of athletic injury and rehabilitation teams. Their expertise coupled with the expertise of the sports medicine team creates an opportunity for the injured athlete to heal physiologically as well as psychologically. There is some debate, however, about who is a sport psychologist. A complete analysis of the debate is beyond the scope of this chapter; suffice it to say that the debate has been ongoing almost since the early beginnings of sport psychology as a formal area of study, research, and practice.[14A] [22A] [39A] [45A] [46A] [46B] [64A] Essentially, the debate is fueled by the presence of two groups calling themselves sport psychologists. Differences in historical roots as well as in the education, training, and respective career pursuits account for the separate emphasis that defines each group. The first group of professionals using the term sport psychologist comes out of the academic disciplines of sport sciences, kinesiology, physical education, and human movement. The target focus of study of these groups centers on (1) achieving a better understanding of the mechanics of human movement and (2) identifying the factors that contribute to athletes' participation in sports and exercise and the benefits that result from their participation in these activities. Research and teaching are the primary means used to carry out their career roles. The second group of sport psychology professionals are persons trained as psychologists who choose to apply their training and expertise to athletes across sports and athletic settings. The target focus of study of this group centers on achieving through scientific inquiry a better understanding of human behavior across settings and within the context of environmental realities. Applied work is the hallmark of this group of sport psychologists, although research and teaching characterize some of their professional activities. Historically, each of these groups came to the sport psychology arena with incomplete training and lacking in the skill sets needed to offer effective consultations to athletes seeking their services. The professionals emanating from the academic traditions of physical education, kinesiology, human movement, and sport sciences contributed their

knowledge and expertise in basic physiologic principles, biomechanics of exercise, motor movement, anatomy, muscle strength and endurance, nutrition, aerobic capacities, and the like to their sport psychology practice. This group was deficient in education and background in psychology, as characterized by a knowledge base rooted in courses having to do with theories of personality; social, biological, and cognitive bases of behavior; psychopathol ogy; and basic counseling skills. On the other hand, psychologists who claimed the title sport psychologist were usually well trained in the discipline of psychology but were deficient in the areas traditionally seen in the sport sciences. Several factors undoubtedly contributed to each group proclaiming itself to be the real sport psychologists. The economics of athletics, however, seems to have played a key role in the development of the territoriality positions of the opposing groups. [40] Over the years, large sums of money have been poured into sports and athletics, so much so that sports has become a multibillion dollar entertainment business. Media, especially television, and endorsement-sponsorship arrangements contributed significantly to the marketing of sports as an industry. Highly skilled and talented athletes were and are paid handsomely in return for their production on the field. Successful athletes and teams bred more success, which often translated into a language of economic prosperity. Sport psychologists were introduced as a means of helping athletes to maximize their performance abilities, thereby protecting owners' and sponsors' investments in their sports commodities. Both groups claiming to be sport psychologists wanted a piece of the lucrative sports enterprise and thus marketed themselves as the consultants who could best take care of the owners' and sponsors' investments. Where does this leave sports medicine professionals with respect to their need to know with whom they can consult regarding the management of an injured athlete? This debate has spawned several professional organizations to grapple meaningfully with the myriad issues associated with the provision of sport psychology services. While the debate about who is a sport psychologist is ever present, attention is being directed to identifying standards that address (1) competency to render psychological interven tions, (2) basic knowledge of human behavior, (3) basic knowledge of sports and athletics, (4) applied training, and (5) ethics. The Association for the Advancement of Applied Sport Psychology has confronted in earnest the task of developing recognized and accepted proficiency standards of the practice for sport psychology. The impact of their work on the respective professions and, more important, on the public and athletes on whose behalf sport psychology professionals are purporting to work remains to be seen. Given the emotional complexities inherent in an athlete's experience of injury and rehabilitation, and given the varied contexts within which the athlete functions and operates, a professional trained with some combination of the described course work, including direct applied experience, seems essential. In the absence of an agreed on set of standards, the following recommendations for working with a sport psychologist are offered. Sports medicine professionals wishing to access services of a sport psychologist might want to inquire about a prospective consultant's credentials to practice psychology. Because psychology is a recognized area of service, and the term psychologist is a protected title, having a license to engage in the independent practice of psychology might be one benchmark by which to assess minimal competence. A

license to practice psychology is granted only to candidates who satisfy national and state requirements, as measured by written and oral examinations.

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It is also important for professionals wishing to consult with sport psychologists to assess the amount and kind of direct, hands on experience a prospective sport psychologist has had working with the specific athletic group for which consultation is desired. Soliciting from the prospective sport psychology consultant information about direct experience with athletes is one means of gathering the data. Securing recommendations in support of the prospective sport psychologist from persons (coaches, colleagues, other athletes) who can attest to his or her work is another way of gathering data about a sport psychologist's experience. Once a consultation agreement between the sport psychologist and the party with whom the sport psychologist is consulting has been entered into, it is important for the party who brought the sport psychologist on board to request or make provisions for a periodic assessment of the work being performed. Periodic stocktaking of promised and rendered services always makes for a good practice. These rules of thumb are offered in the absence of an accepted and acknowledged criterion-referenced document that would otherwise detail competency-based standards for the provision of sport psychology services.

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Conclusion

There are a lot of emotional twists and turns in an athlete's experience of the injury and rehabilitation process. To reiterate a point made earlier, there are methodologic flaws inherent in the empirically based sport psychology research on the athletic injury-rehabilitation process that has been conducted to date. Coupled with the anecdotal descriptions of the athletic injury-rehabilitation process authored by sport psychology practitioners, what emerges is an incomplete picture of the injury-rehabilitation process from the perspective of the athlete. Researchers and practitioners alike continue to chip away, however, at the complexity of the injury-rehabilitation situation in the hope of developing the most accurate picture of the process as it is experienced by athletes. The less than accurate picture of the athletic injury and rehabilitation process that has emerged from existing literature is a byproduct of the way in which the research questions have been framed. Interestingly, the absence of clarity about the athletic injury and rehabilitation process, as demonstrated by available research and anecdotal accounts, actually directs attention to the kinds of questions that could serve as a jump-off point for future scientific inquiry. The following alternative question is offered for consideration by researchers and practitioners with the intent of stimulating a different research direction: How will this particular injury, to this particular athlete, at this particular time in the athlete's life, affect how the individual sees himself or herself now and in the future in relationship to the sport and in relationship to interests and areas other than those related to the sport? This question sets a research direction in that it has the potential to yield responses that are uniquely reflective of the injury-rehabilitation process. As a result, researchers can define terms, organize concepts, and articulate research strategies that seem aligned more closely to an injured athlete's actual experience. The alternative question also sets a clinical direction in that its more exacting focus has the potential to yield responses that are more reflective of the individual's perception of the injury and rehabilitation

experience. One goal of this chapter is to provide a synopsis of the current literature on the athletic injury-rehabilitation process in the hope that the presentation might stimulate discussion of the various concerns, issues, and realities that frame that experience. In presenting the overview and in distilling the current research findings into the least common denominators, what emerges is a two-factor conceptual premise that essentially highlights two themes. The two premises suggest the importance of knowing (1) the type, kind, and degree of actual physiologic impairment and (2) the meaning that the injury has to the athlete who is injured. These premises are offered as a way of highlighting what is agreed on by sport psychology researchers and practitioners. The scenarios are shared to illustrate how what appears on the initial presentation of an injured athlete to be the main focus actually turns out to be a different agenda once further details are gleaned. One Final Note

Athletes, irrespective of age, gender, race, ethnicity, sexual orientation, and disability status, are first and foremost everyday people who, like their nonathlete peers, grapple with life's everyday challenges. On the playing field and in the athletic arenas, they find opportunities to learn what challenge really means and how they can harness their talents and abilities to face the challenges they encounter. In a similar vein, nonathletes use their work or school settings as their challenge arenas. Whereas all athletes enjoy winning, few athletes engage in competition solely for the sake of achieving victory. The real victory comes from athletes' knowing they pushed themselves to the limits of their abilities and skills and thereby overcame the challenges inherent in the victory just achieved. Injury, then, can represent a time of grief, despair, and sometimes helplessness as it removes the athlete from the challenge arena and from continued opportunities to test personal limits. It is an event that is never planned; thus, it catches athletes off guard, and it always comes at the wrong time. Injury can be a minor inconvenience, or it can represent an event that is humbling. Either way, its disruption is unmistakable. Returning athletes to preinjury condition and form is of paramount importance because it signals to them a return to the means that has allowed them to feel important, successful, and accomplished. Therefore, it is incumbent on sports medicine teams employed to assist athletes in the recovery process never to approach an athlete thinking that their intervention efforts are simply routine or that the athlete is just another body. Athletes comply with prescriptive treatment regimens (1) when they have confidence that the intervention efforts will return them to full form, (2) when they have trust in the service provider's competence, and (3) when they believe the service provider has faith and confidence in them.

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Accepting the challenge is a theme that influences the push of an athlete to grow and mature. There are many opportunities on the playing field and in sports arenas for able-bodied, noninjured athletes to put themselves to the test. The physician's office, training room, and rehabilitation facility, however, can serve as alternative venues wherein an injured athlete can continue to accept the challenge, albeit of a different kind. Opportunities to discover inner strength and wisdom are abundant, irrespective of the type of challenge, when athletes begin to see their injury event and subsequent rehabilitation experience as an opportunity to invest in themselves as persons with boundless potential.

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74A. Valliant

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75A. Weiss

MR, Troxel RK: Psychology of the injured athlete. Athletic Training 21:104-154, 1986.

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79A. Williams

JM, Andersen MB: Psychosocial antecedents of sports injury: Review and critique of the stress and injury model. J Appl Sport Psychol 10:5-25, 1998. 79B. Williams

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Chapter 13 - The Female Athlete Letha Y. Griffin MD, PhD

Involvement in sports and physical activity contributes to the physical movement capabilities of girls, the health status of their bodies, the values and ethical behavior they develop, and their personal unique identity. Dr. Linda K. Bunker, Curry School of Education, University of Virginia, Charlottesville, 1998 Involvement of women in athletics is now common in junior high, high school, collegiate, and professional sports. The number of girls participating in athletics in high school has increased from 300,000 three decades ago (before the landmark Title IX legislation that prohibited sex discrimination in intramural sports) to 2.7 million today,[116] and women now represent 33% of all collegiate athletes and 37% of U.S. Olympic athletes. [128] An estimated 55 million women participate in recreational sports and fitness activities. Women represent more than 55% of all volleyball players, 43% of all runners, and 41% of all soccer players.[96] Female athletes representing the United States won gold medals in the 1996 Olympics in multiple sports, including soccer, softball, swimming, track and field, gymnastics, basketball, and others. As additional documentation of improvement in women's sports performance in the last

several decades, in 1972, the women's best time in the Boston Marathon was 3:10.26, whereas in 1999, Fatuma Roba won with a time of 2:23.25. One must remember that the first woman did not compete in an organized marathon until 1967, when Kathrine Switzer entered the Boston Marathon as K. Switzer so as not to reveal her gender and be denied entrance.[106] In the 10K Peachtree Road Race, the winning woman's time has improved from 49:13 minutes (in 1970) to 31:34 minutes (in 1994). Swimming times for women have improved from 25.96 in the 50 meter in 1980 to 24.73 in 2000 and from 17:19.20 in the 1500 meter in 1971 to 15:52.10 in 1988. Despite these significant gains in sports performance by women, the President's Council on Physical Fitness and Sports has stressed a need to provide more quality school-based physical education for girls. Only Illinois requires physical education from kindergarten to 12th grade and encourages girls to get involved in sports and physical activity at early ages. The benefits of physical activity for women are many and include improved mental health and well-being,[16] enhanced self-image and body image,[127] improved social skills and increased confidence,[80] decreased school dropout rates,[162] and a decrease in cholesterol levels, heart disease, and incidence of breast, endometrial, and gallbladder cancers. [18] [84] [156] Until the past several decades, research in sports medicine rarely focused on women. Most impact and performance studies had male subjects, and injury data reports infrequently took gender into account. In 1990, the National Institutes of Health established the Office of Research on Women's Health to develop a comprehensive agenda for research on women's health and to encourage the consideration of gender issues and gender differences in health and disease research. Consumer research and marketing by sporting goods manufacturers have also escalated during the past 20 to 25 years. Shoe manufacturers now make many styles of women's soccer, running, and basketball shoes, as well as other sports equipment. The sports bra industry is very lucrative. Not only do women buy sporting goods for themselves, but now that they are more knowledgeable about sports and sports equipment, they also buy for their children and spouse. For example, female golfers comprise only 20% of all golfers but buy 50% of all golf products, with the exception of golf clubs.[96] Media support of women's sports is increasing but is still far behind that of men's sports. Generally, only 5% of the sports section in most newspapers is dedicated to women's sports,[96] but there has been increased emphasis in most major women's magazines on health, fitness, and exercise techniques. Anatomic and Physiologic Differences between the Sexes That May Affect Performance

Although there are wide variations, the average adult female is shorter and weighs less than her male counterpart. She has shorter limbs and smaller articular surfaces, resulting in less power for striking, kicking, and throwing. [5] [149] Women have narrower shoulders and smaller thoraces than men but wider pelves.[64] [86] The length of their legs per total height is less than men's, resulting in women having a lower center of gravity and, hence, better balance.[5] [64] For example, most men would have a difficult time balancing on a 4½-inch beam, yet women gymnasts do this with ease.

Females have less muscle mass per total body weight than equally trained and conditioned males.[86] [154] Because of this, males can run faster, jump higher, and lift greater weight than equally trained and conditioned females. Female athletes, because they have a greater percent of body fat per body weight, are more buoyant and better insulated than their male counterparts.[86] [154] [158] [159] Therefore, they have an advantage in water sports, particularly those done in cold water. It is not surprising that many English Channel swim records have been set by women. [109] Moreover, women have most of their subcutaneous fat in their hips and lower body, whereas men carry their subcutaneous fat in their abdomen and upper body.[154] This distribution of body fat also contributes to the lower center of gravity in females.

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Greater breast development in the female requires modification of sporting gear, such as wide-strap, maximally supportive bras of soft, sweat-absorbent material. [59] [68] Although at one time there was concern that contact sports and jumping would harm the uterus and the ovaries, such fears have proven to be unfounded. The uterus and the ovaries are well suspended and protected in the pelvis, as are other pelvic organs. Uterine prolapse will not occur unless the abdominal floor is weakened by pathologic processes.[102] Because of their smaller body size, women have a smaller heart size and heart volume, resulting in a smaller stroke volume. This means that they have an increased heart rate for a given submaximal cardiac output (cardiac output = stroke volume × heart rate). [86] [102] [154] Because a woman's stroke volume is less, even with an increased heart rate, her cardiac output is approximately 30% lower than an equally trained man's.[154] Her systolic blood pressure is also lower than a man's.[86] Because men have approximately 6% more red blood cells and 10% to 15% more hemoglobin per 100 mL of blood than women, the blood of men has a greater oxygen-carrying capacity.[6] [46] Adult men, because of their chest size, have a greater vital capacity than women.[5] Vital capacity is the maximal volume of air that can be moved through the lungs from a maximal inspiration to a maximal expiration. A man's residual volume, the volume of air that remains in the lungs after maximal expiration, is also greater. Because vital capacity and residual volume are less in women, total lung capacity is also smaller. In fact, an adult woman's breathing capacity is approximately 10% less than her age-matched male partner's. [154] Furthermore, at the same submaximal minute volume (tidal volume × respiratory rate), women have a smaller tidal volume but a faster respiratory rate than men. [154] Oxygen pulse (i.e., the quantity of oxygen used by the body per heartbeat), which is a measure of the efficiency of the cardiovascular and respiratory systems, is approximately three times higher in adult males.[5] All these differences in physiologic parameters combine to give men a greater maximum oxygen uptake (VO2max ). [102] [154] VO2max is used as a measure of cardiovascular fitness or aerobic ability. It measures the lung's ability to

extract oxygen from the air and deliver it to the blood, the blood's ability to circulate that oxygen to muscle tissue, and the muscle's ability to use oxygen effectively in energy pathways. Before puberty, VO2max is about the same for both sexes. Although both sexes reach their peak VO2max by the late teens, the VO2max of the postpubertal male is greater than that of the female. In fact, expressed per total body weight, men's VO2max is on the average 28% greater than women's.[154] Even if VO2max is expressed relative to fat-free weight rather than total body weight, the differences between the sexes are still considerable. A man's VO2max per fat-free weight is, on the average, 15% to 25% greater than that of a woman.[154] Not only is VO2max an important determinant of endurance performance, but lactate threshold and the economy of movement are also important. Lactate threshold values are similar in male and female endurance athletes.[155] Data on whether economy of motion is similar in both sexes are conflicting. Wells [154] believes that anatomic differences such as pelvic width and stride length affect economy of motion, whereas Williams and associates [157] report no real correlation between economy of motion and gender-related biomechanical differences. At distances greater than 42.2 kilometers, sex differences in running speeds are negligible, with females potentially outperforming men at distances greater than 70 kilometers. One of the potential reasons given for enhanced performance of women in long-distance running events (greater than 42.2 kilometers) is the fatigue resistance of their muscles.[34] [113] At one time, it was felt that women exercising in warm weather were at an increased risk of hyperthermia because, unlike males, they could not effectively decrease core body temperature by sweating. Research has since shown this not to be true. By conditioning in warm weather, both men and women can increase the amount of sweat and the rate of sweating.[54] [69] [153] Women mature physiologically earlier than men. Even in infancy, skeletal ossification is more advanced in girls than in boys. The adolescent growth spurt, which precedes sexual maturation, occurs in girls at about 11 years of age; the adolescent growth spurt in boys does not begin until approximately 1 to 3 years later.[145] Bone growth in girls ceases at about age 20, but in boys growth continues until the early 20s. Tables 13-1 and 13-2 summarize these anatomic and physiologic differences.

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The Preparticipation Physical Examination

The basic components and the format of the preparticipation physical examination are the same for male and female athletes. In women, however, special attention should be given to recognizing conditions that occur more commonly in females, such as anemia, eating disorders, mitral valve prolapse, patellofemoral and shoulder joint laxity, foot abnormalities, and scoliosis. A menstrual history should also be obtained. One should document the date of the first menses, the date of the last period, the average length of periods, the presence of dysmenorrhea, and the pregnancy history. Athletes generally have a delay in menarche. Average age of menarche in nonathletes is reported to be 12.5 years, and the average age in athletes is 13.5 to 15.5 years. [141] The athlete who has not had a period by the age of 16 is considered to have primary amenorrhea and should be referred to a physician for further evaluation to confirm that sports participation and not other diseases has delayed the onset of menses.[140] The normal menstrual cycle is 28 days, with a range of 25 to 35 days (Fig. 13-1 (Figure Not Available) ). Many athletes (approximately 46% of runners) have oligomenorrhea, or infrequent periods (cycles greater than 35 days, but less than 90 days). [56] Five to fifteen percent of athletes have been reported to have secondary amenorrhea, a cessation of menses for greater than 3 months. [152] Secondary amenorrhea is more common in those participating in sports such as running and ballet and is less common in those participating in sports such as swimming and cycling.[137] Physical stress, emotional stress, and weight loss appear to be the biggest contributing factors to the development

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TABLE 13-1 -- Men and Women Athletes: Impact on Performance of Anatomic Differences*

Anatomic Differences Factor

Women

Men

Impact

Height

64.5

68.5

Weight

56.8 kg

70.0 kg

Limb Length

Shorter

Longer

Men can achieve a greater force for hitting or kicking

Articular Surface

Smaller

Larger

May provide men with greater joint stability; men have greater surface area to dissipate impact force

Body Shape

Narrower shoulders

Wider shoulders

Wider hips

Narrower hips

Women have lower center of gravity and therefore greater balance ability; women have an increased valgus angle at the knee which increases knee injuries; women and men have different running gaits

Legs 51.2% Legs 52% of height of height More fat in lower body

More fat in upper body

% Muscle/TBW*

36%

44.8%

Men have greater strength and greater speed

% Fat/TBW

22%-26%

13%-16%

Women are more buoyant and better insulated; they may be able to convert to fatty acid metabolism more rapidly

21-22 yrs

Women develop adult body shape/form sooner than men

Age at Skeletal 17-19 yr Maturation TBW, total body weight.

From Yurko-Griffin L, Harris SS: Female athletes. In Sullivan JA, Anderson SJ (eds): Care of the Young Athlete. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1999, pp 137-148. *Comparisons are made for average postpubertal male and female. Varies somewhat with age, sport, and level of conditioning.

TABLE 13-2 -- Men and Women Athletes: Impact on Performance of Physiologic Differences* Physiologic Differences System/Factor Cardiovascular

Women

Men

Impact

Heart size

Smaller

Larger

Heart volume

Smaller

Larger

Lower

Higher

Systolic blood pressure

Women's stoke volume is less, necessitating an increased heart rate for a given submaximal cardiac output; cardiac output in women is 30% less than men; women may be less at risk of developing hypertension

Hemopoietic Hemoglobin

10-15%> per Men's blood has a greater 100 mL oxygen-carrying capacity blood

Pulmonary Chest size

Smaller

Larger

Total lung capacity in men is greater than in women

Lung size

Smaller

Larger

Vital capacity

Smaller

Larger

Residual volume

Smaller

Larger

Lower

Higher

Higher oxygen pulse provides men an advantage in aerobic activity

Lower

Higher

Men have greater aerobic ability

Metabolism (BMR)

6%-10% lower (when related to body surface area)

6%-10% Women need fewer calories to higher (when sustain same activity level as related to men body surface area)

Thermoregulation

Female = Male

Female = Male

Efficiency of Cardiorespiratory System Oxygen pulse

Level of Aerobic Fitness (reflects performance of cardiorespiratory and muscular systems) VO2max

BMR, basal metabolic rate.

Both sexes can adequately sweat in hot weather to decrease core body temperature

From Yurko-Griffin L, Harris SS: Female athletes. In Sullivan JA, Anderson SJ (eds): Care of the Young Athlete. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1999, pp 137-148. *Comparisons are made for average postpubertal male and female.

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Figure 13-13-1 (Figure Not Available) Normal menstrual cycle. FSH, follicle-stimulating hormone; LH, luteinizing hormone; LHRH, luteinizing hormone-releasing hormone. ( Reproduced by permission from Sloane E: Biology of Women. Albany, NY, Delmar, 1980.)

of secondary amenorrhea. Athletes who have not had a menstrual period for 1 year should not assume that this prolonged amenorrhea is secondary to athletic participation but should be evaluated to exclude other abnormalities. Dysmenorrhea, or painful periods, is less common in athletes than in nonathletes. Nonetheless, this condition can be disabling during competition. Menstrual cramps are caused by endometrial release of prostaglandins, which act on the myometrium to cause contractions. Prostaglandin inhibitors such as naproxen sodium (Anaprox), ibuprofen (Motrin), and naproxen (Naprosyn) may be used to treat dysmenorrhea. Athletes with persistent disabling dysmenorrhea should undergo gynecologic evaluation to rule out other diseases such as endometriosis and pelvic infection. Frequent vaginal infections should be noted in the history. If antibiotics are needed by an athlete who is prone to Candida vaginitis, preventative douches or medicated suppositories may be recommended to avoid development of a Candida infection. Although typically not disabling, this infection is annoying and can interfere with maximal performance. Foot abnormalities secondary to improper shoewear appear to be more common in female athletes. If corns, calluses, blisters, or prominence of a retrocalcaneal bursa is noted, the athlete should be counseled regarding proper shoewear. Bunions are more frequent in women than in men.[55] Shoe modification for symptomatic relief should be tried initially rather than surgery. If the first ray is shortened during a surgical procedure to correct a bunion deformity, the axis of weight-bearing may be shifted to the center of the foot, resulting in stress fractures or metatarsalgia of the middle metatarsals in the running or jumping athlete ( Fig. 13-2 ). Iron deficiency occurs not infrequently in women. It has been estimated that 20% of all adolescent female athletes have iron deficiency anemia and at least an equal number are iron deficient but not anemic. The amount of tissue iron, which can be depleted before the hematocrit falls, can be assessed by measuring serum ferritin levels. Iron is important for optimal sports performance because it not only functions in oxygen transport but also participates in oxidative enzyme functions. Athletes whose iron stores are depleted may experience easy fatigability. Therefore, counseling women regarding incorporating iron-rich foods into their diet is important. The recommended dietary

allowance of iron is 18 mg a day. Female athletes whose performance begins to decline should be screened for iron deficiency. Iron-rich foods include dried fruits (e.g., raisins, dates, prunes), meats (e.g., pork, turkey, beef, liver), and beans (e.g., baked, lima, kidney, pinto). In addition, many foods such as cereal are fortified with iron. During the preparticipation examination, the athlete should be evaluated for increased joint laxity. If patellofemoral, shoulder, or ankle laxity is recognized during the preseason screening examination, conditioning programs to increase the strength of secondary joint stabilizers (i.e., the

509

Figure 13-13-2 Stress fracture of the third metatarsal in a cross-country runner after bunionectomy.

muscles surrounding these joints) can be initiated early in the season to minimize injury during the season. Because idiopathic scoliosis (i.e., scoliosis of unknown cause) is five to eight times more common in adolescent girls than in boys, and adolescent girls have a greater tendency toward curve progression during growth, screening for scoliosis is important as part of the preparticipation examination in adolescent girls.[132] Athletes should be examined from behind, noting the alignment of the spinous processes in the upright posture, and as the athlete bends forward, observing for the prominence of the rib cage secondary to spine rotation. If scoliosis is suspected, further evaluation with radiography is warranted.[95] A nutritional history is important because eating disorders are common (16% to 72% frequency in female athletes), especially in participants in sports in which the lean look is considered an assetballet, gymnastics, skating, and long-distance running.[21] [49] [133] A nutritional history should always be obtained for amenorrheic athletes inasmuch as disordered eating, amenorrhea, and osteoporosis are frequently associated. In fact, the association of these three conditions was termed the female athlete triad by the American College of Sports Medicine in 1992.[2] Although one typically associates osteoporosis with postmenopausal women, it can also occur in young amenorrheic women. Peak bone mass is typically attained between the ages of 18 and 25 years. After this time, men and women lose bone at a rate of 0.3% to 0.5% per year. [11] In women, estrogen is needed to maintain adequate bone mineralization. At menopause, as a result of the lack of estrogen, the rate of bone loss escalates. Hypoestrogenic states seen in amenorrheic athletes may also affect bone density.[47] [130] In fact, stress fractures have been reported to be more frequent in amenorrheic than eumenorrheic athletes ( Table 13-3 ). [151] It is estimated that in secondary amenorrhea, the yearly loss of bone mineral density is approximately 4%. In the case of primary hypoestrogenic amenorrhea (i.e., delayed menarche), it is unclear whether normal bone density accretion is merely postponed until menses begins or whether an irreplaceable period of

bone mineral accumulation is lost forever.[47] The causes for menstrual irregularities in athletes are not very well understood. Strenuous training, psychological stress, and dieting all seem to contribute.[15] [43] [47] [66] Treatment of athletic amenorrhea consists of increasing caloric intake, increasing body fat, and decreasing training.[47] It is often difficult, however, to persuade young athletic women to be compliant with such a program. The literature is not consistent regarding the appropriateness of recommending estrogen supplementation for amenorrheic athletes.[15] [43] The American Academy of Pediatrics does not recommend hormonal therapy for girls within 3 years of menarche, unless there is a history of a stress fracture.[138] Oral contraceptive pills (OCPs), however, can be used in older athletes who are experiencing amenorrhea to help improve bone mineral density.[14] Alendronate sodium and other antireabsorptive therapies are currently recommended only for postmenopausal women.[138] One should not draw the conclusion from the earlier discussion that normal athletic activity is detrimental to the health of a woman's skeleton. It is only when the athlete develops a hypoestrogenic state, typically expressed as menstrual irregularities, that bone health is negatively affected. In general, young athletes have higher bone mineral densities than their nonathletic counterparts. [48] In one study, women who had participated in organized sports or fitness programs had bone mineral density that was 11% greater than women who had not.[104] Swimmers are the exception; those athletes participating in this non-weight-bearing sport appear to have bone mineral densities no greater than sedentary controls.[131] It does appear from dual-energy x-ray absorptiometry (DEXA) studies that the increase in bone mineral density seen in athletes is specific for sites of increased mechanical stress or loading.[97] [143] Although most agree that young women should be encouraged to participate in exercise to maximize bone density, the most effective type, frequency, intensity, and duration of exercise for optimizing bone mass has yet to be defined clearly.[48] In postmenopausal women, exercise also appears to have a TABLE 13-3 -- Incidence of Stress Fractures in Amenorrheic and Eumenorrheic Athletes Reference Sport Amenorrheic (No. of Eumenorrheic (No. of athletes) athletes) Lindberg et al[90A]

Running 49% (11)

0% (15)

Warren[151]

Dancing* 65% (20)

25% (20)

Lloyd et al.[92A]

Mixed

15% (41)

4% (158)

Barrow & Saha[9]

Running 49% (69)

29% (120)

Marcus et al.[100]

Running 55% (11)

17% (6)

Clark et al.[33A]

Running 72% (18)

36% (75)

From Constantini NW: Clinical consequences of athletic amenorrhea. Sports Med 17:213-223, 1994. *Professional ballet dancers.

510

[11] [89]

TABLE 13-4 -- Recommended Dietary Calcium Intake Group (years) Recommendation (mg/day) 1-3

800

4-8

800

9-18

1300

19-50

1000

51 +

1200

Pregnant or lactating

1200

From Dembo L, McCormick KM: Exercise prescription to prevent osteoporosis. ACSM's Health Fitness Journal 4:32-38, 2000. protective, albeit incompletely understood, effect on bone health, especially if combined with adequate calcium in the diet (1200 mg/day) ( Table 13-4 ) and estrogen replacement therapy.[60] The effect of physical activity on peak bone mass is less in older adults than during the years of skeletal growth. As a general rule, however, women at all ages who exercise and maintain normal menstrual cycles have greater bone mass than those who do not. Osteoporosis affects more than 25 million people, with four of five of these being women, and leads to 1.5 million fractures each year at an estimated financial impact of $13.8 billion annually.[111] Therefore, prevention seems critical, and women of all ages should be counseled regarding treatable risk factors (decreased dietary calcium, increased ethanol consumption, cigarette use, intake of caffeinated beverages) as well as the protective effects of estrogen and exercise ( Table 13-5 ).

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Pregnancy and Exercise

In the past, there was concern that exercise during pregnancy could induce premature labor. Most of the studies investigating the effects of exercise on mother and fetus support the conclusion that exercise during pregnancy is beneficial. Concerns that exercise-induced alterations in visceral blood flow and increases in maternal caloric expenditure, body temperature, and biomechanical stresses might have adverse effects on the course and the outcome of pregnancy (i.e., premature labor, abortion, growth retardation, difficult labor, and maternal musculoskeletal injury) are not well supported by the literature. Conversely, it has been shown that exercise during pregnancy reduces TABLE 13-5 -- Risk Factors for Osteoporosis Being female Being postmenopausal Being amenorrheic Being small-boned Eating a diet low in calcium Drinking high quantities of alcohol Drinking high quantities of caffeinated beverages Being sedentary Smoking From Dembo L, McCormick KM: Exercise prescription to prevent osteoporosis. ACSM's Health Fitness 4:32-38, 2000. musculoskeletal complaints, enhances feelings of well-being, and improves body image.[31] [32] [73]

A study conducted by the Melpomene Institute in Minnesota in the 1980s demonstrated no alteration in Apgar scores and normal birth weights in babies of exercising mothers.[91] Moreover, pregnant women who exercised regularly believed that exercising improved their mood, decreased fatigue, and helped them maintain a reasonable weight gain during pregnancy. To avoid overheating during pregnancy, the study advised women to avoid exercising in hot, humid environments; to drink adequate fluids; and to avoid saunas and steam rooms. In 1985, the American College of Obstetrics and Gynecology published guidelines for exercise during pregnancy and the postpartum period (Table 13-6 (Table Not Available) ); however, these guidelines were criticized by some for being too restrictive. For example, the guidelines recommended that all pregnant women, even those who had been very active before pregnancy, keep their heart rate at 140 beats per minute and limit exercise sessions to 15 minutes. A 1992 meta-analysis of 18 studies found that pregnant women can safely exercise three times per week for 43 minutes at a heart rate of 144 beats per minute (i.e., approximately 60% to 70% of the maximum aerobic capacity of most women of childbearing age). [93] The American College of Obstetrics and Gynecology has since revised the 1985 guidelines with updated 1994 guidelines ( Table 13-7 ). Clapp, a leading researcher on the effects of exercise on mother and fetus, cautions that contraindications to exercise during pregnancy include heavier, persistent vaginal bleeding, localized and/or persistent pain, and persistent sensations of uterine contractions.[33] He also recommends that exercise sessions occur 3 or more hours after meals and be followed by a snack to avoid hypoglycemia. Women who exercise during pregnancy tend to continue exercising after the postpartum period. These women tend to return to prepregnancy weight within 1 year, regain abdominal muscle tone more rapidly than nonexercisers, and develop no adverse effects on bladder control during or after pregnancy. One must remember, however, that the type, the intensity, the frequency, and the duration of exercise appear to have an impact on the positive benefits of that activity. [30]

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Conditioning and Rehabilitation

Proper conditioning is as important for women as it is for men. Conditioning programs need to include exercises for flexibility, strength, and neuromuscular conditioning (i.e., proprioceptive skill development). Although girls tend to have greater joint laxity than boys in adolescence, periods of rapid growth may result in decreased muscle flexibility. Stretching exercises should follow a brief period of warm-up calisthenics and should be incorporated in the prepractice and pregame exercises for athletes of all ages. Strength training, or weight training (i.e., adding resistance to the body's natural movements to make those movements more difficult and hence to encourage muscles

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TABLE 13-6 -- American College of Obstetricians and Gynecologists Guidelines for Exercise During Pregnancy and Postpartum (Not Available) From the American College of Obstetricians and Gynecologists: ACOG Home Exercise Programs: Exercise During Pregnancy and the Postnatal Period. Washington, DC, American College of Obstetricians and Gynecologists, 1985. to become stronger or to adapt to the greater resistance) is an integral part of any conditioning program. When muscle is worked near its maximum capacity, its metabolic processes increase to handle the greater load, and the muscle often becomes bigger or hypertrophies. Additionally, neural adaptation within the muscle results in recruitment of

more motor units around the primary muscle. This combination of neural adaptation and increases in metabolic processes within the muscle results in the muscle increasing in size and strength. Men and women respond to strength training similarly (i.e., with the same relative rate of improvement).[19] Because men tend to have greater absolute and relative strength than women initially, however (although these differences diminish when expressed relative to body size), men are still stronger than women after strength training. [129] Increases in muscle size during strengthening programs depend on genetic potential as well as the resistance supplied to the muscles during the training period (i.e., the weight training program used). One's diet also plays a role because muscles need to be supplied with ample raw materials to hypertrophy. Wilmore and others[22] [124] reported minimal muscle hypertrophy in women after resistance training. Cureton[41] and several others,[76] [144] however, reported similar absolute increases in muscle cross-sectional area in men and women after a 16-week progressive resistance training program. The smaller muscle fiber cross-sectional area and the total muscle cross-sectional area of women resulted, however, in sports-specific gender differences in absolute strength. Wells[154] agreed with Wilmore that there are differences in muscle hypertrophy in well-trained men and women, most likely related to androgen levels, particularly testosterone. In men, response to training is believed to be mediated by several anabolic hormones, including testosterone, growth hormone, and cortisone. [144] Hormonal factors that modify muscle hypertrophy and strength in women have not been as fully elucidated. There is controversy whether there is an increase in serum testosterone levels in women during resistance training.[39] [40] Initially, concerns were expressed over the ability of women to tolerate the stresses of an intensive training program, but these have been dispelled. [122] In fact, weight training is an excellent way not only to condition for a particular sport or activity but also generally to improve fitness by increasing muscle strength and endurance, increasing flexibility, maintaining body fat within acceptable limits (i.e., sculpting or reproportioning the body according to individual preferences), enhancing the cardiovascular system (hence, decreasing heart rate), strengthening bones, TABLE 13-7 -- American College of Obstetricians and Gynecologists Recommendations for Exercise in Pregnancy and Postpartum (Abbreviated Version) 1. Exercise is recommended at least three times per week or more if no medical or obstetric contraindications exist. 2. No exercise in the supine position in the first trimester, and avoid prolonged periods of motionless standing. 3. Be aware of the changes and needs of pregnancy. Stop with fatigue; do not exercise to exhaustion. Modifications in exercise routine from weight-bearing such as jogging to non-weight-bearing activities, such as stationary cycling or swimming in later pregnancy, may help with continuing exercise on a regular basis. 4. When good balance is necessary or abdominal trauma is a possibility, exercise should be avoided.

5. Pregnancy requires an extra 300 kcal/day. Supplements are recommended with pregnancy. 6. Exercise in the first trimester requires hydration, clothing, and environment necessary to dissipate heat. 7. Resuming exercise in the postpartum period is individual and determined by physical limitation. Data from American College of Obstetricians and Gynecologists: Exercise during pregnancy and the postpartum period. ACOG Technical Bulletin 189:3-4, 1994. From Wiggins DL, Wiggins ME: The female athlete. In Fadale PD, Halstyn MJ (eds): Clin Sports Med 16:593-612, 1997.

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and increasing self-esteem. Additionally, many women find weight training to be an enjoyable social activity. Similar to the practice in male athletes, designing a weight training program for women must consider which muscle groups need to be exercised, the correct exercises for each muscle group, the number of sets, the repetitions per set, the weight to be lifted, and the amount of rest between exercise sets and between workout days. Seasonal variation (periodization) of the program is also important, especially if the weight training program is to be used to strengthen certain muscle groups to improve performance in a particular sport. Hence, one must establish one's goals for any weight training program before developing the program. If one's goal is merely to exercise for good muscle tone and cardiovascular endurance, one would want to design the weight training program along the lines of a circuit program. The exercise is done at least four times a week for approximately 20 to 30 minutes each session, incorporating minimal rest periods between exercises, typically 30 seconds or less. Such programs generally consist of three sets of 15 to 20 repetitions of an exercise for each major muscle group (i.e., quadriceps, hamstrings, back, biceps, triceps, and so forth). If one's goal is to build muscle strength in a particular muscle group to improve sports participation (e.g., increasing leg strength to improve running speed), one would do a lower-body weight training program, exercising each major muscle group to fatigue and incorporating fewer repetitions (i.e., performing three sets of each exercise and completing only approximately 8 to 10 repetitions per set) with slightly longer rest periods, approximately 60 to 90 seconds between each particular exercise. These programs should be done every other day rather than as frequently as circuit programs. When working for pure strength, one needs to fatigue muscles more maximally; therefore, muscles will need a longer period of rest to recover between exercise days. These principles are the same in female and male athletes. Studies have shown that positive effects of conditioning are possible for women of all ages. One study demonstrated that a moderate-intensity training program for women aged 49 to 62 years resulted in a 20% increase in VO2max . [81] Although it was initially

reported that maximum oxygen uptake did not improve in prepubescent girls after an aerobic training program despite improvement in athletic performance,[7] later studies demonstrated increased VO2max and decreased heart rate in children after vigorous intensive training programs.[87] [110] [135]

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Musculoskeletal Injuries

In general, sports injuries are more sport than gender specific; however, several conditions, including stress fractures, patellofemoral dysfunction, anterior cruciate ligament injuries, foot disorders, frozen shoulder, and problems secondary to shoulder laxity, appear to be more frequent in female than male athletes. An in-depth discussion of these entities can be found in later chapters; the intention of the following section is to highlight pertinent facts in selected areas. Stress Fractures

Stress fractures have been reported to be 10 to 12 times more common in women.[12] Although initially, inadequate conditioning was blamed for this increased incidence, now most investigators relate it to inadequate bone mineral density secondary to hypoestrogenic oligomenorrhea or amenorrhea. Stress fractures are overuse injuries of bone that occur when there is an imbalance between bone reabsorption and bone regeneration due to mechanical, hormonal, and nutritional factors. Bone is dynamic tissue and remodels in predictable patterns in response to stress. The rate of bone repair may be compromised by physical and psychological stresses. Improper training or equipment may increase stress to bone beyond the point at which it is able to repair itself. Inadequate bone stock may also influence the development of stress fractures. The association of the latter with eating disorders and the stress of competition was discussed earlier. Other suggested risk factors for stress fractures are genetic predisposition, bone geometry, diet insufficiencies, training errors, and biomechanical abnormalities.[23] Common sites of stress fractures in athletes include (in order of decreasing frequency) tibia, tarsus, metatarsus, femur, fibula, pelvis, sesamoid, and spine. [103] Tibial stress fractures are common in both men and women; however, women appear to have more femoral, metatarsal, and pelvic stress fractures than men.[13] [74]

In treating stress fractures, it is important to obtain a nutritional and menstrual history from the athlete. In athletes who sustain multiple stress fractures, one should consider obtaining a bone mineral density study, such as the DEXA scan. In some female athletes with abnormal menses, hormone replacement therapy may be appropriate. The use of OCPs in athletes with hypoestrogenic amenorrhea has not been found to increase bone mineral density significantly, but there are numerous studies that seem to show a protective effect of OCPs against stress fractures in runners, and some suggest placing amenorrheic or oligomenorrheic athletes on OCPs.[9] [94] [100] Referral to a physician skilled in the evaluation of the female athlete triad is suggested. In treating stress fractures in athletes, it is important to help the athlete maintain a conditioned state while allowing the injured part to rest. With lower extremity stress fractures, casts are infrequently needed, inasmuch as intact soft tissue can generally supply ample support if crutches or a cane is used initially to unload the injured extremity. Minimal weight-loading, nonimpact types of activities such as cycling, walking, or swimming can be done early in the course of treating a stress fracture to maintain aerobic conditioning without injuring the bone further. A suggested advancement-of-exercise program is given in Figure 13-3 . The rate of activity progression should always be determined by symptoms and physical findings. At all times, activity should be pain free. If bone pain occurs during an activity, that activity should be stopped for 1 to 2 days and then resumed with careful monitoring. One must also address any training areas and correct biomechanical factors that could have contributed to injury.

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Figure 13-13-3 Suggested exercise advancement for females recovering from lower extremity stress fractures. Anterior Cruciate Ligament Injuries

In the 1970s, the classic anterior cruciate ligament (ACL) injury mechanism was thought to be a blow to the lateral aspect of the leg, causing a rotational stress on the knee (as seen in football) and resulting in a combined ligament (anterior cruciate ligament/medial collateral ligament) and meniscal injury. More recent data have revealed, however, that at least 70% of all ACL injuries occur from noncontact mechanisms involving pivoting (cutting), stopping abruptly (decelerating), or landing a jump.[108] Moreover, the vast majority of these injuries occur in late adolescents or young adults, with only 5% of all ACL injuries occurring in patients younger than 16 or older than 45 years.[58] During the past 15 to 20 years, statistics involving team handball, soccer, downhill skiing, volleyball, and gymnastics have revealed that women appear to be more at risk (two to eight times greater) than men of sustaining a noncontact ACL injury when

involved in these high-risk activities.[3] [4] [44] [62] [76] [166] Unfortunately, although the orthopaedics community has gained much knowledge regarding diagnosis and management of noncontact ACL injuries, prevention strategies have been slow to evolve because the mechanism for this injury has not been clearly understood. Arendt and Dick divided the risk factors for injury into intrinsic factors (joint laxity, limb alignment, femoral notch dimension, ligament size, and hormonal influences) and extrinsic factors (muscular strength, neuromuscular control, body movements, shoe-surface interactions, and skill development).[4] Wojtys suggested dividing risk factors into four categories: environmental (shoe-surface interactions, braces), anatomic (size of ligament, size of notch, lower extremity alignment), hormonal, and biomechanical (strength, movement patterns, muscular recruiting, neuromuscular interactions).[161] Although the interaction between the athlete's shoe and the playing surface does play a role in determining forces transmitted to the knee, at present the ideal shoe for each playing surface or the ideal playing surface for a particular shoe has not been developed. The ideal shoe is defined as one that maximizes performance yet minimizes the friction between shoe and surface to decrease stress on the knee. Because shoe-surface interaction is a modifiable risk factor, research in this area is encouraged. Conclusions drawn from multiple studies in the 1980s examining the effect of prophylactic bracing on knee injuries concluded that present-day braces do not seem to be effective in preventing ACL injuries.[134] [148] Anatomic differences between the sexes may play a role in the different rates of ACL injuries. No anatomic factor (notch size, knee valgus, hip varus, pelvic width, or pronation), however, has been definitely associated with an increased risk of ACL injuries in women. Furthermore, anatomic factors will be hard to modify if implicated as significant risk factors in ACL injuries. Because there are mechanoreceptors in ACL ligaments[92] and because hormonal differences are what differentiate men from women, many believed that hormonal influences would be the key to the increased rate of ACL injuries in female athletes. Data relating the time of occurrence of an ACL injury to the athlete's menstrual cycle phase, however, are conflicting. Wojtys and associates found an increased number of ACL injuries in the ovulatory phase of the menstrual cycle (days 10 to 14, when estrogen levels surge) and fewer injuries in the follicular phase (days 1 to 9, when estrogen and progesterone levels are low).[161] Myklebust, however, found significantly fewer injuries during the mid cycle estrogen surge (days 8 to 14) in a group of Norwegian handball players.[115] More recently, a survey of injured National Collegiate Athletic Association basketball players (103 athletes) reported that the majority sustained ACL injuries just before or after the onset of menses.[3] The influence of oral contraceptives in determining the time of occurrence of ACL injuries is also not well understood.[114] Biomechanical factors appear to play a major role in noncontact ACL injuries. Mechanoreceptors have been found in the anterior cruciate ligament, [8] [83] [136] leading to speculation that ligament stress may initiate muscle contraction or alteration in tone to

stabilize the joint in a reflexive manner. A fatigued muscle may be unable to respond adequately to such signals from the ACL. Research by Lephart and coworkers [45] [90] suggests altered afferent feedback mechanisms reflecting proprioceptor deficits, resulting in a decrease in neuromuscular control and an increased risk of ACL injury. Investigations evaluating the differences in body movement between males and females are now under way. Ireland,[78] after analyzing videos of female and male basketball players performing jump shots, rebounds, and pivots, reported differences in body mechanics that may be related to an altered pelvic/knee angle, the woman's lower center of gravity, the overall differences in physique between the sexes, or potentially to training and coaching differences.

514

There are also significant biomechanical differences in the way males and females move during sports. Males cut, pivot, land, and stop with more hip and knee flexion than women.[20] [36] [98] [164] Moreover, women have been found to fire their quadriceps rather than their hamstrings when an anterior translatory force is applied to the proximal tibia.[77] In addition, research has shown that with low levels of knee flexion, the force generated by maximal quadriceps contraction exceeds the tensile strength of the ACL.[101] [121] Griffis and associates, in an abstract presented at the annual American Orthopaedic Society for Sports Medicine meeting in 1989,[63] described what they called the quad-cruciate interaction, or the ability of a maximum quadriceps contraction to tear the ACL when the knee is at or near full extension. In a 10-year review of injuries in Division 1 female basketball players, this group reported that a majority of the ACL injuries sustained were noncontact. The mechanism of injury was planting and cutting (29%), straight knee landing (28%), and one-step stop with the knee hyperextended (26%). They believed that the incidence of ACL injuries could be decreased by modifying these techniques. They suggested substituting an accelerated rounded turn off a bent knee for the pivot and cut, substituting landing on a bent knee for landing on a straight knee, and substituting a three-step stop on bent knees for a one-step stop with the knee hyperextended. Early data reported by this group on a limited number of athletes trained in these modifications did show an 89% decrease in noncontact injuries. Garrett[57] speculated that an ACL injury could occur secondary to the development of a strong eccentric quadriceps contraction occurring simultaneously with a varus or a valgus movement of the knee at or near full extension. He theorized that the quadriceps, preactivated to stop the knee's forward progress at heel strike, when subjected to an unplanned event (a slip or a sudden change in direction in response to another player), results in an unbalanced eccentric maximum quadriceps contraction while the foot is planted. Hewett and associates have designed a three-part prevention program with flexibility, strengthening, and plyometric exercise (jump drills) to improve strength as well as to increase balance and coordination of the stabilizing muscles about the knee joint. Their program (Sportsmetrics) was found to decrease peak loading forces, decrease varus and valgus motions to the knee, increase hamstring power and strength, and increase hamstring-to-quadriceps peak torque ratio.[71] Early data from an initial trial of their prevention program found a two- to fourfold decrease in injury rates.[70] Caraffa,[28] an Italian orthopaedist, believed that a decrease in ACL injuries would be

possible by instituting a prophylactic balance program as part of the preseason and in-season conditioning drills. He established a five-phase skill program using a variety of different balance boards for 300 semiprofessional and amateur Italian soccer players. The program spanned 3 years. In those trained by his program, only 0.15 injuries per team per year occurred, whereas in the untrained group, the ACL injury rate was 1.15 per team per year. Finally, the Vermont Ski Research Association has looked at the strategy of increasing athletes' awareness of injury situations so that they can develop prevention strategies to avoid these situations.[117] It is known that as an individual becomes more accustomed to an activity, central nervous system programming occurs (i.e., activities occur through remembered patterns, allowing faster response times). Participants in the Vermont study included 4700 ski patrollers and instructors in 20 ski areas. The subjects were asked to analyze injury videos and to develop strategies to avoid the events demonstrated on the tapes that resulted in injury.[51] Serious knee injuries significantly declined in the trained group. None of the results of these early prevention studies[28] [51] [63] [71] has been verified by repeat studies. As concluded by a group of biomechanists, orthopaedists, family physicians, and athletic trainers who gathered at the Hunt Valley ACL Prevention Consensus Conference in Hunt Valley, Maryland, in June 1999, neuromuscular factors appear to be significant in the increased risk of ACL injuries in female athletes. Common biomechanical factors involved in many, but not all, injuries include making impact on the foot rather than on the toes during landing, stopping and changing directions, performing awkward dynamic body movements, and experiencing perturbation before injury. Moreover, a strong quadriceps activation during eccentric contraction appears most likely to be a major factor in injury. Present neuromuscular training programs that emphasize enhanced body control (e.g., keeping the hip and the knee flexed and staying on the balls of the feet when pivoting, cutting, landing a jump, or stopping) appear to decrease the risk of ACL injury in female athletes, as does encouraging activation of protective neuromuscular responses based on awareness of ACL injury situations. Hence, the Hunt Valley Conference participants felt it appropriate to suggest that while efforts continue to define risk factors and mechanisms of ACL injury more specifically, the implementation of existing prevention programs seems reasonable as long as these programs continue to be closely monitored, with further improvements and refinements based on ongoing assessments. Shoulder Instability

The shoulder is a joint of remarkable mobility. For review of the complex static (bones, ligaments, and capsule) and dynamic stabilizers (muscles) of the shoulder, which also permit the mobility required of this joint, the reader is referred to the chapters on the shoulder. Some propose that women, because of their increase in joint laxity, are more prone than males to problems with atraumatic shoulder instability.[61] [79] [82] Others agree that ligamentous laxity is more common in women but do not believe that this is related to the development of shoulder instability (the pathologic motion that results in pain,

subluxation, or dislocation of the shoulder).[50] [53] [107] Laxity can occur after significant trauma or can be atraumatic. Atraumatic laxity (multidirectional instability [MDI]) is characterized by excessive glenohumeral translation. Most females who present with MDI are adolescents or young adults who seek care after minor trauma or repetitive injury, such as seen in overhead-throwing athletes. They typically present with vague symptoms of

515

shoulder fatigue, discomfort, apprehension, and pain rather than episodes of instability. A small subset of female athletes present with no precipitating event. On physical examination, these women are often slender and have signs of generalized laxity.[1] [17] [105] [118] In MDI, a large capsular pouch and a defective rotator cuff interval have been described. [142] Such looseness in the shoulder's static stabilizers increases the significance of the dynamic rotator cuff, especially at midrange, where the capsuloligamentous structures are most loose. Evaluation of these structures and the scapulothoracic stabilizers (serratus anterior, trapezius, and rhomboid muscles) is important in assessing athletes with MDI.[99] Multiple tests have been described to assess shoulder instability (see chapters on the shoulder). Treatment of the athlete with MDI is initially conservative and is aimed at improving the coordination and enhancing the muscle tone of the muscles surrounding the scapulothoracic and glenohumeral joints. Such programs have been found to be extremely effective in decreasing shoulder instability.[26] [88] In fact, in a study reported by Burkhead and Rockwood,[26] 88% of the 33 patients in their study had good or excellent results following their exercise program, as outlined in Figure 13-4A and B . For athletes whose symptoms persist despite 6 to 9 months of compliance with a program similar to that of Burkhead and Rockwood, the inferior capsular shift procedure has been suggested as the operative procedure of choice.[17] [27] [118] One must evaluate each athlete carefully to make certain other contributing disorders (i.e., lax rotator interval, Hill-Sachs lesion) do not coexist and, hence, need to be addressed at the time of the operative procedure.[1] [17] Compliance with a postoperative rehabilitation program is essential, and the need for this compliance should be stressed preoperatively. Recently, thermocapsulorrhaphy has been advocated to decrease capsular volume. Early results are encouraging because less depth and more control of the heating temperature are possible with the new monopolar and bipolar electrodes used for thermocapsulorrhaphy. It is anticipated

Figure 13-13-4 A and B, Strengthening exercises for the shoulder. (From Burkhead WZ Jr, Rockwood CA Jr: Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am 74:890,

1992.)

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that results of this procedure will not deteriorate with time, as has been described for the laser-assisted capsular shift procedure popularized several years ago.[139] Frozen Shoulder

Codman[35] originally coined the term frozen shoulder to describe a painful restriction of shoulder motion in an individual whose shoulder radiographs were normal. Adhesive capsulitis (a term introduced by Neviaser[120] ) and pericapsulitis have also been used to describe this syndrome, which occurs in 2% to 5% of the general population. [38] This entity is frequently associated with cervical disease, hyperthyroidism, ischemic heart disease, diabetes, breast surgery, and autoimmune disorders. Often, however, there are no associated disorders or significant precipitating events. Frozen shoulder occurs two to four times more commonly in females than males. [25] [163] It occurs primarily in those 40 to 60 years of age and is not uncommon in the middle-aged female athlete playing a sport requiring repetitive overhead activity. On physical examination, the patient with frozen shoulder syndrome typically has marked restrictive global range of motion of the shoulder passively and actively. Differential diagnosis includes rotator cuff disease with secondary restricted motion, metastatic disease, primary diseases of the apical area of the lung, or referred pain from the cervical spine. Routine radiographs are usually normal, but an arthrogram will show a restricted capsular volume. The exact cause of frozen shoulder is unknown. Shoulder stiffness secondary to trauma or surgery is distinct from the clinical syndrome termed frozen shoulder or adhesive capsulitis. Although the names capsulitis and adhesive capsulitis imply that the disease has an inflammatory basis (and indeed, Neviaser described perivascular inflammation as a component of this syndrome), more recent pathologic evaluation describes fibroblastic proliferation with increased collagen and nodular band formation, similar to that seen in Dupuytren's contracture. [25] [37] Hannafin and associates suggest that the underlying abnormality is synovial

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TABLE 13-8 -- Stages of Adhesive Capsulitis (Not Available) From Hannafin JA, Chiaia TA: Adhesive capsulitis. Clin Orthop 372:95-109, 2000.

inflammation with subsequent reactive capsular fibrosis, and they have described four stages in this disease process (Table 13-8 (Table Not Available) ).[65] They suggest aggressive use of injectable steroids in stages one and two (i.e., aggressively treating the inflammation in an attempt to resolve symptoms before development of fibrosis). Miller and associates suggest an initial period of rest and oral anti-inflammatory medicines followed by a closely monitored home therapy program, claiming that such a program yields complete return to function in the majority of patients, although the course of symptoms may be prolonged (average 14 months).[112] Because of this prolonged treatment period, this disease entity can be frustrating for both patient and physician alike. Connolly[38] suggests a more aggressive approach, to include manipulation of the shoulder with the patient under anesthesia early in the course of treatment (typically after 6 to 8 weeks of conservative management). Pearsall and Speer[125] recommend consideration of arthroscopic capsular release of refractory frozen shoulder, as do Ogilive-Harris and Warner.[123] [150] These authors favor arthroscopic capsular release, as opposed to manipulation under anesthesia or an open surgical release. They also recommend postoperative use of an interscalene block for pain control to facilitate motion postoperatively. Adhesive capsulitis, or the frozen shoulder syndrome, remains an intriguing enigma from both a pathophysiologic and a treatment standpoint.

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Arthritis, Exercise, and the Mature Female Athlete

According to a survey done by the Cooper Clinic of 16,961 patients between the ages of 20 and 87 years, the incidence of osteoarthritis in patients 50 years of age or older was higher in women (7 per 1000 person-years) than in men (4.9 per 1000 person-years). For patients younger than 50 years of age, the incidence of arthritis was similar for men and women (2.6 and 2.7 per 1000 person-years, respectively). [29] These results, indicating a greater predilection for arthritis in women than in men, are similar to those obtained from a survey of 48,218 Canadian patients. This survey, published recently in the New England Journal of Medicine, concluded that 5.3 women of every 1000 merited joint replacement for arthritis of the hip or knee, compared with 1.6 men of every 1000 surveyed.[67] In a recent article, Buckwalter stated that the heterogeneous groups of diseases which cause arthralgia and arthritis are the most common cause of activity limitation and disability among middle-aged and older women.[24] Selected exercises can significantly improve the symptoms of arthralgia or arthritis. [52] Increasing range of motion, decreasing pain, decreasing fatigue, and increasing a sense of well-being are possible through exercise. Exercise in the older adult not only maintains bone mineral density and improves cardiovascular fitness but also strengthens muscles around irritated joints and helps maintain or decrease total body weight and, hence, improves the pain and the stiffness of arthritis. The frequency, the intensity, and the duration of first-time exercises need to be tailored to each individual's level of initial fitness at the time of her entrance into an exercise program. As fitness levels improve, frequency, intensity, and duration of exercise can be increased. To realize the benefits of strength training, a woman needs to work only against a resistance greater than that she usually imposes upon the muscle. For those women with lower extremity arthritis or arthralgia pain, water exercise is a reasonable initial activity. Most find the buoyancy and the therapeutic massage effect of water very beneficial. Tai chi, an exercise that emphasizes controlled rhythmic body motions, has become a popular exercise to increase balance and decrease the potential for falls in elderly women. Ballroom dancing is another enjoyable social activity that improves strength and balance; because of its ability to be performed at a lower

intensity, it is a reasonable exercise for many women who have lower extremity arthritis and arthralgia. Fitness is a lifetime endeavor that should be begun in childhood. One is never too old, however, to embark upon an exercise program, a lifestyle change that has been shown to improve mood, increase energy, and enhance mobility.

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Chapter 14 - The Orthopaedically Disabled Athlete Frank A. Gottschalk MD, FRCSEd, FCS(SA)Orth

Participation in sports by able-bodied individuals has been an accepted way of life for centuries. Undertaking sporting activities provides therapeutic, recreational, motivational, and financial benefits. Sports for the disabled individual have evolved during the past half-century because of the realization that functional impairment need not be a hindrance to many activities, and the overall benefits are significant for daily life. Disability is an alteration of an individual's capacity to meet personal, social, and occupational demands and refers to tasks or activities that the individual cannot accomplish. This chapter focuses only on musculoskeletal disabilities that relate to orthopaedically associated disorders and does not cover disabilities due to mental disorders, visual or hearing impairment, or cerebral palsy. Grouping together all forms of disability is not practical. Athletes, therapists, and trainers realize intuitively that different individuals have different abilities, like the able-bodied individuals with different abilities who perform in different sports. Not everyone can be an Olympic or Paralympic athlete, and different levels of competition should exist to allow all who wish to participate to do so. Younger athletes are encouraged to participate in sports to learn skill sets; they may then continue with sports for recreation and health and occasionally become professional athletes. For many wheelchair users, sport is an important part of their recreational lifestyle.[9]

Orthopaedic impairments include spinal cord injuries; amputation; and neuromuscular disorders, such as poliomyelitis, cerebral palsy, dystrophy, and multiple sclerosis. Sports participation has contributed significantly to rehabilitation and was formally introduced as part of a treatment program by Sir Ludwig Guttman in 1944 at Stoke Mandeville.[38] The recreational opportunities that have become available for the disabled individual have made a major contribution to the increase in quality of life and life expectancy experienced by the disabled athlete.[2] Individuals with paraplegia have been noted to have a marked reduction in activity with a subsequent decrease in physical capacity. Active wheelchair users and athletes appear to be healthier than their less physically active peers.[21] It was also noted that the frequency of hospital admissions, pressure sores, and kidney problems was less among athletic wheelchair users than among their nonathletic counterparts. Concerns about medical problems affecting disabled individuals continue to be a barrier for some, and contributing to a sedentary lifestyle are difficulties with access to various facilities.[16] There has been a lack of programs within facilities that are able to accommodate persons with disabilities. Within North America and Europe, programs do exist to provide exercise classes for the disabled person as well as opportunities to participate in some sports. Scientific literature on sport for disabled individuals has been sparse and has focused predominantly on the physiologic processes (41% of records) and the psychological aspects (29% of records) affecting the disabled athlete[23] ; 58% of records reviewed for these studies had wheelchair users as subjects, resulting in a possibly skewed project. The literature reviewed included amputees, visually impaired subjects, patients with cerebral palsy, and spinal cord-injured patients; few female subjects were studied. Studies regarding the injuries that may be sustained by disabled athletes are sparse.[7] History of Sports for the Disabled Individual

Specialized rehabilitation involving sports was started toward the end of World War II in the United Kingdom for soldiers injured in the line of duty.[29] The first Stoke Mandeville games organized by Sir Ludwig Guttman for paraplegics took place in 1948 for wheelchair athletes. [19] By 1952, disabled athletes from other countries were invited to participate. International games were subsequently held every 4 years. In 1960, these games started to coincide with the International Olympic Games. The term Paralympics was used in 1964, and the International Paralympic Games have been held at the same venue as the International Olympic Games since 1976. Paralympics specifies Games for the Disabled held in parallel with the Olympics and should not be confused with the Special Olympics. Acceptance of the Paralympic Games as a world-class sporting event has been a formidable task, and as recently as the 1996 International Olympic Games in Atlanta, difficulty in gaining recognition for the games was experienced.[1] The International Olympic Committee had always sanctioned the term Paralympics, but the United States Olympic Committee did not approve the term until 1984. Incorporation of the Paralympics as part of the International Olympic Games has not been forthcoming, and it is currently a separate sporting event. Organized sports for disabled individuals in the

United States began with the organization of wheelchair basketball competitions for paraplegics and amputees by the Veterans Administration Hospitals.

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Sports

Organized sports for disabled individuals is impairment specific as well as sports specific. Classification schemes have been developed for athletes with disabilities, and most incorporate specific equipment for the different activities. Organized competition and recreation are now available in most parts of the developed world and exist at all levels to promote exercise, fitness, fun, and a feeling of wellness.[29]

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Integrating sports as part of the rehabilitation for the disabled individual has made a marked contribution to the increase in quality of life and life expectancy. There is no longer a statistical difference between life expectancy of able-bodied people and life expectancy of wheelchair users.[2] The different types of sports and numbers of participants have increased, and limits to performance due to impairment are less of a problem. Sports participation by disabled individuals demonstrates success and achievement to the general public, providing psychological as well as physical benefits (Fig. 14-1 (Figure Not Available) ).[29] Athletes themselves see sports as a pathway to integration into society. There is a range of recreational sports for pleasure and fitness in which the majority of those active in wheelchair sports participate; the level of performance correlates with the underlying physical impairment.[29] A functional classification system for the disabled athlete has been developed that enables organizers, trainers, and medical personnel to group athletes with similar ranges of performance level.[20] A sports-medical assessment protocol has been described that identifies medical problems and therapeutic goals for training programs for athletes with a disability.[24] The assessment provides information about the athlete's functional abilities and limitations and helps identify specific goals that can be included in the training program. The advantage of a sports-medical assessment protocol, in addition to the routine cardiovascular assessment, is that it allows identification of musculoskeletal

problems in the disabled athlete. Sports for the disabled athlete require Figure 14-14-1 (Figure Not Available) Amputee athletes at international track event. (Courtesy of Otto Bock Industries, Minneapolis, Minn.)

Figure 14-14-2 Three-track skiing without prosthesis.

specialized coaching and training as well as different types of adaptive equipment. Sports may be year-round, summer, or winter, like those for the able-bodied athlete. Year-round activities include tennis, golf, cycling, basketball, and swimming as a few examples. Snow skiing has become popular for many disabled athletes. Several forms of adaptive skiing are available and should be individualized to each athlete. Three-track skiing is often used by those individuals with loss of function of one lower extremity ( Fig. 14-2 ). The outrigger skis help provide stability and balance. The sit ski is used by spinal cord-injured athletes for downhill skiing ( Figs. 14-3 and 14-4 ). The athlete may use outrigger skis for control and balance, whereas turning occurs by shifting the upper body to one side. Various adaptations may be required for the different levels of paralysis and residual muscle function, and they often need to be individualized. Appropriate clothing and protective equipment are necessary for skiing.[26] Instruction in use of the sit ski is required before being allowed on the slopes. An increased prevalence of minor injuries has been noted in those athletes who participate in sit ski activities.[26] Water sports include sailing, canoeing, and diving. Suitability for a given sport requires evaluation of the athlete's interest, emotional and motivational factors, physical requirements, and level of skill and determination of the goals the athlete wishes to achieve.[11] Many participants choose activities according to their physical ability, muscle potential and activity, and available limb motion.[20] Other limitations in the choice of activity include the length of time that it takes to become involved, because activities of daily living take more energy and time; the accessibility of appropriate surroundings and facilities; the climate; and various economic influences as well as personal and family resources.[25]

523

Figure 14-14-3 Sit ski with use of outrigger skis. Helmet and protective clothing are worn.

The functional classification used in this chapter is for amputees and wheelchair athletes only and does not include individuals with other disabilities. A medical classification that includes functional and anatomic capability has been developed by Chow and Mindock ( Table 14-1 ). [10] Organization of sports for the disabled athlete is impairment specific, rather than sports specific, and it is applied to all sports.[4] Disability classification and rules for competition differ for each organization. This allows athletes with differing disabilities to compete against each other, but it may not take into account

responses to stress or exercise. For disabled athletes to achieve status equivalent to that of able-bodied athletes, they need to have a talent for the activity and be able to plan their life around the requirements to succeed in high-class sports. [20] A medical classification of the various disabilities has been used for most sports and modified as necessary as circumstances change. [27]

Figure 14-14-4 Specialized sit ski for competition.

A sports medicine protocol has been developed for athletes with a disability.[24] It is designed to identify medical problems and therapeutic goals. It is useful for designing training programs and includes stretching for active muscle groups, range of motion maintenance, compensations, conditioning of functioning muscle groups, cardiorespiratory endurance, and relaxation of muscle groups at risk for injury. Overall, there are fewer disabled athletes than able-bodied athletes, and no gender differences are noted within sports for disabled individuals. Those who were active in sports before becoming disabled may have motivational factors different from those of individuals who took up sports after becoming disabled. Another factor to be considered is inappropriate training, which may have a negative influence on the disabled athlete's ability.[20] As disabled athletes have improved their athletic performances, sports have become a more serious consideration for the elite. Pressure for them to perform has also increased, leading to the potential for misclassification in an attempt to have an unfair advantage over other competitors.[18] The athlete tries to appear more disabled than he or she really is to be placed in a more disabled class. This reinforces the need for trained classifiers and nonpartisan medical personnel to aid in the classification process.

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The Amputee Athlete

The amputee athlete can participate in various activities, with or without use of a prosthesis. The prosthesis may be

Class

TABLE 14-1 -- Functional Classification for Wheelchair Athletes Injury Functional Anatomic Capability Level Capability

F1

C6

No finger control

Functional elbow flexors and wrist extensors

F2

C7

No grasp

Elbow and wrist flexors and extensors

F3

C8

Make fist

Finger flexion and extension

F4

T1-T7

No sitting balance

No functional trunk movement

F5

T8-L1

Good sitting balance

Normal upper limb

No hip flexors

Flail legs

Trunk balance

Weak lower extremities

F6

L2-L5

Some knee extension F7

S1-S2

Poor foot function

Unilateral involvement

Adapted from Chow JW, Mindock LA: Discus throwing performances and medical classification of wheelchair athletes. Med Sci Sports Exerc 31:1272-1279, 1999.

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TABLE 14-2 -- Amputation Categories for Competitive Sport A1 Double transhumeral amputee A2 Single transfemoral amputee A3 Double transtibial amputee A4 Single transtibial amputee A5 Double transhumeral amputee A6 Single transhumeral amputee A7 Double transradial amputee A8 Single transradial amputee the one used for daily activities, or it may be modified for the sporting activity. This applies to upper and lower extremity prostheses. In most activities, crutches and canes are not allowed. There are 8 major categories for various combinations of amputations ( Table 14-2 ). Upper Extremity Amputations

Upper extremity amputations are less frequent than lower extremity amputations; most are due to congenital disorders or trauma. Most athletes with an upper extremity amputation are able to function well without a prosthesis and will not use a prosthesis for most recreational activities. One-handed golf is popular. For those amputees with a wrist disarticulation or transradial amputation who use their prosthesis for golfing, a flexible device attaches from the prosthetic socket directly to the club, enabling a controlled yet powerful stroke.[30] Other adaptable devices that are fitted to the prosthesis are available for different sporting activities. Track events do not require upper limb prostheses, which are likely to be a hindrance in most situations. Many athletes adapt to use of one extremity for throwing and catching. Upper extremity prostheses are not able to provide high activity function for sports and are likely to be burdensome because of weight and difficulty with mobility. Lower Extremity Amputations

In contrast to upper extremity amputees, most unilateral lower extremity amputees use a prosthesis that is modified for their sporting activity. Prosthetic components are available that allow running step over step as well as jumping; for most athletes, these have provided nearly normal athletic activity (Fig. 14-5 (Figure Not Available) ). Continued advances in prosthetic foot components allow amputees to function at an improved level. The use of carbon composite feet with various modifications has more closely approximated normal gait and also improved athletic function (Fig. 14-6 (Figure Not Available) ). A distinction needs to be made between sprint activity and endurance activities. A shock-absorbing mechanism is preferred for endurance activities, whereas it may hinder sprint activity because of a fraction of a second timing delay and a slight increased weight. For sprinting, most athletes are fitted with a carbon foot as stiff as they can tolerate, which increases energy return and helps improve performance (see

Fig. 14-5 (Figure Not Available) ). Nearly normal cadence can be achieved for the transtibial amputee with these prosthetic feet. The kinematics of the prosthetic limb in the transtibial amputee is similar to that of the sound limb, and individuals are able to achieve a running pattern typical of able-bodied sprinting.[6] In sprinting, the duration of stance as a percentage of stride time decreases to 22%. The knee undergoes flexion only during sprinting, contributing little to forward propulsion. With newer types of prosthetic components, transtibial amputees are able to achieve flexion-extension patterns similar to those that are achieved in the sound limb. The carbon fiber leaf spring deforms during loading, creating controlled dorsiflexion as the shank rotates forward over the planted foot, leading to knee flexion. [6] It has been shown that use of older types of prosthetic feet may result in increased time in knee extension during stance, which facilitates proximal transmission of ground reaction force to the spine.[30] It may ultimately predispose the athlete to early onset of fatigue, however. A study by Sanderson and Martin[32] suggests that unilateral transtibial amputee running may be similar to able-bodied Figure 14-14-5 (Figure Not Available) Amputee athletes using various lower extremity prostheses. (Courtesy of Flex Foot Inc., Aliso Viejo, Calif.)

525

Figure 14-14-6 (Figure Not Available) Carbon composite feet with shock absorbers. (Courtesy of Flex Foot Inc., Aliso Viejo, Calif.)

running because of a change in the magnitude of joint moments. Control of the lower limbs during running does not require new joint moment patterns, but adjustment of existing patterns. It has been shown that transtibial amputee runners have a marked reduction in mechanical work done in the stance-phase prosthetic limb. The total amount of energy transferred during swing phase and the energy transferred out of the swing-phase leg into the trunk are greater than for able-bodied runners. A 74% increase in energy transfer of the intact swing-phase limb has been documented. This is thought to be an adaptive mechanism that allows energy redistribution to the trunk to compensate for the reduced power output of the stance-phase prosthetic limb.[14] Running is more difficult for transfemoral amputees. With a traditional prosthesis, swing phase is prolonged on the prosthetic side owing to the inertia of the knee mechanisms. Recently developed knee mechanisms allow a smoother cadence and easier running, however (Fig. 14-7 (Figure Not Available) ). The computer-enhanced hydraulic linked polycentric knee systems propel the shank forward during swing phase, allowing improved cadence. Regardless of the prosthesis, most runners tend to vault and have decreased pelvic rotation and asymmetrical arm movement while running. For high-intensity track athletes, the stump must be in good condition and almost end bearing. A microprocessor hydraulic knee is now available to control swing phase.

There is a decreased need for stance control in sprinting because increased stance phase would slow the athlete. Therefore, some athletes may modify the knee components for sprint events to dampen the swing phase and allow early positioning of the prosthetic foot. For medium- to long-distance events, a rotary hydraulic stance unit allows swing adjustment of the knee to provide enhanced activity. An articulating design is well suited for golfers; the addition of a torsion adapter absorbs the high rotational shear forces at the residual limb. Competitive swimmers often prefer a custom prosthesis incorporating a fin to aid in propulsion. In the future, it is probable that microprocessor control will provide additional improvement for the amputee athlete. Such a unit is currently being tested for walking only. A logical progression of this technology may be the use of electrodes for electromyo-graphically modulated knee mechanisms. The development of improved and advanced prosthetic components can be nullified by poor surgical technique and a disregard for the biologic function of muscle and soft tissue. It is important to adhere to the biomechanical principles of modern amputation surgery for transtibial and transfemoral amputations. These surgical techniques must provide a stump that is easy to fit and has good motor power and adequate sensation to minimize stump-socket interface problems. Myodesis of the transected or detached muscles at the time of surgery helps retain active muscle tension, provided that nearly normal resting tension is restored.

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Spinal Cord Injury

All disabled athletes with spinal cord injuries use a wheelchair for athletic activities. The classification of Figure 14-14-7 (Figure Not Available) Hydraulic knee unit for use in transfemoral prosthesis. ( Courtesy of Flex Foot Inc., Aliso Viejo, Calif.)

526

wheelchair athletes with spinal cord injuries is by severity of disability; it is based on the level of spinal cord involvement and the extent of the injury. The degree of impairment is by neurologic level and completeness of injury with resulting loss of muscle function ( see Table 14-1 ). [10] The paraplegic athletes are predisposed to complications associated with paralysis, over and above overuse injuries related to the sporting activities.[19]

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Exercise Physiology

Wheelchair athletes must use the upper body for strength, movement, and exercise. Muscle strength and endurance are important for the various types of athletic activities.[34] Available muscle power depends on the level of spinal cord injury. The maximal rate at which an individual can consume oxygen (VO2max ) is an important determinant of peak power output and of maximal sustained out put. [19] The amount of available muscle mass is increased with the lower the level of paralysis. Athletes with higher levels of injury involving the thoracic spine, with less muscle mass, may experience peripheral fatigue before cardiovascular maximum is reached, that is, oxygen demand is less than oxygen delivery capacity. In general, when an individual runs, approximately 1 kcal of energy per kilogram of body mass per kilometer traveled is required. In contrast, cycling is more efficient, requiring one third of the output, because of a more level center of gravity. Wheelchair users also have a level center of gravity, but unfortunately, the upper body muscles are much less efficient. The volume of arm muscles is only 20% that of leg muscles, resulting in decreased power.[3] The mean VO2max obtained by wheelchair athletes is comparable to that achieved by sedentary able-bodied athletes.[12] [19] As expected, the highest VO2max values are noted in athletes with the lowest spinal cord injury level. Wheelchair sport generally strengthens the arm muscles, making it possible to develop a given power output and oxygen intake by contracting muscles at a smaller fraction of their maximal voluntary force.[34] Wheelchair athletes have a 10% to 25% reduction in cardiac output and a 15% to 30% lower stroke volume compared with able-bodied athletes in performing similar exercises. Individuals who train in their wheelchairs develop greater peak power than those who use their wheelchairs for activities of daily living. Wheelchair exercise training can improve upper body cardiovascular fitness. Use of arm ergometer training for several weeks may improve muscle power in the proximal upper extremity, but not endurance.[15] Quadriplegic athletes, however, are affected by hypokinetic circulation,

which is an inadequate hemodynamic response to the increased metabolic demand. Below the level of the spinal cord injury, there is no active muscle pump, resulting in venous pooling, decreased venous return, reduced cardiac preload, and reduced myocardial performance. Quadriplegics are frequently hypotensive while exercising in the upright position because of vasodilation in the exercising muscles with lack of compensatory sympathetic vasoconstriction. This is associated with a lower maximal heart rate and a decreased cardiac output. Paraplegics have a reduced ability to sweat below the level of injury. This thermoregulatory dysfunction may cause reduced stroke volume during physical activity, secondary to increased blood pooling in the skin to maintain adequate heat loss during exercise. Spinal cord-injured persons have a higher core temperature in the heat and lower core temperature in the cold because normal autonomic responses for heat dissipation, redistribution of cardiac output, and vasodilation in cutaneous vessels are impaired.[33] The loss of sensory afferent impulses below the level of cord injury may limit hypothalamic responses to exercise and temperature.[19] The normal increase in heart rate at the onset of exercise may be absent because of interference with the sympathetic nerve supply (T2-T4) in paraplegic athletes. Compensation by stroke volume is not sustained because of poor venous return. Ventricular afterloading is increased because of interference in the blood supply to active contracting arm muscles, resulting in elevated blood pressure. Thermoregulation is disrupted as well, resulting in vasoconstriction in the cold and vasodilation in the heat.

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Problems Encountered by Disabled Athletes

Problems encountered by disabled athletes are (1) disability related, such as urinary tract infection and impairment of thermoregulation; (2) disability related and aggravated by competition, such as pressure sores; (3) not disability related but competition related, such as shoulder impingement in the transtibial amputee; and (4) incidental. Urinary Tract Infection

Infections of the urethra, bladder, and kidney as a result of urinary stasis are frequent complications for the paraplegic. Attention to intermittent catheterization or frequent monitoring of an indwelling catheter may reduce the frequency of urinary problems. Inadequate hydration and inaccessible bathroom facilities contribute to complications. Positioning in the racing chair may also produce urinary tract problems by contributing to urinary stasis.[19] Preventive measures include adequate hydration and routine catheterization using proper aseptic techniques. Temperature Regulation

Spinal cord injury impairs temperature regulation.[33] The higher the level of spinal cord injury, the greater the impairment of temperature regulation as a result of loss of sympathetic control for heat loss. Spinal cord-injured persons have higher core temperatures in the heat and lower core temperatures in the cold. Loss of the skeletal muscle pump also contributes to the thermal problem, so that there is a reduced ability to tolerate temperature extremes and perform aerobic exercise.[33] Core body temperature is regulated at approximately 37°C. During exercise, muscle activity

527

may increase up to 100%, and about 75% of the energy used is transformed to heat. Hyperthermia.

The risk of hyperthermia and of its consequences is increased in wheelchair athletes who undertake strenuous exercise in hot climates. For able-bodied individuals, the rise in core temperature is independent of the skeletal muscle mass and dependent on the metabolic rate during exercise. During upper body exercise, there is greater dry heat loss from the torso in able-bodied subjects. In spinal cord injury, the impairment of thermoregulation because of loss of autonomic nervous system function reduces the response for a given core temperature; this is coupled with the loss of normal muscle pump activity from paralyzed limbs. As a result, the spinal cord-injured person has a reduced ability to tolerate thermal extremes and to perform aerobic exercise. [33] [34] The heat loss is from local increased sweating from normally innervated areas of the upper torso, arms, and head, but some limited sweating may occur over insensitive areas. The spinal cord-injured athlete must also rely on heat dissipation from the movement of the arms. Dehydration and medication used for bladder dysfunction (oxybutynin, phenoxybenzamine), pain, or depression may also affect thermoregulation and sweating. [3] [4] Signs and symptoms of hyperthermia are noted in Table 14-3 . The management involves removal of clothing, placement in a cool environment, administration of intravenous fluids, and in severe cases admission for circulatory support. Hyperthermia is prevented by minimizing exposure to heat and direct sunlight, training and competing during cooler times of the day, acclimatization to the environment, adequate replacement of fluids (>1 L/hr), wearing of minimal or light clothing, and use of water spray and cooling towels.[28] Fluid intake may have to be forced before thirst is noted ( Table 14-4 ). The more fit the athlete, the less the risk for development of dangerous hyperthermia because training in a cool environment improves physiologic responses during exercise at high ambient temperatures and speeds heat acclimatization.[3] Hypothermia.

Hypothermia may occur after completion of a competition or training session. Once the activity is completed, heat production ceases and shivering may not occur. The skin remains vasodilated and moist, allowing heat loss.[3] Cold, damp, and windy conditions may exacerbate hypothermia, especially in winter sports.[34] The signs and symptoms are listed in Table 14-5 . Hypothermia is prevented by wearing appropriate clothing that is also insulated and acts as a wind barrier, removal of wet clothing, use of insulated blankets, and fluid replacement.

Symptoms Fatigue

TABLE 14-3 -- Signs and Symptoms of Hyperthermia Signs Vomiting

Weakness

Other neurologic impairment

Lightheadedness Core temperature Headache

Inadequate sweating in normal areas

Myalgia

TABLE 14-4 -- Reducing Risk of Hyperthermia Untrained athletes should not exercise in heat. Acclimate to heat by maintaining fluid and electrolyte balance. Monitor rectal temperature. Limit daily training according to environmental conditions ( /das/book/view/29309971/1103/322.html/top

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Wheelchairs

Wheelchairs for amputees may differ from those for spinal cord-injured athletes in axle positioning, but they will otherwise have similar features for the various activities. The wheelchair is mechanically inefficient for locomotion and relatively cumbersome for rapid changes in direction. Mechanical efficiency depends on several factors, including the wheelchair's mass and design, the athlete's mass and propulsion technique, and the nature of the surface for the activity.[27] Design of the sport wheelchair is important to provide maximal efficiency and maneuverability as well as stability and room for use of sporting equipment. Wheelchairs made of titanium alloy or aluminum are being used more often for most activities of daily living and especially for sporting events ( Fig. 14-8 ). Aluminum and titanium are lightweight materials ideally suited for wheelchairs. Titanium is three times stronger than aluminum, however, and allows strong, durable, and lightweight wheelchairs, but it is also more expensive. Titanium also has better fatigue resistance than aluminum. The modulus of elasticity of titanium is lower than that of aluminum, allowing it to absorb and dampen shocks and vibrations. The different sports may require different modifications for the specific event (Fig. 14-9 (Figure Not Available) ). Ball activities require rapid changes in direction, whereas long-distance athletes require light and sturdy chairs. Wheelchair propulsion has been studied to improve the mechanics involved.[35] [36] Wheelchair sprint performance is dependent on the level of disability and training status of the individual and has wide variation. Those wheelchair athletes who can generate greater force in the appropriate direction within a shorter time span have higher levels of sprint power. At higher speeds, a lot of energy is expended by the upper extremity in accelerating to catch up with the hand rim. [22]

530

Figure 14-14-8 Aluminum racing wheelchair. (Courtesy of New Halls Wheels, Cambridge, Mass.)

The width and size of the wheels also affect speed and maneuverability. The camber of the wheels should be set to provide maximal efficiency and stability as well as use for propulsion. The lowest rolling resistance has been noted with tires 28-mm wide, pressures up to 90 psi, and a wheel camber of 12 to 15 degrees. [22] For elite athletes, custom ergonomic designs to fit the individual together with specialized seating and custom wheels allow maximal performance and improved efficiency ( see Figs. 14-8 and 14-10 (Figure Not Available) ). Propulsion of the wheelchair more efficiently has been linked to the athlete's seated position, which should have the upper body leaning forward.[22] Sports for disabled individuals have progressed from an infancy as a form of rehabilitation to a mature competitive activity providing a means of recreation and socializing Figure 14-14-9 (Figure Not Available) Titanium basketball wheelchair. (Courtesy of Ti Sport, Kennewick, Wash.) Figure 14-14-10 (Figure Not Available) Titanium racing chair. (Courtesy of Ti Sport, Kennewick, Wash.)

for individuals who would otherwise be inactive. Greater recognition needs to be given to the potential abilities of those who are not able-bodied. The perseverance of all those involved in organizing and participating in sports activities for disabled individuals needs to be encouraged and rewarded. The elite able-bodied athletes should encourage the disabled athletes to compete on an equal level. Participation in the Paralympics may be the goal of some, but recreational activities for all should be readily accessible and available.

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Firth FY: Seeking misclassification: Doping in disability sport. Br J Sports Med 33:152, 1999.

Halpern BC, Boehm R, Cardone D: The disabled athlete. In Arendt EA (ed): Orthopaedic Knowledge Update: Sports Medicine. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1999, pp 141-154. 19.

Hansen C: Commitment to fair and competitive classification systems in sports for persons with disabilities. In Steadward RD, Nelson ER, Wheeler GD (eds): Vista '93: The Outlook. Edmonton, University of Alberta, Canada, 1994, pp 82-86. 20.

Heath GW, Fentem PH: Physical activity among persons with disabilitiesa public health perspective. Exerc Sport Sci Rev 25:195-234, 1997. 21.

Higgs C: Sport performance: Technical developments. In Steadward RD, Nelson ER, Wheeler GD (eds): Vista '93: The Outlook. Edmonton, University of Alberta, Canada, 1994, pp 169-186. 22.

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Kratz G, Söderback I, Guidetti S, et al: Wheelchair users' experience of non-adapted and adapted clothes during sailing, quad rugby or wheel-walking. Disabil Rehabil 19:26-34, 1997. 25.

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McCann BC: Thermoregulation in spinal cord injury: The challenge of the Atlanta Paralympics. Spinal Cord 34:433-436, 1996. 28.

McCann BC: Sports for the disabled: The evolution from rehabilitation to competitive sport [editorial]. Br J Sports Med 30:279-280, 1996. 29.

Michael JW, Gailey RS, Bowker JH: New developments in recreational prostheses and adaptive devices for the amputee. Clin Orthop 256:64-75, 1990. 30.

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Chapter 15 - Environmental Stress Section A Heat Intolerance M. Alan Hinton MD Illness resulting from a thermal challenge during exercise presents a spectrum of conditions ranging from benign to fatal. Heat syncope, heat cramps, heat exhaustion, and heat stroke are manifestations of the body's inability to respond to an increased thermal load. Heat stroke and heat exhaustion are the most significant of the heat-related illnesses. This chapter reviews thermoregulatory physiology, recognition of heat intolerance disorders, and treatment of these conditions with an emphasis on prevention. During exercise, an athlete is surrounded by his or her own microclimate. Endogenous heat is produced by muscle work. The amount of heat produced is proportional to the intensity and duration of the exercise. The body's ability to handle this thermal load requires elaborate endocrine, exocrine, circulatory, and neurologic regulatory mechanisms.[7] [13] [54] [56] [77] [81] [93] [106] [114] Heat intolerance problems are associated with a wide variety of athletic activities.[1] [4] [9] [50] [102] [103] [105] [113] [115] Endurance races (10K, marathon, triathlon), preseason football, preseason soccer, sport camps, and other activities in hot weather are potential sites of exercise-induced heat intolerance disorders. The number of endurance athletes who participate in distance runs, marathons, and triathlons has increased significantly. It is estimated that thousands of heat-related illnesses occur each year in the United States

alone. The true incidence of heat intolerance problems in athletes is unknown. Complications from these conditions usually are unreported. From 1955 to 1980, there were 84 reported deaths in high school athletes participating in football in the United States.[2] Many deaths that are reported as cardiac in origin may be secondary to heat stroke, with cardiovascular collapse being the end stage of this circumstance. Basic Thermoregulatory Physiology

The major factors involved in heat intolerance problems are endogenous heat production and the effect of the athlete's environment in terms of temperature and humidity. Thermohomeostasis, the body's complex response to its heat production and the external environment, creates a balanced system in which the heat produced is equal to the heat lost. Humans maintain a constant body temperature despite wide variations in the environmental temperature. Core body temperature (36°C to 37°C [96.8°F to 99.5°F]) is maintained by behavioral and physiologic mechanisms to balance heat gain and heat loss. Exercise in a hot environment magnifies the body's ordinary physiologic response to work.* These responses include increases in body core (absolute central) temperature and skin (surface) temperature, metabolic heat production, pulse rate, blood pressure, and sweat rate. Sweat rate is proportional to the metabolic rate, which is proportional to the level of exertion and the attendant environmental temperature.[1] [20] [33] 41 [76] Resting heat production is the result of thyroid homeothermogenesis (i.e., the metabolic response to circulating thyroid hormones) and the action of adenosine triphosphate (ATP) on the sodium pump of cell membranes. Heat production under resting conditions is 1 kcal/kg/hour or 1700 kcal/day for the average man and 1500 kcal/day for the average woman.[61] Of the chemical energy involved in muscle contraction, 75% to 80% is changed to heat, which then is dispersed to the body through the bloodstream.[1] [8] [21] [74] During vigorous exercise, large muscle mass activity increases the normal resting metabolic demands (which usually are minimal) by factors of 8 to 10.[56] Moderate physical activity increases heat production to 2500 to 3000 kcal/day, whereas heavy activity may increase heat production to 6000 kcal/day.[61] Thermal-sensitive neurons are present in the skin and in the preoptic anterior hypothalamus. The body is 10 times more sensitive to changes in core body temperature than skin temperature. This sensitivity allows the body to accommodate over a wide range of environmental temperatures. Thermal-sensitive neurons relate signals to a central integrative area in the hypothalamus, which directs thermoregulatory effectors to conserve or dissipate heat. The posterior hypothalamus is responsible for heat maintenance, and the anterior hypothalamus functions to dissipate heat. The preoptic area of the hypothalamus functions as a thermostat, regulating the activity of the anterior and posterior hypothalamus.[2] Thermoregulatory effectors function by two mechanisms: the physiologic response and the behavioral response. Physiologic responses include vasomotor alterations in blood flow and its distribution, shivering, and sweating. In the maintenance of temperature, the

physiologic response is more important during heat challenge, whereas the behavioral response is more important during cold challenge. In a cold challenge, the behavioral response is to seek clothing, shelter, and warmth; in a heat challenge, the behavioral response is to seek shelter and cooling. This is one potential explanation as to why the lack of behavioral modification in athletes can lead to serious heat intolerance *See references

[ 1] [ 10] [ 12] [ 27] [ 28] [ 32] [ 38] [ 56] [ 60] [ 70] [ 78] [ 81] [ 93]

and [ 112] .

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problems when mechanisms to prevent difficulties (e.g., shade, shelter, fluids) are present.[61] Heat production is proportional to body weight. Heat loss is proportional to body surface area. For each 1°F rise in core temperature, metabolic demands for oxygen consumption increase 6% to 7% of normal. Metabolic heat production is proportional to the intensity of exercise and the function of exercise efficiency. Marked differences occur between an experienced athlete with efficient motion and a clumsy novice.[29] To prevent excessive rise in body core temperature, the body may dissipate heat by four methods: (1) conduction, (2) convection, (3) radiation, and (4) evaporation. The physiologic reaction to heat stress is by two mechanisms: increased skin blood flow and increased sweating. The increased skin blood flow raises skin temperature and carries heat from the body core to the skin surface. Heat losses by radiation, conduction, and convection constitute only 20% to 30% of the total heat loss from the body. Evaporation is the primary source of heat dissipation. Humans possess two types of sweat glands. The eccrine glands are distributed over the body with greater density in the palms, soles, and scalp. These glands have a cholinergic nerve supply and produce dilute, colorless, and odor less sweat. The apocrine glands develop from hair follicles and are concentrated in the axilla, around nipples, on the labia majora, and on the mons pubis. These glands are stimulated by adrenaline in the bloodstream. Eccrine secretions contribute to most sweat production secondary to thermal sweating and mental (emotional) states. For the normal 70-kg man, sweat production is approximately 1 L/hour of exercise, but it may be 2 L/hour of exercise. One liter of sweat evaporation on the skin leads to loss of 580 kcal of heat from the body. For a 70-kg man, every 100 mm of sweat evaporated decreases mean core body temperature by 1°C. [16] [20] [33] 41 [76] [106] Significant differences exist between children and adults and the ability to handle a thermal load during exercise.[5] [12] [13] [14] [15] Children have increased body surface area to body mass and are slower to become acclimatized to a heat challenge. Children have a higher threshold for sweating and decreased sweat production. In children, the amount of electrolytes lost during sweating is less than lost in adults. Children's sweat is more hypotonic than that of adults. Adults have a lower density of sweat glands than children; however, adults' sweat glands produce 2.5 times as much sweat as children. Children

develop adult-type sweat glands at puberty. Girls have a 10% to 12% higher body surface area-to-mass ratio than boys and have higher amounts of heat loss in response to mild heat stress. In general, boys and girls are equal in response to heat challenges at rest. Boys have higher sweating rates than girls. Because girls have a higher surface area-to-mass ratio, their metabolic rate of heat production is diminished. Adult male and female responses to thermal stress seem to relate more to fitness level and body size than to sex. If cardiovascular fitness level, body size, and acclimation state are standardized, no difference is seen in response to thermal stress. Women have a lower sweat rate than men of equal fitness, size, and acclimation, which is disadvantageous in hot and dry climates, but advantageous in hot and wet climates. Menstrual cycle effects are minimal. Studies correlating male and female differences in response to thermal stress show that aerobic capacity, surface area-to-mass ratio, and state of acclimation are far more important than sex in determining physiologic response to heat stress.[21] [22] [51] [62] [81] With heavy exercise, muscle demands are increased and require increased cardiac output. The muscle, visceral, and skin vascular beds are in complex competition to maintain blood pressure and meet demands to support muscle metabolism and thermal regulation. Muscle blood flow tends to be unchanged with changes in temperature. By contrast, skin blood flow is changed significantly by thermal stress,[60] [76] [77] a reflection of the increase in heart rate and, if blood volume is adequate, increased circulating volume. Traditionally, it has been thought that splanchnic bed vasoconstriction causes a diminution in renal and visceral blood flow. This diminution maintains blood pressure and shunts blood to extremities and skin to provide enough oxygen and nutrients for muscle work and vascular supply for sweat production and heat dissipation.[31] [32] [35] 41 [60]

Heat intolerance problems reflect the body's inability to handle a heat load, producing subsequent cumulative deficits that affect heat transport, sweat production, and failure of temperature regulatory mechanisms. Without volume replenishment, decreased circulatory volume results secondary to fluid loss, sweat production, and blood shunting. To maintain circulatory pressures, sweat production diminishes; this leads to a vicious cycle of increased heat production and inability to dissipate heat. The vascular shunting may be a source of renal, hepatic, and other organ failures that occur in heat stroke. [63] [64] [82] [84] With progressive cardiovascular decomposition owing to hypovolemia, cardiovascular failure occurs with a variety of the collapsed states seen in heat intolerance problems. There are large individual variances in tolerance to an ambient or exercise heat challenge. Individuals at risk include the very young, elderly, unacclimatized, fatigued, obese, unfit, and individuals with a prior history of heat illness. Conditions affecting skin and sweating predispose to heat illness. Skin diseases such as miliaria and burns (sunburns included) are well-recognized risk factors. Arteriosclerotic cardiovascular disease and diabetes mellitus both cause diminution in skin blood flow. A variety of drugs (recreational, over-the-counter, and prescription) may have a negative

precipitating effect in heat-related illness. [26] [44] [66] Medications that compromise the body's thermal response include diuretics, phenothiazines, antihistamines, calcium channel blockers, antidepressants, antiseizure medications, anti-Parkinson medications, caffeine, ethanol, and -blockers. Infections and chronic diseases may contribute to heat intolerance difficulties. Participants in the midst of febrile illness are at risk for heat intolerance problems. It is vital to recognize the athlete who is predisposed to inadequate response to a heat challenge during exercise.[4] [26] [27] [40] [42] [66] [75] These heat intolerance problems constitute a continuum of physiologic inability of the body to respond to heat challenge of exercise in a hostile thermal environment. Heat intolerance problems are seen in athletes in circumstances of intense exercise carried out within rigid systems, either self-imposed or enforced by coaches or peers. Without

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such pressures, most athletes exhibit behavioral modifications to augment the physiologic responses to heat challenge. Behavioral responses include increasing fluid intake, clothing modifications, seeking shade, and going indoors for air conditioning. Only athletes who attempt to continue despite warning signs later develop significant heat intolerance sequelae.

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Environmental Effects

The ambient heat stress imposed on an individual is an integrated function of air temperature, relative humidity, air movement, and solar radiation. [101] The most widely used heat stress index is the wet bulb globe temperature index (WBGT): WBGT = 0.1(Tdb) + 0.2(Tg) + 0.7(Twb) Tdb refers to air temperature measured with a standard dry bulb thermometer not in direct sunlight. Tg is the black globe temperature, and Twb is the wet bulb temperature.[39] [73] Twb is measured with a water-saturated cloth wick over a dry bulb thermometer (not immersed in water). Tg is measured by inserting a dry bulb thermometer into a standard black metal globe (e.g., a toilet tank float painted black). Twb and Tg are measured in direct sunlight. A portable monitor that gives the WBGT index in degrees Celsius or degrees Fahrenheit has proved useful during races and military training.[39] [59] [104] [116] As evidenced by the WBGT index, the measurement of air temperature alone is inadequate. The importance of humidity in total heat stress can be appreciated readily because the Tdb accounts for only 10% of the index, and the Twb accounts for 70%. A Twb reading compared with a Tdb reading yields a measure of relative humidity when each is exposed to a constant rate of air movement. An increase in Twb thermometer value equals no evaporation secondary to atmosphere conditions that produce a high skin residual water vapor. The use of Twb is especially important with individuals who are exercising in heat and humidity. With a relative humidity of 60% or greater, sweat is not evaporated unless there is significant air movement. There is a thermodynamic similarity between a wet bulb thermometer and a man wetted with sweat.[49] The Tg measures radiant heat. Solar radiation may account for 150 kcal/hour of heat gain. Such a radiant source is augmented if the athlete is exposed to a heat sink, such as artificial turf, whose surfaces can be measured at 105°F to 110°F. A WBGT less than 65°F (18°C) indicates a low risk for heat illness; 65°F to 73°F (18°C to 23°C), a moderate risk;

and 74°F to 82°F (23°C to 28°C), a high risk. The general temperature, humidity, and wind speed reported for a general area by the local weather service reflects broad guidelines and may be highly inaccurate for specific exercise locales. Measurement of specific environmental factors should be done at the exercise site so that appropriate assessment of exercise risks in a potential hazardous thermal setting may be made ( Fig. 15A-1 ). Site-specific conditions, such as temperature, humidity, wind

Figure 15-A-1 Assessment of exercise risk in potentially dangerous thermal environments.

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speed, and radiant heat (highly affected by the surface [e.g., color, synthetic versus natural turf]), should be measured. Modification of exercise intensity and duration as well as changes in clothing and equipment may need to be made to eliminate the risk of heat illness.[3]

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Thermal Acclimatization

Acclimatization is a constellation of physiologic adaptations that appear in normal persons as a result of repeated exposure to heat stress.[117] Acclimatization usually requires 7 to 14 days of graduated exposure to increased environmental temperature and humidity. Physiologically, acclimatization to this type of thermal challenge for a given exercise load is shown by earlier onset of sweating at a decreased core and skin temperature, increased sweating rate, decreased electrolytes present within the sweat, decreased pulse rate, and increased ability (in amount of time) to withstand head stress.[16] [21] [37] [44] [48] [86] [99] [112] The cardiovascular system plays a major role in acclimatization and endurance training. Blood volume expands by 10% to 20%.[6] The exact mechanism producing this hypervolemia is unknown and may be related to exogenous thermal stress, associated endurance training, or a combination of both. [32] [37] [43] [99] Heart rate becomes lower and is associated with a higher stroke volume, although no change generally is seen in cardiac output. Other changes include an increase in the level of aldosterone, a fall in total body potassium levels secondary to loss in sweat and urine, and an increase in growth hormone release. Ultimately the acclimated person, subjected to heat stress, exhibits a lower rise in rectal temperature for a given workload, decreased oxygen utilization, and increased maximal oxygen consumption during exercise.[96] All of these measures are designed to improve the body's response to the increased environmental thermal stress. Most athletes are unable to spend time adjusting to the heat challenge, and many challenges occur unpredictably. Although most athletes at the high school and college level are not able to become acclimated to the hot conditions that often exist in late summer preseason practices, acclimatization methods should be kept in mind. If possible, exercise in progressively increasingly hotter circumstances over increasingly longer time periods should be done as part of conditioning programs. Optimization of acclimatization is achieved best by training in an environment

comparable with the one in which the competition will occur. Trained, unacclimatized runners are acclimatized more easily or adapted to heat stress than runners who are untrained. Endurance-trained, acclimatized athletes undergo less cardiovascular strain because of their improved sweat mechanism, which requires diminished peripheral blood flow resistance compared with athletes who are untrained.

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Prevention of Heat Illness

There has been a heightened awareness of exercise-related illness in the athletic population. Despite this awareness, vigilance must be continued to apply preventive measures, identify individuals at risk, and identify heat illness early to initiate treatment. Heat intolerance problems may develop in athletes regardless of training.[40] Assessment of thermal risk existing during exercise must be done by coaching staff and race and tournament officials using guidelines such as the WBGT index. Hydration is crucial to preventing heat illness. The competitive nature of sports and the feeling of invulnerability among athletes must be balanced by the realization that body fluid loss does occur and must be made up in routine and excessive thermal environments.* Hydration needs to be started early in practice and continued throughout the practice or athletic event. Fully acclimated athletes have higher fluid requirements because of enhanced sweating response. [46] [107] An athlete who has sustained cumulative fluid loss for any reason is at significant risk for heat intolerance problems. A loss of greater than 2% to 3% of body fluid from sweating causes an increase in core temperature proportional to the amount of dehydration. Greater than 5% body weight sweat loss causes a marked risk of heat intolerance disorders. Athletes with more than 7% body weight sweat loss are susceptible to potential fatal heat stroke because of cumulative effects of this hypohydration.[14] [31] [34] 41 [54] [75] [93] [115] To counteract the risk of cumulative hypohydration, athletes who engage in successive daily exercise should be weighed nude before and after each practice session. Athletes with body weight loss of more than 2% to 3% per practice should be reminded to drink extra fluids and be permitted to compete within 1 to 2 pounds of the starting weight of the previous day. A weight loss of 5% to 6% represents a mildly severe deficit, and these athletes should be restricted to light workouts after hydration to the normal weight. A loss of 7% or more of body weight represents severe water depletion. These athletes

should not participate in sports and should be examined by a physician.[108] Thirst is an inadequate mechanism for the drive to replace lost fluid. Usually only 50% of the body fluid lost is made up in response to thirst during exercise. Fluid intake must be encouraged between sessions and during sessions to prevent hypohydration. The goal of fluid rehydration is to maximize voluntary intake and gastric emptying so that fluid may enter the small intestine rapidly, where it may be absorbed into the body. Large volumes (500 to 600 mL) and cool temperatures (10°C to 16°C [50°F to 60°F]) accelerate gastric emptying.[88] The primary source of fluid replacement should be water. Commercially available exercise electrolyte replacement drinks may have an excessive amount of glucose and may be hyperosmolar. It has been shown, however, that persons in heat stress conditions provided with cool flavored water consume significantly more fluid than persons given tap water.[54] For practical purposes, cold, flavored water or commercial electrolyte solutions diluted with tap water to one-half to one-third strength provide adequate replacement.[69] [98] No adverse effects have been reported on the use of cool drinks before, during, or after exercise. *See references

[ 31] [ 32] [ 34] 41 [ 47] [ 52] [ 53] [ 56] [ 75] [ 78] [ 93]

and [ 115] .

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The well-conditioned athlete has a more effective sweat mechanism and produces more sweat in response to environmental challenge than athletes in poor physical condition.[11] [29] [43] [66] [99] [100] [114] Poor general conditioning results in inefficient muscle use with a rapid rise in core temperature secondary to excessive muscle activity. Because of poor physical conditioning, workload is less well tolerated. Obesity causes a greater rise in core temperature for a given level of hypohydration and reduced tolerance for prolonged exercise. The group of athletes most commonly afflicted with fatal heat stroke are obese high school football middle linemen.[11] Athletes who have had fluid losses because of gastrointestinal disorders with vomiting and diarrhea are at risk for heat intolerance problems because of their relative state of hypohydration. Such athletes should not be involved in vigorous exercise until normal body weight has been restored. Athletes with chronic disease that may affect oxygen transport (anemia) or sweating (cystic fibrosis) also are at risk for heat-induced disorders. Athletes with a previous history of heat intolerance disorders need to be observed carefully. These athletes tend to be at higher risk for recurrence of these disorders than athletes who have no such history. [66] A variety of drugs (recreational, over-the-counter, and prescription) may have a negative effect on athletic performance in heat.[26] [44] [66] Drugs that can compromise the body's thermal response include diuretics, phenothiazine, antihistamines, calcium channel blockers, antidepressants, antiseizure medication, anti-Parkinson medications, caffeine, ethanol, and soft drinks (that contain caffeine). Appropriate equipment must be chosen to allow maximal surface area exposure for heat

dissipation.[11] [42] [75] Because 50% of heat occurs through the hypervascular scalp and neck area, protective headgear should be worn only at time of direct contact.[27] [42] During the remainder of the time in practice, helmets should be removed to allow body cooling to occur. Practices in sports requiring protective armor, such as football and lacrosse, should be done in shorts and shirts without pads until reasonable acclimatization has occurred. Then periods requiring full equipment contact should be relatively short (25 to 30 minutes) and scheduled for a time of day when thermal challenge is least expected. Light-colored clothing reflects rather than absorbs light. Mesh cutoff jerseys with short sleeves should be worn to increase the amount of surface area exposed for thermal challenge.[94] When clothing inhibits air convection and evaporation, 70% of evaporative cooling may be lost. Sweat must be allowed to evaporate. Sweat that is wiped off or drips away from the body does not allow significant heat lost to occur.[65] The use of salt tablets and salt replacement should not be encouraged. Salt tablet administration decreases gastric emptying time and results in osmotic fluid shifts in the gut and hypernatremic dehydration. Aldosterone is increased with exercise, and sodium is conserved naturally by both kidneys and sweat glands. Excessively high salt intake in relation to salt losses during initial heat exposure may impair acclimatization because of inhibition of aldosterone secretion.[36] Salt is not required in the form of salt tablets because sweat is hypotonic, and sweat loss is primarily water and not electrolyte. The average diet of high school and college students is rich in salt (on the average of 10 to 12 g of sodium per day). It has been shown that the average intake of 6 g of salt a day is sufficient for individuals laboring in the heat, sweating 7 L/day.[30] If dehydration has occurred, it cannot be corrected during exercise. When hypohydration or dehydration has occurred, ingested fluid is excreted as urine, not as sweat.[1] [31] [32] Dehydration decreases total plasma volume, diminishes stroke volume, increases heart rate, and diminishes cardiac output with decreased glomerular infiltration and decreased renal and skin blood flow. Liver glycogen becomes depleted, electrolytes are lost, and muscle strength and endurance are reduced. Mental activity falls, and compromised thermoregulatory mechanisms may result. When hypohydration or dehydration has been identified, the athlete must be removed from the field of competition, beplaced in a cooling environment, be assessed as to the presence of heat illness, and begin fluid rehydration. Dehydration may be minimized by education on exercise-rest cycles and fluid consumption and through provision of cool, pleasantly flavored fluids.[54]

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Heat Intolerance Illness

Heat-induced illnesses include heat cramps, heat syncope, heat exhaustion, and heat stroke. These heat-related illnesses most commonly occur in unacclimated individuals ( Table 15A-1 ). [110] [111] Heat syncope occurs in individuals who are exercising in a hot environment. Peripheral vasodilation and pooling of blood results in decreased cardiac output and stroke volume, producing a transient loss of consciousness. The affected individual quickly regains consciousness when supine. The body temperature is normal. Treatment consists of rest in a cool environment and a gradual resumption of activity. Fluids usually are not required unless a hypohydrated state has been present before the onset of syncope.[65] Elderly individuals are more prone to heat syncope, and a fall may result in serious injury. Heat cramps are painful contractions in large muscle groups, usually in the thigh and buttocks.[1] [28] [33] [53] [56] [70] [78] [105] Because the cramp affects only a few muscle bundles at a time, then moves throughout the muscle, it appears to wander within that large muscle group. These cramps traditionally are thought to be due to decreased hydration as well as a diminution in serum sodium and chloride. A report suggests that the muscle cramps occur when fatigue leads to abnormalities in the mechanisms that control muscle contraction. In short, the theory suggests that cramps occur because Golgi tendon organ units, which normally inhibit the muscle stretch-contraction reflex arc, show decreased activity in fatigued, untrained muscles. This decreased Golgi tendon organ unit activity leads to perpetuation of the reflex arc and continued muscle contraction ( Fig. 15A-2 ). [91] [92] Mainstays of treatment for muscle cramps include passive muscle stretching and fluid and electrolyte replacement. Fluid and electrolyte replacement may consist of 1 to 1.5 L of normal saline solution or ingestion of 1 L of 1% sodium chloride solution. This solution

may be made

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Heat Illness Heat syncope

Heat cramps

TABLE 15-A-1 -- Forms of Heat Illness Prevention Clinical Findings Avoid standing inactivity after vigorous exercise

Normal temperature

Recumbent position with legs elevated

Transient fainting episode

Oral hydration if previously underhydrated

Ensure acclimatization

Normal temperature

Stop exercise

Ensure adequate hydration

Painful contraction of large muscle groups (gastrocnemius, soleus, hamstrings)

Passive stretching of painful muscles

Ensure appropriate conditioning Heat exhaustion

Treatment

See under Heat cramps

Eliminate water and salt deficits Temperature elevated but 104°F)

Emergent condition

Syncope

Remove from thermal environment

Coma

Monitor core temperature (rectal)

Shock

Cooling bath or evaporative fanning

Multisystem failure

IV hydration

Dry, flushed skin (usually but Treat specific organ not necessarily) system compromise IV, intravenous.

Figure 15-A-2 A hypothesis states that muscle cramps occur when fatigue leads to abnormalities in the mechanisms that control muscle contraction. Muscle spindles react to stretch by producing afferent signals, which trigger the motor neurons that cause the muscle to contract; Golgi tendon organs inhibit contraction in response to muscle tension. A, A simplified view. B, During a normal contraction, excitatory and inhibitory signals are in balance. C, In a fatigued muscle, spindle activity increases, and Golgi tendon organ activity decreases, resulting in increased muscle membrane excitability, which can lead to a cramp. Contraction of the muscle in its shortest position (inner range) also inhibits Golgi afferent activity. (From Schwellnus M: Skeletal muscle cramps during exercise. Physician Sportsmed 27:109-115, 1999. )

easily by dissolving two 10-gr sodium chloride tablets in 1 L of water. The intravenous route of fluid administration results in more rapid resolution of symptoms. Oral ingestion of salty solution usually is not palatable, and athletes commonly refuse to ingest the amount necessary to restore normal balance. The best way to prevent such cramps is to ensure adequate hydration before the onset of exercise, conditioning before activity, and stretching of muscle groups prone to cramping. [117] Heat exhaustion is a more severe form of heat intolerance than either heat syncope or heat cramps and is the most common form of heat intolerance in athletes. Heat exhaustion represents an ill-defined spectrum of signs and symptoms, including weakness, dizziness, headache, nausea,

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vomiting, malaise, myalgias, syncope, goose flesh (goose bumps), hypertension, tachycardia, muscle cramps, and hyperventilation.[55] [56] [57] Sweating usually persists and may be profuse. The boundary between heat exhaustion and heat stroke is ill-defined; usually the absence of signs and symptoms of severe central nervous system damage and core temperature of less than 39°C (102°F) differentiates between the two.[58] Temperature is ascertained best by rectal, esophageal, or tympanic membrane probes. Heat exhaustion has been described as hypernatremic (primary water loss) and hyponatremic (primary sodium loss).[67] The hypernatremic form results from inadequate water replacement by persons exposed to heat stress and is seen commonly in military

recruits, laborers, or individuals without access to free water. The hyponatremic form of heat exhaustion results from excessive thermal sweating and pure water replacement.[67] [72] Pure forms of either type of heat exhaustion are rare, and most cases have a mixed salt and water depletion presentation. The hypernatremic (primary water loss) type of heat exhaustion is manifested by thirst and oliguria and presents as lethargy, confusion, nausea, vomiting, and fatigue. [10] [28] [32] [35] [54] [56] [70] [78] [114] The hyponatremic (primary sodium loss) type is not characterized by thirst or relieved by water ingestion alone.[27] [34] [35] It is important to institute treatment for heat exhaustion because continued participation in a hostile thermal environment could lead to heat stroke. Heat exhaustion should not be considered merely as poor conditioning or excessive fatigue during or after a workout. Treatment of heat exhaustion consists of resting the athlete in a cool environment away from direct sunlight and removal of restrictive clothing. Active cooling with ice water immersion, fans, moistening skin, or placement of ice bags in the groin and axilla may be used to lower core temperature. Fluid replacement should be begun immediately and continued until a normal body weight is obtained and polyuria begins. Oral or intravenous methods may be used for fluid replacement, depending on the situation. The most important oral fluid should be water. Controversy exists about whether the addition of glucose helps or hurts.[71] [85] The addition of glucose may be of value if accumulated muscle and liver glycogen depletion has occurred. Such depletion often is noted after the third or fourth day of intense workouts twice a day. A balanced salt intravenous fluid is most appropriate if the victim is vomiting. Intravenous fluids facilitate the most rapid recovery.[55] [79] [80] There is no universal agreement on the ideal fluid to be given intravenously for heat exhaustion therapy. The choice of fluid may be based on clinical findings (i.e., blood pressure, orthostatics, urinary output, and laboratory findings [blood urea nitrogen and hematocrit]). Heat stroke is a catastrophic medical emergency that results from failure of the thermoregulatory mechanisms of the body. Core body temperature elevation exceeds 39°C (102°F) and may reach 41°C (106°F).[1] [7] [11] [27] [35] [50] [54] [56] [66] This condition has a 50% to 70% fatality rate, with 80% of fatalities being due to circulatory collapse. Excessive prolonged vigorous exercise raises body core temperature to 39°C (102°F) or greater. Adequate compensatory mechanisms may not be available in a hostile thermal environment, and heat stroke ensues. The exact temperature that results in tissue damage is difficult to assess. Core body temperature of 45.5°C (114°F) has been measured in some patients who achieve full recovery.[97] The cause of heat stroke is the accumulation of body heat leading to temperatures incompatible with life. Tissue damage appears as a function of temperature and length of exposure time. [23] Extremes of temperature impair coordination of physiologic processes, denature enzymes, liquefy membrane lipids, damage mitochondria, affect coding of proteins, and affect the stability of lipoproteins. [95] Damage on the cellular level results in multiorgan system failure. The classic presentation of heat stroke is hyperthermia (>41°C [104°F]), central nervous system dysfunction, and cessation of sweating with hot dry skin. Not all criteria need to be present for the diagnosis, however. Temperature is ascertained best by rectal, esophageal, or tympanic membrane probes. Oral and axillary temperatures are

inadequate measures of core temperature. Heat stroke patients usually have profound central nervous system disturbances (deliria, seizures, and coma). Early in presentation, headache, mental breakdown, and confusion only may be present. Cessation of sweating may present late in the clinical picture, and many patients may sweat profusely with very increased body core temperature.[45] [87] In addition to the central nervous system failure, other organ systems are affected. Tachycardia usually is present, with hypotension and cardiovascular collapse late in presentation. Coagulopathy may be present and noted clinically by conjunctival hemorrhages, purpura, melena, hemoptysis, hematuria, and central nervous system hemorrhage.[68] Pulmonary edema often is severe, and hemoptysis may be present as a result of coagulopathy. Acute renal failure secondary to acute tubular necrosis is present 20% to 30% of the time. Acute renal failure is due to direct tubal injury from heat, myoglobin precipitation in the tubules, and tubular damage from diminished renal blood flow.[63] Rhabdomyolysis is common as a result of muscle contraction and rigidity. Gastrointestinal manifestations include nausea, vomiting, and diarrhea. Liver involvement usually is associated with central lobular necrosis and cholestasis.[64] Treatment of heat stroke should begin immediately; rapid reduction in body core temperature is the first priority. Morbidity and mortality are related directly to the duration and severity of the hyperthermia.[67] Cooling the patient should begin immediately by removal from the environment, fanning, and removal of clothing and equipment. When in the hospital, a rectal temperature probe should be inserted and monitored. Often, temperature is decreased because of cooling efforts in the field. [24] The most accurate temperature on which to base diagnosis and treatment may be the temperature recorded on site by the paramedics. Controversy exists as to the most effective method for rapid lowering of body temperature. Ice water immersion is effective for rapidly lowering body core temperature.[17] [35] [83] Evaporative cooling also is an effective method. The practice involves exposing and suspending the patient on netting with warm air blowing over the body, keeping the body moist with atomized water spray. [18] [19] One gram of water evaporating dissipates seven times as much heat as melting 1 g of ice.[109] The advantages of evaporative cooling methods are that it does not require water or ice, and it

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avoids vasoconstriction and the counterproductive shivering that may occur with ice water immersion. Cooling measures should be discontinued to avoid hypothermic overshoot when the rectal temperature reaches 39°C (102°F). All heat stroke patients require the emergency department physician to follow the ABCs (airway, breathing, circulation) for stabilization. Airway management may be indicated if the patient is comatose or the airway is compromised. In addition to rectal temperature monitoring, a catheter should be inserted to monitor urinary output. For patients with cardiovascular collapse, hemodynamic monitoring with a pulmonary catheter may be

indicated.[89] Intravenous access should be obtained immediately; however, the fluid requirements are variable. Hypotension is common, usually the result of peripheral vasodilation causing high-output cardiac failure, rather than dehydration. Blood pressure may rise with cooling and peripheral vasoconstriction. Fluid replacement begins with a challenge of 200 to 400 mL of normal saline or lactated Ringer's solution and continues until blood pressure reaches 90/60 mm Hg or central venous pressure exceeds 12 mL of water. Medications should be used cautiously with heat stroke patients. Mannitol and furosemide may be used to increase renal blood flow to prevent acute renal failure from myoglobinuria. Diazepam may be given to control shivering in the cooling bath. Anticholinergics should be avoided because they inhibit sweating. -Adrenergic drugs, such as norepinephrine, should not be used to support pressure because they promote vasoconstriction, resulting in decreased heat exchange.[27] Antipyretics, such as aspirin and acetaminophen, are not indicated and may be harmful. Salicylates may worsen hyperthermia and aggravate bleeding tendencies if disseminated intravascular coagulation is present. Acetaminophen may result in increased hepatic damage.[90]

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Summary Exercise in normothermic conditions is stressful to the body's homeostatic mechanisms. When the challenge of an increased thermal load is superimposed, many athletes cannot cope. Compromise of the thermoregulator mechanism may manifest in a variety of ways, reflecting a spectrum of involvement from rapidly resolving and benign to catastrophic fatal collapse. Responsibility for prevention of heat illness lies with the athlete, coaches, activity directors, and others because the circumstances in which these conditions occur usually are predictable. Appropriate modification of these circumstances benefits all concerned, with the athlete's welfare as the major goal.

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Section B Cold Injury Edward G. Hixson MD Cold injury historically has been most significant in the military. Many armies have suffered more casualties from cold than enemy fire. In 218 BC, Hannibal lost 20,000 of 46,000 men crossing the Alps.[1] Napoleon invaded Russia with 385,000 troops and returned with 3000; there were 250,000 deaths from cold injury.[41] Cold injury accounted for 10% of U.S. casualties in World War II and the Korean War (90,000 in World War II, 9000 in the Korean War). More than 7.5 million U.S. troop days were lost in World War II.[11] The German and especially Russian losses were much greater in World War II. Much of the available information on cold injury comes from the military. The effect of cold on athletic activity is less dramatic. For athletic events in a controlled environment (e.g., swimming or basketball), there is no effect. Athletic activities performed in cold weather are affected, particularly endurance events requiring submaximal exercise for long durations (e.g., cross-country skiing, biathlon). Endurance events now are more frequent in wilderness environments (e.g., marathons, ultramarathons, iron man, triathlon, speed hikes, survival of the fittest). Cold injury is not only more likely, but also the risk is greater. Most peacetime cold injury casualties are seen in wilderness sports (e.g., mountaineering, ski touring, backpacking, trekking, snowmobiling, hunting). Physiology of Cold Injury

Humans evolved in the tropics. Humans can survive in a cold environment only by increased heat production and decreased heat loss achieved by insulation. When thus protected, humans can tolerate extremes of ambient temperature from 50°C to 100°C (58°F to 212°F). Core temperature may vary only through a range of 4°C without impairment of function. Core temperature is the temperature of the internal organs, especially the heart, lungs, and brain, in contrast to surface temperature, which is skin

temperature. Core temperature is relatively constant at 99°F. Skin temperature fluctuates greatly. The living cell can tolerate extremes from 1°C to 45°C (31°F to 113°F) without cell death. The temperature range from 28°C to 34°C (82°F to 93°F) is the thermoneutral zone. If ambient temperatures are in this range, the nude human body does not cool and can dissipate metabolic heat easily. Heat Production

Humans must maintain their core temperature (37.6°C [99.6°F]) within a narrow range (4°C [about 12°F]). The body is able to maintain a core temperature only by constant

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heat production. Under basal conditions of rest, about 1 kcal/kg/hour is produced by the body's metabolic activity. Maximal exercise may increase this by roughly a factor of 10. The body is about 25% efficientit uses about 25% of its energy for work, 75% being released as heat. The source of the energy is foodcarbohydrate, fat, and protein. Carbohydrates produce about 4 kcal/g, protein produces slightly less, and fats produce 9 kcal/g. The average individual requires roughly 2400 kcal daily for nonstrenuous activity. Many athletes require a significantly higher caloric intake to sustain increased muscle activity, 6600 to 10,000 kcal daily. The military recommends 4000 kcal daily for troops training in a cold environment.[39] High-carbohydrate diets generally are preferred for athletes, with carbohydrate accounting for 60%, protein for 15%, and fats for 25% of calories. Heat Loss

Heat production must be balanced by heat loss. The body loses most of its heat through the skin (approximately 90%). This loss is variable by a factor of about 100 from maximum vasodilation to vasoconstriction. Blood flow to the skin is controlled involuntarily. Areas of high blood flow, such as the head and neck, lose heat fastest: The old climbers' dictum states, When your feet are cold, put your hat on. Another area of significant heat loss is the lungs. This loss is variable and is under voluntary and involuntary control; respiratory rate changes dramatically with the level of exercise, response to altitude, and other factors. The body loses heat in four ways: (1) conduction, (2) convection, (3) evaporation, and (4) radiation ( Fig. 15B-1 ). Conduction is direct loss from contact. Because air conducts heat poorly, trapping layers of warm air next to the body is the basic principle of insulation. Contact with water, rock, steel, and other solids that conduct heat better increase conduction losses. Sleeping on the ground is accompanied by increased conduction losses, emphasizing the need for more insulation under the sleeper. Increased conduction losses are most dramatic when the body is wet. Immersion in water increases the rate of cooling 100 times faster than air at the same temperature. [28] As water temperature decreases, cooling increases in a linear fashion.[14] The wet athlete is at great risk, especially if he or she has been immersed accidentally in cold

water, such as in a sailing accident, or his or her own sweat, such as a marathon skier or runner. Convection loss is caused by the motion of air or water across the body surface. Heat is removed relative to the velocity of the air or water. Wind chill is a means of expressing increased heat loss by wind on the human body. Wind chill is expressed most often as the equivalent temperature in motionless air.[35] The rate of heat loss varies directly with the difference in temperature between the body and the air.[42] Heat loss varies directly with the square of the velocity of the wind. Doubling the velocity increases heat loss fourfold. At high wind speeds, the loss is not this great, however, because there is not enough contact time to warm the air. Evaporation is the body's major means of controlling heat loss. Whether through perspiration or external wetting, when water evaporates, heat is absorbed. One gram of water converted to vapor absorbs about 500 calories (heat of vaporization) in addition to increased conduction losses from wetting. Roughly one third of the body's evaporation losses come from the lungs, whereas two thirds come from the skin. The relative humidity of the ambient air is

Figure 15-B-1 The four ways in which heat is lost.

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important. In dry air, evaporation is faster. The respiratory rate increases as altitude increases. Evaporative heat loss is increased greatly as one ascends to high altitude, as is evaporative water loss from the lungs. This loss may require an additional 3 or 4 L of water intake daily to prevent dehydration, and 1500 to 2000 kcal of heat may be lost.[42] Heavy exercise, even in a cold environment, may raise the body temperature as high as 41.1°C (106°F), producing 1.8 L of perspiration hourly.[30] The athlete, especially the high-altitude climber, may lose tremendous amounts of heat and water, especially from the skin and lungs. When the climber stops climbing, he or she is wet, dehydrated, cold, and exhausted. The climber may spend the night in a forced bivouac with limited food and water in subzero windy conditions at an extreme altitude. The greatest amount of heat (approximately 55% to 65% of the body's heat loss) is lost by radiation. A warm body gives off heat as infrared radiation to a colder body or surroundings. The amount of radiation loss is relatively constant and is related to the mass of the body and its surface area. Radiation losses are not affected greatly by clothing. Special reflective surfaces on clothing do not change radiation losses significantly, contrary to the boasts of manufacturers. Children cool faster than adults because they have a greater surface area-to-mass ratio.[20] (This is true for conduction and convection losses as well.) The infrared radiation given off is the basis for the use of infrared radiation detectors to find lost individuals.

Control

Maintenance of a balance between heat loss and heat production is essential to maintain a constant core temperature. With variable climatic conditions, the body is able to control heat loss and heat production through voluntary and involuntary mechanisms. The body senses ambient temperature through the skin, and skin temperature may vary greatly. The thermostat is located in the hypothalamus of the brain and regulates heat loss and production. Voluntary muscular activity produces heat, as does involuntary shivering. Shivering can increase heat production fivefold.[21] The amount of heat production is limited by the body's store of muscle glycogen. Heat loss is controlled largely by vasoconstriction. Cutaneous blood flow may vary by 100 times in the range from maximum vasoconstriction to maximum vasodilation. The body loses 90% to 95% of its heat through the skin. Piloerection, important to animals when they fluff their fur, improves insulation by trapping a layer of motionless air close to the skin. This response is present in nearly hairless humans as goose bumps, which do not increase insulation appreciably. The body may increase heat production involuntarily through nonshivering thermogenesis. The mechanism is complex. Cold causes increased output of epinephrine and norepinephrine. Increased levels of epinephrine and norepinephrine result in increased metabolic work and heat production. The amount of heat produced by this mechanism is insignificant with respect to that produced by shivering.

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Factors Influencing Cold Injury Clothing

Clothing design and materials must make use of physiologic principles to be effective as insulation. The basic principle is to maintain layers of warm, motionless air close to the body. For exercise in a cold environment, the use of layered clothing is important. The elevation of body temperature with exercise should be anticipated. To avoid sweating and soaking insulation as overheating occurs, the athlete should dress down by removing layers. After stopping, the athlete dresses up, adding layers to prevent chilling. The use of warm when wet materials, such as wool, which retains 80% of its insulating value when wet, is important. Fiber pile is similar and lighter. It does not absorb water and may be shaken or wrung out easily. Material that wicks water away from the body (polypropylene for underwear) is beneficial and dry on the body. Down has been the gold standard for loft and insulating ability. Many climbers replace down with newer fibers of materials such as polyester (e.g., Qualofil and Polarguard), which shed water. Down clumps and is useless when wet. Down often is reserved for situations in high, dry, extreme cold. Wind protection is important, and fabrics such as Gore-Tex and Entrant provide wind protection (wool and fiber pile offer little wind protection), while allowing water vapor to escape. These materials provide a reasonable barrier to water droplets in rain or snow. Nylon or plastic rainwear, although waterproof, cause the exercising athlete to become drenched by perspiration because water vapor cannot escape and condenses. Mittens are warmer than gloves. Newton's law states that cooling is proportional to surface area. The lower surface area-to-mass ratio of the mittened hand causes the hand to lose heat more slowly. Adding insulation to fingers of gloves may be counterproductive by increasing surface area and heat loss. Plastic boots using closed-cell foam liners keep and maintain dry insulation. Being rigid, they also prevent

the constricting effect of crampon straps and snowshoe bindings. For cold weather, all clothing should be loose, avoiding constriction of circulation. Dry is best. The military has recommended spraying the feet daily with antiperspirant to keep the feet and socks dry. The vapor barrier concept is applicable for extreme cold. Insensible water loss may be suppressed by a feedback mechanism, preserving heat and avoiding insensible evaporative heat loss. Vapor barriers (an impervious layer of nylon or plastic) generally have been used as liners for socks and sleeping bags. The head and neck area must be protected. Hats, balaclavas, and scarves are important. Nutrition and Hydration

For athletic activity of any kind, nutrition and hydration are important. These two needs are crucial in a cold environment. Stored muscle glycogen is the limiting factor of muscle activity, whether shivering or athletic. Activity of longer duration burns an increased amount of stored fats.

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In response to cold, urinary output is increased, leading to cold diuresis. Vasoconstriction of the skin increases central blood volume and renal blood flow. The usual requirement for about 2 quarts of fluid daily may be significantly increased in the cold. Heredity

There is abundant anecdotal evidence about cold tolerance among certain ethnic and racial groups, including Eskimos, Sherpa, and aborigines. Much adaptation to and tolerance of cold is cultural and learned. A physiologic response, cold-induced vasodilation (CIVD), is measurable. Cold produces vasoconstriction, especially in the hands. After 5 to 10 minutes of constriction, these vessels dilate briefly, avoiding ischemic damage. Inhabitants of cold regions, such as Eskimos and aborigines, have increased CIVD. Blacks have decreased CIVD and an increased risk of frostbite. Mind

Cold injury often accompanies severe adverse environmental conditions compounded by a human catastrophe. It has been shown that a positive attitude, particularly in a leadership position, is the best defense. Individuals afflicted by injury, altitude, starvation, or hypothermia often are apathetic. A positive constructive attitude in one member of the group may mobilize everyone's efforts and enable the group to survive. Another occasionally life-saving quality is knowing when to quit. Mountaineers in particular strive to reach their summit or goal. When reaching this goal risks life and

limb, it is time to turn back. This decision is made best early in the face of deteriorating weather. This recommendation may seem simplistic and self-evident, but it is often a hard decision for a highly motivated mountaineering team to make. Types of Cold Injury

When heat loss exceeds heat production, cold injury results. Cold injury may be one of two types, generalized and localized. Hypothermia is generalized cold injury. Localized injury may be either freezing injury (frostbite) or nonfreezing injury. Several syndromes also are triggered by cold exposure.

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Hypothermia

Hypothermia occurs when the body core temperature decreases to less than 35°C (95°F). There are two classes, primary and secondary. Primary hypothermia occurs accidentally to otherwise healthy individuals. Secondary hypothermia occurs in the course of systemic disease. The former, primary hypothermia, is the subject of this discussion. Hypothermia has been classified as acute and chronic. Acute hypothermia results from sudden exposure to extreme cold. An example is a sudden immersion in icy water (usually /das/book/view/29309971/1103/335.html/top

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Illness Stimulated by Cold

Some disease entities are stimulated by cold but not caused by it. In cold urticaria, hives are produced by cold exposure. The diagnosis is made by a simple provocative test. Applying an ice cube to the skin for 5 minutes produces a wheal. The problem rarely is severe. Life-threatening hypotension is possible if such an individual is immersed in cold water. Systemic symptoms, such as headaches, fever, and arthralgia, can occur.[40] Antihistamines may be useful. Another disease for which cold is the trigger is Raynaud's phenomenon, which is a well-known vasospasm of the fingers in response to cold. Raynaud's phenomenon is intermittent and usually occurs in young women. It occasionally is severe enough to cause ulceration and tissue loss and has been treated with medication and sympathectomy. Pavlovian conditioning at home is simple, inexpensive, and effective and carries no morbidity; it is the treatment of choice. [13] The protocol for this program is well described by Hamlet.[13] Cold often may trigger asthma. Cold-induced bronchoconstriction is a variant of exercise-induced bronchoconstriction and is brought on by the hyperventilation of cold air in susceptible individuals. It is a direct airway effect.[13] Theophylline is minimally effective in blocking bronchoconstriction as a bronchodilator. [23] Cromolyn sodium has been shown to be effective, as have metaproterenol, albuterol, and terbutaline. Metaproterenol is banned by the International Olympic Committee. Theophylline, cromolyn, terbutaline, and albuterol are acceptable. Vigorous training and good warm-up may benefit the patient and make pharmacologic agents unnecessary.

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Summary Whenever athletic activity is performed in a cold environment, cold injury is possible. With knowledge of cold physiology and cold injury, most of the problems presented can be avoided. When accidents occur, they must be treated properly.

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References Bangs C, Hamlet MD: Hypothermia and cold injury. In Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd ed. St. Louis, CV Mosby, 1989. 1.

Bergh V, Ekbloom B: Physical performance and peak aerobic power at different body temperatures. J Appl Physiol 46:885-889, 1978. 2.

Berk JL, Lenner KA, McFadden ED: Cold-induced bronchoconstriction: Role of cutaneous reflexes vs. direct airway effects. J Appl Physiol 63:659-664, 1982. 3.

Burry JH: Adverse effects of topical fluorinated corticosteroids on chilblains [letter]. Med J Aust 146:451, 1987. 4.

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Danzyl DF, Pozos RS: Multicenter hypothermia survey. Ann Emerg Med 16:9, 1987.

Danzyl DF, Pozos RS, Hamlet MD: Accidental hypothermia. In Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd ed. St. Louis, CV Mosby, 1989. 6.

Davies C, Young K: Effect of temperature on the contractile properties and muscle power of triceps surae in humans. J Appl Physiol 55:191-195, 1983. 7.

Faulkner JA, White TP, Markley JM: The 1979 Canadian ski marathon: A natural experiment in hypothermia. In Nagle FJ, Montage JH (eds): Exercise in Health and DiseaseBalke Symposium. Spring-field, IL, Charles C Thomas, 1981. 8.

Federation Internationale de Ski: The International Ski Competition Rules (ICR): Book II. Cross-Country and Nordic Combined. Istanbul, 36th International Ski Congress, 1968. 9.

10.

Fox RH, Woodward PM, Fry AS: Diagnosis of hypothermia in the elderly. Lancet 1:424-427, 1971.

11.

Hamlet MD: An overview of medically related problems in the cold environment. Milit Med

152:393-396, 1987. Hamlet MD: Frostbite and hypothermia. Presented at the 7th Annual Sportsmedicine Meeting, Lake Placid Sports Medicine Society, Lake Placid, New York, 1987. 12.

Hamlet MD: Cold injuries, Raynaud's disease, and hypothermia. In Casey MJ, Foster C, Hixson EG (eds): Winter Sports Medicine. Philadelphia, FA Davis, 1990. 13.

Hayward JS: The physiology of immersion hypothermia. In Pozos RS, Wilttmers LE (eds): The Nature and Treatment of Hypothermia. Minneapolis, University of Minnesota Press, 1958. 14.

Hayward JS: Immersion hypothermia. In Wilkerson JA, Bangs CC, Hayward JS (eds): Hypothermia, Frostbite, and Other Cold Injuries. Seattle, The Mountaineers, 1986. 15.

16.

Heggars JP: Experimental and clinical observations on frostbite. Ann Emerg Med 16:1056, 1987.

17.

Holm PC, Vangaard L: Frostbite. Plast Reconstr Surg 54:544, 1974.

Huang Z, Sun Q, Shen M: Rewarming with microwave irradiation for severe cold injury syndrome. Chin Med J 93:119-120, 1980. 18.

Israel RH, Kohan JM, Poe RH, et al: Inhaled metaproterenol is superior to inhaled cromolyn in protecting against cold air induced bronchoconstriction. Respiration 53:225-231, 1988. 19.

20.

Keating WR: Accidental immersion hypothermia and drowning. Prac titioner 219:183, 1977.

21.

Lampietro PF: Heat production from shivering. J Appl Physiol 15:632, 1960.

Mehta RC, Wilson MA: Frostbite injury: Prediction of tissue viability with triple phase bone scanning. Radiology 120:511-514, 1989. 22.

Merland N, Cartier A, L'Archeveque J, et al: Theophylline minimally inhibits bronchoconstriction induced by dry cold air inhalation in asthmatic subjects. Am Rev Respir Dis 137:1304-1308, 1988. 23.

24.

Merryman HT: Mechanics of freezing in living cells and tissues. Science 123:515, 1956.

Miller JW, Danzyl DF, Thomas DM: Urban accidental hypothermia: 135 cases. Ann Emerg Med 9:456-461, 1980. 25.

26.

Mills WJ Jr: Frostbite. Alaska Med 15:35, 1973.

Myers RA, Britten JS, Crowly RA: Hypothermia, quantitative aspects. J Am Coll Emerg Physicians 8:523, 1979. 27.

28.

Nadel ER: Energy exchanges in water. Underseas Biomed Res 2:149, 1984.

O'Keefe KM: Treatment of accidental hypothermia and rewarming techniques. In Robert JR, Hedger JR (eds): Clinical Procedures in Emergency Medicine. Philadelphia, WB Saunders, 1985. 29.

Pugh LG, Corbett CE, Johnson RH: Rectal temperatures, weight losses, and sweat rates in marathon running. J Appl Physiol 23:347, 1967. 30.

Quiron A, Therminaros A, Pellerei E, et al: Aerobic capacity, anaerobic threshold, and cold exposure with speed skaters. J Sportsmed Phys Fitness 28:27-34, 1988. 31.

Reed MH: Growth disturbances in the hands following thermal injuries in children. J Can Assoc Radiol 39:95, 1989. 32.

Robson MC, Heggars JP: Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg 6:43, 1981. 33.

Schumaker HB: Studies in experimental frostbite: The effect of heparin in preventing gangrene. Surgery 22:900, 1947. 34.

Siple P: Windchill in the Northern Hemisphere. Technical Report Edition 1982. Washington, DC, Falkwaki & Hastings, Quartermaster Research & Engineering Command, 1958. 35.

Smith DJ, Robson MC, Heggers JP: Frostbite. In Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd ed. St. Louis, CV Mosby, 1989. 36.

Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). JAMA 255:2905-2984, 1986. 37.

Therminaros A, Quiron A, Pellerei E, Laurencelle L: Effects of cold exposure on physiologic responses obtained during a short exhaustive exercise. J Sportsmed Phys Fitness 28:27-34, 1988. 38.

U.S. Army Medical Research and Development Command: Report No. T1/78: Behavioral Evaluation of a Winter Warfare Training Exercise. Natick, MA, U.S. Army Medical Research and Development Command, 1977. 39.

40.

Wagner WO: Urticaria: A challenge in diagnosis and treatment. Postgrad Med 83:321-329, 1985.

Whayne TF, DeBakey ME: Cold Injury, Ground Type. Washington, DC, Office of the Surgeon General, Department of the Army, 1958. 41.

Wilkerson JA: Avoiding hypothermia. In Wilkerson JA, Bangs CC, Hayward JS (eds): Hypothermia, Frostbite, and Other Cold Injuries. Seattle, The Mountaineers, 1986. 42.

Wilkerson JA: Other cold injuries. In Wilkerson JA, Bangs CC, Hayward JS (eds): Hypothermia, Frostbite, and Other Cold Injuries. Seattle, The Mountaineers, 1986. 43.

Wilkerson JA, Bangs CC, Hayward JS: Hypothermia, Frostbite, and Other Cold Injuries. Seattle, The Mountaineers, 1986. 44.

Wilmore DW: Fever, hyperpyrexia, hypothermia. In Wilmore DW, Brennan MF, Harken AH, et al (eds): Scientific American, Medical Care of the Surgical Patient, vol 1. New York, Scientific American, 1988. 45.

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Section C Altitude Stress Edward G. Hixson MD High altitude is altitude ranging from 1500 to 3500 m (5000 to 11,000 feet). Below this level, healthy individuals suffer few effects, but above this level, some physiologic effects are noted. Very high altitude ranges from 3500 to 5800 m (10,000 to 19,000 feet). In this zone, humans are able to acclimatize themselves to the physiologic stress of altitude and exercise. Above 5800 m (19,000 feet), which is considered extreme altitude, humans can survive only by acclimatization.[16] No human habitation has ever persisted above 18,000 feet. This region has been referred to as the death zone ( Fig. 15C-1 ). Rate of ascent is important. Rapid ascent is an ascent of minutes or hours in duration; a fast ascent takes place over days, and a slow or gradual ascent takes place over weeks.[20] Commercial airlines are required to pressurize cabins to 436 mm Hg above the outside pressure. For most heights, this pressure is equivalent to experiencing a rapid ascent to 6000 or 7000 feet and is tolerated easily by most people. Rapid ascent to greater than 25,000 feet may be fatal. In 1875, the balloon Zenith made such an epic ascent, and only one of the three occupants survived.[20] If one breathes 100% oxygen, ascent to roughly 45,000 feet is possible. Blood boils at 65,000 feet. The Federal Aviation Administration requires pilots and passengers in unpressurized cabins to use oxygen between 10,000 and 12,000 feet for exposures of more than 30 minutes. Above 12,000 feet, oxygen is required at all times.[9] The summit of Mt. Everest, 29,028 feet (8848 m), is the highest altitude achieved by humans without supplemental oxygen (Reinhold Messner and Peter Habler, 1978 Austrian Everest Expedition). Such a feat requires maximum acclimatization and is attainable by only a few individuals who are able physiologically to tolerate this altitude, perhaps on the basis of genetic advantage. Athletic Events at Altitude

High, very high, and extreme altitudes have been the exclusive realm of the mountaineer. Balloonists, hang gliders, glider pilots, parachutists, and aviators ascend to altitude equipped with oxygen and pressurized suits and cabins when appropriate. Competitive athletic events, such as speed hikes, marathons, and ultramarathons, are becoming more frequent at high and very high altitudes. Many treks go to high altitude, and guided climbs to extreme altitude are available to fit individuals. Approximately 40 million people live at elevations above 8000 feet, and an equal number visit yearly.[28] Hundreds of thousands visit high-altitude regions of the world yearly.[28] There are more than 100,000 active mountain climbers in the United States and many more throughout the world.[26] Thousands of mountaineers ascend extreme altitude yearly, and more than 100 climbers have reached the summit of Mt. Everest.

Figure 15-C-1 Definitions of high altitude.

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Competitive athletic events usually are not held above 2290 m (8700 feet). The International Federation of Sports-medicine banned competition above 3050 m (10,000 feet) in 1974. The International Ski Federation restricts the highest elevation of a cross-country course to 1800 m (6000 feet).[10] Biathlon has a similar rule. For competitive athletes, the concern is not only altitude illness but also the physiologic effects of altitude on the athlete. Concern was great before the 1968 Mexico City Olympics (2300 m [7500 feet]).

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Physiologic Changes at Altitude

Air is 20.93% oxygen, and this remains constant regardless of altitude. As altitude increases, barometric pressure decreases in linear fashion. [11] As barometric pressure decreases, the partial pressure of oxygen (PO2 ) decreases in direct proportion. As the PO2 of ambient air decreases, the partial pressure of oxygen in the blood (PaO2 ) also decreases. Barometric pressure at sea level is 760 mm Hg, normal PaO2 is 90 to 95 mm Hg, PaCO2 is 40 mm Hg, and oxygen saturation of blood is 96%. As one ascends to 3000 m (about 10,000 feet), barometric pressure decreases to 560 mm Hg, and Pa O2 is 60 mm Hg, roughly the level at which most people develop symptoms of altitude stress. As one ascends to 5800 m (19,000 feet), a very high altitude range, barometric pressure decreases to 360 mm Hg, PaO2 is roughly 46 mm Hg, PaCO2 is 20 mm Hg, and oxygen saturation of blood is 80%. Up to this point, humans can become acclimatized without deterioration in performance. At the extreme altitude of the summit of Mt. Everest (8848 m [29,028 feet]), barometric pressure is 253 mm Hg[33] ; on measurement of alveolar air samples, PaO2 at this altitude is computed to be 28 mm Hg, and PaCO2 is 7.5 mm Hg[35] ; corresponding oxygen saturation would be 60%. Under these circumstances, a human would be near death. Maximum oxygen uptake (VO2max ) is calculated to be in the range of 5 mL/minute/kg, [34] barely enough to maintain metabolism. In 1924, Norton reached 28,000 feet on Mt. Everest without supplemental oxygen, but it was not until 1978 that Messner and Habler reached the summit without supplemental oxygen. It took 54 years to climb the last 1000 feet without supplemental oxygen. Acclimatization

Humans must become acclimatized to very high and extreme altitudes by ascending slowly to be able to exercise, to avoid altitude illness, and to survive. The stimulus to acclimatization is hypoxia. The result of acclimatization is maximization of oxygen

delivery to the cell for a given altitude. VO2max decreases roughly 10% for each 1000 m of gain in altitude higher than 1500 m,[16] and this is not changed by acclimatization. VO2max is limited by the oxygen available in the ambient air. Acclimatization occurs by a multitude of complex changes taking place on a systemic as well as a cellular level. Hyperventilation is an important aspect of acclimatization, as shown dramatically by a PaCO2 of only 7.5 mm Hg on the summit of Mt. Everest. That this hyperventilation occurs with a relatively normal pH indicates the acid-base compensation that occurs. Hematopoiesis is stimulated by altitude. An increased number of red blood cells accounts for hematocrits in the range of 50% to 70%.[18] Maximum benefit from increased hematocrit occurs at about 57%; above this level, the decreased blood flow resulting from decreased viscosity may outweigh the benefits of more hemoglobin.[20] Hematocrits greater than 75% are characteristic of chronic mountain sickness, or Monge's disease. [27] This degree of polycythemia is maladaptive. Increased erythropoiesis at altitude has a parallel in illicit blood doping (i.e., athletes may take autologous transfusions to enhance their performance in endurance sports; see later discussion in section on training). It generally is agreed that an altitude above 3000 m (10,000 feet) is needed to stimulate acclimatization. Gradual ascent allows sufficient time. Maximum acclimatization occurs at 3 to 6 weeks. One should allow 1 day for each 1000 feet of ascent above 5000 feet and 1 day for each 500 feet above 14,000 feet. The old climbers' dictum, climb high but sleep low, is appropriate. Deterioration

At extreme altitude (>5800 m [19,000 feet]), the body deteriorates rapidly. This is the death zone. Here the beneficial effects of acclimatization are exceeded by the effects of deterioration. This deterioration is observed as rapid weight loss with attendant loss of strength and vigor. Anecdotally, some climbers have reported a 25% body weight loss during a 3-month expedition. For the China-Everest 1982 expedition, an average 16% body weight loss was observed by the author (unpublished observation). Weight is lost as fat and muscle in roughly equal amounts. There is a myth that if climbers fatten up before an expedition, this fat will be lost, sparing muscle. A high percentage of body fat does not protect against muscle loss. Sherpa, who have low body fat (10% to 15%), generally do not lose weight at high and very high altitudes.[2] Anorexia occurs at high altitude, demanding increased caloric needs to avoid negative nitrogen balance.[17] These needs would be increased greatly at extreme altitude. There is preliminary evidence that increased caloric intake in a fit climber may prevent weight loss during a short exposure to extreme altitude. (G. Roach reached the summit of Mt. Everest and returned with a gain of 2 pounds at the end of the expedition [EG Hixson, unpublished observation].) A high-carbo hydrate diet has the same effect as lowering the summit 2000 feet (EG Hixson, unpublished observation). Carbohydrates use less oxygen when oxidized to produce energy. The deterioration that occurs at altitude has been considered altitude illness and termed high-altitude cachexia by the author. High-altitude deterioration is a generalized deterioration of mind and body. Symptoms are weakness, lethargy, anorexia, and loss of vigor. The most obvious sign is loss of weight and decreased muscle mass as well as fat. Methods of minimizing the effects of deterioration are of benefit to the high-altitude climber, who must function at the highest level of strength, endurance, and mental activity to reach the summit or even to survive.

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High-Altitude Illness

All altitude illness shares a common cause, the hypoxia attendant on decreased barometric pressure, although, for discussion, each syndrome of altitude illness is treated separately here. Often the victim of altitude illness has some symptoms of many of the syndromes discussed, although one syndrome may predominate. High-Altitude Acute Mountain Sickness

Acute mountain sickness (AMS) is usually mild and self-limited. AMS can be minimized or avoided completely by gradual ascent and is uncommon in the acclimatized climber. Symptoms are headache, weakness, shortness of breath, anorexia, nausea, and vomiting. Sleeplessness and Cheyne-Stokes breathing are common. At elevations of 2400 m (8000 feet) in Colorado, 12% of newcomers were noted to be affected. [22] Rapid ascents to high altitude of 3000 to 4392 m (14,400 feet) produced symptoms of AMS in 67%.[15] Some cases do not resolve and progress to more severe altitude illness. At 4243 m, 8% of cases of AMS progress to more severe illness.[14] Symptoms usually are most severe after 48 to 72 hours and are gone by 4 or 5 days. AMS is treated and often can be prevented by acetazolamide. The mechanism of action of acetazolamide is complex. It is a carbonic inhibitor and blocks the enzyme that facilitates the combination of carbon dioxide and water to form bicarbonate in the blood. The rate of breathing is stimulated, and blood pH is lowered. All these changes make acclimatization to altitude easier, and altitude illness, especially AMS, is alleviated. One breathes more easily, receives more oxygen without raising the blood pH, and loses some retained fluid by diuresis because the drug is a mild diuretic. Acetazolamide is approved for treatment and prevention of AMS by the Food and Drug Administration. Acetazolamide for prophylaxis or treatment is given at a dosage of 250 mg twice daily beginning 1 day before ascent. Descent or oxygen administration is effective treatment but is rarely necessary. Rest is important. Exercise exacerbates the symptoms. The

best prophylaxis is gradual ascent, 1 day for each 1000 feet above 5000 feet and 1 day for each 500 feet above 14,000 feet. Hydration, fitness, and a high-carbohydrate diet are helpful; however, physical fitness does not protect one from any high-altitude illness. Many young, fit climbers go too high, too hard, too fast and experience AMS. High-Altitude Pulmonary Edema

High-altitude pulmonary edema (HAPE) is a severe form of altitude illness that is most likely to cause death. HAPE usually is seen 1 to 4 days after arrival at an altitude of 2400 m (8000 feet) or above. A too-high, too-hard, too-fast ascent often precedes HAPE. Fitness is not protective. The disease is most common in young men. HAPE is noted as a reentry phenomenon when acclimatized individuals or high-altitude natives descend for a few days and return. The most significant symptoms are dyspnea and cough. Cyanosis is common, as are elevated heart and respiratory rates. Pulmonary rales lead to frank edema and a copious pink, frothy sputum. Symptoms of AMS may or may not occur concomitantly or may predate HAPE. The incidence of HAPE varies from less than 1 in 10,000 skiers in Colorado, to 2% of climbers on Mt. McKinley, to 15% of Indian recruits flown to altitude.[16] Of those who go rapidly to 9000 feet, 1% get HAPE. Of those who get HAPE, 10% of cases are fatal. [21] Pulmonary hypertension is present.[24] The edema is a permeability edema that results from capillary leakage with normal left heart function.[30] In many ways, HAPE is similar to adult respiratory distress syndrome. Prevention is achieved by ascending gradually. HAPE does strike fit, well-acclimatized mountaineers, however. In these cases, HAPE may be related to excessive exercise at extreme altitude. Treatment is early descent with the first symptom (a descent of only 1000 feet may be sufficient). Oxygen is indicated. Diuretics, such as furosemide, may be useful; however, there is a risk of hypotension with their use. Almost all sick climbers are severely dehydrated, and diuretic therapy has a high risk of hypotension. Morphine has been recommended, as with pulmonary edema of cardiac origin. Respiratory depression from morphine is the main hazard of its use. Descent is the most beneficial treatment that can be done in the field. Many cases resolve as descent is made to the hospital. For severe disease in hospitalized patients, endotracheal intubation with positive end-expiratory pressure ventilation has been beneficial. Some cases progress to a fatal outcome even with the most aggressive respiratory support. Most cases resolve within 24 to 48 hours of descent, however. Radiographs are diagnostic. High-Altitude Cerebral Edema

AMS is a neurologic disorder, mild and self-limited. High-altitude cerebral edema (HACE) is a severe, often fatal neurologic disorder that may result from a progression of AMS. HACE does occur de novo in acclimatized climbers at extreme altitude. In AMS and HACE, there is increased intracranial pressure, which in the latter progresses to frank edema. Cerebrospinal fluid pressure may be greater than 300 mm H2 O in HACE.[23] Edema is noted at autopsy and on computed tomography scans.

The hallmark symptom is severe headache. Ataxia or mental changes, such as confusion and hallucinations, often are present; these may progress to stupor or coma. A variety of focal neurologic signs may occur (i.e., hemiparesis and seizures). Papilledema often is present. HACE rarely occurs below 12,000 feet. It takes 2 to 3 days to develop. HACE is the most severe form of altitude illness and has the highest mortality, morbidity, and likelihood of permanent sequelae. No permanent neurologic effects have been observed to result from altitude exposure alone without altitude illness.[6]

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The treatment is descent. Dexamethasone, 4 to 8 mg given every 6 hours, is indicated, as is oxygen. For the hospitalized patient, intubation and controlled hyperventilation may be helpful in lowering the cerebrospinal fluid pressure. Diuretics may be of benefit but may aggravate injury if, owing to dehydration, hypotension were to occur, decreasing cerebral blood flow. High-Altitude Retinal Hemorrhage

The eye is the window to the brain. In HACE, retinal vessels are engorged with hemorrhage, leading to frank papilledema. Many climbers experience benign asymptomatic retinal hemorrhages. High-altitude retinal hemorrhage is seen in 50% of climbers ascending to 5000 m and in virtually 100% of climbers ascending above 6500 m.[36] High-altitude retinal hemorrhage usually resolves after 1 to 2 weeks without sequelae. If hemorrhage involves the macula, a blind spot or scotoma results. Other High-Altitude Problems

Thrombotic and embolic disease (e.g., phlebitis, pulmonary emboli, cerebral thrombosis) are more common at altitude. As a result of increased hematopoiesis, hematocrits of 70% to 76% occur. In HAPE, a hypercoagulability has been noted.[6] Dehydration aggravates this situation. Neurologic problems ranging from transient ischemic attacks to frank stroke occur. Monge's disease, or chronic mountain sickness, is associated with polycythemia and pulmonary disease in high-altitude natives. High altitude is marked by intense ultraviolet radiation because there is less atmosphere available to filter out these rays. Reflection from snow increases the problems. Severe sunburn or snow blindness may result from only 1 hour of exposure if the eyes or skin is unprotected. Glacier glasses with side panels and maximum ultraviolet block sunscreen are needed. On a glacier at high altitude, the temperature can go from subzero at night to 80°F or 90°F (27°C-32°C) in a matter of hours. Heat injury is possible.

Most altitude illness is decreased in incidence and severity by acclimatization. General advice to mountaineers is summarized as follows: 1. Ascent should be gradual1000 feet daily when higher than 5000 feet and 500 feet daily when higher than 14,000 feet. 2. Decreased workload, especially anaerobic, is recommended after arrival at altitude. 3. Good hydration should be maintained. 4. A high-carbohydrate diet is recommended. 5. A low-salt intake should be maintained. Most people with altitude illness and many new arrivals at altitude note generalized edema. Increased blood pressure may be noted. Many backpack dehydrated foods have a high salt content. 6. In patients with illness worse than AMS, or when AMS does not resolve, descent is advised.

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Athletic Training and Competition at Altitude

Competitive athletic events, even when restricted to moderate altitude, are affected significantly by altitude. Altitude illness is rarely a factor. The main concern is the physiologic effect on performance. In 1968, the Olympic games were held in Mexico City at 2300 m (7349 feet). Since that time, there has been considerable increased interest in the effects of moderate altitude on athletic training and performance. The lowered barometric pressure and its attendant decrease in PO2 are the major factors. At 3000 m, there is 31% less oxygen in the air; at Mexico City, there is a 24% reduction. VO2max decreases roughly 10% for each 1000 m above 1500 m.[16] For endurance events at the altitude of Mexico City, one would have expected time increases of 15% to 20% to occur. Increases of only 7% to 10% were observed, however.[32] Although VO2max cannot be changed for a given altitude by acclimatization, performance, which is related to many variables, can. Temperature

With increasing altitude, ambient temperature decreases 2°C for each 300 m.[31] Concern about cold injury at moderate altitude was not significant for the latitude of Mexico City and its usual weather. Weather and season are more significant factors than altitude for athletic competition. Gravity

Acceleration owing to gravity is decreased 0.3 cm/second[2] for each 1000-m increase in altitude. Conceivably, this fact benefits jumping, pole vault, and ballistic events. Its actual significance is negligible (0.13% at 4000 m), however.[31]

Air Resistance

The thin air at altitude decreases wind resistance, and athletes must expend less energy to overcome it. Work done against wind resistance is proportional to the third power of the velocity.[31] The faster the event, the greater the significance. At sea level, roughly 11% of energy is expended against wind resistance. For the 5000-m run at Mexico City, a 3.4% improved performance would be anticipated based on these data. For 100 m, a 14.38% improvement would be anticipated.[28] Usually in Olympic events, times are 2.9% slower than those in world records. At Mexico City, times were only 0.99% off world record times, [7] and more world records were broken for short events ( /das/book/view/29309971/1103/344.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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Chapter 16 - Imaging Techniques Section A Imaging of Sports-Related Injuries Timothy G. Sanders MD Chris Fults-Ganey MD, PhD Sports-related injuries have become commonplace in society, affecting athletes at all levels, ranging from the poorly conditioned weekend athlete to the professional athlete. Advances in magnetic resonance imaging (MRI) have led to significant improvements in the ability to diagnose these injuries noninvasively. MRI provides superb soft tissue resolution and depicts many of the soft tissue and osseous abnormalities that previously were undetectable by imaging. Although less dramatic, important advances also have occurred in other imaging modalities, including nuclear medicine and computed tomography (CT). As imaging capabilities have improved, the role of imaging modalities in establishing an accurate diagnosis, directing treatment, and providing follow-up has increased in many sports-related injuries. This chapter provides a basic understanding of the various imaging modalities that currently are available and outlines an imaging strategy to aid the clinician in establishing a timely and accurate diagnosis in the injured athlete. Most sports-related injuries are assessed adequately with a thorough clinical evaluation and standard radiographs. Evaluation of complex injuries may require the use of more advanced imaging modalities, however. The first section of this chapter provides a general overview of the various imaging modalities currently available, starting with routine radiography, tomography, and arthrography, followed by an expanded discussion of the more sophisticated technologies, including ultrasonography, bone

scintigraphy, CT, and MRI. The second section maps out fundamental imaging strategies for the evaluation of specific sports-related injuries. In most instances, the initial examination consists of the routine radiograph; however, when specialized studies are required, it is important to choose the modality that would lead to a prompt and accurate diagnosis, while minimizing discomfort and expense to the patient. A basic imaging approach to the commonly encountered sports-related injuries is discussed, including injuries of ligaments, tendons, and cartilage as well as stress or overuse injuries of bones, avulsion injuries, and difficult-to-diagnose fractures. Imaging Techniques Conventional Radiography

Routine radiography is a readily available and inexpensive imaging technique that is easy to perform and typically serves as the initial imaging study after a sports-related injury.[16] [46] To obtain a high-quality diagnostic image, careful attention must be paid to positioning and exposure. A minimum of two perpendicular views is required to evaluate any bone adequately, whereas complex joints, such as the ankle, the wrist, or the elbow, may require additional or specialized views for complete evaluation ( Fig. 16A-1 ).

Figure 16-A-1 Scaphoid fracture. A, Anteroposterior radiograph of the wrist shows a small, thin linear lucency (arrow) in the scaphoid suspicious for a fracture. B, Specialized scaphoid projection clearly delineates a fracture line (arrow) through the waist of the scaphoid.

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The primary purpose of the routine radiograph is to identify and classify various osseous injuries, but the radiograph also may provide valuable clues regarding adjacent soft tissue abnormalities (i.e., soft tissue swelling, joint effusion, or lipohemarthrosis). Chronic soft tissue injuries, including calcific tendinitis or bursitis, can be shown on the routine radiograph, but because of poor soft tissue contrast, little direct information is provided regarding the integrity of soft tissue structures such as ligaments, tendons, and cartilage. Radiographic evaluation is important after treatment to ensure proper postreduction alignment of fracture fragments and to document progression of healing. The conventional radiograph aids in the diagnosis of certain complications, such as infection, avascular necrosis, or post-traumatic osteoarthritis. Tomography

Conventional tomography, or sectional radiography, is a method of imaging that results in blurring of unwanted anatomic structures to provide improved visualization of a desired structure within a given focal plane. This is accomplished by moving the x-ray tube and the x-ray film in the same plane but in opposite directions during exposure. Although CT and MRI largely have replaced this technique, conventional tomography remains a cost-effective method of evaluating certain anatomic structures. It is used primarily as a method of evaluating subtle fractures or fracture healing in the vertebral column, the tibial plateau, the femur, and the carpal bones.[4] [137] The slice thickness (area of anatomy in focus) varies depending on the angle that the tube travels. Tomography can be performed in a linear fashion or by using a complex motion. Complex tomography is generally more effective in showing subtle fractures; however, linear tomography performed in a plane parallel to a metallic internal fixation device minimizes artifact from the adjacent hardware and provides improved visualization of the surrounding osseous structures.[155] Arthrography

Arthrography is an imaging technique in which contrast material is injected into the joint to improve visualization of intra-articular structures. Although conventional arthrography previously was the mainstay of joint imaging, [110] today arthrography frequently is combined with advanced imaging modalities such as CT or MRI.* The combination of intra-articular contrast agent administration with advanced imaging modalities allows exquisite depiction of the intra-articular anatomy as well as the surrounding soft tissue structures, such as tendons and ligaments. Arthrography is a minimally invasive procedure, which is simple to perform and usually well tolerated by the patient. Conventional arthrography of the shoulder has been in use for years as an accurate method of imaging rotator cuff tears. Double-contrast (air and iodinated contrast agent) conventional shoulder arthrography was popularized in the 1980s and improved the accuracy of detecting injuries of the rotator cuff and labrum. [127] [176] CT arthrography further improved the accuracy of detecting labral and capsular abnormalities ( Fig. 16A-2 ). [154] [170] [195] Conventional shoulder arthrography continues to play a role in the evaluation of rotator cuff abnormalities in some practices. MRI arthrography largely has replaced all former arthrographic techniques, however, providing the best overall evaluation of the shoulder, including the articular cartilage, labrum, capsular structures, rotator cuff, and osseous structures ( Fig. 16A-3 ). [28] [55] Arthrography of the elbow is typically performed in conjunction with CT or MRI in the evaluation of osteochondral and ligamentous injuries.[131] [133] [183] CT arthrography provides excellent depiction of osteochondral injuries

Figure 16-A-2 Computed tomographic (CT) arthrography of bony Bankart's and Hill-Sachs fractures. A, Axial CT image through the glenohumeral joint after intra-articular administration of iodinated contrast agent and air shows a small osseous Bankart's fracture ( arrow). B, CT arthrography axial image through

the superior portion of the humeral head shows posterior impaction (arrow). *See references

[ 5] [ 27] [ 28] [ 29] [ 55] [ 85] [ 96] [ 109] [ 131] [ 133] [ 154] [ 169] [ 170] [ 183]

and [ 195] .

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Figure 16-A-3 Magnetic resonance arthrography of Bankart's fracture. Axial T 1 -weighted image with fat saturation after intra-articular injection of gadolinium shows irregularity of the inferior glenoid margin (short arrow) and a displaced osseous Bankart's lesion (long arrow).

of the capitellum and radial head and also aids in the identification of loose bodies. MRI arthrography, however, can identify subtle osseous abnormalities not depicted on CT arthrography including bone marrow edema from compressive forces in the lateral compartment, and also improves detection of collateral ligament injuries. Wrist arthrography is controversial as a method of diagnosing tears of the intercarpal ligaments. This controversy is due in part to an evolving understanding of the role of trauma in the disruption of these ligaments versus age-related change.[25] Conventional arthrography using meticulous technique is an accurate method of showing perforations of the intercarpal ligaments. MRI arthrography has been shown to increase the accuracy of detecting perforations of the intercarpal ligaments and provides a complete evaluation of the adjacent osseous and soft tissue structures.[163] As knowledge in this area expands, MRI arthrography probably will evolve into the imaging modality of choice for the evaluation of intercarpal ligaments. The primary use of hip arthrography in the sports medicine patient is in the detection of labral tears and in the visualization of intra-articular loose bodies. MRI arthrography accurately fulfills this role and shows extra-articular abnormalities, such as tendinitis or bursitis, that may mimic intra-articular pathologic conditions.[34] [105] [108] [151] Conventional knee arthrography was used widely in the past as a method of identifying meniscal tears.[13] [42] [93] [180] Today, routine MRI has replaced conventional knee arthrography as the primary imaging modality in the evaluation of menisci.[12] [32] [87] [128] MRI arthrography plays a valuable role in patients with persistent knee pain after meniscal surgery.[5] MRI arthrography can differentiate accurately postoperative change from a repeat meniscal tear. This modality also is useful in distinguishing between stable and unstable osteochondral fragments of the femoral condyle. MRI arthrography of the ankle is used primarily as a means of evaluating the patient with chronic lateral ankle pain and persistent instability after an inversion injury.[27] Tears of the lateral ankle ligaments and osteochondral injuries of the talar dome ( Fig. 16A-4 ) are depicted accurately and graded by MRI arthrography.[99] [100] Injuries of adjacent soft tissue structures, including the peroneal tendons and sinus tarsi, are evaluated simultaneously.

Ultrasonography

Ultrasound has been available widely as a diagnostic imaging tool since the 1970s, but it was not until the mid-1980s that sonography of the musculoskeletal system was popularized. Advances in musculoskeletal sonography resulted primarily from improved technology and development of high-resolution transducers.[69] [92] Sonography can be used to define the extent of injury in musculoskeletal structures, such as tendons (rotator cuff, Achilles tendon, patellar tendon) and muscles, and can play a role in the evaluation of other musculoskeletal abnormalities, such as soft tissue masses, and in localizing foreign bodies. In the 1990s, musculoskeletal sonography was supplanted widely by MRI, which provides superior soft tissue contrast and is less operator dependent. Nevertheless, sonography is a valuable diagnostic tool, which can provide valuable information about the injured athlete. Ultrasonography uses mechanical pressure waves similar to sound waves rather than ionizing radiation to produce an image and has no known biologically harmful side effects in the diagnostic range. The ultrasound probe functions as a transducer and as a receiver. The sound wave is produced by the probe and directed into a specific body. As the wave encounters various interfaces, such as the interface between two soft tissue structures (i.e., muscle and tendon), a portion of the wave is reflected back and received by the probe, creating an image. Most diagnostic

Figure 16-A-4 Osteochondral lesion of the talus. Coronal T1 -weighted image with fat saturation and intra-articular gadolinium shows a wafer-shaped grade IV osteochondral defect in the lateral talar dome surrounded by gadolinium (arrow), indicating an unstable, minimally displaced fragment.

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Figure 16-A-5 Supraspinatus tendon rupture. A, Sonographic image of an intact left shoulder with medial (M) and lateral (L) aspects of the joint labeled shows a normal supraspinatus (S) muscle and tendon inserting on the greater tuberosity (arrow) of the humeral head (H). The deltoid (D) muscle also is seen. B, Image of the right shoulder shows a massive full-thickness tear of the supraspinatus tendon with retraction (arrows). (Courtesy of Levon Nazarian, MD, Philadelphia, Pa.)

ultrasound images are obtained by using a pressure wave that ranges in frequency between 2.5 and 10 MHz. There always is a trade-off between image resolution and depth of penetration of the sound wave. Because most structures imaged in the musculoskeletal system are superficial, high-frequency transducers are used, usually on the order of 7.5 to 10 MHz. These high-frequency transducers allow for excellent spatial resolution but achieve penetration of only a few centimeters. Imaging of deeper structures can be achieved by using lower frequency probes, but the overall resolution decreases accordingly.

Tendons

Tendons can be imaged sonographically, and a normal tendon appears as an echogenic (bright) structure relative to the surrounding muscle and typically contains longitudinally oriented bundles or strands.[37] [59] [60] [118] The sonographic appearance of tendinitis includes blurring and thickening of the tendon, loss of the normal architecture, and presence of hypoechoic (dark) foci within the tendon. A partial-thickness tear of a tendon is seen as an area of decreased echogenicity within the tendon, and a full-thickness tear appears as a hypoechoic band extending through the entire thickness of the tendon. A massive tear of the tendon shows retraction of the torn ends with a hypoechoic gap between the torn fibers ( Fig. 16A-5 ). The aforementioned criteria can be applied to any tendon, and sonographic imaging has been reported of nearly every tendon in the body. The tendons most frequently imaged sonographically include the Achilles, patellar, and rotator cuff tendons.* Muscles

Evaluation of injured muscles is possible sonographically.[62] [103] [107] [179] Normal skeletal muscle appears as longitudinally *See references

[ 21] [ 23] [ 30] [ 51] [ 58] [ 59] [ 60] [ 79] [ 104] [ 115] [ 122]

and [ 124] .

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arranged hypoechoic (dark) bundles separated by hyperechoic (bright) fascia. Dynamic evaluation of the muscle during contraction allows visualization of these bundles as they contract or relax. A torn muscle is seen sonographically as disorganization of the normal architecture, and a hematoma appears as a hyperechoic (bright) mass dissecting between fascial planes. Shoulder

Ultrasound examination of the shoulder typically is performed with the patient in the sitting position, with the shoulder internally rotated and the hand placed behind the back.[122] [141] [144] This position allows maximal visualization of the crucial portion of the supraspinatus tendon by retracting it from beneath the acromion. The infraspinatus is visualized more posteriorly, whereas the subscapularis muscle is imaged anteriorly in the transverse plane with the arm in the neutral position. The biceps tendon is evaluated in the transverse plane to insure it maintains its normal anatomic position within the bicipital groove. The rotator cuff is evaluated perpendicular and parallel to the long axis of each tendon. The normal tendon shows uniform thickness and echogenicity. Evidence of tendinopathy includes thickening or heterogeneity of the tendon, whereas a partial-thickness tear appears as a focal change in echogenicity. A hyperechoic (bright) area may represent granulation tissue and hemorrhage, whereas a focal hypoechoic

(dark) area may represent fluid extending partially through the tendon. Nonvisualization, focal absence, and discontinuities of the cuff all are criteria for a full-thickness tear. Published reports regarding the accuracy of sonography of the rotator cuff vary widely,[19] [31] [82] [114] [125] [126] [172] ranging from 53% to 100%. Sonographic evaluation of the rotator cuff has a steep learning curve and is extremely operator dependent. This fact, coupled with the fact that MRI provides a global evaluation of the shoulder, has led to the replacement of shoulder sonography by MRI in most practices. Knee

Sonography plays a helpful role in the evaluation of masses located within the popliteal fossa. A palpable mass in this area may represent a Baker cyst, popliteal artery aneurysm, or soft tissue neoplasm. Sonography can detect and differentiate easily between each of these structures.[41] [75] [80] [120] Baker's cyst is a fluid-filled structure located in the posteromedial aspect of the knee, typically arising between the medial head of the gastrocnemius and semimembranosus tendon. Uncomplicated Baker's cyst fulfills the sonographic criteria of a simple cyst, which include (1) an anechoic (black) structure, (2) good through transmission of sound (brighter echoes deep to the cyst), and (3) a well-defined posterior wall. If hemorrhage or infection complicates the cyst, it may not fulfill all three of these criteria. A soft tissue mass shows internal echoes and usually is located in a different anatomic location. Color Doppler can be used to reveal flow in a popliteal artery aneurysm, differentiating it from a Baker cyst. Foreign Body Localization

Ultrasonography is a helpful adjunct in localizing foreign bodies within the soft tissues.[61] [70] [111] Wood, glass, and metal are the most frequently encountered foreign bodies, and they commonly occur in the hands and feet. Although glass and metal are seen 96% to 100% of the time with conventional radiography, wood is identified in only 15% of cases by radiography. Ultrasound accurately localizes all three types of foreign bodies. Pitfalls include the misinterpretation of sesamoid bones and soft tissue calcifications as foreign bodies; radiographs always should be performed for comparison. The leading edge of the foreign body is the only portion visualized sonographically, and as a result, the size and shape cannot be shown adequately by sonography alone. The primary role of sonography with regard to imaging of foreign bodies is in the three-dimensional localization within the soft tissues. Nuclear Medicine

Multiple radionuclide studies are available to the orthopaedic surgeon, and even with the advent of CT and MRI, skeletal scintigraphy is a valuable screening tool because of its high sensitivity and unique ability to image the entire skeleton simultaneously. Indications for skeletal scintigraphy are widespread and include the evaluation of sports-related injuries and associated complications, diagnosis of orthopaedic infections, determination of metabolic activity of incidental bone lesions, and

surveillance for additional lesions. Nuclear medicine differs from other imaging modalities in that it provides physiologic rather than anatomic information. In contrast to routine radiography and CT, which measure x-ray transmission through a patient, nuclear medicine detects gamma ray emission from a patient after parenteral administration of the radiopharmaceutical. Bio-distribution within the body depends on the distinctive chemical and physical properties of the radiopharmaceutical. The radiopharmaceutical contains a radioactive atom that decays, resulting in gamma ray photon emission. These emitted photons are detected by a gamma camera imaging system. The gamma camera system consists of a lead collimator to select photons from a single direction, a sodium iodide crystal detector that produces light when hit by the emitted photon, and a photomultiplier tube to convert light into a voltage to generate an image. Low-energy, all-purpose collimators are used most often for bone scintigraphy. To enhance anatomic detail, a high-resolution collimator or a collimator with magnification properties, such as a converging or pinhole collimator, may be employed. High-resolution collimators are capable of resolving an object 6 to 7 mm.[22] Conventional planar imaging collects and presents data as though it arose from a single plane but lacks tomographic information. Single photon emission computed tomography (SPECT) techniques have become widely available. With SPECT, gamma cameras are mounted on a rotating gantry, and a full 360-degree acquisition can be obtained. Image reconstruction from planar data to tomographic data is accomplished by filtered backprojection,

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which minimizes superimposed radioactivity, resulting in improved image contrast. The reconstructed images can be displayed in axial, coronal, and sagittal planes as well as in a dynamic rotating format, allowing evaluation of the skeleton in multiple projections. The major advantage of SPECT over planar imaging is enhanced tissue contrast resulting in improved sensitivity and specificity of lesion detection and localization.[76] SPECT imaging requires a long acquisition time, however, and image clarity may be degraded by patient motion. Currently used bone scintigraphic agents include technetium-99m (Tc-99m) methylene diphosphonate and Tc-99m hydroxymethylene diphosphonate. These radioactive substances are phosphate analogues, which rapidly localize to bone after intravenous administration by chemisorption on hydroxyapatite crystals in bone and attachment to organic matrix, such as collagen.[22] [52] Blood flow, osteoblastic activity, and extraction efficiency are all related to the degree of uptake. The radiopharmaceutical is cleared rapidly from the plasma and excreted through the urine by glomerular filtration with approximately half of the dose excreted within the first 4 hours. Bone is a dynamic tissue, which undergoes constant remodeling in response to stress. Radionuclide localization provides a metabolic picture reflective of the bone formation

status in the presence of an intact blood supply.[192] Skeletal scintigraphy consists of four imaging phases depending on the indication. McCarthy discussed the mechanisms of radionuclide distribution in the flow, blood pool, and delayed phases of imaging.[119] The arterial phase shows flow of the radionuclide similar to an angiogram. Increased flow occurs in the presence of increased number of mature blood vessels. Immediate static images comprise the second phase and depict blood pool activity with accumulation secondary to leakage of the radionuclide from the blood vessel into the soft tissue. Neovascularization in the setting of granulation or neoplastic tissue often results in increased blood vessel permeability, leading to increased soft tissue activity. Delayed images are acquired 2 to 4 hours after the administration of the radionuclide, allowing for clearance of soft tissue activity and improved detection of bone uptake. Increased activity is attributable to new bone formation by osteoblasts. Finally, a fourth phase can be performed 24 hours after radionuclide administration, which is particularly useful in the evaluation of infection. Trauma

Skeletal scintigraphy can play a significant role in the evaluation of the sports medicine patient, specifically in instances of radiographically occult traumatic or overuse injuries. Shin splints and stress fractures result from repetitive stress; however, the management of these two entities is quite different. Shin splints represent a periostitis, which occurs secondary to disruption of Sharpie's fibers.[86] Delayed bone scintigraphy is characterized by mild, linear, cortically based uptake in the posteromedial or anterolateral tibia involving approximately two thirds of the cortical bone length.[49] If a three-phase technique is employed, the flow and blood pool images typically are normal. Shin splints are not predictive of further injury; the individual can maintain his or her current level of activity without risk of further injury. Treatment consists of the administration of anti-inflammatory medication.[206] Stress fractures occur when repetitive stress exceeds the reparative mechanism of bone. Although structural continuity is maintained, sustained activity may progress to overt fracture. One of the most widely used applications of skeletal scintigraphy is in identifying stress fractures. Bone scintigraphy is considered the gold standard with a sensitivity approaching 100% in the diagnosis of stress fractures, whereas plain films have a sensitivity of 15%.[74] Scintigraphy is characterized by localization of the radiotracer at the site of injury on all three phases ( Fig. 16A-6 ). Stress fractures in the tibia and fibula are particularly common in athletes engaged in running-based sports. Zwas and colleagues proposed scintigraphic staging for tibial stress fractures to aid in patient management.[206] The classification consisted of four grades based on the degree and extent of radiotracer accumulation on delayed images: Grade I is a small region of mild increased activity confined to the cortex; grade II involves a larger region of the cortex; grade III is fusiform accumulation of the tracer with extension into the corticomedullary region; and grade IV is extensive corticomedullary accumulation. Stress fractures of the tibia are treated with rest, and the severity of the stress fracture is a major prognostic indicator, with grades I and II resolving more quickly and completely. Another important site of stress fractures in athletes is in the femoral neck. Increased uptake on all three phases localized to the inferior margin of the femoral neck occurs in compressive-type stress fractures.[53] Recognition is important because

pinning may be necessary for fracture stabilization. Spondylolysis is a defect in the posterior neural arch localized in the region of the pars interarticularis, which is considered a fatigue-type injury secondary to repetitive microtrauma. This injury is often a source of back pain in adolescents and young adults. Spondylolysis may be too subtle to detect with conventional radiography or planar bone scintigraphy. When imaging the lumbar spine, SPECT has a 20% to 50% increase in lesion detection compared with planar scintigraphy.[67] SPECT offers an important advantage over planar imaging in the early detection and localization of lumbar spine lesions ( Fig. 16A-7 ). Skeletal scintigraphy is helpful in determining if a radiographically known spondylolytic lesion is the patient's source of back pain. Lack of radiotracer uptake at the site of abnormality suggests a healed or stable lesion.[53] [117] Occult fractures are true fractures that are not evident on conventional radiographs. Skeletal scintigraphy is a sensitive test to evaluate for the presence of a clinically suspected occult fracture. An acute fracture shows increased radiotracer localization at the site of injury on all three phases ( Fig. 16A-8 ). As a lesion becomes subacute, the rate of healing declines, and the flow and blood pool phases begin to normalize. On delayed images, the radiotracer uptake is less intense and more focal.[86] Scaphoid fractures are the most common carpal injury and often are difficult to diagnose by plain film. If initial radiographs are negative, immobilization typically is performed, and radiographs are repeated in approximately 1 week to re-evaluate for the presence of fracture. Shewring and coworkers suggested substituting bone scintigraphy for the second

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Figure 16-A-6 Tibial stress fracture. A and B, Spot anteroposterior and lateral images of the right lower extremity from delayed bone scintigraphy reveal fusiform accumulation of the tracer in the posterolateral proximal tibia (arrows). C, Lateral radiograph shows linear band of sclerosis in the proximal tibia ( arrow).

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Figure 16-A-7 Spondylolysis. A, Posterior planar bone scintigraphy of the lower spine shows no abnormal accumulation of the radiotracer. B, Sagittal (top), coronal (middle), and axial (bottom) single photon emission computed tomographic images show focal radiotracer localization to the right L4 pars interarticularis (arrows) that was not seen on planar images.

set of conventional radiographs in the evaluation of a suspected acute scaphoid fracture. [167] Plain radiography has a reported sensitivity of 64% in the detection of

scaphoid fracture.[181] Normal scintigraphy performed at least 72 hours after injury is capable of excluding fracture. Scaphoid fractures are at high risk for nonunion, with an increased incidence in the setting of delayed diagnosis and continued motion at the fracture site. The use of three-phase skeletal scintigraphy can decrease the incidence of nonunion by aiding in the identification of radiographically occult non-displaced scaphoid fractures. In a study by Tiel-van Buul and associates, [181] skeletal scintigraphy was shown to be superior to MRI in detection of early scaphoid fractures. Bone scintigraphy can identify other radiographically difficult-to-diagnose carpal fractures, particularly fractures involving the triquetrum, capitate head, and hook of the hamate.[89] The time interval between acute trauma and performance of bone scintigraphy is important and depends on patient age and the presence of osteoporosis. In patients younger than 65 years old, 95% of fractures are identified at 24 hours and 100% at 48 hours after trauma. [53] In elderly or osteoporotic patients, bone turnover occurs at a slower rate, and additional time is required for the study to become positive. Approximately 95% of bone scans in this population are positive by 72 hours after injury.[67] Overall, it is reasonable to perform skeletal scintigraphy shortly after trauma; however, it is important to recognize the possibility of a false-negative study, particularly in older and osteoporotic patients. Traumatic Complications

In addition to identifying acute fractures, scintigraphy can be used in the evaluation of post-traumatic complications. Avascular necrosis can occur in almost any bone and is a potentially serious complication of trauma. Interruption of the blood supply results in edema, increased intraosseous pressure, and death of cellular elements. Skeletal scintigraphy shows a photopenic defect (cold spot) in early avascular necrosis because the necrotic segment is unable to take up the radiotracer.[89] After 1 to 3 weeks, the reparative process begins, and increased uptake is identified on delayed images. The sensitivity of bone scintigraphy in the

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Figure 16-A-8 Occult scaphoid fracture. Three-phase bone scintigraphy obtained 2 weeks after injury with initial negative radiographs. Diffuse increased radiotracer localization to the left carpus ( arrows) is present on initial two phases (flow [top] and blood pool [middle]), with focal scaphoid accumulation (arrow) on the final phase (delayed) (bottom).

detection of femoral head avascular necrosis ranges from 78% to 97%. [53] Given the lack of specificity of scintigraphic findings, however, MRI should be performed for confirmation. A smaller and more focal form of avascular necrosis is an osteochondral lesion. Partial or complete separation of a segment of cartilage together with subchondral bone occurs at an articular surface as a result of joint trauma. Common locations include the medial

femoral condyle, the talar dome, and less often the capitellum. If conventional radiography is normal or equivocal, Urman and colleagues recommended skeletal scintigraphy to screen for the presence and location of a lesion.[190] A negative bone scan obviates the need for additional imaging, whereas further imaging is indicated if skeletal scintigraphy is positive. Scintigraphic findings suggestive of an osteochondral lesion include abnormal localization at the site on all three phases. Early detection and treatment of an osteochondral defect is associated with improved outcome. Reflex sympathetic dystrophy has identifiable antecedent trauma in two thirds of the reported cases. Autonomic dysfunction results in pain, vasomotor disturbances, decreased function, and trophic changes. Conventional radiographic findings are nonspecific, showing patchy demineralization of the bones in the affected extremity. Skeletal scintigraphy can be useful in further evaluation; findings depend on the stage of disease.[63] Stage 1 (0 to 20 weeks after trauma) is characterized by increased radiotracer delivery to the affected limb on flow and blood pool images. Delayed images show increased activity in a juxta-articular distribution ( Fig. 16A-9 ). Stage 2 (20 to 60 weeks after trauma) has normalization of the flow and blood pool images. Stage 3 (>60 weeks after trauma) may show decreased blood pool activity and normal delayed images. The sensitivity of skeletal scintigraphy in the detection of reflex sympathetic dystrophy is related inversely to symptom duration. Reported sensitivities range from 60% to 96% with a specificity of 92% early in the process.[192] Nonunion is another potential complication after fracture. To be classified as a nonunion, the fracture must be at least 9 months old with no evidence of healing for a 6-month period. Differentiation of the type of nonunion as

Figure 16-A-9 Reflex sympathetic dystrophy in a patient with a history of right wrist fracture. Three-phase bone scintigraphy shows increased tracer delivery to the right distal upper extremity diffusely (arrows) on flow (top) and blood pool (middle) images. Delayed images (bottom) reveal diffuse abnormal uptake in the wrist (arrow) and increased activity in a juxta-articular distribution (arrowheads).

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hypertrophic or atrophic has management and prognostic implications. Bone scintigraphy is useful in determining which type of nonunion exists.[49] Hypertrophic nonunion has healing potential and shows hypervascularity and increased activity at the fracture site on blood pool and delayed images. If scintigraphy shows decreased vascularity and a photon-deficient band between the fracture fragments on delayed images, this is indicative of an atrophic nonunion. Atrophic nonunion requires more aggressive treatment for a longer duration. Orthopaedic Infections

Multiple nuclear medicine studies are available to aid in the evaluation of suspected infection in the orthopaedic patient. Although conventional radiography typically is the

initial imaging study performed on a patient with suspected osteomyelitis, classic findings of bone destruction and periosteal reaction usually are absent during the first 10 to 14 days after onset of symptoms. Three-phase or four-phase skeletal scintigraphy can differentiate superficial cellulitis from osteomyelitis in the absence of underlying complicating factors, and a negative study can exclude osteomyelitis. Cellulitis shows diffuse increased uptake in the flow and blood pool phases with normal delayed images. Osteomyelitis manifests as increased activity within the distribution of the involved bone on all phases. The addition of a fourth imaging phase, obtained 24 hours after radiotracer administration, increases diagnostic accuracy by allowing for additional soft tissue clearance and improved localization of focal bone uptake.[150] The sensitivity of bone scintigraphy in the detection of osteomyelitis exceeds 95%; however, the specificity depends on the underlying condition of the bone. The role of bone scintigraphy is limited in bone that has been violated by trauma or surgery. In this setting, imaging with labeled leukocytes or gallium-67 citrate improves specificity. Leukocytes can be labeled with indium-111 or Tc-99m hexamethylpropylene amine oxine (HMPAO) with similar overall results in the detection of infection. The advantage of Tc-99m HMPAO is rapid imaging time, 0.5 to 3 hours after injection.[192] Leukocytes accumulate in hematopoietically active marrow and at sites of infection. A region of focally increased white cell activity or activity outside the normal distribution of active marrow signifies infection.[146] Bone infarction or joint prosthesis placement can alter the distribution of bone marrow, making labeled leukocyte studies difficult to interpret. Dual tracer techniques can be employed with the addition of a Tc-99m sulfur colloid bone marrow template. Both radiotracers accumulate in bone marrow; however, only white cells localize to sites of infection. Discordant leukocyte activity in the absence of corresponding sulfur colloid activity indicates infection.[49] This dual tracer technique has reported accuracies of 89% to 98% in the diagnosis of infection.[146] Vertebral osteomyelitis is a notable exception to the utility of labeled leukocytes in the diagnosis of infection. For reasons not understood completely, false-negative findings occur in 50% of the cases. The best scintigraphic method for the evaluation of suspected vertebral osteomyelitis is the use of combined bone and gallium-67 citrate scintigraphy. Characteristic bone scintigraphic findings include intense uptake in two adjacent vertebral bodies. Gallium enhances specificity and can identify extraosseous extension of the infection.[146] Bone Tumors

Plain films obtained in the setting of trauma may reveal an unsuspected osseous lesion. Bone scintigraphy can be performed to evaluate the metabolic aggressiveness of an incidental skeletal lesion. Scintigraphic findings must be correlated with other imaging modalities and cannot differentiate benign from malignant bone tumors. An additional advantage of bone scintigraphy lies in its ability to survey the entire skeleton, allowing for detection of a polyostotic process. Screening for the presence of osseous metastases in a patient with a known malignancy is one of the most widely used applications of bone scintigraphy. Bone scintigraphy has a limited role, however, in the evaluation of primary bone malignancies.

Although most primary bone tumors avidly accumulate the radiotracer, skip lesions and tumor margins cannot be assessed accurately. The hypervascularity induced by some primary bone tumors results in diffuse increased tracer activity throughout the affected limb, which is not reflective of tumor extent.[1] The primary role of radionuclide bone imaging in this setting is evaluation for distant skeletal metastases. Pediatric Orthopaedics

Pediatric trauma can result in epiphyseal plate injury. The probability of growth disturbance or angular deformity is based on the Salter-Harris classification scheme. Patients with Salter-Harris types III through V injuries are at high risk for complications and may benefit from bone scintigraphy, which is capable of detecting alterations in blood flow and physeal function.[49] The epiphyseal plates in children normally accumulate radiotracer in a homogeneous and symmetric fashion. Soon after injury, bone scintigraphy shows increased blood pool and increased delayed uptake in the affected growth plate.[117] Later, scintigraphy plays a role in assessing growth potential. Premature physeal closure results in decreased flow and decreased radiotracer uptake on delayed images. [76] Apophyseal avulsions are another type of growth plate injury common among young athletes. The tendons, ligaments, and capsular attachments in children are stronger than the physeal cartilage, predisposing to avulsion injury.[76] These injuries may be difficult to identify on plain film if the avulsed fragment is small, minimally displaced, or nonossified. Early after injury, skeletal scintigraphy shows hyperemia and focal abnormal tracer accumulation on delayed images.[53] For suspected nonaccidental trauma, initial evaluation should consist of a radiographic skeletal survey. The advantages of conventional radiography include the ability to date fractures and improved sensitivity in the detection of old fractures, which may no longer have increased osteoblastic activity. Skeletal scintigraphy plays an ancillary role and most often is reserved for cases of suspected abuse with negative or equivocal conventional radiographic findings.[117]

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Computed Tomography

The introduction of CT in the 1970s represented a major advancement in the ability to image musculoskeletal injuries. CT provides significantly better soft tissue contrast than conventional radiography. The narrow x-ray beam used in CT scanning allows for clear depiction of complex anatomy, while overcoming the limitations of conventional tomography by eliminating the blurring of overlying structures. The benefits of CT scanning were realized almost immediately, and CT rapidly evolved into the imaging modality of choice to evaluate radiographically occult fractures and to delineate further fractures of complex anatomic structures, such as the axial skeleton or articular

surfaces. Conventional CT consists of a rotating x-ray tube emitting a collimated radiation beam and multiple detectors to measure transmission through a stationary patient. A computer then processes the data to provide a two-dimensional or simulated three-dimensional image. Technical advances have led to the development of helical or spiral CT scanning. Uninterrupted scanning combined with continuous patient movement through the gantry results in a helical pattern of data acquisition.[91] Advantages of this technique include volumetric data acquisition and significantly shorter scan times, resulting in less patient motion. The volumetric data set can be reformatted into higher quality multiplanar two-dimensional and three-dimensional images than those obtained by conventional CT scanning methods. Scanning parameters, such as collimation, reconstruction interval, and pitch, vary among institutions and influence image quality. With helical CT, slice reconstruction can be performed at any interslice increment regardless of the slice thickness used to acquire the volumetric data set. Images can be reconstructed in a contiguous or overlapping fashion. Slice overlap decreases partial volume averaging and improves two-dimensional and three-dimensional image reconstruction quality. The use of thinner collimation during data acquisition can improve image quality. Typically, small body parts, such as the wrist and foot, are imaged with narrow collimation (1 to 3 mm), and larger areas of interest are scanned with wider collimation (3 to 5 mm).[71] [152] The pitch is defined as the table speed divided by the collimation with higher values resulting in decreased longitudinal resolution. In musculoskeletal imaging, a pitch of 1 to 2 most often is used. One of the most important roles of CT is in the evaluation of acute articular injuries. Although conventional radiography is the initial imaging study of choice in skeletal trauma, CT is a useful adjunct that is readily available, fast (seconds), and able to provide exceptional bone detail in multiple planes. The primary roles of CT in acute skeletal trauma include evaluation of a clinically or radiographically suspected fracture not well delineated on conventional radiographs and more definitive evaluation of a known fracture for preoperative planning. Shoulder

Many patients after shoulder dislocation or trauma benefit from CT examination. Scapular fractures often are subtle, and overlying structures can obscure visualization on conventional radiographs. CT is sensitive in the detection and characterization of scapular fractures and can determine associated injuries to the adjacent osseous structures, chest wall, and lung.[152] Helical CT can be used to evaluate the glenohumeral joint. The glenohumeral joint is visualized best on reformations angled in relation to the joint in the oblique coronal and oblique sagittal planes.[71] After anterior shoulder dislocation, fractures can occur as a result of impaction of the humeral head against the anterior-inferior bony glenoid rim. Small Hill-Sachs and Bankart's fractures often are occult on conventional radiographs but depicted clearly on CT. CT can identify easily cartilaginous Bankart's lesions that are

not visible on conventional radiographs.[153] CT plays a role in the evaluation of complex fractures of the proximal humerus. The Neer classification often is applied to these fractures and aids in determining appropriate management.[134] This classification scheme is based on the number of fragments as well as the degree of fragment rotation and displacement. Although conventional radiography often is adequate in the evaluation of two-part fractures, CT has been shown to be a valuable imaging tool in three-part and four-part fractures of the proximal humerus.[90] [94] CT can provide information about the position and alignment of fragments, course of fracture lines, and status of the articular surface of the humeral head and glenoid. Multiplanar and three-dimensional reformations can display complex spatial information for optimal surgical planning. Spine

The cervical spine is one of the most commonly imaged areas in a trauma patient. Traditionally, conventional radiography is the screening method of choice, and CT plays an adjunctive role, by evaluating further regions of suspected or identified abnormality.[14] CT is employed routinely when conventional radiographs fail to show adequately the craniocervical junction or lower cervical spine. This approach has been challenged, and in several major trauma centers CT has replaced conventional radiography as the initial cervical spine screening examination either exclusively or in select patients.[138] Screening CT has many advantages over conventional radiography, including rapid imaging capability and improved diagnostic accuracy. Previous studies comparing these two imaging modalities in the detection of cervical spine fracture showed the superiority of cross-sectional imaging.[2] [196] The routine use of coronal and sagittal reformations to augment axial images of the cervical spine is essential to evaluate alignment and reduce the risk of missing subtle fractures oriented in the imaging plane.[2] Two-dimensional multiplanar images can be supplemented further with three-dimensional reconstructions. The three-dimensional images provide integrated spatial information useful in evaluation of complex vertebral injuries with associated dislocation or rotation abnormalities.[40] [153] Cost is the major impediment to widespread use of CT in screening suspected cervical spine injuries. A risk-tailored imaging approach has been suggested,[10] and a cost analysis investigation concluded that CT is a cost-effective screening tool in patients with moderate or high risk of injury.[11]

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Conventional radiography is the mainstay in evaluating suspected thoracolumbar spine injuries. If an abnormality is suspected or detected on conventional radiographs, CT often identifies additional injuries, including fractures at the same or adjacent levels. [138] CT can determine osseous fragment location and impingement on the central canal. Pelvis

CT is useful in the evaluation of pelvic and acetabular fractures. Although classification

schemes for acetabular fractures are based on conventional radiographic findings, multiplanar two-dimensional CT can provide additional fracture characterization.[18] One study comparing conventional radiography with CT determined that radiography can classify accurately the type of acetabular fracture, but the articular surface and presence of intra-articular bodies are delineated better by CT.[78] Three-dimensional volumetric CT reconstructions can create oblique, inlet, and tangential views to replace conventional radiographs, obviating problems with patient positioning, overlying material, bowel obscuration, and suboptimal exposure.[166] Three-dimensional CT can identify fracture fragments ( Fig. 16A-10 ) and provide an overview of complex fracture lines helpful in preoperative planning. Patients with major pelvic fractures are at risk for arterial injury. Dynamic contrast-enhanced CT imaging at peak arterial opacification can aid in the detection of vascular injury in the hemodynamically stable patient. Contrast agent extravasation indicates active pelvic hemorrhage. In a review of 30 patients with blunt pelvic trauma, CT had an overall accuracy of 90% in detecting the presence or absence of bleeding.[26] CT can influence management by identifying patients that may benefit from early angiographic intervention. Although often unnecessary, CT can be used to evaluate avulsion injuries. Avulsion injuries tend to occur in the adolescent athlete, and the pelvis is the most common site of injury. Conventional radiography typically is sufficient in the diagnosis of acute avulsion injuries. Healing or chronic avulsions may have mixed lytic and sclerotic components, however, mimicking infection or neoplasm. In this

Figure 16-A-10 Fracture of the posterior acetabulum. Three-dimensional computed tomographic image of the pelvis obtained after reduction of a posterior hip dislocation shows a posterior fracture fragment (arrow). (Courtesy of William Morrison, MD, Philadelphia, Pa.)

situation, CT is helpful in differentiating an avulsion injury from a more aggressive process.[175] Knee

CT typically is not performed in the setting of acute knee trauma. One exception is the use of CT in the evaluation of tibial plateau fractures. Accurate assessment of the degree of comminution, depression, or displacement of fracture fragments influences patient management, and conventional radiographs often underestimate these factors.[135] CT can be performed without removing an overlying splint or cast, and coronal and sagittal reformatted data can provide orthogonal views to optimize evaluation of the articular surfaces ( Fig. 16A-11 ).[153] Hindfoot

The calcaneus is the most commonly fractured tarsal bone, and 75% are complicated by intra-articular extension and involve the subtalar or calcaneocuboid joints (or

both).[135] Two major categories of intra-articular fractures include the joint depression-type and the tongue-type calcaneal fractures. Fractures involving the subtalar joint often divide the sustentaculum tali of the calcaneus into anteromedial and posterolateral fragments. [194] The posterolateral fragment may be fractured further to form a thalamic portion comprising the depressed portion of the posterior facet. These two-part and three-part calcaneal fractures have varying degrees of comminution. In joint depression-type fractures, the fracture line frequently extends anteriorly to involve the calcaneocuboid joint.[44] Helical CT is superior to conventional radiography in characterizing calcaneal fractures. Multiplanar reconstructions are required to determine fracture fragment displacement, rotation, degree of comminution, and articular congruity. All three planes are required for optimal preoperative planning.[45] Coronal images ( Fig. 16A-12A ) accurately display disruption of the superior portion of posterior facet, depression of the sustentaculum tali, and loss of calcaneal height. Axial images ( Fig. 16A-12B ) best show the inferior portion of the posterior facet, widening of the calcaneus, and extension of the fracture into the calcaneocuboid joint. Sagittal images depict rotational displacement of fracture fragments. In addition to providing excellent bone detail, CT can provide important information about adjacent soft tissue structures. [15] Calcaneal widening can displace fragments laterally and medially, resulting in injury to adjacent tendons. Lateral calcaneal widening can damage the adjacent peroneal tendons. A normal tendon is homogeneous in density, well defined, and surrounded by fat. Partial tendon rupture results in tendon enlargement and heterogeneous intrasubstance density ( Fig. 16A-12C ). Obscuration of the adjacent fat plane indicates hemorrhage. A complete tendon tear results in a defect in the tendon. CT can be used to assess peroneal tendon subluxation, dislocation, or impingement. Medial injuries are much less common, and CT can be used to detect changes in the abductor hallucis longus and posterior tibialis tendons.

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Figure 16-A-11 Tibial plateau fracture. Axial (A) Computed tomographic images with sagittal (B) and coronal (C) reformations through the knee show a markedly comminuted tibial plateau fracture with step-off and depression of the articular surface. Magnetic Resonance Imaging

Since the 1980s, MRI has revolutionized the evaluation of sports-related injuries. The superb soft tissue contrast and multiplanar capabilities of MRI provide an excellent means of evaluating noninvasively structures such as muscles, tendons, ligaments, cartilage, and bone marrow. The exquisite ability of MRI to depict normal anatomic detail as well as reveal soft tissue injury is unmatched by other imaging modalities. With the exception of the physical examination and conventional radiography, MRI has become the most useful diagnostic tool to evaluate a sports-related injury. The principles of MRI are complex, and a detailed discussion is well beyond the scope

of this chapter. A basic understanding of MRI principles and terminology is essential, however, for the orthopaedic surgeon to gain the maximal benefit from this technology. This section provides a basic framework of knowledge regarding MRI. The Basics

MRI differs from x-ray-generated images (conventional radiography or CT) in that MRI is based on the number of free water protons present within a tissue sample, rather than the density of the tissue sample and absorption of an

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Figure 16-A-12 Calcaneal fracture. A, Coronal computed tomographic (CT) image through the hindfoot reveals a joint-depression type of comminuted intra-articular calcaneal fracture. B, Axial CT image through the hindfoot shows mild medial-to-lateral calcaneal widening and extension of the fracture into the calcaneocuboid joint (arrow). C, Axial CT image with soft tissue windows shows thickening of the short (short arrow) and long (long arrow) peroneal tendons with surrounding fluid, suggesting injury.

x-ray beam.[47] [130] [197] Water protons precess at a set frequency in a given magnetic field strength; this is known as the Larmour frequency. The Larmour equation states that protons precess at a rate that is directly proportional to the strength of the magnetic field. As the strength of the magnetic field increases, the rate of precession of the free water protons also increases. When a patient is placed in a strong magnetic field, the free water protons align with the external magnetic field ( Fig. 16A-13 ). In MRI, a series of radiofrequency (RF) pulses are applied to the tissue sample, which causes the protons to change their alignment relative to the external magnetic field. The energy released during this realignment of protons is used to create the MRI image. After the RF pulses cease, the protons realign with the external magnetic field, and the process begins again ( Fig. 16A-14 ). The essential components of MRI include a homogeneous magnetic field, gradient coils, RF coils, and one or

571

Figure 16-A-13 Effect of a strong magnetic field on hydrogen protons. The axis of spin of hydrogen protons in the absence of a magnetic field is random. When a tissue sample is placed in a strong magnetic field, the axis of spin of the hydrogen protons aligns with the main magnetic field. B o is the direction of the main external magnetic field.

more computers. The main magnet is responsible for creating the homogeneous

magnetic field, and three types of magnets currently are commercially available: superconducting, resistive, and permanent. The superconducting magnets are used in high field strength systems and are the most common type in use today. Superconducting magnets are capable of creating a magnetic field strength greater than 0.5 Tesla (T). (Tesla is the unit of measure of a magnetic field; 1 T = 5000 Gauss; 1 Gauss = the strength of the earth's magnetic field; 1 T = 5000× the strength of the earth's magnetic field.) Resistive and permanent magnets are used in lower field strength systems, typically less than 0.4 T. Gradient coils provide three-dimensional localization of the precessing protons within a tissue sample. Gradient coils create weaker magnetic fields that are superimposed on the main magnetic field, which results in a predictable

Figure 16-A-14 Effect of the radiofrequency (RF) pulse on the axis of spin. The axis of spin of the hydrogen protons is aligned originally with the main magnetic field. A 90-degree radiofrequency excitation pulse is applied, rotating the axis of spin into the longitudinal plane, which allows the photons to be measured. Over time, the protons realign with the main magnetic field and are ready to begin the process again. B o is the direction of the main external magnetic field.

Figure 16-A-15 Gradient coils. A gradient coil is simply a weaker magnetic field superimposed on the main magnetic field, resulting in a predictable stepwise change in the strength of the magnet. This allows for spatial localization of the signal received from the tissue sample. B o is the direction of the main external magnetic field.

stepwise variation in the strength of the overall magnetic field ( Fig. 16A-15 ). As stated by the Larmour equation, as the strength of the magnetic field changes, the rate of precession of the water protons varies predictably along the course of the tissue sample, allowing for three-dimensional localization of the acquired data. RF coils are radio antennas that transmit and receive RF pulses. The transmitting and receiving of RF pulses may be accomplished by a single coil or by two separate coils. The purpose of the transmitting RF coil is to create an energy pulse, which, in turn, excites the protons within the tissue sample, altering their position relative to the external magnetic field. As the RF pulse subsides, the protons begin to relax and gradually realign with the main magnetic field, resulting in energy emission. The receiving RF coil measures this energy, and computers process the data, creating either a two-dimensional or a three-dimensional image.

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Figure 16-A-16 Standard spin-echo pulse sequence. The standard spin-echo pulse sequence consists

of a 90-degree excitation pulse followed by a 180-degree refocusing pulse. The resulting echo is responsible for creating the magnetic resonance image. Time to echo (TE) is the time interval between the initial excitation pulse and the echo. Time to recovery (TR) is the time it takes to complete one entire cycle of radiofrequency (RF) pulses. In a spin-echo sequence, it is the time interval between the initial 90-degree RF pulse and the subsequent 90-degree RF pulse.

A surface coil is a small RF coil that is placed directly on the body part to be imaged, such as the knee or ankle. The close proximity of the surface coil to the body part results in more precise localization of the energy released from the precessing water protons. The widespread introduction of surface coils in the 1990s resulted in a significant improvement in image quality, allowing improved visualization of subtle abnormalities, such as partial-thickness tendon tears or small cartilage defects. Terminology

Pulse Sequence.

A pulse sequence is a specific series of RF pulses or gradient changes that result in excitation and realignment of water protons in a predictable fashion, allowing for the creation of a MRI image. Spin-echo (SE), gradient echo (GRE), and inversion recovery (IR) sequences are the basic types of pulse sequences used in musculoskeletal imaging, although many variations exist for each type. The SE sequence is a series of RF pulses that begins with a 90-degree RF pulse, causing excitation of the protons, followed by a 180-degree RF pulse, which refocuses the protons. The receiving RF coil listens at a specific time for the energy released (echo) by the realigning protons ( Fig. 16A-16 ). The T1 -weighted and T2 -weighted SE sequences are obtained in this manner. A fast spin-echo (FSE) is a variation of the SE sequence in which the image is obtained by applying multiple 180-degree refocusing pulses to a tissue sample after each 90-degree RF pulse, obtaining several echoes per cycle ( Fig. 16A-17 ). FSE imaging is discussed in greater detail later, but the primary benefit of this type of imaging is a significant reduction in imaging time. The GRE sequence begins with a RF excitation pulse, which is called the flip angle, which typically is less than the 90-degree RF pulse applied in the SE sequence. Rather than a 180-degree refocusing pulse, a reversal of the gradient coils is applied to the excited tissue. After a specified time, the receiver coil listens for the energy being emitted by the relaxing water protons ( Fig. 16A-18 ). The IR sequence is similar to the SE sequence except it begins with a 180-degree RF pulse, followed by a 90-degree excitation pulse, then by a 180-degree RF refocusing pulse ( Fig. 16A-19 ). Numerous variations of the IR sequence exist, but the primary IR sequence used in musculoskeletal imaging is the short tau inversion recovery (STIR) sequence, which is a method of providing fat saturation. Time to Recovery.

The time to recovery (TR) is the time it takes to complete an entire sequence of RF

pulses (measured in milliseconds). In a SE sequence, it is the time interval between the initial 90-degree RF pulse and the subsequent 90-degree RF pulse ( see Fig. 16A-16 ). The length of the TR affects the T1 -weighting of an image and is directly proportional to the length of the imaging time required for a given sequence. If the TR interval is doubled, the imaging time for that sequence also doubles. Time to Echo.

The time to echo (TE) represents the time interval between the initial RF pulse and when the receiver coil listens for the returning signal (measured in milliseconds) ( see Fig. 16A-16 ). The length of the TE is the primary factor determining the T2 -weighting of a pulse sequence (the longer the TE, the heavier the T2 -weighting). Inversion Time.

The inversion time (TI) is the time interval between the initial 180-degree RF pulse and the 90-degree RF excitation pulse applied in an IR sequence (measured in milliseconds) ( see Fig. 16A-19 ). This interval determines the type of tissue suppression that occurs in a particular IR pulse sequence. A specific TI must be chosen to produce fat saturation in the STIR sequence. T1 -Weighted Sequences.

A T1 -weighted sequence is a

Figure 16-A-17 Fast spin-echo pulse sequence. A fast spin-echo sequence differs from a standard spin-echo sequence because multiple 180-degree refocusing pulses are applied during each cycle. This markedly shortens the imaging time because multiple echoes are obtained during each cycle. RF, radiofrequency; TR, time to recovery.

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Figure 16-A-18 Gradient echo pulse sequence. This sequence begins with a radiofrequency (RF) excitation pulse, which is called the flip angle and is typically less than the 90-degree RF pulse applied in a standard spin-echo sequence. The echoes are produced by a reversal of the gradient coils rather than by a 180-degree refocusing pulse.

specific type of SE sequence that has a short TR (400 to 800 msec) and a short TE (2000 msec) and a long TE (>70 msec). The T2 -weighted sequence takes longer to acquire than the T1 -weighted sequence because of the longer TR, which is directly proportional to the imaging time. T2 -weighted images have a decreased signal-to-noise ratio relative to T1 -weighted images, and as a result, the anatomic detail is less well defined. On T2 -weighted images, water is bright, however, and T2 -weighted sequences are sensitive for detecting pathology. T2 -weighted images should be studied closely for evidence of soft tissue injury. Proton Density Sequences.

A proton density (PD) sequence is also a SE sequence, which has a long TR and a short TE. Signal characteristics are similar to T1 -weighted

Figure 16-A-19 Inversion recovery pulse sequence. This sequence is similar to the spin-echo sequence except it begins with a 180-degree radiofrequency (RF) pulse, followed by 90-degree excitation pulse, then by a 180-degree RF refocusing pulse. The time interval between the first 180-degree pulse and the 90-degree excitation pulse is the time to inversion (TI). The length of the TI is responsible for creating the fat saturation in a short tau inversion recovery image.

sequences in that muscle is intermediate; fat is bright; calcium, tendons, and fibrocartilage are dark; however, water signal is brighter than on a T1 -weighted sequence. PD has the highest signal-to-noise ratio of any of the SE sequences, and it provides improved detection of soft tissue abnormalities over T1 -weighted sequences. T1 -weighted and PD images have similar sensitivities for detecting meniscal abnormalities. Fast Spin-Echo Imaging.

FSE imaging is a variation of the SE sequence that uses multiple 180-degree refocusing RF pulses after each 90-degree RF excitation-pulse ( see Fig. 16A-17 ). The number of 180-degree refocusing RF pulses applied per TR (or per cycle) is called the echo train length (ETL). The ETL is inversely proportional to the imaging time required for a particular sequence. If the ETL is 8, the sequence can be obtained in one eighth the

time required to obtain the standard SE sequence, all other imaging parameters being equal. FSE imaging is used primarily in T2 -weighted imaging and can provide significant time savings. A T2 -weighted FSE image is similar to a standard SE T2 -weighted image except that fat is much brighter on a FSE image. As the ETL increases, blurring of the image occurs. Most T2 -weighted FSE sequences in musculoskeletal imaging use an ETL of 8 to 16 without clinically significant blurring of anatomic structures. Gradient Echo Sequences.

A GRE sequence, similar to a SE sequence, begins with a RF excitation pulse (flip angle); however, the flip angle is reduced ( /das/book/view/29309971/1103/346.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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Section B Differences between the Immature and Mature Skeleton George W. Gross MD The evolution of the fetal skeleton, from the immature skeleton and support structures of childhood to the mature skeleton of the adult, involves a progression of histologic and morphologic changes with corresponding changes in appearance on various imaging techniques. This chapter briefly reviews the process of skeletal maturation and demonstrates related radiographic and other imaging findings. Several normal variants and potentially confusing imaging findings as well as a few categories of diseases and disorders occurring in the immature skeleton are discussed and illustrated. Inclusion of the wide variety of disease processes involving the immature and mature skeleton and related structures, however, is beyond the scope of this chapter. Imaging Options

Imaging of the musculoskeletal structures is currently possible by several techniques. Conventional radiography, the oldest and most widely employed, generally provides excellent anatomic detail at relatively low cost, with a limited radiation dosage, and without the need for patient sedation. Although differentiation of a wide variety of normal variants and pathologic conditions from normal osseous structures is possible with conventional radiography, all soft tissue structures other than fat (e.g., muscle, tendon, ligaments, bursae) have the same beam attenuation characteristics on radiography and therefore cannot be distinguished as individual structures. Ultrasonography is excellent at differentiating soft tissue structures that are not mineralized (e.g., cartilage, ligaments, tendons), is relatively low in cost, involves no ionizing radiation, and does not require patient sedation. Except in the youngest child, in whom bone mineralization and cortical thickness are limited, ultrasonography typically cannot penetrate cortical bone and therefore provides no meaningful information

regarding osseous structure. Computed tomography (CT), higher in cost and radiation exposure and often requiring sedation of younger children, generally provides the greatest display of bone detail but provides only limited differentiation of various soft tissue structures. The increasing availability of spiral CT with rapid data acquisition has decreased the need for sedation in younger children.[36] Tissues of differing composition will produce different attenuation values, expressed as Hounsfield units, permitting their differentiation on the CT image. For example, CT images will demonstrate an increase in whiteness as a result of increasing attenuation values in changing from air to fat to soft tissue (e.g., tendons, ligaments, muscles) to calcified structures (e.g., bone). There are several advantages of CT over conventional radiography: cross-sectional anatomic display; the ability to manipulate the gray scale of the image to better define certain types of tissue; and the ability to reconstruct new images in other planes (multiplanar two-dimensional reformatted images and three-dimensional imaging).[36] Contrast resolution of CT is superior to that of radiography but inferior to that of magnetic resonance imaging (MRI).[11] Magnetic resonance imaging provides the best overall differentiation of various soft tissue structures but only limited assessment of cortical bone. MRI provides unique information about internal joint structure and integrity and is the best imaging modality for evaluation of bone marrow. MRI does not involve exposure to ionizing radiation but is relatively highest in cost and may require sedation in young children. MRI of the musculoskeletal system typically involves a variety of pulse sequences: conventional spin-echo for T1 -weighted images; fast (turbo) spin-echo for proton-density and T2 -weighted images; two-dimensional gradient echo; three-dimensional gradient echo; inversion recovery for fat suppression; and magnetic transfer techniques.[11] Discussion of the technical aspects of MRI is beyond the scope of this chapter. Radioisotope imaging of the skeleton is usually obtained with technetium 99m coupled to methylene diphosphonate (Tc 99m MDP).[23] The resultant bone scan may involve several phases: blood flow, blood pool, and delayed imaging to demonstrate isotope incorporation into bone.[23] The bone scan is superior to the other imaging options in providing information on metabolic activity but inferior in terms of displaying anatomic detail.[23] Although the mature, adult skeleton normally demonstrates a relatively homogeneous distribution of isotope, the immature or pediatric skeleton shows a heterogeneous distribution with higher concentrations in the regions of the growth centers ( Fig. 16B-1 ).[23]

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Development and Maturation of the Musculoskeletal System

The imaging findings in the pediatric musculoskeletal structures evolve during childhood in conjunction with the development and maturation of the musculoskeletal structures themselves.[20] The skeletal structures providing support and movement are initially cartilaginous but progressively grow and ossify at a variable rate and to a predetermined degree.[20] The bone marrow is predominantly hematopoietic in the neonate and infant but progressively changes to predominantly fatty marrow during childhood.[20] The fetal skeletal system begins as a condensation of primitive mesenchymal cells, which are then transformed into precursors of membranous bone or cartilage.[20] The

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Figure 16-B-1 Radionuclide bone scan in a child. Increased isotope accumulation occurs normally at sites of increased metabolic activity in the immature skeleton, such as the ends of ribs, physes of long bones, and iliac apophyses (arrows). These hot areas are not normally present in the mature, adult skeleton and could be mistaken for sites of disease in the immature skeleton. LAO, left anterior oblique; RAO, right anterior oblique.

cranial vault and the facial bones originate directly from mesenchyme by the process of intramembranous ossification. The long bones, the vertebrae, and the base of the skull are initially cartilaginous. Via a process known as endochondral ossification, the cartilage is transformed into bone.[20] Immature cartilage differs from adult or mature cartilage in several respects. On gross inspection, immature cartilage appears blue-white in color owing to vascular structures in underlying immature bone and is relatively thicker because it includes both an

articular component and a site for endochondral ossification. There is greater variation in zonal characteristics, and immature cartilage is more uniformly cellular.[24] Articular hyaline cartilage in the adult contains no blood vessels, lymphatics, or nerves and is composed predominantly of extracellular matrix containing a relatively small number of chondrocytes.[27] The extracellular matrix is composed predominantly of water (60% to 80% by weight), collagen, and proteoglycans.[27] Mature hyaline cartilage has been divided into four zones based on microanatomic and ultrastructural features: superficial or tangential zone (3% to 12% of cartilage thickness), intermediate zone (>12%), deep radial zone (>50%), and zone of calcified cartilage.[11] Appendicular Skeleton

Most tubular bones in children have a generally similar structure, consisting of a diaphysis (the shaft), the metaphysis (which is situated between the diaphysis and the growth plate or physis), the growth plate itself, and the epiphysis or apophysis. [20] The epiphysis resides between the growth plate and the adjacent joint.[20] Most epiphyses are entirely cartilaginous at birth.[20] The epiphyseal ossification centers (termed secondary centers of ossification) appear in a predictable pattern within certain age ranges. [20] Appearing spherical initially, the epiphyseal ossifications become progressively hemispherical as they enlarge.[20] The time of appearance and the pattern of growth of the epiphyseal ossification centers are part of the determination of skeletal maturation ( see Fig. 16B-2 ).[20] The epiphyseal margin adjacent to the joint surface is lined by articular cartilage.[20] Most epiphyses of long bones are partly extra-articular. The epiphyseal vessels, which supply the ossification center, the epiphyseal cartilage, and the physis, course directly from their origin into the epiphysis. The apophysis, a secondary center of ossification that is not articular, is typically located at the site of insertion of muscles into bone and generally does not contribute to longitudinal bone growth.[20] Otherwise, apophyses are similar in development and structure to epiphyses.[20] The physis, composed of parallel columns of cartilage cells (chondrocytes) and surrounded by the fibro-osseous zone of Ranvier, is a flat disk at birth but becomes irregularly curved with age.[20] The chondrocytes undergo mitotic activity on the epiphyseal side of the physis in the germinal or resting zone, which consists of stem cells adjacent to the epiphysis.[20] Longitudinal growth of bone occurs at the physis by a process known as endochondral ossification, which reflects both cellular division in the proliferative zone and an increase in the size of the chondrocytes in the hypertrophic zone.[20] [39] The hypertrophied cells ultimately die, and the surrounding matrix mineralizes in the zone of provisional calcification, immediately adjacent to the metaphysis.[20] With approaching skeletal maturity, the physis becomes progressively thinner and more undulating in contour.[20] The pattern of physeal closure usually varies

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according to site.[20] Widening of a bone reflects appositional bone growth by the

periosteum.[38] The junction of the physeal cartilage and the metaphyseal bone is the weakest part of the growing skeleton.[20] This junction is held together in the periphery by a ring of perichondrium, which resists shearing stresses and is also a barrier to the spread of subperiosteal disease. [20] The metaphyseal cortex of tubular bones in children is thin, porous, and breakable, whereas the diaphyseal cortex is thicker and stronger.[20] The physis and the juxtaphyseal metaphysis increase their diameter by membranous growth at the zone of Ranvier complex. [20] Although of considerable structural importance, the diaphysis of tubular bones in children is less metabolically active.[20] The periosteum is loosely attached to the diaphysis.[20] Infections, tumors, and hematomas can easily elevate the periosteum of the diaphysis and spread through the subperiosteal space.[20] In the diaphysis, transverse bone growth is due primarily to deposition of periosteal (intramembranous) new bone along the shaft.[20] The earliest diaphyseal ossification, termed the primary ossification center, occurs around the main nutrient vessel, which penetrates the diaphyseal cortex and branches toward each metaphysis.[20] The terminal branches form tight loops near the physis.[20] Arterial blood subsequently empties into large venous sinusoids in the medullary portion of the metaphysis.[20] By comparison, the epiphysis is invaded by juxta-articular vessels that stimulate the formation of the secondary centers of ossification.[20] During the first 18 months of life, the epiphyseal and metaphyseal vessels anastomose across the physis.[20] During childhood, these anastomoses gradually disappear and the physis becomes an avascular structure that serves as a relative barrier to the spread of infections and tumors.[20] Therefore, during childhood, the physis lies between two vascular beds, one epiphyseal and the other metaphyseal.[20] The epiphyseal vessels supply oxygen and nutrients, and an intact epiphyseal vasculature is essential to sustain the chondrocytes.[20] The metaphyseal vessels interact with the physeal chondrocytes in the hypertrophic zone and may contribute to the death of these cells, a process necessary for endochondral ossification.[20] The metaphyseal vasculature must be intact to sustain normal ossification.[20] Skeletal (striated) muscle consists of muscle fibers grouped in fascicles that are separated by septa of fibroadipose tissue, the perimysium.[11] [12] The entire muscle is enclosed within the epimysium. [11] [12] Tendons consist of dense connective tissue and are highly resistant to traction forces.[13] Separated by a limited amount of ground substance and elongated fibroblasts, the densely packed collagen fibers are arranged in parallel bundles.[11] [13] The peritenon is a layer of loose connective tissue that wraps around the tendon and includes intratendinous septa between the bundles of collagen fibers.[11] [13] At the musculotendinous junction, interdigitation between the muscle fibers and the collagen fibrils occurs.[13] The site of insertion of tendons into bone is associated with heavy calcification of the bone and the presence of some cartilaginous tissue.[13] With aging, the amount of ground substance and the number of fibroblasts decrease while the

number of fibers and fat deposition increase.[13] Spine

The bony spine develops in the fetus in three stages: membrane development and spinal segmentation (up to 6 weeks gestational age); chondrification (6 to 8 weeks); and ossification (9+ weeks).[35] Each half of each vertebral body has two chondrification centers, whereas each half of the posterior vertebral arch has one center, all of which eventually fuse and ossify.[35] Bone Marrow

Bone marrow, located within portions of the trabecular skeleton, is responsible for replenishment of various hematopoietic elements, which include platelets as well as both red and white blood cell lines.[1] [47] Red marrow, beefy red in appearance on gross inspection, is hematopoietically active and is composed of approximately 40% water, 40% fat, and 20% protein.[1] [45] [46] [47] Yellow marrow, so termed because of its yellowish appearance on gross inspection, has only limited blood cell development and is composed of approximately 80% fat, 15% water, and 5% protein.[1] [45] [46] [47] In a healthy person, marrow undergoes conversion from hematopoietically active red marrow to hematopoietically inactive yellow marrow in an orderly and predictable way.[1] [31] [33] [50] At birth, all marrow is hematopoietically active. [1] [5] [33] [47] By 1 year of age, marrow in the epiphyses and apophyses has become inactive.[1] [5] [18] [21] [33] [47] [50] With increasing age during childhood, red marrow continues to convert to yellow marrow but at a slower rate.[1] [5] [47] This change to yellow marrow is from distal to proximal (from the appendicular to the axial portions of the skeleton) and from the diaphyses toward the metaphyses of long bones.[1] [5] [33] [47] [50] Conversion of marrow in the flat bones such as the pelvis lags behind that of the extremities.[1] [5] [47] Marrow in the spine is usually the last to become inactive.[1] [29] [45] By ages 21 to 24 years, the adult marrow pattern has been achieved; the appendicular skeleton has predominantly yellow marrow, whereas almost all remaining red marrow is in the sternum, the pelvis, and the vertebrae. [5] [31] [33] Adult marrow, although predominantly fatty, retains a large reserve that is not used under normal conditions but is available for the formation of blood cells.[31] Activation of quiescent hematopoietic precursors in fatty marrow, termed marrow reconversion, may occur with stress, anemia, and marrow infiltrative disorders. [31] Marrow reconversion occurs in the reverse pattern of conversion of red to yellow marrow and is recognizable with MRI.[31] Bone Remodeling

The long bones of children normally undergo remodeling known as tubulation, during which the diameter of bone decreases from a wide physeal region to a more narrow tubular shaft.[20] Normal tubulation reflects concurrent transverse widening of the physis, longitudinal endochondral lengthening of the physis, and osteoclastic remodeling of the

cortex of the metaphysis. [20] Overtubulation

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results in an increased concavity of the outer margins of the metaphyses and relative thinning of the shafts of long bones. Neuromuscular disorders, disuse of an extremity, and certain syndromes tend to produce overtubulated long bones in children. Undertubulation results in a decreased concavity of the outer margins of the metaphyses and an expanded-appearing bone, especially in the metaphyseal regions. Marrow packing or storage disorders, bone dysplasias, bone tumors, and osteoclastic or osteocytic dysfunction with resultant lack of normal osteolysis may all produce undertubulated long bones in children. Skeletal Maturation

The estimation of gestational age in the newborn is usually by history or physical or neurologic examination. The chest radiograph of the premature or term newborn can provide considerable information for estimating gestational age, based on the humeral epiphyses, tooth mineralization, and thoracic spine length. The proximal humeral ossification center is usually present between 40 and 42 weeks of gestational age in 82% of newborns.[20] [39] Based on the presence or the absence of tooth mineralization within the cusps of the tooth buds of the first and second deciduous molars, a minimum of 33 weeks' gestation is present if the first deciduous molar is mineralized, 36 weeks if the second molar is mineralized.[20] Thoracic spine length in the newborn may be compared with standard tables for determination of gestational age.[20] Estimation of skeletal maturation is important in the diagnosis and management of many pediatric disorders, including endocrinologic disorders, abnormalities of stature, scoliosis, and limb length discrepancies. Skeletal maturity is usually estimated by comparing the child's pattern of ossification in the left hand and wrist with standards developed by Greulich and Pyle ( Fig. 16B-2 ). [10] [14] [20] Other methods are less widely used.

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Bone and Related StructuresImaging Appearances

The imaging modalities used in evaluation of the musculoskeletal system in general demonstrate similar findings in both pediatric and adult skeletons. Some differences do exist, however, and are discussed next. Cortical Bone

Cortical bone appears on conventional radiography as a zone of white density, owing to its maximum x-ray beam attenuation. A narrow zone of markedly increased echogenicity at sonography represents the near-complete if not complete reflection of the incident ultrasound beam at the near cortical surface of bone, accompanied by acoustic shadowing and lack of deeper anatomic definition ( Fig. 16B-3 ). [16] Cortical bone also appears whiter than other musculoskeletal structures on CT imaging, again owing to

Figure 16-B-2 Progressive skeletal maturation as occurs at the hand and wrist. Anteroposterior view of a hand and wrist in three separate male children, aged 6 years (A), 12 years (B), and 18 years (C). In the newborn, the metacarpal and phalangeal epiphyses are unossified and not visible on conventional radiography. In a relatively consistent pattern, development and progressive enlargement of the epiphyseal ossification centers occur. At skeletal maturity, the regional physes (arrows) close as the epiphysis (secondary ossification center) fuses with the metaphysis/diaphysis (the primary ossification center). This pattern of evolution of skeletal maturation occurs throughout the immature skeleton, with the age at individual physeal closure variable at any specific site.

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Figure 16-B-3 Ultrasonography of the neonatal hip. Coronal (A) and transverse (B) images demonstrate the relatively hypoechoic cartilaginous femoral head (large arrow) with numerous punctate echogenic foci. The cartilaginous labrum (arrowheads) is relatively hyperechoic, whereas adjacent striated muscle (small arrows) shows midlevel echogenicity. Cortical bone demonstrates high echogenicity at its near surface, beyond which is acoustic shadowing.

its greater beam attenuation ( Fig. 16B-4 ). The lack of mobile protons and consequent long T2 relaxation time of cortical bone results in a signal void (black zone) appearance at MRI ( Fig. 16B-5 ).[31] The delayed imaging phase of the three-phase Tc 99m MDP bone scan shows low-level, relatively homogeneous isotope activity within cortical bone ( see Fig. 16B-1 ). There is little if any difference in these appearances in the immature as compared with the mature skeleton. The Growth Plate (Physis)

The normal growth plate or physis in the immature skeleton varies in appearance both with age and with type of imaging modality employed. On conventional radiography, the growth plate appears as a zone of soft tissue density between the epiphysis and the metaphysis that is oriented approximately perpendicular to the long axis of a long bone. For flat bones, the contour of the growth plate generally follows that of the bone overall ( Fig. 16B-6 ; see Fig. 16B-2 ). Before the appearance of an epiphyseal or apophyseal ossification center, the growth plate is not defined radiographically as a separate structure. With advancing skeletal maturation, the radiographic growth plate will progressively narrow, in large part owing to ossification of an increasing portion of the adjacent, initially cartilaginous epiphysis. As skeletal maturity approaches, the remaining radiolucent zone will be predominantly, then entirely, growth plate. With achievement of skeletal maturation, the growth plate disappears as a separate structure and does not exist in the mature or adult skeleton.

Figure 16-B-4 Axial plane computed tomography (CT) image of the hip joints in an infant. Ossification of pubic (P) and ischial (I) bones is present. The intervening lucent zone (small arrows) represents a portion of the triradiate cartilage, which will progressively narrow with increasing age, eventually disappearing at skeletal maturity. The femoral heads (large arrows) are entirely cartilaginous at this age and therefore show soft tissue attenuation on CT. A tiny ossific nucleus is suggested in the right femoral head. The ossified proximal right femoral metaphysis (M) is visible in this CT slice.

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Figure 16-B-5 Axial T1 -weighted magnetic resonance image of a knee in a child. Fatty marrow in the patella (P) and the femoral condyles (F) is of typical high signal intensity, as is the subcutaneous fat. Striated muscle bundles (M) are of mid to low signal intensity, whereas cortical bone (long arrow), blood vessels (short arrow), and tendons (arrowheads) all demonstrate a signal void and appear black.

On ultrasonography, the growth plate can be identified as a zone of interruption of the very high echogenicity of adjacent cortical bone, accompanied by through-transmission of the sound wave to deeper tissues, which is not permitted by cortical bone ( see Fig. 16B-3 ). [20] On CT, the growth plate appears as a zone of soft tissue density, similar to unossified cartilage and darker than bone, owing to lower beam attenuation. Because the typical axial-plane imaging of CT tends to be parallel or oblique to the growth plate, volume averaging with inclusion of adjacent mineralized (calcified) bone usually results in an increase in attenuation (greater whiteness) compared with growth plate density alone.[33] Both the physis and the adjacent unossified epiphyseal cartilage are demonstrated on MRI ( Figs. 16B-7 and 16B-8 ). The cartilaginous epiphysis has a lower signal intensity

Figure 16-B-6 Normal unossified zones in the pelvis of the immature skeleton: proximal femoral growth plates adjacent to the apophysis (A) and epiphysis (B); triradiate cartilage (C); and ischiopubic synchondrosis (D). None will be present in the adult, mature skeleton.

Figure 16-B-7 T1 -weighted coronal plane magnetic resonance image of the lower legs in a 13-year-old boy with osteosarcoma of the distal right femur. The zone of low signal intensity (arrow) in the right femoral shaft reflects tumor involvement of the medullary cavity and is accompanied by cortical destruction. The opposite lower leg demonstrates normal high signal intensity of yellow marrow bordered by absence of signal in the intact cortical bone (arrowheads). Tumor or other disease processes originating in the metaphysis or diaphysis of the immature skeleton typically do not cross the physis (curved arrow) to reach the epiphysis and adjacent joint.

than does the physis on T2 -weighted images.[28] The physis is most conspicuous on gradient-recalled echo and fat-suppressed spin-echo proton-density-weighted images.[28] With gadolinium enhancement MRI, enhancement is greater in the physeal than in the epiphyseal cartilage.[1] Physeal enhancement decreases with physeal closure at skeletal maturity.[2] The evolving pattern of ossification of 603

Figure 16-B-8 Sagittal T1 -weighted image of the foot and ankle in a child. The bone marrow (m), including that in the distal tibial epiphysis (e), demonstrates signal intensity characteristic of fat, as does the pre-Achilles fat pad (f). The distal tibial growth plate (straight arrow) is of midlevel signal intensity, typical for growth plates throughout the immature skeleton on T 1 -weighted images. The Achilles tendon (curved arrow) is black, owing to signal void.

different epiphyses can be followed by MRI.[5] [6] [17] Post-traumatic bony bridging of the growth plate is uniquely demonstrated by MRI.[6] [29]

On radionuclide bone scintigraphy employing Tc 99m MDP, the growth plate demonstrates high tracer localization and resultant high imaging brightness owing to its greater osteoblastic activity, which causes intense accumulation of isotope ( see Fig. 16B-1 ). [23] Selective preferential isotope localization at the growth plate continues throughout childhood. At the time of physiologic physeal closure, the osteoblastic activity of the growth plate intensifies and then progressively decreases until closure is completed.[23] The activity on the bone scan of different growth plates varies according to patient age, location in the skeleton, and phase of metabolic activity. [23] The mature, adult skeleton will not demonstrate increased isotope activity at former growth plates that have closed. Cartilage

Normal, healthy cartilage appears as soft tissue density on conventional radiography in both the immature and the mature skeleton ( see Fig. 16B-6 ). In the immature skeleton, articular cartilage cannot be distinguished from unossified epiphyseal or apophyseal cartilage destined to develop into bone. Cartilage appears relatively hypoechoic with ultrasound (US) imaging ( see Fig. 16B-3 ) and is usually accompanied by through-transmission of the sound beam.[11] [16] [22] In children, larger cartilaginous structures such as the proximal humeral epiphysis and the femoral head show tiny specular echoes reflecting vascular channels within the cartilage ( see Fig. 16B-3 ).[16] Blood flow to the unossified neonatal femoral head and its interruption during hip abduction is definable by power Doppler US, an important clinical issue in the management of developmental dysplasia of the hip.[3] Cartilage is of soft tissue attenuation density on CT ( see Fig. 16B-4 ). [33] Hyaline cartilage on T1 -weighted MRI appears uniformly hypointense.[27] On T2 -weighted MRI, hyaline cartilage appears trilaminar: The superficial zone is relatively hypointense; the intermediate zone is hyperintense; and the deep zone is hypointense.[11] [27] Alternating hyperintense and hypointense layers within the deep zone have been described.[11] [48] Contrast-enhanced MRI has shown that in the unossified epiphysis, the vascular channels are mainly parallel but develop a radial pattern with the development of the secondary ossification center.[2] An age-related variation in MRI signal intensity within the cartilaginous epiphysis of the distal femur has been shown to occur normally.[44] Contrast-enhanced MRI of the infant spine demonstrates normal enhancement of cartilage, which is not seen in older children and adults.[40] On the radionuclide bone scan in the immature skeleton, articular cartilage as well as unossified epiphyseal or apophyseal cartilage is relatively photopenic, in contrast to the increased isotopic activity of the growth plate ( see Fig. 16B-1 ). Bone Marrow

Conventional radiography cannot identify bone marrow as such and cannot distinguish between red and yellow marrow. The radiopacity of cortical bone determines the density

of bone, with no contribution from marrow. The inability of the US wave to penetrate the cortex of bone precludes imaging of bone marrow with ultrasonography. CT is excellent at distinguishing cortical bone from the marrow-containing medullary cavity.[47] The ability of CT to differentiate the soft tissue density of red marrow from the fat density of yellow marrow is limited and of little practical value.[47] MRI is the best imaging modality currently available for evaluating bone marrow ( Fig. 16B-9 ; see Figs. 16B-5 , 16B-7 , and 16B-8 ). [30] The lipid component of marrow provides a marker for marrow evaluation with MRI.[30] In the spin-echo technique, the predominance of fat content occurring in yellow marrow produces high signal intensity (whiter image) on T1 -weighted images and intermediate signal intensity (grayish image) on T2 -weighted images.[1] [7] [30] [46] With its lower fat content and higher water content, red marrow has a low-to-intermediate signal intensity on both T1 - and T2 -weighted images.[1] [29] [45] [46] Rapid-acquisition MRI sequences result in higher signal intensity of the fatty marrow than is typically seen on standard T 2 -weighted images.[1] [46] Because the high signal intensity of fat may mask abnormalities within the medullary cavity of bone, suppression of the high fat signal using fat suppression or short inversion time recovery techniques will allow any process with relatively high water content to become more apparent through higher signal intensity.[1] [28] Epiphyseal marrow in newborns is normally hypointense in the newly formed epiphyseal ossification center owing to the presence of red marrow, but within a few months it becomes hyperintense owing to the normal transition to fatty marrow.[19] [31] In marrow of the extremities, gadolinium enhancement on MRI has been shown to be greater in the hematopoietic metaphysis than in the fatty epiphysis, with enhancement decreasing as marrow becomes more fatty.[9]

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Figure 16-B-9 T1 -weighted midsagittal magnetic resonance image of the neonatal spine demonstrates low signal intensity of red, hematopoietic vertebral body marrow (arrows). With increasing age, fatty marrow with high signal intensity will replace the red marrow.

The evolving pattern of red and yellow marrow signal intensity on MRI throughout childhood is consistent in terms of differences in signal intensity but differs in the pattern of distribution within the skeleton, as described previously. [7] [8] [9] [30] [37] [40] Thus, red and yellow marrow on MRI in the child has the same appearance in the adult but with differing ratios and distribution that are age related.[7] [30] Radionuclide evaluation of bone marrow can be direct (physiologic assessment of either hematopoiesis [e.g., radiolabeled iron] or phagocytosis [Tc 99m sulfur colloid]) or indirect (focus on total marrow content, regardless of its components [Tc 99m MDP]).[47] Although scintigraphy can provide a sensitive physiologic survey of the entire skeleton, it has low specificity and lacks anatomic detail.[47]

Ligaments, Tendons, Menisci, Fasciae, and Bursae

Conventional radiography cannot distinguish between ligaments, tendons, menisci, fasciae, and bursae because all appear to be of similar soft tissue density. Although also of similar soft tissue density, fluid within a bursa or a joint may be apparent on radiography if adjacent fat planes are displaced. The appearance of ligaments on US is highly variable, from hyperechoic (usually) to hypoechoic, depending on the angle of insonation.[4] [11] Tendons appear to be of medium-level echogenicity on US, with a fibrillar echotexture that is well seen on longitudinal scans.[4] [11] [12] [13] [15] [22] On transverse scans, most tendons are round to oval.[12] Tendons are not as well visualized at US when surrounded by echogenic fat instead of hypoechoic muscles.[12] Many of the tendons of the extremities can be examined by sonography.[12] Articular disks, menisci, and bursae all appear hyperechoic on the US scan.[11] The margins of a joint bursa appear markedly echogenic.[4] [22] Fluid within a joint or a bursa is usually anechoic or black, owing to a lack of internal reflectors for the US beam.[4] [22] Debris within joint or bursal fluid will produce varying reflectors and therefore variable punctate tiny echogenic foci within the zone of fluid. Fascia appears hyperechoic on US.[11] The normal synovial membrane cannot be detected by US.[4] Ligaments, tendons, bursae, and menisci are all of soft tissue attenuation density on CT.[11] [33] Fascia tends to show increased attenuation on CT.[11] Addition of intravenous contrast enhancement results in little if any increase in density of these structures. The likelihood of greater amounts of adipose tissue occurring in adults will improve delineation of soft tissue planes at CT and differentiation of muscles and other soft tissue components of the skeletal system. On MRI, ligaments appear as linear, low-signal-intensity structures joining adjacent bones and are often delineated by contiguous high-signal fat.[11] [32] [33] [38] When there is interposition of fat between ligamentous fibers, a heterogeneous pattern may occur on MRI.[32] [38] Tendons appear as low-signal-intensity structures with all MRI sequences ( see Fig. 16B-5 ).[33] [38] T 1 -weighted images generally provide good anatomic detail, whereas T2 -weighted images better define various pathologic processes involving tendons.[38] Fascia (e.g., plantar aponeurosis of the foot) has low signal intensity on all MRI sequences, often uniformly hypointense.[11] [43] Articular disks, menisci, and labra appear hypointense on MRI.[11] In general, there is little if any difference in the appearance of the aforementioned structures for the various imaging modalities discussed, when comparing the immature and mature skeleton. Striated (Skeletal) Muscle

On conventional radiography, skeletal muscle appears as homogeneous soft tissue

density unless there are sufficient interspersed zones of fat to provide enough density contrast to differentiate individual muscles or muscle groups. All normal skeletal muscle has a similar appearance on ultrasonography.[12] The perimysium appears on longitudinal scans as oblique, parallel, echogenic striae against a markedly hypoechoic background, representing the mass of muscle fibers; on transverse scans, it appears as finely dotted echoes and short lines scattered throughout the hypoechoic muscle ( see Fig. 16B-3 ).[4] [11] [12] [15] The intermuscular fasciae are brightly echogenic.[4] [12] The echogenicity of striated muscle is generally less than that of tendon and subcutaneous tissue.[4] Contracted muscle is more echoic than relaxed muscle.[4] Striated muscle appears to be of intermediate to low

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signal intensity on T1 -weighted MRI, slightly higher than that of water and much lower than that of fat ( see Fig. 16B-5 ).[25] [26] [43] On T2 -weighted MRI, skeletal muscle shows much lower signal intensity than that of both fat and water. [25] [26] On inversion-recovery and fat-suppressed T2 -weighted images, normal muscle signal intensity is much lower than that of water but higher than that of fat.[26] Spine

Vertebral bodies in the neonate tend to be rectangular in the thoracic region and oval in the lumbar region, as seen on the lateral radiograph ( Fig. 16B-10 ).[35] Between 3 and 6 weeks of life, a bone-within-a-bone appearance is a common finding radiographically.[35] Anterior and posterior vascular channels ( see Fig. 16B-10 ) are normally present in neonates. The anterior channels usually disappear during infancy, whereas the posterior channels may persist into adulthood. [35] Ring apophyses appear in the middle and lower thoracic and upper lumbar regions at approximately 6 years of age.[35] Initially cartilaginous, they are associated with a lucent defect at the respective vertebral body corners ( Fig. 16B-11 ). When ossified, the ring apophyses are recognizable as a structure distinct from the adjacent vertebral body ( Fig. 16B-12 ). The ring apophyses fuse with the vertebral body by the age of 18 years to form the characteristic adult rectangular vertebral body configuration. [35]

Figure 16-B-10 Normal neonatal spine. A lateral view in a newborn demonstrates a relatively oval configuration to the vertebral bodies and a prominent anterior vascular channel notch (arrow)normal appearances for this age.

Figure 16-B-11 Vertebral body corner defect reflecting unossified ring apophyses. The anterosuperior corner of the lumbar vertebral bodies demonstrates a deficiency of ossification (arrows) owing to lack of

ossification of the ring apophysis normally present at this site. This normal appearance will change first to a focus of ossification and later to fusion of the apophysis with the rest of the vertebral body, resulting in the squared-off configuration seen in the mature skeleton. Congenital and Developmental Variants Common to the Pediatric Skeleton

There are a number of anatomic variants limited to the pediatric skeleton that can serve as sources of confusion or misinterpretation, some of which are discussed next. 1. Physiologic periosteal new bone formation. Periosteal new bone can be seen paralleling the cortices of long bones during the first few months of life in at least one third of infants. One or more thin lines that closely parallel the cortex of the diaphysis in a bilaterally symmetrical manner are characteristic of this phenomenon ( Fig. 16B-13 ). 2. Dense transverse metaphyseal bands. Transverse lines of increased radiopacity across the width of the metaphyses of long bones and adjacent to the physis of other bones are normally seen in children aged approximately 2 to 6 years ( Fig. 16B-14 ). Attributed to a relative flattening of bone growth rate, they remain adjacent to the physis and are not left behind with longitudinal bone growth. Confusion with dense metaphyseal bands caused by heavy metal intoxication is possible. 3. Vacuum phenomenon of pediatric joints. Traction on the relatively lax joints of younger children may produce

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Figure 16-B-12 Lateral view of several lower thoracic vertebrae in a 10-year-old girl. Ossification of the ring apophyses of the vertebral bodies (arrows) has occurred. These foci of ossification, which will enlarge and eventually fuse with the adjacent vertebral body, are not present in the mature skeleton.

a crescentic zone of lucency representing negative intra-articular pressure and the production of gaseous nitrogen within the joint ( Fig. 16B-15 ). This occurs most commonly at the shoulder joint with traction restraint of children for chest radiography. 4. Pseudofracture due to contour undulation of

Figure 16-B-13 Physiologic periosteal reaction of the newborn, as represented by periosteal cloaking of the diaphyses of the femora and tibias (arrows). To be considered physiologic, the periosteal reaction must be symmetrical, diaphyseal in location, and not associated with any osseous sclerosis or destructive change.

Figure 16-B-14 The metaphyses of long bones of the immature skeleton, adjacent to the growth plate, will demonstrate relative sclerosis (arrows) compared with the epiphysis and diaphysis that is physiologic but that resolves by skeletal maturity.

the growth plate. Owing to contour undulation of a physis, a portion of a given physis may project at a different level than the rest of the physis, resulting in two separate lucencies, one of which may be misinterpreted as a fracture. This pseudofracture occurs most commonly in the proximal humerus ( Fig. 16B-16 ).

Figure 16-B-15 Fever and hip pain in a 23-month-old. The frog lateral view of the left hip demonstrates a crescent-shaped lucency (arrow) centered in the hip joint space, representing the vacuum phenomenon produced by distraction of the femoral head from the acetabulum by positioning of the leg. The greater joint laxity occurring in younger children permits creation of an intra-articular vacuum, seldom seen in the mature skeleton except in some cases of advanced degenerative arthritis.

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Figure 16-B-16 Pseudofracture due to undulating growth plate contour. An axial view of the proximal humerus in a child demonstrates two separate zones of lucency (arrows) that represent two different segments of the same growth plate, projecting at different levels on the radiograph. The more distal lucent zone could be mistaken for a fracture in the setting of trauma.

5. Ischiopubic synchondrosis. Irregular ossification and expansion of the synchondrosis between the ischium and the pubis frequently occur in prepubertal children, producing a swollen or bubbly appearance of the synchondrosis and resulting in potential confusion with osteomyelitis or fracture ( Fig. 16B-17 ). 6. Irregularities of ischial ossification. Irregularity in the pattern of ossification occurs frequently in the ischia of preadolescents and adolescents and may involve the cortical margin, the tuberosity, or the descending ramus. Confusion with osteomyelitis and avulsion injury is possible.

Figure 16-B-17 The ischiopubic synchondrosis in the immature skeleton frequently appears asymmetrical, with one side demonstrating irregularity of or exuberant ossification (arrow) that may simulate disease but that is a normal variant and of no clinical significance.

Figure 16-B-18 Failure to ambulate after trauma in a 2-year-old. The irregularity of the pattern of ossification of the medial aspect of the distal femoral epiphysis (arrow) represents a normal variation in

epiphyseal ossification, not a pathologic process.

7. Distal femoral epiphyseal irregularity. The ossification of the distal femoral bony epiphysis is commonly irregular in children, especially during the period of most rapid bone growth. It may be unilateral or bilateral; in the latter situation, it may be asymmetrical. Multiple small ossification centers separate from the main osseous epiphysis may be seen ( Fig. 16B-18 ). 8. Benign cortical defects. Benign cortical defects are small cortical fibrous lesions that appear radiographically as eccentric lucent areas with a thin sclerotic rim in up to 40% of boys and 30% of girls ( Fig. 16B-19 ). Typically located near the perichondrium of the physis at sites of ligamentous or tendinous insertion, they eventually fill in and disappear as the child ages and are rarely seen after

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Figure 16-B-19 The expansile, mixed-density lesion with sclerotic margins in the distal tibial shaft reflects a benign fibrous lesion such as a benign cortical defect or nonossifying fibroma. Common in the immature skeleton, this lesion usually heals during childhood and is uncommon in the mature skeleton.

skeletal maturity. An associated pathologic fracture is possible but uncommon. 9. Femoral avulsive cortical irregularity. Situated along the posterior aspect of the medial femoral condyle just above the adductor tubercle, the avulsive cortical irregularity of the distal femur is considered a response to chronic traction stress ( Fig. 16B-20 ). More common in boys and often bilateral, it occurs most frequently between the ages of 10 and 15 years. 10. Irregularity of the tibial tubercle. An anteroinferior extension of the proximal tibial cartilaginous epiphysis, the tibial tubercle frequently ossifies from several small separate centers. The resultant pattern of ossification can simulate avulsion fracture fragments. 11. Increased density of the calcaneal apophysis. The apophysis of the calcaneus in the immature skeleton is normally denser or more sclerotic than the body of the calcaneus ( Fig. 16B-21 ) and is associated with weight-bearing. At skeletal maturity, when the apophysis fuses with the body of the calcaneus, the apophysis assumes the same density as the rest of the calcaneus. 12. Calcaneal pseudocyst. A normal increase in lucency of the calcaneus anterior and inferior to the posterior calcaneal facet is common in children and can mimic a true pathologic cyst. This finding should be symmetrical. 13. Physiologic bowing of the legs in infancy. Occurring typically in later infancy and early childhood, relative bowleggedness (genu vara) occurs commonly and resolves

spontaneously ( Fig. 16B-22 ).

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Pathologic Processes Skeletal Dysplasias

A comprehensive discussion of skeletal dysplasias is beyond the scope of this chapter.[42] [48] Currently, the skeletal dysplasias are divided into five major groups: osteochondrodysplasias; dysostoses; idiopathic osteolysis; chromosomal aberrations or bony disorders due to abnormalities of other organ systems; and primary metabolic disorders. [20] These disorders vary in their radiographic characteristics and the ease with which they can be recognized based on radiographic findings. In addition, the progressive ossification of the initially dysplastic cartilaginous structures that occurs during childhood facilitates characterization of a given dysplasia, being most difficult in the neonate and least difficult as skeletal maturity approaches. MRI provides considerable information about the nonossified components of a given dysplasia and may facilitate earlier recognition or enhanced accuracy of diagnosis. Patients with skeletal dysplasias who survive into adulthood will retain at least a portion of the dysplastic skeletal changes. Fractures in Children

Fractures in children differ from those in adults in regard to patterns of occurrence, diagnosis, and treatment, reflecting differences in anatomy, biomechanics, and physiology.[20] [34] Whereas the child's skeletal elements are in a constantly changing growth mode, the adult skeleton has completed longitudinal growth and is primarily remodeling established structures in response to stresses placed on it.[20] [34] Compared with the mature skeleton of the adult, the following differences can be noted: 1. The immature skeleton has a higher occurrence of fractures, often after limited trauma. 2. The diagnosis of many fractures is more difficult owing to the radiolucent growth plate and variable mineralization of the epiphysis.

3. The increased metabolic activity results in more rapid healing of fractures, with nonunion being rare. 4. Joint injuries, dislocations, and ligamentous disruptions are much less common.[34] The physis is avascular after infancy but interacts with the blood vessels of the epiphysis and the metaphysis.[20] [34] The supply of oxygen and nutrients to the epiphysis and most of the physis comes from the epiphyseal vessels, which usually originate from vessels in the adjacent joint capsule.[20] [34] The diaphysis is supplied by periosteal vessels and by nutrient vessels that enter the bone in the midshaft, at the site of the earliest ossification of the bone, and branch toward the metaphyses.[34] Metaphyseal vessels interact with the chondrocytes of the hypertrophic zone of the physis as part of the process of chondrocyte death and ossification.[34] Injury to the epiphyseal vessels may result in ischemic injury to the physeal chondrocytes and ultimately in growth arrest. Injury to the metaphyseal vessels results in blockage of endochondral ossification and persistence of cartilage within the metaphysis. Small vessels cross from the metaphysis

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Figure 16-B-20 Anteroposterior (A) and oblique (B) views of the knee. Situated along the posteromedial aspect of the distal femoral metaphysis is a short segment of apparent cortical destruction and faint periosteal reaction (arrow), termed the avulsive cortical irregularity. This is a benign, self-limited process that reflects stress reaction from the adductor magnus tendon insertion and is of no clinical significance.

into the epiphysis only during the first 18 months of life and after physeal closure at skeletal maturity. Acute injury to the physeal cartilage can be diagnosed with radiography only by changes in its width, by displacement

Figure 16-B-21 Lateral view of hindfoot demonstrates a relative increase in density of the apophysis (arrow) compared with the rest of the calcaneus. This normal apophyseal hyperdensity will resolve by skeletal maturity.

Figure 16-B-22 Outward bowing of the lower extremities at the knees (genu varum) is a common but physiologic malalignment that is usually symmetrical and spontaneously corrects with age. The primary differential diagnostic considerations are Blount's disease and rickets.

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of the epiphysis from its normal relationship with the metaphysis, or by altered structure of adjacent bone.[20] [34]

Although thicker and stronger in a child and more resistant to disruption than in the adult, the periosteum has less firm attachments to the shaft of bone than in adults and is more readily elevated from the diaphyseal and metaphyseal bone.[34] The firmest attachments are at the ends of long tubular bones at the physeal-metaphyseal junctions.[34] Common in children, post-traumatic subperiosteal collections typically stop at the zone of Ranvier. The child's periosteum is capable of producing exuberant callus after fracture. [34] In a child, periosteal and endosteal reactions after fracture are more active than in the adult, permitting greater correction of post-traumatic longitudinal deformities.[34] Compared with that of the adult, a child's bone is more porous and can tolerate a greater degree of deformation without fracturing.[34] The pediatric bone is more likely to bend without actually fracturing or to sustain only a partial fracture than is the adult bone ( Figs. 16B-23 and 16B-24 ). [20] [34] Growth Plate Injuries and Complications

The epiphyseal-metaphyseal complex (consisting of the epiphysis, the physis, the zone of Ranvier, and the metaphysis)

Figure 16-B-23 An anteroposterior view of the lower leg in an 8-year-old child with trauma to the medial aspect of the ankle region. The resultant greenstick fracture, which involves the medial but not the lateral tibial cortex, is a reflection of the greater flexibility of the immature bone and would be rare in the mature skeleton.

is involved in up to 18% of long bone fractures in children.[20] [34] The physeal region is the weakest part of the child's skeleton, and, because the physeal cartilage is not as strong as the periarticular ligaments and the joint capsule, trauma in the child is more likely to produce separation at the physis than dislocation at the adjacent joint ( Fig. 16B-25 ).[34] The most frequent sites of fracture of the physis are the distal radius, the phalanges of the fingers, the distal tibia, and the distal humerus. [20] [34] Growth arrest may result from direct physeal disruption. Post-traumatic communication between the epiphyseal and the metaphyseal vessels or disruption of the epiphyseal vessels that supply the physeal chondrocytes can produce a bony bridge across the physeal cartilage.[20] [34] Focal or eccentric growth arrest and bony bridging may result in an angulation deformity ( Fig. 16B-26 ). [20] [34] Healing and Remodeling after Fracture

At least partly owing to more rapid osteosynthesis in the immature skeleton, fracture healing occurs much more rapidly in the child than in the adult. Nonunion of a fracture is uncommon in children. Remodeling after fracture healing is also more rapid in children, owing largely to rapid bone turnover. Remodeling usually restores normal alignment in

the plane of motion of the adjacent joint but is less satisfactory when the angular deformity is not in the plane of the joint and when there is rotational deformity. Fracture healing results in longitudinal overgrowth during childhood, so that fractures of long bone shafts are usually allowed to heal with 1 to 2 cm of overriding. Osteomyelitis

Acute osteomyelitis occurs in 1 in 5000 children, a third of whom are younger than 2 years of age. Group B streptococcus is the most common organism in neonates, Staphylococcus aureus in both children and adults.[10] [39] Most acute osteomyelitis in children is hematogenous, arising from transient, asymptomatic bacteriuria or acute sepsis.[20] In children, acute hematogenous osteomyelitis originates in the metaphyses or metaphyseal equivalents of bones ( Fig. 16B-27 ). [20] Owing to local slowing of blood flow in the looping arterial vessels and the sinusoidal venous structures, circulating organisms tend to lodge and proliferate in the metaphysis.[20] The relatively avascular physeal cartilage serves as a relative barrier to the extension of infection into the epiphysis.[20] In children younger than 18 months of age, however, transphyseal vessels still exist, facilitating spread of organisms into the physis, the epiphysis, and even the adjacent joint. [20] Metaphyseal osteomyelitis in adults will more readily spread to the adjacent joint space, in part owing to the absence of the nonvascular physis present in children other than neonates and infants.[39] The increased intraosseous pressure resulting from acute osteomyelitis in the metaphysis often results in spread of infection through the bony cortex, with elevation of the periosteum and invasion of adjacent soft tissues.[20] Infection

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Figure 16-B-24 A, Focal curvature of the distal radial shaft after trauma reflects a bowing or plastic fracture that is a reflection of the greater flexibility of the immature bone and would be rare in the adult, mature skeleton. There is no definable focal cortical disruption. B, Localized periosteal reaction and sclerosis on follow-up radiography (arrow) confirmed the fracture.

Figure 16-B-25 Trauma to the distal right arm in a 10-year-old. Initial radiographs (A) demonstrated considerable regional soft tissue swelling but no apparent fracture or dislocation. Immobilization in a cast was thought to be necessary on clinical grounds because of suspicion of a nondisplaced Salter I growth plate fracture. Follow-up radiographs 1 month later (B) demonstrate widening and irregularity at the growth plate as well as periosteal reaction, confirming the suspected Salter I distal radial fracture.

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Figure 16-B-26 Ankle trauma in a 14-year-old. A, The initial anteroposterior view demonstrates a Salter IV fracture (arrows) of the medial aspect of the distal tibia and a highly probable distal fibular Salter I fracture. B, A 6-month follow-up radiograph demonstrates premature closure of the medial portion of the distal tibial growth plate (arrow).

Figure 16-B-27 Lytic zone with indistinct margins and surrounding sclerosis in the distal radial metaphysis reflects relatively low-grade staphylococcal osteomyelitis. The adjacent growth plate usually acts as a barrier to the spread of infection to the epiphysis and joint space. The metaphysis is the most common site of osteomyelitis in the immature skeleton.

may also spread directly into the medullary cavity and the diaphysis.[20] In the proximal femur and the proximal radius, the joint capsule attaches along the neck of the bone, with most of the metaphysis being intracapsular.[20] At these sites, infection readily extends from the metaphysis into the articular space.[20] Septic arthritis may also result from direct extension from an epiphyseal focus, seen most commonly at the knee joint. [20]

Three fourths of cases of acute hematogenous osteomyelitis in children involve tubular bones, especially the most rapidly growing bones and the largest metaphyses.[20] The proximal and distal ends of the femur are the two most commonly involved sites. [20] The ilium and the vertebrae are the most commonly involved nontubular bones, the site of initial infection being adjacent to bone-forming cartilage.[20] Bone destruction as a reflection of acute osteomyelitis may not be recognizable until 7 to 10 days after the beginning of symptoms owing to insensitivity of radiographs to destruction of less than about 30% of the bone mass.[20] Soft tissue changes, such as deep soft tissue swelling and loss or displacement of adjacent muscle planes, will be apparent much sooner.[20] Three-phase skeletal scintigraphy using Tc 99m MDP is often required to confirm or exclude acute hematogenous osteomyelitis within the first week of active infection. [20] [23] MRI may also demonstrate acute infection earlier than do radiographs, with acute osteomyelitis appearing as a well-defined focal lesion in the metaphysis with a large halo of edema extending into the marrow and soft tissues.[20] The lesion and the halo are of low signal intensity in T1 -weighted images and high signal intensity on T2 -weighted images. MRI is of added imaging value in cases of osteomyelitis of the spine and

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the pelvis and when infection extends into the physis, where it can help focus surgical treatment and decrease the risk of growth arrest.[20] Malignant Bone Neoplasms

There are two main categories of malignant bone neoplasms in children: round cell

tumors and mesenchymal tumors.[20] Round cell tumors such as metastatic neuroblastoma, Ewing's sarcoma, and lymphoma tend to infiltrate bone marrow and do not typically produce tumor matrix.[20] Radiographically, they result in bone destruction, with the response of bone being in the form of periosteal reaction or reactive bone formation.[20] Tumors associated with production of cartilage and bone, such as osteosarcoma and benign cartilaginous tumors, tend to occur near the fastest growing physes and often produce a recognizable tumor matrix.[20] The incidence of malignant bone tumors varies with age and location. [10] [20] [39] Metastatic neuroblastoma is the most frequent cause of tumoral destruction of bone in children younger than 1 year of age.[10] [20] [39] Ewing's sarcoma is the leading primary bone malignancy in children 5 to 10 years of age.[10] [20] [39] Osteogenic sarcoma is the most common malignant bone tumor in adolescents ( see Fig. 16B-7 ).[10] [20] [39] In the adult skeleton, most malignant bone sarcomas occur in those 30 to 40 years of age.[10] [39] Metastatic carcinoma, multiple myeloma, and chondrosarcomas predominate in those older than 40 years of age.[39]

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Conclusion

Although the imaging appearance of the various components of the immature skeleton is often similar to that of the adult, mature skeleton, there are many significant differences, particularly regarding the growth plate of long bones, the appearance of unossified cartilage, the distribution of secondary ossification centers (epiphyses and apophyses), the distribution of isotope on radionuclide skeletal imaging, and the appearance of bone marrow on MRI. In addition, considerable differences in location, appearance, and pattern of healing of fractures exist. There are significant differences in the types of malignant tumors affecting the immature and mature skeleton. Numerous normal variants in the immature skeleton can provide a confusing imaging appearance that may be mistaken for disease.

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Chapter 17 - Special Considerations in the Pediatric and Adolescent Athlete Section A Exercise Physiology Frank A. Kulling EdD Increasing attention is being devoted to the topic of children and physical activity. The reasons are numerous, diverse, and at times based on subjective reasoning. An evolving technology increases personal time but produces sedentary-prone gadgetry for leisure pursuits. Persistent economic woes have affected public education curricula, necessitating a bare bones approach that has increasingly forced the elimination of activity or activity-related classes. Data on the activity and fitness levels of school-aged children, in the last several decades, include the First National Children and Youth Fitness Survey[56] ; The President's Council on Physical Fitness and Sports School Population Fitness Survey[79] ; The Second National Children and Youth Fitness Survey[63] ; and the National School Based Youth Fitness Behavioral Surveillance System.[19] These four surveys disclose the following findings relative to our school-age children: (1) 22% are overweight, a 6% increase from the 1970s; (2) almost 60% do not engage in vigorous physical activity, whereas 25% do not participate in any form of physical activity; (3) upper body strength and aerobic fitness are lower than desirable for at least 50%; and (4) 63% of adolescents have two or more major risk factors for chronic disease. Although the exact interpretation of these results is subject to some debate, experts generally agree that American youth are at increased risk in the future for the chronic, degenerative diseases that ravage our adult population. These concerns and

others have prompted the federal government to publish a number of national health, fitness, and exercise objectives, beginning in 1980[72] and continuing through 2010.[71] If, as these documents recommend, increasing percentages of our school-aged children are to engage regularly in appropriate physical activity to improve fitness and reduce the risk of future chronic disease, it would be prudent to review research directed toward assessing their capacity for, and response to, physical activity. This chapter examines the physiologic systems, organs, and tissues (and their related measures) that could be considered to contribute to health-related fitness.[8] Tanner Classification

The author wishes to acknowledge that the material in this section is derived from the classic work of J. M. Tanner.[70] Interpretation of physiologic phenomena is heavily age and sex dependent. For this reason, it is often necessary to identify developmental benchmarks to impart meaning to physical findings and measures. Often, this is accomplished by using chronologic age; however, because children vary so widely in attaining adolescence and adult maturation, other systems involving the skeleton, dentition, morphology, and secondary sex characteristics have evolved. Because of its close correlation with skeletal maturation and clear delineation of adolescent development, the secondary sex classification system devised by Tanner[70] has received wide acceptance in the medical field. Boys and girls grow and mature at different rates along a chronologic continuum, as depicted in Figure 17A-1 . Tanner, therefore, devised a system for both sexes that judged maturation based on development of the male genitalia, the female breasts, and the pubic hair. Development of each variable occurs in five stages based on size, shape, appearance, and relative changes therein ( Table 17A-1 ). Tanner stage 1 represents preadolescence; stages 2 through 4 represent various levels within adolescence; and stage 5 represents adulthood. The recommended method of assigning a Tanner stage is to average the levels for genitalia or breasts

Figure 17-A-1 Growth curves for boys and girls. (From Tanner JM: Growth at Adolescence. Oxford, Blackwell Scientific Publications, 1962.)

616

TABLE 17-A-1 -- Tanner Stage Ratings for Boys and Girls Pubertal Pubic Hair Genital Breast Stage Development Development 1

None

Testes, scrotum Elevation of about same size and papilla only proportions as in early childhood

2

Sparse growth of long, slightly pigmented downy hair, straight or only slightly curled, appearing chiefly at base of penis or along labia

Enlargement of scrotum and testes; skin of scrotum reddens and changes in texture; little or no enlargement of penis at this stage

Breast bud stage; elevation of breast and papilla as small mound; enlargement of areolar diameter

3

Considerably darker, coarser, and more curled: hair spreads sparsely over junction of pubes

Enlargement of penis, which occurs at first mainly in length; further growth of testes and scrotum

Further enlargement and elevation of breast and areola, with no separation of their contours

4

Hair now resembles adult in type, but area covered is still considerably smaller than in adult; no spread to medial surface of thighs

Increased size of penis with growth in breadth and development of glans; further enlargement of testes and scrotum; increased darkening of scrotal skin

Projection of areola and papilla to form a secondary mound above the level of the breast

5

Adult in quantity and type with distribution of horizontal (or classically feminine) pattern; spread to medial surface of thighs but not up the linea alba or elsewhere above the base of the inverse triangle. In about 80% of Caucasian men and 10% of women, pubic hair spreads further, but this takes some time to occur after stage 5 is reached. This may not be completed until the midtwenties or later

Genitalia adult in size and shape; no further enlargement after stage 5 is reached

The mature stage; projection of papilla only; due to recession of areola to general contour of breast

Adapted from Larson L: Fitness Health and Work Capacity. New York, Macmillan, 1974, pp 516-517. and pubic hair; however, assignment based solely on pubic hair evaluation is often practiced, especially when limited observation precludes relative change comparisons. If pubic hair is used as a maturation variable, 95% of the population begins adolescence (Tanner stage 2) at 10 to 15 years for boys and 8 to 14 years for girls. The progression from Tanner stage 2 to Tanner stage 5 (adulthood) encompasses 4 years on average but may vary by plus or minus 2 years. From this summary, it can be seen that in some

cases, children with the same chronologic age may vary from Tanner stage 1 to Tanner stage 5. Subsequent chapters in this book may mention the Tanner developmental stages, so it is hoped that this cursory introduction will prove beneficial to the reader's understanding. The study of exercise physiology has not relied heavily on the Tanner system, and this author cannot arbitrarily assign such stages to original contributions devoid of such references. For the purposes of this chapter, therefore, ages and maturation levels are reported as they occur in the literature reviewed.

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Differences among Child, Adolescent, and Adult Cardiorespiratory Factors

Information in this section encompasses the cardiovascular and pulmonary organs, tissues, and related measures associated with activity. Cardiorespiratory Potential

A requirement for activity sustained beyond a few moments is the delivery and use of oxygen (O2 ); moreover, the salient associated physiologic variable is maximal O2 uptake (VO2max ). [30] Although it is commonly included in the cardiorespiratory or cardiovascular category, VO2max requires the integrated and effective functioning of several body systems. The heart must provide adequate cardiac output (Q); alveolar tissue must be adequately perfused with air and capillary blood; the circulatory system must deliver O2 and remove the metabolic byproducts of oxidation; and active tissue must be capable of oxidizing food substrates to produce energy. When expressed in absolute terms (L/min), VO 2max increases concomitantly with growth in children until age 18 in boys and age 14 in girls.[12] Until age 12, absolute VO2max values increase at the same rate in both genders, although boys have higher values as early as age 5.[78] Because activity requires the movement of body and body segments through space, VO2max values are often examined relative to body size (mL/kg/min) for comparative purposes. With these relative measures as a criterion, Pate and Blair,[58] Krahenbuhl and colleagues, [46] and Bar-Or[12] all reviewed laboratory studies of children and adolescents and found that VO2max (mL/kg/min) values were significantly in excess of those recorded for an average American adult population. Additionally, Pate and Blair[58] found that children's values were historically consistent for two decades, and Bar-Or[12] found that values in boys remained stable for ages 6 to 17; values in girls were less than those in

boys and remained stable until the age

617

of 11 or 12, then declined each year thereafter. Adult values for a sedentary male tend to remain stable until sometime during the third decade, when progressive decline, averaging somewhat less than 1% per year, begins and continues throughout life.[30] In Bar-Or's review,[12] boys' values encompass a 45- to 57-mL/kg/min range throughout childhood and adolescence, whereas girls' values are approximately 5 mL/kg/min lower until the age of 11 or 12, when a decline begins. An acceptable scientific explanation elucidating the VO2max differences between boys and girls has not been found; however, differences in body composition, particularly during and after adolescence (Tanner stages 2 to 4) constitute a plausible hypothesis. Average relative VO2max values for adults are age and gender dependent; however, using Cooper's data,[24] an average 30to 39-year-old American male would be expected to possess a VO2max of between 30.2 and 39.1 mL/kg/min. Using weight-adjusted VO2max as a criterion, one would likely conclude that children and adolescents are at least the aerobic equals of their adult counterparts. In addition to VO2max , the anaerobic threshold (AT) is often mentioned as a measure of activity potential because it represents the upper limits of activity intensity that can be maintained without subsequent accumulation of endurance-limiting lactate.[75] The reasons for activity cessation in response to lactate accumulation are not completely understood; however, impairment of cellular enzyme activity in response to lowered tissue pH is a possible explanatory factor. When Cooper and colleagues tested 109 boys and girls between the ages of 6 and 17, they found that mean AT was 58% of VO2max . [23] This compares with the results of Davis and colleagues, who found that the mean AT of college-aged males was 58.6% of VO2max .[29] A number of studies have shown that AT in adult males ranges from 49% to 63% of VO 2max , and values for adult women range between 50% and 60% of VO2max . [75] Acute Cardiorespiratory Response

In a closer examination of the acute hemodynamic and ventilatory changes that provide O2 uptake (VO2 ) in support of activity, children respond in a manner that is qualitatively similar to that of adults; however, some quantitative differences may affect activity of high intensity. Specifically, children and adolescents have somewhat higher heart rates (HRs) and arteriovenous oxygen differences (A-VO2 ) and somewhat lower systolic and diastolic blood pressures (SBP, DBP), stroke volumes (SV), and Q at any given level of VO2 . [12] [13] [32] Although research has yet to elucidate the exercise limitations, if any, these differences portend, one could speculate that decreases in Q might be offset by the increased A-VO2 at submaximal activity levels. The same line of reasoning would

predict exercise limitations at maximal or near-maximal activity levels at which A-VO2 extraction rates cannot increase and also during hot, humid conditions, which require increased peripheral blood flow in support of heat dissipation. Children's ventilatory response to exercise is relatively tachypneic, with lower relative tidal volumes (TV) and higher breathing rates (f), ventilation rates (VE ), and ventilatory equivalents (VE /VO2 ) than those occurring in

Figure 17-A-2 Oxygen uptake and age for young males and females walking at various treadmill speeds. (From Astrand PO: Experimental Studies of Working Capacity in Relation to Sex and Age. Copenhagen, Munksgaard International Publishers Ltd, 1952.)

adults.[12] Interpretation of these findings leads to the conclusion that children have a higher relative energy cost associated with breathing and, in this regard, are somewhat inefficient in breathing compared with adults. Changes in these ventilatory variables toward adult equivalents occur both continuously and progressively with growth during childhood and adolescence. [12] This is not surprising because the variable most closely associated with ventilatory volumes is body size. Although children possess more than adequate VO2max and AT levels relative to body size and qualitatively similar hemodynamic and ventilatory responses to acute exercise, they are nonetheless metabolically inefficient at comparable workloads.[12] Daniels and colleagues found that 10-year-old boys expend 26% more energy (VO2 mL/kg/min) than 18-year-olds while running 12 km/hr.[27] Based on the treadmill tests of Astrand,[7] [12] it appears this metabolic inefficiency applies to both boys and girls over a wide range of walking and running speeds until they reach adulthood ( Fig. 17A-2 ). This metabolic inefficiency does not occur during cycling,[80] however, leading to a possible explanatory hypothesis for pediatric gait inefficiency. [27] Musculoskeletal Factors

Information in this section includes factors relating to muscle, bone, joint, and connective and adipose tissue and the related measures commonly associated with activity. The musculoskeletal system provides for movement in two

618

ways: first by converting foodstuffs into chemically usable cellular energy in the form of adenosine triphosphate; and second, by generating and transmitting contractile force that results in the movements of the bony levers that articulate to form bodily joints. [30]

Morphology

It has been known for some time that very young children possess muscle fiber numbers, types, and distribution ratios similar to those of adults. [15] Likewise, resting energy substrates and sources, such as creatine phosphate, adenosine triphosphate, and glycogen, are also similar. [31] Because growth is characterized by a protein anabolic state to support tissue synthesis, children are not likely to be as musculoskeletally stable as adults.[45] The developing tissues most potentially susceptible to instability are bone, articular cartilage, and tendon-bone junctions.[20] At particular risk is the open epiphysis because it is three to five times weaker than the capsular and ligamentous tissues that surround it.[51] Additionally, epiphyseal damage is likely to be of greater consequence in children because it can result in various stages of growth reduction in the affected long bone.[45] The probability of such injury is likely to be the result of a number of interrelated factors in addition to activity itself. [50] The subject of injury will be more completely addressed in subsequent chapters. Strength, Endurance, and Power

Muscular strength, endurance, and power are highly desired attributes in many activities. Maximal muscle strength is usually considered to be the maximum one-effort force that can be exerted against a resistance.[30] Muscle endurance, on the other hand, is the ability to apply repeatedly or sustain a submaximal force over a period of time.[30] Power refers to the amount of work that can be accomplished over time.[30] Although these related concepts are obviously different, many field tests that measure endurance (e.g., sit-ups, chin-ups, pull-ups) are incorrectly labeled as strength measures. Investigators consistently find increases in muscular strength accompanying growth, with maximum values attained during early adulthood in both sexes.[30] Increased strength during maturation is almost entirely due to concomitant increase in muscle tissue growth.[62] The rate of decline in muscle strength in an adult population depends in part on the specific muscle groups tested and on continuing activity levels; however, the decline is generally considered to be somewhat less than 1% per year from the middle of the fourth through the seventh decades of life. [30] Males tend to be stronger than females at any age, particularly with regard to the muscle groups of the upper extremity; however, differences in muscle strength reported by gender and age can be virtually eliminated if strength is expressed per unit of cross-sectional muscle area (kg/cm2 ).[30] Measured as the ability to sustain isometrically a percentage of a maximum voluntary contraction before fatigue occurs, studies of muscle endurance in relation to age are inconclusive.[34] [59] Tests of muscle endurance in both sexes generally show males as superior[2] ; however, most field tests involve only the upper body musculature. One area in which children are markedly inferior to adults is that of anaerobic power production, even when weight-adjusted measures are considered. Using kcal/kg/hr as an objective measure, research has shown that boys are capable of producing more anaerobic power than girls and both steadily progress to adult levels by the end of adolescence.[12] The primary reason for this anaerobic deficiency appears to be the

limited phosphofructokinase activity that occurs in children and early adolescents.[30] Because phosphofructokinase is a key enzyme in glycolysis, this factor alone may cause the reduced anaerobic capacity of children. Although children cannot emulate the activity of adults under anaerobic conditions, the potential detriment may be less than anticipated for a number of reasons. First, most aerobic activities are not significantly above the AT. Second, during activity transitions from a lower to a higher submaximal intensity, children do not require as much time to reach an O2 steady state.[48] Body Composition

Body composition is a difficult area in which to make comparisons because the variables are highly age and gender specific in an adult population and because acceptable and comparable field methods of collecting and assessing data are lacking. As an example, adult skinfold measures commonly employ three to seven sites, whereas children's skinfold measures seldom use more than two. With these shortcomings in mind, if two-site skinfold measures are compared from ages 6 to 18, boys at the 50th percentile show virtually no change, whereas girls show a gradual increase to age 15.[2] Using Lohman and colleagues' equations[3] to estimate body fat from the skinfold sums, it can be shown that body fat in boys at the 50th percentile increases from 10% to 13%, whereas body fat in girls increases from 14% to 25% during the 6- to 18-year time frame. These results are depicted in Figure 17A-3 . These figures remain relatively constant during the college years, [55] but by middle age (40 to 49 years), American males average 20% to 25% body fat, whereas similarly aged American women average 30% to 35% body fat.[67] Using the midpoints of these figures, we can calculate an approximate 8% to 10% increase in body fat between the ages of 25 and 45 for both sexes; therefore, the average increase is approximately 4% to 5% per decade. These figures may be somewhat misleading, however, because body composition comprises lean tissue constituents, primarily muscle and bone, in addition to adipose tissue. Brozek depicted adult changes in body composition as a combination of increasing adiposity and decreasing lean tissue mass.[18] This changed combination could easily be the result of a slowly declining basal metabolic rate[30] and hypokinesis. Flexibility

Flexibility encompasses two basic measures: static or range of motion flexibility and dynamic or motion resistance flexibility.[30] A number of studies[44] [60] [61] indicate that children become less statically flexible as they age, reaching

Figure 17-A-3 Adiposity in young males and females during growth and maturation. The dots on the line with boys' values correspond to (in percents): 10.1, 10.1, 11.1, 12.1, 12.1, 14.1, 13.2, 13.2, 12.1, 12.1, 12.1, 13.2, 13.2. The dots on the line with girls' values correspond to (in percents): 14.1, 15.2, 16.1, 17.1, 18.0, 19.0, 19.0, 19.8, 23.1, 23.8, 23.8, 25.3, 25.3. (Skinfold sums [50th percentile] from AAHPERD: Test Manual: Health Related Physical Fitness. Reston, Va, American Alliance for Health, Physical Education, Recreation, and Dance [AAHPERD], 1980; Percent fat from AAHPERD: Technical Manual: Health

Related Fitness. Reston, Va, American Alliance for Health, Physical Education, Recreation, and Dance, 1984.)

619

minimal levels between 10 and 12 years of age and then improving again toward early adulthood but not sufficiently to emulate childhood results.[30] Because limitations on static flexibility are imposed by muscle, bone, and soft tissue, the early adolescent growth spurt may occasion a short-term tightness about the joints, perhaps as a result of increased tension in connective tissue. Girls appear to be more flexible than boys,[44] [60] [61] an advantage that is likely sustained in adulthood.[30] Static flexibility tends to decrease progressively after early adulthood, and dynamic flexibility decreases with age from childhood.[30] Heat and Cold Adaptability

Heat is a metabolic byproduct of energy production; therefore, the ability to dissipate heat quickly and effectively is crucial to continuance of activity. Because children possess a larger surface area relative to body mass[12] and less subcutaneous fat,[2] [55] [67] one might suspect that they have a disadvantage in dissipating heat and adapting to cold. Additionally, although children possess a higher sweat gland density than adults, they produce far less sweat for evaporative heat dissipation.[10] The result is that children respond with significantly higher skin and rectal temperatures when confronted with heat stress.[12] Additionally, children do not acclimatize to heat as quickly[74] or perceive exercise as intensely as adults.[9] With respect to cold adaptation, a study involving trained male and female swimmers in cold water (20.3°C) showed a linear inverse relationship between core temperature reduction and age.[68]

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Physiologic Response to Training

This section examines documented changes at the systemic, organic, and tissue levels and their associated measures in response to training. Unless otherwise specified, training is assumed to mean those activities that produce the greatest beneficial response in the affected areathat is, endurance activities and cardiorespiratory endurance, resistance activity and musculoskeletal strength, and so on. Cardiorespiratory Function

In response to training, children's absolute performance measures are likely to improve, but VO2max may not.[26] [69] When Rowland examined this subject, he found that 14% mean increases in VO2max occurred, if exercise intensity and duration were commensurate with adult aerobic pre-scriptive criteria.[64] VO2max changes experienced in a healthy adult population depend on age, gender, starting fitness and habitual activity levels, intensity, duration, and frequency of activity, and, most important, heredity. Expected VO2max increases in an average American adult population range from 5% to 25%.[5] Declines in VO2max normally experienced in a sedentary adult population can be effectively forestalled for decades through continued activity.[43] Although more work needs to be done in understanding the pediatric response to endurance exercise, one might speculate that possible improvements in VO2max would tend to be proportionately less because of the relatively high starting values.[12] [46] In both children and adults, training results in lowered heart rates, at rest and at submaximal workloads, whereas stroke volume tends to increase. [17] [30] [41] [69] The resulting combination allows a given Q at a reduced heart rate and an increased Q at maximal and near-maximal workloads. [30] [33] [37] The bottom line, simply put, is attainment of increased physical work capacity, that is, the ability to be active at previously unattainable intensities or to be active for longer periods at similar intensities. Biochemical and cellular explanations supporting increased physical work capacity

response in adults include oxidative cellular shift, increased number and volume of oxidative mitochondria, increased potency of oxidative enzymes, increased glycogen storage, increased efficiency and endurance of accessory ventilatory muscles, increased blood volume, increased total circulating hemoglobin, increased erythrocytic production of 2,3-diphosphoglycerate, increased capillarization of active tissue, increased cellular myoglobin content, increased production of endorphins and enkephalins, and myocardial hypertrophy.[30] [55] Although much needs to be done in determining which activity-induced changes are responsible for increased physical work capacity in children, the available evidence indicates that increased glycogen stores and

620

oxidative enzyme activity[36] as well as increased left ventricular mass[22] [38] are contributing factors. Training has been shown to be capable of increasing both absolute and proportionate (% VO2max ) AT values in adult males.[28] Although more research needs to be done in this area in children and adolescents, at least one study indicated that no such improvement occurred in trained children. [14] Because pulmonary ventilation is so highly correlated with body size, it is difficult to distinguish growth from training-induced changes; moreover, studies involving adequate control group inclusion are few. With these limitations in mind, it appears that children respond in much the same way as adults, showing increases in TV, f, VE , and possibly VE /VO2 . [12] Because these improvements are manifest primarily during the activity bout, one suspects that the increased endurance and efficiency of the accessory ventilatory muscles enhance changes in thoracic volume. Musculoskeletal Function

Morphology

Skeletal muscle hypertrophy has been reported among adolescents participating in sprint training but not endurance training.[36] Although endurance training facilitates a muscle fiber shift toward more oxidative fibers in adults,[30] no such shift has been noted in children.[42] Studies indicate that activity elicits a hypertrophic response in the most heavily loaded areas of immature bone. [6] [49] Strength, Endurance, and Power

A number of investigators have found that most subjects, regardless of age and gender, experience proportionately similar increases in strength in response to a resistive training program.[54] [65] [66] [76] [77] Corresponding increases in muscle hypertrophy are significantly less in females and immature males.[35] [76] [77] A likely explanation for this different hypertrophic response is low circulating androgen levels. Increased strength in

the absence of hypertrophy can be hypothesized to result from neural adaptations[40] or changes in the rate and sequence of motor unit innervation.[25] It has long been known that endurance activities increase the endurance of the muscle groups involved. Cardiorespiratory endurance has been discussed previously; however, we are concerned here with musculoskeletal endurance. The ability of any given activity to induce muscle endurance depends on how closely it incorporates the principles of overload and specificity with respect to the muscles in question.[30] Perhaps the best illustration of these concepts is the fact that a healthy untrained person can increase the number of push-ups, pull-ups, or sit-ups he or she can perform simply by regularly completing such exercises to or near the point of exhaustion. Clarke and Vaccaro[21] found that 9- to 11-year-old boys and girls completing a 7-month swimming program improved arm endurance as measured through push-ups and pull-ups; however, hand grip endurance was not changed. Despite the research that has been accomplished, there is ample room for additional work in this area, particularly in understanding the interrelationship between strength and endurance activities and the extent to which one can influence the other. Body Composition

In adults, activity tends to have both anabolic and metabolic effects and results in increases in lean body tissue and decreases in adipose tissue. The effect of activity on this variable in children is unclear because studies have failed to control for the possibly confounding variables of growth and the amount and composition of food intake. It does appear, however, that obese youths respond to exercise with greater beneficial changes in body composition[53] than their nonobese counterparts.[39] Flexibility

Static stretching can be demonstrated to increase static flexibility in both children and adults.[30] Attempts to elucidate the effects of common activities and exercises on flexibility are likely to be confounded by the fact that they incorporate static stretching as part of their regimen. Connective tissues tend to shorten when placed in a shortened position; therefore, to the extent that hypokinesis reduces motion opportunities among opposing muscle groups, flexibility will tend to decrease. More needs to be done in determining the effects of various activities on flexibility in children, particularly during the growth spurt, when flexibility decreases.[30] Heat and Cold Adaptability

Children and adults become more efficient at dissipating heat when they are exposed to periods of increased activity in a hot environment; however, young adults showed better thermoregulatory responses than either children or older men.[74] More needs to be done in this area, particularly studies that include inactive controls subjected to the same environmental conditions as the subjects of the study.

Health and Disease

Epidemiologic studies conducted in adults show a strong inverse relationship between physical activity or fitness and a number of chronic, degenerative diseases and conditions, including coronary heart disease (CHD); colon, breast, prostate, and lung cancers; hypertension; obesity; type II diabetes; and osteoporosis; and all cause mortality.[16] The degree to which many of these have their inception during childhood is largely unknown; however, CHD is increasingly considered pediatric in origin.[47] Additionally, there is evidence of an inverse relationship between physical activity and CHD risk factors among children.[52] With respect to myocardial infarction, Paffenberger and colleagues found that sedentary Harvard alumni, even those who were physically active as students, were at greater risk than previously

621

sedentary students who became active later.[57] The message here seems to be that children can reduce the risk of at least some degenerative diseases by being active; however, the carryover of this effect into adulthood is likely to depend on maintenance of activity. In this respect, increased attention should be devoted to activities with carryover potential in the hope of increasing adult compliance. Graded Exercise Testing

If increasing percentages of our school-aged children are to become physically active and fit,[71] the use of graded exercise testing for determining pediatric functional capacity may well increase. Contraindications for exercise testing children would be similar to those established for adults.[4] The exercise testing modality would likely use either the treadmill or the cycle ergometer, each possessing unique advantages and disadvantages. The treadmill is likely to be more biomechanically familiar; however, because of the documented metabolic inefficiencies of children during walking and running,[7] [12] [27] accurate calculation of VO2 based on treadmill speed and grade would not be possible. Although this problem has not been shown to exist for cycle ergometry,[80] there may be difficulty in adjusting the ergometer to accommodate the child.[4] Additionally, it may be difficult for the child to adhere to the constant pedaling frequency required. In light of these probable difficulties, VO2 should be directly assessed during pediatric treadmill testing, while close adult supervision and assistance should be available for both modalities. A variety of exercise testing protocols are appropriate for children [4] ; however, specific treadmill and cycle ergometry protocols based on height, weight, and gender, have been published.[11] Criteria for terminating a pediatric exercise test are similar to those published for adults,[4] with the most common physiologic, functional capacity end points being VO2max and attainment of predicted maximal heart rate. Other useful criteria may

include the respiratory exchange ratio and ventilatory threshold.[4] Because children do not perceive exercise as intensely as adults, relative perceived exertion scales may not be useful. Following completion of the exercise test, cool-down and recovery criteria suitable for adults would be appropriate.[4]

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Baseline Data for Treatment Considerations

The vast majority of diseases, illnesses, and conditions that limit activity for children and adolescents are obvious and are diagnosed. Subsequent chapters deal with adapted activities for these special populations; however, it might be beneficial to establish baseline data for some of the measures discussed in this initial chapter. Baseline is interpreted to mean values that encompass the lowest 5% of an age-specific population. Although these values are not in themselves indicative of limiting conditions, they are indicative of limited capacity or undesirable morphology. As such, they should elicit review and investigation by competent personnel with regard to developing an appropriate course of subsequent action. These data include only values for children and adolescents and only values that are applicable by age; therefore, variables correlated with body size are not included. Baseline data are presented in Table 17A-2 .

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Summary and Recommendations

The purpose of this introductory chapter is to examine the physiologic systems, organs, and tissues and their related measures that contribute to health-related fitness[8] in our children and adolescents. The examination is directed toward better understanding the capacity for and response to the increased physical activity thought to be important for children.[71] [72] TABLE 17-A-2 -- Baseline Data (Lowest 5 Percentile) for Health-Related Physiologic Data Age (Years) Measure VO2max (mL/kg/min) AT (mL/kg/min)

Sex

6

7

8

9

10

11

12

M

32

_______________________________

F

26

______________________

M

18

_______________________________

F

16

______________________

27

14

13

14

15

16

17

37 _____________

_______________________ 17 _____________

_______________________

AT (%VO2max )

All 40% ___________________________________________________

Skinfold triceps (mm)

M

13

14

17

20

20

22

23

23

21

21

20

20

F

16

17

20

22

23

23

25

26

27

29

30

29

Skinfold M triceps and subscapularis (mm)

20

24

28

34

33

38

44

46

37

40

37

38

F

26

28

36

40

41

42

48

51

52

56

57

58

M

18

21

24

28

27

30

32

29

30

29

30

30

F

25

26

31

32

33

33

35

35

36

36

36

36

M

6

10

15

15

15

17

19

25

27

28

28

25

F

6

10

12

14

15

19

19

18

20

20

20

19

M

16

_____________

12

12

13

12

15

13

11

15

F

18

16

16

15

17

18

19

14

22

% Body fat Sit-ups (in 1 min) Sit and reach (cm) 23 cm equals level of feet

16

17

17

AT, anaerobic threshold; VO2max , maximal oxygen uptake.

622

The Tanner classification system[70] permits distinction of various maturational levels based on secondary sex characteristics. Using VO2max and AT measures as indicators of cardiorespiratory potential, children and adolescents appear to be at least the equal of their adult counterparts. [12] [23] [24] [29] [46] [55] [75] In response to a single exercise bout, children exhibit cardiorespiratory responses that are qualitatively similar to those of adults. [12] [13] [32] Notable quantitative exceptions include reduced Q[13] and increased VE , f, and possibly VE /VO2 .[12] Partially as a result of these differences, children demonstrate an inverse relationship between relative energy expenditure (VO2 , mL/kg/min) and age while walking and running.[7] [12] [27] This portends difficulty for young children who attempt to emulate absolute adult activity levels. Anaerobically speaking, children are inferior to adults, even when weight-adjusted measures are considered; more-over, progression to adult levels is continuous with growth and maturation.[12] This anaerobic inefficiency is largely due to the limited activity of phosphofructokinase, [30] a key enzyme in the anaerobic glycolytic process. This limitation is not significant at aerobic intensities or during activity transitions within aerobic intensities. Children's muscle tissue is similar to that of adults with respect to the numbers, types, and distribution ratios of muscle fibers[15] ; however, children may be at increased risk of musculoskeletal injury, particularly at the epiphysis.[51] The probability of such injury involves a number of factors in addition to activity itself.[50] Strength continues to

increase with growth to early adulthood, and males tend to be stronger than females at any age, particularly with respect to the upper body musculature. [2] [30] When strength is expressed per unit of cross-sectional muscle area (kg/cm2 ), however, age and sex differences are virtually eliminated.[30] The percentage of body fat tends to increase with age from at least childhood through middle age, with females possessing greater adipose tissue than males throughout life.[2] [3] [55] [67] Flexibility tends to decrease with age, and females are more flexible than males.[2] [30] [44] [60] [61] Because of their relatively large surface area, [12] diminished sweat production,[10] and less subcutaneous fat,[2] [55] [67] children do not adapt to heat[10] [12] [74] or cold [68] as well as adults. Additionally, children do not perceive the intensity of exercise as do adults.[9] In response to appropriate training, children and adolescents also receive most of the beneficial physiologic and performance changes documented for adults,* although there are some questions about the improvements or lack thereof associated with VO2 max,[26] [64] [69] AT,[14] and body composition.[39] [53] Investigators continue to establish inverse relationships between physical activity and degenerative disease risk factors in adult populations.[4] [73] Available evidence indicates that at least CHD may originate in childhood[47] ; moreover, physically active children possess fewer risk factors for CHD.[52] The health protective effects of activity are optimized when activity is continued during the adult years,[57] where physical work capacity and strength, previously thought to decline inevitably with aging, can be maintained at or near maximal levels into the seventh decade of life.[43] [59] Finally, graded exercise testing may play an increasingly important role in determining pediatric functional capacity and potential for physical activity. With appropriate accommodations for size differences and increased assistance and supervision, adult testing criteria are applicable.[4] With respect to graded exercise test protocols, recommendations based on height, weight, and gender have been published.[11]

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Recommendations

Based on the preceding information, it is this author's opinion that children and adolescents have much to gain from beginning and then maintaining an exercise or activity regimen. To optimize the potential benefits and minimize risk, the following recommendations are offered to those involved in the planning and administration of activity programs: 1. An initial physical examination should be required for participants. Ideally, contraindicating or limiting conditions will have been previously diagnosed and known; however, this examination can uncover those conditions that are not known. The examination should include orthopaedic evaluation of the musculoskeletal system and components at greatest risk for injury. 2. Conservative adult criteria should be employed as guides to activity. Activity should be undertaken at the conservative end of relative adult ranges for intensity, duration, frequency, and progression.[5] [55] [80] This author recommends using conservative component ranges owing to proven pediatric metabolic [7] [12] and anaerobic inefficiencies[12] [30] and the increased risk of musculoskeletal injury in children.[20] [45] [51] 3. Activity bouts should include warm-up and cool-down periods. Activity should be preceded and followed by activity of a lesser intensity. Because children do not perceive exercise as intensely[9] and experience shorter O2 uptake transitions,[48] they are more likely to forego warm-ups and cool-downs, thus increasing the risk of musculoskeletal injury. 4. Avoid activity during climatic extremes. Because of their limited response to heat stress,[12] [74] children should restrict their activity during hot, humid conditions. The American Academy of Pediatrics has noted that most heat-related disorders are particularly pronounced in intense activity bouts that exceed 30 minutes' duration.[1] If this restriction is not possible, the intensity of exercise should be reduced, frequent rest

periods should be given, and approximately 150 mL of water should be consumed every 15 to 30 minutes.[12] [80] Drinks containing more than 2.5% solutes should be avoided because gastric emptying will be delayed.[55] Additionally, because children experience greater core body temperature reductions in cold water,[68] exposure to cold water under these conditions should be avoided. 5. Collision or high-risk sports activity should be supervised. To an extent, this is somewhat age dependent. Supervision should be adequate to minimize extraneous hazards and provide required medical attention. 6. The activity environment should emphasize adult carryover potential. Activities should be planned to maximize the participant's potential involvement. Achievement *See references

[ 12] [ 21] [ 30] [ 33] [ 37] [ 38] [ 54] [ 55] [ 65] [ 66] [ 76]

and [ 77] .

623

should be rewarded and recognized for as many participants as possible. Injuries and limiting conditions should receive immediate and appropriate attention, and, if necessary, activity should be suspended to permit proper resolution of problems. Educational components should be included concerning the physiologic and health benefits of the activity. Perhaps the most important attribute of an activity program is its potential for producing active adults.

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Section B Sports and the Neurodevelopment of the Child and Adolescent Helen D. Pratt PhD, DABPS Dilip R. Patel MD, FAAP, FAACPDM Donald E. Greydanus MD, FAAP, FSAM Approximately 20 to 35 million children and adolescents participate in organized sport programs each year, and many more enjoy recreational activities. [39] Participation in sports plays a major role in the lives of parents and children in the United States; for many, it is a means of socialization and physical skill building and a way of teaching prosocial behaviors.[49] [80] Many professionals and parents believe that participation in organized sport activities is essential, and it contributes positively to the growth and development of children and adolescents. Stories of child prodigies who began to learn a specific sport as early as age 3 may encourage parents to question whether or not they too should be enrolling their very young children in sport training programs. This raises the issue of neurodevelopmental maturation and readiness of the child to effectively and safely engage in sports, especially competitive sports. This chapter reviews the definition of neurodevelopment and discusses normal child development (as relevant to sport participation), sport readiness, and growth and maturation during adolescence. The discussion is limited to normally developing children. Some aspects of exercise physiology and sport psychology relevant to this topic will be only briefly reviewed because they are covered in greater detail elsewhere in this book. Several fundamental principles will guide our discussion as follows: Growth and maturation is an ongoing and continuous process.[15] [19] [23] [25] Neurologic, somatic, cognitive, and social development of the child and adolescent progress at the same time as interdependent factors, and therefore must be considered together as one looks at development and sport participation.* Although different developmental milestones are recognized at specific ages,

*See references

[ 34] [ 35] [ 47] [ 52] [ 57] [ 61] [ 63] [ 64] [ 70] [ 81]

and [ 87] .

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appearance of these milestones often varies considerably in different children; however, the sequential nature of development remains the same in normally developing children (i.e., a child must first have neurologic maturity in order to stand and walk; no amount of training will make a child walk before a certain level of neurologic maturity is reached); it is generally well recognized that there will always be children who will be at either end of the developmental spectrum.[3] [7] [29] [32] [34] [57] [61] [72] [81] Health care professionals need to be able to provide information to other professionals, as well as to parents and athletes, about issues of normal growth and development as related to sport participation. A basic understanding of the neurodevelopment of children and adolescents is essential in this regard and will help guide parents and athletes toward making healthy decisions about choosing sport activities appropriate to an athlete's abilities and developmental maturity. In order to effectively engage in and benefit from this involvement, all children and adolescents need to have mastered several fundamental skills.[14] Further refinement of skills is necessary for a child or adolescent to move from participation for fun to participation at a competitive level; at this level, skills must be highly developed to such a degree that limitations will be placed on who can play competitive sports. Children and adolescents who cannot master fundamental skills or who have other impediments to refining those skills can still be involved in sports activities but may require special adaptations or equipment.[49] [84] [87] Virtually all children and adolescents can be involved in sports, with appropriate adaptations to meet the developmental (i.e., physical, cognitive, social, emotional) level of the physically or mentally challenged child.[42] [60] [70] Definition of Neurodevelopment

Neurodevelopment in a broad sense refers to the growth and maturation of the nervous system, as well as of the sensory and perceptual abilities of the child.[29] [30] [32] [35] [43] [63] [64] Normal growth and development is characterized by individual variations in rate of progression and achievement of milestones, and in the sequential nature of this progression. Although development is largely determined by genetic factors, environmental factors (such as opportunity, nutrition, and social context) also play a significant role in the overall development of a child or adolescent. Capute and Accardo[29] noted that motor milestones are mostly influenced by maturation of the neurologic system; on the other hand, social and adaptive skills are influenced largely by environmental factors, such as social expectations, education, and training. The term neurodevelopment encompasses various domains that can be broadly categorized as physical or somatic, neurologic, sensory-perceptual, cognitive, and psychosocial or emotional ( Table 17B-1 ). Gesell[46] described streams of development that include gross motor, fine motor, visual-motor, problem-solving, expressive language, receptive language, and social and adaptive skills. Fagard[40] notes, skill refers to the proficiency with which an integrated activity is carried out. With increasing levels of maturity, levels of integration and interaction among different domains also increase. Although

quantitative TABLE 17-B-1 -- Major Aspects of Normal NeurodevelopmentFunctional Domains and Specific Skills That Represent Aspects of Normal Neurodevelopment Major Aspects of Normal Neurodevelopment Motor Fine motor (precise, specific, and fine neuromotor responses) Gross motor (usually refers to whole body movement; includes coordination, balance, postural control, motor planning, and agility) Muscular strength and endurance Visual Visual acuity, discrimination, tracking, and color vision Extraocular muscle control (resting balance, control of movement, visual-motor coordination) Cognitive Attention (ability to focus selectively and generally on events, actions, and information in the environment) Alertness (or mental processing speed; the ability to respond effectively to environmental cues and stimuli to cause appropriate behavioral adaptation, to optimize positive and minimize negative outcomes) Memory (acquire, store, recall informationshort and long term) Thinking skills (knowledge of specifics; comprehension, application, analysis, synthesis, and evaluation abilities) Decision-making and problem-solving abilities Ability to perform multiple tasks simultaneously Language Receptive language (ability to understand spoken or written language, discriminate meanings; understand semantics, syntax) Expressive language (ability to communicate effectively via spoken or written language) Auditory Normal hearing acuity, processing, selective discrimination of sounds and auditory cues Perceptual Motor Skills Integrated stimulus-specific fine motor and gross motor responses

Visual-spatial discrimination (eye-hand coordination; stereognosis; judgment of speed, direction, spatial orientation of moving objects) Temporal sequencing (awareness of sequential ordering; awareness of time and sequence of events) Proprioceptive and kinesthetic sense Reaction time (time elapsed between stimulus perception and initial neuromotor response) Task-Specific Integrative and Adaptive Skills Development Ability to coordinate, integrate, and adapt various domains to meet the specific demands of a given sport Social and Emotional/Psychosocial Development The ability to make and sustain peer relationships The ability to regulate and monitor emotions The ability to develop healthy interpersonal relationships The ability to establish and maintain mutually beneficial intimate relationships progress (i.e., the number of milestones) in development is more apparent and is often measured, qualitative progress (e.g., not only determining that the child is able to jump or throw, but rather noting how well he or she is able to jump or throw) in motor and developmental skills is of equal or greater importance in terms of sport participation ( Figs. 17B-1 and 17B-2 ). [27] [94] [97] [98] [106] Developmental progression and refinement of certain fundamental sport-related tasks (such as catching, throwing, kicking, various other ball-handling skills, and others) naturally occur over time, along with advancing age and overall neurodevelopmental maturation; these are further enhanced by sport-specific skills training.*

Figure 17-B-1 Qualitative changes from an early to a more mature pattern of a skill: Long jump by a beginner (A) and an advanced long jumper (B). (Adapted from Fagard J: Skill acquisition in children: A historical perspective. In Bar-Or O [ed]: The Child and Adolescent Athlete. Oxford, England, Blackwell Science, 1996, p 84.) *See references

[ 19] [ 23] [ 24] [ 25] [ 27] [ 30] [ 31] [ 55] [ 62] [ 69] [ 83] [ 98]

and [ 105] .

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Physical Growth and Motor Development

Malina refers to an increase in size as growth, and rate of progress toward a mature state as maturation. [71] [72] [103] Different parameters of growth include growth in stature and maturation of specific body systems, as well as changes in body composition.

Maturation is generally considered to occur in skeletal, sexual, and somatic areas.[47] Skeletal age is classified as advanced, average, or delayed in comparison with chronological age. Secondary sexual characteristics have been well described as sexual maturity ratings (SMRs), or Tanner stages.[73] [74] [81] Somatic maturation is indicated mainly by the age at peak height velocity (PHV). Gross motor skills refers mainly to posture and locomotion abilities; these are especially important considerations in a preverbal child.[29] [32] [58] Gesell[46] referred to fine motor and visual-motor problem-solving skills as comprising upper extremity and hand manipulative abilities, as well as eye-hand coordination. Cognitive Development

Cognitive development refers to the level of a child's or adolescent's ability to perform simple to complex mental tasks, including focusing of attention, speed or alertness of mental processing, thinking skills, problem-solving skills, and judgment.* All sport activities require some degree of each of the aforementioned cognitive skills, although the level of sophistication needed varies among sports; sports that require high levels of integration of multiple domains of function (e.g., motor, visual, cognitive, language, auditory, perceptual motor, social, and emotional) require highly sophisticated and complex cognitive skills (i.e., higher-order thinking, such as synthesis and evaluation). [52] [80]

Visual-Motor and Auditory Development

Normal visual acuity, color vision, visual discriminatory ability, and tracking ability allow children to engage in effective sport participation.[47] [52] Visual discrimination skills allow children to identify players, objects (e.g., balls, sticks, goals, end zones, legal play areas, and penalty flags), and markings or colors that designate the function of each player or opposing teams. Children and adolescents also need to be able to track the trajectory of players and moving objects, and to use the trajectory of moving objects in comparison with stationary objects to judge the velocity of moving objects. Normal hearing helps the player to locate the source and direction of the voice, and enables him or her to follow essential instructions or advice from coaches or other players on the field. Youth with normal hearing abilities can also engage in selective attention and hearing; they can make fine discriminations as to which voices and noises are relevant to a specific sport activity. Additionally, they can ignore irrelevant voices and noises. *See references

[ 29] [ 32] [ 37] [ 38] [ 45] [ 46] [ 58] [ 63] [ 64] [ 81] [ 88] [ 89]

and [ 94] .

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Figure 17-B-2 Developmental sequence of throwing behavior. (Redrawn from Seefeldt V, Haubenstricker J: Patterns, phases, or stages: An analytical model for the study of developmental movement. In Kelso JAS, Clark JE [eds]: The Development of Movement Control and Coordination. New

York, John Wiley & Sons, 1982. © John Wiley & Sons Limited. Reproduced with permission. ) Perceptual Motor Development

Perceptual motor skill is the ability to perceive, interpret, and execute an appropriate neuromotor response to a stimulus; perceptual motor development serves to pull the physical skills and functional domain skills into a synthesized whole, allowing the normally developing child to perform most developmentally appropriate sports at an adequate level.[32] [40] [63] [64] Fine motor responses, gross motor responses (including coordination, balance, agility), reaction time, and visual-motor responses are all components of perceptual motor development. Rieser and associates[94] noted that the perceptual and motor systems are mutually calibrated; thus, people fine tune them after brief periods of action under changed circumstances. The abilities to see, hear, think, and move are influenced by a child's level of perceptual motor development. Children begin to learn to coordinate and integrate their physical, cognitive, visual, auditory, and language skills from birth.[7] [18] [32] [40] [43] [45] [58] [63] [99] As children mature, a greater level of sophistication and adaptation occurs. Being able to perform the basic motor skills but not being able to plan complex motor functions, and not having well-developed visual skills of tracking, can result in awkward or clumsy behavior that is seen, for example, in catching.[25] [52] [63] [98] [105] The child might see a ball coming toward him and understand that the thrower said, catch the ball; however, the young child might not be able to think quickly enough through the motor sequence of catching to put his two arms in front of him just far enough apart to fit the dimensions of the ball and close his hands around the ball to catch when it reaches his chest area. This child will more than likely get hit in the chest by the ball, or the ball will bounce off of his hands that closed too quickly to catch. Children who have poor eye-hand coordination or weak fine motor skills may also exhibit these types of sport-related problems.

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Implications for Sport Participation

In addition to having reached an appropriate level of neurodevelopmental maturation, the child must adapt skills to meet the demands of a given sport. [15] [35] [47] [52] [55] Proper training and conditioning are essential for improving sport-specific skills. For example, a child who wishes to play soccer needs to learn how to kick a ball while running, pay attention to who is trying to take the ball, and track the movement of teammates to whom he needs to kick the ball. The child must be alert to know when the ball is coming toward him. He must track the player with the ball as well as the trajectory of the ball as it comes toward him. He must judge the velocity of the ball and lift his foot to stop the ball while maintaining his balance on one leg. As the ball reaches the appropriate spot, the child must put his foot down, stop the ball, and gain control. At the same time, he must be alert and attentive to who is near him and to the direction in which he needs to move the ball, as well as to the position of the player who is going to receive the ball. Once possession and control of the ball are attained, the child must forcefully push the ball with the inside of his foot to propel it along the ground, or with his toes to propel it in

the air, toward the intended receiver. When the child removes his foot from the ball, he risks having it stolen by a member of the other team, so he must be aware of who is near and block such access. The earlier the child is in the developmental process of maturation, the less likely it is that he will be able to carry out such multi-task coordination of all his functional domains. It is apparent that the demands of this sport require functional integration and execution of speed, balance, motor coordination, visual skills, cognitive skills, and perceptual motor skills. The more developmentally advanced the child is, the more likely he is to possess such skills, in addition to the mental processing speed, running speed, physical strength, endurance, agility, and flexibility needed to carry out the demands of this sport. Studies show that in general, reaction time and speed improve with age and practice during childhood and adolescence.[19] [20] [21] [22] [23] [24] [25] [27] [72] [83] [95] [108] [109]

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Neurodevelopmental Readiness

Sports readiness refers to the stage at which the child has reached the necessary maturity to learn a given sport-related task. [18] [28] [34] [35] [37] [52] [103] [106] In other words, it results from a process in which the child acquires the required motor, physical, cognitive, social, and adaptive abilities and is ready to meet the demands of a given sport. Readiness to play and to compete is influenced by biologic, physiologic, psychosocial, and environmental factors.* Participation in sports requires that the child be able to coordinate certain motor, cognitive, and physiologic functions, such as movements of the extremities, breathing, thinking, balancing, and many more. The ability to coordinate different actions is influenced by a child's level of thought processing ability, thinking speed, agility, flexibility, strength, and endurance. Some researchers have proposed that certain critical periods occur, during which sport skills are learned best.[19] [103] On the other hand, it is not necessary that children learn such skills during these periods. Because multiple factors influence readiness and determine the varying rates of growth and development, athletic talent cannot be reliably identified in children, nor can athletic excellence in children be predicted.[10] [23] [34] [37] [47] [52] [97] [103] Seefeldt's classic study showed that by elementary school age, 60% of children were able to perform the following tasks at age-appropriate levels: throwing, kicking, running, jumping, catching, striking, hopping, and skipping ( Fig. 17B-3 ). [97] [98] In general, children younger than age 6 do not have the ability to compare their own abilities with those of others; nor do they have the cognitive maturity to understand the competitive nature of sport before age 9. The ability to fully understand the complex tasks of a given sport may not be fully developed until a child is 12 years of age.

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Stages of Neurodevelopment The Infant and the Toddler

It is not unusual to see many infants and toddlers being initiated into sports programs such as swimming and gymnastics; a crawling race for infants has also been reported. [5] [23] [103] The American Academy of Pediatrics recommends that children are not developmentally ready for swimming lessons until after they have reached 4 years of age.[5] [23] Early participation in swimming programs has not been shown to decrease the later risk of drowning, nor does it increase the skills of swimming in children.[22] [23] Infants attain gross and fine motor skills along a predetermined and sequential path. [15] [23] [25] [32] [88] [97] Attempts at acquisition of specific motor skills by early training usually are not successful.[26] For example, a child must have neuromotor maturation before he can walk, and children who walk earlier than at an average age will not necessarily learn other motor skills earlier as well. During the first year of life, the primary motor reflexes gradually integrate into more complex and coordinated responses.[32] [43] [47] [58] [100] As at any other stage of development, there is a wide range at which infants and toddlers achieve different milestones. For example, most infants can stand alone at between 9 and 16 months; walk sideways when they are between 10 and 20 months of age; jump from the last stair to the floor at between 18 and 30 months; and walk up stairs, alternating a forward foot, at between 23 and 30 months of age.[32] [43] [46] [47] [58] [81] Typically, a toddler can run, jump in place, and throw a large ball overhead. Between ages 2 and 3, children can have full arm swing and are able to run well, hop up to three times, throw a ball with forearm extension, and catch a ball with fixed and outstretched arms.[32] [43] [46] [58] [63] [81] [97] [100] By the end of 2 years, cognitive, language, and social skills also have advanced. Toddlers can engage in pretend play, can remember where an object is hidden, and can retrieve the object.[43] [89] They have a vocabulary of more than 50 words, can speak

several two-word phrases, can

Figure 17-B-3 Age at which 60% of the boys and girls were able to perform at a specific developmental level for selected fundamental motor skills. Numbers refer to developmental stages of that motor skill. (Redrawn from Seefeldt V, Haubenstricker J: Patterns, phases, or stages: An analytical model for the study of developmental movement. In Kelso JAS, Clark JE [eds]: The Development of Movement Control and Coordination. New York, John Wiley & Sons, 1982. © John Wiley & Sons Limited. Reproduced with permission.) *See references [ 23] [ 28] [ 34] [ 37] [ 47] [ 70] [ 98] [ 102] [ 103] and [ 106] . See references [ 15] [ 18] [ 24] [ 25] [ 28] [ 34] [ 37] [ 43] [ 47] [ 52] [ 82] [ 84] [ 98]

[ 103]

and [ 106] .

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follow single-step and two-step commands, and can attend to short stories. [32] [81] [100] A toddler can imitate adults and can engage in parallel play with other children.[37] [43] [63] [89] The Preschool Years

Physical Growth and Motor Development

During the preschool years (from about 3 to approximately 5 or 6 years of age), physical growth slows down compared with that occurring during infancy and toddler stages; however, acquisition of basic neuromotor, language, and cognitive skills increases rapidly.[43] [89] The development of better postural and balance control allows preschoolers to learn how to ride a bicycle without training wheels, to catch a small ball thrown from 10 feet away, and to use their hands to manipulate objects (such as for drawing and elementary writing skills).* Children between 3 and 4 years of age can broad-jump about 1 foot, hop up to six times, and catch a ball against their chest.[32] By the end of 4 years of age, a child can skip on one foot, climb up a jungle gym, throw overhand, and catch a large ball.[32] A child can also stand on one foot for up to 5 seconds, kick a ball forward, catch a bounced ball most of the time, and move backward as well as forward with agility.[17] [22] [25] [30] [43] [47] [65] [100]

By age 5, children have better balance, coordination, body strength, and endurance, although these are still far less developed compared with adolescents and adults. By the end of age 5, children can run smoothly, gallop, do a one-foot skip, hop up to nine times on one foot, throw a ball with a shift of their bodies, catch a ball with both hands, ride a tricycle well, swing, and do somersaults.[7] [32] [100] By age 6, most children can run, throw a small ball at a target, and hit the target; girls can skip but boys may not. Children by 6 years of age can jump up to 1 foot, and broad-jump up to 3 feet.[32] Once children have learned these skills, their continued use results in further refinement. [47] [109] Throughout childhood, the effects of training and skill development are directly

related to age-specific changes in the neuromotor, metabolic, cardiopulmonary, and cognitive/integrative systems.[25] [43] [47] [65] Muscular strength and muscular endurance can be improved during the childhood years with the use of higher repetition-moderate load resistance training programs during the initial adaptation period.[22] [25] [28] [42] [103] Cognitive Development

During the preschool years, children can remember basic information, recall that information on demand, and answer simple who and what questions. Their memory is enhanced by visual aids, and they tend to learn by trial and error.[47] [88] Preschool children generally have short attention spans (5 to 15 minutes) and poor selective attention; they can distinguish simple similarities and differences, and can understand simple analogies; they can identify missing parts of familiar objects. Also, they can follow simple rules but need visual cues and frequent reminders. Language Development

Children by age 5 have a vocabulary of about 2500 words, and by age 6, it includes about 5000 words.[32] Typically, the speech of a preschooler is 100% intelligible to strangers.[7] [32] [46] [81] By age 5, the child can speak sentences *See references

[ 22] [ 25] [ 32] [ 40] [ 43] [ 47] [ 65] [ 81] [ 89] [ 100]

and [ 105] .

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of up to five words, use future tense, name four colors, and count ten or more objects. [32] [46] Children still may have difficulty understanding words that sound alike but have different or multiple meanings. At this age, the ability to comprehend complex or compound sentences is limited. Coaches and trainers who give multiple instructions may find that many of their young players become lost in the words or get distracted. Children are better able to follow instructions given in the form of simple sentences combined with visual cues (such as pictures) that demonstrate the expected action. Sentences should be clear, concise, and devoid of words that have multiple or complex meanings. Use of training tapes to teach a skill may be helpful, if the language used matches the words that will be used during direction of a particular skill; it is also critical that words and skills are shown in a way that depicts the actual intended situation or environment. Coaches and parents can begin to teach children how to communicate when they are frustrated, tired, angry, happy, or excited. This will enhance their overall development of communication skills. Social and Emotional Development

Children between the ages of 3 and 5 or 6 years are egocentric; they thus have difficulty taking the view of another person, or understanding why they cannot always be first.[88] [89] They are learning to interact with their environment and to engage in cooperative play with other children. By age 6, they play best with children of the same gender.

Children learn autonomy and trust through their successes or failures.[88] [89] Preschoolers are unable to compare their own abilities with those of other children.[47] They may become upset when they lose, or may want others to focus only on their performance. They may not understand why one child is allowed more play or demonstration time; they usually want their needs met immediately. Visual Development

At this age, children may not have a fully developed capacity for tracking objects or people, and for judging the velocity of moving objects. [47] [52] Children younger than 6 or 7 are farsighted, and their limited ability to track objects and judge the speed of moving objects is due to their vision limitation, and not to a lack of coordination.[47] [63] In softball, for instance, a pitcher with limited ability to judge velocity might throw the ball too fast. The batter who is accustomed to a slow pitch, but also has a limited ability to track and judge velocity, may be hit in the head because he will not be able to determine the trajectory of the ball, process in time this critical information, and then coordinate his movements to pull his body out of the ball's path. Auditory Development

The ability to understand the sounds they hear is developing rapidly in children in this age range.[43] [63] The multiple sounds that occur in most sport environments can be very confusing for a child at this level of development. In a typical setting, a coach or trainer may be giving the child instructions, while a parent is yelling directions and various members of the audience are also offering advice. Children may have difficulty discriminating which words they should listen to and may become distracted or confused. Other sounds like whistles and bells can simply add to this perceived cacophonous situation. The ability to listen selectively matures as the child grows. All sports require players to listen and comprehend spoken language as well as sounds and to coordinate that information with other events and actions in their specific sport environment. Perceptual Motor Development

These children know their right from their left body parts and can locate the right and left sides of other people or objects.[89] They can also locate themselves in relation to other objects.[89] They have a good orientation of their bodies in space but may not be able to control the intensity and trajectory of a gross motor action.[47] [52] They may throw a ball to another child but at a velocity that is too fast, which may result in the other child's being hurt when the ball hits him. Or the child may kick at a soccer ball, but her aim is off and she kicks another child. A child who runs toward a base may trip and fall in his attempt to beat the ball to the baseman. The act of catching a ball is an example of complex motor planning that involves temporal sequencing, body awareness, eye-hand coordination, and visual-spatial skills ( see Fig. 17B-1 ). [24] [25] [83] [98] [105] Children at this age do better if they are told where the ball will be thrown (e.g., saying and demonstrating: I am going to throw the ball to you; I

will throw it to your chest area; hold your hands up to your chest). The adult throws a medium-sized ball slowly, using exaggerated movements to allow the child time to mentally process and coordinate visual, mental, and gross motor skills; the child also needs time to estimate the temporal sequence, judge the velocity of the ball, determine his body position, move his arms and hands to his chest, and grasp the ball as it reaches the appropriate distance from his body. By following these multiple tasks, the child has just performed the complex motor function of catching. With practice, this child can learn to catch a ball thrown toward other body parts from a distance of up to 10 feet.[19] Implications for Sports Participation

By age 5 or 6, most children can remember simple rules and can play games that require only simple decision-making skills.[47] [52] [88] [89] Their ability to generalize a rule to different aspects of a sport activity other than the context in which it was learned is limited or even nonexistent. Children at the concrete-operational stage of cognitive development understand only clear and concise information. Children before the ages of 6 to 8 do not always understand the purpose or competitive nature of a game, even though they know and understand basic rules.[47] [52] [88] [89] For example, these children will all swarm around a soccer ball to kick it because they know that is what you are supposed to do. They may not understand, however, that they are to engage in a cooperative effort with their peers to move the ball down the field to score points by kicking the ball between their opponent team's goal posts.

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This form of beehive soccer is frustrating to coaches and parents, but it is actually normal behavior for children at this level of cognitive development.[37] [52] [103] All the physical skill and knowledge of the game can be thwarted by a player's stage of cognitive development. If one player kicks the ball in an unanticipated direction, another player may not be able to engage in the rapid decision-making needed to change her position or process a strategy to compensate for this unexpected event. Changes in the demands of the sport during a game or a season will most likely result in chaos; these children are unlikely to be able to change their performance to meet the new competitive requirements of their game.[52] It is best to encourage participation in a variety of different activities that allow preschool-aged children to practice, refine skills, and have fun.[65] In establishing the best learning environment for these children, the best focus is on cooperation and socialization abilities, as well as on critical thinking and perceptual motor skills.[52] [65] Preschool children need to engage in activities that allow them to travel (e.g., hop, skip, run, slide, crawl, creep, slither, and climb) in different directions and on different surfaces (e.g., flat, inclined, wavy, wet, or dry).[65] They also need to exercise postural control and balance (e.g., headstands and hanging). [65] Preschool children should

experience what it feels like to be out of balance and in balance; they need to move their bodies up and down in space while keeping out of contact with the ground (e.g., jumping, hopping, skipping, bouncing, and leaping), and they should experience different means of contorting their bodies (e.g., turning, spinning, rolling, twisting, tumbling, gesturing, bending, stretching, and reaching).[65] It is important for them to learn about directionality (i.e., up, down, sideways, backward, and forward) and about different temporal sequences (i.e., going quickly or slowly, and moving one's body in time to different forms of music, as well as different rhythms or sound patterns). [65] [88] [89] They need to experience a variety of shapes of objects through the visual, symbolic-memory, linguistic, kinesthetic, and proprioceptive properties of each shape (e.g., round, oval, square, thin, twisted, or straight).[65] Also, they should experience physical properties of objects (especially sports objects such as bats, balls, hockey sticks, or rackets), and should experience a variety of concepts and actions (such as strong versus weak, heavy versus light, smooth versus rough or bumpy, smoothly versus jerkily, push versus pull, and receive versus send). Each of these repeated experiences will integrate over time and provide children with foundational skills that will allow them to overcome the physical and mental challenges of various sports. These experiences will also help children develop confidence in their ability to perform skills necessary for participation in most sports and possibly will prevent the development of the fear of being struck by a ball. [47] [52] [65] Middle Childhood

Physical Growth and Motor Development

By the middle years (6 to 10 or 11 years), most children have established adult walking patterns.[43] [59] [63] A synergistic cooperation of the physiologic, neurologic, and musculoskeletal systems allows children at this level of development to adopt a walking frequency to optimize physiologic cost, symmetry, and stability. [59] Physical growth is fairly steady during the elementary school years; gender differences in height and weight are less noticeable than in later developmental stages ( see Fig. 17B-1 ). [43] [63] At this stage, children also develop an initial awareness of how to more effectively and efficiently use their gross motor functions. Gender differences are noted in certain motor tasks during the middle years. [19] [27] [47] [62] [69] [97] [98] [104] As with most fundamental physical skills, boys at this age have a slight advantage in explosive power needed for actions such as vertical jump, long jump, running speed, and throwing for distance. Girls learn to strike objects, jump, kick, and throw later than boys; but girls learn to hop, skip, and catch a little earlier than boys. [97] [98] Girls have the advantage of having better balance than boys at this stage of development. [97] [98] By age 7, children show interest in learning to bat and to pitch and can pedal a bicycle well.[32] [46] [100] By age 8, motor movements are more graceful and rhythmic, and children begin to learn soccer or baseball.[7] [46] By age 9, they can engage in vigorous physical activities, participate in team play, catch a fly ball, and balance on one foot for at least 15 seconds; they like to wrestle, play ball, and be part of a team. [7] [32] [46] [97] [98] [100] By age 10 or 11, most children have mastered all fundamental motor skills.[25] [32] [43] [47]

[52] [103]

Hitting a baseball or tennis ball and shooting a basketball are examples of skills that are easiest to learn at this age. Aerobic and anaerobic capacities increase steadily during middle childhood but are still quite limited compared with those of adolescents. Children now can perform other sophisticated motor functions such as overarm throwing and overhead striking, the latter of which is employed in tennis.[52] [76] As children mature, they continue to experience improvement in posture, balance, and reaction times with practice. The refinement of these skills may be influenced by many factors, including somatotype, gender, training, and motivation; this makes age predictions for a specific child as ready to participate in all sports a difficult task. [18] [22] [34] [52] [84] [97] [102] [103]

Cognitive Development

Children at this age have considerable difficulty with futuristic thinking; they see things as here and now, right or wrong, and black or white. [7] [32] [45] [88] [89] Discussions about morality and future consequences of current behavior are useless. They engage in magical thinking and may believe that they have unique powers that will protect them from harm.[46] [89] These children cannot think through the consequences of their actions to know that jumping from a high place may result in serious injury, as for example, mimicking wrestling stunts seen on television; thus, they believe they have the same abilities as these highly trained athletes. Their attention spans are longer now, but they may still be easily distracted. They can plan and execute simple motor sequences. Further development of memory and rapid decision-making ability takes place; they can understand the intent of instructions given and can follow directions.[52] Critical

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thinking and problem-solving skills are further developed during these middle years. [32] [46] [88] [89] They can apply factual knowledge to familiar situations but may not be able to extrapolate that knowledge to unique or new situations. They are beginning to understand the purpose of the rules they learned earlier. Judgment and decision-making improve significantly by the end of the middle years.[37] [38] Children at this age can adopt another person's spatial perspective much better and can clearly recognize differences between their personal performance and the performance or skill of others.[84] They accurately discriminate between those children who are popular and those who are not. They begin to identify those children who are smart and those who are dumb.[84] They are now very aware of their own body image.[1] [88] [89] Language Development

Use of complex language skills increases considerably during the middle years. By now, children can give complex directions to others and have the cognitive ability to understand a broader range of words and their symbolic use. [32] [46] [84] [100] They understand words with multiple, similar, and different meanings. Children who have

mastered age-appropriate language skills have a better chance of understanding and articulating sports instructions. Language is used as part of the socialization environment in sports, to transmit rules or instructions, give praise, and provide criticism. Social and Emotional Development

At this stage, children are developing a sense of right and wrong and usually like to play by the rules; they become upset with peers who do not follow the rules.[37] [38] [88] [89] They are able to follow limits set by others. During these middle years, children enjoy playing organized games and delight in peer comparisons of athletic prowess. Children at this age generally know it is not okay to make fun of other players. They are now better able to control their anger or hurt feelings when they cannot get their own way. Those children with more advanced skills may not yet understand that their gifts may be time limited; some in fact become less motivated to learn and practice to refine those skills.[84] Special attention from coaches, other players, and their parents (because of their athletic success) may facilitate positive social adaptation of these children. The less gifted or skilled child, however, may become withdrawn and less socially adept. It is important for adults in this environment to recognize these issues and to build into the program confidence-enhancing activities for all children. The focus should be on practice, correcting weak areas, developing overall skills, engaging in multiple activities, and doing one's best. Such a foundation gives children a broader set of criteria on which they can base their self-esteem or belief in their own abilities. They should be involved in more than one sport (at least one noncompetitive type) and in other activities that contribute to other aspects of their development (e.g., music, voice, singing, art, stamp collecting, reading, or debate). The more well-rounded the athlete, the easier it is to maintain a healthy balance. Visual and Auditory Development

These children have improved visual acuity and tracking ability, and a more mature level of visual-perceptual motor integration; however, their sense of directionality may not yet be fully developed. [7] [32] [47] [52] Auditory discrimination is now well developed, and children can begin to listen selectively, so that the confusion they might have experienced during the early childhood years becomes significantly less.[32] [47] [81] They can more clearly distinguish the directions and comments of coaches, trainer, and parents from other noises in the crowd. Perceptual Motor Development

Balance is still somewhat limited because these children are just starting to integrate visual, vestibular, and proprioceptive cues at a more sophisticated level.[52] They have the visual-motor capacity, manual dexterity, basic analytic thinking, problem-solving skills, and motor-planning skills necessary for most sports.[7] [32] [46] [47] [52] [81] [103] Children's ability to estimate the arrival of a simulated moving object onto a target based

on three different motions (constant velocity, constant acceleration, and constant deceleration) was analyzed by Benguigui and Ripoll.[20] Results showed that timing accuracy improved mainly between the ages of 7 and 10 years; tennis practice accelerated the development of timing accuracy; and acceleration or deceleration of the moving object or target had no effect on the timing accuracy of any of the tested groups (ages 7, 10, 13, and 23 years). Additionally, they concluded that with practice, a 7-year-old could develop a level of performance very similar to that of the older participants. Tennis practice induced an accelerated development of the perceptual motor process involved in tennis that requires the player to engage in coincident timing tasks necessary to target the trajectory of a specific moving object in order to intercept it. This study illustrates a child's ability to link sensory input and motor output, even at an early age.[20] Pienaar and colleagues found that they could develop the essential physical and motor skills in 10-year-old rugby players in South Africa.[90] They successfully developed a practical method of selecting and developing the basic skills and abilities needed to play rugbycatching, passing, running, kicking, sprinting, passing for accuracy over a specific distance, two-handed lateral passes, pull-ups, zigzag runs, 50-yard dash, ball-changing skills, strength and endurance training, vertical jumping, throwing a ball through a circle to hit a target, running and throwing at a specific target, making lateral passes, agility runs, sit and reach, flexed arm hang, speed, and endurance.[90] Implications for Sports Participation

The reactions and feedback of coaches, trainers, parents, and other professionals to the behaviors, attitudes, beliefs, and actions of children at this developmental level are crucial to helping these children successfully make the transition from childhood to adolescence. Children during the middle years exhibit early levels of judgment, thinking, and problem-solving, and a variety of physical abilities and emotional reactions; however, they have little history and

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limited perspective to allow them to put their experiences into context.[32] [45] [52] [89] They are still developing their sense of self in terms of confidence, esteem, consciousness, and body awareness.[37] [38] [88] [89] Children's abilities to handle the reactions of others to their words and behaviors are still limited. They do not have abstract thought yet, and may not understand that their ability to hit a pitched ball during a baseball game is related to how much time they spend practicing hitting a ball between games. [45] [84] [87] [88] [89] They may incorrectly assume that being able to hit a ball is something you can either do or not do. For example, a girl at age 10 may think she cannot throw a ball as well as her male peers because when she was age 7, she could not compete with the boys; she may then give up on trying to play ball because she thinks she is not good at that sport. She will need encouragement to continue to play and will need to be told that her skills may develop more fully as she practices.

If sports activities are focused on skill development and incorporate problem-solving and anger management, as well as cooperative play, children can learn to enjoy sports participation and can develop appropriate skills to support competitive play that is both fun and instructive. Children at this age often become confused and very emotional if they are criticized too severely, or if adults (especially coaches and parents) scream, yell, or use harsh tones of voice and animated physical or facial gestures to give feedback. These children attend only to the emotion of the message and not to the message itself. They personalize the negative impact of the message and may not be able to learn or gain an instructive quality from what the adult is saying or is trying to say. Children during these middle years can engage in more complex sports activities that enhance the refinement of the fundamental skills they acquired during preschool years. They should participate in activities that help them learn to use their skills in a variety of settings. Children should receive instructions in a show and tell format, delivered in short intervals and intertwined with free play and drills.[52] Because these children are just beginning to compare their performance with those of their peers, involvement in competitive sports should be minimal.[52] It is more important to work on the perceptual motor skills, decision-making abilities, and problem-solving approaches necessary for participation in a number of different sports, rather than to prematurely specialize in one or two sports.[10] [28] [103] Entry level soccer, baseball, tennis, track, swimming, tumbling, and gymnastics are all examples of appropriate activities.[47] By the end of middle childhood, the normally developing child has mastered the basic skills identified in the functional domains (e.g., as outlined in Fig. 17B-3 , language, auditory, perceptual motor). At this point, the focus shifts to highlight the importance of the adolescent growth spurt, higher-order cognitive functions, and psychosocial development. Transition to the Adolescent Years

During the preschool years, physical growth and neurologic maturation are quite rapid and apparent, with new skills being acquired at a rapid pace. This process continues throughout the middle years at a somewhat slower pace. As the child enters puberty, rapid development of physical and sexual characteristics becomes apparent, accompanied by important psychosocial development. The onset and rate of progression of pubertal events vary considerably among adolescents; however, the changes occur in a predetermined sequence.[57] [61] The adolescent may perceive sports experiences quite differently based on the influences of several variables: the differences in physical and psychosocial development, states of adolescent development (early: 10 to 13 years of age; middle: 14 to 16 years of age; and late: 16 to 20 years of age), and the fact that some mature early and some late.[18] [21] [42] [47] [84] [87] Also, gender differences become more apparent and significant for sports participation during adolescence. Clinically, it is important to assess an adolescent's sexual maturity rating (SMR), or Tanner staging, because chronologic age does not necessarily correlate well with many physiologic and somatic changes.[57] Skeletal maturity is best assessed by measurement of bone age. Selected aspects of somatic, sexual, and skeletal growth and maturation during adolescence (especially relevant to sport participation and performance) and their

developmental continuity and interrelatedness have been the subject of several recent reviews and studies; the key elements are briefly discussed here.* Weight

In males, the average weight gain during its peak is about 9 kilograms (kg) per year, with a range of 6 to 12.5 kg per year; in females, it is about 8 kg per year, with a range of 5.5 to 10.5 kg per year.[57] [63] [81] In males, the peaks of growth spurts in height, weight, and muscle occur at the same time, but in females, these occur in sequence in that order.[61] [71] Height

Peak height velocity (PHV) refers to the maximal rate of linear growth during adolescence. Females reach PHV by 12 years of age during SMR 3, usually 6 to 12 months before menarche (onset of menstruation); their average gain in height is 8 centimeters (cm) per year, and the range is 6 to 10.5 cm per year ( Fig. 17B-4 ). [57] [61] [81] Males usually reach their peak height velocity by 14 years at SMR 4, with an average gain of 9 cm per year and a range of 7 to 12 cm per year ( see Fig. 17B-4 ).[57] [61] [81] During the early growth spurt, growth of the shoulders in males and that of the hips and pelvis in females are the most noticeable changes. In general, linear growth first occurs in the lower extremities, followed by the torso and then the upper extremities. Body Composition

Gender differences in changes in body composition are noted, as described in terms of fat mass (FM), fat-free mass (FFM), and body fat distribution. [14] [54] [72] [87] [95] In general, both males and females tend to increase both FM and FFM from the early to middle adolescent years.[47] Males, *See references

[ 14] [ 16] [ 21] [ 28] [ 53] [ 54] [ 57] [ 61] [ 67] [ 70] [ 71] [ 72] [ 73] [ 81] [ 87] [ 95]

and [ 103] .

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Figure 17-B-4 Normal progression and gender differences in somatic growth of siblings. Seventeen-year record of growth of female (born 3/81) and male (born 11/82) siblings.

however, may show a transient decrease in fat accumulation in the extremities during PHV; females continue to gain fat through late adolescence. By SMR 4 and 5, the fat mass in females can reach twice that in males. There is a relatively predominant deposition of fat in the lower trunk and thighs in females. The pattern of growth of FFM is similar to that noted for growth in height and weight. Body mass index (BMI; weight in kg/stature in meters squared) has been shown to have a better correlation with FM than with weight.[75] The calculated value is compared with the population norm tables. One

limitation of BMI is the fact that factors other than FM, such as muscle mass and bone mass, affect the numerator and may incorrectly yield a high value in someone with high muscle mass and low FM.[72] Application of BMI in sports classified by weight categories has been found useful in such sports as wrestling, bodybuilding, and weightlifting. Flexibility

Typically, skeletal growth precedes musculotendinous growth during early to midadolescence; this partly contributes to a relative decrease in musculotendinous flexibility among some adolescents, especially males. [21] [47] [95] In general, females are more flexible compared with males. In males, overall flexibility tends to decrease from late childhood

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to midadolescence; in females, it tends to show a slight increase during early adolescence, plateauing by age 14 or 15 years.[71] [87] [95] [103] Decreased flexibility is particularly noticeable in hamstrings and ankle dorsiflexors, especially among dancers and gymnasts.[47] [103] Flexibility is influenced by internal factors such as bone structure, muscle volume, and tissue elasticity (i.e., muscles, tendons, joint capsules, and ligaments). External factors that influence flexibility include room temperature, warm-up time, and physical exercise. [51] Muscle Growth and Strength

Growth in muscle mass is seen in both males and females during adolescence. Because androgens partly influence this growth, it is relatively more pronounced among males compared with females. There is also a linear increase in muscle strength among both males and females, with males showing a period of relative acceleration or spurt around age 13 years; females reach a plateau by age 15 years with no apparent spurt.[21] [61] [67] [95] The peak increase in muscle strength follows a peak in muscle mass by about 12 months.[61] [87] [95] The response to strength training is best seen during SMR 4 and 5 in both males and females.[21] [47] [61] [67] [93] Bone Mass

Weight-bearing and loading, along with proper diet, are essential to optimal bone growth. The largest percentage of lifetime acquisition of bone mineral density occurs during the second decade of life.[16] [53] [54] Peak bone mass during adolescence is determined by many factors, including genetic influences, exercise, calcium intake, and hormonal status.[16] [54] Thus, the lack of proper nutrition seen among some athletes who engage in drastic weight-control measures may predispose them to deficiencies in bone

mass accumulation.[54] [87] Implications of Early and Late Maturation

Early development is characterized by advanced bone age compared with chronologic age; and late development, by delayed bone age compared with chronologic age.[57] [61] [81] Early-developing males may have attained PHV before age 13 years, and females may reach PHV before age 11 years; late-developing males may not reach PHV before age 15 years, and females may not reach PHV before age 13 years.[57] [61] [71] [73] [74] [75] [81] [103]

Boys who mature early tend to be taller and to have greater muscle mass, fat mass, and strength (i.e., arm, grip, and explosive) compared with average or late-maturing boys; jumping and sprinting are examples of explosive strength. Adolescent boys who are late maturers are relatively smaller in stature, weaker, and less coordinated; they may experience frustration, anxiety, and disappointment when they are not able to meet performance expectations while playing sports. They may even be ignored by peers and coaching staff. In comparison with average or late-maturing female peers, early-maturing girls tend to be taller and to have greater fat mass and fat-free mass, greater weight for height, relatively shorter legs, and broader hips; however, this gives them only a modest (if any) advantage in sports. In fact, early-maturing girls may be at a disadvantage socially, as well as when performing certain motor tasks, and may not be considered ideal for such sports as gymnastics, dancing, diving, and figure skating.[103] On the other hand, girls who mature later are taller and have lower weight for height, less FM, and relatively longer legs and narrower hips; they may be at an advantage socially, may perform better on tests of upper extremity strength, and are better suited for sports such as gymnastics and figure skating.[103] Early Adolescence

Physical Growth and Development

Rapid changes in physical growth and motor skills characterize early adolescence. Many adolescents, especially males, begin to demonstrate special skills and talents during this time. Because normally girls often experience the onset of puberty earlier than boys, they may become temporarily taller and heavier than boys of the same age ( see Fig. 17B-4 ). Differences in physical performance early in adolescence are more strongly influenced by age at onset of puberty and environmental conditions than by chronologic age.[21] [24] [25] [73] [87] [103] As adolescents become older, gender differences become increasingly a function of environmental factors. Physical differences can be dramatic among some adolescents, especially boys. A wide variability in the rate of progression of growth, physical skills, and overall development may contribute to increased concerns about body image among some adolescents. Increases in muscle mass, strength, and cardiopulmonary endurance that occur during

puberty are greater than at any other age.[47] [61] [82] [95] [103] Males show sharp increases in their ability to perform tasks that require muscle strength, such as vertical or horizontal jumping, throwing, and sprinting; females show a gradual improvement or reach a plateau in their performance of these skills.[47] [71] [73] [103] Cognitive Development

Piaget contends that early adolescents are just beginning the formal operational stage of cognitive development, with improved inductive and deductive reasoning abilities.[1] [45] [88] [89] In addition to developing prepositional logic in which they can think about thinking itself, they may note an awakening sense of morality and altruism. Also, future time perspective has not been fully developed during early adolescence, and children at this age are still at a concrete level of cognitive functioning.[45] [49] [57] [88] It should also be noted that some adolescents may never shift to this stage of thinking and instead remain at the concrete phase of thinking. For many, however, abstract thinking, analytic abilities, problem-solving skills, and transitional skills begin to develop.[1] [3] [37] [39] [88] [89] Selective attention and memory are more mature; early adolescents now have a cognitive ability to

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understand and remember complex strategies for such sports as football and basketball. During adolescence, the focus shifts away from acquisition to the cognitive aspects of language development, such as the ability to understand the semantics of language and the ability to use language to convey the variety and quality of information. Adolescents at this age can understand the basic theories and concepts behind how a sport is played.[52] They can transcribe symbols, signs, and coded words to understand plays the coach or trainer is asking them to perform. They can use such language to communicate with others who understand the special language related to specific sport activities. They may still have some limitations, but with practice and patience, will continue to grow in their use of this vital communication domain. Problems may arise, however, as a result of this developing process. [36] Because behavior and consequences are processed on a here and now basis, early adolescents often fail to extrapolate general rules of the game from one situation to another. They may attribute success or failure in athletics to their own uniqueness and may fail to connect regular training or practice to future athletic success. Early adolescents are preoccupied with physical (bodily) concerns, and may respond to minor injuries with out-of-proportion reactions. Normal comparisons (and noting of differences or similarities) between self and peers may cause the adolescent to either be distressed or feel superior. As reasoning abilities become more sophisticated, some adolescents may argue and disagree with adults; arguments with their coaches, trainers, or referees may result in penalties or ejections from games. Because these adolescents lack life experience, their

magical thinking tendency may be problematic for some. They still need approval from their peers, and may go to great lengths, even get in trouble, to gain their acceptance. They may impulsively engage in high risk-taking behaviors, much to the dismay of parents and coaches. Psychosocial Development

From about age 11 to 14 years, a convergence of body image and motor skills occurs.[52] Sports participation provides an early opportunity for independence and emancipation.[70] [82] Comparison with peers, worry over perceived physical differences, and sexual relationships may occupy much of early adolescents' time.[42] [46] [48] [57] Adolescents are now able to listen to the opinions of peers and adults in the environment and can independently weigh consequences of their decisions before taking action. Peer acceptance is important, but approval and support from family are still significant guiding forces.[88] [89] These adolescents are also able to enjoy and take pride in increasingly complex accomplishments in sports as well as academics, and they begin to improve their self-image. Some studies suggest that adolescents who experience consistent successes tend to develop a positive self-image, and those who experience repeated failures tend to develop a less healthy self-image.[18] [37] [42] [85] [103] Implications for Sports Participation

Most early adolescents are ready for entry level competitive sports, including football, basketball, baseball, and tennis.[52] These young adolescents, however, continue to require a great many demonstrations along with verbal instructions. Although continued participation in different activities is generally preferable, depending on innate abilities and talent, they may begin to specialize in their favorite sport, if they choose this type of concentrated effort. The behavior of adolescents is influenced by the behavior of the adults and peers in their environment. Bullying and teasing may be seen at this developmental stage, with potentially negative effects. Early adolescents cannot often depersonalize criticism, and may even believe the coach or trainer hates them. These adolescents have limited life experiences and may be highly sensitive to negative comments from others (e.g., You are a lousy hitter! You hit like a girl! You shouldn't be in this sport because girls don't belong here! You don't have any talent and should drop out!). At the other end of this continuum, adults might say things that are meant to be positive but may cause problems when the precocious athlete is no longer bigger, stronger, or better than his peers (e.g., You don't need to practice, you are a gifted player! You're better than the other kids! You're going to be a superstar!). Middle Adolescence

Physical Growth and Development

Specialization of gross motor skills continues during middle adolescence. [47] [52] Most adolescents experience continued increases in muscle mass, strength, and

cardiopulmonary endurance that began during early adolescent years. In a study by Hahn and coworkers of competitive athletes ages 14 to 24 years, dynamic strength of the quadriceps muscle was significantly greater in males than in females and was positively associated with body weight, years of jogging, years of soccer, and weekly hours of basketball. [50] Sport-specific adaptation may reflect high levels of running and jumping activity that occur in sports like soccer, European team handball, basketball, badminton, tennis, competitive gymnastics, swimming, and jogging.[50] [51] Improvement in agility, motor coordination, power, and speed continues to occur.[21] [71] [95] Females generally perform better than males in tasks that require balance as a main component. Females generally do not improve in motor performance after age 14, but males continue to improve throughout adolescence. [21] [71] [95] [103] In males, maximal speed peak occurs before PHV, and strength and power peaks follow PHV; no such clear pattern is observed in females.[21] [72] [71] [95] [103] Between 12 and 14 years of age, a transient period of motor incoordination may occur during the adolescent growth spurtprimarily in boys.[21] [71] [87] [103] It typically lasts for only about 6 months and is believed to be due to a temporary disturbance of performance tasks that require balance. Some experts, however, doubt its clinical significance as well as its existence. Multiple factors may account for the differences in motor coordination seen among these adolescents; however, no unique sociocultural, anthropometric, or physical activity characteristics have been identified in these adolescents. If such a period of motor incoordination

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is bothersome to the adolescent or the family, reassurance is all that is needed, in the absence of a specific neuromuscular disorder. Cognitive Development

During middle adolescence, abstract thinking improves, along with the ability to understand consequences of behavior.[1] [47] [57] [88] Adolescents now can perform all levels of thinking as described in Bloom's and Krathwol's taxonomy of the cognitive domain of education ( Table 17B-2 ).[77] With improved ability to understand the sport, the creative use of helpful strategies and techniques along with their execution is now possible.[96] [110] The athlete can now observe her own behavior in a match and analyze what she did correctly and what she did not do well; she can also compare and contrast that behavior with her personal best and other training data, evaluate her strengths and weaknesses, determine what needs to change, modify her action plan, design and formulate a new approach, implement that approach, and begin the process again.[96] [107] [110] She now can perform these functions with or without the aid of a coach or trainer; however, his or her input or feedback is still often valued. Psychosocial Development

During middle adolescence, levels of independence from parents and authority figures increase.[88] [89] Adolescents are capable of multiple relationships, and improved critical thinking skills help expand their roles and options.[48] [57] TABLE 17-B-2 -- Adaptation of Bloom's and Krathwol's Taxonomy for Writing of Educational Objectives* A Developmental Model of a Learning and Thinking Process Knowledge Level At this level, the individual has the ability to define, distinguish, acquire, identify, recall, and recognize. He or she knows specific facts, terms, and rules. Comprehension Level At this level of thinking, the individual has the ability to translate, interpret, and extrapolate information, and can understand the meaning of that information; he or she can explain the concepts. Application Level At this level, the individual can apply knowledge, generalize that knowledge to similar and then new situations; relate, select, organize, transfer, restructure, classify, detect, discriminate, and deduce. Analysis Level At this level, the individual is able to examine (distinguish, detect, identify, classify, discriminate, recognize, categorize, compare, contrast, and deduce). Synthesis Level At this level of thinking, the individual is able to produce, tell, relate, constitute, transmit, originate, modify, document, specify, design, synthesize, classify, develop, and formulate. Evaluation Level At this level, an individual is able to judge, validate, assess, decide, consider, compare, contrast, standardize, summarize, explain (use information to prove a point or support a course of action, outcome, or method), test, rank, grade, and discriminate. *A model of a learning and thinking process that moves from simple to complex thinking patterns. This model is applied to how children and adolescents can be taught the rules and procedures associated with sports participation.

Adolescents now begin to rely more and more on peers as their frames of reference versus parents. They use peer feedback to set personal goals and rules of conduct. They identify with nonparental adults; the coach can become a very influential role model at this stage.[87] During middle adolescence, feelings are very intense and risk-taking behavior can cause conflicts with parents and authority figures. Sports

participation is often used to impress others and to achieve social status; risk taking in sports occurs with increasing frequency.[85] [87] Media images of professional athletes exert greater influence at this stage of development, and can potentially foster unrealistic expectations of fame and fortune attained from participation in sports. [18] [37] [84] [85] [87] [103]

Implications for Sports Participation

During middle adolescence, some adolescents may find it difficult to adjust to the somatic growth spurt. Adolescents who wrestle may find it difficult to maintain a personally desired lower weight in spite of pathogenic weight-control measures. They often refuse to move to a higher weight class for fear of losing in a category in which they would be at the lower end of weight limits. Female athletes may also find that they are now heavier and may engage in as many high calorie-burning sport activities as possible to keep their weight down. Female adolescents who dance may also engage in various excessive weight-control measures to keep their ultra-thin figures. Other adaptations to sports include the need for some to increase bulk, weight, strength, and endurance. The more competitive the sport, the more pressure is on athletes to meet a specific standard and body type. For example, regardless of how talented they may be, adolescents who play defensive tackle in football may not be considered competitive by their coaches and trainers. If they want to be selected for high school varsity or college teams, they are encouraged to gain weight, lift weights, run, engage in multiple activities, and increase their flexibility and agility. Because these adolescents are still at a developmental stage in which peer pressure and the need to please significant adult figures are important, they may engage in unhealthy practices, such as using anabolic steroids or other drugs, in an attempt to achieve weight gain or bulk.[47] [70] [85] These adolescents may understand the consequences of taking steroids, but their caution may be overridden by their stronger need for popularity and peer recognition. Such negative adaptations to sports participation may present significant problems for some adolescents. Adolescents at this stage of development have the requisite skills to recognize and understand the demands of a particular sport and can decide if they want to engage in the necessary behaviors to meet those requirements. Competitive sports are appropriate and can be a rewarding experience; however, it is essential that the emotional needs and personal limitations of each athlete be recognized and that he or she be provided with multiple avenues by which to access peer approval and acceptance. Late Adolescence

Physical Growth and Development

Most adolescents reach full physical maturity by the end of this stage of development, though they continue to

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develop specialization of gross motor skills. Males continue to gain in strength, speed, and size during late adolescence, at a slower rate compared with earlier years; females continue to accumulate fat mass that may negatively affect performance. Muscular strength and aerobic capacity continue to increase into adulthood but at a slower rate than during early puberty Cognitive Development

The late adolescent years are characterized by more realistic goals about one's sports abilities and participation. Other issues, such as dating and future career plans, become more important than sports. Intellectual and functional capacities, as well as abstract thought processes, are now well developed, and decision-making becomes future oriented; personal values are now clearer and better defined.[1] [45] [57] [88] [89] Late adolescents have the cognitive ability to understand and remember complex strategies for participation in sports; their perceptual motor abilities are fully developed. [47] Adolescents are now fully capable of competitive sports and specialization; however, most still prefer to engage in sports for fun. Psychosocial Development

By late adolescence, most issues of emancipation should be essentially resolved, and final pubertal changes have been completed.[88] [89] At this stage, the adolescent is better able to deal with pressures from parents, coaches, and society, and is better able to handle personal failures. The well-adjusted adolescent who is mentally and physically healthy has developed a secure, acceptable body image and gender role. The adolescent athlete now has a more realistic view of the role of sports in the overall scheme of his or her life.[18] [42] [84] [87] Visual-Motor and Perceptual Motor Development

Perceptual motor and visual-motor abilities are now well developed and highly sophisticated.[52] Bardy and Laurent studied how body orientation is controlled during somersaulting in male gymnasts (23 to 26 years of age) by looking at the kinematics of backward standing somersaults. [17] They found that vision plays a significant role in improving the athlete's ability to successfully complete trials over a no-vision condition. Expert gymnasts were able to use their vestibular and somatosensory systems to control their body orientation in the air, help them balance their bodies, control the angle of their jumps, and temporarily stabilize their bodies as they land from a jump. During a no-vision condition, subjects were still able to successfully execute many somersaults, but the authors could not fully explain this ability. They speculated that the gymnasts may have used stored visual representations to control their body orientations in the absence of actual visual cues. The authors concluded that the vestibular and somatosensory systems need the input of vision to be fully operational in these

athletes.[17] Implications for Sports Participation

Late adolescents have the physical, cognitive, social, emotional, visual-motor, and perceptual motor capabilities to adapt their skills to meet the demands of most sports. The adolescent may or may not necessarily achieve the elite skills and psychological motivation to engage in professional or Olympic sports. Adolescents at this stage can participate in any sports for fun, recreation, fitness, and exercise; those who are able to qualify for competitive sports can also make independent determinations as to whether or not they wish to participate in any sport activity.

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Growth, Development, and Training

Studies show that regular training or sports participation does not affect the timing, rate, or magnitude of peak height velocity.[21] [28] [67] [71] [72] [87] [95] [99] [103] Regular weight training may contribute to an increase in FFM and may favorably alter the FM/FFM ratio. Endurance training also may result in improved aerobic capacity; however, the effects of growth itself and of training may be difficult to differentiate, especially among adolescents. Resistance training results in improved muscular strength in preadolescents as well as adolescents.[8] [38] [41] [67] [93] [95] [99] [103] The strength gain in prepubescent children may be more a reflection of improved neuromuscular adaptation than of actual muscle hypertrophy. Many parents wonder whether their child's sports talent can be identified early and developed further to reach an elite or Olympic level. Researchers have used complex measurements of physical, behavioral, and psychological characteristics to identify talented child athletes; however, numerous interrelated variables (such as the continuous process of growth and development, varying selection processes at different levels, different sport-specific demands, and cultural factors) make it extremely difficult to identify and accurately predict athletic excellence at an early developmental stage.[19] [28] [34] [35] [37] [41] [52] [87] [103]

Although research is limited, some reports suggest that early intensive training and specialization in a sport before a child is developmentally ready have not been shown to enhance current performance nor guarantee future athletic success.[10] [28] [37] [83] [90] [101] [103] In fact, some athletes may develop stress-related physical and emotional problems stemming from intense early participation; these problems include overuse injuries (such as stress fractures), over-training syndrome, menstrual disorders, stress injuries to growth plates, depression, anxiety, conversion reactions, and disordered eating behaviors.[10] [28] [37] [102] [103] [106] [107] [109] Regular training enhances neuromuscular adaptive responses and contributes to

improved sport-specific skills and performance.[28] [50] [55] [67] [87] [95] [99] [103] Somatotype, motor skills, age, nutritional status, physiologic and psychological factors, perceived physical abilities, training level, genetic endowment, and injury risk are the major independent variables that influence performance.* Although mesomorphy and, to a lesser extent, ectomorphy are positively associated with enhanced performance, successful athletes *See references

[ 21] [ 22] [ 28] [ 44] [ 68] [ 95] [ 96] [ 102] [ 103]

and [ 109] .

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tend to have or acquire somatotypes characteristic of individuals already successful in a particular sport.[19] [20] For the most part, motor skills are dependent on chronologic age and gender; in general, the efficiency of such skills progressively improves throughout childhood and into early adolescence and is influenced by environmental factors.[21] [22] [24] [25] [27] [69] [71] [104] [105] Lower anaerobic and aerobic capacity to some extent may also reduce performance ability in the child. The relationship between endurance, performance, and aerobic capacity, however, is not strong at any age during childhood. Several mental factors such as motivation, aggression, spirit, and self-confidence are also related to sports performance; however, their specific correlation is unclear at present. Some factors that negatively impact on performance levels include inadequate nutrition, a history of previous injury, excessive training schedules, decreased fitness, decreased endurance, joint looseness, and certain personality traits.

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Neurodevelopment and Injuries

Numerous reports have discussed the implications of a young athlete's growth and development for specific risks, unique characteristics, and short- and long-term complications of sports-related injuries; these reports have suggested appropriate precautionary and preventive measures.* Young children can be predisposed to injuries because of neurodevelopmental immaturity. They may lack the motor skills as well as the cognitive abilities to comprehend the demands and risks of a sport. Sometimes parents or coaches may fail to appreciate the normal developmental readiness of their children and unknowingly push them beyond their limits, resulting in both physical and psychological injury. As was noted earlier, the adverse effects of intensive training begun at an early age have been described by many authors. These include overuse injuries, effects on growth, delayed menarche, amenorrhea, and disordered eating; dysfunctional eating patterns are observed, especially among young gymnasts and dancers. For developing children, certain activities may be more stressful than others. Children participating in triathlons may be exposed to excessive stress, and the American Academy of Pediatrics (AAP) recommends that these events be specifically designed for children with consideration of their developmental stage.[12] Trampolines are associated with a significant risk of injury to young children, and the AAP recommends that trampolines not be used in the home, in routine physical education classes, or in outdoor playgrounds.[5] As has been suggested by recent reports, sports-related, mild, traumatic brain injuries in still-developing young athletes can have significant long-term consequences on cognitive, memory, and fine motor functions.[14] [91] [92] The adolescent years are associated with special risks for injuries related to growth and development.[86] The rapid increase in height and weight during adolescence also re sults in increased force and momentum when two players collide, as, for example, in football and other contact collision sports; this may further increase the risk for injuries.[26] [33] [44] [66] [92] [101] Paradoxically, enhanced motor skills seen in adolescents may lead athletes into a higher, more intense level of competition, also exposing them to

increased risk for injuries.[33] [34] [91] [101] The motor awkwardness and relative decrease in musculotendinous flexibility due to myo-osseous disproportion that characterize adolescence may also contribute to injuries. Because the growth cartilage present at the epiphyseal plate, the joint surface, and the apophyses is the weaker link in the musculoskeletal system, it is especially susceptible to injuries during childhood and adolescence.[26] [56] [66] [79]

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Neurodevelopmental Disabilities and Sports Participation

A wide spectrum of neurodevelopmental disabilities can occur, ranging from mild, with minimal effect on a child's daily life, to severe, with the child being fully dependent on others and on assistive technology.[35] [63] [64] Broadly, these include children with cerebral palsy, mental retardation, communication disorders (i.e., language disorders and autism), learning disorders, attention and cognitive disorders, visual and hearing impairment, and various neuromuscular disorders.[2] [29] [61] [63] [64] The vast majority of these children and adolescents should be able to participate in many sports with careful attention to disability-specific special provisions and adaptations; detailed discussion of this aspect is beyond the scope of this review.

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Conclusion

Neurodevelopmental maturation is a complex, continuous process, encompassing a number of domains. Although the rate of developmental progress varies, the sequence remains the same during normal development. Early training does not seem to enhance achievement of specific abilities at an earlier age; indeed, the neurologic system must first mature at its own normal pace. It is not possible to predict future athletic excellence in children. Different areas of developmentsomatic, neurologic, cognitive, psychosocialfunction in an integrated and interdependent fashion and should be considered together as one looks at the overall development of the child and the adolescent in terms of sport participation. A child's level of physical, neuromotor, cognitive, perceptual motor, and psychological maturation should guide the level of specific sport participation. As was shown by an earlier study, 60% of elementary school-aged children were able to perform the following tasks: throwing, kicking, running, jumping, catching, striking, hopping, and skipping.[97] The sense of social comparison is not achieved until after 6 years of age, and the ability to understand the competitive nature of sports is generally not achieved until 9 years of age. By about 12 years of age, most children are mature enough to comprehend the complex tasks of sports and are physically and cognitively ready to participate and compete in most sports. Sports participation is generally a positive experience for the vast majority of children and adolescents, and it *See references

[ 5] [ 6] [ 8] [ 9] [ 11] [ 12] [ 13] [ 14] [ 26] [ 33] [ 44] [ 56] [ 66] [ 78] [ 79] [ 86] [ 91] [ 92]

and [ 101] .

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should be encouraged. To avoid adverse consequences, however, participation should

be appropriate to the developmental stage and personal interests and abilities of the child and the adolescent; it should not be a reflection of parental dreams or societal expectations. All children can participate in some level of physical activity; however, they may require special adaptations or assistance if they have physical, cognitive, behavioral, social, or emotional disabilities. The level of involvement will be determined by many factors, including neurodevelopmental maturity, age, physical ability, financial ability, transportation resources, motivation, interest of the athlete, and societal expectations. As can be seen from this overview, there are no sure answers to the question of when a particular child is optimally ready to perform a given set of tasks required by a sport. As has been noted by Dyment, common sense and clinical judgment should largely guide such decisions.[35]

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Birrer RB, Levine R: Performance parameters in children and adolescent athletes. Sports Med 4:211-227, 1987. 22.

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Section C Preparticipation Evaluation of the Young Athlete* Keith L. Stanley MD Health care of the healthy adolescent population in the United States is largely crisis oriented. The only youths who have regular encounters with a physician generally are those with congenital or chronic medical illnesses such as congenital heart disease, type I diabetes mellitus, and asthma. One exception is the preparticipation physical examination performed on the more than 20 million young people involved in organized athletics. As a result, interest in this examination is increasing among team physicians and other health care professionals involved in the care of young athletes in this country. The importance of the preparticipation physical examination was recognized by the American Medical Association's Committee on Medical Aspects of Sports, as evidenced by their statement that every athlete has the right to a thorough preseason evaluation.[1] Although most physicians agree on the necessity for an examination, there are many controversies and conflicts about the content of the preparticipation evaluation and the best way to conduct it. As a result, this examination has undergone quite an evolution during the last several years. Many sports medicine physicians, including this author, remember the locker room line-up examination. Fortunately, this has evolved into a better-organized and even sports-specific examination. In many areas of the country, the examination now includes the expertise not only of primary care physicians but also of those in all specialties, both in and out of the sports medicine arena. Some athletic programs even include exercise physiologists, physical therapists, and athletic trainers to evaluate performance and maturity components. Purpose of the Preparticipation Examination

Several authors have offered statements concerning the purpose or goal of this examination.* Most agree that in general terms, the focus of the examination is to

ensure the health and safety of the athlete. In his review, Jones[15] noted that examining and profiling young athletes involves gathering medical and physiologic information that helps determine each child's suitability for participation in sports activities. Linder and associates[18] stated that the major purpose of the preparticipation examination is to screen for conditions that could predispose the athlete to injury or death. Evaluating health risks and relieving the school systems of the legal implications of sports participation by their students were applications of the examination noted by Rowland.[28] Runyan[29] noted that some authors want the examination to serve as a comprehensive interval evaluation; however, this does not appear to be the prevailing attitude among most sports medicine physicians. Strong and Linder [34] mention the identification of conditions that need rehabilitation before sports participation and matching young athletes with an appropriate sport or position as important purposes of the examination. Lombardo [19] summarizes the purposes of the preparticipation examination very nicely in the following six points: (1) to detect additional risks; (2) to detect medical contraindications; (3) to indicate which sports are safe for the individual; (4) to serve as a limited general health screening; (5) to meet legal and insurance requirements; and (6) to evaluate physical maturation. As can be seen from these statements, the purpose of the preparticipation sports examination has undergone *This chapter has been abstracted from Stanley KL: Preparticipation evaluation of the young athlete. Adv Sports Med Fitness 3:69-87, 1990. Reprinted with permission of Year Book Publishing Company, Chicago. *See references [ 6] [ 14] [ 15] [ 18] [ 19] [ 28] [ 29] [ 31] [ 34] and [ 40] .

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significant transition. With the increasing interest in identifying conditions that require rehabilitation before performance and in obtaining performance measurements, it appears that the evolution of the preparticipation examination will continue for some time. All states require that physical examinations be performed before young athletes participate in interscholastic sports in order to identify conditions that may increase the risk of injury.[9] Feinstein and colleagues[11] conducted a survey of all 50 states and the District of Columbia. Out of the 45 replies that they received, they found that 35 states require a yearly examination, three states require an examination every 3 years, one state requires examination only once, and six did not specify their requirements. Several authors now have spoken out in support of requiring only two comprehensive examinations, one to be performed in junior high school and one in senior high school, and annual medical history reviews. If the history indicates something of significance or if there is an injury, a medically specific examination is then recommended. Risser and associates[27] found that, because of the low frequency of significant findings and unfavorable cost-benefit ratio of annual examinations, the University Interscholastic League recommended that the annual examination be required only once or twice in the secondary school years. In the American Academy of Pediatrics publication, Smith[31]

proposed that examinations be performed every 2 years. Other authors support similar requirements.[19] [40] Wood[40] described a pilot program in which examinations are done once in junior high and once in senior high, with the school nurse conducting annual reviews of the medical histories. The school nurse then refers athletes with significant interval histories to a physician. Therefore, although most states still require an annual examination, a growing body of data and an increasing number of sports medicine physicians advocate a reduction in the frequency of the preparticipation examination to two times during the secondary school years. Exceptions are made for athletes who experience an illness or injury that requires an updated examination. Other data that support less frequent preparticipation examinations are those of Thompson and associates,[37] who found that only 1.2% of 2670 athletes had medical problems that excluded them from sports participation. During 2 consecutive years, Linder and associates[18] found that none of 562 athletes were diagnosed with an exclusionary illness or injury the first year, and only 2 (0.3%) of 706 athletes were excluded from sports participation the following year. Of 701 athletes in a study done by Goldberg and colleagues,[12] only 1.3% were excluded from sports participation. Thus, because of the low frequency of significant findings, the trend is to move away from the traditional annual preparticipation examination.

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Method of Examination

The preparticipation examination also has undergone a significant evolution in the manner in which it is conducted. The three most commonly identified means of conducting the examination are having it performed by the personal family physician, as a locker room examination, and using a station-type method. Most sports medicine physicians feel that the locker room examination has no place in the evaluation of athletes, however. Although many authors point out that an examination performed by the family physician offers the advantages of continuity of care, a readily available complete medical history, and better doctor-athlete rapport,[5] [6] [19] [28] [34] there can be drawbacks to this type of examination. Lombardo[19] notes that the accuracy of this type of examination may be limited by the level of interest and knowledge of the private physician. Strong and Linder[34] indicate that an examination done by the private physician may not be sports oriented or sports specific and all too often may be performed in a cursory manner. The group or station method appears to be the type favored by most sports medicine physicians. It is possible to include specialty physicians as well as flexibility and performance testing in this type of examination, and it also appears to be more sports oriented.[36] In addition, at least one study indicates that this type of examination is more sensitive in uncovering significant illness or injury.[5] DuRant and associates [5] found that fewer diagnoses were recognized with single physician examinations than with multiple physician examinations done in a station-type method. Multiple examiners found a higher percentage of abnormalities in 20 of 21 examination categories. The differences were statistically significant in six categories. These included diagnoses of the mouth, teeth, hips, thighs, knees, and ankles. They also noted that only 2.4% of athletes seen by a single physician were referred for further evaluation compared with 6.4% of those seen by multiple physicians. This study lends support to the station method of examination. There is general agreement among sports physicians about the timing of the preparticipation examination. Most agree that it is best to do the examination or medical

history review (if an institution is not conducting annual examinations) 6 to 8 weeks before the beginning of the sports season.[17] [19] [31] [33] [34] [37] In most cases, this leaves adequate time for any additional evaluations that may be needed. It also gives the athlete time to rehabilitate an injury or illness before the start of the season. Special cases may arise in which an athlete may need to be evaluated much earlier than 6 to 8 weeks before the start of the season. This is especially true when significant surgery involving the musculoskeletal system has been performed. Thus, it is important for the sports physician to have a close working relationship with the coaching staff and the athletic trainer. Organization and Set-up

Before going into detail about each area of the medical history and physical examination, some suggestions on how to organize and set up the examination may be timely. First, the number of athletes that will be examined is established. The athletes and their parents are notified of the date, time, and place in advance. This may actually be done by the school administration, athletic directors, or coaches. Second, the number of people that will be participating

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as staff for the examinations is determined. Their capabilities are analyzed, and their appropriate responsibilities are assigned on that basis. If one has fewer personnel, one may have to combine some stations. Also, it is important to ask the athletes to dress in gym shorts and loose-fitting T-shirts to ease and expedite the examination. If possible, one may ask the athlete to complete the medical history form in advance. If this is not possible, then the first station is a check-in to pay the examination fee (if charged) and to get the examination form. This may be staffed by a parent, teacher, or coach. Next in line is the station to review the medical history. As discussed later, this process is very important in the preparticipation evaluation and should be conducted by a nurse, nurse clinician, or physician. Vision testing may follow if it has not been done previously by the school nurse. This can be done at the time of the preparticipation examination by a nurse or other trained personnel. Next, height and weight are obtained. If one is also evaluating the percentage of body fat, it could be done at this station. This station may be manned by a parent. If percentage of body fat is being measured, the staff would have to include an exercise physiologist, nurse, trainer, or some qualified person. Blood pressure and pulse are obtained next. Appropriate personnel include a nurse, trainer, or emergency medical technician. At the next station, the athlete enters the physical examination itself. It is recommended that the ear, nose, and throat examination be conducted first, followed by a dental

examination if a dentist is available at this station. The cardiovascular and pulmonary systems are evaluated next. It is imperative to have a quiet room for this part of the examination. The athlete then goes on to the abdominal examination. Tables are needed to allow comfortable recumbency during this examination. For male athletes, hernia and genitourinary evaluations are done at this station. If flexibility testing is part of the program, it can be done just before the orthopaedic examination. This testing could be conducted by an exercise physiologist, physical therapist, or athletic trainer. The final part of the examination is the orthopaedic assessment. Shoes and socks should be removed. One may also have male athletes remove their T-shirts. Female athletes should wear halter tops or swimsuits. Part of the orthopaedic examination should include evaluation for spinal deformity. The final examiner may also be responsible for reviewing the status of the athlete's sports participation. Again, it should be emphasized that one may have to be flexible depending on the number of personnel available. If stations have to be combined, consolidate those that lead to a smooth-flowing operation (e.g., combine the cardiovascular and pulmonary examination with examination of the abdomen).

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Medical History

A complete medical history is important in every area of medical care, and the sports preparticipation examination is no exception. Runyan[29] indicates that the sports medical history should have a limited scope and should attempt to identify those conditions that are significant to sports participation. Taken in this manner, a medical history can be brief yet effective in identifying potential problems. Ascertaining the accuracy of information given in an athlete's medical history can prove difficult. Athletes themselves may neglect to indicate on the history form an illness or injury that they fear might exclude them from participation. They also may not deem significant something that may in fact be essential to their protection or rehabilitation. Another problem may lie in discrepancies between the medical history provided by the athlete and that provided by the parent. In the study by Risser and colleagues,[27] only 39% of the athletes' histories agreed with those of their parents. Another problem that may sabotage the acquisition of a good medical history is the possible inability of athletes or their parents to read or understand the history form. With illiteracy as high as 25% to 30% in some areas, this can be a significant problem. One solution may be to have one station in the examination include a physician who takes the history.[18] [27] Smith[31] suggests that history taking be assisted by a physician, nurse, or trainer; Wood[40] used the school nurses to obtain the medical history in his program. Other side issues may be important in the medical history. As Lombardo[19] indicates, it is very important to ascertain a history of chemical or substance abuse in a young athlete. He also notes that obtaining a menstrual history in female athletes may be critical in view of the growing concern about exercise amenorrhea and its relationship to bone density and the prevention of osteoporosis in women. The medical history should also include questions about the potential existence of eating disorders. Overall, most sports physicians agree that the medical history should be sports specific and include certain targeted areas. Areas most often noted include musculoskeletal

injuries, neurologic injuries, infectious diseases, cardiac disease, pulmonary disease, hospitalizations, medicine allergies, and surgical procedures. [5] [9] [29] [31] [34] In their study, Strong and Linder[34] indicated that the most frequently reported problems in the medical history were previous injury, hospitalization, and joint problems. Many authors have formulated medical history forms to include those items that they feel are important.[5] [15] [17] [31] [33] [34] Feinstein and colleagues[11] found that 25 states have a standardized medical history questionnaire. Although medical history forms do vary, they all have several areas that consistently are viewed as significant by sports physicians. A question relating to sudden death or myocardial infarction in family members younger than 50 years of age is found on most forms. This means of discovering an athlete with hypertrophic-obstructive cardiomyopathy [3] [8] [20] [22] [23] [24] [35] may be even more sensitive than the physical examination. The responses obtained to an inquiry about syncope or even near-syncope during exercise are deemed important. The ability to complete a quarter- or half-mile run without stopping is also questioned on most forms. The inclusion of questions about arrhythmias, murmurs, hypertension, and previous cardiac surgery on these forms is vital. All of these are necessary for proper screening of an athlete's cardiovascular medical history.

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A neurologic history is also critical, especially as it pertains to head and neck injuries. Because a neurologic deficit can result from the cumulative effect of cerebral contusions, specific questions should be asked about loss of consciousness associated with head injury or any history of diagnosed concussions. A history of a seizure disorder should prompt inquiries about medication because the maintenance of good seizure control must be established. Most forms contain inquiries about infectious diseases, but no specific diseases are usually mentioned. This places the burden on the examiner to be specific and inquisitive about infectious diseases. The most significant question with regard to pulmonary disease in the athletic population is the one relating to asthma or exercise-induced bronchospasm. If the medical history is positive for either of these conditions, the examiner should inquire about any medications being used and their availability during practices and events should they be needed. Inquiries should be made about medications being taken, medication allergies, and environmental allergies. One question that is rarely found on medical history forms for athletes is the presence of allergies to insect stings. In view of the life-threatening potential of these allergies, this question should be included, especially for athletes involved in outdoor sports. Surgeries should be recorded; if any are recent, a proper release should be obtained

from the surgeon of record to be included in the athlete's health record. Any history of chronic illness should be elucidated. If chronic illness exists and requires constant monitoring (as is the case with diabetes mellitus), the medication history is necessary. The musculoskeletal history is of utmost importance when evaluating the athlete. A history of sprains, strains, dislocations, or fractures is often uncovered in the preparticipation examination. DuRant and colleagues[5] found that the most frequent musculoskeletal problems discovered in the health history were previous fractures (22.1%). Other injuries of the musculoskeletal system comprised 20.9% of the responses. The examiner taking the medical history should indicate clearly the presence of any previous musculoskeletal injuries. This allows the physician doing the orthopaedic examination to give special attention to these areas of previous injury. Many other questions may be included in the medical history. It should be kept in mind that the questionnaire should be sports specific, easily understood, and constructed for efficient use by both the athlete and the examiner. Table 17C-1 is a compilation of sports medical history questions that this author views as significant. Although this list is not comprehensive, the questions listed should be found consistently on all medical history formats. The importance of the medical history for sports participation is underscored by the results of two studies. Risser and colleagues[27] found that 67% of all medical problems and 63% of all orthopaedic problems were referred to specialists for further care after being noted in the history. Goldberg and colleagues[12] similarly found that 74% of significant medical and orthopaedic problems were reported. Further, in Goldberg and colleagues' study, seven TABLE 17-C-1 -- Medical History Questions 1. Are you taking medications? 2. Any medication allergies? 3. Any environmental allergies? 4. Any allergies to insect stings? 5. Any hospitalization? 6. Any surgeries? 7. Has any family member had sudden death or heart attack before age 50? 8. Have you had any heart disease, murmur, extra beats, or high blood pressure? 9. Have you ever been dizzy or passed out from exercise? 10. Have you ever been knocked out or had a concussion? 11. Any joint injuries (fractures, sprains, strains, or dislocations)? Neck

Arm

Thigh

Back

Hand

Knee

Shoulders

Finger

Ankle

Elbow

Hip

12. Any organs missing? 13. Any chronic illness? 14. Any chemical or substance use? 15. Any menstrual irregularities? 16. Have you ever induced vomiting, engaged in binge eating or purging? 17. Have you ever been disqualified from participation? 18. Date of last tetanus shot? 19. Do you wear eye glasses, contact lenses, or dental appliances? 20. Any history of seizure disorder? of nine athletes excluded from participation would have been so excluded on the basis of the history alone. Many have recommended that the sports preparticipation physical examination be sports specific.[15] [17] [34] Because most significant findings on the sports preparticipation physical examination involve the musculoskeletal system, emphasis should be placed on this area during the examination.[5] [27] [28] [37] This topic is addressed in more detail later in this chapter. Another area of emphasis should be the cardiovascular examination because most causes of sudden death are cardiac in origin.[3] [8] [10] [23] [24] This subject is addressed in more detail later.

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Specific Areas General Data

Most examinations begin with measurements of height, weight, blood pressure, and pulse. Some also include body fat determination. Goldberg and coworkers [12] found that 32% of the athletes in their study had excessive body fat. Blood pressure parameters, suggested by Smith,[31] are less than 130/75 mm Hg for children aged 6 to 11 years and less than 140/85 mm Hg for children 12 years and older. As pointed out by Strong and Linder,[34] an athlete should not be labeled hypertensive until three abnormal readings are obtained at different times. If hypertension in a child is documented, Strong and Lindner further recommend testing the blood pressure response to exercise. They state that no data have been published indicating that hypertension causes any direct morbidity or mortality during athletic participation. A rapid or irregular pulse should be correlated

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with the cardiovascular examination to determine its clinical significance. Head and Neck

Vision screening should be performed, and an uncorrected vision of less than 20/40 should be referred for further evaluation.[31] This is the time to note whether corrective lenses have been prescribed already. Certain findings in the head, eyes, ears, nose, and throat examination should be noted. Unequal or unreactive pupils should be documented because this finding may be very important later should the athlete incur a head or neck injury. For athletes participating

in water sports, the condition of the external auditory canal and tympanic membranes is important. Proper treatment should be given and proper hygiene practiced by those who have chronic external otitis owing to their constant water exposure. A new area of interest among young athletes is the sport of scuba diving. These young people require a more intense examination of the ear, nose, and throat,[2] [4] because, as noted by Dembert and Keith,[4] most injuries sustained in scuba diving are related to barotrauma or decompression sickness. On inspection, the physician looks for polyps, a deviated septum, or evidence of a necrotic or perforated septum that might indicate substance abuse. Inspection of the mouth should include the teeth. Dentition abnormalities are some of the findings reported most frequently on the physical examination. [34] Note should be made of any dental appliance being worn by the athlete. Skin and Lymphatics

A dermatologic assessment is vital, especially in those participating in contact or collision sports. As Lombardo[19] noted, clearance should not be given to those athletes who have such dermatologic pathologies as herpes, scabies, louse infestations, or impetigo. Other dermatologic conditions such as acne and fungal dermatophytic infections require referral for proper care. Assessment of the lymphatics and abdomen is recommended also. The cervical, supra-clavicular, axillary, and inguinal lymph nodes should be checked for any enlargement or tenderness. The abdomen should be palpated for hepatomegaly or splenomegaly. Should any lymphadenopathy or organomegaly be discovered, referral should be initiated for further evaluation. Genitourinary System

The genitourinary examination has to a great extent been conducted in males and neglected in females. Females with a significant menstrual history, such as primary or secondary amenorrhea, should be referred to their private physicians for further evaluation. A female nurse or female physician may also need to check pubic hair and breast development to assess maturation (this is discussed later). Examination of male athletes should establish the presence or absence of a hernia and whether or not both testes are present and descended. Thompson and associates [37] found three previously undiagnosed cases of cryptorchidism in more than 1700 males examined. Three cases of inguinal hernia were also diagnosed. Strong and Linder[34] reported that 6.5% of all abnormalities found were discovered in the genital and hernia examination. If a hernia is present and an additional risk would be incurred by continued sports participation, surgical correction should be performed before clearance is given.[19] The issue of participation by athletes who are missing a paired organ is discussed later. Cardiovascular System

Because most catastrophic situations involving young athletes are related to sudden death and cardiovascular disease, an in-depth discussion of this topic is appropriate. The highly conditioned athlete is viewed as the epitome of health, and sudden death is such an alarming and unexpected event that it may cause overreaction in an entire community. Because of this, sports physicians and cardiologists have tried to search for

the best screening methods to minimize the risk of this tragic occurrence. Cost containment is one major problem with an extensive cardiovascular screening examination. Another difficulty lies in targeting certain areas in the medical history and physical examination to create the most sensitive protocol. Maron and associates[22] conducted a cardiovascular screening of 501 intercollegiate competitive athletes. The screening protocol included personal and family history, a physical examination, and a 12-lead electrocardiogram. Of these 501 athletes, 102 had positive findings on one or more of the three parameters. Of the 90 who submitted to further evaluation, 75 (84%) had no definitive evidence of cardiovascular disease. Of the other 15, one had mild systemic hypertension and 14 had mild mitral valve prolapse. The authors concluded that performance of an electrocardiogram did not appreciably enhance the sensitivity of the informed history and physical examination and, further, that it was responsible for a high number of false-positive observations. In a study of sudden death that included necropsy in highly conditioned, competitive athletes, cardiovascular abnormalities were found in 28 of 29 athletes (97%) and almost certainly were the cause of death in 22 of the athletes (76%). [23] In only 7 of the 29 patients was cardiac disease suspected, and in only 2 of the 7 had the correct diagnosis been made. Table 17C-2 lists the clinical complaints noted by family members of eight of the athletes when questioned retrospectively, and Table 17C-3 lists the cardiac abnormalities that were found. Hypertrophic-obstructive cardiomyopathy was found in 14 athletes and was the most common cause of death by far. Other diagnoses that were made in more than one athlete included anomalous origin of the left coronary artery from the right sinus of Valsalva, idiopathic concentric left ventricular hypertrophy, coronary heart disease, and ruptured aorta. Other authors have mentioned other, less common causes of sudden death such as prolonged Q-T syndrome, mitral valve

648

TABLE 17-C-2 -- Clinical Complaints in Cases of Sudden Death Reported Symptoms Number Syncope

3

Presyncope

1

Chest pain

2

Periodic mild fatigue

1

Mild fatigue, presyncope, palpitations

1

Reprinted with permission from the American College of Cardiology (Journal of the American College of Cardiology 8:382-385; 1980). prolapse, valvular heart disease, myocardial and pericardial diseases, sarcoidoses, and abnormalities in the cardiac conduction system.[3] [8] [20] [24] [34] [38] Thus far, no author on

the subject of sudden death has recommended including an electrocardiogram or echocardiogram in the screening of athletes. The most cost-effective screening method apparently is an informed medical history and physical examination. The cardiovascular examination should include inspection, palpation (especially of the femoral pulses and precordium), and auscultation of heart sounds. [35] Strong and Steed[35] note that unusual facies and body habitus that are characteristic of syndromes associated with cardiac defects should be recognized. Palpation of the brachial and femoral pulses should be done to rule out the presence of coarctation. A bifid pulse should be recognized as a possible abnormal finding consistent with hypertrophic cardiomyopathy. The carotids and precordium should be palpated for trills. Auscultation should be done to identify S1 and S2 heart sounds. An S3 may be a normal finding in young athletes, but an S4 is always considered pathologic.[35] Murmurs should be identified as systolic or diastolic in origin. The intensity of a murmur itself may not be indicative of either a pathologic or nonpathologic state; the murmur associated with hypertrophic cardiomyopathy may be very soft.[23] Therefore, the intensity of the murmur should not be the only parameter by which one determines the necessity of referral for further evaluation. Most innocent murmurs should diminish with the Valsalva maneuver; however, the murmur of hypertrophic cardiomyopathy increases in the sitting and standing positions as well as with exercise. These parameters may help the examiner determine which athletes should be referred for further evaluation. TABLE 17-C-3 -- Probable Cause of Death in Cases of Sudden Death Probable Cause of Death Number Hypertrophic cardiomyopathy

14

Idiopathic concentric left ventricular hypertrophy

5

Anomalous origin of the left coronary artery

3

Atherosclerotic coronary disease

3

Ruptured aorta

2

Hypoplastic coronaries

1

No cardiovascular disease

1

Reprinted with permission from the American College of Cardiology (Journal of the American College of Cardiology 8:382-385, 1980).

Auscultation of premature beats or frequent dysrhythmias also is an indication that further cardiac evaluation is needed. If the arrhythmia is suppressed with mild exercise, most likely it is benign. But if there is any question, referral for probable exercise testing and 24-hour Holter monitoring may be necessary. The cardiovascular examination should be emphasized during the sports preparticipation physical examination to attempt to identify those athletes who may be at risk for sudden death from cardiovascular disease.

Musculoskeletal System

The musculoskeletal system is another area that should undergo close inspection during the preparticipation examination. Strong and Linder[34] found that 38.3% of abnormal findings on the physical examination were musculoskeletal in origin. Thompson and colleagues[37] reported a much higher incidence of musculoskeletal problems in their series (67%). Although the incidence of musculoskeletal abnormalities identified on a sports preparticipation physical examination may vary, they are still the findings that are most frequently identified and referred for further evaluation in every series. One exception is a study by Goldberg and colleagues[12] in which 60 athletes were reported to have medical problems needing further consultation, 35 of whom had musculoskeletal problems. It should be noted, however, that 40 of the athletes in the medical category were referred for proteinuria. The knees and ankles appear to be the most frequently injured joints in athletes. Linder and colleagues [18] reported findings related to the knee in 6.9% and 8.8% of athletes and to the ankle in 2.1% and 2.5% in two consecutive years, respectively. DuRant and coworkers[5] observed that in the multiple-examiner station examination method, more musculoskeletal problems were identified in more athletes (67%) than in the single-physician examination (5.4%). This fact illustrates the necessity of having an examining physician who is trained in musculoskeletal evaluation and understands a sports-specific examination. Table 17C-4 describes a functional orthopaedic screening examination that is similar to that used by Thompson and colleagues[37] in their series. This type of examination is very efficient in terms of both time and sensitivity in identifying problems. Any problem identified by the screening examination or the medical history may require a more specific, in-depth evaluation. At the time of the examination, it is important to identify problems that require rehabilitation so that a program can be initiated that will allow the athlete to be prepared in time for the sport season. Special emphasis should be placed on those who have had previous surgery. If the surgery has been recent, it is necessary to coordinate the athlete's return to his or her sport with the surgeon of record. In general, laboratory tests have been found to cause added expense with little return in the preparticipation examination. Urinalysis has not proved effective in identifying significant problems; in fact, it creates much anxiety because of the number of referrals it prompts for further evaluation. [31] Hematocrit and hemoglobin determinations also have been found unnecessary; they may be normal even in athletes who are iron deficient. Tissue iron depletion

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TABLE 17-C-4 -- Orthopaedic Screening Examination*

The orthopaedic screening examination requires about 90 seconds. Time studies indicate that it is most efficiently done one athlete at a time rather than in small groups. It is designed to reveal previous inadequately rehabilitated injuries or those few previously unrecognized orthopaedic conditions that might be adversely affected by participation in a sports activity. Positive findings require a more extensive examination and/or history. A more detailed examination should not be attempted at the screening examination. Athletic Activity (Instructions)

Observation

Stand facing examiner

Acromioclavicular joints; general habitus

Look at ceiling, floor, over both shoulders; touch ears to shoulders

Cervical spine motion

Shrug shoulders (examiner resists)

Trapezius strength

Abduct shoulders 90% (examiner resists at 90%)

Deltoid strength

Full external rotation of arms

Shoulder motion

Flex and extend elbows

Elbow motion

Arms at sides, elbows 90% flexed; pronate and supinate wrists

Elbow and wrist motion

Spread fingers; make fist

Hand or finger motion and deformities

Tighten (contract) quadriceps; relax quadriceps

Symmetry and knee effusion; ankle effusion

Duck walk four steps (away from examiner with buttocks on heels)

Hip, knee, and ankle motion

Back to examiner

Shoulder symmetry; scoliosis

Knees straight, touch toes

Scoliosis, hip motion, hamstring tightness

Raise up on toes, raise heels

Calf symmetry, leg strength

From Smith NJ (ed): Sports Medicine: Health Care for Young Athletes. Evanston, Ill, American Academy of Pediatrics, 1983. *May require reflex hammer, tape measure, pin, and examination table.

is best determined biochemically with serum ferritin levels; however, this test should be reserved for athletes who have indications for such evaluation (endurance athletes or female athletes with fatigue or diminished performance).

Maturation Indexing

Currently, areas that are generating interest for inclusion in the sports preparticipation examination include maturation indexing and physiologic testing such as tests of endurance, agility, strength, flexibility, and body composition. [12] [15] [19] [30] [34] Maturation indexing, following guidelines by Tanner,[36] has been recommended to profile athletes to allow them to compete with others who are at similar maturity levels. Proponents believe that this will minimize the higher potential for injury in those with a lower maturity level.[13] [26] They also acknowledge, however, that no data have been reported to indicate that such an increased risk exists. For the clinician, knowing that peak height velocities occur at Tanner stage 2 breast development in girls and at Tanner stage 4 genital development in boys may aid in predicting or even preventing certain injuries that occur with rapid growth.[15] This is especially true of injuries related to inflexibility or diminished agility. In an effort to develop some type of screening method to aid in indexing maturity, Kreipe and Gewanter[16] used a handgrip strength measurement and self-assessed Tanner staging levels. They reported that only 67 of 364 males (18%) had grip strength and self-assessed Tanner staging levels that were discordant. Tanner stage 3 was considered immature. The data indicated a break between Tanner stages 3 and 4 at about 55 pounds of grip strength as measured by a Jamar hand dynamometer. By their data, when self-assessed Tanner staging levels and grip strength were performed together to test for immaturity, the false-negative ratio was 5%. When testing for maturity, the false-positive rate was 1%. Maturity indexing may become a more important part of the preparticipation examination, especially if profiling becomes accepted more widely. This concept is probably very important for many young athletes. In his discussion about the uniqueness of young athletes, Martens[25] lists six major reasons why young athletes drop out of sports. Two of these six are not getting to play and being mismatched. Maturation assessment may prove to be very helpful in screening young athletes and placing them in a healthier sports environment. Physiologic Assessment

Flexibility assessment is being used more often in the preparticipation evaluation also. Goldberg and colleagues[12] have described a flexibility screening technique. Some protocols have included goniometer measurements for selected joints and sit-and-reach measurements. The method described by Goldberg and colleagues is more comprehensive but may not fit into each program's framework of evaluations. As a result, the sports physician may want to have the coaching staff and athletic trainer conduct this protocol at another time and then assess the results with them. Body composition has already been mentioned in the discussion on the physical examination. Body composition can be measured quickly by skin calipers. This

measurement is important from the perspective of athletic performance and also may provide an opportunity for counseling an athlete about health issues that have a lifelong impact. It also may provide important information to wrestlers about the amount of weight loss that is feasible and medically safe. Strength and endurance measurements as well as assessments

650

of agility also are potentially valuable aspects of a preparticipation examination. Each physician or school system, however, may have to develop its own program in these areas because many of these tests do not have well-defined standards. Except for the 12-minute or 1.5-mile run, standards for comparison may not be readily available.

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Classification of Sports Readiness

The final step in the preparticipation examination is the classification of the young athletes according to the safety of their participation. Most authors recommend three clearance options.[19] [34] [37] Clearance A permits unrestricted participation, clearance B permits participation after further evaluation or rehabilitation is completed, and clearance C defers clearance because a high-risk medical contraindication to participation has been detected. The final results should be discussed with the athlete, his or her parents, and coaches if clearance B or C is selected for that particular examination. Much has been written and considerable debate has arisen about which sports are safe for young athletes with certain medical conditions. The American Academy of Pediatrics[7] recently published a statement classifying sports and listing recommendations for the participation of athletes with specific medical conditions in competitive sports ( see Tables 17C-2 and 17C-3 ). Sports are classified as contact or collision, limited contact or impact, and noncontact (which has three levels: strenuous, moderately strenuous, and nonstrenuous). Sports participation by athletes who are missing one organ of a paired set is a controversial topic. Although many physicians and school districts have refused to approve participation in these cases, the courts sometimes have intervened to allow the athlete to perform.[38] Thus, the ultimate decision may not rest with the physician in many cases. In athletes with loss of vision in one eye, an approved eye protection device must be worn for participation in any sport that poses a risk to the eyes. In athletes with an absent testicle, the risks should be discussed with the athlete and his parents, and proper protection should be included in the athletic gear.[21] Athletes with a solitary kidney that demonstrates an abnormal anatomic variant (i.e., ectopic location or a ureteropelvic junction abnormality) or any degree of obstruction or impairment of function, according to Mandell and colleagues,[21] are not allowed to participate in contact or collision sports. It is evident, therefore, that any decision about inclusion or exclusion from participation in sports activities must be made on an individual basis. In tenuous cases, extensive discussion with the athlete, parents, coaches, school

administrators, and physician should take place before a decision is made. It must be recognized that the preparticipation examination does not replace regular continuous care by the athlete's private physician, even though this is the view currently held by most athletes and parents and even by some physicians. The goal of the preparticipation examination should be to ensure as much as possible the health and safety of young athletes. The sensitivity design should be such that potential health risks and medical contraindications to sports participation by the athlete are identified. The examination should be regarded not as an examination designed to exclude young people from participation but as a means of including all young people who can participate safely in athletic endeavors. In addition, the examination should be sport specific, not only designed for the athletic population as a whole but also emphasizing the sport or sports of choice. The examination should convey a positive image of the physician and his or her role in the care of athletes. The athlete should be made to feel comfortable in the relationship that may be built from this encounter. It is also a means by which to bring the physician, athletic trainer, and coaching staff together in a cooperative effort to provide a healthy, safe environment in which young athletes can compete. It should provide an opportunity for each professional involved to gain a better understanding of his or her role in the care of the total person, not just the athlete. Alienation of any of these components is not in the best interest of the young athlete. The preparticipation evaluation is a small but significant investment in our young people. Directly or indirectly, these evaluations affect the physical, psychological, and emotional development of young athletes and provide an opportunity to exert a positive and rewarding influence on their lives.

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References American Medical Association: Medical Evaluation of the Athlete: A Guide, rev. ed. Chicago, American Medical Association, 1976. 1.

Becker D, Parell GJ: Medical examination of the sport scuba diver. Otolaryngol Head Neck Surg 91:246-250, 1983. 2.

Braden DS, Strong WB: Preparticipation screening for the sudden cardiac death in high school and college athletes. Physician Sportsmed 16:128-140, 1988. 3.

Dembert ML, Keith JF: Evaluating the potential pediatric scuba diver. Am J Dis Child 140:1135-1141, 1986. 4.

DuRant R, Seymore C, Linder CW, et al: The preparticipation examination of athletes: Comparison of single and multiple examiners. Am J Dis Child 139:657-661, 1985. 5.

Dyment PG: Another look at the sports preparticipation examination of the adolescent athlete. J Adolesc Health Care 7:130S-132S, 1986. 6.

Dyment PG, Goldberg B, Haefele SB, et al: Recommendations for participation in competitive sports. Pediatrics 81:737-739, 1988. 7.

Epstein SE, Maron BJ: Sudden death and the competitive athlete: Perspectives on preparticipation screening studies. J Am Coll Cardiol 7:220-230, 1986. 8.

Esquivel MT, McCormick DP: Preparticipation sports evaluation, part 1: The station-method examination. Fam Pract Recert 9:41-60, 1987. 9.

Esquivel MT, McCormick DP: Preparticipation sports evaluation, part 2: Recommendations for student participation. Fam Pract Recert 9:107-118, 1987. 10.

Feinstein RA, Soilean EJ, Daniel WA: A national survey of preparticipation physical examination requirements. Physician Sportsmed 16:51-59, 1988. 11.

Goldberg B, Saranit A, Witman P, et al: Preparticipation sports assessment objective evaluation. Pediatrics 66:736-745, 1980. 12.

13.

Goldberg B, Boiardo R: Profiling children for sports participation. Clin Sports Med 3:153-169, 1984.

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Hunter SC: Screening high school athletes. J Med Assoc Ga 74:482-484, 1985.

Jones R: The preparticipation, sport-specific athletic profile examination. Semin Adolesc Med 3:169-175, 1987. 15.

Kreipe RE, Gewanter HL: Physical maturity screening for participation in sports. Pediatrics 75:1076-1080, 1985. 16.

17.

Kulund DN: The Injured Athlete. Philadelphia, JB Lippincott, 1982.

Linder CW, DuRant RH, Seklecki RM, et al: Preparticipation health screening of young athletes. Am J Sports Med 9:187-193, 1981. 18.

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Lombardo JA: Preparticipation physical evaluation. Prim Care 11:3-21, 1984.

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Luckstead EF: Sudden death in sports. Pediatr Clin North Am 29:1355-1362, 1982.

Mandell J, Cromie WJ, Caldemone AA, et al: Sports-related genitourinary injuries in children. Clin Sports Med 1:483-493, 1982. 21.

Maron BJ, Bodison SA, Wesley YE, et al: Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. J Am Coll Cardiol 10:1214-1221, 1987. 22.

Maron BJ, Roberts WC, McAllister HA, et al: Sudden death in young athletes. Circulation 62:218-229, 1980. 23.

Maron BJ, Epstein SE, Roberts WC: Causes of sudden death in competitive athletes. J Am Coll Cardiol 7:204-214, 1986. 24.

Martens R: The uniqueness of the young athlete: Psychologic considerations. Am J Sports Med 8:382-385, 1980. 25.

26.

Nicholas JA: The value of sports profiling. Clin Sports Med 3:3-10, 1984.

Risser WL, Hoffman HM, Bellah G: Frequency of preparticipation sports examinations in secondary school athletes: Are the university interscholastic league guidelines appropriate? Tex Med 81:35-39, 1985. 27.

Rowland TW: Preparticipation sports examination of the child and adolescent athlete: Changing views of an old ritual. Pediatrician 13:3-9, 1986. 28.

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Runyan DK: The pre-participation examination of the young athlete. Clin Pediatr 22:674-679, 1983.

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Smith NJ, Garrick JG: Pre-participation sports assessment. Pediatrics 66:803-806, 1980.

Smith NJ (ed): Sports Medicine: Health Care for Young Athletes. Evanston, Ill, American Academy of Pediatrics, 1983. 31.

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Stanley KL: Pre-participation evaluation of the young athlete. Adv Sports Med Fitness 3:69-87, 1990.

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Strauss RJ (ed): Sports Medicine. Philadelphia, WB Saunders, 1984.

Strong WB, Linder CW: Preparticipation health evaluation for competitive sports. Pediatr Rev 4:113-121, 1982. 34.

Strong WB, Steed D: Cardiovascular evaluation of the young athlete. Pediatr Clin North Am 29:1325-1338, 1982. 35.

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Tanner JM: Growth at Adolescence, 2nd ed. Springfield, Ill, Charles C Thomas, 1962.

Thompson TR, Andrish JT, Bergfeld JA: A prospective study of preparticipation sports examinations of 2670 young athletes: Method and results. Cleve Clin Q 49:226-233, 1982. 37.

Tucker JB, Marron JT: The qualification-disqualification process in athletics. Am Fam Physician 29:149-154, 1984. 38.

VanCamp SP: Exercise-related sudden death: Cardiovascular evaluation of exercises: Part 2. Physician Sportsmed 16:47-54, 1988. 39.

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Section D The Child Athlete with Chronic DiseaseT Charles T. Morton Colonel USAF, MC Because of the technology explosion, children with increasingly severe disabilities are being fully included into the mainstream of life. Both physicians and program directors often previously excluded children with chronic diseases from full participation in sports. Today's athlete may have minor or major disabilities. Special Olympics and camps for children with disabilities have played an important role in moving these children into the mainstream of life.[12] Meeting these new demands challenges today's medical practitioners to become more knowledgeable about chronic medical conditions and available programs. As children with disabilities are living longer and fuller lives, promotion of healthy lifestyles is replacing the disease-oriented medical paradigm. Whereas the annual sports and camp physical remains strongly entrenched in pediatric practice, recommendations for safe participation are also becoming increasingly complex. For example, how quickly may an athlete be returned to sports after a dorsal rhizotomy? Today's athlete may have familiar diseases, like asthma or diabetes, or uncommon disorders, like spina bifida, cerebral palsy, or autism, and may require medications that may have a major impact on participation. Parents and athletes will not accept a denial of participation without data to back up the recommendation. Unfortunately, we will never find every answer to every question. This chapter covers asthma, heart disorders, diabetes, heat injury, and a few uncommon disorders as well as medications that may affect sports participation. Asthma and Exercise

Children with asthma may participate in athletics to the full extent that their disease allows. For most children, there is no restriction on activity. In fact, limited ability to participate in vigorous physical exercise is an indication that a child's asthma is not in

good control. Practice guidelines are now available to guide the practitioner in most aspects of treatment.[13] [18] [20] As new treatment modalities continue to emerge, the treatment of asthma has become both more and less complicated. Prevention of symptoms in children with asthma has become the goal of therapy, and treatment has moved from hospital and emergency department to outpatient and home settings. Unfortunately, deaths due to asthma have not declined in spite of the major advances in diagnosis and treatment. Although regular exercise in children with asthma increases fitness, it does not decrease the incidence or severity of asthma or lessen the frequency or severity of exercise-induced asthma (EIA). Asthma in children is divided into degrees of persistent asthma (mild, moderate, severe) and intermittent asthma (EIA is an example of mild intermittent asthma). Children with persistent asthma usually have worsening of bronchospasm during exercise. Medication treatment of persistent asthma is outside the scope of this discussion; however, The opinions expressed in this chapter are those of the author and do not necessarily reflect those of the United States Air Force, the Department of Defense, or the United States Government.

652

use of corticosteroids to decrease the inflammation associated with asthma is emphasized. The additional availability of other bronchodilators, such as beta-adrenergic agents, nonsteroidal anti-inflammatory medications like cromolyn and nedocromil, and the leukotrienes, has greatly improved exercise tolerance for children with asthma. The long-acting beta-adrenergic agent salbutamol should not be used without steroids in children with persistent asthma (as opposed to EIA). Exercise-Induced Asthma

According to the 1997 National Institutes of Health guidelines, EIA is classified as mild intermittent asthma with a unique triggerexercise. The asthma attack that exercise triggers still has the same basic underlying pathophysiologic mechanism as the other types of persistent asthma. Rapid exposure of the airways to cool or dry air, especially with their subsequent rewarming after exercise, serves as the trigger for bronchospasm. The cooler and dryer the air, the greater the degree of bronchospasm produced. Other environmental triggers (e.g., smoke, pollution, allergens) may also factor into the degree of bronchospasm. The onset is typically within 5 to 10 minutes of beginning to exercise, and it may worsen after exercise is stopped, although it usually remits spontaneously within 20 to 60 minutes. Lack of ability to complete exercise is the usual complaint. With continued exercise, however, symptoms may lessen. A late episode of bronchospasm may occasionally occur 8 to 12 hours after completion of exercise. Recommendations for Treatment of Exercise-Induced Asthma

The treatment of children with EIA focuses on prevention of bronchospasm. A

preventive nonmedical measure that may be helpful is avoidance of activities that cause frequent cooling and rewarming cycles, such as football. Sporting activities that occur in a warm gymnasium are less subject to these cycles that cause EIA. For example, jogging on a cold day is worse than either jogging on a warm day or using an indoor exercise bicycle. Another preventive activity that may help is warm-up exercise. An athlete may experiment with different ways to increase exercise tolerance. Medications are the mainstay of treatment of EIA. These work well. The drug of choice is albuterol, 2 to 4 puffs 30 minutes before exercise. This usually works up to 4 hours and may be repeated at 2- to 4-hour intervals. The drug of choice for exercise of longer duration or for athletes with late bronchospasm (8 to 12 hours after exercise) is salmeterol, 2 puffs 30 to 60 minutes before exercise. Salmeterol must not be given more often than at 12-hour intervals, and it is not to be used to break an asthma episode. Alternative treatment may include the anti-inflammatory agent cromolyn or nedocromil, 2 puffs 30 minutes before exercise. With 1 hour of duration of effect, these agents are shorter acting than the beta-agonists; however, they may be used in conjunction with the beta-adrenergic medications to produce greater effect. The leukotriene antagonist agents may be particularly helpful in certain circumstances, such as the late-phase reaction, but their use in EIA remains to be clearly elucidated. The leukotrienes are typically used in conjunction with other medications in persistent asthma.

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Cardiovascular Disease

The primary care provider often clears children for sports participation who may have known or unknown cardiovascular risk factors or disease. Children with known cardiovascular disease may or may not require restrictions on sports participation. The pediatric sports physical presents an opportunity to increase the health of well children and to prevent morbidity and mortality in those with recognizable risk. Cardiovascular disease in children runs the gamut of the common to the rare, with dramatically changing presentations by age. Disease once thought to be fatal is now commonly treated medically and surgically. The most common cardiovascular diseases in adults are relatively uncommon in children. Through appropriate diet and exercise, children may have a lifelong decrease in the ravages of adult cardiovascular disease. Children with chronic diseases are especially likely to have development of cardiovascular disease, and appropriate interventions to increase their fitness may substantially increase their well-being. All children with known cardiovascular disease should have a pediatric cardiology consultation before initiation of an exercise program. The provider may rely on previous consultations, if appropriate, or request a new consultation. The consultation should answer questions about the particular sports that the child would like to try as well as address warnings about degrees of participation. For example, will the athlete run a 50-meter dash or a marathon? Furthermore, medications may complicate sports participation (see later). Children with heart disease often require ongoing cardiac consultation. Issues of sports participation are often best addressed by the pediatric cardiology consultant. The American Heart Association has published guidelines for the sports physical examination, including complete personal and family history, assessment of vital signs, and physical examination with cardiac auscultation in both standing and recumbent positions. Details are available elsewhere.[6] Assessment of vital signs may disclose hypertension, which will require further investigation. The clinician can often sort out innocent versus pathologic heart sounds appreciated during the examination,

determining which require further evaluation. The personal and family history can give important clues to risk factors for sudden death. Other physical features may lead the provider to suspect conditions such as Marfan's syndrome. Hypertension is relatively uncommon in children and more likely to have an identifiable and treatable cause than in adults. Children with hypertension may have a major benefit from regular aerobic exercise, both lowering their blood pressures and controlling weight. Guidelines regarding hypertension in children have been published by the American Academy of Pediatrics.[4] Children with significant

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(although not severe) hypertension (95th to 98th percentile) without other cardiac disease should not have restrictions if they do not have target organ damage. Children with severe hypertension (99th percentile or higher) who do not have target organ damage should be restricted from strenuous activities and isometric straining activities (i.e., weightlifting) until their hypertension is controlled. Children with end-organ damage should have appropriate consultation to determine safety in exercise. In performing the sports physical examination for children, the clinician must be aware of the often silent syndromes and abnormalities that may result in sudden death with exercise. The body habitus of Marfan's syndrome, the family history of sudden death during exercise with Marfan's syndrome, and a number of other cardiac conditions may provide important treatment and restriction information. Several cardiovascular conditions in children are often asymptomatic until disaster strikes. The most common is hypertrophic cardiomyopathy, present in about 1 of 500 children.[23] These children may present with a murmur (late systolic, retrosternal and apical, worsening with standing or exercise, decreasing with squatting), but 60% have no murmur. The first symptom may be sudden death. More fortunate, however, is the athlete who experiences cardiovascular symptoms while exercising. This event may be sufficient to justify a cardiology consultation, as may the finding of a suspicious murmur in an asymptomatic child. Although this is an autosomal dominant inherited condition, there is not always an early death in a preceding generation. A family history of sudden death in a relative younger than 40 to 45 years especially during exercise may be present. Echocardiography is the diagnostic instrument of choice. Electrocardiography findings are often normal. Even with a high index of suspicion, it is not possible to detect all children with this disorder. Children with hypertrophic cardiomyopathy should be restricted permanently from all strenuous sporting activities and treated with medications to increase diastolic relaxation (such as beta blockers or calcium channel blockers). Prolonged QT syndrome, an often unrecognized familial disorder, may be responsible for up to 4000 deaths per year in children and young adults.[1] With tachycardia, the QT interval must be corrected to a baseline rate of 60 beats per minute (the corrected QT interval, or QTc). A QTc interval is considered normal up to 0.45 to 0.48 second.

Children with prolonged QT interval may have QTc intervals exceeding 0.6 second. Unfortunately, the prolonged QT interval may not be present at all times, and it may be missed on electrocardiography. Thus, the presenting symptom may range from collapse during vigorous exercise to sudden death. Because no prophylaxis is currently recommended, children with prolonged QT syndrome should be restricted permanently from all strenuous sporting activities. Again, cardiology consultation is helpful for diagnosis and treatment. Marfan's syndrome is also a risk factor for sudden death during exercise because of aortic root dissection.[21] Being familiar with the body habitus (long extremities and fingers in typically tall individuals) may provide a clue to the diagnosis. In addition, a family history of aortic root dilation and dissection could provide helpful information. Physical examination may reveal the diastolic murmur of aortic regurgitation. Restriction from isometric exercise is recommended, as is the use of beta blockers. Again, cardiology consultation is helpful for diagnosis and treatment. There are numerous other rare causes of sudde-nonset cardiac disease. Arrhythmogenic right ventricular dysplasia, aortic valve stenosis and regurgitation, Kawasaki's disease, aberrant coronary arteries, hyperlipidemia, and mitral valve prolapse represent rare but potential causes of sudden cardiac death. [10] The athlete may not have warning pain before a life-threatening event occurs. Sudden death in previously healthy athletes is a relatively uncommon but dramatic and often newsworthy event. Cardiovascular symptoms, including chest pain, dizziness, palpitations, and syncope, frequently precede a fatal event, providing a potential opportunity to intervene. In an international study of 27 athletes who died suddenly of coronary artery anomalies, 10 had symptoms that preceded the fatal event. In none of those who had electrocardiography or stress testing were abnormalities found. More appropriate diagnostic studies were recommended by the authors.[9] Knowledge of these disorders may allow the clinician to determine which children need further evaluation by a cardiologist before playing sports.[8]

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Diabetes Mellitus

Type 1 (juvenile-onset) diabetes presents a complex picture to the practitioner. Children with diabetes may be more exercise oriented than their siblings are. Both benefits and risks are clearly associated with exercise in this population. Risk changes with the type and duration of the exercise as well as with the degree of control of diabetes. For example, poorly controlled diabetes inevitably worsens acutely with vigorous exercise owing to the release of catecholamines and increased ketosis, but appropriate exercise is strongly recommended for all children with diabetes. Children with tightly controlled diabetes may experience significant hypoglycemia during or after vigorous exercise. Adults with diabetes have participated in marathon running, with resulting abnormalities in insulin and glucose metabolism exceeding 24 hours. Benefits of exercise include improved glucoregulation in the short term and long-term reduced morbidity of diabetes. Reviews of this subject are available.[16] [24] The key to regulation of type 1 diabetes is blood glucose monitoring during and after exercise. Glucoregulation in the athlete is a complex issue for many reasons. Insulin is often increased in absorption because of higher blood flow to the injection site. Exercise itself will increase the rate of glucose use. Downward adjustment of insulin dosage is usually required, which may range from 5% to 10% of the dose with milder exercise to more than 50% with prolonged, strenuous exercise. Hypoglycemia may occur during or after exercise, including late hypoglycemia, which occurs up to 24 hours after exercise. Increasing calorie intake, especially of complex carbohydrates, may prevent or treat hypoglycemia.[26] Specific recommendations for diet and insulin are required for every individual child, given the large variations

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possible. Adjustment of both insulin (decreasing) and diet (increasing calories and complex carbohydrates) is necessary. Glucose monitoring is crucial to provide guidance for the individual with diabetes. Certain team sports present additional risks of hypoglycemia; an athlete may sit out one game, play a few minutes in another, and play most of a third game. Participation in certain sports, such as rock climbing, parachuting, and scuba diving, may present extreme risks for severe injury or fatality because of poor cognition that occurs during critical moments of severe hypoglycemia. [19] Last, diabetes camp, which introduces educational and behavioral changes that may last a lifetime, may be the most valuable experience for a youth with diabetes. An extremely useful Internet site for diabetes is www.childrenwithdiabetes.com.

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Low-Frequency, High-Severity Disabilities

Children with more severe disabilities represent a significant part of any pediatric practice. These children often have complex medical and developmental problems. They are often observed by subspecialists whose input for sports participation is necessary. Among the more common of these conditions are Down's syndrome, cerebral palsy, spina bifida, and fetal alcohol syndrome, but myriad known and unknown congenital conditions exist, placing a significant burden on the practitioner who must decide on the child's ability to participate in sports. To clear children for sports participation, the clinician must be aware of the physical limitations of the disorder as well as what effects the medications (see later) that the child is taking may have on participation. Last, the sports that the child plans to do must be considered. For example, children with certain metabolic disorders are at high risk for injury if they become hypoglycemic during strenuous or lengthy exercise. One special condition in Down's syndrome meriting mention is atlantoaxial instability. The condition is common and controversial, found in up to 15% of children with Down's syndrome on radiographic studies. The diagnosis is typically made when the routine lateral neck flexion and extension views are obtained. Controversy exists about the value of these films, whether findings are normal or abnormal. Few children with abnormal findings have nervous system symptoms consistent with an unstable cord (easy fatigability, difficulties in walking, abnormal gait, neck pain, limited neck mobility, torticollis or head tilt, incoordination and clumsiness, sensory deficits, spasticity, hyperreflexia, clonus, extensor-plantar reflex, and other upper motor neuron and posterior column signs and symptoms[2] ). A child with Down's syndrome must have normal findings on screening radiography to participate in certain Special Olympics activities, such as gymnastics, diving, the pentathlon, the butterfly stroke and diving starts in swimming, the high jump, soccer, and certain warm-up exercises.[2] In 1995, the American Academy of Pediatrics published a revised statement regarding atlantoaxial instability in children with Down's syndrome.[2] Concern may be merited, however, because examples exist in the literature of children who have been paralyzed during endotracheal intubation. Perhaps the cervical spine of children with Down's syndrome should be evaluated before elective

surgery is done.[3]

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Heat Injury and Chronic Disabilities

Heat illness is a complex subject handled in depth in other settings. [25] The American Academy of Pediatrics has published a statement regarding heat stress in the exercising child and adolescent.[5] Heat injury can develop in anyone, given sufficient heat, humidity, dehydration, and work production. Children with disabilities who participate in sports, exercise, or summer camping programs are at risk for heat injury because they are often unaccustomed to both exercise and high outdoor temperatures. They may take medications or have medical conditions that further increase the risk of heat illness. During the 1996 Connecticut State Special Olympics, a fivefold increase in heat-related illness occurred when the ambient temperature was just 5° higher than the two previous years. [17] Thus, heat illness is an important consideration for both medical practitioners and event planners. Children with disabilities may not easily demonstrate or communicate early signs of heat injury, leading to a missed opportunity for early intervention. Encouraging children with disabilities to drink adequate fluids often represents a major challenge for even the best caretakers. Adequate hydration, cooling, and early recognition of signs of impending heat illness (intense thirst; profuse sweating; nausea and vomiting; cramping; skin erythema; fever; ataxia; tachycardia; hyperventilation; hypotension; changes in mental status, including anxiety, lethargy, apathy, poor judgment, and confusion) are critical to prevention of heat illness or its successful treatment. Signs that the heat illness has progressed to heat stroke are temperature of 104°F or higher; coma; seizures; delirium; and hot, flushed, dry skin. Children with heat stroke (temperature above 104°F, but usually 106°F or higher) emergently require rapid cooling with ice packs or baths, intravenous rehydration, and intensive observation, preferably in a pediatric intensive care unit.[14] Mortality from heat stroke ranges from 10% to 80%. [15] Children with less severe illness require immediate rest, rehydration, and rapid cooling, with consideration given to intravenous rehydration in more severe cases.

Medical Conditions Predisposing to Heat Injury

Any child with a previous heat injury is at higher risk for a repeated event. Children with obesity, a relatively frequent finding in children with disabilities, are at higher risk for heat injury. Some children with brain or spinal abnormalities poorly regulate their internal temperatures and are at risk for hypothermia in cool environments or heat injury in warm environments. A child may rarely present with hyperthyroidism as a cause of poor heat tolerance. Heat illness may develop in a child with an intercurrent

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febrile illness. Children with cystic fibrosis present with special requirements during exercise for increased salt and fluids. Children with rare skin disorders or extensive scarring may sweat inadequately, causing heat injury, or excessively, causing dehydration and potential heat injury. Medications Predisposing to Heat Illness

Numerous medications may present a concern to the practitioner completing the camp or Special Olympics physical examination. The following list of more common medications was generated on the basis of a review of medications used by children with disabilities at the summer Camp CAMP program (Center Point, Texas). Eighty-eight of these children had autism, and 68% were treated with medications. Polypharmacy was the rule of treatment; one child was taking six psychopharmacologic agents. Of these children, 30% were receiving antipsychotic medications; 17%, selective serotonin reuptake inhibitors; 16%, clonidine or other cardiovascular medications; 14%, medications for epilepsy; 9%, stimulants; and 8%, antihistamines. Several patients were receiving medications with potential major side effects, including lithium, tricyclic antidepressants, digitalis, furosemide, and verapamil. Of these children, 13% were taking alternative medications or megavitamin preparations. Information on medications and their potential for heat injury is widely available.[7] [22] The most frequent mechanism by which medications increase the risk for heat injury is through anticholinergic properties that reduce sweating. A less frequent mechanism is increased metabolism, found with thyroid medications and high-dose amphetamines. Medications that have prominent anticholinergic properties include the antipsychotic medications, such as thioridazine, haloperidol, risperidone, and olanzapine. Other medications having anticholinergic properties are atropine, benztropine mesylate, trihexyphenidyl, belladonna alkaloids, and oxybutynin. Antihistamines often dry the mucous membranes through their anticholinergic properties. Baclofen, used to treat spasticity, has significant anticholinergic side effects. Certain medications can become toxic if the child becomes dehydrated. Lithium can be lethal if the child sweats a significant amount of free water. Nonsteroidal anti-inflammatory agents such as ibuprofen may cause renal failure if the patient becomes dehydrated.

A significant number of children with and without disabilities are currently being treated with alternative medications and treatments. Unfortunately, little is known about the risk for heat injury of alternative medications and treatments, although texts are now appearing that will increase the information available to practitioners.[11]

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Summary

Children with disabilities are participating in more activities than ever, presenting ever-greater challenges to the physician performing sports or camp physical examinationsand the physical and psychosocial benefits have been enormous.[12] Role models now include those who are overcoming major obstacles, like Christopher Reeve (actor with a high cervical injury) and Sean Elliott (post-kidney transplantation hero of the 1999 basketball champion San Antonio Spurs). Children with disabilities must overcome obstacles that most never consider, and their victory is often their road to joy and freedom. Neither they nor their parents will accept a response that they should not participate in sports, but they may listen to information provided by an informed expert in these matters. Acknowledgment

The author would like to thank Drs. William Michael Rogers, John Brownlee, and Deanna Dance-Kwan for their review and suggestions.

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References 1.

Ackerman MJ: The long QT syndrome. Pediatr Rev 19:232-238, 1998.

American Academy of Pediatrics, Committee on Sports Medicine and Fitness: Atlantoaxial instability in Down syndrome: Subject review. Pediatrics 96(pt 1):151-154, 1995. 2.

American Academy of Pediatrics, Section on Anesthesiology: Evaluation and preparation of pediatric patients undergoing anesthesia. Pediatrics 98(pt 1):502-508, 1996. 3.

American Academy of Pediatrics: Athletic participation by children and adolescents who have systemic hypertension. Pediatrics 99:637-638, 1997. 4.

American Academy of Pediatrics: Climatic heat stress and the exercising child and adolescent. Pediatrics 106:158-159, 2000. 5.

American Heart Association: Cardiovascular preparticipation screening of competitive athletes. Med Sci Sports Exerc 28:1445-1452, 1996. 6.

Ballester JM, Harchelroad FP: Hyperthermia: How to recognize and prevent heat-related illnesses. Geriatrics 54:20-24, 1999. 7.

Basso C, Corrado D, Thiene G: Cardiovascular causes of sudden death in young individuals including athletes. Cardiol Rev 7:127-135, 1999. 8.

Basso C, Maron BJ, Corrado D, Thiene G: Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coll Cardiol 35:1493-1501, 2000. 9.

10.

Berul CI: Cardiac evaluation of the young athlete. Pediatr Ann 29:162-165, 2000.

11.

Blumenthal M (senior ed), Busse W, Goldberg A, et al (associate eds): The Complete German

Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, Tex, American Botanical Council, 1998. Dykens EM, Rosner BA, Butterbaugh G: Exercise and sports in children and adolescents with developmental disabilities: Positive physical and psychosocial effects. Child Adolesc Psychiatr Clin North Am 7:757-771, 1998. 12.

Emond SD, Camargo CA Jr, Nowak RM: 1997 National Asthma Education and Prevention Program guidelines: A practical summary for emergency physicians. Ann Emerg Med 31:579-589, 1998. 13.

Faunt J: Effects of heat stress. In Rakel R (ed): Conn's Current Therapy 2000. Philadelphia, WB Saunders, 2000, pp 1135-1137. 14.

Fields SA: Heat exhaustion and heat stroke. In Dambro M (ed): Griffith's Five Minute Clinical Consult 2000. Philadelphia, Lippincott Williams & Wilkins, 2000, pp 460-461. 15.

Franz MJ: Lifestyle modifications for diabetes management. Endocrinol Metab Clin North Am 26:499-510, 1997. 16.

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Galena HJ, Epstein CR, Lourie RJ: Connecticut State Special Olympics: Observations and recommendations. Conn Med 62:33-37, 1998. 17.

Matola C: Guideline for the management of chronic asthma in children2000 update. Allergy Society of South Africa Working Group. S Afr Med J 90(pt 2):524-528, 530, 532, 2000. 18.

19.

Mellman MF, Podesta L: Common medical problems in sports. Clin Sports Med 16:635-662, 1997.

National Asthma Education Program Expert Panel report 2: Guidelines for the Diagnosis and Management of Asthma (NIH Publication No. 97-4051). Bethesda, Md, National Institutes of Health, National Heart, Lung, and Blood Institute, 1997. Available at http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm 20.

21.

Pyeritz RE: The Marfan syndrome. Annu Rev Med 51:481-510, 2000.

22.

Schrefer J (ed): Mosby's GenRx, 10th ed. St Louis, Mosby, 2000.

23.

Towbin JA: Pediatric myocardial disease. Pediatr Clin North Am 46:289-312, ix, 1999.

Wheeler ML: Nutrition management and physical activity as treatments for diabetes. Prim Care 26:857-868, 1999. 24.

Yarbrough B, Bradham A: Heat illness. In Rosen P, Barkin R, Danzl D, et al (eds): Emergency Medicine, 4th ed. St Louis, Mosby, 1998, pp 986-1000. 25.

Zinker BA: Nutrition and exercise in individuals with diabetes. Clin Sports Med 18:585-606, vii-viii, 1999. 26.

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Section E The Disabled Pediatric Athlete Frank M. Chang MD Ability Versus Disability

An athlete is an individual who uses his or her body and motor skills to compete in exercises, sports, or games requiring physical strength, agility, and stamina. The desire to compete has been present since the evolution of humans, and athletic competition has been well documented for centuries in all known cultures. An individual who is born disabled or becomes disabled still may have an inherent desire to compete in athletics. Some disabled individuals have a strong desire to participate to prove something to themselves and others. We can assist these potential athletes to achieve their goals by encouraging them to participate; facilitating that participation; and educating parents, coaches, and the children themselves to prevent potential injuries. Stimulating a disabled child to participate, then watching him or her succeed is a gratifying and emotional experience ( Fig. 17E-1 ). The overall sense of accomplishment and the rewards are great for a successful disabled athlete.[16] Participation in sports and recreation is well recognized as a form of rehabilitation of individuals with disabilities.[19] Children with disabilities currently have the best opportunity ever to participate in sports and athletic activities. Disabled children no longer are hidden away from society, in special schools. Strong voices advocating for the disabled, increasing awareness of the lay community, and legislation such as the Americans with Disabilities Act (passed July 26, 1990) have resulted in significant changes in attitudes among the children, parents, and school boards. Disabled children are being mainstreamed into the classroom and given the opportunity to participate in academic and athletic activities with their able-bodied peers.

The spectrum of disabilities is broad and may have a minimal to profound impact on any athletic endeavor depending on the specific disability involved. An amputee has a mechanical handicap, whereas a child with impaired sensory integration or impaired hearing may appear normal to the untrained observer. Classification of the diverse categories of disabilities is important so that competition occurs on an equal level. Almost all sports can be adapted by modifying the rules of the sport or by using adaptive equipment to allow the disabled athlete to participate. Examples include Alpine ski racing, swimming, golf, wheel-chair basketball, wheelchair tennis, wheelchair track, and rock climbing for the visually impaired.

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Classification of Disabilities

The classification of a specific athlete is important and sometimes controversial. The athlete desires to be classified

Figure 17-E-1 Disabled skier with cerebral palsy proudly clutches his trophy after winning a ski race.

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to give him or her the best advantage in whichever competition he or she is competing in. The organization sponsoring the competition wants a fair grouping of the competitors. Experienced, trained classifiers frequently are employed to classify individual athletes. Physicians sometimes are needed to verify medical diagnosis or neurologic deficits. The classification of disabilities varies according to the perspective of the organization responsible for the classification. Similar disabilities must be organized and grouped so that individuals are competing on an equal basis. From an organizational perspective, it is advantageous to group as many similar individuals together as possible. The individuals can be organized into a league or competition comprising large enough groups of athletes to create meaningful competition. If only individuals with a fibular deficiency treated with a Boyd or Syme amputation were included in a group, there would be inadequate participants for meaningful competition. By grouping these individuals with all other participants with a below-knee (BK) amputation, the competitors are functionally equivalent, and there are enough of them to compete. Classification begins by dividing disabilities into broad categoriesneuromuscular

afflictions, amputees, Down's syndrome, orthopaedic deformities, and sensory impairments such as hearing loss or visual impairment. Each broad category is subdivided further into categories to equalize the various differences. Amputees can be classified further into various upper and lower extremity levels (e.g., above-knee [AK], BK, below-ankle). The neuromuscular category is subdivided further into diseases such as cerebral palsy, meningomyelocele, spinal cord injury, head injury, and muscular dystrophies. Meningomyelocele and spinal cord injury can be combined, then subdivided into different spinal cord levels (e.g., cervical, thoracic, lumbosacral) or into specific levels such as T10 or L3. Cerebral palsy and head injuries can be grouped together, then categorized into hemiplegics, diplegics, and quadriplegics or into ambulatory and wheelchair-dependent. The ambulatory group can be subdivided into athletes with or without walking aids, depending on the type of competition and the size of the group competing. The classification must reflect the nature of the sport under consideration. Although arm swing affects cadence and balance, it is unnecessary to subdivide upper extremity amputation levels for running sports. Conversely, the level of the lower extremity amputation (e.g., AK versus BK) significantly affects performance in any sport requiring ambulatory skills but makes relatively little difference in wheelchair sporting competitions. In some team sports, the teams are defined as a specific number of individuals with varying neurologic or functional levels, the aggregate of the team totaling a certain number of functional points. The International Paralympic Committee rules for rugby state:

Everyone playing rugby is assigned a classification based on their func ability. These classifications range from 0.5 points to 3.5 points. A t four players at a time whose classifications total no more than 8.0 poi staff will select a team that allows them to field a variety of eight p in order to maximize the team's ability to adjust in competitive situat (www.paralympic.org; see Appendix) The use of prostheses, wheelchairs, and other adaptive equipment must be defined to prevent any individual or group from receiving an advantage or disadvantage. In national and international disabled Alpine skiing competition, BK amputees must ski with their prosthesis and both skis regardless of the stump length. An AK amputee must ski three-track, regardless of the level of amputation, from knee disarticulation to hip disarticulation. Three-track skiing is skiing with a ski on one leg and two short skis on outriggers supported by the upper extremities ( see Fig. 17E-12D ).[53] The classification process must be consistent and fair. In most situations, the classification is obvious and easy to verify. Amputees fit this category. Other situations require physician input and documentation. At the U.S. National Disabled Skiing Championships, where athletes were competing for national ranking before the international competitions, an allegedly blind skier had been doing exceptionally well locally and was extremely competitive in the national competition. Some of the judges and other race officials noted discrepancies in the stated visual impairment, and after further investigation the competitor was disqualified.

Specific organizations have developed classification systems. Most of these organizations are advocate groups for specific disabilities, such as the National Association of Sports for Cerebral Palsy (NASCP)[52] (which developed a cerebral palsy-based classification) or the United States Cerebral Palsy Athletic Association (www.uscpaa.org; see Appendix) ( Table 17E-1 ). The amputee-based classification system, developed by the United States Amputee Athletic TABLE 17-E-1 -- Cerebral Palsy Eight-Level Classification System* Class Challenge 1

Severe involvement in all four limbs. Limited trunk control. Unable to grasp a softball. Poor functional strength in upper extremities, often necessitating the use of an electric wheelchair for independence

2

Severe to moderate quadriplegic, normally able to propel a wheelchair slowly with arms or by pushing with feet. Poor functional strength and severe control problems in the upper extremities

3

Moderate quadriplegic, fair functional strength and moderate control problems in upper extremities and torso. Uses wheelchair

4

Lower limbs have moderate to severe involvement. Good functional strength and minimal control problem in upper extremities and torso. Uses wheelchair

5

Good functional strength and minimal control problems in upper extremities. May walk with or without assistive devices for ambulatory support

6

Moderate to severe quadriplegic. Ambulates without walking aids. Less coordination. Balance problems when running or throwing. Has greater upper extremity involvement

7

Moderate to minimal hemiplegic. Good functional ability in nonaffected side. Walks and runs with noted limp

8

Minimally affected. May have minimal coordination problems. Able to run and jump freely. Has good balance

*United States Cerebral Palsy Athlete Association Classification System. This classification system is used in all individual sports, including track and field, swimming, cycling, and cross-country, in which athletes compete only against athletes with their same classification. In the remaining sports, athletes are grouped in divisions according to classification.

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TABLE 17-E-2 -- National Wheelchair Athletic Association Junior Medical Classification System*

Age Groups for All Classes (years)

Disability Group Class I

Class II

Class III

A (6-8)

NWAA adult classes NWAA adult IA-IC classes II and III

NWAA adult classes IV-VI

B (9-12)

Cervical spinal level impairment (C1-C7)

Impairment below T10 level; includes amputees

Thoracic level impairment (T1-T10)

C (13-15) D (16-18) *NWAA junior medical classification considers age and neurologic impairment level. Each class is defined by a specific neurologic impairment level and subdivided into four age groups.

Association, is based on level of amputation (AK, BK, above-elbow, below-elbow, and various combinations). The Wheelchair Sports USA (www.wsusa.org; see Appendix) formerly known as the National Wheelchair Athletic Association, classifies its junior division for children 6 to 18 years old divided into four age groups and three neurologic impairment levels ( Table 17E-2 ). Other classification systems have been developed by organizations responsible for organizing various competitions (e.g., the NASCP classification modified by the International Sports Organization for the Disabled for winter sports). Table 17E-3 presents a basic and functional classification system. The interest and participation in disabled sports is growing rapidly. The growth in participation has been accompanied by rapid growth in the organizations and governing bodies responsible for the athletes and the competitions. The classification systems are evolving toward a more functional classification, are changing constantly, and are becoming more detailed. The current classification manual for International Paralympic Committee swimmers is 75 pages.[39] Tables 17E-4 , 17E-5 , and 17E-6 (and the accompanying boxes) display TABLE 17-E-3 -- Basic Classification of Disabilities I. Amputations A. Upper extremity B. Lower extremity, above knee C. Lower extremity, below knee D. Multiple extremities II. Cerebral palsy and head injuries A. Ambulatory 1. Without walking aids

2. With walking aids B. Wheelchair III. Spinal cord disruption (meningomyelocele and spinal cord injuries) A. Cervical B. High thoracic (T1-5) C. Low thoracolumbar (T6-L3) D. Lumbosacral (L4-sacral) IV. Neuromuscular disorders A. Muscular dystrophy B. Spinal muscular atrophy C. Charcot-Marie-Tooth syndrome D. Ataxia V. Others with disease-specific disabilities A. Osteogenesis imperfecta B. Arthrogryposis C. Juvenile rheumatoid arthritis D. Hemophilia E. Skeletal dysplasia F. Down's syndrome

TABLE 17-E-4 -- International Paralympic Committee Classification of Swimmers S1 Very severe quadriplegic with poor head and trunk control (e.g., class 1 cerebral palsy; see Table 17E-1 ) S2

Quadriplegic complete below C5-C6; severe muscular dystrophy; amputation of four limbs

S3

Quadriplegic complete below C6; a lower quadriplegic with an additional handicap; severe muscular dystrophy

S4

Quadriplegic complete below C7; some incomplete C5; polio with nonfunctional hands for swimming; muscular dystrophy comparable with C7

S5

Complete quadriplegia below C8; incomplete C7 or C6 with ability to keep legs horizontal and functional hands for swimming

S6

Complete paraplegia below T1-T8; incomplete C8 with ability to keep legs horizontal

S7

Complete paraplegia below T9-L1; double above-knee amputee shorter than ½

S8

Paraplegia L2-L3 with no leg propulsion but ability to keep legs straight; double above-knee amputee; double below-knee amputee, not longer than

S9

Paraplegia L4-L5; polio with one nonfunctional leg; single above-knee amputee; double below-knee amputee with stumps longer than

S10

Polio or cauda equina lesion with minimal involvement of lower limbs; single below-knee amputee; double forefoot amputation

SB1

Quadriplegic complete below C6; a lower quadriplegic with an additional handicap; severe muscular dystrophy

SB2

Quadriplegic complete below C7; muscular dystrophy comparable with C7 complete quadriplegia with no finger extension

SB3

Complete quadriplegic below C8; complete paraplegic T1-T2; incomplete C7

SB4

Complete paraplegia T6-T10; incomplete C8 or comparable polio

SB5

Complete paraplegia below T10-L1; incomplete T5; double above-knee amputee shorter than ¼

SB6

Paraplegia and polio L2-L3 with no leg propulsion, double above-knee amputation longer than ¼

SB7

Paraplegia and polio L4 poor leg propulsion, below-knee amputation shorter than ½

SB8

Paraplegia L5; polio with one nonfunctional leg; double below-knee amputee longer than ½; single above-knee amputee

SB9

Single below-knee amputee less than ¾

SB10

Single below-knee amputation longer than ¾

SM1-SM10 Individual medley* see formula below *To calculate Individual Medley Class, use the following formula: [(3 × 5 class) + (1 × SB class)] divided by 4 = Individual Medley Class A swimmer can have up to three classes. These are determined by the following strokes: S1-S10 freestyle, backstroke, and butterfly SB1-SB10 breaststroke SM1-SM10 individual medley This information is a general description of classification. Only an official classifier can assign exact classification.

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TABLE 17-E-5 -- Track and Field Functional Classification System: Wheelchair Sports USA Sanctioned Athletics Rules Field New Level

Events

Old Level

Neurologic Level

F1

Club, discus

1A complete

C6

F2

Shot, discus, javelin

1B complete

C7

1A incomplete F3

Shot, discus, javelin

1C complete

C8

1B incomplete F4

Shot, discus, javelin 2

1C incomplete

T1-T7

Upper 3 F5

Shot, discus, javelin

Lower 3

T8-L1

Upper 4 F6

Shot, discus, javelin

Lower 4

L2-L5

Upper 5 F7

Shot, discus, javelin 6

Lower 5

S1-S2

F8

Shot, discus, javelin

Standing athletes

N/A

Standing Sitting

Not more than 70 points in the lower limbs Track

New Level

Events

Old Level

Neurologic Level

T1

All track events

1A complete

C6

T2A

All track events

1B complete

C7

T2B

All track events

1C complete

C8

T3

All track events

1C complete

T1-T7

2 upper 3 T4

All track events

Lower 3

T8-S2

4-5-6 Initially, it is important to know the neurologic level of the athlete, including the motor and sensory level as well as whether the disability is incomplete or complete. The presence of scoliosis (a curved spine) and of joint contracture is noted. (A joint contracture is the inability to move a joint through its normal range.) Difficulties in classification occur more frequently in the athlete who is new or untrained or who has poor technique or poor chair position. The top athletes are generally easier to classify because they are usually at their functional potential.

Track and Field Classification System: Definitions of Codes for Field Events F1 Functional: Have no grip with nonthrowing arm. (Use resin or adhesive-like substance for grip.) DISCUS: Have little control of the discus because finger movements are absent. Throw with a flat trajectory. CLUB: May throw forward or may throw backward over the head. Use either thumb and index finger, or index and middle finger, or middle and ring finger grip. (Clubwhen throwing backward, the athlete is using his or her strong elbow flexors.) Neurologic Level: C6. Anatomic Capability: Have functional elbow flexors and wrist dorsiflexors. May have elbow extensors (up to power 3) but usually do not have wrist palmar flexors. May have shoulder weakness. Have no sitting balance. Old Level: 1A complete. Note: This system applies to the spinal-injured athlete. Athletes whose disability is as a result of polio or other causes may show different movement and function than described here. The total function of the athlete in this specific event would be similar to that of the spinal cord injury description. F2 Functional: Have difficulty gripping with nonthrowing arm.

movement and function than described here. The total function of the athlete in this specific event would be similar to that of the spinal cord injury description. F2 Functional: Have difficulty gripping with nonthrowing arm. SHOT: Unable to form a fist and do not usually have finger contact with the shot at the release point. Unable to spread fingers apart. DISCUS: Have no functional finger flexors; i.e., unable to form a fist. Have difficulty placing fingers over the edge of the discus, but may do so with the aid of contracture or spasticity. JAVELIN: Usually grip the javelin between the index and middle fingers, but may use the gap between the thumb and index finger, or between the middle and ring fingers. These athletes may have slight function between the digits of the hand. Neurologic Level: C7. Anatomic Capability: Have functional elbow flexors and extensors, wrist dorsiflexors, and palmar flexors. Have good shoulder muscle function. May have some finger flexion and extension but not functional. Old Level: 1B completeno sitting balance. Also 1A incomplete with the ability to lift the trunk off the back of a chair and to perform backward and forward movement. Also may be able to rotate the trunk. Note: This system applies to the spinal-injured athlete. Athletes whose disability is as a result of polio or other causes may show different movement and function than described here. The total function of the athlete in this specific event would be similar to that of the spinal cord injury description. F3 Functional: Have nearly normal grip with nonthrowing arm. SHOT: Usually a good fist can be made. Can spread the fingers apart but not with normal power. Use some spreading of the fingers and can grasp the shot put when throwing. DISCUS: Have good finger function to hold discus. May be able to import spin on the discus. Are able to spread and close the fingers, but not with normal power.

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JAVELIN: Usually grip javelin between the thumb and index finger. Have ability to hold javelin because of presence of hand muscles that spread and close the fingers. Neurologic Level: C8. Anatomic Capability: Have full power at elbow and wrist joints. Have full or almost

JAVELIN: Usually grip javelin between the thumb and index finger. Have ability to hold javelin because of presence of hand muscles that spread and close the fingers. Neurologic Level: C8. Anatomic Capability: Have full power at elbow and wrist joints. Have full or almost full power of finger flexion and extension. Have functional but not normal intrinsic muscles of the hand (demonstrable wasting). Old Class: 1C complete (no sitting balance). Also 1B incomplete with trunk movements. F4 Functional SHOT, DISCUS, AND JAVELIN: Have no sitting balance. Usually hold onto part of the chair while throwing. Complete class 2 and upper class 3 athletes have normal upper limbs. They can hold the throwing implement normally. They have no functional trunk movements. Incomplete 1C athletes who have trunk movements, with hand function similar to F3. Neurologic Level: T1-T7. Anatomic Capability: As above. Old Class: 1C incomplete; 2 complete; upper 3 complete. F5 Functional: Three trunk movements may be seen in this class: (1) off the back of a chair (in an upward direction); (2) movement in the backward and forward plane; (3) some trunk rotation. Fair to good sitting balance. Cannot have functional hip flexors, i.e., ability to lift the thigh upward in the sitting position. May have stiffness of the spine, which improves balance but reduces the ability to rotate the spine. SHOT AND JAVELIN: Tend to use forward and backward movements, whereas the discus predominantly uses rotatory movements. Neurologic Level: T8-L1. Anatomic Capability: Normal upper limb function. Have abdominal muscles and spinal extensors (upper or more commonly upper and lower). May have nonfunctional hip flexors (grade 1). Have no adductor function. Old Class: Lower 3; upper 4. F6 Functional

Old Class: Lower 3; upper 4. F6 Functional SHOT, DISCUS, AND JAVELIN: Have good balance and movements in the backward and forward plane. Have good trunk rotation. Can lift the thighs, i.e., off the chair (hip flexion). Can press the knees together (hip adduction). May have the ability to straighten the knees (knee extension). May have some ability to bend the knees (knee flexion). Neurologic Level: L2-L5. Anatomic Capability: As above. Old Class: Lower 4; upper 5. F7 Functional SHOT, DISCUS, AND JAVELIN: Have good sitting balance and movements in the backward and forward plane. Usually have good balance and movements toward one side (side-to-side movements) owing to presence of one functional hip abductor, on the side that movement is toward. Usually can bend one hip backward; i.e., push the thigh into the chair. Usually can bend one ankle downward, i.e., push the foot onto the footplate. The side that is strong is important when considering how much it will help functional performance. Neurologic Level: S1-S2. Anatomic Capability: As above. Old Class: Lower 5, 6. F8 Stand SHOT, DISCUS, AND JAVELIN: Standing athletes with dynamic standing balance. Able to recover in standing when balance is challenged. Not more than 70 points in the lower limbs. International F8 class (must qualify in standing to compete internationally). Sit SHOT, DISCUS, AND JAVELIN: Have normal sitting balance and trunk movements in all planes. Usually are able to stand and possibly walk with braces or by locking knees straight. Are unable to recover balance in standing when balance is challenged and fall when attempting throws with full effort in standing. Not more than 70 points in the

Sit SHOT, DISCUS, AND JAVELIN: Have normal sitting balance and trunk movements in all planes. Usually are able to stand and possibly walk with braces or by locking knees straight. Are unable to recover balance in standing when balance is challenged and fall when attempting throws with full effort in standing. Not more than 70 points in the lower limbs; because of poor dynamic standing balance choose to compete from a seated position. U.S. class only. Note: Any athlete who wishes to be considered for international competition in F8 must (1) not have more than 70 points in the lower limbs; (2) compete from a standing position at regional and national competition. Some Factors to Consider When Observing a Field Athlete The grip of the throwing implement The grip of the nonthrowing arm The starting position The release position of the throwing arm The finishing position The functional use of the nonthrowing arm; e.g., is elbow flexion or elbow extension used, or is the arm used to control trunk movement after release of the implement Trunk movements Off the back of the chair (upward) Forward and backward Rotation Side to side Pelvic stability Leg movements The position of the chair within the throwing circle Attachments to assist throwing, e.g., strapping, hand grip

Definition of Minimal Disability Unable to compete equitably in nondisabled version of the sport owing to a severe, permanent physical disability of the lower extremities. Functional Tests: Trunk rotation test: F4no abdominal function; F5abdominal function; F6abdominal function plus functional

Unable to compete equitably in nondisabled version of the sport owing to a severe, permanent physical disability of the lower extremities. Functional Tests: Trunk rotation test: F4no abdominal function; F5abdominal function; F6abdominal function plus functional movements in the upper parts of the lower limbs; i.e., hip flexors and abductors

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Track and Field Classification System: Definitions of Codes for Track Events T1 Functional: May use elbow flexors to start (back of wrist behind pushing rim). Hands stay in contact or close to the pushing rim, with the power coming from elbow flexion. The old technique is to use the palms of the hands and to push down on the top of the wheel in a forward direction. Neurologic Level: C6. Anatomic Capability: Have functional elbow flexors and wrist dorsiflexors. Have no functional elbow extensors or wrist palmar flexors. May have shoulder weakness. Old Class: 1A complete. T2 Functional: Usually use elbow flexors to start, but may use elbow extensors. Power from pushing comes from elbow extension, wrist dorsiflexion, and upper chest muscles (Matson technique). Additional power may be gained by using the elbow flexors when the hands are in contact with the back of the wheel. The head may be forced backward (by the use of neck muscles), producing slight upper trunk movements.

Additional power may be gained by using the elbow flexors when the hands are in contact with the back of the wheel. The head may be forced backward (by the use of neck muscles), producing slight upper trunk movements. T2A Neurological Level: C7. Anatomic Capability: Have functional pectoral muscles, elbow flexors and extensors, wrist dorsiflexors, radial wrist movements, some palmar flexors. Have no finger flexors or extensors. Old Class: IB complete. T2B Neurologic Level: C8. Anatomic Capability: Have functional pectoral muscles, elbow flexors and extensors, wrist dorsiflexors, palmar flexors, radial and ulnar wrist movements, finger flexors and extensors. Do not have the ability to perform finger abduction and adduction (spread fingers and bring them together). Old Class: 1C complete. T3 Functional: Have normal or nearly normal upper limb function. Have no active trunk movements. When pushing, the trunk is usually lying on the legs. The trunk may rise with the pushing action. Usually use a hand flick technique for power (or friction technique). May use the shoulder to steer around curves. Interrupt pushing movements to steer and have difficulty resuming the pushing position. When braking quickly, the trunk stays close to the pushing position. Note: Scoliosis (curvature of the spine) usually interferes with abdominal and back muscle function. Neurologic Level: T1-T7. Anatomic Capability: Have normal or nearly normal upper limb function. Have

muscle function. Neurologic Level: T1-T7. Anatomic Capability: Have normal or nearly normal upper limb function. Have no abdominal muscle function. May have weak upper spinal extension. Old Class: Incomplete 1C; 2; upper 3. T4 Functional: Have backward movement of the trunk. Usually have rotation movements of the trunk. May use trunk movements to steer around curves. Usually do not have to interrupt the pushing stroke rate around curves. When stopping quickly, the trunk moves toward an upright position. Use abdominals for power particularly when starting, but also when pushing. Neurologic Level: T8-S2. Anatomic Capability: Have back extension, which usually includes upper and lower extensors. Usually have trunk rotation, i.e., abdominal muscles. Old Class: Lower 3; 4-5-6.

TABLE 17-E-6 -- International Paralympic Committee Classification of Athletes with Spinal Cord Lesion, Spina Bifida, and Polio Class 1A

Lower cervical medullary lesions between C4 and C6 with involvement of all four members. Nonfunctional triceps muscles (test = 0-3)

Class 1B

Lower cervical medullary lesions (up to C7) with involvement of all four members. Triceps good or normal (test = 4 or 5). Poor flexion and extension of the wrist (test = 0-3)

Class 1C

Lower cervical medullary lesions (up to C8) with involvement of all four members. Triceps good or normal (test = 4-5). Good or normal function of wrist extensors and flexors (test = 4 or 5). Poor functioning of the interossei and lumbricales of the hand (test = 0-3)

Class 2

Thoracic medullary lesions from T1 to T5. Involvement of the trunk and lower extremities. No use of abdominal muscles. No sitting balance

Class 3

Thoracic medullary lesions from T6 to T10. Involvement of the abdomen and lower extremities. Good upper abdominal muscles. No use of lower abdominal muscles. No use of lower trunk extensors. Slight capacity to maintain sitting balance

Class 4

Thoracic and lumbar medullary lesions from T6 to T10. Involvement of the lower extremities. Good spinal dorsal abdominal muscles and extensors. Fair hip flexors and abductors. Good sitting balance Lower extremity test:* traumatics, 1-20 points; nontraumatics, 1-15 points

Class 5

Lumbar medullary lesion at L4 or L5. Involvement of the lower extremities. Good sitting balance. Good abdominal muscles Lower extremity test:* traumatics, 21-40 points; nontraumatics, 16-35 points

Class 6

Sacrum medullary lesion from S1 to S3, involvement of one lower extremity or slight involvement of both lower extremities Lower extremity test:* traumatics, 41-60 points; nontraumatics, 36-50 points

*Lower extremity tests include testing of muscles involved in hip flexion and extension, hip abduction and adduction, knee flexion and extension, ankle plantar flexion, and dorsiflexion. Points are based on a 0-5 scale: 0-3, nonworking muscle; 4, working with resistance; and 5, normal functioning muscle.

the increasing complexity of the classification of athletes competing with disabilities. The Web pages listed in the Appendix for the specific organizations can be viewed on the World Wide Web for the most up-to-date classifications. These Web sites are a valuable resource for clinicians who would like to learn more about the specific organizations and access links to other related sites.

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Injuries in the Disabled Athlete

The disabled athlete need not intimidate the physician. Injuries are usually the same in disabled children as in able-bodied children. When initially assessing a disabled child with an injury on the field or in the office, the clinician must ignore the disability temporarily and evaluate the patient using a standard routine. The differential diagnosis is essentially the same, disabled or not. The clinician should talk to the child to obtain an accurate history and listen to the child's perception of the symptoms at the time of and subsequent to the injury. If there is a

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history of an acute injury, the child usually can point to an area of tenderness that localizes the injured structure. Obtaining an accurate history from a younger child or a child with an intellectual impairment, such as cerebral palsy or Down's syndrome, is more of a challenge, and the practitioner frequently must rely on a history obtained from parents, siblings, coaches, and day care personnel. If there is no acute episode of trauma, the history may reveal that the child is suffering from an overuse syndrome. In this situation, a detailed history of all activities, including organized sports, running, physical education, and play, must be obtained. If the child is involved in sports, the frequency of participation, training, and practices; the shoes worn; and the temporal association of symptoms all are pertinent aspects of the history. The use of any ambulatory aids, adaptive equipment, or orthoses is pertinent. The clinician must question both parents and especially the child. The clinician must not forget to rule out infectious, neoplastic, or rheumatologic causes and other processes that involve children, such as Legg-Calvé-Perthes disease or diskitis. The clinician should perform a thorough physical examination of at least the entire symptomatic extremity as well as the pelvis and spine if appropriate. Similar to in an able-bodied child, the injured structure almost always is tender to palpation and painful

to manipulation except in a child with a sensory deficit. The clinician must not forget to examine the ipsilateral hip of a symptomatic knee or thigh because referred knee or anterior thigh pain is common in children with hip pathology as a result of referred pain. The multiply disabled child, such as a child with a high-level myelomeningocele with or without shunted hydrocephalus, is more likely to have an acute injury than an overuse injury. The multiply disabled child usually is not as active as an able-bodied child because of an osteopenic skeleton, weaker muscles, and diminished endurance. The evaluation remains the same because the anatomic structures are the same in a disabled child unless there is a congenital absence or duplication of parts. In a child with congenital absence of a structure, for whichever skeletal element is absent or deficient, the normally attached muscular and tendinous counterparts usually also are absent or deficient. Skin and overlying soft tissue lesions should be appreciated. Acute injuries include contusions, abrasions, lacerations, and crush injuries. The skin is vulnerable to sunburn and other thermal injuries. Children with sensory deficits are especially susceptible to these soft tissue injuries and usually are unaware of an injury. When the protective skin layer has been damaged, the risk of cellulitis and deep infection increases. Ligament Sprains

Ligamentous sprains and muscular strains are confirmed with accurate physical diagnosis. Injuries to ligaments are less common in children for two reasons: First, children are more flexible so that the ligaments have more elasticity. Second, the ligaments are generally stronger than the adjacent epiphyseal plates so that the epiphyseal plate is more likely to fail, resulting in an epiphyseal fracture. Ligaments can be torn, especially in adolescent and young adult athletes. Disabled adolescent and young adult athletes with muscular weakness resulting from myelodysplasia or muscular dystrophy are especially vulnerable to sprains because they lack the extra protection normally provided by muscular control. Classification of ligamentous injury (grades 1 to 3) is the same as in adults, indicating the severity of the injury. Treatment of sprains depends on the location and severity of the sprain. Grade 1 sprains are iced and splinted. The joint should be protected until the ligament has healed sufficiently, usually for 3 to 6 weeks. Grade 2 sprains are more severe and take longer to heal. The joint is at higher risk for further injury because the ligament has been weakened significantly. Grade 3 injuries, which involve total disruption, usually require longer periods of immobilization, functional bracing for appropriate joints, and rehabilitation. Some grade 3 injuries require surgical reconstruction. Ligaments such as the anterior cruciate ligament (ACL) pose an additional dilemma. Reconstruction of the ACL is controversial in a skeletally immature patient because currently popular reconstructive procedures involve crossing the distal femoral physis and the proximal tibial physis, which risks growth arrest. At least one third of ACL-deficient knees are asymptomatic, and another third function well with rehabilitation and bracing. If ACL reconstruction is necessary, the procedure should be delayed until skeletal maturity is reached, or else a technique should be used that avoids physeal damage.

Judgment must be used regarding continued competition after ligament injuries. The athlete usually wants to return to competition as soon as possible and definitely as the pain subsides. Some joints, such as finger joints, may not be crucial to performance of the sport and may be protected adequately to enable the athlete to return to competition before complete healing. A severe knee sprain is much more limiting and requires complete treatment and rehabilitation before competition is resumed. Muscle Strains

Muscle strains are common in disabled children. Although children's muscles are more flexible than those of adults, the longitudinal growth of the skeleton is continuous, and the muscles must stretch constantly to maintain relative balance. During a growth spurt, the muscles are relatively tight. Because disabled children are generally less active, they encounter fewer opportunities with activities of daily living for the muscles to stretch. Joint contractures limit muscle excursion. Many neuromuscular conditions cause muscle imbalance, resulting in tighter groups of muscles that are prone to injury. Physicians can help prevent these injuries by educating parents, coaches, and trainers. These individuals should encourage their athletes to stretch the muscles routinely to prevent muscle strains, especially after a warm-up but before participation in practices and competition. Muscle strains are classified into three grades: grade 1, a mild stretch tearing only a few fibers; grade 2, an intermediate tearing of muscle fibers; and grade 3, severe strain with complete disruption. Grade 3 strains are rare in children except when a muscle pulls off its bony apophysis, usually about the pelvis. The diagnosis

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is made by history and physical examination. The location of tenderness and pain when the individual muscle is stressed against resistance confirms the diagnosis. A gap may be palpable between the muscle ends or between the bony fragment and its bed. Radiographs confirm an avulsion injury if the attached bony apophysis is ossified. In the insensate child, local swelling, warmth, and ecchymosis may be the only physical signs. Most muscle strains heal with icing, splinting, and resting for an appropriate length of time. Fractures

The diagnosis of fractures in disabled children is essentially the same as in able-bodied children. In children, the epiphyses are more vulnerable to injury and more difficult to diagnose radiographically. The Salter-Harris classification [58] can be used for prognosis and treatment. Physical examination, coupled with a high index of suspicion, is the key to diagnosis of an epiphyseal fracture. The entire epiphysis is tender circumferentially; this is differentiated easily from a ligament sprain, which is more tender over the joint crossed by the ligament and only on the side of the joint where the injured ligament is located. Diagnosis is more difficult if the child has sensory loss, problems either in perceiving or in interpreting pain, or difficulty in communicating effectively. In the

insensate patient, a fracture is more difficult to diagnose because pain and tenderness are absent. Children with meningomyelocele or spinal cord injuries are more likely to sustain fractures. Because these fractures may occur with minimal trauma, a history of significant trauma is often absent. The location of the fracture is typically metaphyseal, and the fracture may be misinterpreted as an infection[51] of the bone or adjacent joint. Fractures frequently present with erythema, swelling, and warmth near a joint. There is often an associated low-grade fever. Clinical instability, radiographs, appropriate laboratory studies, and a high index of suspicion confirm the correct diagnosis and avoid an embarrassing misdiagnosis. Fractures in disabled children, similar to in able-bodied children, produce pain, swelling, deformity, and ecchymosis. These physical findings are less evident if the involved bone is covered by more soft tissue. If the bones are unstable, there is abnormal motion, crepitus, and severe pain with any motion of the entire injured extremity. Appropriate treatment usually entails reduction and immobilization. Surgery rarely is indicated except in special circumstances, such as in displaced Salter III and IV epiphyseal fractures, displaced fractures difficult to immobilize closed because of excessive spasticity or muscle tone, and displaced fractures around the elbow or hip. Overuse Syndromes

Overuse syndromes may involve almost any anatomic structure under chronic stress. The bones, tendons, skin, and bursae are the most common structures involved. A full discussion of overuse syndromes is found in Section G, Overuse Syndrome in the Pediatric Athlete. Overuse is a relative term. Overuse for a disabled child may be the normal amount of activity for an able-bodied sibling. Neither the parents nor the child may realize that the child is overdoing it. Stress fractures are more common in the lower extremities and are likely to occur just proximal to a brace or prosthesis. In children with normal growth and development, the additional weight and activity as well as increasing length and larger lever arms in the extremities produce increasing forces on the skeleton. The response to the increased forces is an increase in bone strength according to Wolff's law. When the stress forces increase at an accelerated rate (e.g., in a child starting a new sport and playing for hours without an adequate pretraining program), an overuse stress fracture results. The bone involved usually is tender with little associated swelling, deformity, or discoloration of the surrounding soft tissues. Radiographs frequently are normal initially but later show evidence of healing with sclerosis and endosteal, cortical, or periosteal reaction. Technetium bone scans show increased activity at the stress fracture site but are nonspecific. Magnetic resonance imaging can help to differentiate a stress fracture from an infection or neoplastic process. Common overuse problems, such as Osgood-Schlatter disease or Sever's disease, are exacerbated by growth and associated contracted muscles. Sever's disease is overuse of the calcaneal tuberosity. Children typically present with heel pain and a history of increased running or jumping associated with sport participation. The diagnosis is made

by the typical history, location of the symptoms and tenderness about the calcaneal tuberosity, frequently associated tight tendo Achillis, and normal radiographs. Osgood-Schlatter disease is an overuse syndrome involving the anterior tibial tubercle associated with increased quadriceps activity and rapid growth of the distal femur and proximal tibia ( see Chapter 17G ). Disabled children have unique types of overuse syndromes. The locations depend on the type of disability. Children with neuromuscular diseases, such as cerebral palsy, have muscle imbalances that create excessive stress on the musculotendinous unit. Spinal cord injury patients and children with meningomyelocele are prone to blisters and pressure sores on the insensate regions of their lower extremities. In children with congenital deformities or growth-related deformities, such as genu valgus or varus, excessive mechanical stresses are placed on the bones and related joints. Compartment syndromes are rare in children. The deep posterior compartment of the leg is the most common location. Although the problem is rare, children who lack sensation in the lower extremities or lack the ability to communicate effectively cannot recognize or communicate the key symptom, pain. The clinician first must consider the possibility and second evaluate it further if it is suspected. Intercompartment pressures must be measured for children at risk. Summary

The technique used for evaluating an injured disabled or handicapped child is generally the same as that used for

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any other injured child. The clinician starts with a history from the child and the parents. During the physical examination, the clinician looks for specific problems related to the disease process, such as weakness or muscle imbalance, deformity of the skeleton, the presence of braces or a prosthesis, sensation aberrancies, and the usual clinical findings associated with musculoskeletal injuries or syndromes. All these findings are correlated to create a differential diagnosis, then the clinician orders the appropriate radiographs or laboratory studies to confirm the diagnosis.

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Special Considerations for the Disabled Athlete Skin Sensitivity

There are two special areas of concern in regard to skin sensitivity. The first area is the child's awareness of skin sensibility, and the second is the additional risk present at the interface of the skin and an orthotic or prosthetic device or a mobility aid, such as a wheelchair or crutches. Sensibility is a problem for children in general. Children do not seem to have the same regard for their body parts as do adults. In disabled children, this problem is magnified. Children with intellectual and cognitive limitations, such as children with Down's syndrome or cerebral palsy, are even less aware of their bodies. Children with spina bifida or spinal cord injuries have impaired or absent sensation below the neurologic level affected. Although congenital insensitivity to pain is a rare diagnosis, such children are oblivious to pain. Shoes, orthoses, and wheelchairs all can cause excessive localized pressure leading to skin irritation, blisters, skin breakdown, soft tissue infections, and osteomyelitis. Disabled children should be taught to become aware of their skin and its interface with their braces, chairs, and footwear. Coaches, physical education instructors, and parents should be aware of the potential problems and check the skin periodically for erythema, calluses, and blisters. Even if the child never previously has had problems with braces, the added stress of competitive sports can cause excessive skin pressure. In addition, children are constantly growing. With growth, the fit of the braces changes, which eventually leads to altered pressure sites. Children wearing prosthetic limbs are at increased risk. In children with prosthetic lower limbs, the weight-bearing forces must be transferred to the skeleton through the skin and underlying soft tissues. It is more difficult for the prosthetist to transfer these forces successfully in some amputee levels than in others. In the child with a well-done Boyd

or Syme amputation, the stumps are designed to be end bearing. There is a large surface area within the BK prosthesis that distributes the pressure forces, but more important, the heel pad, the organ intended to transmit weight-bearing forces to the skeleton, has been preserved. The heel pad, a specialized structure, acts as a hydraulic cushion,[11] absorbing and dissipating energy or force and transferring the weight-bearing forces. For any lower extremity amputation above the level of the ankle, the skin and soft tissues transferring the weight-bearing forces are more susceptible to breakdown and pressure necrosis. An athlete with a high BK amputation is at a disadvantage. In most competitions, the athlete is grouped, for athletic classification purposes, with other BK amputees. Boyd and Syme amputees look the same externally. Both have a prosthesis that begins below the knee that is connected to a prosthetic foot. A child with a Boyd amputation is bearing weight through the heel pad and into the calcaneus, which approximates the normal situation. A child with a high BK stump is bearing some weight through the skin and whatever soft tissues the surgeon could find to cover the stump, and the remaining pressure is distributed by friction contact to the skin of the lower leg. For day-to-day normal activities, both children may do equally well, but in the arena of competitive sports, the high BK amputee is at a disadvantage, and the added stress to the end-bearing skin interface eventually may provoke skin breakdown. In addition, children must deal with stump overgrowth. Deformities of the Extremities

Deformities need not limit a child's participation in most sports. Psychologically, many children with deformities do not consider themselves disabled. Children with minor deformities often participate and compete with able-bodied children, especially in local neighborhood and sandlot-type games. As the organization and the competition increase in a given sport, the deformities and disabilities may become a relatively greater handicap. At some point, the child or the team may decide that the continued participation of the disabled child is a handicap for the entire team and not just for the disabled child. Type of deformity is an important factor. Deformities can be classified into four groups: congenital, acquired, developmental, and neuromuscular. When considering participation in sports, it is useful to subdivide the deformities

Figure 17-E-2 This child was born with a congenital terminal below-elbow amputation.

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Figure 17-E-3 This child was born with congenital bilateral lower extremity terminal deficiencies, or

congenital above-knee amputations.

further into upper extremity and lower extremity disabilities. Congenital deformities, present at birth, imply that the deformity occurred during fetal development. The most dramatic and distressing to parents is a child born missing some significant parts. The missing part can be terminal (at the end of an extremity) or intercalary (somewhere in the middle of a segment). The understanding of genetic control for embryonic limb development is improving rapidly. [33] An example of a terminal deficiency is illustrated in Figure 17E-2 , a terminal below-elbow amputation. A more severe example is illustrated ( Fig. 17E-3 ) in a child with bilateral lower limb terminal deficiencies. The intercalary deficiency illustrated in Figure 17E-4 is a proximal femoral focal deficiency, which has been renamed congenital femoral deficiency.[39] Problems associated with congenital femoral deficiency depend on the type of deficiency[33] involved but may include limb-length discrepancy, hip instability, and knee deformity. The treatment goal for a terminal deficiency or amputation is to maximize function by providing adequate skin and soft tissue coverage at the distal stump and to fit the child with an appropriate prosthesis. The technology associated with prostheses is evolving and improving. Sophisticated, lightweight, cosmetically attractive materials; high-tech joints; and specialized terminal devices are available.[20] There are several different energy-storing feet, called sports feet, that allow children to jump higher and run faster than the older style of static prosthesis. Specialized lower limbs designed exclusively for swimming are available. Many specialized upper extremity terminal devices are available for specific sports ( Fig. 17E-5 ). A terminal device may be designed to attach to a ski pole ( Fig. 17E-6 ). Treatment for an intercalary deficiency is more challenging. The goal is to optimize function. In the lower extremity,

Figure 17-E-4 A, This child was born with an intercalary deficiency of more than half of the proximal femur (congenital femoral deficiency). B, Note deficiency of right proximal femur.

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Figure 17-E-5 A, Prosthetic adaptive baseball bat attachment. B, Prosthetic adaptive hockey stick terminal device. C and D, Prosthetic adaptive golf club terminal device.

the foot frequently is amputated to facilitate prosthetic fitting, as illustrated in Figure 17E-7 , a case of fibular deficiency[39] (previously called fibular hemimelia). When indicated, this operation is performed at about 1 year of age so that prosthetic fitting can

coincide with independent ambulation. The prosthesis is used to replace foot function and compensate for the difference in limb lengths. In fibular deficiency, the foot is frequently abnormal, missing the lateral rays, and in severe cases the ankle mortise is deficient laterally.[2] [23] [30] In congenital femoral deficiency, the foot usually is normal. The normal foot usually is amputated in this situation to facilitate prosthetic fitting; otherwise, a nonstandard prosthetic fitting would be necessary ( Fig. 17E-8 ). When athletic performance is considered, an alternative is a Van Nes turnaround procedure[64] or a Brown procedure. [13] These procedures rotate the lower extremity 180 degrees and shorten it appropriately, allowing the ankle joint to substitute as an active knee joint ( Fig. 17E-9 ). This 667

Figure 17-E-6 A and B, This child is wearing a below-elbow prosthesis with a Radocy modified terminal device designed to be attached to a ski pole.

Figure 17-E-7 A, This child was born with bilateral fibular deficiency. B, Note absent fibulas, short tibias, and deformed feet with absent lateral rays. C, Postoperative photograph after bilateral Boyd amputation to facilitate prosthetic fitting. D, Standing with bilateral below-knee prosthesis.

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Figure 17-E-8 Nonstandard prosthesis is cosmetically and functionally less desirable than a foot amputation with a more conventional prosthesis.

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Figure 17-E-9 A, Femoral deficiency preoperatively. B, Postoperative view after Van Nes turnaround procedure. C, Active knee extension. D, Active knee extension with prosthesis. E, Ambulation with modified below-knee prosthesis. F, Skiing.

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results functionally in a BK amputation that is athletically much stronger than an AK amputation owing to the active control of the prosthesis at the knee. For a less severe

intercalary deficiency, such as a congenitally short femur, a femoral limb lengthening may offer the best treatment option. [39] Stability of the joint above and below the lengthening (i.e., the hip and knee) is important for a good outcome. In the upper extremity, a similar intercalary deformity might require only therapy to improve the mobility of the joints. The approach to upper extremity deformities is different from that for lower extremity deformities. Lower extremity prosthetics provides an effective replacement for the absent or deficient limb. At the time of this writing, hand function cannot be satisfactorily replaced prosthetically because sensibility is a primary function of the hand that cannot be replaced. Equal upper extremity length is not nearly as important for hand function so that little attempt is made to equalize upper limb-length discrepancies unless they are severe. If sensation and some functional grasp are present, the hand should be preserved. With newer surgical techniques, deformities that previously demanded amputation and prosthetic use for impaired function may now be managed without ablative methods. Significant advances in limb-lengthening techniques using distraction callotasis by ring or cantilever devices have been made in North America,[54] Europe,[28] [64] [65] and Asia.[41] [42] Management of acquired and especially congenital defects is changing as experience grows in the biology and physiology of limb lengthening. Indications for limbs previously thought to be too short to lengthen are now being reevaluated with renewed interest in using these newer techniques.[39] Congenital duplications occur as well as deficiencies. Duplicated toes or fingers are the most common ( Fig. 17E-10 ), and these can be removed easily if they interfere with function or are cosmetically displeasing to the patient. The problems most likely to affect the athlete are problems related to shoe wear, which require modification of the shoe or surgical reconstruction of the foot. Timing of the surgery usually is not crucial. A classic example of failure of segmentation is a simple syndactyly ( Fig. 17E-11 ). In the foot, the problem is mostly cosmetic. In the hand, the deformity is more apparent and functionally disabling, so the fingers usually are separated surgically.

Figure 17-E-10 Polydactyly, congenital duplicated thumb.

Figure 17-E-11 Syndactyly of fourth and fifth digits.

Acquired deformities can be therapeutic or traumatic. An example of a therapeutic deformity is an amputation ( Fig. 17E-12 ) or surgical excision in a child with osteosarcoma using limb salvage techniques for reconstruction ( Fig. 17E-13 ). Traumatic amputations may be primary or secondary. A primary amputation occurs at the time of the injury. A secondary amputation may be necessary if the surviving part is no longer viable or if function would be improved if the part were removed.

Developmental and neuromuscular deformities are grouped together for the purpose of this discussion. Developmental deformities are typically angular or rotational deformities that evolve gradually owing to a growth disturbance, such as Blount's disease ( Fig. 17E-14 ), bone dysplasia, or metabolic disease. Children with neuromuscular imbalance, such as that caused by cerebral palsy, begin with normal skeletal elements that gradually become deformed during growth ( Fig. 17E-15 ) owing to the abnormally balanced forces. The alteration of the normal balance of muscle forces across the skeleton influences the growing bones and produces angular or rotational deformities, shortening, joint deformities, or a combination of these. Growth disturbances have many causes, including (1) bone dysplasia ( Fig. 17E-16 ); (2) traumatic causes ( Fig. 17E-17 ), producing damage to the epiphyseal growth cartilage; (3) acquired conditions, such as an infection that damages the epiphyseal plate ( Fig. 17E-18 ); and (4) idiopathic conditions ( Fig. 17E-19 ). Traumatic or acquired epiphyseal dysfunction may result in angular deformity, shortening, or both ( Fig. 17E-20 ). The clinical significance of these deformities varies. Angular deformities in the lower extremity concentrate abnormal forces across the adjacent joints, increasing the risk for injury and progressive degeneration. The knee and ankle are the joints most susceptible to sprains and progressive degenerative arthritis. In contrast, rotational deformities, such as femoral anteversion or tibial torsion, do not increase the risk for injuries or joint degeneration. Severe rotational deformities may create inefficiencies in the lever arm function of the lower extremities and reduce performance. Sequelae from limb-length inequality depend on the severity of the disorder. Mild limb-length inequalities

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Figure 17-E-12 A, Osteosarcoma of the distal femur with preoperative amputation level marked on radiograph. B, Postoperative above-knee amputation. C, Playing golf with an above-knee prosthesis. D, Skiing three-track without a prosthesis.

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Figure 17-E-13 A, Osteosarcoma of the proximal medial tibial metaphysis. B, Postoperative radiograph: resection arthrodesis with intercalary allograft augmented with ipsilateral vascularized fibula.

of less than 2 cm are rarely symptomatic. Larger limb-length discrepancies, especially when combined with neuromuscular imbalance, may result in pelvic obliquity and progressive spinal deformity, justifying limb-length equalization procedures.

Loss of Coordination, Motor Power, and Endurance

Lack of coordination is a significant disadvantage in many sports. Hand-to-eye and foot-to-eye coordination are important in most sports. Running and jumping also are affected. Neuromuscular conditions affecting the central motor system, such as cerebral palsy, meningomyelocele, and head injuries, are most likely to affect coordination. This situation not only affects performance but also increases the risk for injury. Children with deficient balance should wear protective headgear to prevent potential head injuries. More severely involved children may lack adequate sitting balance or head control. Special adaptations to wheelchairs are necessary to allow participation and to prevent injuries. In addition to coordination defects, mentation may be affected, leading to impaired judgment. Many disabilities affect motor power and control, especially the neuromuscular disabilities. If children are grouped according to similar levels of disability, competition can be fair ( see Tables 17E-1 , 17E-4 , 17E-5 , and 17E-6 ). Endurance is a problem in disabled children. Most children with physical disabilities are not as physically active

Figure 17-E-14 Blount disease. A, Severe genu varus deformity is recurring after a previous osteotomy. B, Same patient showing dysplastic lateral tibial plateau.

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Figure 17-E-15 A child with spastic cerebral palsy who shows progressive neuromuscular hip subluxation with growth.

as able-bodied children. When they decide to participate in a sport, they need to build endurance gradually. If the buildup is too rapid, overuse syndromes may result. When endurance is inadequate and is exceeded in sports, the child becomes fatigued, increasing the risk of injury and decreasing the level of performance. Sphincter Control

Sphincter control is a problem in children with neuromuscular disabilities, especially spina bifida and spinal

Figure 17-E-16 Metatrophic dwarfism with obvious genu valgus.

cord injuries. Frequently, these children are self-conscious of the social stigma, such as the odors and the different bowel and bladder routines they must practice. During participation in sports or athletic competition, the last thing on a child's mind is the status of the bowels or bladder, especially if sensation is lacking. As the bladder becomes distended, reflux can occur, which eventually results in permanent renal damage. The bladder typically is emptied

Figure 17-E-17 This patient suffered a Salter-Harris type III fracture of the lateral femoral condyle that resulted in growth arrest and produced femoral shortening and genu valgus.

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Figure 17-E-18 Septic arthritis with delayed diagnosis in infancy resulted in destruction of the femoral head and growth disturbance, leading to shortening and coxa vara.

on a regular schedule, frequently with assistance by parents. Most children eventually can become independent with these skills. These children and the supervising adults must be made aware of time and schedules and the proper techniques used for bowel and bladder management. If an adequate bowel program is not established, constipation can result in impaction, and incontinence can result in odors and skin breakdown. Children and their families must be educated about proper diet, stool softeners, and the importance of maintaining a regular schedule. Peer and social pressures can affect diet and disrupt regular schedules. High-performance spinal cord injury and spina bifida athletes, especially athletes participating in wheelchair

Figure 17-E-19 A 9-year-old girl with idiopathic genu valgus that does not fit the normal physiologic spontaneous correction pattern.

sports, have been known to clamp Foley catheters to en hance performance. The increased bladder tone produces a vagal response improving performance. This practice is potentially dangerous and should be discouraged.

MD Consult L.L.C. http://www.mdconsult.com 386.html/top"> /das/book/view/29309971/1103/386.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Participation Guidelines Based on Disabilities

Generalized participation guidelines in various sports for disabled athletes are difficult to establish. Participation guidelines must be individualized. The characteristics of the sport and the child's disability should be considered in making a rational decision to participate in a specific sport. A child may want to participate in a specific sport, but the parents may be apprehensive and protective. The Winter Park Seminar on Sports and Recreational Programs for the Child and Young Adult with Physical Disability[62] developed a participation possibility chart, which includes the major physical disabilities and the most common sporting activities ( Table 17E-7 ). Activities are described as recommended, individualized, adapted, not recommended, or no notation if insufficient information is available. Individualized means that although the activity may be inappropriate for some children with certain disabilities, it may be possible for others in the same category to participate, and the activity is not contraindicated for all. Physician judgment and knowledge of the patient are important. Adapted means that in almost all cases adaptations of equipment or rules are necessary. Not recommended is self-explanatory and suggests that the activity is not safe, and the risk of participation in it outweighs its benefits. Amputations

As described earlier, amputations may be congenital or acquired. Congenital amputations are either intercalary or terminal. These groups are subdivided further into transverse or longitudinal defects. Congenital femoral deficiency is an example of an intercalary transverse deficiency because the proximal femur fails to form ( see Fig. 17E-4 ). A terminal transverse congenital wrist amputation describes an absent hand ( see Fig. 17E-2 ). A fibular deficiency may be terminal longitudinal or intercalary longitudinal, depending on the absence or presence of the lateral rays of the foot. Acquired amputations may be either traumatic or therapeutic, for example, when a part may have to be removed owing to a malignancy or vascular insufficiency. A congenital

intercalary amputation may be compounded electively by a terminal acquired amputation to improve prosthetic fitting. This situation occurs commonly in children with fibular deficiency ( see Fig. 17E-7 ). Amputations are classified further by the functional level remaining. Examples in the lower extremity are ankle, BK, AK, and hip disarticulation. Examples of upper extremity amputations are wrist, below-elbow, above-elbow, and shoulder disarticulation. Determining the proper functional level is important because it helps to ensure that athletes compete against others with similar abilities. To illustrate

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Figure 17-E-20 A, Dysplasia epiphysealis hemimelica (Trevor's disease) producing genu valgus and limb-length inequality. B, Note the large cartilaginous lesion deforming the medial femoral condyle. C, Radiographic view of this malformation.

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Archery Bicycling Tricycling Bowling Canoeing/Kayaking

Amputations Upper extremity

RA

R

R

R

RA

Lower extremity AK

R

R

R

R

R

Lower extremity BK

R

R

R

R

R

Ambulatory

R

R

R

R

R

Wheelchair

R

I

I

R

R

RA

RA

RA

IA

High thoracic: T1-T5

R

R

R

R

Low thoracolumbar: T6-L3

R

R

R

R

Cerebral palsy

Spinal cord disruption Cervical

Lumbosacral: L4-sacral

R

R

R

R

R

RA

I

R

R

I

RA

I

R

R

I

Charcot-Marie-Tooth

R

R

R

R

R

Ataxias

R

I

I

R

I

R

I

R

R

R

R

I

I

R

R

RA

I

I

RA

R

RA

R

R

R

R

R

R

R

R

R

Neuromuscular disorders Muscular dystrophy Spinal muscular atrophy

Others Osteogenesis imperfecta Arthrogryposis Juvenile rheumatoid arthritis Hemophilia Skeletal dysplasias

Key: A, adapted; I, individualized; R, recommended; X, not recommended; Blank, no information or no AK, above knee; BK, below knee. *Club throw, discus, javelin, shotput.

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this idea further, we can again look at the previous example of a child with congenital femoral deficiency in whom a Van Nes turnaround procedure was performed instead of a terminal amputation ( see Fig. 17E-9 ). The ankle joint was substituted for the knee joint. This procedure allows the patient to function as a BK amputee instead of an AK amputee. In sports, the presence of an active knee joint provides a competitive advantage. This fact must be weighed against the potential cosmetic disadvantages. Children with congenital deficiencies of the lower extremities usually lack the corresponding muscles and associated soft tissues.[44] These children also may lack other soft tissue structures that are not as obvious. Children with congenitally short femora (congenital femoral deficiency) usually have an associated ACL-deficient knee,[8] [44] manifested by positive drawer and Lachman's signs. This condition should be understood so that it is not mistaken for an acute rupture of the ACL. Many of these patients are fitted with a BK prosthesis. The rigid prosthesis has less flexibility and

elasticity than a normal lower leg, which also increases the risk of injury to the remaining knee ligaments. When participating in sports that carry significant potential for knee injuries, a second prosthesis with medial and lateral hinges and a thigh lacer for additional support and suspension should be prescribed to protect the knee. Stump overgrowth is a constant problem in children with amputations ( Fig. 17E-21 ).[3] [4] [5] [61] Such overgrowth occurs most frequently in the fibula followed by the tibia, humerus, radius, ulna, and femur. [3] [4] During this process, the bone grows through whatever soft tissues the surgeon left to cushion the end of the stump. As the child runs and jumps during athletic competition or during normal play, the skin is at high risk for breakdown. To prevent this skin breakdown, the child, family, coaches, physical education teachers, and anyone else supervising the child should be made aware of the potential problem. If the end of the stump begins to feel bonier or if erythema and skin irritation begin, the child should be evaluated for stump overgrowth. The overgrown stump should be revised surgically to prevent potential complications, such as infection of the soft tissues or osteomyelitis. In a young child, several stump revisions may be necessary at 2- to 3-year intervals [51] before skeletal maturity. In children, the criteria for amputation levels are different from those in adults, particularly at the knee and elbow, where in adults typically an amputation above the level of the joint facilitates placement of the prosthetic joint at the proper anatomic level. In a growing child, the amputation should be a joint disarticulation if possible. Despite creating a more difficult and less cosmetic prosthetic fitting, because the prosthetic joint must be placed distal to the proper anatomic level, a joint disarticulation has distinct advantages. Joint disarticulation minimizes stump overgrowth

Figure 17-E-21 A and B, Stump overgrowth. The tibia has grown right through the skin and the soft tissues.

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and establishes an end-bearing stump. In addition to decreased stump complications, the remaining extremity reaches its full potential length, and the distal growth plate is preserved. At skeletal maturity, the amputation can be revised to allow better cosmetic placement of the involved prosthetic joint. If the epiphysis is sacrificed in a young child at the time of amputation, the potential growth from the epiphysis is lost, and with continued growth the stump becomes relatively shorter and shorter. At skeletal maturity, the functional use of the prosthesis may be compromised owing to inadequate length for suspension or control. If the amputation is done through a joint and the physeal cartilage is left intact, the problem of stump overgrowth does not occur. Marquardt[49] [50] showed that capping the end of a long bone diaphyseal stump with a viable autogenous epiphyseal plate[26] [39] can prevent stump overgrowth. If the amputated stump has an epiphysis, this epiphysis can be used. An AK amputation for a malignant tumor of the distal femoral metaphysis

could be capped with the healthy amputated distal tibial epiphysis. When a healthy epiphyseal autograft is not available, a portion of the iliac apophysis can be substituted to accomplish the same result. Cerebral Palsy

Cerebral palsy is a nonprogressive central nervous system deficiency that is present during early childhood. A deficiency or insult involving the cerebral cortex results in spasticityof the cerebellum in ataxia and of the extrapyramidal tracts with involvement of the basal ganglia in athetosis. In the mixed type, most commonly spasticity and athetosis are combined. The disease is classified further by anatomic involvement. Most common patterns include the following: 1. Monoplegia: One extremity is involved, usually a lower extremity. 2. Hemiplegia: One upper and the lower ipsilateral extremity are involved. 3. Paraplegia: Both lower extremities are involved. 4. Diplegia: All four extremities are involved, but the upper extremities are significantly less involved than the lower. 5. Triplegia: Three extremities are involved, usually sparing one upper extremity. 6. Quadriplegia: All four extremities are significantly involved. 7. Pentaplegia: This term sometimes is used to suggest that the head is involved significantly as well as all four extremities. Pentaplegic children are usually unable to participate in sports. Children with cerebral palsy are susceptible to muscle strains and overuse syndromes. The risk of muscle strains is increased owing to the tightness of the muscles. Because these children are frequently less active, the muscles do not have the opportunity to stretch on a regular or frequent basis. Muscle imbalance, usually caused by spasticity, magnifies the problem, which results in tightness and contractures of major muscle groups. The spastic muscles are usually an agonistic group of muscles. The triceps surae group of muscles attached to the Achilles tendon frequently is spastic, overactive, and tight compared with the antagonistic ankle dorsiflexors. Because the bones usually are of normal strength, the risk of fractures is not increased. The tight contracted muscles result in joint stress. Patellar overload is common and frequently evolves into true chondromalacia. Growth and spasticity result in progressive tightening of the hamstrings and quadriceps muscles. This tightening causes a shortened stride length and increased pressure across the patellofemoral joint. In more severe cases, the tight hamstrings produce a crouched or flexed knee gait. If it is allowed to persist, proximal migration of the patella occurs (patella alta). The increased pressure gradually results in increased wear and damage to the articular surface of the

patella. The symptoms are the same as those seen in able-bodied children with patellar overload symptoms ( see Chapter 17G ), but the problem is accentuated and is more refractory to treatment. The tension on the quadriceps mechanism can produce a syndrome similar to the jumper's knee seen in adolescents.[12] The constant pull of the patellar tendon results in fragmentation of the lower pole of the patella radiographically and causes pain and tenderness clinically. Muscle tightness and imbalance across the hip joint gradually affect the normal development of the hip. In more severe cases, the hip joint subluxes and eventually dislocates ( see Fig. 17E-15 ). In less severe cases, children may develop coxa valga and acetabular dysplasia. Acetabular dysplasia may become symptomatic as the joint undergoes degenerative arthritic changes. As these changes occur, increased activity, such as running and jumping, results in hip pain. Inadequate motor control and lack of coordination are more significant problems for children with cerebral palsy who participate in sports than is their susceptibility to injuries. Impairment of hand-to-eye coordination results in difficulty with controlling athletic equipment, such as rackets, bats, or golf clubs. Difficulty in catching and throwing and perceptual problems, such as judging the speed of a ball, all are hindrances but not insurmountable obstacles. Running with speed is more difficult. These deficiencies in coordination can be improved to some extent with practice and training. Children with head injuries are functionally similar to children with cerebral palsy. Head-injured children have the potential for improvement in neurologic function as the injured tissue recovers. Visual field defects, which are present in some children with head injuries, increase the potential for injuries and can cause problems if an object such as a ball passes through the child's blind spot. Overall, children with spastic monoplegia, diplegia, or hemiplegia and children with athetosis can function relatively well and enjoy participating in sports. Meningomyelocele

Meningomyelocele is the most severe congenital deformity compatible with life. The abnormal spinal canal development results in a damaged spinal cord that is inadequately protected. The patient lacks motor power and

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sensation below the involved level. In addition to motor and sensory deficits, bowel and bladder functions are impaired. Hydrocephalus, which frequently is associated, increases the risk of impaired cerebral function and mentation and damage to the motor cerebral cortex. The resulting damage produces spasticity above the level of spinal cord dysfunction. A team of physicians, including a pediatrician, neurosurgeon, orthopaedic surgeon, urologist, and physiatrist, should provide care.

Participation in sports depends on several factors, the two most important being the functional level of the spinal cord and the severity of hydrocephalus. Hydrocephalus determines the severity of mental retardation and spasticity. The functional level of the spinal cord determines the motor function of the lower extremities. Classification of children with meningomyelocele is based on the functional level (i.e., the lowest nerve root level that is functioning; see Table 17E-6 ). If the ankle can be dorsiflexed actively but cannot be plantar flexed actively, the patient is functioning at the L5 level, or the fifth lumbar nerve root is functioning but nothing below that level. The sensory level usually corresponds to the motor level. The involvement may be asymmetrical. Usually the two sides are within one nerve root level of each other, but children with some spotty function below the primary level are seen. Children with low lumbar and sacral level function can function almost normally. Patients with low lumbar-level function require orthoses to stabilize the foot and ankle. Children with midlumbar-level function may require braces to stabilize the knee. Patients with higher level lesions function best in a seated position. Children with midlumbar-level lesions perform athletic activities better and more safely in a wheelchair than when they are ambulatory in braces. Another concern is lack of sensation. Children wearing braces who participate in sports may develop pressure sores and skin breakdown. Children sitting in wheelchairs for prolonged periods are susceptible to pressure sores and skin breakdown from the seat of the wheelchair. Individuals with normal sensation experience discomfort as the pressure increases or as the tissues start to become ischemic. Such individuals reflexively shift their position to relieve the increasing pressure. Children without adequate sensation do not have these protective mechanisms to guard the skin and underlying soft tissues. To avoid these problems, children, parents, and coaches must be educated to check the skin frequently visually until the skin pressure tolerances can be determined. Children must be taught to shift their weight frequently and to use their upper extremities to lift themselves off their seats. To decrease excessive pressure while sitting in the wheelchair, specially designed cushioned seats are available to distribute the weight evenly and to dissipate pressure. Children with meningomyelocele are more susceptible to fractures secondary to osteopenia. Fractures are more difficult to diagnose. Because of altered or absent sensation, there is less or no associated pain. Because the injured area may appear locally inflamed, a fracture can be mistaken easily for an infection with swelling, erythema, increased local temperature, and low-grade fever. Immobilization of a fractured extremity results in the bone becoming more osteopenic and susceptible to refracture when immobilization ends. Gradual and progressive weight-bearing after a fracture or recent operation and the use of functional braces can help to prevent a refracture. Limiting the time of immobilization and non-weight-bearing decreases the incidence of refracture. Children with meningomyelocele are susceptible to muscle strains. Muscles at the lowest spinal functioning level usually have less than 100% of normal strength. Because children with spinal defects are less active, their overall motor power is not as well developed. Because of muscle imbalance, some muscles are tighter than normal and

are prone to strains caused by decreased flexibility. Children with meningomyelocele are able to participate in sports similar to those suitable for a patient with a spinal cord injury. The one major difference relates to hydrocephalus. Hydrocephalus may result in intellectual compromise with implications for competitive sports ranging from not having the drive to compete and not understanding the rules of the sport to perceptual problems that can affect performance. Children with severe hydrocephalus should wear adequate head protection to prevent head injury and shunt damage. Spinal Cord Injuries

Spinal cord injuries in children, although uncommon, account for 13% to 15% of all spinal cord injuries, with boys predominating 2:1. [40] [45] Spinal cord injuries are typically traumatic and are associated with spinal fractures. Young children less than 10 years of age, because of their generalized ligamentous laxity, may present with spinal cord injuries without associated fractures. Leventhal[48] showed in an infant's spine that the spinal canal can be stretched 2 inches, but the cervical cord can tolerate only ¼inch of stretch. This ligamentous laxity may allow enough motion to damage the cord.[6] [9] [10] [34] [38] [45] [46]

In many respects, the problems experienced with spinal cord injury are similar to those seen with meningomyelocele. Differences include the absence of hydrocephalus or intellectual deficit unless a head injury is associated, the less common presence of mixed levels of dysfunction, and the possible presence of cervical levels of dysfunction. Spinal cord injuries except in special circumstances, such as Brown-Séquard lesions, are typically transverse lesions with symmetrical involvement. Spinal cord injuries can involve the cervical spinal levels, which compromise upper extremity function. Thermal regulation is a problem in patients with spinal cord injuries, especially in higher level lesions. Children with spinal cord injuries above T8 cannot maintain normal body temperature[37] because constant body temperature depends on heat dissipation and heat production. Heat production mechanisms such as shivering and heat dissipation mechanisms such as perspiration are absent below the level of the spinal cord injury. The higher the neurologic level of the injury, the more difficult it is for the individual to compensate for changes in ambient temperature. Children with meningomyelocele have similar problems with thermal regulation. Precautions must be taken when these children participate in winter sports, and they must be observed closely in warm environments. In a survey of competitors

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at the 1990 USA Junior National Wheelchair Games, almost half (49%) of the track participants listed hyperthermia as a problem, and 9% of those competing in swimming listed hypothermia[66] as a concern.

Down's Syndrome

Children with Down's syndrome seem to love sports and can be competitive. They are frequent participants at Special Olympic competitions. Most of the orthopaedic problems in children with Down's syndrome occur because the chromosomal abnormality results in a defect in production of normal collagen. The abnormal collagen produced results in generalized ligamentous laxity and decreased muscle tone. Ligamentous laxity causes hyperflexibility of the joints and related problems, such as flexible flatfeet and joint instability with associated subluxations and dislocations. Judgment may be impaired by intellectual compromise, which is compounded by the fact that children with Down's syndrome frequently do not complain about discomfort or pain and may continue to participate despite the presence of symptoms. Atlantoaxial subluxation is potentially the most devastating problem in the athlete with Down's syndrome. The radiologic incidence of this instability in this population is approximately 15%. The subluxation is due to laxity of the annular ligament of C1 and is magnified by the generalized hypotonia. The space available for the spinal cord consequently diminishes ( Fig. 17E-22 ). Excessive motion at this level can result in permanent damage to the spinal cord. If the motor tracks are injured, the patient is left quadriplegic or quadriparetic with respiratory compromise. There have been sporadic reports of symptomatic atlantoaxial instability in children with Down's syndrome since 1965. Since 1983, the Special Olympics has required screening for atlantoaxial instability in athletes with Down's syndrome before participation in any sport placing excessive stress on the head or neck (gymnastics, diving, pentathlon, butterfly stroke in swimming, diving start in swimming, high jump, and warm-up exercises that place undue stress on the head and neck muscles).[59] [60] This requirement has made families and the medical community

Figure 17-E-22 Sagittal cross section through the base of the upper cervical spine and the skull. A, Normal atlantodens interval (ADI) and available spinal cord space (Space Available for Cord [SAC]). B, In atlantoaxial instability, increased ADI and decreased SAC occur in flexion. C, With neck extension, C1 and C2 are realigned in their normal relationship, and the SAC increases.

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more aware of the existence of the problem. Many school districts require screening before participation of these children in physical education classes. The American Academy of Pediatrics[1] issued a policy statement in 1984 after carefully analyzing the data and statistics reported in the literature, which is paraphrased as follows: 1. Children with Down's syndrome who wish to participate in sports that involve possible trauma to the head and neck should have lateral-view radiographs of the cervical region

in neutral, flexion, and extension positions within the patient's tolerance before beginning training or competition. This recommendation applies to all participants in high-risk sports who have not had normal findings previously on cervical radiographs. Some physicians may prefer to screen all patients with Down's syndrome routinely at 5 to 6 years of age to rule out atlantoaxial instability. 2. When the distance between the odontoid process of the axis and the anterior arch of the atlas is greater than 4.5 mm or the odontoid is abnormal, sports that involve trauma to the head and neck should be restricted, and the patient should be followed up at regular intervals. 3. At present, repeated radiographs are not indicated for patients who previously have had normal findings. Indications for repeated radiographs will be defined by research. 4. Patients with atlantoaxial subluxations or dislocations and neurologic signs or symptoms should be restricted in all strenuous activities, and operative stabilization of the cervical spine should be considered. 5. Patients with Down's syndrome who have no evidence of atlantoaxial instability may participate in all sports. Follow-up is not required unless musculoskeletal or neurologic signs or symptoms develop. Atlantoaxial subluxation is screened by lateral cervical spine radiographs in maximum flexion and extension. The flexion and extension views are compared to assess the atlantodens interval (ADI) ( Fig. 17E-23 ). The ADI is normally less than 2.5 mm, but the highest value acceptable is 4.5 mm in a child with Down's syndrome. In an asymptomatic child with an ADI greater than 4.5 mm, activities that increase the risk to the cervical spine should be restricted. Such sports include tumbling, gymnastics, diving, soccer, high jumping, football, snowboarding, and skiing. If the ADI is excessive (>6.0 mm) or if the child has neurologic symptoms, the child is a candidate for cervical surgical stabilization. Screening should be done before the child is enrolled in any high-risk activities, at the start of school, or if neurologic symptoms are present. Subsequent screening is becoming better defined. Although some physicians still recommend follow-up screening at 3- to 5-year intervals until skeletal maturity is reached, there is no evidence in the literature to support this practice. Pueschel and Scola[55] reported on 404 patients, 95 of whom were followed longitudinally; none showed any progression of the ADI. The time of highest risk is statistically between 5 and 10 years of age. Neurologic symptoms include neck pain, stiff neck, torticollis, progressive weakness or change in sensation in any extremity, decreasing endurance, loss of bowel or bladder control or a change in bowel habits, increased clumsiness, or change in gait pattern. The presence of any of these neurologic symptoms is reason for further evaluation and screening radiographs. An analogous problem can occur between C1 and the occiput, but the parameters for measurement and the norms for Down's syndrome are less well defined. French and colleagues[31] recommended that all children with Down's syndrome be restricted from high-risk sports such as tumbling, trampoline, and gymnastics. These investigators found a 3% incidence of upper cervical ossicles, which they postulated were acquired in

origin because half the patients in the study group had previously documented normal radiographs. The ossicles are thought to be avulsion fractures of the dens, pulled off by the alar ligaments. Two other joints may cause problems in children with Down's syndrome. The patellofemoral joint may be unstable and may become chronically subluxated or dislocated, and occasionally the hip joint may become unstable. Patellofemoral joint laxity can intensify with anatomic abnormalities, such as genu valgus, patella alta, or a hypoplastic medial femoral condyle, resulting in instability. Recurrent subluxations may not produce complaints in a child with Down's syndrome. A dislocation may produce more pain and swelling, but even with an acute dislocation a child with Down's syndrome may complain only a little. Treatment is more difficult because, in addition to ligamentous laxity, children with Down's syndrome are relatively hypotonic. Conservative measures frequently fail. Surgical realignment of the extensor mechanism rarely may be necessary. Hip instability is a more difficult problem to treat. Excessive joint laxity can result in a distended hip capsule, which allows the hip to dislocate. Parents describe audible clunking or popping sounds, with usually little evidence of symptoms. Some children with Down's syndrome intentionally may dislocate the hip to gain attention or for self-stimulation. This problem is similar to the individual with voluntary shoulder dislocation. Conservative measures, such as temporary casting or prolonged abduction bracing, produce inconsistent results. Surgical correction with a femoral or pelvic osteotomy combined with capsulorrhaphy and prolonged postoperative casting does not always ensure permanent hip stability. Although hip damage and eventual degenerative changes occur, the natural history of this problem is not well documented. The instability seems to diminish with progressive growth and development. Flexible flatfeet normally are present in children with Down's syndrome. Most children with flatfeet are asymptomatic. If planovalgus deformities are symptomatic, a UCBL (University of California Berkeley Labs) orthosis or a more flexible custom sport orthosis helps to minimize symptoms and excessive shoe wear. Hearing Impairment

Children with a hearing impairment are not predisposed to any specific injuries and can participate in all sports. Hearing-impaired children are at a disadvantage and have difficulty in participating in some sports. Communication with other participants is compromised. Hearing-impaired children cannot hear someone giving instructions, and their

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Figure 17-E-23 Lateral cervical flexion-extension radiographs. A, Normal extension. B, Normal flexion.

C, Extension measures a normal 2 mm in an abnormal patient with Down's syndrome and atlantoaxial instability. D, Same patient as in C shows laxity in flexion with an abnormal 7.5 mm.

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speech often is impaired. Hearing-impaired children lack the ability to receive auditory cues or to hear other players who are trying to get their attention verbally. Because they do not have any visible physical disability, hearing-impaired children tend to play with other able-bodied individuals, leaving them at some disadvantage. Because the inner ear is connected to the vestibular apparatus, balance may be affected. Hearing aids are useful for some children. Lip reading and signing facilitate communications but have disadvantages during the heat of competition, especially in sports involving other team members or other competitors. For hearing-impaired children to experience maximum success in sports, individual activities, such as tennis, skiing, and running, in which the need for communication is minimal, may be chosen. Hearing-impaired athletes are able to participate in competitions with other hearing-impaired individuals and with able-bodied athletes. To qualify for participation in international competition, an individual must have a hearing loss of 55 dB or greater in the better ear. The use of hearing aids is prohibited in competitions (www.usadsf.org; see Appendix). Visual Impairment

Participation without eyesight in sports is at best a difficult situation. Occasionally, auditory cues can be substituted during some sports, such as skiing. Special programs have been developed at a few ski resorts ( Fig. 17E-24 ). As the proficiency and skills of the skier increase, the skier can ski faster and on more difficult terrain. Other sports have been adapted successfully. Rock climbing,

Figure 17-E-24 A blind skier.

speed skating, tandem cycling, and competitive swimming all are gaining popularity with visually impaired athletes. Children with head injuries may have a limitation in the visual field depending on the anatomic location of the lesion. Awareness of the location of the visual field defect is important for safety and for choosing a sport that would not be affected significantly by the child's blind spot. Official Paralympic sports includes goalball, track, tandem cycling, powerlifting, Nordic and alpine skiing, swimming, and wrestling. The current classification system defines

three groups ( see Table 17E-2 ) (www.uasba.org; see Appendix).

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Special Olympics

The Special Olympics is an international program that promotes physical fitness and athletic competition for mentally impaired children and adults [60] (www.specialolympics.org; see Appendix). The Special Olympics features competition in various sports similar to the Olympic summer and winter games. Participants compete in different divisions based on age and ability. Local and regional competitions are held annually. Winners of the regional competitions go on to compete nationally, and every 4 years an international competition is held similar to the Olympic games. The psychosocial rewards are gratifying for participants. Children and adults with almost any disability may participate. Children with Down's syndrome must be screened for cervical instability before participating in some sports.

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Paralympics

The Paralympics is organized in a similar fashion to the Olympics. Athletes are categorized by their disability and grouped for competitions. This international competition is at a similar level to the able-bodied Olympics. The competitions are held every 4 years at the same venue as the Olympic competitions. The local host decides whether the competitions occur simultaneously or after the regular Olympics have finished. Summer and winter Paralympics are held. Between Olympic seasons, international world cup-level competitions are held. Most of the same countries that send athletes to the Olympics sponsor athletes to the Paralympic Games. As previously mentioned, the interest and participation in disabled sports is growing rapidly nationally and internationally. In the first international Paralympic Games held in Rome in 1960 after the regular summer Olympic Games, 400 athletes from 23 countries participated. The Paralympic Games in Atlanta in 1996 after the summer Olympic Games included more than 10,000 athletes from 197 countries competing in 26 sports. The United States has been competitive in the summer and winter Paralympic games. In 1994 in Lillehammer, Norway, 1054 athletes competed. The United States sent 42 athletes who won 43 medals: 24 gold, 12 silver, 7 bronze ( Fig. 17E-25 ), to place third behind Germany and Norway with 64 each. In the Atlanta Summer Paralympics, the United States sent 318 athletes

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Figure 17-E-25 A, U.S. Olympian Adrienne Rivera wins a gold and a bronze medal competing in the Lillehammer Winter Paralympics. B, On the podium for the gold medal.

that won 157 medals: 46 gold, 46 silver, and 65 bronze, to lead all countries

(www.paralympic.org; see Appendix).

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Adaptive Equipment

Children with disabilities should be given the opportunity and be encouraged to participate in sports. Depending on the disability and the sport, various types of adaptive equipment can be used to enhance their participation, performance, and enjoyment. Some equipment may be simple, such as the ankle-foot orthosis that the child uses every day to stabilize the ankle. At the other end of the spectrum, specialized devices are available that facilitate athletic performance. A child who is a wheelchair ambulator and has a functional chair for daily use may obtain a low-profile, lightweight sports wheelchair to participate in competitive sports. Specialized upper extremity prostheses are available with interchangeable terminal devices that are adapted to hold bats, hockey sticks, golf clubs, rackets, and ski poles ( see Fig. 17E-6 ). Technology has provided specialized energy-storing feet and lighter and stronger materials that enhance athletic performance as well as daily use by individuals who use lower limb prostheses. Some of the terminal device and prosthetic component manufacturers sponsor athletes and teams who use their devices for competitions. A wheelchair-dependent child has many opportunities to participate in athletic competition. In the early 1980s, the NWAA created a junior division for children 6 to 18 years old. Three groups of athletes were defined based on the level of spinal cord function; these were subdivided further into four age groups ( see Table 17E-3 ). Injuries are common in these athletes. Of participants, 97% reported injuries in track competitions at the 1990 Junior Wheelchair National competition.[67] Most of the reported injuries were soft tissue injuries: blisters, 77%; wheel burns, 71%; bruising, 41%; abrasions, 38%; shoulder soft tissue injuries (including sprains, strains, and tendinitis), 19%; pressure sores, 14%; wrist soft tissue injuries, 11%; and elbow soft tissue injuries, 7%. Fractures occurred in 6%, bladder infections occurred in 22%, and overheating or hyperthermia problems were reported in 49% in the same group of children. These problems can be minimized with awareness, vigilance, appropriate protective equipment, clothing, padding, and improved training programs. At the Children's Hospital in Denver, Colorado, we have developed a sophisticated and

successful ski and sports program for children with many different types of disabilities. In the ski program, each child is evaluated individually to determine what adaptive equipment will optimize his or her performance. Depending on the specific disability involved, the child is placed in one of four skier categories. Major skier categories are as follows: 1. Three track: One ski and two outriggers a. AK and higher amputees b. Severely deformed, damaged, weakened, or fragile single lower extremity c. BK amputee with less than a 4-inch stump d. Postpolio (monoplegia) 2. Four track: Two skis and two outriggers a. Midlumbar-level to low lumbar-level spina bifida b. Moderate-to-severe cerebral palsy 3. Two track: Two skis with one, two, or no poles a. Unilateral or bilateral upper extremity amputee b. Spastic diplegic or triplegic cerebral palsy c. BK amputee with 4-inch or longer stump 685

4. Sit skier: Sitting in some modification of a sled device a. High lumbar-level or thoracic-level spina bifida or spinal cord injury b. Any child dependent on a wheelchair 5. Snowboard: A new group evolving using the snowboard a. Midlevel (midlumbar to low lumbar) spina bifida b. Low lumbar to sacral level spinal cord injury c. Spastic diplegic and hemiplegic cerebral palsy and traumatic brain injury The child's stance is analyzed. If there is a limb-length discrepancy, lifts are incorporated between the ski and the binding ( Fig. 17E-26 ). If the child cannot achieve a balanced posture with his or her weight balanced over the feet or slightly forward, heel lifts are incorporated into the ski boot, or the binding and the entire footplate are canted forward in the more severe cases. Canting the footplate appropriately can compensate for the presence of deformed lower limbs (varus or valgus). If the child has compromised balance, weakness in the lower extremities, or difficulty in controlling the legs and feet, a ski bra is used ( Fig. 17E-27 ); this device provides a more stable platform. As the child's skills improve, a bungee cord replaces the ski bra. A bungee cord is elastic, providing some stability but more flexibility. Finally, as the child becomes more proficient and confident, the bungee is removed, and the child is allowed independent control of both skis. This program allows children to participate in sports that enhance many aspects of their lives. Skiing improves strength, endurance, balance, motivation, self-image, and self-confidence. I believe that the handicapped ski program changes the lives of these children in a positive way and ultimately helps them to cope in a world of adults without

handicaps. Involving disabled patients in a sports program is appropriate. Participation in sports is safe, healthy, rewarding,

Figure 17-E-26 A, Preseason ski fitting using platform to equalize limb lengths. B, Binding and boot attached to platform. C, Skiing on the platform fitted to the right ski.

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Figure 17-E-27 Child skiing with ski bra attached to tips of skis.

exciting, and gratifying for patients and their families. Physicians can help and encourage disabled patients to become involved.

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Chang FM: Physically challenged athletes. In Sullivan JA, Anderson JA (eds): Care of the Young Athlete. Rosemont, IL, American Academy of Orthopaedic Surgeons and American Academy of Pediatrics, 2000, pp 149-161. 19.

Chang FM: Sports programs for the child with a limb deficiency. In Herring JA, Birch JG (eds): The Child with a Limb Deficiency. Rosemont, IL, American Academy of Orthopaedic Surgeons, 1998, pp 361-377. 20.

Chang FM: The disabled athlete. In Stanitski CL, DeLee JC, Drez D Jr (eds): Pediatric and Adolescent Sports Medicine, vol 3. Philadelphia, WB Saunders, 1994, pp 48-76. 21.

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Clark MW: Competitive sports for the disabled. Am J Sports Med 8:366, 1980.

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Curtis KA: Injuries in wheelchair athletes. In Sports and Recreational Programs for the Child and Young Adult: Proceedings of the Winter Park Seminar. Park Ridge, IL, American Academy of Orthopaedic Surgeons, 1983. 25.

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Davidson RG: Atlantoaxial instability in individuals with Down syndrome: A fresh look at the evidence. Pediatrics 81:857-865, 1988. 27.

DeBastiani G, Aldefheri R, Renzi-Brivo L, et al: Limb lengthening by callus distraction (callotasis). J Pediatr Orthop 7:129, 1987. 28.

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French HG, Burke SW, Roberts JM, et al: Upper cervical ossicles in Down syndrome. J Pediatr Orthop 7:69-71, 1987. 31.

Giblin PE, Micheli LJ: Management of atlantoaxial subluxation with neurologic involvement in Down syndrome: A report of two cases and review of the literature. Clin Orthop 140:66-71, 1979. 32.

Gillespie R: Classification of congenital abnormalities of the femur. In Herring JA, Birch JG (eds): The Child with a Limb Deficiency. Rosemont, IL, American Academy of Orthopaedic Surgeons, 1998, pp 63-72. 33.

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Kewalramani LS, Tori JA: Spinal cord trauma in children: Neurologic patterns, radiographic features, and pathomechanics of injury. Spine 5:11-18, 1980. 44.

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Lancourt JE, Dickson JH, Carter RE: Paralytic spinal deformity following traumatic spinal cord injury in children and adolescents. J Bone Joint Surg Am 63:47-53, 1981. 46.

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Van Nes CP: Rotation-plasty for congenital defects of the femur: Making use of the ankle of the shortened limb to control the knee joint of a prosthesis. J Bone Joint Surg Br 32:12, 1950. 64.

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APPENDIX: Internet World Wide Web References 1. 2. 3. 4. 5. 6. 7. 8. 9.

Deaf Sports Federation: www.usadsf.org USA Disabled Sports, USA: www.dusa.org International Paralympic Committee: www.paralympic.org National Sports Center for the Disabled (NSCD): www.NSCD.org Special Olympics: www.specialolympics.org United States Association of Blind Athletes: www. usaba.org United States Cerebral Palsy Athletic Association: www.uscpaa.org United States Olympic Committee: www.olympic-usa.org Wheelchair Sports, USA: www.wsusa.org

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Section F Psychological Aspects of Sports in Children and Adolescents William P. Elsass MD Ilaina M. Wingler MA Societal awareness of the need for and benefits of physical fitness has grown in recent years into a full-scale obsession. This awareness, along with a desire to deter disease through personal prevention, has created an explosion of athletic participants at every level from the recreational athlete to the avid competitor. Increased athletic participation has sparked a need to understand the benefits and detriments that accompany this activity. The greatest focus of investigation has been on the physiologic advantages and disadvantages brought about by sports participation; however, society has paid increasingly more attention to the psychological contributions of physical exertion. A complete understanding of the effects of participation in sports and physical fitness should include aspects of physiology, cognition, psychology, and social situation. Children's unique experiences in sports and physical fitness require special approaches, especially because societal realization of the benefits of physical fitness has brought about increasing pressure on children to participate in a wide variety of sports at younger ages. These special approaches, because of unusual age- and sport-related stressors, are best handled by individuals equipped to treat youth developmentally from cognitive, social, and psychological standpoints, such as sports psychologists or behavioral scientists. Sports psychology has been gaining in popularity as

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athletes realize the importance of the mind in sport. It is especially common in the professional arena and is finding a larger role in the sport of recreational athletes. One can easily find articles in the leading sports magazines on how to use psychology to enhance one's athletic performance. There has been interest not only in how to enhance one's performance but also in the negative aspects of sport, such as burnout and stress. Although much of the literature is based on adult populations, there is a good body of information to show that these same principles of psychological enhancement and stress exist in the pediatric athlete as well. Despite a move in recent years toward administration of health care by a team of providers, the physician remains the primary health care provider for virtually all ailments. Although the psychological or behavioral specialist may have a greater understanding of the cognitive, social, or psychological problems faced by these youths, it is the physician who occupies the initial if not central position in the treatment of these problems. Consequently, it is the physician who has the opportunity to identify the psychological issues affecting the child athlete and to organize as well as to coordinate the intervention. Therefore, the physician must understand the psychological issues facing young people in sports and recognize their symptoms. Accurate interventions are potentiated by an understanding of the motivational reasons for participation in sports; the implications of parental, coach, and peer pressures; performance anxiety; winning-losing attitudes along with the associated guilt; the effect of sports injuries on psychological health; and each child's unique disposition. A repertoire of sound and basic approaches enables the practitioner to address many problems seen in the office. Such approaches may include goal setting, imagery, and self-affirmation techniques. The practitioner will find that these and other avenues are not only easy but effective. Should the practitioner find that a particular problem is beyond his or her professional expertise, a referral to a psychological specialist may be the most prudent action. With a basic understanding of some psychological issues and a few methods of intervention, the practitioner will be better prepared to observe a broader spectrum of problems, to coordinate treatment, and thus to facilitate enhanced enjoyment and motivation to participate in sports, a greater sense of accomplishment, and enhanced self-esteem and self-confidence in the young athlete. Practitioners will further promote health by decreasing cognitive, social, psychological, and physiologic disease. Developmental Considerations

Practitioners usually find Erik Erikson's description of developmental stages useful. Briefly, Erikson describes the child from 4 to 6 years of age as in a stage of psychosocial development in which the child experiences an increased identification with parents, an increased motor control and language development, and an expanding imagination. Play is essential for the resolution of internal crises and the management of inner conflicts during this period. If adult figures give punitive or unsupportive treatment, guilt develops.[63] This guilt may become detrimental to the child's entire development should it not be resolved. Simply speaking, at this time in a child's life, play, with adult encouragement and support and without punishment, is the most helpful contribution to

development. The child between the ages of 6 and 11 years, the latency period, begins to solidify the ego through learning. The child feels that she or he is what she or he learns and masters. A healthy ego is based on perceived competence in certain basic skills. Early failures produce feelings of inadequacy and inferiority.[63] Once again, inadequacy and inferiority that are left unresolved can bring about detrimental effects on the child's overall development. In this stage, it is important for young people to set goals, small ones if necessary, and to accomplish these goals with a sense of success. With the onset of adolescence and throughout this developmental period, confusion reigns for both the child and the concerned adult. From approximately 12 to 21 years of age, youth seek identity. This period of confusion and uncertainty is one of social turmoil and search for stability and continuity in life.[63] The adolescent begins the process of separating himself or herself from family and assuming independence, learning to manage intimacy, developing values, and recognizing career goals. Feelings of dependency are overcome as athletic, social, and academic demands take on greater importance.[169] The value of this developmental information has become increasingly apparent in recent years. For the early adolescent, high-schoolaged athletes are some of the most admired individuals in that stage's social milieu. The early adolescent's athletic ability qualifies the athlete for acceptance by peers, support from the family, and support from the community. Moving into the latter years of this developmental stage, the adolescent may find himself or herself in an environment less supportive of psychosocial needs. Increased pressure to perform and more demands to practice are placed on the adolescent athlete. Adolescents who cannot perform up to these increased expectations in the latter part of this stage may experience self-doubt,[169] internal conflict, and stress that are frequently difficult to understand by the athlete or to observe by the interested adult. To maximize involvement of youth at all stages of sport, developmental issues must play a part in the administration of health care. In addition, developmental issues within particular stages must be addressed. Read[174] has suggested that the attempt be made not to develop children for sport activities but to develop sport activities for children.

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Motivation and Rewards for Participating in Sport

Young people are motivated to participate in sport activities for many different reasons, each carrying its own psychological impact. Research has found that youngsters participate in sports primarily for fun and enjoyment. Enjoyment is defined as excitement, personal achievement, performing and improving the specific sport skills, and positively comparing oneself with others in the sport activity. Fun is the feeling of happiness, being friendly and

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cheery as opposed to feeling sad and angry. Some children view being part of a team and having friends as important but second to fun, whereas winning, rewards, and pleasing others are viewed as less important.[214] The need to win is far less important to children than is often assumed by adults, although winning can be a part of the broad concept of fun. As it has been identified that children primarily participate in sport for fun and friendship, studies have looked at what types of programs enhance enjoyment and motivation. One study looked at children involved in martial arts classes. [208] Comparison was made between two teaching programs, traditional and mastery. The mastery program emphasized partner exercises early on, more variety, and use of equipment immediately, whereas the traditional program did not have partner exercises until 4 to 6 years, had less variety, and did not introduce equipment for 1 year. Findings showed that children in the mastery program had significantly more enjoyment and higher levels of motor skill performance. By designing sport instruction around what the children's motivations for participation actually are, instructors can create classes that are more rewarding and beneficial. Rewards and accomplishments are especially important to older youth. Teens in some

studies believe that participation in sports enhances one or more of the following parameters: provides opportunities to make friends, stay in shape, and get exercise; teaches the value of mastery and cooperation; gives people a lifelong physical activity; helps to make athletes good citizens; develops competitive skills; helps individuals obtain a career of status; enhances self-esteem; and develops good social skills that facilitate getting ahead and elevating social status.[49] [54] [162] Coaches and teen athletes rank reasons for dropping out of sports differently.[49] This indicates that adults often do not understand what motivates a child to participate and remain in sport. Parents and coaches could greatly assist young people by designing sporting experiences that emphasize building friendships and creating enjoyment.

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Beneficial and Detrimental Effects of Sport Activities

There is evidence that participation in normal (as opposed to intense) sports activity can facilitate growth in a variety of ways for the athlete. [196] In general, normal physical activity or training enhances the functional capabilities of youth. They experience improvement in their health, physical fitness, and motor skills. Physical involvement is perceived as an effective tool in the development of certain psychosocial aspects of developing youth. Such traits as character development, social adjustment, positive personality traits and attitudes, emotional control, sportsman-like behavior, leadership skills, empathy for others, cooperation, self-discipline, self-confidence, initiative, courage, loyalty, and self-expression have been related to sport and its benefits.[20] [85] [119] [120] [196] It is believed that children, and boys in particular, who participate in sports enjoy greater social status than do their nonparticipating peers. Some studies characterize athletes as more outgoing and socially well adjusted than nonathletes.[196] Evidence indicates that competitive and cooperative behaviors begin at 3 to 4 years of age and that such survival skills can be developed through normal sport experience.[39] In general, evidence points to the fact that young people who participate in normal sport display both physiologic and psychological benefits. Some problems are associated with intense and stressful sport activity, however, and some symptoms appear in normal sport conditions as well. For example, youth who are categorized as elite-level participants and are involved in intense competitive activity have a higher potential for burnout than do those who participate on a less competitive basis.[65] [69] Much of the literature has discussed burnout as stemming from chronic stress, which still has a valid position in the etiology of burnout. An additional perspective that has developed is that burnout is more likely when an athlete feels entrapped by sport. This occurs when athletes do not really want to participate in sport but feel they have to.[171] It has been found that 73% of children drop out of sports programs by the age of 13 years, with a portion of this attributed to burnout. At age 8 or 9 years, a child may have hockey practice at 5 AM two or three times per week, followed by a full day of school and

then, sometimes, another sport after school. Some children adapt to these stressful schedules, but symptoms of burnout develop in others. Some of the symptoms of burnout are emotional and physical exhaustion, withdrawn or depressed mood, irritability, poor behavior, decreased pleasure in sport, back pain, and migraine headaches.[144] Parents need guidance in these cases to help them accept their child for who he or she is and not to force unreasonable expectations on them. Several criticisms related to specific problems in the normal psychological development of youngsters have been leveled against competitive sports programs for young athletes. Certain maladies are brought about by the undue pressure and emotional stress placed on children by over-zealous adult leaders and the extreme emphasis placed by adults on winning. These stressors can cause unhealthy competitive attitudes that can result in serious interpersonally antisocial behavior.[32] [47] [135] [143] [196] When youngsters are threatened with elimination or are left out of play, [227] they often respond with negative stressed states of anxiety and with increased physical strain.[174] These few examples alone re-emphasize the need for parents, coaches, and sport practitioners to understand the psychological aspects of sport involvement and its implications for children and youth. Pressures: Parent, Coach, and Peer

Youth participation in sports, in some instances, may produce detrimental results. Some of the most striking negative effects result from pressures placed on the athlete by parents, coaches, and peers. These pressures frequently coalesce to form a fourth negative psychological influence, the effects of the entire sporting organization on the potentially positive learning experiences inherent in games and sports. In light of the fact that organized sports have been around for a long time, for example, Little League baseball, which was organized in 1936 in Williamsport, Pennsylvania,

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an entire generation of youth have participated in sports without a great deal of psychological support and knowledge. Three pressuresparents, coaches, and peersseem to exert a dynamic influence on the psychological health of young athletes. In a variety of sports, several investigators, including Loy and associates,[129] Greendorfer and Lewko,[81] Snyder and Spreitzer, [199] and Higginson,[97] found that the impact of parent, coach, and peer pressure changed across a child's athletic life span. The predominant socializing influence in the early years of both male and female athletes was the parents. Later, the major socializing agents shifted to peers, coaches, and teachers as parents assumed a less influential role. As major socializing agents, these three groups can be sources of dysfunction as a result of many types of pressures placed on athletes. Parents.

Parents influence their children's attitudes and values. Children's attitudes toward such values as the importance of winning are fixed by 10 to 12 years of age. [164] Furthermore, these values change little after 10 to 12 years of age. Parents have the greatest influence on the young athlete during these early years of life, and it is logical to conclude that parental influence is the most important factor in shaping these values in the child athlete. Therefore, parental influence is a long-term determinant of values. When parents make negative comments to their children or behave in a fashion that results in their being banned from attending events, this would not lead to healthy values and attitudes. Incidents such as a father who trips an opposing player in an under-12-year-olds' rugby game[66] or shouts to his son your father could hit better than that hardly shapes the kind of sportsmanship we desire of our children. Whereas extreme parental behavior is relatively rare in children's sport, negative comments are unfortunately not rare. In one study of parental comments,[111] 34.5% of parental comments were negative, 47.2% positive, and 18.4% neutral. Rugby and soccer showed the highest number of negative comments (45.6% and 40.0%, respectively). The most typical negative comment is correcting (26.8%), such as keep your elbows up, use your feet and watch the ball. Scolding comments, which are the most hurtful, were the second most common (5.3%), comments such as hit hard or you'll be walking home . . . don't sit on your bottom, get up. One can see that this degree of negativity is too high to create a sufficiently supportive environment for children participating in sport. Parents who believe that winning is everything and primary to team building and friendships are likely to contribute to this negativity and contribute to the psychological harm of the children. These actions can produce a negative reaction by the child to the point of the child's avoiding activity and refusing to participate in the sport. When the families of successful athletes are studied, supportive parents are usually found. McClelland[145] and Sears[188] observed that parents who encouraged, joked, made suggestions, and generally supported their child's performance appeared to motivate their children to perform better while positively affecting character development. Children of relaxed, supportive parents were more self-confident, honest, and mature. Balazo[8] found that in 24 female Olympic athletes, both parents were highly support ive of the athlete's efforts from an early age, indicating the importance of family unity. Snyder and Spreitzer[197] found that sport-centered practices supported by the entire family were predictive of both male and female athletic participation in competitive sports. As Devereux[48] commented, a parent who puts the accomplishments of the child before everything else does a grave disservice to the parent, the sport, and especially the child. Coach.

As an athlete continues to mature, the most significant socializing pressure ceases to be the parent and becomes the coach. The coach's influence is not so much on the development of attitudes toward winning and participation but on the player's self-esteem and self-perception. The coaching techniques used by the coach are crucial factors in the way an individual player views himself or herself in the sport and ultimately

in society.[190] Coaching techniques are multifaceted behaviors that are difficult to classify and examine. One of the primary mechanisms by which coaches go about teaching the techniques of a given sport is the use of positive and negative reinforcements. These reinforcements provide feedback to the player on the efficacy of his or her athletic performance. They are also used to shape and develop desired behaviors within and outside sports contexts. When used unwisely, these reinforcements can produce negative, debilitating outcomes that impede the progress and performance of a given athlete.[190] Reinforcement is a broad concept, however. Smith and associates [194] developed a group of categories, the Coaching Behavior Assessment System, to qualify and study coaching behaviors. Included among these categories are reinforcement, nonreinforcement, encouragement, technical instruction in both general and mistake-contingent contexts, punishments, punitive technical instructions, organization, and others. Not only is it important to identify the specific coaching behaviors, it is also essential to understand the effects of these behaviors. Smith and colleagues [194] found that there were important age differences in the athletes' reaction to coaching behaviors. The youngest children paid attention predominantly to variations of negative behavior, children of intermediate ages responded to positive and supportive behaviors, and senior athletes responded to technically instructional and organizational behaviors. In addition, a positive relationship was found between technical instructions, including encouragement in both general and mistake-contingent contexts, and the positive attitudes of players toward the coach. Punishment and punitive technical instructions were associated with negative feelings toward the coach. Although positive or negative feelings toward the coach may not be the most essential factor in sports, it is valid to state that most athletes respond better in any situation if they have positive rather than negative feelings toward the coach. What is ultimately of greatest importance is the athlete's self-concept and self-esteem. Smith and Smoll[195] found that children who were low in self-esteem responded most positively to coaches who were reinforcing and encouraging and most negatively to coaches who were low on this supportiveness dimension. Sinclair and Vealey[190] found that gains in self-confidence were highly associated with immediate feedback provided by coaches. Furthermore, athletes for whom coaches had high expectations were given more immediate feedback than were athletes from whom little

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or no performance was expected. Anshel and Hoosima[6] additionally found that performance stability was more consistent when athletes were exposed to positive rather than negative feedback. Athletes feel good about themselves and perform well when feedback from the coach is immediate and supportive.

Peers.

Because of the nature of sports activity, athletes experience social relationships that are complex. For example, the athlete must both compete and cooperate with teammates at various times and in various ways. On the one hand, an athlete may find that he or she feels more integrated into a team if several friendships are fostered within the team. On the other hand, the outstanding athlete may rise above the athletic performances of his or her peers, and this can create jealousy and resentment, even loneliness. The choice of whether to pursue an outstanding level of performance may be largely dependent on the interplay between the athlete's need to achieve personal recognition and the need for social acceptance. The successful athlete may find that he or she must reject friends to become outstanding among his or her peers. The average athlete may find the social gratification of friendship more rewarding than the infrequent rewards of success. Even the gifted athlete may desire the social rewards more at times and may judiciously lose from time to time to thwart the jealousy of his or her friends. These peer pressures or stressors express themselves through overt observable behaviors.[97] Members of athletic teams tend to like one another more when they are experiencing success. A successful season makes members more likely to do things together outside the context of sports. As a consequence of this friendliness among team members, there may be reluctance to criticize teammates for poor performance, or athletes may adjust their style of play to convey friendship behaviors. This team bonding brings about a unique and sometimes difficult-to-identify quality, that of group cohesion, a team's feeling a oneness that is a positive experience yet at the same time a personal stressor, especially in its development and maintenance. Cohesion essentially reflects the reason that groups of people form and stay together. Group cohesion can best be understood by looking at certain variables. These variables may be divided into categories, such as the personalities and needs of individual members, individual abilities, group size, and the task at hand. In addition, there are dynamic qualities that vary over time, such as the feelings of group success and failure, the stresses imposed by the group on each individual, the clarity and acceptability of group goals, and the type and quality of the leadership. Factors such as homogeneity of the group favor cohesion.[58] High coach or player turnover tends to reduce group cohesion.[61] A group cohesive quality is identified by such behaviors as the ability of individuals on the team to anticipate each other's movements and the timing of one member's actions to maximize another's actions.[36] Group cohesion has been shown to be easier to achieve in winning teams, whereas losing tends to destroy team cohesion.[7] [165] Findings indicate that regardless of whatever individual qualities each team member brings to the task, the quality of the group as a whole, that cohesive quality, is the most important factor in team success. Overall, peer and group interactions are complex and multifaceted components that influence the individual personally, socially, and athletically and also influence the team as a whole. These pressures from parents, coaches, and peers are all stressors, but they become detrimental or negative only if they are overzealously applied. In addition, Devereux[47] points out that these pressures frequently coalesce into an organized sports

environment that can suppress the normal learning experiences that informal game playing can provide. Devereux believes that today's game culture has lost these crucial developmental experiences owing to excessive adult supervision and control. Devereux believes that important educational experiences fostered by play and games are eliminated by rigid and organized sport activities. Children's games and play activities represent miniature safe models of a wide variety of cultural and social situations and concerns. Children can experiment with different personal styles and can more easily practice anxiety management in less rigid experiences.[166] The famed Jean Piaget [167] noted that social rules to developing children originally appear to be part of an external situation that is defined and reinforced by powerful adults. In the early stages of development, children attempt to avoid punishment and maintain the good will of their parents through obedience to these rules, and they do so especially in the rigid context of formal game. Informal games and play with peers offer a unique opportunity for young people to internalize social rules and formulate their own personal guidelines. Parsons and Bales[159] theorized that when an equality of power is perceived by the child as existing between the athlete and his or her peers, the perception allows the child to develop social relationships guided by relative universalistic principles and rules that are observed equally by all participants. What rigid, formal, and organized sports have done is to remove the social opportunities for incidental learning that occur through spontaneous, self-organized, and self-regulated children's games. Whether parents push too hard or not hard enough, whether parents create appropriate values, whether the coach fosters a positive self-esteem or destroys it, whether the athlete's peers participate constructively or destructively, and whether the child has enough informal game playing experiences to facilitate social growth may not be things that practitioners can control or even observe. Nevertheless, knowledge of these psychological effects can allow the practitioner perhaps to intervene, helping young athletes to cope with problems that have become burden-some and negatively stressful. Winning and Losing

Green Bay Packers coach Vincent Lombardi once said winning isn't everything, it's the only thing. This statement typifies a societal value. Leonard[122] pointed out that many scholars believe that a society's basic social structure is characterized by its sports and games. Today, we are witnessing the end of a social structure based on honor and a movement toward one of winning above all else. Competition need not be detrimental if it is put in proper perspective: Like a little salt, it adds zest to the game and

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life itself. But competition produces more losers than winners. Losing can become a habit and can therefore affect self-worth and self-esteem, especially if winning is valued above all else. Losing is an undesirable state to be in, a state of stress, of disequilibriuman unhealthy state. Many parents do not appear to question the impact of the winning above all value on a

child's development because this value is often imparted indirectly and appears to be a cultural norm in American society. Competition and the importance of winning are taught to children at a young age.[164] As stated earlier in this chapter, it is the parents who have the greatest influence on their children in the early years of athletic development. This is the time in which youngsters' attitudes toward participation and winning in competition begin to take form. Piaget stated that competitive behavior begins about the time youngsters start to understand the rules that govern winning and losing, to perceive success and failure, and to compare their efforts with others'. Piaget believed that this development begins around 4 to 5 years of age. In support of these hypotheses, Greenberg[80] found that children younger than 3 years showed no competitive behavior, whereas by the age of 5 years, 10% of surveyed youngsters exhibited some type of competitive response. The findings seem to indicate that competitive behavior is a learned characteristic.[80] Competitive behavior in youngsters has subsequently been characterized as (1) the ability to conceptualize something worth striving for, (2) the realization that the self has an opportunity to acquire that something, and (3) the realization that another individual is also striving to acquire the same goal. White[219] explored competitive development from another perspective. In the early stages, children begin to explore their environment, learning autonomy by relying on themselves as individuals. Subsequently, they pay increasing attention to the acquisition and mastery of motor skills, fostering self-esteem and assertiveness. After the mastery of skills, children begin to impersonate adult behaviors, bringing about knowledge of power roles and their perceived importance in competition and winning. Finally, in the later stages, peer groups begin to take on an increasing degree of importance. Evaluations of performance in competitive situations from both peers and oneself serve to reinforce competitive behaviors positively or negatively. A positive evaluation encourages the development of a competitive mindset, open to feedback and growth, whereas negative evaluations tend to enforce a passive attitude, reducing the exposure. Scanlan[184] noted that with continuous positive evaluations, a child becomes an evaluation seeker, continually displaying behavior that can be considered competitive. Coaches are involved in the development of winning or losing attitudes. Chaumeton and Duda[32] found significant variations among coaching behaviors in competitive environments. Winning had increased significance for coaches with higher levels of competition, reinforcing the competitive attitudes already established by the young athlete's parents early in life. Competition, the increased significance of winning, and the development of winning or losing attitudes affect young people in many ways. In general, the more important winning is, the greater the chance that a loss will be attributed to something or someone other than the individual.[175] In addition, members of successful teams attribute winning to more controllable and stable factors compared with unsuccessful groups. Individuals who evaluate their accomplishments of a task, regardless of the outcome, with more positive attitudes tend generally to perform better than do individuals who evaluate outcomes with a negative bias.[89] The fun of participation can bring about a positive effect that in turn potentiates self-evaluation with a positive attitude, thus bringing about better performance.[214] Hardy and Silva[91] found that athletes who are tense, frustrated, apprehensive, submissive, and humble are more fearful of the consequences of success than are those who are relaxed, self-assured, assertive, venturesome, and

controlled. Guilt, with all of its negative feelings and stressors, naturally follows for the athlete who feels the essential importance of winning and the practical effects of a loss. This situation can leave a young person feeling helpless and unduly stressed. Winning is not everything! The feeling that winning is a desired goal, to be attained at all costs, can be detrimental. As Burke and Kleiber[21] pointed out, it is more constructive to promote cooperation through the forming and main taining of children's self-made games. Competition, winning, and losing are real-life events, and young people need opportunities to experience these normal happenings. What may be most essential and fruitful is to allow children to learn from the experience and to minimize the potential harm. Injury

Despite an estimated 3.3 million injuries that occur every year, minimal investigation has been done on the psychology of athletic injury.[114] This fact again highlights the desperate need for research and treatment strategies aimed at addressing the psychological implications that may accompany athletic injury. The psychology of athletic injury must be examined from two perspectives. On the one hand, there is evidence that a psychological predisposition to athletic injury may exist, and this should be dealt with if the opportunity for diagnosis occurs. On the other hand, an athlete who has a debilitating injury can undergo psychophysiologic responses that untreated can impair or prevent successful rehabilitation and re-entry into sports. A line of research has investigated the relationship between stress and injury. Holmes and Rahe[99] found that individuals with high life stress, which is defined generally as a life filled with major changes, seem to be at greater risk for disease than individuals with low levels of stress. Patterson and colleagues[163] studied psychosocial factors as predictors of injuries in ballet dancers with a mean age of 26.23 years (SD = 4.14). What they found was that major life stressors were predictive of injuries but in dancers who were also low in social support. Dancers who were high in social support did not have a significant correlation between negative life events and injuries. Individuals with high life stress may exhibit a response that brings about increased general muscle tension leading to rapid muscle fatigue, narrowing of the visual field that

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does not allow the individual to attend to the stimuli necessary to avoid athletic injury, and heightened distractibility that demands more attention to extraneous stimuli. These stress responses can be modified by many factors: the social support in one's life, one's cognitive appraisal of the demands of the task, the resources at hand, and the consequences of the task achievement. The individual's personality, such as his or her competitive trait anxiety or achievement motivation, can also influence the response. The individual's history of stress, including life stressors, daily hassles, and previous injury stressors, additionally influences the response. Finally, the individual's coping

resources, such as support systems and stress management skills, have a bearing on this stress reaction. If the practitioner believes that a particular athlete is at high risk for psychosocially mediated sports injury, a number of interventions can be used to prevent injurious outcomes. Through such interventions as relaxation skills, imagery, and desensitization, to name a few, the psychological implications can be managed. Some of these techniques are discussed later in this chapter. Most psychological treatments that are implemented are usually of the postinjury type. The timing is primarily due to the tendency to seek assistance only after an injury or disease has occurred. The practitioner may find opportunities for prevention by intervention in the social support area through families, friends, and community resources. In many cases, the psychological symptoms did not result in the injury but were the result of the injury. Little[126] found that 72.5% of athletes with neuroses experienced some sort of physical illness or injury before the development of their psychological symptoms, whereas only 10.9% of nonathletes experienced similar maladies. Furthermore, despite the finding that the athletic population was more extroverted and vigorous than nonathletes, the prognosis for recovery from injury among athletes was much poorer than that among nonathletes. Little concluded that a preoccupation with fitness and sports placed the athlete in a vulnerable position that predisposed him or her to neuroses as a result of mandatory exercise deprivation. Smith and colleagues[192] examined the presence, type, magnitude, and time course of the emotional responses that occurred throughout the entire injury process from onset to return to participation in sports. With use of an Emotional Response to Injury Questionnaire and the Profile of Mood States evaluation, levels of frustration, depression, and anger were studied. Denial was found to be absent, and global mood disturbances were found. The severity of the injury, the perception of recovery, and the loss of athletic fulfillment were found to be the probable bases for the mood disturbances. In contrast to Smith's results, Weiss and Troxel[216] found that disbelief, rage, depression, tension, fatigue, and somatic complaints were commonly associated with injury. Chan and Grossman[31] found elevated levels of depression, anxiety, and confusion and lower self-esteem in prevented runners. In addition, Morgan[149] found that prevented runners scored higher on a negative mood scale of depression, tension, and confusion than did continuing runners. Morgan attributed this to loss of a coping strategy for those who used physical exertion as a stress management technique. Although none of these studies was conducted with elite athletes, knowledge of these emotional responses after injury in athletes provides the practitioner with some understanding of why certain athletes choose to resume physical activity or sport contrary to the recommendations of their coaches and physicians. [50] These athletes may find that coping with the physical discomfort of the injury is easier than coping with the emotional discomfort experienced in the absence of exercise. Nonetheless, the emotional response to injury is influenced by many personality factors, history of stressors, predisposing psychological influences, and normal coping skills. Tunks and Bellissimo[209] organized normal coping skills into three categories: (1) the

appraisal-focused coping strategy, in which the athlete attempts to understand and find meaning in a crisis; (2) the problem-focused strategy, in which the athlete confronts the reality of a crisis by dealing with the tangible consequences through constructing a more gratifying situation; and (3) the emotion-focused strategy, in which the athlete aims to cope with the feelings brought about by the crisis and to maintain an effective balance. Carmen and colleagues[27] and Pierce[168] noted that noninjured athletes seem to prefer physical exertion to verbalization as a normal means of coping with stress. Scanlan and associates[185] found that 23% of the elite figure skaters they interviewed believed that skating was an adequate means of coping with stressors. The development of neuroses in athletes after an injury may be due to deprivation of a perceived normal method of coping.[126] [127] Wiese and Weiss[220] proposed a four-stage model of injury rehabilitation. The first stage is simply the state of recognition, the actual injury that is a stressor itself. Second, the athlete appraises the situation that caused the injury. The injury may be ascribed to such things as self, equipment failure, opponents or teammates, the inherent risk of the sport, or a coaching error. The injury may also be appraised with regard to its severity and impact on the athlete's future goals. These factors influence the emotional response, which is the third stage. This stage may influence such factors as the immune response, which can be counter-productive to the healing process. The psychological (coping techniques) and physiologic consequences of injury finally follow in the last stage. Injury is important in the life of an athlete. Thus, the prevention and care of injuries must bring together every possible resource available to hasten the participants' re-entry into athletics. This care must address the psychological implications because neglect of these factors can slow recovery and increase the likelihood of recurrence. Performance Anxiety

Anxiety is frequently defined as an emotional state consisting of feelings such as worry, apprehension, nervousness, and tension combined with an arousal of the autonomic nervous system.[201] Anxiety is an unpleasant reaction; if persistent, it can lead to such stress-related disorders as insomnia and headaches.[202] Chronically high levels of anxiety can interfere with the performance and enjoyment of almost any aspect of sports participation.[137]

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Although anxiety reactions occur infrequently in youth sports, there is a need to address the problem. There is a belief that performance anxiety is ultimately related to perceptions of competence and motives for participation in sports. Harter [94] [95] proposed a theory about anxiety, expanding on former thoughts. Competence motivation theory suggests that

individuals possess an innate desire to feel and express competence and control in any achievement-oriented situation. A positive result is associated with successful mastery of a particular experience. This positive response or mastery results in reinforcement of the competence motive. An athlete who perceives the lack of requisite competence for mastery or the lack of adequate situational control experiences a negative effect, which takes the form of performance anxiety. This performance anxiety weakens the competence motive and feelings of competence. Anxiety is a complex phenomenon, and despite much study in the past few decades, it is a condition that still defies clear understanding and treatment. Conceptualization and measurement of anxiety have been enormously aided and advanced by Spielberger's study,[200] which divides the general anxiety response into two types: state anxiety (A-state), which designates an individual's reaction to a perceived situational threat; and trait anxiety (A-trait), which is related to personal anxiety characteristics that remain constant throughout many different situations. Building on these thoughts and theories, a growing body of anxiety research specifically related to sports has developed in the form of competitive trait anxiety and competitive state anxiety. [200] Competitive trait anxiety is a construct that describes individual differences in the tendency to perceive competitive situations as threatening. [137] High levels of competitive trait anxiety occur when athletes perceive that they do not have the basic requisites needed for success in the competitive task. In one study, boys who experienced frequent physical competitive trait anxiety symptoms were found to have lower self-esteem, felt greater upset after a poor performance, and preferred to avoid sport competition and the anxiety related to possible negative results.[123] Cognitive competitive trait anxiety symptoms were more likely to occur in the presence of perceptions of parental or coach shame and upset, greater negative adult evaluation, and conditions of general parental pressure. It was found by Lewthwaite and Scanlan[123] that individuals with high competitive trait anxiety tended to avoid stress-inducing events. The second division of general anxiety in the sport context is competitive state anxiety. Davidson and Schwartz[43] and Liebert and Morris[124] used a multidimensional view of state anxiety that separated the mental or cognitive component from the physical or somatic part. The cognitive component of state anxiety was defined by negative thoughts, difficulty with concentration, and disbursed attention, whereas the physical component encompassed strong body signs of anxiety such as autonomic arousal. Cues to somatic state anxiety are thought to be of short duration and include conditioned responses to environmental stimuli, such as the locker room, the stadium, or the fans. These cues many times remain unchanged throughout a season, and therefore somatic anxiety shows a characteristic and consistent pattern before competition; anxiety rises as competition draws near, peaks as competition begins, and then rapidly falls off after the onset of competition.[23] Cognitive state anxiety is believed to arise when personal expectations of success become negative. This type of anxiety accounts for the worry athletes experience several days before competition. This worry remains constant up to and during competition unless changes in expectations occur. Research has consistently shown an inverted U relationship between performance and

general state anxiety. The inverted U hypothesis states that for any given task, optimal performance is achieved at some intermediate level of anxiety. Thus, performance is predicted to be poor at low levels of anxiety, good at moderate levels of anxiety, and poor again at high levels of anxiety. When an athlete goes into such a high level of anxiety that performance is hindered, anecdotal evidence suggests that small reductions in anxiety do not bring the athlete back into a state of optimal performance. [93] Therefore, the prevention and management of anxiety before it reaches a critical point are desirable. The following section deals with management of performance anxiety together with other sports psychology management issues.

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Management Techniques

Although research on management techniques in sports for youth is limited, the management of sport-related issues from a psychological standpoint demands that serious consideration be given to developmental issues. Understanding of development includes physical, intellectual, social, and psychological perspectives. Although both developmental issues and management techniques are briefly addressed in this chapter, it is suggested that a more thorough review of these subjects be undertaken by the reader, using references given at the end of the chapter. With regard to management techniques, the most basic, simple, and easy methods are usually the most effective. Common sense is, in addition, an excellent guide. If basic nonintrusive techniques and common sense do not have an observable effect, expert advice is readily available. The following suggested management aids are a few of the many that exist and are meant to be only examples of possible approaches. Many of these aids overlap and can be used with individuals or with groups or teams to deal with motivation and fun, performance anxiety, pressures (parent, coach, and peer), team organization, winning and losing, and injuries. Management techniques can be divided into several categories. First, recognizing and dealing with stress while facilitating concentration and control require relaxation, anxiety management, and attention control techniques. Second, techniques helpful in improving practice and activating an athlete include imagery, motivation, and the psych-up pep talk. Third, young people need positive attitudes and definite objectives to potentiate success. This can be accomplished through the techniques of goal setting, self-esteem and confidence building, and reward and reinforce ment. Last, many general issues need to be addressed, such as persistence, toughness and aggression, and competition

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and cooperation. Injury, burnout, and dropping out are areas of concern, but suggested interventions for these involve all of the preceding techniques. Expert counseling should be sought if basic techniques and common sense fail. Dealing with Stress, Anxiety, and Control

The most effective management techniques are those that are basic and simple because they are generally needed by athletes at one point or another. The following techniques can usually be incorporated into the athlete's repertoire of skills fairly easily. Stress Anticipation, Stress Management, and Relaxation Techniques

Simply stated, the practitioner of sports medicine can do many things to lessen stress and reduce uncertainty through answering any questions the athlete may have about stressors or management techniques, removing hazards that may produce anxiety (such as poor equipment), eliminating surprise, avoiding humiliation, being consistent, letting the athlete know that the contributions he or she makes are a valuable asset to the team, diminishing the importance of the activity for the athlete by diminishing the vital importance of winning without displaying disinterest, and downplaying or eliminating practice or recognition awards and elite groups. All of these may be avenues for consideration.[138] In addition, it is important to work with the parents of the athlete as well. Family dynamics and unrealistic expectations can be great sources of stress for the pediatric athlete. Educating parents about realistic goals and expectations can be a valuable technique for reducing the athlete's stress. Anticipating stress before an athletic event means that one does the job of worrying before the event. Anticipation can prove to be one of the most useful stress management techniques if the athlete understands the physiologic and cognitive components of the stressor and can effectively use techniques to control the impact. Effective techniques include cognitively going through the details of the athletic experience, practicing feedback, increasing real situational awareness, and shifting control from external to internal cues.[71] The first step toward managing stress is recognition by the athlete that she or he is experiencing stress. Symptoms can be observed physiologically, psychologically, or behaviorally. Physiologic symptoms include increased heart rate, sweating, increased respiration, pupil dilation, increased muscle tension, cotton mouth, and frequent urination. Psychological changes include worry, feelings of being overwhelmed, inability to make decisions, confusion, inability to concentrate, out of control feelings, and feeling different. Behavioral manifestations of stress may be rapid talking, nail biting, foot tapping, pacing, scowling, increased blinking, yawning, trembling, or a broken voice.[138] The physiologic symptoms of stress result from in creased somatic arousal. As such, one of the most beneficial ways of managing stress is through the use of relaxation techniques that target the body's sympathetic nervous system. The simplest of these techniques is diaphragmatic breathing. In this technique, the athlete focuses his or her attention on breathing. The athlete then concentrates on using the muscles of the

diaphragm, rather than the muscles of the chest, to pull in deep, slow, rhythmic breaths. Progressive muscle relaxation is another technique commonly used for relaxation. This technique involves the systematic tension and relaxation of muscle groups. Biofeedback is also available for relaxation training. A practitioner trained in biofeedback uses electronic equipment to measure such processes as respiration, heart rate, muscle tension, and temperature. The athlete then practices relaxation techniques, such as those described, while receiving feedback about these processes. Many of the psychological changes associated with stress are mediated by negative self-talk. This is what the athlete is saying to himself or herself about a given situation. The athlete's negative self-talk may include predictions, such as I'll never be able to make this shot, or labels, such as I'm no good. Elimination of negative self-talk and thought-stopping is a viable approach in the management of cognitive stress.[138] In managing this self-talk, it is important first to monitor and become aware of negative self-talk. Once the athlete is successful in doing this, techniques such as thought-stopping or disputing negative thoughts become important. For example, when the athlete experiences the negative thought I'll never be able to make this shot, he or she can replace this negative thought with the disputation That is not true. I have practiced very hard and I have made this shot before. Like the physical and cognitive response to stress, the behavioral response also requires monitoring. Some behaviors may exacerbate an already stressful situation. Stress and Anxiety Management

Whereas the techniques described in the preceding section can help the athlete manage stress, they can also help the athlete maintain the optimal level of anxiety discussed earlier in this chapter. An athlete can experience detrimental levels of anxiety in either the somatic or cognitive area or in both areas. In the area of sport psychology, research indicates that somatic anxiety and cognitive anxiety should be considered separate entities that require different intervention strategies. [24] Further, research indicates that a moderate level of somatic anxiety facilitates performance, whereas even small levels of cognitive anxiety can hinder performance.[139] As such, it appears that cognitive anxiety should be addressed with every athlete, whereas somatic anxiety should be addressed with those athletes who report experiencing detrimental levels of somatic anxiety. For those athletes experiencing more intense anxiety, one helpful technique for controlling anxiety is stress inoculation training.[133] The three-phase technique is made up of five to seven sessions, each approximately 45 minutes in duration. The first contact with the athlete is an educational one in which the athlete is given information about stress, how stress occurs, and the relationship between

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stress and performance. The participant is encouraged to describe his or her feelings

and experiences during any period of the athletic performance. Each session that follows this initial encounter teaches the athlete how to relax progressively, rehearse mentally, visualize anxiety-provoking situations, and make positive self-remarks. In these sessions, the athlete cognitively experiences situations that provoke increasing anxiety. An intentional attempt is made to intensify subsequent encounters. Thus, through simulated experiences, the athlete develops the ability to cope with his or her anxiety. The three phases of stress inoculation are the education phase, in which the athlete learns about the impairment; the rehearsal phase, in which the athlete learns to use coping skills appropriate to the particular problem and to develop coping self-statements, visualizations, and mental exercises; and the last phase, in which the athlete has an opportunity to practice these coping skills in gradually more stressful situations. Such interventions are normally best accomplished with the guidance of a skilled behavioral scientist. Attention Control

The ability to concentrate and to prevent inappropriate distractions is essential for an athlete. Attention can be impaired by arousal levels that are too high or too low. If an athlete is too highly aroused, he or she may disregard relevant situational and performance cues. If an athlete is too low in arousal, he or she may pay attention to irrelevant cues. Loss of attention control is recognized by the loss of the normal ability to focus or attend. Other signs may include increased muscle tension; changes in breathing; twitching movements in or around the face; increased jaw muscle tension; and extraneous behaviors, such as yawning, stretching, laughing, or crying. Positive impacts of attention control have been documented. For example, children in one study were told to place themselves in a bubble, cocoon, or chrysalis, depending on age, while playing tennis.[60] They were then instructed to leave irrelevant cues, such as self-doubts, noises, and negative comments, outside, while relevant cues were let inside. Experimental subjects experienced continued improvement in concentration skills throughout the program, compared with control subjects. Furthermore, the children in the experimental group experienced dramatic improvement in their tennis performance compared with that of the control subjects. To facilitate attention control, it is important to understand that there are two different attentional dimensions, width (broad and narrow) and direction (internal and external). Different tasks involve different attentional demands and thus should be approached with the correct attentional perspective. For example, a basketball player may need to cultivate a broad external focus of attention during regular play but then shift to a narrow external focus of attention when attempting a free throw. It is important for the athlete to know when to use the appropriate attentional perspective and to be able to identify task-relevant and task-irrelevant cues.[154] It is also important not to overload the athlete with information. One or two pieces of constructive advice, spoken slowly, provide structure and clear direction. For example, asking the athlete to repeat what has been verbalized and making eye contact enable the athlete to focus on listening. During a performance, encouraging the athlete to focus his or her attention on a few specific critical cues, such as a location in the arena, gives some structure. It is important that

the athlete not focus on motor tasks that have become automatic through practice, however; this can actually inhibit the smooth execution of the task. Repeating attention cue words or phrases that remind the athlete of the proper attentional focus for a given situation may be helpful as well.[173] Distracting the athlete from the event during breaks reduces possible anxiety that may be the result of ongoing attention control problems. Most of all, reassuring the athlete that his or her feelings are normal and that they will pass is extremely beneficial.[153] The centering procedure is a training exercise that can be practiced physically and mentally and is especially effective in gaining attention control. The procedure is more complex than other procedures, but after a few practice sessions, it can become incorporated into a repertoire of behaviors that is available to the athlete should concentration become a problem during performance. [153] Practice and Activation

To prepare for a performance and to psych up for the actual event, mental exercises such as the following are effective. Imagery

Imagery is cognitively experiencing a situation in the absence of external stimuli. In other words, imagery simulates a real-life experience through mental exercise.[138] It involves the mental visualization of a task before or while engaging in the task and helps athletes practice motor skills, rehearse strategies, and acquire psychological dexterity. Imagery can be used in two different situations, either in precompetition practice or in conjunction with competition. As a learning aid in practice, athletes mentally picture themselves performing a task in a specific setting. For example, a basketball player may spend 20 minutes each day mentally practicing a free throw. As an aid during ongoing competition, either immediately before or during a contest, this basketball player may visualize a successful free throw before attempting the shot. Research in this area indicates that athletes are more likely to use imagery in conjunction with competition rather than as a learning aid in practice.[86] [182] Athletes who use imagery both before and during a competition, however, are taking maximal advantage of this performance-facilitating technique. The positive performance-enhancing effects of imagery have been shown in a number of studies looking at various sports, including basketball,[170] [206] soccer,[182] skating,[177] and track and field.[210] The performance-depleting effects of negative imagery, such as visualizing a negative performance, have also been documented.[140] [151] Individuals will differ in their ability to produce mental images. As with any skill, however, this can be improved with practice. Even for those individuals with strong imagery skills, most important to success with imagery is accurate

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and systematic practice of the technique. It is important to practice the technique initially in a quiet setting, while as relaxed as possible. Mental accuracy, even with the use of

guided instruction or videotape, can be beneficial. Combining imagery with self-modeling may also increase the effectiveness of imagery.[206] By videotaping and viewing his or her successful performance, an athlete may be better able to develop a highly vivid image for use in mental practice. The use of sight, sound, touch, smell, and taste stimulation also intensifies sensory awareness and the vividness of the experience.[138] A facilitator or practitioner can aid in the development of this technique. Motivation, Activation, and Psych-Up

Motivating an athlete requires an understanding of the individual and a knowledge of the techniques that are most effective in certain situations. Motivation is an interactive process between the motivator and the athlete. Some athletes are intrinsically motivated, whereas others are extrinsically motivated. In almost all cases, positive reinforcement accomplished by catching the athlete doing something right and reinforcing the behavior through praise or encouragement motivates and activates the athlete. Reinforcement should be given as soon as possible after the event and should be as clear and specific as possible. It should be given continually during the initial learning phases and intermittently once skill has been developed to maximize the effect. Positive reinforcement should not be given for undesirable behaviors, and punishment should be avoided if possible. The practitioner should control the sport environment to reduce stress and chaos while exciting, arousing, or activating the athlete. Generally most exciting for an athlete is goal setting. Athletes are automatically motivated when they are involved in setting goals for practice or performance. Sport practitioners can psych up athletes through the pep talk. The purpose of such an experience is to motivate athletes. The pep talk is no more than a last-minute effort to maximize psychological and physiologic readiness. The best motivation is guidance, direction, support, and excitation of the athlete throughout preparation in a constant and devoted manner, even during times when results are not optimal.[26] Building Positive Attitudes and Objectives for Success

When success occurs, self-esteem is enhanced and the athlete grows psychologically. Success is potentiated through techniques of goal setting, confidence building, and as stated before, reinforcement. Goal Setting

The satisfaction generated by collaborative team goal setting in sports cannot be understated. Studies support the idea that young people are capable of setting performance standards and that they will use these standards to evaluate their performance.[100] This is particularly true if long-term goals are reduced to a series of achievable, intermediate, and short-term goals. Two types of goals, product and process, can be used. Product goals define an end

result to be achieved through performance of the athletic task, whereas process goals define the steps in the performance that the participant will take in preparing for or actually performing the task. These goals should specify measurable milestones that are achievable, realistic, and worthwhile to the performer. The availability of feedback is necessary to provide a means of evaluating progress. Most important, the athlete must accept and be committed to the defined goals for the process to work.[92] Use of this technique will help the practitioner to circumvent the onset or development of burnout and performance anxiety as well as to facilitate a sense of accomplishment. Self-esteem and Confidence Building

Self-confidence is always enhanced when an athlete has realistic expectations about achieving success, not necessarily when the athlete believes that he or she will win. Self-confidence is based on a person's feelings of self-worth and self-esteem. Athletes who feel successful become more self-confident, gain greater self-esteem, and feel more worthy, making them more motivated. On the other hand, athletes who experience initial failure become insecure and feel less worthy. A mistake does not destroy a self-confident athlete, but insecure athletes fear the anxiety brought on by a mistake or failure so intensely that they are easily intimidated and act timidly, increasing the possibility of failure. A spiraling exposure ensues from negative expectations to failure to insecurity to further negative expectations, failure, and more insecurity. Self-fulfilling prophecies need not be negative. Positive yet realistic expectations can potentiate positive results. Affirmation techniques, such as I can, I will statements, can be used to encourage athletes. These statements aid in the self-affirmation that athletes may need to form a stable basis for self-esteem. Self-affirmation can generate self-confidence. Wholesome self-confidence in athletes is also facilitated through learning the techniques and tactics of the sport well. In addition, positive feedback about the athlete's self-worth apart from the sport is affirming and generally aids in the overall resultconfidence. [138] Reward and Reinforcement

Although reinforcement and reward are addressed earlier in the chapter, the division between intrinsic and extrinsic rewards is briefly addressed here. If an athlete performs to feel delight or joy, he or she is seeking intrinsic or internal rewards. On the other hand, if an athlete performs to gain recognition and rewards from others, she or he needs extrinsic and external reinforcements. It is only when an athlete perceives success and reinforcement that the athlete will feel fulfilled and have fun.[26] It is helpful to identify the reinforcements that appear to be best for each young athlete. It is the immediate and personal feedback, however, rather than the external

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rewards of status or winning, that conveys the quality that is of primary importance to

young athletesthe growth of self-esteem and self-worth.[26] Individual and Group Issues

Unique and sometimes conflicting issues exist in athletics, such as the need to be tough in an environment that encourages aggressive behavior and the need to compete and cooperate at the same time. Toughness and Aggression

Great athletes are thought to have a strong will to win. The will to survive and the need to be tough at all times are present in all living organisms. Sport participation may be similar to life in that many athletes describe sport involvement as survival, persistence, total concentration, commitment, motivation,[26] and even aggression.[51] A number of factors may heighten the probability of an aggressive act. These factors include an unfit player, a player with a hostile group of spectators, a losing team, a loss by a close score, the competition between two teams that are close in rank or standing, the competition between teams that are different (racially, ethnically, or politically), a competitive situation that has a history of hostility, and an aggressive act by one individual that goes undisciplined or brings about an unfair advantage.[39] Recognizing these factors and dealing with them before an aggressive act occurs teach discipline and good sportsmanship to young athletes. In attempting to understand and manage aggression, it is necessary to determine which athletes are likely to be aggressive in competition, to ascertain the requirements of the sport and the content of the behavior that constitutes excessive aggression, to predict situations that are likely to cause team aggression, and to be able to calm an overly aggressive athlete or the team as a whole. Some guidelines for managing aggression in sport have been suggested and are summarized by Anshel. [5] For example, teaching athletes to cope with failure and abusive treatment, discouraging violent behavior during the game in pregame talks, providing positive reinforcement to athletes who control their temper, and ensuring that parents reinforce to the athlete to play within the rules and with minimal or no hostility are techniques that may reduce the likelihood of aggressive acts. Another technique for reducing aggression between teams is to encourage interaction among opposing teams. If the opposing team is seen as a respected opponent rather than as a feared enemy, aggression may be reduced.[38] Competition and Cooperation

Competitive and cooperative behaviors are present in practice as well as in actual performance situations and may bring about anxiety that can be self-defeating. It is important to note individual differences in practice situations before competition. Helping athletes to realize appropriate sportsman-like values and attitudes toward success is usually more easily accomplished than demanding competitive behavior from them in a nondestructive cooperative manner.

If the stress aroused during intersquad competition becomes too great, it is important to direct the athlete to an unstructured fun program during a particular practice. If the stress of a forthcoming competition is inordinate, it will help to lessen the threat of losing, to encourage the athlete to see the rivals in human terms, or to try to put the forthcoming competition into a proper gamesman-like perspective.[39] Above all, it is essential to develop not only competitive athletes for sport activity but also cooperative citizens for a future society. Injury, Burnout, and Counseling

If the sample strategies given earlier, including counseling as an alternative, are used by leaders in youth sports, they will have a positive impact on the problems of injury burnout, and dropout. In addition, education of parents is important in the prevention and treatment of burnout. Research has consistently shown that the important aspects of sport for the child athlete are having fun and learning new skills. For example, one study with 822 youth sport participants found that the excitement of the sport and improving one's skills were rated most important, whereas winning the game was consistently rated least important.[213] Adults place great emphasis on winning, however. In doing so, they place a great deal of pressure on the child athlete, which may result in burnout. This seems to be supported by a review of related literature conducted by Gould,[75] which found that the primary reason for the young athlete's quitting was an overemphasis on winning. Focusing on the child's strengths, encouraging the child after failure, and allowing breaks from sport are important in the prevention and treatment of burnout. If these techniques, as well as those discussed previously, are implemented, sporting activities will be a joy, a pleasure, and a growing experience for children and adolescents.

MD Consult L.L.C. http://www.mdconsult.com 396.html/top"> /das/book/view/29309971/1103/396.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Conclusion

Educational philosophers and leaders such as Socrates, Aristotle, Comenius, John Locke, and John Dewey advocated play and sporting activity as an important educational experience for children. As Lawther states, children's physical activity and sport loses much of its meaningful pleasure, educational and recreational value, mental health value, and skill-attainment value if it becomes an obligation, without joy or fun. Our job is to ensure that the value of fun endures and that the benefits are experienced by children and youth today and always.[203]

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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Section G Overuse Injuries in the Skeletally Immature Athlete Carl L. Stanitski MD Overuse injuries are caused by unresolved submaximal stress in previously normal tissues. The first reported sports overuse injury was a pediatric onelittle leaguer's elbowwhich was believed to be caused by excessive baseball throwing.[1] All sports require repetitive motion, and increased musculoskeletal stress is common among young athletes.[2] [23] [34] Training intensity, training duration, and competition levels have been increased at younger ages, and athletes commonly go directly from one sport season to the next or participate in prolonged seasons without respite. Intense activity at sports camps imposes additional musculoskeletal system overload. For some young athletes, life becomes a year-round cycle of focused training and competition. Nonosseous Stress Disorders

Mechanical stress is essential for normal connective tissue homeostasis. [12] [34] [39] In the upper and lower extremities, a baseline of tensile, compressive, and rotational forces is needed for maintenance of normal soft tissue and bone formation, growth, and remodeling. The specific minimal activity necessary for such growth and maturation is unknown. Limited data exist about musculoskeletal exercise tolerance in skeletally immature humans and laboratory animals. Previous laboratory evaluations of soft tissue and bone stress were largely acute test-to-failure models following a single maximum load, most commonly given with tension and performed at nonfunctional rates of loading in mature animal models (e.g., canines, lapins, rodents). In contrast, most sports produce cyclic submaximal stresses with an occasional acute maximal load in an unpredictable direction. Stress injuries are an extension of physiologic adaptation that occurs in response to

training stimuli. Repetitive excessive rates or magnitudes of loading, with inadequate time for resolution of these stress effects, lead to injury. Time compression is seen with training demands in a setting in which peers, parents, and coaches insist on and encourage efforts that at that time are too much or too soon, or both, in the unconditioned or unprepared athlete. Soft tissues and bone act as heterotopic, viscoelastic mechanical units whose properties, highly determined by collagen, depend on the rate and direction of the applied load. Superimposed on the sports demands are the adaptation requirements of growth. In rapidly growing children, whose rate of bony growth outstrips their rate of soft tissue adaptation, diminished flexibility is commonly seen, along with deficits in strength and endurance; the resultant enhanced stresses at various musculoskeletal junctional sites act as foci for symptoms. These junctional problems occur at bone-muscle, muscle-tendon, tendon-bone, or ligament-bone interfaces ( Fig. 17G-1 ) and are clinically recognized as the Osgood-Schlatter condition, Sever's apophysitis[32] ( Fig. 17G-2 ), and little leaguer's elbow ( Fig. 17G-3 ).[29] Young athletes are not all equally prepared for sports demands. Natural selection based on sports interest and ability occurs at about age 9 to 10 years. Children with genetically limited kinesthetic sense feel like motor morons because their bodies simply will not do what is requested of them during sports. [8] Much emphasis is placed on sports that require eye-hand coordination. Unfortunately, many children are not as adroit at this type of coordination but have excellent foot-foot, hand-hand, or hand-foot coordination. These children should be encouraged to pursue sports in which they can make use of these skills (e.g., soccer, swimming, wrestling, or dance). A transient period of uncoordination is commonly seen during the adolescent growth spurt, a time during which intensification of sports interests and demands occurs. Fortunately, this dyscoordination does pass, and a more normal motor capability returns. In boys and girls with exaggerated growth, several years may pass before they feel that they have grown into their bodies. Because of ungainliness coupled with limited speed, strength, and endurance, the adolescent is awkward at sports, and overuse may result from his or her limited sports skills. Children commonly feel that they must engage in sports because of peer or parental pressures, even though they have neither the psyche nor the soma for sports activities. If sports participation is an important part of their social scheme, these less-than-willing (and able) participants (whom I call atheloids) are prone to injury during athletic

Figure 17-G-1 Symptomatic medial malleolar ossification center in a 10-year-old hockey player.

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Figure 17-G-2 Radiographs of calcanei of a symptomatic 10-year-old soccer player. Calcaneal apophyseal fragmentation is normal and not pathognomonic of Sever's condition.

activities. These children need to be guided into sports that are appropriate for them, often the more nontraditional ones. If these children are forced to continue in the standard sports menu, overuse injuries commonly occur, resulting in a lifelong disdain for any type of athletic activity. Musculoskeletal fitness is a goal, not an event. Fitness occurs through adaptation of the biological system to graduated stresses ( Fig. 17G-4 ). Until the system adapts to one level of stress, it cannot respond appropriately if higher demands are placed on it. Overuse symptoms and injury occur in the overloaded unit. Overuse injury occurrence is bimodal. Injuries are most common among underused participants, that is, the ones who are previously unfit or partially conditioned and are placed in demand situations (e.g., preseason football or cross-country training). Musculoskeletal stresses in these settings are usually limited by fatigue and by minimal cardiopulmonary reserve. The second most common injury peak occurs in the extremely fit athlete who, through adaptation, is close to the innate breakdown boundary of his or her system. Tissue reserve is depleted as efforts are focused to obtain the final bit of adaptation. If symptoms do not cause discontinuance of the activity, tissue failure occurs and a complete stress condition becomes manifest. Diagnosis

Most overuse injuries are diagnosed by clinical examination, with a focus on determining the factor or factors that produced the injury. These factors fall into two broad categories. Intrinsic factors include the patient's genetic composite of body habitus, alignment, coordination, and response to training stress. Extrinsic factors encompass training regimen, equipment, sports venue (e.g., field, mats, floor), and sports technique demands. The clinical history must include an assessment of these factors. Overuse injuries usually cause a mechanical type of pain, one that increases with activity and diminishes with rest. I characterize this pain as being one of three levels: Level I occurs with strenuous sports activity; level II happens with limited sports activity; and level III is associated with routine, nonsports daily activity. Previous injury and treatment must be considered for determination of patient compliance with treatment programs; this gives one a sense of patient commitment. Inappropriately sized balls, racket grips or excessive string tension, swimming hand paddles, and gymnastic dowel grips, as well as inappropriately supervised strength training equipment and inadequate footwear, are common sources of overuse injuries ( Fig. 17G-5 ). Uneven running

Figure 17-G-3 Radiographs of a 30-year-old man who was a high-level pitcher/shcatcher from the ages of 9 to 22 years. Tricompartmental degenerative joint disease is present. A, Maximum extension. B, Maximum flexion. (Courtesy of Greg Houser, MD.)

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Figure 17-G-4 Relationship between training effort, conditioning response, and tissue tolerance. Note the inverse relationship between the latter two factors.

surfaces, rigid gymnasium floors, and floor mats that are too firm or too soft also generate unfriendly forces. Incorrectly performed sport-specific techniques cause excessive stresses. In young athletes, whose enthusiasm often greatly surpasses their technical skills, incorrect throwing, jumping, or running motions are sources of excessive submaximal forces. As sports tasks become more complex to accommodate the improved sports skills (e.g., gymnastics training intensifies), such increased demands may overwhelm a system that easily withstood lesser stresses. Abnormal anatomic alignment due to a fixed or dynamic deformity adds stress to the active site. Congenital or developmental conditions such as tarsal coalition or cavus feet can predispose the athlete to injury ( Fig. 17G-6 ).[16] [26]

Figure 17-G-5 Soccer ball size is appropriate for the age group involved.

The factor that most often contributes to the development of overuse injury is the training program itself. In uncontrolled athletic systems such as free play, acute injuries occur, but stress injuries are rare. It is only when parental, peer, and coaching pressures result in unreasonable demands that overload occurs. During the clinical examination, one must look for rapid changes of frequency, intensity, magnitude, and duration of the workout, to greater than 10% that of the previous week ( Table 17G-1 ). Clinical evaluation must include multiple factors in the upper extremities, spine, and lower extremities. Lower extremity alignment is checked for excessive ligamentous laxity and angular, rotational, and longitudinal deformities ( Fig. 17G-7 ). Joint range of motion is compared with that of the contralateral normal side. Normal range of motion may not be adequate for specific sports demands, such as those of gymnastics or dance. Focal tenderness, swelling, and warmth are common findings in various -itises (e.g., tendinitis, bursitis, apophysitis), as well as with stress fractures. Routine radiographic findings are usually normal and at times misleading. Technetium bone scanning and magnetic resonance imaging (MRI) are more sensitive than routine radiographs for stress fracture definition. Single photon emission computed tomographic (SPECT) scintigraphy is useful in determining radiographic image-negative spondylolysis.[4] Ultrasonography is useful in the diagnosis of tendinopathies such as jumper's knee. Treatment

Treatment for overuse problems consists of five phases that are not isolated but are

often concurrent. Phase one involves identification of overuse factors. Phase two is

Shoes

TABLE 17-G-1 -- Running Injury Analysis: Six Ss Wear status or pattern

Surface

Uneven topography

Speed

Too much, too soon

Stretching Flexibility Strength

Muscle group imbalance

Structure

Anatomic malalignment

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Figure 17-G-6 Clinical photograph (A) and radiograph (B) of rigid symptomatic pes planus due to a calcaneonavicular coalition in an 11-year-old soccer player.

characterized by modification of the offending factor(s), which includes a review of sport-specific mechanics. Communication with the coach expedites this process. Elimination or modification of inappropriate equipment (to a size adequate for the young athlete) may be required. Relative rest requires reduction in the duration, intensity, magnitude, and frequency of training to levels that do not cause symptoms. Providing cross-training and substitution of activities such as swimming and cycling is helpful and allows fitness to be maintained while avoiding the negative effects of disuse and misuse. In phase three, pain control is introduced once the appropriate diagnosis is made. Pain management allows gradual, supervised rehabilitation. Pain control can be attained by means of a variety of physical modalities, such as contrast and nonsteroidal anti-inflammatory medications.

Figure 17-G-7 Miserable malalignment, which may produce symptoms anywhere in the lower extremity.

Phase four is characterized by progression of functional activity, with emphasis on restoration of full flexibility, endurance, and strength. This progressive phase leads to sports-readiness tasks and return to play. Phase five is a maintenance program that is used to prevent recurrence. The value of this phase must be emphasized to the athlete as a means of avoiding new injury and

preventing return of previous injuries ( Table 17G-2 ). A fine line exists between acceptable training loads and ones that produce bony and soft tissue injury. Incidence and prevalence of overuse injuries rival those of acute injuries. The most common etiologic factor in overuse injury is training error. The five-step management plan listed here allows symptom resolution and healing and prevents recurrent injury. Patient, parental, and coach education is a significant component of treatment and focuses on training abuses and the use of improper equipment.

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Bone Stress Disorders

Bone is a viscoelastic, anisotropic material whose properties depend on load magnitude, rate, and direction. Adaptation to mechanical stress is a function of the magnitude, direction, and frequency of the loading cycle, as well as its rate and duration. Bone collagen resists tensile stresses TABLE 17-G-2 -- Overuse Treatment Protocol Identify risk factors Modify offending factors Institute pain control Undertake progressive rehabilitation Continue maintenance Note: Phases are often concurrent (e.g., pain control and rehabilitation).

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better than mineral phase bone, which in turn is more resistant to compressive loads. This complex interplay between gravitational and muscle forces within bone's organic and mineral matrix is reflected in Wolff's law, which states that deforming strain causes mechanically induced bone remodeling (i.e., bone develops a structure that is most suited to resist the forces acting upon it). [9] [12] [34] [39] The specific trigger mechanism, be it physical, chemical, or a combination signal, that causes the conversion of mechanical stresses and strains to a biological response is unknown. Bone homeostasis is related to mechanical and hormonal stimuli. Female athletes are

especially prone to calcium balance disorders because of dietary factors (e.g., weight loss for body image, competitive weight) often associated with eating disorders (e.g., anorexia, bulimia), as well as exercise-induced menstrual irregularities, including secondary amenorrhea leading to osteoporosis, the so-called female triad.[5] [15] [18] [22] [37] Increased endurance training in males lowers testosterone levels, with loss of inhibition of interleukin-6; the result is an increase in both osteoclast production and bone resorption.[37] Bone exists in a soft tissue envelope with muscle forces that generate as well as attenuate bone stress. The effect of repetitive muscle forces has been hypothesized as an etiologic factor in stress fractures ( Table 17G-3 ).[33] Other authors suggest that muscle fatigue reduces the muscle's capability to attenuate loads transmitted to bone, leading to stress injury.[17] Fyhrie and associates[17] suggest that changes in bone strain rate associated with muscle fatigue have a greater impact on stress injury production than does strain magnitude, based on animal and human evaluations. Li and colleagues [24] demonstrated that there is a greater initial osteoclastic than osteoblastic response to increased bone stress. This period of accelerated bone remodeling in response to mechanical loads occurs during the first 2 to 3 weeks of training, resulting in a transient period of diminished bone mass before the appearance of enhanced bone formation in response to exercise. This vulnerable time at 3 weeks is when occurrence of stress fracture is most common.[9] [18] [25] Stress fractures result from abnormal forces in normal bone, in contrast to insufficiency fractures, which happen in abnormal bone. Only three animals are known to sustain stress fractures on a regular basis: racing greyhounds, racehorses, TABLE 17-G-3 -- Muscle Forces Leading to Stress Fracture Increased muscle force + Change of remodeling rate Resorption and rarefaction Focal microfractures Periosteal/cortical/endosteal response (stress fracture) Linear fracture (Stress fracture) Displaced fracture and humans. All three are placed in situations in which repetitive musculoskeletal

demands are made without adequate time between training cycles or competitions to allow resolution of subclinical bone stress injury. The physiologic response of bone during exercise can be considered as a dose-response curve and the outcome as a spectrum in response to the various factors mentioned earlier. A stress reaction of bone reflects bone weakness; it should be considered a first response in those patients whose dose is modified in various ways so that a true stress fracture is not produced but a more diffuse periosteal injury is engendered, which may be symptomatic. If the activity continues unabated, stress fracture production may ensue. Stress fractures were originally described in marching military recruits. The incidence and prevalence of stress fractures in athletic populations are functions of the population studied and the methods of detection used to identify the fracture. Stress fractures usually (>90% of the time) involve the lower extremity. Upper extremity stress fractures occur in throwing athletes, and rib stress fractures are seen in oarsmen and oarswomen. Lumbar spine stress fractures are seen in gymnasts and other athletes who place hyperlordotic stress on their lower backs. In children, age plays a direct role.[13] [34] [38] [40] In an extensive literature review completed in 1988, Yngve[40] found 113 stress fractures reported in children younger than 14 years of age. Multiple sites were cited, with the tibia accounting for about half of the fractures. Children have fewer stress fractures than adolescents, who have fewer fractures than adults. In a review of 368 stress fractures, Orava and Hulkko[27] found that 9% of these injuries occurred in children younger than 15 years old, and 32% were seen in 16- to 19-year-olds, with the tibia being the most commonly fractured bone in both groups. Stanitski et al[34] reviewed 16 exercise-induced stress fractures in 14 patients younger than 16 years old. The tibia was the site of fracture in 11 of the 16 patients. Lower extremity dominance and tibial proclivity were also noted by later authors.[13] [18] Epiphyseal stress injuries have been reported in the radii of gymnasts by Caine and Roy and associates and others.[10] [11] [31] [41] The fractures were directly exercise dose related to the weight-bearing done by the upper extremities, and clinical and radiographic evidence of recovery required up to 3 months following cessation of the initiating activity. Dowel grips, vaulting, soft mats, and tumbling maneuvers were added factors in the production of injury. Diagnosis

Most stress disorders of bone can be detected clinically. Patients complain of mechanical types of pain at varying stages of the exercise cycle. Pain levels should be graded (as noted earlier in the chapter), as done for soft tissue stress injuries. Factors that cause the injury should be identified. Exquisite, focal tenderness and swelling to palpation with associated pain on juxta-articular motion are found on examination. Imaging studies may be confusing in this type of disorder.

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Routine radiographs reflect the duration and magnitude of the process and are normal early in the condition. Bone response to stress can be periosteal, endosteal, or intracortical ( Fig. 17G-8 ). Periosteal reaction is diffuse in stress reactions, especially in the tibia. The periosteal response should not be confused with bone malignancy ( Fig. 17G-9 ). If bone architecture is compromised by a cyst or benign tumor, a stress fracture may occur through this weakened area ( Fig. 17G-10 ). Technetium-99m bone scintigraphy is helpful in the early detection of stress fractures, if questions about the diagnosis remain after clinical and routine radiographic examinations. Although nonspecific, nuclear imaging is sensitive. It documents the site of the injury and may uncover sites of previously unresolved stress fractures and reactions ( Figs. 17G-11 and 17G-12 ). Because resolution of the scintigraphic activity lags 6 to 18 months behind clinical healing, bone scintigraphy is not of value for monitoring healing. MRI is reported to be a sensitive means of early detection of stress injury of bone because periosteal and marrow edema is evident along with a fracture line. Arendt and Griffiths[3] developed a grading system for comparing findings on routine radiographs, bone scan, and MRI sequences. This system is based on the premise that MRI is as sensitive as but more specific than scintigraphy. The grading system considers subtle changes of the bone marrow in cases of stress reactions and stress fractures. These authors define grade I and II changes as low-grade changes that are equivalent to stress reactions. Grades III and IV are high-grade and equal stress fractures. Results derived from any imaging modalities must be clinically correlated before treatment is begun.

Figure 17-G-8 Proximal tibial stress fracture with periosteal and endosteal responses in a 13-year-old cross-country runner.

Figure 17-G-9 Distal femoral stress fracture in a 14-year-old soccer player. The lesion was originally diagnosed as an osteosarcoma.

Differential diagnoses of exercise-induced stress disorders include compartment syndrome, tendinitis, bursitis, and muscle tear or herniation. The term shin splints is nonspecific and should be discarded. Treatment

Treatment of stress fractures should follow the general guidelines outlined earlier for treatment of nonbone injuries, especially identification of the factor(s) causing the stress disorder. The vast majority of fractures will resolve with activity modification for 2 to 3 weeks. A gradual return of function is needed so that recurrence is avoided. Dickson and Kichline,[14] as well as Swenson and associates,[35] advocate the use of a pneumatic leg brace for nontension-type tibial and fibular stress fracture management. Rapid return to full sports activity with complete fracture healing was seen in all patients. Stress distribution and force attenuation by the pneumatic layer appear to be the mechanisms of action when this device is used. Most stress fractures (e.g., medial tibia, ribs, radius, second and third metatarsals) are the low-risk type (i.e., ones that heal without difficulty

once the offending activity is removed). High-risk stress fractures, so called because of their propensity for healing difficulty and nonunion, include stress fractures of the midanterior tibia, patella, medial malleolus, talus, tarsal navicular, and fifth metatarsal base.[7] [18] [22] [25] [28] Anterior, midtibial, tension-type stress fractures, especially in children and adolescents involved with jumping sports,

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Figure 17-G-10 Femoral deformity and periosteal and cortical responses from stress fractures through a large nonossifying fibroma in a 13-year-old boy who was symptomatic while playing soccer.

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Figure 17-G-11 Diffuse increased bilateral tibial isotope uptake, indicating a stress reaction in an 18-year-old hockey player who complained of shin splints.

Figure 17-G-12 Increased isotope uptake in both femora of an 18-year-old cross-country runner. She was symptomatic in her left leg and, on further questioning, recalled similar symptoms in her right leg 7 months previously.

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Figure 17-G-13 High-risk, anterior tibial transverse stress fracture in an 18-year-old basket ball player.

can be particularly vexing to treat once they become established with focal fibrosis, necrosis, and minimal activity ( Fig. 17G-13 ). [6] [19] [27] [30] They may require bone grafting and, in cases in which significant bone deformity exists, realignment osteotomy to normalize forces. Tarsal navicular stress fractures require non-weight-bearing, short-leg cast immobilization.[20] [21] [22] [25] [36] Femoral neck stress fractures are rare among children and uncommon in adolescents. They require internal fixation to prevent fracture completion and displacement, particularly in tension types involving the superior femoral neck.

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References Adams RE: Injuries to the throwing arm: A study of traumatic changes in the elbow joints of boy baseball players. Calif Med 102:127-129, 1965. 1.

Adams RE: Little League shoulder osteochondrosis of the proximal humeral epiphysis in boy baseball pitchers. Calif Med 105:22, 1966. 2.

Arendt EA, Griffiths HJ: The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes. Clin Sports Med 16:291-306, 1997. 3.

Bellah RD, Summerville DA, Treves ST, Micheli LJ: Low-back pain in adolescent athletes: Detection of stress injury to the pars interarticularis with SPECT. Radiology 180:509-512, 1991. 4.

Bennell KL, Malcolm SA, Wark JD, Brukner PD: Skeletal effects of menstrual disturbances in athletes. Scand J Med Sci Sports 7:261-273, 1997. 5.

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Blank S: Transverse tibial stress fractures. A special problem. Am J Sports Med 15:597-602, 1987.

Boden BP, Osbahr DC: High-risk stress fractures: Evaluation and treatment. J Am Acad Orthop Surg 8:344-353, 2000. 7.

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Burke BL Jr, McGee DP: Sports deficit disorder. Pediatrics 85:1118, 1990.

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Burr DB: Bone, exercise, and stress fractures. Exerc Sport Sci Rev 25:171-194, 1997.

Caine D, Roy S, Singer KM, Broekhoff J: Stress changes of the distal radial growth plate. A radiographic survey and review of the literature. Am J Sports Med 20:290-298, 1992. 10.

Carter SR, Aldridge MJ, Fitzgerald R, Davies AM: Stress changes of the wrist in adolescent gymnasts. Br J Radiol 61:109-112, 1988. 11.

Chamay A, Tschantz P: Mechanical influences in bone remodeling. Experimental research on Wolff's law. J Biomech 5:173-180, 1972. 12.

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Coady CM, Micheli LJ: Stress fractures in the pediatric athlete. Clin Sports Med 16:225-238, 1997.

Dickson TB Jr, Kichline PD: Functional management of stress fractures in female athletes using a pneumatic leg brace. Am J Sports Med 15:86-89, 1987. 14.

Drinkwater BL, Nilson K, Chestnut CH III, et al: Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med 311:277-281, 1984. 15.

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Elkus RA: Tarsal coalition in the young athlete. Am J Sports Med 14:477-480, 1986.

Fyhrie DP, Milgrom C, Hoshaw SJ, et al: Effect of fatiguing exercise on longitudinal bone strain as related to stress fracture in humans. Ann Biomed Eng 26:660-665, 1998. 17.

Giladi M, Milgrom C, Simkin A, Danon Y: Stress fractures. Identifiable risk factors. Am J Sports Med 19:647-652, 1991. 18.

Green NE, Rogers RA, Lipscomb AB: Nonunions of stress fractures of the tibia. Am J Sports Med 13:171-176, 1985. 19.

Hunter LY: Stress fracture of the tarsal navicular. More frequent than we realize? Am J Sports Med 9:217-219, 1981. 20.

Khan KM, Fuller PJ, Brukner PD, et al: Outcome of conservative and surgical management of navicular stress fracture in athletes. Eighty-six cases proven with computerized tomography. Am J Sports Med 20:657-666, 1992. 21.

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Knapp TP, Garrett WE Jr: Stress fractures: General concepts. Clin Sports Med 16:339-356, 1997.

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Leadbetter WB, Buckwalter JA, Gordon SL: Sports-Induced Inflammation. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1990. 23.

Li GP, Zhang SD, Chen G, et al: Radiographic and histologic analyses of stress fracture in rabbit tibias. Am J Sports Med 13:285-294, 1985. 24.

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McBryde AM, Barfield WR: Stress fractures of the foot and ankle. Foot Ankle Clin 4:881-909, 1999.

O'Neill DB, Micheli LJ: Tarsal coalition. A followup of adolescent athletes. Am J Sports Med 17:544-549, 1989. 26.

Orava S, Hulkko A: Delayed unions and nonunions of stress fractures in athletes. Am J Sports Med 16:378-382, 1988. 27.

Orava S, Karpakka J, Taimela S, et al: Stress fracture of the medial malleolus. J Bone Joint Surg Am 77:362-365, 1995. 28.

Panner HJ: A peculiar affection of the capitellum humeri, resembling Calve-Perthes' disease of the hip. Acta Radiol 8:617, 1927. 29.

Rettig AC, Shelbourne KD, McCarroll JR, et al: The natural history and treatment of delayed union stress fractures of the anterior cortex of the tibia. Am J Sports Med 16:250-255, 1988. 30.

Roy S, Caine D, Singer KM: Stress changes of the distal radial epiphysis in young gymnasts. A report of twenty-one cases and a review of the literature. Am J Sports Med 13:301-308, 1985. 31.

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Sever JW: Apophysitis of the os calcis. N Y Med J 95:1025-1029, 1912.

Stanitski CL, McMaster JH, Scranton PE: On the nature of stress fractures. Am J Sports Med 6:391-396, 1978. 33.

Stanitski CL: Repetitive stress and connective tissue. In Sullivan JA, Grana WA (eds): The Pediatric Athlete. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1988. 34.

Swenson EJ Jr, DeHaven KE, Sebastianelli WJ, et al: The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med 25:322-328, 1997. 35.

Torg JS, Pavlov H, Cooley LH, et al: Stress fractures of the tarsal navicular. A retrospective review of twenty-one cases. J Bone Joint Surg Am 64:700-712, 1982. 36.

Voss LA, Fadale PD, Hulstyn MJ: Exercise-induced loss of bone density in athletes. J Am Acad Orthop Surg 6:349-357, 1998. 37.

Walker RN, Green NE, Spindler KP: Stress fractures in skeletally immature patients. J Pediatr Orthop 16:578-584, 1996. 38.

Wolff J: Concerning the interrelationship between form and function of the individual parts of the organism. Clin Orthop 228:2-11, 1988. 39.

Yngve DA: Stress fractures in the pediatric athlete. In Sullivan JA, Grana WA (eds): The Pediatric Athlete. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1988. 40.

Yong-Hing K, Wedge JH, Bowen CV: Chronic injury to the distal ulnar and radial growth plates in an adolescent gymnast. A case report. J Bone Joint Surg Am 70:1087-1089, 1988. 41.

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Section H Physeal Injuries in Young Athletes Daniel C. Wascher MD Enrico J. Stazzone MD Gerald A. M. Finerman MD Over the past 20 years, a large increase in organized athletic participation by children has been noted. Today, more than 20 million children participate in sports programs outside of school. Approximately 800,000 new coaches are needed each year for these programs. The majority of these coaches are volunteers with little formal training in coaching the young athlete. Although these programs promote fitness and health consciousness among youth, sporting activities also carry inherent risks of injury. In the growing child, excessive force applied to the appendicular skeleton often results in growth plate injuries. Sports trauma remains an important cause of physeal injuries, particularly physeal damage about the knee.[34] [71] Fortunately, a majority of these injuries heal without permanent sequelae; however, accurate recognition and prompt, appropriate treatment are required to minimize complications. The first description of physeal injuries may well date back to the time of Hippocrates. Poland[62] published an extensive review of growth plate injuries in 1898 that included an early classification system. With the advent of roentgenograms in the late 19th century, physicians were able to diagnose physeal injuries more easily. Over the past 25 years, our understanding of physeal anatomy and biomechanics has improved and a variety of newer classification systems have been developed. This information has led to improved recognition and treatment of these injuries. When growth arrest follows trauma to the physis, the surgeon can now employ a variety of techniques to correct the deformity. In addition to detecting acute traumatic damage to the physis, the physician caring for young athletes must also be aware of chronic injuries to the growth plate. The increased

organized sports participation by youths has led to a rise in the number of overuse injuries. These injuries are caused by excessive training demands placed on the immature musculoskeletal system. The physis is not immune from chronic, repetitive damage, and many examples of physeal stress injuries have been reported over the past few years.[15] [20] [48] [56] Anatomy of the Physis

In the embryo, the limb buds appear at about the fifth week. A condensation of mesenchymal cells in the buds differentiates into a cartilaginous precursor of the long bones. Vascular invasion of this cartilage anlage causes ossification in the central portion, producing the primary ossification center. At various times, the cartilage caps at the ends of bone are invaded by blood vessels, causing formation of secondary ossification centers. A well-organized layer of cartilage separates the primary and secondary ossification centers until late adolescence. This cartilage layer is the physis, which is where the axial and circumferential growth of the bone occurs. Eventually, the physis is penetrated by metaphyseal vascular channels, resulting in ossification of the growth plate and bony fusion of the ossification centers. Various physes close at various ages, but the progression of closure follows an organized, predictable sequence. The growth plate can be divided into several anatomic layers ( Fig. 17H-1 ). Beginning at the top, the epiphysis with its layer of articular hyaline cartilage is the first layer. Beneath this lies the true cartilaginous physis, and below

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Figure 17-H-1 Histologic section of a proximal femur at low power. The physis is a cartilaginous layer lying between the metaphysis and the epiphysis. The wavelike structure of the physis helps to increase its strength against shear stresses.

this lies the metaphyseal bone. The physis is not a flat plane of cartilage. Viewed macroscopically, the physis is a wavelike layer that separates the ossification centers. The nature and complexity of these convolutions vary with the different physes. On a microscopic level, small surface irregularities can be noted along the physeal-metaphyseal junction; these are known as mammillary processes. It is theorized that these major and minor interdigitations help to increase the strength of the physis to shear forces.[9] These interdigitations appear to play a greater role in physeal strength during puberty.[19] Histologically, the growth plate can be divided into several discrete layers[12] [67] (Fig. 17H-2 (Figure Not Available) ). On the epiphyseal end of the physis is a zone of small, isolated chondrocytes. This layer is referred to as the reserve zone. It was previously called the resting zone or the germinal zone; however, these cells are metabolically quite active but proliferate only sporadically. They do not give rise to the columns of

cells seen in the deeper zones of the physis. The cells in the reserve zone are spherical, exist singly with occasional couplets, and are surrounded by an abundant extracellular matrix. The exact function of these cells is unclear; a high lipid body and vacuole content suggests that this layer provides storage for later nutritional requirements. Below the reserve zone lies the proliferative zone. This layer contains the true mother cells that divide, forming palisading columns of chondrocytes. The amount of growth of the physis is equal to the rate of production of new chondrocytes multiplied by the maximum size of the chondrocytes at the bottom of the hypertrophic zone. Cell division occurs, and these cells play a role in matrix production. The bottom layer of the physis is the hypertrophic zone. In this zone, the proliferating chondrocytes become spherical and undergo a fivefold enlargement. The cells in the upper portion of the hypertrophic zone remain metabolically active, but as the cells are pushed farther away from the physeal blood supply, they eventually undergo a process of vacuolization and ultimately cell death. At the bottom of each column of chondrocytes lie empty lacunae. Cell death leads to calcium release from the mitochondria, which probably plays a role in initiation of calcification of the matrix. Some authors refer to the bottom area of this layer as the zone of provisional calcification.[66] Beneath the physis lies the metaphyseal bone. There is a transverse septum of bone adjacent to the physis; then the normal pattern of trabecular metaphyseal bone is encountered. Figure 17-H-2 (Figure Not Available) Schematic drawing illustrating the layers of the physeal plate. The epiphyseal side of the growth plate is at the top of the drawing. (From Brighton CT: Structure and function of the growth plate. Clin Orthop 136:24, 1978.)

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Figure 17-H-3 (Figure Not Available) Histologic section through the peripheral portion of a rodent's growth plate. The ossification groove of Ranvier, the wedge of fibrous tissue at the rim of the physis, is clearly visible. The perichondral ring of Lacroix lies peripheral to the ossification groove and provides mechanical support to the growth plate. (From Rockwood CA, Green DP [eds]. Children's Fractures, 3rd ed. Philadelphia, JB Lippincott, 1991.)

Vascular invasion of the physeal extracellular matrix occurs from the metaphyseal capillary loops, which deliver osteoprogenitor cells. The vascularized, calcified cartilage layer is referred to as the primary spongiosum. Just below this layer, osteoblasts cause endochondral ossification on the calcified cartilage bars; this is the secondary spongiosum. Below this layer, the calcified cartilage and the woven bone initially produced are replaced with lamellar bone. Osteoclasts are seen in this region of remodeling, which takes on the characteristics of trabecular bone. Surrounding the physeal cartilage is a wedge-shaped groove of cells, called the ossification groove of Ranvier[73] (Fig. 17H-3 (Figure Not Available) ). This groove has been shown to contain three cell types that allow circumferential growth of the physis to

occur. An osteoblast-like cell forms the bony portion of the perichondrial ring at the metaphysis, and a chondrocyte-like cell divides to contribute latitudinal growth of the physis. Fibroblast cells in the groove of Ranvier help to anchor the growth plate to the perichondrium of the hyaline cartilage above the growth plate. [30] In addition to the groove of Ranvier, a dense fibrous band encircles the growth plate at the physeal-metaphyseal junction. This band has been labeled the perichondrial ring of Lacroix. This ring is contiguous with the periosteum of the metaphysis and the fibroblasts in the groove of Ranvier. [67] The ring of Lacroix provides mechanical support, acting as a limiting membrane to the physis. Chung and colleagues[19] showed that the perichondrial ring provides much of the resistance to shear forces seen in younger children. As the child matures, the perichondrial ring thins out and plays a smaller role in the strength of the physis. Injury to these peripheral structures can cause formation of peripheral physeal bars.[66]

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Vascularity of the Physis

Each portion of the growth plate has a unique blood supply (Fig. 17H-4 (Figure Not Available) ).[84] The metaphyseal circulation is derived primarily from branches of the nutrient artery. Additional blood supply occurs from perforating vessels from the periosteal arteries. These metaphyseal vessels end in vascular capillary loops just below the base of the cartilaginous zones. No vascular channels cross the bone-cartilage junction; hence, the metaphyseal vessels do not contribute at all to the nutrition of the physeal cartilage cells. The epiphysis is supplied by epiphyseal arteries. The majority of physes are located extracapsularly[6] ; in these physes, arteries penetrate the epiphysis through soft tissue attachments. The proximal radial and the proximal femoral physes are unique, however. These physes are located completely intracapsularly, and they have no soft tissue attachments to the epiphysis. Their epiphyseal vessels arise from soft tissue overlying the metaphysis; these vessels then crawl along the surface of the epiphysis to penetrate it intracapsularly. The proximal femoral and proximal radial epiphyseal vessels are thus at great risk for injury with physeal disruption. Branches of the epiphyseal vessels supply the reserve and the proliferating zones of the physis; Figure 17-H-4 (Figure Not Available) The blood supply to the growth plate can arrive by one of two paths. Most commonly, the vessels enter from soft tissues surrounding the epiphysis (left). When the entire physis is located intracapsularly (right), the vas culature arises from soft tissues overlying the metaphysis; the blood vessel must then travel along the articular surface before penetrating the epiphysis. ( From Dale GG, Harris WR: Prognosis of epiphyseal separation. An experimental study. J Bone Joint Surg Br 40:117, 1958.)

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no vessels pass through the proliferative zone to supply the hypertrophic zone. Hence,

the hypertrophic zone is avascular and relies on diffusion for its nutrition; cell death eventually occurs when the hypertrophic cells become too remote from the physeal vessels. This avascularity also plays an important role in matrix calcification, which results in part from decreased oxygen tension in the lower portion of the hypertrophic zone.[12] The peripheral fibrous structures receive a rich blood supply from perichondrial arteries.[74] The vascular supply of the growth plate has important implications for physeal injuries. Even minor physeal injuries of the proximal femur and the proximal radius can completely disrupt the physeal blood supply, leading to premature closure of the physis and avascular necrosis of the epiphysis. In addition, disruption of the physis that allows communication between the metaphyseal and epiphyseal circulations allows osteoprogenitor cells to enter the physis, resulting in localized or complete growth plate arrest. As is discussed later in this chapter, the vascular damage that occurs at the time of physeal injury is an important predictor of complications.

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Incidence of Physeal Injury

Sports-related injuries in children are relatively common. One recent European study found the incidence of sports injuries in school-age children (ages 6 to 17) to be 73 per 1000 per year.[78] In this study, boys and girls were most often injured in soccer, skateboard, rollerskating, horseback riding, gymnastics, handball, and basketball. By comparison, a recent prospective study in the United States reported the incidence of sports injuries in children to be 49 per 1000 per year.[44] High school students were most often injured in the gym, middle/junior high students on the athletic field, and elementary students on the playground. A number of authors have analyzed the incidence of growth plate injuries[28] [45] [47] [54] [57] [62] [69] ; although the exact numbers vary from study to study, remarkably constant findings are seen. Some general conclusions are readily drawn. Approximately 15% to 30% of injuries to the long bones of children involve the growth plate. Of all physeal injuries that occur in children, 10% are sports related.[51] Soccer, alpine skiing, gymnastics, weightlifting, and baseball are the sports most often associated with physeal injuries. The upper extremities are involved more frequently than the lower extremities by a ratio of 2:1. The distal radial physis is the most commonly injured, accounting for approximately one third of all growth plate injuries. Although this information was not included in early reports, it is now recognized that collectively, the phalangeal physes constitute the second most common site of growth plate injury,[28] [42] [83] followed closely by the distal tibial physis. Physeal disruptions about the knee are rare, constituting only about 2% of all growth plate injuries; however, they represent half of all growth arrests requiring surgical correction. Most studies have found that the incidence of physeal injuries in boys is twice that in girls. This is thought to be secondary to an increased exposure to trauma in young males as well as to a longer period of exposure because physeal closure occurs at a later date in males. Hormonal differences may also cause a qualitatively weaker growth

plate in males during puberty.[55] The peak incidence of injury occurs during the period of rapid growth in early adolescence ( Fig. 17H-5 ). This occurs at about age 11 in girls and at ages 12 to 13 in boys. Again, these peaks result from increased exposure to trauma at this age combined with a weakening of the growth plate during puberty. Peterson and Peterson[62] and Rogers[69] noted in their studies that the distal humeral physis was an exception in that it was associated with an early peak incidence of injury (occurring at ages 4 to 5 in girls and 5 to 8 in boys), as well as the peak seen during adolescence. These authors suggested that the early peak represented complete epiphyseal separation, whereas the adolescent injuries involved predominantly only the medial or lateral epicondyle. It should also be noted that most

Figure 17-H-5 Incidence ratio of acute physeal injuries in females (A) and males (B). Note that boys have an incidence of growth plate fracture that is twice that of girls; the peak incidence for males (ages 12 to 16) also occurs later than that for females (ages 8 to 13). (From Peterson CH, Peterson HA: Analysis of the incidence of injuries to the epiphyseal growth plate. J Trauma 12:279. Copyright Williams & Wilkins, 1972.)

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epidemiologic studies excluded slipped capital femoral epiphyses and vertebral physeal injuries. The physician frequently has difficulty in differentiating traumatic and chronic injuries of the proximal femoral physis. Physeal injuries have been reported in the cervical, thoracic, and lumbar spine, but they appear to be unusual.[41] Athletics is an important cause of physeal injuries in children, accounting for 10% of all physeal injuries. Several studies suggest that sports cause a large proportion of physeal injuries, especially those to the shoulder and elbow in the throwing athlete. Furthermore, the physes around the knee and ankle are often sites of physeal growth injury that may require surgical treatment.[22] [46] [82] In one study, 15 of 23 triplane fractures of the distal tibia occurred during sporting activities. [22] Twenty percent of all distal femoral epiphyseal injuries in one series were related to athletic pursuits.[46] More than half of Salter-Harris III injuries of the medial femoral condyle are reported to be secondary to clipping injuries in football or soccer.[68] [82] Certainly, sports trauma represents a significant source of physeal injury, particularly about the knee, a location prone to physeal bar formation and subsequent growth deformity.

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Mechanisms of Injury

A variety of forces, both acute and chronic, can result in physeal injury. The most common form of injury results from acute mechanical overload. The cartilaginous physis represents the weakest biomechanical link in the growth plate. [72] This physis is most susceptible to shear forces. Bright and colleagues[11] showed that the physis exhibits viscoelastic properties, requiring higher loads before failure occurs with increasing rates of load. Bright and associates[11] and others[19] [55] also observed that female physes are stronger than those of their male counterparts. A decrease in physeal strength has been noted at puberty.[55] Chung and colleagues[19] noted the importance of the ring of Ranvier in resisting shear stress in younger children; this role decreased concomitantly with the thinning of the ring seen during puberty. These observations may explain some of the increased incidence of physeal injury noted in pubescent males. Salter and Harris[72] noted that the plane of cleavage in physeal separations almost always occurs between the hypertrophic zone and the metaphyseal bone. The strength of the physis is derived from the extracellular matrix. At the bottom of the hypertrophic zone is a paucity of matrix, and intuitively, one would expect physeal failure at this level. Bright and associates[11] noted cleavage of the physis through this plane, but they also observed short, linear cracks deep within the physis. Subfailure loads of 50% also initiated these cracks (Fig. 17H-6 (Figure Not Available) ). They suggested that the primary failure occurred through these short linear breaks in the deeper layers of the physis along the planes of highest shear stress. With continuing load, a tensile failure occurred, causing a secondary crack along the cleavage plane between the zone of hypertrophy and the metaphysis. The secondary cracks often coalesced with the primary cracks, especially in older animals. With additional load application, rupture of the periosteal sleeve occurred, Figure 17-H-6 (Figure Not Available) Histologic sections through proximal tibial physes of rats subjected to shear loads. A, The typical failure path when the physis is loaded to failure. The majority of the separation occurs between the hypertrophic zone and the metaphyseal bone. B, A physis loaded to 48% of failure energy. A short linear crack (arrow) is seen deep within the physis, where primary failure to

shear stress occurs. (From Bright RW, et al: Epiphyseal-plate cartilage. A biomechanical and histological analysis of failure modes. J Bone Joint Surg Am 56:699, 1974.)

allowing epiphyseal displacement. Using torsional forces, Peltonen and associates [59] observed a pure cleavage plane through the physeal-metaphyseal junction in younger animals. In older animals, however, a more sinuous separation pattern appeared, with the fracture also occurring through metaphyseal bone. In summary, the major cleavage plane in physeal injuries occurs through the zone of hypertrophy. Both clinical experience and animal studies suggest that younger children sustain a greater number of pure physeal separations without bone fractures. Other areas fail also, more frequently in older children, giving rise to varied physeal fracture patterns. Pressure applied perpendicular to the growth plate can have profound effects on physeal function. Arkin and Katz[4] used serial casts to apply pressure to rabbit tibial physes and demonstrated marked angular deformities with relative growth arrest on the side of the physis exposed to increased pressure from the casts. They also observed increased physeal longitudinal growth in rabbit limbs that were kept non-weight-bearing. Slight and even intermittent pressures were shown to slow or hinder physeal growth. Simon[78] found that excessive dynamic loading could decrease physeal growth, but he noted that slight increases in dynamic loading could cause increased growth. Basic science studies on proteoglycan gene expression in the separate layers of

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the bovine calf growth plate have demonstrated increased activity in the reserve and proliferative zone chondrocytes after short-term pulses of static load, confirming that the growth plate does indeed respond to the mechanical stresses to which it is exposed.[81] Short-acting high-energy forces cause metabolic changes in the physeal layers, indicative of permanent growth plate injury.[25] Distal radius growth arrest has been noted in young gymnasts who train excessively. Markolf and colleagues[52] studied the forces generated in gymnasts' wrists and showed that forces almost three times body weight (BW) are applied to the distal radius during pommel horse routines. Loading rates reached 28 BW/sec. This repetitive, rapid, high loading probably produces the physeal changes in the distal radius observed in young gymnasts. Physeal damage also results from nonmechanical causes. Children with frostbite have been noted to have premature physeal closure[73] ; this effect results from both ischemia and thermal damage. Stark and associates[80] showed that 7 hours of warm ischemia causes severe damage to the central region of the physis; 12 hours of warm ischemia leads to infarction. Infection due to metaphyseal hematogenous osteomyelitis or open physeal injuries often causes growth arrest.[60] A stable environment must be maintained for continued physeal growth to be ensured. Iatrogenic physeal arrest has also been demonstrated. Epiphysiodesis has been used as a surgical procedure to correct limb length discrepancies. Siffert [77] showed that staples bridging the physis caused permanent growth arrest of the physis. Large or threaded wires crossing the physis have been reported to cause growth arrest. Makela

and colleagues[49] demonstrated that destruction of only 7% of the cross-sectional area of the growth plate caused permanent growth disturbances. When internal fixation is required for physeal injuries, the surgeon should use thin, smooth wires and avoid fixation that crosses the physeal cartilage, if possible.[9] [72]

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Classification of Physeal Injuries

Many classification schemes for physeal injuries have been proposed. [1] [18] [23] [63] [64] [72] Foucher[23] in 1860 was the first to propose a system for classifying physeal injuries. Poland[63] in 1898 proposed four types of epiphyseal injuries. His types I to III are identical to the types I to III used today in the Salter-Harris system. Poland's type IV was an intercondylar T-type fracture. Aitken[1] and later Weber[86] categorized physeal injuries based on the presence or absence of intra-articular extension. Pollen[64] describes three groups: fracture separation of the epiphysis, transepiphyseal fractures, and crushing injuries of the growth plate. Today in North America, the most commonly used classification system is the Salter-Harris system[72] ( Fig. 17H-7 ). Types I to IV of this system are similar to the types listed in the previous classification systems. The Salter-Harris classification is based on the pathoanatomy of the fractures, which is readily apparent from radiographic studies. This feature facilitates communication between physicians when physeal injuries are discussed. Salter-Harris type I injuries involve a purely transphyseal separation with no visible osseous fracture lines. If the periosteal sleeve remains intact, there may be very little displacement. These injuries are more commonly seen in younger children and in rachitic patients. Type II fractures comprise a transphyseal separation with an extension through the metaphysis on the compression side of the bone. This metaphyseal fragment, which remains attached to the epiphysis, is referred to as the Thurston Holland sign. The size of the metaphyseal piece can be quite variable. The intact periosteal sleeve on the compression side usually facilitates closed reduction. Type II injuries are by far the most common type of physeal injury.[62] [69] Salter-Harris type III injuries involve a partial separation through the physis with extension of the fracture line through the epiphysis and exiting out of the joint surface. This injury is uncommon and is usually found around the knee joint or at the distal tibial

physis. Anatomic reduction of the fracture fragment is necessary to restore a smooth articular surface. A type IV Salter-Harris injury is a fracture that extends from the joint surface through the epiphysis and physis, exiting through metaphyseal bone. This injury is most commonly seen about the lateral humeral condyle and the medial malleolus. Anatomic reduction is necessary to restore joint congruity and to prevent metaphyseal-epiphyseal bony bridging. Salter-Harris type V injuries involve a crush injury of the epiphyseal plate. Radiographs at the time of injury often appear normal. This diagnosis is usually made retrospectively after growth arrest has occurred following compression injury to a physis. Some authors doubt the existence of this injury[61] ; most agree that it occurs but is rare. Distal radial physeal growth disturbances from chronic stresses seen in young gymnasts probably represent a variant of the type V injury.[15] [70] Rang[66] later added a type VI to the Salter-Harris classification. This injury involves damage to a portion of the perichondrial ring. Minimal damage occurs to the true physis, but a bony bridge can develop across the peripheral site of injury, resulting in angular deformity of the physis. Ogden[58] proposed a classification system that subdivides the Salter-Harris groups and adds three additional paraphyseal injury types. With 20 different categories, this system appears overly complex for routine use in practice. The Salter-Harris classification system was originally intended to serve as a prognostic indicator for the chances of subsequent growth arrest. The authors stated that types I, II, and III had an excellent prognosis for continued physeal function because the blood supply to the injured physis remained intact. Type IV injuries were thought to have a poor prognosis if they were not anatomically reduced because of the communication of the metaphyseal and epiphyseal circulations and subsequent bony bridge formation. Type V injuries were considered to have the worst prognosis because microscopic bony bridges formed through the crushed physis, causing growth disturbance. Many studies have subsequently found a poor correlation between Salter-Harris type and subsequent development of physeal bars.[9] [18] [46] [60] This discrepancy arises from the failure of the Salter-Harris classification to take into account macroscopic or microscopic physeal vascular damage

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Figure 17-H-7 The Salter-Harris classification of physeal injuries is the most commonly used system in North America. Rang added type VI (perichondral ring injuries) to the initial scheme. (From Rang M: The Growth Plate and Its Disorders. Edinburgh, Churchill Livingstone, 1969.) Figure 17-H-8 (Figure Not Available) Shapiro's pathophysiologic classification of growth plate injuries. Type B injuries, which result in communication between the epiphyseal and metaphyseal circulations, have the potential to produce physeal bars and subsequent growth disturbances. (From Shapiro F:

Epiphyseal growth plate fracture-separations. A pathophysiologic approach. Orthopedics 5:721, 1982. )

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at the time of injury. For example, even type II radial head fractures cause a high incidence of growth arrest and avascular necrosis because of the precarious epiphyseal blood supply. Additionally, as has been shown in the experimental work of Bright and colleagues,[11] physeal separation is usually not a pure cleavage through the hypertrophic zone. Other cracks and fissuring occur in the physis that can lead to the formation of bony bridges, even in type I and II injuries. Shapiro[76] has proposed a pathophysiologic classification scheme to be superimposed on the Salter-Harris system (Fig. 17H-8 (Figure Not Available) ). In Shapiro's approach, type A injuries have an intact epiphyseal vascularity with no communication between the epiphyseal and metaphyseal circulations. Type B injuries have intact epiphyseal vessels, but communication exists between the epiphyseal and metaphyseal systems. Type B1 injuries result from gross displacement (i.e., Salter-Harris type IV); type B2 injuries result from microscopic or macroscopic crushing or fissuring of the physis. Type C injuries have disrupted epiphyseal circulation with subsequent death of the growth plate cartilage. This system helps to explain the poor correlation of Salter-Harris type with eventual outcome, but it remains difficult for clinicians to identify type B2 injuries prospectively. Currently, we continue to use the Salter-Harris classification. It is an anatomic classification, and identification can easily be made from roentgenograms. Although it does not accurately predict the incidence of subsequent growth plate arrest, the Salter-Harris system does help in treatment planning. The pathophysiologic approach of Shapiro accurately emphasizes that vascular injury is the best predictor of potential growth plate damage; however, until better diagnostic techniques for studying the microcirculation in physeal injuries become available, it will have only limited value.

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Assessment Patient History and Physical Examination

An injury at the end of a long bone in any child should be suspected of being a physeal injury. Likewise, a joint dislocation or ligament injury in any young athlete should be considered to be a physeal injury unless proven otherwise. The physeal plate is by far the weakest structure around the joint in growing children; physeal injuries are far more common than dislocations and ligament tears in this age group. A history should be obtained in an attempt to elicit the mechanism of the injury. For example, distal femoral physeal injuries are commonly caused by clipping injuries in football.[68] The possibility of child abuse also should always be kept in mind. Physical examination should include a careful examination of the entire injured extremity; patients with injuries resulting from high-energy trauma should have a complete examination to rule out visceral injury. Bilateral physeal injuries have been reported.[53] In children with physeal trauma, pain and swelling are almost invariably present. Deformity is often present but may be slight if the fracture is minimally displaced. Crepitus may be absent in patients with pure physeal separations. A careful distal neurovascular examination should be performed before any reduction or casting is undertaken. Although physeal injuries about the knee are more common in children than are ligament disruptions, the presence of a physeal separation does not rule out concomitant ligament injury. Bertin and Goble[5] reported a series of 29 patients with physeal injuries about the knee. At follow-up examination, 14 (48%) had evidence of ligament instability about the knee. Eleven of the fourteen had anterior cruciate ligament (ACL) laxity, and 5 of the 14 had medial collateral ligament (MCL) laxity of 2+ or greater; two of the patients had combined ACL/MCL instability patterns. Of note, 11 patients in this series were injured during athletic activities, and 6 of these showed demonstrable ligamentous instability. In physeal injuries about the knee, the physician must maintain a

high index of suspicion for coexisting ligamentous injury; re-examination after fracture treatment is mandatory, and treatment is dictated by the patient's age, physical demands, and desires. Diagnostic Studies

Radiographic examination is required for every child in whom a growth plate injury is suspected. Plain radiographs in two views are requisite; often oblique views are necessary to demonstrate small metaphyseal fragments in Salter-Harris II injuries[69] ( Fig. 17H-9 ). The presence of normal physeal lines is often confusing. Fractures can mimic physiologic physeal lines and vice versa.[40] The physician should

Figure 17-H-9 Radiograph of a 14-year-old boy who sustained a Salter-Harris type II injury to the proximal humeral physis. The fracture line was not readily visible on other views of the shoulder.

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Figure 17-H-10 This 14-year-old boy sustained a valgus injury to his knee in a football game. Examination revealed marked valgus laxity. The initial radiograph (A) shows only subtle evidence of a growth plate injury. A stress radiograph (B) clearly demonstrates a Salter-Harris type II injury of the distal femur.

not hesitate to obtain comparison views of the contralateral extremity to settle any doubts. If no obvious physeal disruption is seen on initial radiographs and physical examination suggests ligamentous laxity, stress radiographs should be taken to look for occult physeal fractures[68] ( Fig. 17H-10 ). Computed tomographic (CT) scanning has been reported to be helpful in the evaluation of triplane fractures of the distal tibia,[22] but it is not required in the evaluation of most physeal injuries. In fact, the CT scan in triplane fractures is used to assess the joint articular surface injury and not the physeal injury. The triplane fracture only occurs in the distal tibial physis when it has started to close; therefore, future growth disturbance is rare. We are not aware of any reports of magnetic resonance imaging (MRI) for physeal injuries, but MRI may have the potential to provide more detailed information about injury to the growth plate. Likewise, bone scanning is being investigated in children with growth plate trauma,[75] [88] but its usefulness in predicting subsequent physeal arrest remains to be proved. Plain radiographs remain the workhorse for evaluating physeal injuries.

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Treatment of Physeal Injuries

A great majority of physeal injuries in children heal without any significant or clinically important growth disturbance. Significant growth disturbance will occur, however, in approximately 10% of physeal injuries. The treating physician should warn the parents of the possibility of physeal arrest at the time of injury. Follow-up examinations after fracture healing are required to search for any signs of altered physeal growth. Some authors recommend clinical and radiographic follow-up until the child attains skeletal maturity, but this seems excessive. A careful clinical examination combined with attention to radiographic detail will allow detection of almost all cases of growth arrest within 1 year of injury. Hynes and O'Brien[29] pointed out that observation of the Harris growth lines after physeal trauma can provide early evidence of partial physeal arrest. If these growth disturbance lines remain parallel to the physis with longitudinal bone growth, then physeal growth is occurring normally. Almost all Salter-Harris I and II fractures can be treated with closed reduction and immobilization. The intact periosteal hinge on the compression side of the injury prevents overreduction. The manipulation must be done gently. Adequate anesthesia is mandatory; the physician should not hesitate to use general anesthesia if necessary. An imperfect reduction has a great capacity for remodeling in children if the angle of deformity is in the same plane as the angle of joint motion. [9] [72] The younger the child and the greater the contribution of the physis to the overall length of the bone, the greater the capacity for remodeling. For example, in

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proximal humeral fractures, remodeling of almost any residual angulation occurs with excellent final functional results. Occasionally, a flap of periosteum is interposed at the fracture site and blocks reduction.

If success is not obtained after one or two attempts at closed reduction, the physician should not be reluctant to proceed with an open reduction. Excessive closed manipulation can lead to further physeal damage and may increase the potential for growth plate arrest.[71] After open reduction, many Salter-Harris I and II injuries do not require internal fixation. Salter-Harris III and IV physeal injuries require anatomic reduction. [72] [82] Because these are intra-articular fractures, articular congruity is requisite for accurate restoration and fixation of the fracture fragments. In addition, type IV injuries require accurate alignment to prevent the formation of bony bridges between metaphyseal and epiphyseal bone. If these injuries are nondisplaced on all radiographic views, they can be treated with immobilization alone. Some authors believe that all of these injuries should be treated with internal fixation[9] ; however, with close follow-up, any displacement should be readily detected. If any displacement of the fragments is suggested on initial or subsequent radiographs, immediate open reduction and internal fixation should be performed ( Fig. 17H-11 ). The surgeon should use only small-diameter smooth pins for fixing the fracture fragments and should avoid crossing the physis with the pins, if possible. [77] These injuries heal rapidly; fixation does not need to be rigid, but only secure enough to prevent loss of reduction. Because the Salter-Harris III physeal injuries predominantly occur in the older adolescent, these physes have less remaining growth potential and seldom result in significant shortening or angular deformity. The main goal in treatment of these injuries is to anatomically realign the joint surface. This is in contrast to the Salter-Harris I and II physeal injuries that often occur in younger children with several years of growth remaining at the injured physis. Type V and VI injuries are usually impossible to detect on initial presentation. The physician must maintain a high index of suspicion for significant physeal trauma from a compression injury or direct blow. If the physician is concerned about an occult physeal injury, he or she should immobilize the patient and keep him or her non-weight-bearing on the affected extremity. Serial radiographs can be taken to detect the occurrence of any physeal bars. As a rule of thumb, physeal injuries can be expected to heal in half the time of a purely bony injury at the same location.[9] This applies to type I injuries and, if the metaphyseal fragment is small, to type II separations. Thus, if a metaphyseal fracture of the distal radius requires 6 weeks of immobilization, a Salter-Harris type II injury of the distal radial physis will require only 3 weeks of immobilization. Type III and IV injuries will require the same period of immobilization for healing as that needed for nonphyseal injuries in the same location. The decision about when a patient can return to sports is a difficult one. No good guidelines exist, but the patient should have full use of the injured joint and normal strength for several weeks before returning to contact sports. The physician must use discretion and decide each case on an individual basis, using clinical and radiographic information as well as the social factors involved in the child's need to return to athletics.

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Growth Arrest

Bony bars have been seen following all Salter-Harris types of physeal injuries.[60] Based on the studies by Shelton and Canale and Burkhart and Peterson, the risk of proximal tibia physeal arrest was 50% for Salter-Harris type I physeal injuries, 25% for type II, 6% for type III, and 55% for type IV fractures.[32] Growth disturbance is also much more common following open fractures involving the physis. Various authors have reported an incidence of growth disturbance following physeal injuries ranging from 1%[54] to 30%.[31] This discrepancy results from the authors' criteria for growth disturbances. If one uses strict radiographic measurements of limb shortening or angulation, a high incidence of growth arrest is found. Fortunately, a majority of these cases do not require treatment for two reasons. First, the incidence of physeal injury is much higher among adolescents near the end of their skeletal growth period. There is not enough longitudinal growth left in this age group for clinically significant deformities to occur. Second, physeal injuries are much more common in the upper extremity, where small angular deformities or limb length discrepancies are not functional liabilities. Complete growth arrest is unusual following trauma to the growth plate. This usually occurs only in type V compression injuries or in cases of ischemic damage to the physis. Ischemic damage can result from frostbite, from amputation, or from trauma to the vulnerable epiphyseal vessels in the proximal radial or proximal femoral physes. Complete growth arrest is readily detected on plain radiographs. Clinically, these children present with a limb length discrepancy. The long-term functional deficit is dependent on the patient's age and the specific physis involved. Older patients near skeletal maturity have only minor shortening; younger children have a much more noticeable limb length discrepancy. The amount of growth contributed by a particular physis to a bone also plays a role. Complete arrest of the proximal humerus or distal femur results in marked shortening. Likewise, complete physeal arrest in a two-bone unit such as the forearm or calf may cause joint deformities if untreated. There is some evidence that growth is accelerated at the other end of a bone with a complete growth arrest.[60] It is difficult to quantitate the growth potential of this remaining physis, but this

phenomenon must be considered before treatment is undertaken. Patients with partial physeal arrest present clinically with angular deformities or limb shortening ( Fig. 17H-12 ). Again, the age of the patient and the location of the physis play a major role in predicting the long-term effects of the growth arrest. Bright[9] classified partial growth arrest into three types (Fig. 17H-13 (Figure Not Available) ). Type I is a peripheral bony bar. These injuries can cause rapid angular deformity of the involved physis. Type II partial growth arrest is a central bony bridge with a perichondrial ring that is completely intact. Growth of the peripheral plate continues, and a tenting phenomenon occurs with the apex pointing toward the metaphysis. Type III lesions are combination injuries

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Figure 17-H-11 This 15-year-old competitive skier sustained a Salter-Harris type III injury to her right distal femoral physis during a skiing accident. A and B represent anteroposterior and lateral knee radiographs. C and D are preoperative coronal and sagittal plane magnetic resonance images of the injured right knee. E and F are postoperative anteroposterior and lateral radiographs after arthroscopic assisted reduction and percutaneous screw fixation of this intra-articular physeal fracture.

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Figure 17-H-12 This 10-year-old girl sustained a Salter-Harris type IV injury to her left distal tibial physis (A). Despite an anatomic reduction, 1 year later she had developed a peripheral physeal bar and an angular deformity of her left ankle (B).

that are usually associated with Salter-Harris type III or IV fractures. A linear bone bridge occurs along the fracture plane, involving portions of the periphery as well as the central areas. In his series of patients requiring surgery for partial growth arrest, Bright reported that 60% of injuries were type I, 21% were type II, and 19% were type III. A majority of bony bars requiring treatment occur after physeal injuries about the knee.[9] [60] These physes account for most of the growth occurring in their respective bones. Angular deformity about the knee causes marked cosmetic deformity and functional disability. Therefore, although physeal injuries about the knee account for only 3% of physeal injuries, they account for more than 50% of patients requiring operative correction for partial growth arrest. An attempt should be made in all patients with bony bars to assess the complete extent of involvement. Historically, tomograms using thin cuts (1 mm) taken every 3 mm in both the anteroposterior and lateral planes have been used to evaluate bony bars.[16] [60]

Careful evaluation of the tomograms allows the surgeon to construct a map of the physeal bar on graph paper, from which he or she can then estimate the percentage of physeal involvement. In the past, CT scanning was not useful because the irregularity of the physis caused undulations of the physis to be misinterpreted as bony bars. Over the past decade, the quality of CT scan and MRI images has markedly improved so that these modalities are now superior to polytomograms for mapping physeal bars. Furthermore, many institutions no longer have the equipment necessary to do polytomograms. Scanograms should also be obtained to assess the shortening of the involved bone and to get a baseline measurement. Bone age determination is required for the remaining growth potential to be evaluated. Accurate determination of the extent of the physeal bar and assessment of future growth of the physis are mandatory before treatment is undertaken for partial physeal arrest. [33] Treatment of Growth Arrest

The orthopaedic surgeon evaluating a child with growth arrest has a variety of treatment options at his or her disposal. First, it must be remembered that many physeal arrests cause no significant disability. Central physeal bars in adolescents with little growth remaining often do not require treatment. Leg length discrepancies less than 2 cm cause little functional impairment except perhaps a mild compensatory (nonstructural) scoliosis and can be readily treated with a shoe lift.[60] Early angular deformities in adolescents should be treated by arresting the remaining physis if the projected limb length discrepancy is minor. In two-bone units such as the forearm, arrest of the physis of the adjacent bone is also required. Contralateral epiphysiodesis can be performed to prevent any worsening of the limb length discrepancy. These techniques can be combined with angular osteotomies to correct any existing angular deformity. Osteotomy without epiphysiodesis will lead to recurrent angular deformity and the need for future correction. Surgeons prefer to avoid using physeal arrest to prevent limb length discrepancy or angular deformity in the younger child. The overall loss of height and the malproportion of the extremities that result from the previous options make these choices unattractive in preadolescents. In this situation, the surgeon can attempt a bone-lengthening procedure. Osteotomy can correct angular deformities; however, if the physeal bar remains in a younger child, the deformity will recur. Recently, epiphyseal distraction has

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Figure 17-H-13 (Figure Not Available) Bright's classification of partial growth arrest. Type I results from a peripheral bony bar and causes rapid angular deformity. Type II is a central growth arrest that results in limb shortening. Type III partial growth arrests are linear bony bridges that occur after Salter-Harris type III or IV fractures. (From Rockwood CA, Green DP [eds]: Children's Fractures, 3rd ed. Philadelphia, JB Lippincott, 1991.)

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Figure 17-H-14 (Figure Not Available) Technique for excision of central physeal bony bar. A, The bar is approached from a transmetaphyseal exposure; a dental mirror is used for visualization. B, After resection of the bar, only enough cranioplast is inserted in the defect to bridge the physeal gap. C, The remainder of the metaphyseal defect is bone grafted. (From Lovell DD, Winter D: Pediatric Orthopaedics. Philadelphia, JB Lippincott, 1986.)

been used to correct angular deformities, and the correction has been maintained in 77% of patients.[3] The physeal bar should not occupy more than 20% to 30% of the growth plate area; this procedure is more successful in children who are near the end of skeletal growth. During the past 20 years, much progress has been made in surgical resection of physeal bars. Bony bridges should involve less than 50% of the physeal area to be suitable for resection.[13] [36] [37] [60] Type I bars can be approached directly from the periphery; central bars require a transmetaphyseal approach (Fig. 17H-14 (Figure Not Available) ). For the central bar, a cortical window is made in the metaphyseal bone in the appropriate position above the physeal bar. A high-speed burr is then used to tunnel toward the bar and resect the entire bony bar. An arthroscope can then be inserted into the defect that has been created to assess whether growth plate material is now visible circumferentially. Small curets can be used to remove any residual bar that is present. Metallic surgical clips are placed to determine if physeal growth resumes after the physeal bar resection. A generous local fat graft or other interpositional material is placed in the defect, and the cortical window is put back into place. Protected weight-bearing is necessary until the cortical window heals ( Fig. 17H-15 ). If no interpositional material is placed in the defect following bar excision, the bony bridge will re-form rapidly. A variety of interpositional materials have been used; these include autogenous fat,[35] [38] methyl methacrylate,[60] and Silastic material. [10] The reader is referred to the original articles for the details of these materials. No clear guidelines exist regarding the need for removal of foreign interpositional material. Fat has the disadvantage of weakening the bone if a large bar is excised. Silastic is strong but has the disadvantage of being a substance controlled by the Food and Drug Administration (FDA). Methyl methacrylate is strong and provides excellent hemostasis. Cranioplastic does not contain barium and aids in the detection of postoperative bar re-formation. During bar excision, metal markers can be placed within the bone to aid in measuring subsequent growth. Repeat bar formation can be successfully treated by re-excision. After successful bar excision, growth of the bone varies from 0% to 200% of the normal size, with an average of 94%.[60] Some physes, although they resume active growth, appear to undergo physiologic closure at an earlier age than their contralateral physes. Even when complete growth is not achieved, this technique can prevent further deformity or may allow the use of other modalities such as contralateral epiphysiodesis. Experimental work is being done in the area of microvascular growth plate transfer.[7] [8] Successful revascularization in animals requires restoration of both the epiphyseal and metaphyseal circulation; subsequent growth of the physis continues at a rate 85% of normal. Much work remains to be done before this technique is widely used in humans.

Transplantation of chondrocytes into physeal defects is another treatment that is currently being studied for the treatment of growth arrest.[39] [43]

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Stress Injuries of the Growth Plate

In addition to assessing acute physeal injuries in children, the physician caring for young athletes must be aware of chronic stress injuries that can cause physeal damage. As athletes embark on rigorous training programs at younger ages, the number of these injuries is bound to increase. Repetitive stress, particularly a sudden increase in training, can lead to physeal failure with no history of direct trauma. Stress fractures have been reported in runners through the distal femoral and proximal tibial physes[14] [24] [86] (Fig. 17H-16 (Figure Not Available) ). These injuries can be misinterpreted as neoplastic or infectious processes. Careful attention to the history, the detection of localized tenderness over the involved physis, and close scrutiny of the radiographs will lead to the correct diagnosis. Treatment includes avoidance of running activities for 6 weeks followed by a gradually progressive training program. Most young athletes have been able to return to full sports activity 3 months after treatment is initiated. In the upper extremity, unilateral bony overgrowth of the entire arm and associated muscle hypertrophy have been seen in high-caliber tennis players. [65] Dotter[21] was the first to describe physeal injuries to the proximal humerus in baseball pitchers, coining the term Little League shoulder. Other authors have reported similar cases involving pitchers and tennis players.[26] [27] These patients have shoulder pain during throwing activities. Radiographs reveal widening of the proximal humeral physeal plate and adjacent osteoporosis. These are thought to represent a Salter I injury due to repetitive rotational stress. The marked irregularity of the proximal humeral physis prevents severe slippage. Treatment is rest from throwing activities, which leads to prompt resolution of the symptoms. It has been recommended that tennis players wait until the next season before resuming their sport; baseball pitchers are advised

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Figure 17-H-15 Radiographs of a 2 + 7-year-old child with a left distal femur partial physeal arrest and progressive varus knee deformity. A, Preoperative radiograph of the physeal bar. B, Preoperative computed tomography scan of the physeal bar. C, Intraoperative image after curettage of the physeal bar. D, Two-year postoperative radiograph of the left knee, demonstrating recovery of normal physeal growth after bar resection.

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Figure 17-H-16 (Figure Not Available) This 15-year-old long distance runner had gradual onset of right knee pain. He was running 40 to 50 miles per week. Radiographs of the proximal tibia show a small, triangular metaphyseal fragment on the medial tibia typical of a Salter-Harris type II fracture (arrow). This represents a stress fracture of the proximal tibial physis. (From Cahill BR: Stress fracture of the proximal tibial epiphysis: A case report. Am J Sports Med 5:186, 1977.) Figure 17-H-17 (Figure Not Available) Radiographs of a young gymnast's wrist, illustrating stress injury to the distal radial growth plate. Note the widening of the radial margin of the distal radial physis, and the cystic changes and irregularity of the metaphyseal margin. ( From Roy S, Caine D, Singer KM: Stress changes of the distal radial epiphysis in young gymnasts. Am J Sports Med 13:304, 1985.)

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that until physeal closure has occurred, they should play a position other than pitcher. Perhaps the most common physeal stress injury occurs in the distal radius growth plate in gymnasts. Roy and colleagues[70] reported on 21 young, elite gymnasts with wrist pain. Radiographs showed widening of the growth plate with occasional haziness of the physis, cystic changes on the metaphyseal side of the growth plate, and a beaked effect of the distal aspect of the epiphysis on the radial and volar sides pointing toward the physeal plate (Fig. 17H-17 (Figure Not Available) ). They felt that these findings represented stress changes and possibly stress fractures of the distal radial physis. Carter and Aldridge[17] reported similar findings in 21 gymnasts and also noted that the skeletal age of their patients was retarded, which increased the length of time the physis was at risk. Yong-Hing and colleagues[87] found changes on both the distal radial and ulnar growth plates in a gymnast and attributed these changes to a dowel grip worn by the patient during training. Others have noted premature growth arrest of the distal radius in gymnasts,[2] [15] and an acquired Madelung-like deformity has been reported. An average 3-mm positive ulnar variance was found in UCLA male gymnasts, possibly representing premature arrest of the distal radial physis.[50] The positive ulnar variance that results can lead to ulnar impingement and may be the cause of the wrist pain reported by many gymnasts even after skeletal growth has been completed. Although physical activity is felt to be required for normal bone formation and growth, detrimental effects to the physis undoubtedly occur from repetitive, excessive stress. [25] A fine line exists between the beneficial effects of a training regimen and overuse that can cause permanent growth arrest. The exact tolerance of a particular physis in an individual patient is impossible to predict. Education of athletes and coaches can

reverse the trend to play with pain and may lead to early referral of children with suspected physeal injuries. Young athletes involved in strenuous training programs who develop pain at the end of a long bone should undergo radiologic evaluation of the adjacent physes. Any evidence of physeal widening or other abnormality should lead the physician to recommend avoidance of the offending activity for up to 3 months. Alternative exercises can be prescribed to maintain aerobic conditioning and flexibility and to satisfy the patient's desire for physical activity. If the patient remains asymptomatic, he or she can then begin a graduated training program with the goal of returning to the desired sport. The physician must maintain careful follow-up to guard against any recurrence of physeal injury.

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Summary The physician caring for young athletes frequently encounters physeal injuries. He or she must comprehend the complex anatomy of the physeal plate and the mechanisms of failure. Although not useful for prognosis, the Salter-Harris classification allows communication between health care providers and has implications for treatment. Most physeal fractures can be treated using closed methods; however, open reduction should be used in displaced type III and IV injuries. Fortunately, most physeal injuries heal with no growth arrest or only minor growth disturbances. A variety of options exist for treating premature physeal arrest when it does occur. Finally, the physician needs to be aware of chronic stress injuries that can occur in young athletes who undertake excessive training regimens.

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Section I Strength Training in Children and Adolescents Bettina M. Gyr MD Millions of children and adolescents participate in scholastic or community-based organized sports programs in the United States. Children are participating in competitive sports at younger ages and face increasing demands for peak performance. These young athletes are being asked to increase their level of performance and their pace of improvement more than ever before, thus creating the need to find ways to enhance their athletic abilities. The most popular and fastest-growing means of enhancing athletic abilities is resistance and strength training. The medical and athletic communities are routinely asked to evaluate the safety and the efficacy of strength training programs for these young athletes. For many years, the prevailing attitude was that strength training for children and adolescents was inappropriate and even dangerous. There were several misconceptions about strength training that prevailed for decades: Strength training for children is of no benefit owing to low levels of circulating hormones; strength training leads to decreased flexibility and loss of range of motion; and strength training carries a high risk of injury. [14] These misconceptions have all been refuted recently. In 1990, the American Academy of Pediatrics Committee on Sports Medicine published a position statement on strength training for children, stating short-term programs in which prepubescent athletes are trained and supervised by knowledgeable adults can increase strength without significant injury risk. [1] In addition, guidelines of the American College of Sports Medicine, the American Orthopaedic Society for Sports Medicine, and the National Strength and Conditioning Association all suggest that strength training for youths can be a safe and worthwhile activity provided that the program is appropriately designed and supervised.[9] Despite this information, the medical community's knowledge and understanding of these topics remain inconsistent, often creating confusion and uncertainty among parents and coaches about the value and the safety of strength training. This chapter presents current knowledge about strength training in

the child and adolescent athlete. Definitions

This chapter addresses the issues surrounding strength training in the pediatric athlete. Strength training (also referred to as weight training and resistance training) is the use of a variety of methods, including exercises with free weights and weight machines, to increase muscular strength, endurance, and/or power for sports participation or fitness enhancement.[1] Youth sports programs should include an overall conditioning program that includes aerobic activity, endurance training, strength training, flexibility, and instruction in physical and sports skills and sportsmanship. For the purpose of this chapter, the terms weightlifting, powerlifting, and bodybuilding refer to specific competitive sports rather than training modalities. The term children refers to boys and girls who have not developed secondary sex characteristics, usually boys younger than the age of 13 years and girls younger than age 11 who are in Tanner stage 1 or 2. This stage of development is also referred to as preadolescence. The term adolescent refers to boys between the ages of 14 and 18 and girls between the ages of 12 and 18 who are in Tanner stage 3 or 4 of development. The terms youths and young athletes are used broadly to refer to children and adolescents, respectively.

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Biology and Physiology of Children

Parents and coaches must realize that the pediatric athlete is not a miniature adult. Because of the lack of research on the appropriate way to train a child or an adolescent, coaches and trainers often use exercise protocols based on their experience with training more mature athletes. Young athletes are special people with age and developmental differences in their response to exercise and training. Treating them like adults can lead to injury, burnout, and loss of interest. Physicians, parents, coaches, and athletes must be aware of the different kinds of musculoskeletal problems that arise in children. The unique features of a child's skeletal system can lead to specific injury patterns. The peak incidence of physeal fractures is in the 12- to 13-year-old age group, right at the end of the preadolescent growth spurt. The hypertrophic zone of the physeal cartilage is its weakest part; this zone increases in size just before the onset of sexual maturation, thus making it prone to injury. The secondary growth centers are sites of increased concentration of stress owing to the large muscle forces applied through the tendon attachments at these sites, which can lead to fracture or separation of the cartilage. The prevailing attitude used to be that strength training in children would make them more prone to injury and growth arrest. [13] Review of the recent literature, however, reveals that there is no reason to prevent children from strength training in a well-supervised, well-designed program.[9] Children have less ability to perform anaerobic exercise than do adults and adolescents, although they have similar ability to perform endurance activities. Aerobic exercises are designed to work the body at an intensity level that will not result in rapid fatigue because the energy requirements can be met by the oxidative system. Anaerobic exercise, however, is of higher intensity and duration, thus causing the glycolytic system to become activated. Children do not use glycogen as effectively as adults owing to their reduced levels of phosphofructokinase, a key enzyme in the glycolytic pathway. This physiologic difference

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needs to be considered when designing a strength training and conditioning program for children.

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Physiologic Effects of Strength Training

Although it is now well accepted that young athletes can safely participate in a strength training program, the physiologic effects of strength training are not well established in the child and the adolescent. Muscle strength in children is related to growth, and there is some controversy whether strength gains come from training or growth. The largest changes in muscle growth occur during and after puberty. Sewall and Micheli showed that muscle strength in 10- and 11-year-old children increases in response to resistance training.[21] Muscle hypertrophy, however, does not occur. A study of children in a 10-week strength training program found increases in isometric and isotonic strength but no change in cross-sectional area of their muscles.[4] To study the neuromuscular adaptations to strength training, Ozmun and associates evaluated strength, integrated electromyography, and anthropometrics in 16 children after 8 weeks of strength training. [20] They observed significant increases in isotonic and isokinetic strength, as well as increased integrated electromyographic amplitudes, without changes in arm circumference. Strength gains in children and adolescents are most likely caused by neurogenic adaptations (improved recruitment of motor units, improved motor skills, and decreased inhibition) and myogenic adaptations (increase in contractile proteins, enlargement and thickening of connective tissues, and increase in energy sources, such as creatine phosphate).[8] Training-induced strength gains are possible in both boys and girls, with no differences in muscle strength adaptations between the sexes in the young athlete.[3] [17] This finding is due to the fact that neural adaptations, rather than an increase in size, are primarily responsible for these strength gains, and these adaptations are the same in males and females. During and after puberty, strength gains in males are associated with increased muscle mass caused by the influence of testosterone, whereas female muscle development is caused by other hormones and growth factors (i.e., insulin-like growth factor and growth hormone).[9] There may be some potential for muscle hypertrophy in children undergoing longer training periods, more intense training, and more precise measuring techniques, but this area requires further research.

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Benefits of Strength Training

Although children used to be discouraged from strength training owing to the perceived risk of injury and growth disturbance, there are clear benefits to strength training in the pediatric age group. Strength training can improve athletic performance, decrease injury risk in other sports, improve self-esteem, and reduce obesity among young people. Children should be encouraged to participate in a variety of physical activities to enhance their development, and strength training can be a part of a comprehensive physical fitness program. According to Faigenbaum, youth strength training carries many health benefits, including improvements in cardiorespiratory fitness, body composition, bone mineral density, and blood lipid profile.[9] Despite the traditional belief that strength training could damage young bones, the bone mineral density of junior Olympic weightlifters and elite gymnasts as young as 7 years old was found to be higher than in age-matched controls.[6] [7] Childhood obesity is becoming a major public health problem in the United States. Increasing the physical activity of obese children and adolescents can decrease their risk of developing cardiovascular disease and diabetes. A study of 19 children aged 7 to 12 years who were enrolled in a 1-year weight management program (including resistance training, flexibility exercises, and aerobic exercises) showed that resistance training can be safely incorporated into a weight management program.[22] Resistance training may be a good alternative to weight-bearing exercise in the obese child. During activities such as walking and jogging, these children are at risk of overuse injuries owing to their weight. They can, however, benefit from the moderate caloric expenditure and increase in aerobic fitness provided by a resistance training circuit.[22] With a decrease in resistance and an increase in the number of repetitions, which potentially increases heart rate, a well-supervised strength training program could be an integral part of a weight management program in the obese child or adolescent. Because of the increasing number of young athletes competing in various sports, the benefits of strength training on motor skills and sports performance are of renewed interest to coaches, trainers, and parents. Many studies have noted improvements in

long and vertical jump performance after strength training, whereas others have reported improved running speed and agility.[12] [16] [17] Because athletic ability is a difficult variable to quantify and involves many factors, it is difficult to say that strength training enhances sports performance. There is, however, enough evidence to show that a well-designed, supervised strength training program will not have negative effects on sports performance or the general health of the childhood athlete. Strength training can be of further benefit to the young athlete by actually helping to prevent injuries. The development of fundamental fitness skills can lead to a lifetime of fitness and sports participation. Many parents and coaches are steering children toward earlier sports specialization, whereas others feel that broad-based participation in a variety of activities is more related to later sports success. Because children develop certain motor skills at varying ages, youth sports programs should focus on the development of fundamental fitness skills rather than sports-specific skills. A strength training program can be a valuable part of a generalized fitness program, thereby preparing children and adolescents for the increasing demands of later sports participation. Fewer and fewer children are participating in free-time physical activity, preferring instead to watch television or surf the net. Some of these same children, however, then become aspiring teenage athletes whose bodies are not prepared to handle the demands of sports training and competition. According to Arendt and Dick, this is a particular problem in female athletes, who are prone to knee injuries.[2] Participating in a conditioning

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Figure 17-I-1 Partner twist exercises with a medicine ball for stretching and strengthening core muscles. (From Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593-619, 2000.)

program of strength, aerobic, and flexibility training could reduce or prevent acute and overuse injuries ( Fig. 17I-1 ). Faigenbaum discusses several studies in which strength training reduced the number and severity of injuries in high school football players, adolescent swimmers, and other athletes in a variety of sports.[9] There are 750,000 sports-related injuries in children younger than 15 years of age seen in United States emergency rooms annually; strength training may be of significant benefit in reducing injuries by better preparing young athletes for the rigors of sports participation.[23]

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Safety of Strength Training

There is little evidence that strength training, as defined previously, is responsible for large numbers of acute or chronic musculoskeletal injuries. There are a reported 17,000 weightlifting and powerlifting injuries annually in the United States that require emergency room visits.[19] These injuries are primarily due to unsupervised activity in home and school weight rooms. The large majority of these injuries are strains and sprains, with isolated case reports or small series of more severe injuries. Many of these injury reports come from data from the United States Consumer Product Safety Commission's National Electronic Injury Surveillance System, which projects the total number of injuries related to exercise and equipment. They fail to distinguish between injuries associated with supervised, properly designed strength training programs and those associated with unsupervised weightlifting, poorly designed equipment, or free access to equipment. [9] The most common clinical complaint after strength training is low back pain. Adolescents involved in strength training are at risk of both flexion-torsion lumbar injuries (herniated intervertebral disk and paraspinous muscle strain) and extension lumbar injuries (facet syndrome and pars interarticularis stress fracture). Skeletally immature athletes may be at increased risk of developing spondylolisthesis, spondylolysis, and pars interarticularis stress fracture.[24] Physicians should have a high index of suspicion for these injuries in young football players, gymnasts, cheerleaders, and weightlifters. Coaches and trainers should emphasize proper lifting techniques, avoiding lifts that involve hyperextension of the lumbar spine. The risk of physeal injury during youth strength training continues to be a common concern. There have been some isolated reports of distal radius physeal fractures in young weightlifters, but these were all in adolescents involved in competitive weightlifting.[9] These types of injuries have not been reported in any prospective study on youth strength training, and the risk of these injuries is minimal if children and adolescents are taught proper techniques and use proper training loads. Overuse physeal injuries, such as those seen in baseball pitching (e.g., little leaguer's elbow),

have not been reported as a result of strength training. Knee and shoulder injuries occurring during strength training programs are largely muscle and tendon overuse injuries. These can be prevented by a thorough warm-up, appropriate stretching before each strength training session, and avoidance of maximal lift attempts. The effects of weight training on blood pressure and hemodynamics can influence both children and adolescents. While performing maximal lifts in Olympic-style powerlifting, as well as in unsupervised competition-type lifting by adolescents, Valsalva's maneuver is performed. This can lead to weightlifter's blackout, during which blood pressure falls acutely and blackout follows. [24] As with all other risks already mentioned, this can be prevented by proper supervision and by lifting appropriate amounts of weight. The safety of strength training in children and adolescents had been judged largely by case reports and weight room accident reports. When the literature on strength training is systematically reviewed, however, the findings are that strength training is no more dangerous than many other sports and activities in which young people regularly participate. When evaluating strength training injuries in 13- to 16-year-old adolescents, Hamill found that strength training resulted in remarkably fewer injuries than soccer, basketball, and football.[15] There are currently no justifiable safety reasons to preclude youths from participating in properly designed and supervised strength training programs.

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A Sample Program and Training Guidelines

A strength training program for the young athlete should focus on learning lifting technique, improving coordination, and developing motor skills. Parents often ask at what age their child can safely begin to lift weights, and the answer to that question must be based on the individual child. A child should be able to accept and follow directions,

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Figure 17-I-2 Child-sized seated-row machine. (From Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593-619, 2000.)

and he or she should be able to understand the objectives associated with a strength training program. Usually, if a child is considered mature enough to participate in organized sporting activities, he or she should be able to strength train.[9] A young athlete's training regimen requires use of lower weights and higher repetitions, focusing on the development of good technique and safe training procedures for a variety of strength training exercises. Determining an appropriate resistance weight requires adult supervision, and it is better to underestimate the amount of weight a child can lift and to build a program from there. The child should be given the opportunity to develop proper form on a variety of exercises before progressing to heavier weights or more repetitions. Owing to the size of most child athletes, they are unable to use standard adult-sized weight machines safely. With the use of extra pads and boards, most adolescents are able to use these machines, but the weight increments are often too large. It is thus recommended that young athletes use child-sized weight machines or simple free-weight equipment, such as barbells ( Fig. 17I-2 ).

The repetition maximum (RM) can be a guide in building a strength training program. One RM is the maximum amount of weight that can be lifted with proper form one time, but not two times. Ten RM is the maximum amount or weight that can be lifted with proper form 10 times, but not 11. Recent data suggest that a 13- to 15-RM load (high repetition, moderate weight) can be more beneficial to the adolescent athlete than a 6to 8-RM load (low repetition, heavy load).[10] With high-repetition, moderate-weight strength training, the young athlete is more likely to notice positive changes in muscle performance. The number of repetitions that can be performed with different exercises often varies and is most likely the result of differing amounts of muscle mass involved in each exercise. Each of the major muscle groups should be included in a strength training program for balanced strength increases. Many coaches and trainers focus only on the development of the primary muscles involved in a given sport. This ignores the importance of synergistic and antagonistic muscles in injury prevention. As mentioned previously, one of the goals of strength training in the young athlete is injury prevention, accomplished by strengthening the muscles susceptible to injury. The progression of a strength training program requires the supervision of a qualified adult. The young athlete should first be taught the fundamental form and technique of each exercise with very light weights. If the emphasis is on form, technique, and appropriate weights, children can even be safely taught Olympic-style lifts ( Fig. 17I-3 ). Training is begun with a weight that can be lifted 10 times correctly. This amount of resistance should be used until two sets of 10 to 15 repetitions can be performed without fatigue, and resistance should then be increased by 5% to

Figure 17-I-3 Practicing proper technique for the snatch lift using a lightweight bar. (From Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593-619, 2000. Courtesy of Chris Polakowski, BS, CSCS, Essex, Vt.)

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TABLE 17-I-1 -- Recommended Specific Exercises Exercise 1. Leg press 2. Bench press 3. Leg curls (hamstring) 4. Lateral pulls or bent-over rows (using bench for support) 5. Leg extension (quadriceps) 6. Lateral raises (elbows bent, arms raised to shoulder level)

7. Back extension (avoid hyperextension) 8. Triceps extension 9. Abdominal crunches 10. Biceps curls Beginner

1-2 sets

10-15 repetitions

Intermediate 2-3 sets

10-15 repetitions

Advanced

8-12 repetitions

2-3 sets

10% (usually 2 to 5 pounds). After consistent training over a 1- to 3-month period, the program can be increased to two to three sets of a 10- to 15-RM load. More advanced athletes can then further increase their supervised training to include two to three sets of an 8- to 12-RM load, each to fatigue, with a 2- to 3-minute rest interval between sets. Both single-joint (e.g., leg press, biceps curls) and multi-joint exercises (e.g., squats) ought to be incorporated into the training program ( Table 17I-1 ). The single-joint exercises target specific muscle groups, whereas the multi-joint exercises involve the coordinated action of multiple muscles. Because sports movements require coordination, stabilization, and balance, athletes preparing for sports participation should include multi-joint weight training in their workout program.

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Summary The major benefits of strength training in child and adolescent athletes are improvements in strength, coordination, and self-image. The potential for protection against injury is also a well-recognized benefit. Although the risk of injury during strength training is real, it is not greater than is seen in many other sports. To have a safe and effective youth strength training program, the following guidelines have been set forth[9] : Include supervision and instruction by qualified adults Wear appropriate clothing and footwear in the training area Ensure that the training environment is safe and free of hazards Set realistic goals according to the needs and the abilities of each participant Include a warm-up with 10 minutes of light aerobic exercise and stretching Use appropriate exercises and workloads for each participant; begin with one light set of 10 to 15 repetitions of six to eight exercises Focus on technique and participation, rather than amount of weight lifted Use workout cards and regularly review progress Use two to three nonconsecutive training sessions per week Increase resistance gradually as strength improves Vary training program to optimize adaptations and prevent boredom Include strength training as part of a well-balanced fitness program

Figure 17-I-4 Physical activity recommendations for children and adolescents. (From Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593-619, 2000. )

A well-designed, supervised strength training program is in no way detrimental to the

young athlete. Children and adolescents today face many of the risks of a sedentary lifestyle, including obesity, heart disease, and diabetes. They should be encouraged to begin a lifetime of good fitness and nutritional habits at an early age, and strength training has many benefits for long-term health ( Fig. 17I-4 ).

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References American Academy of Pediatrics Committee on Sports Medicine: Strength training, weight and power lifting, and body building by children and adolescents. Pediatrics 86:801-803, 1990. 1.

Arendt E, Dick R: Knee injury patterns among men and women in collegiate basketball and soccer: NCAA data and review of literature. Am J Sports Med 23:694-701, 1995. 2.

Blimkie C: Age- and sex-associated variation in strength during childhood: Anthropometric, morphologic, neurological, biomechanical, endocrinologic, genetic, and physical activity correlates. In Gislofi C, Lamb D (eds): Perspectives in Exercise Science and Sports. Indian-apolis, Benchmark, 1989, pp 99-163. 3.

Blimkie C: Resistance training during preadolescence: Issues and controversies. Sports Med 15:389-407, 1993. 4.

Cahill B, Griffiths E: Effect of preseason conditioning on the incidence and severity of high school football knee injuries. Am J Sports Med 6:180-184, 1978. 5.

Cassell C, Benedict M, Specker B: Bone mineral density in elite 7-to 9-year old female gymnasts and swimmers. Med Sci Sports Exerc 28:1243-1246, 1996. 6.

Conroy B, Kraemer WJ, Maresh CM, et al: Bone mineral density in elite junior Olympic weightlifters. Med Sci Sports Exerc 25:1103-1109, 1993. 7.

8.

Cook P, Leit M: Issues in the pediatric athlete. Orthop Clin North Am 26:453-464, 1995.

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9.

Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593-619, 2000.

Faigenbaum A, Wescott W, Micheli L, et al: The effects of strength training and detraining on children. J Strength Cond Res 10:109-114, 1996. 10.

Faigenbaum A, Zaichkowsky L, Wescott W, et al: Psychological effects of strength training on children. J Sport Behav 20:164-175, 1997. 11.

Falk B, Mor G: The effects of resistance and martial arts training in 6 to 8 year old boys. Pediatr Exerc Sci 8:48-56, 1996. 12.

Falk B, Tenenbaum G: The effectiveness of resistance training in children: A meta-analysis. Sports Med 22:176-186, 1996. 13.

Guy J, Micheli L: Strength training for children and adolescents. J Am Acad Orthop Surg 9:29-36, 2001. 14.

15.

Hamill B: Relative safety of weight lifting and weight training. J Strength Cond Res 8:53-57, 1994.

Hetzler R, DeRenne C, Buxton B, et al: Effects of 12 weeks of strength training on anaerobic power in prepubescent male athletes. J Strength Cond Res 11:174-181, 1995. 16.

Lillegard W, Brown EW, Wilson DJ, et al: Efficacy of strength training in prepubescent to early postpubescent males and females: Effects of gender and maturity. Pediatr Rehabil 1:147-157, 1997. 17.

18.

Lillegard W, Terrio J: Appropriate strength training. Med Clin North Am 78:457-477, 1994.

Mazur L, Yetman RJ, Risser WL: Weight-training injuries: Common injuries and preventative methods. Sports Med 16:57-63, 1993. 19.

Ozmun J, Mikesky AE, Surburg PR: Neuromuscular adaptations following prepubescent strength training. Med Sci Sports Exerc 26:510-514, 1994. 20.

21.

Sewall L, Micheli L: Strength training for children. J Pediatr Orthop 6:143-146, 1986.

Sothern M, Loftin JM, Udall JN: Safety, feasibility, and efficacy of a resistance training program in preadolescent obese children. Am J Med Sci 319:370-375, 2000. 22.

23.

Stanitski C: Pediatric and adolescent sports injuries. Clin Sports Med 16:613-633, 1997.

24.

Webb D: Strength training in children and adolescents. Pediatr Clin North Am 37:1187-1210, 1990.

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Chapter 18 - The Team Physician: The Preparticipation Examination and On-Field Emergencies Christopher C. Madden MD W. Michael Walsh MD Morris B. Mellion MD

Philosophy

In the June 18, 1989, Philadelphia Inquirer, a headline blared Team Doctors: A Crisis in Ethics. In the article that followed, staff writers Angelo Cataldi and Glen Macnow pointed out that under pressure from coaches and owners to keep players on the field, doctors often must choose between winning and the health of their patients. Former National Football League (NFL) star lineman Charlie Krueger put it more bluntly: The doctor works for the team, and he doesn't know what the Hippocratic oath means as it pertains to you. The same article quoted one well-known team physician as saying, Being a team physician is a bum deal. Another said, It's a lousy job. Malpractice insurance carriers often offer high rates or refuse to insure physicians with team doctor roles. Even at the college level, doctors are open to such legal charges as those brought in the widely publicized Buonicanti vs. Citadel team physician case, in which the team doctor was accused of contributing to a disastrous cervical spine injury. Grim reading for the young orthopaedist or family physician who is contemplating taking on the care of an athletic team!

Is that all there is? Headaches, ethical conflicts, and threats of lawsuits? Fortunately not. Especially at the grass-roots level, few positions offer as much enjoyment, satisfaction, and stimulation as that of team physician. Being a team physician may be a privilege, a challenge, or a threat. Usually, the experience is a mixture of the three. In ideal circumstances, the privileges and challenges far outweigh the threatening aspects. Caring for an athletic team adds new dimensions to the practice of medicinethe pressures of time, society, and money on the athlete. At all levels of competition, the element of time is paramount. The season's schedule marches inexorably on. If the athlete is not fit to play, the coach must use others in his or her place. The challenge for the physician is to find the fastest safe treatment, thus allowing the athlete to return to play quickly and with smallest chance of re-injury. The importance placed by our competitive society on winning further complicates the decision-making of the team physician. The value of an individual player to the competitive success of the team is often blown out of proportion. This is particularly true at younger ages and lower levels of competition, where the welfare of the athlete must come before any thought of team victory. At higher levels of play, the margins of safety often become obscure. What would be an easy decision about a junior high school quarterback may be extremely difficult when it involves a National Collegiate Athletic Association (NCAA) Division I competitor leading a team into postseason play. Medical decisions may influence not only the athlete and his or her teammates but also the coach and the institution. When injuries plague a team and key athletes are sidelined, their loss may affect the coach's ability to keep his or her job, the school's opportunity to participate in lucrative postseason play, and the professional team's success in selling tickets. Our purpose in this chapter is to discuss the various functions, relationships, and responsibilities of the team physician to maximize the pleasures of that job while minimizing the frustrations.

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Roles and Functions of the Team Physician Who Serves as Team Physician?

A variety of doctors serve as team physicians. Family physicians, general practitioners, and orthopaedists make up the majority of team physicians. Other specialties involved include osteopathy, internal medicine, general surgery, pediatrics, and obstetrics/gynecology.[97] A good team physician must address the physical, emotional, and spiritual needs of the athletes. The job requires a comprehensive approach.[48] [63] [77] [99] It is performed within the context of the sport and the needs of the team. The real success of the specialist as team physician depends on his or her ability to meet the athletes' varied medical and psychosocial needs. This ability depends on a broad knowledge base that includes athletics as well as medicine. Caring for athletes requires a detailed knowledge not only of the musculoskeletal system but also of the processes of growth and development, cardiorespiratory function, gynecology, dermatology, and neurology. The physician must be well versed in psychology and human behavior, particularly as they relate to issues of performance anxiety, motivation, and group interactions. To achieve a high level of success, the physician must understand and appreciate the role of rehabilitation in the care of the athlete. Three areas of pharmacology are also critical: therapeutics, performance-enhancing substances, and recreational drugs. Finally, the team physician must be well grounded in exercise physiology, biomechanics, and the physical demands of specific sports.

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Often, an orthopaedist and a family physician or other generalist share the responsibility for an athletic team. This may be an ideal situation because even though the majority of

injury problems are musculoskeletal, they constitute only a fraction of the athlete's health care needs.[98] Lombardo has referred to the primary care physician as the captain of the ship, director of the symphony, and jack of all trades. [63] Availability

Availability is a cornerstone for success as a team physician. [48] [88] [98] Personal presence and a well-organized coverage system are essential. The most common service team physicians provide is game coverage. Sidelines are the front lines of sports medicine, especially in contact and collision sports. A physician who covers a team solely from the stands or the office does not truly deserve the title of team physician. A second venue of coverage is the athletic training room. The physician can demonstrate interest in the team by seeing athletes in their own environment rather than in the office. Athletes are more relaxed in their familiar setting and generally provide a better history and a higher level of compliance with recommendations given there. On the other hand, team physicians often make special accommodations in their office schedules to squeeze in athletes from their teams who have urgent problems. Most athletic activity goes on during the normal workday, and it is not reasonable for the team physician to be continuously available on site. The team physician or other appropriate back-up should always be available to the coach or athletic trainer. An additional but extremely important element of an effective relationship is some unstructured time spent with the athletic trainer or coach. Often, it is the informal conversations that cement a good working relationship. Qualifying Athletes to Play

Decisions about qualifications to play are always difficult. With youngsters in community leagues, a very conservative approach may be warranted. Sometimes, however, coaches and parents may have an expanded notion of why it is important for a particular player to be on the field on a given day. At the high school level, the opportunity to compete often influences scholarship opportunities. For a few performers at the highest level, a scholarship may mean an opportunity to attend NCAA Division I schools. For the majority of these high school athletes, however, athletic scholarships may represent their only opportunity to afford an education at Division II or Division III NCAA schools as well as universities, colleges, and junior colleges with many other affiliations. For these athletes, the ability to play well may truly be their only option for financing a college education. College level participation carries an even larger set of economic and social rewards. Although only a tiny percentage of college athletes advance to the professional level, many more gain employment and social opportunities from their achievements in athletics. Finally, in professional sports, there is a phalanx of young recruits knocking at the door to replace any injured player. Medical decisions are very difficult in this context.

Preparticipation Evaluation

Team physicians are now involved in a variety of preventive aspects of athletic medical care. Foremost among these is the preparticipation evaluation. Even before the physician-athlete relationship exists, the prospective participant must be accepted as a member of the team. In most circumstances this means undergoing some type of preparticipation physical evaluation. The completeness, complexity, and sophistication of this evaluation vary widely with the level of competition and the nature of the sport. At the junior high school level this examination may require only a general health evaluation to rule out conditions that contraindicate participation in certain sports. The major challenges at this level are the wide range of musculoskeletal maturation that exists in peripubertal athletes and the possibility of discovering previously unidentified congenital defects that could pose serious health threats. [16] [44] [61] [95] [103] By the time the athlete reaches senior high school and college level participation, natural selection processes have been at work, and the likelihood of finding a serious congenital problem is much less. Here the usual finding is a previous orthopaedic injury, so examiners must be extremely adept at performing musculoskeletal examinations and appropriate preparticipation rehabilitation techniques. By the time professional level competition has been reached, much has usually occurred in the athlete's past. Examinations are usually rigorous and sophisticated because of the economic aspects of professional sports. Extensive performance testing, routine radiographic screening, and the use of computerized musculoskeletal testing techniques are commonplace. These topics are beyond the scope of this chapter, which is oriented more toward the volunteer team physician at the high school level. The role of the team physician in the preparticipation evaluation is to determine the qualifications of athletes, both general and sport-specific, in order to counsel them on appropriate sports and to treat and rehabilitate deficits. An excellent policy statement, guide, and form for use in the preparticipation physical evaluation was developed jointly by members of the American Academy of Family Physicians, the American Academy of Pediatrics, the American Medical Society for Sports Medicine, the American Osteopathic Academy of Sports Medicine, and the American Orthopaedic Society for Sports Medicine. It is the only publication on sports physicals endorsed by five major medical societies (Fig. 18-1 (Figure Not Available) ).[2] Objectives.

Overall, the primary goal of any preparticipation physical examination is to help maintain the health and safety of the athlete. Beyond that, its mandatory objectives are to: 1. Detect conditions that may be life-threatening or disabling. 2. Detect conditions that might limit competition. 3. Detect conditions that might predispose the athlete to injury.

4. Meet certain legal and insurance requirements.

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Figure 18-18-1 (Figure Not Available) Preparticipation physical evaluation. (Reprinted with permission from American Academy of Family Physicians, American Academy of Pediatrics, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Society for Sports Medicine: Preparticipation Physical Evaluation, 2nd ed. Physician Sportsmed [monograph], 1997.)

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In an ideal situation these objectives can be expanded to include the following: 1. 2. 3. 4.

Determination of general health status. Physician counseling. Maturity assessment. Fitness evaluation.

Timing.

The timing of the preparticipation examination is always something of a dilemma. Ideally, it should take place approximately 6 weeks before the beginning of the sports season to allow for correction or rehabilitation of any defects that are identified. This often means the middle of the summer, however, when few athletes are available and when the physician's schedule may already be over-committed. Frequency.

The frequency of the preparticipation examination has been the subject of much controversy. Untold man-hours have been wasted in performing routine full examinations on the same group of healthy high school athletes year after year. We believe that, ideally, a complete screening examination should be performed on entry into any given level of school, that is, junior high school, senior high school, and college. After the initial full examination, in subsequent years an interim health questionnaire would be filled out and a limited physical examination performed focusing on the new areas of illness or injury disclosed by the questionnaire. This approach has been adopted by the NCAA, but at the moment few states have seen fit to follow suit. Consequently, in many locales, a full screening examination must be done annually to fulfill state requirements.

In 1996, the American Heart Association (AHA) published a scientific statement on screening for cardiovascular abnormalities in young athletes that recommends both a history and physical examination before participation in organized high school and collegiate sports. Repeat screening is then recommended every 2 years, and an interim history should be obtained in intervening years.[10] In 1997, the NCAA Committee on Competitive Safeguards and Medical Aspects of Sports challenged the AHA's recommendations, indicating that there was minimal scientific evidence supporting the efficacy of a routine second examination after 2 years of competition detecting more collegiate athletes with cardiovascular abnormalities. The AHA addressed the NCAA's concerns by changing their recommendations for collegiate athletes only. They now recommend that an interim history and blood pressure measurement should be obtained in each of the subsequent 3 to 4 years after the initial comprehensive preparticipation examination. Changes or abnormalities detected during interim screens may lead to another complete physical examination and possibly further testing. Recommendations for high school athletes remain unchanged.[9] Methodology.

The venue for the preseason examination has also been the subject of much discussion. Office-based and station-based examinations are the two most common methods used.[2] [16] [41] Undoubtedly, there are great advantages to having this examination done in the athlete's primary care physician's office. A physician-patient relationship already exists. Past records are available. There is a great measure of privacy for counseling. Overall, such a setting greatly enhances continuity of health care. On the other hand, many athletes may not have a primary care physician. Many physicians may have extremely limited appointment time, especially during the time of year when every athlete needs an examination. There are certainly varying interest and skill levels among primary care physicians in dealing with athletes and sports. Such examinations also tend to be significantly more costly. Because of these disadvantages, the preseason screening examination is often carried out as a multistation examination using a medical team. The advantages are those of personnel with specialized interests in sports, efficiency in handling large numbers of athletes, the ability to move into nontraditional areas such as performance testing, and an immediate line of communication open to coaches, trainers, and school nurses. The disadvantages of such a setting are apparent. This is usually a noisy environment with fairly hurried examinations. It is almost impossible to counsel athletes on delicate issues in such a setting. Follow-up is often spotty. A word should also be said about what appears to be the worst of both worlds, that is, one overworked physician trying to examine a gymnasium or locker room full of athletes on one day after office hours. This setting tends to promote the warm body type of evaluation. The final station is the most important. Having an experienced head team physician available there to review all of the data to determine clearance, and to make appropriate recommendations, is vital to the station-based approach. The locker room examination is a variant of the station-based examination. Rather than

having each physician take responsibility for a specific station, this approach focuses on a one-on-one encounter that requires that each physician complete a full preparticipation examination on each individual athlete. Concerns are similar to those of the station-based examination. This method may be the quickest and most widely used, but concerns have been raised about the lack of personalized attention and continuity of care.[16] [41] We believe, however, that this may vary greatly with each setting. The ideal situation appears to be a private office setting in which the examination is done by a knowledgeable team physician who is also the athlete's family physician or pediatrician. This is seldom practical. When it is not, a well-organized station-to-station examination is a good alternative. If one chooses to organize such a screening program, the following information may be of benefit. Adequate manpower is a must. Team members can include physicians, dentists, house officers, medical students, physician assistants, nurse practitioners, athletic trainers, physical therapists, exercise physiologists, and dietitians. A variable number of stations can be used depending on the space and manpower available. A typical set-up might include the stations shown in Table 18-1 . Stations 1 through 8 are required. Stations 9 and 10, in addition to stations addressing nutrition, strength, speed, agility, power, endurance, and balance, are optional.[2] Some additional clarification is relevant. Station 1 ideally should not include actually filling out the medical history form. The forms

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Station Number

TABLE 18-1 -- Stations for Preparticipation Examination Function Required Personnel

1

Sign-in

Athletic director or coach

2

Review history

Physician, physician assistant (PA), nurse, or senior athletic trainer

3

Height and weight

Coach, athletic trainer, other volunteer

4

Visual acuity

Athletic trainer or nurse

5

Vital signs

Athletic trainer, PA, or nurse

6

Medical examination

Physician(s), PAs, nurse practitioners

7

Orthopaedic examination

Physician(s), PAs, nurse practitioners

8

Reviewreassessment

Team physician

9

Body composition

Exercise physiologist, athletic trainer, or physical therapist

10

Flexibility

Physical therapist or athletic trainer

should be completed in advance, with young athletes receiving assistance at home from parents or guardians. One recent study demonstrates a system of completing a detailed history on the Internet. [83] Station 2 is one of the most important. Here the validity of the written health history is ascertained. All athletes have a tendency to pencil whip the history form. Unless it is double-checked by a health care professional, major points in the history may go overlooked. Station 6 may well be divided into more stations, at each of which only a portion of the medical examination is done. If the entire examination is done at one station, plenty of help should be available because otherwise this will undoubtedly become a bottleneck. Station 7, the orthopaedic examination, may take various forms. If physicians without sports medicine training are performing the examination, or if time is a factor, a quick 13-point general orthopaedic screening examination may be used.[2] [65] [102] If the evaluation is performed by orthopaedic surgeons or other sports physicians, they may wish to use joint-specific testing to go into much more detail, especially regarding the examination of ankles, knees, elbows, and shoulders. Station 8 is undoubtedly the most difficult. Here a physician, preferably the team physician, must review all of the data generated during the examination and decide whether the athlete may safely participate. The physician is responsible for the final clearance section on the preparticipation evaluation form. This not only involves clearing an athlete for play but also involves making appropriate recommendations for follow-up of specific concerns. The physician is responsible for facilitating communication between other primary or consulting physicians, athletic trainers, coaches, and parents. This process can be enhanced by carefully documenting problems and specific recommendations in the clearance section of the preparticipation evaluation form. History.

A comprehensive history and physical examination make up the bulk of the preparticipation examination. A careful history is the most important part of the preparticipation evaluation. Two studies in high school settings and one study in a collegiate setting point out that the medical history alone uncovered 65% to 74% of abnormal preparticipation examination findings.[39] [62] [89] Parental input also may be important. Risser and colleagues showed that only 39% of athlete-reported histories correlated with histories reported by parents.[90] Joint completion of history forms by athletes and their parents is recommended when possible. Special emphasis in the history should be placed on screening for significant recent illnesses, allergic reactions, cardiac or pulmonary problems, musculoskeletal problems, skin problems, previous head injuries and other neurologic problems, previous heat illness, medication problems, inadequate immunizations, and in the female athlete, menstruation abnormalities and disordered eating. The specific set of questions found

on the recommended preparticipation evaluation form is aimed at detecting these potential problems, and the questions should be reviewed carefully with each athlete (see Fig. 18-1 (Figure Not Available) ). [2] Sudden death is one of the greatest tragedies in sport, and it deserves special mention. Over 95% of sudden deaths in athletes younger than 30 years of age are secondary to cardiovascular problems, the most common problem being hypertrophic cardiomyopathy. There are currently no universally accepted screening standards for high school and college athletes.[10] A recent analysis of high school preparticipation questionnaires revealed that eight states have no approved history and physical examination questionnaires to guide examiners. Of the remaining 43 states (includes District of Columbia), only 40% have history and physical examination forms addressing at least 9 of the 13 AHA recommendations. [38] Although preparticipation screening may be of limited value in detecting cardiovascular causes of sudden death, the AHA recommends that some form of preparticipation cardiovascular screening for high school and collegiate athletes is justifiable and compelling, based on ethical, legal, and medical grounds.[10] [68] Specific historical questions and examination components recommended by the AHA are listed in Table 18-2 . Each athlete deserves a comprehensive cardiovascular screen, and if abnormalities are detected or suspected, the athlete should be referred for further evaluation. Physical Examination.

The physical examination focuses on the areas of greatest importance in sports participation, and it specifically addresses problems uncovered by the history. Standard components of the preparticipation examination can be found in Table 18-3 .[2] Adequate exposure is important during the examination. Height and Weight.

Height and weight should be recorded with each physical examination. Excessive weight change should alert physicians to possible underlying problems such as eating disorders and steroid abuse.

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TABLE 18-2 -- American Heart Association Recommendations for Cardiovascular Screening in the Preparticipation Examination History Physical Examination Sudden death in family member 60 mm Hg) or radial pulses (>80 mm Hg). If the athlete is pulseless, immediately activate the emergency medical system. Early defibrillation with a standard defibrillator or an automatic external defibrillator may have the single greatest impact on survival. [9] [69] [101] Hypotension following injury should be considered hypovolemia until proven otherwise, and hemorrhage should be sought immediately. Disability (D) is evaluated by performing a limited neurologic examination to establish level of consciousness and pupillary size and reaction. Level of consciousness may be described using the mnemonic AVPU: Alertness, response to Vocal stimuli, response to Painful stimuli, and Unresponsive.[7] The Glasgow Coma Scale may also be used.[105] Head injuries are the most common cause of disability in organized sporting events. The D may also stand for defibrillation or drugs, which may be required for successful cardiopulmonary resuscitation. Exposure (E) should be adequately evaluated by inspecting the extremities and other body parts for bleeding, fractures, or severe contusions. Blood pressure may be checked at this time. The E can also stand for environment. Moving the athlete out of direct physical danger, or applying rewarming or cooling techniques, may be required. Airway protection, CPR, and other lifesaving measures may begin as soon as a problem is identified, even before the completion of the primary survey ( Table 18-9 ). Once an identified problem is stabilized, the survey is resumed. In addition to CPR, large-caliber (18-gauge) intravenous catheters, oxygen, and electrocardiographic monitoring (IV-O2 -Monitor) should be used appropriately when available. Enough information is usually obtained during the primary survey and resuscitation to decide about immediate transfer to a referral facility. A secondary survey is performed in athletes whose injuries do not warrant immediate transfer. The secondary survey is a head-to-toe evaluation for injuries, and it includes assessment of the vital signs (including temperature) and continual reassessment of the ABCs. If the athlete makes it through the secondary survey without being transferred, decisions must ultimately be made about disposition and follow-up. The team physician must address the issues of whether it is safe to return to play. Any athlete expressing concern or hesitation about returning to play should be held out despite medical

clearance opinions. Figure 18-4 summarizes the primary surveyresuscitationsecondary survey approach and the decision-making process regarding hospital transfer, follow-up, and return to play.[65] The injuries listed in the table all can be associated with life-threatening complications, and they should be diligently ruled out. Specific Injuries and Illnesses.

Specific injuries will be identified during both primary and secondary surveys. Immediately life-threatening injuries compromising the airway, breathing, and circulation must be recognized during the primary survey and treated immediately to ensure a better chance for survival. Other life-threatening injuries, either because of a more delayed presentation or because they indirectly affect the ABCs, should be sought during the secondary survey. Less serious injuries can be dealt with only after the athlete is deemed stable. Head and Neck.

Head and neck injuries are the most common cause of catastrophic athletic injuries. Loss or alteration of consciousness signifies head injury, and the athlete should be immediately assumed to have a cervical spine injury. Be aware that hypoxia, hypovolemia (shock), hypoglycemia, seizures, heatstroke, hypothermia, and therapeutic or abusive drugs (e.g., alcohol, cocaine) can cause alteration or loss of consciousness. Cerebral concussion is the most common head injury encountered by team physicians. Kelly defines concussion as a trauma-induced alteration in mental status that may or may not involve loss of consciousness.[52] Its hallmarks are confusion and amnesia.[6] Other associated findings include headache, dizziness or vertigo, blurriness of vision, tinnitus, nausea and/or vomiting, gross incoordination, emotional lability, seizures, slowness to answer questions, easy distractibility, disorientation, slurred or incoherent speech, vacant staring, repetitive asking of questions (e.g., what happened?), amnesia, and generalized lack of awareness of surroundings. Amnesia can be retrograde (can't remember events before the injury) or anterograde (can't remember events after the injury). Severe retrograde amnesia may indicate a more serious injury. Head injury evaluation is subdivided into on-field and sideline phases. The most important objective of the initial field examination is to make an accurate diagnosis of the TABLE 18-9 -- A Summary of Current Guidelines for Cardiopulmonary Resuscitation Adult (>8 yr) Adult (>8 yr) Child (1-8 yr) Infant ( /das/book/view/29309971/1103/425.html/top

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Chapter 19 - Head Injuries Section A Head Injuries in Adults Robert C. Cantu MA, MD, FACS, FACSM The head and cervical spine are unique structures because their contents, the brain and spinal cord, are largely incapable of repair and regeneration and subserve important functions for the individual. Therefore, although injuries to the central nervous system may occur less frequently than other sports-related injuries, they can have a major impact on the affected individual and the sport. Sports-related injuries of the head receive substantial public attention and are responsible for some of the most catastrophic athletic injuries,[2] causing 70% of traumatic deaths and 20% of permanent disability related to sports.[26] Mild to moderate concussion has been recognized as an epidemic in sports, and it can have an impact on the scholastic performance of the athlete. Even a single, mild sports-related concussion can temporarily affect neuropsychological test responses.[19] This chapter reviews the epidemiology of head injuries, basic pathophysiologic mechanisms of injury, and criteria for return to play of the athlete after a head injury. Epidemiology

The incidence of traumatic central nervous system injury is estimated to be 150 to 430 cases per 100,000 for brain injury. The percentage of these injuries related to sporting activities is believed to be 3% to 25%.[16] Although it might be expected that nervous system injuries are limited solely to contact and collision sports, in actuality they can occur in most sports. The injuries that are most visible in the public eye tend to occur in organized and professional sports, but many sports-related head injuries appear to

occur during unsupervised activities, such as skiing.[20] These tend to be sporadic and less widely publicized, leading to an underestimation of the magnitude of the problem. Certain trends are prevalent in sports-related injuries. It has been observed that the risk for serious head injury in organized sports generally increases with age. Football is an excellent example of this. There is virtually no death or quadriplegia at the Pop Warner level, but the incidence steadily rises from junior high to high school, college, and the professional level. This is because the force of impact, a product of the individual's weight and speed, is low in young athletes compared with skeletally mature participants. Organized Sports

The following list demonstrates the sports that are most hazardous to the head and spine: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Auto racing Boxing Cycling Equestrian sports Football Gymnastics Hang-gliding Ice hockey Lacrosse Martial arts Motorcycling Parachuting Rugby Skating, rollerblading Skiing Skydiving Soccer (goalie) Track (pole-vaulting)

The most effective method of handling central nervous system injuries is to prevent their occurrence. According to statistics from the National Center for Catastrophic Sports Injury Research, the sports with the highest risk for head injury per 100,000 participants are football, gymnastics, and ice hockey. Although there is no statistically significant difference between the three on the basis of incidence per 100,000 participants, the absolute numbers of severe head injuries are highest from football because 1,500,000 play football annually, and there are fewer than 100,000 participants in each of the other sports. Fortunately, rules change, and better equipment and techniques seem to have dramatically decreased the rate of serious nervous system injury in football. Other sports have a position or event with high risk for head injury, whereas the overall risks for serious injury in the sport are low. For instance, pole-vaulting is a high-risk position, as is being on top of the pyramid in cheerleading. Because the risks for and incidence of

injury are well established for most popular organized sports, some sports of emerging popularity that have significant rates of injury are cited. Although the sport of soccer is generally considered safe, goaltender is a position known to have risk for serious neurologic injury. Contrary to conventional thinking, however,

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new information from the Netherlands has revealed that concussion and chronic traumatic brain injury may be significant problems for all players in soccer. A study of neuropsychological test results of 53 professional soccer players revealed impaired memory, planning, and visual perceptual processing compared with control subjects, with a direct relationship between the number of concussions and the frequency of heading the ball.[22] Interestingly, a soccer ball weighs about 1 pound and can travel at speeds of 30 to 60 miles per hour at the professional level, giving an indication of the force it may apply to the player's head. These findings need to be confirmed by prospective studies. Notably, a related event, cheerleading, has risks similar to those of gymnastics. This is of concern because as a sport, cheerleading is poorly regulated. Whereas gymnastic events are closely monitored, cheerleaders may perform pyramids, jumps, and flips with little guidance in technique or safety. Recreational Sports

Many unsupervised activities, including skiing, skating, and equestrian sports, have reports of catastrophic head injuries, but statistics on relative rates of injury are not widely studied or reviewed. Indeed, because the number of participants in any given recreational sport can never be determined, the rate of injury per participant can only be estimated. Golf has had a recent surge in popularity owing in large part to the successes of Tiger Woods. Along with this, a sharp rise in golf-related head injuries has been seen in some regions. In a 3-month period at one institution in New York, 50% of operative head trauma was golf related and generally caused by careless swinging of the club.[30] A study from Scotland revealed golf to be one of the most common sports-related causes of head injury.[22] Equestrian accidents are also prevalent among recreational athletes. In the United States, more than 2300 are hospitalized annually because of equestrian injuries.[28] Neurologic injury is the leading cause of serious injury and death[23] ; head injury occurs in 92% of patients and is responsible for most deaths. With more than 30 million horseback riders in the United States, the magnitude of the problem is potentially enormous. For an unclear reason, more women than men are affected, with falls from the horse being the most common mechanism. [28] Fortunately, safety measures such as

helmets seem to have reduced the rate of serious neurologic injury over time. Winter sports also pose significant dangers to the head. As with horseback riding, severe injuries in celebrities, like the death of actor and politician Sonny Bono, have brought the dangers of skiing to public attention. A Canadian series [24] reported 145 nervous system injuries in skiers in a 5-year period in Calgary. In this group, five deaths were related to neurologic injury, usually caused by a collision with a tree. Risk factors include reckless skiing, manufactured snow, and poor course design. In related sports, up to 54% of snowboarding accidents result in a closed head injury.[29] Tobogganing and sledding[31] are also culprits, with an estimated 59% of injuries affecting the head. [15]

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Pathophysiology of Injury to the Head Causes of Brain Injury

An understanding of the forces that produce skull and brain injuries requires an understanding of the following principles: A forceful blow to the resting, movable head usually produces maximal brain injury beneath the point of cranial impact (coup injury). A moving head colliding against an unyielding object usually produces maximal brain injury opposite the site of cranial impact (contrecoup injury). Such lesions are most common at the tip and the undersurfaces of the frontal and temporal lobes. If a skull fracture is present, the preceding two principles do not pertain, because the bone itself, whether it is transiently (linear skull fracture) or permanently (depressed skull fracture) displaced at the moment of impact, may directly injure brain tissue. In discussing brain injuries, it is essential to realize that three types of stresses can be generated by an applied force: compressive, tensile (the opposite of compressive, sometimes called negative pressure), and shearing (a force applied parallel to a surface). Uniform compressive stresses are tolerated fairly well by neural tissue, but shearing stresses are tolerated poorly. The cerebrospinal fluid acts as a shock absorber, cushioning and protecting the brain by converting focally applied external stresses to a more uniform compressive stress. This is accomplished because the fluid follows the contours of the sulci, thus setting up damaging shearing forces. Despite the presence of cerebrospinal fluid, shearing stresses may still be imparted to the brain. If rotational forces are applied to the head, shearing forces will occur at those sites where rotational gliding is hindered. These areas are characterized by (1) rough, irregular surface contacts between the brain and skull, hindering smooth movement; (2)

dissipation of the cerebrospinal fluid between the brain and skull; and (3) impedance of brain motion by dura mater brain attachments. The first condition is most prominent in the frontal and temporal regions and explains why major brain contusions occur at these sites. The second condition explains the coup and the contrecoup injuries. When the head is accelerated before impact, the brain lags toward the trailing surface, thus squeezing away protective cerebrospinal fluid and allowing the shearing forces to be maximal at this site. Brain lag actually thickens the layer of cerebrospinal fluid under the point of impact, which explains the lack of coup injury in moving head injury. On the other hand, when the head is stationary before impact, there is neither brain lag nor disproportionate distribution of cerebrospinal fluid, accounting for the absence of contrecoup injury and the presence of coup injury. The scalp also has energy-absorbing properties; 10 times more force is required to produce a skull fracture in a cadaveric head with the scalp in place than in one with the scalp removed. In addition, Newton's lawforce equals mass times accelerationmust be appreciated. An athlete's

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head can sustain far greater forces without brain injury if the neck muscles are tensed at the moment of impact. In the relaxed state, the mass of the head is essentially its own weight. With the neck rigidly tensed, however, the mass of the head approximates the mass of the body.

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Types of Brain Injury Concussion

Universal agreement on the definition of concussion does not exist. This fact renders evaluation of the epidemiologic data extremely difficult. A working definition of concussion that has gained general acceptance is the one proposed by the Committee on Head Injury Nomenclature of the Congress of Neurological Surgeons: a clinical syndrome characterized by immediate and transient post-traumatic impairment of neural function, such as alteration of consciousness, disturbance of vision, equilibrium, etc., due to brainstem involvement.[7] Maroon and Bailes,[20] in attempting to simplify the clinical problem, divided concussion into three grades on the basis of duration of unconsciousness. The three grades are mild (no loss of consciousness), moderate (loss of consciousness with retrograde amnesia), and severe (unconsciousness longer than 5 minutes). Different schools of thought exist on grading the severity of concussion. Some concussion classifications place greater emphasis on the duration of confusion and post-traumatic amnesia,[13] whereas others place more emphasis on loss of consciousness regardless of the amnestic period. Lovell and colleagues[18] evaluated 383 patients with mild head injury, with and without loss of consciousness, admitted to the trauma service at Allegheny General Hospital. They hypothesized that patients who had experienced a loss of consciousness would perform worse on neuropsychological tests known to be sensitive for mild traumatic brain injury. In comparing concussed patients, however, they found no support for weighing loss of consciousness more heavily than other markers of concussion, such as amnesia or confusion, in making decisions about return to previous activities. Loss of consciousness did not result in greater neuropsychological impairment in this large group compared with patients without loss of consciousness. Their results seem to question the continued emphasis on loss of consciousness as the most important determinant of when an athlete should return to the playing field after a concussion.[26] I have devised a well-accepted, on-the-field grading scale by combining elements of the

various definitions of concussion[4] ( Table 19A-1 ). Whichever scale is preferred by a practitioner, what is important is that consistent return-to-play criteria be used to prevent an athlete with ongoing symptoms of head injury from returning to play. On a public health note, the epidemic of concussion is significant enough to have promoted task forces of the National Football League and the National Hockey League to investigate the magnitude and impact of this problem on their sports. The grade 1, mild concussion (based on the Cantu grading scale [4] ; see Table 19A-1 ) is the most difficult to recognize and judge. The patient does not lose consciousness TABLE 19-A-1 -- Cantu Grading System for Concussion Grade 1 (mild) No loss of consciousness; post-traumatic amnesia for less than 30 minutes Grade 2 (moderate)

Loss of consciousness for less than 5 minutes or post-traumatic amnesia lasting longer than 30 minutes but less than 24 hours

Grade 3 (severe)

Loss of consciousness for more than 5 minutes or post-traumatic amnesia for more than 24 hours

From Cantu RC: The Exercising Adult. New York, Macmillan, 1987. but suffers impaired intellectual function, especially in remembering recent events and in assimilating and interpreting new information. Grade 1 concussion occurs most frequently (>90% of concussions) and often escapes medical attention. [34] Players commonly are dinged or have their bell rung and continue to play. Dave Meggyesy, a professional football player turned author, described this condition: Your memory's affected, although you can still walk around and sometimes continue playing. If you don't feel pain, the only way others know that you have been dinged is when they realize you can't remember the plays. [25] Initial treatment of a mild concussion requires the player to be removed from the game and observed on the bench. After a sufficient time (as short as 15 to 30 minutes), if the athlete has no headache, dizziness, or impaired concentration (including orientation to person, place, and time and full recall of events that occurred just before the injury), return to the game may be considered.[21] [34] Before being allowed to return, the player should be asymptomatic at rest and demonstrate movement with the usual dexterity and speed during exertion. If an athlete has any symptoms during rest or exertion ( Table 19A-2 ), continued neurologic observation is essential. With grade 2, moderate concussion (unconsciousness lasting less than 5 minutes), initial management should be the same as for grade 3. At this grade, however, if the period of unconsciousness is brief and if the athlete has no neck problems after regaining consciousness, clinical judgment may dictate that removal on a fracture board is not necessary. The athlete should be removed from the game and evaluated by a neurologist at a medical facility. It is not difficult to recognize a grade 3, severe concussion (unconsciousness lasting 5 minutes or more). Initial treatment should be the same as treatment of a suspected

cervical spine fracture. The athlete should be transported TABLE 19-A-2 -- Checklist of Postconcussion Signs and Symptoms Headache Anterograde or retrograde amnesia Nausea, vomiting

Fatigue

Drowsiness

Trouble falling asleep

Feeling slowed down

Excess sleep

Feeling in a fog

Sadness

Numbness, tingling

Nervousness

Dizziness, balance

Memory disturbance

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on a fracture board, with the head and neck immobilized, to a hospital with a neurosurgery service. All athletes with severe concussions should be admitted to check for possible intracranial bleeding.[12] [17] Postconcussion Syndrome

This syndrome consists of headache (especially with exertion), labyrinthine disturbance, fatigue, irritability, and impaired memory and concentration. [27] The true incidence of this syndrome is not known. Persistence of symptoms reflects altered neurotransmitter function[27] and usually correlates well with the duration of post-traumatic amnesia,[10] and it suggests that the athlete should be evaluated by computed tomography and neuropsychiatric testing. Before an athlete is allowed to return to play after a head injury, the criteria in Table 19A-3 should be met. To not do so risks cumulative brain injury as well as the second impact syndrome. Guidelines for Return to Play after Concussion

In general, return to competition after concussion must be deferred until all symptoms have abated and diagnostic study findings are normal. Most scales have incorporated a specific duration of recovery time based on grade of concussion to assist with this clinical decision-making. These scales generally refer to the asymptomatic state as the baseline on which to judge return-to-play criteria, but these older concepts may soon be replaced by more sensitive, athlete-specific examinations. A number of centers are looking into the efficacy of various neuropsychiatric tests and tests of balance and coordination in predicting whether the athlete may return safely to the sport sooner.[10] [11] Whereas these tests may play important roles in university and professional sports, their complexity and expense may preclude routine use. Again, before an athlete is allowed to return to play after a head injury, all the criteria in Table 19A-3 should be met.

Second Impact Syndrome

Second impact syndrome is defined as rapid brain swelling and herniation after a second head injury, and it is more common than previously reported in the medical literature.[2] [3] [5] Between 1980 and 1998, the National Center for Catastrophic Sports Injury Research in Chapel Hill, North Carolina, identified 35 probable cases of second impact syndrome among football players alone. Autopsy TABLE 19-A-3 -- Criteria for Return to Play after Concussion All postconcussion symptoms cleared at rest and exertion Neurologic examination findings normal If done, neuropsychological test scores baseline or above If done, neuroimaging study findings normal or without lesions of risk or surgery and magnetic resonance imaging findings confirmed 17 of these cases. An additional 18 cases, although not conclusively documented with autopsy findings, most probably are cases of second impact syndrome. Careful scrutiny excluded this diagnosis in 22 of 57 cases originally suspected. What Saunders and Harbaugh[32] called the second impact syndrome of catastrophic head injury in 1984 was first described by Schneider[33] in 1973. The syndrome occurs when an athlete who has had a head injuryoften a concussion or worse injury, such as cerebral contusionsustains a second head injury before symptoms associated with the first have cleared. The athlete typically suffers postconcussive symptoms after the first head injury. These may include visual, motor, or sensory changes and difficulty with thought and memory processes. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head. The second blow may be remarkably minor, perhaps involving a blow to the chest, side, or back that merely snaps the athlete's head and indirectly accelerates the brain. The athlete may appear stunned but usually does not lose consciousness and often completes the play. The athlete usually remains on his or her feet for 15 seconds to 1 minute or so but seems dazed, like someone suffering from a grade 1 concussion, without loss of consciousness. The athlete often remains on the playing field or walks off under his or her own power. What happens in the next 15 seconds to several minutes sets this syndrome apart from a concussion or even a subdural hematoma. Usually within seconds to minutes of the second impact, the athlete, conscious yet stunned, precipitously collapses to the ground, semicomatose, with rapidly dilating pupils, loss of eye movement, and evidence of respiratory failure. The pathophysiologic mechanism of second impact syndrome is thought to involve loss of autoregulation of the brain's blood supply.[2] [3] [14] [32] [33] This loss of autoregulation

leads to vascular engorgement within the cranium,[5] [14] which in turn markedly increases intracranial pressure and leads to herniation of the medial surface (uncus) of the temporal lobe or lobes below the tentorium or of the cerebellar tonsils through the foramen magnum. The usual time from second impact syndrome to brain stem failure is rapid (2 to 5 minutes). Once brain herniation and brain stem compromise occur, coma, ocular involvement, and respiratory failure precipitously ensue. This demise occurs far more rapidly than that usually seen with an epidural hematoma. Second impact syndrome is not confined to football players, and physicians who cover athletic events, especially those in which head trauma is likely, must understand second impact syndrome and be prepared to initiate emergency treatment. Head injury reports of athletes in other sports almost certainly represent the syndrome but err by not labeling it as such. Fekete,[8] for example, described a 16-year-old high-school hockey player who fell during a game, striking the back of his head on the ice. The boy lost consciousness and afterward complained of unsteadiness and headaches. While playing in the next game, 4 days later, he was checked forcibly and again fell, striking

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his left temple on the ice. His pupils rapidly became fixed and dilated, and he died within 2 hours while in transit to a neurosurgical facility. An autopsy report revealed occipital contusions of several days' duration, an edematous brain with a thin layer of subdural and subarachnoid hemorrhage, and bilateral herniation of the cerebellar tonsils into the foramen magnum. For a catastrophic condition that has a mortality rate approaching 50% and a morbidity rate nearing 100%, prevention takes on the utmost importance. An athlete who is symptomatic from a head injury must not participate in contact or collision sports until all cerebral symptoms have subsided, and preferably at least not for 1 week after. Whether it takes days, weeks, or months to reach the asymptomatic state, the athlete must never be allowed to practice or compete while he or she has postconcussion symptoms. Players, parents, and the physician and medical team must understand this. Files of the National Center for Catastrophic Sports Injury Research include cases of athletes who did not report their cerebral symptoms because, above all, they wanted to return to play. Intracranial Hemorrhage

Although concussion is a major public health problem in youth sports, the leading cause of death from athletic head injury is intracranial hemorrhage. There are four types of hemorrhage, of which the examining trainer or physician must be aware in every head injury: epidural, subdural, intracerebral, and subarachnoid. Because all four types of intracranial hemorrhage may be fatal, rapid and accurate initial assessment and appropriate follow-up are mandatory after an athletic head injury. Epidural Hematoma

An epidural hematoma is usually the most rapidly progressing intracranial hematoma. It is frequently associated with a fracture of the temporal bone and results from a tear of the middle meningeal artery supplying the covering (dura) of the brain. This hematoma accumulates between the skull and the covering of the brain and may reach a fatal size in 30 to 60 minutes. The athlete may have a lucid interval, although this does not always occur. Thus, the athlete may initially remain conscious or regain consciousness after the head trauma and then experience an increasing headache and a progressive decline in level of consciousness. This occurs as the clot accumulates and the intracranial pressure increases. This lesion, if present, will almost always declare itself within 1 or 2 hours from the time of injury. The brain substance is usually free from direct injury; thus, if the clot is promptly evacuated, full recovery is to be expected. Because this lesion may be rapidly fatal if missed, all athletes receiving a major head injury must be observed closely and frequently, preferably during the ensuing 24 hours. This observation should be done at a facility where full neurosurgical services are immediately available. Subdural Hematoma

A subdural hematoma occurs between the brain surface and the dura, and so it is located directly on the brain. Subdural hematoma usually results from a torn vein running from the surface of the brain to the dura or from diffuse injury to the surface of the brain. It may also result from a torn venous sinus or even a small artery on the surface of the brain. Unlike epidural hematoma, subdural hematoma is often associated with injury to the brain tissue. If the symptoms of a subdural hematoma are severe enough to necessitate emergent surgery, the mortality rate is high, not because of the clot itself, but because of the associated brain damage. With a subdural hematoma, the athlete usually does not regain consciousness, and the need for immediate neurosurgical evaluation is obvious. This is the most common fatal athletic head injury. On occasion, the brain itself is not injured, and a subdural hematoma may develop slowly during a period of days to weeks. This chronic subdural hematoma, although often associated with headache, may initially cause a variety of mild, almost imperceptible mental, motor, or sensory signs and symptoms. Because its recognition and removal will lead to full recovery, it must always be suspected in an athlete who has previously sustained a head injury and who, days or weeks later, is not quite right. A computed tomographic or magnetic resonance imaging scan of the head shows such a lesion. Intracerebral Hematoma

An intracerebral hematoma is the third type of intracranial hemorrhage seen after head trauma. In this instance, the bleeding is into the brain substance itself, usually from a torn artery. It may also result from the rupture of a congenital vascular lesion, such as an aneurysm or arteriovenous malformation. Intracerebral hematomas are not usually associated with a lucid interval and may be rapidly progressive. Death occasionally

occurs before the injured athlete can be moved to a hospital. Because of the intense reaction such a tragic event precipitates among fellow athletes, family, students, and the community, and because of the inevitable rumors that follow, it is imperative to obtain a complete autopsy to clarify the causative factors. The autopsy often reveals a congenital lesion that may indicate that the cause of death was other than presumed and ultimately unavoidable. Only by such full, factual elucidation will appropriate feelings of guilt in fellow athletes, family, and friends be assuaged. Subarachnoid Hematoma

A fourth type of intracranial hemorrhage is subarachnoid, confined to the cerebrospinal fluid space along the surface of the brain. After head trauma, such bleeding is usually the result of disruption of the tiny surface brain vessels and is analogous to a bruise, but it can also result from a ruptured cerebral aneurysm or arteriovenous malformation. As with the intracerebral hematoma, there is often brain swelling. Because bleeding is superficial, surgery is not usually required unless a congenital vascular anomaly is present.

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Contusion or injury of the brain, as seen with any hematoma, usually causes headache and, often, an associated neurologic deficit, depending on the area of the brain involved. The irritative properties of the blood may also precipitate a seizure. If a seizure occurs in a head-injured athlete, it is important to roll the patient onto the side. By this maneuver, any blood or saliva rolls out of the mouth or nose, and the tongue cannot fall back to obstruct the airway. A padded tongue depressor or oral airway can be inserted between the teeth. Under no circumstances should fingers be inserted into the mouth of an athlete who is having a seizure because a traumatic amputation can easily result from such a maneuver. Such a traumatic seizure will usually last only 1 to 2 minutes. The athlete will then relax, and transportation to the nearest medical facility can be effected. After intracranial hemorrhage, prophylactic anticonvulsant therapy is usually given for 1 week, and a longer course may be indicated if the patient actually experienced a seizure. Because the chance of post-traumatic epilepsy is less than 10% with a concussion or contusion, anticonvulsant therapy is given in these conditions only if late epilepsy actually occurs.[9]

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Summary Careful study of the pathophysiology and epidemiology of sports-related head injuries brings to light many common features. The incidence increases as the sport becomes increasingly violent and aggressive. Poor conditioning and lack of knowledge of the proper techniques of the sport put the athlete at significant risk for head injury. Improper helmet fit and the use of the head as an offensive weapon are also common features of injury. Although recognition of these features has resulted in a dramatic reduction in catastrophic neurologic injury, the athlete remains at risk for less severe head injury, and concussion remains at epidemic proportions at high-school, university, and professional levels. It is hoped that careful recognition of the signs of concussion and knowledge of return-to-play criteria will prevent catastrophic complications from minor head injuries, although the long-term effects of multiple concussions on cognition may be a problem.

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References Cantu RC, Mueller FO: Fatalities and catastrophic injuries in high school and college sports. Physician Sportsmed 27:35-50, 1999. 1.

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Cantu RC: Second impact syndrome: Immediate management. Physician Sportsmed 20:55-60, 1992.

Cantu RC, Voy RO: Second impact syndrome: A risk in any contact sport. Physician Sportsmed 23:27-34, 1995. 3.

4.

Cantu RC: The Exercising Adult. New York, Macmillan, 1987.

Cantu RC: Guidelines for return to contact sports after a cerebral concussion. Physician Sportsmed 14:76-79, 1987. 5.

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Cantu RC: Health Maintenance Through Physical Conditioning. Littleton, Mass, Wright-PSG, 1981.

Committee on Head Injury Nomenclature of the Congress of Neurological Surgeons: Glossary of head injury including some definitions of injury to the cervical spine. Clin Neurosurg 12:386-394, 1966. 7.

Fekete JF: Severe brain injury and death following minor hockey accidents. Can Med Assoc J 99:1234-1239, 1968. 8.

Gruber R, Bubl R, Fruttiger V: Anticonvulsant therapy after juvenile craniocerebral injuries: A retrospective evaluation. Z Kinderchir 40:199-202, 1985. 9.

Guskiewicz K, Perrin D, Gansneder B: Effect of mild head injury on postural sway. J Athletic Training 81:300-306, 1996. 10.

Guskiewicz K, Riemann B, Perrin D, et al: Alternative approaches to the assessment of mild head injuries in athletes. Med Sci Sports Exerc 29:213-221, 1997. 11.

Hugenholtz H, Richard MT: Return to athletic competition following concussion. Can Med Assoc J 127:827-829, 1982. 12.

Jennett B: Late effects of head injuries. In Critchley M, O'Leary JL, Jennett B (eds): Scientific Foundations of Neurology. Philadelphia, Davis, 1971. 13.

Kelly JP, Nichols JS, Filley CM, et al: Concussion in sports: Guidelines for the prevention of catastrophic outcome. JAMA 266:2867-2869, 1991. 14.

Kim PC, Haddock G, Bohn D, et al: Tobogganing injuries in children. J Pediatr Surg 30:1135-1137, 1995. 15.

Kraus JF: Epidemiologic features of injuries to the central nervous system. In Anderson DW (ed): Neuroepidemiology. Boca Raton, Fla, CRC Press, 1991. 16.

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Lindsay KW, McLatchie G, Jennett B: Serious head injury in sport. Br Med J 281:789-791, 1980.

Lovell MR, Iverson GL, Collins MW, et al: Does loss of consciousness predict neuropsychological decrements after concussion? Clin J Sport Med 9:193-198, 1999. 18.

Macciocchi SN, Barth JT, Alves W, et al: Neuropsychological functioning and recovery after mild head injury in collegiate athletes. Neurosurgery 39:510-514, 1996. 19.

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Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21:2294-2299, 1996.

Maroon JC, Steele PB, Berlin R: Football head and neck injuries: An update. Clin Neurosurg 27:414-429, 1980. 21.

Matser JT, Kessels AGH, Jordan BD, et al: Chronic traumatic brain injury in professional soccer players. Neurology 51:791-796, 1998. 22.

McAbee GN, Ciminera PF: Intracranial hematoma in experienced teenage equestrians. Pediatr Neurol 15:235-236, 1996. 23.

McGuffie AC, Fitzpatrick MO, Hall D: Golf related head injuries in children: The little tigers. Scott Med J 43:139-140, 1998. 24.

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Meggyesy D: Out of Their League. Berkeley, Calif, Ramparts, 1970.

Mueller FO, Cantu RC, Van Camp S: Football. In Mueller FO, Cantu RC, Van Camp S (eds): Catastrophic Injuries in High School and College Sports. Champaign, Ill, Human Kinetics, 1996. 26.

Murphey F, Simmons JC: Initial management of athletic injuries to the head and neck. Am J Surg 98:379-383, 1959. 27.

Nelson DE, Bixby-Hammett D: Equestrian injuries in children and young adults. Am J Dis Child 146:611-614, 1992. 28.

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Prall JA, Winston KR, Brennan R: Severe snowboarding injuries. Injury 26:539-542, 1995.

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Rosenow JM, Hahn MS, Moore KD, et al: Pediatric cranial golf injuriesan emerging contemporary

phenomenon? Surg Neurol 50:608, 1998. 31.

Rowe BH, Bota GW: Sledding deaths in Ontario. Can Fam Physician 40:68-71, 1994.

Saunders RL, Harbaugh RE: The second impact in catastrophic contact sports head trauma. JAMA 252:538-539, 1984. 32.

Schneider RC: Head and Neck Injuries in Football: Mechanisms, Treatment and Prevention. Baltimore, Williams & Wilkins, 1973. 33.

34.

Yarnell PR, Lynch S: The ding amnestic states in football trauma. Neurology 23:196-197, 1973.

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Section B Pediatric Sports-Related Head Injuries Kevin L. Stevenson MD P. David Adelson MD, FACS, FAAP Sports-related head injuries are common in all age groups but are of particular concern in children because of the potential for lifelong effects. In the pediatric population, although only approximately 10% of all head injuries are related to athletics,[45] 70% of traumatic deaths and 20% of permanent disabilities that occur in athletic or recreational pursuits are from injuries to the head.[19] Deaths are infrequent, but they occur more frequently as a result of head and neck injuries in young athletes; 26 such fatalities were reported between 1985 and 1994 among high-school football players alone.[53] Although most children are sub-lethally injured, many suffer an injury that is significant enough to result in long-term cognitive and other permanent deficits. When one considers that more than 36 million children between the ages of 6 and 21 years participate in organized athletics each year,[21] and countless others in nonorganized athletics, it becomes obvious that the proper recognition, treatment, and prevention of head injury can have an impact on a significant number of young athletes. With the exception of bicycle accidents, athletics-related head injuries are rare in children younger than 12 years. Young children's bodies are typically incapable of generating forces sufficient to produce a significant injury, and the attitude of the younger athlete is typically less aggressive than that of older children. Regardless of age, although the majority of athletic head injuries are not life-threatening and do not require hospitalization, it is important for the physician and allied health care providers to recognize the short- and long-term consequences of head injury in children so that they can be accurately diagnosed and properly treated. This chapter reviews the mechanisms and pathophysiologic events, including secondary sequelae that follow head injury in children; acute injury assessment; differential diagnosis; acute management; and return-to-play guidelines after a concussive head injury. The last

section includes comments on specific sports. Mechanism of Injury

Acute head injuries generally result from acceleration-deceleration injuries due to angular (rotational) acceleration, linear (translational) acceleration, focal impact, or a combination of these forces. Angular acceleration injuries are caused by rapid turning of the head and result in shearing forces transmitted deep within the brain parenchyma. This type of force is poorly tolerated by the brain and is maximal where rotation is impaired by dural attachments to the skull: the falx cerebri and tentorium cerebelli. Impaired rotation at these structures imparts increased shearing forces to the structures in proximity: the brain stem and corpus callosum. Depending on the magnitude of the applied angular acceleration force, the severity of injury may range from mild concussion to death. A linear acceleration injury occurs when force is applied in a vector perpendicular to the skull. The applied force causes tensile and compressive forces within the brain. Because the brain is floating in cerebrospinal fluid (CSF), the brain can accelerate or decelerate relative to the skull, resulting in injurious contact with the skull at the site of impact or opposite the site of impact. These injuries had previously been termed coup and contrecoup, respectively. In addition, as the brain accelerates or decelerates within the skull, the rough surface of the skull base can impart direct injury to the cortex and parenchyma. The most common regions injured in this way are the frontal lobes in the anterior fossa and the temporal lobes in the middle fossa. The brain, in part owing to the cushioning effect of CSF, better tolerates this type of force. Impact forces result in the application of maximal stress at the point of contact, leading to skull fractures and injury to the structures (brain parenchyma, blood vessels, dura) directly underlying the point of applied force. Although the focal injury can be severe, distant neural structures are commonly spared because of the dissipation of the force by the skull and the cushioning effect of the CSF. Two points about the effects of forces applied to the brain should be kept in mind. First, injury due to brain acceleration (angular or linear) does not require direct head impact.[48] For example, an athlete who receives a blow to the chest can suffer a brain injury from brain acceleration imparted by a whiplash effect of the cervical spine. Second, acceleration of the brain is lessened if the athlete prepares for the oncoming force by contracting the cervical musculature. Contracted cervical musculature renders the mass of the head essentially that of the entire body and lessens the effects of acceleration applied to the body as well as the whiplash effect.

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Concussion

The most common athletic head injury is concussion. It was previously believed that approximately 20% of high-school football players could expect to suffer at least one concussion each playing season.[31] More recently, this number has more accurately been estimated at approximately 7%. [15] When one considers that more than 1.3 million high-school students participated in organized football in 1974,[54] the number of adolescents sustaining concussions is staggering. Commonly described as getting your bell rung, a concussion has often been treated as a minor consequence of athletics. The minor effects of concussion, though, have been disproved; experimental concussion models have shown extensive physiologic injury and anatomic neuronal dysfunction in the brain stem reticular activating system, cerebral ischemia, edema, neuronal depolarization with widespread acetylcholine release, neuronal disruption, and brain stem capillary damage with a variety of levels of

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force.[33] [73] Even when tissue damage is minimal, a cascade of pathophysiologic events occurs, including excitotoxicity,[43] intracellular calcium accumulation,[27] inflammation, and cerebrovascular dysautoregulation leading to membrane destabilization and a resultant rise in the energy demands of the membrane in an attempt to restore homeostasis. These energy demands are initially met through increased glucose use by glycolysis with a resultant lactic acidosis.[76] Within 24 hours, the brain enters a phase of metabolic depression that can last upward of 10 days, during which protein synthesis and other cellular functions are diminished, leading to an overall state of cerebral depression.[1] These cellular postconcussive derangements are likely to contribute to the postconcussive syndrome, postconcussive neuropsychological deficits, and second impact syndrome. There is no such thing as a minor head injury, and a concussion, no matter how minor, is a head injury with potential long-term consequences.

Definition

Considerable disagreement exists regarding the definition of a concussion. In 1966, the Committee of Head Injury Nomenclature of the Congress of Neurological Surgeons defined concussion as a clinical syndrome characterized by immediate and transient post-traumatic impairment of neural functions, such as alteration of consciousness, disturbance of vision, equilibrium, etc. due to brainstem involvement.[20] Since that time, numerous other descriptions and definitions have been put forth. Despite the semantic disagreement, the cardinal feature of every concussion is an alteration in mental status, with or without loss of consciousness. Confusion and amnesia are universally present to some degree in every athlete who suffers a concussion, requiring astute examination to detect even the mildest of cases and to prevent further injury. An athlete who has lost consciousness, no matter how briefly, has suffered a concussion.[73] Other common features of a concussion are headache, disorientation, blank stare, slurred speech, delayed verbal responses to questions, slow and uncoordinated motor function, dizziness, emotional lability, and short-term memory deficits. Differential Diagnosis

Concussions can be associated with other intracranial pathologic processes. Although most occur in isolation, there is the potential for coexisting intracranial injuries with every concussion, some of which can be lethal if undetected. These injuries include subdural hematomas, epidural hematomas, intracerebral hemorrhage, subarachnoid hemorrhage, cerebral contusions, diffuse axonal injury, and skull fractures. These injuries rarely occur without a coexisting concussion, whereas concussions are occasionally associated with a second intracranial pathologic process. Subdural Hematoma

Acute subdural hematomas are the leading cause of death in athletes, [32] with an approximate incidence three times that of acute epidural hematoma.[73] Between 1945 and 1994, 352 football players died of acute subdural hematomas, the majority of them at the high-school level.[53] Acute subdural hematomas result most commonly from laceration of a vein traversing the space between the dura and cortex and less commonly from a dural sinus or cortical artery laceration. As such, the hematoma forms directly on the brain surface ( Fig. 19B-1 ). Because of the force necessary to produce a subdural hematoma, the underlying brain is also often injured. As the hematoma enlarges, often rapidly, a mass lesion forms, compressing and further injuring the underlying brain. Untreated, acute subdural hematomas can lead to coma and death from herniation-induced brain stem dysfunction with a mortality rate of 30% to 40% even with expert neurosurgical treatment.[17] The athlete with an acute subdural hematoma is typically unconscious after injury and usually does not regain consciousness. Focal neurologic signs, if not present immediately, may appear rapidly in the form of hemiparesis, aphasia, unilateral pupillary dilation, or another focal finding. In the comatose athlete, a blown pupil may be the first

finding suggestive of the intracranial mass lesion. In many athletes, the neurologic findings are due to the underlying brain injury rather than the compressive effects of the subdural hematoma.[11] Given the lethal nature of subdural hematomas, an unconscious athlete should be transported to a neurosurgical center for computed tomographic (CT) imaging and emergent craniotomy as needed. Even if the mass lesion is emergently evacuated, the morbidity and mortality of subdural hematomas are high because of the associated brain injury. Chronic subdural hematomas can develop in athletes who incur a subdural hematoma that is not recognized and surgically evacuated.

Figure 19-B-1 Large right frontotemporal subdural hematoma in a child tackled during a football game. The athlete was rendered immediately unconscious and rapidly transported to a trauma center. Despite emergent craniotomy, the athlete suffered a significant brain injury with a poor functional outcome.

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Figure 19-B-2 Computed tomographic scan showing a large left frontotemporal epidural hematoma in a 14-year-old boy. Note the different densities of blood within the lesion, characteristic of an ongoing hemorrhage.

In these instances, the injury to the underlying brain is minimal and the athlete often did not have significant symptoms at the time of injury. During a period of weeks, the clot is broken down into a viscous motor oil-like fluid that expands and compresses the underlying brain. Any athlete suffering a minor head injury that did not require imaging who complains of persistent headache, nausea, or lethargy or who has a delayed focal neurologic finding (e.g., pronator drift, aphasia) should undergo CT scanning despite the length of time after the injury. Epidural Hematoma

Classically associated with skull fractures, epidural hematomas are the most rapidly progressing intracranial hemorrhage ( Fig. 19B-2 ). The meningeal arteries lie just under and often partially imbedded within the inner table of the skull. A skull fracture can tear one or more of these vessels and lead to formation of a hematoma in the extradural space. The most common scenario involves a temporal bone fracture lacerating the middle meningeal artery, although epidural hematomas can occur in any location. On occasion, an epidural hematoma can be secondary to venous bleeding, and in younger children, epidural hematomas can even occur from bleeding from the skull itself without laceration of a meningeal vessel.[73] The classically described presentation of an epidural hematoma is an immediate loss of consciousness after injury due to the concussion. Consciousness is then regained (the so-called lucid interval) for a period of minutes to hours, after which the patient lapses into coma and suffers a herniation syndrome with an ipsilateral pupillary dilation and

contralateral hemiparesis or posturing due to the expanded hematoma and cerebral shift. This classic scenario occurs in only 33% of presentations, however.[11] As previously mentioned, an acute epidural hematoma can accumulate rapidly, producing lethal consequences in as little as 15 to 30 minutes.[17] The emergent need for neurosurgical intervention cannot be overstated, and a high index of suspicion is required for correct diagnosis and treatment of this mass lesion. Although epidural hematomas can be rapidly fatal, a good outcome can be expected if craniotomy and evacuation are performed expeditiously because the injury to the brain itself is generally minimal or altogether absent.[11] Intracerebral Hemorrhage

Intracerebral hemorrhage is associated with a sudden, severe acceleration-deceleration injury to the brain.[17] After injury, the athlete is usually rendered unconscious and typically remains so. Most commonly occurring in subcortical structures (subcortical white matter, basal ganglia, thalamus, brain stem), traumatic intracerebral hemorrhages are often neurologically devastating ( Fig. 19B-3 ). The primary pathologic process in intracerebral hemorrhage is most commonly traumatic arteriolar laceration with subsequent intraparenchymal bleeding. Rupture of a preexisting vascular lesion, such as an arteriovenous malformation or aneurysm, can also lead to this lesion and should be suspected when the resultant injury is far greater than is expected from the mechanism of injury. Although diagnostic and localizing signs are beyond the scope of this chapter, coma can quickly progress to death in these patients, even before they can be removed from the field, and therefore rapid transport to a neurosurgical facility is critical.

Figure 19-B-3 Computed tomographic scan of a 7-year-old boy with a right intraparenchymal (basal ganglia) hemorrhage.

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Depending on the extent of injury, there is potential for complete recovery. Subarachnoid Hemorrhage

Despite the association between intracranial aneurysms and subarachnoid hemorrhage, trauma is the most common cause of this form of intracranial hemorrhage [74] and is most commonly due to laceration of small cortical surface vessels. In this situation, consciousness may or may not be lost, headache is typically prominent, and nuchal rigidity is found secondary to meningeal irritation. Traumatic subarachnoid hemorrhage, in and of itself, does not cause mass effect, and surgical intervention is not required unless the hemorrhage extends into the ventricular system, causing hydrocephalus. Subarachnoid hemorrhage secondary to intracranial aneurysm or arteriovenous malformation rupture should be considered in the differential diagnosis of this form of

intracranial hemorrhage, even in the setting of athletic trauma. Any suspicion of these vascular anomalies should prompt cerebrovascular angiography to exclude their presence ( Fig. 19B-4 ). Cerebral Contusion

Cerebral contusions can be thought of as a bruise of the brain parenchyma. Contusions can occur in the setting of skull fracture, especially a depressed fracture, whereby the bone is forced inward, making focal impact with the cortical surface. Because the brain, floating in CSF, has the ability to move independently within the cranium, acceleration-deceleration forces can cause the brain to impact the inner table of the skull without fracture. Sudden deceleration of the head, as when a falling athlete's head makes contact with the playing surface, causes the brain to impact the skull directly under the point of contact. The most common locations of contusions are the frontal, temporal, and occipital poles ( Fig. 19B-5 ). Contusions are commonly associated with a concussion, and consciousness is often lost because of the forces necessary to produce this injury. Symptoms can range from headache to focal neurologic deficit (e.g., right hemiparesis if the contusion is in the left motor cortex), depending on the location of the contusion. Although resolution without surgical intervention is the typical course, cerebral contusions can enlarge and coalesce (blossom) during the first 24 to 48 hours ( Fig. 19B-6 ), leading to focal mass effect and sudden neurologic decline, particularly if the contusion is in the temporal lobe or cerebellum. After diagnosis, frequent neurologic checks and close monitoring by a neurosurgeon are mandatory. A follow-up CT scan of the head is frequently obtained 12 to 24 hours after the injury to assess changes in the size of the contusion. Diffuse Axonal Injury

Diffuse axonal injury is a primary injury produced by rotational acceleration-deceleration of the brain.[28] Rotational forces cause shearing of multiple axons, widespread white matter axonal damage, and discrete focal hemorrhagic lesions in the corpus callosum and rostral brain stem. Diffuse axonal injury is the most common cause of persistent vegetative state and disability after traumatic

Figure 19-B-4 Two examples of traumatic subarachnoid hemorrhage. A, Focal subarachnoid hemorrhage in the left sylvian fissure in a defensive lineman after he tackled a running back. Also present is layering of blood along the tentorium. B, Diffuse subarachnoid hemorrhage after a blow to the right side of the head. Severe, diffuse subarachnoid hemorrhage like this should prompt a search for an intracranial vascular anomaly, such as an aneurysm or an arteriovenous malformation, by means of cerebral angiography.

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Figure 19-B-5 Diffuse frontal contusions in a 16-year-old boy who lost consciousness after being tackled in a football game. Although the contusions enlarged slightly during the ensuing days, management was nonoperative.

Figure 19-B-6 A, Immediate postinjury computed tomographic scan of a 9-year-old child found unconscious next to his bicycle. Except for a scant amount of blood along the falx anteriorly, this scan is normal. The child improved for the first 24 hours, then deteriorated. B, A follow-up scan revealed a large left frontal intracerebral hemorrhagic contusion with surrounding edema. The hemorrhage resolved without surgical intervention, and the child recovered without serious deficits.

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brain injury,[73] and it occurs in nearly half of all severe head injuries.[33] Most commonly associated with severe head injury during motor vehicle accidents, diffuse axonal injury is occasionally seen in athletic head injury. Diffuse axonal injury renders the athlete immediately comatose after injury, with an absence of focal neurologic deficits (assuming there is no associated intracranial mass lesion). Immediate CT imaging is indicated and typically fails to show any major abnormality, although petechial hemorrhages can occasionally be appreciated in the subcortical areas. Magnetic resonance imaging is confirmatory in these instances, often showing discrete lesions in the corpus callosum and brain stem. Skull Fractures

Common in the pediatric population, a skull fracture may lessen or prevent significant injury to the underlying brain by dissipating the force of impact. Skull fractures can be divided into four general categories: linear, depressed, basilar, and open. Linear fractures ( Fig. 19B-7 ), the most common skull fracture in children,[34] require no immediate treatment. Most are found incidentally during imaging directed at discovering intracranial mass lesions. Depressed skull fractures involve displacement of the skull or skull fragments inward ( Fig. 19B-8 ). On occasion, a depression under the scalp can be palpated, but overlying soft tissue swelling often prevents diagnosis in this way. Focal neurologic deficits can occur if the fracture fragment exerts pressure on the underlying cortex or if the depressed fracture has caused a contusion or penetrating injury to the underlying brain. Although most depressed skull fractures heal spontaneously, immediate neurosurgical evaluation is required to determine whether the fracture should be elevated. Indications to elevate a depressed skull fracture include an open laceration, depression of 10 mm

Figure 19-B-7 Linear frontal skull fracture involving the inner and outer tables of the frontal sinus. Frontal sinus fractures typically do not require surgical intervention, and assuming that a cerebrospinal fluid leak

is not present, they are treated like any other linear skull fracture.

Figure 19-B-8 Computed tomographic image of a depressed left frontotemporal fracture in an 11-year-old girl hit in the left frontal area with a baseball.

or more, neurologic deficit related to underlying brain injury, CSF leak due to dural laceration, and depression in a cosmetically obvious location (i.e., forehead). Basilar skull fractures are linear fractures occurring in or involving the skull base. Basilar fractures differ from calvarial fractures in that they often involve the numerous vascular and nervous structures that are intimately involved with the skull base. Some common associated injuries are carotid artery injury (dissection, carotid-cavernous sinus fistula), cranial nerve palsy or injury (especially of cranial nerves I, II, VI, VII, and VIII), CSF leak (CSF otorrhea, rhinorrhea), and meningitis (from fracture through an air sinus). Signs, which may take hours to develop, include CSF rhinorrhea or otorrhea, postauricular ecchymoses (Battle's sign), periorbital ecchymoses (raccoon's eyes), hemotympanum, anosmia, facial palsy, deafness, and extraocular muscle palsy. Major neurologic deficits (e.g., hemiparesis, aphasia) or coma may be seen with compromise of the carotid artery. Open skull fractures, by definition, involve interruption of the scalp overlying the fracture. Complications of open skull fractures include CSF leak (if an associated dural laceration is present), meningitis, and cerebral abscess. Blood loss from scalp lacerations can be impressive and can lead to hemorrhagic shock in rare instances. CT scanning is indicated in most cases, prophylactic antibiotics are mandatory, and surgical débridement and irrigation are required if the wound or brain is contaminated.

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Secondary Sequelae of Athletic Head Injury

The majority of children who suffer a sports-related head injury will recover without permanent morbidity. With

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adequate time away from contact sports and understanding on the part of parents, coaches, and educators, the most common athletic head injury, the grade 3 concussion, resolves. The goal in the evaluation and treatment of head injuries is to prevent second insults and to provide an optimal environment for recovery. With accurate diagnosis and swift transfer to a head trauma center, a significant number of athletes who sustain an intracranial hemorrhage can make a meaningful if not complete recovery. In contrast, even the mildest of concussions carries with it the risk of post-traumatic complications, including death. This is often due to a second injury too close in time to the primary impact or to the secondary sequelae of the primary injury. The long-term outcome is often predicated on the extent that these variables affect the acute and chronic issues. Acute Sequelae

Second Impact Syndrome

The term second impact syndrome (SIS) was coined by Saunders and Harbaugh in 1984[62] for a condition first described in 1973.[63] The most feared of postinjury complications, SIS is a potentially fatal condition that can occur after a seemingly trivial second head injury. This devastating condition is completely preventable. SIS occurs when an initial head injury is followed by a second, often trivial head injury before resolution of the first. The second injury need not even involve a blow to the

head. For example, a force that causes secondary head acceleration-deceleration may be sufficient to set in motion a rapid sequence of events that can lead to sudden death.[18] After the second injury, the player typically remains conscious but may appear dazed, as if suffering from a grade 1 concussion. Within seconds to minutes, the player collapses and becomes rapidly comatose. In a matter of minutes, brain stem signs such as dilated pupils, posturing, and respiratory arrest appear. The feature that differentiates SIS from an intracranial hematoma is the rapidity with which the player deteriorates. Often within minutes, and even before being removed from the playing field, the player progresses rapidly to a moribund state or death. The mechanism of SIS is not completely understood, but it is thought to be due to loss of cerebral autoregulation.[18] In the normal state, cerebral blood flow and pressure to the brain are tightly regulated through cerebral vasodilation or constriction so that within limits, the brain receives a constant volume and pressure of blood regardless of the volume and pressure delivered to it from the cardiovascular system. In SIS, the autoregulatory mechanisms of the cerebral vasculature fail; an abnormally high blood volume enters the cerebral vasculature, leading to a rapid rise in intracranial pressure and an often fatal herniation syndrome. Management of SIS requires rapid transport of the athlete to a neurosurgical center, where CT examination of the head usually shows a tremendously edematous brain and usually little more. Measures to control increased intracranial pressure are often futile, and 50% of athletes with SIS die secondary to brain stem compromise.[18] Survivors have a nearly 100% certainty of severe neurologic morbidity.[18] Because of the grave prognosis, and often the inefficacy of treatment, the best management scheme for SIS is prevention. Under no circumstance should an athlete return to play or practice until he or she is absolutely symptom free. Because SIS is preventable, education of coaches, players, and parents about this catastrophic complication of head injury should be an integral part of organized athletics. Diffuse Cerebral Swelling Syndrome

Unique to the pediatric population, malignant cerebral edema or diffuse cerebral swelling syndrome is not truly a secondary phenomenon of head injury, but it is discussed here because of its often delayed presentation. The primary pathophysiologic mechanism of diffuse cerebral swelling syndrome has been hypothesized to be similar to that of SIS: intracerebral vascular engorgement. What differentiates this syndrome from SIS is that diffuse cerebral swelling syndrome can occur after the first head injury. The child athlete typically sustains a head injury, such as a grade 2 concussion that seemingly resolves. Within minutes to several hours, the initially awake and alert athlete undergoes neurologic deterioration that can culminate in coma and death due to herniation.[18] Whereas diffuse cerebral hyperemia, rather than a focal intracranial mass lesion, has previously been implicated in the potentially lethal rise in intracranial pressure, [47] [52] the true etiology is probably multifactorial, involving excitotoxicity, inflammation, neurotransmitter dysfunction, and other cellular derangements. Although uncommon, with an incidence of 4.34% in one series,[65] this phenomenon can be rapidly fatal if it is not properly identified. Any young athlete who sustains any head injury, no matter how minor, must be observed by a responsible adult for the remainder of the day or evening because immediate neurosurgical intervention aimed at lowering intracranial

pressure is required as soon as neurologic deterioration is first detected. [10] Chronic Sequelae

Postconcussion Syndrome

Consisting of headache, irritability, minor personality changes, decreased concentration and memory, fatigue, and dizziness, the postconcussion syndrome can occur after any grade of concussion and may persist for several months. Several reports have shown that approximately 20% of patients who have suffered a concussion will report some or all symptoms of the postconcussion syndrome.[3] [41] [75] This syndrome is believed to be secondary to alterations in neurotransmitter function [40] and metabolic derangements,[76] and it is not associated with intracranial imaging abnormalities. Non-narcotic analgesics, such as ibuprofen and naproxen, can be helpful in relieving headache, but for the most part, treatment of the postconcussive syndrome is largely based on rest and the prevention of further injuries while symptoms persist. Irritability, minor personality changes, and poor concentration can have a negative impact on scholastic performance, and time away from school

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in the first few weeks after injury may prove beneficial in the long term. Symptoms that persist beyond several weeks or are progressive should prompt CT scanning to rule out intracranial disease, such as a chronic subdural hematoma. Imaging, including magnetic resonance imaging, may still not be diagnostic because this syndrome is most often based on the clinical examination findings. Athletics of any kind are strictly prohibited if any symptoms of the postconcussive syndrome are present. Neuropsychological Impairment

Although most young athletes appear asymptomatic relatively soon after most head injuries, in-depth neuropsychological testing often reveals some degree of impairment after even the most minor of injuries.[5] [25] [49] Poor performance in tasks requiring auditory concentration, eye-hand coordination, short-term memory, and other cognitive functions can be found in nearly every athlete who sustains a concussion or other head injury. In most athletes, neuropsychological functions return to baseline within 5 days,[49] but a small percentage of players will experience cognitive difficulty for months after injury. It is well known that a player who has suffered an initial concussion is four to six times more likely than a previously nonconcussed athlete to suffer a second concussion. [31] One possible explanation is that the neurocognitive deficits uniformly present after the first concussion place the athlete at higher risk for a second head injury because of decreased concentration, coordination, and attentiveness. Post-traumatic Migraine

Especially common among adolescents, migraine headache complete with aura, nausea, and vomiting can occur soon after athletic head injury as well as persist for variable periods thereafter.[7] [38] Although the exact mechanism of trauma-induced migraine is not completely understood, cerebral vasospasm[46] and spreading depression[56] have been implicated. Like classic migraine, post-traumatic migraines can be preceded by an aura involving a focal neurologic deficit, raising concern of an intracranial mass lesion. Any athlete exhibiting the onset of a focal neurologic deficit or a new severe headache should undergo CT scanning immediately to rule out intracranial hemorrhage as the cause. Once the diagnosis of post-traumatic migraine has been established, medical therapy can be undertaken for management of this frequently disabling condition. The management of post-traumatic migraine usually involves treatment with nonsteroidal anti-inflammatory drugs, although escalation to antimigraine (sumatriptan, beta-blockers) or antiepileptic (gabapentin) medications may be necessary. Seizures

Immediate post-traumatic seizures are a concern with any head injury; they occur in 2.6% of all children who suffer a primary brain injury.[4] Fortunately, when they do occur, post-traumatic seizures tend to be relatively short-lived and self-limited. [15] Immediate management of the young athlete having a seizure involves ensuring an adequate airway and protecting the athlete from harming himself or herself. If a mouthguard is in place and can be removed, removal should be done without placing a finger into the player's mouth to avoid severe injury to the finger. Because seizures are more common after focal brain injury (e.g., contusion, subdural hematoma), an emergent CT scan should be obtained in every child who has a seizure after trauma. Chronic epilepsy requiring long-term antiepileptic medication will develop in 7.4% of children with severe head injury. In children with moderate and mild head injuries, epilepsy will develop in 1.6% and 0.2%, respectively, a frequency that does not differ significantly from that of the noninjured pediatric population.[4] Young athletes with epilepsy unrelated to trauma, with few exceptions, are at no increased risk for sustaining injuries than their nonepileptic peers are, [16] and frequent exercise may actually improve their condition. Clinical and experimental data show that seizure activity decreases during exercise,[6] [72] possibly because of changes in blood pH or increased concentrations of gamma-aminobutyric acid and beta-endorphins.[16] It has also been shown that epileptic children are not at increased risk for post-traumatic seizures after athletic head injury,[8] suggesting that contact sports pose no increased threat to young athletes with epilepsy. With the exception of unsupervised swimming, the child with epilepsy should be able to participate in any athletic endeavor that she or he chooses.

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Acute On-Field Injury Assessment

The first step in assessing the athlete with a potential head injury is recognizing that a head injury has occurred. This process is relatively easy in the unconscious athlete; it is the child who walks off the field under his or her own power who presents the larger challenge. Of football players who are knocked out during play, 70% return to the contest the same day,[2] possibly owing in part to lack of recognition of the head injury. Concussion Grading

Multiple grading schemes have been developed in an attempt to stratify the severity of concussions[14] [55] [58] [59] [71] ( Table 19B-1 ). Although no one grading system is universally accepted, all grading scales provide the physician, trainer, and coach with a reproducible means of identifying concussion and advising a young athlete when it is safe to return to play. In this discussion, Cantu's concussion grading scale is used.[13] Grade 1 concussions are defined by the absence of a loss of consciousness and less than 30 minutes of post-traumatic amnesia; they represent more than 90% of cases of concussion.[17] Despite their relative frequency, grade 1 concussions are often the most difficult to detect. The young athlete, often unaware of the seriousness of the injury, may dust off the cobwebs and continue playing. In this situation, it is often a teammate who notices subtle changes in the injured athlete, such as forgetting the snap

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TABLE 19-B-1 -- Concussion Grading Scales

Grade 1 (Mild)

Grade 1a Grade 2 (Moderate)

Grade 3 (Severe)

Cantu[14]

No LOC or PTA 24 hr

Colorado Medical Society[59]

No LOC, confusion without amnesia

No LOC, confusion with amnesia

LOC

AAN[58]

No LOC, symptoms 15 min

LOC

Torg[71]

No LOC or amnesia (PTA allowed) [grade I-II]

LOC for a few minutes, PTA or retrograde amnesia [grade III-IV]

LOC with coma, confusion, amnesia [grade V-VI]

VNI[55]

Brief LOC, PTA /das/book/view/29309971/1103/436.html/top

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Comments on Specific Sports

Nearly every child and adolescent participates in athletics of some sort, the majority being unorganized sandlot team sports and individual activities such as bicycling and skateboarding. Although organized athletics make up a smaller percentage of the total of athletic endeavors, the numbers are still substantial, and most of the sports-related head injury data is derived from organized athletics. Team sports involving frequent contact, such as football, baseball, basketball, and soccer, are the most frequent activities producing injury of any type, surprisingly more often than unsupervised activities such as skateboarding and in-line skating. [23] Football-related head injuries are by far the best studied and observed, with a small body of data collected to date on several other sports commonly associated with head injury. Football

Halfway through the 1905 collegiate football season, President Theodore Roosevelt met representatives of several Ivy League schools in an attempt to save the sport from being banned because of the brutal nature of play. During that single season, 18 players died of head injury at the college level,[22] and a complete rewriting of the rules occurred in response. Since that time, football-related head injury deaths have declined, but they have not been eliminated. Before 1976, an average of more than 12 head injury-related deaths occurred annually; 36 fatalities occurred during the 1968 season alone.[53] In 1976, spearing (initiating contact with another player using the helmet) was outlawed in football, and this is considered the greatest advancement in head and neck injury prevention in football.[57] Although joint injuries and fracture account for the majority of high-school level football injuries,[24] head injuries are the leading cause of death in high-school football players. Despite modifications of rules and safety equipment, an average of 3.2 deaths due to head injury occurred each year during the early 1990s; 2.6 of these deaths occurred at the high-school level.[53] The majority of these deaths are due to subdural hematoma [2]

[53]

that occurred during incidental collision or deliberate tackling.[53]

Hockey

Despite improvements in safety equipment and education, head injury in hockey occurs in 18% to 28% of players.[12] [30] [42] The most common head injury sustained by young hockey players is concussion, with an incidence of up to 0.8 per 1000 player-hours in the 5- to 14-year-old age group and an incidence of 2.7 at the high-school level.[39] Unlike in football, head injury occurs less commonly in children and adolescents than in collegiate and professional players,[39] probably because of the mandatory use of face-shielded helmets and mouthguards in this population. Bicycling

With an estimated 33 million participants younger than 20 years, [66] bicycling may be the most popular athletic activity of children and adolescents. Head injury is the most common cause of death and serious disability in bicycling[26] [67] ; an average of 247 deaths and 140,000 head injuries occur annually in participants younger than 20 years.[66] The majority of these deaths occur in unhelmeted riders, making death due to bicycle-related head injury largely preventable. Although it had no significant impact on the total number of head injuries, New York State's Bicycle Helmet Law requiring the use of approved safety helmets in children younger than 14 years has shifted the type of injury sustained toward concussion and away from more serious injury, such as cerebral contusion and hemorrhage.[64] Safety helmets have been shown to reduce the risk for brain injury by 88%,[70] and all physicians involved in the care of children should strongly advocate their use. Other Sports

Focal injuries, such as depressed skull fracture and epidural hematoma, are the most common head injuries associated with golf and baseball. At one pediatric trauma center, only 9% of all head trauma was related to golf, but this sport accounted for 50% of all operative head injuries.[60] Downhill skiing head injuries are more common in children than in adults,[9] presumably because of less developed judgment and a tendency to ski fearlessly beyond their limits ( Fig. 19B-11 ). The most common severe injury incurred during equestrian activities is also head injury, most commonly occurring in unhelmeted riders.[37] Because few young athletes participate in the sport, boxing is mentioned only to discourage its support. Deserving of its own discussion, boxing is the only organized sport in which the primary goal is intentionally to inflict a brain injury on one's opponent. Between 1918 and 1983, 645 boxers died of head injury[1] ; 42 boxers died of head injury between 1984 and 1996 in the era of boxing safety.[61] In addition, the chronic effects of boxing on the brain are well known. The punch-drunk state refers not to the acute effects of concussion but rather to dementia pugilistica, a condition resembling Parkinson's and Alzheimer's diseases leading to permanent, severe neurologic impairment due to repeated violent blows to the head. [1] In short, any child or teenager

interested in pursuing the sport of boxing should be well supervised, and injury guidelines for concussion should be strictly adhered to in an attempt to avoid long-term effects.

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Figure 19-B-11 Classic lentiform epidural hematoma in a child who struck a tree while skiing. Note the thin-rimmed subdural hematoma along the frontal and temporal lobes on the left, opposite the epidural hematoma.

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Conclusion

Head injury is a significant contributor to athletic morbidity and mortality. Identification is the critical first step to proper management of head injury in a child, and this is especially important with mild head injuries such as grade 1 concussion, for which a missed diagnosis can have fatal consequences. The evaluation of the head-injured athlete requires a rapid yet thorough assessment of mental status and of the cranial nerve, motor, sensory, and cerebellar functions of the brain. On-field evaluation of the head-injured athlete is not a single event but rather an ongoing process that terminates in resolution of all symptoms or further off-field evaluation. The awake and alert athlete may be harboring a life-threatening hematoma, which requires constant vigilance on the part of the members of the injury team. Treatment of the head-injured young athlete varies according to the nature of the injury. In every case, however, the cervical spine is assumed to be unstable until it is proved otherwise. With the exception of grade 1 concussions, every head-injured athlete should be evaluated by a neurosurgeon or neurologist acutely, and mechanisms should be in place to provide rapid transfer to a trauma center in the event of head injury. It is the rare child who will be considered for a return to competition the day of head injury. Return-to-play guidelines are well established and should be strictly adhered to for prevention of a catastrophic neurologic injury that can occur when these guidelines are not observed. Despite advances in the neurosurgical management of head injury, the single most important aspect of head injury management is prevention. With proper supervision, training, and equipment, the young athlete can have a productive, enjoyable, and safe athletic experience.

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Kelly JP, Rosenberg JH: Diagnosis and management of concussion in sports. Neurology 48:575-580, 1997. 44.

Kraus JF, Fife D, Cox P, et al: Incidence, severity and external causes of pediatric head injury. Am J Dis Child 140:687-693, 1986. 45.

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McQuillen JB, McQuillen EN, Morrow P: Trauma, sport, and malignant cerebral edema. Am J Forensic Med Pathol 9:12-15, 1988. 52.

Mueller FO: Fatalities from head and cervical spine injuries occurring in tackle football: 50 years' experience. Clin Sports Med 17:169-182, 1998. 53.

Mueller FO, Blythe CS: Can we continue to improve injury statistics in football? Physician Sportsmed 12:79-84, 1984. 54.

Nelson WE, Jane JA, Gieck JH: Minor head injury in sports: A new system of classification and management. Physician Sportsmed 12:103-107, 1984. 55.

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Saunders RL, Harbaugh RE: Second impact in catastrophic contact-sports head trauma. JAMA 252:538-539, 1984. 62.

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Snoek JW, Minderhoud JM, Wilmink JT: Delayed deterioration following mild head injury in children. Brain 107:15-36, 1984. 65.

Sosin DM, Sacks JJ, Webb KW: Pediatric head injuries and deaths from bicycling in the United States. Pediatrics 98:868-870, 1996. 66.

Spence LJ, Dykes EH, Bohn DJ, et al: Fatal bicycle accidents in children: A plea for prevention. J Pediatr Surg 28:214-216, 1993. 67.

Swenson T, Lauerman W, Blanc R: Cervical spine alignment in the immobilized football player: Radiographic analysis before and after helmet removal. Am J Sports Med 25:226-230, 1997. 68.

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Warren JWL, Bailes JE: On the field evaluation of athletic head injuries. Clin Sports Med 17:13-26, 1998. 73.

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Chapter 20 - Cervical Spine Section A Cervical Spine Injuries in the Adult Joseph S. Torg MD This chapter presents guidelines for classification, evaluation, management, and return to play criteria for injuries that occur to the cervical spine and related neural structures as a result of participation in competitive and recreational activities. Although all athletic injuries require careful attention, the evaluation and management of cervical spine injuries should proceed with particular caution. The actual or potential involvement of the nervous system creates a high-risk situation in which the margin for error is low. An accurate diagnosis is imperative, but the clinical picture is not always representative of the seriousness of the injury at hand. An intracranial hemorrhage may present initially with minimal symptoms yet follow a precipitous downhill course, whereas a less severe injury, such as neurapraxia of the cervical spinal cord associated with alarming paresthesias and paralysis, will resolve swiftly and allow a return to activity. Although the more severe injuries are rather infrequent, this low incidence coincidentally results in little, if any, management experience for the on-site medical staff. Emergency Management

There are several principles that should be considered by individuals responsible for athletes who may sustain injuries to the cervical spine.[97] [98] 1. The team physician or the trainer should be designated as the person responsible for supervising on-the-field management of the potentially serious injury. This person is the

captain of the medical team. 2. Previous planning must ensure the availability of all necessary emergency equipment at the site of potential injury. At a minimum, this should include a spine board, a stretcher, and equipment necessary for helmet removal and the initiation and maintenance of cardiopulmonary resuscitation. 3. Previous planning must ensure the availability of a properly equipped ambulance as well as a hospital equipped and staffed to handle emergency neurologic problems. 4. Previous planning must ensure the immediate availability of a telephone for communicating with the hospital emergency room, ambulance, and other responsible individuals in case of an emergency. Managing the unconscious or spine-injured athlete is a process that should not be done hastily or haphazardly. Being prepared to handle this situation is the best way to prevent actions that could convert a repairable injury into a catastrophe. Be sure that all the necessary equipment is readily accessible and in good operating condition and that all assisting personnel have been trained to use it properly. On-the-job training in an emergency situation is inefficient at best. Everyone should know what must be done beforehand so that on a signal, the game plan can be put into effect. A means of transporting the athlete must be immediately available in a high-risk sport such as football and on call in other sports. The medical facility must be alerted to the athlete's condition and estimated time of arrival so that adequate preparation can be made. The availability of the proper equipment is essential! A spine board is necessary and is the best means of supporting the body in a rigid position. It is essentially a full-body splint. By splinting the body, the risk of aggravating a spinal cord injury, which must always be suspected in the unconscious athlete, is reduced. In football, appropriate instruments are also essential if it becomes necessary to remove the facemask. A telephone must be available to call for assistance and to notify the medical facility. Oxygen should be available and is usually carried by ambulance and rescue squads, although it is rarely required in an athletic setting. Rigid cervical collars and other external immobilization devices can be helpful if properly used. Manual stabilization of the head and neck is recommended if other means are not available. Properly trained personnel must know, first of all, who is in charge. Everyone should know how to perform cardiopulmonary resuscitation and how to move and transport the athlete. They should know where emergency equipment is located, how to use it, and the procedure for activating the emergency support system. Individuals should be assigned specific tasks beforehand, if possible, to prevent duplication of effort. Being well prepared helps alleviate indecisiveness and second-guessing. Prevention of further injury is the single most important objective. Do not take any action that could possibly cause further injury. The first step should be to immobilize the head and neck by supporting them in a stable position ( Fig. 20A-1A and B ). Then, in the

following order, check for breathing, pulse, and level of consciousness. If the victim is breathing, simply remove the mouth guard, if present, and maintain the airway. It is necessary

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Figure 20-A-1 A, Athlete with suspected cervical spine injury may or may not be unconscious. All who are unconscious, however, should be managed as though they had a significant neck injury. B, Immediate manual immobilization of the head and neck unit. First check for breathing. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

to remove the facemask only if the respiratory situation is threatened or unstable or if the athlete remains unconscious for a prolonged period. Leave the chin strap on. Once it is established that the athlete is breathing and has a pulse, evaluate the neurologic status. The level of consciousness, the response to pain, the pupillary response, and any unusual posturing, flaccidity, rigidity, or weakness should be noted. At this point, simply maintain the situation until transportation is available or until the athlete regains consciousness. If the athlete is face down when the ambulance arrives, change his or her position to face up by logrolling the athlete onto a spine board. Gentle longitudinal traction should be exerted to support the head without attempting to correct alignment. Make no attempt to move the injured person except to transport him or her or to perform cardiopulmonary resuscitation if it becomes necessary. If the athlete is not breathing or stops breathing, the airway must be established. If face down, he or she must be turned to a face-up position. The safest and easiest way to accomplish this is to logroll the athlete. In an ideal situation, the medical support team is made up of five members: the leader, who controls the head and gives the commands; three members to roll; and another to help lift and carry when it becomes necessary. If time permits and the spine board is on the scene, the athlete should be rolled directly onto it. Breathing and circulation are much more important at this point, however. With all medical support team members in position, the athlete is rolled toward the assistantsone at the shoulders, one at the hips, and one at the knees. They must maintain the body in line with the head and spine during the roll. The leader maintains immobilization of the head by applying slight traction and by using the crossed-arm technique. This technique allows the arms to unwind during the roll ( Fig. 20A-2A , B , and C ). The following guidelines are outlined by Kleiner[33] : Heavy persons, including many athletes, can be handled more efficiently with a six-plus-person lift; this is also preferred for suspected spine injuries. The

Inter-Association Task Force recommends that the six-plus-person lift be used along with a scoop stretcher whenever possible. In the athletic arena, there are usually a sufficient number of certified athletic trainers, physicians, and EMS personnel on hand to effectively administer the six-plus-person lift. For the six-plus-person lift, rescuer 1 immobilizes the neck. The rescuer's hands are placed on the athlete's shoulders (under the shoulder pads) with the thumbs pointed away from the athlete's face. The athlete's head will then be resting between the rescuer's forearms. The other six rescuers position themselves along the athlete's sides: one on each side of the chest, pelvis, and legs. The hands are slid under the athlete and equipment, if any, to provide a firm, coordinated lift. To lift, rescuer 1 gives the command prepare to lift; lift. The assistants lift the athlete 4 to 6 inches off the ground. It is imperative to maintain a coordinated lift and to prevent any movement of the spine. One of the rescuers at the thigh level must control the legs with his or her arms toward the feet so the splint can be slid into place from the foot end. After the splint is in place, while positions are maintained, rescuer 1 gives the command prepare to lower; lower, and the athlete is lowered onto the splint. In the case of larger athletes, as many as 10 individuals should participate in the lift, with one on each side of the chest and pelvis, two at the legs, one at the head, and one with the splint. The Inter-Association Task Force does not recommend the use of fewer than four-plus-persons to lift athletes suspected of having a spinal injury, even smaller athletes and children, in part due to the weight of the athlete while wearing protective equipment.[33] The facemask should be removed from the helmet as quickly as possible any time a player is suspected of having a spinal injury, even if still conscious and regardless of

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Figure 20-A-2 A, Logroll to a spine board. This maneuver requires four individuals: the leader to immobilize the head and neck and command the medical-support team, and the remaining three individuals positioned at the shoulders, hips, and lower legs. B, Logroll. The leader uses the crossed-arm technique to immobilize the head. This technique allows the leader's arms to unwind as the three assistants roll the athlete onto the spine board. C, Logroll. The three assistants maintain body alignment during the roll. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

respiratory status. The type of mask that is attached to the helmet determines the method of removal. Bolt cutters are used with the older single- and double-bar masks. The newer masks that are attached with plastic loops should be removed by cutting the loops with an instrument capable of cutting through the newer loop straps made of harder plastic, such as Dura shears, EMT scissors, or the Trainer's Angel. Remove the entire mask so that it does not interfere with further rescue efforts ( Fig. 20A-3A and B ). Once the mask has been removed, initiate rescue breathing following the current standards of the American Heart Association.

Once the athlete has been moved to a face-up position, quickly evaluate breathing and pulse. If there is still no breathing or if breathing has stopped, the airway must be established. The jaw thrust technique is the safest first approach to opening the airway of a victim who has a suspected neck injury because in most cases it can be accomplished by the rescuer grasping the angles of the victim's lower jaw and lifting with both hands, one on each side, displacing the mandible forward while tilting the head backward. The rescuer's elbows should rest on the surface on which the victim is lying ( Fig. 20A-4 ). If the jaw thrust is not adequate, the head tilt-jaw lift should be substituted. Care must be exercised not to overextend the neck. The fingers of one hand are placed under the lower jaw on the bony part near the chin and are lifted to bring the chin forward, supporting the jaw and helping tilt the head back. The fingers must not compress the soft tissue under the chin, which might obstruct the airway. The other hand presses on the victim's forehead to tilt the head back ( Fig. 20A-5 ). The transportation team should be familiar with handling a victim with a cervical spine injury, and they should be receptive to taking orders from the team physician or the trainer. It is extremely important not to lose control of the care of the athlete; therefore, be familiar with the transportation crew that is used. In an athletic situation, arrangements with an ambulance service should be made ahead of time. An appreciation of the controversy that currently exists

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Figure 20-A-3 Head and helmet must be securely immobilized. A, Remove cage-type masks by cutting the plastic loops with Dura shears, EMT scissors, or Trainer's Angel. Make the cut on the side of the loop away from the face. B, Remove the entire mask from the helmet so that it does not interfere with further resuscitation efforts. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

Figure 20-A-4 Jaw-thrust maneuverury.

Figure 20-A-5 Head tilt-jaw lift maneuver for opening the airway. Used if jaw thrust is inadequate or if a helmet is being worn.

for opening the airway of a victim with a suspected cervical spine inj between emergency medicine physicians and technicians on one hand and team physicians and athletic trainers on the other regarding helmet removal is in order. Existing emergency

medical services guidelines mandate removal of protective headgear before transport of an individual suspected of having a cervical spine injury to a fixed medical installation. These guidelines were implemented with motorcycle helmets in mind to facilitate both airway accessibility and application of cervical spine immobilizing devices. Clearly, such a procedure contradicts the long standing principle adhered to by team physicians and athletic trainers of leaving the helmet in place on the football player suspected of having a cervical spine injury until he or she is transported to a definitive medical facility. It must be emphasized that this particular problem is of more than academic interest. Specifically, there have been occasions in which emergency medical technicians under the direction of emergency room physicians unfamiliar with the nuances of the relationship between helmet, shoulder pads, and the injured cervical spine have precipitated turf battles by refusing to move the injured player before helmet removal. Again, such episodes represent more than an honest difference of opinion. Such episodes are clearly detrimental to the health and well-being of the injured player. It is my view that removal of the football helmet and shoulder pads on site exposes the potentially injured spine to both unnecessary and awkward manipulation and disruption of the immobilizing capacity of the helmet and shoulder pads. Also, removal of the helmet alone subjects a potentially unstable spine to hyperlordotic deformity. I agree with the National Collegiate Athletic Association Guidelines for helmet removal.[44] Unless there are special circumstances, such as respiratory distress coupled with an inability to access the airway, the helmet should never be removed during the prehospital care of the athlete with a potential head and neck injury unless the following conditions are present: 1. The helmet does not hold the head securely, such that immobilization of the helmet does not immobilize the head. 2. The design of the sport helmet is such that even after

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removal of the facemask, the airway cannot be controlled and ventilation cannot be provided. 3. After a reasonable period of time, the facemask cannot be removed. 4. The helmet prevents immobilization for transportation in an appropriate position. When helmet removal is necessary in any setting, it should be performed only by personnel trained in this procedure. If removal of the helmet is needed to initiate treatment or to obtain special radiographic studies, a specific protocol needs to be followed. With the head, the neck, and the helmet manually stabilized, the chin strap can be cut. While stability is being maintained, the cheek pads can be removed by slipping the flat blade of a screwdriver or bandage scissors under the pad snaps and

above the inner surface of the shell. One individual provides manual stability of the chin and the neck, and the other workers stabilize the head by placing their thumbs or index fingers into the earholes on both sides. By pulling both laterally and longitudinally, the helmet shell can be spread and eased off. If a rocking motion is necessary to loosen the helmet, the head and neck unit must not be allowed to move. Those individuals participating in this important maneuver must proceed with caution and must coordinate every move. Supporting the concept of leaving the helmet on is the work of Swenson and associates[71] and Gastel and colleagues. [21] Swenson and associates studied sagittal cervical alignment in live subjects with various combinations of helmets, shoulder pads, and no equipment. They concluded that football players with a potential cervical spine injury should be immobilized for transport with both helmet and shoulder pads left in place, thereby maintaining the neck in a position most closely approximating normal. Gastel and colleagues performed a similar study using stable and surgically destabilized cadaver spines. They concluded that to maintain a neutral position and minimize secondary injury to the cervical neural elements, both the helmet and the shoulder pads should be either left on or removed in the emergency setting. Lifting and carrying the athlete requires five individuals; four to lift, and a leader to maintain immobilization of the head. The leader initiates all actions with clear, loud verbal commands ( Fig. 20A-6A and B ). The same guidelines apply to the choice of a medical facility as to the choice of an ambulance: Be sure it is equipped and staffed to handle an emergency head or neck injury. There should be a neurosurgeon and an orthopaedic surgeon to meet the athlete on arrival. Radiographic facilities should be standing by. Once the athlete is in a medical facility and permanent immobilization measures have been instituted, the helmet can be removed. The chin strap may now be unfastened and discarded. The following protocol is recommended:[33] [44] The helmet be removed in a controlled environment after radiographs have been obtained and only by qualified medical personnel with training in equipment removal. Helmet removal should never be attempted without thorough communication among all involved parties. One person

Figure 20-A-6 A, Four members of the medical support team lift the athlete on the command of the leader. B, The leader maintains manual immobilization of the head. The spine board is not recommended as a stretcher. An additional stretcher should be used for transporting the patient over long distances. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

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should stabilize the head, neck, and helmet while another person cuts the chin strap. Accessible internal helmet padding, such as cheek pads, should be removed, and air

padding should be deflated before removal of the helmet, while a second assistant manually stabilizes the chin and back of the neck, in a cephalad direction, making sure to maintain the athlete's position. The pads are removed through the insertion of a tongue depressor or a similar stiff, flat-bladed object between the snaps and helmet shell to pry the cheek pads away from their snap attachment. If an air cell-padding system is present, deflate the air inflation system by releasing the air at the external port with an inflation needle or large-gauge hypodermic needle. The helmet should slide off the occiput with slight forward rotation of the helmet. In the event the helmet does not move, slight traction can be applied to the helmet, which can then be gently maneuvered anteriorly and posteriorly, although the head/neck unit must not be allowed to move. The helmet should not be spread apart by the ear holes [33] [44] as this maneuver only serves to tighten the helmet on the forehead and occiput region ( Fig. 20A-7A and B ). Despite the advent of such high-tech imaging modalities as computed tomography (CT) and magnetic resonance imaging (MRI), the initial radiographic examination of a patient with suspected or actual cervical spine trauma remains a routine radiographic examination. The preliminary study, performed while immobilization of the head, the neck, and the trunk is maintained, includes an anteroposterior and lateral examination of vertebrae C1 to C7. If major fracture, subluxation, dislocation, or evidence of instability is not evident, the remainder of the routine examination, including open mouth and oblique views, should be obtained. Depending on the neurologic and comfort status of the patient, lateral flexion and extension views should be obtained at some point. CT and MRI may provide more detailed information; however, horizontally oriented fractures and subtle subluxations are best identified on the routine radiographs. The choice of imaging technique depends on the results of the routine examination, the neurologic status of the patient, the preference of the responsible physician, and the availability of the imaging modalities.

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Cervical Spine Injuries

Athletic injuries to the cervical spine may involve the bony vertebrae, the intervertebral disks, the ligamentous supporting structures, the spinal cord, the roots, the peripheral nerves, or any combination of these structures. The

Figure 20-A-7 A, The helmet should be removed only when permanent immobilization can be instituted. The helmet may be removed by detaching the chin strap, removing cheek pads, deflating air padding, and gently pulling the helmet off in a straight line with the cervical spine. B, The head must be supported under the occiput during and after removal of the helmet. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

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panorama of injuries observed runs the spectrum from the cervical sprain syndrome to fracture-dislocations with permanent quadriplegia. Fortunately, severe injuries with neural involvement occur infrequently. Those responsible for the emergency and subsequent care of the athlete with a cervical spine injury should possess a basic understanding of the variety of problems that can occur. The various athletic injuries to the cervical spine and related structures are the following: 1. 2. 3. 4. 5. 6.

Nerve root-brachial plexus injury Stable cervical sprain Muscular strain Nerve root-brachial plexus axonotmesis Intervertebral disk injury (narrowing-herniation) without neurologic deficit Stable cervical fractures without neurologic deficit

7. 8. 9. 10. 11. 12. 13. 14.

Subluxations without neurologic deficit Unstable fractures without neurologic deficit Dislocations without neurologic deficit Intervertebral disk herniation with neurologic deficit Unstable fracture with neurologic deficit Dislocation with neurologic deficit Quadriplegia Death

Criteria for return to contact activities after congenital and traumatic problems of the cervical spine are included at the end of this chapter. Nerve Root-Brachial Plexus Injury

The most common and poorly understood cervical injury is pinch-stretch neurapraxia of the nerve roots and the brachial plexus ( Fig. 20A-8 ).[61] Typically, after an impact involving with head, neck, or shoulder, a sharp burning pain is experienced in the neck on the involved side that may radiate into the shoulder and down the arm to the hand. There may be associated weakness and paresthesia in the involved extremity lasting several seconds to several minutes. Characteristically, there is weakness of shoulder abduction (deltoid), elbow flexion (biceps), and external humeral rotation (spinatis). The key to the nature of this lesion is its short duration and the presence of a full, pain-free range of neck motion. Although the majority of these injuries are short lived, they are worrisome because of the occasional plexus axonotmesis that occurs. The youngster whose paresthesia completely abates and who demonstrates full muscle strength in the intrinsic muscles of the shoulder and upper extremities, and who, most important, has a full, pain-free range of cervical motion may return to his or her activity.[25] [26] The burner syndrome has been attributed to different mechanisms. Bateman[6] believed that root lesions were rarely involved in injuries to athletes, whereas peripheral nerve lesions were common. He recognized that direct blows as well as other mechanisms could result in varying peripheral nerve injuries about the shoulder.

Figure 20-A-8 Diagram of the brachial plexus demonstrating the location of Erb's point (arrow). Presumably, brachial plexus stretch injuries result from traction of the plexus at this point. (From Torg JS: Athletic Injuries to the Head, Neck and Face, 2nd ed. St. Louis, Mosby-Year Book, 1991.)

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Chrisman[11] described lateral neck flexion away from the involved side resulting in cervical sprain and traction injury to the cervical nerve roots. Rockett[91] reported operative findings in patients with persistent burners. He noted scarring of the C5 and C6 nerve roots at their point of emergence from the vertebra between the anterior and middle scalene. He suggested that repetitive tightening of the scalenes causes trauma

to the nerve roots with resultant scarring. Clancy and associates[12] [13] suggested a more distal injury. They believed that burners were brachial plexus injuries. Electrodiagnostic evidence indicated that plexus axonotmesis involved only the upper trunk. They noted different mechanisms of injury and suggested that the point of plexus injury may vary depending on neck, arm, and shoulder position. Neck hyperextension, shoulder depression, neck hypertension with lateral bend to the side of injury, and contralateral neck flexion with ipsilateral shoulder depression were some mechanisms reported. Clancy and associates[12] [13] also recommended classifying these injuries based on the staging system of Seddon. [66] Neurapraxia, the mildest form of injury, represents a reversible aberration in axonal function. Focal demyelinization can occur, producing an electrophysiologic conduction block or conduction slowing. Complete recovery usually occurs immediately or within a maximum of 2 weeks. Axonotmesis is an injury in which the axon and the myelin sheath are disrupted, but the epineurium remains intact. Wallerian degeneration occurs distal to the point of injury; functional recovery may occur, but it can be incomplete and unpredictable. The most severe injury, neurotmesis, is rarely seen in athletes and results in complete disruption of the nerve. Prognosis is poor, and generally recovery does not occur. Clancy and associates[12] [13] define cervical nerve pinch syndrome as those injuries that recover within 2 weeks; most likely, these represent neurapraxia. The term brachial plexus injury is reserved for injuries with weakness or sensory changes lasting longer than 2 weeks. In our opinion, the term brachial plexus injury should be reserved for anatomic localization. Many of these injuries are mixed lesions, and classification by Seddon's system[66] serves mainly to aid in describing a potential recovery course and prognosis. Robertson[54] indicated that brachial plexus injury at Erb's point is most likely to be a stretch injury. He reported that all patients became symptomatic after contact, causing ipsilateral shoulder depression and lateral neck flexion to the opposite side. Kelly and coworkers[30] [31] investigated the relationship between burners and cervical stenosis in younger patients aged 15 to 18 years. A review of 69 cervical spine radiographs demonstrated a significant decrease in the Torg ratio (the ratio of the anteroposterior diameter of the spinal cord to the anteroposterior diameter of the vertebral body) as compared with the control group. They hypothesized that developmental cervical stenosis predisposes an athlete to experience burners as a result of concomitant foraminal narrowing with nerve root compression. Meyer[43] studied 40 patients with stingers at the University of Iowa from 1987 to 1991. The mechanism was reported as extension-compression in 34 subjects and brachial plexus stretch in 6 subjects. Cervical spine radiographs were analyzed and compared with a control group of asymptomatic football players. Players with stingers demonstrated a statistically significant incidence of spinal stenosis of at least one cervical segment as defined by a Torg ratio of lower that 0.8. For the stinger group, 47.5% had a ratio less than 0.8 for at least one level versus 25.1% in the asymptomatic

group. No patient in the group with brachial plexus stretch injuries had a Torg ratio of lower than 0.8. He concluded that there is a relationship between cervical stenosis and the occurrence of nonparalyzing extension-compression injuries. It is clear that the typical burner can be caused by various injury mechanisms. History, physical examination, and appropriate diagnostic studies help differentiate between brachial plexus and cervical nerve root lesions. Brachial plexus injuries are more likely to occur in younger patients with less well-developed neck musculature. Usually, these are traction injuries resulting from lateral neck flexion away from the involved area and shoulder depression to the side of involvement. Neck pain can be present but is usually not a prominent feature. When pain is present, cervical spine radiographs are necessary. Typically, pain and paresthesias involving the arm and the shoulder are transient. On examination, a Spurling's test result is negative ( Fig. 20A-9 ). Weakness typically involves the deltoid, the spinati, and the biceps and might not be evident initially on clinical examination, making a follow-up visit necessary. Root lesions result from compression of the nerve root or dorsal root ganglion in the intervertebral foramen and are generally associated with radiologic evidence of cervical disk disease and developmental stenosis. In football players, these injuries usually occur when the player reaches the college or professional level. Hyperextension

Figure 20-A-9 Spurling's maneuver. The examiner applies pressure to the head, forcing the cervical spine into extension and lateral flexion toward the symptomatic side. This reproduces the pathomechanics of those injuries resulting from compression of the cervical nerve roots or the dorsal root ganglion in the involved intervertebral foramen.

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with lateral neck flexion is the common mechanism of injury. Neck pain and a decreased cervical range of motion may be present. Spurling's test result is positive. Plain radiographic findings may be normal or may demonstrate loss of normal cervical lordosis and the changes of degenerative disk disease. MRI is indicated in patients with a persistent neurologic deficit and prolonged or recurrent symptoms and will demonstrate either acute disk herniation or degenerative disk disease with asymmetrical disk bulging. In our experience, patients often have developmental spinal stenosis, degenerative disk disease, and asymmetrical disk bulging that results in root irritation with cervical hyperextension. Persistence of paresthesia, weakness, or limitation of cervical motion requires that the individual be protected from further exposure and that he or she undergo neurologic, electromyographic, and roentgenographic evaluation. Persistent or recurrent episodes require a complete neurologic and radiographic/imaging work-up. If routine roentgenographic films of the cervical spine are negative and a preganglionic root lesion

is suspected, MRI, plain myelography, or CT myelography should be considered. Disk herniation, foraminal narrowing, and extradural intraspinal masses should be considered in the differential diagnosis. A complete electromyographic examination, including both nerve conduction studies and a needle electrode examination, may be helpful. These studies should be delayed for 3 to 4 weeks from the time of the initial injury. Nerve conduction studies should include both routine conduction as well as sensory nerve action potential evaluations. Electrode evaluation of the cervical spine musculature will differentiate between preganglionic root injuries and plexus disorders. Initial management must be directed at evaluation of the cervical spine, the shoulder girdle, the affected upper extremity, and the peripheral nervous system. The first obligation of the physician is to rule out a serious cervical spine injury. A patient history of bilateral symptoms or symptoms including the lower extremities should alert the physician to the possibility of cord neurapraxia, cervical spine fracture, or ligamentous injury. In this instance, the spine should be immobilized until injury is ruled out. If a player complains of neck pain, a complete cervical spine evaluation is mandatory, including radiographic examination. Characteristically, the signs and symptoms are transient and resolve within minutes. In athletes whose pain and paresthesias abate, a normal neurologic examination is required and, most important, a full pain-free range of cervical motion must be seen before return to activity is allowed. Also, players must demonstrate normal strength on clinical examination before they return to participation. Those patients who have recurrent symptoms without weakness require careful follow-up; continued symptoms associated with weakness preclude further athletic participation. In brachial plexus injuries, prevention is based on an aggressive neck and shoulder strengthening program ( Fig. 20A-10 ). Neck rolls, or devices such as the cowboy collar, and high-profile shoulder pads also help prevent injuries by limiting the extent of lateral flexion and extension( Fig. 20A-11A and B ). Electrodiagnostic studies may be helpful but are not

Figure 20-A-10 Crucial in the effective management of the athlete with recurrent burners is the implementation of an aggressive, year-round neck and shoulder muscle strengthening program. Effective are variable-resistance isotonic neck machines.

mandatory in the management of burners secondary to brachial plexus injury. Speer[68] demonstrated that although there was no correlation between initial physical findings and the results of electrodiagnostic testing, evidence of muscular weakness 72 hours after the injury did correlate with positive electromyographic results. Bergfeld [8] reported that electromyographic changes continue to appear long after weakness has apparently been resolved according to clinical examinations; therefore, abnormal electromyographic findings should not be used as a criterion for exclusion from athletic participation.

In summary, the burner pain syndrome results from either of two distinct injury patterns: traction to the brachial plexus or compression of the cervical nerve roots. Brachial plexus injuries are typically traction neurapraxias occurring in younger athletes as a result of shoulder depression and lateral neck flexion away from the side of injury. Cervical root injuries typically occur in older players. They are hyperextension injuries and are associated with degenerative disk changes, often in combination with developmental cervical stenosis.[37] Criteria for return to athletic participation include absence of symptoms, normal strength, and painless, full range of motion of the cervical spine. Players who experience one or more burners should wear appropriate neck rolls or a cowboy collar to prevent extreme hyperextension and lateral bending of the cervical spine ( Fig. 20A-12 ). A year-round neck and shoulder muscle strengthening program will aid in the prevention of the burner syndrome.[91]

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Figure 20-A-11 Frontal (A) and lateral (B) views of the cowboy collar. This device, which is worn under the shoulder pads, effectively limits the extremes of extension and lateral bending of the cervical spine. Acute Cervical Sprain Syndrome

An acute cervical sprain is a collision injury frequently seen in contact sports. The patient complains of having jammed his or her neck with subsequent pain localized to the cervical area. Characteristically, the patient presents with limitation of cervical spine motion but without radiation of pain or paresthesia. Neurologic examination is negative, and roentgenograms are normal. Stable cervical sprains and strains eventually resolve with or without treatment. Initially, the presence of a serious injury should be ruled out by performing a thorough neurologic examination and determining the range of cervical motion. Range of motion is evaluated by having athletes perform the following actions: actively nod their head,

Figure 20-A-12 The combined action of the football helmet, the cowboy collar, and the shoulder pads effectively limits the extremes of lateral bend of the neck.

touch their chin to their chest, extend their neck maximally, touch their chin to their left shoulder, touch their chin to their right shoulder, touch their left ear to their left shoulder, and touch their right ear to their right shoulder. If the patient is unwilling or unable to perform these maneuvers actively while standing erect, proceed no further. The athlete with less than a full, pain-free range of cervical motion, persistent paresthesia, or weakness should be protected and excluded from activity. Subsequent evaluation should include appropriate roentgenographic studies, including flexion and extension

views to demonstrate fractures or instability. In general, treatment of athletes with cervical sprains should be tailored to the severity of the injury. Immobilizing the neck in a soft collar and using analgesics and anti-inflammatory agents until there is a full, spasm-free range of neck motion is appropriate. Individuals with a history of collision injury, pain, and limited cervical motion should have routine cervical spine roentgenograms. Also, lateral flexion and extension roentgenograms are indicated after the acute symptoms have subsided. Marked limitation of cervical motion, persistent pain, or radicular symptoms or findings may require MRI to rule out intervertebral disk injury. Intervertebral Disk Injuries

Acute herniation of a cervical intervertebral disk associated with neurologic findings and occurring as an isolated entity is rare in the athlete. Acute onset of transient quadriplegia in an athlete who has sustained head impact but has negative cervical spine roentgenographic findings should prompt consideration of an acute rupture of a cervical intervertebral disk. The syndrome of acute anterior spinal cord injury, as described by Schneider, may be observed in individuals with instability associated with acute disk herniation[63] [64] : The acute anterior cervical spinal cord injury syndrome may be characterized as an immediate

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acute paralysis of all four extremities with a loss of pain and temperature to the level of the lesion, but with preservation of posterior column sensation of motion, position, vibration and part of touch. The pressure of the disk is exerted on the anterior and lateral columns, whereas the posterior columns are protected by the denticulate ligaments. MRI or a CT myelogram should be performed to substantiate the diagnosis. Anterior diskectomy and interbody fusion for a patient with neurologic involvement or persistent disability because of pain should be considered. Albright and colleagues[3] studied 75 University of Iowa freshmen football recruits who had had roentgenograms of their cervical spines after playing football in high school but before playing in college. Of this group, 32% had one or more of the following: occult fracture, vertebral body compression fracture, intervertebral disk-space narrowing, or other degenerative changes. Of this group, only 13% admitted to a positive history of neck symptoms. The development of early degenerative changes or intervertebral disk-space narrowing in this group was attributed to the effect of repetitive loading on the cervical spine as a result of head impact from blocking and tackling. Acute and chronic cervical intervertebral disk injury without frank herniation or neurologic findings occurs with considerable frequency in the athlete. Associated with a history of injury are neck pain and limited cervical spine motion. Roentgenograms may demonstrate disk-space narrowing and marginal osteophytes. Magnetic resonance imaging frequently demonstrates disk bulge without herniation. In general, management

is conservative; permission to engage in activity is withheld until the youngster is asymptomatic and has a full range of cervical spine motion. Cervical Vertebral Subluxation without Fracture

Axial compression-flexion injuries incurred by striking an object with the top of the helmet can result in disruption of the posterior soft tissue supporting elements with angulation and anterior translation of the superior cervical vertebrae. Fractures of the bony elements are not demonstrated on roentgenograms, and the patient has no neurologic deficit. Flexion-extension roentgenograms demonstrate instability of the cervical spine at the involved level, manifested by motion, anterior intervertebral disk-space narrowing, anterior angulation and displacement of the vertebral body, and fanning of the spinous processes. Demonstrable instability on lateral flexion-extension roentgenograms in young, vigorous individuals requires aggressive treatment. When soft tissue disruption occurs without an associated fracture, it is likely that instability will result despite conservative treatment. When anterior subluxation greater than 20% of the vertebral body is due to disruption of the posterior supporting structures, posterior cervical fusion is recommended. Cervical Fractures or Dislocations: General Principles

Fractures or dislocations of the cervical spine may be stable or unstable and may or may not be associated with neurologic deficit. When fracture or disruption of the soft tissue supporting structure immediately violates or threatens to violate the integrity of the spinal cord, implementation of certain management and treatment principles is imperative. These include the following: 1. 2. 3. 4.

Protection of the cord from further injury Expeditious reduction Attainment of rapid and secure stability Implementation of an early rehabilitation program

The first goal is to protect the spinal cord and the nerve roots from injury through mismanagement. It has been estimated that many neurologic deficits occur after the initial injury. That is, if a patient with an unstable lesion is carelessly manipulated during transportation to a medical facility or subsequently managed inappropriately, further encroachment on the spinal cord can occur. Second, once appropriate roentgenograms have been obtained and qualified orthopaedic and neurosurgical personnel are available, the malalignment of the cervical spine should be reduced as quickly and gently as possible. This will effectively decompress the spinal cord. When dislocation or anterior angulation and translation are demonstrated roentgenographically, immediate reduction is attempted with skull traction using Gardner-Wells tongs. These tongs can be easily and rapidly applied under local anesthesia without shaving the head in the emergency room or in the patient's bed. Because these tongs are spring-loaded, it is not necessary to drill the outer table of the skull for their application. The tongs are attached to a cervical-traction pulley, and

weight is added at a rate of 5 pounds per disk-space, or 25 to 40 pounds for a lower cervical injury. Reduction is attempted by adding 5 pounds every 15 to 20 minutes and is monitored by lateral roentgenograms. Unilateral facet dislocations, particularly at the C3-C4 level, are not always reducible by using skeletal traction. In such instances, closed skeletal or manipulative reduction under nasotracheal anesthesia may be necessary. The expediency of early reduction of cervical dislocations must be emphasized.[87] It has been proposed that the presence of a bulbocavernous reflex indicates that spinal shock has worn off and that except for recovery of an occasional root at the site of the injury, neither motor nor sensory paralysis will be resolved regardless of treatment. The bulbocavernous reflex is produced by pulling on the urethral catheter. This stimulates the trigone of the bladder, producing a reflex contraction of the anal sphincter around the examiner's gloved finger. Although the presence of a bulbocavernous reflex is generally a sign that there will be no further neurologic recovery below the level of injury, this is not always true. The presence of this reflex does not give the clinician license to handle the situation in an elective fashion. Malalignments and dislocations of the cervical spine associated with quadriparesis should be reduced as quickly as possible, by whatever means necessary, if maximum recovery is to be expected. In most instances in which a vertebral body burst fracture is associated with anterior compression of the cord, decompression is logically effected through an anterior approach with interbody fusion. Likewise, intervertebral disk herniation with cord involvement is best managed

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through anterior diskectomy and interbody fusion. In patients with cervical fractures and dislocations, posterior cervical laminectomy is indicated only rarely when excision of foreign bodies or bony alignment of the spine is the most effective method of decompression of the cervical cord. Indications for surgical decompression of the spinal cord have been delineated. A documented increase in neurologic signs is the clearest mandate for surgical decompression. Further observation, expectant waiting, and procrastination in this situation are contraindicated. Persistent partial cord or root signs, with objective evidence of mechanical compression, are also an indication for surgical intervention. The use of parenteral corticosteroids to decrease the inflammatory reactions of the injured cord and the surrounding soft tissue structures is indicated in the management of acute cervical spinal cord injuries. The efficacy of methylprednisolone in improving neurologic recovery when given in the first 8 hours has been recently demonstrated. The recommended regimen is a bolus of 30 mg/kg of body weight of methylprednisolone administered intravenously followed by an infusion of 5.4

mg/kg/hour for 23 hours.[10] The third goal in managing fractures and dislocations of the cervical spine is to effect rapid and secure stability to prevent residual deformity and instability with associated pain as well as to prevent the possibility of further trauma to the neural elements. White and coworkers recognized that the literature is neither always clear nor consistent in describing what constitutes an unstable cervical spine. Using fresh cadaver specimens, they performed load displacement studies on sectioned and unsectioned two-level cervical spine segments to determine the horizontal translation and rotation that occurred in the sagittal plane after each ligament was transected. The experiments constituted a quantitative biomechanical analysis of the effects of destroying ligaments and facets on the stability of the cervical spine below C2 in an attempt to determine cervical stability. The express purpose of the study was to establish indications for surgical treatment to stabilize the spine. Although the intent of the study was to define clinical instability to formulate treatment standards and was not intended to establish criteria for a return to contact athletics, it appears that their findings are relevant to the latter issue.[99] [100] White and his colleagues described clinical stability as the ability of the spine to limit its patterns of displacement of physiologic loads to prevent damage or irritation of the spinal cord or the nerve roots.[99] [100] They delineated four important findings. First, in sectioning the ligaments, small increments of change in stability occur followed without warning by sudden, complete disruption of the spine under stress. Second, removal of the facets alters the motion segment such that in flexion there is less angular displacement and more horizontal displacement. Third, the anterior ligaments contribute more to stability in extension than the posterior ligaments, and in flexion the posterior ligaments contribute more than the anterior ligaments. The most relevant finding from the standpoint of criteria for return to contact sports is the fourth one. The adult cervical spine is unstable, or on the brink of instability, when one or more of the following conditions is present: (1) all the anterior or all the posterior elements are destroyed or are unable to function; (2) more than 3.5 mm of horizontal displacement of one vertebra exists in relation to an adjacent vertebra, measured on lateral roentgenograms (resting or flexion-extension); or (3) there is more than 11 degrees of rotation difference compared with that of either adjacent vertebra measured on a resting lateral or flexion-extension roentgenogram (Figs. 20A-13 (Figure Not Available) and Figs. 20A-14 (Figure Not Available) ). The method of immobilization depends on the postreduction status of the injury. Thompson and colleagues have concisely delineated the indications for using nonsurgical and surgical methods to achieve stability.[76] These concepts for managing cervical spine fractures and dislocations may be summarized as follows: 1. Patients with stable compression fractures of the vertebral body, undisplaced fractures of the lamina or lateral masses, or soft tissue injuries without detectable neurologic deficit can be adequately treated with traction and subsequent protection with a cervical brace until healing occurs. 2. Stable, reduced facet dislocation without neurologic deficit can also be treated conservatively with a halo jacket brace until healing has been demonstrated by negative lateral flexion-extension roentgenograms. 3. Unstable cervical spine fractures or fracture-dislocations without neurologic deficit

may require either surgical or nonsurgical methods to ensure stability. 4. Absolute indications for surgical stabilization of an unstable injury without neurologic deficits are late instability Figure 20-A-13 (Figure Not Available) Abnormal angulation between two vertebrae at any one interspace is determined by comparing the angle formed by the projection of the inferior vertebral body borders with that of either the vertebral body above or the vertebral body below. If the angle at the interspace in question is 11 degrees or greater than either adjacent interspace, it is considered by White and associates to be clinical instability. (From White AA, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 109:85, 1975. )

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Figure 20-A-14 (Figure Not Available) The method for determining translatory displacement, as described by White and colleagues. Using the posteroinferior angle of the superior vertebral body as one point of reference and the posterosuperior angle of the vertebral body below, the distance between the two in the sagittal plane is measured. A distance of 3.5 mm or greater is suggestive of clinical instability. (From White AA, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 109:85, 1975.)

after closed treatment and flexion-rotation injuries with unreduced locked facets. 5. Relative indications for surgical stabilization in patients with unstable injuries without neurologic deficit are anterior subluxation greater than 20%, certain atlantoaxial fractures or dislocations, and unreduced vertical compression injuries with neck flexion. 6. Cervical spine fractures with complete cord lesions require reduction followed by stabilization by closed or open means, as indicated. 7. Cervical spine fractures with incomplete cord lesions require reduction followed by careful evaluation for surgical intervention. The fourth and final goal of treatment is rapid and effective rehabilitation started early in the treatment process. A more specific categorization of athletic injuries to the cervical spine can be made. Specifically, these injuries can be divided into upper cervical spine, midcervical spine, and lower cervical spine injuries. Upper Cervical Spine Fractures and Dislocations

Upper cervical spine lesions involve C1 through C3. Although they rarely occur in sports, several specific injuries that can occur to the upper cervical vertebrae deserve mention. The transverse and alar ligaments are responsible for atlantoaxial stability (Fig. 20A-15 (Figure Not Available) ). If these structures are ruptured from a flexion injury with translation of C1 anteriorly, the spinal cord can be impinged between a posterior aspect of the odontoid process and the posterior rim of C1. The patient gives a history of head trauma and complains of neck pain, particularly with nodding, and may or may not present with cord signs. Roentgenographically, lateral views of the C1-C2 articulation demonstrate increase of the atlantodens interval. This interval is normally 3 mm in the adult. With transverse ligament rupture, it may increase up to 10 to 12 mm depending

on the status of the alar and accessory ligaments. Note that increase in the atlantodens interval may be seen only when the neck is flexed. Fielding states that atlantoaxial fusion may be the conservative treatment for this lesion.[18] He recommends posterior C1-C2 fusion using wire fixation and an iliac bone graft. Fractures of the atlas were described by Jefferson in 1920.[29] These may be of two types: posterior arch fractures or burst fractures. Posterior arch fractures are more common, and with a brace support they go on to satisfactory fibrous or bony union. Burst fractures result from an axial load transmitted to the occipital condyles, which then disrupt the integrity of both the anterior and posterior arches of the atlas ( Fig. 20A-16 ). Roentgenograms demonstrate bilateral symmetrical overhang of the lateral masses of the atlas in relation to the axis, with an increase in the paraodontoid space on the open mouth view. Clinically, the patient characteristically has pain and imitates the nodding Figure 20-A-15 (Figure Not Available) The atlantoaxial complex as seen from above (A). The disruption of the transverse ligament (TAL) with intact alar ligaments results in C1-C2 instability without cord compression (B). (Redrawn from Hensinger RN: Congenital anomalies of the atlantoaxial joint. In The Cervical Spine Research Society Editorial Committee: The Cervical Spine, 2nd ed. Philadelphia, JB Lippincott, 1989, p 242.)

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Figure 20-A-16 Schematic representation of the four-part comminuted burst fracture of the atlas as seen from above. (Redrawn from Jefferson G: Fracture of the atlas vertebra. Br J Surg 7:407-422, 1919. By permission of the Publishers Butterworth-Heinemann Ltd.)

motion. These fractures are considered stable when the combined lateral overhang of the atlas measures less than 7 mm. When the transverse diameter of the atlas is 7 mm greater than that of the axis, a transverse ligament rupture should be suspected (Fig. 20A-17 (Figure Not Available) ). Treatment, as recommended by Fielding, includes head-halter traction until muscle spasm resolves, followed by a brace support. [18] If flexion-extension roentgenograms subsequently demonstrate significant instability, fusion may be indicated. Fractures of the odontoid have been classified into three types by Anderson and D'Alonzo.[5] Type I is an avulsion of the tip of the odontoid at the site of the attachment of the alar ligament and is a rare and stable lesion. Type II is a fracture through the base at or just below the level of the superior articular processes. Type III involves a fracture of the body of the axis ( Fig. 20A-18 ). When the odontoid is not displaced, planograms may be required to identify the lesion. The mechanism of odontoid fractures has not been clearly delineated; however, they appear to be due to head impact. All routine cervical spine roentgenographic studies should include the open mouth view to identify lesions involving the odontoid as well as the atlas. If these are negative, and if a lesion in this area is suspected, planograms or

bending films may further delineate pathologic changes in this area. Managing type II fractures is a problem. It has been reported that 36% to 50% of these lesions treated initially with plaster casts or reinforced cervical braces fail to unite. Figure 20-A-17 (Figure Not Available) Illustration of a comminuted Jefferson fracture with both the transverse ligament intact (stable configuration) and a transverse ligament rupture (unstable configuration). (Redrawn from White AA, Panjabi MM: Clinical Biomechanics of the Spine. Philadelphia, JB Lippincott, 1978, p 204.)

Cloward has reported that 85% of his patients heal within 3 months when treated with the halo brace.[14] Current management involves more aggressive surgical management with early posterior stabilization by means of wiring and fusion. It is necessary to stabilize fibrous unions or nonunited fractures of the odontoid surgically if they are demonstrated to be unstable on flexion and extension views. Stabilization may be effected through either posterior C1-C2 wire fixation and fusion or anterior odontoid screw fixation. Fractures through the arch of the axis are also known as traumatic spondylolistheses of C2, or hangman's fractures. These are relatively rare lesions. The mechanism of injury is generally recognized to be hyperextension. This injury is inherently unstable, but it has been shown to heal with predictable regularity without surgical intervention. Midcervical Spine Fractures and Dislocations

Acute traumatic lesions of the cervical spine at the C3-C4 level are rare and are generally not associated with fractures. These lesions are classified as follows: (1) acute rupture of the C3-C4 intervertebral disk; (2) anterior subluxation of C3 on C4; (3) unilateral dislocation of the joint between the articular processes; and (4) bilateral dislocation of the joint between the articular processes.[80] [81] [87] An episode of transient quadriplegia in an athlete who has sustained head impact but has a cervical spine roentgenogram with negative findings suggests acute rupture of the C3-C4 intervertebral disk. The syndrome of acute anterior spinal cord injury, as described by Schneider and associates,[63] [64] may be observed. A cervical myelogram or an MRI will substantiate the diagnosis. Anterior diskectomy and interbody fusion may be the most effective treatment of this lesion. Anterior subluxation of C3 on C4 is a result of a shearing force through the intervertebral disk space that disrupts the interspinous ligament as well as the posterior supporting structure. Roentgenograms demonstrate narrowing of the intervertebral disk space, anterior angulation and translation of C3 on C4, an increase in the distance between the spinous processes of the two vertebrae, and instability without fracture of the bony elements ( Fig. 20A-19 ). Spinal fusion may be necessary for adequate stabilization

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Figure 20-A-18 Illustration of the three types of odontoid fractures in both the anteroposterior and lateral planes. Type I is an oblique avulsion fracture from the upper portion of the odontoid. Type II is a fracture of the odontoid process at its base. Type III is an odontoid fracture through the body of C2. (Redrawn from Anderson LD, D'Alonzo RT: Fractures of the odontoid process of the axis. J Bone Joint Surg Am 56:1663-1674, 1974.)

in such cases, in contrast to cervical spine instability caused by fracture, in which adequate reduction and subsequent bony healing result in stability. When the patient has posterior instability, posterior fusion is preferable to an anterior interbody fusion. Unilateral facet dislocation at C3-C4 may result in immediate quadriparesis. This injury involves the intervertebral disk space, the interspinous ligament, the posterior ligamentous supporting structures, and the one facet with resulting rotatory dislocation of C3 on C4 without fracture ( Fig. 20A-20 ). At this level, strong skeletal traction does not usually yield a successful reduction, and closed manipulation under general anesthesia is necessary to disengage the locked joint between the articular processes. Bilateral facet dislocation at the C3-C4 level is a grave lesion ( Fig. 20A-21 ). Skeletal traction may not reduce the lesion, and the prognosis for this injury is poor. Lower Cervical Spine Fractures and Dislocations

Lower cervical spine fractures or dislocations are those involving C4 through C7. In injuries resulting from various athletic endeavors, the majority of fractures or dislocations of the cervical spine, with or without neurologic involvement, involve this segment. Although unilateral and bilateral facet dislocations occur, they are relatively rare. The vast majority of severe, athletically incurred cervical spine injuries are fractures of the vertebral body with varying degrees of compression or comminution.[36] Unilateral Facet Dislocations

Unilateral facet dislocations are the result of axial loading, flexion-rotation types of mechanisms. The lesion may be truly ligamentous without an associated vertebral fracture. In such instances, the facet dislocation is stable and is usually associated with neurologic involvement. Roentgenograms demonstrate less than 50% anterior shift of the superior vertebra on the inferior vertebra. Attempts should be made to reduce the facet dislocation by means of skeletal traction. As with similar lesions described at the C3-C4 level, it may not be possible to effect a closed reduction. In this instance, open reduction under direct vision through a posterior approach with supplemental posterior elementbone grafting should be performed.

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Figure 20-A-19 Roentgenogram demonstrates C3-C4 subluxation as manifested by anterior intervertebral disk space narrowing, anterior angulation, displacement of the superior vertebral body, and fanning of the spinous processes. (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17-25, 1991.)

Figure 20-A-20 Unilateral C3-C4 facet dislocation resulting in complete motor and sensory deficit distal to the lesion. There is fanning of the spinous processes of C3 and C4 and more than 20% anterior displacement of the body of C3 on C4. (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17-25, 1991.)

Figure 20-A-21 Bilateral facet dislocation at the C3-C4 level demonstrates anterior angulation as well as translation greater than 50% of the width of the vertebral body associated with spinous fanning. The lesion resulted in quadriplegia. (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17-25, 1991.) Bilateral Facet Dislocations

Bilateral facet dislocations are unstable and are almost always associated with neurologic involvement. These injuries are associated with a high incidence of quadriplegia. Lateral roentgenograms demonstrate greater than 50% anterior displacement of the superior vertebral body on the inferior vertebral body. Immediate treatment, as described previously, consists of closed reduction with skeletal traction. Such lesions are generally reducible by means of skeletal traction and are then treated by halo-brace stabilization and posterior fusion. It should be noted that instability is directly related to the ease with which the lesion is reduced because the easier it is to reduce, the easier it is to redislocate. If skeletal traction is unsuccessful, either manipulative reduction under sedation or general anesthesia or open reduction under direct vision is recommended. When the dislocation is reduced closed and the reduction is maintained, immobilization should be effected by use of the halo brace for 8 to 12 weeks. Corrective bracing should continue for an additional 4 weeks. Vertebral Body Compression Fractures

Compression fractures of the vertebral body are a result of axial loading. Vertebral body fractures of the cervical spine can be classified into five types.[4] Type I.

Simple wedge or vertebral end plate compression fractures of the cervical vertebrae are

common injuries

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Figure 20-A-22 A and B, Type I vertebral body end plate compression fracture involving the superior aspect of C6 (arrow). Extension and flexion views demonstrate absence of evidence of instability. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

that respond to conservative management and rarely if ever are associated with neurologic involvement ( Fig. 20A-22A and B ). It is important to differentiate these lesions from compression fractures that are associated with disruption of the posterior element soft tissue supporting structures. The latter lesions are unstable and are frequently associated with neurologic involvement, including quadriplegia. Figure 20-A-23 (Figure Not Available) Type II anterior-inferior vertebral body fracture demonstrates the characteristic isolated teardrop fracture. Lateral roentgenograms of the lesion demonstrate maintenance of adjacent disk space height as well as a lack of subluxation or spinous process fanning. If there is no disruption of the posterior elements, this is a relatively stable lesion. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.) Type II.

An isolated anterior-inferior vertebral body or teardrop fracture is without displacement, has intact posterior elements, and is not associated with neurologic involvement (Fig. 20A-23 (Figure Not Available) ). This is a relatively stable fracture and may be treated conservatively. [34] [65] Type III.

Comminuted burst vertebral body fractures have intact posterior elements, but displacement of bony

Figure 20-A-24 Type III comminuted burst fracture of C4 with displacement of fragments into the vertebral canal (arrow). (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

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fragments into the vertebral canal may place the cord in jeopardy. Late settling of the fracture with deformity can occur. Surgical stabilization is recommended ( Fig. 20A-24 ).

Type IV.

The axial load three-part-two-plane vertebral body fracture consists of three fracture parts: (1) an anteroinferior teardrop; (2) a sagittal vertebral body fracture; and (3) disruption of the posterior neural arch.[35] [40] [50] [79] [88] This lesion is unstable and is almost always associated with quadriplegia. Careful evaluation of the routine anteroposterior roentgenogram or CT scan is necessary to appreciate the sagittal vertebral body fracture, a finding that portends a grave prognosis ( Fig. 20A-25A , B , C , and D ). Type V.

This is a vertebral body three-part-two-plane compression fracture associated with disruption of posterior elements of an adjacent vertebra. This is an extremely unstable fracture ( Fig. 20A-26A and B ). Cervical Spinal Stenosis with Cord Neurapraxia and Transient Quadriplegia

Characteristically, the clinical picture of cervical cord neurapraxia (CCN) with transient quadriplegia involves an

Figure 20-A-25 A, A three-part-two-plane fracture of C6. Lateral view demonstrates prevertebral soft tissue swelling and an anteroinferior fracture fragment of C6 involving the entire vertebral body height and one third of the vertebral body width. There is approximately 1 mm of posterior displacement of the inferior aspect of the posterior vertebral body. The C6-C7 intervertebral disk space is minimally narrowed posteriorly with associated capsular disruption and fanning. ( From Torg JS, Pavlov H, O'Neill MJ, et al: The axial load teardrop fracture. Am J Sports Med 19:355-364, 1991.) B, Frontal view demonstrates a faint, linear radiolucency through the C6 vertebral body indicating a sagittal vertebral body fracture (arrow). There is mild lateral mass displacement. C, Computed tomographic examination demonstrates the sagittal fracture extending completely through the vertebral body with disruption of the lamina on the right. D, Diagrammatic representation of the three-part-two-plane vertebral body compression fracture demonstrates the anteroinferior teardrop as well as the sagittal vertebral body fractures and associated fracture through the lamina.

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Figure 20-A-26 A, Type V compression fracture of the vertebral body associated with fractures of the neural arch of an adjacent vertebra. Settling and posterior displacement of the superior vertebral segment occur. B, Distraction of the superior vertebral segment with skeletal traction permits visualization of fractures through the pedicles (arrow) of C6 in addition to the three-part-two-plane fracture of the body of C5. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

athlete who sustains an acute transient neurologic episode of cervical cord origin with sensory changes that may be associated with motor paresis involving both arms, both legs, or all four extremities after forced hyperextension, hyperflexion, or axial loading of the cervical spine.[78] [89] Sensory changes include burning pain, numbness, tingling, or loss of sensation; motor changes consist of weakness or complete paralysis. The episodes are transient, and complete recovery usually occurs in 10 to 15 minutes, although in some cases gradual resolution does not occur for 36 to 48 hours. Except for burning paresthesia, neck pain is not present at the time of injury. There is complete return of motor function and full, pain-free cervical motion. Routine roentgenograms of the cervical spine show no evidence of fracture or dislocation, but a demonstrable degree of cervical spinal stenosis is present. Determination of Spinal Stenosis: Method of Measurement

To identify cervical stenosis, a method of measurement is needed. The standard method, the one most commonly employed for determining the sagittal diameter of the spinal canal, involves measuring the distance between the middle of the posterior surface of the vertebral body and the nearest point on the spinolaminar line. Using this technique, Boijsen[9] reported that the average sagittal diameter of the spinal canal from the fourth to the sixth cervical vertebra in 200 healthy individuals was 18.5 mm (range, 14.2 to 23 mm). The target distance he used was 1.4 m. Others have noted that values of less than 14 mm are uncommon and fall below the standard deviation for any cervical segment. Other measurements reported in the literature vary greatly. The variations in the landmarks and the methods used to determine the sagittal distance as well as the use of different target distances for roentgenography have resulted in inconsistencies in the so-called normal values. Therefore, the standard method of measurement for spinal stenosis is a questionable one. The Ratio Method.

An alternative way to determine the sagittal diameter of the spinal canal was devised by Pavlov and colleagues and is called the ratio method.[47] It compares the standard method of measurement of the canal with the anteroposterior width of the vertebral body at the midpoint of the corresponding vertebral body ( Fig. 20A-27 ). The actual measurement of the sagittal diameter in millimeters,

Figure 20-A-27 The ratio of the spinal canal to the vertebral body is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line (a) divided by the anteroposterior width of the vertebral body (b). (From Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354-1370, 1986.)

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as determined by the conventional method, is misleading both as reported in the

literature and in actual practice because of variations in the target distances used for roentgenography and in the landmarks used for obtaining the measurement. The ratio method compensates for variations in roentgenographic technique because the sagittal diameter of both the canal and the vertebral body is affected similarly by magnification factors. The ratio method is independent of variations in technique, and the results are statistically significant. Using the ratio method of determining the dimension of the canal, a ratio of the spinal canal to the vertebral body of less than 0.80 is indicative of cervical stenosis. I believe that the ratio of the anteroposterior diameter of the spinal canal to that of the vertebral body (SC/VB ratio) is a consistent and reliable way to determine cervical stenosis ( Fig. 20A-28A and B ) in those individuals who have experienced episodes of CCN. The ratio has a very low predictive value, however, and should not be used as a screening tool. On the basis of these observations, it may be concluded that the factor that explains the described neurologic picture of CCN is diminution of the anteroposterior diameter of the spinal canal, either as an isolated observation or in association with intervertebral disk herniation, degenerative changes, post-traumatic instability, or congenital anomalies. In instances of developmental cervical stenosis, forced hyperflexion, or hyperextension of the cervical spine, the caliber of an already narrow canal is further decreased, as explained by the pincer mechanism of Penning ( Fig. 20A-29 ).[48] In patients in whom stenosis is associated with osteophytes or a herniated disk, direct pressure can occur, again when the spine is forced in the extremes of flexion and extension. It is further postulated that with an abrupt but brief decrease in the anteroposterior diameter of the spinal canal, the cervical cord is mechanically compressed, causing transient interruption of either motor or sensory function, or both, distal to the lesion. The neurologic aberration that results is transient and completely reversible. A review of the literature has revealed few reported cases of transient quadriplegia occurring in athletes. Attempts to establish the incidence indicate that the problem is more prevalent than may be expected. Specifically, in a population of 39,377 exposed participants, the reported incidence of transient paresthesia in all four extremities was 6 per 10,000, whereas the reported incidence of paresthesia associated with transient quadriplegia was 1.3 per 10,000 in the one football season surveyed. From these data, it may be concluded that the prevalence of this problem is relatively high and that an awareness of the causes, manifestations, and appropriate principles of management is warranted.[78] Characteristically, after an episode of CCN with or without transient quadriplegia, the first question raised concerns the advisability of restricting activity. In an attempt to

Figure 20-A-28 A and B, A comparison between the ratio of the spinal canal to the vertebral body of a stenotic patient and the same ratio in a control subject is demonstrated on lateral roentgenograms of the cervical spine. The ratio is approximately 1:2 (0.50) in the stenotic patient compared with 1:1 (1.00) in the control subject. (From Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354-1370, 1986.)

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Figure 20-A-29 The pincers mechanism, as described by Penning, occurs when the distance between the posteroinferior margin of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the subjacent vertebra decreases with hyperextension, resulting in compression of the cord. With hyperflexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior margin of the inferior vertebra would be the pincers. ( Redrawn from Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354-1370, 1986.)

address this problem, 117 young athletes have been interviewed who sustained cervical spine injuries associated with complete permanent quadriplegia while playing football between the years 1971 and 1984. None of these patients recalled a prodromal experience of transient motor paresis. Conversely, none of the patients in this series who had experienced transient neurologic episodes subsequently sustained an injury that resulted in permanent neurologic injury. On the basis of these data, it was concluded that a young patient who has had an episode of CCN with or without an episode of transient quadriplegia is not predisposed to permanent neurologic injury because of it.[78] Subsequent to the description of neurapraxia of the cervical cord with transient quadriplegia, a number of issues concerning the disorder have arisen. An epidemiologic study evaluating 45 athletes who had an episode of transient neurapraxia of the cervical spinal cord revealed the consistent finding of developmental narrowing of the cervical spinal canal. The purpose of the study was to determine the relationship, if any, between a developmentally narrowed cervical canal and reversible and irreversible injury of the cervical cord with use of various cohorts of football players and a large control group. Cohort 1 was composed of 227 college football players who were asymptomatic and had no known history of transient neurapraxia of the cervical cord. Cohort 2 consisted of 97 professional football players who also were asymptomatic and had no known history of transient neurapraxia of the cervical cord. Cohort 3 was a group of 45 high school, college, and professional football players who had at least one episode of transient neurapraxia of the cervical cord. Cohort 4 was composed of 77 individuals who were permanently quadriplegic as a result of an injury while playing high school or college football. Cohort 5 consisted of a control group of 105 male subjects who were not athletes and had no history of a major injury of the cervical spine, an episode of transient neurapraxia, or neurologic symptoms. [95] The mean and standard deviation of the diameter of the spinal canal, the diameter of the vertebral body, and the ratio of the diameter of the spinal canal to that of the vertebral body were determined for the third through sixth cervical levels on the radiographs of each cohort. In addition, sensitivity, specificity, and positive predictive value of the ratio of the diameter of the spinal canal to that of the vertebral body of 0.90 or less was evaluated. The findings of this study demonstrated that a ratio of 0.80 or less had a high sensitivity (93%) for transient neurapraxia. These findings also support the concept that the symptoms result from a transient reversible deformation of the

spinal cord in a developmentally narrowed osseous canal. The low predictive value of the ratio (0.2%), however, precludes its use as a screening mechanism for determining the suitability of an athlete for participation in contact activities. Axial load, degree of instability, and the period of time from injury to reduction have been implicated as factors in permanent neurologic injury in athletes who play tackle football. None of the 77 quadriplegic individuals (cohort 4) had an episode of neurapraxia of the spinal cord before the catastrophic injury. Also, none of the 45 high school, college, and professional players who had an episode of transient neurapraxia (cohort 3) became quadriplegic. These data, in combination with the absence of developmental narrowing of the cervical canal in the quadriplegic group (cohort 4), provide evidence that transient neurapraxia of the cervical cord and an injury associated with permanent catastrophic neurologic sequelae are unrelated ( Fig. 20A-30 ). Therefore, developmental narrowing of the cervical canal in a spine that has no evidence of instability is neither a harbinger of nor a predisposing factor for permanent neurologic injury. The data did not reveal an association between developmental narrowing of the cervical canal and quadriplegia. The major factor in the occurrence of cervical quadriplegia in football players is a tackling technique in which the head is used as the primary point of contact, with resulting transmission of axial energy to, and subsequent failure of, the cervical spine. The findings of this study demonstrated the high sensitivity, low specificity, and low predictive value of the ratio of the diameter of the cervical spinal canal to that of the vertebral body, precluding its use as a screening mechanism for determining the suitability of an individual for participation in contact sports. Developmental narrowing of the cervical canal without associated instability does not predispose an individual to permanent catastrophic neurologic injury and therefore should not preclude an athlete from participation in contact sports.

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Figure 20-A-30 Profile plot of the mean diameter of the spinal canal, demonstrating a significantly smaller value in cohort 3 compared with that in all other cohorts (P < 0.05). With the numbers available, no significant difference was found among cohorts 1, 2, 4, and 5. (From Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 178:1308-1313, 1996.)

More recently, a group of 110 patients with CCN has been studied. In this report, a classification system of CCN was developed, and MRI data were analyzed using a new computerized measurement technique.[96] CCN was classified according to the type of neurologic deficit: plegia for episodes with complete paralysis; paresis for episodes with motor weakness; and paresthesia for episodes that involve only sensory changes without motor involvement. The CCN grade was defined by the length of time that the neurologic symptoms persisted: grade I, less than 15 minutes; grade II, greater than 15 minutes but less than 24 hours; and grade III, greater than 24 hours. The CCN pattern

was defined by the anatomic distribution of all the neurologic symptoms: quad, episodes that involve all four extremities; upper, episodes involving both arms; lower, episodes involving both legs; and hemi, episodes involving an ipsilateral arm and leg. Using this classification system, the incidence of CCN type was plegia in 44 cases (40%), paresis in 28 (25%), and paresthesia in 38 cases (35%). CCN was grade I in 81 cases (74%), grade II in 17 (15%), and grade III in 12 cases (11%). The pattern was quad in 88 cases (80%), upper in 17 (15%), lower in 2 cases (2%), and hemi in 3 cases (3%). To study the relationship of the spinal cord to the spinal canal, a computerized system was developed to analyze magnetic resonance images. This system consisted of a personal computer and a color scanner with a transparency adapter. Images were digitized on the scanner and then uploaded using an imaging software package. The midsagittal T1 - and T2 -weighted images were digitized. Using a graphics digitizer pad with a resolution of 0.01 mm, the following measurements were made at levels C3-C7: To quantify spondylitic narrowing, the disk level canal diameter was measured as the shortest distance between the intervertebral disk and the body posterior elements; the cord diameter was determined by measuring the transverse diameter of the spinal cord at the appropriate level; and the space available for the cord was calculated by subtracting the spinal cord diameter from the disk level canal diameter. Follow-up evaluation was obtained by questionnaire, telephone interview, or office evaluation and was available for 105 of the 110 cases. Sixty-three patients (57%) returned to contact activities after their first episode of CCN. Of this group, 35 patients (56%) experienced a second episode of CCN. Once again, there were no permanent or catastrophic neurologic injuries related to the occurrence of CCN. Patients returning to football had a higher recurrence rate that those returning to other sports. Thirty-two of 52 football players (62%) who returned to the sport experienced a recurrence, compared with 3 of 11 players (27%) who returned to other sports. All radiologic measure ments except spinal cord diameter were predictive or recurrent. The patients' age, level of sports participation, radiographic findings, MRI findings, clinical CCN classification, and radiologic classification did not have predictive value in determining which patients were at risk of recurrence. The presence of disk herniation, cord compression, degenerative disk disease, or any other finding was not an indicator of whether patients would suffer future episodes of CCN. Based on the finding that narrowing of the canal is a causative factor of CCN, the recurrence and diameter data were analyzed and correlated. Graphic plots were constructed using logistic regression analysis or the percentage risk of recurrence versus the disk-level canal diameter and the SC/VB ratio. The plots demonstrated a strong inverse correlation between the risk of recurrence and the disk-level canal diameter and SC/VB ratio ( Fig. 20A-31A and B ).

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Prevention

Athletic injuries to the cervical spine that result in injury to the spinal cord are infrequent but catastrophic events.

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Figure 20-A-31 Graphs developed using regression analysis in which the risk of recurrence can be plotted as a function of the disk-level diameter measured on magnetic resonance imaging (A) and the spinal canal/vertebral body ratio calculated on the basis of x-ray films (B). The construction of these plots is based on the result that increased risk of recurrence is inversely correlated with canal diameter. Future patients with cervical cord neurapraxia can be counseled regarding their individual risk of recurrence based on the particular size of their spinal canal.

Accurate descriptions of the mechanism or mechanisms responsible for a particular injury transcend simple academic interest. Before preventive measures can be developed and implemented, identification of the mechanisms involved in the production of the particular injury is necessary. Because the nervous system is unable to recover significant function after severe trauma, prevention assumes a most important role when considering these injuries. Injuries resulting in spinal cord damage have been associated with football,[16] [20] [82] [83] [84] water sports,[1] [2] [15] [32] [59] wrestling,[101] rugby, [39] [56] [58] [60] [67] trampolining,[24] [70] [77] and ice hockey.[72] [74] The use of epidemiologic data, biomechanical evidence, and cinematographic analysis has (1) defined and supported the involvement of axial load forces in cervical spine injuries occurring in football; (2) demonstrated the success of appropriate rule changes in the prevention of these injuries; and (3) emphasized the need for employment of epidemiologic methods to prevent cervical spine and similar

severe injuries in other high-risk athletic activities. Identification of the cause of football-related cervical quadriplegia and its prevention center on four areas: (1) the role of the helmet-facemask protective system; (2) the concept of the axial loading mechanism of injury; (3) the effect of the 1976 rule changes banning spearing and the use of the top of the helmet as the initial point of contact in tackling; and (4) the necessity for continued research, education, and enforcement of rules. The protective capabilities provided by the modern football helmet have resulted in the advent of playing techniques that have placed the cervical spine at risk of injury, with associated catastrophic neurologic sequelae. Available cinematographic and epidemiologic data clearly indicate that cervical spine injuries associated with quadriplegia occurring as a result of football are not hyperflexion accidents. Instead, they are due to purposeful axial loading of the cervical spine as a result of spearing and head-first playing techniques ( Fig. 20A-32A , B , C , and D ). As an causative factor, the modern helmet-facemask system is secondary, contributing to these injuries because of its protective capabilities that have permitted the head to be used as a battering ram, thus exposing the cervical spine to injury. Classically, hyperflexion has been emphasized as playing a role in cervical spine trauma, whether the injury was due to a diving accident, trampolining, rugby, or American football. Epidemiologic and cinematographic analyses have established that most cases of cervical spine quadriplegia that occur in football have resulted from axial loading. Far from being an accident or an untoward event, techniques are deliberately used that place the cervical spine at risk of catastrophic injury ( Fig. 20A-33A , B , C , and D ). Recent laboratory observations also indicate that athletically induced cervical spine trauma results from axial loading.[82] [83] [84] [86] Mertz and colleagues,[42] Hodgson and Thomas,[28] and Sances and colleagues[55] measured stresses and strains within the cervical spine when axial impulses were applied to helmeted cadaver head-spine-trunk specimens. They were able to produce fractures of the lower cervical spine when the impulse was applied to the crown of the helmet. Hodgson and Thomas determined that direct vertex impact imparted a larger force to the cervical vertebrae than forces applied further forward on the skull. Gosch and associates [23] investigated three different injury modes (hyperflexion, hyperextension, and axial compression) in anesthetized monkeys and concluded that axial compression produced cervical spine fractures and dislocations. Maiman and coworkers,[38] Roaf,[51] [52] [53] and White and Punjabi[99] demonstrated vertebral body fractures in the lower cervical spine caused by the axial loading of isolated spinal units. Roaf subjected spinal units to forces differing in direction and magnitude and concluded that hyperflexion of the cervical spine was an anatomic impossibility. In contrast, he was able to produce almost every variety of spinal injury with a combination of compression and rotation. Bauze and Ardran[7] postulated that axial loads were responsible for cervical spine dislocations as well as fractures. They demonstrated that failure of the facet joints and posterior ligaments occurred when axial loads were applied to cadaveric spines. When the lower portion of the spine was flexed and fixed, and the upper part extended and free to move forward, vertical

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Figure 20-A-32 A, With the advent of the polycarbonate helmet-facemask protective device, use of the top or crown of the helmet as the initial point of contact in blocking and tackling became prevalent. Contact is made, the head abruptly stops, the momentum of the body continues, and the cervical spine is literally crushed between the two. In this instance, the fracture-dislocation transected the spinal cord. B, The injured player collapses, having been rendered quadriplegic. C, Further collapse is noted. D, The player is evacuated on a spine board and stretcher. (Photos by Randy Green, Vanderbilt Student Communications.)

compression produced bilateral dislocation to the facet joints without fracture. If lateral tilt or axial rotation occurred as well, a unilateral dislocation was produced. The forces observed were all less than those required for bony failure and allowed facet dislocation without associated bony injury. Nightingale and associates[45] analyzed the relationships among head motion, local deformations of the cervical spine, and injury mechanisms using a cadaver head and neck model that had experienced impact in an anatomically neutral position. They observed that classic concepts of flexion and extension of the cervical spine do not apply as a mechanism of injury to a vertically impacted head. They further conclude that straightening of the cervical spine before injury may be a necessary element of the compressive flexion mechanism. In the course of a collision activity, such as tackle football, most energy inputs to the cervical spine are effectively dissipated by the energy-absorbing capabilities of the cervical musculature through controlled lateral bending, flexion, or extension motion. The bones, the disks, and the ligamentous structures can be injured when contact occurs on the top of the helmet when head, neck, and trunk are positioned in such a way that forces are transmitted along the longitudinal axis of the cervical spine. When the neck is in the anatomic position, the cervical spine is extended as a result of normal cervical lordosis. When the neck is flexed to 30 degrees, the cervical spine straightens ( Fig. 20A-34A and B ). In axial loading injuries, the neck is slightly flexed, and normal cervical lordosis is eliminated, thereby converting the spine into a straight segmented column. Assuming head, neck, and trunk components to be in motion, rapid deceleration of the head occurs when it strikes another object, such as another player, trampoline bed, or lake bottom. This results in the cervical spine being compressed between the rapidly

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Figure 20-A-33 A, Subject (No. 37, foreground) lines up in front of ball carrier in preparation for tackling.

B, Preimpact position shows tackler about to ram ball carrier with the crown of his helmet. C, At impact, contact is made with the top of the helmet. Although the neck is slightly flexed, it is clearly not hyperflexed. The major force vector is transmitted along the axial alignment of the cervical spine. D, The tackler recoils following impact.

Figure 20-A-34 A, When the neck is in a normal upright anatomic position, the cervical spine is slightly extended because of the natural cervical lordosis. B, When the neck is flexed slightly, to approximately 30 degrees, the cervical spine is straightened and converted into a segmented column.

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Figure 20-A-35 (Figure Not Available) Biomechanically, a straight cervical spine responds to an axial load force like a segmented column. Axial loading of the cervical spine first results in compressive deformation of the intervertebral disks (A and B). As the energy input continues and maximum compressive deformation is reached, angular deformation and buckling occur. The spine fails in a flexion mode (C), with resulting fracture, subluxation, or dislocation (D and E). Compressive deformation to failure with a resultant fracture, dislocation, or subluxation occurs in as little as 8.4 msec. ( From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sport Med 1:12-27, 1991.)

decelerated head and the force of the oncoming trunk. When the maximum amount of vertical compression is reached, the straightened cervical spine fails in a flexion mode, and fracture, subluxation, or unilateral or bilateral facet dislocation can occur (Fig. 20A-35 (Figure Not Available) ).[46] Refutation of the freak accident concept with the more logical principle of cause and effect has been most rewarding in dealing with problems of football-induced cervical quadriplegia. Definition of the axial loading mechanismin which football players, usually defensive backs, make a tackle by striking an opponent with the top of their helmethas been a key element in this process. Implementation of rule changes and coaching techniques eliminating the use of the head as a battering ram has resulted in a dramatic reduction in the incidence of quadriplegia since 1976. Data on cervical spine injuries resulting from participation in football have been compiled by a national registry since 1971.[82] [84] Analysis of the epidemiologic data and cinematographic documentation clearly demonstrates that the majority of cervical fractures and dislocations were due to axial loading. On the basis of these observations, rule changes banning both deliberate spearing and the use of the top of the helmet as the initial point of contact in making a tackle were implemented at the high school and college levels. Subsequently, a marked decrease in cervical spine injury rates has occurred. The incidence of permanent cervical quadriplegia decreased from 34 cases in 1976 to 5 in the 1984 season ( Fig. 20A-36 ). We believe that the majority of athletic injuries to the cervical spine associated with quadriplegia also occur as a result of axial loading. Tator and colleagues studied 38 acute spinal cord injuries caused by diving accidents. They observed, In most cases the cervical spine was fractured and the spinal cord crushed. The top of the head struck the bottom of the lake or pool.[73] Scher, reporting on vertex impact and cervical dislocation in rugby players, observed, When the neck is

slightly flexed, the spine is straight. If significant force is applied to the vertex when the spine is straight, the force is transmitted down the long axis of the spine. When the force exceeds the energy-absorbing capacity of the structures involved, cervical spine flexion and dislocation will result.[58] Tator and Edmonds[72] reported the results of a national questionnaire by the Canadian Committee on the Prevention of Spinal Injuries due to Hockey, which recorded 28 injuries involving the spinal cord, 17 of which resulted in complete paralysis. They noted that in this series, the most common mechanism involved was a check,

Figure 20-A-36 The yearly incidence of permanent cervical quadriplegia for all levels of participation (1975 to 1995) decreased dramatically in 1977 following initiation of the rule changes prohibiting the use of head-first tackling and blocking techniques.

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in which injured players struck the boards with the top of their heads, while their necks were slightly flexed. Reports in the recent literature on the mechanism of injury involved in cervical spine injuries resulting from water sports (diving), rugby, and ice hockey support our thesis.

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Pathophysiology of Cervical Cord Injury as It Relates to the Principles of Cord Resuscitation

Cervical cord injuries have resulted in reversible, incompletely reversible, and irreversible neurologic deficits. An explanation for this variable response to injury has been obtained from the study of the histochemical responses of a squid axon injury model to mechanical deformation.[92] The spinal cord is considered an element with a low modulus of rigidity in which compressive macroscopic loads applied to the cord result in localized tension within the tissue. Various macroscopic deformations result in local elongation. With axial elongation of the cord, all elements experience stretch. With extension or flexion, the tension in the cord will vary across the diameter. Highly localized loading, such as shearing from subluxation of the vertebral elements, or focal compressions, such as a weight-drop experiment, result in elongation of the elements in the direction of the long axis of the cord. The effects of mechanical deformation of the axon membrane lead to an alteration in membrane permeability as a result of the development of nonspecific defects in the membrane. This allows calcium to flow into the cell and results in depolarization of the membrane. The giant axon of the squid was used as the tissue model to determine the effects of high strain and uniaxial tension to various degrees of stretch in concert with the neurophysiologic changes of the single axon. These experiments showed that the degree of mechanical injury to the axon influences the magnitude of the calcium insult and the time course of the recovery phase. A low rate of deformation produces only a small reversible depolarization. The axon responds to the increased intracellular calcium by pumping it extracellularly with no residual deficit. As the rate of loading was increased, the magnitude of the depolarization and the recovery time to the original resting potential increase in a nonlinear fashion. The axon may or may not fully recover depending on the ability of the cell to pump calcium. With a large influx of calcium, intracellular calcium pumps may be overwhelmed, resulting in irreversible injury. The excess intracellular calcium results in activation of calcium activated neutral proteases, which lead to cytoskeletal depolymerization and the accumulation of proteins intracellularly. The resulting increased osmotic pressure causes the cell to swell and eventually rupture ( Fig. 20A-37 ). In addition to the immediate and direct effect of

mechanical deformation on the cytosolic calcium concentration within the axon, it has been shown that high strain rate elongation of isolated venous specimens elicits a spontaneous constriction. This mechanically induced vasospasm has the effect of altering blood flow in various regions as a function of the level of vessel stretch. Ultimately, the outcome for the neural tissue will depend synergistically

Figure 20-A-37 Schematic representation of the effects of elevated intracellular calcium concentration on cell viability. Specifically, elevated cytosolic-free calcium in excess of 50 micromolar will result in calcium-activated neutral protease (CANP), which can damage protein structures of the cell.

on the level of calcium introduced into the cytosol and the degree to which the metabolic machinery of the cell may be compromised by regional reduction in blood flow.[92] >

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Clinical Correlation

The clinical evidence of varying degrees of recovery to cervical spine injury correlate with the squid axon model. Cord neurapraxia and transient quadriplegia, a completely reversible lesion, are associated with developmental narrowing of the cervical spine. Cord deformation occurs rapidly and is attributable to a hyperflexion or hyperextension mechanism. Disruption of cell membrane permeability leads to a small increase in intracellular calcium, but spinal stability and cell anatomy are not disturbed, and the deleterious effects of local anoxia secondary to venous spasm do not impede recovery of axonal function. Cervical cord lesions with incomplete reversibility are often associated with instability such as seen with subluxation or unilateral facet dislocation whereby the cord undergoes maximal elastic deformation. It is proposed that lack of full recovery is attributable to prolonged duration of deformity with local anoxia inhibiting cell membrane function and a reduction of intracellular calcium concentrations.

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Irreversible cord injury with permanent quadriplegia results from an axial load mechanism, which causes a fracture or dislocation that renders the spine markedly unstable. The cord undergoes functional plastic deformation with anatomic disruption of axonal integrity.

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Management Implications: Principles of Cervical Cord Resuscitation

These observations support the concept that acute spinal cord injury with concomitant subluxation and dislocation should be reduced promptly. This approach contradicts previous approaches that recommended gradual reductions of cervical dislocations over a prolonged period of time. Recent studies have documented the efficacy of methylprednisolone in the management of acute spinal cord injuries. These observations suggest the possible efficacy of other pharmacologic agents that would increase vasodilatation and local blood flow and counteract the effects of local cord anoxia or enhance the removal of intracellular calcium. Correlation of both reversible and irreversible spinal cord injury with the effect of neuronal and small vessel deformation have clearly indicated the potential for neurologic recovery by reversing the effects of increased intracellular calcium ion concentration and tissue anoxia. Presumably, these observations suggest that it is secondary cord injury caused by hypoxia and aberration in cell membrane potential that are largely responsible for irreversible neurologic deficits. Thus, the concept of spinal cord resuscitation is proposed as an attempt to reverse secondary changes that occur to obtain maximal neurologic recovery. Such measures would include prompt relief of cord deformation, administration of intravenous corticosteroid, measures to facilitate spinal cord perfusion, and pharmacologic agents to facilitate the return of the calcium pump mechanism.[93]

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Criteria Used to Gauge Return to Contact Activities after Cervical Spine Injury

Injury to the cervical spine and associated structures as a result of participation in competitive athletic and recreational activities is not uncommon. It appears that the frequency of these various injuries is inversely proportional to their severity. Whereas Albright[3] has reported that 32% of college football recruits sustained moderate injuries while in high school, catastrophic injuries with associated quadriplegia occur in fewer than 1 in 100,000 participants per season at the high school level. As indicated, the variety of possible lesions is considerable and the severity variable. The literature dealing with diagnosis and treatment of these problems is considerable. However, conspicuously absent is a comprehensive set of standards or guidelines for establishing criteria for permitting or prohibiting return to contact sports (boxing, football, ice hockey, lacrosse, rugby, wrestling) following injury to the cervical spinal structures. The explanation for this void appears to be twofold. First, the combination of a litigious society and the potential for great harm should things go wrong makes no the easiest and perhaps most reasonable advice. Second and perhaps most important, with the exception of the matter of transient quadriplegia, there is a lack of credible data pertaining to postinjury risk factors. Despite a lack of credible data, this chapter will attempt to establish guidelines to assist the clinician as well as the patient and his or her parents in the decision-making process.[90] Cervical spine conditions requiring a decision as to whether or not participation in contact activities is advisable and safe can be divided into two categories: (1) congenital or developmental conditions, and (2) post-traumatic conditions. Each condition has been determined to present either no contraindication, relative contraindications, or an absolute contraindication on the basis of a variety of parameters. Information compiled from over 1200 cervical spine injuries documented by the National Football Head and Neck Injury Registry has provided insight into whether various conditions may or may not predispose to more serious injury.[82] [83] [84] A review of the literature in several instances provides significant data for a limited number of specific conditions. Analysis of many conditions predicated on an understanding of recognized injury mechanisms has permitted categorization on the basis of educated conjecture. And last, much

reliance has been placed on personal experience that must be regarded as anecdotal. The structure and mechanics of the cervical spine enable it to perform three important functions. First, it supports the head as well as the variety of soft tissue structures of the neck. Second, by virtue of segmentation and configuration, it permits multiplanar motion of the head. Third, and most important, it serves as a protective conduit for the spinal cord and cervical nerve roots. A condition that impedes or prevents the performance of any of the three functions in a pain-free manner either immediately or in the future is unacceptable and constitutes a contraindication to participation in contact sports. The following proposed criteria for return to contact activities in the presence of cervical spine abnormalities or following injury are intended only as guidelines. It is fully acknowledged that for the most part they are at best predicated on anecdotal experience, and no responsibility can be assumed for their implementation. Critical to the application of these guidelines is the implementation of coaching and playing techniques that preclude the use of the head as the initial point of contact in a collision situation. Exposure of the cervical spine to axial loading is an invitation to disaster and makes all safety standards meaningless. Congenital Conditions

Odontoid Anomalies

Hensinger[27] has stated that patients with congenital anomalies of the odontoid are leading a precarious existence. The concern is that a trivial insult superimposed on already weakened or compromised structure may be catastrophic. This concern became a reality during the

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Figure 20-A-38 (Figure Not Available) Inherent instability at C1 in a patient with an os odontoideum. This condition resulted in respiratory-dependent quadriplegia following a spear tackle by this 18-year-old high school football player. The reduction in the space available for the cord is vividly demonstrated by the lateral extension (A) and flexion (B) views postinjury. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sports Med 1:12-27, 1991.)

1989 football season when an 18-year-old high school player was rendered a respiratory-dependent quadriplegic while making a head tackle that was vividly demonstrated on the game video. Postinjury roentgenograms revealed an os odontoideum with marked C1-C2 instability (Fig. 20A-38 (Figure Not Available) ). Thus, odontoid agenesis, odontoid hypoplasia, and os odontoideum are all absolute contraindications to participation in contact activities. Spina Bifida Occulta

This is a rare, incidental roentgenographic finding that presents no contraindication. Atlanto-occipital Fusion

This rare condition is characterized by partial or complete congenital fusion of the bony ring of the atlas to the base of the occiput. Signs and symptoms are referable to the posterior columns as a result of cord compression by the posterior lip of the foramen magnum and usually occur in the third or fourth decade. They usually begin insidiously and progress slowly, but sudden onset or instant death has been reported. Atlanto-occipital fusion as an isolated entity or coexisting with other abnormalities constitutes an absolute contraindication to participation in contact activities. Klippel-Feil Anomaly

This eponym is applied to congenital fusion of two or more cervical vertebrae. For purposes of this discussion, the variety of abnormalities can be divided into two groups: type Imass fusion of the cervical and upper thoracic vertebrae (Fig. 20A-39 (Figure Not Available) ); and type IIfusion of only one or two interspaces (Fig. 20A-40 (Figure Not Available) ). To be noted, a variety of associated congenital problems have been associated with congenital fusion of the cervical vertebrae and include pulmonary, cardiovascular, and urogenital problems. Pizzutillo[49] has pointed out that children with congenital fusion of the cervical spine rarely develop neurologic problems or signs of instability. However, he further states that the literature reveals more than 90 cases of neurologic problems...that developed as a consequence of occipital cervical anomalies, late instability, disk disease, or degenerative joint disease. These reports included cervical radiculopathy, spasticity, pain, quadriplegia, and sudden death. Also, more than two thirds of the neurologically involved patients had single level fusion of the upper area, whereas many cervical patients with extension fusions of five to seven levels had no associated neurologic loss. Despite this, a type I lesion, a mass fusion, constitutes an absolute contraindication to participation in contact sports. A type II lesion with fusion of one or two interspaces with associated limited motion or associated occipitocervical anomalies,

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Figure 20-A-39 (Figure Not Available) Type I Klippel-Feil deformity with multiple-level fusions and deformities as demonstrated on the lateral roentgenogram. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sport Med 1:12-27, 1991.) Figure 20-A-40 (Figure Not Available) Type II Klippel-Feil deformity with a one-level congenital fusion at C3-C4 involving both the vertebral bodies and the lateral masses. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12-27, 1991.)

involvement of C2, instability, disk disease, or degenerative changes also constitutes an absolute contraindication to participation. On the other hand, a type II lesion involving

fusion of one or two interspaces at C3 and below in an individual with a full cervical range of motion and an absence of occipitocervical anomalies, instability, disk disease, or degenerative changes should present no contraindication. Developmental Conditions

Developmental Narrowing (Stenosis) of the Cervical Spinal Canal

This condition and its association with CCN and transient quadriplegia has been well defined.[78] [92] [95] The definition of narrowing or stenosis as a cervical segment with one or more vertebrae that have a SC/VB ratio of 0.8 or less is predicated on the fact that 100% of all reported clinical cases have fallen below this value at one or more levels. To be noted, 12% of asymptomatic controls also fell below the 0.8 level, as did 32% of asymptomatic professional and 34% of asymptomatic college players. In the group of reported symptomatic players, there was in every instance complete return of neurologic function, and in those who continued with contact activities, recurrence was not predictable. Clearly, the presence of developmental narrowing of the cervical spinal canal does not predispose to permanent neurologic injury. Eismont and colleagues have indicated, on the basis of experience of cervical fractures or dislocations resulting from automobile accidents, that the degree of neurologic impairment was inversely related to the anteroposterior diameter of the canal.[17] As a result of the all-or-nothing pattern of axial load football spine injuries, this phenomenon has not been observed in sports-related injuries. The presence of a SC/VB ratio of 0. 8 or less is not a contraindication to participation in contact activities in asymptomatic individuals. We further recommend against preparticipation screening roentgenograms in asymptomatic players. Such studies will not contribute to safety, are not cost effective, and will only contribute to the hysteria surrounding this issue. In individuals with a ratio of 0.8 or less who experience either motor or sensory manifestations of CCN, there is a relative contraindication to return to contact activities. In these instances, each case must be determined on an individual basis depending on the understanding of the player and his or her parents and their willingness to accept any presumed theoretical risk (Fig. 20A-41 (Figure Not Available) ). An absolute contraindication to continued participation applies to those individuals who experience a documented episode of CCN associated with ligamentous instability, MRI evidence of cord defects or swelling, symptoms or positive neurologic findings lasting more than 36 hours, or more than one recurrence. Spear Tackler's Spine

Analysis of material more recently received by the National Football Head and Neck

Injury Registry has identified

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Figure 20-A-41 (Figure Not Available) The ratio of the spinal canal to the vertebral body is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line divided by the anteroposterior width of the vertebral body. A ratio of less than 0.8 indicates the presence of developmental narrowing (stenosis). Lateral roentgenogram of a 20-year-old intercollegiate football player who had one episode of transient quadriplegia that lasted 10 minutes following a hyperflexion injury. The canal-vertebral body ratios are narrow from C3 through C7. Specifically, the ratio at C4 measures 0.6. This player returned to active playing for two seasons without a recurrence. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12-27, 1991.)

a subset of football players with spear tackler's spine.[85] The entity consists of (1) developmental narrowing (stenosis) of the cervical canal; (2) persistent straightening or reversal of the normal cervical lordotic curve on an erect lateral roentgenogram obtained in the neutral position; (3) concomitant preexisting post-traumatic roentgenographic abnormalities of the cervical spine; and (4) documentation of the individual employing spear tackling technique ( Fig. 20A-42A and B ). In two instances in which preinjury roentgenograms as well as video documentation of axial loading of the spine due to spear tackling were available, a C3-C4 bilateral facet dislocation resulted in one instance and C4-C5 fracture-dislocation in the other, both players being rendered quadriplegic. It is postulated that the straightened segmented column alignment of the cervical spine combined with head-first tackling techniques predisposed these individuals to an axial loading injury of the cervical segment. Thus, this combination of factors constitutes an absolute contraindication to further participation in collision sports. Traumatic Conditions of the Upper Cervical Spine (C1-C2)

The anatomy and mechanics of the C1-C2 segments of the cervical spine differ markedly from those of the middle or lower segments. [22] Lesions with any degree of occipital or atlantoaxial instability portend a potentially grave prognosis (Fig. 20A-43A (Figure Not Available) and B (Figure Not Available) ). Thus, almost all injuries involving the upper cervical segment that involve a fracture or ligamentous laxity are an absolute contraindication to further participation in contact activities (Fig. 20A-44A (Figure Not Available) and B (Figure Not Available) ). Healed, nondisplaced Jefferson fractures, healed type I and type II odontoid fractures, and healed lateral mass fractures of C2 constitute relative contraindications providing the patient is pain free, has a full range of cervical motion, and has no neurologic findings.[5] Because of the uncertainty of the results of cervical fusion, the gracile configuration of C1, and the importance of the alar and transverse odontoid ligaments, fusion for instability of the upper segment constitutes an absolute contraindication regardless of how successful the fusion appears roentgenographically.

Traumatic Conditions of the Middle and Lower Cervical Spine

Ligamentous Injuries

The criteria of White and Panjabi for defining clinical instability were intended to help establish indications for surgical stabilization (see Figs. 20A-13 (Figure Not Available) and 20A-14 (Figure Not Available) ). [99] [100] However, although the limits of displacement and angulation correlated with disruption of known structures, no one determinant was considered absolute. In view of the observations of Albright and colleagues that 10% (7 of 75) of the college freshmen in their study demonstrated abnormal motion, as well as on the basis of our own experience, it appears that in many instances some degree of minor instability exists in populations of both high school and college football players without apparently leading to adverse effects. The question, of course, is what are the upper limits of minor instability? Unfortunately, there are no data available relating this question to the clinical situation that allow reliable standards. Clearly, however, lateral roentgenograms that demonstrate more than 3.5 mm of horizontal displacement of either vertebra in relation to another or more than 11 degrees of rotation than either adjacent vertebra represent an absolute contraindication to further participation in contact activities. With regard to lesser degrees of displacement or rotation, further participation in sports enters the realm of trial by battle, and such situations can be considered a relative contraindication depending on such factors as level of performance, physical habits, position played (i.e., interior lineman vs. defensive back), and so on. Fractures

The following healed stable fractures in an asymptomatic patient who is neurologically normal and has a full

822

Figure 20-A-42 Roentgenograms of a 19-year-old intercollegiate linebacker with spear tackler's spine. On the anteroposterior view (A), the cervical spine is noted to be tilted toward his left. This represents a wry neck attitude frequently seen in those with either acute or chronic cervical injury. The lateral view (B) demonstrates several manifestations of spear tackler's spine: (1) a cervical kyphosis, (2) developmental narrowing of the cervical canal, and (3) an old compression injury of C5. The kyphotic deformity was fixed in both flexion and extension. He subsequently sustained a bilateral C3-C4 facet dislocation and was rendered quadriplegic as a result of spear tackling. Figure 20-A-43 (Figure Not Available) The atlas-dens interval (ADI) is the distance on the lateral roentgenogram between the anterior aspect of the dens and the posterior aspect of the anterior ring of the atlas. In children, the ADI should not exceed 4.0 mm, whereas the upper limit in the normal adult is less than 3.0 mm. C1-C2 instability is vividly demonstrated in the above extension (A) and flexion (B) views. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury.

Clin J Sport Med 1:12-27, 1991.)

823

Figure 20-A-44 (Figure Not Available) A, Lateral roentgenogram of the cervical spine in the erect neutral position of a 21-year-old college football player demonstrates anterior translation of C6 on C7 of greater than 3.5 mm (arrows). B, A computed tomographic scan of C6 in the sagittal plane demonstrates a fracture through the lateral mass (arrow). Persistent displacement despite healing of the fracture constitutes an absolute contraindication to further participation in contact sports. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.)

range of cervical motion can be considered to present no contraindication to participation in contact activities: 1. Stable compression fractures of the vertebral body without a sagittal component on anteroposterior roentgenograms and without involvement of either the ligamentous or the posterior bony structures (Fig. 20A-45 (Figure Not Available) ). Figure 20-A-45 (Figure Not Available) Lateral roentgenogram of the cervical spine taken in the erect neutral position demonstrates an anterosuperior compression defect in the vertebral body of C5 (arrow). This limbus deformity resulted from a previous compression injury to the ring epiphysis. There is no evidence of angulation, displacement, or instability of the spine. Such a radiographic finding would not constitute a contraindication to further participation. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.)

2. A healed stable end plate fracture without a sagittal component on anteroposterior roentgenograms or involvement of the posterior or bony ligamentous structures ( see Fig. 20A-22A and B ). 3. Healed spinous process clay shoveler fractures. Relative contraindications apply to the following healed stable fractures in individuals who are asymptomatic and neurologically normal and have a full pain-free range of cervical motion: 1. Stable undisplaced vertebral body compression fractures without a sagittal component on anteroposterior roentgenograms. The propensity for these fractures to settle, causing increased deformity, must be considered and carefully followed (Fig. 20A-46A (Figure Not Available) and B (Figure Not Available) ). 2. Healed stable fractures involving the elements of the posterior neural ring in individuals who are asymptomatic, neurologically normal, and have a full pain-free range of cervical motion (Fig. 20A-47A (Figure Not Available) and B (Figure Not Available) ). In evaluating radiographic and imaging studies to find the location and subsequent healing of a posterior neural ring fracture, one must understand that a rigid ring cannot break in one location.[72] Thus, healing of paired fractures of the ring must be demonstrated. Absolute contraindications to further participation in contact activities exist in the presence of the following fractures: 1. An acute fracture of either the body or posterior elements with or without associated

ligamentous laxity constitutes an absolute contraindication to participation. 2. Vertebral body fracture with a sagittal component ( see Fig. 20A-25A , B , C , and D ). 3. Fracture of the vertebral body with or without displacement with associated posterior arch fractures or ligamentous laxity (Fig. 20A-48 (Figure Not Available) ).

824

Figure 20-A-46 (Figure Not Available) A, Lateral roentgenogram of the cervical spine taken while in a cervical brace demonstrates undisplaced compression fracture of the vertebral body of C5. Notable is the fact that there is no associated angulation, displacement, intervertebral disk space narrowing, facet incongruity, or fanning of the spinous processes. B, Lateral flexion view demonstrates pathologic angulation as defined by White and associates. There is no translation, disk space narrowing, facet incongruity, or fanning of the spinous processes, suggesting a stable lesion. The increased angulation is attributed to the deformity of the vertebral body. Assuming that no progression of the deformity or evidence of instability occurred and that the patient had a pain-free neck with a normal range of motion, this situation would constitute a relative contraindication to participation in contact activities depending on the player's level, position, and willingness to accept risk of reinjury. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.) Figure 20-A-47 (Figure Not Available) A, Computed tomographic scan of a vertebral neural arch in the transverse plane demonstrating a hairline fracture through the lateral mass (open arrow) as well as a more evident nondisplaced fracture through the ipsilateral lamina (closed arrow). B, The patient was treated in a halo brace with satisfactory evidence of healing as demonstrated on CT scan. Following immobilization and the return of normal pain-free motion, he was permitted to return to contact activity after rehabilitation was fully effected and pain-free cervical range of motion and paravertebral muscle strength returned. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.)

825

Figure 20-A-48 (Figure Not Available) Lateral roentgenograms of the cervical spine in the erect neutral position demonstrate an anterosuperior compression defect in the vertebral body of C6 (large arrow). In addition, there is fanning of the C5-C6 spinous process, indicating posterior instability due to disruption of the intraspinous and posterior longitudinal ligaments (small arrows). This situation constitutes an absolute contraindication to contact sports. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.)

4. Comminuted fractures of the vertebral body with displacement into the spinal canal. 5. Any healed fracture of either the vertebral body or the posterior components with associated pain, neurologic findings, and limitation of normal cervical motion. 6. Healed displaced fractures involving the lateral masses with resulting facet incongruity. Intervertebral Disk Injury

There is no contraindication to participation in contact activities in individuals with a healed anterior or lateral disk herniation treated conservatively (Fig. 20A-49 (Figure Not Available) ) or in those requiring an intervertebral diskectomy and interbody fusion for a lateral or central herniation who have a solid fusion, are asymptomatic and

neurologically negative, and have a full pain-free range of motion. A relative contraindication exists in individuals with either conservatively or surgically treated disk disease with residual facet instability. An absolute contraindication exists in those with an acute or chronic hard disk herniation with associated neurologic findings, pain, or significant limitation of cervical motion (Fig. 20A-50 (Figure Not Available) ). Status after Cervical Spine Fusion

A stable one-level anterior or posterior fusion in a patient who is asymptomatic, neurologically negative, and Figure 20-A-49 (Figure Not Available) Magnetic resonance sagittal image of the cervical spine in a 17-year-old high school football player with a history of neck injury. An anterior intervertebral disk herniation with disk space changes at the C5-C6 level is seen (arrow). At the time of follow-up examination, the youngster was asymptomatic and neurologically normal and had a pain-free range of cervical motion. He was permitted to return to contact activities. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.) Figure 20-A-50 (Figure Not Available) A sagittal magnetic resonance imaging scan of the cervical spine of a 17-year-old high school football player who complained of posterior neck pain while butt blocking as well as a right unilateral transient radiculopathy or burner. Visualized are intervertebral disk herniations at C4-C5 and C5-C6 that are indenting the spinal cord at both levels (arrows). Although the neurologic examination was normal, the presence of a wry neck attitude, limited neck extension, congenital canal narrowing (stenosis), and reversal of a normal cervical lordosis on roentgenogram precluded the individual from participation in contact sports. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.)

826

Figure 20-A-51 (Figure Not Available) Lateral roentgenogram of a 28-year-old professional ice hockey player who underwent a successful one-level interbody fusion at C5-C6 for instability. He subsequently played 2 years without a problem. (From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.) Figure 20-A-52 (Figure Not Available) Lateral roentgenogram of the cervical spine of a 28-year-old former professional football player who had undergone a C4-C5-C6 posterior fusion for a post-traumatic instability. He subsequently returned to play 2 years of professional football; however, he developed stiffness, neck discomfort, and limited motion. The individual who elects to return to contact activities following more than a two-level fusion must understand that the probability of symptoms resulting from degenerative changes at the articulations above and below the fusion is increased. ( From Torg JS, Glasgow SG: Clin J Sport Med 1:12-27, 1991.) Figure 20-A-53 (Figure Not Available) Lateral roentgenograms of an 18-year-old who had injured his neck playing football when he was 13 years old. At that time, a three-level posterior fusion and wiring was performed; however, it appears that periosteal stripping of adjacent vertebrae above and below resulted in a five-level fusion. Such a situation is an absolute contraindication to participation in contact activities. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12-27, 1991.)

pain free and has a normal range of cervical motion presents no contraindication to

continued participation in contact activities (Fig. 20A-51 (Figure Not Available) ). Individuals with a stable two- or three-level fusion who are asymptomatic and neurologically negative and have a pain-free full range of cervical motion have a relative contraindication. Because of the presumed increased stresses at the articulations of the adjacent uninvolved vertebrae and the propensity for development of degenerative changes at these levels, it appears to be the rare exception who should be permitted to continue contact activities (Fig. 20A-52 (Figure Not Available) ). In individuals with more than a three-level anterior or posterior fusion, an absolute contraindication exists as far as continued participation in contact activities (Fig. 20A-53 (Figure Not Available) ).

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Sances A Jr, Myklebust JB, Maiman DJ, et al: Biomechanics of spinal injuries. Crit Rev Biomed Eng 11:1-76, 1984. 55.

Scher AT: The high rugby tackleAn avoidable cause of cervical spinal injury? South Afr Med J 53:1015-1018, 1978. 56.

Scher AT: Diversity of radiological features in hyperextension injury of the cervical spine. South Afr Med J 58:27-30, 1980. 57.

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Scher AT: Crashing the rugby scruman avoidable cause of cervical spinal injury. South Afr Med J 61:919-920, 1982. 60.

Schneck CD: Anatomy of the innervation of the upper extremity. In Torg JS (ed): Athletic Injuries to the Head, Neck and Face, 2nd ed. St. Louis, Mosby-Year Book, 1991. 61.

Schneider RC: A syndrome in acute cervical spine injuries for which early operation is indicated. J Neurosurg 8:360-367, 1951. 62.

Schneider RC, Charie G, Pantek H: The syndrome of acute central cervical spinal cord injury. J Neurosurg 11:546-577, 1954. 63.

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Schneider RC, Kahn EA: Chronic neurologic sequelae of acute trauma to the spine and spinal cord. Part I. The significance of the acute-flexion or tear-drop fracture dislocation of the cervical spine. J Bone 65.

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Seddon H: Surgical Disorders of the Peripheral Nerves. Edinburgh, Churchill-Livingstone, 1972.

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Steinbruck J, Paseslack V: Trampolinspringen-ein gefahrlicher Sport? (Is trampolining a dangerous sport?) Münch Med Wochenschrift 120:985-988, 1978. 70.

Swenson TM, Lauerman WC, Blanc RO, et al: Cervical spine alignment in the immobilized player. Radiographic analysis before and after helmet removal. Am J Sports Med 25:226-230, 1997. 71.

Tator CH, Edmonds VE: National survey of spinal injuries in hockey players. Can Med Assoc J 130:875-880, 1984. 72.

Tator CH, Edmonds VE, New ML: Diving: A frequent and potentially preventable cause of spinal cord injury. Can Med Assoc J 124:1323-1324, 1981. 73.

Tator CH, Ekong CEU, Rowed DA, et al: Spinal injuries due to hockey. Can J Neurol Sci 11:34-41, 1984. 74.

Thibault LE, Gennarelli TA: Biomechanics and craniocerebral trauma. In Povlishock J, Becker D (eds): Central Nervous System Trauma Status Report. Bethesda, Md, National Institute of Neurological and Communicative Disorders and Stroke, 1985, pp 370-390. 75.

Thompson RC, Morris JN, Jane JA: Current concepts in management of cervical spine fractures and dislocations. Am J Sports Med 3:159, 1975. 76.

Torg JS, Das M: Trampoline-related quadriplegia: Review of the literature and reflections on the American Academy of Pediatrics' position statement. Pediatrics 74:804-812, 1984. 77.

Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354-1370, 1986. 78.

Torg JS, Pavlov H, O'Neill MJ, et al: The axial load teardrop fracture: A biomechanical, clinical, and roentgenographic analysis. Am J Sports Med 19:355-364, 1991. 79.

Torg JS, Sennett B, Vegso JJ, Pavlov H: Axial loading injuries to the middle cervical spine segment: An analysis and classification of twenty-five cases. Am J Sports Med 19:6-20, 1991. 80.

Torg JS, Truex RC, Marshall J, et al: Spinal injury at the level of the third and fourth cervical vertebrae from football. J Bone Joint Surg Am 59:1015, 1977. 81.

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Section B The Cervical Spine in the Child Peter D. Pizzutillo MD The pursuit of excellence in athletic endeavors has resulted in the development of highly effective training programs for adolescent atheletes that have made them bigger, stronger, and faster than young athletes of a generation ago. The emphasis on winning is generated by pressures within the athlete and is enhanced by peers, parents, coaches, and society in general. Society likes a winner. Tremendous pressures are placed on young athletes to perform well not only for the satisfaction enjoyed in sports but also as a passport to a lifetime of success. This milieu has led to significant medical problems in athletes with the popularization of steroids, psychological turmoil due to unrealistic expectations, and the burnout phenomenon. Competitive behavior has become more aggressive and physical. Even a highly skilled finesse sport such as basketball is now played as a contact sport. Football and ice hockey have evolved from contact sports to the level of collision sports. The result is an increased incidence of injury in young athletes. Forty-four percent of injuries sustained in students 14 years of age or older are due to sports activity.[41] In a high school survey conducted by Paulson,[41] 80 of 100 participants in football sustained an injury during the playing season. This compares to 75 of 100 participants in wrestling, 44 of 100 participants in softball, 40 of 100 female participants in gymnastics, 28 of 100 male participants in gymnastics, 35 females and 29 males of 100 participants in track and cross-country, 31 of 100 male participants in basketball, 30 of 100 participants in soccer, and 18 of 100 male participants in baseball. This survey reflects all levels of severity; however, it is significant

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that 7% of high school students were hospitalized as the result of sports injuries.

Football injuries accounted for 20% of these cases, and basketball injuries accounted for 17.4%. A review of patients with spinal cord injury at several regional rehabilitation centers revealed that 10% to 20% of spinal cord injuries were due to sports-related accidents. [7] [49] From 1950 to 1989, 90% of fatal football injuries involved head or neck injuries. [8] The modern helmet and face mask were developed in the 1950s and 1960s, and these devices led to increased use of the head in blocking and tackling techniques, resulting in an increase in deaths from head injury.[51] In the 1970s, helmets were improved to protect the brain. A subsequent decrease in fatalities due to head injury followed, but the level of cervical spine injuries was sustained, primarily owing to spearing techniques in tackling. [60] In January 1976, the National Collegiate Athletic Association (NCAA) and the National Federation of State High School Associations (NFSHSA) formally adopted high school, college, and coaching rules that prohibited tackling or blocking with a helmeted head because of the vulnerability of the cervical spine to injury in this position. This single step has resulted in a significant decrease in serious cervical spine injury.[64] Since 1977, there has been one fatality for every 10 million athlete exposures in football at the high school, college, and professional levels. The incidence of nonfatal but catastrophic injuries is difficult to report reliably because of incomplete recording of injuries.[37] [47] The National Football Head and Neck Injury Registry has been functional since 1955 and has provided much of the information that is used today for analysis. The decreasing rate of cervical spine injury in football is attributed to improvements in equipment, changes in game rules that better protect the athlete, more effective conditioning of the athlete, and better coaching in basic playing techniques, especially blocking and tackling. Similar developments are necessary to reverse the increasing incidence of cervical spine injury in other sports. From 1978 to 1982, the National Registry of Gymnastic Catastrophic Injuries documented 20 incidents of injury, including 17 patients with permanent quadriplegia and three deaths.[9] These injuries occurred in skilled performers during practice settings. Analysis of this group revealed that permanent spinal cord injury was closely associated with use of the trampoline, [53] especially when attempting to perform a somersault. In many states, the trampoline has now been banned from physical education classes and is used only with spotters and physical restraints in teaching new skills in gymnastics. Catastrophic neurotrauma involving the cervical spinal cord has also occurred in diving,[6] [31] [38] rugby,[9] [25] [35] ice hockey, [15] [16] and wrestling. [30] Diving injuries account for 4% to 14% of spinal cord injuries in young patients [17] ; the majority of these occur outside of organized programs.[6] Downhill skiing had a reported mortality of 1.7% in 430 patients reported from Lake Tahoe in a 14-year study.[20] Thirteen patients in this group had permanent radiculopathy, and four had permanent myelopathy. Cervical spine injury in skiers is frequently associated with concurrent head injury. The martial arts have contributed to cervical spine fractures and dislocations, usually as the result of a forceful foot strike to the head or a fall onto the head and neck area. At least 17 deaths have been reported in judo and karate as a result of this mechanism.[5] Interestingly, soccer[5] and boxing[29] have not been associated with a high incidence of cervical spine

injury. Anatomy of the Cervical Spine

Cervical spine injury in children younger than 8 years of age is uncommon and differs from injury in older adolescents and adults by virtue of site and mechanism of injury. [24] [26] The problem of evaluation of the cervical spine in childhood is complicated by the fact that much of the cervical spine is unossified and is undergoing progressive radiographic changes as ossification and growth proceed. By 8 years of age, the cervical spine has developed the adult configuration. Before the age of 1 year, the anterior ring of C1 is unossified, and it may be difficult to determine whether the upper cervical spine is unstable ( Fig. 20B-1 ). At 3 to 6 years of age, the basilar synchondrosis becomes visible and may be mistaken for fracture at the base of the odontoid. By 6 years of age, the inner diameter of the spinal canal of the entire cervical spine has reached the adult level. In the child younger than 8 years of age, extension of the spine causes a spurious impression of subluxation of the anterior arch of the atlas over the superior aspect of the dens, which is not yet ossified. From infancy to 8 years of age, lateral neutral radiographs of the cervical spine reveal an increase in the angulation of the facet joint from 30 degrees to 60 degrees. In the younger child with a facet joint angle of 30 degrees, a greater

Figure 20-B-1 Lateral radiograph of the immature cervical spine reveals absence of the anterior arch of C1, presence of the basilar synchondrosis, and apparent wedging due to unossified vertebral bodies.

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degree of freedom in flexion and extension exists, which may contribute to the appearance of pseudosubluxation commonly seen at the C2-C3 and C3-C4 levels. In the first decade of life, flexion-extension lateral radiographs of the cervical spine may reveal an atlantodens interval up to 5 mm, whereas the adult interval should not exceed 3.5 mm. Incomplete ossification of the cervical spine creates the appearance both of a truncated odontoid (until its tip ossifies at 10 to 12 years of age) and of apparent wedging of the vertebral bodies on lateral radiographs (until ossification is more complete at 10 years of age). Whereas the majority of fractures in adults occur in the lower cervical spine, the upper cervical spine is involved in up to 70% of cervical spine fractures in children. The relatively large size of the child's skull may be a significant factor in injury of the upper cervical spine in this age group. A marked differential in elasticity between the spinal column and the spinal cord has been identified in the young child. The clinical expression of this differential in elasticity has been popularized by Pang and Wilberger[39] in their report of spinal cord injury without radiographic abnormality (SCIWORA) in children. Pang and Wilberger's study

documents the presence of serious neurologic damage of the upper cervical cord in the absence of cervical spine osseous damage on initial radiographic evaluation in children younger than 8 years of age.

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Recognition and Primary Treatment

The lifelong consequences of catastrophic spinal cord injury are of such magnitude that it is imperative that personnel dealing with athletes on a regular basis be well educated about the possibility of injury during practice and game conditions. Education alone can increase awareness of this problem and may indeed spare the injured athlete from further neural damage caused by mismanagement on the field. There is considerable difficulty in maintaining a high index of suspicion for spinal injury because severe neck injury does not occur frequently. The very mention of spinal cord injury creates an immediate emotional response among athletes, coaching staff, and the athletes' families. In competitive conditions, whether in practice or in actual game situations, it can be quite difficult to evaluate the injured athlete adequately and manage problems on the field. Preparation and education of everyone involved in the athlete's care in the event of nonfatal catastrophic spinal cord injury are of the utmost importance. A properly equipped ambulance with attendants trained in safe transport of individuals with neurologic damage as well as identification of hospital facilities that have the capability of dealing with catastrophic neurologic injury is necessary well in advance of injury in order to provide the optimal environment for the athlete's treatment. The development of regional spinal cord injury centers has provided a network of experienced staff throughout the country that can provide the very best care for the spinal cord-injured athlete. Education of emergency medical technicians has significantly decreased the incidence of secondary neural injury formerly caused by improper immobilization during transport. Ongoing educational efforts are needed to maintain current proficiency and to improve our existing level of care. The management of the athlete with a severe spinal injury requires rapid assessment with protection of vital structures.[4] If the athlete is unconscious, quadriparetic, or quadriplegic or has significant paresthesias or dysesthesias involving the upper and lower extremities, the cervical spine must be considered unstable and must be protected.[33] The head and neck should immediately be immobilized in a neutral position. If the patient is in the prone position, an organized logroll maneuver may be performed, in which the head and neck are turned as one unit with the patient's trunk.

This can be managed by having one member of the emergency team control the head and neck while grasping the shoulder area to prevent changes in flexion or extension. In addition to level of consciousness, it is important to determine the patient's respiratory and circulatory status. If the athlete uses a mouthpiece during sports activity, the mouthpiece should be removed. Football players should have their facemasks removed, but the helmet and chin strap should be left in place until the athlete is evaluated neurologically. If the patient is not breathing, it is important to position the jaw in an appropriate forward attitude to open the airway without overextending the neck. If the jaw thrust maneuver is not successful in restoring breathing, rescue breathing must be initiated. The athlete must be transported in an expedient manner but under safe conditions to an appropriately identified medical facility capable of dealing with these problems. In athletes younger than 8 years of age, care must be taken to avoid the forced flexion of the cervical spine that occurs on a flat spine board because of the relatively increased size of the head in relation to the size of the chest.[23] A standard flat board can be used with a towel roll beneath the shoulders to create a more neutral position of the cervical spine. The minimum requirements for the evaluating facility should include access to a neurosurgeon and an orthopedic surgeon and adequate radiographic capability.

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Acute Soft Tissue Injury

Acute soft tissue injury of the cervical spine may involve disk, ligaments, muscle, and fascia. Typically, these injuries are the result of a collision or a fall onto the head and neck complex. The athlete usually complains of neck pain or neck and shoulder pain without distal radiation of pain or paresthesias. Physical examination reveals a limited range of motion of the cervical spine, usually in the presence of mild to moderate paraspinal muscle spasms, with no evidence of motor, sensory, or reflex changes in the upper or lower extremities. Radiographs of the cervical spine have normal findings and show no evidence of subluxation or dislocation but may reveal straightening of the cervical lordosis. Acute injury involving fascia, muscle, or ligaments of the neck without disruption and instability should be treated symptomatically. A rehabilitation program comprising range of motion exercises and restitution of strength of the neck and shoulder girdle is important before gradual

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resumption of sports activity. The painful phase of soft tissue injury usually does not last more than 5 to 10 days, after which the athlete can resume sports activity. If rehabilitation is not included as an integral part of the return-to-play program, the athlete will demonstrate a chronic decrease in range of motion of the cervical spine and diminished strength of the neck, especially in the flexor muscle group. Limitation of motion and weakness of the neck may lead to secondary injury with low-grade fascial, muscular, or ligamentous injury, which perpetuates a vicious cycle of disability. Effective treatment of chronic cervical sprains and strains, therefore, includes a rehabilitation program designed to stretch out contracture of the cervical soft tissues and reconstitute the strength of the surrounding cervical and shoulder musculature.

It is extremely important that children and adolescents who have sustained apparent innocuous injury to the cervical spine be re-evaluated on a serial basis. Herkowitz and Rothman[21] reported development of instability of the cervical spine in individuals who initially demonstrated no radiographic evidence of bony or soft tissue abnormality. Subacute instability of the cervical spine is due to elastic and plastic deformation of the ligamentous and disk structures and may result in neurologic deficits in individuals who were initially neurologically normal. Children in the first decade of life who sustain neck injuries but appear to be normal by radiographic and neurologic testing need careful follow-up. Pang and Wilberger's report[39] primarily involved victims of vehicular injury and included only four sports injuries, but it demonstrated that 52% of patients with spinal cord injury without radiographic abnormality experienced the onset of serious neurologic problems an average of 4 days after initial injury. Pollack and colleagues[45] reviewed 42 children with spinal cord injury and found that within 10 weeks of the first injury, eight children had a second spinal cord injury with more serious neurologic consequences; central or partial cord injury occurred in all eight, and three patients had severe quadriparesis or paraparesis. Pollack and colleagues proposed an arbitrary protocol that includes immobilization of the cervical spine in a brace for 3 months with no sports activity, close clinical follow-up, and repeat somatosensory evoked potentials at 6 weeks. If dynamic radiographic studies and physical examination of the cervical spine are normal at the 3-month follow-up examination, the individual is ready to begin the return to sports. Full range of motion of the neck with demonstrated stability of the cervical spine on flexion-extension lateral radiographs and the absence of sensory or motor loss are required before the athlete is allowed to return to competitive sports activity. Acute herniation of the cervical nucleus pulposus has been reported in adult sports activity[28] but is rare in the child or adolescent athlete. Its presence can result in catastrophic neurologic injury with compromise of the anterior spinal cord.[36] These patients experience a sudden onset of neck pain with radiation to both shoulders, arms, and hands and tend to hold the head tilted to the side of the disk lesion. Interscapular pain is commonly reported. When the head is tilted to the side of the lesion and then extended, there is an increase in pain. Herniation of the cervical disk most commonly occurs at the C5-C6 and C6-C7 levels. The immediate concern is to differentiate the acute herniated disk from the burner lesion, which results in searing pain in a radicular distribution. A detailed neurologic assessment as well as an appropriate radiographic evaluation including computed tomographic (CT) scan and magnetic resonance imaging (MRI) are usually required. Treatment of acute disk herniation in adolescent athletes requires decompression of the spinal canal. Repetitive axial compression of the cervical spine may result in chronic changes involving the disk. Albright and colleagues[2] [3] reported radiographic evidence of neck injury in 32% of freshman college football players in their preseason evaluations. Half of this study group had a past medical history of neck pain and showed abnormal radiographic findings involving the cervical spine. Linebackers and defensive halfbacks were most commonly involved; running backs and wide receivers were at greater risk than linemen. Among athletes in whom the preseason physical examination or past medical history suggested a cervical spine problem, half demonstrated radiographic abnormalities of the cervical spine involving disk degeneration. Most of the athletes were unaware of any significant neck problems

and had not sought medical evaluation previously. Axial loading appears to be the most important injury of the cervical spine. Torg and colleagues[57] demonstrated that axial forces transmitted to the cervical spine in slight extension are dissipated primarily by the cervical muscles. When the neck is flexed 30 degrees, it becomes a straight segmented column. Axial forces applied under these conditions are transmitted directly to vertebrae, ligaments, and disk rather than being dissipated by muscle. These observations have led to improvements in tackling and blocking techniques to reduce the frequency of cervical spine injury.

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Fractures and Dislocations Atlanto-occipital Instability

Atlanto-occipital instability is usually the result of violent forces and is frequently fatal.[10] [14] [32] Although atlanto-occipital instability has not been reported in sports injuries, it is conceivable that its incidence may be higher than suspected because appropriate diagnostic tests for spinal stability are not always conducted after acute fatalities, and there has not been very much attention directed at the atlanto-occipital junction in the past. Athletes with Down's syndrome are of special concern. The recent observation that individuals with Down's syndrome may have atlanto-occipital hypermobility that excludes them from contact sports and from axial loading sports is important. In addition to the more commonly reported atlantoaxial instability, atlanto-occipital instability must be ruled out before athletes with Down's syndrome can be medically cleared for sports activities ( Fig. 20B-2 ). Injury to the Atlas and the Axis

Jefferson's Fracture

When a high axial load is delivered from the apex of the skull to the cervical spine, tremendous forces are generated

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Figure 20-B-2 Lateral radiograph of the upper cervical spine reveals significant anterior translation (arrows) of the occiput on the cervical axis.

at the junction of the occipital condyle and the ring of the atlas. Low-level forces result in fractures of the posterior atlantal arch that are stable and can be successfully treated with immobilization by orthotics.[27] When severe force is applied, a burst fracture of the atlas involving disruption of both anterior and posterior arches allows progressive displacement of the lateral masses of the atlas, producing consequent vascular and neurologic compromise. The great majority of patients who have sustained injuries to the ring of the atlas are neurologically intact and must be evaluated in an expedient manner to avoid delay in diagnosis and secondary neurologic compromise. Patients with an injury of the ring of the atlas complain of neck pain and have severely restricted motion of the cervical spine in flexion, extension, lateral side bending, and lateral rotation. In the presence of a normal neurologic examination, a high index of suspicion for fracture of the atlas is required when evaluating patients with a skull fracture or severe laceration of the scalp that suggests axial loading. Routine radiographs of the upper cervical spine are difficult to interpret, especially when the head is tilted in response to paravertebral muscle spasm. Detailed inspection of the ring of the atlas on both lateral and open-mouth anteroposterior (AP) radiographs is required to determine the relationship between the lateral masses of the atlas and the axis. When the open-mouth AP radiograph reveals combined overhang of the lateral masses of the atlas on the axis of more than 7 mm, instability and disruption of the transverse ligament must be assumed. If there is difficulty in obtaining adequate information from routine radiographs, CT scans provide excellent detail in evaluation of an injury of the atlas ( Fig. 20B-3 ). Fractures of the anterior and posterior arches of the atlas as well as the relationship of the odontoid to the anterior arch of the atlas can be precisely evaluated on CT scans. Although the majority of fractures of the atlas heal by nonoperative immobilization techniques, such as a halo brace, there is an occasional need for surgical fusion.[18] Acute Atlantoaxial Instability

Acute atlantoaxial instability is usually the result of severe flexion forces imposed on the cervical spine. If the atlas-dens interval is greater than 5 mm in children, the transverse ligament is compromised, and instability is present ( Fig. 20B-4 ). Posterior fusion of the atlas and axis is required to avoid spinal cord compression. Special concern exists about individuals with Down's syndrome who are athletically active. The standard radiographic parameters for stability of the cervical spine in individuals without Down's syndrome are not appropriate for judging stability in individuals with Down's syndrome. Natural history studies indicate that one third of adults with Down's syndrome demonstrate a radiographic appearance of instability at all levels of the cervical spine, but only 3% of these individuals experience neurologic problems. Caution must be exercised in evaluating individuals with Down's syndrome to avoid undertreatment or overtreatment. Many children and adolescents with Down's syndrome are actively involved in sports activities such as basketball, swimming, and

horseback riding. Like other athletes, these individuals and their families derive a great deal of satisfaction, pride, and joy from their athletic accomplishments. A blanket prescription against sports involvement needlessly deprives these athletes of the sense of accomplishment that accompanies athletic endeavor and diminishes their self-esteem. On the other hand, children and adolescents with Down's syndrome who demonstrate radiographic evidence of cervical instability should be advised against participation in sports activities that potentially endanger neural function, such as diving and gymnastics. In the presence of neurologic dysfunction and radiographic cervical instability, surgical stabilization of the cervical spine is necessary to preserve existing neural function and to prevent progressive loss. Rotary Atlantoaxial Subluxation

Children may demonstrate the insidious onset of wry neck deformity in association with posterior pharyngeal inflammation. Clinical examination of the involved child reveals a cock-robin attitude of the head with tilt of the head toward one shoulder and rotation of the chin toward the opposite shoulder. The patient demonstrates mild to moderate limitation of flexion and extension and nearly full lateral rotation to the side opposite the head tilt. In contrast, there is minimal lateral rotation toward the side of the head tilt. Cervical muscle spasm or localized soft tissue tenderness is usually absent. In addition, there is no prominence of the sternocleidomastoid muscle on the side

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Figure 20-B-3 A, Lateral radiograph reveals a break in the cortex of the posterior arch of C1. B, Open-mouth view reveals bilateral symmetrical overhang of the lateral masses of C1 on C2. C, Computed tomography scan reveals a disruption in the ring of C1 in both the anterior and posterior arches.

of the head tilt, as is seen in congenital muscular torticollis. The great majority of involved children are neurologically intact. Routine radiographs of the cervical spine should be supplemented by open-mouth as well as lateral flexion-extension views of the upper cervical spine. Adequate lateral evaluation may be quite difficult to obtain if the radiology technician aligns the patient in the standard fashion for a lateral view of the cervical spine because of the rotation and tilt of the skull and the atlas. To avoid the confusing features caused by rotation and lateral tilt, the technician should be instructed to obtain a lateral radiograph of the skull to include the upper cervical spine. A lateral view of the skull using this technique will reveal a true lateral view of the atlas and will permit more reliable interpretation of the relationship between the atlas and the axis. In the presence of malrotation, the lateral radiograph may spuriously suggest instability at the atlanto-occipital junction as well as at the atlantoaxial junction. In addition, the lateral mass of the atlas may appear anteriorly as a triangular wedge, the so-called sail sign ( Fig. 20B-5A ). Lateral flexion-extension radiographs in neutral rotation are needed to evaluate reliably the degree of stability of the upper cervical spine as well as the existence of fixed rotary

displacement between the atlas and the axis. CT scans have been extremely helpful in documenting the degree of displacement of the lateral mass of the atlas in relationship to the axis, the spatial relationship of the odontoid to the anterior arch of the atlas, and the space available for the cord dorsal to the odontoid ( see Fig. 20B-5B ). Parke and colleagues[40] demonstrated a rich network of sinusoidal vessels draining directly from the posterior pharynx to the soft tissues about the atlas and the axis. During inflammatory states, such as those occurring with upper respiratory tract infection, hyperemia results in dissolution of the attachment of the transverse ligament to the anterior arch of the atlas. With progressive dissolution, gross instability occurs with loss of orientation of the lateral masses of the atlas and the axis. Treatment initiated before 4 weeks of clinical expression is successful in resolving rotary subluxation of the atlas and the axis by nonsurgical methods. After 4 weeks, surgical stabilization is frequently required to maintain stability even when anatomic alignment can be regained by traction techniques ( see Fig. 20B-5C ). [42] Children and adolescents who present with a mild degree of rotary subluxation of the atlas and the axis should

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Figure 20-B-4 Lateral flexion radiograph of the cervical spine reveals significant anterior displacement of the ring of C1 from the odontoid in a patient with Down's syndrome with hypoplastic odontoid.

be placed in a cervical collar and prohibited from recreational and sports activity. With more severe degrees of subluxation or fixed rotary subluxation, the patient should be protected and treated as an inpatient. Patients are initially treated by means of halter cervical spine traction or by means of halo traction in mild hyperextension and longitudinal traction. Once anatomic reduction has been obtained, the patient is immobilized in either a halo vest or a Minerva cast. After a 6- to 8-week period of immobilization, lateral flexion-extension radiographs of the cervical spine out of the cast or the brace are needed to document stability. If stability is proved, the patient may be weaned to a soft cervical collar and begun on gentle range of motion exercises as well as isometric strengthening exercises. Repeat lateral flexion-extension radiographs of the cervical spine should be obtained 6 weeks later to rule out recurrent instability. If instability persists following immobilization or if recurrent instability develops, posterior atlantoaxial surgical fusion is indicated. Fracture of the Odontoid

Fractures of the odontoid in children may be difficult to assess, especially in the presence of an unossified basilar synchondrosis. Acute separation of the odontoid through the basilar synchondrosis can occur in children younger than 7 years of age. Spontaneous reduction may occur, but marked widening of the retropharyngeal space is

usually observed on radiographic evaluation of these patients.[10] MRI evaluation may also reveal occult injury. With ossification of the ossiculum terminale, avulsion of the tip of the odontoid may be inadvertently suspected on radiographs. Lateral flexion-extension radiographs document the presence or the absence of stability. In children older than 7 years, a type II odontoid fracture is more common and may be associated with nonunion, as it is in adults. The majority of type II odontoid fractures heal through the use of nonsurgical techniques of immobilization such as halo vest stabilization but may require surgical fusion.[19] Hangman's Fracture

The term hangman's fracture refers to fractures involving the pedicle of the second cervical vertebra. These fractures are frequently the result of motor vehicle accidents or falls and do occur in children and adolescents.[43] The most common mechanism of injury is extension and distraction, although other mechanisms have been suggested, including axial loading in extension and flexion. With bilateral disruption of the axial pedicles, the atlas and the anterior elements of the axis move as a single unit in flexion and extension. Schneider and associates described anterior displacement of the cervicocranium with enlargement of the upper cervical spinal canal in flexion, which spares the spinal cord from injury. [50] The patient with hangman's fracture may present with neck pain and cradling of the head in the absence of objective neurologic abnormalities. With persistent anterior displacement of the cervicocranium, neurologic deficits will eventually develop. Early identification is of paramount importance. In addition to routine radiographs, CT scans of the cervical spine have allowed precise delineation of fracture patterns. The majority of patients with hangman's fracture may be treated with gentle traction followed by use of a halo vest or a cast for 3 months. Lateral flexion and extension radiographs are necessary to demonstrate osseous healing and intersegmental stability. In the presence of nonunion or disruption of the C2-C3 disk, surgical fusion is indicated, either by anterior fusion of C2 to C3 or by posterior cervical fusion involving C1, C2, and C3. The Subaxial Cervical Spine

Injury to the lower cervical spine from C3 to C7 may involve injury to the anterior elements of the spinal column, to the posterior elements, to the lateral elements, or to a combination of sites. Clinical problems include facet dislocation with or without fracture, laminar fractures, and avulsion fractures of the spinous processes. Lateral mass fractures and pedicle fractures are uncommon in the subaxial spine compared with the incidence of injury in the upper cervical spine. The anterior elements of the spinal column are usually injured in flexion, with resultant compression fractures of the vertebral body and injury to the disk. Although disruption of the posterior longitudinal ligament is not common in athletic injuries, disruption may occur, especially with a flexion-distraction mechanism associated with significant intersegmental instability and the potential for neurologic catastrophe. As with injury at other

835

Figure 20-B-5 A, Lateral radiograph of the cervical spine in a patient with rotary subluxation of C1-C2 presents a triangular wedged appearance of the anterior arch of C1. B, Computed tomography scan of C1-C2 reveals malalignment of the axis of the vertebrae with anterior translation of the lateral mass of C1 on C2. C, Lateral flexion radiograph reveals solid fusion between C1 and C2 without evidence of displacement.

levels, immediate immobilization of the spine is of extreme importance to prevent additional loss of neurologic function. Fracture at the C3-C4 vertebral level is rare.[32] Athletic injuries most commonly result in injury at vertebral levels ranging from C4 to C7.[1] [11] [12] [13] [30] [45] [46] [56] [59] Facet dislocation may be unilateral or bilateral and may occur with or without associated fracture. Unilateral facet dislocation is usually the result of axial loading in combination with flexion and rotation and does not usually result in neurologic damage. In the absence of facet fracture, the injury is primarily ligamentous and capsular, and the spine maintains its stability. Lateral radiographs of the cervical spine with unilateral facet dislocation reveal anterior translation of one vertebra on another of approximately 25%. Reduction of facet dislocation is obtained by closed traction techniques; occasionally, inability to reduce facet dislocation caused by closed methods necessitates open reduction with posterior fusion of the involved levels. Bilateral facet dislocation is a much more serious injury and occurs primarily through a mechanism of flexion. The spine is unstable in this situation and is associated with severe neurologic deficit, including quadriplegia. Lateral radiographs of the cervical spine with bilateral facet dislocation reveal translation of more than 50% of one vertebra on another. These dislocations can usually be reduced by traction, immobilized in a halo cast, and stabilized by posterior fusion of the involved cervical vertebrae. Laminar fractures are difficult to diagnose on routine radiographs owing to the obliquity of the lamina in relation to the axis of the radiograph. CT scan is more reliable in identification of laminar fractures. Fractures of the lamina do not usually participate in compression of neural tissue and heal with immobilization. Avulsion fractures of the spinous process are the result of vigorous exertion and are termed clay shoveler's fractures. The spinous process of the seventh cervical vertebra is most frequently involved. Treatment of the clay shoveler's fracture is symptomatic because no subsequent instability results from this avulsion fracture. Injury of the anterior elements of the spinal column primarily involves axial loading resulting in compression fracture of the vertebral body. The extent of injury varies from a wedge fracture, which is stable, to the severely comminuted burst fracture, which is unstable and involves intrusion of bony elements into the spinal canal. The wedge

836

fracture is common and is not associated with neurologic compromise. The posterior elements, including the ligamentous structures, are intact, and the spinal column remains stable. If disruption of the posterior elements is associated with anterior compression fracture of the vertebral body, stability is most likely compromised, and surgical stabilization is necessary. When progressive escalation of forces is experienced by the neck with axial loading, more severe injury of the vertebral body occurs, ranging from nondisplaced fracture fragments to wide displacement of bone and compromise of the spinal canal. Disruption of the posterior elements is more frequent with severe flexion and distraction forces and creates an extremely unstable clinical situation with severe neurologic compromise, including quadriplegia. Anterior decompression of the spinal canal with fusion is required followed by posterior spinal fusion. Patients with facet dislocation or moderate to severe degrees of compression fracture require evaluation of the spinal canal to eliminate the possibility of concomitant extrusion of disk material ( Fig. 20B-6 ). Neurologically intact individuals with facet dislocation have been rendered quadriplegic following closed reduction owing to compromise of the anterior spinal cord by extruded disk material. If a disk is extruded, anterior surgical decompression of the disk should be performed, followed by reduction of facets with anterior and posterior spinal stabilization. Subacute or late instability of the cervical spine should be suspected in the presence of facet dislocation. Herkowitz

Figure 20-B-6 Patients with a severe compression fracture and disruption of the posterior soft tissues require further evaluation to rule out disk extrusion into the spinal canal.

and Rothman[21] reported on six neurologically intact patients with no bone or soft tissue abnormalities on initial radiographs. Four patients had unilateral facet dislocations; one had a perched facet at C5-C6; and one had subluxation at C4-C5. Each patient subsequently developed radiographic changes indicating intersegmental instability with attendant neurologic compromise. It is important to perform repeat physical examinations and radiographic studies within 3 weeks of injury to rule out the existence of subacute instability. Once instability has been identified, surgical stabilization is required.

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Spinal Cord Injury

Spinal cord injury results from violent forces imposed on the spinal column. Injury may be direct, as in complete transection or bony compression of the spinal cord, or indirect, as a result of hemorrhage, swelling, or secondary ischemia. With the clinical presentation of complete motor and sensory loss, transection of the spinal cord is likely and is irreversible. Incomplete lesions of the spinal cord usually present as mixtures of described syndromes. When severe forces are imposed by axial loading on the cervical spine, a burst fracture of the vertebral body may result, producing bony impingement on the anterior spinal artery with motor loss below the injury level and loss of sensations of pain and temperature. These deficits are usually permanent, and the degree of loss is equal in both upper and lower extremities. Severe flexion-extension moments applied to the cervical spine in the presence of spinal stenosis or secondary degenerative changes, which may occur in high school athletes, result in central cord hemorrhage and ischemia with primary involvement of the corticospinal tracts. Nonspecific sensory loss may be observed in the presence of incomplete motor loss involving all extremities. The upper extremities are usually significantly weaker than the lower extremities. Central cord involvement has a relatively favorable prognosis and is associated with varying degrees of recovery. Hemisection of the spinal cord results in loss of ipsilateral motor function and contralateral pain and temperature and is designated Brown-Séquard's syndrome. Posterior spinal cord syndrome is a rare lesion in sports, with ischemia of the posterior spinal artery resulting in loss of dorsal column function and preservation of anterior cord function. These clinical syndromes do not usually appear in pure form but rather as parts of more complex lesions, most commonly involving a combination of central cord injury and Brown-Séquard's syndrome. The burning hands syndrome was first described by Maroon in 1977 as severe burning dysesthesias and paresthesias of both hands due to injury to the central fibers of the

spinal tract.[34] The injury is usually the result of ischemia. Wilburger and colleagues[63] used MRI and somatosensory evoked potentials to demonstrate that the burning hands syndrome was a reversible insult to the sensory pathways of the spinal cord. Vascular insults may result in thrombosis or embolization. In 1970, Schneider and associates[52] reported seven

837

cases of cervicomedullary injury in football players that resulted from spearing. Five of the athletes had no radiographic evidence of fracture or dislocation, although two showed evidence of atlantoaxial instability. Schneider and coworkers postulated that vertebrobasilar insufficiency with hypoperfusion of either the vertebral or the basilar arteries could result in intramedullary cavitation and hemorrhage. A second possible mechanism of injury suggested by these authors involved acute arterial or venous obstruction from the brain due to uncal herniation through the tentorial notch. The final mechanism postulated by Schneider and colleagues involved high-velocity impact to the top of the head such that the brain interacts with the cervicomedullary junction, which is tethered by the dentate ligaments, resulting in secondary hemorrhages of the cervicomedullary junction. Fortunately, vascular injury of this sort in athletic events is uncommon. Of great concern is the problem of transient quadriplegia. Torg and his colleagues[58] [59] described this problem as acute but transient episodes of sensory changes that may be associated with motor paresis in both arms, both legs, or all four limbs following forced hyperextension, hyperflexion, or axial load to the cervical spine. Complete recovery usually occurs in less than 15 minutes. Of interest is Torg's report of 32 athletes with transient quadriparesis and associated developmental cervical spine stenosis.[58] The degree of canal stenosis may be enhanced in flexion and extension by the pincer mechanism described by Penning[41A] or by infolding of the laminar ligaments, which are capable of narrowing the spinal canal by 30% in hyperextension. Torg notes that 17 of the reported 32 athletes demonstrated developmental spinal stenosis. Only 4 of the 17 were able to return to play without permanent problems. Of the remaining 15 athletes without stenosis, five had congenital cervical fusions, and only one of these returned to play; four athletes had evidence of cervical instability, and one of these returned to competition; and of six athletes with degenerative disk changes, none returned to sports without problems. Therefore, of the group of 32 patients reported by Torg and associates, only six were able to return to play without problems. Although Torg and his group imply that athletes who have sustained transient quadriplegia with coincident developmental spinal stenosis should be discouraged from returning to competition, they conclude that athletes with transient quadriplegia and no demonstrated stenosis should be able to return to sports activity without a predisposition to permanent neurologic injury. The subset sample size is small in this study and does not allow formulation of a firm conclusion about the safety of return to competition. Transient quadriplegia in young athletes demands a detailed orthopaedic, neurologic, and imaging evaluation to rule out factors that may prohibit continued sports participation. [54] [68] Evaluation of larger study groups of involved athletes is required before strong

recommendations can be formulated about return to competition. The human cost of premature conclusions is too great. Burners are described as episodes of searing pain in the upper extremities that follow the radicular distribution.[8] [22] [44] [48] [57] [62] Burners tend to occur after acute extension of the neck or a lateral stretch of the neck to the side opposite the painful arm with depression of the shoulder, as in a tackling maneuver. The symptoms usually last a few seconds in the initial episodes. The involved athlete allows his arm to hang limply at the side and then shakes or rubs the hand or arm vigorously to diminish the unpleasant searing pain. Numbness tends to last longer than the weakness; however, with repeated episodes, progressive residual weakness is observed. College football players have reported that burners last longer with increased frequency, and occasionally persistent weakness, sensory loss, and pain are experienced whenever the arm is used. Rockett's obervations[48] during surgical exploration of patients with burners document scarring at the C5-C6 nerve roots as they emerge between the anterior and the posterior lamellae of the transverse processes. He subsequently recommended decompression of the nerve roots with lysis of nerve adhesions. Poindexter and Johnson[44] performed electromyographic (EMG) evaluation of burners and suggested that they are the result of C6 radiculopathy rather than stretch of the brachial plexus. The initial complaints of athletes with burners suggest the diagnosis of acute herniated nucleus pulposus; however, with burners the range of motion of the cervical spine remains normal, and symptoms are short lived. Burners, or, as they are also called, stingers have been reported at least once in the careers of more than 50% of football players.[22] During on-field evaluation, the affected player holds his head in a forward, stiff position to avoid extension and rotation of the neck. The presence of motor or sensory loss or arm or neck pain precludes return to play during that game until further evaluation is performed. In players who have sustained repeated injuries, full range of motion of the cervical spine as well as normal strength of the neck and the shoulder girdle should be present before the athlete is permitted to return to competition. [61] If weakness persists despite rest and rehabilitation, radiographic evaluation, EMG analysis, and MRI are needed to rule out less common lesions such as a herniated nucleus pulposus. EMG changes may persist in the absence of objective neurologic deficits for several years and cannot be used as a parameter for determining return to competition. Preventive measures that have been recommended to decrease the frequency of burners include employing neck and shoulder strengthening exercises, increasing the thickness of shoulder pads, and using neck rolls.

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Congenital Anomalies

Congenital anomalies of the cervical spine primarily involve failure of formation or failure of segmentation of the vertebrae. Occipitalization of the atlas has been associated in the neurosurgical literature with neurologic compromise; however, occipitalization is not usually associated with stenosis at the foramen magnum or with instability. The exception is the patient with occipitalization of the atlas and congenital fusion of C2-C3 in whom secondary hypermobility and instability frequently develop at the atlantoaxial junction. Instability has also been reported in individuals with hypoplasia of the odontoid in the presence of occipitalization of the atlas. Instability at this level requires posterior fusion of the occiput to the axis.

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Congenital absence of the posterior arch of the atlas is a rare congenital anomaly that is not usually associated with instability ( Fig. 20B-7 ). Lateral flexion-extension radiographs of the cervical spine as well as MRI evaluation are helpful to rule out cervical spine instability and chronic spinal cord impingement. In the absence of the posterior arch of the atlas, it is the author's recommendation that athletes refrain from high-impact loading activities such as contact or collision sports and diving. Os odontoideum may be the result of nonunion or fracture through the body of the odontoid or congenital deformity. Lateral flexion-extension radiographs are required to document stability. Athletes with a stable os odontoideum should avoid impact-loading sports, including contact and collision sports. Individuals with an unstable os odontoideum require posterior surgical stabilization of the atlas and the axis. The normal spine that has undergone single-level spinal fusion should not be considered normal, and such an individual should not be allowed to return to full sports activity. There are no scientific data on the response of the surgically fused spine to forces imposed by sudden motion and the forces experienced in athletic activity. High-impact loading in the

form of contact and collision sports and high diving should be avoided by this patient population. Congenital absence of the pedicles is a rare congenital anomaly that is usually alarming when viewed radiographically. If lateral flexion-extension radiographs demonstrate stability, however, there is no known reason to restrict the athlete's activity. Congenital scoliosis of the cervical spine is not associated with instability. Mixed bony lesions may be noted

Figure 20-B-7 Lateral radiograph of the cervical spine reveals a complete absence of the posterior arch of C1 with no instability at C1-C2.

Figure 20-B-8 Lateral radiograph of the cervical spine reveals congenital fusion of C1 and C2 and also of C3, C4, C5, and C6.

with widening of the interpedicular distances, suggestive of intraspinal lesions such as diastematomyelia. If appropriate radiographic studies and MRI eliminate the existence of intraspinal lesions and instability, involved athletes should be permitted to participate in all sports activities. Congenital fusion of the cervical spine, referred to as the Klippel-Feil syndrome, presents with a host of patterns from one-level fusion to multiple levels of fusion to complete fusion from C2 to C7 ( Fig. 20B-8 ). It is extremely important to document the integrity of the occipitocervical junction in patients with Klippel-Feil syndrome to rule out instability. In the subaxial cervical spine, lateral flexion-extension radiographs may demonstrate anteroposterior translation of vertebrae as well as anterior gaping of open disk spaces. In the absence of progressive radiographic changes in stability and of neurologic deficits, individuals with Klippel-Feil syndrome should be observed; however, progressive translation or angular deformation at an open disk space should lead to exclusion of these patients from contact and collision sports and possibly to surgical stabilization of the unstable segment. The high incidence of renal anomalies in those with congenital scoliosis or congenital fusion of the cervical spine demands evaluation of the renal system by ultrasound to rule out clinically important anomalies. Unilateral absence of a renal system is the most common anomaly and is a significant factor in restricting involved individuals from contact sports ( Fig. 20B-9 ).

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Conclusion

Neglect of injury to the cervical spine can result in catastrophic neurologic damage as well as death. The study

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Figure 20-B-9 Intravenous pyelogram demonstrates complete absence of one renal system with hydronephrosis of the remaining system.

of mechanisms of sports injuries involving the neck has resulted in a significant decrease in the incidence of catastrophic and fatal injuries involving the cervical spine by means of alterations in competitive rules and the education of athletes and coaches in safe techniques of play. Comprehensive conditioning programs tailored to the neck and the shoulder girdle improve the athlete's ability to resist damaging forces. Equipment deficits have been responsibly addressed by manufacturers with design improvement in such items as football pads, cervical rolls, and helmets. The unexpected contributes to the excitement experienced in sports. Unfortunately, it is a limiting factor that precludes the reduction of serious or fatal injury to zero. The majority of serious cervical spine injuries can be eliminated by strict adherence of coaches and officials to the rules of competition, use of effective equipment, instruction of athletes in safe techniques, and identification of high-risk athletes combined with subsequent conditioning before competition.[4] Team orthopaedic surgeons should educate the coaching staff about the serious nature of injury to the cervical spine. Injury to the soft or hard tissues of the neck requires attention to treatment guidelines and a comprehensive rehabilitation program that fosters full range of motion of the neck as well as normal strength. There have been no rigorous studies designed to prove that

proper conditioning and preparation for competition decrease the incidence of injury of the cervical spine; however, the uncertainty of sports demands that the competitive athlete be in optimal physical condition during competition. Safe and effective competition requires appropriate mental and psychological preparation as well as physical conditioning to complement the state-of-the-art equipment available. It is only by adherence to a disciplined program that the incidence of serious and catastrophic cervical spine injuries can be lowered.

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Chapter 21 - Shoulder Section A Functional Anatomy and Biomechanics of the Shoulder 1. FUNCTIONAL ANATOMY AND BIOMECHANICS OF THE ADULT SHOULDER Patrick J. McMahon MD James E. Tibone MD Marilyn M. Pink PhD, PT The goal in treating the injured shoulder is not simply to eliminate pain but also to obtain normal function. Today, knowledge of shoulder anatomy, pathoanatomy, and biomechanics has dramatically improved treatment of shoulder injuries. An enormous range of mobility is essential at the shoulder to place the hand in all the positions required of everyday life. As a consequence, there is less bony stability at the shoulder than at other diarthrodial joints, so soft tissues guide and limit motion. A significant loss of function can occur when the physiologic limits of the tissues are exceeded or impaired; this is less common in the general population, but it is a frequent finding in individuals who participate in competitive overhead athletics. When one considers that simple shoulder motion necessitates the coordinated actions of four separate articulations, it is apparent that appreciable demand is placed on the shoulder during rigorous athletics. In this chapter, the anatomy and biomechanics of the shoulder are described. The normal and adaptive mechanics of two overhead sport paradigms are then discussed (the pitcher and the freestyle swimmer). The adaptive mechanics may be indicative of a

pathologic process, or they may lead to pathologic change. The vulnerable muscles during each paradigm are also reviewed. Functional Anatomy and Biomechanics

Before shoulder anatomy and biomechanics are described, some definitions of terms are necessary. Even though the term shoulder is often used to refer to the glenohumeral joint, normal function of the shoulder requires the coordinated function of four articulations: the sternoclavicular, the acromioclavicular, the glenohumeral, and the scapulothoracic ( Fig. 21A1-1 ). Furthermore, the shoulder is composed of 30 muscles and three bones (humerus, clavicle, and scapula) in addition to the upper thorax. In this chapter, shoulder motion refers to the complex interaction of all these structures. The actions (either translations or rotations) between the humerus and the glenoid are as follows. Small linear movements that take place between the articular surfaces of the humeral head and the glenoid are termed translations. When large and symptomatic, these translations are exhibited clinically as glenohumeral joint instability. Large angular rotations also occur between the humerus and the scapula. In normal shoulders, motion is composed of large angular rotations and small glenohumeral translations.[37] [73] For clarity, we define the three possible translations as anterior-posterior, superior-inferior, and medial-lateral. The three rotations are internal-external, adduction-abduction in the scapular plane, and adduction-abduction in the horizontal plane ( Fig. 21A1-2 ). Sternoclavicular and Acromioclavicular Anatomy and Motion

The sternoclavicular joint is the only true synovial joint connecting the upper extremity and the axial skeleton. Although it lacks bony stability, four ligaments and the

Figure 21-A1-1 Normal function of the shoulder requires the coordinated function of scapulothoracic, sternoclavicular, acromioclavicular, and glenohumeral joints.

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Figure 21-A1-2 Only three axes are needed to describe rotation at the shoulder: internal-external, adduction-abduction in the scapular plane, and adduction-abduction in the horizontal plane. Description of rotation about other axes, such as flexion and extension, causes confusion.

intra-articular disc stabilize it. The interclavicular ligament provides restraint to superior joint motion and is taut when the shoulder is at the side. [76] Anterior and posterior motion is prevented by the anterior and posterior capsular structures, the anterior being the stronger.[6] The anterior structures also resist superior motion. The joint is also stabilized by the costoclavicular ligaments, which run obliquely and laterally from the first rib to the

inferior surface of the clavicle. The intra-articular disc restrains medial displacement of the clavicle ( Fig. 21A1-3 ). In the coronal plane, the acromioclavicular joint is inclined 20 to 50 degrees,[20] [104] which may affect joint stability. Unlike at the sternoclavicular joint, there is meaningful stability from structures other than the joint capsule. The clavicle is stabilized to superior motion at the acromioclavicular joint by the conoid and trapezoid coracoclavicular ligaments; the joint capsule is a restraint to anterior and posterior motion. Acromioclavicular ligaments are thickenings of the capsule. The inferior ligament is the primary

Figure 21-A1-3 The sternoclavicular joint is stabilized by the interclavicular ligament, the anterior and posterior capsular structures, the costoclavicular ligaments, and the intra-articular disc. Ant., anterior; lig., ligament.

restraint to anterior translation.[45] The trapezoid coracoclavicular ligament has been determined to be the primary restraint to posterior translation[45] ( Fig. 21A1-4 ). The clavicle moves with shoulder motion; however, large axial rotations initially reported by Inman and coworkers[39] have been questioned. By placing pins in the clavicle and the acromion, Rockwood and Green[76] have shown that the clavicle rotates axially less than 10 degrees over the entire arc of shoulder abduction. This finding is supported by the clinical observation that fixing the clavicle to the scapula does not significantly limit shoulder motion. Scapulothoracic Anatomy and Motion

The scapulothoracic muscles include the trapezius (upper, middle, and lower portions), levator scapulae, serratus anterior, pectoralis minor, and rhomboids. They all act to position the scapula in the proper orientation on the thoracic

Figure 21-A1-4 The conoid and trapezoid coracoclavicular ligaments and the joint capsule stabilize the acromioclavicular joint. Acromioclavicular ligaments are thickenings of the capsule. lig., ligament.

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cage for a given shoulder motion. The levator scapulae and the upper trapezius provide postural support. The middle trapezius and rhomboids retract the scapula, whereas the serratus anterior protracts the scapula. Upward rotation of the scapula is accomplished with the trapezius and serratus anterior. The upper trapezius and levator scapulae can also elevate the scapula. These muscles position the scapula to provide maximal stability at the glenohumeral joint while maintaining a large range of motion.

Motion between the scapula and the thorax, the scapulothoracic articulation, is an integral part of normal shoulder function. Other than muscle attachments, only the acromioclavicular joint and the coracoclavicular ligaments support the scapula. The scapula is mobile in many directions because of this unique articulation. The relative motion between the scapulothoracic articulation and the glenohumeral joint during abduction is termed the scapulothoracic rhythm. For the first 30 degrees of abduction, glenohumeral motion is much greater than scapulothoracic motion; the ratio of motions has been reported to range from 4:1 to 7:1.[23] [73] Thereafter, both joints move approximately the same amount.[23] [73] In summary, over the entire arc of abduction, the glenohumeral joint moves more than the scapulothora cic joint; however, the difference is large at the beginning of abduction and minimal at the end. In the resting position, the superior edge of the scapular spine is rotated anterior from the frontal plane a mean of 31 degrees. [44] As the shoulder abducts, the scapula rotates not only in the plane of abduction but also in a plane perpendicular to it. The superior edge of the scapula first rotates anterior about 6 degrees with the first 90 degrees of shoulder abduction. Past 90 degrees, 16 degrees of posterior scapular rotation occurs.[14] Shoulder Muscle Anatomy

Glenohumeral Muscles

Four muscles compose the rotator cuff: the supraspinatus, subscapularis, infraspinatus, and teres minor ( Fig. 21A1-5 ). The supraspinatus has its origin on the posterior-superior scapula, superior to the scapular spine. The anterior portion is more than two times larger than the posterior. [78] It passes under the acromion, through the supraspinatus fossa, and inserts on the greater tuberosity with an extended attachment of fibrocartilage. The tendon has parallel independent collagen fascicles that probably allow differential excursion of portions of the tendon[25] needed for the enormous range of shoulder mobility. The supraspinatus is active during the entire arc of scapular plane abduction; paralysis of the suprascapular nerve results in an approximately 50% loss of abduction torque.[15] The infraspinatus and the teres minor muscles originate on the posterior scapula, inferior to the scapular spine, and insert on the posterior aspect of the greater tuberosity. Despite their origin below the scapular spine, their tendinous insertions are not separate from the supraspinatus tendon. The insertion of the teres minor tendon can be distinguished from the others by a small separate tubercle that can be palpated on the most posteroinferior aspect of the greater tuberosity. These muscles function together to

Figure 21-A1-5 A and B, The supraspinatus, the subscapularis, the infraspinatus, and the teres minor are the four muscles of the rotator cuff.

externally rotate and extend the humerus. Both account for approximately 80% of external rotation strength in the adducted position. The infraspinatus is more active with the arm at the side; the teres minor activates mainly with the shoulder in 90 degrees of elevation. The subscapularis muscle arises from the anterior scapula and is the only muscle to insert on the lesser tuberosity. The subscapularis is the sole anterior component of the rotator cuff and functions to internally rotate and flex the humerus. The tendinous insertion of the subscapularis is continuous with the anterior capsule; therefore, these two structures have been considered responsible for providing anterior glenohumeral stability.[91] [96] In the superior two thirds of the muscle, there is a consistent pattern of tendinous bands evenly dispersed in the midportion of the muscle that condense laterally into a single large flat tendon.[43] The inferior third of the subscapularis is muscular from origin to insertion. The deltoid is the largest of the glenohumeral muscles and covers the proximal humerus on a path from its tripennate origin at the clavicle, acromion, and scapular spine to its insertion midway on the humerus at the deltoid tubercle. Abduction of the joint results from activity of the anterior and middle portions. The anterior portion is also a forward flexor. The posterior portion does not abduct the joint but instead adducts[109] and extends the humerus. The deltoid is active throughout the entire arc of glenohumeral abduction; paralysis of the axillary nerve results in a 50% loss of

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abduction torque.[15] The deltoid muscle can fully abduct the glenohumeral joint with the supraspinatus muscle inactive. The teres major muscle originates from the inferior angle of the scapula and inserts on the medial lip of the bicipital groove of the humerus, posterior to the insertion of the latissimus dorsi. The axillary nerve and the posterior humeral circumflex artery pass superior to it through the quadrilateral space that is also bordered by the teres minor, the triceps, and the humerus. Because of its proximity to the rotator cuff, the tendon of the teres major muscle has been proposed as a donor in rotator cuff reconstruction. This muscle contracts with the latissimus dorsi muscle,[69] and the two muscles function as a unit in humeral extension, internal rotation, and adduction. The neuromuscular pedicle and muscle-tendon unit length allow its use in unipolar transfer.[97] Biceps Brachii Muscle

Both heads of the biceps brachii muscle have their origin on the scapula. The short head originates from the coracoid and with the coracobrachialis muscle forms the conjoined tendon. The long head of the biceps originates just superior to the articular margin of the glenoid from the posterosuperior labrum and the supraglenoid tubercle and is inside the synovial sheath of the glenohumeral joint.[17] It traverses the glenohumeral joint, passing over the anterior aspect of the humeral head to the bicipital

groove, where it exits the joint under the transverse humeral ligament. The tendon is normally widest at its origin and becomes progressively narrower toward the muscle belly. The two muscle bellies are jointed at about the level of the insertion of the deltoid on the humerus. Although closely approximated, the two bellies are separable until about 7 cm from the elbow.[83] Its origin on the scapula and insertion on the radius give the long head of the biceps brachii muscle the potential to function at both the shoulder and the elbow. Elbow function has been well established to include both flexion and supination. The function of the long head of the biceps tendon at the shoulder has been the subject of much controversy, however. Enlargement of the tendon in the presence of large rotator cuff tears had led to the postulate that it is a depressor of the humeral head. In five cases at arthroscopy, Andrews and coworkers[2] observed glenohumeral joint compression when the biceps was electrically stimulated. The role in limiting superior humeral head instability was sub sequently supported by in vitro study by Flatow and coworkers.[27] They used a cadaveric model and simulated muscle activity with a cable system. The biceps tendon restrained superior migration of the humeral head most meaningfully in the presence of a large rotator cuff tear. Biomechanical studies also demonstrated that the long head of the biceps brachii tendon contributes to anterior stability by limiting resistance to torsional forces[77] and decreasing joint translation.[67] In an in vivo study of patients with isolated rupture of the long head, there was mild superior positioning of the humeral head.[98] The role of the active biceps has been questioned, however, because electromyographic study indicated that there is little or no activity of the biceps when elbow motion is controlled.[33] [108] The long head was not observed to be active during surgery in patients under local anesthesia during elbow flexion.[51] Specifically, the humeral head did not compress against the glenoid with biceps contractions. This does not preclude a passive role or an active role associated with elbow motion because tension in the tendon may contribute to glenohumeral joint stability. Thoracohumeral Muscles

Shoulder muscles that do not originate on the scapula should also be considered. Because of its proximity to the rotator cuff, the tendon of the latissimus dorsi muscle can be a donor in rotator cuff reconstruction. Its neurovascular pedicle and muscle-tendon length allow its use in unipolar transfer.[29] Muscles that have origin on the thorax contribute to glenohumeral stability and may have roles in instability as well. For example, the pectoralis major and the latissimus dorsi muscles are powerful movers of the shoulder; in doing so, they contribute to the joint force that in turn usually stabilizes the glenohumeral joint. The pectoralis major muscle may also contribute to anterior joint instability in some instances. In a biomechanical study, addition of a pectoralis muscle force resulted in significant change in the joint force, such that it became directed significantly more anterior.[24] Likewise, chronic spasm of the pectoralis major muscle was a factor in irreducible anterior glenohumeral dislocation because treatment with botulinum toxin injection resolved the instability.[84] In such a manner, abnormal action of the pectoralis major muscle, if it is

chronic, may contribute to joint instability. It has long been known that the pectoralis major muscle has ideal orientation to affect anteroinferior instability. Arciero and Cruser[3] additionally indicated that there is no need for contraction of the pectoralis major muscle for it to contribute to instability. In concurrent anterior dislocation and pectoralis major tendon rupture, they theorized that tendon rupture occurs from eccentric lengthening. The pectoralis major muscle arises as a broad sheet of two distinct heads with the lowermost fibers of the sternal head inserting most proximally on the humerus. When the shoulder is placed in horizontal abduction, similar to the apprehension position, these lowermost fibers of the sternal head are stretched to an extreme.[106] Because anterior instability also occurs from forcible horizontal abduction of the shoulder, the humeral head can be pulled out of the glenoid by passive tension in the pectoralis major. Such study is preliminary; the roles of the pectoralis major and other thoracohumeral muscles should be considered further. Glenohumeral Joint Anatomy and Stability

Static Stability

Articular Surfaces.

The size of the glenohumeral articular surfaces correlates directly with differences in size and height of both men and women and therefore is extremely variable.[38] The humeral head represents approximately one third of a 45-mm-diameter sphere and is spherical[86] or

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slightly elliptical, larger in the vertical dimension than in the horizontal.[38] It has a mean thickness of 19 mm.[38] [68] The articular surface spans an arc of 150 to 160 degrees,[40] and the angle between its inferior margin and the shaft (the head-shaft angle) is a mean of 45 degrees.[38] The superiormost point on the humeral head articular surface is a mean of about 8 mm above the greater tuberosity. [38] [70] Lateral humeral offset, the distance from the base of the coracoid to the lateralmost point of the greater tuberosity, is a mean of 56 mm.[38] Last, there is both medial and posterior offset of the head relative to the shaft, that is, the center of the humeral head is about 3 mm posterior[10] and nearly 1 cm medial to a line through the middle of the humeral shaft.[70] The proximal humerus is generally separated anatomically into four parts: the articular surface, the greater tuberosity, the lesser tuberosity, and the diaphyseal humeral shaft. The humeral head is angulated medially 45 degrees to the long axis of the humeral shaft and retroverted 30 degrees relative to the transcondylar axis of the distal humerus[39] [71] ( Fig. 21A1-6 ). Between the two tuberosities is the intertubercular groove, in which lies the tendon of the long head of the biceps brachii muscle. This tendon is held in place by the coracohumeral ligament and the transverse humeral ligament. During abduction of the glenohumeral joint, the proximal humerus slides on the tendon of the long head of the biceps brachii. If the tendon ruptures, translation of

the humeral head increases.[98] The mean size of the glenoid is about 35 mm in vertical diameter and 25 mm in horizontal diameter.[13] [18] [38] [40] [92] Relative to the plane of the scapula, the fossa is angled slightly superior and posterior, [28] [73] offering little bony support to inferior instability with the arm at the side ( Fig. 21A1-7 ). In the first 2 years of life, the glenoid is normally retroverted about 6 degrees, but by the end of the first decade of life, it reaches adult retroversion of 2 to 6 degrees. [59] There has been considerable controversy about the conformity of the two articular surfaces,[79] [80] partly because the bony glenoid is relatively flat, whereas the articular surface is not. Articular cartilage is thicker at the periphery of the glenoid than at the center; conversely, the articular surface of the humeral head is thicker at the center than at the periphery.[99] Unfortunately, radiographs lead to the mistaken impression that the articular surface of the glenoid is flatter

Figure 21-A1-6 The humeral head is angulated medially 45 degrees relative to the long axis of the humeral shaft and is retroverted 30 degrees relative to the transcondylar axis of the distal humerus.

Figure 21-A1-7 Relative to the plane of the scapula, the fossa is angled slightly superiorly and posteriorly, offering little bony support to inferior instability with the arm at the side.

than that of the humeral head. A stereophotogrammetric study by Soslowsky and coworkers[86] provided direct measurement of the articular surfaces and indicated that the articular surfaces are matched nearly perfectly with similar radii of curvature, and during joint motion, the humeral head maintained uniform contact with the glenoid. This point is controversial, however, and others believe that the surfaces are noncongruent, with the radius of curvature of the articular surface of the glenoid being slightly larger than that of the humerus. [11] [38] This is important because three actions are possible in the glenohumeral joint: spinning, sliding, and rolling. Spinning occurs when the contact point on the glenoid remains the same while the contact point on the humeral head is changing. Sliding is pure translation of the humeral head on the articular surface of the glenoid. At the extremes of motion, and certainly in unstable joints, glenohumeral translations occur. In this circumstance, the contact point on the glenoid is moving while that on the humerus remains the same. The third type of action, rolling, may also occur at the glenohumeral joint. Rolling is a combination of humeral head translation and spinning with respect to the glenoid, and the contact point changes on both the glenoid and the humeral head.[61] All three motions may take place at the glenohumeral joint [61] as dictated by the conformity of the articular surfaces. The position of the glenohumeral articular surfaces contributes to joint stability. Because the glenoid is concave and tilted slightly superior when it is viewed in an anteroposterior direction, inferior joint translation is coupled to lateral translation of the humeral head. The lateral translation tightens the superior capsular structures and the supraspinatus,

maximizing inferior joint stability. [5] Knowledge of normal glenohumeral joint anatomy is important for minimizing the ramifications of imprecise surgical repair. Nonunion may occur if the tuberosities are not positioned in contact with the humeral shaft in treatment of four-part proximal humerus fractures. A greater tuberosity malpositioned above the articular surface of the humeral head may lead to pain from abnormal contact

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Figure 21-A1-8 The thin redundant joint capsule has almost twice the surface area of the humeral head, allowing a tremendous range of joint motion. lig., ligament, Sup., superior.

with the coracoacromial arch. Failure to reproduce humeral thickness and offset may lead to weakness and diminished range of motion. Abnormal soft tissue tensioning and glenoid impingement may be responsible. Excessive glenoid retroversion may also lead to joint instability. Such alterations from the normal articular surface geometry are unusual unless they are the result of glenoid hypoplasia or trauma. After shoulder arthroplasty, however, alterations of joint geometry are not unusual. Whereas limitations of prosthetic design may sometimes make reconstruction of the glenohumeral joint difficult,[68] surgeons remain responsible for precisely positioning head and glenoid components. Capsuloligamentous Structures.

The thin redundant joint capsule has almost twice the surface area of the humeral head[20] ( Fig. 21A1-8 ). This allows a tremendous range of joint motion. Selective tightening of capsular portions, depending on shoulder position, provides passive stability. With the arm at the side in the dependent position, the superior portion of the capsule is taut and the inferior portion is lax.[42] With overhead elevation, this relationship reverses. Although originally disputed, it is now agreed that the glenohumeral ligaments provide structural reinforcement of the anterior capsule. Named for their humeral insertions, variations in the insertion sites have been described. In most joints, all three glenohumeral ligaments are present, [90] and only the pattern of the anterior synovial recesses varies. The superior glenohumeral ligament, present in 94% of shoulders, [90] originates anterior to the tendon of the long head of the biceps brachii. If the glenoid had the markings of a clock with the 12-o'clock position superior and the 3-o'clock position anterior, the origin of the superior glenohumeral ligament would correspond to the area from the 12-o'clock to the 2-o'clock positions. The superior glenohumeral ligament runs inferior and laterally and inserts into the fovea capitis on the humerus, just superior to the lesser tuberosity. The superior glenohumeral ligament has been shown to be important in resisting inferior

subluxation with the arm at the side.[101] The middle glenohumeral ligament is present in 70%[21] to 85%[90] of shoulders. It usually arises from the neck of the glenoid[32] just inferior to the origin of the superior glenohumeral ligament and inserts on the humerus just medial to the lesser tuberosity. Viewed from inside the joint, it crosses over the superior margin of the subscapularis tendon. The presence of the middle glenohumeral ligament is the most variable.[21] [90] There are four types: cordlike, bandlike yet separate from the inferior glenohumeral ligament, bandlike yet confluent with the inferior glenohumeral ligament, and poorly defined. The middle glenohumeral ligament limits anterior translation of the humeral head with the arm in moderate (45 degrees) abduction and external rotation.[96] The inferior glenohumeral ligament is located in the inferior redundant part of the capsule and is absent in only 7% of glenohumeral joints. [90] It is identified as a broad structure with closely packed collagen fiber bundles[32] and is a complex structure that consists of an anterior band, a posterior band, and an axillary pouch in between.[66] It has been likened to a hammock, which supports the humeral head. With abduction and external rotation, the anterior band fans out and the posterior band becomes cordlike. Likewise, with internal rotation, the posterior band fans out and the anterior band appears cordlike. The anterior band of the inferior glenohumeral ligament arises from various areas corresponding to the 2-o'clock to 4-o'clock positions on the glenoid. The posterior band originates at the 7-o'clock to 9-o'clock positions and inserts on the humerus either adjacent to the anterior band or on the posterior articular margin of the humerus. With the arm at the side, both the anterior and posterior bands pass through a 90-degree arc and insert on the humerus. In addition to resisting anterior translation with the shoulder abducted and externally rotated, the anterior band of the inferior glenohumeral ligament is a secondary restraint to inferior instability with the arm at the side.[102] The posterior band is probably important in resisting inferior subluxation in the joint abducted more than 45 degrees.[101] Last, the importance of the anterior capsuloligamentous structures in resisting posterior glenohumeral instability has been implied.[93] [105]

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Whether it occurs alone or in combination with a Bankart lesion, stretching of the capsuloligamentous soft tissues has been hypothesized to contribute to anterior instability. There is still considerable debate about the amount of stretching that occurs with an initial dislocation episode, however. Part of the problem lies in the differences in the definition of stretching. When a ligament fails, the change in length has both recoverable and permanent components. The total ligament midsubstance strain, representing the recoverable and permanent components, reported by Bigliani and coworkers,[9] Mow and coworkers,[63] and Ticker and coworkers[94] was 11%, 9.1%, and 10.8%, respectively. The change in total ligament length of the anterior band of the inferior glenohumeral ligament was larger because it represented change of both insertion sites and the ligament midsubstance. It was 24%[9] to 30.4%[94] of the total ligament length. Only the permanent component of the stretching needs to be corrected with surgical repair, however. The amount of permanent stretching can be gauged in

two manners. First, the difference between the strain at failure and the strain at yield represents the permanent strain. This is small, a mean of less than 4% regardless of the failure mode.[57] In the second method, the permanent deformation represents permanent stretching of both insertion sites and the ligament midsubstance. In the anterior band of the inferior glenohumeral ligament that failed at the glenoid insertion region, this was only 2.3 ± 0.4 mm.[57] Tensile testing of the anterior band of the inferior glenohumeral ligament[9] [57] reveals that most fail at the origin from the glenoid bone, representing the Bankart lesion. More specifically, the labrum can be avulsed from the glenoid bone, along with a ligament attachment to the anterior neck of the glenoid. The ligament can be avulsed alone, representing failure at the ligament-labrum junction, with the labrum being left intact on the glenoid. This is usually not seen clinically. More rarely, failure can occur at the humeral insertion region or at the ligament midsubstance. [57] After injury other than the Bankart lesion, the anterior band probably heals, albeit in a lengthened state. In this way, the manner of tearing rather than permanent stretching of the capsuloligamentous structures may be responsible for the spectrum of glenohumeral instability that is observed clinically. Permanent stretching of the capsuloligamentous soft tissues at the time of ligament failure occurs not only in the medial to lateral direction but also in the superior to inferior direction.[88] This concurs with the empirical finding that permanent lengthening of the capsule occurs not only along the anatomic alignment of the glenohumeral ligaments but also in the superior to inferior direction. Plication of the capsule in both directions leads to an acceptable out-come.[8] [60] The optimal amount of ligament plication after repetitive episodes of instability remains unknown and may be different in individuals of different ages at the time of injury.[48] Findings of biomechanical studies indicate, however, that the amount of plication necessary after an initial instability episode is small, probably less than a few millimeters.[57] [88] [89] Rotator Interval and Coracoacromial Ligament.

At the anterosuperior aspect of the glenohumeral joint is the interval between the supraspinatus and the subscapularis. The rotator cuff tendon is thin or absent altogether because the muscle origins are separated by the coracoid. The rotator interval consists of the superior glenohumeral ligament and the coracohumeral ligament. The coracohumeral ligament originates on the base of the coracoid and passes between the supraspinatus and subscapularis tendons to blend with the insertion of the subscapularis tendon on the lesser tuberosity. It helps to support the dependent arm and acts as a restraint to external rotation in this shoulder position.[64] The coracohumeral ligament has anterior and posterior bands originating at the coracoid. [75] The anterior band inserts onto the lesser tuberosity and becomes most taut with external rotation when the arm is at the side. The posterior band inserts onto the greater tuberosity and becomes most taut with internal rotation when the arm is at the side. The coracohumeral ligament may also restrain glenohumeral translations when the arm is at the side and positioned in internal or external rotation.[47] Injury to the rotator interval results in posteroinferior instability,

[35] [101]

and in a human

cadaveric model, tightening of these tissues significantly decreased the posterior and inferior translation of the joint.[35] Schwartz and coworkers[81] found that posterior dislocation would not occur after sectioning of the entire posterior capsule unless the rotator interval was also sectioned. The coracoacromial ligament has been implicated as an important soft tissue structure contributing to the symptoms of impingement syndrome. Its release has traditionally been performed liberally because the coracoacromial ligament was thought to have little functional importance. Studies indicate that the coracoacromial ligament plays an important role in normal shoulder function,[1] [85] however, and capricious release should be avoided. The coracohumeral ligament is a barrier to anterosuperior translation of the humeral head, especially after rotator cuff rupture. Detachment of the coracoacromial ligament also results in increased anterior and inferior translation of the internally and externally rotated glenohumeral joint.[47] This is due to impairment of interaction between the coracoacromial ligament and the coracohumeral ligament. The coracoacromial ligament has an extension, termed the falx, that runs lateral to the coracoid process; it is also composed of fibers from the conjoined tendon.[47] [72] Because the falx inserts on the clavipectoral fascia and specifically into the area of the rotator interval, the coracoacromial ligament acts as a support for the coracohumeral ligament. When the coracoacromial ligament is detached from the acromion, the falx becomes lax, then the coracohumeral ligament does also. These interactions can be likened to a suspension bridge, with the coracoacromial ligament as the primary suspension cable and the falx as the secondary suspension cable. When the primary suspension cable becomes lax, so does the secondary suspension cable and then in turn the coracohumeral ligament ( Fig. 21A1-9 ). In this manner, release of the coracoacromial ligament from the acromion impairs function of the coracohumeral ligament. Labrum.

The labrum surrounds the periphery of the glenoid and is composed of dense fibrous connective tissue; it is the insertion of the capsuloligamentous structures. [62] The anatomy of the anteroinferior region, which is the glenoid insertion site of the anterior band of the inferior glenohumeral ligament, is more complex. The insertion site of this ligament has two attachments, one to the glenoid

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Figure 21-A1-9 The coracoacromial ligament can be likened to the primary suspension rope of a suspension bridge, with the falx being the secondary vertical cables.

labrum and the other directly to the anterior neck of the glenoid.[57] The size of each attachment relative to the other is variable, but both are likely to be important in resisting anterior translation of the humeral head. The labral attachment demonstrates similarities to some direct ligament or tendon insertions, such as that of the supraspinatus.[7]

Characteristic of direct insertions, the collagen fibers meet the attachment at a right angle in a sequence of four distinct zones (ligament, fibrocartilage, mineralized fibrocartilage, and bone).[107] In contrast to other direct insertion sites, wherein the four morphologically distinguishable zones span a distance of less than 1 mm, the labral attachment of the anterior band of the inferior glenohumeral ligament is relatively long. The zone of fibrocartilage is particularly long at the superior margin of the anterior band. The glenoid neck attachment near the 3-o'clock location is similar to the tibial insertion of the medial collateral ligament as described by Woo and associates.[107] Dense collagen fibers approach the bone at an acute angle and attach as an indirect insertion. Both superficial and deep fibers are present. The superficial fibers run parallel to the bone surface, blending in with the periosteum, and the deep fibers attach straight to the bone. At the 6-o'clock location, as the collagen bundles approach the glenoid, they appear disorganized, but this finding probably represents a change in direction of the collagen bundles; that is, the collagen bundles of the anterior band midsubstance are primarily oriented in a radial fashion, but they change direction near the glenoid and form the labrum as a circular system of collagen bundles. [32] The labrum in this region consists mainly of fibrous tissue.[17] [62] The glenoid labrum may act not only as an attachment site for the capsuloligamentous structures but also as an extension of the articular cavity. [74] It serves to increase the surface area of the glenoid.[11] [87] Howell and Galinat[36] showed that the labrum deepens the glenoid socket by nearly 50%. Lippitt and coworkers[50] have shown that removal of the labrum decreases joint stability to shear stress by 20%. In this way, the triangular cross section of the labrum acts as a chock to help prevent subluxation. Intracapsular Pressure.

The contribution of normal intracapsular pressure to joint stability is described in Gray's Anatomy[34] the looseness of the capsule is so great that the arm will fall about an inch from the scapula when the muscles are dissected and a hole is made in it to remove the [negative intracapsular] pressure. Anatomic studies, surgical findings, and magnetic resonance imaging studies confirm that a layer of synovial fluid less than 1 mm in thickness is present in the normal glenohumeral joint.[54] Because joint volume is finite, a negative intracapsular pressure is generated with attempts to distract the glenohumeral joint. In this way, slightly negative intracapsular pressure, which is present in the normal joint,[49] aids in centering the humeral head.[30] The negative intracapsular pressure is likely to be of particular importance in limiting inferior subluxation of the humeral head.[12] [102]

Dynamic Stability (Concavity-Compression)

Large forces are generated in the shoulder muscles to move the shoulder against gravity. In the normal shoulder, this contributes meaningfully to joint stability through the application of a compression force. This is the component of the glenohumeral joint force that acts perpendicular to the glenoid fossa such that the concave humeral head is compressed into the glenoid fossa. Termed concavity-compression by Lippitt and coworkers,[50] this action was initially reported to be important in maintaining joint stability at the midranges of shoulder elevation[50] when the static restraints are lax.[100]

The shoulder muscles that are active in elevation of the arm [4] [16] [19] [55] include the rotator cuff and are directed toward the glenoid fossa. The anterior capsuloligamentous structures are lax, so the compression force maintains stability. In addition to the rotator cuff muscles, any muscle that crosses the glenohumeral joint can contribute to concavity-compression. For example, a weight lifter bench-presses while exercising and a large force is generated in the pectoralis muscle. The component of the pectoralis muscle force that acts perpendicular to the glenoid contributes to concavity-compression while the shoulder is moving. The muscle orientation in addition to the magnitude of the muscle force determines how much a muscle contributes to concavity-compression. Concavity-compression is also important at the end range of elevation. [24] [46] Because muscle forces are larger with the arm in 90 degrees of elevation than at lower levels, [55] concavity-compression should also be larger, as long as the humeral head remains centered on the glenoid. Interplay of Static and Dynamic Stability

In the apprehension position, precise interplay of the dynamic and static restraints results in anterior joint stability.[58]

849

The way in which the anterior band of the inferior glenohumeral ligament acts with concavity-compression can be likened to the manner by which a rider controls a powerful horse. In this example, the horse represents concavity-compression force and the reins represent the anterior band of the inferior glenohumeral ligament. When the horse is running straight ahead, little control on the reins is needed to maintain it on a path. If the horse begins to turn, a light tug on the opposite rein redirects the horse onto the path. In the same way, the anterior band of the inferior glenohumeral ligament, which alone has biomechanical properties[9] [48] [57] insufficient to resist the large force of dislocation, can maintain the humeral head in the glenoid. A study indicated that concavity-compression is not significantly altered after injury to the anteroinferior static restraint.[58] In fact, the compression force, that is, the component oriented perpendicular to the glenoid, is large even after anteroinferior static restraint injury. As in the example, if the horse is running straight ahead, the rider can drop the reins and the horse will not initially deviate from the path. Unfortunately, in the shoulder with pathologic change, other joint forces that contribute to instability can offset concavity-compression. For example, in the shoulder with a supraspinatus tendon tear, the glenohumeral joint force is oriented superior rather than perpendicular to the glenoid as in the normal shoulder. Over time, this results in erosion of the superior rim of the glenoid, and the humeral head can sublux a small amount superior.[53] This serves only to direct the glenohumeral joint force more superior. Eventually, the entire superior rim of the glenoid becomes worn, and the humeral head

ends up abutting the acromion. In a similar manner, if a traumatic anterior dislocation results in damage to the anteroinferior glenoid, the humeral head subluxes a small amount anteroinferior. The glenohumeral joint force is no longer directed perpendicular to the glenoid but instead is directed a small amount anteroinferior. The static restraints fail in time, and the instability worsens. Scapula Positioning

The scapula has long been thought to have a role in glenohumeral stability because it positions the glenoid. Therefore, treatment of glenohumeral instability includes scapula muscle strengthening for correction of scapula muscle deficits.[56] As the scapula protracts, it slides laterally and tilts forward to maintain conformity with the convex thorax. In the protracted position, the laterally located glenoid is angled anterior. Intuitively, this scapula position would lead to increased anterior glenohumeral translation because the humeral head would move down the bony slope of the glenoid. This is not the case; instead, as the glenoid is angled anterior, anterior translation decreases.[103] With simulated scapular protraction, the anteroinferior capsule that contains the anterior band of the inferior glenohumeral ligament becomes increasingly taut. In this manner, normal scapulothoracic motion is important to pain-free shoulder function because the position of the scapula on the thorax determines the position and inclination not only of the glenoid but also of its attached capsuloligamentous structures, including the inferior glenohumeral ligament. Repetitive or chronic abnormal scapula positioning may result in excessive strain and ultimately insufficiency in the anterior band of the inferior glenohumeral ligament. It is important to consider the scapula's position in treating patients with anterior glenohumeral joint instability.

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Kinematics and Muscle Function of the Shoulder

Inman and coworkers[39] provided the first comprehensive biomechanical analysis of shoulder function in 1944. With use of anatomic, radiographic, and electromyographic systems of analysis, a dynamic model of the shoulder was created and yielded several tenets of shoulder mechanics. They proposed that the supraspinatus and the deltoid muscles acted as a single unit throughout elevation of the shoulder. The subscapularis, infraspinatus, and teres minor acted as a functional unit to depress the humerus continuously throughout this motion. An understanding of shoulder biomechanics is of paramount importance to sports medicine physicians because athletic injuries to the shoulder are common. It was Jobe's[41] observation that athletes often experience a selective weakness of specific rotator cuff muscles rather than the generalized muscle impairment predicted by Inman's model. This led to laboratory investigation of whether Inman's conclusions regarding single-plane motion analysis could be applied to sport-specific activities. The Centinela Hospital Biomechanics Laboratory in Inglewood, California, began to study shoulder motion during baseball pitching and other overhead sports activities with the goal of providing a basis for optimal treatment and prophylaxis of athletic injuries. In addition, the effects of selected common pathologic processes of the shoulder were studied. Dynamic electromyography and high-speed analysis were used to identify the functions of major muscles that control the shoulder. Data were collected with use of the Basmajian single-needle technique.[4] Dual 50-m insulated wires with 2-mm-bared tips were inserted into the muscle with use of a 25-gauge needle as a cannula. Manual muscle examination and signal display on an oscilloscope determined the accuracy of placement. The subject wore an FM transmitter belt pack, and the telemetered electromyographic information was recorded on multichannel tape for later retrieval and

review. Motion analysis was conducted with the aid of 16-mm cameras that were set at speeds varying from 50 to 200 frames per second. The subjects were photographed from two or three points of view (anterior, posterior, lateral, or overhead), depending on the needs of the study. The cameras were pin-registered to ensure accurate simultaneous recording. An electronic pulse marked the film and electromyographic records simultaneously to synchronize the data. After processing, the films were reviewed on a stop-action projector that permitted single-frame viewing. The electromyography data were converted from analog to digital signals and quantitated by computer integration with sampling at 2500 times per second. After exclusion

850

Figure 21-A1-10 Phases of the baseball pitch.

of the low-level activity identified as the resting signal, the greatest 1-second electromyographic signal during the manual muscle strength test was selected as the normalizing base value. Results were expressed as percentages of the manual muscle strength test. Overhand Pitcher

The phases of the baseball pitch are found in Figure 21A1-10 . The description is of a right-handed pitcher. Whereas some of the mechanics discussed are of the lower extremities and trunk, the eventual effect can be on the shoulder. It is in the lower extremities that the build-up of energy is begun. From there, the energy is transmitted through the trunk and up to the arm. If faulty mechanics are initiated lower in the chain, the ultimate pathologic process may manifest itself in the shoulder. Normal Mechanics

Wind-up.

The wind-up can have much personality. Many pitchers have their own stylistic adaptations to this phase. Some basic components in this phase are found in all successful stylistic adaptations, however, and these basics determine the success of the delivery. If the mechanics are properly executed during wind-up, they will flow naturally and easily throughout the rest of the pitch. The basic components of this phase begin with the feet parallel to one another and perpendicular to the rubber on the mound. The hips are level to one another and are perpendicular to the plate. The hands

are together. The body is aligned with good balance. The left leg takes a small, comfortable step back, in line with home plate. The right foot is then positioned parallel to the rubber, and some coaches have the pitcher wedge the foot with the lateral half on top of the rubber. The left lower extremity is picked up in a controlled, active fashion, and the hips remain level while pointing toward home plate. As the hips begin to move forward, a V is formed with the hips at the apex; the torso and right leg form the two sides of the V. The hips point toward the batter. In the final event of wind-up, the hand holding the ball comes out of the glove. Although these key points in wind-up are necessary for a successful delivery, the shoulder is relatively nonchallenged. The shoulder moves slowly, the hands are together, and the muscle activity is low.[22] Early Cocking.

As the hand comes out of the glove, it must stay on top of the ball. The hand on top of the ball helps the shoulder stay in more internal rotation, which is a safer position for the glenohumeral joint. The shoulder is elevated in the scapular plane to 104 degrees and externally rotated to 46 degrees.[26] The V, which was initiated in wind-up, becomes more pronounced in early cocking as the hips continue to advance toward home plate ( Fig. 21A1-11 ). The hips stay level. Rotation of the hips is delayed as long as possible. From the perspective of the batter, the ball is hidden, because the batter cannot yet determine which type of pitch will be delivered. The early cocking phase ends as the left leg slowly, easily, and comfortably comes down and the foot contacts the mound. Late Cocking.

As the left foot makes contact with the mound, it lands within the width of the right foot. The foot points toward home plate. The weight is evenly distributed on the legs, and the legs are firm. The torso is balanced in

Figure 21-A1-11 In early cocking, the V (which was initiated in wind-up) becomes more pronounced as the hips advance toward home plate and the foot wedges into the rubber.

851

an upright position between the legs. The pitcher stays closed (delays trunk rotation) as long as possible. The point of the late cocking phase is to move the humerus into maximal external rotation. The humerus maintains its level of elevation in the scapular plane and externally rotates from 46 degrees to 170 degrees.[26] Acceleration.

Once the humerus begins to internally rotate, the acceleration phase is initiated. Within approximately 0.05 second, the ball is released from the hand at 90 miles per hour. This motion occurs on a firm base provided by the lower extremities, with both feet planted on the mound throughout the phase. Deceleration.

After the ball is released, the right hip comes up and over the left leg. The right foot disengages from the mound, and the body does a controlled fall forward. The excess kinetic energy that was not transferred to the ball is dissipated, beginning with the arm. Follow-through.

As the arm continues to be brought down, the forces are much less to the arm. This phase appears to be fairly inconsequential. Adaptive Mechanics

Wind-up.

In that the stage is set during wind-up, numerous problems are actually initiated in this phase, but the pathologic repercussions are not noted until later. For example, if the hips are pointing in a direction other than home plate during wind-up, the leg will later land in the faulty direction. The trunk will then exhibit compensatory rotation, and the timing of the arm will be off. Similarly, if the trunk leans back as the left leg is raised, the balance will be off throughout the pitch with excessive motion in the anterior-posterior plane (and perhaps medial-lateral motion as well). Yet, as mentioned before, the arm is at relatively low risk during wind-up because it is moving slowly, and torque is low, as is the muscle activity. An astute clinician will pay careful attention to the basics during the wind-up phase, however, because any problems here will later be magnified. Early Cocking.

One of the more common faulty habits of a pitcher is to place the hand under the ball during early cocking. This is most notable in youths who are learning to pitch or in people who have not had proper coaching. Some players will take the ball out of the glove with the hand underneath it. Others will take the ball out of the glove with the hand on top, but as they bring the arm back, they rotate the hand to beneath the ball. This erroneous technique is called pie-throwing. With the hand under the ball, the humerus moves into external rotation. As the arm is swinging back (behind the body) and up (into the throwing position), the faulty external rotation leaves the humeral head at risk to sublux anterior. Thus, there is potential for instability, which can lead to anterior subluxation and subsequent injury. Another common problem in early cocking is excessive early trunk rotation. During this

phase, the left leg is not yet in contact with the mound. A pitcher who begins excessive rotation of the trunk will obviously not have a stable, balanced base from which to rotate. In addition to a loss of balance, a lot of potential energy will be lost. An individual who begins excessive rotation in early cocking also opens up too soon in late cocking. Opening up refers to the chest facing the batter. When the hips rotate too quickly, the trunk follows, and the upper torso has not rotated to face the batter. The pitcher who opens too soon attempts to replace the lost potential energy by heaving the ball forward in acceleration. Late Cocking.

The position of the left foot as it contacts the mound is an indicator of the earlier position of the hips (in which they pointed toward home plate) as well as an indicator of whether the pitcher will open up too soon. If the left foot lands pointing to the first-base side, the pitcher will open up too soon. If it lands pointing to the third-base side, the pitcher will stay closed too long, throw too far to the inside, or become off balance. If a pitcher opens up too soon, the arm is typically left behind the scapular plane (hyperangulation) while the humerus is externally rotating to 170 degrees.[26] This leaves the humeral head angled so that it can stretch the anterior structures and creates the potential for anterior instability and the resultant injury ( Fig. 21A1-12 ). If the muscles of the anterior wall are weak or fatigued, the probability of injuring them in the hyperangulated position is even higher. Opening up too soon also has an effect on the elbow. If the arm is left behind the scapular plane, the valgus load on the elbow is increased. The stress is largely borne by the ulnar collateral ligament. Hence, this mechanical deviation can lead to medial elbow instability. Several muscles are vulnerable during the late cocking phase. The first is the serratus anterior. The serratus anterior is significantly less active in pitchers with unstable shoulders than in pitchers with normal shoulders.[31] This can be related clinically because one of the subtlest signs of impending injury is scapular winging, asymmetry, or premature elevation. When the serratus anterior is no longer able to perform adequately, no other muscle can effectively substitute. Without the serratus anterior to tether down the inferior angle of the scapula, the scapula elevates early or wings. The serratus anterior is one of the few muscles that are constantly active. Therefore, it is more vulnerable to fatigue. A therapist would wisely focus on strengthening and endurance training for the serratus anterior. In the subtle stage of diminished serratus anterior activity, the astute eye of the coach or medical practitioner may note that the player tends to drop the elbow. The dropped elbow is really decreasing the degree of necessary scapular rotation and elevation. This, in turn, requires less from the serratus anterior. As the pathologic process progresses, the player may begin with the compensatory mechanics of moving the humerus into or behind the coronal plane. The player also loses some humeral external rotation, and the back typically begins to move into hyperlordosis.

Experience has shown that if the scapular asynchrony can be identified at the earliest stage, even before there are complaints of pain or before there is a tangible consistent drop in performance, the athlete can be pulled off the field. A specific strengthening program to prevent anatomic damage to the static stabilizers can then be initiated. Chronically unstable shoulders have also demonstrated significantly less activity in the subscapularis and pectoralis major.[31] The result of this is obviously a lack of support for the anterior wall of the glenohumeral joint. Thus, another concept to reinforce in an exercise program is strengthening

852

Figure 21-A1-12 If a pitcher opens up too soon, the arm is left behind the scapular plane, which causes potential for anterior instability and the resultant injury. A, Normal mechanics. B, Pathologic mechanics; the arm is behind the scapular plane.

of these muscles. In that the subscapularis inserts more closely to the axis of rotation than the pectoralis major does, it would be more closely related to shoulder stability. For these reasons, it is more important to focus on the subscapularis in the strengthening program. Not all of the pathologic mechanics are what they seem. The pathologic mechanics are sometimes a substitution pattern for a downstream problem. For example, if a pitcher has back pain, the arm may move into the coronal plane for reasons unrelated to the previous discussion. If the back is sore, the pitcher may not be able to transmit the forces from the legs up through the trunk and out the arms. Thus, as a substitution, the pitcher may attempt to regain the lost power by heaving the ball. The arm may move into the coronal plane to heave the ball forward. If this is done, the pitcher still ends up with anatomic damage to the shoulder, yet the shoulder damage is really symptomatic of another problem. Perhaps the shoulder will undergo a rehabilitation program, and the pitcher is then returned to the mound. If the core problem of a back injury had not been addressed, it could flare up again, causing another spate of injuriesperhaps at the shoulder, perhaps to the elbow, or perhaps at a different weak link in the chain. For this reason, the total picture of the mechanics and the effect of one body part must be considered. If an athlete presents with more than one overuse injury, it is pointing toward a mechanical deficit somewhere else in the chain. This concept applies not just to the late cocking phase of the pitch or just to the pitcher, but to all phases of all sports. Acceleration.

The problems mentioned in the cocking phases are also present in acceleration. The lordotic position of the back is most evident at this time. The arm behind the body is also

noted, as is a dropped elbow. A whipping action occurs to substitute for the hyperangulated arm. This action brings the arm forward. The whipping in combination with the valgus forces at the elbow in late cocking causes microtrauma of the ulnar collateral ligament and, in some cases, an acute rupture of the ligament. In either case, medial instability of the elbow results. In terms of shoulder muscle function, the serratus anterior and subscapularis continue with the pattern of decreased activity in unstable shoulders that was apparent in the late cocking phase. The effect and rehabilitation implications are the same as those discussed earlier. In another mechanical deviation that may be noted in acceleration, the right foot comes off the ground. If this occurs, the pitcher can easily be off balance. If there is not a stable, bilateral base, it is much more difficult to accumulate and transmit the large forces to throw the ball. Thus, compensatory mechanics in the upper extremity may occur. If the pitcher is off balance, the chances are much higher that the ball will be inaccurately placed. Deceleration.

During deceleration, the teres minor demonstrated the highest level of activity of all glenohumeral muscles.[22] This has clinical relevance in that a subtle sign of injury is pain localized to the teres minor during deceleration. The prevention and rehabilitation programs consist primarily of strengthening the teres minor. Clinicians tend to think of the teres minor and infraspinatus muscles as one unit, yet work on muscle function during pitching[22] as well as on exercise programs[95] demonstrates that these two muscles function differently and need to be strengthened differently. The infraspinatus can be strengthened optimally with the arm held at 20 degrees of abduction. The teres minor is strengthened optimally at 70 degrees of abduction. Follow-through.

Any faulty mechanics that are noted at this point had their genesis much earlier, and the outcome (pathologic change, ball speed, or placement) has already been determined. Freestyle Swimmer

The arm motion in the freestyle stroke is reciprocal, and arm position marks the different phases of the stroke. The phases are found in Figure 21A1-13 . Normal Mechanics

Early Pull-through.

The hand enters the water forward of and lateral to the head and just medial to the shoulder.

853

Figure 21-A1-13 Phases of the freestyle swim stroke. (Adapted from Pink MM, Perry J, Browne A, et al: The normal shoulder during freestyle swimming. Am J Sports Med 19:569-576, 1991.)

The elbow is flexed and positioned above the hand, so the fingers are the first to enter the water. The hand then reaches forward under the water, and the palm begins to rotate down. Thus, the first action in pull-through is really a forward reach. Only after maximal arm length is obtained is the motion reversed to a pull. At the point of maximal elbow extension, the hand initiates an S-shaped pattern of pulling. The first part of the S-shaped pull is called the catch. It occurs as the opposite arm releases pressure on the water. The elbow begins to flex as the head and shoulders start to be propelled over the arm. This is one of the more propulsive phases of the stroke.[52] The next motion is in a downward and outward direction. As the hand approaches the deepest point, the downward motion is rounded off into an inward, upward, and backward motion. The hand moves toward the midline of the body. The humerus becomes perpendicular to the long axis of the torso (i.e., mid pull-through) while the hand is still forward of the shoulder. Late Pull-through.

After the humerus reaches a 90-degree angle with the torso, the hand continues to move toward the midline. The humerus is now extending for the hand to exit the water eventually. The swimmer continues to push the water back as the hand passes the hip. At this point, the push moves outward and upward as the hand approaches the anterior thigh. The elbow breaks the surface of the water while the hand is completing the pull-through phase. The motion from the midline to anterior thigh is the most propulsive phase of the stroke.[52] The palm then rotates toward the thigh to exit the water. Recovery.

Recovery is a much shorter phase than pull-through. The purpose of recovery is simply to bring the arm into position to pull once again. The humerus is internally rotated as it is lifted out of the water. It then abducts and rotates externally to a small degree (i.e., not

beyond neutral rotation) to bring the forearm around. In freestyle swimming, the arm functions in internal to neutral rotation, which is one of the main differences from baseball pitching. The pitch and most overhead activities require the arm to move into maximal external rotation. The position of maximal external rotation is a vulnerable position. The shoulder of the freestyle swimmer is also vulnerable; however, its mechanics are different because the humerus never moves into external rotation. Pathologic Mechanics

Early Pull-through.

A swimmer with a painful shoulder may demonstrate a wider hand entry and a flatter pitch to the hand. Coaches note this position as a dropped elbow and remark that they can tell when swimmers are hurt, tired, or lazy because they fail to hold the elbow up. In that the hand entry position for the normal shoulder closely approximates the Neer test for impingement,[65] it is understandable that the swimmer would adapt her or his mechanics to avoid the painful position. The altered hand entry position in swimmers with painful shoulders is consistent with the significant decrease in muscle activity in the anterior and middle deltoids.[82] In addition, the scapula does not need to be upwardly rotated or retracted as much in this position. Accordingly, there is significantly less activity in the upper trapezium and rhomboids. Mid Pull-through.

During mid pull-through, the most dramatic significant differences in muscle activity are noted. The serratus anterior reveals a drop in muscle activity while the rhomboids increase their activity.[82] Most likely, the serratus anterior fatigues in swimmers with painful shoulders and produces a floating scapula. To compensate, the rhomboids contract to stabilize the scapula. It is of interest that these two muscles are antagonists. When the serratus anterior cannot perform, there is no muscle that can assist by doing a similar action. The only way the body can stabilize the scapula is to call on antagonistic muscles, the rhomboids, which attempt to substitute for a deficient serratus anterior. Thus, the optimal synchrony of firing seen in normal scapular rotation is disturbed at the time of propulsion. The swimmer with shoulder pain may also exhibit excessive body roll throughout pull-through. This may be leading up to an early hand exit. Because the hand exit in the normal swimmer entails a large degree of humeral internal rotation (which is painful), the swimmer with pathologic change may compensate by hand exit before that point. One way to facilitate an early hand exit is to have excessive body roll toward the side of the hand exit. As the body rolls to that side, the hand is able to come out of the water. This usually happens shortly after the hand passes the umbilicus. Because the most propulsive portion of the stroke is after that point, quite a bit of power can also be lost. The altered muscle action in the swimmer with painful shoulders supports the point of decreased internal rotation at an early hand exit. The infraspinatus demonstrates

significantly more activity in the painful shoulders as it externally rotates the humerus.[82] Recovery.

As the swimmer with a painful shoulder demonstrates an early hand exit with decreased internal rotation, the elbow is also dropped. The dropped elbow (decreased internal rotation) is carried through for all of recovery. Even as the hand enters the water in a wider

854

position, the elbow is dropped. Once again, coaches note this as a dropped elbow. By keeping the arm lower and shortening the arc of motion, these swimmers avoid the painful impingement. Likewise, the altered muscle activity in the swimmer with painful shoulders suggests the dropped elbow. As the hand exits the water, the anterior deltoid shows significantly less activity[82] as lifting, abducting, and forward flexing of the humerus are blunted. There is also diminished activity in the subscapularis at mid recovery. In that the subscapularis places the arm in the painful position of internal rotation, it is understandable that it would decrease its activity as the elbow drops and the arm avoids the extreme of internal rotation. As with the serratus anterior, the muscle activity of the subscapularis stays above 20% of its maximum in normal shoulders throughout the stroke. This suggests its vulnerability to fatigue, so the diminished activity in recovery may be a response to fatigue.

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Summary

Understanding of the shoulder's function requires knowledge of its anatomy and biomechanics. Information on dynamic shoulder function presented in this chapter correlates well with the original work of Inman and coworkers.[39] Although elevation presents a prolonged three-dimensional challenge in stabilizing the shoulder, the humeral rotator muscles act in synchrony with the deltoid. During sporting activities, rapid, precise motion stimulates selective muscle activity and specific periods of great muscle intensity. At these times, the rotator cuff muscles do not always act in synergy with the deltoid but act according to their mechanical qualities and are function or sport specific. The rotator cuff is always important in stabilization of the arm in space, whereas the roles of other muscles vary. Although baseball pitching provides the clearest model, similar patterns are evident in other sports as well. The importance of the serratus anterior muscle activity in stabilizing and protracting the scapula is a consistent finding. Such information has provided a physiologic basis for exercise protocols[95] to minimize injury. Expansion of this research to include subjects with pathologic processes of the shoulder strengthens therapeutic guidelines. It is critical to have an understanding of the demands placed on the shoulder during a particular activity to be able to understand and treat the pathologic conditions.

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2. ANATOMY, BIOMECHANICS, AND KINESIOLOGY OF THE CHILD'S SHOULDER Ralph J. Curtis Jr. MD The shoulder is a complex series of four jointsthe glenohumeral joint, the acromioclavicular joint, the sternoclavicular joint, and the scapulothoracic articulation. The shoulder provides the only connection between the upper extremity and the axial skeleton. The anatomy of the shoulder has evolved to accommodate its primary function of providing prehensile use of the upper extremity. The shoulder is well suited for this purpose because of the minimal bony constraints and elaborate soft tissue attachments that allow a large degree of freedom and multiplanar range of motion at the joint. This premium on shoulder motion is accomplished by sacrificing inherent stability. The unique aspects of pediatric anatomy are based on the body's need for continuing growth throughout this period of life. The growth plates or physes are characteristic of immature, growing bone. They provide longitudinal growth of the major bones around the shoulder but are also more vulnerable to injury by compression and shearing forces. Both the physes and the thick periosteum found in children allow growth and contribute to the rapid healing and remodeling in cases of fracture. In addition, the soft tissues about the shoulder have a tendency toward more elasticity, which allows increased flexibility in an already unstable joint. Prenatal Development

The embryonic period extends from conception to the eighth week of development. It is characterized by rapid formation and differentiation of structures. The limb buds develop as small elevations on the ventrolateral body wall during the fourth week of gestation. The upper limb buds develop opposite the lower six cervical and first and second thoracic segments. By the fifth week, peripheral nerves grow into the mesenchyme of the limb buds from

the brachial plexus, stimulating the development of limb musculature. Simultaneously, the central core of the humerus begins to chondrify. The scapula appears and is positioned at the level of C4 and C5. The precursor to the shoulder joint, called the interzone, appears between the humerus and scapula at this stage. Also during the fifth week of gestation, the clavicle

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begins to ossify through intramembranous ossification from two centers; it is one of the first bones to ossify. During the sixth week, the hands begin to develop, and bending occurs at the elbow. The interzone of the shoulder develops a true layered configuration with a chondrified layer on either side of a loose layer of central cells. Bone formation occurs in the primary ossification center of the humerus. The scapula enlarges and extends from C4 to T7 . In the seventh week, the upper limbs rotate laterally through 90 degrees on their longitudinal axis with the elbows and the extensor muscles facing laterally and posteriorly. The radius assumes a lateral position. The shoulder joint is now well formed. The scapula descends to its position between the first and fifth ribs. By the eighth week of gestation, the shoulder joint has developed into a fully formed adult-like glenohumeral joint with capsular ligamentous thickenings apparent. It is during this embryonic period that certain toxins and environmental factors can lead to congenital deformities around the shoulder joint.[2] [7] [12] [16] [17] [18] [19] [20] [25] [29] [31] The fetal period, the time from 8 weeks of gestation to birth, is characterized mainly by enlargement of the structures differentiated and developed during the embryonic period. The primary center of ossification for most long bones appears in the diaphysis between the 7th and 12th week of development. The muscular, tendinous, and ligamentous structures around the shoulder appear to become distinct by the 13th week and continue to mature throughout the gestational period. [2] [12] [16] [17] [18] [19] [20] [25] [29]

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Postnatal Development

The shoulder joint complex is fully formed by the time of birth. Postnatal development through childhood consists of further growth and enlargement with maturation of the bony, cartilaginous, musculotendinous, and ligamentous tissues. Several factors involving this rapid growth of the musculoskeletal system distinguish the pediatric athlete from the adult. In the pediatric patient, open growth plates include primary physes and secondary apophyses, both of which are more vulnerable to injury.[12] [25] [28] [29] Injuries to the growth plate are characterized by rapid healing but also by the potential for growth arrest or disturbance. The physis itself is an area of rapidly growing cartilage that has much less tensile strength than the surrounding epiphysis or metaphysis. The histologic appearance of the growth plate is well recognized; it has a typical columnar orientation of cartilage cells with progressive cellular hypertrophy, provisional calcification, and finally endochondral ossification. The zone of hypertrophy and the zone of provisional calcification have most often been implicated as the anatomic sites of growth plate fractures ( Fig. 21A2-1 ). Long bones in skeletally immature individuals are characterized by a primary ossification center within the diaphysis (shaft), a physis (growth plate), and an epiphysis or secondary ossification center at either end. In children, the diaphysis is surrounded by a thick periosteal sleeve that provides appositional growth and remodeling. The growth plate or physis is the primary site of longitudinal bone

Figure 21-A2-1 The physis of the proximal humerus. Note that fractures through the growth plate often occur through the zone of hypertrophy and the zone of provisional calcification.

growth that occurs by endochondral ossification. The epiphysis or secondary

ossification center begins as a completely cartilaginous anlagen at the ends of long bones. As maturity approaches, this model is progressively ossified, leaving only the articular surface as cartilage. The external surface of the epiphysis or perichondrium serves as a direct attachment point for muscles, tendons, and ligaments. This anatomic arrangement increases the vulnerability of the physeal plate to injury, such as fracture. Injuries to the growth plate have been classified in detail by Salter and Harris, Rang, and more recently Ogden.[12] [28] The Salter-Harris classification, the most commonly used in practice, describes five types of injuries involving the physeal plate ( Fig. 21A2-2 ). The plasticity of young bone is greater than that in an adult. This relates to the thick periosteal tube that surrounds immature bone. Bone tends to get stiffer and more brittle with age. Immature bone is susceptible to plastic deformation characterized by the greenstick type of fracture. In addition to injury associated with acute macrotrauma, the athletic pediatric population is especially susceptible to repetitive overuse microtrauma-type activities. Repetitive stress in a tensile fashion across the epiphysis or apophysis can lead to stress-related injuries, such as osteochondroses and stress fractures.

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Bone Development

The humerus is completely ossified throughout its diaphysis and metaphyseal portions at birth. The secondary ossification center of the proximal humerus is rarely ossified until after the first 6 months postnatally. Only approximately 20% of newborn infants demonstrate radiographic evidence of ossification of the proximal humeral epiphysis

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Figure 21-A2-2 The Salter-Harris classification as applied to the proximal humerus. Type 1 is a transverse fracture through the physis. Type 2 is a transverse fracture through the physis with a small metaphyseal fragment. Type 3 is a transverse fracture through the physis including a fracture through the epiphysis. Type 4 is a longitudinal fracture across the epiphysis and the metaphysis through the physis. Type 5 is a crushing-type injury to the physis involving a central portion.

at birth. The ossification center of the greater tuberosity appears between the seventh month and third year of age. The center of the lesser tuberosity appears approximately 2 years after the appearance of the greater tuberosity. By the age of 5 to 7 years, the three proximal ossification centers of the humeral head, greater tuberosity, and lesser tuberosity coalesce to become a single proximal ossification center ( Fig. 21A2-3 ). The proximal humeral physis usually closes between 19 and 22 years of age. This proximal humeral physis accounts for approximately 80% of the longitudinal growth of the humerus.[6] [20] [22] [28] > The clavicle forms by intramembranous ossification. It is one of the first bones in the human to ossify and begins in the fifth gestational week from two different areas in the

Figure 21-A2-3 Radiograph demonstrating the single proximal humeral ossification center. This physis usually closes between 19 and 22 years of age.

central portion of the bone. The medial physis of the clavicle provides up to 80% of the remaining longitudinal growth of this bone ( Fig. 21A2-4 ). Interestingly enough, it is one of the last to ossify; its secondary ossification center appears between 12 and 19 years of age. Fusion to the shaft of the clavicle does not occur until the age of 22 to 25 years. The lateral clavicular epiphysis is usually inapparent radiographically because it appears, ossifies, and then fuses during a period of a few months at about 19 years of age. This is significant during evaluation and treatment of distal clavicular injuries in the adolescent. Many times, these injuries are actually physeal fractures as opposed to true acromioclavicular dislocations. [1] [6] [11] [22] [26] [33] The scapula first appears as a chondrified anlagen in the fifth gestational week. It begins at the level of C4-C5 and then migrates to occupy a position extending from C4 to T7 during the sixth and seventh gestational weeks. After formation of the shoulder joint at about the seventh week, the scapula descends from the cervical area to its more adult-like position overlying the first through fifth ribs. Failure of the scapula to descend results in Sprengel's deformity. The body of the scapula forms by intramembranous ossification throughout its primary center, which is usually completely ossified by birth. The remaining multiple ossification centers are highly variable in terms of number and position ( Fig. 21A2-5 ). At approximately 1 year, an ossification center for the coracoid process appears. By 10 years of age, a common physis appears for the base of the coracoid and upper glenoid. A third, somewhat variable ossification center can appear at puberty at the tip of the coracoid and may be misidentified as an avulsion fracture. By the age of 15 to 16 years, these three centers usually coalesce. The acromion ossifies by forming between two and five ossification centers. These usually appear by puberty and are completely fused by the age of 22 years. Failure of fusion of one of the acromial physes results in an unfused os acromiale ( Fig. 21A2-6 ). [23] [27] At puberty, the center for the vertebral border and inferior angle of the scapula and a horseshoe-shaped epiphysis for the lower three quarters of the glenoid appear. They fuse to the remaining scapula by the 22nd year. Because of the multitude of centers of ossification, many anomalies of the scapula have been described, including bipartite coracoid, duplication of the acromion process, dysplasia of the glenoid, and scapular clefts.[6] [22] [24] [31]

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Surgical Anatomy Bone Anatomy

Clavicle

The clavicle is a subcutaneous S-shaped bone that extends from the sternoclavicular joint medially to the acromioclavicular joint laterally. The clavicle has a more cylindrical configuration medially but becomes somewhat flattened and narrow laterally. It provides attachment for many of the major shoulder girdle muscles, including the trapezius, deltoid, sternocleidomastoid, and pectoralis major muscles. It provides a bony protective roof over the thoracic outlet through which pass the axillary vessels and brachial plexus.

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Figure 21-A2-4 Radiograph of the clavicle in a child with inapparent physis medially and laterally.

The clavicle is capable of motion in multiple planes. Most of this motion occurs through the sternoclavicular joint and includes rotation, translation, and an ability to pivot anterior to posterior as well as superior to inferior. When the shoulder is taken through a full range of motion, the clavicle rotates about its long axis approximately 50 degrees and is elevated upward approximately 30 degrees. Only a small amount of motion occurs laterally through the acromioclavicular joint. [1] [2] [20] [26] Scapula

The scapula is a large flattened, triangular bone positioned at the posterolateral aspect

of the bony thorax situated approximately between the third and ninth ribs. The scapula provides a framework for attachment of many of the major muscles about the shoulder and a mobile base

Figure 21-A2-5 The multiple ossification centers of the scapula.

for the glenohumeral joint at the glenoid. It has five major componentsthe body, neck, spine, glenoid, and coracoid. The body of the scapula is oriented at a 30- to 45-degree angle to the coronal plane of the body. It is somewhat concave on its costal surface with slight convexity on the dorsal surface. Dorsally, the body of the scapula is divided by a thin rigid bone known as the spine of the scapula. It separates the dorsal aspect of the scapula into the supraspinatus and infraspinatus fossae. At the lateral edge of the scapular spine, these two fossae communicate by way of the spinoglenoid notch. The acromion is an extension of the spine of the scapula that rotates to form a flattened roof above the shoulder joint itself. The acromion is a flattened structure with some variability in terms of its angle of inclination and morphologic features. Bigliani has described this morphologic appearance as one of three types. The type I acromion has a relatively high angle and flat undersurface. The type II acromion has a downward curve and a decreased angle of inclination. The type III

Figure 21-A2-6 Axillary radiograph of the shoulder demonstrating an unfused os acromiale.

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acromion has a hooked configuration along the anterior portion and a further reduction of the angle of inclination.[4] [20] The lateral portion of the scapular body narrows to form the scapular neck, which supports the glenoid fossa. The glenoid is a concave, pear-shaped structure that is oriented laterally at approximate right angles to the long axis of the scapular body. The glenoid has an average of 5 degrees of superior tilt and a retroversion of 3 degrees to 9 degrees in relationship to the long axis of the scapula. The coracoid process is a bony projection off the anterior surface of the scapula just medial to the scapular neck. It projects anteriorly and laterally and has a hooked configuration. It serves as the origin of several muscles and ligaments that provide stability at the acromioclavicular joint. Superiorly and medial to the coracoid is the supraspinous notch, which contains the suprascapular nerve.[5] [20]

Proximal Humerus

The proximal humerus consists of the humeral head, greater tuberosity, lesser tuberosity, bicipital groove, and metaphyseal portion of the shaft. The humeral head articulates with the glenoid and has a large convex oval shape. It is in 25 to 35 degrees of retroversion as it relates to the humeral epicondyles. The head forms an upward head-shaft angle between 130 and 140 degrees in relationship to the shaft. With the arm in the anatomic position, the intertubercular or bicipital groove is anterior. It is covered by a transverse humeral ligament and allows access for the long head of the biceps tendon into the shoulder joint. Immediately distal to the articular surface and posterior to the intertubercular groove lies a prominent projection of bone known as the greater tuberosity. Anterior and medial to the bicipital groove is a smaller prominence of bone known as the lesser tuberosity. The lesser tubercle is the insertion for the subscapularis tendon, and the greater tubercle bears the insertion of the supraspinatus, infraspinatus, and teres minor in superior to inferior order. The anatomic neck is that space between the articular cartilage and the ligamentous and tendinous attachments.[20] Articulations

Glenohumeral Joint

The articulation between the humerus and the glenoid is the most mobile major joint in the body. The unique anatomic configuration of this joint accommodates motion while sacrificing inherent stability. The articular surface area of the humeral head is greater than the relatively small articular surface of the glenoid. The radius of curvature of the glenoid is somewhat greater than that of the humeral head, however. This mismatch allows inherent translation of the humeral head on the glenoid with range of motion. The glenoid labrum deepens and provides stability for the joint by decreasing this relative difference in radius of curvature.[20] The capsule of the glenohumeral joint is reinforced by thickened areas known as the glenohumeral ligaments.

Figure 21-A2-7 The glenohumeral joint capsule and its relationship to the proximal humeral physis. Note that the physis is predominantly extra-articular except on the medial side, where it becomes an intra-articular structure.

These primary stabilizers attach to the glenoid labrum and circumferentially attach to the rim of the glenoid. The humeral attachment of the capsular ligaments occurs along the region of the anatomic neck except medially, where the attachment extends distally along the shaft. The proximal humeral physis lies in an extracapsular position except along this medial side, where it is intra-articular ( Fig. 21A2-7 ). The glenoid labrum, in addition to deepening the glenoid, provides a strong area of attachment for the capsular ligaments.[8] These capsular ligamentous bands have more precisely been defined in the

anterior capsule as the superior, middle, and inferior glenohumeral ligaments. The capsular ligaments of the glenohumeral joint form a complex functional unit. With the arm adducted at the side, the inferior capsule and ligaments are highly redundant, but as the arm is taken through a range of abduction, elevation, flexion, or extension, these ligaments sequentially tighten to provide stability for the joint.[9] [12] [14] [15] [20] [21] [30] [32] With the arm in the anatomic position, the intertubercular groove between the greater tuberosity and the lesser tuberosity lies approximately 1 cm lateral to the midline. This groove is covered by a transverse ligament and permits access for the long head of the biceps into the joint. The long head of the biceps attaches superiorly to the glenoid rim and labrum as a prominent intra-articular structure. The rotator cuff tendons form a sleeve of thickened tissue that covers the joint anteriorly, posteriorly, and superiorly. The tendinous contributions from the subscapularis muscle attach to the lesser tuberosity; the supraspinatus, infraspinatus, and teres minor tendons coalesce to form a posterior sleeve of tissue that attaches to the greater tuberosity. The rotator cuff inserts immediately adjacent to the insertion of the capsular ligaments.[20] [32] Acromioclavicular Joint

The acromioclavicular joint is formed by the lateral end of the clavicle and its articulation with the medial aspect of the acromion. The clavicle becomes more flattened in

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Figure 21-A2-8 The distal clavicle and its relationship to the acromioclavicular joint in the immature patient. Note the thickened periosteal tube surrounding the distal clavicle, which is continuous with the acromioclavicular and the coracoclavicular ligaments. C, coracoid; HH, humeral head.

its outer third and is surrounded by an extremely thick periosteal tube. This periosteum is continuous laterally with the acromioclavicular ligaments that span the acromioclavicular joint and inferiorly with the coracoclavicular ligaments that provide stability for the distal clavicle ( Fig. 21A2-8 ). The acromioclavicular joint is a diarthrodial joint stabilized primarily by these strong coracoclavicular ligaments that extend from the coracoid to the undersurface of the distal third of the clavicle. There are two portions to the coracoclavicular ligament, the conoid and trapezoid, that extend from the level of the joint medially for approximately 3 cm along the clavicle. In the mature individual, an intra-articular disk covers the end of the distal clavicle and protects the two adjacent incongruous surfaces. The acromioclavicular joint is protected by thick muscular attachments of both deltoid and trapezius. The deltoid attaches all along the anterior aspect of the distal clavicle and anterior acromion. Posteriorly on the distal clavicle is the strong insertion of the trapezius muscle. These multiple muscular and ligamentous attachments surrounding the distal clavicle provide relative protection compared with the

clavicular shaft. In children, injury more commonly consists of a fracture through the clavicular shaft or through the distal physis with splitting of the periosteal tube. [1] [2] [11] [20] Sternoclavicular Joint

The sternoclavicular joint is a diarthrodial joint composed of the large medial end of the clavicle, the sternum, and the first rib ( Fig. 21A2-9 ). The medial clavicle becomes somewhat bulbous at its medial end and articulates with a portion of the sternum and first rib that form a relatively flat and shallow surface for articulation. This joint is extremely incongruous and has little inherent bony stability. A fibrocartilaginous disk provides further cushioning and stability for this joint, which is surrounded by a strong series of ligaments. The anterior and posterior capsular ligaments provide the major support. The anterior portion of the capsular ligament is stronger and heavier and provides the primary support against upward and anterior displacement of the medial clavicle. These ligaments attach primarily to the epiphysis of the medial clavicle, which helps to explain why medial clavicular physeal injuries in children are more common than true sternoclavicular dislocations.[11] [20] In addition, the intra-articular disk ligament is a dense fibrous structure extending from the first rib through the joint and attaching both anteriorly and posteriorly to the strong capsular ligaments. Further stability for the joint is provided by the interclavicular ligament and costoclavicular ligaments. The interclavicular ligament runs from clavicle to clavicle, attaching to the superior aspect of the manubrium. The costoclavicular ligaments run from the first rib to the inferior surface of the medial clavicle. They help suspend the clavicle much like the boom of a crane.[3] [10] [13] [15] [20]

Most clavicular motion occurs through the sternoclavicular joint. This joint has the capability of allowing 30 to 35 degrees of upward clavicular elevation (pivot), 35 degrees of anterior to posterior glide (translation), and 45 to 50 degrees of rotation about the long axis of the clavicle. This motion is extremely important for normal shoulder function as the scapula rotates to allow normal abduction and elevation of the arm. In addition to its important function in mobility, this joint provides the only true bony

Figure 21-A2-9 The medial clavicle and its relationship to the sternum and the first rib through the sternoclavicular joints. Note the complex series of ligaments and the extra-articular position of the medial physis of the clavicle.

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articulation between the upper extremity and the axial skeleton. Its position anterior to the mediastinum also gives it a protective function. In posteriorly displaced fractures and dislocations about the medial clavicle and sternoclavicular joint, injury can occur to the major neurovascular structures exiting the mediastinum.[3] [20] [26] [30]

Scapulothoracic Articulation

The scapulothoracic articulation does not represent a true joint in the strictest sense. This articulation is surrounded by heavy musculature and allows a gliding action of the scapula on the posterior thorax. It is through this motion that the scapula provides a mobile base for the glenohumeral joint. Muscles

Trapezius

This muscle originates from the spinous processes of the C7 through T12 vertebrae, the ligamentum nuchae, and the external occipital protuberance. Insertion is over the distal third of the clavicle, the acromion, and the spine of the scapula ( Fig. 21A2-10 ). It is innervated by the accessory spinal nerve (cranial nerve XI). The nerve runs parallel and medial to the vertebral border of the scapula in the medial 50% of the muscle. The trapezius acts as a scapular retractor.[20] Rhomboids

The rhomboids originate from the lower ligamentum nuchae, C7 and T1 for the rhomboid minor and T2 through T5 for the rhomboid major. They insert on the posterior portion of the medial base of the spine of the scapula and

Figure 21-A2-10 The posterior periscapular musculature, including the trapezius, the levator scapulae, and the rhomboids.

into the posterior surface of the medial border to the inferior angle of the scapula ( see Fig. 21A2-10 ). Innervation to the rhomboid muscles is by the dorsal scapular nerve (C5). The action of the rhomboids is retraction of the scapula with some participation in elevation of the scapula.[20] Levator Scapulae

This muscle originates from the posterior tubercle to the transverse processes of the first through fourth cervical vertebrae and inserts into the superior angle of the scapula and along the medial border of the scapula to approximately the level of the scapular spine ( see Fig. 21A2-10 ). The innervation of this muscle is from the cervical plexus and occasionally the dorsal scapular nerve. The levator acts to elevate the superior angle of the scapula, and in conjunction with the serratus anterior, it produces upward rotation of the scapula.[20]

Serratus Anterior

The serratus anterior originates from the outer surface of the first eight ribs and follows the curvature of the ribs to insert along the medial aspect of the scapula on its costal surface. It is innervated by the long thoracic nerve. The serratus protracts the scapula and participates in upward rotation. Absence of serratus activity produces a winging of the scapula with forward flexion of the arm.[20] Deltoid

This is the largest and most important of the glenohumeral muscles. It originates from the lateral third of the clavicle, the acromion, and the scapula and inserts into the deltoid tuberosity along the anterolateral aspect of the proximal humerus ( Fig. 21A2-11 ). It has a multipennate configuration with an anterolateral raphe. The deltoid receives it innervation from the axillary nerve. The deltoid functions in elevation in the scapular plane through the action of the anterior and middle thirds. Abduction in the coronal plane decreases the contribution of the anterior third and increases the contribution of the posterior third. Flexion is a product of the anterior and middle thirds of the deltoid, whereas extension involves the posterior and middle thirds. The deltoid is active in any form of elevation, therefore, and loss of deltoid function is significant.[20] Rotator Cuff

The rotator cuff consists of four muscles having their origin on the scapula with a combined tendinous insertion surrounding the humeral head on the greater and lesser tuberosities. These muscles are the supraspinatus, the infraspinatus, the teres minor, and the subscapularis ( Fig. 21A2-12 ). The supraspinatus muscle arises from the supraspinatus fossa and passes laterally under the coracoacromial arch, inserting into the greater tuberosity. It is innervated by the suprascapular nerve. This muscle is active in any motion

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Figure 21-A2-11 The deltoid muscle, with its origin on the clavicle, the acromion, and the scapula and its insertion into the deltoid tuberosity distally along the anterolateral aspect of the humerus.

involving elevation at the shoulder. It exerts maximal effort at about 30 degrees of elevation and is the center for the head-depressing effect of the rotator cuff. The infraspinatus muscle arises from the infraspinous fossa and travels laterally to insert on the posterior aspect of the greater tuberosity. It is innervated by the

suprascapular

Figure 21-A2-12 The muscles and the tendons of the rotator cuff. These muscles include the supraspinatus, the infraspinatus, the teres minor, and the subscapularis.

nerve. It is one of the two main external rotators of the humerus and accounts for as much as 60% of external rotation force. It also functions as a glenohumeral head depressor through its common attachment with the remaining rotator cuff. The teres minor originates from the middle portion of the lateral border of the scapula and the dense fascia of the infraspinatus. It inserts into the lower posterior aspect of the greater tuberosity. It is innervated by a posterior branch of the axillary nerve. The teres minor also functions as an external rotator at the shoulder. The subscapularis muscle arises from the costal surface of the scapula and converges to insert on the lesser tuberosity of the humerus. It is innervated by the subscapular nerve. It functions as an internal rotator and passive stabilizer against anterior subluxation and serves in its upper fibers to depress the humeral head.[20] Pectoralis Major

The pectoralis major consists of three portions. The upper portion originates on the medial one half to two thirds of the clavicle and inserts along the lateral lip of the bicipital groove distal to the subscapularis. The middle portion originates from the manubrium and upper two thirds of the body of the sternum and ribs two through four and inserts directly behind the clavicular portion. The inferior portion originates from the distal body of the sternum, the fifth and sixth ribs, and the external oblique muscle fascia and inserts along with the other two portions into the humerus by rotating through 90 degrees ( Fig. 21A2-13 ). The pectoralis major is innervated by the lateral pectoral nerve (C5, C6, and C7) to the clavicular portion and by the medial pectoral nerve (C8 and T1) to the remaining portion. The muscle is a powerful adductor of the shoulder but can also participate in flexion, extension, and internal rotation, depending on arm position. Biceps Brachii

The biceps originates proximally by two heads: the long head from the supraglenoid tubercle and labrum within the

Figure 21-A2-13 The relationship of the three portions of the pectoralis major: the clavicular portion, the sternal portion, and the costal portion.

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shoulder joint, and the short head from the tip of the coracoid with the coracobrachialis. It inserts distally into the bicipital tuberosity of the radius. Innervation of the biceps is through the musculocutaneous nerve (C5, C6). The biceps functions primarily in flexion and supination at the elbow. It has a secondary humeral head-depressing effect at the shoulder.[20]

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Biomechanics

The primary function of the shoulder is to position the arm and hand in space to carry out desired sports activity. A multiplanar range of motion is required to accomplish this task, and stability is sacrificed to allow this wide range of mobility. The function of the shoulder girdle requires the integrated motion of all four jointsthe sternoclavicular, acromioclavicular, glenohumeral, and scapulothoracic. The acromioclavicular and sternoclavicular joints provide a stable strut that supports the action of the more mobile glenohumeral and scapulothoracic articulations. This complex interaction of four joints depends on precise function of articular surfaces, ligaments, and muscle-tendon units to provide coordination for shoulder mobility. Sternoclavicular Joint

The sternoclavicular joint is a shallow, relatively incongruous joint supported by a strong ligamentous complex. The sternoclavicular joint is oriented somewhat posterior, lateral, and upward. It contains an intra-articular disk or meniscus that helps provide congruity and stability. Four main ligamentous groups provide support for the sternoclavicular joint. The anterior capsule is supported by anterior sternoclavicular ligaments, which provide support against anterior translation of the joint. Posteriorly, the capsule is supported by the posterior sternoclavicular ligament and the costoclavicular ligament that extends from the first rib to the clavicle. The interclavicular ligaments extend from clavicle to clavicle across the superior manubrium and provide superior constraint. The costoclavicular ligaments run from the first rib to the inferior surface of the medial clavicle. With the arm adducted to the side, these ligaments are tightened; with the arm elevated, they are lax.[36] [42] [65] [67] Most clavicular motion occurs through the sternoclavicular joint. Motion at the sternoclavicular joint includes approximately 30 to 35 degrees of upward rotation (pivot), 35 degrees of anterior to posterior glide (translation), and up to 45 to 50 degrees of axial rotation. Stability at the joint is provided by tightening of ligaments opposite the direction

of motion ( Fig. 21A2-14 ). Acromioclavicular Joint

The articular surfaces of the acromioclavicular joint are not perfectly congruent and are supported by an intra-articular disk or meniscus. This plane-type joint is oriented somewhat posterior to the perpendicular from the coronal plane.

Figure 21-A2-14 Motion of the clavicle occurs predominantly through the sternoclavicular (SC) joint, including 30 to 35 degrees of upward rotation, 35 degrees of anterior-to-posterior glide, and 45 to 50 degrees of axial rotation. The clavicle moves through the acromioclavicular (AC) joint approximately at 30 degrees of elevation.

Ligamentous stability is provided by the acromioclavicular capsular ligaments and the more important coracoclavicular ligaments. The coracoclavicular ligaments consist of two components, the conoid ligament and the trapezoid ligament. The clavicle moves at the acromioclavicular joint through approximately 30 degrees of elevation. Joint motion includes anterior to posterior translation, inferior to superior rotation, and compression. The coracoclavicular ligaments are the primary restraints to displacement in both an anterior to posterior and a superior to inferior direction ( see Fig. 21A2-14 ). [36] [42] [44] [65] [67]

Glenohumeral and Scapulothoracic Joint Motion

The humeral head is composed of 120 degrees of the arc of a sphere. It is inclined superiorly in relation to the shaft, with a neck-shaft angle of 130 to 140 degrees. The articular surface is retroverted in relation to the transepicondylar axis approximately 30 degrees ( Fig. 21A2-15 ). The glenoid surface has been described as pear shaped. In the superior to inferior plane, it represents 75 degrees of an arc with a length of approximately 3.5 to 4 cm. In an anterior to posterior plane, it describes a 50-degree arc with a length of 2.5 to 3 cm. It is retroverted 7 degrees in relation to the scapular axis, and there is a 5-degree superior tilt. The glenoid labrum attaches circumferentially to the rim of the glenoid and deepens the socket. It has been found that the labrum increases the relative contact of the humeral head with the glenoid from approximately one fourth to one third. [36] [65] [67] Saha has described the glenohumeral ratio as 0.8 in the coronal plane and 0.6 in the horizontal plane ( Fig. 21A2-16 ). [80] [81] The range of motion at the shoulder complex is greater than at any other joint in the body. By convention, any

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Figure 21-A2-15 The relationship between the glenoid, the humeral head, and the coronal axis of the humerus. The humeral head is retroverted approximately 35 degrees in relation to the transepicondylar axis of the humerus.

upward motion of the shoulder, whether in forward flexion, abduction, or extension, is defined as elevation.[43] [46] [51] [59] [64] [65] [66] [67] The shoulder can be carried through an arc of elevation from 0 to 180 degrees. In addition, there is an internal rotation to external rotation arc of approximately 150 degrees. There is a horizontal plane range of motion in adduction and abduction of approximately 170 degrees. Although complementary motion in the sternoclavicular and acromioclavicular joints is necessary, the majority of this shoulder motion occurs through the glenohumeral and scapulothoracic joints. The relative contribution of the glenohumeral joint and scapulothoracic articulation to overall shoulder motion has been well studied. This motion is described as scapulothoracic rhythm. The average ratio of glenohumeral-to-scapulothoracic motion is approximately 2:1. There is general agreement that in the first 30 degrees of abduction, there is a much greater contribution from the glenohumeral joint to this range of motion.[46] [49] [55] [59] [65] [67] There is a variably decreasing contribution from the glenohumeral joint beyond 30 degrees of abduction and an almost equal contribution between glenohumeral and scapulothoracic joints during the last 60 degrees of elevation ( Fig. 21A2-17 ). An obligatory external rotation of the humerus occurs to allow complete elevation. This external rotation of the humerus clears the greater tuberosity and loosens the inferior capsular ligamentous structures to allow full elevation.[36] [38] [39] [42] [65] [67]

Figure 21-A2-16 The humeral head and its relationship to the glenoid. The glenoid socket is deepened by the glenoid labrum, which provides both congruity and increase in contact area.

The glenohumeral joint itself undergoes three types of motion at the joint surface. Spinning is rotation of the humeral head at a single instant center of rotation on the glenoid. Sliding is pure translation of the humeral head on the glenoid with a change in the instant center of rotation. Rolling is motion between the rotating humeral head and glenoid in which the instant center also changes. At any given time, only approximately one third of the humeral head is in contact with the glenoid. This is maximized with the shoulder at a functional position between 60 and 120 degrees of elevation.[40] [42] [50] [55] [59] [65] [67] [74] [75]

The instant center of rotation within the humeral head has a small amount of upward translation in the first 30 degrees of elevation equal to about 3 mm. Above 30 degrees, there is a further increase in elevation of approximately only 1 mm. With regard to translation in an anterior to posterior plane, this is relatively small through normal shoulder motion. Pathologic states, such as cuff deficiency, increase superior translation, and in cases of shoulder instability, there is increased anterior to posterior

translation.[36] [56] [60] [65] [67] Static Glenohumeral Stability

Both humeral and glenoid version contributes to the static stability of the glenohumeral joint. The 30-degree retroversion of the humeral head matches the amount of glenoid version with the scapula positioned at 30 to 45 degrees on the thorax in relation to the coronal plane. The 5-degree superior tilt of the glenoid has also been recognized as a static stabilizer against inferior instability.[35] [36] [39] [46] [62] [65] [67] [84] The surface areas of the humeral head and glenoid as well as articular conformity also contribute to stability of the joint. Although this is a relatively shallow ball-and-socket type of joint, the joint conformity does provide some stability. The glenohumeral articulation is usually described with the radius of the glenoid surface being greater than the radius of the humeral head. The glenoid-labral socket has recently been described to have a radius nearly equal to that of the humeral head. The labrum functions as a static stabilizer by deepening the socket, providing as much as 50% of its depth. In addition, it increases the surface area for contact with the humeral head and provides a buttress to translation and an attachment point for the glenohumeral ligaments. This is more consistent with studies that reveal little translation within a normal shoulder range of motion or only a slight degree of anterior translation with flexion and a slight degree of posterior translation with extension.[36] [46] [56] [65] [67] Interestingly enough, in static cutting studies, creation of a Bankart lesion alone does not lead to instability.[65] [67] [69] [78] [83] Another factor with regard to stability is the normal negative intra-articular pressure within the closed glenohumeral joint capsule. Many studies have shown that venting the capsule leads to immediate increased translation both in the anterior to posterior plane and in the superior to inferior plane. The magnitude of this effect depends on arm position.[52] [65] [67] The glenohumeral joint capsule provides the primary

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Figure 21-A2-17 A to C, The average ratio of glenohumeral (GH) to scapulothoracic (ST) motion is approximately 2:1. For the first 30 degrees of abduction, it is all glenohumeral motion. In the last 60 degrees of elevation, there is an almost equal contribution between the glenohumeral and the scapulothoracic joints.

static constraint for the shoulder joint. It is a continuous layered capsule of collagen fiber bundles with various thicknesses and orientations. With the advent of arthroscopy, better definition of the anatomy of the glenohumeral joint capsule has been obtained ( Fig. 21A2-18 ). Four major ligamentous structures are found within the capsulethe coracohumeral ligament, the superior glenohumeral liga ment, the middle glenohumeral

ligament, and the important inferior glenohumeral ligament complex.[42] [46] [49] [50] [65] [67] [78] [82] [85]

Figure 21-A2-18 Arthroscopic view of the glenohumeral ligaments. G, glenoid; H, humeral head; I, inferior glenohumeral ligament; M, middle glenohumeral ligament; S, subscapularis tendon.

The coracohumeral ligament extends from the lateral base of the coracoid as two separate bands attaching to the greater tuberosity and lesser tuberosity in the region of the rotator interval. In the adducted arm, it provides a primary restraint to inferior translation as well as external rotation. When the arm is adducted, flexed, and internally rotated, it also provides restraint to posterior translation. [65] [67] [69] [72] [76] The superior glenohumeral ligament is somewhat variable in its size and relative contribution. It runs parallel to the much larger extra-articular coracohumeral ligament from the superior rim of the glenoid adjacent to the biceps insertion to the lesser tuberosity. It functions as a primary restraint to external rotation as well as inferior translation in the adducted arm. Similar to the coracohumeral ligament, it is a secondary restraint to posterior translation in the adducted, flexed, and internally rotated arm. [36] [65] [67] [69] [72] [76]

The middle glenohumeral ligament is highly variable with its origin along the anterior-superior labrum, the scapular neck, or the supraglenoid tubercle and insertion into the lesser tuberosity along with the subscapularis tendon. This ligament can be either a distinct cordlike band or a sheetlike structure that blends with the inferior glenohumeral ligament. In ligament cutting studies, it has been shown to be a primary stabilizer against anterior translation when the arm is abducted up to 45 degrees. It is also thought to be important in limiting external rotation above 60 degrees of abduction.[65] [67] [69] [76] The inferior glenohumeral ligament complex is an important structure that has been described as having a hammock-like appearance.[68] [69] It extends from the glenoid labrum anteriorly, inferiorly, and posteriorly and runs laterally to the humeral head, attaching between the subscapularis and the triceps. It is characterized by substantially thicker areas anteriorly and posteriorly called the superior bands. The inferior glenohumeral ligament is the primary stabilizer in the shoulder above 60 degrees of abduction to

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both anterior and posterior translation. In the abducted shoulder, external rotation places the inferior glenohumeral ligament in a more anterior position to resist anterior translation; in the internally rotated shoulder, the inferior glenohumeral ligament is positioned posteriorly to resist posterior translation ( Fig. 21A2-19 ). [49] [65] [67] [68] [69] [70] [76] [85] [86] [87]

Figure 21-A2-19 With the shoulder abducted and externally rotated, the inferior glenohumeral ligament becomes the primary restraint to anterior translation of the glenohumeral joint. AIGH, anterior-inferior glenohumeral ligament. Dynamic Glenohumeral Stability

Contraction of the rotator cuff compresses the humeral head into the glenoid, providing increased joint compressive forces and resisting translation. The entire rotator cuff acts in concert to provide joint compression and stability. This effect of the cuff may be more important than any of the static capsular constraints in stabilizing the glenohumeral joint. The dynamic effect of the rotator cuff as an active counterbalancing restraint against the shear forces resultant to the muscular power of the deltoid, pectoralis, and latissimus has been well demonstrated ( Fig. 21A2-20 ). The muscles of the rotator cuff may also serve in a dynamic way to pretension the glenohumeral ligament complex through the common insertion of glenohumeral joint capsule and rotator cuff at the humerus. Specialized nerve endings in the rotator cuff and glenohumeral joint capsule provide proprioception, which is another component of dynamic stabilization of the glenohumeral joint.[54] [60] [62] [65] [67]

Figure 21-A2-20 The rotator cuff acts as a dynamic stabilizer resisting the shear forces exerted on the glenohumeral joint by the larger muscles, including the deltoid, the pectoralis major, and the latissimus dorsi.

The biceps tendon may also play a role in stability. The biceps can increase joint compression, and it has been demonstrated that sectioning of the long head of the biceps increases force across the inferior glenohumeral ligament complex in the abducted and externally rotated arm.[53] [65] [67] [71] [78] [79] In summary, the glenohumeral joint has a great degree of motion because of the complex interrelationship between the articular surfaces, capsular ligamentous restraints, and dynamic muscle stabilizers. The glenohumeral ligament complex, particularly the inferior component, is the primary restraint against anterior and posterior displacement. Translation is also limited by the geometry of the articular surfaces, the labrum, and the normal negative intra-articular pressure. The rotator cuff and biceps exert a dynamic element to stability by counterbalancing the forces of the larger power muscles acting at the shoulder.

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Kinesiology

The primary function of the shoulder is to allow the hand to be positioned in space to carry out prehensile function. The shoulder has evolved into an efficient anatomic structure to carry out the wide range of multiplanar motion required for this task. Unfortunately, stability is sacrificed anatomically for this goal of motion to be accomplished. When the shoulder is taken through a range of elevation, motion occurs primarily at the glenohumeral and scapulothoracic articulations. Secondary supportive motion occurs at the sternoclavicular joint and to a lesser degree at the acromioclavicular joint. Stability of the glenohumeral joint has both static and dynamic components. The humeral head is normally located within a 6-mm area on the center of the glenoid in a superior to inferior plane while remaining nearly neutral in an anterior to posterior translation plane during motion. Synergy between the rotator cuff and the deltoid is a key to normal function of the shoulder. The deltoid has a mobile point of origin on the acromion, clavicle, and scapula that allows it always to function within its most efficient length-tension curve. At the initiation of abduction, the long lever arm of the deltoid applies a force across the shoulder with a tendency to cause upward displacement or shear force across the humeral head. This force exerted by the deltoid becomes a more compressive force once the shoulder is abducted more than approximately 45 degrees. All four components of the rotator cuff work in concert to help improve deltoid function by serving as a humeral head depressor and stabilizer against this superior shear force that is created. The rotator cuff is therefore extremely important in providing dynamic stability in its force-couple relationship with the deltoid.[34] [36] [37] [38] [41] [43] [50] [60] [65] [67] The biomechanics and kinesiology of the throwing motion have been studied intensively by high-speed cinematography

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and by electromyographic analysis, which have provided information about the kinematics of the shoulder.[34] [41] [45] [47] [57] [58] [73] The demand on the shoulder during throwing is intense in terms of both the extremes in range of motion required and the large muscle forces involved ( Fig. 21A2-21 ). The kinesiology of the shoulder during the throwing motion shows many similarities to kinematics found in other overhand sports activities, such as the tennis serve, volleyball spike, javelin throw, and freestyle swimming stroke, and it can therefore be used as a model.[45] [73] [77]

Figure 21-A2-21 The baseball throw has been studied extensively and has become a model for study of biomechanics and kinesiology of the shoulder. The three phases of pitching include wind-up/cocking phase (A), acceleration phase (B), and follow-through phase (C).

The pitch has been broken down into three major phases of action: the wind-up/cocking phase, the acceleration phase, and the follow-through phase. The wind-up/cocking phase begins as the arm is elevated to approximately 90 degrees and then is horizontally extended or abducted. With these motions, the shoulder is externally rotated, tightening the anterior-inferior capsule. The anterior-inferior glenohumeral ligament complex is maximally tightened across the anterior-inferior surface of the joint. The subscapularis tendon begins as both a dynamic and static stabilizer, but as the wind-up/cocking phase is completed, it is elevated into a more superior position, decreasing its effectiveness. This phase is complete when the shoulder reaches its maximal point of external rotation. Electromyographic studies have shown that deltoid activity is high during this phase. The posterior deltoid serves as the prime source of extension, whereas the anterior and lateral components of the deltoid provide elevation and some external rotation. The supraspinatus, infraspinatus, and teres minor act sequentially throughout external rotation and abduction. With their combined stabilizing effect, they provide relief from anterior to posterior translation across the joint. Adequate strength in the rotator cuff musculature in this phase is of critical importance. The acceleration phase consists of a rapid unwinding of the potential energy stored in the soft tissues as they are positioned in the wind-up/cocking phase. Initiation of the acceleration phase occurs as the subscapularis and pectoralis major begin internal rotation. This phase is brief, lasting only 0.01 second. Peak rates of internal rotation of up to 7000 degrees per second have been measured. Although this represents a relatively passive activity from the standpoint of electromyographic activity, tremendous rotational stress is applied across the glenohumeral joint soft tissues in multiple planes. The follow-through phase consists of the shoulder's final continuation of internal rotation and horizontal adduction after the ball leaves the hand. Many muscle groups are active during this phase, including the deltoid, rotator cuff, biceps brachii, latissimus dorsi, and pectoralis major. These muscles fire in an attempt to decelerate the arm during this phase. Stress across the posterior capsule is at its peak.

The pitching cycle has revealed the complex function and interaction of joints, muscles, and tendons required to support normal shoulder activity. Further study of highly sport-specific activities, such as pitching, should enable us to continue to learn more about the kinesiology of the shoulder. This will help in the design and implementation of programs for both prevention and rehabilitation of injuries.

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Section B Imaging of the Glenohumeral Joint Timothy G. Sanders MD Shoulder pain is a frequent complaint of the competitive athlete as well as of the weekend athlete and provides an important indication for diagnostic imaging procedures. Several different imaging procedures are available for evaluation of the glenohumeral joint, but unfortunately, no single test reliably detects and fully evaluates all glenohumeral abnormalities that may be encountered. During the past decade, magnetic resonance (MR) imaging has evolved into the modality of choice for the evaluation of the painful shoulder in most cases. Other imaging modal ities, however, including conventional radiography, computed tomography (CT), and ultrasonography, continue to play a vital role in the evaluation of shoulder disease. The initial imaging evaluation of any shoulder condition should be the conventional radiograph, which reveals abnormalities such as fracture, dislocation, arthritis, tumor, and other unexpected conditions. After conventional radiography, several different imaging procedures are available to provide a more complete evaluation of the soft tissue and osseous structures of the glenohumeral joint. These include conventional arthrography, CT imaging, CT arthrography, ultrasonography, MR imaging, and MR arthrography. The role of the various imaging modalities as they pertain to the evaluation of shoulder disease is discussed, with special emphasis on the role of MR imaging and the emerging role of MR arthrography ( Table 21B-1 ). TABLE 21-B-1 -- Anatomy Key Ac

Acromion process

AC

Anterior capsule

AGL

Anterior glenoid labrum

Ax

Axillary recess

Bi

Bicipital tendon sleeve

BT

Bicipital tendon

Bu

Subacromial-subdeltoid bursa

C

Clavicle

Co

Coracoid process

D

Deltoid

G

Glenoid process

GT

Greater tuberosity

H

Humeral head

IGhL

Inferior glenohumeral ligament

ISM

Infraspinatus muscle

IST

Infraspinatus tendon

LT

Lesser tuberosity

MGhL Middle glenohumeral ligament PBF

Peribursal fat plane

PC

Posterior capsule

PGL

Posterior glenoid labrum

S

Scapula

SSM

Supraspinatus muscle

SST

Supraspinatus tendon

Su

Subscapularis recess

SuSM Subscapularis muscle SuST Subscapularis tendon TMM

Teres minor muscle

TMT

Teres minor tendon

Conventional Radiography

Conventional radiography is often the initial imaging examination performed for a patient presenting with shoulder pain, and although radiographs provide only a limited evaluation of the rotator cuff and glenoid labrum, they occasionally offer important information about the source of the patient's symptoms. Radiographs depict an assortment of osseous abnormalities, including fracture, arthritis, and tumor, and they are frequently complementary to the more advanced imaging modalities, such as CT

and MR imaging. A wide variety of radiographic views has evolved to aid in the evaluation of the glenohumeral joint, and knowledge about the advantages and disadvantages of each will assist in optimizing imaging protocols, depending on the clinical presentation.[22] [64] [112] The role of conventional radiography, including the use of specialized views, is discussed in separate sections of this chapter dealing with specific abnormalities.

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Conventional Shoulder Arthrography

Conventional arthrography of the shoulder ( Fig. 21B-1 ) has long been considered the gold standard for preoperative diagnosis of full-thickness tears of the rotator cuff ( Fig. 21B-2 ); reported accuracies range as high as 98% to 99%. [81] Partial-thickness rotator cuff tears involving the undersurface ( Fig. 21B-3 ) as well as adhesive capsulitis ( Fig. 21B-4 ) are also accurately depicted with use of this method. Partial-thickness rotator cuff tears involving the bursal surface and intrasubstance tears, on the other hand, are not demonstrated by conventional shoulder arthrography, and its usefulness in the evaluation of glenohumeral instability is limited.[82] Conventional arthrography remains a cost-effective and highly accurate method of identifying full-thickness tears of the rotator cuff. During the past decade, however, MR imaging has largely supplanted it as the primary imaging modality for evaluation of the rotator cuff, and in many practices, MR arthrography has evolved into the modality of choice for the evaluation of glenohumeral instability. The primary factors contributing to the shift from conventional arthrography to MR imaging are the superb soft tissue contrast and multiplanar capabilities provided by MR imaging. This allows a global assessment of the painful shoulder, including the rotator cuff, labrum and capsular structures, osseous outlet, acromion, and articular surfaces.

Figure 21-B-1 Normal shoulder, arthrography. Spot radiographs from single-contrast (A) and double-contrast (B, C, D, and E) glenohumeral arthrograms demonstrate the appearance of a normal arthrogram. Ax, axillary recess; Bi, bicipital tendon sleeve; Su, subscapularis recess.

Figure 21-B-2 Rotator cuff tear, shoulder arthrography. A, Frontal external rotation radiograph demonstrates air and radiographic contrast agent within the subacromial-subdeltoid bursa (Bu) after glenohumeral arthrography. B, An initial radiograph after joint injection appears normal. C, In a

postexercise radiograph, a prominent air collection (arrowheads) within the bursa is readily evident.

Figure 21-B-3 Incomplete rotator cuff tear, shoulder arthrography. A, Spot radiograph demonstrates a small collection of contrast material within the supraspinatus tendon (white arrow) near its insertion into the greater tuberosity (black arrow) of the humerus. B, Internal rotation spot radiograph demonstrates radiographic contrast agent (arrow) dissecting within the substance of the supraspinatus tendon.

Figure 21-B-4 Adhesive capsulitis, shoulder arthrography. External rotation arthrographic spot films in neutral (A) and abducted (B) positions demonstrate the typical changes of adhesive capsulitis with small capsular volume and abbreviation of the subscapularis recess and axillary pouch. Note the marked limitation of motion; virtually all abduction occurs through scapulothoracic rotation with almost no glenohumeral motion. C, An external rotation spot radiograph in a patient with a history of seven previous shoulder operations demon strates similar changes with a tight capsule and plication defects. Note the feathered appearance of the capsular margins in all radiographs.

Conventional shoulder arthrography ( see Fig. 21B-1 ) may be performed as either a single-contrast[61] or double-contrast[45] procedure. The double-contrast technique is generally considered preferable,[81] providing accuracy similar to that of the single-contrast method in the diagnosis of full-thickness tears while improving the detection rate of partial-thickness undersurface tears and cartilage defects. Although many variations in technique exist, a standard method for performing double-contrast arthrography typically begins with the appropriate scout films of the affected shoulder. This ensures proper radiographic technique and identifies abnormalities, such as soft tissue calcifications, that may be obscured by the radiopaque contrast agent. Standard scout films include anteroposterior projections of the shoulder in internal and external rotation, an axillary lateral projection, and a bicipital groove view. The patient is then placed supine on the fluoroscopic table with the arm positioned next to the body in slight external rotation. The anterior skin is prepared and draped in a sterile manner, and the sight of joint puncture is determined fluoroscopically. A point is chosen overlying the lower third of the humeral head approximately 0.5 cm lateral to the medial cortex of the humeral head. The skin is anesthetized with 1% lidocaine (Xylocaine) with a 25-gauge 3/4-inch needle. Deeper anesthesia is achieved with a 22-gauge 11/2-inch needle. A 22-gauge 31/2-inch spinal needle is then used to enter the joint. Correct position is verified fluoroscopically by injecting a small amount of radiopaque contrast material. If the needle is correctly positioned within the joint, the contrast material will outline the medial surface of the humeral head and spill into the subscapularis recess. A total of 2 to 5 mL of radiopaque contrast material is injected, followed by 10 mL of air. A total volume of 12 to 15 mL of air and contrast material provides adequate distention of the shoulder joint without undue discomfort. Injection of a larger volume often leads to decompression of the joint through a weak point of the capsular insertion along the medial aspect of the subscapularis recess, resulting in leakage of contrast material and air into the adjacent soft tissues. This degrades the quality of the examination and should be avoided if possible. Rotator cuff tears are identified fluoroscopically as the contrast agent leaks through the defect. The diagnosis of adhesive capsulitis ( see Fig. 21B-4 ) is made by identifying increasing resistance to

the contrast material with a small injected volume as well as by noting an abnormally small axillary pouch and a small or absent subscapularis recess. If increased pressure is encountered during injection of the contrast agent, fluoroscopic observation should be performed to ensure that the needle tip remains intra-articular. If the contrast agent is intra-articular, the diagnosis of adhesive capsulitis is made, injection of contrast material is ceased, and the needle is withdrawn. After injection of the contrast agent, spot radiographs are obtained of any abnormality noted fluoroscopically. Radiographs are then obtained, repeating the anteroposterior projections of the shoulder in internal and external rotation, an axillary lateral projection, and a bicipital groove view. If no abnormality of the rotator cuff is noted on these images, the patient exercises the arm for a total of 5 minutes, and the same views are repeated. The exercise portion of the examination ( see Fig. 21B-2 ) is important because an inadequately stressed articulation is the most common reason for a false-negative study result. Spot radiographs ( see Fig. 21B-3 ) can be obtained of any abnormality to localize and quantify the rotator cuff tears more precisely.

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Although conventional shoulder arthrography was in the past considered the gold standard for identifying full-thickness tears of the rotator cuff, it has many limitations, and MR imaging has largely replaced conventional arthrography in the evaluation of the rotator cuff. It is less invasive and provides a more thorough evaluation of the shoulder. When shoulder arthrography is performed, it is now frequently combined with a more advanced imaging modality, such as CT or MRI, in an attempt to evaluate the labrum and capsular structures better.

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Computed Tomography

Computed tomography of the shoulder ( Fig. 21B-5 ) is performed primarily to evaluate the osseous anatomy after trauma and fracture.[28] [31] The shoulder is a complex articulation, and CT is capable of accurately defining the extent of fracture. High-resolution bone-imaging algorithms are usually performed with thin (1.5 to 3 mm) contiguous sections through the joint in the axial plane. Sagittal and coronal reconstructions can provide additional information about the location of fracture fragments and the integrity of the articular surfaces.

Figure 21-B-5 Fractures about the shoulder, computed tomography. A, A computed tomography section in this patient demonstrates a fracture of the surgical neck of the humerus as well as an irreducible posterior dislocation of the humeral head (H), which is impacted on the posterior glenoid (G). B, In another patient, a computed tomography section through the inferior glenoid demonstrates a fracture of the anterior glenoid (Bankart's fracture) with the fragment (arrow) displaced posteriorly. C, A glenoid neck fracture is accompanied by a displaced fracture involving the posterior third of the glenoid (arrow) as well as by an impaction fracture of the anterior aspect of the humeral head (reverse Hill-Sachs lesion).

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Computed Arthrotomography

Computed arthrotomography of the shoulder ( Fig. 21B-6 ) was widely used in the past and for years was considered the gold standard in the imaging of labral abnormalities.[109] [120] [121] [143] The combination of CT with intra-articular

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injection of contrast material provides a highly sensitive method of evaluating the glenoid labra and articular cartilage. It has been shown to be as sensitive as conventional shoulder arthrography in the detection of full-thickness rotator cuff defects and provides improved accuracy in detecting abnormalities of the glenoid labrum.[30] [47] In recent years, MR imaging and MR arthrography have largely replaced CT arthrography in the evaluation of rotator cuff abnormalities and glenohumeral instability.[19] [42] A short discussion of CT arthrography is warranted because it may occasionally be useful in the evaluation of the glenoid labrum in a patient with a contraindication to MR imaging.

Figure 21-B-6 Normal shoulder, computed arthrotomography. Normal anatomy is demonstrated by computed arthrotomographic sections at the level of the bicipital tendon origin (A), the coracoid process (B), the subscapularis tendon (C), and the inferior joint level (D). AGL, anterior glenoid labrum; BT, bicipital tendon; Co, coracoid process; G, glenoid process; GT, greater tuberosity; H, humeral head; LT, lesser tuberosity; PGL, posterior glenoid labrum; SuST, subscapularis tendon.

The technique of joint injection for computed arthrotomography [30] [65] [109] [120] is similar to that for conventional double-contrast shoulder arthrography. A smaller volume of contrast material (usually 2 to 3 mL) and a smaller total volume (10 to 12 mL) are used to prevent spontaneous decompression of the joint through the subscapularis recess, which results in a significant degradation of the diagnostic accuracy of the study. The iodinated contrast agent is mixed with 0.1 to 0.3 mL of 1:1000 epinephrine to prolong retention of the contrast agent within the joint to allow adequate time for transportation of the patient to the CT scanner and imaging. CT should be performed as soon as possible after injection of the contrast agent to minimize resorption of the air and contrast material. Two sets of contiguous 3-mm axial images are obtained through the shoulder with the arm in internal and external rotation. Sagittal and oblique coronal reformatted images may also be obtained to provide a better evaluation of the rotator cuff and superior labrum.[24] [50] [120] Although CT arthrography clearly depicts rotator cuff abnormalities and many of the lesions associated with glenohumeral instability, MR imaging and MR arthrography improve sensitivity in the detection of many labral abnormalities, and they use no ionizing radiation. Relative to CT arthrography, MR imaging and MR arthrography provide superior soft tissue contrast and multiplanar imaging capabilities, resulting in a more accurate depiction of nondisplaced labral tears as well as tendinopathy and partial-thickness tears of the rotator cuff. Another limitation of CT arthrography is that air is rapidly absorbed into the adjacent soft tissues, and any delay in imaging will significantly diminish the diagnostic accuracy of the examination.

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Ultrasonography

Sonography of the rotator cuff ( Fig. 21B-7 ) was popularized in the 1980s as a simple and noninvasive method of evaluating the rotator.[13] [25] [49] [78] [80] Ultrasound examination of the shoulder requires a high-resolution transducer (7.5 to 10 MHz). Evaluation of the shoulder is performed with the patient in the sitting position. The examination begins with the arm in neutral (thumb up) position. In this position, the bicipital tendon ( Fig. 21B-7C ) is clearly visualized at the superolateral margin of the shoulder, and the presence or absence of fluid can be noted in the subacromial-subdeltoid bursa. Before evaluation of the rotator cuff, the shoulder is rotated internally and the arm is placed behind the back. This maneuver results in retraction of the critical portion of the supraspinatus tendon from beneath the acromion, allowing maximal visualization of this portion of the rotator cuff.[26] The rotator cuff should be evaluated in both the sagittal and coronal planes.

Figure 21-B-7 Normal shoulder, sonography. Images from a normal shoulder sonogram demonstrate the appearance of the supraspinatus tendon in axial (A) and sagittal internal rotation (B) projections. C, The bicipital groove (arrows) is demonstrated in an axial sonographic section. BT, bicipital tendon; GT, greater tuberosity; H, humeral head; SST, supraspinatus tendon.

The normal rotator cuff ( Fig. 21B-7A and B ) is sharply defined, uniform in thickness, and homogeneous in echo texture; it measures 4 to 6 mm in thickness anteriorly, normally being somewhat thinner posteriorly. [25] A thin echogenic band paralleling the upper surface of the cuff characterizes the subacromial-subdeltoid bursa. [37] The overlying deltoid muscle is characterized by a speckled appearance that is distinct from the normal overlying cuff. Sonographic signs of rotator cuff tendinopathy ( Fig. 21B-8 ) include thickening and a heterogeneous appearance. A partial-thickness tear can be seen as a focal change in echogenicity. A focal area of increased echogenicity ( Fig. 21B-9C and D ) may

represent granulation or hemorrhage, whereas a focal hypoechoic area may represent fluid extending partially through the tendon. A full-thickness tear ( Fig. 21B-9A ) may present sonographically as nonvisualization of the tendon, focal absence, or discontinuities of the cuff.[11] [37] [53] [125] Fluid within the subacromial-subdeltoid bursa ( Fig. 21B-9B ) is seen as a band of decreased echogenicity filling the bursa.

Figure 21-B-8 Supraspinatus tendinitis, shoulder sonography. Transaxial (A) and sagittal internal rotation (B) sonographic images demonstrate increased echogenicity within the substance of the supraspinatus tendon (between arrows). Subsequent shoulder arthrography did not demonstrate a rotator cuff tear. GT, greater tuberosity; H, humeral head.

Figure 21-B-9 Rotator cuff tears, shoulder sonography. Sonographic abnormalities that may be associated with rotator cuff tears are demonstrated. A, Absence of the normal supraspinatus insertion into the greater tuberosity (GT) of the humerus. B, Morphologic alteration of the supraspinatus tendon (arrowheads) consisting of an area of indentation is associated with an overlying bursal effusion (Bu) in this transaxial sonographic section. Sonographic sections in C (transaxial) and D (sagittal internal rotation) show a bright spot (arrows) within the substance of the supraspinatus tendon tears. E, A bursal effusion (Bu) is demonstrated as an elliptical anechoic fluid collection associated with a deeper zone of hyperechogenicity, which is characteristic of a fluid collection.

The accuracy of sonography of the rotator cuff varies widely, and it is clear that sonographic evaluation of the shoulder has a steep learning curve and is extremely operator dependent. Reports suggest that sonography is inferior to both conventional arthrography and MR imaging in the

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evaluation of the rotator cuff.[11] This coupled with the fact that MR imaging provides a more thorough evaluation of the shoulder, including the labrum and osseous structures, has led to the replacement of shoulder sonography by MR imaging in most cases.

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Magnetic Resonance Imaging

During the past decade, MR imaging has evolved into the imaging modality of choice for the evaluation of shoulder impingement.[38] [42] [46] [52] [57] [66] [146] It offers soft tissue contrast that is superior to any other imaging modality and provides an excellent overall assessment of the osseous outlet and acromion, tendons, muscles, capsular structures, and labrum. The addition of intra-articular contrast material has also been shown to increase sensitivity in the detection of undersurface partial-thickness tears of the rotator cuff[42] [52] [101] and abnormalities of the labrum.[19] [42] The type of magnet and various pulse sequences that are used to evaluate the shoulder differ according to equipment availability and the preference of the imager. Numerous commercial coils are suitable for MR imaging of the shoulder. Surface coils come in a variety of configurations and are generally adequate for the majority of clinical applications. Recent advances in coil design include the quadrature and phased-array coils, which offer the highest signal-to-noise ratio and best overall image quality. The arm is typically positioned next to the side; for specialized views, it may be placed over the head. The arm should not be positioned on the abdomen because this transmits respiratory motion to the shoulder, with subsequent image degradation. The arm should be placed in the neutral position with the thumb up to provide the most comfort for the patient, thus limiting motion artifact. External rotation tends to be uncomfortable for the patient and tightens the anterior capsule, resulting in poor visualization of the anterior labrum.[29] [70] Internal rotation may obscure the posterior

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labrum. The abduction-external rotation (ABER) position ( see Fig. 21B-35C ) reportedly improves visualization of the undersurface of the rotator cuff as well as of the anterior band of the inferior glenohumeral ligament and the anterior labroligamentous complex.[27] [70] [131]

The shoulder is usually imaged in three planes, the axial ( Figs. 21B-10 and 21B-11 ), oblique sagittal, and oblique coronal ( Fig. 21B-12 ) planes. A typical imaging protocol includes a T1 -weighted sequence in the oblique coronal plane. The T1 -weighted images provide the best overall signal-to-noise ratio and are thus excellent for depicting anatomy. T1 -weighted images also nicely demonstrate the osseous anatomy of the shoulder, and because fat is bright, this sequence will demonstrate fatty atrophy of the rotator cuff. Fast spin-echo T 2 -weighted images with frequency-selective fat saturation are commonly obtained in the oblique coronal and oblique sagittal planes. Fluid is bright on T2 -weighted images, thus allowing the most accurate detection of shoulder disease, including rotator cuff abnormalities ( see Fig. 21B-24 ), labral tears, bone marrow edema, and paralabral cysts. Axial imaging may be performed with use of either fast spin-echo T2 -weighted or gradient-echo sequences and typically provides the best opportunity for evaluation of the anterior and posterior labra as well as of the glenohumeral ligaments and subscapularis tendon.

Figure 21-B-10 Normal shoulder, magnetic resonance imaging, transaxial orientation. Representative transaxial intermediate-weighted sections are demonstrated from superior (A) to inferior (H). See Table 21B-1 for definition of abbreviations.

Figure 21-B-11 Normal shoulder, magnetic resonance imaging, transaxial MPGR/30 orientation. Transaxial MPGR/30 sections from superior (A) to inferior (I) demonstrate superior visualization of the capsular structures and glenoid labrum. See Table 21B-1 for definition of abbreviations.

Figure 21-B-12 Normal shoulder, magnetic resonance imaging, coronal oblique orientation. Representative coronal oblique intermediate-weighted sections are demonstrated from posterior (A) to anterior (D). E, Same section as shown in B with T2 weighting. See Table 21B-1 for definition of abbreviations.

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Magnetic Resonance Arthrography

Although conventional MR imaging has been established as the imaging modality of choice in the evaluation of shoulder impingement syndrome, MR arthrography is steadily gaining acceptance as the method of choice for the evaluation of glenohumeral instability.[19] [42] Many of the lesions associated with instability are subtle and may undergo partial healing. This coupled with the fact that the normal anatomic structures of the shoulder lie in proximity can make the diagnosis of these lesions difficult even with high-quality conventional MR imaging.[3] [94] [95] [106] MR arthrography, on the other hand, is performed by distending the joint with fluid (saline or dilute gadolinium), which more accurately depicts subtle labral tears ( see Fig. 21B-33 ), cartilage ( see Fig. 21B-42 ) and ligamentous abnormalities, and partial-thickness tears of the undersurface of the rotator cuff ( see Fig. 21B-45 ). The standard injection technique for MR arthrography of the shoulder is similar to that for conventional double-contrast shoulder arthrography or computed arthrotomography described in previous sections. The injection is typically performed through an anterior approach under fluoroscopic guidance with a 22-gauge 31/2-inch spinal needle. A small amount (1 to 2 mL) of an iodinated contrast agent is first injected to confirm intra-articular placement of the needle tip. Approximately 12 to 15 mL of gadolinium diluted 1:200 with normal saline is then injected. The patient is taken directly to the MR unit, and imaging is initiated within 30 minutes to avoid excessive resorption of the intra-articular gadolinium. Unlike postinjection exercise in conventional shoulder arthrography, which increases the sensitivity of detection of subtle tears, exercising the shoulder after injection of gadolinium is neither beneficial nor detrimental.[12] Imaging protocols vary, but a standard set of imaging sequences typically includes T1 -weighted images with frequency-selective fat saturation in the axial, oblique sagittal, and oblique coronal planes. The T1 -weighted images have a high signal-to-noise ratio, resulting in exquisite anatomic detail critical in detecting the subtle lesions associated with glenohumeral instability. A T2 -weighted sequence performed in the oblique coronal plane is the most important sequence for depicting rotator cuff abnormalities. A T2

-weighted sequence may also be helpful in detecting other pathologic processes, such as a paralabral cyst ( see Fig. 21B-29 ) or bone marrow edema ( see Fig. 21B-40C ).

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The ABER view may be added to the standard imaging protocol for any patient thought to have an anterior labral pathologic process.[27]

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Imaging of Specific Shoulder Abnormalities

The shoulder is a complex joint, and the interpretation of a shoulder MR examination is complicated, requiring the evaluation of numerous images obtained in several imaging planes and with various pulse sequences. A comprehensive MR examination of the shoulder requires a search pattern that encompasses all of the pertinent anatomic structures. The following sections provide a systematic approach for MR evaluation of the shoulder that includes a thorough review of the basic anatomy as well as of the imaging basis for recognizing common pathologic processes; when appropriate, complementary imaging modalities are discussed. The important structures that must be thoroughly evaluated on each MR examination are the osseous outlet and acromion, rotator cuff, labrum and capsular structures, biceps tendon, and osseous structures and articular surfaces. Osseous Outlet and Acromion

The clinical syndrome of shoulder impingement refers to a painful compression of the soft tissues of the anterior shoulder (rotator cuff, subacromial bursa, and bicipital tendon) between the humeral head and the coracoacromial arch (coracoid process, acromion process, coracoacromial ligament, and acromioclavicular joint).[11] [62] [89] [90] Pain occurs when the arm is elevated forward and internally rotated or placed in the position of abduction and external rotation.[89] In the normal shoulder, the powerful upward pull of the deltoid on the proximal humerus is resisted by an intact rotator cuff so that the humeral head remains centered on the glenoid in all arm positions. If this stabilizing mechanism becomes weakened secondary to repeated trauma, overuse, or age, the humeral head is pulled upward under the structures of the coracoacromial arch. Impingement is initially followed by subacromial bursitis and rotator cuff tendinopathy. Over time, irreversible cuff trauma occurs with fibrosis and degeneration. In the latter stages, a bony excrescence (subacromial enthesophyte) tends to form at the anteroinferior margin of the acromion where the

coracoacromial ligament inserts. Tears of the rotator cuff are frequent in this stage, undoubtedly in part owing to direct cuff trauma from the spur. After massive tears of the rotator cuff, bone-to-bone contact may result between the humeral head and the undersurface of the anterior third of the acromion, causing sclerosis and proliferative changes in this area. Neer[90] first introduced the term impingement syndrome and described three stages in the rotator cuff disorder. Reversible hemorrhage and edema characterize stage 1, typically seen in individuals younger than 25 years. Stage 2 consists of cuff fibrosis and tendinitis and occurs in individuals between 25 and 40 years of age. In stage 3, osteophyte formation occurs along the anteroinferior margin of the acromion, and rotator cuff tears are common; this group is typically older than 40 years. Impingement is common in young athletes who participate in sports requiring repetitive overhead activities, such as tennis, baseball, and swimming. Neer postulated that chronic impingement is the most common cause of rotator cuff tear,[90] although other authors have suggested that additional causes including degeneration of the cuff secondary to aging, acute trauma, and inflammatory diseases may also result in rotator cuff tear.[20] [100]

The diagnosis of impingement syndrome is usually a clinical one based on appropriate historical and physical examination findings. A thorough history and physical examination by an experienced physician have an 84% to 90% sensitivity and a 75% to 95% specificity for diagnosis of a tear of the rotator cuff. [77] [126] Many imaging modalities are available to assist in the evaluation of the progressively painful shoulder, and their role is both to assess the extent of abnormality of the rotator cuff and to identify configurations of the osseous outlet that may predispose to rotator cuff impingement. Conventional radiography has met with limited success in the evaluation of the clinical syndrome of impingement. Many of the osseous changes that occur with impingement are seen late in the process and thus offer little in establishing an early diagnosis and preventing progression of the associated soft tissue injuries. Osseous abnormalities that may be associated with the clinical syndrome of impingement include enthesophyte formation off the anteroinferior aspect of the acromion ( Fig. 21B-13 ), long anterior portion of the acromion with anterior or lateral downsloping, configuration of the undersurface of the acromion, os acromiale, and hypertrophy of the acromioclavicular joint.[9] [86] [89] [141] Optimal conventional radiographic views have been described for identifying these variations of the osseous

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outlet.[22] [64] [96] [112] The anteroposterior radiograph at a 30-degree caudal angle ( see Fig. 21B-13 ) is helpful in visualizing the anterior aspect of the acromion and in detecting inferiorly directed enthesophytes.[64] A modified transcapular lateral view obtained with 10 to 15 degrees of caudal angulation (supraspinatus outlet view) helps further identify the anteroinferior aspect of the acromion.[91] Fluoroscopy has also been shown to aid in the detection of subacromial enthesophytes.[96] A high-riding humeral head with remodeling of the undersurface of the acromion and sclerosis of the greater tuberosity

are conventional radiographic findings ( Fig. 21B-14 ) that are pathognomonic of a chronic rotator cuff tear. Although conventional arthrography, ultrasonography, and CT offer improved visualization of the rotator cuff relative to conventional radiography, they add little in the direct evaluation of the osseous outlet.

Figure 21-B-13 Subacromial spur, conventional radiography. A frontal radiograph of the shoulder with a 30-degree caudal tilt demonstrates a large hooklike bony excrescence (S) arising from the anteroinferior margin of the acromion process in this patient with shoulder impingement syndrome.

Figure 21-B-14 Chronic rotator cuff tear, conventional radiography. A frontal radiograph of the shoulder demonstrates a high-riding humeral head (arrows) resulting in remodeling of the undersurface of the acromion and sclerosis of the greater tuberosity. An osteophyte (arrowhead) extends off the inferior aspect of the humeral head, resulting from osteoarthritis of the glenohumeral joint. Magnetic Resonance Imaging of the Osseous Outlet and Acromion

Magnetic resonance imaging provides an excellent evaluation of the entire osseous outlet. This is due to its multiplanar capabilities and its ability to demonstrate the

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relationship of the entire osseous outlet to the underlying rotator cuff. Bigliani and colleagues[9] described three different acromial shapes ( Fig. 21B-15 ) and related the configuration of the undersurface of the acromion to the presence of rotator cuff tears. A type I acromion ( Fig. 21B-15A ) has a flat undersurface, a type II acromion ( Fig. 21B-15B ) has a curved undersurface, and a type III acromion ( Fig. 21B-15C ) has an anterior hook. The acromial types II and III have an increased association with rotator cuff tear.[9] [86] A type IV acromion with a convex undersurface has subsequently been described, but no definite correlation has been shown to exist between the type IV acromion and impingement.[39] On MR images, the shape of the acromion ( see Fig. 21B-15 ) is best assessed on the oblique sagittal view just lateral to the acromioclavicular joint. One study, however, suggests poor correlation of acromial arch shape between conventional radiography and MR imaging.[105] Anterior and lateral downsloping of the anterior acromion ( Fig. 21B-16 ) can also narrow the coracoacromial outlet and potentially result in impingement.[2] [119] Anterior downsloping ( Fig. 21B-16B ) is demonstrated on the oblique sagittal MR images; lateral downsloping ( Fig. 21B-16C ) is best seen on the oblique coronal images. An enthesophyte ( Fig. 21B-17 ) extending off the anteroinferior aspect of the acromion can also be clearly demonstrated on MR imaging. It typically appears as a marrow containing osseous excrescence ( see Fig. 21B-17 ), which should have MR signal characteristics similar to the adjacent acromion marrow (bright on T1 -weighted images). Potential pitfalls include the attachment of the coracoacromial ligament and the deltoid tendon insertion ( see Fig. 21B-16A and C ) on the anterior acromion. These structures may mimic an osseous

excrescence, but they can be differentiated from enthesophytes because they lack marrow signal and appear dark on all pulse sequences. The acromion should also be evaluated for os acromiale ( Fig. 21B-18 ). This is an accessory ossification center along the outer edge of the anterior acromion. It is normally fused by 25 years of age. There is an association between persistent os acromiale and impingement of the rotator cuff.[33] [56] [88] The deltoid muscle attaches to the inferior aspect of the accessory ossicle, and contraction of the deltoid results in a downward motion of the unstable segment, potentially leading to impingement of the underlying rotator cuff.[88] Os acromiale is demonstrated best on axial images ( Fig. 21B-18A ), but it can also be seen on oblique sagittal ( Fig. 21B-18B and C ) or oblique coronal images, on which it should not be confused with the adjacent acromioclavicular joint.

Figure 21-B-15 Acromial types, magnetic resonance imaging, oblique sagittal T1 -weighted images of the acromion one section lateral to the acromioclavicular joint. A, Type I acromion demonstrates a flat undersurface (arrows). B, Type II acromion demonstrates a gentle curvature to the undersurface of the acromion (arrows). C, Type III acromion demonstrates a hook (arrow) extending off the anterior aspect of the acromion.

Figure 21-B-16 Acromial downsloping, magnetic resonance imaging. A, Oblique sagittal T1 -weighted image demonstrates no evidence of anterior downsloping (arrows). The deltoid tendon (arrowhead) is noted as it inserts onto the anterior aspect of the acromion. B, Oblique sagittal T2 -weighted image demonstrates marked anterior downsloping of the acromion (arrows) with resulting mass effect on the underlying supraspinatus muscle. C, Oblique coronal image demonstrates lateral downsloping of the acromion (white arrow). The black arrow demonstrates the insertion site of the deltoid tendon onto the anterolateral acromion.

Figure 21-B-17 Acromial enthesophyte, magnetic resonance imaging. Oblique sagittal image demonstrates marrow containing osseous excrescence (arrowheads) extending off the anterior aspect of the acromion (arrow). Note that an enthesophyte contains marrow signal that is bright on T1 -weighted images. This differs from the deltoid tendon attachment, which is of low signal intensity on all pulse sequences ( see Fig. 21B-16A and C ).

Figure 21-B-18 Os acromiale, magnetic resonance imaging. A, Axial MPGR/30 section at the level of the acromioclavicular joint demonstrates an accessory ossification center, the os acromiale (long arrows), which remains unfused to the remainder of the acromion (short arrows). AC, acromioclavicular joint. B, T 1 -weighted oblique sagittal image demonstrates a normal-appearing acromioclavicular joint (arrow). C, T 1 -weighted oblique sagittal image of the same patient, two images more lateral, demonstrates an unfused os acromiale (arrow). This can easily be misinterpreted as the acromioclavicular joint, and this finding has been referred to as the double acromioclavicular joint sign on both oblique sagittal and oblique coronal magnetic resonance images.

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Hypertrophic changes of the capsule and osteophyte formation of the acromioclavicular joint ( Fig. 21B-19 ) can also be associated with impingement.[89] MR imaging clearly demonstrates these changes as well as associated mass effect on the underlying rotator cuff. The coracoacromial ligament ( Fig. 21B-20 ) is a soft tissue structure that forms part of the coracoacromial arch. It extends from the coracoid to the acromion and is well seen on oblique sagittal MR images. It normally measures less than 2 mm in thickness ( Fig. 21B-20A ) and extends across the rotator interval and anterior aspect of the supraspinatus tendon. The role of the coracoacromial ligament in impingement remains controversial; some believe that its thickening ( Fig. 21B-20B ) may be a potential cause of impingement, whereas others believe that its thickening results from impingement.[116]

Figure 21-B-19 Acromioclavicular joint hypertrophy, magnetic resonance imaging. Coronal oblique T 1 -weighted image demonstrates marked capsular hypertrophy (arrows) of the acromioclavicular joint. No significant mass effect is noted on the underlying supraspinatus muscle.

Figure 21-B-20 Coracoacromial ligament, magnetic resonance imaging. A, Oblique sagittal T1 -weighted image demonstrates a normal coracoacromial ligament (arrows) extending from the coracoid process to the anterior acromion. The normal ligament measures less than 2 mm in thickness. B, Oblique sagittal T1 -weighted image demonstrates a thickened coracoacromial ligament (arrows). Rotator Cuff

The rotator cuff is composed of four tendons ( see Figs. 21B-10 , 21B-11 , and 21B-12 ): the supraspinatus superiorly, the subscapularis anteriorly, and the infraspinatus and teres minor posteriorly. These tendons are important dynamic stabilizers of the glenohumeral joint, and any review of rotator

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cuff disease will rapidly expose the supraspinatus tendon as the weak link of the rotator cuff. The majority of cuff failures originate in the supraspinatus tendon at or near its insertion onto the greater tuberosity of the humeral head.[21] Many investigators attribute this propensity for cuff failure within the supraspinatus tendon to its blood supply. The supraspinatus tendon receives its arterial supply from the anterior humeral circumflex, subscapular, suprascapular, and posterior humeral circumflex arteries.[72] [111] A zone of relative avascularity has been described in the tendon proximal to its attachment site and may represent a critical zone for cuff failure. [72] [111] Other authors have found this zone to be richly vascularized by anastomosing vessels from the tendon and humeral

tuberosity.[87] Arterial filling of the cuff vessels in the critical zone depends greatly on the position of the arm; poor filling is present when the arm is adducted. [110] A high correlation has also been shown to exist between rotator cuff tears and subacromial impingement.[90] It is probably some combination of avascularity and subacromial impingement that leads to the majority of rotator cuff abnormalities originating in the critical zone of the supraspinatus tendon. Conventional radiography plays only a limited role in the direct evaluation of the rotator cuff, although it is frequently the initial imaging study performed for the patient with the clinical syndrome of impingement. Radiographs allow identification of associated pathologic change, especially of the osseous outlet and acromion. Conventional radiography may also demonstrate calcific tendinitis or bursitis ( Fig. 21B-21 ). In the patient with a chronic rotator cuff tear ( see Fig. 21B-14 ), radiographs may demonstrate a high-riding humeral head ( /das/book/view/29309971/1103/474.html/top

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Section C Injuries to the Acromioclavicular Joint in Adults and Children Augustus D. Mazzocca MD Robert Sellards MD Ralph Garretson MD Anthony A. Romeo MD The acromioclavicular (AC) joint is a robust structure that anchors the clavicle to the scapula. Approximately 9% of shoulder girdle injuries involve damage to the AC joint. Other similar studies have shown that most AC joint injuries occur in adults in their 20s (43.5%), that acromioclavicular dislocation is overwhelmingly more common in males (5:1), and that these dislocations are more often incomplete than complete (2:1).[102] This chapter also addresses other entities such as degenerative AC joint disease, atraumatic osteolysis of the distal clavicle, and intra-articular distal clavicle fractures as they pertain to athletics. The anatomy and design of the AC joint make it a resilient joint that can accept a significant amount of force before disruption. Numerous procedures and protocols have been devised to treat the AC joint. It is this multitude of research with various conflicting outcomes that can make choosing an appropriate treatment confusing. For this reason, it is important to understand the anatomy and biomechanics of the joint so that basic principles can be applied. An understanding of these basic principles can then allow the physician, the therapist, or the health care provider to evaluate certain clinical situations and apply a multitude of treatments to specific patient disorders and needs. This chapter defines and explains the anatomy and biomechanics of the AC joint as well as describing evaluation, diagnosis, and nonoperative and operative treatment of various disorders of the AC joint. Anatomy and Biomechanics

The AC joint is diarthrodial and has six degrees of freedom moving in the anterior/posterior as well the superior/inferior planes. It is surrounded by a joint capsule that has synovium and an articular surface that is made up of hyaline cartilage containing an intra-articular meniscustype structure (Fig. 21C-1 (Figure Not Available) ). This intra-articular disk has tremendous variation in size and shape. DePalma, Petersson, and Salter have demonstrated that with age, this meniscal homologue undergoes rapid degeneration, until it is no longer functional beyond the fourth decade.[35] [97] [104] Its actual function in the joint is negligible. Figure 21-C-1 (Figure Not Available) Normal anatomy of the acromioclavicular joint. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.)

The AC joint is stabilized by both static and dynamic stabilizers. The static stabilizers include the acromioclavicular ligaments (superior, inferior, anterior, and posterior), the coracoclavicular ligaments (trapezoid and conoid), and the coracoacromial ligament. The dynamic stabilizers include the deltoid and the trapezius muscles. Fibers from

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the superior acromioclavicular ligament blend with the fascia of the trapezius and the deltoid, adding stability to the joint when they contract or stretch. The AC joint capsule and the capsular ligaments are the primary restraints of the distal clavicle to anterior-to-posterior translation ( Fig. 21C-2 ).[90] These ligaments insert an average of 16.7 mm posterior-superior on the capsule and 12.8 mm anterior-superior. The maximum average distance was 16.1 mm from the joint line, and the greatest was 20 mm from the joint line. These numbers should be kept in mind during distal clavicle resection.

Figure 21-C-2 Resection or injury of the acromioclavicular ligaments causes horizontal instability and, if in excess, can cause abutment of the posterior clavicle into the anterior portion of the scapular spine.

These ligaments are primarily involved in horizontal stability. [41] Posterior horizontal instability of the distal clavicle can cause abutment of the posterolateral portion of the clavicle into the spine of the scapula. Clinically, resistance to posterior translation is critical to avoid painful horizontal instability of the AC joint with abutment of the posterolateral end of the clavicle onto the spine of the scapula.[67] Serial sectioning of the AC joint ligaments revealed that the superior ligament contributed 56% of the resistance to posterior displacement of the clavicle, with the posterior ligament contributing 25%. Consequently, surgical treatment of the AC joint should be designed to avoid rendering the superior and posterior ligaments incompetent. The coracoclavicular ligament's main contribution is in vertical stability, preventing

superior and inferior translation of the clavicle ( Fig. 21C-3 ). This complex is made up of two structures: the trapezoid and the conoid ligaments. These ligaments span the space (1.3 cm) between the coracoid and the clavicle.[14] The trapezoid is anterior and lateral to the conoid, and both the trapezoid and the conoid are posterior to the pectoralis minor attachment on the coracoid. Bearden reported a range of values for the coracoclavicular space of 1.1 to 1.3 cm. [10] This distance becomes clinically important when differentiating between incomplete and complete AC joint separations. The larger the distance between the coracoid and the clavicle, the more likely it is that a complete dislocation has occurred. The coracoclavicular ligaments perform two major functions: (1) They mediate synchronous scapulohumeral motion by attaching the clavicle to the scapula, and (2) they strengthen the acromioclavicular articulation.

Figure 21-C-3 Injury to both the coracoclavicular ligaments frequently occurs in the face of acromioclavicular ligament injury and causes an inferior translation of the scapulohumeral complex from the clavicle. It is important to note in this diagram that the clavicle stays in its normal anatomic position, tethered by the sternoclavicular joint, and the scapulohumeral complex subluxates inferiorly.

Fakuda has reported that with small displacements, the acromioclavicular ligaments are the primary restraints to posterior (89%) and superior (68%) translation of the clavicle.[41] With larger displacement, the conoid ligament was found to be the primary restraint (62%) to superior translation, whereas the acromioclavicular ligaments were still the primary restraints to posterior translation. The trapezoid ligament was found to be the primary restraint to compression of the AC joint at both small and large displacements. Recent studies have shown that the acromioclavicular and, especially, the coracoclavicular ligaments do not act in isolation. When the acromioclavicular ligaments have been resected, the coracoclavicular ligaments have been shown to take an increased load, especially with anterior and posterior displacement. The conoid increases its force significantly with an anterior load.[33] The coracoacromial ligament is important as a secondary glenohumeral stabilizer to prevent anterosuperior displacement of the humeral head in longstanding massive rotator cuff disease (cuff tear arthropathy).

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Motion of the Acromioclavicular Joint

Rockwood, Williams, and Young have reported that there is approximately 5 to 8 degrees of motion detected at the AC joint, with forward elevation and abduction to 180 degrees.[102] The clavicle rotates between 40 and 50 degrees during full overhead elevation (Fig. 21C-4 (Figure Not Available) ). This motion is combined with scapular rotation rather than occurring through the AC joint. This synchronous motion

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between the clavicle, which is rotating upward as the scapula rotates downward during abduction, and forward elevation was described by Codman[26] as synchronous scapular-clavicular rotation. This is coordinated by the coracoclavicular ligaments. Figure 21-C-4 (Figure Not Available) Motions of the clavicle and the sternoclavicular joint. A, With full overhead elevation, the clavicle is elevated 35 degrees. B, With adduction and extension, the clavicle displaces anteriorly and posteriorly 35 degrees. C, The clavicle rotates on its long axis 45 degrees as the arm is elevated to full overhead position. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.)

The motion of the AC joint is important clinically in that both fusion of the AC joint and implantation of a coracoclavicular screw to stabilize the clavicle to the scapula allow full forward elevation in abduction. This motion has also caused these screws and this hardware to migrate as well as to break over time.

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Classification of Acromioclavicular Dislocation

The pathologic process of AC joint dislocations was originally described by Cadenat; it involves sequential injury, beginning with the acromioclavicular ligaments, extending to the coracoclavicular ligaments, and finally affecting the deltoid and trapezial muscles and fascia.[22] Tossy, Mead, and Sigmond later classified the injury as types I, II, or III.[115] Rockwood expanded the classification in 1984 to include types IV, V, and VI (Fig. 21C-5 (Figure Not Available) ).[102] The expanded classification recognized a variety of complete AC joint dislocations. These classifications correlate with increasing soft tissue injury and are as follows: Type IAcromioclavicular ligament sprain with the AC joint intact Type IIAcromioclavicular ligament tear, coracoclavicular ligament intact; AC joint subluxed Type IIIAcromioclavicular and coracoclavicular ligaments torn; 100% dislocation in joint Type IVComplete dislocation with posterior displacement of distal clavicle into or through the trapezius muscle Type VExaggerated superior dislocation of the joint of 100% to 300%, increasing the coracoclavicular ligament distance two to three times, including disruption of the deltotrapezial fascia Type VIComplete dislocation with inferior displacement of distal clavicle into a subacromial or subcoracoid position

Figure 21-C-5 (Figure Not Available) The classification of the ligamentous injuries that can occur to the

acromioclavicular joint. In a type I injury, a mild force applied to the point of the shoulder does not disrupt either the acromioclavicular or the coracoclavicular ligament. In a type II injury, a moderate to heavy force applied to the point of the shoulder disrupts the acromioclavicular ligaments, but the coracoclavicular ligaments remain intact. In a type III injury, when a severe force is applied to the point of the shoulder, both the acromioclavicular and the coracoclavicular ligaments are disrupted. In a type IV injury, not only are the ligaments disrupted, but also the distal end of the clavicle is displaced posteriorly into or through the trapezius muscle. In a type V injury, a violent force applied to the point of the shoulder not only ruptures the acromioclavicular and coraclavicular ligaments but also disrupts the muscle attachments and creates a major separation between the clavicle and the acromium. A type VI injury is an inferior dislocation of the distal clavicle in which the clavicle is inferior to the coracoid process and posterior to the biceps and coracobrachialis tendons. The acromioclavicular and coracoclavicular ligaments have also been disrupted. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.)

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Mechanism of Injury

The mechanism of most AC joint injuries and distal clavicle fractures is simply direct trauma. The subcutaneous position of this joint, which does not have large amounts of muscle protecting it, theoretically puts it at an increased risk of injury. Direct trauma is caused by a fall or blow to the acromion with the arm adducted. The stability of the sternoclavicular joint transfers the energy to the acromioclavicular and coracoclavicular ligaments ( Fig. 21C-6A and B ).

Figure 21-C-6 Mechanism of acromioclavicular joint injury. A, Direct trauma as result of a fall or blow to the acromium with the arm adducted. B, Indirect injury caused by falling on an adducted outstretched hand or elbow causing the humerus to translocate superiorly.

Indirect injury can result from a fall onto an adducted outstretched hand or elbow, which causes the humerus to translocate superiorly, driving the humeral head into the acromion and causing damage.

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Diagnosis and Physical Examination

Pain originating from the superoanterior aspect of the shoulder may be challenging to localize to one specific

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structure. A likely explanation of this phenomenon is the innervation of the AC joint and the superior aspect of the glenohumeral joint. The lateral pectoral nerve provides sensation to the anterior aspect of the shoulder. Gerber evaluated patterns of pain and found that irritation to the AC joint produced pain over the AC joint, in the anterolateral neck, and in the region of the anterolateral deltoid ( Fig. 21C-7A and B ). [47] Irritation of the subacromial space produced pain in the region of the lateral acromion and the lateral deltoid muscle but did not produce pain in the neck or the trapezius region.

Figure 21-C-7 A, Innervation of the acromioclavicular joint in the superior aspect of the glenohumeral joint is by two nerves. The lateral pectoral nerve provides sensation to the anterior aspect of the shoulder. The suprascapular nerve provides innervation of the posterior aspect of the acromioclavicular joint and posterior structures. B, Superficial pain pattern produced by irritation of the acromioclavicular joint and irritation of the subacromial space. (As per Gerber CR, Galantay R, Hersche O: The pattern of pain produced by irritation of the acromioclavicular joint and the subacromial space. J Shoulder Elbow Surg 7:71-77, 1998.)

The history and the mechanism of injury are important in making an accurate diagnosis. A direct blow to the AC joint or a fall on the elbow forcing the head of the humerus into

the AC joint is the mechanism associated with an AC separation. A painful symptomatic AC joint without a history of discrete injury resulting in separation of the joint can generally be termed an arthrosis (degenerative condition). Pathologic processes of the AC joint are identified by a triad of point tenderness, positive pain at the AC joint with cross-arm adduction, and relief of symptoms by injection of a local anesthetic agent. The cross-arm adduction test is performed with the arm elevated to 90 degrees and then adducted across the chest with the elbow bent at approximately 90 degrees. This cross-arm adduction will produce pain specifically at the AC joint ( Fig. 21C-8A ). It may sometimes produce pain in the posterior aspect of the shoulder associated with a tight posterior capsule or at the lateral aspect of the shoulder, which can also be associated with rotator cuff disease. The reason that the cross-arm adduction test causes pain at the AC joint specifically is compression across the AC joint with that motion.

Figure 21-C-8 A, Cross-arm adduction test is performed with the arm flexed to 90 degrees in adduction across the body with a finger placed on the acromioclavicular (AC) joint indicating pain at that spot only. It is important to understand that this test may produce pain posteriorly if there is a tight posterior capsule decreasing internal rotation or in the glenohumeral joint if there is glenohumeral arthritis. It is only positive for AC joint disease if cross-arm adduction produces pain at the AC joint itself. B and C, O'Brien's test is performed with the arm flexed to 90 degrees with the elbow in extension and adducted 10 to 15 degrees with maximum supination; it is then performed again in maximal pronation. Symptoms referred to the AC joint with either of these maneuvers or with the arm in supination indicate more of an AC joint disorder, whereas symptoms referred to the anterior glenohumeral joint that are increased in maximal pronation indicate more of a superior labral disorder.

O'Brien ( Fig. 21C-8B ) recommended the active compression test for diagnosis of AC joint abnormalities. The O'Brien test may be particularly helpful when attempting to differentiate symptoms of AC joint arthrosis from intra-articular disease, especially with lesions of the superior glenoid labrum. The test is performed with the arm elevated to 90 degrees, the elbow in extension, adduction of 10 to 15 degrees, and maximum pronation of the forearm with

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obligate internal rotation of the arm. The examiner applies a downward force resisted by the patient. Symptoms referred to the top of the shoulder and confirmed by examiner palpation of the AC joint indicate damage to this structure. Symptoms referred to the anterior glenohumeral joint suggest labral or biceps disease. Other conditions associated with AC joint pain have been associated with pseudogout and synovial chondromatosis. Aseptic inflammation in the joint has been reported in Crohn's disease. Acromioclavicular joint cysts have been associated with glenohumeral arthritis, and there is significant involvement of the AC joint with rheumatoid arthritis. The following are the basic mechanisms and the radiographic and clinical examination findings for the six types of AC joint injuries.

Type I

Direct force to the shoulder produces a strain to the acromioclavicular ligament. The coracoclavicular and acromioclavicular ligaments are intact, and the x-ray examination is normal. Type II

Increased force to the point of the shoulder is severe enough to rupture the AC joint but not severe enough to rupture or affect the coracoclavicular ligaments. There is pain with motion, and the distal clavicle is unstable in the horizontal plane. On x-ray examination, the lateral end of the clavicle may be slightly elevated; however, stress views fail to demonstrate a 100% separation of the clavicle and acromion (Fig. 21C-9 (Figure Not Available) ). Figure 21-C-9 (Figure Not Available) Radiographic appearance of a type II acromioclavicular joint injury to the right shoulder (A). With stress, the coracoclavicular distance in both shoulders measures 1.5 cm. In the injured right shoulder, however, the acromioclavicular joint is widened compared with the normal left shoulder (B). (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.) Type III

This injury is a complete disruption of both the acromioclavicular and the coracoclavicular ligaments without significant disruption of the deltoid or trapezial fascia. The

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upper extremity is usually held in an adducted position with the acromion depressed while the clavicle appears high-riding. The clavicle is unstable in both the horizontal and vertical planes, and stress views on x-ray examination are abnormal. Although the clavicle appears high on the radiograph, in reality the acromion and the remainder of the upper extremity are displaced inferior to the horizontal plane of the lateral clavicle (Fig. 21C-10 (Figure Not Available) ). Pain with motion is severe typically for the first 1 to 3 weeks. Figure 21-C-10 (Figure Not Available) Radiographic appearance of a type III injury to the right shoulder. Stress radiographs were made to compare the right ( A) with the left (B) shoulder. Not only is the right acromioclavicular joint displaced compared with the left, but, more significantly, there is a great increase in the coracoclavicular interspace in the injured right shoulder compared with the normal left shoulder. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.) Type IV

The distal clavicle is posteriorly displaced into the trapezius muscle and may tent the posterior skin. The posteriorly displaced clavicle is easily seen on an axillary radiograph. It is important to evaluate the sternoclavicular joint because there can be an anterior dislocation of the sternoclavicular joint and posterior dislocation of the AC joint ( Fig. 21C-11 ).

Figure 21-C-11 Type IV dislocation of the acromioclavicular joint. A, The anteroposterior radiograph reveals obvious deformity of the acromioclavicular joint. The distal end of the clavicle appears to be inferior to the acromion. B, The axillary view confirms that the clavicle is displaced posteriorly away from the acromion process. C, Computed tomography scans reveal that the left clavicle is in its normal position adjacent to the acromion. Note that the right clavicle is completely absent. D, A lower cut demonstrates the posterior displacement and also confirms the fact that the clavicle is inferior to the acromion. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.) Type V

This is a more severe form of a type III injury, with all the trapezial and deltoid fascia being stripped off the acromion as well as the clavicle. It is manifested by a two- to threefold increase in the coracoclavicular distance or a 100% to 300% increase in the clavicle-to-acromion radiographic distance. The shoulder manifests as a severe droop secondary to downward displacement of the scapula and humerus with stabilization of the clavicle (Fig. 21C-12A (Figure Not Available)

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and B (Figure Not Available) ). An effective physical examination marker to differentiate type III from type V can be noted by having the patient shrug the shoulders. If the AC joint reduces, this is not a type V injury; however, if it does not reduce, then it is, indicating that the trapezial and deltoid fasciae have been stripped off the clavicle. Figure 21-C-12 (Figure Not Available) A, This is a type V injury and is differentiated from a type III injury by the two-to threefold increase in the coracoclavicular distance as well as a stripping of the deltoid and trapezial fascia from the clavicle. This can be clinically differentiated from a type III injury by having the patient shrug his or her shoulders. If the acromioclavicular (AC) joint reduces and the deformity diminishes, this indicates a type III injury. If the deformity persists and the AC joint does not reduce, then this indicates a type V injury. This phenomenon is due to the stripping of the trapezial and deltoid fascia. B and C, Clinical photographs of patient with type V AC dislocation. B, A severe upward displacement of the right clavicle has occurred into the base of this patient's neck. C, Note the severe upward displacement of the clavicle in this patient's right shoulder. There was so much tension on the skin that it was becoming necrotic. (B and C, From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.) Type VI

This is an inferior dislocation of distal clavicle. Gerber and Rockwood have reported

three cases.[48] This injury is associated with severe trauma and frequently accompanied by multiple other injuries. The mechanism is thought to be severe hyperabduction and external rotation of the arm combined with retraction of the scapula. The distal clavicle goes in two directions, either subacromial or subcoracoid. With the subcoracoid dislocation, the clavicle becomes lodged behind the intact conjoined tendon. In a type VI injury, transient paresthesias are present in most patients before reduction and subside afterward.

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Radiologic Evaluation

An important aspect of radiologic evaluation of the AC joint is that it requires one third to one half of the radiographic penetration required for the denser glenohumeral joint. This is why in a standard anteroposterior (AP) view of the shoulder, the AC joint will be overpenetrated (dark), and small or subtle disease may be overlooked. When the history and physical examination indicate possible disease in the AC joint, specific directions must be given to the radiology technician to perform the appropriate view. AP and lateral views are standard for the shoulder; however, a Zanca view is the most accurate in looking at the AC joint. This view is performed by tilting the radiologic beam 10 to 15 degrees toward the head and using only 50% of the standard shoulder AP penetration strength (Fig. 21C-13A (Figure Not Available) and B (Figure Not Available) ). Figure 21-C-13 (Figure Not Available) Explanation of why the acromioclavicular joint is poorly visualized on routine shoulder radiographs. A, This routine anteroposterior view of the shoulder shows the glenohumeral joint well. The acromioclavicular joint is too dark to be interpreted, however, because that area of the anatomy has been overpenetrated by the x-rays. B, When the usual exposure for the shoulder films is decreased by two thirds, the acromioclavicular joint is well visualized. The inferior corner of the acromioclavicular joint, however, is superimposed on the acromion process. C, Tilting the tube 15 degrees upward provides a clear view of the acromioclavicular joint. D, Position of the patient for the Zanca viewa 10- to 15-degree cephalic tilt of the x-ray tube for visualizing the acromioclavicular joint. (A-C, From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984; Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.) Stress View

Stress views are performed with 5 pounds placed on the wrists. A comparison is made on the AP radiograph between the coracoclavicular distance on the normal side and that on the investigative side. These are mainly used to differentiate between type II and type III injuries. The literature has shown that the usefulness of these views does not outweigh the added cost, patient discomfort, and time consumption. Patients who

present with a clinically obvious

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acromioclavicular injury and deformities suggestive of complete dislocation (types III, IV, V, or VI) often demonstrate maximum coracoclavicular interspace widening on routine AP views (Fig. 21C-14 (Figure Not Available) ). Figure 21-C-14 (Figure Not Available) Technique of obtaining stress radiographs of the acromioclavicular joint. A, Anteroposterior radiograph are made of both acromioclavicular joints with 10 to 15 pounds of weight hanging from the wrists. B, The distance between the superior aspect of the coracoid and the undersurface of the clavicle is measured to determine whether the coracoclavicular ligaments have been disrupted. One large horizontally positioned 14- by 17-inch x-ray cassette can be used in small patients to visualize both shoulders on the same film. In large patients, it is better to use two horizontally placed smaller cassettes and take two separate films to obtain the measurement. The arrow indicates the inferior subluxation of the scapulohumeral complex. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.)

When there is a normal coracoclavicular interspace but a complete dislocation of the AC joint, a coracoid fracture should be suspected. A Stryker notch view is helpful in diagnosing this condition ( Fig. 21C-15 ).

Figure 21-C-15 Stryker notch view. Normal Radiologic Findings

The configuration of the AC joint on AP radiographs varies significantly. Zanca reported that the AC joint width is normally between 1 and 3 mm.[124] Petersson and associates reported that the AC joint space diminishes with increasing age, so a joint space of 0.5 mm is normal in 60-year-old patients.[97] The coracoclavicular interspace can also exhibit variability. Bosworth[13] stated that the average distance between the clavicle and the coracoid process is usually between 1.1 and 1.3 cm. Bearden [10] reported that an increase in the coracoclavicular distance of 25% to 50% more than on the normal side indicated complete coracoclavicular ligament disruption.

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Treatment

A multitude of opinions exist in the literature regarding the treatment of AC joint injuries. In most AC joint separations, incomplete injuries (types I and II) are treated nonoperatively with a sling, ice, and a brief period of immobilization, typically lasting 3 to 7 days. Complete AC joint injuries (types IV, V, and VI) are usually treated operatively

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owing to the significant morbidity associated with persistently dislocated joints and severe soft tissue disruption. Treatment of type III injuries remains controversial, with a trend toward initial nonoperative treatment in most cases. This controversy is in part a result of early literature reports that evaluated all AC joint injuries using a type I through III classification system. Type III injuries included what are now considered types IV, V, and VI injuries by Rockwood's addition.[102] Rockwood reported that type III injuries are usually treated nonoperatively, particularly in patients who participate in contact sports (football, hockey, soccer, and lacrosse), in which the risk of re-injury is high. [102] There is a subset of patients who will have persistent pain and will be unable to return to their sport or job with nonoperative treatment. In these cases, successful surgical stabilization has allowed return to sport or work. Evidence supporting nonoperative treatment of type III acromioclavicular dislocations has been provided by a meta-analysis. [99] In a review of 1172 patients, 88% of the operatively treated and 87% of the nonoperatively treated patients had satisfactory outcomes. Complications included the need for further surgery (59% operative vs. 6% nonoperative), infection (6% vs. 1%), and deformity (3% vs. 37%). Pain and range of motion were not significantly affected. The authors did not recommend surgery for type III AC joint injuries in young patients.

In 1997, McFarland published the results of a survey of major-league baseball team physicians evaluating treatment modalities for a type III injury in a pitcher. [80] Sixty-nine percent reported that they would opt for nonoperative treatment. Of the 32 patients with type III injuries, 20 were treated nonoperatively and 12 operatively. There was complete pain relief and normal function in 80% of the nonoperatively treated and 91% in the operatively treated patients. Larson and Hede[70] prospectively compared nonoperative and operative treatment with similar rates of persistent symptoms (2/25 [8%] operative vs. 3/29 [10%] nonoperative).

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Nonoperative Treatment

Most type I and type II AC joint separations are treated in a nonoperative fashion, and type III injuries are usually

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evaluated on a case-by-case basis, taking into account hand dominance, occupation, heavy labor, position/sport requirements (quarterbacks, pitchers), scapulothoracic dysfunction, and a risk for re-injury. Types IV, V, and VI are generally treated operatively. There is some literature information to support reduction of the clavicle in types IV, V, and VI injuries, turning them into a type III injury and then treating them conservatively.[93] The main goals of treatment, whether surgical or nonsurgical, are to achieve a pain-free shoulder with full range of motion, strength, and no limitations in activities. The demands on the shoulder will differ from patient to patient, and these demands should be taken into account during the initial evaluation. Gladstone and colleagues[49] discussed a four-phase rehabilitation program for athletes. The four phases are as follows: (1) pain control, immediate protective range of motion, and isometric exercises; (2) strengthening exercises using isotonic contractions; (3) unrestricted functional participation with the goal of increasing strength, power, endurance, and neuromuscular control; and (4) return to activity with sports-specific functional drills. Phase One

The first phase of nonoperative treatment ( Fig. 21C-16 ) is to decrease pain, allowing

early range of motion to nourish the cartilage and to maintain maximal soft tissue function. Ice and some short-term immobilization can be used in this phase to decrease pain and reduce inflammation. Active assisted range of motion is begun as early as possible for shoulder internal/external rotation and elevation/depression of the arm in the plane of the scapula (30 to 45 degrees of abduction, 30 to 40 degrees of forward flexion). It is important for the patient to reach the range of motion where pain begins but not go beyond this. Arm elevation in abduction allows the clavicle to rotate upward, which stresses the acromioclavicular ligament. This can

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further increase pain and inflammation, so that the athlete is instructed not to perform this motion. Other motions to decrease the atrophy of the surrounding muscular groups in the shoulder are shoulder flexion and internal and external rotation. These exercises are done in an isometric fashion so as not to cause the clavicle to rotate. The patient or athlete is transitioned to the second phase when the range of motion and forward elevation are relatively pain free or with minimal pain up to 140 degrees of flexion and maximum external rotation compared with the contralateral arm. The criteria to advance to phase two are (1) 75% full range of motion, (2) minimal pain and tenderness on palpation of the AC joint, and (3) a manual muscle test grade of 4 out of 5 for the anterior deltoid, middle deltoid, and upper trapezius.

Figure 21-C-16 Phase 1nonoperative treatment. Active assisted range of motion for external rotation. Phase Two

The main goal of phase two ( Fig. 21C-17 ) is to advance a patient to full painless range of motion and to increase the strength in an isotonic arc. Active assisted motion exercises, allowing up to full forward flexion and internal and external rotation, are performed with 90 degrees of shoulder abduction as well as with the arm at the patient's side. Strengthening exercises are directed toward the deltoid, trapezius, and rotator cuff. Press maneuvers such as the bench press or the military shoulder press are limited because they increase the stress in the AC joint. Gladstone and coworkers' criteria [49] for advancing from phase two to phase three are a nonpainful range of motion, no pain or tenderness on palpation, and strength that is 75% of the contralateral side.

Figure 21-C-17 Phase 2Advance to active assisted motion exercises allowing up to full forward flexion. Internal and external rotation is performed with 90 degrees of shoulder abduction as well as with the arm at the patient's side. The L bar is used for active assisted range of motion, allowing the patient to participate in his or her care.

Phase Three

The main goal of phase three ( Fig. 21C-18 ) is to increase strength of the entire shoulder complex musculature. Specific exercises emphasized during this phase are isotonic dumbbell shoulder flexion, abduction, shrugs, and bench press. Wilke[122] has described a complete list of upper extremity plyometric drills that also start during phase three ( Fig. 21C-19 ). Transition to phase four, which is the last rehabilitative stage involving sports-specific exercises, is allowed when the patient achieves (1) full range of the motion, (2) no pain or tenderness, (3) satisfactory clinical examination, and (4) if available, isokinetic test data with close to 100% of strength and range of motion compared with the contralateral uninjured side. These isokinetic tests are performed at 180 degrees per second and 300 degrees per second.

Figure 21-C-18 Phase 3Increased strength and endurance of both the scapula stabilizers as well as specific rotator cuff muscles are attained using Thera-Bands and isometrics.

Figure 21-C-19 Phase 4The last rehabilitative stage involves sport-specific exercise and allows throwing.

It is important to emphasize that patients with type III injuries treated nonoperatively versus operatively demonstrate no difference in strength at 2 years' follow-up.[114] If symptoms persist, including an increased amount of instability and pain, especially posterior instability with the clavicle contacting the anterior portion of the spine of the scapula, then operative procedures may be indicated.

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Operative Techniques

Despite the prevalence and the success of nonoperative management of AC joint injuries, much of the literature has focused on surgical treatment. Operative treatment of types IV, V, and VI is generally recommended because of morbidity associated with persistent marked displacement of the distal clavicle, although there are reports of good results with conservative management.[85] A closed reduction

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maneuver should be attempted, because these types of dislocations can sometimes be reduced into a position that mimics a type III injury, then treated nonoperatively. There have been four basic types of surgery recommended: (1) acromioclavicular ligament repair, (2) dynamic muscle transfer, (3) coracoclavicular ligament repair, and (4) distal clavicle resection. Some authors have advocated combinations of these procedures. Acromioclavicular Ligament Repair

Sage and Salvatore[103] advocated acromioclavicular ligament repair and reinforcement of the superior acromioclavicular ligament with joint meniscus ( Fig. 21C-20 ). Many have recommended transarticular smooth or threaded pins to supplement repair. * In a comparison of smooth pins, threaded pins, and a cortical screw by Eskola,[39] 13 of 86 patients available for follow-up had symptomatic osteolysis, and 8 of these 13 patients were among the 25 who had been treated with a Bosworth screw. Other authors have reported on the use of an acromioclavicular joint plate for complete separations. [16] [38] [57] [59] [119] Results have been good or excellent in 60% to 94% of patients. Broos[16] compared the Wolter plate with the Bosworth screw and found no significant difference in outcome.

Figure 21-C-20 Acromioclavicular ligament repair. The acromioclavicular joint is fixed internally with two unthreaded Kirschner wires. The wires are generally removed approximately 8 weeks after surgery. (Reproduced with permission from Justis EJ Jr: Traumatic disorders. In Canale ST [eds]: Campbell's Operative Orthopedics, 7th ed, vol 3. St. Louis, Mosby, 1987.) Dynamic Muscle Transfer

Transfer of the short head of the biceps with or without the coracobrachialis has been described,[6] [7] [17] [18] [36] [50] [109] usually with acceptable results (Fig. 21C-21 (Figure Not Available) ). However, Skjeldal[109] reported 10 complications in 17 patients, including coracoid fragmentation, infection, and pain. Figure 21-C-21 (Figure Not Available) Transfer of the short head of the biceps with or without the coracobrachialis, shown here as the Dewar technique. The coracoid process is transferred with the attached muscles by screw fixation to the undersurface of the clavicle. (Adapted from Dewar FP, Barrington TW: The treatment of chronic acromioclavicular dislocation. J Bone Joint Surg Br 47b:32, 1965.) Coracoclavicular Ligament Repair

Coracoclavicular ligament repair ( Fig. 21C-22 ) was introduced by Bosworth in 1941,[13] who referred to it as a screw suspension procedure, which he performed percutaneously. Tsou reported on 53 patients in 1989 who underwent percutaneous cannulated screw coracoclavicular fixation and found a 32% technical failure rate.[116] In 1968, Kennedy reported on use of a coracoclavicular screw with *See references

[ 1] [ 5] [ 8] [ 10] [ 20] [ 32] [ 42] [ 61] [ 81] [ 84] [ 89] [ 103]

and [ 125] .

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acromioclavicular débridement and trapeziodeltoid repair.[66] Jay[62] reported on 31 patients who underwent coracoclavicular ligament repair and Bosworth screw fixation with deltotrapezial repair. Lowe and Fogarty[75] used a similar technique in 21 patients.

Figure 21-C-22 Coracoclavicular ligament repair and Bosworth screw fixation with deltoid trapezial repair.

Bearden[10] and Albrecht[2] recommended using wire loops around the clavicle and the coracoid. Many others have used loops of other material.[45] [52] [63] [88] [95] [113] Bunnell in 1928[21] and Lom in 1988[74] used fascia lata to reconstruct the coracoclavicular ligaments.

There have been numerous recent reports of coracoclavicular ligament repair by polydioxanone (PDS) suture or cerclage.[51] [53] [60] [77] [83] [98] Clayer [25] found that a PDS coracoclavicular sling did not maintain reduction, but good results were obtained in 6 patients. Gohring[51] and Pfahler[98] separately compared PDS cerclage with other techniques. Gohring compared surgical treatment of 64 complete AC joint dislocations with three techniques: tension band, Wolter hook-plate, or PDS cord (braided). Early postoperative complications occurred in 43% of patients treated by use of a tension band, 58% of those treated by use of a hook plate, and 17% of those treated by use of a PDS cord. Acromioclavicular joint instability at a 35-month average follow-up was seen in 32% with a tension band, 50% with the plate, and 24% with the PDS cord. The author recommended limiting surgery to younger, athletic patients. Coracoacromial Ligament Transfer

Neviaser[89] introduced coracoacromial ligament transfer without coracoclavicular ligament repair. Variations on this principle have been reported.[1] [4] [9] [22] [61] [84] [94] [111] Several authors have emphasized imbrication of the deltotrapezial fascia as part of any surgical treatment.[8] [20] [73] De la Caffiniere[34] felt that transfer of the coracoacromial ligament, which he attributed to Cadenat, is usually too weak and too short for the treatment of acromioclavicular dislocation. He used a reinforcement flap made by lateral supraclavicular detachment of the superior fibrous capsular sheath. Out of 26 patients, all 19 who had undergone reinforced repair had no recurrence of dislocation, whereas all 7 without reinforcement had recurrence. Kumar[69] treated 14 acromioclavicular dislocations with coracoacromial ligament transfer and coracoclavicular fixation with a screw. All 14 patients had excellent or good results. Guy[56] treated 23 chronic separations with coracoacromial ligament transfer and a Bosworth screw. Nineteen of 23 showed good to excellent results. The four patients with fair or poor results had a previous distal clavicle resection. At the time of a complete acromioclavicular dislocation, the coracoclavicular ligaments may avulse the coracoid instead of tearing. Hak[58] reported one case of coracoid avulsion in association with acromioclavicular dislocation, which he treated nonoperatively with a favorable outcome. Previous reports indicated similar outcomes with either surgical or nonsurgical treatment. Hak[58] recommended treating an acromioclavicular dislocation with coracoid avulsion as if it were an isolated type III injury. Eyres[40] reported treating 12 coracoid fractures that were not associated with acromioclavicular dislocation. The 10 patients without extension into the glenoid were treated nonoperatively, with good results. Results after more severe injuries may not be as good. Verhaven and associates[118] achieved a 71% good or excellent outcome in 28 patients treated surgically for type V injuries. Outcome was unrelated to reduction of the joint, osteolysis, or calcifications. Athletes involved in throwing or contact sports are sometimes considered a special case. Some argue that throwing requires an anatomic reduction of the AC joint. Recent reports of successful nonoperative treatment of major league baseball pitchers suggest that this is not the case. Therefore, the preferred treatment of type III injuries remains

nonoperative, with surgical treatment reserved for those patients who present with persistent symptoms after 3 to 6 months, even in high-level athletes. Distal Clavicle Resection and Coracoclavicular Ligament Reconstruction

Distal clavicle resection is undertaken as a salvage procedure for persistent pain after acromioclavicular dislocation, especially type I or type II injuries, or as treatment of degenerative or osteolytic AC joint arthrosis. In either case, reports indicate that a high rate of success can be expected, although patients with fractures or instability do not demonstrate the same outcome. Distal clavicle resection was reported separately in 1941 by Mumford[86] and by Gurd.[55] Mumford excised the distal clavicle in patients with persistent subluxation and degenerative changes and emphasized the need for coracoclavicular ligament reconstruction when the distal clavicle was noted to be tender. In general, when the distal clavicle is unstable, distal clavicle resection is accompanied by coracoclavicular ligament reconstruction with or without augmentation. In a classic article by Weaver and Dunn[120] published in

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1972, 15 patients with type III injuries were treated with distal clavicle resection and coracoclavicular ligament reconstruction using the coracoacromial ligament (Fig. 21C-23 (Figure Not Available) ). Rauschning[101] reported that 18 patients all had stable painless shoulders after this procedure. Kawabe[64] and Shoji[108] transferred the coracoacromial ligament with an acromial bone block to the distal clavicle and fixed it with a screw. Figure 21-C-23 (Figure Not Available) Dr. Charles Rockwood's method of reconstructing a chronic type III, IV, V, or VI acromioclavicular dislocation. A, The incision is made in Langer's lines. B, The distal end of the clavicle is excised. C, The medullary canal is drilled out and curetted to receive the transferred coracoacromial ligament. D, Two small drill holes are made through the superior cortex of the distal clavicle. The coracoacromial ligament is carefully detached from the acromion process. E, With the coracoacromial ligament detached from the acromion, a heavy nonabsorbable suture is woven through the ligament. F, The ends of the suture are passed out through the two small drill holes in the distal end of the clavicle. The coracoclavicular lag screw is inserted, and when the clavicle is reduced down to its normal position, the sutures used to pull the ligament snugly up into the canal are tied. (From Rockwood CA, Green DP [eds]: Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984.) Distal Clavicle Resection without Ligament Reconstruction

Much of the recent literature involves the development of the technique for arthroscopic distal clavicle resection and comparison of classic open and new arthroscopic methods. A summary of recent literature regarding resection of the distal clavicle is presented in Table 21C-1 . Snyder[112] and Levine[71] reported results of arthroscopic resection; their combined results were good or excellent in 92%. Many authors have contributed to the development of techniques for arthroscopic distal clavicle resection.[11] [46] [65] [112]

Eskola,[39] Flatow,[44] and Levine[71] have all reported worse outcomes for resection in patients with instability of the lateral clavicle. A stabilization procedure in addition to resection is indicated for patients with AC joint arthrosis and instability. Eskola reported poorer results for patients with a history of fracture of the distal clavicle.

Author

TABLE 21-C-1 -- Resection of the Distal Clavicle Patients Injury Treatment Outcome

Auge[4]

10

Osteolysis

Resection

Returned to sport 3.2 months avg.

Cook[28]

17

Type II in athletes

Resection

16/17 returned to sport

Eskola[39]

73

Mixed

Resection

21 good, 29 satisfactory, 23 poor; poor result more common in fractures

Flatow[44]

41

Arthrosis vs instability

Resection

27/29 good or excel for arthrosis, 7/12 instability

Levine[71]

24

Arthrosis

Arthroscopic 71% excellent, 16.5 good, 12.5 failures; failures in instability

Novak[92]

23

Arthrosis

Resection

18/23 good or excellent with normal motion and strength

No instability

Resection

All satisfied

Arthrosis

Arthroscopic 47 good or excellent

Petchell[96] 18/39 [112]

Snyder

50

Excessive posterior translation after distal clavicle resection can be associated with pain, and the AC joint capsule helps restrain this motion. Blazar[12] looked at translation of the clavicle after distal clavicle resection. Motion in the anteroposterior direction was 8.7 mm, compared with 3.2 mm on the contralateral side. Visual analog pain scores correlated with the amount of translation. Translation and pain did not correlate with amount of apparent joint space after surgery. Klimkiewicz[67] used a cadaver model to evaluate the contributions of the superior, inferior, anterior, and posterior portions of the capsule. Sectioning of the anterior and inferior capsular ligaments had no significant effect on posterior translation; however, sectioning of the superior and posterior ligaments had significant effects (56% and 25%, respectively). To avoid posterior translation, techniques that spare the posterior and superior capsular ligaments should be used. Branch[15] demonstrated in a cadaver model that only a 5-mm resection of the distal clavicle is required to ensure that no bone contact between the distal clavicle and the acromion occurs with elevation. He found

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no difference between removal of the superior or the inferior ligament for joint access. Also in a cadaver model, Matthews[77] compared arthroscopic with open distal clavicle

resection. No significant differences were found between the two methods in terms of displacement. There is conflicting evidence regarding the effect of resection on strength and range of motion. Auge[4] reported that all 10 of their patients who underwent resection of the distal clavicle were able to return to their previous sports. Novak[92] reported no clinically perceptible loss of motion or strength in 18 of 23 patients, although objective strength testing was not performed with a calibrated measuring device. Petchell[96] found that motion and strength were not restored in his patients who underwent resection for arthrosis without instability. Although all his patients self-reported that they were satisfied, more than 50% had ongoing difficulties with activities of daily living, sleeping, or working. Twenty-nine percent of patients who wanted to participate in their previous sports activities were unable to do so. Cook[28] reported on open resection in 17 athletes with type II injuries and chronic pain. Sixteen of 17 returned to their previous level of activity, although some complained of decreased strength, which was seen on Cybex testing at low speed but not high. There remains some controversy regarding the development of AC joint symptoms after arthroscopic acromioplasty for impingement syndrome. Neer[87] recommended the removal of any osteophytes from the inferior aspect of the distal clavicle when performing open subacromial decompressions. He thought that these osteophytes could contribute to narrowing of the space available for the rotator cuff. With the development of arthroscopic techniques for subacromial decompression, some surgeons have suggested removing osteophytes from the inferior clavicle. After arthroscopic acromioplasty, however, part of the native distal clavicle is exposed, and certainly some techniques have included removal of this inferior aspect of the clavicle in the co-planing procedure. Fischer[43] reviewed 183 subacromial decompressions and divided them into three groups. The group in which the distal clavicle was not co-planed and the group who underwent formal arthroscopic distal clavicle resection had no postoperative symptoms referable to the AC joint. However, the group that also underwent partial distal clavicle resection (co-planing) along with the subacromial decompression showed a high incidence of postoperative AC joint symptoms (14 of 36, or 39%). Because of these results, an all or none philosophy has developed. In other words, the distal clavicle is left alone for routine subacromial decompression, or a formal distal clavicle resection is performed if the patient has significant acromioclavicular disease.

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Authors' Preferred Method of Treatment

Treatment of AC joint disease ( Fig. 21C-24A , B , C , D , E , F , and G ) always involves a detailed history, physical examination, and an understanding of the patient's goals and needs. Overall, type I and II injuries are treated with the previously described nonoperative protocol. These athletes show a return to sports in 1 to 4 weeks depending on the amount of contact or collision in the sport. Type III are treated nonoperatively; however, close follow-up and scrutiny of stability and pain is important. After 3 to 6 months, operative intervention is warranted if the patient is not improved. Type IV through type VI injuries are treated operatively with an anticipated return to sport at 6 months after surgery. When discussing return to play the type of sport, position, and level must be considered.

Figure 21-C-24 A, Saber-type incision (dashed line) starting slightly medially and posterior to the acromioclavicular joint and extended to just above the coracoid. This is accomplished after diagnostic glenohumeral arthroscopy and an arthroscopic distal clavicle excision have been performed. B, A horizontal incision is made in the deltoid trapezial fascia across the acromioclavicular joint. The joint is completely exposed with careful anterior and posterior subperiosteal dissection to assure full thickness of the flaps. C, The coracoacromial ligament is dissected off the acromium and a No. 2 permanent Ethibond suture is placed in a Krakow-type manner. The clavicle is secured. D, A curet is used to hollow out a trough for the coracoacromial ligament in the distal clavicle, and a large hole is made in the clavicle approximately a centimeter from the edge using a 4.5-mm drill. It is then made larger either with a curet or using the drill as a reamer. Two smaller holes are made on either side of this with a 3.2-mm drill. E, The two limbs of the Ethibond suture tied around the coracoacromial ligament are then placed through the small holes, and the ligament is placed into the bone tunnel. (Inset shows this with magnification.) Upward pressure is placed on the scapulohumeral complex to reduce the coracoclavicular distance. A suture can be placed around the coracoclavicular ligaments if possible. F, A tinaculum clamp is used to hold the reduction that has been accomplished with upper traction on the scapulohumeral complex. This facilitates easy and tight fitting of the coracoacromial ligament into its bone tunnel and passage of the semitendinosus graft. G, Shown is the placement of the semitendinosus graft and the braided Ethibond suture in a figure-of-eight pattern around the base of the coracoid and through the large hole in the distal clavicle, with concomitant fixation of the coracoacromial ligament in the bone tunnel. Of note and not shown in these illustrations is repair of the deltotrapezial fascia with nonabsorbable sutures, which is

extremely important.

Operative treatment begins with a diagnostic glenohumeral and subacromial arthroscopy. The coracoacromial ligament is released, preserving its overall length. A suture can be placed in the end of the ligament and brought out the anterior portal. An arthroscopic distal clavicle excision is completed. Typically, this involves removing 2 to 3 mm from the medial edge of the acromion and 7 to 8 mm from the lateral edge of the clavicle for a space of greater than

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1 cm. A small saber-type incision is made starting slightly medial and posterior to the AC joint and extending to just above the coracoid. A horizontal incision is made in the deltotrapezial fascia across the AC joint. The joint is completely exposed with an anterior and posterior subperiosteal dissection using a needle-tip bovie. Care is taken to maintain the strength of the periosteum and deltotrapezial fascia to allow a secure anatomic closure. Two drill holes with a 1.6-mm drill are made 5 mm medial to the distal end of the clavicle. The coracoacromial ligament is dissected out and a No. 2 permanent Ethibond suture is placed into its end. This is then placed into the end of the clavicle and tied over the holes. Downward stabilization of the clavicle and upward reduction of the scapula are maintained during this procedure. The gracilis or semitendinosus autograft is then harvested

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in the usual fashion. Of note, if a previous procedure has taken these tendons, a section of fascia lata, palmaris longus, or hamstring allograft can be used. A drill hole is placed in the coracoid and using a loop of suture or a Hughson suture passer, the autograft is passed though the hole, twisted in a figure-of-eight fashion and tied to itself with permanent suture.

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Postoperative Care

A variety of factors affect postoperative management of surgery involving the AC joint. If the procedure includes only a distal clavicle resection, then a short (1 to 3 days) period of immobilization is followed by a range of motion program. Strengthening begins at 4 to 6 weeks. Heavy weight training can begin at 3 months, but power athletes will often require 6 to 12 months to return to peak strength. After a coracoclavicular reconstruction, the arm is supported with an external device such as a sling and immobilizer. Gentle range of motion activities in the supine position can begin after 7 to 10 days. Range of motion with the arm unsupported in an upright position should be delayed until the reconstruction has had time to develop early biologic stability. For an acute repair, this takes 4 to 6 weeks. A chronic repair with severe soft tissue involvement, for example a type V separation, a period of 6 to 12 weeks may be indicated. Strengthening begins at 6 to 12 weeks, with weight training started at 3 to 4.5 months. Power athletes and heavy physical demand workers generally take 9 to 12 months to reach peak strength, especially with pressing activities or lifting from the floor (example: dead lift). Historically, motion is limited until pins are removed at 6 to 8 weeks. After coracoclavicular screw fixation, range of motion begins when pain subsides. Bosworth recommended no heavy activity for 8 weeks. Alldredge[3] recommended no immobilization, Bearden[10] a sling for 10 to 14 days, Jay[62] a sling for 4 weeks, and Gollwitzer[53] a Velpeau cast for 4 weeks. Recommendations regarding hardware removal have varied.[3] [10] [13] [62] [66] [121] After coracoid transfer, Brunelli[18] recommended 90 degrees of elbow flexion with gradual straightening starting on day 5 to reduce the AC joint, and protected activities for 6 to 8 weeks.

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Complications

Hardware migration, the most serious complication of AC joint injury, is associated with surgical treatment of dislocations. The frequency of pin migration and seriousness of potential complications have prompted most surgeons to abandon their use, especially the use of smooth pins. Those who still use pins check their position with frequent radiographs and remove them after some interval of healing. Pin migration into the lung and spinal canal has been reported.[79] [91] Lindsey[72] reported migration into a patient's neck posterior to the carotid sheath. Eaton [37] and Urban[117] reported migration into the pleural cavity. Sethi[106] reported laceration of the subclavian artery by a migrated pin. Grauthof and Klammer [54] reported five cases of migration into the aorta, subclavian artery, or lung. Loss of reduction of the AC joint is not uncommon. The weight of the arm and scapula places a tremendous static force on the coracoclavicular reconstruction. Younger patients have a tendency to discontinue efforts at supporting the arm for the first 6 weeks, which is necessary to protect the reconstruction. Efforts at augmentation of the repair and reconstruction have helped to reduce the incidence of complete failure, but partial loss of reduction remains common. In one report, Mayr[78] reported a lost reduction rate of 28%, with a less satisfactory outcome in these patients. Other surgical complications include infection, aseptic reaction to the reconstruction, calcifications, erosion through the clavicle from nonabsorbable materials used to augment the repair and reconstruction, fracture of the coracoid, osteolysis, and persistent pain. Reported rates of infection range from 0 to 9%, with an average of 6% taking into account numerous reports.[53] [60] [77] [123] Colosimo[27] reported an aseptic foreign body reaction to Dacron graft used to reconstruct the coracoclavicular ligaments. Calcification in the reconstructed ligament has been noted, but does not appear to affect results. [60] In fact, if the reduction is maintained and calcification occurs, the stability of the reconstruction seems to be enhanced.

Erosion of cerclage material through the clavicle or coracoid is a well-documented complication.[30] [31] [52] A modification of the cerclage technique to place material through an osseous tunnel in the clavicle rather than completely around it decreases the severity of this complication because erosion does not create a complete discontinuity between the medial and lateral clavicle. Fracture of the coracoid may occur with placement of a coracoid screw.[82] Osteolysis associated with acromioclavicular fixation has been reported.[39] Smith and Stewart[111] recommended resection of the distal clavicle at the time of surgical reduction to avoid this complication. The complication of late AC joint arthrosis is avoided and therefore distal clavicle resection has become an integral part of any acromioclavicular instability reconstruction. Chronic pain after surgical treatment of acromioclavicular instability can be another challenging complication. Many possible causes need to be considered, including horizontal instability (anterior to posterior) of the clavicle, subacromial disease, and neurologic injury. Neurologic injury can occur with the initial trauma or with the surgical procedure. For example, suprascapular neuropathy may occur after distal clavicle resection and has been associated with resections of greater than 1 cm.[76]

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Osteolysis of the Distal Clavicle

Atraumatic osteolysis of the distal clavicle ( Fig. 21C-25[COMP1]A ) is a stress overload syndrome of the distal clavicle. It occurs predominantly in young athletes who have a history of intense weight training associated with bench press activities and military shoulder press.[19] [23] [24] [107]

Figure 21-C-25 A, Radiograph of acromioclavicular (AC) joint demonstrating widening of the AC joint and loss of subchondral cortical detail of the distal clavicle (arrow). B, Radiograph of AC joint demonstrating osteoporosis of the distal clavicle and cortical thinning. C, Radiograph of AC joint demonstrating cystic changes (arrows) and loss of subchondral integrity. D, Radiograph of AC joint demonstrating cystic changes of the clavicular portion of the acromium (solid arrows) and widening of the AC joint. (Reproduced with permission from Pitchford MR, Cahill BR: Osteolysis of the distal clavicle in the overhead athlete. Operative Tech Sports Med 5:74, 1997.)

Scavenius and Iversen[105] found a link between weightlifting and atraumatic osteolysis of the distal clavicle. They reported in 25 elite weightlifters compared with age-matched controls that 28% of the weightlifters exhibited radiographic evidence of atraumatic osteolysis of the distal clavicle. On average, this group tended to be active, lifting heavy weights twice as long, and subjects were older as well as heavier when compared with the controls.[100] Typically, the athlete presents with a slow onset of pain in the area of the AC joint with occasional radiation to the surrounding deltoid muscle or superior border of the trapezius. The pain is intensified by activity, especially bench press on a flat bench, typically using greater than 200 pounds (>90 kilograms). Slawski and Cahill[110] reported a 79% bilateral involvement with weightlifters once they present to the physician with symptoms. Radiographically, a Zanca view (cephalic tilt of 10 to 15 degrees) when taking AP

radiographs of the AC joint provides the best image of the distal clavicle. The changes are represented by a loss of subchondral bone detail at the distal clavicle, cystic appearance in the subchondral area and osteoporosis to the distal one third of the clavicle. Late manifestations include a distinct widening of the AC joint with cysts and lucency at the clavicular end of the acromion. A bone scan is useful in assessing the biologic activity at the distal clavicle and can be used to support the diagnosis of distal clavicle osteolysis. Pitchford and Cahill's [100] conservative treatment of atraumatic osteolysis of the distal clavicle is directed toward eliminating the provocative maneuvers causing it. Unfortunately, many power athletes require the weight training to maintain and increase strength as well as their overall body mass if they want to remain competitive. Pitchford and Cahill[100] suggested the following surgical indications for the treatment of distal clavicle osteolysis: (1) a confirmed diagnosis of atraumatic osteolysis and (2) an unwillingness on the part of the athlete to accept a lower level of performance. The surgical procedure is a distal clavicle resection that can be performed with open or arthroscopic techniques. In summary, atraumatic osteolysis of the distal clavicle is a cumulative stress on the distal clavicle caused by muscular forces across the AC joint with press-type maneuvers. This entity predominantly occurs in weightlifters but may be seen in athletes who use weightlifting for strength and conditioning. The clinical history and examination, combined with appropriate radiographs, allows for the correct diagnosis. The diagnosis is supported by a positive bone scan. The treatment of choice is avoidance of the activities associated with increased symptoms. When this fails, distal clavicle resection may be indicated.

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Intra-articular Acromioclavicular Joint Fractures

Minimally displaced distal clavicle fractures or acromial fractures are relatively stable due to the ligamentous stability provided by the acromioclavicular, coracoclavicular, and coracoacromial ligaments. These are generally treated nonoperatively with success unless there are extenuating effects (open injury, neurovascular compromise). A sling for comfort, then early range of motion and shoulder strengthening exercises when pain permits, is recommended. Some of these fractures may predispose the joint to early post-traumatic arthrosis. When indicated by the persistence of pain unrelieved with nonoperative treatment, a distal clavicle resection is performed.

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Acromioclavicular Injuries to the Child

The developmental anatomy of the shoulder provides insight regarding the type of injuries that occur in a skeletally immature athlete. At 1 year of age there is an ossification center seen at the tip of the coracoid. At age 10, the base of the coracoid and upper fourth of the glenoid has ossified, and these fuse to the scapula by the age 15. Near puberty, the acromion forms between two and five ossification centers that fuse by the age of 22. Failure of the acromion ossifications to fuse can occur without any loss of shoulder function. In children, the classification of acromioclavicular injuries is based on the position of the clavicle with respect to the periosteal sleeve and intact ligaments. This classification system has been reported by Curtis and colleagues and is organized in a similar progression as the adult or skeletally mature patient classification scale ( Fig. 21C-26 ). [29]

Type I injury: sprain of acromioclavicular ligaments with the periosteal sleeve intact Type II injury: partial disruption of the periosteal sleeve with slight winding of the AC joint Type III injury: periosteal tube disrupted with instability of the distal clavicle, superior displacement 25% to 100% of the distal clavicle on the AP radiograph Type IV injury: periosteal tube disrupted, distal clavicle displaced posterior through or into trapezius muscle seen on axial lateral radiograph Type V injury: periosteal tube disrupted, deltoid and trapezial detachment, clavicle displaced subcutaneously greater than 100% of the normal Type VI injury: inferior displacement of the clavicle behind the coracoid process

Figure 21-C-26 Acromioclavicular ligament injuries. Displacement of the distal clavicle occurs through a tear in the periosteal tube. This occurs in children who sustain a severe force to the shoulder. The acromioclavicular and costoclavicular ligaments remain intact through the periosteal tube. (From Beim GM, Warner JP: Clinical and radiographic evaluation of the acromioclavicular joint. Oper Tech Sports Med 5:68, 1997.)

Fracture of the coracoid through the common growth plate with the upper glenoid fossa may mimic an acromioclavicular injury, but the coracoclavicular interspace remains intact.[96] The axillary view will best demonstrate a fracture to the coracoid. This should be suspected in acromioclavicular injuries within the first three decades of

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life. A computerized tomographic scan is indicated if there is any concern of a displaced fracture involving the glenohumeral joint.

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Treatment in Children

The treatment of AC joint injuries in skeletally immature athletes is typically nonoperative because the most common injuries are type I, II, and III. Nonoperative treatment consists of a sling for pain control over the first 3 to 7 days, ice, nonsteroidal anti-inflammatory medications, and mild analgesics as needed. Most athletes in this age group do not require physiotherapy, but if limitations in range of motion are present after 2 to 4 weeks, a short course of physiotherapy is beneficial. Eidman[38] has reported that conservative treatment of these injuries have gone on to heal without clinically relevant sequelae. Nuwber and Bowman report in their chapter that surgical treatment of type IV, V, and VI injuries is successful. Replacement of the clavicle into its periosteal sleeve with suturing the sleeve closed and then fixation of the coracoclavicular lag screw or transacromial fixation is recommended. The fixation is then removed at 4 to 6 weeks before physical therapy is started in the child.

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Section D Injuries to the Sternoclavicular Joint in the Adult and Child Michael A. Wirth MD Charles A. Rockwood Jr. MD A review of the early literature indicates that Rodrigues[72] most likely published the first case of traumatic posterior dislocation of the sternoclavicular joint, a case of dislocation inward of the internal end of the clavicle. The patient's left shoulder was against a wall when the right side of the chest and thorax were compressed almost to the midline by a cart. Immediately, the patient experienced shortness of breath, which persisted for 3 weeks. When first seen by the physician, the patient appeared to be suffocating and his face was blue. The left shoulder was swollen and painful, and there was a depression on the left side of the superior extremity of the sternum. Pressure on the depression greatly increased the sensation of suffocation. In the late 19th century, a number of articles appeared from England, Germany, and France, but it was not until the 1930s that articles by Duggan, [33] Howard and Shafer,[47] and Loman[52] appeared in the American literature.

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Surgical Anatomy

The sternoclavicular joint is a diarthrodial type of joint and is the only true articulation between the clavicle of the upper extremity and the axial skeleton (Fig. 21D-1 (Figure Not Available) ). The articular surface of the clavicle is much larger than that of the sternum, and in the adult, both are covered with fibrocartilage. The enlarged, bulbous medial clavicle presents a saddle-type joint with the clavicular notch of the sternum.[39] [40] The clavicular notch of the sternum is curved, and the joint surfaces are not

congruent. Figure 21-D-1 (Figure Not Available) Normal anatomy around the sternoclavicular and acromioclavicular joints. Note that the tendon of the subclavius muscle arises in the vicinity of the costoclavicular ligament from the first rib and has a long tendon structure. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

Because less than half of the medial clavicle articulates with the upper angle of the sternum, the sternoclavicular joint has the distinction of having the least amount of bony stability of any major joint in the body. If a finger is placed in the superior sternal notch, one can feel that with motion of the upper extremity, a large part of the medial clavicle is completely above the superior margin of the sternum. Ligaments of the Sternoclavicular Joint

There is so much joint incongruity that the integrity has to come from its surrounding ligaments: the intra-articular disk ligament, the extra-articular costoclavicular ligament (rhomboid ligament), the capsular ligament, and the interclavicular ligament. Intra-articular Disk Ligament

The intra-articular disk ligament is a very dense, fibrous structure that arises from the synchondral junction of the first rib to the sternum and passes through the sternoclavicular joint, dividing the joint into two separate joint spaces ( Fig. 21D-2 ).[39] [40] The upper attachment is on the superior and posterior aspects of the medial clavicle. Anteriorly and posteriorly, the disk blends into the fibers of the capsular ligament. The disk acts as a checkrein against medial displacement of the inner clavicle ( see Fig. 21D-2 ).

Figure 21-D-2 A, Normal anatomy around the sternoclavicular joint. Note that the articular disk ligament divides the sternoclavicular joint cavity into two separate spaces and inserts onto the superior and posterior aspects of the medial clavicle. B, The articular disk ligament acts as a checkrein for a medial displacement of the proximal clavicle. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.) Costoclavicular Ligament

The costoclavicular ligament, also called the rhomboid ligament, is short and strong and consists of an anterior and a posterior fasciculus (see Fig. 21D-1 (Figure Not Available) ).[11] [25] [40] The two different parts of the ligament have a twisted appearance.[40] The costoclavicular ligament is attached below to the upper surface of the first rib and at the adjacent part of the synchondral junction with the sternum and above to the margins of the impression on the inferior surface of the medial end of the clavicle, sometimes known as the rhomboid fossa.[39] [40] The fibers of the anterior and posterior components cross to allow for stability of the joint

during rotation and elevation of the clavicle. The two-part costoclavicular ligament is in many ways similar to the two-part configuration of the coracoclavicular ligament on the outer end of the clavicle. Interclavicular Ligament

The interclavicular ligament connects the superomedial aspects of each clavicle with the capsular ligaments and the upper sternum ( see Fig. 21D-2 ). According to Grant,[39] this band may be homologous with the wishbone of birds. This ligament assists the capsular ligaments to produce shoulder poise, that is, to hold up the shoulder. This can be tested by putting a finger in the superior sternal notch;

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with elevation of the arm, the ligament is lax, but as soon as both arms hang at the sides, the ligament becomes tight. Capsular Ligament

The capsular ligament covers the anterosuperior and posterior aspects of the joint and represents thickenings of the joint capsule (see Figs. 21D-1 (Figure Not Available) and 21D-2 ). The anterior portion of the capsular ligament is heavier and stronger than the posterior portion. According to the original work of Bearn,[11] this may be the strongest ligament of the sternoclavicular joint, and it is the first line of defense against the upward displacement of the inner clavicle caused by a downward force on the distal end of the shoulder. The clavicle attachment of the ligament is primarily onto the epiphysis of the medial clavicle, with some secondary blending of the fibers into the metaphysis.[18] [30] [67] Although some authors report that the intra-articular disk ligament greatly assists the costoclavicular ligament in preventing upward displacement of the medial clavicle, Bearn[11] has shown that the capsular ligament is the most important structure in preventing this

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upward displacement. In experimental postmortem studies, he evaluated the strength and the role of each of the ligaments at the sternoclavicular joint to see which one would prevent a downward displacement of the outer clavicle. In experimental postmortem studies, he evaluated the strength and the role of each of the ligaments at the sternoclavicular joint ( Fig. 21D-3 ).

Figure 21-D-3 The importance of the various ligaments around the sternoclavicular joint in maintaining

normal shoulder poise. A, The lateral end of the clavicle is maintained in an elevated position through the sternoclavicular ligaments. The arrow indicates the fulcrum. B, When the capsule is divided completely, the lateral end of the clavicle descends under its own weight without any loading. The clavicle will seem to be supported by the intra-articular disk ligament. C, After division of the capsular ligament, it was determined that a weight of less than 5 lb was enough to tear the intra-articular disk ligament from its attachment on the costal cartilage junction of the first rib. The fulcrum was transferred laterally so that the medial end of the clavicle hinged over the first rib in the vicinity of the costoclavicular ligament. D, After division of the costoclavicular ligament and the intra-articular disk ligament, the lateral end of the clavicle could not be depressed, as long as the capsular ligament was intact. E, After resection of the medial first costal cartilage along with the costoclavicular ligament, there was no effect on the poise of the lateral end of the clavicle, as long as the capsular ligament was intact. (From Beam JG: Direct observation on the function of the capsule of the sternoclavicular joint in clavicular support. J Anat 101:159-170, 1967. Reprinted with the permission of Cambridge University Press.) Range of Motion of the Sternoclavicular Joint

The sternoclavicular joint is freely movable and functions almost like a ball-and-socket joint in that the joint has motion in almost all planes, including rotation. [49] [53] The clavicle, and therefore the sternoclavicular joint, in normal shoulder motion is capable of 30 degrees to 35 degrees of upward elevation, 35 degrees of combined forward and backward movement, and 45 degrees to 50 degrees of rotation around its long axis ( Fig. 21D-4 ). It is likely to be the most frequently moved joint of the long bones in the body, because almost any motion of the upper extremity is transferred proximally to the sternoclavicular joint.

Figure 21-D-4 Motions of the clavicle and the sternoclavicular joint. A, With full overhead elevation, the clavicle elevates 35 degrees. B, With adduction and extension, the clavicle displaces anteriorly and posteriorly 35 degrees. C, The clavicle rotates on its long axis 45 degrees as the arm is elevated to the full overhead position. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.) Epiphysis of the Medial Clavicle

Although the clavicle is the first long bone of the body to ossify (fifth intrauterine week), the epiphysis at the medial end of the clavicle is the last of the long bones in the body to appear and the last epiphysis to close (Fig. 21D-5 (Figure Not Available) ).[39] [40] [67] The medial clavicular epiphysis does not ossify until the 18th to 20th year, and it fuses with the shaft of the clavicle around the 23rd to 25th year.[39] [40] [67] Webb and Suchey,[81] in an extensive study of the physis of the medial clavicle in 605 males and 254 females at autopsy, reported that complete unions may not be present until 31 years of age. This knowledge of the epiphysis is important because we believe that many of the so-called sternoclavicular dislocations are fractures through the physeal plate. Figure 21-D-5 (Figure Not Available) Tomogram demonstrating the thin, wafer-like disk of the epiphysis of the medial clavicle. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

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Applied Surgical Anatomy

The surgeon who is planning an operative procedure on or near the sternoclavicular joint should be completely knowledgeable about the vast array of anatomic structures immediate posterior to the sternoclavicular joint. There is a curtain of muscles, comprising the sternohyoid, sternothyroid, and scaleni, that is posterior to the sternoclavicular joint and the inner third of the clavicle, and this curtain blocks the view of the vital structures. Some of these vital structures include the innominate artery, the innominate vein, the vagus nerve, the phrenic nerve, the internal jugular vein, the trachea, and the esophagus ( Fig. 21D-6 ). If one is considering the possibility of stabilizing the sternoclavicular joint by running a pin down from the clavicle and into the sternum, it is important to remember that the arch of the aorta, the superior vena cava, and the right pulmonary artery are also very close at hand.

Figure 21-D-6 Applied anatomy of the vital structures posterior to the sternoclavicular joint. A and B, Sagittal views in cross section demonstrating the structure posterior to the sternoclavicular joint. C. Diagram demonstrating the close proximity of the major vessels that are posterior to the sternoclavicular joint. D. Aortogram showing the relationship of the medial end of the clavicle to the major vessels in the mediastinum. (A and C, From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984; B and D, from Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Another structure to be aware of is the anterior jugular vein, which is between the clavicle and the curtain of muscles. The anatomy books state that this vein can be quite variable in size. We have seen it as large as 1.5 cm in diameter. This vein has no valves, and when it is nicked, it looks as though someone has opened up the flood gates.

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Mechanism of Injury

Because the sternoclavicular joint is subject to practically every motion of the upper extremity and because the joint is so small and incongruous, one would think that it would be the most commonly dislocated joint in the body. On the contrary, the ligamentous supporting structure is so strong and so designed that it is one of the least commonly dislocated joints in the body. Traumatic dislocation of the sternoclavicular joint usually occurs only after tremendous forces, either direct or indirect, have been applied to the shoulder.

939

Direct Force

When a force is applied directly to the anteromedial aspect of the clavicle, the clavicle is pushed posteriorly behind the sternum and into the mediastinum (Fig. 21D-7 (Figure Not Available) ). This may occur in a variety of ways: An athlete lying on his back on the ground is jumped on and the knee of the jumper lands directly on the medial end of the clavicle, a kick is delivered to the front of the medial clavicle, a person is run over by a vehicle, or a person is pinned between a vehicle and a wall. Because of our anatomy, it would be most unusual for a direct force to produce an anterior sternoclavicular dislocation. Figure 21-D-7 (Figure Not Available) Cross section through the thorax at the level of the sternoclavicular joint. A, Normal anatomic relations. B, Posterior dislocation of the sternoclavicular joint. C, Anterior dislocation of the sternoclavicular joint. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Indirect Force

A force can be applied indirectly to the sternoclavicular joint from the anterolateral or posterolateral aspect of the shoulder. This is the most common mechanism of injury to the sternoclavicular joint. Mehta and coworkers[57] reported that three of four posterior sternoclavicular dislocations were produced by indirect force, and Heinig[45] reported that indirect force was responsible for eight of nine cases of posterior sternoclavicular dislocation. It was the most common mechanism of injury in our series of 168 patients. If the shoulder is compressed and rolled forward, an ipsilateral posterior dislocation results; if the shoulder is compressed and rolled backward, an ipsilateral anterior dislocation results (Fig. 21D-8 (Figure Not Available) ). One of the most common causes that we have seen is a pile-on in a football game. In this instance, a player falls on the ground, landing on the lateral shoulder; before he can get out of the way, several players pile on top of his opposite shoulder, which applies significant compressive force on the clavicle down toward the sternum. If, during the compression, the shoulder is rolled forward, the force directed down the clavicle produces a posterior dislocation of the sternoclavicular joint. If the shoulder is compressed and rolled backward, the force

940

directed down the clavicle produces an anterior dislocation of the sternoclavicular joint. Figure 21-D-8 (Figure Not Available) Mechanisms that produce anterior or posterior dislocations of the sternoclavicular joint. A, If the patient is lying on the ground and a compression force is applied to the posterolateral aspect of the shoulder, the medial end of the clavicle will be displaced posteriorly. B, When the lateral compression force is directed from the anterior position, the medial end of the clavicle is dislocated posteriorly. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott. 1984.) Most Common Cause of Injury to the Sternoclavicular Joint

The most common cause of dislocation of the sternoclavicular joint is vehicular accidents; the second is an injury sustained during participation in sports.[59] [63] [80] Omer,[63] in his review of patients from 14 military hospitals, accumulated 82 cases of dislocation to the sternoclavicular joint. He reported that almost 80% of these cases occurred as the result of vehicular accidents (47%) and athletics (31%). We reviewed 19 patients with posterior sternoclavicular joint injuries that were managed at the University of Texas Health Science Center at San Antonio. Seventy-nine percent of these injuries were the result of motor vehicle accident or sports-related trauma. [83] Probably the youngest patient to have a traumatic sternoclavicular dislocation was a 7-month-old girl with an anterior dislocation reported by Wheeler and associates.[82] The injury occurred when she was lying on her left side and her older brother accidentally fell on her, compressing her shoulders together. The closed reduction was unstable, and the child was immobilized in a figure-of-eight bandage for five weeks. At 10 weeks, the child had a full range of motion, and there was no evidence of instability. The senior author has seen an anterior injury in a 3-year-old patient that occurred as a result of an

automobile accident (Fig. 21D-9 (Figure Not Available) ). Figure 21-D-9 (Figure Not Available) Radiograph of a 3-year-old child with traumatic anterior dislocation of the left sternoclavicular joint. The chest film demonstrates that the left clavicle is superior to the right, suggesting an anterior displacement of the left medial clavicle. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

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Classification of Problems of the Sternoclavicular Joint

There are two types of classifications. One is based on the cause of the dislocation, and the other on the anatomic position that the dislocation assumes. Classification Based on Anatomy

Detailed classifications are confusing and difficult to remember, and the following classification is suggested.

941

Anterior Dislocation

The anterior dislocation is the most common type of sternoclavicular dislocation. The medial end of the clavicle is displaced anteriorly or anterosuperiorly to the anterior margin of the sternum (Fig. 21D-10 (Figure Not Available) ). Figure 21-D-10 (Figure Not Available) A, Clinically, there is an evident anterior dislocation of the right sternoclavicular joint (arrow). B, When the clavicles are viewed from down around the level of the patient's knees, it is apparent that the right clavicle is dislocated anteriorly. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Posterior Dislocation

Posterior sternoclavicular dislocation is uncommon. The medial end of the clavicle is displaced posteriorly or postero-superiorly with respect to the posterior margin of the sternum (Figs. 21D-11 (Figure Not Available) and 21D-12 (Figure Not Available) ).

Figure 21-D-11 (Figure Not Available) A, Posterior dislocation of the left sternoclavicular joint as seen on the 40-degree cephalic tilt radiograph in a 12-year-old boy. The left clavicle is displaced inferiorly to a line drawn through the normal right clavicle. B, Following the closed reduction, the medial ends of both clavicles are in the same horizontal position. The buckles are a part of the figure-of-eight clavicular harness that is used to hold the shoulders back after reduction. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott. 1984.) Figure 21-D-12 (Figure Not Available) Posterior dislocation of the right sternoclavicular joint. A, A 16-year-old boy has a 48-hour-old posterior displacement of the right medial clavicle that occurred from direct trauma to the anterior right clavicle. He noted immediate onset of difficulty in swallowing and some hoarseness. B, The 40-degree cephalic tilt radiograph confirmed the presence of posterior displacement of the right medial clavicle as compared with the left clavicle. Because of the patient's age, this was considered most likely to be a physeal injury of the right medial clavicle. C, Because the injury was 48 hours old, we were unable to reduce the dislocation with simple traction on the arm. The right shoulder was surgically cleansed so that a sterile towel clip could be used. D, With the towel clip securely around the clavicle and with continued lateral traction, a visible and audible reduction occured. E, Postreduction radiographs showed that the medial clavicle had been restored to its normal position. The reduction was quite stable, and the patient's shoulders were held back with a figure-of-eight strap. F. The right clavicle has remained reduced. Particularly note the periosteal new bone formation along the superior and inferior borders of the right clavicle. This is the result of a physeal injury whereby the epiphysis remains adjacent to the manubrium while the clavicle is displaced out of a split in the periosteal tube. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Classification Based on Cause

Traumatic Injury

Sprain or Subluxation.

Acute sprains to the sternoclavicular joint can be classified as mild, moderate, or severe.

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In a mild sprain, all the ligaments are intact and the joint is stable. In a moderate sprain, there is subluxation of the sternoclavicular joint. The capsular, intra-articular disk, and costoclavicular ligaments may be partially disrupted. The subluxation may be anterior or posterior. In a severe sprain, there is complete disruption of the sternoclavicular ligaments, and the dislocation may be anterior or posterior. Acute Dislocation.

In a dislocated sternoclavicular joint, the capsular and intra-articular ligaments are ruptured. Occasionally, the costoclavicular ligament is intact but stretched out enough to allow the dislocation.

Recurrent Dislocation.

If the initial acute traumatic dislocation does not heal, mild to moderate forces may produce recurrent dislocations. This is a rare entity.

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Unreduced Dislocation.

The original dislocation may go unrecognized, it may be irreducible, or the physician may decide not to reduce certain dislocations. Atraumatic Problems

For a variety of nontraumatic reasons, the sternoclavicular joint may sublux or enlarge. Spontaneous Subluxation or Dislocation.

One or both of the sternoclavicular joints may spontaneously sublux or dislocate anteriorly during overhead motion. The problem is usually not painful ( Fig. 21D-13 ).

Figure 21-D-13 Spontaneous anterior subluxation of the sternoclavicular joint. A, With the arms in the overhead position, the medial end of the right clavicle spontaneously subluxes out anteriorly without any trauma. B, When the arm is brought back down to the side, the medial end of the clavicle spontaneously reduces. This is usually associated with no significant discomfort. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.) Congenital or Developmental Subluxation or Dislocation.

Newlin[60] reported a case of a 25-year-old man who had bilateral congenital posterior dislocation of the medial ends of the clavicle that simulated an intrathoracic mass. Guerin[41] first reported congenital luxations of the sternoclavicular joint in 1841. Congenital defects with loss of bone substance on either side of the joint can predispose to subluxation or dislocation. Cooper[28] described a patient with scoliosis so severe that the shoulder was displaced forward enough to dislocate the clavicle posteriorly behind the sternum.

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Incidence of Injury to the Sternoclavicular Joint

Sternoclavicular injuries are rare, and many of the authors apologize for reporting only three or four cases. Attesting to this rarity is the fact that some orthopaedists have never treated or seen a dislocation of the sternoclavicular joint. [46] [74] The incidence of sternoclavicular dislocation, based on the series of 1603 injuries of the shoulder girdle reported by Cave,[26] is 3%. (The total incidence in the study was glenohumeral dislocations, 85%; acromioclavicular, 12%; sternoclavicular, 3%.) In the series by Cave and in our experience, dislocation of the sternoclavicular joint is not as rare as posterior dislocation of the glenohumeral joint. Ratio of Anterior to Posterior Injuries

Undoubtedly, anterior dislocations of the sternoclavicular joint are much more common than is the posterior type. However, the ratio of anterior to posterior dislocations is only rarely reported. Theoretically, one could survey the literature and develop the ratio of anterior dislocations to posterior dislocations, but most of the published material on sternoclavicular dislocations is on the rare posterior dislocation. Of the references listed at the end of this subchapter that deal with injuries of the sternoclavicular joint, more than 60% discuss only the rare posterior dislocation of the sternoclavicular joint and the various complications associated with it. The largest series from a single institution is reported by Nettles and Linscheid,[59] who studied 60 patients with sternoclavicular dislocations (57 anterior and three posterior). This gives approximately a 20:1 ratio of anterior dislocations to posterior dislocations of the sternoclavicular joint. Waskowitz[80] reviewed 18 cases of sternoclavicular dislocations, none of which was posterior. However, in our series of 185 traumatic injuries, there have been 135 patients with anterior dislocation and 50 patients with posterior dislocation.

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Signs and Symptoms of Injuries to the Sternoclavicular Joint Mild Sprain

In a mild sprain, the ligaments of the joint are intact. The patient complains of a mild to moderate amount of pain, particularly with movement of the upper extremity. The joint may be slightly swollen and tender to palpation, but instability is not noted. Moderate Sprain (Subluxation)

A moderate sprain results in a subluxation of the sternoclavicular joint. The ligaments are either partially disrupted

944

or severely stretched. Swelling is noted and pain is marked, particularly with any movement of the arm. Anterior or posterior subluxation may be obvious to the examiner when the injured joint is compared with the normal sternoclavicular joint. Severe Sprain (Dislocation)

A severe sprain is analogous to a joint dislocation. The dislocation may be anterior or posterior. The capsular ligament and the intra-articular disk ligament are ruptured. Regardless of whether the dislocation is anterior or posterior, there are characteristic clinical findings of sternoclavicular joint dislocation.

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Signs Common to Both Anterior and Posterior Injuries

The patient has severe pain that is increased with any movement of the arm, particularly when the shoulders are pressed together by a lateral force. The patient usually supports the injured arm across the trunk with the normal arm. The affected shoulder appears to be shortened and thrust forward when compared with the normal shoulder. The head may be tilted toward the side of the dislocated joint. The patient's discomfort increases when he or she is placed into the supine position, at which time it will be noted that the involved shoulder will not lie back flat on the table.

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Signs and Symptoms of Anterior Injury

The medial end of the clavicle is visibly prominent anterior to the sternum (see Fig. 21D-10 (Figure Not Available) ) and can be palpated anterior to the sternum. It may be fixed anteriorly or may be quite mobile.

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Signs and Symptoms of Posterior Injury

The patient with a posterior dislocation has more pain than a patient with anterior sternoclavicular dislocation. The anterosuperior fullness of the chest produced by the posteriorly dislocated clavicle is less prominent and visible when compared with the normal side. The usually palpable medial end of the clavicle is displaced posteriorly. The corner of the sternum is easily palpated compared with the normal sternoclavicular joint. Venous congestion may be present in the neck or in the upper extremity. Breathing difficulties, shortness of breath, or a choking sensation may be noted. Circulation to the ipsilateral arm may be decreased. The patient may have difficulty swallowing or a tight feeling in the throat, may be in a state of complex shock, or possibly may have a pneumothorax. We have seen a number of patients who clinically appeared to have an anterior dislocation of the sternoclavicular joint but, on radiograph, were shown to have complete posterior dislocation. The point is that one cannot always rely on the clinical findings of observing and palpating the joint to make a distinction between the anterior and posterior dislocations.

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Radiographic Evaluation

Occasionally, routine anteroposterior or posteroanterior radiographs of the chest or sternoclavicular joint suggest that something is wrong with one of the sternoclavicular joints. One or the other of the medial clavicles may appear to be displaced. Ideally, a second view in a plane orthogonal to the anteroposterior view may be taken (Fig. 21D-14A (Figure Not Available)

945

and B (Figure Not Available) ). However, normal anatomic constraints do not allow this. Figure 21-D-14 (Figure Not Available) A, Positioning of the patient for radiographic evaluation of the sternoclavicular joint, as described by Heinig. B, Heinig view demonstrating a normal relationship between the medial end of the clavicle (C) and the manubrium (M). (From Rockwood CA, Green DP, Bucholz RW, Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996.)

Rockwood described a 40-degree cephalic tilt view of both sternoclavicular joints. He called this view the seren-dipity view because of the manner in which it was discovered. The patient is positioned supine in the center of the x-ray table with an 11 × 14 nongrid cassette beneath his or her shoulders and neck. The tube is tilted 40 degrees cephalic and centered directly on the sternum. The distance from the beam to the patient's sternoclavicular joint varies with the thickness of the thorax to project both clavicles onto the film. In children, the tube should be 45 inches from the sternoclavicular joint. In adults, whose anteroposterior chest diameter is greater, the distance should be 60 inches (Fig. 21D-15 (Figure Not Available) ). Figure 21-D-15 (Figure Not Available) Positioning of the patient to take the serendipity view of the sternoclavicular joints. The x-ray tube is tilted 40 degrees from the vertical position and is aimed directly at the manubrium. The nongrid cassette should be large enough to receive the projected images of the medial halves of both clavicles. In children, the tube distance from the patient should be 45 inches; in

thicker-chested adults the distance should be 60 inches. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Tomograms

Tomograms can be very helpful in distinguishing between a sternoclavicular dislocation and a fracture of the medial clavicle. They are also helpful in questionable anterior and posterior dislocation of the sternoclavicular joint to distinguish fractures from dislocations and to evaluate arthritic changes (Fig. 21D-16 (Figure Not Available) ). Figure 21-D-16 (Figure Not Available) Tomogram demonstrating a fracture of the left medial clavicle. The clinical preradiographic diagnosis was an anterior dislocation of the left sternoclavicular joint. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Computed Tomography Scans

Without question, the computed tomography (CT) scan is the best technique to study any or all problems of the sternoclavicular joint ( Fig. 21D-17 ). It clearly distinguishes injuries of the joint from fractures of the medial clavicle and defines minor subluxations of the joint. The orthopaedist must remember to ask for CT scans of both sternoclavicular joints and the medial one half of both clavicles so that the injured side can be compared with the normal side. The patient should lie flat in the supine position. If one requests a study of the right sternoclavicular joint, the x-ray technician may rotate the patient to the affected side and provide views of only the one joint.

Figure 21-D-17 Computed tomography scans of the sternoclavicular joint demonstrating various types of injuries. A, A posterior dislocation of the left clavicle compressing the great vessels and producing swelling of the left arm. B, A fracture of the medial clavicle that does not involve the articular surface. C, A fragment of bone displaced posteriorly into the great vessel. D, A fracture of the medial clavicle into the sternoclavicular joint. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Hartman and Dunnagan[43] reported on the use of CT arthrography to demonstrate capsular disruption in a patient after a traumatic injury to the joint.

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Treatment of Traumatic Injuries Mild Sprain

The joint is stable but painful. Application of ice for the first 12 to 24 hours followed by heat is helpful. The upper

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extremity should be immobilized in a sling for 3 to 4 days, and then, gradually, the patient can regain use of the arm in everyday activities. Moderate Sprain (Subluxation)

For subluxation of the sternoclavicular joint, application of ice is recommended for the first 12 hours, followed by heat for the next 24 to 48 hours. The joint may be subluxed anteriorly or posteriorly, and the subluxation may be reduced by drawing the shoulders backward as if reducing and holding a fracture of the clavicle. A clavicle strap can be used to hold the reduction. A sling and swath should also be used to hold up the shoulder and to prevent motion of the arm. The patient should be protected from further possible injury for 4 to 6 weeks. Occasionally, after conservative treatment of a type II injury, the pain lingers or the symptoms of popping and grating persist. This situation may require joint exploration. Bateman[10] has commented on the possibility of finding a tear of the intra-articular disk, which should be débrided.

Severe Sprain (Dislocation)

The dislocation of the sternoclavicular joint may be anterior or posterior. Nonoperative Treatment

Anterior Dislocation.

There is still some controversy regarding the treatment of acute or chronic anterior dislocation of the sternoclavicular joint. In 1990, deJong and Sukui[29] reported long-term follow-up results in 10 patients with traumatic anterior sternoclavicular dislocations. All patients were treated nonoperatively with analgesics and immobilization. The results of treatment were good in seven patients, fair in two patients, and poor in one patient at an average follow-up of 5 years. Most acute anterior dislocations are unstable after reduction, and many operative procedures have been described to repair or reconstruct the joint. Technique of Closed Reduction.

Closed reduction of the sternoclavicular joint may be accomplished with local or general anesthesia or, in stoic patients, without anesthesia.

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Most authors recommend the use of narcotics or muscle relaxants. The patient is placed supine on the table, lying on a 3- to 4-inch-thick pad between the shoulders. In this position, the clavicle may reduce with direct gentle pressure over the anteriorly displaced clavicle. However, when the pressure is released, the clavicle usually dislocates again. Postreduction Care.

If, with the shoulders held back, the sternoclavicular joint remains reduced, the shoulders can be stabilized with a soft figure-of-eight dressing. Immobilization should be maintained at least 6 weeks, and then the arm should be protected for another 2 weeks before strenuous activities are undertaken. If the sternoclavicular joint again dislocates when the reduction pressure is released, as it usually does, a figure-of-eight dressing or a sling can be used until the patient's symptoms subside. Posterior Dislocation.

A careful examination of the patient is extremely important. Complications are common with posterior dislocation of the sternoclavicular joint, and the patient should receive

prompt attention. A very careful history and physical examination should be done to rule out damage to the pulmonary and vascular systems. The sternoclavicular joint must be carefully evaluated by all available x-ray techniques, including, when indicated, combined aortogramCT scan for potential vascular injuries (Fig. 21D-18 (Figure Not Available) ). If specific complications are noted, appropriate consultants should be called in before reduction is performed. Figure 21-D-18 (Figure Not Available) A, Computed tomography scan revealing a posterior fracture-dislocation of the sternoclavicular joint with significant soft tissue swelling and compromise of the hilar structures. B, Duplex ultrasound study revealing a large pseudoaneurysm of the right subclavian artery. Note the large neck of the pseudoaneurysm, which measured approximately 1 cm in diameter (arrow). (From Rockwood CA, Green DP, Bucholz RW, and Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996.) Techniques of Closed Reduction.

Many different techniques have been described for closed reduction of a posterior dislocation of the sternoclavicular joint. Abduction Traction Technique.

For the abduction traction technique,[32] [36] [56] [58] [69] [74] the patient is placed on his or her back with the dislocated shoulder near the edge of the table. A 3- to 4-inch-thick sandbag is placed between the patient's shoulders (Fig. 21D-19 (Figure Not Available) ). Lateral traction is applied to the abducted arm, which is then gradually brought back into extension. This may be all that is necessary to accomplish the reduction. The clavicle usually reduces with an audible snap or pop, and it is almost always stable. Too much extension can bind the anterior surface of the dislocated medial clavicle on the back of the manu-brium. Occasionally, it may be necessary to grasp the medial clavicle with one's fingers to dislodge it from behind the sternum. If this fails, the skin is prepared and a sterile towel clip is used to grasp the medial clavicle to apply lateral and anterior traction (see Fig. 21D-12 (Figure Not Available) ). Figure 21-D-19 (Figure Not Available) Technique of closed reduction of the sternoclavicular joint. A, The patient is positioned supine with a sandbag placed between the shoulders. Traction is then applied to the arm against countertraction in an abducted and slightly extended position. In anterior dislocations, direct pressure over the medial end of the clavicle may reduce the joint. B, In posterior dislocations, in addition to the traction it may be necessary to manipulate the medial end of the clavicle with the fingers to dislodge the clavicle from behind the manubrium. C, In stubborn cases of posterior dislocations, it may be necessary to prepare the medial end of the clavicle sterilely and to use a towel clip to grasp around the medial clavicle to lift it back into position. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.) Adduction Traction Technique.

In this technique,[22] the patient is supine on the table with a 3- to 4-inch bolster between the shoulders. Traction is then applied to the arm in adduction while a downward

pressure is exerted on the shoulders. The clavicle is levered over the first rib into its normal position. Postreduction Care.

After reduction, to allow ligament healing, the shoulders should be held back for 4 to 6 weeks with a figure-of-eight dressing or one of the commercially available figure-of-eight straps used to treat fractures of the clavicle. If closed maneuvers fail in the adult, an operative procedure should be performed because most adult patients cannot tolerate the posterior displacement of the clavicle into the mediastinum. Technique of Operative Treatment

The operative procedure should be performed in a manner that disturbs as few of the anterior ligament structures as possible. If the procedure can be performed with the

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anterior ligaments intact, the reduction may be stable with the shoulders held back in a figure-of-eight dressing. If all the ligaments are disrupted, a significant decision has to be made to try to stabilize the sternoclavicular joint or to resect the medial 1 to 1½ inches of the medial clavicle and stabilize the remaining clavicle to the first rib. Some of the older literature of the 1960s and 1970s recommended stabilization of the sternoclavicular joint with pins. Elting[35] used Kirschner wires to stabilize the joint and supplemented ligament repairs with a short toe extensor tendon. Denham and Dingley[30] and Brooks and Henning[18] used Kirschner wires. DePalma[31] and Brown[20] recommended a repair of the ligaments and stabilized the sternoclavicular joint with one or two Steinmann pins. Habernek and Hertz,[42] Nutz, [62] Pfister and Weller,[66] Kennedy,[50] Tagliabue and Riva,[78] Hartman and Nunnagan,[43] Bankart,[4] Ecke,[34] and Stein[77] avoided the use of pins across the sternoclavicular joint and used loops of various types of suture wires across the joint. Burri and Neugebauer[23] recommended the use of a figure-of-eight loop of carbon fiber. Maguire,[55] Booth and Roper,[14] Barth and Hagen,[7] and Lunseth and coworkers[54] reconstructed the sternoclavicular joint using local tendons of the sternocleidomastoid, subclavius, or pectoralis major tendons for repair. Haug [44] reported on the use of a special plate to stabilize the joint. The complications of fixation of the sternoclavicular joint with Kirschner wires or Steinmann pins are horrendous and are discussed in the section on complications.

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Authors' Preferred Method of Treatment Traumatic Problems

Type I Injury (Mild Sprain)

For mild sprains, we recommend the use of cold packs for the first 12 to 24 hours and a sling to rest the joint. Ordinarily, after 5 to 7 days, the patient can use the arm for everyday living activities. Type II Injury (Subluxation)

In addition to the cold pack, we may use a soft, padded figure-of-eight clavicle strap to hold the shoulder back

949

gently to allow the sternoclavicular joint to rest. The figure-of-eight harness can be removed after a week or so; then either put the patient into a sling for a week or so or allow the patient to gradually return to everyday living activities. Type III Injury (Dislocation)

In general, we manage almost all dislocations of the sternoclavicular joint in children and in adults by either a closed reduction or a nonoperative skillful neglect form of treatment. The acute traumatic posterior dislocations are reduced closed and become stable when the shoulders are held back in a figure-of-eight dressing. Most of the anterior dislocations are unstable, but we accept the deformity because it is less of a

problem than the potential problems of operative repair and internal fixation. Anterior Dislocation

Method of Reduction.

In most instances, knowing that the anterior dislocation will be unstable, we will still try to reduce the anterior displacement. Muscle relaxants and narcotics are administered intravenously, and the patient is placed supine on the table with a stack of three or four towels between the shoulder blades. While an assistant gently applies downward pressure on the anterior aspect of both shoulders, the medial end of the clavicle is pushed backward where it belongs. On some occasions, rare as they may be, the anterior displacement may stay adjacent to the sternum. However, in most cases, either with the shoulders still held back or when they are relaxed, an anterior displacement promptly recurs. We explain to the patient that the joint is unstable and that the hazards of internal fixation are too great, and we prescribe a sling for a couple of weeks and allow the patient to begin using the arm as soon as the discomfort improves. Criteria for Return to Athletics.

Regardless of whether or not the reduction is stable, athletes involved in contact sports should not be allowed to participate until 6 to 8 weeks after injury to allow soft tissue healing. Return to noncontact sports may be attempted after the athlete has received a full range of motion and is pain free. This normally occurs around the 4-week mark. Posterior Dislocation

It is most important to take an extremely careful history and to perform a very careful physical examination. The physician should obtain radiographs, tomograms or CT scans, or angio-CT scans to document whether there is any compression of the great vessels in the neck or arm or any difficulty in swallowing or breathing. It is also important to determine if the patient has any feeling of choking or hoarseness. If any of these symptoms is present, indicating pressure on the mediastinum, the appropriate specialist should be consulted. We do not believe that operative techniques are usually required to reduce the acute posterior sternoclavicular joint dislocation. Furthermore, once the joint has been reduced closed, it is usually stable ( Fig. 21D-20 ).

Figure 21-D-20 Posterior dislocation or type I epiphyseal separation of the left sternoclavicular joint in a 12-year-old boy. A, The 40-degree cephalic tilt serendipity radiograph reveals that the left clavicle is significantly lower on the horizontal plane than the normal right clavicle. B, Before reduction, the medial end of the left clavicle was displaced posteriorly compared with the normal right clavicle. The only remaining prominence of the left sternoclavicular joint was the prominence of the superomedial corner of the manubrium. C, Under general anesthesia, closed reduction was performed by traction on the arm out into abduction and extension. The clavicle reduced with an audible pop back into position. It was restored

to the same horizontal level as the normal right clavicle. D, Clinically, both clavicles were palpable at the same level following reduction. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Although we used to make the diagnosis of anterior or posterior injury of the sternoclavicular joint on physical examination, we know now that one cannot rely on the anterior swelling and firmness as being diagnostic of an anterior injury. We have been fooled on several occasions when, from physical examination, the patient appeared to have an anterior dislocation but radiographs have documented a posterior problem. Therefore, we recommend that the clinical impression always be documented with appropriate radiographs before any decision to treat or not to treat is made. Method of Closed Reduction.

The patient is placed in the supine position with a 3- to 4-inch-thick sandbag or three or four folded towels between the scapulae to extend the shoulder. The dislocated shoulder should be over the edge of the table so that the arm and the shoulder can be abducted and extended. If the patient is having extreme pain and muscle spasm and is quite anxious, we use general anesthesia; otherwise, narcotics, muscle relaxants, or tranquilizers are given through an established intravenous route in the normal arm. First, gentle traction is applied on the abducted arm in line with the clavicle while countertraction is applied by an assistant who steadies the patient on the table. The traction on the abducted arm is gradually increased while the arm is brought into extension. Reduction of an acute injury usually occurs with an audible pop or snap, and the relocation can be noted visibly. If the traction in abduction and extension is not successful, an assistant grasps or pushes down on the clavicle in an effort to dislodge it from behind the sternum. Occasionally, in a stubborn case, especially in a thick-chested person or a patient with extensive swelling, it is impossible for the assistant's fingers to obtain a secure grasp on the clavicle. The skin should then be surgically prepared, and a sterile towel clip should be used to gain purchase on the medial clavicle percutaneously (see Fig. 21D-12 (Figure Not Available) ). The towel clip is used to grasp completely around the shaft of the clavicle. The dense cortical bone prevents the purchase of the towel clip into the clavicle. Then, the combined traction through the arm plus the anterior lifting force on the towel clip will reduce the dislocation. After the reduction, the sternoclavicular joint is stable, even with the patient's arms at the sides. However, we always hold the shoulders back in a well-padded figure-of-eight clavicle strap for 3 to 4 weeks to allow for soft tissue and ligamentous healing. Technique of Open Reduction.

The complications of an unreduced posterior dislocation are numerous, for example, thoracic outlet syndrome,[37] vascular compromise,[16] and erosion of the medial clavicle into any one of the many vital structures that lie posterior to the sternoclavicular joint. Therefore, in adults, if closed reduction fails, an open reduction should be performed. The patient is supine on the table and three or four towels or a small sandbag is placed

between the scapulae. The upper extremity should be draped free so that lateral traction can be applied during the open reduction. In addition, a folded sheet should be placed around the patient's thorax so that it can be used for countertraction during the traction on the involved extremity. An anterior incision is used that parallels the superior border of the medial 3 to 4 inches of the clavicle and then extends downward over the sternum just medial to the involved sternoclavicular joint ( Fig. 21D-21 ). As previously described, this should usually

950

be done with a thoracic surgeon. The trick is to remove sufficient soft tissues to expose the joint but to leave the anterior capsular ligament intact. The reduction can usually be accomplished with traction and countertraction while lifting up anteriorly with a clamp around the medial clavicle. Along with the traction and countertraction, it may be necessary to use an elevator to pry the clavicle back to its articulation with the sternum. When the reduction has been obtained and with the shoulders held back, the reduction will be stable because the anterior capsule has been left intact. If the anterior capsule is damaged or is insufficient to prevent anterior displacement of the medial end of the clavicle, we recommend excising the medial 1 to 1½ inches of the clavicle and securing the residual clavicle to the first rib with 1-mm Dacron tape. The medial clavicle is exposed by careful subperiosteal dissection (Fig. 21D-22 (Figure Not Available) ). When possible, any remnant of the capsular or intra-articular disk ligaments should be identified and preserved because these 951

structures can be used to stabilize the medial clavicle ( Fig. 21D-23 ). The capsular ligament is primarily attached to the epiphysis of the medial clavicle and is usually avulsed from this structure with posterior sternoclavicular dislocations. Similarly, the intra-articular disk ligament is usually intact where it arises from the synchondral junction of the first rib and sternum and is avulsed from its attachment site on the medial clavicle.

Figure 21-D-21 Proposed skin incision for open reduction of a posterior sternoclavicular dislocation. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.) Figure 21-D-22 (Figure Not Available) A and B, Subperiosteal exposure of the medial clavicle. Note the posteriorly displaced medial end of the clavicle. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1996.)

Figure 21-D-23 Forceps hold the anterior portion of the sternoclavicular ligament, which was avulsed from its attachment on the medial clavicle. The sternal attachment site of this ligament was intact. (From

Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

If the sternal attachment site of these structures is intact, a nonabsorbable No. 1 cottony Dacron suture is woven back and forth through one or both ligaments so that the ends of the suture exit through the avulsed free end of the tissue. The medial end of the clavicle is resected, being careful to protect the underlying structures (Fig. 21D-24 (Figure Not Available) ). The medullary canal of the medial clavicle is drilled out

952

953

and curetted to receive the transferred capsular or intra-articular disk ligament ( Fig. 21D-25 ). Two small drill holes are then placed in the superior cortex of the medial clavicle, approximately 1 cm lateral to the site of resection ( Fig. 21D-26 ). These holes communicate with the medullary canal and will be used to secure the suture in the transferred ligament. The free ends of the suture are passed into the medullary canal of the medial clavicle and out the two small drill holes in the superior cortex of the clavicle ( Fig. 21D-27 ). While the clavicle is held in a reduced anteroposterior position in relationship to the first rib and sternum, the sutures are used to pull the ligament tightly into the medullary canal of the clavicle. The suture is tied, thus securing the transferred ligament into the clavicle ( Fig. 21D-28 ). The stabilization procedure is completed by passing several 1-mm cottony Dacron sutures around the medial end of the remaining clavicle and securing the periosteal sleeve of the clavicle to the costoclavicular ligament ( Fig. 21D-29 ). Postoperatively, the patient's shoulders should be held back in a figure-of-eight dressing for 4 to 6 weeks to allow for healing of the soft tissues. Figure 21-D-24 (Figure Not Available) A and B, Excision of the medial clavicle is facilitated by creating drill holes at the intended site of osteotomy. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

Figure 21-D-25 The medullary canal of the medial clavicle is curetted in preparation for receiving the transferred sternoclavicular capsular ligament. (From Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Figure 21-D-26 A and B, Drill holes are placed in the superior cortex of the clavicle, approximately 1 cm lateral to the osteotomy site. (A, From Rockwood CA, Green DP, Bucholz RW, Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996.)

Figure 21-D-27 A and B, The free ends of the suture are passed into the medullary canal and out the

two holes in the superior cortex. (A, From Rockwood CA, Green DP, Bucholz RW, Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996; B, from Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Figure 21-D-28 A and B, The transferred capsular ligament is secured into the medial clavicle by tying the sutures exiting from the superior cortex of the clavicle. (A, From Rockwood CA, Green DP, Bucholz RW, Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996; B, from Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998.)

Figure 21-D-29 A and B, Closure of the periosteal sleeve around the medial clavicle and secure fixation of these structures to the costoclavicular ligament. (A, From Rockwood CA, Green DP, Bucholz RW, Heckman JD [eds]: Fractures in the Adult. Philadelphia, JB Lippincott, 1996.)

Note: We do not recommend the use of Kirschner wire or Steinmann pins or any other type of metallic pins to stabilize the sternoclavicular joint. Criteria for Return to Athletics.

Following either closed or open reduction, return to sports should be postponed for a total of 10 to 12 weeks after reduction. The complications associated with chronic or recurrent posterior dislocations are so severe that complete ligament healing should be ensured prior to return to competition.

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Complications of Injuries to the Sternoclavicular Joint

Serious complications that occur at the time of dislocation of the sternoclavicular joint are primarily limited to

954

the posterior injuries. About the only complication that occurs with the anterior dislocation of the sternoclavicular joint is a cosmetic bump or late degenerative changes.[84] [85] [86] Many complications have been reported secondary to the retrosternal dislocation: pneumothorax and laceration of the superior vena cava,[65] venous congestion in the neck, rupture of the esophagus with abscess and osteomyelitis of the clavicle,[15] pressure on the subclavian artery late in a patient who was not treated,[76] compression of the right common carotid artery by a fracture-dislocation of the sternoclavicular joint,[47] brachial plexus compression,[56] and hoarseness of the voice, onset of snoring, and voice changes from normal to falsetto with movement of the arm (Figs. 21D-30 (Figure Not Available) and 21D-31 ). [15] [50] [58] [74] [79] Figure 21-D-30 (Figure Not Available) A computed tomography scan demonstrates posterior dislocation of the clavicle back into the mediastinum, displacing the trachea.

Figure 21-D-31 Open reduction of a posterior dislocation of the left sternoclavicular joint causing compression of the great vessels in the mediastinum and resultant swelling in the patient's left arm. A, Chest film does not suggest any serious problem with the left medial clavicle. B, Clinically, the patient had a depressed medial end of the left clavicle compared with the right. C, The computed tomography scan reveals posterior displacement of the medial clavicle back into the mediastinum, compressing the great

vessels and slightly displacing the trachea. D, The patient was carefully prepared for a surgical repair in cooperation with a cardiovascular surgeon. The patient was prepared from the base of his neck down to the umbilicus so that we could manage any type of vascular problem or complication. Open reduction was accomplished without any vascular incident. The medial end of the clavicle was totally unstable, so the medial 2 cm was resected, and the remaining clavicle was stabilized to the first rib. E, Four months following surgery, the patient's slight anterior displacement of the clavicle was essentially asymptomatic, and the remaining clavicle was stable.

Several of our patients have had unusual complications that resulted from traumatic injuries to the sternoclavicular joint. One patient, as the result of a posterior dislocation and rupture of the trachea, developed massive subcutaneous emphysema ( Fig. 21D-32 ). Another had an anterior dislocation on the right and a posterior dislocation on the left. When first seen, his blood pressure was very low. After reduction of the posterior dislocation, his blood pressure, as recorded on his monitor, instantly returned to normal ( Fig. 21D-33 ).

Figure 21-D-32 Complications of sternoclavicular dislocation. As a result of posterior dislocation of the sternoclavicular joint, the patient had a lacerated trachea and developed massive subcutaneous emphysema. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

Figure 21-D-33 Complications of sternoclavicular joint dislocation. This patient had an anterior dislocation on the right and a posterior dislocation on the left. As a result of the posterior dislocation, he had sufficient pressure on the mediastinal structures to cause significant hypotension. When the posterior dislocation was reduced, the blood pressure on the continuous monitor promptly returned to normal. (From Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

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Complications of Operative Procedures

Through 1992, seven deaths[27] [38] [51] [59] [74] [75] and three near deaths[20] [64] [87] had been reported from complications of transfixing the sternoclavicular joint with Kirschner wires or Steinmann pins. The pins, either intact or broken, migrated to the heart, pulmonary artery, innominate artery, or aorta. Tremendous leverage force is applied to pins that cross the sternoclavicular joint, and fatigue breakage of the pins is common. To our knowledge, there were no deaths reported that occurred as a result of migrating pins from the sternoclavicular joint until the report in 1984 by Gerlach, Wemhoner, and Ogbuihi[38] from West Germany. They reported two deaths that resulted from migrating nails that caused cardiac tamponade. The physicians were charged with manslaughter by negligence. We do not recommend any type of transfixing pinslarge or smallacross the sternoclavicular joint.

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Special Considerations in the Pediatric Athlete Incidence

The true incidence of injuries to the medial end of the clavicle in children is unknown. Knowledge of these injuries is contained in case reports and in small series that define a variety of treatments with short-term follow-up. [1] [2] [3] [6] [8] [9] [13] [20] [21] [23] [24] Rowe reports that fractures and dislocations of the medial clavicle constitute less than 6% of all injuries of the clavicle for all age groups.[73] Rang estimates that injuries to the medial clavicle comprise only 1% of all clavicle injuries in children.[68] Nordquist and Peterson found that Allman type II injuries constitute 3% of all clavicle fractures.[61] Classification

Extraphyseal fractures of the medial clavicle in children have been reported,[4] [5] but the majority of repaired injuries to this region in children are Salter-Harris type I and type II injuries ( Fig. 21D-34 ).[1] [2] [8] [9] [13] [23] [24] The displacement can be anterior or posterior. Anterior displacements of sternoclavicular joint injures occur twice as often as do posterior displacements[17] [18] in large series, but most case reports in the literature are for retrosternal displacements owing to the morbidity associated with these injuries. True dislocation of the sternoclavicular joint in children is rare. Most reported cases of younger patients are part of a larger series of adults and do not exclude Salter-Harris injuries as a possibility.[6] [12] [19] [20]

Figure 21-D-34 Diagram depicting a Salter-Harris type I injury to the medial clavicular physis. Healing is by periosteal new bone formation with significant potential for remodeling.

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Treatment

As has been described earlier in this section, the epiphysis on the medial end of the clavicle is the last epiphysis in the body to appear on radiograph and the last one to close. The epiphysis on the medial end of the clavicle does not appear on radiographs until about the 18th year and does not unite with the clavicle until the 23rd to 25th year.[39] [40] [81] If children and young adults younger than 23 to 25 years of age have symptoms from the pressure of the posteriorly displaced clavicle into the mediastinum, an operative procedure should likewise be performed. Children, however, may have no symptoms, and the physician can wait and watch to see if the physeal plate remodeling

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process removes the posteriorly displaced bone.[71] Indeed, as with other childhood fractures, the potential for remodeling is significant and may extend until the 23rd to 25th year. The senior author[70] has demonstrated a similar mechanism to support conservative treatment of adolescent acromioclavicular joint injuries or pseudodislocations, in which there is a partial tear of the periosteal tube containing the distal clavicle. The coracoclavicular ligaments remain secured to the periosteal tube. Because of its high osteogenic potential, spontaneous healing and remodeling to the preinjury reduced position occur within this periosteal conduit. Zaslav and associates[88] have reported successful treatment of a posteriorly displaced medial clavicle physeal injury in an adolescent athlete with CT documentation of remodeling, most probably within an intact periosteal tube. Similarly, Hsu and associates[48] reported successful treatment of a posterior epiphyseal fracture dislocation of the medial end of the clavicle in a 15-year-old patient. Anterior Displacement of the Medial Clavicle

If the physeal injury is recognized, or if the patient is younger than 25 years of age, closed reduction, as has been described for anterior dislocation of the sternoclavicular joint, should be performed. The shoulders should be held back in a clavicular strap of figure-of-eight dressing for 3 to 4 weeks, even if the reduction is unstable. Healing is prompt, and remodeling will occur at the site of the deformity. Posterior Displacement of the Medial Clavicle

Closed reduction of this injury should be performed in the manner described for

posterior dislocation of the sternoclavicular joint. The reduction is usually stable with shoulders held back in a figure-of-eight dressing or strap. Immobilization should continue for 3 to 4 weeks. If the posterior physeal injury cannot be reduced and if the patient is not having symptoms, one can treat the injury expectantly while remodeling occurs. Open reduction of the physeal injury is seldom indicated except for the irreducible posterior displacement in a patient with symptoms of compression of the vital mediastinal structures. Criteria for Return to Athletics.

Return to noncontact sports can be attempted at 6 weeks after injury or when the athlete has regained full, painless range of motion and the fracture site and medial clavicle are nontender. Contact sports should be avoided for an additional 4 to 6 weeks to allow remodeling and strengthening of the medial clavicle. The true incidence of medial clavicular physeal injury is unknown. Because the medial clavicular epiphysis does

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not ossify until age 18, the diagnosis is difficult to verify radiographically. Because the capsule attaches mainly onto the epiphysis, however, it is conceivable that the majority of dislocations in patients younger than 25 years of age are actually physeal separations rather than true dislocations. This distinction is clinically relevant because residual displacement in this injury can potentially diminish with time as remodeling occurs.

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Hsu HC, Wu JJ, Lo WH, et al: Epiphyseal fracture-retrosternal dislocation of the medial end of the clavicle: A case report. Chin Med J 52:198-202, 1993. 48.

Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1-30, 1944. 49.

50.

Kennedy JC: Retrosternal dislocation of the clavicle. J Bone Joint Surg Br 31:74-75, 1949.

Leonard JW, Gifford RW: Migration of a Kirschner wire from the clavicle into pulmonary artery. Am J Cardiol 16:598-600, 1965. 51.

Lowman CL: Operative correction of old sternoclavicular dislocation. J Bone Joint Surg 10:740-741, 1928. 52.

53.

Lucas DB: Biomechanics of the shoulder joint. Arch Surg 107:425-432, 1973.

Lunseth PA, Chapman KW, Frankel VH: Surgical treatment of chronic dislocation of the sterno-clavicular joint. J Bone Joint Surg Br 57:193-196, 1975. 54.

Maguire WB: Safe and simple method of repair of recurrent dislocation of the sternoclavicular joint [abstract]. J Bone Joint Surg Br 68:332, 1986. 55.

McKenzie JMM: Retrosternal dislocation of the clavicle: A report of two cases. J Bone Joint Surg Br 45:138-141, 1963. 56.

57.

Mehta JC, Sachdev A, Collins JJ: Retrosternal dislocation of the clavicle. Injury 5:79-83, 1973.

58.

Mitchell WJ, Cobey MC: Retrosternal dislocation of clavicle. Med Ann DC 29:546-549, 1960.

59.

Nettles JL, Linscheid R: Sternoclavicular dislocations. J Trauma 8:158-164, 1968.

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Newlin NS: Congenital retrosternal subluxation of the clavicle simulating an intrathoracic mass. AJR Am J Roentgenol 130:1184-1185, 1978. 60.

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Nordquist A, Petersson C: The incidence of fractures of the clavicle. Clin Orthop 300:127-132, 1994.

62.

Nutz V: [Fracture dislocation of the sternoclavicular joint]. Unfallchirurg 89:145-148, 1986.

Omer GE: Osteotomy of the clavicle in surgical reduction of anterior sternoclavicular dislocation. J Trauma 7:584-590, 1967. 63.

Pate JW, Wilhite J: Migration of a foreign body from the sternoclavicular joint to the heart: A case report. Am Surg 35:448-449, 1969. 64.

65.

Paterson DC: Retrosternal dislocation of the clavicle. J Bone Joint Surg Br 43:90-92, 1961.

66.

Pfister U, Weller S: [Luxation of the sternoclavicular joint]. Unfallchirurg 8:81-87, 1982.

Poland J: Separation of the epiphyses of the clavicle. In Traumatic Separation of Epiphyses of the Upper Extremity. London: Smith, Elder and Co, 1898. 67.

68.

Rang M: Clavicle. In Rang M (ed): Children's Fractures. Philadelphia, JB Lippincott, 1983, pp 139-142.

Rockwood CA Jr: Dislocation of the sternoclavicular joint. In Rockwood CA Jr (ed): Fractures. Philadelphia, JB Lippincott, 1975, pp 756-787. 69.

Rockwood CA Jr: Injuries to the sternoclavicular joint. In Rockwood CA Jr (ed): Fractures in Adults. Philadelphia, JB Lippincott, 1984, pp 910-948. 70.

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Rockwood CA Jr: The shoulder: Facts, confusions, and myths. Int Orthop 15:401-405, 1991.

Rodrigues H: Case of dislocation inwards of the internal extremity of the clavicle. Lancet 1:309-310, 1843. 72.

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Rowe CR: An atlas of anatomy and treatment of midclavicular fractures. Clin Orthop 58:29-42, 1968.

74.

Salvatore JE: Sternoclavicular joint dislocation. Clin Orthop 58:51-54, 1968.

Smolle-Juettner FM, Hofer PH, Pintner H, et al: Intercardiac malpositioning of a sternoclavicular fixation wire. J Orthop Trauma 6:102-105, 1992. 75.

76.

Stankler L: Posterior dislocation of the clavicle: A report of 2 cases. Br J Surg 50:164-168, 1962.

77.

Stein AH: Retrosternal dislocation of the clavicle. J Bone Joint Surg Am 39:656-660, 1957.

78.

Tagliabue D, Riva A: Le lussazioni sterno-claveari. Minerva Ortopedica 36:867-871, 1985.

Tyler HDD, Sturrock WDS, Callow FM: Retrosternal dislocation of the clavicle. J Bone Joint Surg Br 45:132-137, 1963. 79.

Waskowitz WJ: Disruption of the sternoclavicular joint: An analysis and review. Am J Orthop 3:176-179, 1961. 80.

Webb PAO, Suchey JMM: Epiphyseal union of the anterior iliac crest and medial clavicle in a modern multiracial sample of American males and females. Am J Phys Anthropol 68:457-466, 1985. 81.

82.

Wheeler ME, Laaveg SJ, Sprague BL: S-C joint disruptions in an infant. Clin Orthop 139:68-69, 1979.

Wirth MA, Jensen KL, Rockwood CA: Treatment of traumatic posterior sternoclavicular joint injuries. Paper presented at the 12th open meeting of the American Shoulder and Elbow Surgeons, 1996, Atlanta, Ga. 83.

Wirth MA, Rockwood CA: Chronic conditions of the acromioclavicular and sternoclavicular joints. In Chapman M (ed): Operative Orthopaedics. Philadelphia, JB Lippincott, 1992, pp 1683-1693. 84.

Wirth MA, Rockwood CA: Complications following repair of the sternoclavicular joint. In Bigliani L (ed): Complications of the Shoulder. Baltimore, Williams & Wilkins, 1993, pp 139-153. 85.

Wirth MA, Rockwood CA: Complications of treatment of injuries to the shoulder. In Epps C (ed): Complications in Orthopaedic Surgery. Philadelphia, JB Lippincott, 1994, pp 229-253. 86.

Worman LW, Leagus C: Intrathoracic injury following retrosternal dislocation of the clavicle. J Trauma 7:416-423, 1967. 87.

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Section E Clavicle Fractures 1. CLAVICLE FRACTURES IN ADULT ATHLETES Carl J. Basamania MD ...a fracture of the clavicle has been greatly underrated in respect to pain and disability. ...the usual or routine treatment is perhaps far short of satisfying, relieving therapy. Carter R. Rowe, 1968 Clavicle fractures are some of the most common shoulder girdle injuries sustained during athletic endeavors, with collision sports being the most frequent causative agents. The vast majority of these injuries heal uneventfully no matter what we do. As evidence of this, consider the variety of treatment options available for treating a simple midshaft clavicle fracture. These include benign neglect, sling alone, sling and swathe, Velpeau dressing, Sayre bandage, various figure-of-eight bandages, figure-of-eight bandages with a sling, figure-of-eight bandages with a collar and cuff, external fixation, open reduction, and internal fixation, just to name a few. They all work about equally well and all are associated with some degree of shortening at the fracture site, or some type of residual deformity. Even the occasionally seen untreated fracture will generally heal if left to nature's good graces. Fractures of the clavicle are not without potential complications, however. Management of both the early and late complications possible with these fractures can be difficult. The orthopaedic surgeon caring for a sporting population must be aware of these potential complicating factors and must be able to recognize the atypical clavicle fractures that may require more or even urgent intervention to help avoid potential late complications. We all have our own favorite method of treating the simple clavicle fracture. I endeavor

to remain concise while pointing out my treatment philosophies for both the simple and the potentially problematic clavicle fracture. I emphasize recognition of atypical fracture patterns because early recognition of a problem fracture is the single best way to avoid devastating late complications. The ultimate goal of treatment is to ensure a safe and rapid return to sports participation.

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Epidemiology

The clavicle is the bone most commonly fractured during childhood. [8] [49] In adults, clavicle fractures have a bimodal incidence by both age and sex. Most clavicle fractures occur in men and women before the age of 25. Some of this distribution is due to participation in contact and collision sports, and some of it is likely due to the ever-present feeling of being both immortal and bulletproof before age 25. Except in certain individuals and isolated populations, this type of sports participation and these inherent feelings rapidly decline after age 25. According to the American Academy of Orthopaedic Surgeons, clavicle fractures occur with a frequency of about 1 in 1000 people per year.[14] Eighty percent of these fractures occur in the middle one third of the bone, 12% to 15% in the lateral one third, and 5% to 6% in the medial one third.

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Anatomy

The clavicle is the first bone in the body to ossify (usually by the fifth fetal week). It ossifies through a combination of intramembranous and endochondral ossification. Epiphyseal growth plates develop at both the medial and lateral ends of the bone, but it is the medial ossification center that is responsible for the majority of the longitudinal growth of the bone (approximately 80%). [38] The medial ossification center first appears on radiograph between the ages of 12 and 19. This physis does not fuse until well into young adulthood (between ages 22 and 25).[20] [52] This is important to remember because many medial clavicle fractures and sternoclavicular injuries in young adults are actually physeal injuries. The clavicle is S-shaped with a flat cross section laterally, a tubular section in the middle, and a more oblong cross section at the most medial aspect. It is firmly anchored at both ends by very strong capsular ligamentous attachments, as well as by extra-articular ligaments that attach the clavicle to the first rib, the sternum, and the scapula via the coracoid. Proximally, the clavicle is supported by muscles, including the sternocleidomastoid, the pectoralis major, and the subclavius. Distally, the clavicle is also supported by muscular attachments to the deltoid, and by the trapezius. The middle section of the clavicle is relatively unsupported by muscular or ligamentous attachments and is also the transition point between the flatter cross section laterally and the more tubular cross section medially.[27] This area, just distal to the subclavius muscle insertion, is mechanically the weakest point.[3] [16] [18] [27] [37] This is likely the reason that most fractures of the clavicle occur exactly in this area with uncanny regularity. Another possible explanation for the high incidence of fractures in this area is that, because of the S shape of the clavicle, axial load forces have to virtually take a right turn at the midpoint. This creates very high tensile forces along the anterior midcortex of the clavicle. The superior surface of the clavicle is essentially subcutaneous over its course, with only the thin platysma providing any muscular coverage, and then only to the inner two thirds of the bone. The supraclavicular nerves, which provide sensation to the overlying skin, are consistently found just deep to the platysma muscle layer. These

nerves have been known to cause painful neuroma when damaged by fracture shards or iatrogenic injury. The middle and inner thirds of the clavicle have a thick cross section and a well-defined medullary canal that provides bony protection for the underlying subclavian artery and vein, as well as the cords of the brachial plexus. These structures are further protected by a dense fascial layer lying in front of them that is composed of the clavipectoral fascia and its extensions. This layer begins on the clavicle, envelops the subclavius muscle, and then unites to form a single layer before enveloping the pectoralis minor muscle. This layer thus forms a wall between the clavicle and the chest wall, behind which the important neurovascular structures are found. The neurovascular structures traverse the space between the inferior surface of the clavicle and the superior surface of the first rib, called the costoclavicular space. This space is relatively small and is well surrounded by bony structures. This sword is indeed double-edged in that the bony structure provides great protection for the underlying structures. In the event of an injury to one of the bones, however, this tight space allows little extra room for these same important structures. Because of its anatomic position at the most narrow region of the costoclavicular space, the medial cord of the brachial plexus, which provides the majority of nervous tissue to the ulnar nerve, is most at risk. Direct trauma by sharp fracture ends, clavicular nonunion, clavicular malunion, or healing with exuberant callus can place any of the structures in the costoclavicular space at risk, but the most commonly affected are the medial cord and the ulnar nerve.[3] [5] [23] [28] [44] The most medial portion of the clavicle lies anterior to the root of the internal jugular vessels and is near the trachea and esophagus. These structures are potential sites of injury or compression with fractures of the medial growth plate of the clavicle or sternoclavicular fractures/dislocations.

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Biomechanics and Function

The clavicle provides the only bony link between the thorax and the entire upper extremity. In the upright, resting position, the clavicle is under constant bending load from the force of gravity relentlessly pulling down on the combined mass of the upper extremity and any load carried therein. Structurally, the clavicle can be thought of as analogous to the wing of an aircraft parked on the ramp, with the weight of the wing and engines causing the wing to droop under the load. The wing is firmly anchored to the fuselage centrally; likewise, it is firmly attached to the load of the engines distally. If the wing is disrupted anywhere along its length, the weight of the distal unsupported portion with its attached engines will fall under the force of gravity. The central portion of the wing, now set free of its load, will recoil and elevate to a new resting position consummate with current load configuration. Disruption of the middle third of the clavicle, likewise, will result in depression of the distal segment with the attached upper extremity. The medial segment, when released from its load, will elevate. On the question of whether the distal

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fragment is depressed or the proximal fragment elevated, the answer is clearly yes to both questions. Resting muscular tone modifies this basic mechanical description. The pull of the sternocleidomastoid pulls the proximal fragment superiorly and posteriorly. The pectoralis major muscle causes shortening at the fracture site and medial rotation of the distal segment and attached upper extremity through its attachments and action on the proximal humerus. The clavicle can be regarded as the force multiplier for the upper extremity for two main reasons. First, it provides stability to the arm by supplying a firmly attached bone linkage to the axial skeleton. Second, and perhaps more importantly, the clavicle provides a fixed-length strut through which the muscles attached to the shoulder girdle can

generate and transmit large forces to the upper extremity. The clavicle thus enhances the power and stability of the upper extremity through force transmission from the axial skeleton to the extremity. This multiplication of force and stability is especially important in movements above shoulder level.[33] This force multiplication role is most important in the movements of the overhead-throwing ath lete. Clavicular disruption anywhere along its length will affect a patient's ability to generate and transmit forces to the upper extremity. Congenital absence of the clavicle, as occurs in cleidocranial dysostosis, may result in some weakness in the support of overhead loads.[17] It is known that excision of the clavicle results in drooping of the shoulder girdle anteriorly and medially. These patients have weakness and pain that can be disabling. [41] [47] Significant shortening of the clavicle, as occurs in malunion, can result in a vague feeling of weakness in the shoulder, especially in overhead activity.[2B] This effect can be measured through strength testing of the pectoralis major muscle in patients with shortened malunion of the clavicle. The measurable weakness in this muscle group is likely attributable to the decreased distance between the origin and the insertion of the muscle. Because it is known that a muscle has maximum effectiveness within a range of fiber length (according to Blick's curve), it maybe surmised that shortening beyond a certain point will begin to manifest as weakness in the muscle group. In addition, there can be a significant change in the orientation of the glenohumeral joint with a clavicle malunion. Clavicle malunions represent fixed or static anteriomedial displacements of the shoulder, whereas clavicle nonunions are more like acromioclavicular (AC) separations in that they are more dynamic. The key question is, How much shortening is too much? Some authors have suggested that as much as 15 mm of shortening can lead to poor long-term results and patient dissatisfaction.[13A] [14A] Nonunion of a clavicle fracture can add another variable to the equation because the clavicle can be both short and unstable. The instability denies the shoulder girdle muscles the rigid post against which they generate their force, particularly in the overhead position. A muscle deprived of a stable post to pull against is unable to generate the magnitude of force required for most activities. A similar situation occurs in the case of chronic severe instability of the AC joint. The problem is essentially the same, although at a slightly different location. Disruption of the coracoclavicular (CC) and AC ligaments allows the shoulder girdle to rotate anteromedially beneath the distal clavicle. Patients complain of vague shoulder weakness and pain.

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Classification of Fractures

Several classifications of clavicle fractures are available, from the simple to the highly comprehensive, depending on whether you are a lumper or a splitter. All of these classifications are more useful for academic comparison of fractures than for treatment decision-making. I ascribe to the KISS (Keep It Simple, Stupid) principle and discuss my treatment philosophy by region of injury, as well as methods of treatment at our disposal for these specific regions. The reader is encouraged to consult one of the many fine published classification systems for a more comprehensive classification.[37] [50]

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Mechanism of Injury

Several large studies of clavicle fractures detailing the apparent mechanism of injury have been published.[9] [45] [46] [48] In the vast majority of these fractures, the reported mechanism resulted from a fall onto the point of the shoulder or a lateral blow to the shoulder. A small percentage of patients recalled a fall onto the outstretched hand. [45] [48] Stanley and colleagues also suggested that even these patients may have fractured owing to a laterally applied force in that the shoulder may have been the next point of contact with the ground after the hand. [48] A direct blow to the bone inflicted by a hard instrument is another recognized mechanism of fracture, particularly in stick sports such as hockey and lacrosse. A force applied to the top of the shoulder, driving the clavicle against the first rib, is another recognized mechanism of producing a middle third fracture. In practice, a majority of clavicle fractures have remarkably consistent injury patterns. Stanley and associates were able to produce fractures at every site along the length of the clavicle in cadaver specimens through application of a laterally directed force to the shoulder.[48] In most clavicle fractures caused by sports-related injuries, the bone generally fails to bend at the middle third, thereby producing an oblique fracture. As the energy of the fracture is increased, the most common pattern observed is a comminuted, shortened middle third fracture with a consistent inferior butterfly fragmentagain a failure in bending. The rarer lateral third clavicle fractures may occur in a manner more analogous to AC joint injuries, whereby force is applied superolaterally onto the point of the shoulder. The even rarer medial clavicle fracture may occur in a manner as suggested for injuries to the sternoclavicular joint, whereby a laterally directed force on the shoulder causes the shoulder to fold either anteriorly or posteriorly before fracture occurs. This mechanism is similar to that seen in SC separations.

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Assessment Patient History

In the awake and alert athlete, the history is usually quite clear in cases of clavicle fracture. In collision sports,

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the patient may report a high-energy collision or being injured at the bottom of a pile. In other sports, a common story is a collision with a fixed structure such as the wall, a post, or the boards. In stick sports, occasionally a patient reports a direct blow to the top of the clavicle inflicted by a stick. The athlete generally complains of pain at the site of fracture, and he or she cradles the injured extremity with the other uninjured arm. The patient may also complain of deformity of the collar bone, along with severe pain coinciding with attempts to actively lift the extremity. Occasionally, the patient may complain of persistent numbness or weakness in the affected upper extremity. An important consideration at this point is to elicit a history of previous stingers and the patient's assessment of whether this feels similar. Very rarely, a patient may complain of difficulty swallowing, fullness in the chest, difficulty breathing (not just pain with deep inspiration that can pull on the clavicle), or swelling in the entire affected upper extremity. An extremely rare presentation is the patient seen on the field or brought in by emergency medical services (EMS) in shock or already dead. In the more typical presentation of a clavicle fracture, the odds are good that the injury will be fairly innocuous. In the atypical presentation, it is prudent for clinicians to increase their level of concern. Although rare, serious associated injuries to the great vessels, brachial plexus, or lungs and pleura can occur, and these may become life threatening.[10] Failure to recognize these injuries or delayed treatment can result in disaster.

Physical Examination

A careful physical examination, actually involving laying hands on the patient, is important for several reasons. A careful examination can occasionally enable the clinician to make the diagnosis, but even if it does not, it can help in the identification of other associated injuries and in ruling out potentially serious problems that can be life threatening. A well-done physical examination will help to ensure that the clinician orders the appropriate radiographs or special studies to allow diagnosis of the disease. A complete neurovascular examination of the upper extremity takes very little time, and it can reveal uncommon brachial plexus or vascular injuries. The chest should be auscultated and the results documented. On visual inspection, the athlete with a clavicle fracture frequently has a notable edematous or ecchymotic area at the site of fracture. The affected extremity may droop both downward and forward if it is unsupported by the other arm. The site of fracture is tender to palpation, and crepitus may be felt. In fact, if crepitus is not felt, the possibility must be considered that interposed soft tissue may be impairing fracture healing. This is a more high-energy injury and requires a greater level of concern on the part of the clinician. The skin over the fracture site should be examined for open wounds or severe tenting. Tented, blanched skin can signify that the area is in jeopardy of necrosis. Lack of normal contour in the clavicle, or lack of or increased normal prominence of the sternoclavicular joint, can signify medial clavicle fracture or sternoclavicular disruption. Radiographic Evaluation

The appropriate radiographic evaluation will vary according to the location of the clavicle injury and the presence of any associated injuries. Potentially life-threatening associated injuries will obviously take precedence. In the unconscious athlete, a chest film and cervical spine films should be the first radiographs completed. A chest film should also be completed when the history or physical examination suggests possible thoracic injury. An abnormal vascular examination of the upper extremity may require an arteriogram.[15] [19] [24] [26] [30] [51] If an institution is incapable of performing these specialized studies or does not have the personnel to deal with a potential thoracic injury, transport to another facility must be considered. Delay can be deadly. Fractures of the medial third of the clavicle can be particularly difficult to image owing to the superposition of the ribs, sternum, spine, and mediastinum. Routine films should include an anteroposterior (AP) film centered on the sternoclavicular joints. Because an orthogonal view of the medial clavicle is difficult to obtain and nearly impossible to interpret, the serendipity view as popularized by Rockwood offers a reasonable alternative. This view is shot with the patient supine and the beam directed 40 degrees cephalically and centered on the sternoclavicular joints. The cassette must be wide enough to display both sternoclavicular joints and the majority of both clavicles to allow accurate interpretation. Although this view is most useful for sternoclavicular joint disruptions, it provides a fairly good image of the entire medial clavicle. Also, because many presumed sternoclavicular joint disruptions in patients younger than 25 years old are in reality physeal injuries, this view may differentiate between the diagnoses. If the diagnosis cannot be confirmed with these plain radiographs, a computed tomographic

(CT) scan is necessary. The CT scan is currently the best available technique for evaluating injuries to the medial clavicle and the sternoclavicular joint. It provides the true orthogonal views unobtainable with plain films. The scan must include both sternoclavicular joints and at least half of both clavicles to allow side-to-side comparison. Magnetic resonance imaging (MRI) may be useful, particularly in cases of diseased fractures and stress fractures, and in the identification of associated soft tissue injuries. Fractures of the middle third of the clavicle are more straightforward when it comes to imaging. Clavicular shaft fractures are generally easy to see when viewed in an AP projection centered on the midshaft of the clavicle. A 45-degree cephalic tilt film will more clearly delineate the fracture anatomy, amount of displacement, and extent of comminution. The typical pattern in a low-energy injury is an oblique fracture. The proximal fragment is displaced superiorly and posteriorly by the pull of the sternocleidomastoid muscle. The distal fragment is depressed by the weight of the upper extremity. If there is complete displacement of the fracture or comminution, the distal fragment is most commonly pulled medially by the pectoralis major, which underrides the proximal fragment. To evaluate the amount of shortening at the fracture site, we recommend an AP view of both clavicles on a wide cassette, including

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the sternum and the AC joints. This radiograph allows fairly accurate measurement of clavicular lengths. It should be pointed out, however, that clavicle fractures represent multiplanar deformities, and it is very difficult, if not impossible, to get an accurate estimate of shortening with the use of plain radiographs. Greater accuracy of measurement of clavicular shortening can be obtained with a CT scan, especially with three-dimensional (3D) reconstructions, including both clavicles from sternum to AC joint. This level of accuracy is rarely required. Fractures of the distal third of the clavicle are also more difficult to image. Standard radiographic technique for either the clavicular shaft or the shoulder overexposes the distal clavicle. Also, a straight AP view of the region obscures the distal clavicle and the AC joint in the overlap of the scapula and the acromion. Subtle fractures, and particularly intra-articular fractures, are inadequately displayed using standard techniques. Routine films of this region should include a 15-degree cephalic tilt AP view centered on the AC joint using soft tissue technique (Zanca view), as well as an axillary lateral view. Another view that may be useful for imaging this difficult region reveals the arm in the cocked position as if about to throw a ball. This view is shot with 10 degrees cephalic tilt, and soft tissue technique is centered on the AC joint. Intra-articular disease is highlighted on this view, and an unobstructed lateral view of the AC joint is obtained. To assess the ligaments about the AC joint, special views must be obtained. Traditionally, the integrity of the CC and AC ligaments is ascertained by use of weighted and unweighted views of both AC joints. When this technique is used, it is imperative that the weights be tied to the wrists rather than held in the hands; otherwise, splinting by the patient can reduce the accuracy of the assessment.[3] We prefer to use a different view to assess the integrity of these ligaments. The cross-body adduction view

highlights medial rotational instability of the shoulder complex. This is important because it simplifies the treatment algorithm. This is discussed further in the treatment section. This AP radiograph is shot with the patient pulling the affected upper extremity across the body in adduction. Maximal internal rotation of the humerus (thumb-down position) accentuates the instability, and soft tissue technique highlights the AC joint. Medial rotational instability is present if the distal fragment grossly underrides the proximal fragment. This signifies either that CC ligamentous disruption has occurred or that all ligaments are attached to the distal fragment. Intra-articular fractures or stress fractures involving the AC joint occasionally require CT scan or MRI for elucidation. Concomitant glenohumeral joint dislocation with a clavicle fracture is relatively rare, but the potential complications caused by failure to diagnose a posterior shoulder dislocation are very great. For this reason, we recommend that at least an AP shoulder view and an axillary lateral view be taken. The AP shoulder view may have already been obtained or at least caught on one of the previous films. An axillary lateral radiograph is easy to obtain and interpret and sets to rest any questions regarding the glenohumeral joint. Because of the surrounding edema and tenderness, the active glenohumeral motion and the physical examination itself can be limited. The clinician does not wish to miss a glenohumeral dislocation because he or she could not complete a good physical examination. It is always better to be safe now, than very, very sorry later on.

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Treatment Options

Clinicians are advised to keep their goals in mind when discussing what could be done and what should be done to treat clavicle fractures. In treating the athlete, the primary goal is to obtain solid union of the clavicle fracture while at the same time avoiding undue risks of complications, both late and iatrogenic. The next goal is to restore function to the injured upper extremity to allow the athlete to return to play at his sport of choice. In the professional athlete or the champion amateur competitor, return to play at the same level as before the injury is required as soon as possible. In general, only three options are available for achieving the first goal. These include (1) partial immobilization and support of the upper extremity, (2) closed reduction and partial immobilization, and (3) closed or open reduction and internal fixation. Attainment of the second goal may require early application of a rehabilitative protocol or sport-specific rehabilitation. This may merely involve maintaining aerobic fitness or instituting a strengthening program designed to maintain strength in the other uninjured extremities. A good working relationship with the patient, the trainer, or the coach can assist the clinician in attaining this goal. Partial Immobilization and Support of the Upper Extremity

This option is preferable when the fracture alignment is acceptable, and there are no other indications for reduction or operative fixation of the fracture. Choices include sling, sling and swathe, Sayre bandage, Velpeau dressing, and modified Velpeau, to name only a few. If what is seen on the initial injury films is acceptable, this method is likely to maintain adequate partial immobilization at the fracture site to allow healing in this position. Both functional and cosmetic results can be expected to be essentially the same as those achieved with a figure-of-eight bandage. [1] Closed Reduction and Partial Immobilization (with or without Support of the Closed Upper Extremity)

Because the proximal fragment cannot be controlled, reduction maneuvers are

designed to bring the depressed and medially rotated distal fragment(s) up to and back to the proximal fragment. Various forms of figure-of-eight bandages, both with and without support of the upper extremity, have been designed to help achieve this goal. The various figure-of-eight dressings all require periodic adjustments. Occasionally, patients may be unable to tolerate the dressing secondary to pain at the fracture site or

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neurovascular compromise while the figure-of-eight bandages are worn.[42] There is no evidence that a figure-of-eight bandage or variant provides any better functional or cosmetic result than partial immobilization and support alone.[2] [31] In fact, these studies have found the results to be identical, and furthermore, unchanged from the initial fracture displacement noted on the injury films.[2] [31] This suggests that the amount of displacement that is seen on the initial injury films is the most that clinicians can ultimately hope to achieve after fracture healing when treatment by closed means of any type is provided. With this in mind, the choice of figure-of-eight variants versus sling variants is made according to physician and patient preference. Thompson noted that a 100% displaced middle third clavicle fracture is at particular risk for nonunion unless bony contact can be achieved and maintained.[12] Clearly, none of the aforementioned closed means can reliably maintain any reduction obtained. All of this information raises the following question: Should a reduction maneuver ever be performed? The answer is yes, but more as a diagnostic test than as a form of treatment. In the case of a 100% displaced middle third fracture, if a reduction maneuver is performed, and crepitus is felt on palpation of the fracture site, we can be more confident that the bone ends are in the same ballpark. We can then advise the patient that we are more optimistic that the fracture will heal by closed means alone. If no crepitus is felt with a reduction maneuver, we must assume that there is some interposed soft tissue at the fracture site, which may prevent the bone ends from ever finding one another and may potentially lead to nonunion. Soft tissue interposition was thought to be a major contributing factor in the formation of clavicular nonunion in a study by Manske and Szabo. They found that one of the fragments is frequently impaled in the trapezius muscle.[29] In several acute fractures treated with open reduction and intramedullary fixation, and in one malunion, we have found that one of the supraclavicular nerves was entrapped in the fracture site. From personal experience, we can confirm that soft tissue interposition is real and does occur in clavicle fractures. In higher-energy fracture patterns, we have found soft tissue interposition to be a very frequent finding. Others have reported that this is uncommon, however.[21] A reduction maneuver is also indicated when there is evidence of neurovascular compromise that is persistent or progressive, and in cases in which the overlying skin is in jeopardy of necrosis. Closed or Open Reduction and Internal Fixation

The methods available include soft tissue and suture procedures alone (SC joint suturing), intramedullary devices,[4] [25] [32] [35] [36] [39] [40] [43] [53] plate fixation,[22] [34] external fixation, and, for distal clavicle fractures, CC screw fixation.[2A] The indications for

operative treatment of acute clavicle fractures include the following: Open fractures Medial clavicle fractures, including growth plate injuries with posterior displacement that is impinging on vital structures or causing symptoms such as thoracic outlet syndrome, difficulty swallowing, difficulty breathing, and brachial plexopathy Neurovascular compromise requiring immediate exploration, or that is progressive or unresponsive to closed reduction maneuvers. Even if closed reduction relieves the symptoms, these patients must be closely monitored because reduction is very difficult to maintain and redisplacement is common Displacement severe enough to tent the skin and impair its blood flow, possibly leading to necrosis. This may be improved by a closed reduction maneuver, which may make the problem less urgent. Even if this is initially successful, this skin must be watched closely for signs of impending necrosis because the reduction is very difficult to maintain, and re-displacement is common The so-called floating shoulder combination of fractures Displaced, comminuted, and shortened fractures of the middle third of the clavicle, particularly in the dominant extremity of the throwing athlete Displaced midclavicle fractures in patients who routinely wear a backpack or shoulder harness directly over the midclavicle because malunion or abundant callus in this region can cause disability Patients unable to tolerate closed treatment, such as patients with Parkinson's disease, seizures, or other ataxias[53] Distal clavicle fractures that are completely displaced and irreducible with intact CC ligaments Displaced distal clavicle fractures with rupture of the CC ligaments Multi-trauma patients, especially those with lower extremity fractures that require use of the upper extremities for transfers and crutch ambulation The very rare patient who for some good reason is unable to tolerate the cosmetically unappealing lump of the healed clavicle, and is willing to trade a scar for a lump (We would also modify this trade to include the scar and the inherent risks of surgery)

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Treatment Philosophy Medial Clavicle Fractures

These fractures are rare, accounting for about 5% of all clavicle fractures in adults. As was stated previously, the medial clavicular physis is the last in the body to close, and this occurs between ages 22 and 25.[20] [52] Many medial clavicle fractures are therefore physeal injuries, which inherently have great healing potential. Physeal arrest is not a concern. Even in cases in which the medial physis has already fused, these fractures heal well. Anterior displacement, even if complete, is not a concern. The great majority of these fractures are best treated nonoperatively with figure-of-eight bandages or a sling. Healing can be expected to be rapid with a very low risk for nonunion. This being said, it must be emphasized that accurate diagnosis is important for several reasons. These injuries can be misdiagnosed as sternoclavicular joint injuries, which can confound treatment. Medial clavicle fractures that include extension

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into the sternoclavicular articulation carry some risk of post-traumatic arthrosis. This is something to consider when one is counseling the patient about his or her injury. The medial clavicle fracture that can be very problematic is that with posterior displacement severe enough to impinge on the vital structures at the root of the neck. Patients with complaints of difficulty swallowing or breathing, or with any neurovascular compromise, will require operative reduction of the fracture. Furthermore, patients without symptoms, but with documented CT scan evidence of impingement of the fragments on vital structures, should be considered for operative reduction. Reduction maneuvers or a towel clip reduction should not be performed in the clinic or the emergency room unless the posterior position of the fragment is causing an airway or

hemodynamic emergency. This reduction must be performed in the operating room with the patient under general anesthesia. The chest must be prepared as for a sternotomy, and a thoracic surgeon must be available in case a vascular problem develops. A towel clip can be used to grasp the distal fragment and pull it forward to the proximal fragment. Traction on the upper extremity, or a towel placed between the shoulder blades, may assist the clinician in unlocking the fragments and allowing reduction. The reduction is generally stable. In cases in which the reduction is unstable or unobtainable, open reduction will be necessary. Removing interposed soft tissue will likely allow reduction and should stabilize the fracture. Fixation may be obtainable with heavy suture and repair of the soft tissue envelope. In some cases, plate and screw fixation may be necessary. In these cases, the vital structure beneath the clavicle must be protected with a curved Crego or other such retractor to prevent plunging with the drill. The clinician must use all available will power to resist pinning across the fracture and into the sternum. The literature includes many reports of broken hardware that migrated to the mediastinum, to the neck, and even into the great vessels and heart.[41] Middle Third Fractures

The great majority of middle third fractures or shaft fractures of the clavicle can be managed best by closed means, with either a figure-of-eight splint or a sling. One must keep in mind, however, that what is seen clinically and on the original injury films is likely to foretell the ultimate result after healing has occurred. Reduction maneuvers and figure-of-eight bandages have not been conclusively shown to hold a reduction or improve cosmesis in patients with these fractures. A fracture that is completely displaced or severely shortened is likely to stay in this position or revert to this position despite the physician's best efforts at reduction and use of the tightest figure-of-eight bandage. As was stated previously, an attempt at reduction can be useful in several circumstances. In cases in which there is acute neurovascular compromise to the extremity as a result of the clavicle fracture, an attempt at reduction may be helpful. These cases are rare, but when they occur, a reduction maneuver can turn an emergency into just urgency. This may give the clinician the necessary time for planning or for calling in appropriate equipment. Another case for which a reduction maneuver may be useful is that of the completely displaced middle third fracture. This fracture is at greater risk for nonunion according to Thompson and others.[2B] [14A] [50] Crepitus felt with a reduction maneuver would suggest that the fracture fragments are at least in the same area and are less likely to include interposed muscle or other soft tissues. If crepitus is felt and the fracture has no other indications for operative intervention, one may wish to attempt nonoperative treatment of this fracture, realizing that there may still be an increased risk of nonunion. If no crepitus is felt, one must assume that this is because something is interposed between the fracture fragments. This raises concern for the development of a nonunion. The problematic fractures of the midshaft of the clavicle are generally those that have absorbed greater energy. In our experience, these higher-energy fractures tend to have a remarkably consistent pattern. They are generally shortened and comminuted with a butterfly fragment that is consistently inferior. Soft tissue injury and stripping are usually significant, and greater instability is frequent. All of these things raise the risk of

nonunion in any fractured bone. We believe that these fractures are best treated with open reduction and internal fixation. For this, we have essentially two optionsplate and screw fixation and intramedullary fixation. For plate and screw fixation, one must use dynamic compression or reconstructive plates. The forces across this bone are too great to tolerate semitubular or one-third tubular plates. Even though they fit better, these will fail. It is best to obtain at least three screws for each fragment, and preferably six cortices. The exposure must be large enough to allow placement of all these screws and, much more importantly, the exposure must allow protection of the structures directly beneath the clavicle. This will require the placement of a curved Crego retractor or other protective device beneath the clavicle while the holes are drilled. Although physicians are unlikely to admit it, even the best among us occasionally plunge with the drill. Plunging in this region is flirting with disaster. Most catastrophes occur when physicians fail to protect themselves from themselves. Although plate and screw fixation can provide good stability, it requires significant soft tissue stripping. Besides leaving an unsightly scar, this soft tissue stripping may compromise clavicle healing because most if not all of the blood supply to the clavicle is periosteal. Furthermore, if the patient is displeased with the feel of a subcutaneous plate or wishes to have the hardware removed for any other reason, a second invasive procedure is required that leaves the patient with multiple stress risers in the clavicle. This may place active patients at risk for subsequent re-fracture. For most of these fractures, I prefer intramedullary fixation using a modified Hagie pin (DePuy AcroMed, Raynham, Mass). We believe this method to be superior for several reasons. The exposure necessary to place an intramedullary pin is significantly less than that needed to perform a formal open reduction and internal fixation with plates and screws. This limits further damage to the already decimated soft tissue envelope. The intramedullary pin allows for compression at the fracture site and load sharing, both of which have been advantageous in the healing of

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other long-bone fractures. The intramedullary pin is easily removable with the patient under local anesthesia. Intramedullary pins come in different sizes, allowing canal fill, which again has been shown to be advantageous in other fractures treated with intramedullary devices. Unlike plate and screw fixation, placement of the intramedullary pin does not require physicians to drill perpendicularly through the clavicle. This fact decreases the risk to neurovascular structures and obviates the need to strip the soft tissues to allow for protection of these structures. Removal of the pin can be accomplished in the clinic with the patient under local anesthesia; this procedure leaves the patient with only one stress riser in the metaphyseal posterior distal clavicle. We have never seen a subsequent re-fracture through this region.

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Technique for Intramedullary Pin Fixation

The operating room setup for this procedure is similar to that for other shoulder procedures. The patient is placed in the beach chair position on a table or shoulder positioner that allows penetration with a C-arm. The C-arm is positioned to obtain an unobstructed cephalic tilt AP view of the clavicle. Once it is confirmed that the view is appropriate, the C-arm can be removed for later use, or, as we now prefer to do, it can be draped into the field to allow easy visualization with less risk of contamination. The entire upper extremity is prepared and draped free. The clavicle, fracture site, and surrounding anatomy are drawn on the skin. The C-arm is used to locate the appropriate position for the incision, which is centered directly over the fracture site. The incision is 2 to 3 cm in length and is made in the normal skin creases around the neck. This is referred to as a necklace incision because the skin lines follow the same path as a necklace that is sitting on the neck. The subcutaneous tissues are divided with the electrocautery down to the platysma muscle, which is usually a well-defined layer. This layer is important because a branch of the supraclavicular nerves consistently lies directly beneath this layer and almost always right over the fracture site. The platysma is divided bluntly to expose the nerve, which is protected by blunt retraction. The fracture site is then opened and cleared of debris. A curved Crego elevator or a small bone clamp is useful for delivering the bone ends out of the incision. Care is taken to avoid stripping the butterfly fragment of soft tissue attachments. An appropriately sized long drill bit is then used to ream the canal of both the proximal and distal fragments. The average male canal can accommodate a 3.2-mm drill bit, whereas most female canals require a 2.5-mm drill bit. The C-arm is used during reaming to confirm that the drill is in the canal at all times. The modified Hagie pin system has different drills that correspond to the size of the pin chosen. The pins come in four diameters and one length. Most frequently, a medium or large pin gives the appropriate fit in males and older patients, whereas a small- or medium-sized pin is used for smaller and younger patients. The drill size that most closely approximates the canal size is chosen and is used to ream the canal of the proximal fragment under C-arm guidance. Because the butterfly fragment is routinely anterior and inferior, the drill will have a tendency to walk inferiorly and go under the proximal fragment rather than into the canal. The C-arm will help avoid this

problem. Allow the drill to seek the canal. During treatment of more medial fractures, the curvature of the clavicle may require that you drill slightly into the anterior cortex to allow enough length for the intramedullary pin. We avoid drilling completely through the anterior cortex because this can create a stress riser and can cause discomfort for the patient while the pin is in place. The lateral fragment is then again delivered into the wound. The lateral fragment medullary canal is then drilled with a drill bit of the same size. On the lateral fragment, the posterior cortex is most often intact, and the drill can be run along this cortex to find the canal. The drill is then allowed to seek out the canal. When the canal is visualized with the C-arm, the drill should exit the posterolateral cortex of the clavicle just above and slightly lateral to the conoid tubercle of the clavicle. If the C-arm is not used, the surgeon can place his finger at the posterolateral bend of the clavicle and then use his finger as an aiming point. The drill should not exit too far superiorly or inferiorly because this will compromise the chances of getting an anatomic reduction of the fracture with the pin once it is passed into the medial fragment. Both the medial and lateral fragments are tapped with an appropriately sized tap until all threads are in the fragment. This will facilitate later pin placement. A pin of the appropriate size is then placed in the drill chuck with the grips on the smooth tip of the pin only to avoid damage to the threaded portion. The side of the pin with the fine threads is then drilled into the canal of the lateral fragment, allowing the pin to seek the canal. The C-arm is used to confirm that the pin is in the canal at all times. Because of the curvature of the clavicle, the pin will exit just lateral to the conoid tubercle of the clavicle on the posterior aspect of the clavicle along the path previously drilled. The pin is driven posteriorly until it tents the skin near the spine of the scapula. A No. 15 blade scalpel is used to make about a 1-cm incision over the pin, and the pin tip is delivered out of this wound. Incidentally, a battery-powered reamer allows more control than a drill for this procedure because it is has low rpm and high torque. The chuck is then placed onto the smooth tip of the pin that is exiting posteriorly, again avoiding damage to the threads of the pin. The pin is then backed into the lateral fragment with just the smooth tip of the medial aspect of the pin protruding at the fracture site to allow reduction of the fracture. The pin can now be used to manipulate the lateral fragment and assist reduction. Manual traction on the upper extremity may also assist reduction. With the fracture held reduced, and under C-arm guidance, the pin is then driven antegrade across the fracture site and into the proximal fragment. This can be done with the reamer/drill or with a T-handle chuck. Because of its morphology, the fracture again will tend to push the pin inferiorly rather than allowing it to enter the canal. Prevent this by use of the C-arm. It should also be remembered that the weight of the arm pulls the distal fragment inferiorly, and it may become necessary to lift up on the arm to get the pin to pass into the medial fragment. Sometimes a Crego elevator can help force the pin into the

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canal of the medial fragment. All of the large threads must be placed across the fracture site. If the pins seems too tight to pass safely into the medial fragment, you may need to

widen the canal by toggling the drill bit in it, or if all else fails, choose the next smaller pin size. The fit should be snug, but the pin should be fairly easy to drive. Beware, because forcing too large a pin into the canal can result in explosion of the proximal fragment or, worse yet, shearing off of the pin in the bone, which can be very difficult to remove. With good reduction and fixation achieved, two nuts are then placed on the small, threaded end of the pin and tightened into position. A T-handle wrench provides for compression at the fracture site and fixes length. Overtightening of these nuts can strip them or shear the pin, so just snug them up. The excess pin is cut as close to the nuts as possible. The butterfly fragment can be laid in place or cerclaged with polydioxanone or other absorbable suture. The wounds are closed in layers. AP cephalic tilt and axillary lateral radiographs are obtained in the operating room to confirm position of the hardware and reduction. The patient is placed into a sling and swathe postoperatively for comfort. When comfortable, the patient may forego the sling. Activity is limited to lifting of no more than 5 pounds and abduction and forward flexion to no higher than 90 degrees. The intramedullary pin is removed at 10 to 12 weeks through the small posterior incision, usually under local anesthesia.

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Distal Clavicle Fractures

These fractures comprise a group with differing treatments and prognoses, depending on their location and displacement. In this section, we consider those fractures that involve or are distal to the conoid tubercle of the clavicle. This distinction is made because fractures that are medial to the conoid tubercle generally can be treated as middle third fractures are treated, but those lateral to the conoid present different concerns and treatment requirements. Obviously, this is so because of the presence of the CC ligaments and their effects on fracture stability. Nondisplaced fractures of the distal clavicle are best treated with a sling. As symptoms allow, the patient is weaned from the sling and is started on a shoulder rehabilitation program. The earliest return to sports activity generally occurs around 6 to 8 weeks after injury. In collision sports, extra padding or a fiberglass shell may be necessary to protect the distal clavicle. Even though he feels good-to-go, the patient must be advised that early return to sports is a compromise that involves some risk of re-fracture or displacement. Nondisplaced fractures that involve the AC joint deserve special note. Their treatment is the same as that provided for nondisplaced fractures of the distal clavicle; however, the patient must be informed that the involvement of the joint increases the likelihood of chronic pain and post-traumatic arthrosis of the AC joint. If this occurs, a later surgical procedure may be required to alleviate these symptoms; the patient needs to know this fact. The treatment of displaced distal clavicle fractures hinges on the integrity of the CC and AC ligaments. More precisely, the treatment generally depends on whether or not the conoid portion of the CC ligaments is still attached to the medial fragment of the clavicle. If the conoid remains attached to the medial fragment, this strong ligament will maintain the CC interval, and thereby will help prevent large displacement at the fracture site. In fact, it is rare to have a markedly displaced distal clavicle fracture if the conoid ligament

remains intact and attached to the medial fragment of the clavicle. The ligamentous stability does not easily allow displacement to occur. Therefore, the first question you have to ask yourself is: Is some portion of the CC ligaments (i.e., at least the conoid) still attached to the medial clavicular fragment? When the answer to this question is yes, the CC interval will be maintained. This means that the ligamentous/bony anatomy will help prevent the distal clavicular fragment from undergoing marked displacement. The fracture fragments should remain relatively close to one another, and this fracture can be expected to heal with sling treatment. When the answer to this question is no, the distal clavicle fragment with the attached scapula (through AC and CC ligaments) will droop inferiorly and medially under the weight of the attached upper extremity. The medial clavicular fragment, now unencumbered, will elevate away from the distal fragment. This raises the risk for nonunion and chronic medial rotational instability of the shoulder through the fracture site. Essentially, two possibilities exist. Both conoid and trapezoid can be attached to the distal fragment with the fracture occurring just medial to them, or the trapezoid ligament can be attached to the distal fragment and the conoid ruptured. When the conoid is detached from the medial fragment, this allows medial rotational instability of the shoulder. Whether this occurs completely through the fracture site, as when both ligaments are attached to the distal fragment, or partially through the fracture site and partially through a torn conoid ligament, does not make a difference. The overall effect is the same, and the requisite treatment is the same. This fracture will require operative fixation to increase the odds of healing. Several clues can be used to ascertain the integrity of the conoid ligament. Often, rupture of the conoid ligament is obvious on radiograph by occurrence of the fracture lateral to the conoid tubercle, with marked increase in the CC interval, and marked fracture displacement. With fractures occurring at or very near the conoid tubercle, this call sometimes becomes more difficult. When both CC ligaments are attached to the distal fragment, the fracture line is usually oblique, with the CC interval maintained with the lateral fragment. Fracture displacement is usually wide. In equivocal cases, medial rotational instability at the fracture site can be demonstrated by a cross-body adduction view of the shoulder. This stress radiograph will accentuate conoid ligament detachment from the medial clavicular fragment. Generally, an increase in fracture displacement, an increase in the CC interval, and marked underriding of the distal fragment are seen beneath the proximal fragment. This is medial rotational instability occurring through the fracture site. Failure of this to occur suggests that the conoid ligament is still attached to the medial fragment of the clavicle. A good MRI scan will also clearly demonstrate the CC ligaments. For the unstable variety of this fracture, we generally

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prefer placement of a CC screw, which will reduce the CC interval and thereby bring the fragments into close proximity to allow healing. Other options include plate fixation, CC suture circlage, and K-wire fixation. Plate fixation of this fracture can be problematic.

The required exposure is relatively large. The distal fragment is small, and the AC joint limits the length of plate that can be used. A small T-plate sometimes allows enough screws in the distal fragment for adequate fixation. K-wire fixation down the intramedullary canal of the distal clavicle can create problems as well. The forces on this area are large, and hardware breakage is quite possible. Migration of broken hardware within this region is well documented, and we prefer to avoid this possibility. The use of a CC screw is limited by comminution that extends medial to the conoid tubercle. Comminution distal to the conoid tubercle is not a factor. The CC screw offers several advantages. The required exposure is small, and sometimes the fracture site does not even have to be opened. The fixation is solid, and under C-arm guidance, this procedure can be performed almost percutaneously. After fracture healing has occurred, the screw can be removed easily under local anesthesia, thereby avoiding breakage of the hardware.

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Technique for Coracoclavicular Screw Fixation

The beach chair position is required to obtain the necessary medial oblique view of the coracoid and clavicle. We use the Schlien shoulder table to facilitate the beach chair position, but any radiolucent table will suffice. The C-arm is positioned before the patient is prepared to confirm that the appropriate view is obtainable. The operating table must be rotated a full 90 degrees to the anesthesia equipment to allow enough room for the C-arm. The base of the machine is positioned at the head of the table, with the C-arm over the top of the shoulder. The receiver is placed as far medially as the bed will allow. Usually, the receiver is impacting the back of the bed in the beach chair position. The plane of the radiographic beam is perpendicular to the CC interval. The beam is thus directed from anterolateral to posteromedial. The view of the coracoid obtained in this way must be down the barrel of the coracoid, which produces a nearly perfect dense circle. The circle or target is the radiographic shadow of the combined cortical density of the shaft of the coracoid, with the intramedullary cancellous bone as the clear central region of the target. This target view with a nearly perfect circle must be obtained before proceeding. If it cannot be obtained, the C-arm or the table must be readjusted to provide this view. More often than not, the base of the receiver is not far enough medially. This view will allow placement of the CC screw in perfect position every time. Acceptance of anything less risks malposition of the screw and fixation failure. The shoulder and upper extremity are prepared in standard fashion, with the upper extremity draped free to allow full motion if necessary. The local anatomy is drawn on the skin, including the clavicle, acromion, AC joint, and coracoid. The C-arm is brought into position to provide the target view of the coracoid. This is the important step. The clinician who spends time here will be repaid with the ease of the rest of the procedure. The site for the skin incision is located under C-arm guidance. The appropriate position for this is one that overlies the clavicle just medial to the conoid tubercle on the inferior surface of the clavicle. The incision extends from the posterior border of the clavicle to its anterior border. The anterior and posterior borders of the clavicle are identified using subperiosteal dissection. We prefer to use the Rockwood screw set marketed by DePuy AcroMed. The 3/16 (large) drill bit is centered on the dorsal surface of the medial

fragment of the clavicle just medial to the conoid tubercle. The drill tip is aimed toward the base of the coracoid, which usually requires that the drill hand be up against the ipsilateral side of the patient's head. Both cortices of the clavicle are drilled, and the hole is then widened by toggling of the drill in the hole. This allows some latitude with the small (9/64) drill bit to allow placement in the exact center of the coracoid base. The 9/64 (small) drill bit is then passed through the clavicular drill hole and is used to palpate the base of the coracoid. The tip of the drill bit is used to locate the medial and lateral borders of the coracoid. These positions are confirmed with the C-arm. The drill bit is then positioned at the top of the target circle so as to pierce the center of the target from superior to inferior. With the fracture held in a reduced position, the first cortex is drilled. This is usually relatively weak bone. The intramedullary bone provides no resistance to the drill. The inferior cortex is solid bone and provides good tactile and auditory feedback at the point of penetration. High drill rpm and good control help prevent plunging. The upper extremity should be in a relaxed, adducted position across the front of the abdomen to take the tension off the neurovascular structures and give maximal distance between them and the base of the coracoid. Drill penetration of the inferior cortex is confirmed on C-arm. A depth gauge is used to measure screw length and to confirm the angle of screw placement. Usually, a 40- or 45-mm screw with a washer is appropriate. The screw is passed through the clavicle; then the screw tip should be placed at the top of the target to allow the nipple of the screw to seat inside the drill hole. This is felt and then confirmed using the C-arm. The screw is then tightened into position, piercing the center of the target under C-arm guidance. The inferior cortex must be engaged to obtain solid fixation. The CC interval can be reduced by bringing the shoulder girdle and arm up to the medial clavicle fragment, which allows ease of placement of the screw. It is important to never overreduce the CC interval because this can result in unrelenting pain until the screw is loosened a turn or two. We have also successfully used this same procedure for nonunion of a distal clavicle fracture. Because the fracture occurs in a more cancellous portion of the clavicle, good healing can usually be obtained once the nonunion site is curetted and bone grafted. Postoperatively, the patient is placed into a sling and swathe, with later transition to a sling for comfort only. The patient is allowed to perform activities of daily living with the extremity and to lift up to 5 pounds. Motion is limited to that below 90 degrees of abduction (i.e., no overhead activity). When the fracture shows radiographic

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healing, the screw is removed, generally with the patient under local anesthesia.

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Rehabilitation after Clavicle Fracture

Rehabilitation following clavicle fracture in the athlete is started almost immediately, regardless of the treatment modality used. Assuming there are no associated injuries, the athlete is allowed to continue lower body strengthening exercises as before the injury occurred. Aerobic conditioning on an exercise bike or other stationary apparatus is encouraged. The athlete is allowed to immediately perform wrist and elbow range of motion exercise, as well as grip strength maintenance exercise. Running is discouraged until the acute pain has resolved. As soon as the acute pain resolves, the athlete is started on gentle pendulum exercises, as well as isometric strengthening of the rotator cuff, deltoid, biceps, and triceps. Normal use of the ipsilateral hand for activities of daily living is also encouraged. Generally, active range of motion is limited to less than 90 degrees of forward flexion or abduction if any operative fixation has been performed. This helps limit the initial stresses on the hardware. In the absence of hardware, the patient is allowed to advance active range of motion within the arc of pain tolerance. If no operative fixation is performed, full, active range of motion is allowed when the athlete is completely pain-free, which usually occurs after between 4 and 6 weeks of healing. When the athlete has achieved a full, pain-free range of motion, and there is radiographic evidence of callus, resistive exercises may be instituted. When the athlete has attained near-normal strength in the injured upper extremity, he or she may be started on a plyometric program. This is particularly useful in the throwing athlete.

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Return to Play Criteria

The criteria for return to sport activities are always controversial and essentially equate to a judgment call by the treating orthopaedist. This decision may be affected by several factors, including the personality of the athlete, the specific fracture, the sport, the position played, the level of sports competition, the level of compensation, and the needs of the team. Occasionally, these factors are sometimes in direct opposition to common sense. The treating surgeon must realize that this decision is ultimately a compromise, and all compromises come with inherent risks. The athlete, coaches, and team may be willing to take risks that the orthopaedist is unwilling to shoulder. It is our job to protect the athlete from these competing forces just long enough to allow adequate healing at the clavicle fracture. The key word here is adequate. Physicians know that fracture remodeling is a long and ongoing process that takes 9 months to 1 year or longer. In theory, the risk of re-fracture is increased until the bone remodels completely. Stopping sports participation for a year is obviously overkill. The clinician must make the athlete understand that returning to sports earlier than recommended is a compromise, and that by doing so, he or she increases the risk of re-injury. The goal is using caution to allow adequate healing without providing overprotection. For the noncontact athlete, return to sports may be allowed when there is a painless, full, active range of motion; near-normal strength; and evidence of bridging callus. This usually occurs about 6 weeks after fracture. Contact athletes, particularly those involved in collision sports, are obviously at greater risk for re-fracture. The position played and the type of fracture incurred will also affect this risk. Even if the physician cannot allow a return to full participation, frequently he or she can allow the athlete to return to practice with the team on a noncontact basis. This allows the athlete to remain at least mentally in synch with the team. This is generally allowed when the athlete meets the same criteria as those required for the noncontact athlete. The team trainer can be extremely valuable in keeping the athlete from doing too much too soon because he or she is with the team every day at practice. Generally, between 2 and 3 months after injury would be the earliest recommended time for return to contact sports. In football, extra protection at times can be afforded by use of donut pads or fabrication of a fiberglass shoulder

shell to dissipate impact forces to the clavicle. If the fracture required operative fixation of any type, generally the season is over for this athlete.

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References 1.

Abbot LC, Lucas DB: Function of the clavicle. Its surgical significance. Ann Surg 140:583-599, 1954.

Anderson K, Jensen P, Lauritzen J: Treatment of clavicular fractures. Figure of eight bandage vs a simple sling. Acta Orthop Scand 57:71-74, 1987. 2.

Ballmer FT, Gerber C: Coracoclavicular screw fixation for unstable fractures of the distal clavicle. A report of five cases. J Bone Joint Surg Br 73:291-294, 1991. 2A.

Basamania CJ: Claviculopasty and intramedullary fixation of malunited clavicle fractures. Presented at the International Congress of Shoulder Surgery, 1999, Sydney, Australia. 2B.

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Berkheiser EJ: Old ununited clavicular fractures in the adult. Surg Gynecol Obstet 64:1064-1072, 1937.

Breck L: Partially threaded round pins with oversized threads for intramedullary fixation of the clavicle and the forearm bones. Clin Orthop 11:227-229, 1958. 4.

Campbell E, Howard WB, Breklund CW: Delayed brachial plexus palsy due to ununited fracture of the clavicle. JAMA 139:91-92, 1949. 5.

6.

Copeland SM: Total resection of the clavicle. Am J Surg 72:280-281, 1946.

Cumming WA: Neonatal skeletal fractures. Birth trauma, or child abuse? J Can Assoc Radiol 30:30-33, 1979. 7.

Dameron TB, Rockwood CA: Fractures of the shaft of the clavicle. In Rockwood CA, Wilkins KE, King RE (eds): Fractures in Children. Philadelphia, JB Lippincott, 1984, pp 608-624. 8.

9.

Depalma A: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.

Dugdale TW, Fulkerson JB: Pneumothorax complicating a closed fracture of the clavicle. A case report. Clin Orthop 221:212-214, 1987. 10.

Echtermeyer V, Zwipp H, Oestern HJ: Fehler und gefahren in der behandlung der fracturen und pseudarthrosen des schlusselbeins. Langenbecks Arch Chir 364:351-354, 1984. 11.

Edvardsen P, Odegard O: Treatment of posttraumatic clavicular pseudoarthrosis. Acta Orthop Scand 48:456-457, 1977. 12.

13.

Elliot AC: Tripartite injury of the clavicle. A case report. S Afr Med J 70:115, 1986.

13A. Eskola

A, Vainionpaa S, Myllynen P, et al: Outcome of clavicular fracture in 89 patients. Arch Orthop Trauma Surg 105:337-338, 1986.

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Grazier KL, Holbrook TL, Kelsey JL, Stauffer RN: The Frequency of Occurrence, Impact, and Cost of Musculoskeletal Conditions in the United States. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1984. 14.

14A. Hill

JM, McGuire MH, Crosby LA: Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J Bone Joint Surg Br 79:537-539, 1997. Howard FM, Schafer SJ: Injuries to the clavicle with neurovascular complications. A study of fourteen cases. J Bone Joint Surg Am 47:1335-1346, 1965. 15.

Hoyer HE, Kindt R, Lippert H: Zur Biomechanik der menschlichen Clavicula. Z Orthop Ihre Grenzgeb 118:915-922, 1980. 16.

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Inman VT, Saunders JB: Observation in the function of the clavicle. Clif Med 65:158-165, 1946.

Jablon M, Sutker A, Post M: Irreducible fractures of the middle third of the clavicle. J Bone Joint Surg Am 61:296-298, 1979. 18.

19.

Javid H: Vascular injuries of the neck. Clin Orthop 28:70-78, 1963.

Jit I, Kulkrani M: Times of appearance and fusion of epiphysis at the medial end of the clavicle. Indian J Med Res 64:773-792, 1976. 20.

21.

Jupiter JB, Leffert RD: Nonunion of the clavicle. J Bone Joint Surg Am 69:753-760, 1987.

22.

Khan MAA, Lucas HK: Plating of fractures of the middle third of the clavicle. Injury 9:263-267, 1978.

Kay SP, Eckardt JJ: Brachial plexus palsy secondary to clavicular nonunion. A case report and literature survey. Clin Orthop 206:219-222, 1986. 23.

Klier I, Mayor PB: Laceration of the innominate internal jugular venous junction. Rare complication of fracture of the clavicle. Orthop Rev 10:81-82, 1981. 24.

Lengua F, Nuss JM, Lechner R, et al: The treatment of fracture of the clavicle by closed mediolateral pinning [French]. Rev Chir Orthop 73:377-380, 1987. 25.

Lim E, Day LJ: Subclavian vein thrombosis following fracture of the clavicle. A case report. Orthopedics 10:349-351, 1987. 26.

27.

Ljunggren AE: Clavicular function. Acta Orthop Scand 50:261-268, 1979.

Luskin R, Weiss CA, Winer J: The role of the subclavius muscle in the subclavian vein syndrome (costoclavicular syndrome) following fracture of the clavicle. Clin Orthop 54:75-84, 1967. 28.

28A. Lyons

FA, Rockwood CA: Current concepts review: Migration of pins used in operations on the shoulder. J Bone Joint Surg Am 72:1262-1267, 1990. Manske DJ, Szabo RM: The operative treatment of mid-shaft clavicular non-unions. J Bone Joint Surg Am 67:1367-1371, 1985. 29.

Matry C: Fracture de la clavicule gauche au tiers interne. Blessure de la vein sour-claviere. Osteosynthese Bull Mem Soc Nat Chir 58:75-78, 1932. 30.

McCandless DN, Mowbray M: Treatment of displaced fractures of the clavicle. Sling vs figure of eight bandage. Practitioner 223:266-267, 1979. 31.

32.

Moore TO: Internal pin fixation for fracture of the clavicle. Am J Surg 17:580-583, 1951.

33.

Moseley HF: Shoulder Lesions. Edinburgh, Churchill Livingstone, 1972, pp 207-235.

34.

Mueller ME, Allgower N, Willenegger H: Manual of Internal Fixation. New York, Springer-Verlag, 1970.

35.

Murray G: A method of fixation for fracture of the clavicle. J Bone Joint Surg 22:616-620, 1940.

Neviaser RJ, Neviaser JS, Neviaser TJ: A simple technique for internal fixation of the clavicle. Clin Orthop 109:103-107, 1975. 36.

Neer CS II: Fractures of the clavicle. In Rockwood CA, Green DP (eds): Fractures in Adults. Philadelphia, JB Lippincott, 1984, pp 707-713. 37.

Ogden JA, Conologue GJ, Bronson NL: Radiology of postnatal skeletal development. III. The clavicle. Skeletal Radiol 4:196-203, 1979. 38.

Paffen PJ, Jansen EW: Surgical treatment of clavicular fractures with Kirschner wires. A comparative study. Arch Chir Neerl 30:43-53, 1978. 39.

40.

Perry B: An improved clavicular pin. Am J Surg 112:142-144, 1966.

41.

Rockwood CA: Personal communications, 1993-1997.

42.

Rowe CR: An atlas of anatomy and treatment of mid-clavicular fractures. Clin Orthop 58:29-42, 1968.

Rush LV, Rush HL: Technique of longitudinal pin fixation in fractures of the clavicle and jaw. Mississippi Doctor 27:332, 1949. 43.

44.

Sakellarides H: Pseudoarthrosis of the clavicle. J Bone Joint Surg Am 43:130-138, 1961.

45.

Sankarankutty M, Turner BW: Fractures of the clavicle. Injury 7:101-106, 1975.

Silloway KA, Mclaughlin RE, Edlichy RC, et al: Clavicular fractures and acromioclavicular joint injuries in lacrosse: Preventable injuries. J Emerg Med 3:117-121, 1985. 46.

47.

Spar I: Total clavulectomy for pathologic fractures. Clin Orthop 129:236-237, 1977.

Stanley D, Trowbridge EA, Norris SH: The mechanism of clavicular fracture. J Bone Joint Surg Br 70:461-464, 1988. 48.

49.

Tachdjian MO: Pediatric Orthopaedics. Philadelphia, WB Saunders, 1972.

Thompson JS: Classification of clavicle fractures has an impact on operative indications [abstract]. Proceedings of the Fourth International Conference on Surgery of the Shoulder, 1989, New York. 50.

Tse DH, Slabaugh PB, Carlson PA: Injury to the axillary artery by a closed fracture of the clavicle. J Bone Joint Surg Am 62:1372-1373, 1980. 51.

Tyrnin AH: The Bohler clavicle splint in the treatment of clavicular injuries. J Bone Joint Surg 19:417-424, 1937. 52.

Zenni EJ Jr, Krieg JK, Rosen MJ: Open reduction and internal fixation of clavicular fractures. J Bone Joint Surg Am 63:147-151, 1981. 53.

Zanca P: Shoulder pain: Involvement of the acromioclavicular joint: Analysis of 1,000 cases. AJR Am J Roentgenol 112:493-506, 1971. 54.

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2. CLAVICLE INJURIES IN THE PEDIATRIC AND ADOLESCENT ATHLETE Edmund G Witkowski MD Carl J. Basamania MD Anatomy

The clavicle is the first bone in the body to ossify (usually by the fifth fetal week). It ossifies through a combination of intramembranous and endochondral ossification. Epiphyseal growth plates develop at both medial and lateral ends of the bone, but, much like the distal end of the femur and the proximal end of the humerus, it is the medial ossification center that is responsible for the majority of the longitudinal growth of the bone (approximately 80%).[38] The medial ossification center first appears on radiograph between the ages of 12 and 19 years. This physis does not fuse until well into young adulthood (between ages 22 and 25 years).[20] [56] This is important to remember because many medial clavicle fractures and sternoclavicular injuries in children and young adults are actually physeal injuries. Although little growth occurs at the lateral end of the clavicle, one should keep in mind that acromioclavicular (AC) injuries in children and young adults also represent Salter-Harris type I and II injuries, although true AC injuries can occur in older children. The periosteum of the lateral clavicle is quite thick, and the coracoclavicular (CC) ligaments are strongly attached to this periosteum. In children up to about 16 years of age, most distal clavicle injuries are really sleeve avulsion-type injuries with the lateral clavicle actually ripping out of the periosteal sleeve. Because of the strong attachment of the

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AC and CC ligaments to the periosteal sleeve, what appears as an AC separation or dislocation in the patient is actually a lateral clavicle physeal fracture. The clavicle is S-shaped with a flat cross section laterally, a tubular section in the middle, and a more oblong cross section at the most medial aspect. It is firmly anchored at both ends by very strong capsular ligamentous attachments, as well as by extra-articular ligaments that attach the clavicle to the first rib, the sternum, and the scapula via the coracoid. Proximally, the clavicle is supported by muscles, including the sternocleidomastoid, the pectoralis major, and the subclavius. Distally, the clavicle is also supported by muscular attachments to the deltoid, and by the trapezius. The middle section of the clavicle is relatively unsupported by muscular or ligamentous attachments and is also the transition point between the flatter cross section laterally and the more tubular cross section medially.[27] This area, just distal to the subclavius muscle insertion, is mechanically the weakest point.[3] [16] [18] [27] [37] This is likely the reason that most fractures of the clavicle occur exactly in this area with uncanny regularity. Another possible explanation for the high incidence of fractures in this area is that, because of the S shape of the clavicle, axial load forces have to virtually take a right turn at the midpoint. This creates very high tensile forces along the anterior midcortex of the clavicle. The superior surface of the clavicle is essentially subcutaneous over its course, with only the thin platysma providing any muscular coverage, and then only to the inner two thirds of the bone. The supraclavicular nerves, which provide sensation to the overlying skin, are consistently found just deep to the platysma muscle layer. These nerves have been known to cause painful neuroma when damaged by fracture shards or iatrogenic injury. The middle and inner thirds of the clavicle have a thick cross section and a well-defined medullary canal that provides bony protection for the underlying subclavian artery and vein, as well as the cords of the brachial plexus. These structures are further protected by a dense fascial layer lying in front of them that is composed of the clavipectoral fascia and its extensions. This layer begins on the clavicle, envelops the subclavius muscle, and then unites to form a single layer before enveloping the pectoralis minor muscle. This layer thus forms a wall between the clavicle and the chest wall, behind which the important neurovascular structures are found. The neurovascular structures traverse the space between the inferior surface of the clavicle and the superior surface of the first rib, called the costoclavicular space. This space is relatively small and is well surrounded by bony structures. This sword is indeed double-edged in that the bony structure provides great protection for the underlying structures. In the event of an injury to one of the bones, however, this tight space allows little extra room for these same important structures. Because of its anatomic position at the most narrow region of the costoclavicular space, the medial cord of the brachial plexus, which provides the majority of nervous tissue to the ulnar nerve, is most at risk. Direct trauma by sharp fracture ends, clavicular nonunion, clavicular malunion, or healing with exuberant callus can place any of the structures in the costoclavicular space at risk, but the most commonly affected are the medial cord and the ulnar nerve.[3] [5] [23] [28] [44] The most medial portion of the clavicle lies anterior to the root of the internal jugular vessels and is near the trachea and esophagus. These structures are potential sites of injury or compression with fractures of the medial growth plate of the clavicle or sternoclavicular fractures/dislocations. Both the AC and sternoclavicular joints are diarthrodial joints; an intra-articular disk or

meniscus covers the joint surfaces of both. Both of these joints have strong ligamentous sleeves that are contiguous with the joint capsules. Unlike the AC joint, which allows only about 10 degrees of rotation about the long axis of the clavicle, the sternoclavicular joint allows for considerable motion, with approximately 30 to 35 degrees of movement in the horizontal and vertical planes and 40 to 50 degrees of rotation along the axial plane of the clavicle.

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Biomechanics and Function

The clavicle provides the only bony link between the thorax and the entire upper extremity. In the upright, resting position, the clavicle is under constant bending load from the force of gravity relentlessly pulling down on the combined mass of the upper extremity and any load carried therein. Structurally, the clavicle can be thought of as analogous to the wing of an aircraft parked on the ramp, with the weight of the wing and engines causing the wing to droop under the load. The wing is firmly anchored to the fuselage centrally; likewise, it is firmly attached to the load of the engines distally. If the wing is disrupted anywhere along its length, the weight of the distal unsupported portion with its attached engines will fall under the force of gravity. The central portion of the wing, now set free of its load, will recoil and elevate to a new resting position consummate with current load configuration. Disruption of the middle third of the clavicle, likewise, will result in depression of the distal segment with the attached upper extremity. The medial segment, when released from its load, will elevate. On the question of whether the distal fragment is depressed or the proximal fragment elevated, the answer is clearly yes to both questions. Resting muscular tone modifies this basic mechanical description. The pull of the sternocleidomastoid pulls the proximal fragment superiorly and posteriorly. The pectoralis major muscle causes shortening at the fracture site and medial rotation of both the distal segment and the attached upper extremity through its attachments and action on the proximal humerus. The clavicle can be regarded as the force multiplier for the upper extremity for two main reasons. First, it provides stability to the arm by supplying a firmly attached bone linkage to the axial skeleton. Second, and perhaps more importantly, the clavicle provides a fixed-length strut through which the muscles attached to the shoulder girdle can generate and transmit large forces to the upper extremity. The clavicle thus enhances the power and stability of the upper extremity through force transmission from the axial skeleton to the extremity. This multiplication of force and stability is especially important in movements above shoulder level.[1] [33] This force multiplication role is most important in the movements of the overhead-throwing athlete.

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Clavicular disruption anywhere along its length will affect a patient's ability to generate and transmit forces to the upper extremity. Congenital absence of the clavicle, as occurs in cleidocranial dysostosis, may result in some weakness in the support of overhead loads.[17] It is known that excision of the clavicle results in drooping of the shoulder girdle anteriorly and medially. These patients have weakness and pain that can be disabling. [41] [47] Significant shortening of the clavicle, as occurs in malunion, can result in a vague feeling of weakness in the shoulder, especially during overhead activity.[56] This effect can be measured through strength testing of the pectoralis major muscle in patients with shortened malunion of the clavicle. The measurable weakness in this muscle group is likely attributable to the decreased distance between the origin and the insertion of the muscle. Because it is known that a muscle has maximum effectiveness within a range of fiber length (according to Blick's curve), it may be surmised that shortening beyond a certain point will begin to manifest as weakness in the muscle group. In addition, there can be a significant change in the orientation of the glenohumeral joint with a clavicle malunion. Clavicle malunions represent fixed or static anteromedial displacements of the shoulder, whereas clavicle nonunions are more like AC separations in that they are more dynamic. The key question is, How much shortening is too much? Some authors have suggested that as much as 15 mm of shortening can lead to poor long-term results and patient dissatisfaction. [56] Nonunion of a clavicle fracture can add another variable to the equation because the clavicle can be both short and unstable. The instability denies the shoulder girdle muscles the rigid post against which they generate their force, particularly in the overhead position. A muscle deprived of a stable post to pull against is unable to generate the magnitude of force required for most activities. A similar situation occurs in the case of chronic severe instability of the AC joint. The problem is essentially the same, although at a slightly different location. Disruption of the CC and AC ligaments allows the shoulder girdle to rotate anteromedially beneath the distal clavicle. Patients complain of vague shoulder weakness and pain.

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Classification of Fractures

Several classifications of clavicle fractures are available, from the simple to the highly comprehensive. All of these classifications are more useful for academic comparison of fractures than for treatment decision-making. In the following sections, we discuss our treatment philosophy by region of injury, as well as methods of treatment at our disposal for these specific regions. The reader is encouraged to consult one of the many fine published classification systems for a more comprehensive classification.[37] [56]

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Mechanism of Injury

Several large studies of clavicle fractures detailing the apparent mechanism of injury have been published.[9] [45] [46] [48] In the vast majority of these fractures, the reported mechanism resulted from a fall onto the point of the shoulder or a lateral blow to the shoulder. A small percentage of patients recalled a fall onto the outstretched hand. [45] [48] Stanley and colleagues also suggested that even these patients may have fractured owing to a laterally applied force in that the shoulder may have been the next point of contact with the ground after the hand. [56] A direct blow to the bone inflicted by a hard instrument is another recognized mechanism of fracture, particularly in stick sports such as hockey and lacrosse, although in our experience, this is rather rare. A force applied to the top of the shoulder, driving the clavicle against the first rib, is another recognized mechanism of producing a middle third fracture. In practice, a majority of clavicle fractures have remarkably consistent injury patterns. Stanley and colleagues were able to produce fractures at every site along the length of the clavicle in cadaver specimens through application of a laterally directed force to the shoulder.[56] In most clavicle fractures caused by sports-related injuries, the bone generally fails to bend at the middle third, thereby producing an oblique fracture. As the energy of the fracture is increased, the most common pattern observed is a comminuted, shortened middle third fracture with a consistent inferior butterfly fragmentagain a failure in bending. The rarer lateral third clavicle fractures may occur in a manner more analogous to AC joint injuries, whereby force is applied superolaterally onto the point of the shoulder. The even rarer medial clavicle fracture may occur in a manner as suggested for injuries to the sternoclavicular joint, whereby a laterally directed force on the shoulder causes the shoulder to fold either anteriorly or posteriorly before fracture occurs. This mechanism is similar to that seen in SC separations. Stress fractures of the clavicle have been reported; however, these too are quite unusual.

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Assessment Patient History

In the awake and alert athlete, the history is usually quite clear in cases of clavicle fracture. A majority of the clavicle fractures seen in our clinic are secondary to bike accidents in which the patient is thrown off the bike and lands on the lateral aspect of the shoulder. In collision sports, the patient may report a high-energy collision or being injured at the bottom of a pile. In other sports, a common story is a collision with a fixed structure such as the wall, a post, the boards, or, most commonly, the ground. In stick sports, occasionally a patient reports a direct blow to the top of the clavicle inflicted by a stick. The athlete generally complains of pain at the site of fracture, and he or she cradles the injured extremity with the other uninjured arm. The patient may also complain of deformity of the collar bone, along with severe pain coinciding with attempts to actively lift the extremity. Occasionally, the patient may complain of persistent numbness or weakness in the affected upper extremity. An important consideration at this point is to elicit a history of previous stingers and the patient's assessment of whether this feels similar. Very rarely, a patient may complain of difficulty swallowing,

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fullness in the chest, difficulty breathing (not just pain with deep inspiration that can pull on the clavicle), or swelling in the entire affected upper extremity. Although rare, serious associated injuries to the great vessels, brachial plexus, or lungs and pleura can occur, and these may become life threatening.[10] Failure to recognize these injuries or delayed treatment can result in disaster. Physical Examination

Fortunately, clavicle fractures do not represent a diagnostic dilemma for the treating physician. A careful physical examination, however, actually involving laying hands on the patient, is important for several reasons. A careful examination can occasionally enable the clinician to make the diagnosis, but even if it does not, it can help in the identification of other associated injuries and in ruling out potentially serious problems that can be life threatening. A well-done physical examination will help to ensure that the clinician orders the appropriate radiographs or special studies to allow diagnosis of the disease. A complete neurovascular examination of the upper extremity takes very little time, and it can reveal uncommon brachial plexus or vascular injuries. The chest should be auscultated and the results documented. On visual inspection, the athlete with a clavicle fracture frequently has a notable edematous or ecchymotic area at the site of fracture. The affected extremity may droop both downward and forward if it is unsupported by the other arm. The site of fracture is tender to palpation, and crepitus may be felt. In fact, if crepitus is not felt, the possibility must be considered that interposed soft tissue may be impairing fracture healing. This is a more high-energy injury and requires a greater level of concern on the part of the clinician. The skin over the fracture site should be examined for open wounds or severe tenting. Tented, blanched skin can signify that the area is in jeopardy of necrosis. Lack of normal contour in the clavicle, or lack of or increased normal prominence of the sternoclavicular joint, can signify medial clavicle fracture or sternoclavicular disruption. Radiographic Evaluation

The appropriate radiographic evaluation will vary according to the location of the clavicle injury and the presence of any associated injuries. Potentially life-threatening associated injuries will obviously take precedence. In the unconscious athlete, a chest film and cervical spine films should be the first radiographs completed. A chest film should also be completed when the history or physical examination suggests possible thoracic injury. An abnormal vascular examination of the upper extremity may require an arteriogram.[15] [19] [24] [26] [30] [56] If an institution is incapable of performing these specialized studies or does not have the personnel to deal with a potential thoracic injury, transport to another facility must be considered. Delay can be deadly. Fractures of the medial third of the clavicle can be particularly difficult to image owing to the superposition of the ribs, sternum, spine, and mediastinum. Routine films should include an anteroposterior (AP) film centered on the sternoclavicular joints. Because an orthogonal view of the medial clavicle is difficult to obtain and nearly impossible to interpret, the serendipity view as popularized by Rockwood offers a reasonable alternative. This view is shot with the patient supine and the beam directed 40 degrees cephalad and centered on the sternoclavicular joints. The cassette must be wide enough to display both sternoclavicular joints and the majority of both clavicles to allow accurate interpretation. Although this view is most useful for sternoclavicular joint disruptions, it provides a fairly good image of the entire medial clavicle. Also, because many presumed sternoclavicular joint disruptions in patients younger than 25 years old are in reality physeal injuries, this view may differentiate between the diagnoses. If the diagnosis cannot be confirmed with these plain radiographs, a computed tomographic (CT) scan is necessary. The CT scan is currently the best available technique for

evaluating injuries to the medial clavicle and the sternoclavicular joint. It provides the true orthogonal views unobtainable with plain films. The scan must include both sternoclavicular joints and at least half of both clavicles to allow side-to-side comparison. Magnetic resonance imaging (MRI) may be useful, particularly in cases of diseased fractures and stress fractures, and in the identification of associated soft tissue injuries. Fractures of the middle third of the clavicle are more straightforward when it comes to imaging. Clavicular shaft fractures are generally easy to see when viewed in an AP projection centered on the midshaft of the clavicle. A 45-degree cephalic tilt film will more clearly delineate the fracture anatomy, amount of displacement, and extent of comminution. The typical pattern in a low-energy injury is an oblique fracture. The proximal fragment is displaced superiorly and posteriorly by the pull of the sternocleidomastoid muscle. The distal fragment is depressed by the weight of the upper extremity. If there is complete displacement of the fracture or comminution, the distal fragment is most commonly pulled medially by the pectoralis major, which underrides the proximal fragment. To evaluate the amount of shortening at the fracture site, we recommend an AP view of both clavicles on a wide cassette, including the sternum and the AC joints. This radiograph allows fairly accurate measurement of clavicular lengths. It should be pointed out, however, that clavicle fractures represent multiplanar deformities, and it is very difficult, if not impossible, to get an accurate estimate of shortening with the use of plain radiographs. Greater accuracy of measurement of clavicular shortening can be obtained with a CT scan, especially with three-dimensional (3D) reconstructions, including both clavicles from sternum to AC joint. This level of accuracy is rarely required. Care should be taken to avoid mistaking a congenital pseudarthrosis for an acute fracture or nonunion of the clavicle. The pseudarthrosis often has a benign history and typically causes minimal dysfunction. The ends of fragments often have a rounded or pencil-tip appearance. Although these occasionally can cause problems, most patients have full painless function.60 Fractures of the distal third of the clavicle are also more difficult to image. Standard radiographic technique for either the clavicular shaft or the shoulder overexposes the

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distal clavicle. Also, a straight AP view of the region obscures the distal clavicle and the AC joint in the overlap of the scapula and the acromion. Subtle fractures, and particularly intra-articular fractures, are inadequately displayed using standard techniques. Routine films of this region should include a 15-degree cephalic tilt AP view centered on the AC joint using soft tissue technique (Zanca view),59 as well as an axillary lateral view. To assess the ligaments about the AC joint, special views must be obtained. Traditionally, the integrity of the CC and AC ligaments is ascertained by use of weighted and unweighted views of both AC joints. When this technique is used, it is imperative that the weights be tied to the wrists rather than held in the hands; otherwise, splinting by the patient can reduce the accuracy of the assessment. [3] We prefer to use a different view to assess the integrity of these ligaments. The cross-body adduction view highlights medial rotational instability of the shoulder complex. This is important

because it simplifies the treatment algorithm. This is discussed further in the treatment section. This AP radiograph is shot with the patient pulling the affected upper extremity across the body in adduction. Maximal internal rotation of the humerus (thumb-down position) accentuates the instability, and soft tissue technique highlights the AC joint. Medial rotational instability is present if the distal fragment grossly underrides the proximal fragment. This signifies either that CC ligamentous disruption has occurred or that all ligaments are attached to the distal fragment. Intra-articular fractures or stress fractures involving the AC joint occasionally require CT scan or MRI for elucidation. Concomitant glenohumeral joint dislocation with a clavicle fracture is relatively rare, but the potential complications caused by failure to diagnose a posterior shoulder dislocation are very great. For this reason, we recommend that at least an AP shoulder view and an axillary lateral view be taken. The AP shoulder view may have already been obtained or at least caught on one of the previous films. An axillary lateral radiograph is easy to obtain and interpret and sets to rest any questions regarding the glenohumeral joint. Because of the surrounding edema and tenderness, the active glenohumeral motion and the physical examination itself can be limited. The clinician does not wish to miss a glenohumeral dislocation because he or she could not complete a good physical examination.

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Types of Clavicular Fractures Medial Clavicle Fractures

These fractures are rare, accounting for about 5% of all clavicle fractures in adults. As was stated previously, the medial clavicular physis is the last in the body to close, and this occurs between ages 22 and 25 years.[20] [56] Many medial clavicle fractures are therefore physeal injuries, which inherently have great healing potential. Physeal arrest is not a concern. Even in cases in which the medial physis has already fused, these fractures heal well. Anterior displacement, even if complete, is not a concern. The great majority of these fractures are best treated nonoperatively with figure-of-eight bandages or a sling. Healing can be expected to be rapid with a very low risk for nonunion. This being said, it must be emphasized that accurate diagnosis is important for several reasons. These injuries can be misdiagnosed as sternoclavicular joint injuries, which can confound treatment. Medial clavicle fractures that include extension into the sternoclavicular articulation carry some risk of post-traumatic arthrosis. This is something to consider when one is counseling the patient about his or her injury. The medial clavicle fracture that can be very problematic is that with posterior displacement severe enough to impinge on the vital structures at the root of the neck. Patients with complaints of difficulty swallowing or breathing, or with any neurovascular compromise, will require operative reduction of the fracture. Furthermore, patients without symptoms, but with documented CT scan evidence of impingement of the fragments on vital structures, should be considered for operative reduction. Reduction maneuvers or a towel clip reduction should not be performed in the clinic or the emergency room unless the posterior position of the fragment is causing an airway or hemodynamic emergency. This reduction must be performed in the operating room with the patient under general anesthesia. Reductions are best performed within the first 72 hours after injury. The chest must be prepared as for a sternotomy, and a thoracic surgeon must be available in case a vascular problem develops. A towel clip can be used to grasp the distal fragment and pull it forward to the proximal fragment. Traction

on the upper extremity, or a towel placed between the shoulder blades, may assist in unlocking the fragments and allowing reduction. The reduction is generally stable. In cases in which the reduction is unstable or unobtainable, open reduction will be necessary. Removing interposed soft tissue will likely allow reduction and should stabilize the fracture. Fixation may be attainable with heavy suture and repair of the soft tissue envelope. The clinician must use all available will power to resist pinning across the fracture and into the sternum. The literature includes many reports of broken hardware that migrated to the mediastinum, to the neck, and even into the great vessels and heart.57 Middle Third Fractures

Unlike adult fractures, the vast majority of middle third fractures or shaft fractures of the clavicle in children and younger adolescents can be managed best by closed means, with either a figure-of-eight splint or a sling. Midshaft fractures are often greenstick, or minimally displaced, fractures. Reduction maneuvers and figure-of-eight bandages have not been conclusively shown to hold a reduction or improve cosmesis in patients with these fractures. In patients with minimally displaced fractures, motion, although painful, is usually full, with minimal deformity over the fracture site. These can be treated quite adequately in a sling rather than with a figure-of-eight splint.[2] It has been our experience that the figure-of-eight offers little advantage over the standard sling. It is much more cumbersome for parents to deal with and must be adjusted daily for adequate tension to be maintained. Often, it is difficult

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to keep the figure-of-eight from resting directly over the fracture; this typically causes more discomfort than relief. If parents are insistent on a figure-of-eight, they must be instructed in its application and adjustment. We typically have parents mark the straps with a pen as they pass through the buckles. This way, they can see if they are putting it at a proper level of tension each day. It is also important to warn parents that there will be a persistent bump over the fracture site that will remodel. Even grossly displaced fractures in children younger than 12 years of age will remodel. This is sometimes met with skepticism on the part of parents. To convince them of the remodeling potential, one can compare the length of the child's clavicle to the parent's own. This usually impresses on them the amount of growth the clavicle still has to undergo. There is greater controversy about treatment of older adolescents with a displaced fracture. Many authors advocate a reduction of the fracture and use of a figure-of-eight splint or even a cast61 ; however, it has been our experience that even if a reduction is obtained, bones almost always revert to the position seen immediately after the injury. A fracture that is completely displaced or severely shortened is likely to stay in this position or revert to this position despite the physician's best efforts at reduction and use of the tightest figure-of-eight bandage. As was stated previously, an attempt at reduction can be useful in several circumstances. In cases in which there is acute neurovascular

compromise to the extremity as a result of the clavicle fracture, an attempt at reduction may be helpful. These cases are rare, but when they occur, a reduction maneuver can turn an emergency into just urgency. This may give the clinician the necessary time for planning or for calling in appropriate equipment. The problematic fractures of the midshaft of the clavicle are generally those that occur in patients who are nearly skeletally mature who have absorbed greater energy. In our experience, these higher-energy fractures tend to have a remarkably consistent pattern. They are generally shortened and comminuted with a butterfly fragment that is consistently anterior and inferior. Soft tissue injury and stripping are usually significant, and instability is common. All of these conditions raise the risk of nonunion in any fractured bone. Although most of these fractures heal, the near-skeletally mature patient is often left with a nonunited clavicle. This can be problematic for the highly competitive athlete, particularly for the overhand thrower. Recent research has suggested that these fractures can cause more problems than were previously recognized.[55] [56] Young contact athletes with recurrent fractures have also been reported. It would appear that the angulations of these fractures, even though well healed, make the biomechanical forces around the clavicle even more prone to fracture with axial loading. We believe that these fractures should be considered for treatment with open reduction and internal fixation, especially when recurrent fractures occur in contact athletes. For this, we have essentially two options: plate and screw fixation and intramedullary fixation. Treatment Methods

Plate and Screw Fixation.

For plate and screw fixation, one must use dynamic compression or reconstructive plates. The forces across this bone are too great to tolerate semitubular or one-third tubular plates. Even though they fit better, these will fail. It is best to obtain at least three screws for each fragment, and preferably six cortices. The exposure must be large enough to allow placement of all these screws and, much more importantly, the exposure must allow protection of the structures directly beneath the clavicle. This will require the placement of a curved Crego retractor or other protective device beneath the clavicle while the holes are drilled. Although physicians are unlikely to admit it, even the best among us occasionally plunge with the drill. Plunging in this region is flirting with disaster. Most catastrophes occur when physicians fail to protect themselves from themselves. Although plate and screw fixation can provide good stability, it requires significant soft tissue stripping. Besides leaving an unsightly scar, this soft tissue stripping may compromise clavicle healing because most if not all of the blood supply to the clavicle is periosteal. Furthermore, if the patient is displeased with the feel of a subcutaneous plate or wishes to have the hardware removed for any other reason, a second invasive procedure is required that leaves the patient with multiple stress risers in the clavicle. This may place active patients at risk for subsequent re-fracture. Intramedullary Fixation.

For most of these fractures, we prefer intramedullary fixation using a DePuy Clavicle Pin (DePuy AcroMed, Raynham, Mass). We believe this method to be superior for several

reasons. The exposure necessary to place an intramedullary pin is significantly less than that needed to perform a formal open reduction and internal fixation with plates and screws. This limits further damage to the already decimated soft tissue envelope. The intramedullary pin allows for compression at the fracture site and load sharing, both of which have been advantageous in the healing of other long-bone fractures. The intramedullary pin is easily removable with the patient under local anesthesia. Intramedullary pins come in different sizes, allowing canal fill, which again has been shown to be advantageous in other fractures treated with intramedullary devices. Unlike plate and screw fixation, placement of the intramedullary pin does not require physicians to drill perpendicularly through the clavicle. This fact decreases the risk to neurovascular structures and obviates the need to strip the soft tissues to allow for protection of these structures. Furthermore, the pin can be inserted without violating the medial or lateral physis. Removal of the pin can be accomplished in the clinic with the patient under local anesthesia; this procedure leaves the patient with only one stress riser in the metaphyseal posterior distal clavicle. We have never seen a subsequent re-fracture through this region.

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Surgical Technique for Intramedullary Pin Fixation Step 1: Patient Positioning

Place the patient in a beach chair position on the operating table. Both visualization of the clavicle and shoulder access are facilitated by using a radiolucent shoulder-positioning

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device. An image intensification device, or C-arm, greatly facilitates pin placement and can help reduce the anxiety that may be associated with drilling of the clavicle. The C-arm base should be brought in from the head of the bed with the C-arm gantry rotated slightly away from the operative shoulder and oriented with a cephalic tilt. The C-arm can then be draped into the field to decrease the need for the C-arm to be brought into and out of the field and to allow monitoring of the procedure at any point. Step 2: Incision

A 3-cm incision is made in Langer's lines over the distal end of the medial fragment. This is done because the clavicle skin is moved medially more easily than it is moved laterally. Most patients have a deep skin crease in the same area where the incision is made. Placement of the incision in this crease results in a more cosmetically pleasing scar. Because little subcutaneous fat is found in this region, care must be taken to prevent injury to the underlying platysma muscle. Scissors are used to free the platysma muscle from the overlying skin. Once the platysma muscle has been identified, its fibers are divided longitudinally. One must take care to prevent injury to the middle branch of the

supraclavicular nerve, which is usually found directly beneath the platysma muscle near the midclavicle. The nerve is identified and retracted to prevent injury. With acute fractures, the periosteum over the fracture site is disrupted and usually requires no further division. In most cases, interposed muscle and soft tissue are noted. These must be carefully removed with an elevator or curet. Small butterfly fragments, usually found anteriorly, must be left attached to their soft tissue envelope. Step 3: Drilling and Tapping the Intramedullary Canal

The proximal end of the medial clavicle is elevated through the incision using a towel clip, elevator, or bone-holding forceps. Because the drills, taps, and intramedullary pins are packaged in sets, either the smooth end of the taps or the drills should be used to size the canal. With care taken not to penetrate the anterior cortex, the intramedullary canal is drilled. The fit should not be too loose because this may compromise fixation, or too tight because this may split the bone. The C-arm can be used to check orientation of the drill. Then, the drill is removed from the medial fragment and the same-sized tap is attached to the T-handle. The intramedullary canal is also tapped to the anterior cortex. Next, the lateral fragment must be elevated through the incision. The same-sized drill used in the medial fragment is connected to the ratchet T-handle and the intramedullary canal is drilled. The drill is passed under C-arm guidance out through the posterolateral cortex of the clavicle, which will be posterior to the AC joint. The drill should then penetrate the posterolateral cortex at a point just above and slightly lateral to the conoid tubercle. Next, the drill is removed from the lateral fragment, the same-sized tap is attached to the T-handle, and the intramedullary canal is tapped so that the large threads are advanced fully into the canal. Step 4: Insertion of the Clavicle Pin

While still holding the distal fragment with a bone clamp, the physician must pass the trocar end of the DePuy Clavicle Pin into the medullary canal of the distal fragment. The pin should exit through the previously drilled hole in the posterolateral cortex. Once the pin exits the clavicle, its tip can be felt subcutaneously. A small incision is then made over the palpable tip and the subcutaneous tissue is spread with a hemostat. The tip of the hemostat is placed under the tip of the clavicle pin to facilitate its passage through the incision. Then, the pin is drilled out laterally until the large, medial threads start to engage the cortex. The Jacobs chuck is attached to the end of the pin protruding laterally, and the medial end of the clavicle pin is carefully advanced into the lateral fragment until only the smooth tip is protruding from the lateral fragment. The weight of the arm usually pulls the arm downward; therefore, the shoulder needs to be lifted to facilitate pin passage into the medial fragment. The medial nut must be placed on the pin, followed by the smaller lateral nut. The two nuts are cold-welded together by grasping the medial nut with a needle driver or needlenose pliers and tightening the lateral nut against the medial nut using the lateral nut wrench. The

fracture is reduced and the pin is passed into the medial fragment with the use of the T-handle and wrench on the lateral nut until it comes in contact with the anterior cortex. This position can be verified by C-arm or by radiograph. Step 5: Securing the Pin

The cold weld between the nuts is broken by grasping the medial nut with a needle driver or pliers and quickly turning the lateral nut counterclockwise with the insertion wrench. The medial nut is advanced until it is against the lateral cortex of the clavicle. Then, the lateral nut is tightened until it engages the medial nut. Next, the pin cutter is used to cut the pin near the lateral nut. Step 6: Soft Tissue Closure

To reapproximate the anterior butterfly fragments, the Crego elevator is passed beneath the clavicle in an anterior-to-posterior direction to protect the underlying structures. Absorbable Ethicon 0 or 1 polydioxanone or Panacryl sutures loaded on a CTX or CT1 needle are used and passed through the periosteum attached to the butterfly fragment. Then, they are passed around and beneath the clavicle. The needle is carefully directed toward the Crego elevator

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so that it will be deflected by the elevator. The needle is then retrieved posteriorly. The suture is passed in a figure-of-eight manner, or multiple simple sutures are used, to cerclage the butterfly fragment to the main fracture fragments. Next, the periosteum overlying the fracture is closed with multiple figure-of-eight 0 absorbable sutures. The platysma muscle is reapproximated with simple nonabsorbable Ethicon 2-0 Vicryl sutures. Both incisions are closed with a running subcuticular suture. The patient is placed into a sling and swathe postoperatively for comfort. When comfortable, usually the next day, the patient may forego the sling. Activity is limited to lifting no more than 5 pounds; abduction and forward flexion are restricted to no higher than 90 degrees for 4 weeks, or until the fracture site is nontender. The intramedullary pin is removed at 8 to 12 weeks through the small posterior incision, usually with the patient under local anesthesia.

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Rehabilitation after Clavicle Fracture

Rehabilitation following clavicle fracture in the athlete is started almost immediately, regardless of the treatment modality used. Assuming there are no associated injuries, the athlete is allowed to continue lower body strengthening exercises as before the injury occurred. Aerobic conditioning on an exercise bike or other stationary apparatus is encouraged. The athlete is allowed to immediately perform wrist and elbow range of motion exercise, as well as grip strength maintenance exercise. Running is discouraged until the acute pain has resolved. As soon as the acute pain resolves, the athlete is started on gentle pendulum exercises, as well as isometric strengthening of the rotator cuff, deltoid, biceps, and triceps. Normal use of the ipsilateral hand for activities of daily living is also encouraged. Generally, active range of motion is limited to less than 90 degrees of forward flexion or abduction if any operative fixation has been performed. This helps limit the initial stresses on the hardware. In the absence of hardware, the patient is allowed to advance active range of motion within the arc of pain tolerance. If no operative fixation is performed, full, active range of motion is allowed when the athlete is completely pain free, which usually occurs after 4 to 6 weeks of healing. When the athlete has achieved a full, pain-free range of motion, and there is radiographic evidence of callus, resistive exercises may be instituted. When the athlete has attained near-normal strength in the injured upper extremity, he or she may be started on a plyometric program. This is particularly useful in the throwing athlete.

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Return to Play Criteria

The criteria for return to sport activities are always controversial and essentially equate to a judgment call by the treating orthopaedist. This decision may be affected by several factors, including the personality of the athlete, the specific fracture, the sport, the position played, the level of sports competition, and the needs of the team. Unfortunately, some of the most problematic factors associated with this decision are the parental demands and expectations. Even when the child is happy to sit out the season, parents may have unrealistic expectations about the child's need to return to the sport as soon as possible. The surgeon can be put into an awkward situation when he or she sees disappointment or fear on the patient's face while the parents discuss the need to get their child back to playing as soon as possible. Occasionally, these factors directly oppose common sense. The treating surgeon must realize that this decision is ultimately a compromise, and all compromises come with inherent risks. The athlete, coaches, team, and parents may be willing to take risks that the orthopaedist is unwilling to shoulder. It is our job to protect the athlete from these competing forces just long enough to allow adequate healing at the clavicle fracture. Physicians know that fracture remodeling is a long and ongoing process that takes 9 months to 1 year or longer. In theory, the risk of re-fracture is increased until the bone remodels completely. Stopping sports participation for a year is obviously overkill. The clinician must make the athlete understand that returning to sports earlier than recommended is a compromise, and that by doing so, he or she increases the risk of re-injury. The goal is using caution to allow adequate healing without providing overprotection. For the noncontact athlete, return to sports may be allowed when there is a painless, full, active range of motion; near-normal strength; and evidence of bridging callus. This usually occurs about 4 to 6 weeks after injury in younger patients, with longer time required in older patients. Contact athletes, particularly those involved in collision sports, are obviously at greater risk for re-fracture. The position played and the type of fracture incurred will also affect this risk. Even if the physician cannot allow a return to full participation, frequently he or she can allow the athlete to return to practice with the team on a noncontact basis. This allows the athlete to remain at least mentally in touch

with the team. This is generally allowed when the athlete meets the same criteria as those required for the noncontact athlete. The team trainer can be extremely valuable in keeping the athlete from doing too much too soon because he or she is with the team every day at practice. Generally, between 2 and 3 months after injury would be the earliest recommended time for return to contact sports. In football, extra protection at times can be afforded by the use of donut pads, or fabrication of a fiberglass shoulder shell, to dissipate impact forces to the clavicle. If the fracture required operative fixation of any type, generally the season is over for this athlete. We have treated athletes who returned to contact sports with the intramedullary pin still in place after 4 to 6 weeks; however, we do not encourage this. If the portion of the pin that is protruding from the posterolateral aspect of the clavicle is not causing skin irritation, if the area about the pin is nontender, and if the pin itself is not too prominent, the patient may return to contact sports once the fracture site is nontender and there is radiographic evidence of callus. We prefer to have the athlete wait until at least 2 weeks after pin removal before returning to contact sports. We have not known any patients who experienced re-fracture

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after pin removal when these criteria were followed.

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Injuries to the Lateral Clavicle

Although no specific data are available on the incidence of lateral clavicle fractures in children and adolescents, it is probably the same as that reported in adults by Neer and Rowe,[37] [44] which is about 10% to 15% of all clavicle fractures. The mechanism of these fractures is the same as that seen with AC joint injuries in adults, namely, a fall on the point of the shoulder. The resultant force typically loads the scapula in an inferior, anterior, and medial direction. Although this mechanism was proposed by Codman, most authors have suggested that the mechanism of fracture is merely a downward force on the scapula. The magnitude of these various forces determines both the severity and the resultant displacement of the fracture. As was noted earlier, children and adolescents typically rupture the distal end of the clavicle out of the periosteal sleeve, rather than rupturing the AC and CC ligaments.62 This represents a true distal clavicle fracture rather than an AC joint disruption. Surgical Treatment of Lateral Clavicle Injuries

Surgical treatment of lateral clavicle injuries is carried out with the patient in a beach chair position. A C-arm can be used to help visualize the reduction. A 3-cm strap-type incision is made just medial to the distal end of the clavicle. Most cases will require complete stripping of the soft tissue off the lateral end of the clavicle. In the case of type IV injuries, the trapezius will have to be inspected and the clavicle pulled out of its buttonholed position. The defect in the trapezius can then be repaired with absorbable sutures. The lateral clavicle is then reduced and the periosteal sleeve is repaired using multiple figure-of-eight absorbable sutures. We typically use long-acting absorbable sutures such as 2-0 or 0 Panacryl because there is no need for nonabsorbable sutures. In older adolescents, or in patients with significant disruption of the periosteal tube, consideration should be given to supplementing CC fixation.58 Although a CC screw can be used, this requires very exacting placement in the center of the base of the coracoid.

This can be facilitated by the use of a C-arm; however, it can be rather demanding. Furthermore, if the screw is not perfectly centered in the coracoid base, one can have a loss of fixation. If a CC screw is used, it should be removed 6 to 8 weeks later. Although it is not typically a problem in adults, we have seen significant bony overgrowth over the head of the screw even in this short period of time, which can complicate screw removal. Because of torque on the screw, we also recommend that patients avoid lifting and overhead activity until at least 4 weeks postoperatively. Because of these problems and in view of the rapid healing seen in adolescents, we prefer to use absorbable CC sutures passed in a cerclage fashion around the coracoid. Care must be taken to avoid injury to the coracohumeral ligament. We typically pass a loop of suture around the base of the coracoid with a ligament passer. This loop is then used to pass braided strands of 0 Panacryl sutures that are tied over the clavicle. Again, in view of the rapid healing seen in these patients, nonabsorbable suture is not necessary. Furthermore, nonabsorbable suture can erode through the clavicle or coracoid. Postoperatively, the patient is kept in a sling for 3 to 4 weeks and is not allowed to return to sports until full strength and painless range of motion are restored, typically after 8 to 12 weeks. Owing to the difficulty in placement of AC pins and the associated potential for injury to the acromion and for pin migration, we cannot recommend this type of fixation.

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Distal Clavicle Injuries in Children Classification

Rockwood has classified these fractures in a manner that is roughly analogous to his classification system of AC joint injuries in adults. This system is based on the amount of energy imparted to the distal clavicle, which determines the degree of displacement and the direction of the applied forces; these determine the direction of the displacement. The subtypes are based on the position of the distal clavicle relative to the periosteal tube.62 Rockwood's classification is as follows: Type I: A minor strain of the AC ligaments without disruption of the periosteal sleeve of the clavicle. The patient with this injury may have tenderness to palpation of the AC joint but no significant side-to-side radiographic changes. Type II: Some disruption of the periosteal sleeve with a minimal increase in the CC interval noted on radiographs in comparison with the uninjured side. The AC interval may appear to be slightly widened. Type III: Gross disruption of the dorsal aspect of the periosteal sleeve, with the clavicle appearing to be displaced upward relative to the scapula. On plain radiographs taken with both shoulders on the same cassette, the clavicles appear to be of the same relative height with the scapula on the injured side drooping downward. This is usually confirmed clinically. The CC interval may appear to be increased by 50% to 100% more than that on the uninjured side. Swelling and ecchymosis may be noted over the dorsal aspect of the AC joint and distal clavicle, in addition to ecchymosis over the posterolateral aspect of the acromion. If the CC interval is not widened but the AC space is significantly widened, the physician should be suspicious of a coracoid base fracture. In these injuries, the forces are

dissipated during fracture of the coracoid before the periosteal tube is disrupted. The fracture of the base of the coracoid can sometimes be seen on the axillary view, but it is best seen on the Stryker notch view. Type IV: Posterior displacement of the clavicle relative to the acromion. In reality, the clavicle remains in the same position owing to its strong medial attachments; however, the scapula is driven anteriorly relative to the clavicle. The CC interval may not appear to be 978

significantly increased, thereby leading the physician to conclude that this is a less significant injury. It is key to (1) examine the patient by palpating the distal clavicle relative to the acromion and (2) obtain a good axillary view to look for the relative posterior displacement of the clavicle. In our experience, these are the most problematic injuries among children and adolescents, just as the type IV injury in adults is so disabling. This is so because the distal clavicle can be buttonholed out of the trapezius muscle, which not only prevents reduction but also causes considerable pain for the patient. Type V: Essentially a severe type III injury with complete disruption of the dorsal periosteal tube and significant superior displacement of the distal clavicle relative to the acromion. This is presumably due to the additional disruption of the deltotrapezial fascia. Again, the distal clavicle stays in its anatomic position while the scapula drops away. The CC interval is typically increased by more than 100%. Type VI: Extremely rare and associated with displacement of the clavicle under the coracoid process (similar to adult type VI injuries).

Radiographic evaluation of these injuries has been described earlier in the chapter. Treatment

Similar to pediatric midshaft clavicle fractures, distal clavicle injuries represent periosteal sleeve avulsions. Because there is tremendous remodeling potential with these injuries, the type I to type III injuries can usually be treated nonoperatively. We believe, as does Dr. Rockwood, that consideration should be given to operative intervention in type IV and V injuries owing to the gross displacement of the fragments. All type VI injuries, although very rare, should be treated operatively. As was noted earlier, we have found that type IV injuries seem to be the most problematic when treated nonoperatively owing to the buttonholing of the distal clavicle out through the trapezius. The remodeling potential of this injury is low, and the injury causes considerable pain for the patient. Furthermore, this represents a fixed deformity, which typically requires operative reduction. Once reduced, this injury tends to be rather unstable because of the injury to the periosteal tube and deltotrapezial fascia; therefore, it is a rather simple task to

reduce the clavicle and repair the periosteal sleeve. With type I to III injuries, most patients can be managed by means of a period of short immobilization and support with a sling. Ice should be applied to the shoulder. Progressive motion and strengthening exercises should be started once the fracture site is nontender, typically after 3 to 6 weeks. As with any other shoulder injury, return to sports should not be allowed until the patient has regained full strength and painless range of motion. In older adolescents, typically older than age 14, consideration can be given to treating this as an adult injury. Although considerable disagreement is recorded in the literature about the proper treatment of these injuries in adults, we feel that most type III injuries and some type II injuries, particularly in the overhead athlete, respond better to operative treatment. Because we have seen numerous injuries that initially appeared minor but went on to become more obvious deformity and dysfunction, we prefer to base our operative decisions on the presence of medial instability, as assessed by means of a cross-body adduction view. (This was noted earlier in the radiographic section.) If the older adolescent has developed medial instability, we typically treat with operative stabilization, as is provided for an adult.

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Depalma A: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.

Dugdale TW, Fulkerson JB: Pneumothorax complicating a closed fracture of the clavicle. A case report. Clin Orthop 221:212-214, 1987. 11.

Echtermeyer V, Zwipp H, Oestern HJ: Fehler und Gefahren in der Behandlung der Fracturen und Pseudarthrosen des Schlusselbeins. Langenbecks Arch Chir 364:351-354, 1984. 12.

Edvardsen P, Odegard O: Treatment of posttraumatic clavicular pseudarthrosis. Acta Orthop Scand 48:456-457, 1977. 13.

14.

Elliot AC: Tripartite injury of the clavicle. A case report. S Afr Med J 70:115, 1986.

Eskola A, Vainionpaa S, Myllynen P, et al: Outcome of clavicular fracture in 89 patients. Arch Orthop Trauma Surg 105:337-338, 1986. 15.

Grazier KL, Holbrook TL, Kelsey JL, Stauffer RN: The Frequency of Occurrence, Impact, and Cost of Musculoskeletal Conditions in the United States. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1984. 16.

Hill JM, McGuire MH, Crosby LA: Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J Bone Joint Surg Br 79:537-539, 1997. 17.

Howard FM, Schafer SJ: Injuries to the clavicle with neurovascular complications: A study of fourteen cases. J Bone Joint Surg Am 47:1335-1346, 1965. 18.

Hoyer HE, Kindt R, Lippert H: Zur Biomechanik der menschlichen Clavicula. Z Orthop Ihre Grenzgeb 118:915-922, 1980. 19.

20.

Inman VT, Saunders JB: Observation in the function of the clavicle. Clif Med 65:158-165, 1946.

Jablon M, Sutker A, Post M: Irreducible fractures of the middle third of the clavicle. J Bone Joint Surg Am 61:296-298, 1979. 21.

Jit I, Kulkrani M: Times of appearance and fusion of epiphysis at the medial end of the clavicle. Indian J Med Res 64:773-792, 1976. 22.

23.

Khan MAA, Lucas HK: Plating of fractures of the middle third of the clavicle. Injury 9:263-267, 1978.

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Kay SP, Eckardt JJ: Brachial plexus palsy secondary to clavicular nonunion: A case report and literature survey. Clin Orthop 206:219-222, 1986. 24.

Klier I, Mayor PB: Laceration of the innominate internal jugular venous junction: Rare complication of fracture of the clavicle. Orthop Rev 10:81-82, 1981. 25.

Lengua F, Nuss JM, Lechner R, et al: The treatment of fracture of the clavicle by closed mediolateral pinning. Rev Chir Orthop 73:377-380, 1987. 26.

Lim E, Day LJ: Subclavian vein thrombosis following fracture of the clavicle: A case report. Orthopedics 10:349-351, 1987. 27.

28.

Ljunggren AE: Clavicular function. Acta Orthop Scand 50:261-268, 1979.

Lyons FA, Rockwood CA: Current concepts review: Migration of pins used in operations on the shoulder. J Bone Joint Surg Am 72:1262-1267, 1990. 29.

Manske DJ, Szabo RM: The operative treatment of mid-shaft clavicular non-unions. J Bone Joint Surg Am 67:1367-1371, 1985. 30.

McCandless DN, Mowbray M: Treatment of displaced fractures of the clavicle: Sling vs figure of eight bandage. Practitioner 223:266-267, 1979. 31.

32.

Moore TO: Internal pin fixation for fracture of the clavicle. Am Surg 17:580-583, 1951.

33.

Moseley HF: Shoulder Lesions. Edinburgh, Churchill-Livingstone, 1972.

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Mueller ME, Allgower N, Willenegger H: Manual of Internal Fixation. New York, Springer-Verlag, 1970.

35.

Murray G: A method of fixation for fracture of the clavicle. J Bone Joint Surg 22:616-620, 1940.

Neviaser RJ, Neviaser JS, Neviaser TJ: A simple technique for internal fixation of the clavicle. Clin Orthop 109:103-107, 1975. 36.

Neer CS II: Fractures of the clavicle. In Rockwood CA, Green DP (eds): Fractures in Adults. Philadelphia, JB Lippincott, 1984, pp 707-713. 37.

Ogden JA, Conologue GJ, Bronson NL: Radiology of postnatal skeletal development: Volume 3, the clavicle. Skeletal Radiol 4:196-203, 1979. 38.

Paffen PJ, Jansen EW: Surgical treatment of clavicular fractures with Kirshner wires: A comparative study. Arch Chir Neerl 30:43-53, 1978. 39.

40.

Perry B: An improved clavicular pin. Am J Surg 112:142-144, 1966.

41.

Rang M: Clavicle. In Rang M (ed): Children's Fractures, 2nd ed. Philadelphia, JB Lippincott, 1983.

42.

Rockwood CA: Personal communications, 1993-1997.

Rockwood CA: Fractures of the outer clavicle in children and adults. J Bone Joint Surg Br 64:642, 1982. 43.

44.

Rowe CR: An atlas of anatomy and treatment of mid-clavicular fractures. Clin Orthop 58:29-42, 1968.

Rush LV, Rush HL: Technique of longitudinal pin fixation in fractures of the clavicle and jaw. Mississippi Doctor 27:332, 1949. 45.

46.

Sakellarides H: Pseudoarthrosis of the clavicle. J Bone Joint Surg Am 43:130-138, 1961.

47.

Sankarankutty M, Turner BW: Fractures of the clavicle. Injury 7:101-106, 1975.

Shalom A, Khermosh O, Wientroub S: The natural history of congenital pseudarthrosis of the clavicle. J Bone Joint Surg Br 76:846-847, 1994. 48.

Silloway KA, Mclaughlin RE, Edlichy RC, et al: Clavicular fractures and acromioclavicular joint injuries in lacrosse: Preventable injuries. J Emerg Med 3:117-121, 1985. 49.

50.

Spar I: Total clavulectomy for pathologic fractures. Clin Orthop 129:236-237, 1977.

Stanley D, Trowbridge EA, Norris SH: The mechanism of clavicular fracture. J Bone Joint Surg Br 70:461-464, 1988. 51.

52.

Tachdjian MO: Pediatric Orthopaedics. Philadelphia, WB Saunders, 1972.

Tse DH, Slabaugh PB, Carlson PA: Injury to the axillary artery by a closed fracture of the clavicle. J Bone Joint Surg Am 62:1372-1373, 1980. 53.

Tyrnin AH: The Bohler clavicle splint in the treatment of clavicular injuries. J Bone Joint Surg 19:417-424, 1937. 54.

Zanca P: Shoulder pain: Involvement of the acromioclavicular joint: Analysis of 1,000 cases. AJR Am J Roentgenol 112:493-506, 1971. 55.

Zenni EJ Jr, Krieg JK, Rosen MJ: Open reduction and internal fixation of clavicular fractures. J Bone Joint Surg Am 63:147-151, 1981. 56.

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Section F Glenoid and Scapula Fractures in Adults and Children Allen Deutsch MD Gerald R. Williams MD The scapula is intimately linked to shoulder function and mobility. It links the appendicular and axial skeletons through the clavicle and the acromioclavicular, sternoclavicular, and glenohumeral joints and presents a stable platform for the upper extremity. Injury to the scapula may disrupt normal shoulder function. The incidence of scapular fracture has been reported to be 3% to 5% of shoulder girdle injuries [22] [61] and 0.4% to 1% of all fractures. [49] [76] The low incidence of scapular fracture is due to its protected position along the rib cage, the enveloping musculature, and its relative mobility, which permits dissipation of forces. Scapular fractures most commonly involve the scapular body (49% to 89%), the glenoid neck (10% to 60%), and the glenoid cavity (10%).[1] [2] [14] [27] [40] [74] Scapular fractures are usually sustained as the result of severe trauma. Most series report motor vehicle or motorcycle accidents as the cause of injury in more than 50% of the cases.[1] [2] [27] [40] [74] Associated injuries are common, including rib fracture, pneumothorax, and head injury. Rowe[62] reported that 71% of the patients in his series of scapular fractures had other associated injuries: 45% had fracture of other bones, including the ribs, sternum, and spine; 3% sustained a pneumothorax; 4% sustained brachial plexus injuries; and 19% sustained other shoulder girdle dislocations. Several classification systems for scapular fractures have been reported in the literature. Zdravkovic and Damholt[78] divided scapular fractures into three types: type I fractures, or fractures of the body; type II fractures, or fractures of the apophyses (including the coracoid and acromion); and type III fractures, or fractures of the superior lateral angle (i.e., scapular neck and glenoid). Zdravkovic and Damholt[78] considered the type III fracture to be the most difficult to treat; these represented only 6% of their

series. Thompson and coworkers[69] presented a classification system that divided these fractures according to the likelihood that associated injuries would be present. Their cases resulted from blunt trauma. Class I fractures included fractures

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of the coracoid and acromion process and small fractures of the body. Class II fractures comprised glenoid and scapular neck fractures. Class III fractures included major scapular body fractures. Thompson and colleagues[69] reported that class II and class III fractures were much more likely to have associated injuries. Wilber and Evans[74] described 40 patients with 52 scapular fractures. The patients were divided into two groups on the basis of fracture location: group I, which included patients with fractures of the scapular body, neck, and spine; and group II, which included patients with fractures of the acromion process, coracoid process, or glenoid. They reported unsatisfactory results of treatment of patients in group II because of residual pain and loss of glenohumeral motion. Ideberg[25] [26] devised a classification system of five types of scapular fracture with an associated intra-articular glenoid component. This system was modified by Goss[18] [20] with inclusion of six types. Type I fractures involve the glenoid rim and are subdivided into Ia, anterior rim, and Ib, posterior rim. Type II to type V fractures extend from the glenoid fossa to various exit points along the scapula. Type II fractures exit the lateral border of the scapula, below the infraglenoid tubercle. Type III fractures exit the superior border and typically extend medial to the base of the coracoid. Type IV fractures extend directly across the scapula to the medial border and usually exit superior to the scapular spine. Type V fractures are combinations of types II to IV. Type VI fractures encompass glenoid fractures with extensive intra-articular comminution[18] ( Fig. 21F-1 ).

Figure 21-F-1 Classification of fractures of the glenoid cavity: type Ia, anterior rim fracture; type Ib, posterior rim fracture; type II, fracture line through the glenoid fossa exiting at the lateral scapular border; type III, fracture line through the glenoid fossa exiting at the superior scapular border; type IV, fracture line through the glenoid fossa exiting at the medial scapular border; type Va, combination of types II and IV; type Vb, combination of types III and IV; type Vc, combination of types II, III, and IV; type VI, comminuted fracture. (© 1995 American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 3[1], pp 22-33 with permission.)

Goss[19] described the superior shoulder suspensory complex, consisting of the glenoid, coracoid, acromion, distal clavicle, coracoclavicular ligaments, and acromioclavicular ligaments. This bone-soft tissue ring maintains the normal, stable relationship between the upper extremity and the axial skeleton. Single disruptions of the superior shoulder suspensory complex, such as an isolated scapular neck fracture, are usually anatomically stable because the integrity of the complex is preserved, and nonoperative

management yields good functional results. When the complex is disrupted in two places (double disruption), such as a scapular neck fracture with an acromioclavicular joint disruption, a potentially unstable anatomic situation is created. Because the superior shoulder suspensory complex includes the glenoid, acromion, and coracoid, many double disruption injuries involve the scapula. Open reduction is indicated for double disruptions that are accompanied by significant displacement, which may lead to delayed union, malunion, or nonunion as well as long-term functional deficits. Anatomy

The scapula is enveloped by multiple layers of muscles. The anterior surface provides attachment for the subscapularis,

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the serratus anterior, the omohyoid, the pectoralis minor, the conjoined tendon of the coracobrachialis and short head of the biceps, the long head of the biceps, and the long head of the triceps ( Fig. 21F-2 ). The posterior surface of the scapula provides muscle attachment sites for the levator scapulae, the rhomboid major, the rhomboid minor, the latissimus dorsi, the teres major, the teres minor, a portion of the long head of the triceps, the deltoid, the trapezius, the supraspinatus, the infraspinatus, and a portion of the omohyoid ( Fig. 21F-3 ). The intramuscular position of the scapula provides it with great mobility and a protective cushion that are no doubt responsible for the low incidence of scapular injury.

Figure 21-F-2 The muscle attachments to the anterior surface of the scapula. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-3 The muscle (m.) attachments to the posterior surface of the scapula. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

The closeness of neurovascular structures to the scapula places them at risk for injury. The pectoralis minor tendon inserts at the base of the coracoid process and the lateral border of the suprascapular notch. The brachial plexus and axillary artery travel posterior to the pectoralis minor tendon. The suprascapular nerve traverses the suprascapular notch to innervate the supraspinatus muscle, whereas the suprascapular artery passes over it. The suprascapular nerve continues through the spinoglenoid notch, or the junction between the base of the acromion and the neck of the scapula, to innervate the infraspinatus muscle. At the medial border of the scapula, the dorsal scapular and spinal accessory nerves course along with the branches of the transverse cervical artery.

The osseous components of the scapula, which consist of the body and spine, the coracoid process, the acromion process, the glenoid, and the inferior angle, arise from several ossification centers.[41] [53] [68] At birth, the body and spine form one ossified mass. The coracoid process, the acromion process, the glenoid, and the inferior angle are cartilaginous, however. The coracoid process is a coalescence of four or five centers of ossification. The center of ossification for the midportion of the coracoid appears at the age of 3 to 18 months and may be bipolar. The ossification center for the base of the coracoid, which includes the upper third of the glenoid, appears at 7 to 10 years. Two ossification centers appear at the age of 14 to 16 years: a center for the tip and a shell-like center at the medial apex of the coracoid process. The ossification centers for the base and the midportion of the coracoid coalesce during adolescence at 14 to 16 years of age. The other ossification centers fuse at the age of 18 to 25 years ( Figs. 21F-4 and 21F-5 ).

Figure 21-F-4 A normal ossification pattern at the base of the coracoid. A crescent-shaped center is seen at the apex of the coracoid. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-5 An epiphyseal line is seen across the upper third of the glenoid because this portion of the glenoid ossifies in common with the base of the coracoid. This may be confused with a fracture and is the precise location of most type III glenoid fractures. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

The acromion is a coalescence of two or three centers of ossification that appear between the ages of 14 and 16 years, coalesce at the age of 19 years, and fuse to the spine at the age of 20 to 25 years. Failure of the anterior acromion ossification center to fuse to the spine gives rise to the os acromiale. This unfused apophysis is present in 2.7% of random patients and is bilateral in 60% of cases.[33] The size of the os acromiale depends on which of the four ossification centers of the acromion have failed to fuse ( Fig. 21F-6 ). The most common site of nonunion is between the mesoacromion and the meta-acromion, which corresponds to the mid-acromioclavicular joint level. An axillary lateral radiograph clearly demonstrates the lesion ( Fig. 21F-7 ). Norris[52] has reported that the os acromiale has been mistaken for fracture and that there is an association between the os acromiale and a rotator cuff tear.

Figure 21-F-6 A, The diagram represents the ossification centers of the acromion. B, The most common site of failure of ossification lies between the mesoacromion and the meta-acromion. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-7 Os acromiale. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB

Saunders, 1990.)

The inferior angle of the scapula arises from an ossification center that appears at the age of 15 years and fuses with the remainder of the scapula at the age of 20 years. The vertebral border arises from an ossification center that appears at 16 to 18 years of age and fuses by the 25th year. The glenoid fossa ossifies from four sources: (1) the coracoid base (including the upper third of the glenoid), (2) the deep portion of the coracoid process, (3) the body, and (4) the lower pole, which joins with the remainder of the body of the scapula at 20 to 25 years of age.

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Because many athletes are adolescents and because many of the apophyses do not fuse until the age of 25 years, caution must be exercised in interpreting radiographs of the scapula. The os acromiale is the most frequently quoted unfused apophysis and can be confused with fracture.[33] [52] In addition, the physes at the base of the coracoid and the tip of the coracoid process can be difficult to distinguish from fracture. In the appropriate setting, a radiograph of the contralateral scapula is useful in determining whether a radiographic line is truly a fracture or an unfused apophysis.

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Clinical Evaluation History

Scapular fractures in athletes can result from either direct or indirect mechanisms of injury. Although most athletes are not subjected to the high-energy trauma associated with motor vehicle accidents, direct blows to the scapula can occur with enough force to cause fracture in contact sports such as hockey and football. Direct blows to the acromion can cause either acromion fracture or acromioclavicular separation. In addition, direct blows to the scapula or to the lateral aspect of the shoulder can cause scapular body fractures or glenoid fractures. Alternatively, glenoid fractures can be the result of indirect trauma incurred during a violent glenohumeral dislocation or a fall on an outstretched arm. Physical Examination

The athlete with a scapular fracture typically presents with the arm adducted and protected from all movements.

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Abduction is especially painful. Although ecchymosis is less than expected from the degree of bone injury present, severe local tenderness is a reliable finding.[8] Athletes with scapular body fractures or coracoid process fractures often complain of increasing pain with deep inspiration secondary to the pull of the pectoralis minor or serratus anterior muscles. Frequently, rotator cuff function is extremely painful and weak secondary to inhibition from intramuscular hemorrhage. This has been described as a pseudorupture of the rotator cuff [47] and usually resolves within a few weeks.

Scapular fracture is often associated with other injuries that need more urgent treatment. Significant associated injuries have been reported to occur in 35% to 98% of all patients with scapular fractures.[8] The highest incidence of serious associated injuries occurs in fractures sustained during high-speed motor vehicle accidents.[2] [15] [27] [40] [69] [74] McLennen and Ungersma[43] reported 16 pneumothoraces in 30 patients who presented with fractured scapulae. Of the 16 pneumothoraces, 10 were delayed in onset from 1 to 3 days. The authors recommended a follow-up chest radiograph, physical examination, and blood gas determination for all patients with scapular fractures. Other series have reported an overall incidence of pneumothorax associated with scapular fracture between 11% and 38%. [2] [15] [69] Ipsilateral rib fractures,[69] pulmonary contusion, [15] [69] arterial injury,[15] and brachial plexus injury[2] [15] [27] [40] [69] have also been reported in association with scapular fractures. Physical examination should be directed toward detecting any of these possible associated injuries. Radiographic Evaluation

Most scapular fractures can be adequately visualized on routine radiographic views. A true anteroposterior view of the scapula combined with an axillary or true scapular lateral view demonstrates most scapular body or spine fractures, glenoid neck fractures, and acromion fractures ( Figs. 21F-8 , 21F-9 , and 21F-10 ). Special views may be required in selected circumstances. The Stryker notch view, as described later in this chapter, is useful for coracoid fractures [8] ( Fig. 21F-11 ). The apical oblique view described by Garth[17] and the West Point lateral view[59] [60] are useful for evaluating anterior glenoid rim fractures.

Figure 21-F-8 A true anteroposterior view of the glenoid showing an anterior-inferior glenoid fracture. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-9 A tangential scapular lateral view (trauma series lateral view) showing a displaced scapular body fracture with a bayonet position. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-10 The fractured base of the acromion is well seen on a tangential scapular lateral view. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-11 A fracture of the base of the coracoid, seen best on a Stryker notch view. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Computed tomography is a useful adjunct in evaluating intra-articular glenoid fractures.

The contralateral normal shoulder as well as the involved shoulder may be scanned to provide a means for comparison of the pathologic findings noted in the involved shoulder, especially in adolescents.[8] Computed tomography allows confirmation of the size, location, and degree of displacement of fracture fragments

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and detects the presence of instability. Three-dimensional images can be generated as well ( Fig. 21F-12 ). These three-dimensional computed tomographic reconstructions are useful in surgical planning. With appropriate software, the humeral head can be subtracted from the image so that an unobstructed view of the scapula and glenoid can be obtained ( see Fig. 21F-12 ).

Figure 21-F-12 Anteroposterior radiograph (A) and scapular Y view (B) of a type V scapular fracture. Computed tomographic scan (C) and three-dimensional reconstructions (D) illustrate the amount of displacement of the inferior intra-articular component with extension across the scapular body.

Glenoid rim fractures associated with glenohumeral instability pose perhaps the most difficult decisions for treatment of fractures of the scapula among athletes. The athlete does not always relay a history of glenohumeral dislocation in association with the initial injury. Because the decision regarding operative or nonoperative treatment of these glenoid rim fractures depends on whether they are associated with instability,[8] the physician should make every attempt to verify the presence or absence of instability. In this regard, stress views with or without fluoroscopic control or an examination under anesthesia may be helpful.

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Treatment Options in Adults

The recommended treatment of specific types of scapular fracture varies according to whether the fracture is intra-articular or extra-articular. Most extra-articular fractures (i.e., glenoid neck, scapular body or spine, acromion, and coracoid fractures) are managed nonoperatively.[5] [13] [34] [42] [58] Intra-articular fractures, particularly those associated with glenohumeral instability, are managed operatively.[13] [25] [57] [62] [63] Extra-articular Fractures

Glenoid Neck Fracture

Fracture of the neck of the scapula is the second most common scapular fracture. [8] The glenoid articular surface is intact, and the fracture line most often extends from the suprascapular notch area across the neck of the scapula to its lateral border inferior to the glenoid. The glenoid and coracoid may be comminuted or may remain as an intact unit. Although glenoid neck fractures are often impacted, their displacement is limited by an intact clavicle and by the acromioclavicular and coracoclavicular ligaments.[22] Most authors recommend closed treatment of glenoid neck fractures. [5] [13] [34] [58] For displaced fractures, DePalma[13] recommended closed reduction and olecranon pin traction for 3 weeks followed by a sling. Bateman[5] favors closed reduction and a shoulder spica cast for 6 to 8 weeks in cases in which shortening of the neck is sufficient to favor subluxation or interfere with abduction. McLaughlin [42] casts doubt on the usefulness of closed reduction in these fractures because most of them are impacted and difficult to move. Lindholm and Leven[34] studied a series of scapular neck and body fractures and concluded that if untreated, all fractures healed in the position displayed at the time of the original injury (i.e., without additional displacement). Other authors[16] [22] have recommended open reduction of glenoid neck fractures. Gagey and colleagues[16] reported only one good result among 12 displaced glenoid neck

fractures with closed treatment. They theorized that healing of the glenoid neck in the displaced position would disorganize the coracoacromial arch. Therefore, they recommended open reduction and internal fixation. Suprascapular nerve paralysis (confirmed by electromyography) that results from a glenoid neck fracture extending into the suprascapular notch is an indication for early exploration, open reduction, and internal fixation. [14] [66] Ada and Miller[1] described 24 patients with displaced scapular neck fractures. Of the 16 treated conservatively, 50% complained of night pain, 40% had weakness of abduction, and 20% had decreased range of motion. Open reduction with internal fixation was used to treat eight

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patients with scapular neck fractures having greater than 40 degrees of angulation or more than 1 cm of medial displacement of the glenoid surface. None of these patients complained of night pain, and all regained at least 85% of abduction. Ipsilateral scapular neck and clavicle fractures are thought to produce a floating shoulder.[23] These injuries have been managed both conservatively and operatively, with good functional results reported for both treatment methods. Ramos and associates[56] reported 92% good or excellent results in 16 patients treated conservatively with aggressive rehabilitation. Williams and associates[75] correlated functional outcome with medial glenoid displacement in nine patients treated nonoperatively. Six patients with 2.2 cm or less of medial displacement had good or excellent results. They recommended that nonoperative management be considered in fractures with less than 3 cm of medial displacement of the glenoid. Van Wellen and colleagues[70] described successful treatment of ipsilateral displaced glenoid neck and clavicle fracture with balanced traction. Hardegger and coworkers[22] recommended open reduction and scapular fixation for displaced glenoid neck fractures associated with a fracture of the clavicle or disruption of the coracoclavicular ligaments. They postulated that a severe displacement in these injuries would result in functional imbalance of the shoulder mechanism. Leung and Lam[32] managed these injuries with open reduction of both the clavicle and scapula fractures because of loss of the normal lever arm of the cuff. They reported good or excellent functional results in all but 1 of the 15 patients they treated. Herscovici and associates[23] believed that this injury disrupts the suspensory structures, leading to anteromedial displacement of the glenoid and ptosis of the shoulder due to muscle forces and the weight of the arm. They used open reduction of the clavicle in seven patients with excellent functional results. Most series report good functional results in patients with glenoid neck fractures regardless of the method of treatment[9] [11] [14] [33] ( Fig. 21F-13 ). Hitzrot and Bolling[24] in 1916 stated that manipulation and traction had no effect on displaced glenoid neck fractures and that the results were so satisfactory without reduction that attempts to

achieve reduction were unnecessary. Armstrong and Vanderspuy[2] reported that six of seven of their patients with glenoid neck fractures had some residual stiffness, but no patient

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had a functional disability. Zdravkovic and Damholt[78] came to the same conclusion in their report, in which patients had an average of 9 years of follow-up.

Figure 21-F-13 A healed glenoid neck fracture with marked medial displacement and full range of motion. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.) Scapular Body Fracture

Fracture of the body of the scapula is the most common type of scapular fracture and is correlated with the highest incidence of associated injury. [8] When injury is the result of high-energy trauma, these fractures may be comminuted and displaced. Cain and Hamilton[9] reported five scapular fractures in professional football players that were the result of direct blows to the shoulder. The musculature surrounding the scapula makes nonunion a rare occurrence. Scapular malunion is rarely associated with clinical symptoms. [13] [58] [61] [62] Consequently, most authors favor a sling, ice, and supportive measures until the initial pain subsides.[42] [58] [61] [62] Neer[44] and Bateman[5] reported immobilization using cross-strapping with adhesive moleskin in a nonambulatory patient with a scapular body fracture. This type of immobilization, however, has occasionally been associated with residual shoulder stiffness.[42] On occasion, scapular malunion results in painful crepitus interfering with range of motion that may require removal of a bone prominence.[36] Nordqvist and Petersson[51] found poor long-term results in some patients with more than 10 mm of displacement. Unusual causes of scapular body fractures include indirect injury, low-energy injury, and stress fracture. These injuries are treated nonoperatively with early mobilization. Wyrsch and coworkers[77] reported a scapular body fracture in a professional boxer who sustained the injury during an attempted punch that completely missed the opponent. This injury was caused by a voluntary muscle contraction and was treated successfully with progressive active range of motion and physical therapy. Deltoff and Bressler[12] described the case of a scapular fracture sustained while a man was performing push-ups. McAtee[39] reported an isolated scapular body fracture in a 41-year-old man playing touch football. Scapular body stress fracture has been reported in an elderly woman who had used a cane for ambulation.[54] All these fractures were treated with a short period of protection and progressive range of motion. Acromion Fracture

Although fracture of the acromion is rare, when it does occur, it is usually the result of one of two mechanisms. First, an acromion fracture can result from a downward blow directly applied to the superior aspect of the acromion. Second, acromion fracture can result from superior displacement or dislocation of the humeral head. When the injury is a result of a downward blow to the acromion, acromioclavicular dislocation is much more common than acromion fracture. When a fracture does occur, however, it is usually minimally displaced. Caution should be used in distinguishing this minimally displaced fracture from an os acromiale. In questionable cases, a radiograph of the contralateral side may be helpful because the os acromiale is bilateral in 60% of the cases.[33] The supraspinatus outlet view may be useful in estimating the amount of displacement if any is present.[46] Significant displacement of an acromion fracture resulting from a downward blow to the acromion should alert the clinician to possible associated brachial plexus avulsions.[8] [45] Significant superior displacement of the acromion associated with superior displacement or dislocation of the humeral head should alert the clinician to possible injury to the rotator cuff.[45] The majority of acromion fractures, because they are minimally displaced, should be treated closed.[45] [58] [61] [62] [74] McLaughlin[42] stated that bony union is the rule, despite the presence or absence of immobilization, provided the fragments are in apposition. Neer[45] recommended symptomatic treatment only. Wilber and Evans,[74] on the other hand, reported residual stiffness in patients with acromion fractures. They recommended cast immobilization in 60 degrees of abduction, 25 degrees of flexion, and 25 degrees of external rotation for 6 weeks. Most authors recommend open reduction and internal fixation for markedly displaced acromion fractures to reduce the acromioclavicular joint and prevent nonunion, malunion, and secondary impingement.[44] [45] [62]

Kuhn and associates[29] recommended a classification system to help determine the need for operative intervention. Type I fractures with minimal displacement and type II displaced fractures without a decrease in the subacromial space warrant nonoperative treatment. In type II displaced fractures in which the subacromial space is diminished by the inferior pull of the deltoid on the acromial fragment, open reduction with internal fixation is required to prevent secondary impingement. Stress fractures of the acromion may occur in athletes. These injuries should be managed nonoperatively. Ward and colleagues[72] reported a stress fracture at the base of the acromion in a professional football player resulting from repeated microstresses secondary to weightlifting and blocking assignments. Veluvolu and associates[71] reported a case of an acromial stress fracture in a jogger using arm weights while running. Hall and Calvert[21] described a woman golfer who sustained a stress fracture at the base

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of the acromion as a result of repetitive stress by repeated shots and contraction of the

posterior deltoid as the club struck the golf ball. Stress fractures have also been reported after subacromial decompression secondary to thinning of the acromion. [35] [37] [73]

Glenoid (Intra-articular) Fractures

Historically, intra-articular glenoid fracturesin the absence of associated glenohumeral instabilityhave been managed nonoperatively.[8] [74] Intact glenohumeral ligaments act to prevent gross displacement of the fracture. Many authors have reported good early functional results in patients treated nonoperatively with intra-articular glenoid fractures without associated instability[25] [57] [58] [62] ( Figs. 21F-14 and 21F-15 ). Surgical intervention was initiated only for glenoid fractures associated with glenohumeral instability.[3] [13] These reports were limited because standardized outcome measures were lacking and the incidence of late glenohumeral arthritis was unknown. Surgical treatment of glenoid fractures has received greater attention

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recently.* Indications for open reduction and internal fixation of intra-articular glenoid fractures depend on fragment size, fracture displacement, and stability of the glenohumeral joint. (Figure Not Available)

Figure 21-F-14 A combined glenoid articular fracture with satisfactory position. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 21-F-15 This fracture healed well without problems and with good preservation of the joint surface. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Glenoid rim fractures (type I) are usually sustained during traumatic glenohumeral subluxation or dislocation. In the setting of recurrent anterior instability, Rowe and coworkers[62] [63] recommended excision of an anterior rim fragment of up to 25% of the articular surface with repair of the capsule back to the remainder of the glenoid. DePalma [13] believed that glenohumeral instability will result if the fragment is greater than 25% of the anterior rim, greater than 33% of the posterior rim, or displaced more than 10 mm. He recommended immediate open reduction for these situations.[13] Rockwood [57] recommended open reduction of the fragment with screw fixation if the fracture involves at least 25% of the glenoid and is associated with instability. Whereas debate exists among surgeons about the amount of displacement and the size of the fragment that are acceptable, it is well accepted that rim fractures associated with persistent or recurrent instability should undergo open reduction and internal fixation.[3] [8] [13] [22] [25] [50] [57] [65] The size of the glenoid rim fragment and the quality of the bone determine the method of fixation to stabilize the fragment. Anterior glenoid rim

fragments that are too small to accommodate a screw can be reduced and stabilized with suture anchors in the glenoid, with sutures passed through the fragment and tied ( Fig. 21F-16 ). Screw fixation can be used for large enough fragments with good bone quality ( Fig. 21F-17 ). Arthroscopically assisted reduction and percutaneous fixation of a displaced intra-articular glenoid fracture has been reported with good results.[10] [11] Careful monitoring of fluid extravasation and assessment for compartment syndrome are recommended. If the rim fracture is comminuted, the fragment can be excised, and a tricortical graft harvested from the iliac crest can be internally fixed to the glenoid rim.[18] The results of operative fixation of glenoid rim fractures have been successful; most authors reported restoration of glenohumeral stability and good functional results. [3] [4] [7] [8] [10] [11] [50] [65]

Figure 21-F-16 Anteroposterior radiograph (A) and computed tomographic scan (B) of an anterior glenoid rim fracture (type Ia) involving approximately 33% of the articular surface, resulting in anterior instability of the shoulder. The fracture was repaired with five suture anchors through an anterior deltopectoral approach. Postoperative radiographs show anatomic reduction (C) and a reduced glenohumeral joint (D).

Figure 21-F-17 Anteroposterior radiograph (A) and magnetic resonance image (B) demonstrate a posterior glenoid fracture involving approximately 40% of the articular surface, leading to posterior subluxation of the humeral head. Note the comminution extending down into the articular surface and lateral scapular body. This fracture was repaired by limited internal fixation to restore the posterior glenoid rim and glenohumeral stability (C).

For glenoid fossa fractures of type II to type V, the *See references [ 4] [ 6] [ 10] [ 11] [ 18] [ 20] [ 28] [ 30] [ 32] [ 38] [ 48] [ 50] and [ 65] . See references 4[ 4] , 6[ 6] , 10[ 10] , 11[ 11] , 13[ 13] , 18[ 18] , 20[ 20] , 25[ 25] , 28[ 28] , 30[ 30] , 32[ 32] , 38[ 38] , 48[ 48] , 50[ 50] , 57 [ 57] , 62[ 62] , 63[ 63] , and 65[ 65] .

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amount of articular displacement and the degree of comminution determine the need for open reduction and internal fixation ( Fig. 21F-18 ). Goss[20] recommended open reduction and internal fixation for an articular step-off of 5 mm or more. Kavanagh and associates [28] described successful surgical treatment of displaced (4 to 8 mm) intra-articular fractures of the glenoid fossa. They emphasized that uncertainty still remained with regard to the amount of glenoid articular incongruity that could be accepted without risking long-term pain, stiffness, and post-traumatic degenerative arthritis. Poppen and Walker[55] demonstrated that transarticular forces of 0.9 times body weight can be generated at 991

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the glenohumeral joint by lifting a 5-kg mass to shoulder height with the elbow extended. This suggests that disruption of articular congruence probably leads to unacceptable joint contact stress. Soslowsky and coworkers[67] demonstrated that the maximal thickness of glenoid articular cartilage is 5 mm. On the basis of this information, several surgeons have adopted displacement of 5 mm or more as the indication for reduction and stabilization.[3] [6] [28] [31] [64] The results of operative fixation of glenoid fossa fractures have been less predictable. Bauer and colleagues[6] reported greater than 70% good or very good functional results for patients treated surgically for grossly displaced fractures of the glenoid rim, neck, fossa, and acromion. Leung and associates[31] reported 9 excellent and 5 good results in 14 patients treated surgically for displaced intra-articular glenoid fractures. Mayo and associates[38] reviewed 27 displaced glenoid fossa fractures treated with open reduction and internal fixation at 43 months of follow-up and found that 82% of patients had good or excellent results. Three patients had articular incongruities measuring 2 mm or less. Ruedi and Chapman[64] maintain that glenoid fractures that result in incongruity and instability benefit from open reduction and internal fixation to prevent arthritic changes.

Figure 21-F-18 A, Anteroposterior radiograph shows an intra-articular glenoid fracture involving the superior half of the glenoid (type III). B, Computed tomographic scan demonstrates involvement of the coracoid process. C and D, The fracture was reduced and fixed with a superior-to-inferior lag screw and an anterior plate. E, The patient regained full forward elevation and had an excellent result.

Type V fractures are treated operatively if the degree of comminution is minor and will allow stable fixation. If comminution is too severe to permit fixation of all fragments, limited reduction and stabilization of the articular segment is performed. If fracture comminution prevents even limited fixation, nonoperative management is employed. For type VI fractures, the degree of comminution dictates the method of treatment. The comminution associated with type VI fractures is typically too severe to allow internal fixation except in rare instances when limited fixation of larger fragments can be accomplished. To maximize functional results after operative intervention, fixation must be rigid enough to allow early passive mobilization. Severe comminution that prevents stable fixation is best managed nonoperatively with early motion. Type VI fractures in which the humeral head is well centered are managed nonoperatively.

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Treatment Options in Children

The criteria for operative treatment of scapular and glenoid fractures in children and adolescents are not known. These types of injuries are extremely uncommon in children and adolescents. In addition, the capacity for remodeling in children makes the amount of tolerable displacement less certain. The amount of glenoid or scapular remodeling possible as a function of age is not known. Therefore, treatment recommendations must be made intuitively, based on the age and projected growth remaining. Nonoperative treatment is recommended for the vast majority of scapular fractures in children. The only potential exceptions to this rule are displaced glenoid fossa fractures, floating shoulders with greater than 3 cm of displacement of the glenoid fragment, and glenoid rim fractures that are associated with recurrent or persistent glenohumeral instability.

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Authors' Preferred Method of Treatment in Adults Glenoid Neck Fracture

The majority of glenoid neck fractures are impacted and stable and do not require any reduction to obtain a good clinical result. Symptomatic local care, followed by passive exercises, will result in a rapid return of motion. Strengthening exercises may be instituted at 4 to 6 weeks. In the case of a double disruption of the superior shoulder suspensory complex, including the glenoid neck and another portion of the superior shoulder suspensory complex, surgical management becomes necessary if displacement at one or both sites in unacceptable. Reducing and stabilizing one of the disruptions will usually indirectly reduce and stabilize the other, if the reduction is performed acutely (within 1 week of injury). Ipsilateral glenoid neck and clavicle fractures are managed operatively if medial displacement of the glenoid neck fracture is more than 3 cm. In most acute cases, reduction and stabilization of the clavicle will reduce and stabilize the glenoid neck. If clavicular fixation fails to reduce the medial displacement of the glenoid neck, reduction and fixation of the glenoid neck are carried out. Criteria for Return to Athletics.

Healing is normally complete after approximately 6 weeks. Return to sports should be delayed, however, until range of motion has returned to normal and the strength of the shoulder is 90% of that of the uninvolved extremity. This normally takes 3 to 4 months. Body and Spine Fractures

Assuming that serious associated injuries have been ruled out, symptomatic treatment is indicated for virtually all patients with this type of fracture. Ice and sling immobilization

are used initially. Within 1 to 2 weeks, passive range of motion and stretching exercises can be instituted. As pain and swelling subside, active range of motion and progressive-resistance exercises can be instituted. Criteria for Return to Athletics.

The athlete should be withheld from competition until the fracture has healed and there is a full range of motion (typically 6 to 12 weeks). Foam padding over the posterior aspect of the scapula helps cushion blows that may be encountered when the athlete returns to contact competition. Acromion Fractures

Most acromion fractures are stable and are minimally displaced. Therefore, a sling is required for only 3 to 5 days. When pain diminishes enough to permit exercise, active and passive range of motion exercises are begun. Resisted deltoid exercises are avoided for 6 weeks to allow fracture union. In the instance of a displaced acromion fracture, open reduction and internal fixation are performed with tension band or compression screw fixation for distal

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fractures or a 3.5-mm malleable reconstruction plate for more proximal injuries. Caution should be exercised to rule out the presence of os acromiale, rotator cuff tear, or brachial plexus injury. Criteria for Return to Athletics.

The athlete with an acromion fracture, regardless of whether it was displaced and required fixation, should be withheld from competition until fracture union is complete and range of motion is pain free. This normally requires between 6 and 12 weeks. If the fracture was accompanied by a complication, such as a rotator cuff tear or brachial plexus injury, appropriate treatment should be instituted and return to sport delayed accordingly. Glenoid Fractures

Stable Glenohumeral Joint

Glenoid fossa fractures with less than 5 mm of displacement that are not associated with instability are treated symptomatically, with a sling for immobilization, until pain permits range of motion exercises (7 to 10 days). Glenoid rim or fossa fractures involving 20% or more of the articular surface that are displaced more than 5 mm are treated surgically.

Type II to type V glenoid fossa fractures with displacement of 5 mm or more are treated surgically. The approach depends on whether extensile exposure of the lateral angle of the scapula is required. Extensile exposure of the anterior aspect of the lateral scapular border is limited because of the axillary nerve. The posterior approach is the most utilitarian and is used for most type II, type IV, and type V fractures. An extensile exposure may be obtained by reflecting the posterior deltoid origin from its attachment on the scapular spine ( Fig. 21F-19 ). Displaced type III glenoid fossa fractures usually do not require exposure of the lateral scapular border and can frequently be stabilized through an anterior deltopectoral approach. If the posterior cortex is comminuted, a posterior deltoid-splitting approach may be used in place of an anterior approach.

Figure 21-F-19 Posterior extensile exposure of the glenoid. The skin incision begins at the base of the scapular spine and extends laterally, parallel to the scapular spine. At the posterolateral corner of the acromion, the incision turns distally and medially and parallels the lateral border of the scapula (A). The posterior deltoid is reflected from its origin on the scapular spine from its most medial attachment to the posterolateral corner of the acromion. The interval between the infraspinatus and teres minor is indicated by the curved arrow (B). The infraspinatus insertion is sharply divided and retracted medially, thereby protecting the supraspinatus nerve at the supraspinatus notch (C). The teres minor and the axillary nerve are retracted laterally, providing excellent exposure to the posterior scapula (D). A plate is applied to the posterior aspect of the glenoid (E).

Rehabilitation is similar for operatively and nonoperatively treated glenoid fossa fractures without glenohumeral instability because both are stable. Passive mobilization is instituted within the first week of injury or surgery. Active-assisted range of motion is added at 4 weeks. Strengthening exercises are added as range of motion is restored and absence of pain permits (typically 6 to 8 weeks). When nonoperative management is undertaken (i.e., less than 5 mm of displacement), close follow-up with radiographs and physical examination is necessary to document maintenance of glenohumeral stability. Criteria for Return to Athletics.

Return to sport is possible after fracture union has occurred, range of motion has reached its maximal level, and strength has returned to within 90% of that of the opposite extremity (typically 3 to 4 months, depending on the type of fracture). The athlete should be warned about the possibility of the development of glenohumeral arthritis, particularly if he or she is involved in a sport that places a large demand on the shoulder. Unstable Glenohumeral Joint

Anterior glenoid fractures (type Ia) associated with glenohumeral instability are best treated with surgical repair. If the fragment is of good quality and large enough to accept a small fragment screw, open reduction with internal fixation through an anterior deltopectoral approach is performed. The fragment is reduced and held provisionally with a temporary wire, and a standard 3.5-mm cortical or partly threaded cancellous

screw is used for definitive fixation. Smaller fractures may be fixed with suture anchors placed in the glenoid and sutures passed through the fragment. If the fragment is too small to accommodate a screw or suture, it is excised, and the anteroinferior capsule is repaired to the raw surface of the remaining glenoid. Pendulum exercises are begun immediately postoperatively. At 2 to 3 weeks postoperatively, the patient is encouraged to use the arm for everyday living activities, and gentle passive flexion and external rotation exercises are begun. At 6 to 8 weeks, stretching and strengthening exercises are instituted. Posterior glenoid fractures (type Ib) with significant displacement or posterior glenohumeral instability require operative intervention through a posterior approach. A deltoid-splitting approach is usually adequate. If the fragment is not too large, this may be combined with a muscle-splitting, internerve approach between the infraspinatus and teres minor or an infraspinatus-splitting approach. The more distal interval (i.e., between infraspinatus and teres minor) is preferred if the fragment involves the inferior third of the glenoid or if the fragment is large. This exposure can be made extensile by reflecting the infraspinatus and elevating the dorsal portion of the teres minor origin. If exposure of the midportion of the posterior glenoid is required, an infraspinatus-splitting approach may be more appropriate. If the fragment represents 25% or more of the articular surface, it is reduced and stabilized with a screw. Smaller fragments are excised, and the capsule is reattached to the remaining glenoid. Criteria for Return to Athletics.

Regardless of whether the fragment has been excised or fixed, the presence of glenohumeral instability dictates postponement of a return to competition. Rehabilitative efforts should concentrate on passive range of motion until fracture union has occurred. Further therapy should emphasize restoration of glenohumeral stability through rotator cuff and scapular stabilizer muscle exercises. Return to sport is possible after glenohumeral stability has been achieved, range of motion is restored, and strength has returned to within 90% of that of the opposite extremity (typically 4 to 6 months for anterior instability and 6 to 9 months for posterior instability). The athlete should be warned about the possibility of the development of glenohumeral arthritis, particularly if he or she is involved in a sport that places a large demand on the shoulder.

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Authors' Preferred Method of Treatment in Children

All extra-articular scapular fractures in children who are 12 years and younger are treated nonoperatively initially.

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This recommendation is based on the belief that most if not all of these fractures will heal and that the potential for remodeling is significant. The only exception to this rule is a displaced (>3 cm) glenoid neck fracture in combination with a displaced, ipsilateral clavicle shaft fracture (i.e., a floating shoulder). Under these circumstances, the clavicle is reduced anatomically and fixed rigidly with a plate and screws. Glenoid rim fractures in children who are 12 years and younger are not treated operatively unless they are associated with recurrent or persistent glenohumeral instability or are displaced 1 cm or greater. The indications in children older than the age of 12 for operative treatment are the same as for adults. The surgical techniques for stabilization of glenoid rim fractures in children are the same as those described for adults. In children who are 12 and younger,

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the technique of placing suture anchors within the remaining, uninvolved glenoid and passing sutures through the osseocartilaginous glenoid rim is preferred. Anchors with long-term absorbable (i.e., 3 months) sutures are preferred. Glenoid fossa fractures in patients older than 12 are treated similarly to glenoid fossa fractures in adults. The potential for remodeling is greater in children who are 12 and

younger. The amount of residual displacement that is capable of being remodeled is not known. Open reduction with internal fixation is currently performed in glenoid fossa fractures with 1 cm or greater of articular displacement. The surgical techniques, postoperative rehabilitation, and timing for return to athletics are the same as for adults.

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Rockwood CA Jr: Fractures and dislocations of the shoulder. Part II. Subluxations and dislocations about the shoulder. In Rockwood CA Jr, Green DP (eds): Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984, pp 722-950. 57.

58.

Rockwood CA Jr: Management of fractures of the scapula. Orthop Trans 10:219, 1986.

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Rockwood CA Jr: Personal communication, 1989.

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Rokous JR, Feagin JA, Abbott HG: Modified axillary roentgenogram. Clin Orthop 82:84-86, 1972.

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Rowe CR: Fractures of the scapula. Surg Clin North Am 43:1565-1571, 1963.

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Rowe CR: The Shoulder. New York, Churchill Livingstone, 1987, pp 373-381.

Rowe CR, Patel D, Southmayd WW: The Bankart procedurea long-term end-result study. J Bone Joint Surg Am 60:1-16, 1978. 63.

Ruedi T, Chapman MW: Fractures of the scapula and clavicle. In Chapman M (ed): Operative Orthopaedics. Philadelphia, JB Lippincott, 1988, pp 197-202. 64.

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Sinha J, Miller AJ: Fixation of fractures of the glenoid rim. Injury 23:418-419, 1992.

Solheim LF, Roaas A: Compression of the suprascapular nerve after fracture of the scapular notch. Acta Orthop Scand 49:338-340, 1978. 66.

Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop 285:181-190, 1992. 67.

68.

Tachdjian MO: Pediatric Orthopedics. Philadelphia, WB Saunders, 1972, pp 1553-1555.

Thompson DA, Flynn TC, Miller PW, Fischer RP: The significance of scapular fractures. J Trauma 25:974-977, 1985. 69.

Van Wellen PAJ, Casteleyn PP, Opdecam P: Traction-suspension therapy for unstable glenoid neck fracture. Injury 23:57-58, 1992. 70.

Veluvolu P, Kohn HS, Guten GN, et al: Unusual stress fracture of the scapula in a jogger. Clin Nucl Med 13:531-532, 1988. 71.

Ward WG, Bergfeld JA, Carson WG Jr: Stress fracture of the base of the acromion process. Am J Sports Med 22:146-147, 1994. 72.

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Warner JJP, Port J: Stress fracture of the acromion. J Shoulder Elbow Surg 3:262-265, 1994.

Wilber MC, Evans EB: Fractures of the scapulaan analysis of forty cases and review of literature. J Bone Joint Surg Am 59:358-362, 1977. 74.

Williams GR, Silverberg DA, Iannotti JP, et al: Nonoperative treatment of the ipsilateral clavicle and glenoid fracture. Presented at 15th Open Meeting of the American Shoulder and Elbow Surgeons, October 1999, Anaheim, Calif. 75.

Wilson PD: Experience in the Management of Fractures and Dislocations (Based on an Analysis of 4390 Cases) by the Staff of the Fracture Service Massachusetts General Hospital, Boston. Philadelphia, JB Lippincott, 1938. 76.

Wyrsch RB, Spindler KP, Stricker PR: Scapular fracture in a professional boxer. J Shoulder Elbow Surg 4:395-398, 1994. 77.

Zdravkovic D, Damholt VV: Comminuted and severely displaced fractures of the scapula. Acta Orthop Scand 45:60-65, 1974. 78.

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Section G Fractures of the Coracoid in Adults and Children Allen Deutsch MD Gerald R. Williams MD Fractures of the coracoid process of the scapula are uncommon and have received especially little attention in the sports medicine literature. Injury may occur as an apparently isolated phenomenon or in association with other injuries about the shoulder girdle. The coracoid process of the scapula serves as an anchoring point for the attachment of multiple ligaments and muscles. Ligaments include the coracohumeral and coracoacromial ligaments and the conoid and trapezoid components of the coracoclavicular ligaments. These last two ligaments perform an essentially suspensory function, exerting a static upward force on the scapula through the coracoid process.[7] On the contrary, the muscular attachments exert a dynamic, active, and largely inferior force on the coracoid. The muscular origins comprise the pectoralis minor from the body and tip of the coracoid and the conjoined tendon from the tip incorporating the coracobrachialis and the short head of the biceps brachii. Consideration of these ligamentous and muscular attachments to the coracoid will give some insight into the proposed mechanisms of coracoid fracture. The location of the coracoid fracture (i.e., tip, body, or base in relation to the musculoligamentous structures) will also determine the stability of the fracture and hence the propensity for displacement. Mechanism of Injury

Mariani[16] has suggested that direct and indirect mechanisms cause acute coracoid fracture. The direct type of injury appears to be a relatively rare phenomenon, probably because of the coracoid's deep-seated, sheltered anatomic location. Therefore, a direct external blow to the coracoid severe enough to result in fracture usually involves massive trauma more common to motor vehicle accidents than to sporting endeavors. Direct trauma to the coracoid from the interior may arise in two circumstances, however. Anterior translation of the humeral head in subcoracoid glenohumeral dislocations may

result in a direct coracoid impact that is sufficient to cause fracture.[1] [10] [30] [32] This too must be considered an uncommon injury, but it has been proposed that the combination of glenohumeral dislocation with coracoid fracture may be underdiagnosed. As is discussed later, this shortcoming may be related to the difficulty of obtaining a good axillary lateral radiograph in an acutely painful shoulder or to the widespread practice of relying on the more difficult-to-interpret and less readily reproducible scapular lateral radiograph. McLaughlin[15] considered glenohumeral dislocation the most common cause of coracoid fracture. It has also been suggested that an undetected coracoid fracture might account for occasional cases of prolonged convalescence after glenohumeral dislocation[1] and may conceivably be confused with recurrent anterior instability or rotator cuff disease. Wong-Chung described fracture of the coracoid tip that prevented closed reduction of an anterior glenohumeral dislocation.[31] The other direct mechanism of coracoid fracture would in theory involve a blow to the lateral clavicle causing inferior displacement and impact with the coracoid. [16] This would result in acromioclavicular ligamentous

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disruption but would preserve the coracoclavicular ligaments. Although this scenario appears not to have received specific attention in the literature, it is possible that some apparently isolated, undisplaced coracoid fractures might arise in this manner. The stress radiograph, discussed later, would be of particular relevance in this situation. So-called indirect mechanisms probably account for the majority of fractures of the coracoid process. An indirect mechanism is probably most often responsible for isolated coracoid fractures.[4] [16] Smith[26] described this mechanism in terms of a sudden, violent, and resisted contraction of the conjoined tendon and pectoralis minor. Wyrsch and associates described a case of an extra-articular scapula fracture with extension into the coracoid process in a professional boxer resulting from to a violent muscle contraction.[33] Mariani[16] concluded that the coracoid is especially vulnerable to the stress of muscular action when the arm is in the position of abduction and extension. Benton and Nelson[2] drew attention to the stress placed on the coracoid when the arm is in this position. Another indirect mechanism of coracoid fracture involves a direct blow or fall onto the point of the shoulder,[22] causing superior subluxation or dislocation of the lateral clavicle. Rather than the more common rupture of the coracoclavicular ligaments, the coracoid (proximal to the coracoclavicular ligaments) may fail.[3] [14] [18] [20] [26] [27] The pain accompanying the coracoid fracture may overshadow the acromioclavicular disruption so that, again, this injury may be misinterpreted as an isolated coracoid fracture if stress radiographs are not obtained.[16] [26] More commonly, however, the acromioclavicular dislocation is recognized and the coracoid process fracture is unappreciated. Avulsion fractures of the coracoid resulting from strong traction forces have also been reported.[21] In addition to these direct and indirect mechanisms involving significant trauma,

repetitive forces of a lesser degree have been reported by a number of authors to be a source of coracoid stress fracture. Boyer [4] and Sandrock[25] in separate reports described a fracture of the coracoid base in a young female trapshooter. The position of the gun butt directly over the coracoid tip was confirmed radiologically. Symptoms resolved, and the fracture healed when shooting was stopped. This appears to be an example of repetitive direct trauma resulting in stress fracture. A case of indirect trauma resulting from repetitive muscular action and leading to coracoid stress fracture in its distal half was reported by Benton and Nelson.[2] They described a 19-year-old tennis player with a 4-year history of shoulder pain. It had been of insidious onset and was aggravated during serving. This patient eventually required excision of the distal fragment and reattachment of the conjoined tendon. Nontraumatic causes of coracoid fractures have also been described secondary to nonresorbable coracoclavicular tape fixation for acromioclavicular reconstruction, as well as in association with massive rotator cuff tears.[17]

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Pattern of Coracoid Fracture

The pattern of coracoid fracture is variable. Most such fractures occur through the base of the process,[1] [4] [13] [16] [23] and this is almost invariably the case with associated acromioclavicular injuries. Basal coracoid fractures may very rarely involve a significant portion of the superior portion of the glenoid articular surface. Fractures of the body or tip of the coracoid process of the scapula without acromioclavicular injury seem to be related more to violent muscular action[2] [7] [10] [34] but have been associated with anterior glenohumeral dislocation.[32] These more distal fractures also appear to be more troublesome in terms of delayed union or nonunion and the related problem of displacement.[10] Both these problems are well demonstrated in the previously mentioned case report by Benton and Nelson[2] of a distal stress fracture in a young tennis player. These problems of union and displacement and hence the possibility of persistent symptoms seem to be related to the location of the fracture in relation to the coracoclavicular ligaments.[7] A fracture within the broad area of the attachment of these ligaments is likely to be splinted and minimally displaced. As the fracture line moves toward the tip and hence beyond the attachments of the conoid and trapezoid ligaments, however, the coracoid tip becomes increasingly subject to the displacing action of the pectoralis minor and the conjoined tendon.[2] [10] Coracoid fracture has been described in association with acromioclavicular separation and glenohumeral dislocation. Montgomery and Loyd[18] described two adolescents with coracoid apophyseal avulsion at the site of attachment of the coracoclavicular ligament. Combalia and colleagues described a case of a 12-year-old boy who sustained an acromioclavicular dislocation with epiphyseal separation of the coracoid process as a result of a fall during a soccer match.[5] Certain other associations have also been recognized. Zilberman and Rejovitzky[34] encountered coracoid fractures in conjunction with clavicular shaft and acromion fractures. Wolf and colleagues[30] described a combination of coracoid base fracture and avulsion of a thin spicule from the superior border of the scapula medial to the coracoid. This pattern of injury may be due to the fact that the fragments are connected by the suprascapular ligament ( Fig. 21G-1 ). Acromioclavicular separation with coracoclavicular ligament disruption and coracoid

fracture has also been described.[28] [29]

Figure 21-G-1 An anteroposterior radiograph of a patient with a fracture through the base of the coracoid process that includes the superior border of the scapula.

Neurologic injuries may also be seen with coracoid fractures. [22] The brachial plexus deep to the coracoid and pectoralis minor may be contused, resulting in either specific or subtle patchy neurologic deficits. Basal coracoid fractures may especially result in suprascapular nerve entrapment and may be confused with rotator cuff tears[22] ( Fig. 21G-2A and B ).

Figure 21-G-2 A, The coracoid process serves as the insertion of the pectoralis minor and the origin of the conjoined tendon of the coracobrachialis and the short head of the biceps. Reflection of the pectoralis reveals the proximity of the underlying brachial plexus. B, The suprascapular nerve is at risk with fractures of the coracoid base that extend into the superior scapular notch.

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Clinical Features of Coracoid Fractures History

The history of coracoid fractures caused by shoulder injury is not particularly specific. Approximately one third of reports of coracoid fractures attribute the injury to a motor vehicle accident.[3] The next most common history obtained is that of a fall onto the point of the shoulder or

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a direct blow to the shoulder. It is of interest that football injuries involving both these mechanisms appear regularly in the literature. Typical football injuries have included a fall onto the shoulder, a direct blow from running into a goalpost, and apparently impact sustained during a rugby scrum.[16] A fall backward onto the extended abducted and externally rotated arm also appears to be a well-established mechanism[7] [10] and may be brought out in the history. As previously discussed, coracoid stress fracture appears to be a real entity in sportsmen.[2] [4] [25] A history of acute injury is conspicuously absent, and recalcitrant symptoms of insidious onset may pose a diagnostic dilemma. Pain is an invariable complaint with acute fracture of the coracoid but may be poorly localized at the front of the shoulder. Pain may be aggravated by arm movements that exert muscular forces onto the coracoid. The patient may recognize these particular movements, which include elbow flexion,[9] shoulder flexion with the elbow extended,[2] [16] and combined shoulder abduction, extension, and external rotation.[9] Similarly, the patient may volunteer the fact that the pain is aggravated by deep inspiration owing to pectoralis minor activation.[2] [16]

As with all shoulder girdle injuries, neurologic symptoms[22] may be prominent, especially in the form of transient paresthesias. This is not surprising in view of the intimate relationship of the major neurovascular structures to the coracoid and pectoralis minor. Physical Examination

Unless there has been an associated injury to the acromioclavicular joint or a glenohumeral dislocation, there will

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usually be no striking external abnormality. Falls onto or direct blows to the shoulder may, of course, result in localized areas of contusion or abrasion. Despite the deep-seated location of the coracoid process, swelling or loss of definition in the deltopectoral interval may be detected.[9] Marked localized tenderness on palpation is a key finding. Specific stress tests[2] [9] [16] such as resisted elbow flexion, resisted straight arm raising, and coughing may also sharply localize discomfort to the coracoid region. Whenever suspicion of a coracoid injury is raised, attention should be specifically directed to the acromioclavicular joint and vice versa. Local acromioclavicular tenderness, swelling, subluxation, or obvious superior dislocation of the lateral clavicle may be apparent. As always, comparison with the normal shoulder may be of considerable assistance. Neurologic examination is mandatory in cases of coracoid fracture. Because deficits may be patchy and subtle, a thorough brachial plexus assessment is essential. Special emphasis should be placed on suprascapular nerve evaluation because of the risk of entrapment. [22] Diagnostic Studies

The anteroposterior view should be part of the routine shoulder series and is of particular relevance in detecting associated acromioclavicular injuries or fractures[30] [34] ( Fig. 21G-3 ). Although it is possible to diagnose some coracoid fractures with a plain anteroposterior radiograph, [9] it is likely that most will be overlooked without additional views[2] ( Fig. 21G-4 ). This is because the coracoid process is foreshortened and projected over the acromion and the spine of the scapula in this view. [12] Many authors have stressed the value of the axillary lateral view in diagnosing coracoid fractures,[1] [2] [3] [4] [22] [32] but even this view may fail to demonstrate a basal coracoid fracture [12] ( Fig. 21G-5 ). Froimson[9] has also pointed out that the abduction required for a good axillary lateral view may be difficult to obtain because of the pain it provokes in patients with acute coracoid fractures. A much better profile of the coracoid, including the base, can be obtained by tilting the x-ray beam in a cephalic direction. This obviates the need to move the patient's arm. Most authors recommend a supine position with a 30- to 35-degree cephalic tilt. [12] [16] [20] [32] [34] Froimson found that a cephalic tilt of as much as 45 to 60 degrees was quite useful. Although the Stryker notch view was originally intended to identify the Hill-Sachs lesion characteristic of anterior glenohumeral dislocations, the authors have found this technique especially useful in studying

coracoid fractures[11] ( Fig. 21G-6 ). Kopecky and colleagues[13] reported on the value of computed tomography scanning when doubt exists. The authors have also found that this modality is helpful in clarifying coracoid fracture morphology ( Fig. 21G-7 ).

Figure 21-G-3 Combined coracoid process fracture and acromioclavicular dislocation as demonstrated on routine anteroposterior radiograph.

Figure 21-G-4 A, A coracoid process fracture that is well visualized on a routine anteroposterior radiograph. B, Fractures of the base of the coracoid process can be difficult to visualize on routine anteroposterior views.

Figure 21-G-5 A, Fractures of the tip of the coracoid process are frequently well visualized on an axillary lateral radiograph. B, Basal fractures of the coracoid process can be difficult to demonstrate, even on an axillary lateral radiograph.

Figure 21-G-6 The Stryker notch view is very helpful in demonstrating basal coracoid process fractures that are difficult to visualize on other routine views.

Figure 21-G-7 Computed tomography scanning is occasionally useful for clarifying the morphology of certain coracoid fractures.

Specific attention should be paid to the acromioclavicular joint in the presence of coracoid fracture. Despite acromioclavicular dislocation, the coracoclavicular distance will be maintained[3] [16] [26] ( Fig. 21G-8 ). Erect anteroposterior films of both shoulders are necessary to compare the coracoclavicular distance on the injured side with the uninjured side. Although stress views may be helpful in some cases, most often they are not required.

Figure 21-G-8 An anteroposterior stress radiograph of this patient with a combined coracoid process fracture and an acromioclavicular dislocation reveals that the coracoclavicular interspace has been maintained.

Normal coracoid epiphyses or apophyses should not be confused with fractures.[2] [11] The coracoid process forms from two ossification centers. The basal ossification center also forms the upper third of the glenoid, whereas the other forms the main body of the coracoid. The basal epiphyseal plate fuses at puberty. Smaller accessory ossification centers that are shell-like and rounded may be seen medial to the coracoid base or at

its very tip ( Fig. 21G-9 ). Cottalorda and colleagues described a case of a 15-year-old boy who suffered a displaced epiphyseal separation as a result of a direct fall onto the shoulder while participating in judo.[6]

Figure 21-G-9 A, The normal basal coracoid physis as demonstrated on the Stryker notch view. B, The normal ossification center at the tip of the coracoid process.

The only other diagnostic study apart from radiography that may be necessary is electromyography, which is indicated if suprascapular nerve entrapment is suspected.[22] This most often occurs subacutely when the pain associated

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with the acute fracture has subsided and strength of the supraspinatus and infraspinatus can be accurately assessed.

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Treatment Options

Acute isolated fracture of the coracoid base is almost invariably nondisplaced and is treated conservatively with the expectation of a good result. [7] If the acromioclavicular joint is sound, the basal fracture is splinted by the coracoclavicular ligaments, and displacement is minimal. Fracture surfaces are relatively large and predominantly cancellous. Prompt union is generally anticipated. Nonunion is infrequent, may be related to premature return to vigorous activities, and may require bone grafting and screw fixation ( Fig. 21G-10 ). Essentially, the basic treatment ought to be symptomatic, resting the affected arm in a sling, administering analgesia for the initially severe pain, and gradually mobilizing the shoulder as symptoms regress and radiographic healing occurs. Basal coracoid fracture with suprascapular nerve palsy is a rare indication for early operative exploration, especially if there is any displacement of the fracture with narrowing of the suprascapular notch. The prognosis for recovery from suprascapular entrapment appears to be poor once cancellous bone has formed in the region of the suprascapular notch.[22]

Figure 21-G-10 A, Stryker notch view demonstrating nonunion of the base of the coracoid process in an 18-year-old football player. B, The nonunion was fixed through an anterior deltopectoral approach with an interfragmentary screw and bone graft.

As the location of an isolated coracoid fracture approaches the tip of the coracoid process, opinions about treatment diverge. The closer the fracture gets to the tip of the coracoid process, the smaller is the stabilizing effect of the coracoclavicular ligaments and the greater is the propensity for displacement or nonunion exerted by the muscular attachments at the tip. Rowe[24] recommends simple approximation of fragments with nonresorbable sutures in this situation, whereas McLaughlin[15] considers that fibrous union is not uncommon and is rarely accompanied by any residual symptoms ( Fig. 21G-11 ). Benton described late surgical treatment of a displaced coracoid fracture that irritated the surrounding soft tissue structures. [2] Marked displacement and delayed

union of these more distal fractures may significantly delay recovery. [2] [7] [10] Moreover, surgical management of significantly displaced fractures frequently

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yields satisfactory results. When surgical management is selected, the choice is between fixation of the fragment and, if it is especially distal, excision of the fragment and reattachment of the pectoralis minor and conjoined tendon to the residual coracoid stump.

Figure 21-G-11 A, Axillary lateral view demonstrating an acute fracture of the coracoid in a 42-year-old woman who sustained a glenohumeral dislocation. This patient also suffered concomitant suprascapular nerve palsy and was managed nonoperatively. B and C, At 2 years' follow-up, the suprascapular nerve palsy had resolved, the patient had returned to all previous activities, and physical examination revealed small deficits in forward elevation and internal rotation.

Similarly, for a combined coracoid fracture and acromioclavicular dislocation, there appears to be no single best line of management. Bernard and associates, [3] in a comprehensive review of this dual injury, found that surgical and nonsurgical methods of treatment appear to offer equally favorable results. It is also of interest that coracoid non-union appeared to be no more common with this injury. Should nonunion arise, its combination with complete acromioclavicular dislocation appears to be compatible with a functional pain-free result.[14] Eyres and coworkers recently described a classification system for coracoid fractures that is based on the size of the coracoid fragment and whether a clavicle fracture or an acromioclavicular separation is present.[8] They recommend surgical treatment of displaced fractures that extend into the glenoid or scapular body, fractures associated with clavicle fracture or acromioclavicular separation, and fractures with interposed coracoid fragments preventing reduction of glenohumeral joint dislocation. Ogawa and colleagues described their experience with treatment of 67 coracoid fractures.[19] Most patients had associated injuries, including acromioclavicular separations, clavicle fractures, and scapula fractures, that disturbed the link between the scapula and the clavicle. They recommended open reduction and internal fixation of coracoid fractures that were posterior to the attachment of coracoclavicular ligaments to restore the scapuloclavicular connection to permit early therapy. When one is dealing with athletes with combined acromioclavicular dislocation and a displaced coracoid base fracture, the unusual physical demands of their sport may influence treatment more toward anatomic restoration. If this course is taken, the fracture location itself may preclude coracoclavicular fixation techniques, and transarticular pins may become necessary[26] ( Fig. 21G-12 ). Screw fixation of the coracoid back to the body of the scapula is technically difficult but may be indicated if the fracture is not fixed acutely. Under these circumstances, direct fracture exposure is

necessary to accomplish reduction.

Figure 21-G-12 Combined coracoid process fracture and acromioclavicular dislocation treated with reduction and acromioclavicular wires.

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Authors' Preferred Method of Treatment Without Acromioclavicular Dislocation

Because the coracoclavicular and acromioclavicular ligaments remain intact in this injury, the fracture is stable. Therefore, treatment with a sling for comfort is sufficient. Pendulum exercises should be encouraged to prevent loss of motion in the shoulder; however, overhead elevation is restricted for 4 to 6 weeks to allow healing to occur at the base of the coracoid process. Criteria for Return to Athletics.

The athlete may return to competition after complete healing of the fracture and return of a full, painless range of motion. This usually requires 6 to 10 weeks. With Acromioclavicular Dislocation

When a coracoid process fracture is accompanied by a severely displaced acromioclavicular dislocation, open reduction with internal fixation is usually indicated. The displacement criteria for fractures of the coracoid base that involve the articular surface of the glenoid are more stringent than the criteria for fractures without articular involvement. Articular displacement of 5 mm or greater is treated with open reduction and internal fixation. Fixation options are limited because of the fracture of the coracoid process. Reduction and fixation of the acromioclavicular joint must be accompanied by reduction of the coracoid base/intra-articular glenoid component. Therefore, in spite of the small risk of acromioclavicular arthritis, fixation with transarticular smooth pins is indicated. The pins are removed at 6 to 8 weeks when radiographs reveal healing of the fracture. Before the pins are removed, the patient is not permitted to raise his or her arm overhead.

If the fracture is not reduced within 1 week, reduction of the acromioclavicular dislocation will most likely not result in simultaneous reduction of the coracoid fracture. Under these circumstances, direct exposure of the coracoid base fracture is required. Interfragmentary screw fixation is performed. Criteria for Return to Athletics.

After pin removal, fracture healing, and restoration of a full, pain-free range of motion, the athlete may return to competition. It is not necessary to wait for screw removal in those treated with interfragmentary screw fixation. Return to competition is encouraged after restoration of a full, pain-free range of motion. This normally requires 8 to 12 weeks.

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Fractures of the Distal Coracoid Process

Treatment for these fractures is symptomatic. The majority of patients become asymptomatic in 8 to 10 weeks regardless of the presence or absence of nonunion. Should a symptomatic nonunion result, excision of the fragment and reattachment of the pectoralis minor or conjoined tendons to the residual coracoid stump are curative. Criteria for Return to Athletics.

The athlete can return to competition when pain allows a full range of motion. This normally occurs approximately 4 to 6 weeks after injury.

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Postoperative Management and Rehabilitation

The postoperative rehabilitation of coracoid process fractures is the same as the nonoperative management of fractures that do not require surgery. This is because fractures selected for nonoperative management are either minimally displaced and stable or displaced without the need for anatomic reduction. Likewise, operatively treated fractures have been rendered stable. Pendulum exercises are instituted within 7 to 10 days of injury or surgery. Supine passive flexion to 90 degrees or less and passive external rotation are added 3 to 4 weeks after injury or surgery. External rotation is particularly important in coracoid base fractures because scarring at the coracohumeral ligament attachment site may result in loss of passive external rotation. Passive and active assisted overhead elevation is permitted 6 weeks after injury or surgery. An overhead pulley is very useful in allowing the athlete to improve overhead elevation progressively. Rotator cuff and deltoid strengthening exercises are added 6 to 8 weeks postoperatively. As these exercises are progressed, the important scapular rotators are also strengthened. Return to athletic competition is determined individually based on attainment of a pain-free range of motion and strength that approaches 90% of the uninjured side.

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Bernard TN Jr, Brunet ME, Haddad RJ Jr: Fractured coracoid process in acromioclavicular dislocations. Report of four cases and review of the literature. Clin Orthop 175:227-232, 1983. 3.

Boyer DW Jr: Trapshooter's shoulder: Stress fracture of the coracoid process. Case report. J Bone Joint Surg Am 57:862, 1975. 4.

Combalia A, Arandes JM, Alemany X, Ramon R: Acromioclavicular dislocation with epiphyseal separation of the coracoid process: Report of a case and review of the literature. J Trauma 38:812-815, 1995. 5.

Cottalorda J, Allard D, Dutour N, Chavrier Y: Fracture of the coracoid process in an adolescent. Injury 27:436-437, 1996. 6.

Derosa GP, Kettlekamp DB: Fracture of the coracoid process of the scapula. Case report. J Bone Joint Surg Am 59:696-697, 1977. 7.

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Froimson AI: Fracture of the coracoid process of the scapula. J Bone Joint Surg Am 60:710-711, 1978.

Garcia-Elias M, Salo JM: Nonunion of a fractured coracoid process after dislocation of the shoulder. A case report. J Bone Joint Surg Br 67:722, 1985. 10.

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Hall RH, Isaac F, Booth CR: Dislocations of the shoulder with special reference to accompanying

small fractures. J Bone Joint Surg Am 41:489-494, 1959. Kohler A, Zimmer EA: Borderlands of the Normal and Early Pathologic in Skeletal Roentgenology, 3rd Am ed. New York, Grune & Stratton, 1968, pp 156-159. 12.

Kopecky KK, Bies JR, Ellis JH: CT diagnosis of the coracoid process of the scapula. Comput Radiol 8:325-327, 1984. 13.

Lasda NA, Murray DG: Fracture-separation of the coracoid process associated with acromioclavicular dislocation: Conservative treatmenta case report and review of the literature. Clin Orthop 134:222-224, 1978. 14.

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16.

Mariani PP: Isolated fracture of the coracoid process in an athlete. Am J Sports Med 8:129-130, 1980.

Moneim MS, Balduini FC: Coracoid fracturesa complication of surgical treatment by coracoclavicular tape fixation. A case report. Clin Orthop 168:133, 1982. 17.

Montgomery SP, Loyd RD: Avulsion fracture of the coracoid epiphysis with acromioclavicular separation: Report of two cases in adolescents and review of the literature. J Bone Joint Surg Am 59:963-965, 1977. 18.

Ogawa K, Yoshida A, Takahashi M, Ui M: Fractures of the coracoid process. J Bone Joint Surg Br 79:17-19, 1997. 19.

Protass JJ, Stampfli FV, Osmer JC: Coracoid process fracture diagnosis in acromioclavicular separation. Radiology 116:61-64, 1975. 20.

Ramin JE, Veit H: Fracture of the scapula during electroshock therapy. Am J Psychiatry 110:153, 1953. 21.

Rockwood CA Jr: Dislocations about the shoulder. In Rockwood CA Jr, Green DP (eds): Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984, pp 719-721. 22.

23.

Rounds RC: Isolated fracture of the coracoid process. J Bone Joint Surg Am 31:662-663, 1949.

24.

Rowe CR: Fractures of the scapula. Surg Clin North Am 43:1565-1571, 1963.

Sandrock AR: Another sports fatigue fracture. Stress fracture of the coracoid process of the scapula. Radiology 117:274, 1975. 25.

Smith DM: Coracoid fracture associated with acromioclavicular dislocation. A case report. Clin Orthop 108:105-167, 1975. 26.

27.

Urist MR: Complete dislocations of the acromioclavicular joint. J Bone Joint Surg 28:813-837, 1946.

Wang KC, Hsu KY, Shih CH: Coracoid process fracture combined with acromioclavicular dislocation and coracoclavicular ligament rupture. Clin Orthop 300:120-122, 1994. 28.

Wilson KM, Colwill JC: Combined acromioclavicular dislocation with coracoclavicular ligament disruption and coracoid process fracture. Am J Sports Med 17:697-698, 1989. 29.

Wolf AW, Shoji H, Chuinard RG: Unusual fracture of the coracoid process. A case report and review of the literature. J Bone Joint Surg Am 58:423-424, 1976. 30.

Wong-Chung J, Quinlan W: Fractured coracoid process preventing closed reduction of anterior dislocation of the shoulder. Injury 20:296, 1989. 31.

Wong-Pack WK, Bobechko PE, Becker EJ: Fractured coracoid with anterior shoulder dislocation. J Can Assoc Radiol 31:278-279, 1980. 32.

Wyrsch RB, Spindler KP, Stricker PR: Scapula fracture in a professional boxer. J Shoulder Elbow Surg 4:395-398, 1995. 33.

34.

Zilberman Z, Rejovitzky R: Fracture of the coracoid process of the scapula. Injury 13:203-206, 1981.

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Section H Scapulothoracic Crepitus and Bursitis in Athletes John E. Kuhn MD Scapulothoracic crepitus and bursitis are related conditions that are not infrequently seen in the athletic population. These conditions are often related to alterations in normal scapulothoracic kinematics. Before these conditions are described, it is important to discuss the anatomy of the scapulothoracic articulation. Anatomy and Biomechanics of the Scapulothoracic Articulation

Seventeen muscles have their origin or insertion on the scapula ( Table 21H-1 , Fig. 21H-1 (Figure Not Available) ), making it the cornerstone for coordinated upper extremity activity. These muscles include the rhomboideus major and minor, the levator scapulae, the serratus anterior, the trapezius, the omohyoid, and the pectoralis minor. Scapular winging or scapulothoracic dyskinesia may occur as a result of dysfunction of these muscles. The rotator cuff muscles (i.e., supraspinatus, infraspinatus, subscapularis, and teres minor) contribute to control activities of the glenohumeral articulation. Disorders of these muscles are common among athletes and are discussed in other sections of this text. The scapulohumeral muscles provide power to the humerus and include the deltoid, the long head of the biceps, the short head of the biceps, the coracobrachialis, the long head of the triceps, and the teres major. Almost every functional upper extremity movement has components of scapulothoracic and glenohumeral motion. TABLE 21-H-1 -- Muscles with Origins or Insertions on the Scapula Scapulohumeral muscles Long head of biceps Short head of biceps

Deltoid Coracobrachialis Teres major Long head of triceps Scapulothoracic muscles Levator scapulae Omohyoid Rhomboid major Rhomboid minor Serratus anterior Trapezius Pectoralis minor Rotator cuff muscles Supraspinatus Infraspinatus Subscapularis Teres minor From Kuhn JE: The scapulothoracic articulation: Anatomy, biomechanics, pathology and management. In Iannotti JP, Williams GR Jr. Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams & Wilkins, 1999. pp 817-845.

Figure 21-H-1 (Figure Not Available) Muscles with origins or insertions on the scapula. Posterior (A) and anterior (B) views of the scapula demonstrate the multiple attachment sites for muscles of the scapula, making it the center for coordinated upper extremity motion. (From Kuhn JE: The scapulothoracic articulation: Anatomy, biomechanics, pathology and management. In Iannotti JP, Williams GR Jr [eds]: Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams & Wilkins, 1999, pp 817-845.

While at rest, the scapula is anteriorly rotated relative to the trunk by approximately 30 degrees.[22] [45] The medial border of the scapula is also rotated, with the inferior pole diverging away from the spine by approximately 3 degrees. The scapula is also tilted forward about 20 degrees in the sagittal plane when viewed from the side.[22] It is thought by some that deviations in this normal alignment may contribute to glenohumeral instability, and that they likely contribute to scapulothoracic crepitus and bursitis.

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Bursae About the Scapula

The normal, smooth, gliding motion of the scapula on the chest wall occurs as a result of multiple scapulothoracic bursae. Three major or anatomic bursae and four minor or adventitial bursae have been described for the scapulothoracic articulation[22] ( Table 21H-2 , Fig. 21H-2 (Figure Not Available) ). The major bursae are easily and reproducibly found,[19] [50] whereas the adventitial bursae are not. The first major bursa is found in the space between the serratus anterior muscle and the chest wall. The second major bursa is located between the subscapularis and the serratus anterior muscles. [7] [19]

TABLE 21-H-2 -- Bursae Around the Scapula Major/Anatomic Bursae Infraserratus bursaeBetween serratus anterior and chest wall Supraserratus bursaeBetween subscapularis and serratus anterior muscles Scapulotrapezial bursaeBetween superomedial scapula and the trapezius Minor/Adventitial Bursae Superomedial Angle of the Scapula Infraserratus bursaeBetween serratus anterior and chest wall Supraserratus bursaeBetween supscapularis and serratus anterior Inferior Angle of the Scapula Infraserratus bursaeBetween serratus anterior and chest well Spine of Scapula Trapezoid bursaeBetween medial spine of scapula and trapezius

From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP, Gerber C (eds): Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 357-375.

Figure 21-H-2 (Figure Not Available) Bursae of the scapula. The locations of both anatomic (black) and adventitial (hatched) bursae are shown. (From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP, Gerber C [eds]: Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 357-375.)

The superomedial angle and the inferior angle of the scapula seem to be the two anatomic regions involved in patients with scapulothoracic bursitis. When the patient is symptomatic, these areas tend to develop inflamed bursae; however, these bursae may be adventitious in that they are not found reliably.[8] [19] [37] When scapulothoracic bursitis affects the inferior angle of the scapula, most authors agree that the inflamed bursa lies between the serratus anterior muscle and the chest wall.[9] [29] [42] This bursa has been called the infraserratus bursa,[9] and the bursa mucosa serrata.[42] [48] The second and more common site of scapulothoracic bursitis occurs at the superomedial angle of the scapula. Codman[9] believed that the inflamed superomedial angle bursa was also an infraserratus bursa, lying between the upper and anterior portions of the scapula and the back of the first three ribs. O'Donoghue [35] also believed that the bursa between the serratus anterior and the chest wall was the involved bursa in athletes with pain and crepitus. Von Gruber[48] on the other hand identified a bursa in this region between the subscapularis and the serratus anticus muscles, which he called the bursa mucosa angulae superioris scapulae. Williams and associates[50] identified a third major bursa, the scapulotrapezial bursa, which lies between the superomedial scapula and the trapezius muscle. This bursa contains the spinal accessory nerve, but is not thought to be a source of scapulothoracic crepitus or bursitis. A third minor or adventitial bursa, which Codman[9] believed was the site of painful crepitus in scapulothoracic crepitus, was called the trapezoid bursa, and is found over the triangular surface at the medial base of the spine of the scapula under the trapezius muscle. Some believe that these

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minor bursae are adventitial and develop in response to abnormal pathomechanics of the scapulothoracic articulation.[8] [19] [37] It would not be surprising, then, to find these bursae inconsistently or in different soft tissue planes.[22]

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Scapulothoracic Crepitus Pathophysiology

Symptomatic scapulothoracic crepitus has been described by several different authors and has been called the snapping scapula,[29] the washboard syndrome,[10] the scapulothoracic syndrome,[33] the rolling scapula,[8] the grating scapula,[34] and the scapulocostal syndrome.[41] Boinet[4] was the first to describe this disorder in 1867. Thirty-seven years later, Mauclaire [25] classified scapulothoracic crepitus into three groups: froissement was described as a gentle friction sound and was thought to be physiologic, frottement was a louder sound with grating and was usually pathologic, and craquement was a loud snapping sound and was always pathologic. These scapular noises are thought to occur from two sourceseither from anatomic changes in the tissue

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interposed between the scapula and the chest wall, or from incongruence in the scapulothoracic articulation ( Table 21H-3 ). Extrapolating from Milch,[29] frottement may suggest soft tissue disease or bursitis, and craquement may suggest bony disease as the source of symptomatic scapulothoracic crepitus. [22] It is interesting to note that Codman[9] was able to make his own scapula . . . sound about the room without the slightest pain, and was likely demonstrating froissement. In every instance, the air-filled thoracic cavity acts as a resonance chamber, much like a string instrument, [2] and amplifies these noises. TABLE 21-H-3 -- Causes of Scapulothoracic Crepitus Interposed Tissue Muscle Atrophy

Fibrosis Anatomic variation Bone Rib osteochondroma Scapular osteochondroma Rib fracture Scapular fracture Hooked superomedial angle of scapula Luschka's tubercle Reactive bone spurs from muscle avulsion Other Soft Tissue Bursitis Tuberculosis Syphilitic lues Abnormalities in Scapulothoracic Congruence Scoliosis Thoracic Kyphosis From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP Gerber C (eds): Complex and Revision Problem in Shoulder Surgery, Philadelphia, Lippincott-Raven, 1997, pp 357-375.

Pathologic conditions affecting the muscle in the scapulothoracic articulation include atrophied muscle,[29] fibrotic muscle,[29] [30] [48] and anomalous muscle insertions.[43] The most common bony disease in the scapulothoracic space that may give rise to scapulothoracic crepitus is the osteochondroma, arising from either the ribs[12] or the scapula[30] [31] [36] ( Fig. 21H-3 ). Malunited fractures of the ribs or scapula are also capable of creating painful crepitus.[29] [30] [44] Abnormalities of the superomedial angle of the scapula, including a hooked superomedial angle,[31] [38] or Luschka's tubercle (which originally was described as an osteochondroma, but subsequently has come to mean any prominence of bone at the superomedial angle[29] [44] [49] ), have also been implicated as sources of scapulothoracic crepitus. Others[2] [39] [46] implicate reactive spurs of bone that are created by the microtrauma of chronic, repeated small periscapular muscle avulsions.

Figure 21-H-3 Osteochondroma of the scapula causing scapulothoracic crepitus. Note the increased

signal in the bursa surrounding this osteochondroma of the scapula.

Certainly, any bony disease that causes scapulothoracic crepitus is capable of forming a reactive bursa around the area of disease.[11] [40] In fact, at the time of resection of bony disease, a bursa is frequently seen. Bursae can become inflamed and painful in the absence of bony disease, and may, by themselves, become a source of crepitus. Other soft tissue pathologies that have been implicated in scapulothoracic crepitus include tuberculosis lesions (in the scapulothoracic region) and syphilitic lues,[29] which are exceedingly rare in athletes. A common source of scapulothoracic crepitus in athletes involves abnormalities in congruence of the scapulothoracic articulation. Both scoliosis[14] [47] and thoracic kyphosis[8] have been implicated as sources of scapulothoracic crepitus. In many athletes, thoracic kyphosis is common[16] [51] and may be the most likely source of scapulothoracic crepitus. Scapulothoracic dyskinesia[17] [18] may position the scapula in such a way as to promote contact between the superomedial angle and the ribs. Morgan has recognized a disorder of the normal scapulothoracic kinematics, which he calls the S.I.C.K. (scapula infra coracoid dyskinesis) scapula syndrome (personal communication). In this disorder, frequently seen in throwing athletes, the scapula assumes a protracted and depressed position, with the inferior angle deviated laterally. Morgan believed that this altered position of the scapula leads not only to glenohumeral joint disease, but to scapulothoracic crepitus as well. Clearly, our understanding of scapulothoracic dyskinesia and its

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relationship to other disorders about the shoulder is evolving. Winging of the scapula has also been associated with scapulothoracic crepitus. Winging may be described as primary, secondary, or voluntary.[21] Primary scapular winging results from identifiable anatomic disorders that directly affect the scapulothoracic articulation. Secondary scapular winging usually accompanies some form of glenohumeral disease. This type of winging resolves once the glenohumeral disease has been addressed. Voluntary winging, although rare, often has psychological overtones. Any form of winging may be associated with scapulothoracic crepitus. The more common causes of scapular winging in athletes are neurologic and include damage to the fifth cervical nerve root, causing rhomboideus palsy; damage to the spinal accessory nerve, causing trapezius palsy ( Fig. 21H-4 ); and as has been described in a number of athletic events, damage to the long thoracic nerve, causing serratus anterior palsy ( Fig. 21H-5 ). Long thoracic nerve injury causing scapular winging is typically a neurapraxic or stretch injury to the nerve that occurs during play and typically will resolve spontaneously within 1 year.[21]

Figure 21-H-4 Scapular winging associated with spinal accessory nerve injury and trapezius palsy. A, Anterior view. B, Posterior view. The scapula assumes a depressed and laterally deviated position.

Figure 21-H-5 Scapular winging associated with long thoracic nerve injury and serratus palsy. A, The scapula assumes a superior and medial position at rest. B, Winging is accentuated with elevation of the arms. Evaluation

The patient with symptomatic scapulothoracic crepitus may be able to identify the location of the crepitus by pointing to the superomedial angle or the inferior angle. Athletes who participate in sports that require repetitive overhead activity are commonly affected.[35] There may be a familial tendency toward the development of symptoms.[8] Patients may relate a history of mild trauma that precipitates symptoms,[5] and scapulothoracic crepitus may be bilateral in some patients.[7] A space-occupying lesion, such as an osteochondroma, should be suspected if fullness or winging is identified on inspection of the scapula. Neurologic evaluations using electromyography should be employed if winging is observed in the absence of a space-occupying lesion. Palpation or auscultation while the shoulder goes through a range of motion may help to identify the source and location of the periscapular crepitus.[1] [7] Supplemental radiographs, which include tangential views of the lateral scapula, computed tomography (CT), or magnetic resonance imaging (MRI) scans may be helpful in identifying anatomic disease. Treatment

As exemplified by Codman,[9] it is important to recognize that scapulothoracic crepitus is not necessarily a pathologic condition. Scapular crepitus has been found in 35% of normal asymptomatic people.[15] As a result of this, patients with hidden agendas or psychiatric conditions may not

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respond to treatment as well as other patients. If the athlete presents with pain, winging, or other disorders of the scapulothoracic articulation, however, the scapulothoracic crepitus is considered to be pathologic. Most athletes will not require surgical treatment of their scapulothoracic crepitus, particularly if the crepitus is related to soft tissue abnormalities, altered posture, scapular winging, or scapulothoracic dyskinesia.[7] [27] Treatment in these athletes should include postural exercises designed to prevent sloping of the shoulders.[7] [26] A figure-of-eight harness may be a useful tool for reminding patients to maintain upright posture. Exercises to strengthen periscapular muscles are also thought to be

important.[7] [27] [35] Systemic nonsteroidal anti-inflammatory drugs, as well as local modalities such as heat, massage, phonophoresis, and ultrasound, and the application of ethyl chloride to trigger points may also prove useful. [7] [27] [35] Injections of local anesthetics and corticosteroids into the painful area have also been recommended. [5] [8] [24] [27] [35] Caution must be used because there is a risk of creating a pneumothorax.[5] When scapular winging accompanies scapulothoracic crepitus, the source of the winging must be determined. If neurologic injury is suspected, electromyographic studies at 3-month intervals will typically demonstrate reinnervation, which is associated with a decrease in symptoms. Using these means, most athletes are expected to improve significantly[24] [35] ; however, for those who fail to benefit from these approaches, several operations have been described. In addition, athletes with clearly defined bony disease such as an osteochondroma are unlikely to improve with conservative treatment.[27] Resection of the bony disease is usually necessary to alleviate symptoms, with a high likelihood of success.[28] [30] [35] Historically, some authors have used muscle plasty operations to treat scapulothoracic crepitus, including those described by Mauclaire,[25] who reflected a flap of the rhomboids or trapezius and sutured it to the undersurface of the scapula. This is thought to be inadequate, however, because the muscle flap may atrophy with time and symptoms could return.[27] Rockwood has excised a rhomboid muscle avulsion flap with the elimination of snapping and pain.[5] The most popular method for the surgical treatment of scapulothoracic crepitus involves a partial scapulectomy, which has been performed on the medial border of the scapula, [6] and more commonly on the superomedial angle.[1] [8] [20] [27] [36] [44] [50] The surgical technique for the resection of the superomedial angle of the scapula begins with the patient in the prone position (Fig. 21H-6 (Figure Not Available) ). An incision following Langer's lines is made just lateral to the medial border of the scapula, from the superior angle to the scapular spine. The soft tissue is dissected down to the spine of the scapula. The periosteum over the spine is incised, and a plane is developed between the superficial trapezius and the underlying scapula. Next, a plane is developed between the supraspinatus and the rhomboids, and the levator scapulae muscles along the medial border of the scapula, starting at the spine of the scapula. The supraspinatus is elevated in a subperiosteal plane from the supraspinatus fossa. The medial scapulothoracic muscles are dissected from the medial border of the scapula, and the dissection in this subperiosteal plane is carried around the medial border to the subscapularis fossa, thus elevating the serratus and subscapularis with the rhomboids and the levator. The superomedial angle of the scapula is resected with an oscillating saw. Caution is warranted as the resection is carried laterally, to avoid injury to the dorsal scapular artery and the suprascapular nerve in the suprascapular notch. After the bone is resected, the reflected muscles fall back into place, and the medial border of the supraspinatus is repaired to the rhomboid/levator flap. Inferiorly, the periosteum is repaired back to the spine of the scapula using sutures passed through drill holes. Postoperatively, the patient is placed in a sling, and passive motion is begun immediately. Active motion is begun at 6 weeks, and resistance exercises follow at 8 to 12 weeks. Figure 21-H-6 (Figure Not Available) Surgical approach for excision of superomedial angle of the scapula. A, Trapezius is elevated from the spine of the scapula. B, The supraspinatus, rhomboids, and

serratus are elevated in a subperiosteal plane from the medial border, and the superomedial scapula is resected while protecting the suprascapular nerve and artery. C, The supraspinatus is sutured back to the spine of the scapula. (From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP, Gerber C [eds]: Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 357-375.)

Complications associated with partial scapulectomy include pneumothorax and postoperative hematoma. In younger patients, bone may try to form again; however, this rarely produces symptoms. The reported results for this procedure are generally good.[8] [20] [27] [36] It must be remembered, however, that athletes typically do not require surgical intervention; therefore, there are few data in the literature regarding the effect of superomedial angle resection of the scapula on athletic performance. It is also important to note that the bone resected is not pathologic and appears normal histologically, which has prompted some to perform bursectomies, thereby avoiding a partial scapulectomy. [25] [40]

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Scapulothoracic Bursitis

Symptomatic scapulothoracic crepitus is typically accompanied by an inflamed scapulothoracic bursa. It is important to realize that although these two conditions are frequently found together, an athlete may have crepitus without pain, and another may have scapulothoracic bursitis without creptitus. As has been described, symptomatic scapulothoracic bursitis seems to affect two areas of the scapulathe superomedial angle and the inferior angle. These bursae, when inflamed, are thought to be adventitious.[8] [19] [35]

Evaluation

Scapulothoracic bursitis may accompany painful scapular crepitus or may exist as a separate entity. The diagnosis of scapulothoracic bursitis is made clinically, but there are few predictable signs of its presence. Patients generally complain of pain with activity and may have audible and palpable crepitus of the scapulothoracic articulation. Usually, the scapular crepitus associated with bursitis is of a much lesser quality and nature than that described with bony disease. Periscapular fullness is frequently appreciated in thinner athletes. This may become significant enough to produce a noticeable scapular winging, which has been identified in 50% of patients with a snapping scapula and no bony abnormalities.[35] Patients may describe minor trauma as a predisposing event.[1] [25] More commonly, repetitive overhead activities in work or athletics have been implicated.[24] [25] [40] The repetitive motion may irritate soft tissues until a chronic bursitis and inflammation develop.

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The bursa then undergoes scarring and fibrosis, with crepitus and pain to follow. Like scapulothoracic crepitus, this scapulothoracic bursitis in athletes is related to postural

abnormalities and scapulothoracic dyskinesia. O'Donoghue[35] recommended injecting local anesthetic into the bursa as a diagnostic aid. MRI will occasionally demonstrate increased signal and even fluid collections in an inflamed bursa. When these are seen, this is highly specific for bursitis, but the condition may also be present with a normal study result. Therefore, MRI is not very sensitive for the condition. Treatment

The initial treatment of scapulothoracic bursitis regardless of its location is conservative, beginning with rest, analgesics, and nonsteroidal anti-inflammatory drugs. Physical therapy to improve posture, heat, and local steroid injections have also been recommended.[24] [40] Efforts to strengthen periscapular muscles and stretching are frequently added.[24] [40] For patients who continue to have symptoms despite conservative treatment, surgery may be beneficial. Sisto and Jobe[42] described an open procedure for resecting a bursa at the inferior angle of the scapula in four major league baseball pitchers. All pitchers had pain during the early and late cocking phases, as well as during acceleration, and they could no longer pitch (Fig. 21H-7 (Figure Not Available) ). Only one of the four patients presented with scapulothoracic crepitus, but all had a palpable bursal sac ranging in size from 1 to 2 cm, which was best seen with the arm abducted to 60 degrees and elevated forward 30 degrees. All four pitchers failed conservative therapy and underwent a bursal excision via an oblique incision just distal to the inferior angle of the scapula. The trapezius muscle, then the latissimus dorsi muscle, were split in line with their fibers, thus exposing the bursa. The bursa was sharply excised, and any bony prominence on the inferior pole of the scapula or ribs was removed. The wounds were closed routinely over a drain, and a compression dressing was applied. Physical therapy that stressed motion was begun after 1

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week and progressed to allow gentle throwing at 6 weeks. This progressed, as symptoms permitted, to full-speed throwing. After this procedure, all four pitchers were able to return to their former level of pitching. Figure 21-H-7 (Figure Not Available) Bursa at the inferior angle of the scapula in throwers. This is an infraserratus bursa and has been described in baseball pitchers, in whom an excision of the bursa has allowed a return to throwing. (From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP, Gerber C [eds]: Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 357-375.)

Similarly, McCluskey and Bigliani[26] [27] performed an open excision of a symptomatic superomedial scapulothoracic bursa in nine patients, noting a thickened, abnormal bursa between the serratus anterior and the chest wall at the time of surgery. Their surgical technique involved making a vertical incision medial to the vertebral border of the scapula. The trapezius was dissected free and a subperiosteal dissection was used to free the levator scapulae and rhomboids from the medial border of the scapula. A

plane was developed between the serratus anterior and the chest wall. The thickened bursa was resected and any bony projections removed. The medial periscapular muscles and trapezius were reapproximated to the scapula. The skin was closed in a routine fashion. The patient used a sling for comfort and began passive motion and pendulum exercises immediately. At 3 weeks, active motion was allowed, with strengthening begun at 12 weeks. With this technique, 88% of patients with symptomatic scapulothoracic bursitis had good or excellent results. One patient with a fair result also required muscle transfers for trapezius winging.[25] Resection of the symptomatic scapulothoracic bursa has been performed endoscopically as well.[3] [7] [13] [19] [22] Ciullo and Jones[7] have the largest endoscopic series to date, with 13 patients who underwent subscapular endoscopy after failing a conservative treatment program for symptomatic scapulothoracic bursitis. Débridement was performed for fibrous adhesions found in the bursa between the subscapularis and serratus muscles, as well as in the bursa between the serratus and chest wall. In addition, débridement or scapuloplasty of changes at the superomedial angle or inferior angle was performed. All 13 patients returned to their preinjury activity level, except for physician-imposed restrictions in a few patients, thus limiting the assembly line use of vibrating tools.[7] Matthews and colleagues[24] have described the technique for scapulothoracic endoscopy. Patients can be placed in the prone or lateral position; however, the lateral position is preferred because it allows for arthroscopic evaluation of the glenohumeral joint and the subacromial space. In addition, if the arm is extended and maximally internally rotated, the scapula will fall away from the thorax, thereby improving access to the bursae. Three portals are used, which are placed at least 2 cm from the medial border of the scapula in the region between the scapular spine and the inferior angle. For the middle portal, a spinal needle is inserted into the bursa between the serratus anterior and the chest wall. This needle should be inserted midway between the scapular spine and the inferior angle, at least 3 fingerbreadths medial to the medial border of the scapula, to avoid injury to the dorsal scapular artery and nerve. The bursa under the serratus anterior can be distended with fluid before a stab wound is made in the skin and the blunt obturator and endoscope are inserted. Deep penetration may traverse the serratus entering the axillary space and should be avoided. Once this initial middle portal has been established, a superior portal placed 3 fingerbreadths medial to the vertebral border of the scapula just below the spine will penetrate the interval between the rhomboideus major and the rhomboideus minor. This portal will allow access to the superomedial angle of the scapula. Portals placed superior to the scapular spine jeopardize the dorsal scapular nerve and artery, the spinal accessory nerve, and the transverse cervical artery, and should be avoided. A third inferior portal can be made in a similar fashion at the inferior angle of the scapula. In the bursa between the serratus anterior and the chest wall, landmarks are generally absent, except for the ribs.

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A motorized shaver and electrocautery are required to perform the bursectomy and obtain hemostasis. The arthroscopic pump should be kept at low pressure throughout the procedure. After the bursectomy is complete, the portals are closed in a standard fashion and the patient is placed in a sling for comfort. Physical therapy, beginning with active range of motion, is initiated as tolerated by the patient. As presented at numerous meetings, the arthroscopic techniques for performing a scapulothoracic bursectomy seem to have early promising results and to date, no cases of injury to the long thoracic nerve, dorsal scapular artery, suprascapular nerve, axillary contents, or thoracic cavity have been reported. Despite this, few series of patients treated arthroscopically for scapulothoracic bursitis have been published in the peer-reviewed literature, and this technique remains investigational at this time.

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Summary

Scapulothoracic crepitus and scapulothoracic bursitis are two related conditions, but they may be found independently in athletes with periscapular pain. In general, treatment for athletes is nonoperative and requires postural exercises designed to prevent sloping of the shoulders[7] [26] and to strengthen periscapular muscles.[7] [27] [35] A figure-of-eight harness may be a useful tool to remind patients to maintain upright posture. Local modalities, nonsteroidal anti-inflammatory drugs, and local injections have also been recommended.[5] [7] [8] [24] [27] [35] In athletes with refractory symptoms, other accompanying sources of disease, such as scapular winging, must be ruled out. In athletes who fail nonoperative treatment, surgical correction may be considered; however, there are only a few reports in the literature for this select population. Therefore, it is difficult to predict outcomes with regard to returning to sport.

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References Arntz CT, Matsen FA III: Partial scapulectomy for disabling scapulothoracic snapping. Orthop Trans 14:252, 1990. 1.

2.

Bateman JE: The Shoulder and Neck, 2nd ed. Philadelphia, WB Saunders, 1978.

Bizousky DT, Gillogly SD: Evaluation of the scapulothoracic articulation with arthroscopy. Orthop Trans 16:822, 1992-1993. 3.

4.

Boinet W: Bull Soc Imperiale de Chirurge, 2nd series. 8(2 series): 458, 1867.

Butters KP: The scapula. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 335-366. 5.

6.

Cameron HU: Snapping scapulae. A report of three cases. Eur J Rheumatol Inflamm 7:66-67, 1984.

Ciullo JV, Jones E: Subscapular bursitis: Conservative and endoscopic treatment of snapping scapula or washboard syndrome. Orthop Trans 16:740, 1992-1993. 7.

8.

Cobey MC: The rolling scapula. Clin Orthop Rel Res 60:193-194, 1968.

Codman EA: The anatomy of the human shoulder. In Codman EA (ed): The Shoulder, Supplemental edition. Malabar, Fla, Kreiger Publishing, 1984, pp 1-31. 9.

Cohen JA: Multiple congenital anomalies. The association of seven defects including multiple exostoses, von Willebrand's disease, and bilateral winged scapula. Arch Intern Med 129:972-974, 1972. 10.

Cuomo F, Blank K, Zuckerman JD, Present DA: Scapular osteochondroma presenting with exostosis bursata. Bull Hosp Jt Dis 52:55-58, 1993. 11.

12.

DeMarquay J: Exostosis of rib. In Dictionaire de Medicine et de Chirugie Pratique, 1868.

Gillogly SD, Bizouski DT: Arthroscopic evaluation of the scapulothoracic articulation. Orthop Trans 16:196, 1992-1993. 13.

Gorres H: Ein fall von schmerzhaften skapularkrachen durch operation geheilt. Deutsch Med Wchnschr 472:897-898, 1921. 14.

Grunfeld G: Beitrag zur Genese des Skapularkrachens und der Skapulargerausche. Arch Orthop J Unfall Chir 24:610-615, 1927. 15.

Hellstrom M, Jacobsson B, Sward L, et al: Radiologic abnormalities of the thoracolumbar spine in athletes. Acta Radiol 31:127-132, 1990. 16.

17.

Kibler WB: Role of the scapula in the overhead throwing motion. Contemp Orthop 22:525-532, 1991.

Kibler WB, Chandler TJ, Uhl T: Functional scapular instability in throwing athletes. Orthop Trans 10:240, 1990. 18.

Kolodychuk LB, Regan WD: Visualization of the scapulothoracic articulation using an arthroscope: A proposed technique. Orthop Trans 17:1142, 1993-1994. 19.

20.

Kouvalchouk JF: Subscapular crepitus. Orthop Trans 9:587-588, 1985.

21.

Kuhn JE, Plancher KP, Hawkins RJ: Scapular winging. J Am Acad Orthop Surg 3:319-325, 1995.

Kuhn JE, Plancher KP, Hawkins JR: Scapulothoracic crepitus and bursitis. J Am Acad Orthop Surg 6:267-273, 1998. 22.

Laumann U: Kinesiology of the shoulder joint. In Kolbel R, et al (eds): Shoulder Replacement. Berlin, Springer-Verlag, 1987. 23.

Matthews LS, Poehling GC, Hunter DM: Scapulothoracic endoscopy: Anatomical and clinical considerations. In McGinty JB, Caspari RB, Jackson RW, Poehling GG (eds): Operative Arthroscopy, 2nd ed. Philadelphia, Lippincott-Raven, 1996, pp 813-820. 24.

Mauclaire M: Craquements sous-scapulaires pathologiques traites par l'interposition musculaire interscapulo-thoracique. Bull Mem Soc Chir Paris 30:164-168, 1904. 25.

McCluskey GM III, Bigliani LU: Scapulothoracic disorders. In Andrews JR, Wilk KE (eds): The Athlete's Shoulder. New York, Churchill-Livingstone, 1994, pp 305-316. 26.

McCluskey GM III, Bigliani LU: Surgical management of refractory scapulothoracic bursitis. Orthop Trans 15:801, 1991. 27.

Michele A, Davies JJ, Krueger FJ, Lichtor JM: Scapulocostal syndrome (fatigue-postural paradox). N York J Med 50:1353-1356, 1950. 28.

29.

Milch H: Snapping scapula. Clin Orthop Rel Res 20:139-150, 1961.

30.

Milch H: Partial scapulectomy for snapping scapula. J Bone Joint Surg Am 32:561-566, 1950.

Milch H, Burman MS: Snapping scapula and humerus varus: Report of six cases. Arch Surg 26:570-588, 1933. 31.

Morse BJ, Ebrahem NA, Jackson WT: Partial scapulectomy for snapping scapula syndrome. Orthop Rev 22:1141-1144, 1993. 32.

33.

Moseley HF: Shoulder Lesions, 2nd ed. New York, Hocher Publishing, 1933.

Neer CS II: Less frequent procedures. In Neer CS II (ed): Shoulder Reconstruction. Philadelphia, WB Saunders, 1990, pp 421-485. 34.

35.

O'Donoghue DH: Treatment of Injuries to Athletes. Philadelphia, WB Saunders, 1962, pp 14-144.

Parsons TA: The snapping scapula and subscapular exostoses. J Bone Joint Surg Br 55:345-349, 1973. 36.

Percy EL, Birbrager D, Pitt MJ: Snapping scapula: A review of the literature and presentation of 14 patients. Can J Surg 31:248-250, 1988. 37.

Richards RR, McKee MD: Treatment of painful scapulothoracic crepitus by resection of the superomedial angle of the scapula. Clin Orthop Rel Res 247:111-116, 1989. 38.

Roldan R, Warren D: Abduction deformity of the shoulder secondary to fibrosis of the central portion of the deltoid muscle. In Proceedings of the American Academy of Orthopaedic Surgeons. J Bone Joint Surg Am 54:1332, 1972. 39.

Shogry ME, Armstrong P: Case report 630: Reactive bursa formation surrounding an osteochondroma. Skel Radiol 19:465-467, 1990. 40.

41.

Shull JR: Scapulocostal syndrome: Clinical aspects. South Med J 62:956-959, 1969.

Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192-194, 1986. 42.

43.

Ssoson-Jaroschewitsch JA: Uber skapularkrachen. Arch Klin Chir 123:378, 1923.

Steindler A: Traumatic Deformities and Disabilities of the Upper Extremity. Springfield, Ill, Charles C Thomas, 1946, pp 112-118. 44.

Steindler A: Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, Ill, Charles C Thomas, 1955. 45.

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46.

Strizak AM, Cowen MH: The snapping scapula syndrome. J Bone Joint Surg Am 64:941-942, 1982.

47.

Volkmann J: Uber sogenannte skapularkrachen. Klin Wchnschr 37:1838-1839, 1922.

Von Gruber W: Die bursae mucosae der inneren aschselwand. Arch Anatomie Physiologie Wissenschaftliche Medizin 358-366, 1864. 48.

Von Luschka H: Uber ein costo-skapular-gelenk des menschen. Vierteljahrsheft Praktische Heilkunde 107:51-57, 1870. 49.

Williams GR Jr, Shakil M, Klimkiewicz J, Ianotti JP: The anatomy of the scapulothoracic articulation. Clin Orthop Rel Res 357:237-246, 1999. 50.

Wojtys EM, Ashton-Miller JA, Huston LJ, Moga PJ: The association between athletic training time and the sagittal curvature of the immature spine. Am J Sports Med 28:490-498, 2000. 51.

Wood VE, Marchinski I: Congenital anomalies of the shoulder. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 98-148. 52.

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Section I Sternum and Rib Fractures in Adults and Children Augustus D. Mazzocca MD Ralph Garretson MD Anthony A. Romeo MD Rib and sternum injuries are relatively rare in athletes and more commonly result from motor vehicle accidents.[11] [15] In the pediatric case, this type of fracture can be a marker of either severe trauma or abuse.[25] This chapter defines the classification of rib and sternal fractures, the mechanism of injury, the physical assessment, and the treatment for both pediatric and adult athletes. Rib Fractures

Rib fractures can be divided into two main categories: stress fractures (indirect) and traumatic fractures (direct). Traumatic fractures are caused by either a blow from a blunt object, which fractures the ribs in direct contact, or compression of the entire thorax, which results in fractures of multiple ribs. [28] Stress fractures can occur in ribs that are subjected to repetitive mechanical loading during a particular activity. The complete history will generally provide insight into which of these categories applies. Traumatic Rib Fractures

The mechanism of traumatic rib fracture or injury is a direct blow from a blunt object. In athletics, this blow generally comes from an anterior direction, causing a more lateral rib fracture or an injury to the costochondral junction.[31] Athletes will recall the injury and will sometimes report that the wind was knocked out of them. It is important to identify which and how many ribs are injured because fractures of the first four or last two ribs, multiple fractures, and flail segments may result in injury to surrounding structures. [26] The definition of a flail chest used to be involvement of three or more ribs that are fractured in two or more places. Clinically, this term has changed to include any chest

segment that exhibits paradoxical motion during respiration. Injuries to the kidney, the spleen, or the liver may not be readily clinically apparent. Splenic trauma has been reported in up to 20% of left lower rib fractures, and liver trauma has been reported in 10% of right lower rib fractures. Pneumothorax and hemothorax must be ruled out by auscultating the chest and palpating for subcutaneous air. Progressive shortness of breath is also an ominous indicator in this situation. Examination

Physical examination usually will elicit pain during palpation as well as during deep inspiration. A hematoma is an indicator of a displaced rib fracture produced by injury to the intercostal vessel. In palpating the costochondral junction, one may also palpate a step-off, which aids in the diagnosis of costochondral fracture-dislocation. Two radiographic examinations (chest series and rib series) are important in diagnosing rib fractures. A chest series (posterior to anterior and lateral) is needed to rule out pneumothorax. A rib series includes oblique views of the clinically involved segment. Injuries to the costochondral junction are not well seen on radiographs. Magnetic resonance imaging or computed tomography may be needed to confirm the suspected diagnosis of a costochondral injury. Treatment

Treatment of traumatic rib injuries is primarily symptomatic. Most of these fractures are stable. Stable rib fractures are nondisplaced or minimally displaced and do not involve more than two consecutive segments. The first mode of treatment is oral analgesic medication to relieve pain, which mainly occurs during inspiration. If this does not relieve the pain, an intercostal rib block may offer some temporary relief of spasm. A long-acting medication such as bupivacaine is used. It is infiltrated along the intercostal nerve of the fractured rib and the ribs above and below it. Some success has also been reported with the use of rib binders, which may splint the fracture, keeping it more stable so that activities of daily living are more comfortable.[30] Criteria for Return to Athletics

The criteria for return to play with rib fractures are stability of the injury with no soft tissue complications

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(e.g., pneumothorax, hemothorax, or liver, spleen, or kidney contusion) and an improvement in pain. This is usually seen approximately 2 to 3 weeks after injury. The athlete can return to play at this time using a rib belt; he or she is further protected for approximately 6 to 8 weeks by a flak jacket ( Fig. 21I-1 ) so that the rib can heal completely. It has been reported that nonunion is not a complication of this type of

traumatic fracture, and malunion is of little importance.[30] It is also important for the team physician to note that training can be started as early as 1 week after injury if the pain has significantly decreased.

Figure 21-I-1 A and B, Flak jacket used to protect the athlete with rib fractures.

Costochondral injuries have a history of healing much more slowly. Computed tomography and magnetic resonance imaging may be helpful in evaluating these injuries if there is persistent pain lasting longer than 6 to 8 weeks. Stress Fractures

Stress fractures or indirect injury to the ribs usually involves muscle contractions that result in subthreshold bending, causing microfracture. This microfracture is additive and eventually causes pain. A stress fracture is caused by the inability of the bone to withstand subfracture threshold force in a repetitive fashion. There is an imbalance between bone formation and bone resorption. It is also important to realize that a stress fracture is a normal response to an abnormal stress, whereas an insufficiency fracture is the abnormal response to a normal stress. Stress fractures have been reported to occur in the first rib in baseball players [6] [14] [21] [32] (Fig. 21I-2 (Figure Not Available) ) and also as a more acute phenomenon in basketball players. Fractures of the lower ribs have been reported in golfers and rowers.[3] [13] [19] [23] Karlson[19] reviewed rib stress fractures in rowers and found that those occurring in the anterolateral to posterolateral aspects of ribs five through nine are most often associated with long-distance training and heavy load per stroke. It was also noted that the similarity between these stress fractures and fractures caused by chronic coughing suggests

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a similar mechanism of injury. The actions of both the serratus anterior and the external oblique abdominal musculature on the rib may cause these stress fractures because of the repeated bending forces of both rowing and coughing. Mintz[27] used a magnetic resonance imaging analysis technique, and McKenzie[24] analyzed rowing mechanics to implicate the serratus anterior in the causation of stress fractures. Avulsion fractures of the floating ribs may also result from the opposing pulls of the latissimus dorsi, the internal obliques, and the serratus posterior inferior muscles (Fig. 21I-3 (Figure Not Available) ). [32] Specific radiographs can be directed to the posterolateral portion of the rib cage because most stress fractures associated with rowers occur in this area. Figure 21-I-2 (Figure Not Available) Activities such as pitching may result in a stress fracture of the first rib. (From Tullos HS, Erwin WD, Woods GW, et al: Unusual lesions of the pitching arm. Clin Orthop 88:169-182, 1972.) Figure 21-I-3 (Figure Not Available) Avulsion fractures of the floating ribs may result from the opposing pulls of the latissimus dorsi, internal obliques, and serratus posterior inferior. (From Tullos HS, Erwin WD,

Woods GW, et al: Unusual lesions of the pitching arm. Clin Orthop 88:169-182, 1972.)

Rib stress fractures have been reported to occur in golf as well. The leading side of the trunk in the posterolateral part of the rib is the most common site. Poor technique, frequent strokes, and large divots place the beginner or the poorly skilled golfer at greatest risk. These symptoms can also be confused with back strain, which is also quite common in this athlete. Electromyographic examination has shown that the serratus anterior muscle is the main force on the rib during these motions. Examination

The diagnosis of rib stress fractures is confirmed if deep inspiration causes significant pain. This motion causes the accessory muscles of inspiration to contract, pulling the periosteum of the rib under tension and causing an increase in pain. This test can differentiate a stress fracture from back strain, which is common in this population. Bone scanning and oblique radiographs of the ribs can also aid in diagnosis. Treatment

These injuries are treated in a symptomatic manner with analgesics and rest. The key difference in this type of injury is that the mechanics must be addressed. Strengthening and stretching of the serratus anterior muscle with physical therapy is critical, as is kinesiologic evaluation of the basic mechanics of motion in the particular sport in question followed by correction of those mechanics. There are very few long-term sequelae associated with this.

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Sternal Fracture

The sternum is a flat bone that forms a portion of the anterior wall of the thorax ( Fig. 21I-4 ). It is composed of three parts: the manubrium, the body, and the xiphoid process. The upper portion of the manubrium forms the jugular notch. It also articulates with the clavicle, forming the sternoclavicular joint. The first and second costal cartilages articulate with the upper and lower borders of the manubrium. The manubrium itself then articulates with the body of the sternum. This articulation forms the sternal angle. This level is generally associated with the fourth and fifth thoracic vertebrae and can be palpated. The seventh costal cartilage generally fits into the notch by the body in the xiphoid process. The xiphisternal joint is at the apex of the infrasternal angle. It lies at about the level of the tenth or eleventh thoracic vertebra.[31]

Figure 21-I-4 Structure of the sternum.

Injuries to the sternum in athletes are rare. Most sternal injuries occur in automobile racing.[12] Fowler reported three

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mechanisms: direct, indirect, and muscular (Fig. 21I-5 (Figure Not Available) ). [12] Direct injuries occur when either a helmet or a steering wheel strikes the sternum directly. The relatively flexible lower portion of the sternum is displaced inward in a fracture, or a sternomanubrial dislocation can occur (Fig. 21I-6 (Figure Not Available) ). This direct mechanism can also be associated with posterolateral rib fractures as well as cardiac lung contusions. The indirect injury results from a flexion-compression injury of the cervical thoracic spine (Fig. 21I-7 (Figure Not Available) ). This type of injury leads to fracture-dislocation of the sternomanubrial joint with posterior displacement of the

manubrium and anterior displacement of the body of the sternum. The chin's striking the chest may aid this mechanism. Increased intrathoracic pressure along with the mobility of the lower ribs may actually drive the body of the sternum forward. A wedge fracture of the thoracic vertebrae can also be associated with this condition.[31] The last mechanism proposed by DeTarnowski[10] and Fowler [12] is muscular action. This supposedly tears the sternum into proximal and distal fragments through the action of the opposing muscle groups. Figure 21-I-5 (Figure Not Available) Mechanistic classification of sternal fractures. (From Fowler AW: Flexion-compression injury of the sternum. J Bone Joint Surg Br 39:487-497, 1957.) Figure 21-I-6 (Figure Not Available) Sternomanubrial dislocation caused by hyperflexion of the cervical spine combined with axial load. (From Johnson CD, MacKenzie JW, Zawadsky JP: Manubriosternal dislocation in a football athlete. Surg Rounds Orthop 2:45-50, 1989.) Figure 21-I-7 (Figure Not Available) A fall or blow to the upper part of the spine (A) or to the back of the head and neck (B) can result in sternal fracture. Posterior displacement of the manubrium can be exaggerated by a blow from the chin as the neck is hyperflexed (B). (From Fowler AW: Flexion-compression injury of the sternum. J Bone Joint Surg Br 39:487-497, 1957.)

Although this is rare in sports, Johnson[18] reported an indirect sternomanubrial fracture-dislocation in a football player as a result of a flexion-compression mechanism. Woo[33] reported traumatic sternomanubrial joint subluxation in two basketball players from violent blows from the elbow to the sternum. Stress fractures of the sternum have been reported in both a wrestler and a golfer. [1] [20] Examination

Patients presenting with a sternal fracture have a history of a direct blow with pain and tenderness over the sternum. Sternal and rib fractures may be associated. These patients may also complain of shortness of breath that is not prolonged. [4] Historically, sternal fractures have been thought to be associated with myocardial contusion and therefore a potential for arrhythmia. This has not been borne out by more recent studies. Isolated sternal fractures are not a significant risk factor for myocardial contusion.[29] Peek and Firmin[29] found no cases of arrhythmia in 162 consecutive isolated sternal fractures. Similarly, others have been unable

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to link sternal fractures to myocardial injury.[2] [5] [7] It is believed that the energy is absorbed by the sternum and the fracture as opposed to being transmitted through the sternum to the cardiac muscle and then causing a contusion. Obviously, trauma protocol dictates that sternal injuries causing ecchymosis to the chest require 24-hour monitoring for arrhythmia. The diagnosis is confirmed if there is pain on palpation in the area of fractures as well as palpable crepitation at the level of the injury with respiration and any type of

movement. Adequate radiography is the study of choice when a sternal fracture is suspected, particularly a lateral view of the sternum. [4] There should be an increase in penetration over that normally used for chest radiography so that the sternum can be better penetrated and fractures can be appreciated ( Fig. 21I-8 ). Huggett and Roszler[17] reviewed data from a small series of sternal fractures, comparing computed tomographic scans with plain radiographs. Computed tomography identified only six of nine sternal fractures, whereas radiography identified eight of nine. A retral sternal hematoma, which is a specific finding for sternal fractures, was seen in only three of nine computed tomography scans. Hendrich[16] used ultrasonography to correctly identify 16 of 16 sternal fractures, whereas radiography identified 15 of 16.

Figure 21-I-8 Lateral radiograph of the chest revealing a sternomanubrial dislocation.

In the pediatric population, it is important to recognize that the time of fusion commonly varies for the four segments of the body of the sternum. [28] At 7 years of age, the third and fourth segments fuse. At 14 years of age, the second and third fuse, and at age 21, the first and second fuse. Fusion of these segments may be delayed at any stage, possibly leading to an incorrect diagnosis of fracture.[22]

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Treatment

Most sternal fractures do not require more than symptomatic treatment. [9] Pain around the fracture site will last for an average of 11 weeks but persists longer in older patients.[8] Rarely, displacement may warrant a reduction attempt. Once pain has diminished, the patient may return to athletics in a general conditioning and training program and is limited only by pain. Reduction of a dislocated sternomanubrial joint can be performed with the patient supine in Trendelenburg's position with a sandbag underneath the scapula ( Fig. 21I-9 ). Manual pressure on the manubrium as well as gentle traction on the arms may aid in reduction of the sternomanubrial dislocation.[9]

Figure 21-I-9 Method of reduction of fractured sternum. If necessary, an assistant may apply traction by grasping the patient's arm at the axilla and pulling cephalad. Inset shows detail of the forces applied in reduction. (From DePalma AF: The Management of Fractures and DislocationsAn Atlas, 3rd ed. Philadelphia, WB Saunders, 1981.) Return to Athletics

Sternal contusion and most fractures are stable injuries that can be treated

conservatively. Conservative measures consist of rest, ice, and various oral analgesics. Contact sports should be avoided until pain subsides. It has been reported that pain persisting beyond 6 to 12 weeks is rare.[30] Sternomanubrial dislocations are generally felt to be stable after reduction. Treatment is similar to that for sternal fracture. [30]

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References 1.

Barbaix E: Stress fracture of the sternum in a golf player. Int J Sports Med 17:304-305, 1996.

2.

Brooks J, Dunn T: Sternal fractures: A retrospective analysis of 272 cases. J Trauma 35:46-54, 1993.

Brukner P, Khan K: Stress fracture of the neck of the seventh and eighth ribs: A case report. Clin J Sport Med 6:204-206, 1996. 3.

Buckman R, Trooskin S, Flancbaum L, Chandler J: The significance of stable patients with sternal fractures. Surg Gynecol Obstet 164:261-265, 1987. 4.

Chiu W, D'Amelio L, Hammond J: Sternal fractures in blunt chest trauma: A practical algorithm for management. Am J Emerg Med 15:252-255, 1997. 5.

6.

Curran J, Kelly D: Stress fracture of the first rib. Am J Orthop 8:16-18, 1966.

Cuschieri J, Kralovich K, Patton J, et al: Anterior mediastinal abscess after closed sternal fracture. J Trauma 47:551-554, 1999. 7.

de Oliveira M, Hassan T, Sebewufu R, et al: Long-term morbidity in patients suffering a sternal fracture following discharge from the A and E department. Injury 29:609-612, 1998. 8.

DePalma AF: The Management of Fractures and DislocationsAn Atlas, 3rd ed. Philadelphia, WB Saunders, 1981. 9.

10.

DeTarnowski G: Contrecoup fracture of the sternum. Ann Surg 41:253-264, 1905.

11.

Foley N, Mattox K: Fractures of the sternum. Curr Concepts Trauma Care 9-11, 1985.

12.

Fowler AW: Flexion-compression injury of the sternum. J Bone Joint Surg Br 39:487-497, 1957.

13.

Gaffney K: Avulsion injury of the serratus anterior: A case history. Clin J Sport Med 7:134-136, 1985.

Gurtler R, Pavlov H, Torg J: Stress fracture of the ipsilateral first rib in a pitcher. Am J Sports Med 13:277-279, 1985. 14.

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Helal B: Fracture of the manubrium sterni. J Bone Joint Surg 46:602-607, 1964.

Hendrich C, Finkewitz U, Berner W: Diagnostic value of ultrasonography and conventional radiography for the assessment of sternal fractures. Injury 26:493-497, 1995. 16.

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Huggett J, Roszler M: CT findings of sternal fracture. Injury 29:623-626, 1998.

Johnson CD, MacKenzie JW, Zawadsky JP: Manubriosternal dislocation in a football athlete. Surg Rounds Orthop 2:45-50, 1989. 18.

Karlson D: Rib stress fractures in elite rowers. A case series and proposed mechanism. Am J Sports Med 26:516-519, 1998. 19.

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Keating T: Stress fracture of the sternum in the wrestler. Am J Sports Med 15:92-93, 1987.

Lankenner P, Micheli LJ: Stress fracture of the first rib. A case report. J Bone Joint Surg Am 67:159-160, 1985. 21.

Lyons F, Rockwood C: Fractures of the sternum. In DeLee JC, Drez D (eds): Orthopaedic Sports Medicine. Philadelphia, WB Saunders, 1994, pp 572-576. 22.

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Maffulli N, Pintore E: Stress fracture of the sixth rib in a canoeist. Br J Sports Med 24:247, 1990.

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McKenzie D: Stress fracture of the rib in an elite oarsman. Int J Sports Med 10:220-222, 1989.

Merten DF, Osborne RS, Radhowski MA: Craniocerebral trauma in the child abuse syndrome: Radiological observations. Pediatr Radiol 14:272-278, 1984. 25.

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Miles J, Barrett G: Rib fractures in athletes. Sports Med 12:66-69, 1991.

Mintz A, Albano A, Reisdorff E, et al: Stress fracture of the first rib from serratus anterior tension: An unusual mechanism of injury. Ann Emerg Med 19:411-414, 1990. 27.

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Peek G, Firmin R: Isolated sternal fracture: An audit of 10 years' experience. Injury 26:385-388, 1995.

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Orthopaedic Knowledge Update, Sports Medicine. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1999. 31.

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Section J Glenohumeral Instabilities 1. GLENOHUMERAL INSTABILITY IN ADULTS Marianne Backer MD Russell F. Warren MD Instability of the shoulder joint ranges from subtle increased laxity, in which the instability is clinically assessed as increased translation of the humeral head over subluxation in the joint, to acute frank dislocation, in which the increased translation is easily diagnosed. The most common complaints related to the glenohumeral joint are instability and increased laxity. In the earliest reports, shoulder instability covered frank dislocation of the shoulder, and treatment covered reduction of that dislocation. Later, surgical treatment of recurrent shoulder dislocation evolved, and atraumatic multidirectional instability became a recognized shoulder disease. With increasing quality of magnetic resonance imaging (MRI), biomechanical studies of shoulder instability, and increasing skills in shoulder arthroscopy, glenohumeral instability is now known to cover a wide variety of disorders in the shoulder. No single disease or lesion is responsible for instability in the shoulder, and the joint should be looked on as a circle wherein increased translation in one direction demands laxity of the soft tissue opposite the translation to allow the increased motion. Treatment of shoulder instability has become more lesion oriented, and the goal of treatment and rehabilitation now includes full stability with full range of motion in the joint. Increasing demands from young athletic patients suggest that early surgical repair is indicated in some cases, whereas protection and rehabilitation still constitute the primary treatment of shoulder instability in most cases. Familiarity with the anatomy and the biomechanics of the shoulder is mandatory to understand the different instability patterns in the shoulder and to be able to make a diagnosis. This chapter concentrates on the anatomy important to the stability of the

shoulder joint and on the influence of dynamic and static stability in the shoulder. Indications for treatment and the different treatment modalities together with the expected results are included. Anatomy of the Stability of the Shoulder Joint

The shoulder joint has the greatest range of motion of all the joints in the body. There are few bony restraints to movement and only a small area of articular contact. This increases the demand on the surrounding tissues of the shoulder joint, with primary dependency on the capsule, the ligaments, and the surrounding muscles for stability. [42] Glenohumeral Joint.

The glenohumeral joint is the joint between the glenoid of the scapula and the humeral head. The glenoid, which is oval, is longest in its inferior-superior diameter. It is connected to the body of the scapula by the glenoid neck with an angle of approximately 7 degrees posterior and slightly superior version[48] ( Fig. 21J1-1 ). The bony articular surface of the glenoid is almost flat; the center of the glenoid is only slightly deeper than the periphery. In the center of the glenoid, called the bare area, the articular surface is thin, sometimes almost transparent. Compared with the hinged joint of the knee or the ball-and-socket joint of the hip, the shape of the glenoid does not contribute much to the stability of the joint.

Figure 21-J1-1 A and B, The scapular plane. The glenoid is connected to the scapular body in a slightly posterior and superior version. (A and B modified from Matsen FA III, Lippitt SB, Sidles JA, Harryman DT II: Practical Evaluation and Management of the Shoulder. Philadelphia, WB Saunders, 1994.)

The body of the scapula lies on the posterior thoracic wall facing the glenoid articular surface anterior and superior toward the humeral head. The position of the scapula on the thoracic wall constitutes the scapular plane of motion, with the glenoid articular surface directed in 35 degrees of anterior and 5 degrees of superior version to the sagittal plane. This version of the glenoid increases the posterior and inferior stability of the joint. The shoulder joint superiorly is covered by the acromion of the scapula. The acromion arises posteromedially from the spine of the scapula, has a free posterior and lateral edge, and is connected to the coracoid of the scapula by the coracoacromial ligament anterior and to the clavicle through the acromioclavicular joint medially. The roof of the shoulder joint is important for superior and anterior stability. The humeral head is retroverted 30 to 40 degrees to the distal humeral epicondyles to meet the anteversion of the scapula. The articular surface of the humeral head is half a circle connected to the humerus at the level of the surgical neck, with the lesser tuberosity anterior to the biceps groove and the greater tuberosity posterior to the groove and lateral to the joint. Labrum.

The fibrous labrum is firmly attached to the rim of the glenoid inferiorly and to a looser meniscus-like structure superiorly, where it ends in the origin of the tendon of the long head of the biceps. It contributes to the stability of the joint by adding depth and increasing the surface of the glenoid and allows attachment of the capsule, the ligaments, and the biceps tendon to the glenoid. A mobile attachment of the labrum to the superoanterior rim of the glenoid is occasionally seen as a superoanterior labral foramen. This is a normal anatomic variant and does not necessarily compromise the stability of the joint. Capsule.

The capsule of the glenohumeral joint is normally redundant and lax to allow the great range of motion in the joint. It is attached to the rim of the glenoid, often connected to the labrum, and surrounds the joint going lateral to the surgical neck of the humeral head, where it attaches underneath and blends with the insertion of the rotator cuff tendons. Inside the capsule, the pressure in the joint is negative, accounting for the vacuum effect that is known to be important for the stability of the joint. [19] The capsule should be looked upon as a circle. Instability in one direction requires capsular damage on the opposite

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side of the joint to allow abnormal motion.[40] [41] [52] [56] The area between the superior edge of the subscapular tendon and the anterior border of the supraspinatus is the rotator interval, where the capsule, the coracohumeral and superior glenohumeral ligaments, and the tendon of the long head of the biceps are the only restraints to superior migration.[17] [36] This interval is relatively thin, allowing the rotator cuff to slide back and forth around the coracoid process when the arm moves. The size of the rotator interval is important for the stability of the joint; increased size increases the inferior instability of the joint, whereas contracture of the rotator interval inhibits external rotation of the joint.[17] [22] Ligaments.

The ligaments of the glenohumeral joint are reinforcing bands in and around the capsule that restrict motions in the joint to those that can be stabilized by muscle balance. The most important ligaments for stability of the shoulder are the superior glenohumeral, middle glenohumeral, and inferior glenohumeral ligaments. [11] The superior glenohumeral ligament is the most consistent of the ligaments. It runs from the superoanterior rim of the glenoid across the rotator interval and above the biceps tendon to its insertion with the capsule on the humeral head superior to the lesser tuberosity close to the bicipital groove.

The middle glenohumeral ligament is the most variable of the ligaments, and different anatomic variations that do not compromise the stability of the joint are seen. The ligament normally arises from the anterior upper third of the glenoid rim and the labrum and runs underneath and across the subscapular tendon to its humeral attachment. A normal anatomic variant is seen when the superoanterior part of the labrum is missing and a cordlike middle glenohumeral ligament runs as a band in front of the joint; this is called the Buford complex. The anterior band of the inferior glenohumeral ligament runs from the anteroinferior rim of the glenoid to the undersurface of the humeral head. It is attached to the inferior labrum and becomes lax with a detachment lesion of the inferior labrum from the glenoid rim, as in a Bankart's lesion. The posterior band is the only reinforcing band in the posterior capsule and runs from the posteroinferior rim of the glenoid to the posterior part of the humeral head. Between the posterior band and the anterior band of the inferior glenohumeral ligament, there is a soft capsular area called the axillary pouch. The axillary nerve runs close to the joint just outside the capsule in this area. Both bands of the inferior glenohumeral ligament are important structures for the stability of the glenohumeral joint. The coracohumeral ligament in the anterior part of the rotator interval runs between the base of the coracoid and the humeral head and inserts in the transverse humeral ligament, which acts as a roof of the bicipital groove between the lesser and the greater tuberosities. Both ligaments have minor roles in the stability of the joint. [3] [8] Muscles.

The muscles that surround the shoulder joint are dynamic stabilizers of great importance. The muscles of the rotator cuff, whose tendons run anterior, superior, and posterior to the joint, act as stabilizers because of their compression of the humeral head into the glenoid cavity during motion.[6] [26] [27] [28] The subscapularis muscle originates from the undersurface of the body of the scapula and runs anterior to the shoulder joint. The muscle inserts on the lesser tuberosity with a cordlike strong tendon as its upper part and is more muscular in its lower part of insertion along the lesser tuberosity. The part of the subscapular tendon that crosses anterior to the joint can be seen arthroscopically through the capsule as an anterior landmark in the joint. The upper edge of the subscapular tendon is the lower border of the rotator interval. The subscapularis muscle is innervated by the subscapular nerve from the posterior cord of the brachial plexus. The muscle applies an anterior compression load to the joint and an internal rotation force to the humeral head; with increased abduction of the arm, it functions as a humeral head depressor. The supraspinatus muscle originates from the anterosuperior part of the scapula above the spine and runs along the upper surface of the glenoid above the shoulder joint, where it becomes a tendon that inserts on the greater tuberosity lateral on the humeral

head. The part of the tendon that crosses above the shoulder joint can be seen

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arthroscopically through the capsule as the roof of the joint. Its anterior edge is the superior border of the rotator interval. The supraspinatus is innervated by the suprascapular nerve. The nerve arises in the posterior cord of the brachial plexus and runs underneath the suprascapular ligament in the suprascapular notch on the superior edge of the scapula, into and underneath the supraspinatus muscle in the supraspinous fossa. The supraspinatus functions as an important humeral head depressor and humeral joint compressor and stabilizer with increased abduction of the arm. Between the insertion of the subscapularis and the supraspinatus tendons on the humeral head, the tendon of the long head of the biceps comes from distally underneath the pectoralis major insertion, underneath the transverse humeral ligament in the biceps groove and penetrating the capsule on top of the humeral head, and then courses intra-articularly to its origin on the superior glenoid labrum. The long head of the biceps is a humeral head depressor in the beginning of abduction in the shoulder joint. The infraspinatus muscle is posterior and inferior to the supraspinatus. It originates from the inferior surface of the scapula below the spine and runs lateral to its insertion on the posterior part of the greater tuberosity and posterior part of the humeral head, crossing the shoulder joint on its most superoposterior aspect. It is innervated by the suprascapular nerve as well. When the nerve leaves the supraspinatus muscle through the supraspinous fossa, it runs distally laterally around the base of the spine of the scapula through the spinoglenoid notch to the infraspinous fossa, where it innervates the infraspinatus muscle. The muscle functions as an external rotator of the shoulder and, with increasing abduction in the shoulder, as a humeral head depressor. The trapezius, rhomboids, latissimus dorsi, serratus anterior, and levator scapulae are important scapular stabilizers in that they position the glenoid in an anteverted and superior position to articulate with the retroverted humeral head. The position of the glenoid in relation to the humeral head increases the posterior and inferior stability of the glenohumeral joint under motion. Other muscles surrounding the shoulder joint function in shoulder motion but have less effect on stability. The deltoid muscle originates anterior from the lateral part of the clavicle and from the anterior, lateral, and posterior border of the acromion. It inserts on the lateral upper third of the humeral shaft and is an important and forceful abductor and flexor of the shoulder. It is innervated by the axillary nerve that comes from the quadrangular space posterior and runs on the undersurface of the muscle. The pectoralis major and pectoralis minor originate medial to the deltoid from the medial clavicle and from the anterior chest wall and insert on the humeral shaft just medial to the deltoid and above the long head of the biceps. They are important internal rotators and flexors of the shoulder joint. The coracobrachialis muscle and the biceps brevis head connect the elbow and the lower part of the humeral shaft with the coracoid, where they insert as the conjoint tendon and flex the shoulder. Posterior to the shoulder joint, below the infraspinatus muscle, the teres minor and teres

major are external rotators and extensors of the shoulder. Vessels and Nerves.

The vessels and nerves important to the shoulder originate from the axillary artery and the brachial plexus. The subclavian artery becomes the axillary artery just medial to the coracoid, where it dives into the axilla and medially down the arm as the brachial artery. When it passes the axilla, the anterior and posterior circumflex arteries to the humeral head run anterior and posterior to the shoulder. The posterior circumflex artery runs with the vein and the axillary nerve underneath the capsule in the axilla and underneath the teres minor through the quadrangular space posterior. The anterior circumflex artery runs with its two veins along the lower border of the subscapularis tendon to its insertion on the lesser tuberosity. The axillary nerve continues from the quadrangular space posterior to the undersurface of the deltoid approximately 5 cm below the lateral edge of the acromion, where it can easily be damaged during surgery if it is not protected. The musculocutaneus nerve arises medially to the conjoint tendons and passes behind them approximately 5 to 7 cm below the coracoid, where it can be damaged during surgery, especially if retractors are placed under the conjoint tendon. The nerves innervating the rotator cuff and the muscles surrounding the shoulder have already been mentioned. The cephalic vein lies in the deltopectoral groove and runs medially and inferior to the coracoid. The nerves and the vessels are important landmarks and should be located and protected during shoulder surgery. Lesions to the nerves and the vessels are often seen after major shoulder dislocations.

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Biomechanics of Shoulder Stability

The influence of bone on the stability of the shoulder joint is small and mostly related to the position of the glenoid anterior and superior toward the humeral head. When the arm is adducted, the bare area in the center of the glenoid represents the articular area of contact, and articular contact becomes more peripheral with increasing abduction. At the extremes of motion, rotation of the humeral head is coupled with translation on the glenoid cavity,[21] [26] [27] [43] but translation of the humeral head on the glenoid is normally confined to only a few millimeters during motion.[5] [27] [43] [44] [55] With extension and external rotation, the head translates posterior owing to the development of tension in the periarticular soft tissues and the fact that the articular surfaces of the humeral head and the glenoid fossa are not perfectly congruous.[42] In internal rotation and flexion, the humeral head translates anterior. In the unstable shoulder, the lack of restraint to motion increases the translation in the direction toward the lack of restraint. The shoulder is dependent on the surrounding soft tissue for its stability in various positions of motion. At rest, the joint is held in position partly by the vacuum effect of the negative pressure inside the capsule.[21] [22] As soon as the arm moves, however, a complex interaction between dynamic stabilization from the muscles and static stabilization from the ligaments around the shoulder takes place. The ligaments serve as the final check for keeping the joint in positions that allow the muscle to create its dynamic stabilizing effect. With the arm adducted, the main stabilizers against inferior translation of the humeral head are the superior glenohumeral ligament, the coracohumeral

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ligament, and the rotator interval.[56] These structures are under tension in both flexion and extension with the arm adducted and externally rotated. They also resist posterior

translation but have no major role against anterior translation. With increasing abduction of the shoulder to 45 degrees, the middle glenohumeral ligament becomes the major restraint against anterior translation of the humeral head; with the arm in external rotation, the ligament comes under maximal tension.[37] [38] [39] When the arm is abducted farther toward 90 degrees, the inferior glenohumeral ligament comes under increasing tension, resisting inferior translation of the humeral head; and at 90 degrees of abduction, the inferior glenohumeral ligament is the primary restraint to inferior translation. The anterior and posterior bands of the inferior glenohumeral ligament have important roles in the stability of the joint. With the arm in abduction and external rotation, the anterior band moves from inferior to more anterior, restraining anterior translation of the humeral head, and the posterior band moves from posterior to more inferior, restraining inferior translation. When the arm is internally rotated, the anterior band moves inferior and the posterior band moves posterior, protecting against translation of the humeral head in these directions. When the shoulder is flexed, the posterior band of the inferior glenohumeral ligament is under tension and is the primary restraint to anterior and posterior translation of the humeral head; during extension, the tension shifts to the anterior band as the primary restraint to translation. [5] [37] [39] These reciprocal movements of the different portions of the inferior glenohumeral ligament are thought to contribute to the rollback of the head on the glenoid during motion.[42] Dynamic stabilization by the muscles of the shoulder joint, like static stabilization by the ligaments, is related to the position of the arm. The muscles function in a complex balance to keep the joint stabilized during the full range of motion. The rotator cuff muscles are the main stabilizers in that they compress the humeral head into the glenoid cavity during motion, so it stays centered. The scapular stabilizing muscle positions the glenoid cavity to the humeral head during motion, increasing the inferior and posterior stability of the joint.

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Lesions and Biomechanics of Instability in the Shoulder

In the unstable shoulder, the main reason for the instability is most often lack of soft tissue restraint to translation of the humeral head on the glenoid. With increasing knowledge of the complex pattern of static and dynamic stability in the shoulder, an unstable shoulder should be considered a multifactorial disease, for which all the factors contributing to the instability need to be addressed in treatment. The capsule should be looked on as a circle around the shoulder joint. A capsular lesion in one direction of the joint requires laxity in the opposite direction to allow the increased translation of the humeral head in the joint. If the capsule suffers general laxity, the increased translation is in all directions, as in multidirectional instability of the shoulder. If the negative pressure inside the capsule is lost, as with labrum and capsule detachments, increased inferior translation of the humeral head occurs. Lesions in the shoulders in which the labrum and the capsule are detached from the rim of the glenoid result in an increased laxity of the bands of the inferior glenohumeral ligament and the capsule. Detachment lesions of the anterior labrum from the glenoid rim are called Bankart's lesions. Bankart's lesions increase the anterior translation of the humeral head in abduction and external rotation, increase anterior and posterior humeral head translation in flexion, and increase inferior translation in extension and internal rotation of the shoulder joint because of increased laxity of the anterior band of the inferior glenohumeral ligament and a lax anterior capsule. In a reverse Bankart's lesion, in which the lesion is on the posterior and inferior part of the labrum, the laxity of the posterior band of the inferior glenohumeral ligament and of the posterior capsule increases. Reverse Bankart's lesions increase posterior translation of the humeral head in abduction and internal rotation, increase anterior and posterior translation of the humeral head in extension, and increase inferior translation in flexion and external rotation of the shoulder joint. Labrum lesions and increased ligament and capsule laxity are closely connected in the unstable shoulder joint.

In a detachment lesion to the upper part of the labrum classified as a type II SLAP (superior labrum anterior-posterior) lesion, the biceps anchor and the superior labrum are detached and unstable. This can result in instability of the shoulder, depending on the size and extension of the lesion. An increased size of the rotator interval and a lesion of the coracohumeral ligament and superior glenohumeral ligament crossing the interval may result in increased inferior translation when the arm is adducted. Decreased muscle function around the shoulder joint due to nerve compressions or tendon lesions influences the dynamic stability in the shoulder. Nerve entrapment due to bone changes or nerve compression due to a ganglion along the glenoid leads to muscle atrophy and decreased muscle function. Decreased function of one of the rotator cuff muscles increases the stress on the joint in the opposite direction and may lead to increased instability in the shoulder joint. Patients with winging scapula, as in serratus anterior muscle palsy due to a lesion to or compression of the long thoracic nerve, lose the anterior and superior positioning of the glenoid to the humeral head and may experience increased posterior and inferior instability in the shoulder joint. Bony retroversion of the glenoid or an altered version of the humeral head, as can be seen after fractures, is rarely responsible for instability in the shoulder joint. If there is a bony Bankart's lesion on the anterior rim of the glenoid, however, the bony restraint to anterior translation is lost and instability may occur. Hill-Sachs lesions, impact fractures on the humeral head from the glenoid edge, are due to shoulder dislocation. The impact fracture is on the posterior area on the humeral head if the shoulder is anteriorly dislocated and on the anterior area of the humeral head if the shoulder is posteriorly dislocated. Hill-Sachs lesions are the result of the instability, not the cause of it, and they are associated with increased instability only if

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there is a concomitant capsular lesion[23] or more than 30% of the humeral articular surface is involved.[47]

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Classification of Shoulder Instability

Glenohumeral instability encompasses a spectrum of disorders ranging from the dislocated shoulder to more subtle instability and covers a wide range of disabilities due to increased translation in the shoulder joint ( Table 21J1-1 ). Proper classification of shoulder instability is important in establishing the correct diagnosis and in planning the treatment of the disability. [1]

Degree

TABLE 21-J1-1 -- Classification of Shoulder Instability Direction

Dislocation

Unidirectional

Subluxation

Anterior

Microinstability

Posterior

Frequency Acute (primary) Chronic Recurrent Fixed Etiology Traumatic (macrotrauma) Atraumatic Voluntary (muscular) Involuntary Acquired (microtrauma)

Inferior Bidirectional Anterior-inferior Posterior-inferior Multidirectional

Degree

Shoulder instability is classified by degree as dislocation, subluxation, and microinstability. Dislocation.

Shoulders that have sustained a frank dislocation of the humeral head often have a disruption of the labrum-capsule complex in the direction of the dislocation. The capsule opposite the dislocation is normally stretched, but it can sometimes be seen to be totally detached laterally from the humeral head, in which case it may need to be reattached surgically for the stability of the joint to be regained. Subluxation.

In shoulders with increased laxity, in which the humeral head translates to the edge of the glenoid without true dislocation, the instability is called a subluxation of the humeral head. Subluxation can be the primary instability or the resultant instability after a true dislocation of the shoulder. Subluxation in the glenohumeral joint can evolve because of increased laxity in a shoulder with a preexisting genetic instability. Microinstability.

Microinstability in the shoulder joint has a more subtle instability pattern and can be difficult to diagnose. The symptom is often pain from internal impingement of the undersurface of the rotator cuff due to the increased laxity, rather than symptoms of instability in the shoulder joint. In these cases, the labrum attachment tends to be intact or only frayed, and the microinstability in the joint is due to increased capsular laxity. Whereas instability with dislocation and subluxation tends to be in one direction, microinstability is often in more than one direction. Frequency

In the treatment of shoulder instability, it is important to know whether it is an acute or recurrent complaint. Acute.

An acute dislocation or subluxation of the shoulder joint will usually involve an acute injury to the capsule-labrum complex. These injuries have a certain potential to heal if they are given rest, leaving the shoulder more or less stable after the instability episode.

Chronic.

If the capsule and labrum detachment lesions do not fully heal after an acute dislocation, a certain amount of instability remains in the shoulder joint, and the patient suffers recurrent instability. Each time an instability episode occurs, the capsule and ligaments become progressively stretched, with increased laxity in the shoulder joint as a result. Recurrent instability in the shoulder joint has no major potential to heal and must be treated surgically for stability to be regained in the joint if rehabilitation fails. There will often be concomitant laxity of the capsule and the ligaments, which must be treated together with a labrum tear to gain full stability in the joint. If the dislocation of the shoulder joint is not recognized acutely, as is common in posterior dislocations, and the shoulder stays dislocated for more than a few days, the dislocation is fixed and can normally no longer be treated with closed reduction alone. Even if it is possible to reduce a fixed dislocated shoulder without surgery, the joint is usually rendered so unstable because of the capsular injury and the muscle contractions that the shoulder will redislocate immediately if it is not stabilized surgically. Etiology

Traumatic.

Frank acute dislocation of the shoulder is often due to an acute traumatic event with a falling accident on an outstretched arm. Certain sports, such as football and skiing, are known to cause many shoulder dislocations or subluxations, as do other contact sports. Traumatic dislocation or subluxation in the shoulder joint is often a unidirectional injury to the capsule-labrum complex with a stretch of the capsule opposite the injury. The soft tissue injury is often more extensive when there has been a traumatic event and may result in major instability in one direction in the shoulder. Atraumatic.

Atraumatic shoulder instability is often a microinstability or slight subluxation increased laxity in the joint. There may be a genetic increased laxity of the capsule, often with bilateral and multidirectional instability. Involuntary atraumatic true dislocations, however, can be seen as a result of recurrent traumatic dislocations; the shoulder capsule has become so lax that the joint dislocates without any new trauma. Dislocation of the shoulder joint can be voluntary and be associated with certain psychologically disturbed patients (who try to get attention by dislocating the shoulder)

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or drug abusers (who try to get pain medication by dislocating the shoulder voluntarily). Patients with voluntary dislocation often have a multidirectional instability pattern with a

global increased laxity in the joint. Although classic teaching has been to avoid operation in all patients with voluntary instability,[46] there is a subgroup of patients who can demonstrate their instability but do not have an underlying psychiatric disease. In general, these patients have a more positional type of instability in which the humeral head slides out posteriorly with flexion, adduction, and internal rotation of the arm. [16] These patients know their instability pattern well and know how to dislocate and reduce the shoulder voluntarily. They may benefit from stabilizing surgery. Acquired.

It has never been shown that microtrauma, due to repetitive overhead motions, increases capsular laxity in an otherwise stable shoulder. People participating in overhead sports often have shoulder disabilities, however; some of them are due to a preexisting increased laxity in the shoulders that increased with increasing stress to the stabilizing structures. The primary shoulder symptom is often pain due to internal impingement of the rotator cuff because of the increased laxity in the joint,[29] not a complaint of instability. Direction

It is important to establish the direction of the instability in the shoulder joint. The majority of acute traumatic dislocations are anterior; the remainder are posterior or inferior. Unidirectional.

Unidirectional anterior instability is often related to a traumatic event, with an anterior labrum detachment lesion and inferior capsular laxity together with laxity of the anterior band of the inferior glenohumeral ligament. If rehabilitation fails, surgery often includes arthroscopic or open Bankart repair and anterior capsular shift, especially in recurrent dislocations. Unidirectional posterior instability and dislocations can be difficult to diagnose and require careful examination of the injured shoulder. Posterior dislocations rarely become recurrent, but a subluxation disability may remain and will need careful rehabilitation. A posterior labrum lesion is often found, and the instability is merely a capsular laxity and a laxity of the posterior band of the inferior glenohumeral ligament, which needs to be addressed if surgery is planned. A posterior approach to the shoulder is then recommended. Bidirectional.

If acute unidirectional anterior or posterior dislocations become recurrent, they tend to increase instability in the inferior direction because of increasing inferior capsular and

ligament stretching. The direction of the instability is then bidirectional, and the increased laxity of the axillary pouch should be addressed in the treatment. Multidirectional.

Multidirectional instability of the shoulder tends to be due to a generalized increased capsular laxity as is seen in atraumatic genetic instability. The diagnosis of multidirectional instability requires an inferior instability pattern, and it will often show global increased laxity. Multidirectional instability can be the result of laxity after a unidirectional recurrent dislocation with increasing laxity of the capsule and the ligaments. Most often, however, multidirectional instability is a subtle instability seen as a complaint of shoulder pain in a patient with genetic bilateral and generalized increased joint laxity.[9]

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Diagnostic Evaluation

A careful history and physical examination are essential to uncover the nature of the shoulder instability. Even though the shoulder instability may be due to an acute traumatic unidirectional dislocation, it is still important to perform a careful examination to identify concomitant injuries to the stabilizing structures of the shoulder, which will need to be addressed in the treatment.[1] History

By obtaining a careful history from patients with shoulder instability, it is often possible to differentiate between acquired and genetic instability. Patients may describe a history of a frank dislocation after an acute traumatic event, repetitive microtrauma linked to the overhead actions of specific sports, or generalized joint laxity. To ascertain the dominance of the involved arm, the age of the patient and the type of sport played are important. An increased rate of recurrent dislocation is seen in younger individuals, and the fact that a full range of motion in the dominant shoulder in some sports is more important than an absolutely stable shoulder influences treatment decisions. If both shoulders are involved and the humeral head instability is multidirectional, it is likely that the instability is due to a genetic basis. A family history of shoulder instability may support this, as would a history of other diffuse joint complaints. These patients can often be treated nonoperatively with rehabilitation; but if rehabilitation fails, surgery with capsular shrinkage is needed. The pain pattern in shoulder disability is helpful in establishing the diagnosis. Pain in the neck and radiating arm pain may indicate a neurologic condition, which should be ruled out. Dead arm syndrome, a complaint of neurologic disturbances in the arm, occurs especially during throwing because of stretch of the brachial plexus of a subluxating humeral head.[14] Pain at rest, pain that radiates down to the elbow, and night pain are often associated with subacromial impingement and rotator cuff disease. Inquiring about pain with specific movements or in specific positions can help uncover the direction in

which the laxity in the joint is increased. Pain is the main symptom in patients with internal impingement of the rotator cuff because of increased laxity in the shoulder.[29] Physical Examination

The physical examination of a patient with shoulder instability begins with inspection of the skin and the muscles around the joint. In major traumatic dislocations, the humeral head can be seen dislocating out through the skin.

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Muscle atrophy can be seen in neurologic diseases, in local nerve compression by a ganglion or a tumor, and when a torn tendon is responsible for the shoulder disability. If the shoulder is dislocated at the time of examination, the normal configuration of the joint is lost. If the humeral head is anteriorly dislocated, the lateral deltoid region is hollow and the humeral head is anterior, inferior, and medial to the normal shoulder joint. The arm is held in a fixed, slightly externally rotated, slightly abducted position. Posterior dislocation can be difficult to see from the configuration of the joint, but a posterior prominence may be noted. With a posterior dislocation, the arm is held in fixed internal rotation and adduction. Patients with inferior dislocation can be seen with the humeral head dislocated down into the axilla and the arm held fixed above the head because of humeral head entrapment under the inferior rim of the glenoid. Pain, local tenderness, and swelling over the shoulder joint line and the tendons are recorded, as is any tenderness over the adjacent acromioclavicular and sternoclavicular joints. Patients with shoulder instability should be evaluated for neck pain, and cervical spine mobility should be examined as well. A brief neurologic examination of the upper extremity can rule out most neurologic causes of shoulder disability. After acute dislocations, the function of the axillary nerve is evaluated by testing sensibility in the deltoid region and contraction of the deltoid muscle; the vascular integrity of the arm should be evaluated as well. Nerve lesions are common after shoulder dislocation.[32] Passive and active mobility in the shoulder joint and scapular stability are evaluated and compared with the opposite shoulder. A decrease in shoulder mobility can result from pain and discomfort stemming from shoulder instability; however, other diseases in the joint, such as subacromial impingement and rotator cuff tear, may be responsible. If the shoulder is dislocated at the time of the examination, the shoulder and arm are held fixed in the dislocated position, and both passive and active motion in the shoulder is restricted. Patients with increased mobility in the shoulder should be examined for bilateral increased mobility and for generalized joint laxity by evaluating thumb hyperabduction. The strength of the muscles surrounding the shoulder joint is compared with the opposite site and graded 0 to 5; grade 5 is normal strength. Abduction and external and internal rotation strength in the shoulder is an indication of the dynamic stability in the joint. In dealing with shoulder instability, it is also important to evaluate scapular stability

and the patient's ability to hold the scapula fixed during motion in the shoulder. Specific tests for shoulder instability enable the clinician to classify the instability pattern. It is often advisable to evaluate the opposite shoulder first to gain the patient's confidence during the examination and for comparison.[1] These tests should be conducted in every examination for shoulder instability to establish the degree and direction of the instability. The inferior instability test is conducted with the patient standing ( Fig. 21J1-2 ). The test establishes the sulcus sign, which is the inferior translation of the humeral head, leaving a gap between the undersurface of the acromion and the upper surface of the humeral head when a direct inferior force is applied to the arm. The sulcus sign is graded 1+ when the gap is less than 1 cm, 2+ when the gap is between 1 and 2 cm, and 3+ when the gap is more than 2 cm. Inferior laxity is also tested with the arm in 90 degrees of abduction and application of an inferiorly directed force to the joint.

Figure 21-J1-2 The sulcus sign test for inferior instability. The test is graded 1 to 3, depending on the distance between the undersurface of the acromion and the humeral head.

The patient is best evaluated for anterior and posterior instability in the supine position, with the arm and shoulder on the border of the table. The anterior apprehension test ( Fig. 21J1-3 ) is performed with the arm in 90 degrees of abduction. The arm and shoulder are externally rotated, and the patient's apprehension (i.e., the anxiety and muscle defense against the motion) is observed. A positive response typically indicates anterior instability. If the patient experiences pain with the movement, it may be a symptom of internal impingement of the rotator cuff undersurface on the posterosuperior glenoid labrum inside the shoulder joint due to the instability. The response to the anterior relocation test (Jobe's test) ( Fig. 21J1-4 ) is positive if the pain and the apprehension disappear on relocation of the humeral head with application of a posteriorly directed force to the shoulder joint. The posterior pain test is conducted with the arm in forward flexion at a 90-degree angle and the shoulder internally rotated. Again, the test response is positive if the patient experiences discomfort with this motion. The apprehension and relocation tests are specific for instability and internal impingement in the shoulder joint and should be conducted in every evaluation for shoulder instability.

Figure 21-J1-3 The anterior apprehension test for anterior instability with the patient supine. The arm is abducted 90 degrees, and the shoulder is increasingly externally rotated to stress the anterior capsule.

Figure 21-J1-4 The response to Jobe's relocation test is positive when the apprehension from the anterior apprehension test disappears with the application of a posteriorly directed force to the shoulder.

The axial load test ( Fig. 21J1-5 ) is conducted with the

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patient supine and the arm in 90 degrees of abduction and neutral rotation. While one hand applies an axial load, crepitation and humeral head translation are noted when the other hand applies anterior and posterior stress to the joint. Grading reflects the degree of humeral head translation anterior and posterior to the glenoid rim. The grade is 1+ if the translation of the humeral head is to the edge of the glenoid, 2+ if the humeral head can be subluxated over the glenoid rim but reduces spontaneously, and 3+ if a frank dislocation of the humeral head over the glenoid rim does not reduce spontaneously. The axial load test must be performed carefully if there is a risk for dislocating the patient's shoulder. The grading system is used for microinstability and subluxations or when the patient is evaluated under anesthesia.

Figure 21-J1-5 The axial load test is performed with the patient supine and the arm abducted 90 degrees and in neutral rotation. While one hand applies an axial load, crepitation and translation are noted when the other hand applies an anteriorly and posteriorly directed force to the shoulder joint. Imaging Tests

Radiography

Radiographs of the shoulder are mandatory in evaluating shoulder instability. After an acute traumatic event, anteroposterior, lateral, and axillary views are recommended to rule out dislocations and fractures. An anteroposterior view is deviated 30 to 45 degrees from the sagittal plane of the body to parallel the plane of the glenohumeral joint. A trans-scapular (Y) lateral view and an axillary view are extremely valuable for assessing glenoid version, demonstrating humeral head impression fractures, and revealing the position of the humeral head relative to the glenoid. These three views are the trauma series.[42] In the assessment of more chronic shoulder instability, additional views are helpful in determining bony anatomy and pathologic changes. The West Point view[45] often reveals a bony Bankart's fracture or ectopic bone production at the anterior glenoid rim that may not be visualized in other projections. The West Point view is obtained by placing the patient prone with the arm in 90 degrees of abduction and neutral rotation. The cassette is placed at the superior aspect of the shoulder. The radiographic beam comes from inferior and is projected cephalad at an angle of 25 degrees from the horizontal and medially at an angle of 25 degrees. In the Stryker notch view, the patient is supine and the palm of the hand is placed on top of the head. The shoulder is in 90 degrees forward flexion and neutral abduction to expose the humeral head. The cassette is placed posterior to the shoulder. The Stryker notch view will show the

Hill-Sachs lesion. [20] These bony compression fractures of the humeral head occur when the shoulder is dislocated and the humeral head presses against the glenoid rim. The Hill-Sachs lesion is found on the posterosuperior region of the humeral head if the dislocation is anterior

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and on the anterior neck if the dislocation is posterior. The Stryker notch view is also useful in revealing the Bennett lesion of the shoulder,[10] which is a crescent-shaped region of mineralization at the posteroinferior rim of the glenoid where the posterior capsule inserts. The Bennett lesions are most often seen in baseball pitchers and can be connected with labrum and rotator cuff disease. Magnetic Resonance Imaging

During the past 5 years, MRI has become an important tool in the evaluation of shoulder instability. Because image quality has increased dramatically, it is now possible to evaluate glenoid labrum lesions, to detect ligament and capsule detachment from the glenoid rim, and to assess the humeral head with great accuracy. [18] MRI of the shoulder of a young athletic patient is important after an acute traumatic dislocation to rule out a Bankart's lesion that needs repair. MRI pinpoints the site of injury before surgery and may uncover additional ligament and tendon lesions due to the instability. Computed Tomography

Computed tomography with or without three-dimensional reconstruction can be helpful in selected cases, especially if there is a fracture of the glenoid rim that needs to be addressed with surgery and treated by open reduction with internal fixation.[51]

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Treatment

A treatment algorithm is presented in Figure 21J1-6 .

Figure 21-J1-6 Treatment algorithm. Reduction

Acute dislocations of the shoulder are reduced as gently and expeditiously as possible to minimize the damage to the surrounding structures. Trauma series radiographs of the shoulder are taken before and after the reduction to rule out fractures of the glenoid or the humeral head. Early relocation of the joint can sometimes be performed without sedation of the patient or with local anesthetic injections in the joint if it is done before muscle spasm of the pectoralis major sets in and if the patient can cooperate. Recurrent dislocations can be easier to reduce because they more easily dislocate and may need less sedation. At the other extreme, dislocations may need total sedation or regional brachial anesthesia to secure a gentle and safe closed reduction. Anterior and posterior shoulder dislocations are best reduced with the patient supine, applying traction against countertraction to the shoulder. The elbow is flexed to relax the structures around the shoulder. Traction is applied in the inferior direction of a slightly abducted arm while countertraction is applied by use of a sheet around the shoulder, pulling the humeral head out lateral and upward from the inferior edge of the glenoid. When the humeral head is free of the inferior glenoid edge, anterior dislocation is reduced with internal rotation; posterior dislocation is reduced with external rotation of the arm. Inferior dislocation of the humeral head, in which the patient presents with the arm held fixed above the head, is reduced with the patient supine by gently releasing the humeral

head from the inferior glenoid edge with a slightly inferior pull and lateral traction on the shoulder. As soon as the humeral head is free of the edge, the arm can be brought down in adduction during the reduction. If a gentle attempt at closed reduction fails or if the dislocation is fixed with the passage of time, open reduction is the most secure way of relocating the joint and avoiding a secondary fracture. Care should be taken of the neurovascular bundle; its location may be altered because of the

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dislocation of the humeral head. The subscapularis tendon and the anterior capsule are incised near their insertion on the lesser tuberosity to allow external rotation to release the humeral head underneath the coracoid. If the dislocation is still locked, osteotomy of the coracoid may be necessary to relocate the joint. Rehabilitation

Except for a young patient who is participating in contact sports or has other high physical demands, rehabilitation is the cornerstone in the management of shoulder instability. If the patient has suffered a true dislocation or a traumatic subluxation of the shoulder, protection for 3 to 4 weeks is mandatory to enhance healing of the capsule-labrum complex.[12] The emphasis of the rehabilitation program is on regaining safe and protected full-range motion, starting with passive range of motion and pendulum exercises. External rotation above neutral and abduction above 90 degrees are restricted until 6 weeks after anterior shoulder dislocation to protect the healing soft tissue. If the dislocation is posterior, internal rotation is limited for 4 to 6 weeks. Terminal stretch of the joint, to gain full range of motion, should not be allowed before 9 to 12 weeks, but full range of motion in the joint is an important goal.[31] If range of motion is restricted in the shoulder joint itself, motion of the scapula on the thoracic wall will take place during shoulder motion, leading to pain in the shoulder joint.[34] Strengthening of the rotator cuff is essential to restore and increase the dynamic stabilization of the joint, as is strengthening of the scapular stabilizing muscles to position the glenoid toward the humeral head.[31] Muscle rehabilitation can be started early with isometric contractions. Unstable shoulders and shoulders with increased laxity may have a defect in proprioception. A rehabilitation program concerning shoulder stability should emphasize the neuromuscular control of the joint. The goal of rehabilitation is to restore function in the shoulder to a level that allows the patient to return safely to previous activity. Each rehabilitation program should include a final sport- or activity-specific test that proves the patient's ability to return to the sport or activity. Return to sport and physical activities is allowed after 8 to 10 weeks. If the patient is not able to return to the previous level of activity because of pain or instability

in the shoulder, an MRI scan of the shoulder should be considered to rule out underlying injuries that may need surgical intervention. When rehabilitation fails, surgery should be considered to restore the stability of the shoulder joint. Rehabilitation after stabilizing surgery depends on the surgical approach. In general, arthroscopic stabilization is followed by a faster rehabilitation with rapid restoration of motion. Open stabilization with capsular shifting either posterior or anterior has the same general guidelines for rehabilitation as an acute shoulder dislocation, except that contact sports and overhead sports are first allowed after 4 months. Surgical Treatment of the Unstable Shoulder

Patients younger than 25 years are at high risk for redislocation after one acute traumatic shoulder dislocation if they have been treated conservatively with rehabilitation.[24] [25] [31] [46] [47] [53] They will have difficulty in returning to their previous level of activity, reducing their quality of life.[31] In a young, active individual with a first-time dislocation of the shoulder and a Bankart's lesion of the labrum shown on MRI evaluation, primary early repair of the labrum should be considered. Otherwise, surgery should be considered secondary to a failed rehabilitation program, when pain and instability are consistent. An MRI scan of the shoulder before the surgery is planned may help pinpoint specific and additional injuries to the joint that need to be addressed in the treatment. Examination under anesthesia is mandatory before stabilizing shoulder surgery to plan the surgical approach. With the patient anesthetized and in the beach-chair position, the shoulder is examined for laxity. The axial load test is performed to establish the direction and degree of instability in the joint and to determine whether it is a unidirectional or a more general unstable joint disease. In unstable shoulder joints, especially if the instability is in more than one direction, the surgical approach leans toward an open capsular stabilization. Arthroscopic Stabilization

Arthroscopy is performed as an adjunct to open shoulder stabilization. Arthroscopy allows improved visualization of the capsule-labrum complex and identification of other articular lesions. To be an effective alternative to open stabilization, however, arthroscopic stabilization should have comparable success and failure rates, and the technique must allow treatment of multiple lesions in the joint. Arthroscopic stabilization has evolved from staples[30] to transglenoid sutures[34] to cannulated bioabsorbable implants[54] and suture anchors, and the recurrence rate of instability and the surgical complications improved significantly. The reported failure rate with use of biodegradable implants to secure the labrum and ligament complex to the glenoid rim varies from 0% to 21%,[3] [50] depending on the quality of the labrum tissue to be repaired. Bioabsorbable implants are useful in arthroscopic repair of shoulder instability due to an isolated Bankart's lesion that does not extend too far inferior on the glenoid and with labrum tissue of good quality, as is

normally found in young patients with only a short history of instability. Biodegradable implants can also be used with other stabilizing procedures, such as an open stabilizing capsular shift or arthroscopic capsular shrinkage, or with suture anchors to secure the more inferior labrum lesions that can be difficult to address with the implants. The benefits of the cannulated biodegradable implants are the relative short learning curve and the good results after repair of simple lesions. The disadvantages are the limitation in addressing capsular laxity and the reported 6% incidence of intracapsular synovial reaction, a reaction that normally subsides with the oral

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administration of nonsteroidal anti-inflammatory drugs or responds to arthroscopic lavage or intra-articular administration of steroids.[13] Arthroscopic placement of suture anchors for repair of labrum and capsule detachments in the shoulder joint can be a technical challenge for the surgeonnot only the placement of the anchors, but also the arthroscopic knot tying. The problem of knot tying is resolved by the knotless suture anchors, although they are still technically demanding. The failure rate with the newest methods is reported to be less than 10%,[14] and the benefit of the use of anchors is the ability to address both inferior lesions and more extensive lesions including capsular laxity. The disadvantages, in addition to the technical issues, are the risk of loosening or migration of the metal anchor, suture breakage, and difficulty in removing the anchor if malposition or infection occurs. Thermal shrinkage of the capsule can be employed in shoulders with minor multidirectional instability when there is a generalized capsular laxity but no labrum tear, or it can be applied in combination with a labrum repair if a slight capsular laxity remains. The optimal amount of heat that will shrink the capsule without damaging the strength of the tissue is in the range of 60° to 67.5°C; the depth of the effect is between 700 and 1200 m, depending on the device.[49] Several factors remain unknown about the use of thermal shrinkage of the capsule in unstable shoulders. What effect does the temperature have on the proprioceptive nerve endings in the shoulder? How long does it take to fully re-form normal tissue after the shrinkage, and how long does the effect last? Despite the unknown issues, including the risk for nerve damage, thermal capsular shrinkage has been useful in selected cases.[49] To be able to use and control the technique of all these modalities is essential in performing arthroscopic shoulder stabilization. In selected cases, the results of arthroscopic stabilization will then be comparable to those of open stabilization with the benefit of having arthroscopic surgery with quicker recovery, better cosmesis, greater return in postoperative range of motion, and less morbidity. Surgical Approach

Arthroscopy.

Local regional anesthesia with an interscalene block or general anesthesia is needed to obtain the amount of shoulder muscle relaxation that allows uncomplicated shoulder arthroscopy. The patient is secured in the beach-chair or lateral decubitus position. The landmarks on the shoulderthe acromion, the acromioclavicular joint, and the coracoidare marked. If regional anesthesia is used, supplementary local anesthesia in the area of the posterior portal is needed. An evaluation under anesthesia is performed to determine the pattern of instability that needs to be addressed in the treatment. If the patient is in a beach-chair position, an arm-holder can be beneficial. The arthroscope is passed through the posterior portal 2 cm below and medial to the posterior corner of the acromion. The anterior working portal just lateral to the coracoid is placed under vision with use of an inside-out or outside-in technique. If the labrum lesion is on the posterior rim, the scope is placed in the anterior portal and the instruments are used through the posterior portal, which may have to be moved more lateral to gain the right working angle to the glenoid. If the lesion responsible for the instability is an isolated labrum lesion, or if only slight capsular laxity coexists, and if the tissue that needs repair is of good quality, the instability is suitable for arthroscopic repair. The lesion area between the labrum and the glenoid is débrided of scar tissue, and the glenoid edge is prepared down to bleeding bone with either a rasp or the shaver. This increases the area of healing tissue. Depending on the extension, the tissue, and the area of the labrum lesion, either biodegradable tacks or suture anchors or both are used. It is important to bring the labrum repair all the way up to and above the edge of the glenoid to get the labrum effect of increased depth of the glenoid. If thermal capsular shrinkage is planned, the labrum lesion is repaired first before shrinkage of the capsule; otherwise, there is a risk that the repair will be too tight. Open Capsular Shift and Shoulder Stabilization

Patients with recurrent shoulder dislocations, who have had shoulder instability for a longer time, will often have an increased capsular laxity that cannot be treated arthroscopically with satisfying results. Shoulders that on evaluation under anesthesia show major instability in more than one direction and shoulder instability in young patients who want to participate in contact sports are better treated with open capsular stabilization. Surgical Approach

Open Anterior Capsular Shift.

Open capsular stabilization can be performed with either general anesthesia or regional interscalene block anesthesia and supplementary local anesthesia in the axillary region. The patient is placed supine in a slightly elevated position. An evaluation is performed under anesthesia. If the shoulder has grade 3 instability with frank dislocation and instability in more than one direction or if the patient is young and is participating in

contact sports, the instability is suitable for an open stabilizing procedure. An arm-holder enables the surgeon to place the arm in specific positions during the capsular repair to secure the proper tightness of the repair. The skin incision is marked from just lateral to the coracoid process following the deltopectoral fold distally going lateral to the axilla. Administration of epinephrine into the skin and subcutaneous tissue before incision decreases bleeding. Incising the fascia above the deltoid allows localization of the cephalic vein, an important landmark that normally runs in the deltopectoral interval. The remainder of the major vessels and the brachial plexus are located medial and inferior to the coracoid process. Splitting the deltopectoral interval just medial to the cephalic vein, keeping the vein laterally to preserve the venous drainage of the deltoid muscle, takes the surgeon to the next layer. If the patient is older, however, and a more extensive exposure is needed, the cephalic vein should be kept medially to release the tension on the vein to avoid rupture. With the shoulder held in slight flexion, the muscles are relaxed, which facilitates access to the joint. The coracoid process and the conjoint tendons are medial in the incision. The fascia is incised lateral to the muscle and tendon of the biceps brevis, allowing exposure of the subscapularis

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tendon and the anterior circumflex vessels, which helps define the lower border of the tendon. The subscapularis tendon blends laterally with the capsule before it inserts on the lesser tuberosity. If self-retractors are used to facilitate exposure, care should be taken not to place too much tension on the blades underneath the conjoint tendon because of the risk of damaging the musculocutaneus nerve that runs 5 cm below the coracoid medially and under the conjoint tendons. The subscapularis tendon is released from its lateral insertion by separating the muscle medially from the underlying capsule going laterally to where it becomes tendon and blends with the capsule. Care should be taken not to go too far medially because that may jeopardize the nerve supply to the muscle. The tendon is released from its lateral insertion, leaving some tendon tissue for the repair of the tendon. It may be necessary to coagulate the three circumflex vessels below the subscapularis tendon to improve exposure for release of the muscle tissue from the capsule all the way medial to the joint line. Retention sutures placed in the subscapularis tendon secure it from retraction medially. The capsule and shoulder joint are now exposed. The capsular shift can be performed either medially or laterally ( Figs. 21J1-7 and 21J1-8 ). In a lateral capsular shift, the capsule is incised along its lateral insertion on the humeral head. The rotator interval is opened from the humeral side going medially to the coracoid. Placement of the arm in abduction and external rotation while the capsule is being incised distally allows the most inferior part of the posterior capsule to be exposed. The axillary nerve should be protected during the inferior and posterior capsular incision. The capsule should be released inferiorly going slightly posteriorly to bring the capsule shift far enough superior to tighten the inferior lax capsule. The capsule is split horizontally between the upper third and the lower two thirds from its

lateral border going medial to its insertion on the glenoid. The joint is now open, and the capsule can be brought medially to check for a Bankart's lesion along the glenoid rim. A Bankart's lesion can be repaired with suture anchors along the glenoid edge. The rim of the glenoid is débrided of scar tissue, and the capsule and labrum are released to be brought up to the edge. It is important to obtain fresh bleeding bone along the edge of the glenoid to enhance healing between bone and capsule. Two to four suture anchors, depending on the size of the lesion, are inserted along the glenoid rim close to the articular surface in a 45-degree angle. The sutures are brought through the capsule-labrum complex and tied on the outside, with enough tension on the tissue to make the repair stable. Three or four suture anchors are needed to shift the capsule back to its insertion along the humeral head, starting inferior to secure the most inferior limb of the capsule. The most superior anchor is placed just below the rotator interval and the biceps tendon. The inferior limb of the capsule is pulled up and lateral to tighten it, and sutures are brought through the capsule tissue to create the desired tension. The superior limb of the capsule is then sutured on top of the inferior limb to close the defect. Finally, the rotator interval is closed. To ensure that the shift is not too tight, the arm is held in a 45-degree abducted, 45-degree externally rotated position during the inferior shift and in adduction and external rotation when the rotator interval is closed. This allows the desired range of motion after the shift.

Figure 21-J1-7 A to E, Medial capsular shift with repair of a Bankart's lesion: drawing of surgical approach. (C, D, and E from O'Brien SJ, Warren RF, Schwartz E: Anterior shoulder instability. Orthop Clin North Am 18:395-408, 1987.)

Figure 21-J1-8 Lateral capsular shift: drawing of surgical approach.

In medial shift of the capsule, the incision in the capsule is made parallel and close to the glenoid rim going from superior all the way inferior past the 6-o'clock position of the glenoid.[2] The axillary nerve should be protected during the inferior capsular incision. A horizontal incision in the capsule from medial to lateral divides the capsule into an inferior and superior limb. The Bankart's lesion is repaired with suture anchors as described before, and the same anchors are used to shift the inferior capsule limb superiorly and the superior limb medially. After the capsule shift, the subscapularis tendon is repaired back to its insertion with the arm in 45 degrees of external rotation, and the remainder of the wound is closed. Open Posterior Capsular Shift.

If the instability is mostly posterior, it can be difficult to get enough tension on the posterior capsule by shifting it from an anterior approach, and a posterior approach is needed. General anesthesia or regional interscalene block anesthesia may be used. The patient should be placed in a sitting position, which allows good exposure of the

posterior part of the shoulder joint. The skin incision extends from 1 cm medial to the posterior corner of the acromion distally toward the axillary fold. The deltoid is split vertically between its middle and posterior thirds. The approach to the joint begins through a horizontal split in the infraspinatus muscle and tendon that will expose the capsule. The capsular shift is performed by opening the capsule along the glenoid rim and shifting the capsule medially and superiorly, using suture anchors as described before. Alternatively, an oblique capsulotomy can be used to repair the labral tear. In the posterior approach to the shoulder, care should be taken to avoid interference with the quadrangular space containing the axillary nerve and circumflex vessels. The space is just below the teres minor muscle and can be jeopardized if the incision and the split in the deltoid are too low. Results.

Open capsular reconstruction is a versatile procedure capable of addressing both detachment lesions and capsular disease when necessary with an expected success rate between 91% and 97%.[46] [47] Open procedures tend to gain better stabilization at the expense of full range of motion, however.[4] Therefore, before treating patients with instability, it is important to ascertain whether full range of motion or complete stability of the joint is required after surgery. Throwing athletes and athletes participating in overhead sports will have difficulty in returning to their previous level of activity if they lack full range of motion, whereas patients participating in contact sports or mountain climbing are more dependent on complete stability. Postoperative Rehabilitation.

The repair of the capsule and the subscapularis tendon needs to be protected for 4 to 6 weeks. The arm should be protected in a sling, not allowing external rotation and abduction above neutral for the first 3 weeks. Passive motion of the shoulder with pendulum exercises is allowed immediately after surgery in addition to motions of the hand and elbow. Active range of motion is allowed after 6 weeks with increasing external rotation and isometric exercises. After 9 weeks, terminal

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stretch to regain full range of motion is allowed. The patient can return to contact sports after 4 months. Combination of Arthroscopic and Open Shoulder Stabilization

Shoulder instability is a complex disease, and the treatment requires advanced surgical skills. Different arthroscopic repair and stabilization modalities should be available to the

surgeon, who should be able to shift to an open stabilizing procedure when it is needed. Some patients will benefit from an arthroscopic labrum repair in conjunction with an open capsular shift. Patients who have a posterior Bankart's lesion with increased anterior capsular laxity can be treated with a posterior arthroscopic labrum repair using tacks or suture anchors followed by open anterior capsular

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stabilization. Patients with recurrent shoulder instability who have an anterior Bankart's lesion and increased capsular laxity can be treated with arthroscopic labral repair as described and either anterior or posterior open capsular shift, depending on the instability pattern.

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Summary

An increasing knowledge of the biomechanics of the shoulder joint has improved the diagnosis and treatment of shoulder instability. Frank dislocations of the joint are often easily diagnosed, but a thorough knowledge of the pathoanatomy and biomechanics of the shoulder is required with subtler instability patterns for a correct diagnosis to be established and a correct treatment plan formulated. With increasing aid from MRI scans of the shoulder together with a careful history and examination, a specific diagnosis of the instability pattern in the shoulder joint is possible. Physicians treating patients with shoulder disabilities should be familiar with this, and patients with shoulder complaints should be routinely examined for instability of the joint. Except for specific cases, rehabilitation is the cornerstone of treatment of shoulder instability. In the future, however, as skills increase in both arthroscopic and open surgery, more patients may benefit from primary surgical shoulder stabilization. Newer tools with bioabsorbable tacks and knotless anchors for labrum repair make the surgery less traumatic to the patient and the rehabilitation after surgery easier. The ability to switch between different surgical approaches is important for surgeons dealing with shoulder instability to achieve a high success rate with few recurrences while an almost normal postoperative range of motion is maintained in the shoulder. Salvage procedures are rarely necessary. Humeral or glenoid osteotomies and other bone and soft tissue salvage procedures, such as Bristow and Putti-Platt procedures, should be considered the last choice for treatment of shoulder joint instability.

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DeMaeseneer M, Jaovisidhas S, Jacobsen JA, et al: The Bennett lesion of the shoulder. J Comput Assist Tomogr 22:31-34, 1998. 10.

DePalma AF, Callery G, Bennett GA: Variational anatomy and degenerative lesions of the shoulder joint. Instr Course Lect 6:255-281, 1949. 11.

Dines DM, Levinson M: The conservative management of the unstable shoulder including rehabilitation. Clin Sports Med 14:797-816, 1995. 12.

Edwards D, Howy G, Saies AD, Hayes MG: Adverse reactions to an absorbable shoulder fixation device. J Shoulder Elbow Surg 3:230-233, 1994. 13.

Field L, Savoie F, Griffith P: A comparison of open and arthroscopic Bankart repair [abstract]. J Shoulder Elbow Surg 8:195, 1999. 14.

Field LD, Warren RF, O'Brien SJ: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557-563, 1995. 15.

Fronek J, Warren RF, Bowen M: Posterior subluxation of the glenohumeral joint. J Bone Joint Surg Am 71:205-216, 1989. 16.

Gartsman G, Taverna E, Hammerman S: Arthroscopic rotator interval repair in glenohumeral instability: Description and operative approach. Arthroscopy 15:330-332, 1999. 17.

Gusmer PB, Potter HG, Schatz JA, et al: Labral injuries: Accuracy of detection with unenhanced MRI of the shoulder. Radiology 200:519-524, 1996. 18.

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Habermeyer P, Schuller U, Wiedemann E: The intra-articular pressure of the shoulder: An experimental study on the role of the glenoid labrum in stabilizing the joint. Arthroscopy 8:166-172, 1992. 19.

Hall RH, Isaac F, Booth CR: Dislocations of the shoulder with special references to accompanying small fractures. J Bone Joint Surg Am 41:489-494, 1959. 20.

Harryman DT, Sidles JA, Clark JM, McQuade KJ: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990. 21.

Harryman DT, Sidles JA, Harris SL, Matsen FA: Role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 72:53-66, 1992. 22.

Hill HA, Sachs MD: Grooved defect of the humeral head: A frequently unrecognized complication of dislocation of the shoulder. Radiology 35:690-700, 1940. 23.

Hoelen MA, Burgers AMJ, Rozing PM: Prognosis of primary anterior dislocations in young adults. Arch Orthop Trauma Surg 110:51-54, 1990. 24.

Hovelius L: Anterior dislocation of the shoulder in teenagers and young adults. J Bone Joint Surg Am 69:393-399, 1987. 25.

Howell SM, Galinat BJ: The glenoid labral socket. A constrained articular surface. Clin Orthop 243:122-125, 1989. 26.

Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232, 1988. 27.

Howell SM, Imobersteg AM, Seger OH, Marone PJ: Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am 68:398-404, 1986. 28.

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Jobe FW, Pink M: The athlete's shoulder. J Hand Ther 7:107-110, 1994.

Johnson L: Techniques of anterior glenohumeral ligament repair. In Arthroscopic Surgery: Principles and Practice, vol 2, 3rd ed. St Louis, Mosby, 1986, pp 1405-1420. 30.

Kirkley A, Griffin S, Richards C, et al: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder. Arthroscopy 15:507-514, 1999. 31.

Kumar VP, Balasubramaniam P: The role of atmospheric pressure in stabilizing the shoulder. An experimental study. J Bone Joint Surg Br 67:719-721, 1985. 32.

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Morgan C, Bodenstab A: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111-122, 1987. 34.

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Nobuhara K, Ikeda H: Rotator interval lesion. Clin Orthop 223:44-50, 1987.

O'Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 37.

O'Brien SJ, Schwartz RE, Warren RF, Torzilli PA: Capsular restraints to anterior/posterior motion of the shoulder. Orthop Trans 12:143, 1988. 38.

O'Connell PW, Nuber GW, Mileski RA, Lautensclager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 39.

Oveson J, Nielson S: Anterior and posterior instability: A cadaver study. Acta Orthop Scand 57:324-327, 1986. 40.

Oveson J, Nielson S: Posterior instability of the shoulder: A cadaver study. Acta Orthop Scand 57:436-439, 1986. 41.

Pagnani MJ, Galinat BJ, Warren RF: Glenohumeral instability. In DeLee JC, Drez D, Miller MD (eds): Orthopaedic Sports Medicine: Principles and Practice, vol 1. Philadelphia, WB Saunders, 1994, pp 580-623. 42.

Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 58:195-201, 1976. 43.

Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop 135:165-170, 1978. 44.

Rokous JR, Feagin JA, Abbott HG: Modified axillary roentgenogram: A useful adjunct in the diagnosis of recurrent instability of the shoulder. Clin Orthop 82:84-86, 1972. 45.

Rowe CR, Sakellarides HT: Factors related to recurrences of anterior dislocation of the shoulder. Clin Orthop 20:40-48, 1961. 46.

Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863-871, 1981. 47.

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Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491-505, 1971.

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Speer K, Warren RF, Pagnani M, Warner JJP: An arthroscopic technique for anterior stabilization of the shoulder with a bioabsorbable tack. J Bone Joint Surg Am 8:1801-1807, 1996. 50.

Stevens KJ, Preston BJ, Wallace WA, Kerslake RW: CT imaging and three-dimensional reconstruction of shoulder with anterior glenohumeral instability. Clin Anat 12:326-336, 1999. 51.

Terry GC, Hammon D, France P, Norwood LA: The stabilizing function of passive shoulder restraints. Am J Sports Med 19:26-34, 1991. 52.

Yoneda B, Welsh RP, MacIntosh DL: Conservative treatment of shoulder dislocations in young males. J Bone Joint Surg 64:254-255, 1982. 53.

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2. GLENOHUMERAL INSTABILITIES IN THE CHILD Ralph J. Curtis Jr. MD The glenohumeral joint of the shoulder is susceptible to dislocation and subluxation in high-demand sports activities. The anatomy of the glenohumeral joint provides a high degree of functional mobility with the sacrifice of stability. Although the glenohumeral joint is commonly affected by instability in adolescents and adults, it is much less commonly affected in children. Traumatic forces applied to the shoulder in the skeletally immature child are more likely to result in fracture of the proximal humeral physis as opposed to damage to the soft tissues of the joint leading to dislocation.[14] [17] [19] [30] [61] Therefore, traumatic dislocation of the shoulder in a child is rare. In the adolescent with open physes, however, patterns of instability begin to resemble those found in the adult. Varying degrees of atraumatic instability based on multidirectional laxity of the shoulder are not uncommon and must be recognized for appropriate treatment. Incidence

Incidence data for glenohumeral instability in skeletally immature patients are difficult to extrapolate from the literature.* A review of 500 dislocated shoulders by Rowe[68] *See references

[ 5] [ 8] [ 9] [ 18] [ 28] [ 36] [ 37] [ 41] [ 42] [ 45] [ 47] [ 52] [ 54] [ 64] [ 65] [ 70]

and [ 73] .

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listed only 8 patients younger than 10 years, whereas 99 patients were between 10 and 20 years of age. Wagner and Lyne[76] presented a series of 9 children with open epiphyses of 212 patients with traumatic glenohumeral dislocations, representing a 4.7% incidence rate. Heck[33] and Foster and colleagues[22] reported cases of true glenohumeral dislocation due to trauma in children younger than 10 years. Endo and

coworkers[21] presented two cases of traumatic dislocation of the shoulder in children younger than 10 years. Many reports in the literature include patients between 11 and 20 years of age, but data for skeletal maturity are not included.* Most of these studies involve traumatic instability treated by surgical reconstruction and do not address instability treated by nonoperative means. Other studies describing multidirectional laxity with subluxation of the shoulder demonstrate this problem to be more common in younger age groups.[49] [59] [72] Certainly, true traumatic glenohumeral dislocation in children younger than 10 years is rare. True traumatic instability of the shoulder in skeletally immature adolescents is more common, probably approaching the incidence in adults.

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Classification

Glenohumeral joint instability can be classified by degree, direction, frequency, and etiology of the dislocation. All of these factors are important in formulating treatment options and in predicting prognosis. Degree of instability 1. Dislocation 2. Subluxation Dislocation represents complete disassociation between the humeral head and glenoid. This is more likely to be associated with traumatic events and usually requires a manipulative reduction. Subluxation represents varying degrees of instability without complete dislocation. This can be associated with both traumatic and atraumatic types of instabilities. Direction of instability 1. 2. 3. 4.

Anterior Posterior Inferior (luxatio erecta) Multidirectional

Anterior dislocation of the glenohumeral joint is thought to be the most common direction of instability, constituting more than 90% of traumatic cases. Cases of posterior dislocation in children and adolescents have been reported, but as in the adult, true traumatic posterior instability of the shoulder is rare. [22] Luxatio erecta due to extreme trauma has been described in children and has been reported in at least two cases.[23] This is not commonly associated with sports injuries. Multidirectional shoulder instability in association with generalized joint laxity is becoming more readily recognized and

appreciated.[49] This is undoubtedly a common form of instability in young athletes. Etiology of instability 1. Traumatic instability 2. Atraumatic instability a. Voluntary b. Involuntary For classification of a case as traumatic instability, a history of significant high-energy trauma and an appropriate mechanism of injury should exist. This scenario is common in sports activities resulting in classic traumatic instability. Atraumatic instability of the glenohumeral joint occurs only in the presence of multidirectional joint laxity. Many patients report some element of trauma as an inciting event of atraumatic instability, but in most cases, the insignificance of the trauma and the lack of an appropriate mechanism give the physician a clue to the diagnosis of atraumatic instability. Frequency of instability 1. Acute instability 2. Chronic instability 3. Recurrent instability An acute dislocation of the shoulder is associated with a single episode of instability. Chronic instability represents a case of locked dislocation that has been neglected in a dislocated position. Recurrent instability is a common consequence after treatment of acute instability and is associated with repetitive episodes of instability.

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Clinical Evaluation and Treatment Traumatic Anterior Instability

Anterior instability of the glenohumeral joint is the most common type associated with trauma. This type represents more than 90% of traumatic dislocations and is frequently seen in all collision and contact sports. In a true traumatic dislocation, there is a history of significant injury and an appropriate mechanism. Anterior dislocation is usually associated with a fall on the outstretched hand, which forces the shoulder into an abducted and externally rotated position. The humeral head is translated anteriorly, damaging the anterior glenohumeral ligaments and eventually dislocating. The posterior aspect of the humeral head is impacted against the anterior rim and neck of the glenoid. The resulting impaction fracture on the posterior-superior aspect of the humeral head is called a Hill-Sachs lesion. The capsular injury that results in stripping of labrum from the insertion on the rim of the glenoid is termed a Bankart's or Perthes' lesion ( Fig. 21J2-1 ).

Figure 21-J2-1 Diagram in the coronal plane of the relationship between the humeral head (HH) and the glenoid in anterior traumatic instability. Note the Perthes'/Bankart's lesion, which includes stripping of the anterior ligaments off the glenoid rim. Also note the Hill-Sachs compression fracture on the posterior aspect of the humeral head. A, anterior; P, posterior.

Patients with traumatic glenohumeral anterior dislocation present with obvious deformity, often with swelling and always with pain. The acromion is prominent with a void below it. The humeral head is located anteriorly, and it can sometimes be visualized or palpated in the axilla. The affected arm is usually supported by the opposite hand and held in a slightly abducted and externally rotated position ( Fig. 21J2-2 ). There is pain with any attempted motion and occasionally crepitus. Careful examination of the neurologic and vascular status is mandatory. The axillary nerve is

the most commonly injured neurologic structure, *See references

[ 1] [ 6] [ 9] [ 18] [ 36] [ 41] [ 42] [ 45] [ 47] [ 55] [ 65] [ 70]

and [ 80] .

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but there may be additional brachial plexus involvement. Axillary nerve injury has been reported in between 5% and 35% of first-time anterior shoulder dislocations. Careful examination of the axillary nerve can be accomplished easily. The sensory distribution of the axillary nerve is along the upper lateral arm and can be tested by light touch or pinprick. The motor innervation of the axillary nerve includes the deltoid and teres minor muscles. This motor innervation can be tested by support of the affected elbow with the examiner's hand while the deltoid is palpated with the opposite hand during voluntary contraction of the deltoid in an attempt to abduct the elbow. This can be accomplished without causing the patient undue pain and confirms function of the axillary nerve ( Fig. 21J2-3 ). The presence of both the radial and ulnar pulses is noted. Absence of the pulses in association with massive swelling or rapidly expanding hematoma suggests a vascular injury. Appropriate consultation with a vascular surgeon is therefore indicated.[7] [15]

Figure 21-J2-2 A patient with acute traumatic anterior dislocation of the shoulder. Note the prominent acromion with characteristic deformity of the shoulder.

Figure 21-J2-3 Clinical examination of the axillary nerve should be carried out in every patient with anterior dislocation. A, Sensory distribution noted in the upper lateral arm. B, Motor testing for deltoid function.

Routine radiography of the shoulder includes three views: the standard anteroposterior view, an axillary view, and a trans-scapular Y view. The humeral head can be seen situated anterior and inferior to the normal position in the glenoid ( Fig. 21J2-4 ). There is overlapping of the humeral head with the glenoid on the anteroposterior view. The lateral radiographs confirm the anterior position of the

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head. Postreduction films in both planes are important to confirm reduction. The postreduction films often reveal the common posterolateral humeral head impaction fracture (Hill-Sachs lesion). The glenoid rim is best evaluated for fracture or deficiency on an axillary lateral or modified axillary lateral view (West Point view).[67] Magnetic resonance imaging scans have improved our ability to assess soft tissue injury in the shoulder. Anterior capsular and labral injury can be successfully visualized in a high percentage of cases.[29] [62] [63]

Figure 21-J2-4 Anterior dislocation of the shoulder. A, Prereduction radiograph demonstrating an anteroinferior dislocation of the left shoulder. B, Postreduction radiograph demonstrating a prominent posterolateral compression fracture known as the Hill-Sachs lesion.

After completion of a thorough examination, initial treatment is accomplished by closed reduction. If the dislocation is treated promptly, reduction can be carried out without anesthesia. If significant pain and muscle spasm have ensued, appropriate intra-articular anesthesia, analgesia, or intravenous sedation is used.[57] [66] Several safe and effective methods for closed reduction of an anterior dislocation have been described, including the traction-countertraction technique, the Stimson's maneuver, and the abduction maneuver.[16] [56] [64] [66] The traction-countertraction technique ( Fig. 21J2-5 ) is accomplished with the patient in the supine position. Longitudinal traction is applied to the arm on a continuous basis while countertraction is applied to the thorax by means of a sheet passed around the patient through the axilla. The humeral head is disimpacted from the anterior glenoid rim by overcoming the muscle spasm with traction, leading to reduction.

Figure 21-J2-5 The traction-countertraction maneuver for reduction of anterior dislocation of the shoulder.

In the Stimson's maneuver ( Fig. 21J2-6 ), the patient is placed prone on an examination table. The dislocated arm is allowed to hang off the edge of the table while up to 10 to 15 pounds is suspended from the patient's wrist. Spontaneous reduction occurs as the shoulder musculature is relaxed by the gravity-assisted traction.

Figure 21-J2-6 Stimson's maneuver for reduction of anterior dislocation of the shoulder.

Closed reduction by the abduction maneuver is performed with the patient in the supine position. The arm is supported by the examiner with the elbow flexed. The shoulder is gently abducted and externally rotated into the overhead position, reproducing the mechanism of injury. As the arm is then adducted and gently internally rotated, reduction occurs. It is important to repeat examination of the neurologic and vascular status after reduction. Postreduction radiographs are also obtained to confirm the position of the humeral head and to rule out the possibility of associated fracture. After reduction, the arm is immobilized in a sling for protection. This is usually followed by a period of supervised rehabilitation. The length of immobilization and the type and length of rehabilitation are somewhat controversial. Recurrent dislocation is the single biggest problem in shoulder instability after an acute traumatic dislocation. At least two studies

have demonstrated lower recurrence rates in young, at-risk patients treated with 4 to 6 weeks

1038

of immobilization and a 3- to 6-month delay in return to athletic activities.[4] [12] [79] Other reports suggest that neither the length of immobilization nor the type or duration of rehabilitation alters the natural history of recurrence.[34] [37] [69] [73] [74] Aggressive rehabilitation focuses on strengthening the rotator cuff, deltoid, and periscapular muscles. Plyometric exercises are added in the later rehabilitation phase in an attempt to improve proprioceptive function for return to sports-specific activities.[46] Investigation of acute surgical stabilization in the treatment of initial traumatic anterior dislocation in the young, at-risk athlete has been reported. Arthroscopic findings have documented the presence of a Bankart's lesion and hemarthrosis in a large number of cases after initial traumatic dislocation, providing a milieu favorable to arthroscopic fixation. Studies from the U.S. Military Academy using either an arthroscopic transglenoid suture technique or an arthroscopic bioabsorbable fixation device have resulted in an 88% success rate.[2] [3] This is appealing because the recurrence rate in patients younger than 20 years after anterior dislocation has been cited as low as 48% and as high as 100%. Further study is necessary, including comparison of results by open surgical techniques with the baseline arthroscopic data. Traumatic Posterior Instability

Posterior dislocation of the shoulder is uncommon. When all age groups are included, posterior dislocation represents approximately 4% of traumatic dislocations of the shoulder. Many large series of posterior dislocations include adolescent patients, but no data are available as to whether these patients have completed skeletal maturity. [10] [11] [19] [31] [35] [53] Foster, Ford, and Drez[22] have described a case of an isolated traumatic posterior shoulder dislocation in a 10-year-old child. Most cases of posterior instability in young patients are associated with multidirectional atraumatic instability. Both direct and indirect mechanisms can result in posterior dislocation. A force directed on an outstretched arm with the shoulder adducted, internally rotated, and flexed can commonly drive the shoulder out posteriorly ( Fig. 21J2-7 ). A direct blow to the anterior aspect of the shoulder can also result in posterior shoulder dislocation. Either of these mechanisms can occur in the course of contact sports. In addition, posterior dislocation can occur indirectly as a result of a seizure or electrical shock. During seizure activity, violent contraction of the strong shoulder internal rotators levers the humeral head out posteriorly. Any complaint of shoulder pain in an athlete who has suffered a convulsion should be taken seriously and a posterior dislocation suspected.

Figure 21-J2-7 Posterior dislocation of the shoulder can occur in contact sports both by a direct blow to

the front of the shoulder or indirectly owing to a fall on an outstretched arm with the shoulder adducted, internally rotated, and flexed.

Posterior dislocation is less apparent on clinical examination compared with the more common anterior dislocation and can easily be overlooked. The arm is usually held across the abdomen with the shoulder internally rotated and adducted. The shoulder is painful, and the patient avoids motion. Only on close inspection is deformity noted. There is flattening of the anterior aspect of the shoulder with prominence of the coracoid. A fullness posteriorly created by the dislocated humeral head can sometimes be appreciated ( Fig. 21J2-8 ). These features are best appreciated when they are visualized by the examiner from above. The hallmark of the diagnosis is a lack of shoulder external rotation and inability to supinate at the forearm. These examination findings are subtle and sometimes difficult to elicit in the acute situation because of swelling and pain. The lack of clinical findings can lead the examiner to a delay in diagnosis.

Figure 21-J2-8 A patient with a locked posterior dislocation of the shoulder.

The radiographic evaluation of posterior instability of the shoulder includes a three-view seriesthe anteroposterior view, the axillary lateral view, and the trans-scapular Y view. Findings on the anteroposterior view are subtle with overlapping of the humeral head on the glenoid. The diagnosis is confirmed with a lateral radiograph, either axillary or trans-scapular Y view, demonstrating the posterior dislocation of the humeral head. On the axillary view, the empty glenoid is apparent with the humeral head lodged on the posterior aspect of the glenoid ( Fig. 21J2-9 ). Postreduction films are important in both the anteroposterior and lateral planes to confirm the position of reduction. Common radiographic findings include a reversed Hill-Sachs impaction fracture on the anterior surface of the humeral head and fractures of the posterior glenoid rim. [10] [53] [66]

Figure 21-J2-9 Magnetic resonance imaging scan depicting a posterior Bankart's lesion in recurrent posterior instability of the shoulder in a college football player.

Initial treatment of posterior dislocation of the shoulder

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includes adequate diagnosis followed by closed reduction. Appropriate analgesia and intravenous sedation are used. With the patient in the supine position, reduction is carried out by applying traction in line with the deformity. The arm is usually in an adducted position. Countertraction is applied to the chest while lateral pressure is placed on the upper arm, lifting the humeral head back into the glenoid fossa. The arm is usually stable at the side and can be immobilized in a sling. If instability is present after reduction, an external rotation splint or spica cast can be applied. Six weeks of

immobilization is usually recommended for soft tissue healing followed by an aggressive rehabilitation program. The incidence of recurrent dislocation after posterior instability is lower than that documented for anterior instability. Surgery is occasionally indicated after an acute traumatic posterior dislocation when it is associated with fracture of the lesser tuberosity or with a major fracture of the posterior glenoid rim resulting in instability. Open reduction and internal fixation of the fracture are usually sufficient to provide stability. Recurrent Traumatic Instability

The age at the time of a first dislocation and the activity level of the patient are the most important factors in assessing the risk of whether an acute dislocation will go on to recurrent instability. The literature is filled with studies confirming that the risk for recurrence is inversely proportional to the patient's age.* For patients younger than 25 years who want to continue to be athletically active, the risk for recurrent dislocation ranges between 50% and 100%. Rowe, [68] in 1963, reported a 100% incidence of recurrence in children younger than 10 years. He reported a 94% incidence of recurrence in adolescent and young adult patients 11 to 20 years old. He did not distinguish in these patients whether they had open growth plates. Rockwood[16] reported in 1975 a recurrence rate of 50% in a series of adolescent patients between 13.8 and 15.8 years of age. This was a mixed group of patients with traumatic and atraumatic instability. Wagner and Lyne[76] reported an 80% recurrence rate in 10 patients with clearly open proximal humeral epiphyses. Marans and associates[50] reported on the natural history of dislocation in 21 children between the ages of 4 and 15 years with open physes at the time of initial dislocation. They found a 100% recurrence rate no matter what postreduction treatment program was used. By contrast, Heck[33] reported a case of traumatic anterior dislocation in a 7-year-old boy who remained stable at 5-year follow-up. Endo and coworkers[21] reported two cases of traumatic anterior dislocation in children, both of whom remained stable with nonoperative treatment at more than 1-year of follow-up. Evaluation of the patient with recurrent instability complaints begins with a careful history and physical examination. Careful consideration of the initial trauma should be given to rule out the possibility of atraumatic instability. Patients may present with pain rather than complaints of recurring instability after an initial dislocation. This may represent recurrent traumatic subluxation, which can be confirmed by examination. Clinical examination usually reveals a full range of motion. Guarding in the abducted, externally rotated position is common. Provocative tests include the anterior apprehension test and the relocation test. The anterior apprehension test ( Fig. 21J2-10 ) is performed with the patient upright or seated with the examiner positioned at the side. *See references

[ 3] [ 4] [ 12] [ 16] [ 34] [ 36] [ 37] [ 54] [ 68] [ 69] [ 73]

and [ 79] .

1040

The examiner stabilizes the scapula with one palm, placing the thumb on the posterior aspect of the shoulder joint while the opposite hand is used to bring the patient's arm into abduction and external rotation. The result is positive when the test elicits a feeling of apprehension with or without pain in this position.[24] [32]

Figure 21-J2-10 The anterior apprehension test.

The relocation test ( Fig. 21J2-11 ) is performed with the patient supine. The examiner performs the apprehension test in this position, then repeats the test with one hand on the anterior shoulder, applying a posteriorly directed force with resultant decrease in apprehension.

Figure 21-J2-11 A and B, The relocation test.

Radiographic work-up consists of the anteroposterior view, axillary lateral view, and trans-scapular Y view. Special views, such as the West Point axillary lateral view for imaging the anterior glenoid and the Stryker notch view for evaluating the posterior humeral head, may also be indicated. Common findings include the Hill-Sachs compression fracture on the posterolateral aspect of the humeral head and anterior glenoid rim lesions associated with a bony Bankart's defect. A magnetic resonance imaging scan can be useful in assessing capsulolabral insufficiency as well as other soft tissue damage about the shoulder ( Fig. 21J2-12 ).[29] [62] [63]

Figure 21-J2-12 Magnetic resonance imaging scan of the shoulder demonstrating an anterior Bankart's lesion in recurrent anterior instability.

Recurrent traumatic dislocation of the shoulder, when it is confirmed by appropriate history, physical examination, and radiographic studies, should be treated surgically. Many types of procedures have been used effectively in the treatment of recurrent dislocation. The most common types of open anterior reconstruction of the shoulder are

1041

bone block-type procedures (Bristow), subscapularis-shortening procedures (Putti-Platt, Magnuson-Stack), and capsular procedures (Bankart, du Toit).* All of these procedures are reported to have good success with regard to eliminating instability, but the bone block and subscapularis-shortening procedures are associated with higher risk for both short-term and long-term complications, including implant loosening, decreased motion, and arthritis. For patients with open epiphyses, it would seem prudent to consider capsular procedures about the shoulder for reconstruction to decrease risks to the

physis and long-term complications. In the report by Wagner and Lyne,[76] 10 shoulders were treated by surgical reconstruction with use of the Magnuson-Stack procedure in 8 and the Bristow procedure in 2. No long-term follow-up was included for their series. Marans and associates[50] described 13 of 21 recurrent dislocations of the shoulder treated surgically with soft tissue procedures. No long-term follow-up was given in this series as well. Most authors today use the Bankart repair or some variation of the capsular shift procedure with good results.[9] [41] [66] [70] Today, arthroscopic Bankart and capsular repairs are becoming more popular but have yet to be proven to match the results of open reconstruction for recurrent shoulder instability. [2] [3] [25] [26] [27] [28] [52] [58] [77] [78] [80] Atraumatic Instability

Atraumatic instability of the glenohumeral joint in children and adolescents probably represents the most common type. Many patients present with complaints of pain and not instability; therefore, atraumatic instability is often not recognized on initial presentation. An underlying multidirectional laxity of the shoulder is a prerequisite for pathologic atraumatic instability. Multidirectional laxity may be associated with a true syndrome of collagen deficiency, such as Marfan's or Ehlers-Danlos syndrome. For most of these patients, however, the excessive joint laxity of the shoulder is just an extreme variant of normal. Emery and Mullaji[20] have reported signs of instability in 57% of shoulders in boys and 48% in girls in a study of normal school-children. Atraumatic instability can be categorized as voluntary or involuntary. All of these patients have multidirectional shoulder laxity with increased translation in at least three directions: anterior, posterior, and inferior. A shoulder dislocation in a child or adolescent without a clear-cut, significant history of trauma suggests that this may be an instance of atraumatic instability. These patients have inherent joint laxity, and the glenohumeral joint can be dislocated voluntarily or involuntarily as a result of minimal trauma. Episodes of instability may occur with activities such as throwing, hitting an overhead serve in tennis and volleyball, and swimming. These episodes do not constitute significant trauma, and a high index of suspicion should be maintained in these cases for atraumatic instability. Voluntary instability can be accomplished in patients with multidirectional laxity by conscious firing of certain muscle groups while their antagonists are inhibited and combining these muscle manipulations with certain arm positions that lead to subluxation of the glenohumeral joint ( Fig. 21J2-13 ). A most notable finding in cases of voluntary instability is the lack of pain associated with the subluxation or dislocation. Pathologic voluntary instability can be associated with psychological or emotional instability. Huber and Gerber[40] have described 25 children who presented with voluntary subluxation of the shoulder at an average 12-year follow-up; 18 children were managed by skillful neglect, whereas 7 children had undergone stabilizing operations. At long-term follow-up, the nonoperative *See references

[ 1] [ 6] [ 8] [ 9] [ 18] [ 38] [ 39] [ 41] [ 42] [ 45] [ 47] [ 55] [ 65]

and [ 70] .

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treatment group had 16 of 18 who were considered to have successful outcomes; in the surgical group, only 3 had good results. Their conclusion was that voluntary subluxation of the shoulder in children has a favorable prognosis, and there is no indication for surgical intervention during childhood.

Figure 21-J2-13 A and B, A 10-year-old boy with voluntary instability of the shoulder.

In the subset of patients who have involuntary atraumatic instability of the shoulder, only half of these patients present with complaints of instability. Most present with complaints of pain, and many do not recognize the inherent instability in the glenohumeral joint. The instability is commonly exacerbated by high-demand overhead sports, such as throwing, serving, and swimming. These patients commonly present with inflammatory complaints due to secondary impingement phenomena associated with the instability. Subluxation is more characteristic than dislocation in these patients, and rarely do they require reduction. On the examination, signs of multidirectional laxity of the glenohumeral joint are present. The sulcus sign ( Fig. 21J2-14 ), a dimpling of the skin below the acromion when manual longitudinal traction is applied to the arm, is present. It is due to inferior subluxation of the humeral head within the glenohumeral joint. Significant humeral head translation is often present on the anterior and posterior drawer test as described by Gerber and Ganz.[24] The drawer test ( Fig. 21J2-15 ) is performed with the examiner seated at the side of the patient. The scapula is stabilized with one hand while the opposite hand manually translates the humeral head anteriorly and posteriorly. During the acutely painful phase, the affected shoulder may not demonstrate these signs because of guarding. If multidirectional laxity is suspected, the opposite noninvolved shoulder should be examined to confirm the diagnosis. Many of these patients demonstrate evidence of joint hyperlaxity in multiple other joints ( Fig. 21J2-16 ). Examples include hyperextension at the elbows, knees, and metacarpophalangeal joints. Skin hyperelasticity and striae may also be present and may be suggestions of underlying collagen abnormality.*

Figure 21-J2-14 The sulcus sign.

Figure 21-J2-15 A and B, The anterior-posterior drawer test.

Figure 21-J2-16 Note the hyperextension at the elbow (A) and the knees (B) often associated with multiple joint laxity.

The findings on radiographic examination of patients with atraumatic instability are usually normal. Stress radiographs can be used to supplement the clinical examination to demonstrate instability in the anterior, posterior, and inferior directions. The inferior component is easily demonstrated by applying weights to the arm during an anteroposterior radiographic film. Traumatic lesions, such as the Hill-Sachs lesion of the humeral head and anterior glenoid fracture, are not characteristic of atraumatic instability. Treatment of patients with atraumatic instability begins with a careful diagnosis, thorough history, and physical examination. A nonoperative approach is indicated as initial treatment in every case of atraumatic instability. This nonoperative treatment emphasizes a vigorous rehabilita tion program involving strengthening of the dynamic stabilizers, improvement of proprioception, and avoidance of provocative activities. Most patients who do not have significant *See references

[ 13] [ 32] [ 43] [ 48] [ 49] [ 53] [ 57] [ 59] [ 60] [ 71]

and [ 75] .

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emotional or psychiatric problems improve their symptomatic shoulder instability with this program. Burkhead and Rockwood[12] have reported an 80% success rate in the treatment of atraumatic instability with a vigorous rehabilitation program alone ( Fig. 21J2-17 ). Neer and Foster,[59] [60] in the classic description of multidirectional laxity, restricted surgical intervention to patients whose 12-month rehabilitation program failed.

Figure 21-J2-17 Rehabilitation of the rotator cuff is important to provide dynamic stability of the shoulder.

For patients with multidirectional atraumatic instability who fail to improve after a thorough rehabilitation program, the inferior capsular shift procedure has been popularized.[49] [57] [59] [60] This procedure addresses the capsular redundancy directly by diminishing the overall capsular volume. Mizuno and associates[57] have reported two cases of surgical treatment in young children with disabling multidirectional instability who were treated successfully with the inferior capsular shift. Many adolescent patients have been included in other large studies on surgical treatment of this difficult problem and appear to have successful results proportional to those reported for adults.*

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Author's Preferred Method of Treatment

Careful history of the mechanism of injury, thorough physical examination to elicit signs of multidirectional laxity, and appropriate radiographs help the treating physician to elucidate the direction, degree, and frequency of instability as well as to determine whether the instability is traumatic or atraumatic in nature. Once the etiology of the instability has been determined, a rational treatment program can be outlined. For acute traumatic dislocations, whether anteriorly or posteriorly in direction, closed reduction is the initial treatment. Physical examination of the neurologic status, specifically of the axillary nerve and *See references

[ 43] [ 44] [ 48] [ 49] [ 57] [ 59] [ 60] [ 71] [ 72]

and [ 75] .

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brachial plexus, is performed before and after reduction. Radiographic evaluation with a trauma series is performed to confirm the diagnosis and to rule out associated fracture. For stable dislocations, a sling is adequate for postreduction immobilization. Despite the high incidence of recurrence in young patients, nonoperative treatment is still used. Immobilization is continued for 3 to 4 weeks. This is followed by a vigorous rehabilitation program and avoidance of provocative sports activities for at least 3 months. For adolescent athletes in high-risk collision sports who have documented traumatic lesions, primary surgery is occasionally recommended. In the skeletally immature patient who has recurrent shoulder instability, surgical reconstruction is indicated. I prefer the capsular imbrication procedure described by Rockwood performed either anteriorly or posteriorly along with direct repair of the Bankart's lesion if it is present[66] ( Fig. 21J2-18 ). A sling is used postoperatively for 3 to 4 weeks, followed by a vigorous 6- to 9-month rehabilitation program before return to

competitive sports.

Figure 21-J2-18 The capsular shift reconstruction as described by Rockwood. A, The Bankart's lesion is repaired directly with suture anchors or through drill holes. B, The medial capsular flap is passed beneath the lateral capsular flap, and the rotator interval is closed. C, The lateral flap is then closed over the medial flap. D, The end result with repair of Bankart's lesion and shrinkage of overall capsular volume.

In the case of atraumatic instability, physical examination should confirm multidirectional shoulder laxity. Initial treatment includes nonsteroidal anti-inflammatory medications and avoidance of the provocative activity, followed by a diligent rehabilitation program. Improving dynamic stability through a strict rehabilitation program is undertaken for 9 to 12 months before any more aggressive intervention is considered. In the patient with multidirectional instability who has failed to improve with the rehabilitation program, an inferior capsular shift reconstruction is performed to accomplish global tightening of the redundant capsule. Care must always be taken to exclude the voluntary dislocator, who will have a greater risk for poor outcome after surgical treatment.

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Mallon WJ, Speer KP: Multidirectional instability: Current concepts. J Shoulder Elbow Surg 4:54-64, 1995. 49.

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Matthews LS, Vetter WL, Oweida SJ, et al: Arthroscopic staple capsulorrhaphy for recurrent anterior shoulder instability. Arthroscopy 4:106-111, 1988. 52.

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Mizuno K, Itakura Y, Muratsu H: Inferior capsular shift for inferior and multidirectional instability of the shoulder in young children: Report of two cases. J Shoulder Elbow Surg 1:200-206, 1992. 57.

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Palmer WE, Caslowitz PL: Anterior shoulder instability: Diagnostic criteria determined from prospective analysis of 121 MR arthrograms. Radiology 197:819-825, 1995. 62.

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Rockwood CA Jr, Thomas SC, Matsen FA III: Subluxations and dislocations about the glenohumeral joint. In Rockwood CA Jr, Green DP, Bucholz RW (eds): Rockwood and Green's Fractures in Adults, 3rd ed. Philadelphia, JB Lippincott, 1991, pp 1021-1179. 66.

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Section K Superior Labral Injuries Mark W. Maffet MD Walter R. Lowe MD The recognition of the importance of the superior labrum and biceps tendon complex in normal shoulder function as well as in shoulder pathophysiology is shown in the creation of a new section in this chapter. This section summarizes biomechanics, diagnosis, and treatment of injuries to the superior labrum. The importance of the superior labrum and the biceps tendon in shoulder pathology was emphasized in the 1990s. Modern thought regarding impingement syndrome and rotator cuff pathophysiology dates back to Neer's writings in 1972. [40] The literature has evolved subsequently to include secondary impingement[61] and internal impingement associated with overhead throwing athletes.[28] [63] Literature regarding shoulder instability treatment dates back to the hot poker days centuries ago. Although more modern treatment has evolved in the form of anatomic reconstructions and recognition of subtle instabilities associated with athletes, the acceptance of shoulder looseness as a source of morbidity is long-standing. The superior labrum and biceps tendon complex as a possible source of shoulder pain and dysfunction first was recognized by Andrews and colleagues in 1985.[1] In an electromyography study, these investigators successfully showed that biceps contraction could lift the biceps tendon off its glenoid insertion. Andrews and colleagues[1] postulated that tensile overload during eccentric biceps contraction in the follow-through phase of throwing in athletes could lead to injuries to this area. In 1990, Snyder and coworkers[56] coined the term SLAP lesion, an acronym for superior labrum, anterior to posterior, for these injuries to the superior labrum and biceps tendon complex. This term seems to have stuck in the orthopaedic dialogue similar to the Bankart lesion. Confusion exists regarding what exactly constitutes a SLAP lesion. The

incidence of SLAP lesions found during shoulder arthroscopy varies in the literature from 4%[10] to 11%. [58] Snyder and colleagues[57] and Maffet and coworkers[36] found a 6% occurrence in their studies. The widespread use of shoulder arthroscopy in the 1990s expanded knowledge of superior labrum injuries as well as increasing questions surrounding the superior labrum. This section updates current thought in relation to underlying superior labrum and proximal biceps insertional anatomy, describes injury patterns and their relationship to suspected mechanisms of injury, describes new diagnostic methods, and discusses the treatment of these lesions. Anatomy

Understanding of the anatomic relationships of the rotator cuff and glenohumeral ligaments of the shoulder is based on decades of research and study. Only in the 1980s and 1990s, however, has work attempting to understand the anatomy of the superior labrum been published.[11] [36] [38] [62] Many surgeons may not have a thorough understanding of the anatomy of the superior labrum and biceps tendon complex and its normal variants. The importance of this understanding cannot be overemphasized; otherwise the surgeon at arthroscopy will not know what needs repair and what should be left alone. The glenoid labrum peripherally surrounds the glenoid and deepens the socket. Perry[47] showed that humeral head contact area increased 75% vertically and 67% horizontally when the labrum was intact. The glenoid often is thought of as being flat because of its radiographic appearance. Differences in the glenoid articular cartilage depth (thicker peripherally narrowing to a central clear area) along with the presence of the glenoid labrum cause the glenoid to be more cup-shaped, however. This deepening effect appears to help stabilize the glenohumeral joint. When the labrum is intact, some authors[24] have suggested a bumper effect stabilizing the humeral head within the glenoid. This effect appears to be more important in the superoinferior direction than in the anteroposterior direction.[35] Others[18] [66] have studied the suction effect of an intact labrum and capsule and its shoulder-stabilizing properties. In addition to these biomechanical effects, the labrum is the point of attachment of the supporting shoulder ligaments. Specifically the superior labrum is the seat of attachment of the superior glenohumeral ligament, the middle glenohumeral ligament, and the posterosuperior capsule.[11] [13] It is readily apparent based on these biomechanical and anatomic facts that the glenoid labrum serves an important function in the shoulder. The normal appearance of the labrum can vary significantly depending on the position around the glenoid. The inferior labrum anatomically appears to be an elevated extension of the articular cartilage blending into the capsule (Fig. 21K-1 (Figure Not Available) ), whereas the superior labrum above the midglenoid notch typically carries a more meniscoid appearance. This normal appearance can vary significantly. Some shoulders show a minimal labral fold all the way around the glenoid; other shoulders have an abundant meniscal appearance circumferentially ( Fig. 21K-2 ). The histologic appearance of the glenoid labrum, once thought to be cartilaginous,[39] appears to be

more fibrous in nature, consistent with its appearance as an extension of the glenohumeral ligaments (see Fig. 21K-1 (Figure Not Available) ).[25] There is a fibrocartilaginous transition zone from the articular cartilage to the fibrous labral tissue. Figure 21-K-1 (Figure Not Available) Histologic stain of a normal inferior labral attachment to the glenoid. Note the firm attachment to the glenoid rim. I, inferior glenohumeral ligament complex; L, labrum. (From Cooper DE, Arnoczky SP, O'Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum: An anatomical study. J Bone Joint Surg Am 74:46-52, 1992.)

Figure 21-K-2 Arthroscopic pictures of the superior labrum. A, A nonmeniscoid type of superior labrum; B, a more meniscoid appearance.

The labrum above the midglenoid notch can have a significant amount of variability. The anterosuperior labrum can be attached firmly to the glenoid rim or can be detached with a sublabral foramen present. This normal variant can be seen in 12% of shoulders [67] and should not be confused with a pathologic labral detachment (Fig. 21K-3 (Figure Not Available) ). A sublabral

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hole communicates anteriorly with the subscapularis recess, both of which can vary in size. The middle glenohumeral ligament (MGHL) attaches onto the anterosuperior portion of glenoid labrum forming a continuous structure. Commonly in shoulders with a prominent sublabral foramen, the MGHL has a cordlike appearance that merges with the anterosuperior labrum to insert at the anterior base of the biceps tendon ( Fig. 21K-4 ). A small percentage of these cordlike variants can have a prominent recess below the MGHL that has the overt appearance of a capsular rent. Williams and associates[67] called this normal variant a Buford complex. The clinician must be aware of the appearance of this variation to avoid unnecessary repairs. Figure 21-K-3 (Figure Not Available) Anterosuperior sublabral hole. Cadaveric specimen demonstrating a normal sublabral hole under the anterosuperior labrum. (From Cooper DE, Arnoczky SP, O'Brien SJ, et al: Anatomy, histology and vascularity of the glenoid labrum: An anatomical study. J Bone Joint Surg Am 74:46-52, 1992.)

Figure 21-K-4 Arthroscopic photograph of a cordlike middle glenohumeral ligament (arrowheads) as visualized from the posterior portal. This normal variant should not be confused with a capsular tear.

Superiorly the biceps tendon has a close relationship with the glenoid labrum. The biceps tendon inserts onto the supraglenoid tubercle after its entry into the joint through the rotator interval. This tendon insertion begins approximately 5 mm medially from the superior edge of the glenoid. The articular cartilage often extends superiorly over the top of the glenoid 5 mm to the biceps. The fibers of the biceps tendon blend into the fibers

of the labrum and capsule surrounding this insertion.[11] Normal variations can exist as well in the biceps insertion into the labrum. In the sagittal plane, as one faces the glenoid, four types of attachments are seen (Fig. 21K-5 (Figure Not Available) ). [62] The tendon's labral attachment can be (1) entirely to the posterior labrum, (2) entirely to the anterior labrum, (3) equally to both, or (4) mostly posterior with a small anterior contribution. Differences in the biceps insertion have implications in the type of superior pathology that develops during an injury. These differences determine the approach and type of repair that is performed. Figure 21-K-5 (Figure Not Available) Subtypes of superior labral attachment. Type I superior labral attachment is entirely posterior (A). In type II, it is mostly posterior (B). Type III is equally distributed anteriorly and posteriorly (C). In type IV, most of the attachment is to the anterior labrum (D). (From Vangsness CT, Jorgenson SS, Watson T, Johnson DL: The origin of the long head of the biceps from the scapula and glenoid labrum. J Bone Joint Surg Br 76:951-954, 1994.)

Cooper and colleagues[11] carefully evaluated the cross-sectional anatomy of the biceps tendon and superior labral complex. Evaluating normal biceps insertional anatomy in the frontal plane shows an intimate relationship between the proximal biceps insertion and the superior glenoid labrum. Some authors have described the labrum as inserting onto the tendon,[11] whereas other authors describe the tendon as inserting onto the labrum.[25] The point is

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probably moot because the superior labrum itself appears typically to have only a loose connection to the glenoid periphery (Fig. 21K-6 (Figure Not Available) ). The supraglenoid tubercle onto which the biceps tendon attaches is about 5 mm medial to the glenoid rim. Because the superior labrum does not always attach firmly to the superior glenoid over this distance, a small synovial recess often exists beneath a meniscoid-appearing superior labrum. This particular cross-sectional anatomy is important to understand because it may explain why certain patterns of superior labral tears are seen. Figure 21-K-6 (Figure Not Available) Histologic picture of a cross section of the superior labrum (L), the glenoid, and the biceps tendon (B). This photomicrograph demonstrates primary attachment of the superior labrum to the biceps tendon before it inserts onto the supraglenoid tubercle. Note the lack of firm attachment of the superior labrum to the glenoid itself. (From Cooper DE, Arnoczky SP, O'Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum: An anatomical study. J Bone Joint Surg Am 74:46-52, 1992.)

We have found a new superior labrum and biceps tendon complex variation ( Fig. 21K-7 ). Two patients have been found to have this atrophic biceps tendon entering the joint normally through the rotator interval but blending into the supraspinatus portion of the rotator cuff instead of inserting onto the superior glenoid. There were no signs of traumatic injury to the biceps or superior labrum. Both patients had bicipital tendon signs on preoperative examination.

Figure 21-K-7 New superior labral variant (A and B). This pattern, seen recently in two patients, shows an atrophic biceps tendon (arrowheads) that enters the joint normally through the rotator interval. Instead of attaching to the superior glenoid (arrows), however, it blends into the articular surface of the rotator cuff. No signs of trauma or previous labral attachment of the biceps are seen on inspection of the superior glenoid.

The vascularity of the glenoid labrum originates from the suprascapular artery, the posterior circumflex artery, and the circumflex scapular branch of the subscapular artery.[11] Apparently there is no vascular contribution to the labrum from the underlying bone. The penetration of vascular branches from the periphery into the substance of the labrum varies. Similar to the knee meniscus, most of the labral vascularity in the meniscoid variety is limited to its periphery. The superior and anterosuperior labrum is less vascular than the inferior and posterior portions. This diminished vascularity may contribute to delayed or incomplete healing after injury and higher rates of failure after repair. The vascularity of the glenoid labrum often appears to decrease with increased age of the individual.

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Pathoanatomy

Snyder and colleagues in 1990[56] originally tried to classify the pathoanatomy they found in the superior labrum. Snyder and colleagues[56] described four main patterns of injury ( Fig. 21K-8 ). Type I lesions involved fraying of the superior labrum but no detachment of the biceps tendon insertion. Type II lesions were characterized by detachment of the biceps tendon from the supraglenoid tubercle. In type III lesions, a bucket-handle tear of a meniscoid-type superior labrum occurred. Type IV lesions involved a superior labrum detachment that extends into the substance of the biceps tendon.

Figure 21-K-8 The original Snyder classification of SLAP lesions. Type I has degenerative superior labrum tearing but attached biceps (A). Type II has detachment of the superior labrum/biceps tendon complex from the superior glenoid (B). Type II has a bucket handle tear of a meniscoid superior labrum but attached biceps (C). Type IV has tearing of the superior labrum up into the biceps tendon (D). Variable amounts of the biceps are left attached. (From Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990.)

Others[36] later found pathologic patterns that did not fit within Snyder's classification: (1) a biceps insertion detachment extending anterior to include a Bankart lesion in a continuous labral detachment, (2) a cordlike MGHL with detachment of the biceps, and (3) a flap tear of the superior labrum with biceps separation ( Fig. 21K-9 ). It is possible the flap-type tear described previously simply is a further injury to a type III lesion with separation of one limb of the bucket handle. It is also easy to confuse a cordlike MGHL and the Buford complex with a truly pathologic lesion.

Figure 21-K-9 Additional patterns of superior labrum/biceps tendon complex injury. An anterior Bankart's lesion continues superiorly to include separation of the biceps tendon ( A). An unstable flap tear of the

labrum is present in addition to biceps tendon separation (B). The superior labrum/biceps tendon avulsion extends anteriorly beneath the middle glenohumeral ligament (C). (From Maffet MW, Gartsman GM, Moseley JB: Superior labrum/biceps tendon complex lesions of the shoulder. Am J Sports Med 23:93-98, 1995.)

Orthopaedists appear confused regarding Snyder's original classification. Of Snyder's four types, only the type II

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lesion involved an actual detachment of the biceps insertion. The biceps attachment remains intact in types I, III, and IV lesions. Other authors have used the term SLAP lesion only when the biceps detachment is found. The basic classification of SLAP lesion should not be made complicated. There should be two categories of superior labral lesion: (1) lesions with the biceps detached and (2) lesions with the biceps attachment intact. These two categories have significant bearing on the mechanism of injury that causes the lesion, associated pathology found, and the surgeon's treatment plan. Morgan and coworkers[38] divided type II lesions (biceps detached) based on whether the detachment is (1) primarily posterior, (2) primarily anterior, or (3) primarily anterior and posterior. These subtypes probably are important to know because they may be related to certain injury mechanisms, affect the type of repair attempted, and affect postoperative care. When evaluating a suspected type II SLAP lesion, one thing not always clear is how much biceps tendon must be detached to consider the lesion to be pathologic. Complete detachments are not a problem diagnostically ( Fig. 21K-10 ). One often sees a tendon, however, that appears partially separated. The surgeon has to incorporate the superior labrum and biceps tendon complex appearance with other arthroscopic clues (see later) and with the patient's history and physical complaints in deciding if the anatomy seen is pathologic and in need of repair. The biceps tendon typically begins attachment to the supraglenoid tubercle 5 mm from the edge of the glenoid.[11] Using the 3-mm probe as a guide, one must determine whether the biceps is attached or not. One thing is clear: The surgeon must be familiar with normal superior labral anatomy and its many variants before diagnosing and classifying a SLAP lesion.

Figure 21-K-10 Photograph of a type II SLAP lesion (A and B). Note the area of denuded articular cartilage on the superior glenoid rim (arrow), which is often seen in unstable SLAP lesions.

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Biomechanics

The structural importance of the biceps tendon and superior labrum complex to the glenohumeral joint became increasingly clear in the 1990s. Good biomechanical studies showed that this complex is important in normal shoulder function and that disruption of it has detrimental effects.

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The biceps tendon function as a humeral head depressor has been established previously.[23] [33] That function and its relationship to rotator cuff pathology have been well studied. Warner and McMahon[65] showed the importance of the biceps tendon in superior stability of the glenohumeral joint as the arm is abducted in the scapular plane. Increased superior translation was noted varying 2 to 6 mm when the biceps tendon was ruptured in vivo compared with the contralateral control shoulder. More recently, the importance of the biceps tendon in supporting the anterior shoulder has been studied.[43] [51] Pagnani and associates[43] looked at translations of the glenohumeral

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joint with and without detachment of the superior labrum and biceps tendon complex. Significant increases of superoinferior and anteroposterior translations were found in

shoulders with created SLAP lesions when the arm was in the abducted position. Pagnani and associates[43] created SLAP lesions not involving detachment of the biceps insertion as well and found no increase in translation. Rodosky and coworkers,[51] using a dynamic cadaver shoulder model, showed that the biceps contributed to torsional rigidity of the shoulder in abduction and external rotation. With the shoulder in this position, the biceps seemed to support the function of the inferior glenohumeral ligament (IGHL). Next, the authors created SLAP lesions with biceps tendon detachment and found decreased torsional rigidity of the joint and increased strain on the IGHL. The results of this work are complemented by electromyography studies performed at the Kerlan-Jobe Clinic.[19] [20] During the overhead throwing motion, high electromyography activity was found in the biceps during the late cocking phase when the shoulder was at an extreme of abduction and external rotation ( Fig. 21K-11 ).[19] In a comparative study done on pitchers with known instability of the shoulder, there was higher biceps electromyography activity in these subjects compared with normal controls (Fig. 21K-12 (Figure Not Available) ). All of these data point to the biceps tendon normally functioning to resist anterior translation and supporting the IGHL when the shoulder is in abduction and external rotation.

Figure 21-K-11 Baseball pitcher in the cocking phase of the throw. Note the pitching arm in 90 degrees of abduction and external rotation with posterior rotation on the biceps in this position. Figure 21-K-12 (Figure Not Available) A chart of electromyographic activity of the biceps as a percentage of maximal manual muscle test for each phase of the overhand throw. Comparison is made between biceps activity in normal shoulders and in those with instability. Note increased biceps activity in the unstable shoulder. (From Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988.)

Fleisig and colleagues[16] found increased biceps firing on electromyography testing in pitchers during arm acceleration and deceleration. These investigators postulated that a loose shoulder may cause a need for increased compressive forces from the biceps resulting in increased demand from, and stress to, the superior labrum and biceps tendon complex. It is postulated that the shoulder-stabilizing effects of the biceps occur through (1) compression of the joint, (2) tension on periligamentous fibers, (3) anterior and superior barrier function of the tendon, (4) placement of the joint into a position that secondarily tightens the ligamentous structures.[27] [44] It is likely a combination of these effects comes into play.

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Mechanism of Injury

What causes damage to the superior labrum and biceps tendon complex? Opinion varies greatly, and several types of injury have been implicated ( Table 21K-1 ). Different mechanisms may cause different types of superior labral pathology. TABLE 21-K-1 -- Mechanisms of Injury Fall on the outstretched arm Overhead throw Traction injury Underlying shoulder instability Torsional peel-back

In their original study, Snyder and colleagues[56] found that many of their patients described a fall on the outstretched arm as the inciting trauma to the shoulder. Snyder and colleagues[56] extrapolated a superior translation and compression of the humeral head damaging the superior labrum. In a case report, Lee and Harryman [34] noted the occurrence of superior labral damage in a paralytic patient. The mechanism of persistent superior compression force in a patient using the upper extremity as a weight-bearing joint is assumed.

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Andrews and coworkers[1] noted that firing of the biceps muscle caused elevation of the superior labrum off the glenoid. Because their electromyography studies showed the greatest biceps firing during the deceleration phase of the overhead throw, Andrews and

coworkers[1] speculated that injuries to the superior labrum and biceps insertion occurred during this portion of the throw. Studies at the Kerlan-Jobe clinic [19] [20] support this finding of high levels of biceps firing during the overhead throw. Others[16] evaluating the overhead throw noted that 1090N of shoulder compression force was produced shortly after ball release and believed this could explain the high incidence of SLAP lesions in overhead athletes. It is possible that biceps firing versus compression mechanisms during the throw may cause different types of SLAP lesions. Traction injuries have been suggested to cause SLAP lesions. Maffet and associates[36] polled 84 patients and found many describing a typically sudden traction injury as the onset of shoulder pain. A fall onto the point of the shoulder, pulling superiorly on a heavy object, water-skiing injuries, and traumatic dislocations were described. Bey and coworkers [4] in a cadaver study found that stress on the superior labrum and biceps complex was enhanced significantly when inferior instability was introduced. These investigators noted that the direction of pull of the biceps tendon changed when inferior subluxation was produced. Bey and coworkers[4] speculated this change caused the increased stress on the superior labrum found in their study. Burkhart and colleagues[7] described a torsional peeling-back mechanism. This mechanism occurs with the humerus abducted and external rotation occurring with glenohumeral joint compression as in the overhead throw ( Fig. 21K-13 ). These authors speculated that this mechanism may either cause a posterior subtype SLAP lesion or cause extension of a type II lesion posteriorly. This mechanism could cause injury in the late cocking phase of the overhead throw. Burkhart and colleagues [7] discussed the contribution of posterior capsular tightness in the evolution of SLAP lesions in pitchers. These authors speculated that tightness postero-inferiorly adjusts the resting position of the humeral head superiorly and anteriorly, causing torsional peel back of the biceps and superior labrum more likely to occur during the cocking phase of the throw.

Figure 21-K-13 The torsional peel-back mechanism of injury to the superior labrum and the biceps tendon. Note the difference between the resting position (A) and the position at 90 degrees of abduction and external rotation (B). The biceps tendon rotates posteriorly, peeling the posterosuperior labrum off the glenoid. (From Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair and rehabilitation. Arthroscopy 14:637-640, 1998.)

All of these mechanisms likely contribute to injury to the superior labrum and biceps tendon. It is likely that different types of SLAP lesions occur with different injury mechanisms. This fact has not been documented yet and is under study. The more one understands the relationship between a specific mechanism and the pathology it typically creates, the more accurate the clinical diagnosis in the office will be.

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Diagnosis

Determining whether a patient has a superior labral lesion as the source of shoulder pain can be a challenge. The most important part of the work-up is to maintain a high level of suspicion for these problems. Symptomatic superior labrum and biceps tendon complex lesions can act like almost anything. The patient can present with complaints similar to an impingement syndrome, chronic acromioclavicular (AC) joint pain, refractory bicipital tendinitis, or a case of symptomatic instability. The most common presenting symptoms are pain often with overhead activities and mechanical catching, popping, or grinding. Depending on what secondary pathology accompanies the SLAP lesion, a combination of the above-mentioned symptom complexes may be present. Current thought suggests that SLAP lesions are associated with shoulder instability, often subtle instability. It is still unclear whether the SLAP lesion leads to secondary instability or whether underlying instability leads to a SLAP lesion. Either way, an instability examination can be positive. True laxity in the anteroinferior direction may be detectable. More often, the patient complains of pain only with provocative instability testing. The apprehension test can cause pain anteriorly or posteriorly if there is secondary involvement of the posterosuperior rotator cuff. The Jobe relocation test also may be positive.

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Persistently positive biceps tendinitis signs may be found, but not always. A positive Speed or Yergason test makes sense given the involvement of the proximal biceps insertion. One always must consider superior labral and biceps tendon pathology when a biceps tendinitis fails to improve despite adequate conservative management. Because of the common association of rotator cuff damage with SLAP lesions, typically in the posterosuperior portion, a clinical examination entirely consistent with

impingement or rotator cuff tendinitis or tear often is seen.[12] This association is one reason we and others believe all rotator cuff patients should have diagnostic arthroscopy before any open repair. A SLAP lesion probably would be missed from a purely open approach and may lead to persistent shoulder pain after rotator cuff repair. The tear may recur if an unrecognized SLAP lesion and its resultant posterosuperior laxity are missed ( Fig. 21K-14 ).

Figure 21-K-14 Rotator cuff damage associated with SLAP lesion. Type III SLAP lesion with unstable biceps insertion in a volleyball coach (A). Note the undersurface fraying of the posterosuperior portion of the rotator cuff (arrow). This patient had previously had an open rotator cuff repair that recurred owing to this unrecognized SLAP lesion. The subacromial arthroscopic view from the posterior portal of the same injury shows a full-thickness rotator cuff tear that was repaired along with the SLAP lesion ( B).

Berg and Ciullo[2] studied a group of patients who had persistent shoulder pain after an AC joint resection. These patients were diagnosed clinically with AC joint pain and had had a distal clavicular resection. Berg and Ciullo[2] found 75% of these failed AC resections had SLAP lesions that had not been diagnosed at or before the first surgery. Attempts have been made to improve the preoperative clinical diagnosis of SLAP lesions. Several clinical tests have been described with varying degrees of accuracy.[3] [30] [31] [37] [41] Most of these tests seem to be variations of maneuvers that either try to pinch a torn labrum between the humeral head and glenoid causing pain, clicking, or popping, similar to a McMurray test in the knee, or place traction on the biceps tendon. Mimori and colleagues[37] noted a difference in pain provoked when alternately pronating and supinating the forearm with the humerus at 90 degrees abduction and external rotation. Increased pain in the pronated position relative to supination was considered positive for superior labral pathology. The pilot study by Mimori and colleagues[37] showed a 100% sensitivity rate with 90% specificity. Similarly, O'Brien and associates [41] and Berg and Ciullo [3] described a test in which the patient has the arm extended in front with the elbow extended. The arm is adducted across the body with the forearm pronated, then with it supinated ( Fig. 21K-15 ). Increased pain in the pronated position versus supination was consistent with a SLAP lesion. Pain in both positions more likely would indicate AC joint pathology. It is believed that increased biceps tension in the pronated position provokes pain.

Figure 21-K-15 O'Brien's clinical test for SLAP lesions (A and B). The arm is brought into adduction across the body with 90 degrees of forward flexion. A positive test shows improvement of the patient's symptoms with a supinated forearm, and reproduction of pain with pronation (thumb down) of the forearm.

Other authors have described more specificity in the preoperative clinical examination. Morgan and colleagues[38] believed they could differentiate between posterior versus anterior type II SLAP lesions. Posterior lesions would show a positive Jobe relocation test, whereas anterior SLAP lesions would have positive Speed and O'Brien test. Kim and coworkers[31] devised a test they thought could differentiate between anterior

shoulder instability alone and anterior instability with a SLAP lesion. A standard apprehension test with the arm in the abducted and externally rotated position was performed with a positive result present in the anteriorly unstable patient. Active elbow flexion against resistance in the stressed position would improve symptoms unless a SLAP lesion also was present. No change or worsening pain with active elbow flexion was considered diagnostic of a SLAP lesion accompanying anterior instability in Kim's study. More commonly in our experience, SLAP lesions are difficult to diagnose accurately by clinical examination. The above-mentioned tests are useful when employed in the context of the entire clinical history and examination along with a high level of suspicion. The clinical picture may be entirely consistent with rotator cuff pathology or entirely consistent with instability, depending on associated shoulder pathology. Imaging studies can be helpful diagnostically. Magnetic resonance imaging (MRI) scans of the shoulder can show the anatomy of the superior labrum and the proximal biceps tendon insertion well. Limitations exist in the sensitivity of nonenhanced MRI scans to detect superior labrum detachments. Although some authors [10] have shown good success in detecting SLAP pathology on plain MRI scans, the presence of a highly qualified musculoskeletal radiologist directing scan parameters and interpretation in their study makes a huge difference. Not all orthopaedists in the community

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have access to this skill level or interest from a MRI radiologist so that most series show a high level of missed pathology.[57] [69] The use of gadolinium-enhanced MRI scans in the shoulder has increased greatly accurate preoperative diagnosis of superior labral pathology.[29] [32] If appropriate slices are obtained, dye often can be seen leaking between a detached superior labrum and biceps tendon complex and the glenoid ( Figs. 21K-16 ). This appearance can be diagnostic of a SLAP lesion. The orthopaedist must be cognizant of and familiar with normal superior labral variants, however, when interpreting these scans. The normal anterosuperior labral detachment and the normal sublabral recess under a meniscoid-type superior labrum can lead to false-positive readings of MRI scans. The orthopaedist must become familiar with interpreting superior labral anatomy on gadolinium-enhanced MRI. All younger patients with refractory shoulder pain being evaluated by MRI should have a gadolinium-enhanced MRI scan to increase diagnostic accuracy.

Figure 21-K-16 Gadolinium-enhanced magnetic resonance images of SLAP lesions. A-C, Note the leakage of the dye under the biceps tendon insertion in three separate cases (arrowheads). These images are clearly diagnostic of a type II SLAP lesion. D, A type IV SLAP lesion is suspected owing to the imaging appearance. This same case is viewed arthroscopically in Fig. 21K-19 .

Arthroscopy is the gold standard in the diagnosis of superior labral lesions. The diagnosis more often than not is made or modified at arthroscopy. The surgeon should be aware of repair techniques and have necessary equipment available to handle SLAP repairs when performing shoulder arthroscopy.

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Pathomechanics

It is not clear based on research until now whether shoulder instability puts stress on the biceps insertion leading to a detachment or whether a biceps avulsion leads to shoulder instability. It probably can occur both ways. The cause of superior labral pathology not involving the biceps insertion probably is related to a compression mechanism either through a sudden injury, as in a fall, or through repetitive compression, as occurs in the overhead throw.[16] [19] A sudden compressive blow or persistent grinding on a meniscoid-type superior labrum can cause type I or III injuries or one of the other types that do not involve detachment of the biceps insertion.[36] Instability and its subsequent problems typically do not occur. The torn labrum may cause a functional instability[46] resulting from the mechanical disruption of normal shoulder function but not a true laxity-induced symptom of instability. The treatment is simple débridement of the torn labrum. Things become more complex if the biceps tendon is detached. The mechanism for this is more likely a traction injury that occurs either suddenly or related to the overhead throw. A sudden pull on the biceps by mechanisms previously described can avulse the superior labrum and biceps tendon complex, causing a type II SLAP lesion. The bulk of the posterosuperior labrum is composed of extended biceps periarticular fiber bundles.[25] A more complicated symptom complex can evolve from there. The patient initially may complain of mechanical popping and clicking related to the torn labrum, or the patient may describe bicipital tendinitis symptoms. Because studies[44] have proved the association of increased glenohumeral laxity anteroposterior and superoinferior with these SLAP lesions, the patient may complain of instability symptoms. Alternatively, the patient may have pain just with provocative activities or examination maneuvers. Pitchers often develop a dead arm sensation. This circle concept of shoulder stability explains the elimination of the positive drive-through sign seen by surgeons[38] after the repair of a type II SLAP lesion. If this anteroinferior-posterosuperior pseudoinstability continues, especially in an overhead throwing athlete, the additional occurrence of secondary impingement is well

accepted.[61] In this case, however, the underlying instability is related more to a type II SLAP lesion than to detachment or laxity of the glenohumeral ligaments. It now is believed that increased superior laxity from the loss of the biceps insertion may lead to damage to the posterosuperior portion of the rotator cuff selectively. [4] [26] [38] Snyder and coworkers[58] noted a 31% incidence of rotator cuff injury in chronic SLAP lesions but found none in acute SLAP lesions.

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The concept of internal impingement of the shoulder has been described previously.[28] [63] The rotator cuff injury these authors describe occurs to this same posterosuperior portion of the rotator cuff. The authors report that subtle anterior instability leads to anterior translation of the humeral head on the glenoid during the cocking phase of the overhead throw. No mention is made in studies of the presence of, or any association with, superior labral pathology. It is unclear presently how these two different descriptions of pathomechanical injury to the same part of the shoulder are related. Burkhart and Morgan[7] described a torsional peel-back mechanism of superior labral injury. These authors thought this twisting of the biceps insertion at the crucial position of abduction and external rotation might not create a biceps tendon avulsion but would extend the injury to involve the posterosuperior labrum. This extension occurs through the intimate association of collagen fibers as described by Huber and Reinhard.[25] This pathomechanical description explains the large number of posterior SLAP subtypes that occur in overhead throwing athletes. Morgan and coworkers[38] believed that the torsional peel-back mechanism could stand alone as a cause of type II SLAP lesions. If one understands normal superior labrum and biceps insertional anatomy as well as how possible mechanisms of injury affect that anatomy, SLAP lesions make more sense. Type III SLAP lesions probably occur as a compression injury against a meniscoid-type superior labrum ( Fig. 21K-17 ). Often type III lesions have an intact biceps insertion. Type V [36] or the flap-type superior labrum probably is just a type III variant with bucket-handle tear further avulsed anteriorly or posteriorly to create a labral flap ( Fig. 21K-18 ). Type IV lesions probably occur as a result of the same superior compression injury; however, because of the patient's variable anatomy, the meniscoid superior labrum does not detach cleanly from its insertion onto the biceps but rather tears up into the biceps substance ( Fig. 21K-19 ). Depending on the amount of involvement of the biceps, instability can result in type IV lesions even if all the biceps is not detached.[5]

Figure 21-K-17 Photograph of a type III SLAP lesion pattern with detachment of the biceps insertion. Note the bucket handle portion of the injury below (arrow).

Figure 21-K-18 Flap-type SLAP lesion. As viewed from the posterior portal, the posterior-based unstable

superior labral flap (arrow) can be noted. This variety is very similar in origin and treatment to the type III SLAP lesion.

Figure 21-K-19 Arthroscopic photograph of a type IV SLAP lesion. One can see the extension of the tear into the substance of the biceps tendon.

The combination of a Bankart lesion with a superior labral detachment (type VI)[36] [64] makes more sense given the understanding of the association between SLAP lesions and instability. Two studies[22] [60] have shown a 10% incidence of SLAP lesions in first-time dislocators confirmed during arthroscopy. Repair of the entire detached labrum is important in reestablishing normal shoulder function.[64] This association reinforces our belief that all shoulders should

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have diagnostic arthroscopy before open repair. Missed pathology is a major cause of failed shoulder surgery.

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Treatment Conservative Treatment

Conservative treatment has no proven role in the treatment of superior labral injuries. Although judicious use of nonsteroidal anti-inflammatory medications and isolated corticosteroid injections may decrease symptoms, they do not cure the mechanical problems created by a superior labral lesion. A shoulder rehabilitation program centered around rotator cuff exercises, scapular stabilization exercises, and regaining a full normal range of motion no doubt would optimize any surgical treatment that ensues and help improve symptoms of associated instability or rotator cuff disease. This program may alleviate symptoms of SLAP lesions in which the biceps anchor is stable. Also, familiarity with this rehabilitation program benefits the patient recovering from any surgical procedures required to correct the superior labral pathology. Surgical Management

Arthroscopic surgical techniques are invaluable in the evaluation and treatment of superior labral lesions. Variations in the normal anatomy of the superior labrum, superior glenohumeral ligament, and MGHL make interpretation of pathologic lesions and the extent of these lesions difficult. A thorough understanding of normal superior labral anatomy and normal superior labral anatomic variants as discussed earlier is essential. A cordlike MGHL (Buford complex) may confuse the surgeon and result in surgical treatments that may worsen the patient's overall shoulder condition.[67] Recognition of the pathologic aspects of the superior labrum is equally important in dictating the surgical treatment. Classifying superior labral pathology is the first step in the surgical management of SLAP lesions. Type I through IV lesions have been well described. More complex superior labral lesions also must be appreciated, however.[36] [38] Recognition of these lesions as well as in the associated pathology, such as concomitant anterior capsulolabral injury, allows arthroscopic and open surgery to be

planned. Complex types of SLAP lesions are the most difficult to treat. Any information available preoperatively, such as the appearance of the anterior, posterior, and superior labrum on gadolinium MRI scan, may be helpful in planning not only the surgical repair, but also the surgical positioning for that repair. Diagnostic Arthroscopy

Diagnostic arthroscopy of the shoulder joint may be performed in either the beach chair or the lateral decubitus

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position. The advantages and disadvantages of these two positions are debated among shoulder surgeons. Surgeon familiarity with either position is paramount to a successful surgical procedure. Each position has its benefits when addressing particularly complex lesions that involve not only the superior labrum, but also the anterior or posterior labrum. A type II SLAP lesion with concomitant anterior capsulolabral avulsion may be addressed in the beach chair position for access to the anterior shoulder should open repair of the capsulolabral lesion be required. Conversely, reparable superior labral lesions that are associated with significant posterior instability may be addressed best in the lateral decubitus position, which allows easier access to the posterior shoulder for open surgical procedures. Snyder[55] described a 15-point arthroscopic examination visualizing all shoulder structures from posterior and anterior arthroscopic portals. Familiarity with diagnostic arthroscopy of the shoulder through both of these portals greatly aids the arthroscopic surgeon in repair of superior labral lesions. Probing of the superior labrum allows the surgeon to assess the stability of the biceps anchor on the supraglenoid tubercle. When superior labral pathology has been visualized and biceps anchor stability assessed, surgical treatment can proceed. Operative Arthroscopy

Many advanced arthroscopic skills are required to treat superior labral lesions successfully. The surgeon should be familiar with the use of arthroscopic tacks, suture anchors, knot tying, and suture passing techniques. Any or all of these skills may be required to address repair of superior labral tears successfully. Historically, transglenoid surgical repairs have been used, but these techniques largely have been replaced by the aforementioned techniques. The surgical treatment of SLAP lesions can be difficult. Proper portal placement is essential to success in repairing lesions that extend anterior and posterior to the biceps anchor. Several arthroscopic portals may be required, including a straight posterior portal for scope visualization, a high anterior portal, a low anterior portal, and a posterolateral portal typically located 1 cm lateral and 1 cm anterior to the posterolateral corner of the acromion. When a posterior arthroscopic portal has been established and

the pathology assessed, subsequent portals are established based on what structures need repairing. The principles of treatment of these lesions are simple after proper portal placement and include the following: 1. 2. 3. 4.

Débridement of degenerative labral tissue Preparation of the superior glenoid for biceps anchor repair Biceps anchor repair Repair of other pathology

Each of these steps is addressed separately. Débridement of Superior Labral Lesions

Most SLAP lesions have associated degenerative edges, flap tears, or bucket-handle tears of the central edge of the superior labrum. Débridement of this pathologic tissue is simple. Care must be taken to ensure that the labral change is pathologic because normal variants and age-related fraying are much more common than true superior labral pathology. Débridement is performed with an arthroscopic shaver, arthroscopic baskets, or thermal devices to ablate and smooth the lesion. Care must be taken no matter what the débridement technique to avoid injuring the articular cartilage surface of the glenoid and preserving all normal functional labral tissue. Any of the available devices may cause injury if not used with care. Preparation of the Superior Glenoid

The superior labrum is known to be an area of questionable vascularity. Cooper and associates[11] and Rouse and coworkers [52] have shown abundant vascularity of the entire labrum with the exception of the superior portion. This area where SLAP lesions occur is vascularized only at the periphery with a relatively avascular central edge. Anything the arthroscopic surgeon can do to promote healing in this area is beneficial. Although there are no basic science studies comparing biceps anchor repair with or without abrasion of the superior glenoid, common sense dictates that preparation of the superior glenoid bony surface is necessary to maximize the healing of labral tissue to the bone ( Fig. 21K-20 ). Preparation of the bony glenoid surface can be done with an arthroscopic shaver, bur, or arthroscopic rasps; this part of the procedure is performed easily through a properly placed anterosuperior or anteroinferior portal.

Figure 21-K-20 Abrasion of the superior glenoid rim with an arthroscopic rasp. It is very important to stimulate a bleeding surface before repair. The superior labrum typically has a poor blood supply from the underlying bone.

Repair of the Biceps Anchor

There are many different techniques to repair or stabilize the biceps anchor. Each of these techniques has its proponents. Surgeons who are not acquainted with arthroscopic knot-tying techniques should choose tack-type repairs. Surgeons who possess knot-tying skills may prefer suture anchor-type repairs. Becoming acquainted with both of

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these techniques significantly increases the likelihood that an anatomic repair can be obtained. The principles of each of these techniques are discussed. Arthroscopic Tack Repairs.

Several arthroscopic tacks are available for use in the shoulder joint. The techniques are similar for each of these devices. The posterior portion of the SLAP lesion is repaired through the posterolateral portal, and the anterior portion is repaired through the high anterior portal. Important to these techniques is the ability to penetrate the superior labral tissue with a guide pin and cannulated drill setup. A drill hole is made in the superior glenoid. The drill is removed, leaving the guide pin crossing the labral tissue while remaining in the bony drill hole. A bioabsorbable tack is loaded on the guide pin and hammered into place, compressing torn labral tissue up against the prepared bony glenoid surface ( Fig. 21K-21 ). Controversy exists regarding the high posterolateral portal as to whether significant injury is caused to the rotator cuff during this process. Inspection of the rotator cuff arthroscopically after tack placement can identify whether a significant rotator cuff lesion has been caused by a posterolateral portal placement. If significant injury has been caused to the rotator cuff tendon, it can be repaired by arthroscopic suture techniques after labral repair has been accomplished. Similarly, these arthroscopic tacks may be used to repair additional anterior or posterior labral detachments that may be associated with the superior labral lesion.

Figure 21-K-21 Repair of SLAP lesion using bioabsorbable tacks. Type II SLAP lesion before repair ( A). Posterior tack impacted into place (B). Note orientation with glenoid (arrowhead) and biceps tendon (arrow). Anterior tack impacted into place (C). Final repair with stable superior labrum (D).

Alternatively to this technique, the drill/guide pin construct can be used to establish a superior glenoid drill hole without first traversing labral tissue. Both then are removed from the glenoid. The guide pin is advanced down the cannula and across labral tissue, minimizing surgical injury to the labral tissue. Tack placement is as described previously.

Arthroscopic Suture Anchor Repair.

The technique for repairing the biceps anchor back to the supraglenoid tubercle using suture anchor techniques is technically more demanding than arthroscopic tack repairs. We believe an anatomic repair can be accomplished best through this technique. Many factors affect the surgeon's ability to accomplish this type of repair, including the ability to place suture anchor constructs into the superior glenoid, pass suture through the avulsed labral tissue, and tie secure arthroscopic knots to complete the repair. There are many suture anchors on the market to choose from for this type of repair. Surgeon familiarity with suture anchor techniques is paramount to successful use. Metallic and bioabsorbable suture anchors are available. Braided nonabsorbable No. 1 or No. 2 suture is preferred. There are many ways to pass sutures through torn labral tissues, including using a Caspari punch, penetrating instruments using suture hand-off techniques, and suture lasso techniques. Whether a simple suture with one pass through the labral tissue or a mattress-type suture with two passes through the labral tissue is used depends on the surgeon's

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preference. Our technique is described later. To facilitate suture passage through the torn labral tissue, generally three arthroscopic portals are required. The surgeon must ensure that all arthroscopic tools fit easily through the cannulas used in these portals. After sutures have been passed through the labral tissue, secure surgical knots must be tied arthroscopically to complete the repair. Sliding and nonsliding knots may be used, according to the surgeon's preference. The operating surgeon should be familiar with both types of knots because both might be needed to complete a repair. To use sliding knots successfully, the knot must be tied through the same arthroscopic cannula in which the suture anchor was placed into the glenoid. All sliding knots, regardless of how secure they may seem, should be backed up with several nonsliding knots for additional security. Review of the Literature

In reviewing the salient orthopaedic literature regarding the treatment of SLAP lesions, it is apparent that the orthopaedic surgeon's options continue to evolve. Simple débridement alone has failed to achieve satisfactory long-term results, especially in athletes. In 1993, Cordasco and associates[12] reported on 27 patients with unstable SLAP lesions treated with débridement alone. Although 78% of patients showed excellent pain relief at 1 year, these results deteriorated to 63% at 2 years, and only 45% of the patients were able to return to their previous level of athletic performance.

Cordasco and associates[12] attributed these unsatisfactory and diminishing results to instability associated with the superior labral lesion. No patients in this study had a history of dislocation or instability on clinical examination. Of patients, 70% had instability on examination under anesthesia. This finding suggests that even subclinical instability associated with unstable biceps anchor may be the reason unrepaired SLAP lesions cause symptoms. Failure to regain the stability of the biceps anchor predictably leads to continued symptoms. Other authors have reported similarly poor results with débridement of unstable superior labral lesions.[9] [57] Because of the uncertain results after simple débridement regarding pain relief and return to athletic activity, the evolution of treatment of superior labral injuries has focused more recently on repair of the biceps anchor to the bony glenoid. Many techniques have been described for repair of the unstable biceps anchor, involving metal staples, metal screws, bioabsorbable tacks,[53] transosseous suture techniques, and suture anchor techniques. In the largest study to date, Snyder and colleagues[58] reported their results with 140 patients treated with a variety of methods. Second-look arthroscopies were performed on 18 of the 140 patients. Of these 18 patients, five type II lesions were treated with abrasion and débridement alone. Three of the five had healed at second-look arthroscopy. Of five type II lesions treated with tack fixation, four of the five had healed. These five second-look procedures were to remove loose bioabsorbable tack material. Three type III lesions and a type IV lesion that were treated with débridement alone had a normal appearance on inspection. The biceps anchor at initial arthroscopy in these types was believed to be stable. Two unstable type IV lesions and a complex type II/III lesion were treated with suture anchor repair, and all were found to have healed at second-look arthroscopy. Snyder's work laid the foundation for surgical treatment of unstable superior labral lesions. Suture anchor repair appeared to yield the highest percent of surgical success and was not associated with the need to remove surgical implants. For these reasons, attachment of the unstable biceps anchor using suture anchor techniques is preferred. Field and Savoie[15] reported their experience using transosseous suture techniques for SLAP lesion repair. They reported on 15 type II and 5 type IV repairs at 12 to 42 months postoperatively. All patients had good-to-excellent results. Six throwing athletes all were able to return to their sport without limitations. Ten patients had work-related injuries, and all were able to return to their previous type of work. Only one complication was reported in this study; one patient developed adhesive capsulitis, which required further surgery. Yoneda and associates[68] in 1991 reported on the repair of 10 superior labral lesions with a high profile staple. Yoneda and associates[68] reported 80% good or excellent results at 2 years. Repeat arthroscopy was performed in all patients at 3 to 6 months for staple removal. At this second-look arthroscopy, four of the superior labral lesions were healed completely, whereas six showed good stability with partial healing. There were no noted problems with the staple other than the necessity for removal. Fair and poor results in this study were related to patients with other problems, such as subacromial impingement or multidirectional instability.

Resch and associates[50] described their experience with repair of 14 of 18 SLAP lesions. Six lesions were repaired with a 2.7-mm cannulated titanium screw and washer. Eight were stabilized with a 6.5-mm absorbable tack. Follow-up at 6 to 30 months showed eight patients returned to sports at the same level they had before injury. Four other patients returned to sports but at a lower level. Of the four patients with débridement alone for an unstable superior labral lesion, only one showed improvement. Complications in this study included two instances of glenoid articular cartilage penetration with the metal screw and one instance of screw loosening necessitating a second surgery at 11 weeks for removal. Stetson and coworkers[59] presented their results of 23 SLAP lesions without associated additional pathology that were repaired. One type I SLAP lesion was treated with débridement. Six type II SLAP lesions were treated with débridement and glenoid abrasion. Twelve type II lesions were treated with suture anchor repair. One type II lesion was treated with débridement. Two type IV lesions were treated with débridement, and one complex type II/III lesion was treated with a combination of débridement and suture anchor fixation. Using the Rowe scoring system, 82% of the patients had good or excellent results, 9% had fair results, and 9% had poor results. Multiple fixation devices were used in this study, including absorbable tacks and nonabsorbable suture anchors. The poor results included a type II lesion treated with débridement alone and

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a type IV lesion treated with débridement that was thought to be unstable on further evaluation. The complex type II/III SLAP lesion was treated with absorbable tacks and needed further surgery to remove fragmented tacks that were symptomatic. Burkhart and colleagues[8] reported on 102 type II SLAP lesions treated surgically from 1992 through 1997. Repair was accomplished using suture anchor techniques with only one limb of the suture passed through the labral tissue. Absorbable No. 1 and No. 0 nonabsorbable-type sutures were used. Using the UCLA score at 1 year, 83% excellent, 14% good, 3% fair, and no poor results were recorded. The three patients with fair results all had full-thickness rotator cuff tears that were treated with concomitant repair and acromioplasty. Each of these patients required second surgeries for motion complications. Of patients, 44 were baseball pitchers and, of these, 37 (84%) returned to preinjury levels of activity. Pagnani and associates[43] reported on 13 patients with type II lesions. All lesions were repaired using a bioabsorbable tack. At 2 years, 86% of the patients reported satisfactory results, with 12 of 13 returning to full overhead activities. These authors reported no complications with the biodegradable implant. Authors' Preferred Technique for Superior Labral Repair

Understanding the pathology when planning a repair of the superior labrum is paramount to achieving a successful result. As stated earlier, a thorough diagnostic arthroscopy performed through posterior and anterior portals as well as a methodical examination under anesthesia for shoulder instability greatly aids the surgeon in planning surgical repairs. When operating on a shoulder with superior labral pathology, débridement and repair of multiple structures frequently is necessary. A planned approach to addressing these multiple pathologies simplifies the surgery. We prefer the following order of débridement and repair. Initially, débridement is performed on the rotator cuff and torn labral structures. This is followed by posterior and superior labrum repair, anterior capsulolabral repair, thermal capsulorrhaphy, subacromial débridement, and rotator cuff repair. A routine approach during a shoulder arthroscopy greatly simplifies the surgical experience. Débridement of soft tissue, cartilage, and bone generally is performed through an anterior portal using a mechanical shaver with a 4.0-mm concave curve-tip shaver blade. Limit the extent of labral débridement to preserve as much tissue as possible for repair. A thermal instrument, such as the Oratec 3.0 Vulcan 60-degree ablator (Oratec Interventions, Inc, Menlo Park, CA) may be used to seal the margins of the injured tissues. A surgeon should avoid using thermal energy around a planned suture repair site to prevent potential weakening of the repair tissue. For superior labral repair, three arthroscopic portals are required. Two anterior portals, one high in the rotator interval and the other low entering the joint just above the subscapularis tendon, are employed ( Fig. 21K-22 ). These two portals generally are established before arthroscopic débridement. A third portal is created just lateral to the acromial border to facilitate repair of the posterosuperior labrum. An 18-gauge needle is used to determine the appropriate anteroposterior position for the portal. Generally, this portal is 1 cm anterior to the posterior lateral corner of the acromion. Most superior labral injuries in throwers are posterosuperior and require this more posterior portal placed through the supraspinatus tendon. After establishing the correct position, a No. 11 blade is passed into the subacromial space in line with the fibers of the rotator cuff, staying as medial as possible within the tendon ( see Fig. 21K-22 ). The path of the blade should follow that of the 18-gauge needle. A Wissenger rod is then inserted through the incision and into the shoulder joint while visualizing through the posterior portal. An 8-mm transparent cannula (Arthrex Clear Cannula [Arthrex, Naples, Fla] or Acufex Clear-trac Cannula [Acufex Microsurgical, Mansfield, Mass]) is loaded on its cannulated introducer and placed over the Wissenger rod and directed into the shoulder joint. The cannulated introducer is crucial to the success of establishing this portal. This method provides access to the superoposterior margin with minimal trauma to the rotator cuff tendon. The articular opening of the portal is through the muscle tendon junction of the supraspinatus and should heal without the need for closure. If desired, however, the rotator cuff incision from the portal may be closed easily with a side-to-side repair using arthroscopic suture techniques during evaluation of the subacromial space.

Figure 21-K-22 Repair of SLAP lesion using suture anchor technique. High and low anterior portals with cannulas in front of biceps tendon (arrow) (A). Placement of posterolateral portal with No. 11 blade in

view (B). Placement of anterior suture anchor (C). Anterior and posterior suture anchor repairs in place (D).

Next, repair of the superior labrum is performed from posterior to anterior. Débridement of the labrum is limited to preserve tissue for repair. The 4.0-mm concave curve-tip shaver generally is used for débridement of the superior labrum and the superior rim of the glenoid. If further bony débridement is necessary, an arthroscopic rasp is preferred instead of an arthroscopic bur. Bony débridement facilitates labral healing to the superior glenoid, where little potential for spontaneous healing exists. The number of suture anchors and their position needed for anatomic repair of the superior labrum are determined next. Current preference is for the 3.5-mm corkscrew suture anchor (Arthrex, Naples, Fla). This anchor may be inserted with or without predrilling by hand ( see Fig. 21K-22 ). Ensuring an easy insertion helps prevent injury to the anchor head and suture eyelet. The handle for anchor insertion has a laser mark indicating the alignment of this suture eyelet. Proper alignment of this suture anchor eyelet has been shown to be advantageous for tying tight suture loops. The eyelet should be positioned perpendicular to the glenoid rim to allow vertical mattress sutures to be placed across the circumferential fibers of the labrum. This positioning, although probably creating a stronger repair, also facilitates repairing the labrum up onto the glenoid rim in its normal anatomic position. Two suture anchors are used routinely to repair the unstable biceps anchor. More anchors may be required, however, should the lesion extend further in an anterior or posterior direction. The suture anchors placed posterior to the biceps are introduced through the posterior lateral portal, and suture anchors positioned anterior to the biceps are placed through the high anterior portal. The order in which anchors are placed probably is not important. We typically place anchors from

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posterior to anterior to get the difficult part of the repair done first. Proper orientation of the suture anchor with respect to the glenoid rim is important. Viewing the angle at which the anchor is to be inserted from posterior and anterior may be helpful in achieving proper orientation. Anatomic dissections in our laboratory show the typical angle of insertion through the posterolateral portal to be extremely variable, making anchor insertion unpredictable. Initially, attempts are made to place the anchor without predrilling the glenoid bone. A mallet is used to tap the anchor into place, while screwing in the anchor at the same time. Should difficulty be encountered, the anchor is removed, and glenoid bone is drilled before reinserting the suture anchor. Noting the etched laser mark on the anchor inserting device, the eyelet of this suture anchor is positioned perpendicular to the glenoid rim. When the anchor is inserted, the insertion handle is removed, leaving the attached No. 2 braided suture exiting the cannula through which the anchor was inserted. The most difficult part of suture anchor repair for SLAP lesions is passing sutures through the detached labral tissue. Many devices can be helpful during this process,

including a Caspari punch (Linvatec Corporation, Largo, Fla), SutureLasso (Arthrex, Naples, Fla), and curved arthroscopic suture passing needles (OBL, Scottsdale, Ariz). Cannulas 8 mm in size are required for all suture passing devices. The 90-degree curved SutureLasso is currently the favorite for suture passage. It is introduced adjacent to the selected anchor penetrating the labrum as medial as possible. The labrum is lifted off of the superior glenoid, and the lasso is passed through the labrum, exiting immediately above the glenoid rim. The monofilament suture loop within the lasso is advanced into the joint. A suture retriever (Arthrex, Naples, Fla) is introduced through a separate cannula to capture the monofilament suture loop and the braided suture from the anchor. Both of these sutures are pulled out through an anterior cannula. The braided suture is passed through the monofilament suture loop, and the suture is pulled back through the labrum and through the original cannula. The lateral limb of the mattress suture pair is placed in a similar manner except this time the SutureLasso should pierce the labrum directly over the suture anchor entry site. Suture passage is as described previously. When sutures are passed, they are tied using arthroscopic knot-tying techniques. The process is repeated for each successive suture anchor. It is preferable to tie knots as soon as suture is passed for each anchor; this prevents many suture tangles if all suture is passed for all anchors before tying. Several principles are important regarding suture handling

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and knot tying during superior labral repair. The sutures to be tied should exit the cannula through which their attached anchor was placed; this allows the suture to slide easily through the labrum and anchor eyelet. The anchor eyelet must be aligned with the direction of the suture passing through the labrum. The suture must pass through the labrum, through the eyelet, and back through the labrum without twisting or crossing. A knot pusher must be used to tighten the loop before locking the knot. The surgeon must be adept at tying sliding and nonsliding knots ( see Fig. 21K-22 ). One type of arthroscopic knot will not work in all situations. There are two types of knots, sliding and nonsliding. Sliding knots can be divided into groups that lock themselves and those that must be locked. Nonsliding knots (square knot, Revo knot) are the most difficult to produce tight loops and suture knots. When the suture does not slide well, however, these techniques are essential. Sliding knots (e.g., Tennessee slider, Duncan loop, Roeder knot) and sliding-locking knots (Westin knot, giant knot) produce tighter loops but must be secured with three reversed half-hitch throws on alternating posts. Current preference is for the Westin knot, which is easy to tie and reliably produces tight loops and secure knots with a low profile. The ability to tie secure arthroscopic knots is important to the successful completion of these superior labral repairs. The surgeon performing arthroscopic repairs must be aware of the differences in knot strength and security of different suture materials and knot patterns. Familiarity with one sliding knot and one nonsliding knot is essential to

handle any clinical situation. Rehabilitation after Biceps Anchor Repair

As with the diagnosis and treatment of superior labral lesions, the rehabilitation program associated with superior labral repair continues to evolve. Burkhart and colleagues[8] summarized their program for superior labral repair in throwers as follows: Week 1Sling immobilization at all times. Week 2 to 3Codman circumduction, passive range of motion from 0 to 90 degrees of abduction and external rotation in adduction, sling immobilization when not doing passive range-of-motion exercises. Week 3 to 6Discontinue sling, progress to full passive range of motion in all planes, begin passive posterior capsular and internal rotation stretching, begin passive and manual scapular mobility program, begin active external rotation in abduction, may use the operative extremity for light activities of daily living. Week 6 to 16Continue all stretching and flexibility programs as previously listed; begin progressive strengthening of the rotator cuff, scapular stabilizers, and biceps. Month 4Begin interval return to throwing program, continue stretching and strengthening regimen with particular emphasis on posterior capsular stretching. Month 6Begin throwing from the mound.

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Conclusions

Lesions of the superior labrum and biceps anchor are being recognized increasingly as the cause of shoulder symptoms. Differentiating between normal and abnormal superior labral anatomy can be difficult. Surgeon experience is invaluable in recognizing and successfully treating these lesions. Diagnostic shoulder arthroscopy is the gold standard for accurate diagnosis of superior labral lesions. The association of superior labral pathology with rotator cuff tears, anterior and posterior instability, and AC joint injury and degeneration necessitates diagnostic shoulder arthroscopy as an important part of all shoulder procedures. Missed superior labral pathology continues to be a cause of failed open surgical procedures that could be prevented by recognition of these injuries through shoulder arthroscopy performed before open shoulder procedures. Similar to the debate involving the instability and impingement continuum of the late 1980s and 1990s, understanding of the relationship between superior labral lesions and shoulder instability continues to evolve. Treatment of these lesions is accomplished best through arthroscopic surgical techniques. Surgeons should be familiar with placement of the multiple shoulder portals using outside-to-inside techniques. Familiarity with suture anchor placement, suture passage through reparable tissue, and knot-tying techniques is essential for successful repair. Although there are multiple classifications of superior labral lesions, we suggest viewing these lesions as (1) those that have an unstable biceps anchor and (2) those with a stable biceps anchor. Other shoulder pathology associated with these lesions, such as rotator cuff tears, splits within the biceps tendon, and capsulolabral avulsions, can be addressed separately. The unstable biceps anchor needs repairing, whereas débridement of lesions in which the anchor is stable is adequate treatment.

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Section L Rotator Cuff and Impingement Lesions in Adult and Adolescent Athletes Sumant G. Krishnan MD Richard J. Hawkins MD, FRCSC(c) Historical Review

Rotator cuff disease and impingement lesions are among the most commonly encountered disorders of the shoulder in the general population. In 1788, Monro illustrated a tear in the supraspinatus and infraspinatus. John Smith in 1834 published the first detailed series of rotator cuff ruptures. The earliest published report of a rotator cuff repair appears to have been submitted by Muller in 1889. [133] However, the modern evolution of rotator cuff injury, evaluation, and management began with the comprehensive work of Codman in 1934. Codman thoroughly delineated the pathology and pathophysiology of these lesions and described both the associated clinical findings and appropriate treatment recommendations. [35] [36] [37] Rotator cuff injuries and impingement syndromes in the athlete are much less common than in the sedentary populace, and they have only recently been documented as a separate subset of injuries.[3] [15] [19] [57] Furthermore, the cause of impingement and rotator cuff lesions in athletes may differ from the commonly described causes. Codman purported a purely traumatic cause for rotator cuff injury. This was refuted by Meyer in 1937, who argued that repetitive minor trauma caused the disease in the cuff. He was the first to describe what is now the concept of classic outlet impingement, between the greater tuberosity and the acromion.[126] Charles S. Neer expanded on this idea, publishing the technique of anterior acromioplasty for the relief of outlet impingement.[137] Neer further classified impingement and rotator cuff injury into a spectrum of three stages: inflammation and edema in the cuff (stage I), fibrosis and tendinitis (stage II), and partial or complete rotator cuff tearing (stage III).[138] [139] With regard to athletic endeavors, Neer intimated that pitching and overhead-motion sports may be related to

the development of the first two stages of outlet impingement in the athlete.[140] Recently, several authors have documented that outlet impingement and rotator cuff lesions in young athletes often do not clearly fall into this scheme. [3] [12] [19] [66] [76] [81] [82] [161] In older athletes, a primary tendinopathy may occur within the substance of the cuff, leading to secondary acromial changes and compression of the cuff under the coracoacromial arch.[74] [76] In younger overhead-motion athletes, classic outlet impingement is most often caused by subtle glenohumeral laxity/instability, leading to muscle imbalance and subsequent subacromial space impingement.[3] [161] [162] Additionally, the recently published findings in overhead-motion athletes of impingement of the articular surface of the rotator cuff under the posterosuperior glenoid rim (posterosuperior glenoid impingement, or internal impingement) underscore the differences in the types and causes of rotator cuff and impingement lesions in the athlete.[44] [65] [205]

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Epidemiology

The incidence of rotator cuff tears has been reported to be between 39% and 60% of cadaveric specimens, although this may not accurately reflect the incidence in either the general or the athletic population.[36] [47] [57] Eighty percent of swimmers have been reported to experience shoulder pain.[166] [177] In football, shoulder injuries are usually traumatic dislocations or acromioclavicular separations with a lesser incidence of rotator cuff or bicipital tendinitis.[20] Nirschl reported, in a series of world-class tennis players, that more than 50% of these athletes suffered from shoulder problems involving the rotator cuff and biceps tendon.[150] Though the original descriptions of rotator cuff tears involved laborers, rotator cuff lesions have been demonstrated as a considerable concern in athletes (especially overhead-motion athletes). Because the shoulder is primarily involved in many overhead-motion sporting activities (such as baseball, golf, and volleyball), the true incidence of both outlet and internal impingement lesions of the rotator cuff may be much higher than in the general populace.

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Current Concepts and Controversies

Since the pioneering work of Neer in the 1970s, the primary disorder underlying rotator cuff disorders was felt to be outlet impingement from narrowing of the subacromial spaceowing to edema of the inflamed cuff or bony encroachment from the overlying bony and soft tissue superior to the coracoacromial arch. [137] [138] [139] [140] However, in the athletic population, this extrinsic impingement appears to be a secondary phenomenon related to eccentric overload

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of the cuff or to subtle glenohumeral instability, creating a relative narrowing of the subacromial space.[81] [82] Overuse and fatigue related to eccentric overload that results in intrinsic fiber failure of the rotator cuff and biceps tendon constitute a common causation in the young athletic population, especially those involved in repetitive overhead use of the extremity. This intrinsic fiber failure may lead to secondary coracoacromial impingement.[3] [81] [82] [162] Glenohumeral instability may also be related to both rotator cuff and bicipital disorders.[197] [207] Excessive translation of the glenohumeral joint (especially in the anterior direction) may create secondary subacromial impingement of the overlying rotator cuff. Even overwork or overstretching of the shoulder in those patients with multidirectional laxity may lead to secondary cuff tendinitis and shoulder pain. Walch and associates and Davidson and colleagues have documented the phenomenon of posterosuperior glenoid impingement (or internal impingement) of the articular surface of the rotator cuff in overhead-motion athletes.[44] [205] Walch and coworkers demonstrated arthroscopically physiologic contact between the cuff and the

posterosuperior glenoid rim when the arm is abducted to 90 degrees and then maximally externally rotated. Lesions of the articular surface of the cuff have been demonstrated as a result of repetitive use of the arm in this position with overhead-motion sports involving throwing. Davidson and associates have suggested that a subtle increase in anterior glenohumeral translation can also cause internal impingement. In the throwing shoulder, fatigue of the shoulder musculature may result in stretching of the anterior band of the inferior glenohumeral ligament, leading to hyperangulation of the proximal humerus during the throwing motion. In the late cocking and early acceleration phases of throwing, this may result in internal impingement, with more of the rotator cuff contacting the posterosuperior glenoid rim because of the subtle anterior glenohumeral translation. The true origin of pathologic internal impingement that causes a painful shoulder in the overhead-motion athlete is likely a spectrum from repetitive physiologic contact to subtle but pathologic anterior glenohumeral translation. Despite these controversies relating to rotator cuff disorders in the athlete regarding underlying disease, there is a general consensus that nonoperative management of these problems in the athlete should be aggressively pursued.[19] [81] [82] [98] [135] Such nonoperative management involves muscular strengthening and appropriate stretching. Surgical treatments, though uncommon, remain controversial. Advances in arthroscopic techniques have opened a new set of debates regarding appropriate treatment of the damaged rotator cuff when nonoperative measures fail or when the underlying diagnosis mandates surgical management.[57] [60] [161]

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Pertinent Anatomy

The shoulder is a ball-and-socket joint linking the axial trunk and appendicular upper extremity. The glenohumeral joint is the most mobile in the body, allowing for precise positioning of the hand in space. The shoulder is also the fulcrum for the long lever arm of the upper limb and consequently absorbs the majority of forces in sports that require propulsive action of the upper extremity. The rotator cuff is vitally linked to these motions in terms of both precision and propulsion. The cuff comprises the confluent tendon of the supraspinatus, infraspinatus, subscapularis, and teres minor muscles ( Fig. 21L-1A ).[189] The tendon of the long head of the biceps is intimately associated with the cuff and has been called the fifth tendon of the rotator cuff.

Figure 21-L-1 A, Posterior view of shoulder. B, Anterior view of shoulder.

The cuff surrounds and is united with the glenohumeral capsule on all sides, except at the redundant inferior pouch. The biceps tendon originates at the supraglenoid tubercle and traverses the glenohumeral joint as an intra-articular but extrasynovial structure because it is lined by a synovial sheath. The biceps passes deep to the interval between the supraspinatus and the subscapularis (the rotator interval) and exits the joint in the intertubercular sulcus, which is bounded by the coracohumeral ligament superiorly and the superior glenohumeral ligament inferiorly. These ligaments form a pulley for the biceps tendon as it enters the intertubercular groove. The groove has a variable shape and depth, and the bony anatomy of the supratubercular region has been implicated in degenerative lesions of the biceps tendon.[57] [133] [171] Distal to its articular portion, the

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biceps is held in the intertubercular groove by the transverse humeral ligament ( see Fig. 21L-1B ). The vascular supply of the biceps and rotator cuff has been extensively studied.[39] [134] [174] [181] Anatomic studies have demonstrated that the supply from the axillary artery involves six branches, with the largest contribution arising from the suprascapular and the anterior and posterior humeral circumflex arteries.[181] The pattern of arterial supply appears to result in an anastomotic area known as the critical zone, which is the area of the cuff in which most degenerative changes occur and in which most rotator cuff tears begin.[35] [36] [134] Areas of hypovascularity in the supraspinatus tendon immediately proximal to its insertion into the greater tuberosity correspond to this critical zone.[174] Nevertheless, these theories of vascular deficiency of the rotator cuff predisposing to injury remain controversial. The biceps tendon also demonstrates an area of hypovascularity in its intra-articular portion related to tension or pressure from the humeral head when the tendon is in the anatomic position. With arm abduction, these areas demonstrate complete vascular filling.[174] Superficial to the rotator cuff are the deltoid and the coracoacromial arch ( Fig. 21L-2 ). The acromion is an extension of the spine of the scapula; it has a variable shape and a slope that forms the posterolateral bony roof of the arch.[7] The acromion provides bony protection to the glenohumeral joint but also creates a finite space between its undersurface and the humeral head. The coracoacromial (CA) ligament extends from the outer edge of the coracoid and widens to insert onto the anteromedial aspect and the undersurface of the acromion. The CA ligament encompasses the anterior extent of the coracoacromial arch and, with the anteroinferior edge of the acromion and the coracoid process, is implicated in classic extrinsic impingement of the rotator cuff ( Fig. 21L-3 ). [18] [137] However, it remains controversial whether acromial arch morphology and potential extrinsic compression are clearly related to primary rotator cuff degeneration, or if they constitute a secondary phenomenon.[111]

Figure 21-L-2 Superficial shoulder girdle muscles with deltoid (middle arrowhead) overriding sloping acromion (diamond), trapezius (arrow at top), and latissimus dorsi (lower arrow).

Figure 21-L-3 Coracoacromial arch.

Deep to the coracoacromial arch lies the filmy, synovium-lined sac known as the subacromial bursa, which attaches at its base to the greater tuberosity, with its roof fixed to the undersurface of the acromion and the CA ligament ( Fig. 21L-4 ).[2] The remainder of the superior and inferior surfaces of the bursa loosely articulates with the deltoid and the rotator cuff, respectively. Although the roof and base of the bursa are in intimate contact, the two layers are separated by a thin interface of synovial fluid that allows

relatively frictionless motion between the cuff and the overlying deltoid and the coracoacromial arch.

Figure 21-L-4 Subacromial bursa between overlying coracoacromial arch and underlying cuff tendons attached to greater and lesser tuberosities.

Inferior to the subacromial bursa, the rotator cuff and biceps tendon reside within the glenohumeral joint. The four tendons insert as a composite into the greater and lesser tuberosities ( see Fig. 21L-4 ). The rotator interval is an anatomic space defined by the inferior edge of the supraspinatus tendon and the superior edge of the subscapularis tendon. [89] [197] [207] The superficial roof of the rotator interval is the coracohumeral (CH) ligament, and the floor of the interval is the superior glenohumeral ligament (SGHL). This interval is occupied by the biceps tendon as it enters the shoulder joint, with the CH ligament and SGHL forming a pulley for the biceps tendon ( Fig. 21L-5 ). The rotator interval has been demonstrated biomechanically to function as a suspensory structure for the humeral head, and lesions of the rotator interval have been recognized as an important disorder in the genesis of shoulder pain.[17] [189]

Figure 21-L-5 Anterior cuff structures with coracohumeral ligament depicted as a superficial structure to the rotator interval between the subscapularis and supraspinatus tendons.

As was mentioned previously, some authors have suggested that the shape and slope of the acromion may be related to extrinsic rotator cuff disease. [18] [137] However, it remains controversial whether the variability in acromial shape is the result or the cause of the underlying cuff degeneration ( Fig. 21L-6 ).[111]

Figure 21-L-6 A, Normally shaped acromion, lateral view. B, Hooked acromion, lateral view.

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Relevant Biomechanics

The rotator cuff provides muscular forces to generate movement in the shoulder and is intimately involved in stabilizing and controlling the humeral head in the glenoid during overhead and athletic activity.[184] [185] The effectiveness of the cuff depends on its force of action, which is

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related to its size, the type of contraction, and the speed of contraction. Effectiveness is also related to the moment arm or leverage of the cuff and to its angle of pull. Cuff Function

The supraspinatus, although previously thought to initiate abduction, is presently thought to function primarily as a stabilizer of the glenohumeral joint. Its angle of insertion at 70 degrees with respect to the glenoid provides a compressive force ( Fig. 21L-7 ).[163] This allows the powerful deltoid to function more efficiently by maintaining its fulcrum of action at the glenohumeral interface. Without the synergistic action of the supraspinatus, the fulcrum would displace superiorly and allow impingement of the rotator cuff between the humeral head and the undersurface of the acromion.[163] [215]

Figure 21-L-7 Angle of pull of supraspinatus with direct line of force (solid arrow) and compressive component of force (dotted arrow).

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The infraspinatus and teres minor are primarily external rotators and humeral head depressors.[91] Recent work has demonstrated that the infraspinatus is the primary depressor of the humeral head. The subscapularis internally rotates and depresses the humeral head. The infraspinatus and subscapularis are two of the most important stabilizing muscles of the shoulder, especially during eccentric contraction and overhead activity.[101] The large superficial muscles around the glenohumeral joint (such as the deltoid, trapezius, latissimus dorsi, and pectoralis major [ see Fig. 21L-2 ]) provide power for movements of the shoulder; the rotator cuff provides for the fine tuning of those movements. Concentric contraction provides propulsive movement, but eccentric control is crucial to the balance of muscular function about the shoulder and to stabilization of the joint during motion. Biceps

The long head of the biceps, though implicated as a humeral head depressor, is most likely a passive player during most shoulder motions ( Fig. 21L-8 ).[185] [193] Yamaguchi and associates recently demonstrated no significant shoulder-related activity of the biceps muscle when elbow function was controlled with the use of a brace. [216] No significant increase was seen in patients with rotator cuff tears. Nevertheless, in the presence of a rotator cuff tear, the biceps may also be torn or may become enlarged through compensatory functional requirements, especially if the tear involves the subscapularis and the anterosuperior cuff. Rodosky and colleagues demonstrated an in vitro contribution of the biceps to anterior stability of the glenohumeral joint by increasing the resistance of the shoulder to torsional forces, particularly in the positions of abduction and external rotation.[207] Hence, the biceps may be important in combined shoulder and elbow function in the overhand or throwing motion during athletic activity.

Figure 21-L-8 Biceps tendon showing potential humeral head depressive action (dotted arrow). Static Stabilizers

The static structures of the shoulder such as the glenohumeral ligaments are important for stability but also may be implicated in the impingement phenomenon ( Fig. 21L-9 ). [197] For example, tight posterior structures cause greater anterior translation of the humeral head with forward elevation and thus may contribute to secondary impingement.[73] Similarly, anterior laxity and subluxation may result in compromise of the available subacromial space, leading to classic outlet impingement, or may result in increased hyperangulation of the humeral head in the abduction/external rotation position, leading to posterosuperior glenoid or internal impingement.[44] [72]

Figure 21-L-9 Inside view of the shoulder joint showing the relationship between the rotator cuff biceps tendon and the static stabilizers, including the superior, middle, and inferior glenohumeral ligaments. The Throwing Motion

Overhead motion, as exemplified by throwing, is the most common motion affecting the shoulder in sports.[3] [149] This action can be divided into three phases.[22] [23] [66] [163] [202] Wind-up or Cocking Phase

The wind-up or cocking phase involves abduction, extension, and external rotation ( Fig. 21L-10 ). Some authors

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divide the wind-up and cocking phases, and further subdivide the cocking phase into early cocking and late cocking. However, from a muscular standpoint, the deltoid is primarily involved during this phase, resulting in a levering action anteriorly. This may cause superior migration of the humeral head (especially in late cocking or abduction/external rotation) with the natural consequences of secondary impingement and tension on the anterior joint structures. The supraspinatus provides a stabilizing force through its action in compressing the humeral head in the glenoid. The actions of the infraspinatus and teres minor maintain the humeral head within the glenoid fossa through inferiorly directed forces while also providing a concentric external rotation contraction. The subscapularis, aided by the pectoralis major, restricts the terminal external rotation of this first phase through eccentric control and stabilizes the humeral head within the glenoid fossa through a tethering effect.

Figure 21-L-10 Wind-up or cocking phase of throwing motion. Acceleration Phase

The acceleration phase then begins instantaneously with a complete reversal of motion ( Fig. 21L-11 ). The internal rotators, the subscapularis and the sternal head of the pectoralis major, provide the force. It may be that no synergistic relaxation of the posterior cuff muscles actually occurs but rather eccentric contraction of these muscles contributes to a stabilizing balance in the joint. The latissimus dorsi, serratus anterior, and triceps provide additional force through concentric activity.

Figure 21-L-11 Acceleration phase of throwing motion. Deceleration or Follow-through Phase

The final phase, deceleration or follow-through, involves the entire rotator cuff ( Fig. 21L-12 ). The subscapularis is continuing to rotate internally. The posterior cuff is working to decelerate the arm and maintain the humeral head within the glenoid. The supraspinatus is active through all phases of the throwing motion, but its intensity of activity is only moderate and probably reflects its role in maintaining the humeral and glenoid articulating surfaces. The long head of the biceps tendon, apart from being active during the cocking phase in which the elbow is actively bent, also comes into play during deceleration. It is at peak activity following ball release when it acts eccentrically to decelerate terminal elbow extension.

Figure 21-L-12 Deceleration or follow-through phase of throwing motion.

This constitutes the active or dynamic description of the throwing motion. Passively, it has been demonstrated that there are obligator translations of the glenohumeral joint during this motion. The humeral head moves posteriorly with extension or external rotation, and anteriorly with flexion or cross-body motion. The humeral head also hyperangulates during late cocking in abduction/external rotation. However, a clear understanding of the interplay between the dynamic and passive motions in the shoulder

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remains elusive. Recognition of these components implies that an even greater complexity of these functions exists. The actions involved in the overhead throw, the tennis serve, the javelin throw, and the various swimming strokes are all made up of relatively similar mechanisms. Differences exist in the equipment involved, the associated body motions, and the position of the shoulder in each action. Of importance are the degree, repetitiveness, and nature of the forces involved and whether any impact occurs, such as in spiking a volleyball. Because of the biomechanical action of the rotator cuff, dysfunction due to injury or disease can easily lead to significant problems, particularly in the athlete's shoulder in which the stresses are so great. Concentric Versus Eccentric Muscular Contraction

Recent work in biomechanics suggests that significant interplay between concentric and eccentric action of the muscles on opposite sides of a joint occurs, particularly in the

shoulder with the rotator cuff. With external rotation of the arm, the infraspinatus contracts concentrically; however, the subscapularis shows significant electromyographic (EMG) action, obviously as a result of eccentric contraction. [95] [96] [97] [98] [99] [100] [101] [102] This action is related to the propulsive action of power movements on one side of the joint, and perhaps to tethering stabilizing control on the opposite side of the joint. This balance is important biomechanically for fine-tuning the movements in the athlete's shoulder. Recent work suggests that emphasis should be placed more on eccentric strengthening. Scapular Lag

Biomechanically, the scapula plays an intimate role in shoulder function. Many pathologic situations such as impingement and various instabilities result in subtle winging through dysfunction of the scapula as it moves on the chest wall. Fatigue of the scapular rotators on the chest wall may lead to inability of the scapula to rotate properly; therefore, the acromion may fail to clear out of the way when the arm is elevated. This situation, called scapular lag, may result in secondary impingement.[66] [75] [76] Eccentric and Intrinsic Failure

In many shoulder problems, early musculotendinous fiber failure is likely, with resultant secondary changes.[54] [55] [156] [157] [158] [159] With time and superior migration of the humeral head, degenerative changes develop, causing wearing and thinning with eventual tearing of the rotator cuff. Many years are usually required to develop a rotator cuff tear; however, in the younger throwing athlete, partial tears may occur because of the severe stresses placed on the cuff structures. The incidence of partial articular surface tears of the rotator cuff in the athletic population is unknown but may approach 30% to 40%.[57] In addition, other mechanisms may come into play such as instability with secondary impingement, causing further stresses on the already weakened musculotendinous cuff. Classic full-thickness tears are not usually seen until the athlete is older, usually over the age of 50 years. These tears are related to chronic degeneration and attrition, occurring over an extended period. This process leads to changes in the biomechanical function of the shoulder, with abnormal instant centers of rotation and resultant compensation by the biceps, deltoid, and other shoulder girdle muscles.

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Clinical Evaluation History

An athlete initially diagnosed as having a rotator cuff or biceps tendon problem in the shoulder may present with

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one or a variety of chief complaints. The majority of patients have pain. They may complain of such things as fatigue, functional catching in the shoulder, stiffness, weakness, and symptoms of instability. On occasion, an athlete may present simply with complaints about deterioration in athletic performance, for example, a pitcher who loses velocity on his fastball. When one is considering an athlete's shoulder problem, it is important to categorize carefully the sport involved, the intensity of participation (recreational vs professional), the offending activity (such as throwing in baseball or pass-blocking in football), and the arm position and activity causing the problem and the painful shoulder.[74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86]

The chief complaint must be matched with various constitutional factors such as age and sex. The older athlete who has experienced an overhead smash in tennis or a fall on the outstretched arm could sustain a rotator cuff tear, but this would be quite unusual in someone younger than 40 years of age. Female athletes are more likely to demonstrate the generalized hyperlaxity that has been implicated in chronic painful shoulder conditions. Hand dominance also plays a role. In the older nonathletic population, rotator cuff disease may be distributed equally between the dominant and nondominant shoulders. However, among athletes, it is likely to be bilateral only in such

athletes as swimmers or gymnasts. When these considerations are taken into account, it is usually possible to characterize these complaints into two main categories: (1) the acute, or macrotraumatic presentation, in which it is necessary to identify as clearly as possible the mechanism of injury; and (2) the overuse, or microtraumatic presentation, in which it is helpful to analyze the pattern of training and competition. It is also important to realize that an acute episode may be superimposed on a chronic situation. As was previously stated, the most common complaint is that of pain. Although pain can be difficult for the patient to localize accurately, it commonly radiates into the upper arm in the region of the deltoid tuberosity. Biceps tendon pain is usually located anteriorly and can radiate down the belly of the long head of the biceps toward the elbow. Most athletes associate their pain with their sporting activity. It is important to gauge the severity of the complaint. The associated symptoms of fatigue, functional catching, stiffness, or weakness must also be characterized carefully with respect to individual constitutional factors and how they relate to the particular sporting activity ( Table 21L-1 ). Other symptoms, such as clicking in the shoulder, a feeling of instability, numbness, or radiating sharp pain or paresthesias down the arm into the hand, neck, or elbow, suggest an alternative or associated diagnosis to rotator cuff and biceps tendon disease.[12] [13] [14] [26] [27] [142] [143] [144] [145] [146] [147] [148]

TABLE 21-L-1 -- Rotator Cuff Problems in Adult and Adolescent Athletes Pain Difficult with overhead activities Night pain Loss of endurance during activities Deterioration in sporting performance Catching, grinding (crepitus) Weakness Stiffness

History taking in the athletic population does not lead to a clear-cut diagnosis as easily as it does in more sedentary people. This is a direct result of the fact that the cause of rotator cuff and biceps tendon disease can be attributed to a number of different factors. Stresses placed on the shoulder joint by the athlete can lead to problems such as eccentric overload of the surrounding musculature, impingement (either primary or secondary), acute traumatic injury, or unidirectional or multi-directional instability. This understanding, combined with constitutional factors, the severity of the complaint, and the specific sporting activity involved, encompasses the diagnostic process during the

history taking. The main concern with respect to the differential diagnosis is ruling out glenohumeral instability of one form or another.[98] This can be particularly difficult, and indeed instability may be combined with rotator cuff or biceps tendon disease. Referred pain from the surrounding joints should always be considered. Radicular pain, numbness, or paresthesias may point to cervical disease, thoracic outlet syndrome, or a primary neurologic problem such as suprascapular neuropathy ( Table 21L-2 ).[26] [27] TABLE 21-L-2 -- Differential Diagnosis of Rotator Cuff Problems in Adult and Adolescent Athletes Rotator cuff or biceps tendon Strain Tendinitis Tear Glenohumeral instability Glenohumeral instability with secondary impingement Primary impingement of the cuff or biceps tendon Calcific tendinitis Acromioclavicular joint disease Glenohumeral arthritis Cervical spine disease Thoracic outlet syndrome Adhesive capsulitis Suprascapular neuropathy Angina, lung tumor, gallbladder disease

Finally, it should be stated that a diagnosis of rotator cuff or biceps tendon disease based on the history alone is not as specific or sensitive as is a diagnosis of other athletic injuries made in this way. Confirmation by physical examination and further investigation is usually required. Physical Examination

The physical examination should include the necessary evaluation of the general health of the individual in order to consider systemic or regional diseases that can cause shoulder pain. Usually, the history is sufficient in this regard; nevertheless, a lack of local shoulder findings could point toward conditions such as angina, cervical disk

disease, or cholecystitis as the cause of the shoulder pain. The

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initial impression considers the athlete's age, overall health, and level of specific distress related to the shoulder problem. An organized and comprehensive approach to the physical examination is necessary. Inspection, palpation, range of motion, strength testing, and neurologic and vascular stability assessment constitute an orderly sequence.[74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [95] [96] [114] Inspection considers symmetry (one must appreciate that pitchers or tennis players may have unilateral drooping of their dominant shoulder) or deformities such as old acromioclavicular injuries and muscle wasting, which are most often located in the infraspinatus fossa with a rotator cuff tear ( Fig. 21L-13 ). A ruptured biceps tendon shows the diagnostic bulging of the distal retraction with muscle contraction.

Figure 21-L-13 Right-sided dominant tennis player showing compensatory droop of the right shoulder girdle.

The location and degree of tenderness found on palpation often provide a reliable physical sign, leading to an accurate diagnosis. Tenderness in the bicipital groove (2-5 cm distal to the anterior acromion and midway between the axilla and the lateral deltoid with the arm in the anatomic position) is a reliable sign of bicipital tendinitis ( Fig. 21L-14 ). Tenderness in this region with palpation and passive external rotation of the arm (rolling the bicipital groove under the examiner's fingers) is another reliable sign of bicipital disease.[80] The supraspinatus insertion (Codman's point) is palpated through the deltoid just distal to the anterolateral border of the acromion, with the shoulder extended and internally rotated.[36] Maximal tenderness over the acromioclavicular joint may also indicate specific disease.

Figure 21-L-14 Palpation of the biceps tendon in the bicipital groove. Demonstration of Yergason's test with resisted supination and palpation in the bicipital groove.

Range of motion requires documentation. A true discrepancy between active and passive ranges of motion is suggestive of a rotator cuff tear. However, in the athlete, superior strength and flexibility may easily mitigate against this finding. Many athletes such as swimmers and gymnasts may appear to have a greater range than normal, and it is important to recognize that there is great variation in the normal range. The unilateral overhead-motion athlete may demonstrate an obvious discrepancy with increased external rotation and decreased internal rotation compared with the opposite side ( Fig. 21L-15 ). However, the total arc of motion is the same on both sides.[44] It is believed that this decreased internal rotation is an adaptive mechanism in athletes engaging in overhead throwing, possibly resulting from hyperangulation of the humerus

with relative stretching of the anterior capsular structures and relative tightening of the posterior capsular structures. This may be a contributing factor in rotator cuff overuse syndromes

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through excessive obligatory anterior translation and secondary impingement. Stressing the shoulder at the extremes of motion can also provide clues to disease in the shoulder.

Figure 21-L-15 Increased external rotation in the right dominant shoulder.

Ranges of motion that should be documented in degrees are active and passive elevation in the scapular plane, active and passive external rotation with the arm at the side, and internal rotation in which the hitchhiking thumb (or index finger) reaches in reference to the posterior vertebral anatomy ( Figs. 21L-16 , 21L-17 , and 21L-18 ). It is also important, especially in athletes, to document external rotation (particularly passively in the 90-degree abducted position in the coronal plane). This position represents a more functional measure of external rotation ( Fig. 21L-19 ).[80]

Figure 21-L-16 Elevation in the scapular plane.

Figure 21-L-17 External rotation, neutral position.

Figure 21-L-18 Internal rotation.

Figure 21-L-19 External rotation in the 90-degree abducted position.

Strength testing is considered, along with range of motion. Although it is part of the neurologic examination, assessment of strength is particularly important in athletes with rotator cuff disease. Objective weakness beyond that considered due to pain or a neurologic deficit is a very specific sign of rotator cuff deficiency. The remainder of the neurologic examination will help to rule out disease such as a cervical root, brachial plexus, or a peripheral nerve lesion. The assessment of shoulder stability is very important because rotator cuff signs and

symptoms are often a secondary manifestation of an underlying problem in stability. It has been suggested in high-profile throwing athletes that shoulder pain is due to instability related to anterior subluxation with secondary impingement until proven otherwise. Stability is assessed by translating the humeral head in the glenoid fossa anteriorly, posteriorly, and inferiorly (the load-and-shift and sulcus tests, respectively) with the arm in varying degrees of abduction and rotation ( Figs. 21L-20 and 21L-21 ).[80] The presence of an anterior apprehension sign is also important, which can be positive either for anterior instability or for pain from internal impingement.

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This is performed by passively placing the arm in increasing degrees of abduction and external rotation.[55] [56] [85] The relocation test (Fowler's sign or Jobe's relocation test) is a variation of the apprehension sign ( Fig. 21L-22 ). The arm is placed in the abducted/externally rotated position until pain or apprehension is elicited. The maneuver is then repeated with the arm supported in a posterior direction. Relief of pain or apprehension with improved external rotation is indicative of internal impingement or anterior subluxation, respectively ( Fig. 21L-23 ).

Figure 21-L-20 The load and shift test.

Figure 21-L-21 The sulcus sign.

Figure 21-L-22 Anterior apprehension testing.

Figure 21-L-23 The relocation test, or Fowler's sign.

Examination of the regional vascular supply is necessary as a baseline and also for consideration of conditions such as thoracic outlet syndrome. Finally, a number of special tests should be considered. The signs of impingement are characteristic of rotator cuff tendinitis and tears. These include a painful arc of abduction between 60 and 120 degrees, pain on forced forward flexion in which the greater tuberosity is forced against the anterior acromion (Neer's sign), and pain on forcible internal rotation of the 90-degree forward flexed arm (Hawkins' sign or the impingement reinforcement test) ( Figs. 21L-24 and 21L-25 ). [106] [138] The latter maneuver causes impingement against the coracoacromial ligament. Biceps tendon involvement is demonstrated by Speed's test, in which pain is reproduced on resisted forward elevation

of the humerus against an extended elbow ( Fig. 21L-26 ). Yergason's test is performed with the elbow flexed to 90 degrees and the forearm pronated.[216] The examiner grasps the wrist and resists active supination by the patient. Pain in the area of the bicipital groove suggests disease in the long head of the biceps ( see Fig. 21L-14 ). The active compression test (O'Brien's test, with resisted elevation and the arm at 90 degrees of forward flexion and 10 to 15 degrees of adduction) may also be positive with disease of the long head of the biceps without a superior labral-anterior posterior (SLAP) lesion.[152]

Figure 21-L-24 Impingement sign: forced forward flexion.

Figure 21-L-25 Impingement sign: abduction internal rotation.

Figure 21-L-26 Speed's test.

Biceps tendon instability (medial subluxation or dislocation) can be determined by passively abducting the shoulder to 80 to 90 degrees and eliciting a palpable snap in the region of the bicipital groove with internal and external rotation.[92] [93] [164] [171] [175] This is a rare presentation as an isolated entity, and it usually indicates a lesion to the superior fibers of the subscapularis tendon, or the SGHL.

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The history and physical examination will lead to an appropriate diagnosis. As was previously stated, in athletes, the main differential diagnosis is between instability and primary rotator cuff disease. Shoulder pain in the athlete can create a vicious cycle, with an overlap between shoulder instability or laxity and rotator cuff and biceps tendinitis or impingement. Whether or not instability causes tendinitis or tendinitis causes instability remains unclear ( Fig. 21L-27 ).

Figure 21-L-27 Causes of tendinitis. Diagnostic Studies

The use of diagnostic studies to evaluate the athlete with a rotator cuff or proximal biceps tendon problem aids in the confirmation of the clinical findings. These studies are also important in ruling out other pathologic entities.

The Impingement Test

This test, as described by Neer, involves injection of local anesthetic into the subacromial region after a positive Neer's sign ( Fig. 21L-28A ).[137] [138] [139] The injection is performed under sterile conditions with insertion of the needle anteriorly, laterally, or posteriorly into the subacromial space ( see Fig. 21L-28B ). Impingement signs should be sought, as was previously described. Subjective relief of pain and diminution of the previously present painful signs demonstrated that impingement may be a component of the problem. Nevertheless, it should be emphasized that this is a nonspecific test and can be misleading, in that it may be positive in patients with either primary impingement or secondary impingement due to instability.[27] [214]

Figure 21-L-28 A, Impingement test showing needle in subacromial region. B, Impingement test, lateral approach.

Although not strictly an impingement test, injection of local anesthetic into the acromioclavicular joint or into the bicipital groove can provide additional information about

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the source of the pain. Subacromial anesthetic can mask or minimize the symptoms from these two areas. The clinical examination is critical in guiding the selection and the sequence of injection sites. Radiographic Studies

Plain Radiographs.

Plain radiographs of the normal athlete with a rotator cuff complaint are most often normal.[40] These should include an anteroposterior (AP) film at right angles to the scapular plane, a lateral film in the scapular plane with the beam tilted 10 degrees to evaluate acromial shape and slope, and an axillary view ( Fig. 21L-29 ). The characteristic changes of advanced rotator cuff disease include sclerosis and cystic changes in the greater tuberosity, osteophyte formation on the acromion, a more prominent notch between the greater tuberosity and the articular surface, changes in the shape of the acromion, and, in the presence of a cuff tear, sometimes a narrowed acromiohumeral distance (less than 6 mm). There may

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be osteophyte formation on the inferior surface of the acromioclavicular joint as part of chronic rotator cuff disease. One value of these films is in ruling out other conditions that may present with shoulder pain such as glenohumeral arthritis and calcific tendonitis, which would not be considered primary problems in the athlete.

Figure 21-L-29 Supraspinatus, outlet view.

Plain radiographs can also be used to evaluate the bicipital groove. A shallow groove may indicate a very rare biceps tendon instability problem. Osteophytes around the groove may be implicated in pathologic degenerative conditions of the biceps. Arthrography.

Single- or double-contrast arthrography was considered the gold standard for determining the presence of a full-thickness rotator cuff tear before the advent of magnetic resonance imaging ( Fig. 21L-30 ).[24] [180] Arthrography is now most commonly used in combination with other imaging modalities (such as computed tomography or magnetic resonance imaging) to increase conspicuity for subtle lesions of the cuff and glenohumeral joint.

Figure 21-L-30 Single-contrast arthrogram showing contrast in the subacromial bursa. Rotator cuff tear.

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Ultrasonography.

Diagnostic ultrasound is a noninvasive form of examination of the rotator cuff.[1] [192] [196] It allows comparison with the other side and can provide a great amount of anatomic detail ( Fig. 21L-31 ). It has a reported 91% sensitivity and specificity, with a 100% positive predictive value when it shows nonvisualization or focal thinning. It has also been reported to be very useful in diagnosing bicipital disease and is helpful in patients who have previously undergone a rotator cuff repair. However, the results are related to the operator's experience, and the technique has inherent limitations because of the surrounding bony anatomy.

Figure 21-L-31 Normal supraspinatus, ultrasound. The tendon lies between the cortical surface of the humerus (white arrowheads) and the linear echogenic interface with subacromial fat, bursa, and tendon (long arrow). There is a small irregular focus of increased echogenicity within the tendon (short arrow).

Magnetic Resonance Imaging.

Magnetic resonance imaging (MRI) has become the gold standard for the investigation of rotator cuff disease, with sensitivities and specificities exceeding 90% in most current series ( Fig. 21L-32 ).[180] [192] [201] [219] MRI can demonstrate the size, location, and characteristics of the cuff diseasewhether full-thickness, partial-thickness, or intratendinous ( Fig. 21L-33 ). Cost and reimbursement, which used to be important issues, appear to be resolving problems in the current orthopaedic environment. The main drawback of MRI usage is an occasional instance of patient intolerance because of the required lack of movement during the procedure and because of claustrophobia (which has been addressed by the advent of open scanners). The addition of intra-articular or intravenous gadolinium to the MRI may increase the conspicuity of the rotator cuff and intra-articular disease, and may be of particular benefit in the identification of partial cuff tears and labral lesions in the athletic population.

Figure 21-L-32 Magnetic resonance imaging showing a normal supraspinatus tendon between the humeral head and acromion.

Figure 21-L-33 Magnetic resonance imaging demonstrating torn rotator cuff (black arrow). Open white arrows show fluid in the subacromial space. Examination Under Anesthesia

Performing an examination under general anesthesia (EUA) allows assessment of translation of the humeral head within the glenoid fossa and an accurate assessment of the passive range of motion of the shoulder. [22] [30] [44] [86] The load-and-shift test can be applied to document translation clinically and to evaluate the relationship of the humeral head to the glenoid rim with anterior, posterior, and inferior stress in differing positions of abduction and rotation ( see Fig. 21L-20 ). In patients with multi-directional instability, the humeral head can frequently be displaced over the glenoid rim both anteriorly and posteriorly. An inferior sulcus sign is an important indicator of multi-directional instability and is documented under anesthesia by determining in centimeters the amount of inferior translation of the superior part of the humeral head away from the undersurface of the acromion ( see Fig. 21L-21 ). More than 2 centimeters of inferior translation suggests excessive inferior laxity. Sometimes a diagnosis of adhesive capsulitis

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(decreased passive motion compared with the normal contralateral side) is not determined until EUA.

Arthroscopy

Arthroscopy can play an important role in the evaluation of a patient with a painful shoulder.* Arthroscopy provides direct visualization of the intra-articular structures. The biceps tendon, the articular surfaces, the status of the labrum and ligamentous structures, and the undersurface of the cuff can be observed. Combined with an examination under anesthesia, the clinical picture, and other investigations, arthroscopy can usually allow a definitive diagnosis to be made. The subacromial space may be less reliably assessed by looking at the cuff on its superficial surface, and débridement of the subacromial bursa may be required for accurate visualization (introducing an operative component to the diagnostic arthroscopy). In the athletic population, the specific lesions to be identified are partial- or full-thickness rotator cuff tears; biceps tendinitis and other disease; SLAP lesions; antero-inferior labral avulsions or damage suggestive of associated instability; and chondral changes, or even a frank Hill-Sachs lesion. It is surprising how often multiple lesions are identified through the arthroscope, and management of each of these lesions requires careful individualized consideration. Challenging situations prompt investigations such as MRI, EUA, and arthroscopy. Sometimes in the overhead-motion athlete with a painful shoulder, the diagnosis of impingement versus instability versus eccentric overload can be confusing. However, the history and physical examination remain the most reliable diagnostic procedures in the majority of situations.

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Treatment Options

In the majority of athletes, treatment of a rotator cuff and biceps tendon problem is nonoperative. Three important items to be considered are (1) the cause of the condition, (2) the sport and level of performance, and (3) the severity of the problem. Causes

Patients with primary outlet or extrinsic impingement fit into Neer's three-stage classification: stage 1, edema and hemorrhage (at any age); stage 2, fibrosis and tendinitis (usually in patients over the age of 25); and stage 3, degeneration, bony changes, and tendon ruptures (usually in patients over the age of 40). [137] [138] [139] [140] Overuse and fatigue of the scapular stabilizers may lead to scapular lag and secondary impingement. Eccentric overload of the cuff tendons leads to fatigue and pain. Long-term repetitive overuse combined with the inherent poor blood supply of the tendon can lead to degeneration and tearing, particularly in older invidivuals. [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86]

Instability may be due to one of two causes. True multi-directional instability can lead to secondary rotator cuff-related pain and disease. Anterior subluxation can lead to secondary impingement with pain. In the overhead-motion athlete, anterior subluxation is a common cause of secondary impingement, especially in patients with tight posterior structures and limited internal rotation.[3] [23] Recent authors have described posterosuperior glenoid or internal impingement in overhead-motion (particularly throwing) athletes.[44] [72] [205] This is a secondary impingement of the articular surface of the cuff under the posterosuperior glenoid rim. Contact between the cuff and the posterosuperior glenoid is physiologic when the arm is maximally abducted and externally rotated. However, repetitive contact in this area (such as in throwers) leads to partial tearing of the supraspinatus and often the

infraspinatus tendons on their articular surface (usually 1 cm posterior to the biceps tendon). Others have illustrated that subtle anterior glenohumeral laxity may exacerbate this internal impingement by allowing the humerus to hyperangulate in the late cocking (maximal abduction/external rotation) phase of throwing. Acute trauma to the cuff secondary to either a dislocation of the glenohumeral joint or direct/indirect damage can also be implicated as a cause.[74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86]

Although the great majority of athletes with these problems can be treated nonoperatively, the surgical management varies dramatically between an athlete with primary *See references

[ 4] [ 5] [ 6] [ 28] [ 29] [ 60] [ 107] [ 160] [ 161] [ 173] [ 180] [ 194] [ 198] [ 199] [ 205]

and [ 211] .

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impingement and one with primary instability and secondary impingement. Sport and Performance

A number of generalizations can be made with respect to the type of sport. A soccer player with a rotator cuff problem will have only minimal if any disability. The baseball pitcher, on the other hand, may be significantly disabled and may be unable to throw at all. The gymnast can avoid the rings and concentrate on vaulting, and a swimmer may be able to change from freestyle to breaststroke. The same consideration should be given to the level of performance. Enforcement of therapeutic rest has dramatically different implications for a weekend tennis player than for a professional quarterback in midseason. Severity

Finally, the severity of the problem, whether measured in terms of the clinical picture or in terms of the underlying disease, has obvious implications with respect to the proposed treatment.

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Types of Treatment

With these principles in mind, we can divide the suggested treatments into three categories: (1) preventive, (2) nonoperative, and (3) operative. Preventive Treatment

First and foremost when dealing with athletes, the sports medicine physician, surgeon, trainer, therapist, or coach should consider prevention of injury and problems.* Prevention is of particular importance in relation to the shoulder, in which the majority of injuries are related to overuse. The countless hours of training and practice are to be condemned if faulty technique or improper methods lead to damage of the rotator cuff or biceps. The underlying principle of prevention is applied common sense. A musculotendinous unit is capable of resisting only as much as it has been prepared to resist. A 50-year-old who plays 2 hours of doubles tennis once per week cannot expect his shoulder to tolerate up to 12 hours over a 2-day weekend tournament. The same argument can be applied to the college or professional level pitcher who arrives in training camp with little or no off-season training. The basis of prevention is preparation.[135] This involves overall body conditioning, flexibility, strengthening, and careful attention to technique, with recognition of the stresses of training and competition. It may appear from the examples given earlier that this is possible in the organized sporting situation but unrealistic for the weekend tennis player. Prevention in the latter circumstance refers to avoidance of re-injury and minimization of the current problem, as well as to sport-related education. It has been recommended that the Little League pitcher develop the fastball as his primary pitch.[186] From there, the emphasis should be on improving velocity while maintaining consistent mechanics and control before developing the full repertoire of pitches. The off-season is the key to an athlete's development, with a general fitness and weight-training/flexibility program being essential. It is during this time that the

specific adaptation to imposed demand (SAID) principle is applied to training. For a pitcher, this involves alternating between long-toss and short-toss throwing at half speed, with enforced rest at least 2 days per week. During the season, the same principle applies, with a proportionate increase in the frequency and duration of training. The warm-up is also of critical importance.[135] A satisfactory warm-up leads to increases in tissue temperature with improved oxygen uptake and nerve impulse transmission, and increased activity of metabolic enzymes. The influence of shoulder flexibility has been demonstrated in swimmers.[166] [167] [168] Published reports have demonstrated a clear correlation between anterior shoulder inflexibility and shoulder pain. It follows that stretching is an important preventive measure. The particular goal in stretching is to try to maintain internal rotation and adduction ( Fig. 21L-34 ). It is not necessarily the intention to normalize internal rotation compared with the opposite side. The intention is to avoid posterior capsular contractures and maladaptive loss of internal rotation and adduction. Stretching is equally important in older athletes, in whom the potential for stiffness is greater.

Figure 21-L-34 Internal rotation and adduction stretching.

A well-balanced strong shoulder musculature is critically important in the prevention of overuse injuries.[74] [75] [76] [77] [78] [79] [80] [135] The rotator cuff can be strengthened with the use of many *See references

[ 34] [ 43] [ 59] [ 62] [ 67] [ 71] [ 88] [ 90] [ 94] [ 105] [ 108] [ 116] [ 117] [ 135] [ 136] [ 150] [ 158] [ 176]

and [ 179] .

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aids, such as free weights, Thera-Bands, or surgical tubing. Isokinetic machines are also recommended. It is evident that any strengthening program must be well controlled, particularly in the young athlete. In addition, the use of some isokinetic equipment does not allow eccentric muscle contraction. This may be of considerable importance, given our understanding of the pathophysiology of rotator cuff lesions, which involves eccentric overload. A preventive strengthening program for shoulder problems in athletes is critical, and the emphasis should be placed on eccentric exercises.[74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] These can be easily performed by the athlete on a daily basis with some form of resisted Thera-Band or rubber tubing. The exercises consist of: 1. Resisted external rotation exercises with the arm at the side and also in the 90-degree abducted position ( Fig. 21L-35 ) 2. Resisted internal rotation exercises ( Fig. 21L-36 ) 3. Push-ups with the arm adducted for scapular rotator control ( Fig. 21L-37 ) 4. Sitting rows for serratus and rhomboid scapular control

5. Shrugs for trapezius strengthening 6. Latissimus pull-downs for latissimus control, important in the deceleration phase of overhead motion and change 7. Supraspinatus strengthening exercises: Resisted abduction in the scapular plane with internal rotation ( Fig. 21L-38 )

Figure 21-L-35 Resisted external rotation.

Figure 21-L-36 Resisted internal rotation.

Figure 21-L-37 Inside push-ups.

Figure 21-L-38 Supraspinatus strengthening.

Finally, it is incumbent upon the coaches to teach the correct technique, avoid overtraining, allow for rest periods, and (ideally) recognize the fatigued athlete who is heading for a painful shoulder problem. Nonoperative Treatment

Overall, nonoperative treatment is really an extension of preventive management with the addition of specific measures dealing with the injury.[74] [76] It can be divided into four components: (1) modification of activity, (2) local or systemic measures to reduce and relieve the symptoms, (3) stretching and strengthening exercises, and (4) re-evaluation and maintenance treatment. Modification of Activity

In the athlete with mild symptoms, modification of activity means reducing the frequency and duration of the specific activity. It also involves activity substitution, or what is sometimes called active rest. For a tennis player, avoiding the service action but still hitting groundstrokes may be all that is required. For a baseball pitcher, it would be helpful to cut back on the daily number of pitches and to slow velocity. A swimmer should decrease yardage or use the kickboard. Other methods of treatment involve specific changes in technique, such as throwing side-arm

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for a pitcher, or using a higher arm entry for a freestyle swimmer. Changing equipment may also be of benefit. Over time, these patients usually improve, but return to sport is a longer term goal and more involved treatment may be necessary. Local and Systemic Methods to Relieve Symptoms

Although the athlete who experiences pain with activity that is not disabling may be able to manage with various methods of modified activity, most patients have a more involved problem and require more complicated therapies. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is ubiquitous. There is no question that they provide symptomatic relief. However, we are dealing with injury and, whether acute or due to overuse, the inflammatory response to this injury is a normal part of the healing mechanism. There is also evidence that in chronic overuse-type injuries, the surgical pathologic tissue is non-inflammatory. The value of these medications lies in the initial treatment given to decrease pain and to allow rehabilitation. Ice treatment is also a recognized local treatment modality with its action of reducing vascularity, numbing the pain, and possibly reducing swelling and inflammation. Ice is particularly useful after an acute episode or injury. It is commonly advocated after overuse activity to minimize the pain and lessen the immediate inflammatory response after activity. Therapeutic ultrasound may be helpful in the treatment of rotator cuff and biceps tendinopathies. It is believed to increase the local vascular response to injured tissue. This in turn allows the release of the products of injury and the influx of the raw materials needed for repair. Other modalities include high-voltage electrical stimulation, transcutaneous nerve stimulation, electromagnetic field therapy, and the use of lasers. The specific benefits of some of these modalities are not clear, yet many patients seem to gain relief with few side effects. The use of local corticosteroid injections is a more invasive form of therapy. The deleterious effects of steroid injections have been documented. Critical analysis of the literature cannot lead to the conclusion that they are of any long-term benefit. Their use is still advocated, however, and they may be of value in a patient with an acutely painful lesion to halt the vicious circle of pain related to overuse. This would then allow earlier institution of corrective rehabilitation. Stretching

Stretching exercises are not only therapeutic but are quite clearly preventive and provide the basis for maintenance treatment. [74] [135] The warm-up, including stretching, not only helps the athlete improve timing and control but also allows the muscles to function efficiently. Stretching increases muscle blood supply and improves contractility. Lack of flexibility has been associated with a higher incidence of shoulder problems in swimmers. An increased range of external rotation compared with internal rotation is also associated, especially in throwers. These factors in the athlete with a painful

shoulder require specific attention to the treatment regimen. Stretching should be generalized but should focus on internal rotation and adduction across the chest and internal rotation and extension behind the back ( see Figs. 21L-18 and 21L-34 ). These exercises should be performed before activity, in addition to the usual routine. Strengthening

Strengthening is the mainstay of treatment for the majority of athletes with rotator cuff or biceps tendon problems.[3] [12] [15] [19] [74] [98] Whether the problem is due to an acute direct injury or to eccentric overload, the athlete is left with a compromised, weakened musculotendinous unit. This unit is usually contracted either primarily as a result of muscular imbalance or secondarily owing to the injury mechanism. A complete tear or disruption of the tendons will obviously need to heal or be approximated through surgery before active use, but this is an uncommon circumstance among the young athletic population. Strengthening should emphasize the external rotators ( see Fig. 21L-35 ).[74] The use of rubber tubing is simple and effective for both prophylaxis and treatment. Initially, the exercises need to be performed with the arm at the side until the pain has been relieved. When pain is present, it is important to avoid the 90-degree abducted position with resisted rotational strengthening. The arm can be brought into the abducted position gradually, initially to 45 degrees

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until the pain has completely disappeared, and then to the functional range. Most recreational and nonthrowing athletes do not require strengthening at 90 degrees of abduction. The associated musculature, particularly the scapular stabilizers, should also be considered. These muscles, when overused, fatigued, or overstretched, may develop scapular lag and secondary impingement. This can be treated with exercises such as shoulder shrugging, both upward and backward, and push-ups (arms adducted) ( see Fig. 21L-37 ). In addition to the specific components of shoulder strengthening, it is important to understand that the shoulder cannot be viewed in isolation. Equal concern should be paid to the associated joints and muscles to ensure that appropriate body mechanics are used in the rehabilitation of the athlete. Re-evaluation and Maintenance

It is during re-evaluation that the treatment phase blends into that of prevention of further injury. Throughout the process of treatment, the athlete, coach, trainer, and (if applicable) parent should be part of an educational program. This involves education

about the clinical problem, its course, and its ultimate prognosis. Most athletes are willing to perform a daily routine of exercises if it means participating in the sports they love. Unfortunately, compliance with this routine is more likely to occur following, rather than preceding, an injury. Operative Treatment

It cannot be restated enough that the surgical management of athletes with rotator cuff or biceps tendon disease should be emphasized less than nonoperative treatment. The great majority of athletes will recover, modify their activities, or even give up their sport before undergoing surgery. The maturing athlete may have not only acute and overuse injuries but also the added concern of degenerative tendon disease, which involves a far greater incidence of rotator cuff and biceps tears. These athletes have the same symptoms as any individual of a similar age with rotator cuff disease, but usually they have greater demands and expectations. Greater understanding of the pathophysiology of shoulder pain has led to the realization that sometimes stabilization procedures rather than surgery are required to deal with primary cuff or biceps disorders. Surgical management involves open or arthroscopic procedures. * Historically, the procedures designed to correct these problems involved various forms of cuff repair and biceps tenodeses and used a variety of approaches, including acromionectomy. Even a paraglenoid osteotomy was devised to deal with subacromial bursitis and supraspinatus tendinitis. Today, only three procedures are really used in the athletic population: subacromial decompression (and its variants such as débridement), rotator cuff repair, and biceps tenodesis. Open Techniques

Neer was the first to describe anterior acromioplasty based on the fact that extrinsic impingement occurred under the anterior third of the acromion. [137] His initial patient population was nonathletic and included a heterogeneous group of patients with and without cuff tears, with satisfactory results in 80%. Neer's method of anterior acromioplasty has been modified by others to avoid detachment of the deltoid, to include distal clavicle excision, or to release only the CA ligament.[74] The other main open procedure is that of rotator cuff repair. Usually this involves an anterior acromioplasty (though this remains controversial) with both direct side-to-side (McLaughlin or margin convergence technique) and tendon-to-bone repair.[74] [75] [119] Many other techniques have been advocated in dealing with an athletic population, including arthroscopic procedures. However, restoration of normal anatomy is the obvious goal. Many factors relating to sport, level of activity, and arm dominance influence results. [90] The demands are different for athletes versus nonathletes and throwers versus non-throwers. Surgery for cuff tendinitis produces different results in a soccer player than in a pitcher.

The use of CA ligament resection has been successful in 95% of a series of patents who had failed to benefit from nonoperative management for impingement syndrome secondary to CA ligament entrapment.[103] The use of this procedure, which has a 70% success rate in athletes, has been advocated as an alternative to the more surgically invasive anterior acromioplasty. [94] Comparison of these two procedures in a group of athletes showed similar results.[162] Of the patients with CA ligament resections, 13 of 17 returned to full activity with no further symptoms at an average follow-up of 3.5 years. These series did not clearly define the level of activity or throwing capability postoperatively. In a report of open anterior acromioplasty in athletes, 89% reported improvement subjectively, but only 43% showed good functional results. Of the athletes classified as primarily pitchers and throwers, the results are even less satisfactory, with only 22% achieving a good functional result.[199] It is very difficult to compare these results. Patient selection is critical to the outcome in this type of operation, and there are no adequate control series. For athletes with rotator cuff tears, the decision to operate is easier in those with a complete cuff lesion but is not so clear with partial-thickness tears. In a series of 45 patients who underwent rotator cuff repair for both full-thickness and partial-thickness tears, 39 (87%) were satisfied and experienced subjective pain relief.[200] Analysis based on sports participation showed that among pitching and throwing athletes performing at the college or professional level, only 32% had a good result. The results of surgery in similar athletes with complete cuff tears were slightly better, with 5 of 9 experiencing good results. Most authors recommend early surgical repair for full-thickness cuff tears that are symptomatic.[11] [38] [45] [46] [54] [74] However, many older athletes can manage by modifying their functional demands, provided the pain has resolved. In an athlete with higher demands, a prediction of full return to the pre-morbid level of play is not possible based on a current review of the literature. This caution applies *See references and [ 218] .

[ 2] [ 3] [ 4] [ 6] [ 28] [ 49] [ 50] [ 51] [ 60] [ 61] [ 62] [ 63] [ 75] [ 90] [ 112] [ 161] [ 194] [ 198] [ 199] [ 200] [ 208] [ 209] [ 210] [ 211] [ 213] [ 215]

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both to decompression of the cuff, regardless of the method used, and to rotator cuff repair. A symptomatic full-thickness tear without surgery yields predictably poor results, and a large tear (greater than 3 cm) has a poor functional recovery, even with surgery.[46] [51] [67] [68] [90] Surgery related to biceps tendon disease is even less clearly delineated in the literature.[138] [142] [143] [144] [145] [210] It is usually assumed that the biceps is involved along with the rotator cuff, based on similar pathophysiology, mechanisms of injury, and repair. It therefore follows that the treatment involves decompression of the

coracoacromial arch. Again, it is very difficult to ascertain the results of surgical management, but success similar to that achieved with rotator cuff repair has been reported. With respect to subluxation or dislocation of the biceps tendon from the bicipital groove, the treatment is relatively straightforward, with tenodesis being the recommended approach in the athletic populace.[153] [171] One series reported that 77% of athletes resumed their sport and could throw satisfactorily after tenodesis. In another report, excellent results were cited; however, no specifics were documented about either the patient population or the actual results. It should be remembered that primary biceps instability in athletes is an extremely rare entity. Arthroscopic Techniques

Arthroscopic evaluation is now the standard-of-care for athletes with rotator cuff and impingement lesions.* Diagnostic arthroscopy allows confirmation of the diagnosis. The intra-articular structures are visualized, and evidence of articular damage or instability is documented. SLAP lesions with undersurface cuff degeneration may be a manifestation of overuse associated with instability. The undersurface of the cuff is carefully examined. Partial-thickness tears can be examined and evaluated. Snyder and Ellman[50] [194] have both proposed classifications for the arthroscopic evaluation of rotator cuff tears. A spinal needle or a marker suture can be placed through the articular surface partial tear for later bursal surface identification and evaluation. Most authors currently recommend débridement and sub-acromial decompression if the partial tear involves less than 50% of the cuff ( Fig. 21L-39 ).[28] [60] [116] [211] If the tear involves more than 50% of the cuff, repair and decompression are indicated. Recent work has demonstrated that partial tears may significantly predispose to the development of a full-thickness tear.[57] Hence, some have advocated repair for all partial-thickness tears, though this clearly remains controversial, especially in the athletic population.

Figure 21-L-39 Arthroscopic subacromial decompression with removal of anterior acromion and coracoacromial ligament.

Posterosuperior glenoid impingement, or internal impingement, can be evaluated only arthroscopically.[44] [72] [205] Results have been mixed with débridement alone for this lesion. Some have reported improved functional results in the athletic population with the addition of anterior thermal capsulorrhaphy in this population of athletes, with a presumed diagnosis of subtle anterior instability, thus allowing excessive hyperangulation of the humerus and causing the internal impingement. These results, however, have not been reported in the peer-reviewed literature, and such treatment remains controversial until further studies clarify the issue.

The results of subacromial decompression in 24 patients active in sports who had a diagnosis of primary impingement revealed that 87.5% returned to active participation.[8] The overall success rate in another heterogeneous series (including both sport- and non-sport-related causes) was 88%.[49] The complications of arthroscopic procedures are relatively few in all reported series.[183] The arthroscope has also allowed the identification and treatment of lesions in the intra-articular portion of the biceps tendon.[5] Biceps tenosynovitis is often located in the intertubercular groove portion, and can be visualized and débrided arthroscopically. Partial tears of the biceps can be débrided, and if more than 25% to 50% of the tendon is disrupted, a tenodesis can be performed. Recently, arthroscopic biceps tenodesis has been described in a mixed population of patients, with successful early results (Boileau and Krishnan, personal communication). SLAP lesions, which are discussed elsewhere, can be appropriately treated arthroscopically. Evaluation of the anterior-inferior labrum can identify labral disease responsible for anterior subluxation and secondary cuff disease and impingement. Anterior stabilization procedures can be performed arthroscopically or as open procedures to prevent the secondary impingement occurring in this situation.

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Postoperative Management and Rehabilitation

The postoperative routine follows principles similar to those governing nonoperative management of cuff and biceps tendon disease.[71] [81] [82] [83] [84] With arthroscopic débridement procedures, immobilization in a sling is not necessary, although it is useful simply for comfort until the inevitable swelling has subsided in 24 to 72 hours. Range of motion *See references

[ 4] [ 5] [ 6] [ 28] [ 29] [ 60] [ 107] [ 160] [ 161] [ 173] [ 180] [ 194] [ 198] [ 199] [ 205]

and [ 211] .

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exercises can begin in the recovery room and thereafter can progress as tolerated, with the goal of attaining a full range of motion. Activities of daily living can be resumed as pain relief permits. Strengthening exercises stressing the rotators with the use of rubber tubing are recommended before a return to sporting activities, especially sports involving throwing. It has been recommended that strenuous overhead-motion sports be avoided for at least 4 to 6 weeks following simple débridement, and longer following decompression, until strength has been restored. This recommendation is sport- and activity-related. Throwers usually require much longer than other athletes. With reconstructive procedures and repair of the cuff, two separate issues determine the postoperative course of management: (1) the status of the deltoid, and (2) whether or not a rotator cuff repair was performed, as well as the quality of the repair. Postoperative management involves the same considerations in the athlete as in any other individual undergoing these procedures. The main difference relates to the timing and intensity of the postoperative regimen. In the high-performance athlete, there is a great deal of pressure to get back to the playing field. There are also considerably

higher expectations with regard to ultimate function. The available literature offers little reason to hope for a full functional recovery, regardless of the type of rotator cuff surgery performed.[83] [90] [199] [200] In spite of this, there is a consistent and predictable response in terms of pain relief. This dual result leads to the dilemma of wanting to push the rehabilitation as quickly as possible for the sake of improving performance while realizing that repair of tissues after the surgical insult takes time. Most surgeons advocate a sling postoperatively, with initial rehabilitation involving passive range of motion and pendulum exercises for 6 weeks. [74] This stage is followed by active motion. Once a full range of motion has returned, strengthening and stretching are advocated. It is recommended that athletes not return to sport until 6 months after the operation (12 months for pitchers). The use of abduction splints has been advocated for patients undergoing cuff repair surgery, especially for large cuff defects. The use of isokinetic machines in the postoperative period has become very popular, but there are few published guidelines on how to use these devices. It has been shown that strength measured objectively by an isokinetic device improves during the first year following cuff repair. At 1 year, the ultimate strength attained is still less than that on the contralateral normal side. Overall, there is little evidence to provide clear recommendations for rehabilitation of an athlete following these surgical options. The most important guideline for postoperative management is to use techniques similar to those used in the nonoperative management of these problems. The bottom line is the need to appreciate the functional demands of the athlete's sport and to ensure that he or she is prepared during the postoperative period to withstand the severe stresses anticipated by return to the sport.

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Criteria for Return to Sports Participation

The literature provides few recommendations regarding specific criteria governing return to sports participation after either surgery or nonoperative rehabilitation. [98] Determining factors must be individualized for each patient, based on the level of participation anticipated, the particular sport, and the specific activity requirement. For example, in a high-profile pitcher following surgical treatment, 1 year has been suggested as the time needed for full return to function. Many guidelines can be used. The first is pain. To return to sports activity, pain must be relieved sufficiently to allow normal biomechanical function. The range of motion should be within normal limits for that athlete, given the specific sport. Strength also needs to be near normal. Endurance is an important component of strength and should be assessed. This, however, is particularly difficult because there is no accurate way to determine an athlete's endurance. It follows that careful control of return to activity is required. Gradually increasing the intensity and duration of training is the only way to ensure adequate endurance. Finally, performance of the sport must be considered. This can be viewed from two points: (1) physical performance, such as pitch velocity or previous swimming event times, and (2) mental performance. A high-performance athlete requires a high degree of motivation and confidence before he or she is able to return to his or her previous level of competition. It must be clear that these considerations also apply to the weekend tennis player with his sore shoulder. The recreational athlete can often return to sports activity earlier because he has lower demands and expectations and need not necessarily perform at 100% capability. The major difference is that the physician has less ability to control the circumstances of return to sport in such people. It is here that the principle of applied common sense overrides any specific criteria. The return to sport is always based on the relative severity of the original problem, and there is no way of speeding up the process of recovery. It is imperative that careful

control be maintained to avoid re-injury and to determine the optimum time for full return.

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Authors' Preferred Method of Treatment [74] [75] [76]

[77] [78] [79] [80] [81] [82] [83] [84] [85] [86]

First and most important in the management of any athlete with a rotator cuff, impingement, or biceps problem, is establishing the correct diagnosis. We place strong emphasis on a careful history, thorough physical examination, plain radiographs, and the judicious use of diagnostic injections. Further investigation (usually in the form of an MRI) is reserved for athletes with an atypical presentation, those who are older, those with a significant traumatic episode, and those in whom a lesion requiring surgery is suspected. The diagnosis and treatment of the rotator cuff or biceps injury are based on the cause: 1. 2. 3. 4. 5. 6.

Acute trauma Primary impingement Instability and secondary impingement Internal impingement Overuse: (a) scapular lag with secondary impingement, or (b) eccentric overload Combined etiology

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The type of management used follows from this etiologic classification. It should be emphasized that the focus of treatment is nonoperative in the great majority of individuals. It is estimated that within a busy tertiary subspecialty shoulder practice, less than 20% of athletes with these problems require surgery. Acute Trauma

Patients with acute traumatic episodes resulting in a strain of these musculotendinous

units require rest until the symptoms have subsided, and then a rehabilitation program involving a gradually increasing regimen of stretching an strengthening. Immobilization should be avoided, and anti-inflammatory agents are sometimes helpful in this situation. The prognosis is good, and an early return to sport is possible depending on the severity of the injury. In an older individual (older than 40 years of age), acute trauma could suggest a disruption of the rotator cuff. This should be treated with temporary rest to allow sufficient healing to take place, followed by range of motion and strengthening exercises. Persistent pain or weakness requires further investigation. Surgical repair should be considered early (within 2 months) to minimize the chronic effects of such an injury. Primary Impingement

Patients with primary impingement more commonly present at an older age. This diagnosis implies an anatomic narrowing of the subacromial space. We advocate surgical decompression at an earlier date than in someone with secondary impingement following failure of nonoperative management. Instability and Secondary Impingement

Patients with associated instability are treated nonoperatively, especially if multi-directional instability is diagnosed. The emphasis is on strengthening the cuff after symptoms have subsided. Following failure of a prolonged nonoperative program, surgical management involves stabilization (arthroscopic or open). Anterior subluxation causing secondary impingement and pain can produce both a diagnostic and a therapeutic challenge. In such cases, prolonged nonoperative measures are appropriate. If surgery is considered, the choice between anterior stabilization (arthroscopic or open), subacromial decompression, or a combined procedure remains unclear. We use our EUA and arthroscopic evaluation to determine the most appropriate course of action, and usually perform all technical procedures (both stabilization and decompression) arthroscopically. Internal Impingement

Patients with internal impingement are similarly treated nonoperatively, with restriction of the extreme abduction/external rotation position until symptoms resolve. A program emphasizing deltoid, rotator cuff, and scapular stabilizer exercises is begun, with a gradual return to throwing. Intra-articular cortisone injections are employed on a selected basis to reduce pain in the early stages. Caution should be exercised in the management of these athletes, as this can be a very difficult entity to treat. Surgical management is indicated with refractory symptoms and an adequate trial of rehabilitation. Again, the EUA and arthroscopic evaluation will aid in identifying and treating any subtle but disease-associated anterior laxity. Overuse Problems

Overuse problems should be treated extensively with nonoperative methods. Surgery is recommended in chronic situations in which nonoperative management has failed, or when the problem has progressed to the point of a cuff tear. Combined Causes

It must be appreciated that in athletes, combined causes and underlying disease often run hand-in-hand. It is in such cases that treatment is very difficult. A nonoperative approach is prudent until the specific components can be determined, and the treatment is modified accordingly.

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Authors' Preferred Method of Nonoperative Management

Nonoperative treatment, regardless of the level of performance, follows the same generic plan: 1. 2. 3. 4. 5. 6.

Activity modification Medications Stretching Strengthening Ice Physiotherapy

Usually a period of rest is advised, with specific avoidance of the overhead-motion sporting activity involved. It should be emphasized that this is an active form of rest. This means that although the specific activity causing the symptoms is avoided, substitute activities are used (e.g., practicing groundstrokes and avoiding serving and overhead swings in tennis, changing from a butterfly to a breaststroke). This active rest is particularly important in the high-profile athlete who will not accept the prescription of total rest. We then prescribe NSAIDs, initially for a 2- to 4-week period, with the understanding that they can be used on an as-needed basis thereafter. The use of a steroid is reserved for patients not responding to this regimen of anti-inflammatory medications, in addition to the other aspects of the protocol. Subacromial or intra-articular injections of 40 mg of water-soluble steroid combined with 6 to 8 mL of lidocaine and bupivacaine are used as a one-time measure.

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A peritendinous injection at the level of the transverse humeral ligament is used for bicipital tendinitis, with the same amount of steroid and 2 to 4 mL of lidocaine and bupivacaine. The injection is rarely repeated. Occasionally, for severely refractory cases, we use a tapered oral steroid protocol, but this is a rare circumstance. Stretching is used to maintain range of motion and to correct any obvious discrepancies or contractures, in particular posterior capsular tightness ( see Fig. 21L-18 ). Cross-arm adduction and overhead adduction stretching are important in the athlete, particularly one with tight posterior structures. Strengthening is the hallmark of nonoperative management of the adult or adolescent athlete with a biceps or rotator cuff lesion. The use of rubber tubing or simple free weights is the most practical method of strengthening the rotator cuff. The scapular muscles cannot be ignored, however, especially when they are implicated in the cause. Rotator cuff strengthening exercises are performed initially at the side using the rubber tubing. The individual then progresses to 45 degrees of abduction and then to a more functional level above 90 degrees in selected athletes (especially throwers). The supraspinatus muscle is isolated by abducting the arm in the plane of the scapula with the forearm and shoulder internally rotated ( Fig. 21L-40 ). The infraspinatus and teres minor are exercised in external rotation, and the subscapularis in internal rotation ( Fig. 21L-41 ). Biceps function is improved through elbow flexion and forearm supination. Scapular stabilizers are strengthened by resisted scapular elevation, retraction, and protraction. In addition, the inside push-up with hands placed inside the parasagittal plane of the shoulder has been helpful ( see Fig. 21L-37 ). Sitting rows for the serratus and rhomboids, shrugs for the trapezius, and latissimus pull-downs for the latissimus dorsi muscle help control, strengthen, and stabilize the scapula.

Figure 21-L-40 Supraspinatus strengthening with weights.

Figure 21-L-41 External rotation strengthening with weights.

Local ice application after workouts and competition can prove beneficial and is frequently employed, depending on the athlete's level of participation and response. Physiotherapy is instituted with specific modalities such as ultrasound, transcutaneous nerve stimulation, muscle stimulation, and laser therapy, depending on the individual athlete's response to these modalities. We employ these modalities only occasionally in resistant cases. Nonoperative management of the athlete with a rotator cuff or biceps tendon problem initially involves regular visits to the therapist. However, it should be emphasized that long-term benefit will be gained through a regular and almost obsessive home exercise program rather than relying on specific physical therapy modalities or medications. Failure of this regimen over a prolonged period of 6 to 12 months constitutes an

indication for surgery. The treatment of the high-profile athlete may differ in subtle ways from the generic program previously outlined. Included in this group are individuals who may not necessarily be competing at a professional, national, or international level. Nevertheless, they take their sport very seriously and have the same motivation to compete and perform to capacity within their own level. The main differences between their treatment and the generic program concern the intensity and volume of the exercises prescribed. Because these individuals place great demands on their shoulders, the overall management should reflect the stresses involved. Isokinetic machines can be of value, especially those allowing eccentric training of the musculature. Strengthening again is the key to long-term success. Depending on whether the sport involves primarily aerobic or anaerobic shoulder function, strengthening exercises should be low-intensity/high-volume or high-intensity, respectively. The other main difference encountered in treatment of these high-profile athletes is that communication with the coach, team trainer, and parent (if applicable) is essential. Communication creates the best possible environment with all relevant people involved. Specific techniques may need to be changed, equipment modified, and short- and long-term competition goals identified. This approach helps the athlete to focus and maintain a positive attitude during the rehabilitation process.

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Authors' Preferred Method of Surgical Management

The primary indication for surgery is the failure of an adequate nonoperative management program. Inherent in defining failure is the presence of sufficient pain and disability to warrant intervention. In general, this program should be carefully coordinated and the patient followed for a minimum of 1 year before surgery is considered. With an acute traumatic injury, especially in an older

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athlete, the possibility of a full-thickness rotator cuff tear must be entertained. MRI is the gold standard in providing a diagnosis in this situation. If a full-thickness tear of the rotator cuff is present, surgical repair is performed. Another situation in which surgery may be considered earlier is the presence of very obvious primary impingement due to bony overgrowth of the acromion or an abnormally angled acromion, usually in an older athlete. In both of these situations, the pathologic status of the anatomy dictates a surgical solution. Overall, the choice of surgical procedure depends on a number of factors, including the underlying cause and the extent of the abnormality. If a full-thickness tear of the rotator cuff is present, open surgical repair is preferred. The method of repair involves an anterosuperior approach centered between the acromioclavicular (AC) joint medially and the lateral edge of the acromion. The incision is 5 to 7 cm long, with one third superior and two thirds inferior to the anterior tip of the acromion ( Fig. 21L-42 ). The skin and subcutaneous tissues are incised and blunt dissection performed to allow identification of the AC joint, the lateral acromion, and the muscular attachments overlying the acromion. Formal detachment of the deltoid can be performed ( Fig. 21L-43 ); however, we prefer a deltoid-on approach to avoid the potential for

postoperative deltoid dehiscence. The junction between the anterior and middle parts of the deltoid is identified. The aponeurosis of the muscle is then incised over the anterior acromion in line with the deltoid fibers. The deltoid is then elevated medially and laterally off the acromion. This affords adequate access to perform acromioplasty and to repair all rotator cuff tears. The deltoid is then split distally in line with its fibers, taking care to avoid distal extension beyond 5 cm, where the axillary nerve could be in jeopardy ( see Fig. 21L-43 ). [84] A straight retractor is placed under the acromion to protect the underlying cuff. An anterior acromioplasty is then performed. A 2.5-cm osteotome is used, commencing at the anterosuperior edge of the acromion and aiming

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posteriorly to exit the osteotomy at a distance of 1.5 to 2.0 cm. This results in excision of the anterior inferior portion of the acromion and a portion of the coracoacromial ligament ( Fig. 21L-44 ). Any remaining ligament is excised. Bleeding is frequently encountered in this area owing to incising of the acromial branch of the thoracoacromial artery. The bony margins are smoothed down using a burr or rasp, including any prominence of the inferior surface of the acromioclavicular joint. This completes the subacromial decompression. Although impingement is not considered in the pathophysiology of the acute traumatic tear, residual swelling in the cuff tissues and that resulting from the surgical insult will likely cause impingement. Decompression also allows adequate exposure to perform the necessary repair. Visualization of the cuff is improved by removing the bursa, and the entire extent of the cuff can be brought into view by careful manipulation of the arm. The cuff defect is then repaired as dictated by the extent of the lesion, either with a side-to-side repair ( Fig. 21L-45 ) or, more commonly, by securing it to a trough in bone ( Figs. 21L-46 and 21L-47 ). The deltoid is re-approximated very carefully to maintain its normal length of attachment to the acromion. [67]

Figure 21-L-42 Anterosuperior approach to the shoulder.

Figure 21-L-43 Approach through the deltoid with split distally and detachment from anterior acromion.

Figure 21-L-44 Excision of anteroinferior acromion and associated coracoacromial ligament.

Figure 21-L-45 Side-to-side repair of cuff defect.

Figure 21-L-46 Repair of cuff through a trough in bone.

Figure 21-L-47 Combined side-to-side and repair through trough in bone.

Postoperatively, a shoulder immobilizer is used. Passive assisted motion is started immediately.[77] The patient progresses to active motion at approximately 6 weeks, depending on the extent of the tear.[74] [84] Active motion is combined with terminal stretching, and resistive motion is added according to each individual's progress, usually at the 8-week mark.[83] The remaining postoperative regimen includes the components outlined in the nonoperative section. With regard to partial-thickness cuff tears, we currently perform only a débridement of the cuff if the tear involves less than 50% of the tendon. If the tear involves more than 50% of the tendon, we consider excision of the damaged tissue and formal repair to bone. At the same time, we prefer to perform a subacromial space decompression (whether or not the cuff requires repair). If a repair is not necessary, the arthroscopic method of subacromial decompression is employed and has been used for the past few years. For arthroscopic subacromial decompression, insertion is initially made from a posterior portal to perform a diagnostic evaluation of the intra-articular structures. An EUA is also considered an integral part of the procedure. The purpose of the EUA and diagnostic arthroscopy is to rule out alternative or associated disease. In particular, instability can be diagnosed by evidence of increased translation of the humeral head, associated labral disease, or even a Bankart's lesion. Internal impingement is diagnosed based on the pathologic changes of the posterosuperior glenoid labrum and the articular surface of the cuff. The

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biceps tendon and its intertubercular portion are drawn into the joint and evaluated. If the biceps tendon is implicated as a contributing factor, synovitis and partial tearing can be débrided. Operative arthroscopy is performed through an anterior portal in the rotator interval. If the biceps is not implicated, attention is directed to the undersurface of the rotator cuff, and the appearance of the cuff tendons is documented. A partial-thickness cuff tear can be visualized more easily from the joint than from the bursa. We place an absorbable marker suture in the partial tear for later bursal surface identification. The arthroscope is then inserted into the subacromial space to pursue the subacromial decompression ( Fig. 21L-48 ). A lateral portal is established 2 to 3 cm inferior to the lateral edge of the acromion and 1 cm posterior to the anterior border. The appearance of the bursa is irregular, and visualization can be very difficult. Epinephrine (1:1000 ampule to 3 L of irrigation fluid) added to the irrigation fluid will help to minimize the inevitable bleeding during the procedure. Initially, the bursal tissue is removed using a

full-radius resector. The landmarks can then be visualized, along with the bursal surface of the rotator cuff, where the previously placed marker suture can be used to evaluate the extent of the cuff tear. A needle can be used percutaneously to help in identification of the acromioclavicular joint, the anterolateral edge of the acromion, and the coracoacromial ligament. The flattened oval-shaped or spherical burr is then inserted through the lateral portal into the subacromial space ( see Fig. 21L-36 ). The posterior extent of the acromioplasty is measured directly; it should be 1.5 to 2 cm from the anterior border. The depth of the resection can be difficult to determine; however, we suggest that the anterior border be resected until the soft tissue of the deltoid insertion can be seen. The resection is then tapered to the posterior extent, as was previously determined. The medial extent is determined by identification of the acromioclavicular joint. Any prominence of the undersurface of the joint is smoothed off using the same burr. Because the anatomic insertion of the coracoacromial ligament extends to the anterior border and undersurface of the acromion, adequate bony removal usually renders the ligament nonfunctional. It should be débrided further with a full-radius resector to ensure that it does not reconstitute itself. We have found it unnecessary to use cutting cautery for this purpose. However, if significant bleeding is encountered, cautery is used.

Figure 21-L-48 Arthroscopic subacromial decompression.

Postoperatively, passive assisted motion and stretching are started immediately. The patient progresses rapidly to active and resisted motion, as tolerated. The nonoperative routine is then instituted to build strength and regain function. For those athletes with internal impingement, we débride the posterosuperior labral lesion and the corresponding cuff lesion. We use the EUA to determine whether subtle but pathologic differential anterior laxity is present, and perform an anterior stabilization (usually thermal capsulorrhaphy with or without capsulolabral suture fixation), depending on the disease present. It should be emphasized again that this is a very difficult population of patients to diagnose and treat, and the surgeon should be certain of the appropriate treatment before proceeding with any surgical management that might result in postoperative failure to regain external rotation in the throwing athlete. With respect to surgical management, the biceps tendon must be considered separately from the rotator cuff. Acute rupture of the biceps tendon in an athletic individual is more common at the elbow with severe trauma and requires surgical management.[9] Ruptures at the shoulder are usually due to chronic attrition with or without an acute episode, usually in an older athlete.[169] Although this is a relatively common finding, surgery is only rarely required. A surgical tenodesis within the bicipital groove is indicated in an athlete with a specific need for strong elbow flexion and forearm supination. This is a rarity, and we have not performed a tenodesis in an elite-level throwing athlete. When necessary, we currently perform this tenodesis with an arthroscopic technique (Boileau and Krishnan, personal

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communication). A subacromial decompression for concomitant rotator cuff disease will usually benefit a symptomatic bicipital tendinitis, but it is not indicated for the isolated bicipital problem. For symptomatic biceps tenosynovitis and partial tearing (less than 25% of the tendon), we perform a débridement only. SLAP lesions are dealt with appropriately, based on the disease present. For degenerative biceps tendons with greater than 25% tearing, we perform a tenodesis. Usually, this is in conjunction with a rotator cuff repair. Postoperative management is geared toward the procedure, especially if a concomitant rotator cuff repair is performed. A tenodesis will require sufficient healing time before full activity is recommended. We allow immediate active elbow flexion postoperatively but restrict resisted flexion for 6 weeks. With an arthroscopic débridement, we progress our patients as quickly as tolerated using the principles of nonoperative management. Those patients presenting with symptoms and signs of primary instability of their biceps tendon in our experience are extremely rare in the athletic population. If necessary, we would recommend a biceps tenodesis, although we have not ever had to perform this procedure in the athletic population. It has been our experience that despite our best efforts to make a clear diagnosis, some patients have problems actually related to both instability and rotator cuff disease. Under these circumstances, both a decompression procedure and an anterior stabilization procedure have been performed in the same patient arthroscopically. We must emphasize the overlap between instability and rotator cuff and biceps tendon disease. The vicious cycle concept that was outlined earlier attempts to explain this difficulty in diagnosis and the necessity of paying attention to two pathologies. In summary, it is unlikely for elite overhead-motion athletes to gain full functional recovery after an operation for rotator cuff or biceps tendon disease. The real benefit comes from pain relief and, indeed, a secondary improvement in function is likely. However, normality in terms of stressful overhead-motion athletic competition is achieved in the minority. This is not the case with nonoperative management, with which full functional recovery is a reasonable goal. The difference in prognosis is obviously related to the severity, chronicity, and nature of the disease.

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Section M Injuries of the Proximal Humerus 1. INJURIES OF THE PROXIMAL HUMERUS IN ADULTS Dan Guttmann MD Chang-Hyuk Choi MD Frances Cuomo MD Proximal Humerus Fractures

Fractures of the proximal humerus are an uncommon sports injury, [137] [202] [289] representing 4% to 5% of all fractures. [16] [119] They are most common in the early adolescent patient who has open physes and in the older, osteoporotic patient. In the more active young and middle-aged groups, the bony structure of the proximal humerus is less vulnerable to injury than the soft tissue structures about the shoulder. When proximal humeral fractures do occur in the athlete, they are usually the result of high energy or some insidious pathology.[202] [245] [284] Most proximal humerus fractures are minimally displaced and can be treated nonopera tively. In athletes, however, in order to allow rapid return to competitive sport, rigid fixation with anatomic reconstruction is often the goal of treatment. In the significantly displaced fracture, a reproducible classification system is essential to make the correct diagnosis and to choose appropriate treatment options. Minimal internal fixation techniques have proved in recent years to be of great benefit in efforts to maximize results and minimize complications. For severely comminuted fractures and fracture dislocations that compromise the blood supply, the final surgical option most often is primary humeral head replacement. The surgical techniques and designs for prostheses have evolved since first reported by Neer in 1955. In spite of the impressive developments in surgical techniques and

implants, controversies still exist when choosing treatment methods of severely displaced fractures. Also as important is an early and aggressive rehabilitation program designed to prevent residual stiffness and dysfunction, which can compromise treatment of these fractures.[165] [204] Anatomy

The proximal humerus consists of four major bony components: the humeral head, the lesser tuberosity, the greater tuberosity, and the humeral shaft ( Fig. 21M1-1 ). The humeral head is retroverted 30 to 35 degrees and is tilted upward 45 degrees in relation to the humeral shaft. The anatomic neck lies at the junction between the head and the greater and lesser tuberosities, whereas the surgical neck is the area below the tuberosities at the junction with the shaft. The anatomic neck is located between the articular cartilage and the attachment of the rotator cuff, which supplies the primary blood supply to the head.[147] [191] [207] [229] [240] Fractures involving the anatomic neck can disrupt the blood supply to the humeral head and can lead to avascular necrosis ( Fig. 21M1-2 ). The lesser tuberosity provides the insertion for the subscapularis muscle and anterior capsule of the glenohumeral joint. The bicipital or intertubercular groove lies between the greater and lesser tuberosities and can vary considerably in width and depth. The biceps tendon lies within the bicipital groove as it enters the glenohumeral joint and is covered by the transverse humeral ligament. The greater tuberosity is much larger than the lesser and lies posterior and superior on the humeral shaft. Its three facets provide attachment for the supraspinatus, infraspinatus, and teres minor muscles. Closure of the proximal humeral physis leaves an area of dense bone or scar that remains until the sixth or seventh decade. The medullary canal begins distal to the epiphyseal scar, leaving the entire proximal humeral area composed of dense cancellous bone surrounded by a cortical shell. In the older patient, osteoporosis leads to a decrease in density of this cancellous bone.[99]

Figure 21-M1-1 The bony structure of the proximal humerus and its relationship to the scapula. Note the four major portions of the proximal humerus: (1) head, (2) greater tuberosity, (3) lesser tuberosity, and (4) shaft.

Figure 21-M1-2 Vascular supply to the humeral head. The anterior humeral circumflex artery, through the ascending arcuate branch, enters the humerus at the intertubercular groove, providing the major source of proximal humeral vascularity.

The glenoid or socket of the glenohumeral joint is shallow and concave. It has approximately one third the surface area of the humeral head. Superior to the humeral head lies the acromion. It is a broad, thin shelf of bone extending laterally from the spine of the scapula. The acromion provides a superior origin for the deltoid muscle and a protective bony cover for the glenohumeral joint. Together with the coracoacromial ligament and coracoid, it forms the coracoacromial arch, under which the proximal humerus, rotator cuff, and subacromial bursa pass when the arm is abducted and elevated. Residual displacement in fractures of the proximal humerus can result in

impingement underneath this arch. The subacromial bursa is a large synovial-lined structure that lies between the proximal humerus

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and the undersurface of the coracoacromial arch and the deltoid muscle. Adherent scar within this bursa after fracture can cause limitation of motion by reducing the normal ability of the bursa to reduce friction, therefore preventing the gliding mechanism. [47] The displacement of tuberosity fragments and shaft is dependent upon the direction of pull of muscle fibers attached to the tuberosities and the proximal shaft. The subscapularis muscle attaches to the lesser tuberosity and functions as a strong internal rotator of the humerus. The supraspinatus, infraspinatus, and teres minor tendons attach to the greater tuberosity and function in abduction and external rotation. [118] In fractures involving the greater tuberosity, the pull of the supraspinatus, infraspinatus, and teres minor can displace the greater tuberosity fragment both posteriorly and superiorly.[34] Similarly, fractures of the lesser tuberosity will be displaced by the attached subscapularis muscle anteriorly and medially. The long head of the biceps sends its tendon through the intertubercular groove, which lies between the greater and lesser tuberosities, to enter the glenohumeral joint and attach to the superior pole of the glenoid.[118] The long head of the biceps tendon can act as a tether in closed reduction, although intraoperatively it is a useful landmark in identifying the rotator interval and relative position of the tuberosity fragments. The deltoid muscle originates from the lateral one third of the clavicle, the acromion, and the spine of the scapula. It inserts into the deltoid tuberosity distally approximately halfway down the lateral shaft of the humerus. [118] The deltoid can cause displacement of fractures of the proximal humerus due to the shearing action imparted to the fracture during muscular contraction ( Fig. 21M1-3 ).

Figure 21-M1-3 The muscular attachments and the direction of their pull (arrows) can influence displacement in proximal humeral fractures. These forces must be taken into account when one is attempting to reduce a fracture in this region.

The pectoralis major is a large fan-shaped muscle that originates from the clavicle, upper ribs, and sternocostal area. It inserts on the lower portion of the lateral lip of the bicipital groove distal to the tuberosities. It functions as a strong adductor and internal rotator, and it often displaces the proximal shaft of the humerus medially in fractures of the surgical neck.[118] Blood Supply

The major blood supply to the humeral head is through the intraosseous vessels that

cross the anatomic neck from the metaphysis.[147] Proximal humerus fractures depend upon the presence of an adequate blood supply to ensure union. Laing and Gerber have reported that the anterolateral branch of the anterior humeral circumflex artery provides the main blood supply to the humeral head.[85] [147] At the superolateral aspect of the bicipital groove, it becomes the arcuate artery within the humeral head. The arcuate artery anastomoses with posteromedial branches of the posterior humeral circumflex artery and is responsible for supplying the greater tuberosity ( see Fig. 21M1-2 ). Injury to this main blood supply of the humeral head with significant displacement of fracture fragments may result in avascular necrosis. Nerve Supply

The brachial plexus lies anterior to the scapula, passing below the coracoid to enter the upper arm ( Fig. 21M1-4 ). The axillary nerve arises from the posterior cord and courses first inferiorly along the anterior surface of the subscapularis muscle belly and then below the glenohumeral joint to innervate the deltoid and teres minor. The musculocutaneous nerve arises from the lateral cord, penetrating the coracobrachialis muscle as near as 2 cm distal to the coracoid process.[77] The brachial plexus therefore is tethered in its position anteromedial to the proximal humerus and is vulnerable to injury in displaced fractures. The axillary nerve is the most frequently injured portion of the plexus in proximal humerus fractures.

Figure 21-M1-4 The relationship of the proximal humerus to the brachial plexus and the axillary nerve, along with its prominent branches, is demonstrated.

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The subscapularis muscle arises from the medial two thirds of the costal surface of the scapula and is innervated on its costal surface by the upper and lower subscapular nerves. The supraspinatus muscle arises from the medial two thirds of the bony walls of the supraspinatus fossa of the scapula, and from the dens fascia that covers the muscle. It is innervated from its underside by the suprascapular nerve. This nerve is relatively fixed at its origin from the superior transverse scapular ligament, where a traction injury rarely may occur. The infraspinatus muscle originates from the infraspinatus fossa of the scapula and from the dense overlying infraspinatus fascia. The suprascapular nerve passes through the spinoglenoid notch and under the inferior transverse scapular ligament. Electrophysiologic evidence of nerve injury is found in up to 45% of humeral neck fractures and primary dislocations, most commonly involving the axillary nerve, followed by the suprascapular, radial, and musculocutaneous nerves. Older patients and those with hematomas have more neurologic injuries. Most patients with low-energy injuries recover partially or completely in less than 4 months. In patients with permanent motor loss from brachial plexus injuries, treatment is focused on preservation of hand

function.[54] Biomechanics

The shoulder is the most mobile major joint in the body. The articular surface of the humeral head is two to three times larger than the surface area of the glenoid. The range of motion of the glenohumeral joint is two times that of scapulothoracic motion, and their combined motion approximates 180 degrees of elevation. The humeral neck shaft angle is approximately 45 degrees, and the head is 30 to 40 degrees retroverted relative to the epicondyles at the elbow.[47] The synergy between the stabilizing effect of the rotator cuff and the biceps combined with the power of the deltoid provides normal dynamic shoulder function. The deltoid is the primary motor source for the shoulder but also creates shear stress across the joint. The rotator cuff and biceps provide stability by counterbalancing the humeral head against the deltoid shear. As internal rotation and external rotation components are added, the rotator cuff muscles provide not only humeral head depression but also stability against excessive anterior and posterior translation within the joint. Fractures of the proximal humerus that disrupt this fine anatomic balance can alter the biomechanics of the shoulder and therefore lead to limitation of motion and function. Restoration of this anatomy along with appropriate muscle strength and coordination is necessary to return the shoulder to normal function.[47] [287] Incidence and Causes of Proximal Humeral Fractures

Proximal humeral fractures are more common in females than in males, by a ratio of 2:1.[239] This difference is largely attributable to osteoporosis of the humerus. The injury usually is sustained after a simple fall onto the outstretched limb or onto the shoulder itself. In males, high-energy trauma is more common with a higher incidence of associated dislocations. Sports-related fractures tend to be the result of high-energy impact or avulsion type injuries often associated with dislocations. Classification

The most commonly adopted classification is the four-segment classification described by Neer in 1970.[197] The AO/ASIF system, described in 1990 by Muller and based on the work of Jakob, is much less frequently employed. [126] [194] The Neer classification ( Fig. 21M1-5 ) is based on the concept of four fragments of the proximal humerus as first proposed by Codman in 1934.[39] When any of the four major fragments is displaced greater than 1 cm, or angulated more than 45 degrees, the fracture is considered displaced. The central focus of this fracture classification is the status of the blood supply to the humeral head and the relationship of the humeral head to the displaced parts and glenoid. Neer also emphasized the term fracture-dislocation,

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which is classified according to direction as well as number of fracture fragments. Other special features of the articular involvement are the head-splitting fractures and impression fractures. Because the Neer classification system is a pathoanatomic classification of fracture displacement, difficulties arise evaluating a three-dimensional image with a two-dimensional radiograph. Sidor and Zuckerman reported fair interobserver and intraobserver agreement with the Neer classification.[259] It should be noted that there was a wide range of experience within the observers and predictably, the most experienced reviewer was found to have a much higher reliability. Siebenrock and Gerber assessed the reliability and reproducibility of the AO classification and compared it with the classification by Neer. Results were somewhat better using the AO three-type classification, but once the fractures were further classified according to groups and subgroups, results deteriorated predictably.[260] Despite the reported difficulties of reproducibility, which tend to be radiograph and experience related, the Neer classification is the most widely used classification system because of its simplicity and rationale for surgical management.

Figure 21-M1-5 Neer four-segment classification of displaced fractures. A fragment is considered displaced when greater than 1 cm of displacement or 45 degrees of angulation is present. A fracture-dislocation is present only if the articular segment is no longer in contact with the glenoid. (From Neer CS: Displaced proximal humeral fractures. Part I. Classification and evaluation. J Bone Joint Surg Am 52:1077-1089, 1970.)

Soft tissue pathology associated with fractures of the proximal humerus is important when determining treatment. It is often not well defined by conventional imaging procedures. Schai performed arthroscopic examination in a series of 80 fractures about the shoulder.[248] Significant numbers of labral, capsuloligamentous, and rotator cuff lesions as well as cartilage damage were reported. Arthroscopic assessment in shoulder fractures has recently been found to be a useful tool in better understanding the extent of the injury. It is expected that the role of arthroscopy

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will increase in the treatment of fracture reduction, fixation, and correction of any associated soft tissue injuries. Clinical Evaluation

History and Mechanism of Injury

The patient with a proximal humeral fracture typically describes specific trauma and can often outline the mechanism of injury.[56] [137] [202] [222] [242] Pain, swelling, and inability to

use the shoulder are seen immediately. The most common mechanism of fracture is a fall on an outstretched arm, and it can occur in both contact and noncontact sports. In the older patient with osteoporotic bone, fracture of the proximal humerus may occur without significant trauma. In the younger patient, however, significant high-energy trauma is necessary, and the resultant fracture is often more serious. These younger patients commonly have displaced fractures or fracture-dislocations with substantial soft tissue disruption. Neurologic or vascular injury can also occur and is related to the gravity of the soft tissue component of the injury. An additional mechanism of fracture of the proximal

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humerus occurs with excessive external rotation of the arm, especially in an abducted position in association with a dislocation. A direct blow to the lateral arm can also cause injury to the proximal humerus but is less common. This mechanism usually results in a fracture of the greater tuberosity, a minimally displaced fracture, or a fracture involving the articular surface. Fractures associated with primary dislocation of the shoulder, both anterior and posterior, are usually caused by the forced abducted, externally rotated position (for anterior fracture-dislocations) and forced adduction with posterior displacement (for posterior fracture-dislocations). [47] Physical Examination

Physical examination reveals in most cases swelling and tenderness to palpation about the shoulder.[20] [38] [199] Disruption of the normal bony contour of the shoulder is seen in displaced fractures and fracture-dislocations. Crepitus may be present if there is significant displacement of the fracture fragments. Ecchymosis occurs over 2 or 3 days and discoloration may occur in the arm extending past the elbow and along the chest wall and upper back. These patients often hold the arm adducted to help protect it against motion. It is difficult for the patient to initiate active motion, which usually results in painful muscle spasm. A detailed neurovascular examination is essential. Brachial plexus and axillary artery injuries have been associated with proximal humerus fractures. [24] [66] [111] [308] The axillary nerve is the most commonly injured, but the entire plexus can be involved. The sensory distribution of the axillary nerve over the lateral upper arm should be examined for light touch and pin-prick. Deltoid motor activity can be evaluated by palpating the muscle belly with one hand while supporting the elbow to resist abduction or extension with the other ( Fig. 21M1-6 ). It is difficult to test the suprascapular nerve in isolation. The suprascapular nerve innervates the supraspinatus and infraspinatus muscles. The supraspinatus and the deltoid are both primary shoulder abductors, whereas the infraspinatus and teres minor are involved primarily in external rotation. While testing the relative strength in abduction and external rotation, there will subsequently be some degree of overlap.

Figure 21-M1-6 A, Clinical examination of axillary nerve motor distribution. The deltoid muscle is palpated while an attempt to abduct the arm is made. B, This football player has sustained an injury to the axillary nerve. Note atrophy of the deltoid muscle. C, The lined area on the upper lateral arm depicts the region of decreased sensation in axillary nerve injury. Imaging

Accurate radiographic evaluation is essential for diagnosis and treatment of proximal humerus fractures. The mandatory

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trauma series consists of anteroposterior and lateral views in the scapular plane and an axillary view. A true anteroposterior view in the scapular plane is performed with the affected shoulder placed against the x-ray cassette and the body rotated toward that side approximately 40 degrees ( Fig. 21M1-7 ). The true lateral view in the scapular plane is also termed the tangential view, Y view, or true scapular lateral view. The lateral view in the scapular plane is accomplished by placing the x-ray cassette laterally against the point of the affected shoulder while the plane of the x-ray beam is directed along the scapular spine ( Fig. 21M1-8 ). This can best be accomplished by drawing a line along the scapular spine to help align the x-ray tube with the spine.

Figure 21-M1-7 The technique for taking a true anteroposterior radiograph of the shoulder is demonstrated. The affected shoulder is rotated approximately 40 degrees toward the cassette. This eliminates the bony overlap between the humeral head and the glenoid. ( A and B, From Rockwood CA, Matsen DD [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.) (C-E from Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

Figure 21-M1-8 The technique for true scapular lateral radiography of the shoulder is demonstrated. The cassette is placed lateral to the affected shoulder, and the x-ray beam is directed along the scapular spine. (A and B, From Rockwood CA, Matsen DD [eds]: The Shoulder. Philadelphia, WB Saunders, 1990; C, from Rockwood CA, Green DP [eds]: Fractures, 2nd ed. Philadelphia, JB Lippincott, 1984.)

The axillary view allows evaluation in the axial plane ( Fig. 21M1-9 ). The supine position is preferable but not mandatory. The arm can be held in slight abduction with slight flexion in the plane of the scapula while the plate is placed along the superior aspect of the shoulder. The tube is angled approximately 20 degrees off the horizontal and vertical axes and is directed toward the axilla. Alternatively, a Velpeau axillary lateral view may be taken, allowing the patient to keep the arm immobilized in the sling

without abduction. The patient leans back and the

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tube is directed from superior to inferior, so that the beam is directed vertically through the shoulder onto the cassette. On this view the humerus appears foreshortened and the glenohumeral joint is magnified but still demonstrates the relationship of the humeral head to the glenoid[25] (Fig. 21M1-10 (Figure Not Available) ).

Figure 21-M1-9 The technique for taking an axillary lateral radiograph of the shoulder is demonstrated. The beam is angled approximately 20 degrees off the horizontal and vertical axes toward the cassette, which is positioned above the shoulder. (A and B, From Rockwood CA, Matsen DD [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.) Figure 21-M1-10 (Figure Not Available) A Velpeau axillary view may be taken; this allows the patient to keep the arm immobilized in the sling. The patient leans back and over the plate while the beam is directed from superior to inferior. (From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 143.)

The axillary view often provides the best information about the relationship of the humeral head and glenoid fossa (anterior or posterior dislocation versus rotary subluxation of the head). In addition, posterior displacement of the greater tuberosity and medial displacement of the lesser tuberosity are best delineated in this projection. [44] Computed tomography (CT) is extremely helpful in evaluating the amount of articular involvement with head-splitting fractures, impression fractures, chronic fracture-dislocations, and glenoid rim fractures. CT may also aid in judging the amount of displacement of tuberosity fragments.[22] [190] Recently, however, Sjoden investigated whether the addition of three-dimensional reconstruction would increase the reproducibility of the Neer and AO fracture classifications. Seven observers independently classified 24 fractures of the proximal humerus using both plain radiographs and three-dimensional CT reconstructions. Moderate interobserver agreement was noted with Neer's four-segment classification, but only fair agreement with the AO classification. Intraobserver reproducibility was fair for both the Neer and AO classifications. The authors concluded that the addition of CT and three-dimensional reconstructions did not improve reproducibility when classifying these injuries.[265] Treatment

Historically, many different types of treatment have been described for proximal humerus fractures including a

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variety of external immobilization devices such as spica and hanging arm casts, traction, and splints as well as internal fixation devices such as percutaneous pinning, plates and screws, rods, staples, and the humeral head prosthesis.* In the competitive overhead athlete who requires the arm for throwing or motion, (baseball, football, javelin, swimming, and so forth), a more rigorous effort should be made to restore anatomy and obtain rigid fixation. Many factors contribute to the decision-making process of fracture treatment. There is an increasing trend toward minimal osteosynthesis employing either tension band sutures or percutaneous fixation of the fragments. Even in special cases of plating, conventional T-plates are being replaced by LC-condylar plates or applied with less aggressive soft tissue stripping. Some controversy remains regarding the management of four-part fractures and fracture-dislocations.[223] [278] Correlation of treatment modality and functional outcome remains difficult, as seen in a prospective multicenter study by Weber where confusion regarding classification and numerous techniques of fixation made statistical analysis impossible.[290] Nonoperative Treatment

Most proximal humerus fractures are minimally displaced and can be treated with sling and early passive range of motion exercises. Koval and colleagues reported outcomes at an average of 41 months in 104 patients treated for one-part fractures. Results were excellent in 77% of patients, fair in 13%, and poor in 10%. The authors report that an age over 70 years and a delay of passive range of motion exercises (14 days) had detrimental effects on range of motion outcome.[141] Zyto reported the results of nonoperative treatment of three- and four-part fractures. Seventeen shoulders with a minimum follow-up of 10 years were included. The mean Constant score in the three-part fracture group was 59, and 47 in the four-part fractures. Despite low functional scoring, poor fracture reduction and mean flexion and abduction of 90 degrees, the authors suggest that nonoperative treatment should be considered.[309] *See references

[ 1] [ 2] [ 33] [ 53] [ 66] [ 70] [ 81] [ 115] [ 120] [ 130] [ 131] [ 132] [ 164] [ 183] [ 188] [ 199] [ 225] [ 230]

and [ 254] .

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Operative Management

Percutaneous Reduction and Pinning.

Percutaneous pinning may be indicated after closed reduction if the reduction is deemed to be unstable. It is technically demanding but offers the advantage of less disruption of soft tissue and minimal fixation, thus reducing the prevalence of avascular necrosis. Williams recommended that the most suitable indication for closed reduction

and percutaneous pinning is in select two-part surgical neck fractures and valgus-impacted fractures with good bone quality and minimal comminution. This technique has also been reported with good results in three- and four-part fractures of younger patients without osteoporosis[301] ( Fig. 21M1-11 ).

Figure 21-M1-11 A, Anteroposterior view of a two-part angulated surgical neck fracture. B, Anteroposterior view after placement of percutaneous pins; C, axillary lateral view after pin placement. The most proximal pin is first placed into the greater tuberosity and head fragment so that it can be used as a joystick to aid in reduction. It is then driven distally into the cortex medially in conjunction with lateral pins placed from distal to proximal into the head.

Biomechanically, multiplanar pins are required to augment torsional stiffness, and it has been shown that the addition of two bicortical tuberosity pins enhances bending rigidity.[195] Jaberg reported satisfactory results in 70% (34/48) of patients who underwent percutaneous pinning, including 32 two-part fractures.[125] In another study, the results of 31 percutaneous pinnings in patients averaging 68 years, including 7 two-part, 20 three-part, and 4 four-part fractures were studied. [267] The mean Constant score was 80, with avascular necrosis seen in five cases. The authors

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concluded that transitory percutaneous pinning was a reasonable technique for the management of displaced three-part fractures even in an older population but was not satisfactory for the management of four-part fractures. Some modification of percutaneous pinning was attempted by several authors.[37] Resch and associates also reported satisfactory results with percutaneous pin fixation of three- and four-part fractures.[233] Avascular necrosis was seen in only 11% of four-part fractures. Bungaro and coworkers discussed preliminary results of osteosynthesis with percutaneous wiring. They found the use of a traction device applied to the surgical table simplified reduction maneuvers and osteosynthesis.[31] Plate Fixation.

Although the trend is away from classical open reduction and internal fixation (ORIF) to minimal fixation techniques, concern has been expressed regarding the ability of newer techniques to afford adequate fixation without increasing the risk of soft tissue and vascular injury. Hessmann evaluated the use of indirect reduction and internal fixation using a buttress-plate in 99 cases of two-, three-, or four-part fractures of the proximal humerus. The mean age was 63 years and average follow-up period was 30 months. Good to excellent results were reported in 69% of cases. Complete and partial humeral head necrosis developed in 3% and 1% of cases, respectively.[114] Wanner employed double-plate stabilization to 57 displaced two-, three-, and four-part fractures of the proximal humerus. Two one-third tubular plates were applied to the anterior and lateral aspects of the proximal humerus. At an average follow-up of 16.8 months, 32% of patients were graded as excellent, 37% good, 21% satisfactory, and 10%

unsatisfactory.[288] T-plate osteosynthesis has also been used for the treatment of fracture-dislocations in 33 patients. The rate of osteonecrosis of the humeral head was 39%, with poor results in almost 50%. These authors concluded that the functionally poor results correlated more with dislocated fragments and persistent axial deviation than with the type of fracture or the development of necrosis of the humeral head.[156] The use of the AO buttress plate technique for three-part fractures has also been reported.[144] [214] [293] This method has been successful in younger patients with good bone stock and limited comminution. The advantage of this technique is the ability to achieve rigid internal fixation, facilitating early range of motion exercises. However, several authors have reported a substantial complication rate using this technique, including avascular necrosis, plate impingement requiring removal, and failure of fixation in osteoporotic bone.[144] [247] [275] Kirschner Wire and Tension Band.

Darder presented 64% excellent or satisfactory results in 33 patients (average age 59 years) with four-part fractures employing modified K-wires through the tuberosities in conjunction with tension band techniques.[49] Zyto found no benefit from tension band fixation in a more elderly group with a mean age of 74 years compared to nonoperative management.[309] These papers illustrate the need to consider the patient's age, lifestyle, and bone quality as well as the fracture pattern in making a management decision. Screw and tension band technique has also been reported with 80% good results.[42] Intramedullary FixationEnder Nails.

Originally, a retrograde approach was recommended to avoid rotator cuff injury. Ogiwara described the effectiveness of stabilization of displaced surgical neck fractures with retrograde Ender nailing. Thirty-four patients were evaluated at the average follow-up of 9.9 months. Bone union occurred by 5.9 weeks in all but 1 patient. [211] Others have reported good results with antegrade modified Ender nails in conjunction with suture or wire tension band fixation in an attempt to achieve better rotational and longitudinal control[44] [301] ( Fig. 21M1-12 ).

Figure 21-M1-12 A, Anteroposterior view of a three-part proximal humerus fracture treated with Ender nails and tension band fixation. B, Anteroposterior view after treatment; C, axillary lateral view after treatment. Intramedullary Nailing.

Lin reported 86% excellent or satisfactory results with locked intramedullary nailing in 21 proximal humerus fractures. Union occurred at an average of 14.8 weeks with one case of postsurgical impingement.[158] Twenty-one two- and three-part proximal humerus fractures treated by the Kapandji nailing technique were also reviewed. Pin migration was frequent but the technique was felt to be technically easy, noninvasive, and

inexpensive.[187] There has been increasing interest in the technique of retrograde intramedullary fixation to avoid injury to the greater tuberosity and rotator cuff. Retrograde intramedullary fixation was used in 74 unstable proximal humerus fractures, resulting in 60% good or excellent results, 30% satisfactory, and 10% unsatisfactory or poor. The main complications associated with the procedure especially in marked osteoporosis were secondary loss of reduction (16%) and pin migration (21%). [117] Loitz reported satisfactory results of retrograde unreamed nailing in 120 fractures of displaced two-part and occasionally three- and four-part fractures. This study included 110 cases of unreamed humeral nails with deployable proximal locking and 10 cases of solid interlocking nails. Functional results averaged 87% of the opposite side with complications including nail migration (8.3%), instability (3.8%), nonunion (5.8%), and iatrogenic fractures (5.8%). The results again revealed that patients with high-grade osteoporosis, small proximal fragments, and poor compliance were poor candidates for this procedure[163] ( Fig. 21M1-13 ).

Figure 21-M1-13 A, Anteroposterior view of a three-part proximal humerus fracture treated with intramedullary rodding; B, axillary lateral view before treatment. C, Anteroposterior view after treatment; D, axillary lateral view after treatment. Biomechanical Evaluation of Internal Fixation

Ruch examined biomechanical stability of three constructs currently used for the management of three-part proximal humerus fractures. Sixteen stripped cadaveric specimens were used in an effort to eliminate variables such as the quality, function, and integrity of the rotator cuff. They found cloverleaf plates and intramedullary nails provided greater torsional and bending stiffness than fixation with tension band wires with supplemental Ender nails.[243] The results were not consistent with data reported by Weinstein, who studied AO buttress plating and tension band wire supplemented with Rush rods. The authors reported superior torsional stability in the tension band construct. This study evaluated cadavers with an intact rotator cuff which may explain the enhanced stability with the tension band construct.[291] Wheeler compared biomechanical stability between intramedullary nail and percutaneous pin fixation in simulated three-part proximal humerus fractures. The intramedullary device was found to provide a

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stronger, more stable and durable fixation option than did percutaneous pins for large fragment three-part proximal humerus fractures with minimal comminution. [298] Humeral Head Replacement

Shoulder hemiarthroplasty is a well-accepted surgical procedure for the treatment of select proximal humerus fractures, including four-part fractures and fracture-dislocations, three-part fractures associated with severe osteoporosis, head splitting, and severe head impression fractures. The role of prosthetic replacement in treating acute proximal humeral fractures requires special consideration. Surgical reconstruction requires restoration of humeral length, center of rotation, and anatomic retroversion. Adequate positioning of the tuberosities and osteosynthesis are most critical to the successful outcome of prosthetic replacement surgery.[45] [97] Hartsock reported satisfactory results in approximately 80% of cases in young patients, with acute fractures faring better than chronic cases.[103] Balmer pointed out the value of proper evaluation of the patient and accurate fracture assessment. In young individuals with good-quality bone, they recommended careful techniques of reduction and fixation, even in the case of possible impairment of the vascular supply to the humeral head. In elderly patients with osteoporotic bone and limited compliance throughout aftercare, humeral head replacement is a superior indication with a more predictable expectation of a pain-free shoulder[12] ( Fig. 21M1-14 ).

Figure 21-M1-14 A, Anteroposterior view of a four-part proximal humerus fracture. B, Intraoperative radiographs of a trial prosthesis can be used to assess humeral height and the relationship of the humeral head to the greater tuberosity and the glenoid. C, Anteroposterior view after treatment with a humeral head replacement.

Most investigators have recommended arthroplasty as a primary rather than secondary procedure.* Generally, *See references

[ 41] [ 63] [ 68] [ 76] [ 80] [ 124] [ 142] [ 185] [ 198] [ 209] [ 278]

and [ 279] .

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secondary intervention requires a more demanding surgical approach as a result of soft tissue contracture, scarring, and altered anatomy with poor functional results. Gobel evaluated the results of shoulder hemiarthroplasty in patients with 9 acute and 13 old fractures of the proximal humerus. The mean Constant score improved 28 points (27 to 55), especially distinct in the group with acute fractures.[90] Bosch compared outcome results after primary ( /das/book/view/29309971/1103/594.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

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MD Consult L.L.C. http://www.mdconsult.com 596.html/top"> /das/book/view/29309971/1103/596.html/top

DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

2. FRACTURES OF THE PROXIMAL HUMERUS IN THE CHILD Kaye E. Wilkins MD Epidemiology Incidence of Shoulder Injuries

Uncommon

Shoulder injuries are relatively uncommon in the overall picture of injuries to the pediatric musculoskeletal system. Although fractures to the upper extremities per se are the most common injuries seen in the pediatric age group, most are distal rather than proximal. In his study of 8682 fractures in children, Landin[31] found that 22.7% involved the distal forearm, 8.1% involved the clavicle, and only 2.2% involved the proximal end of the humerus. Most clavicular fractures after the age of 10 occurred in boys and occurred during ball or contact sports. In a more recent review of 6493 children's fractures by Cheng and coworkers,[9] fractures about the shoulder accounted for less than 5% of all fracture types. Horseback RidingHigh Risk

In Landin's series, the sporting event that produced the highest percentage of shoulder injuries was horseback riding

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( Fig. 21M2-1 ). Twenty-eight percent of the injuries sustained from horseback riding

involved the proximal humerus, and another 9% involved the clavicle.

Figure 21-M2-1 Horseback riding injury. Proximal humeral metaphyseal greenstick fracture in an 11-year-old girl who fell off a horse. Almost No Sequelae

In looking at long-term sequelae of pediatric sports-related injuries, Marchi and coworkers[34] found that none of those injures occurring in the shoulder region had any long-term sequelae in young athletes. The highest incidence of injuries with long-term sequelae occurred in the ankle and elbow regions. Social Factors

Organized Sports

In Landin's overall global review of all pediatric fractures, only 21% occurred in organized sporting events. In fractures associated with sporting events, there have been increases not only in participation but also in the number of injuries. Landin[31] found that in the three decades from 1950 to 1980, there was a fivefold increase in the incidence of injuries to children from sporting activities. Nonorganized SportsHigher Risks

In the pediatric age group, most sports activity occurs outside the organized educational setting. This has been a popular trend over the past 20 years. In the pediatric age group setting, many studies[12] [23] [31] have found that far more injuries occur in organized play activities. It was estimated in 1980 that nearly 30 million young people aged 6 to 21 were involved in nonscholastic athletic programs.[11] On the other hand, in organized interscholastic sports in 1981,[37] only 5.35 million young people were active participants. In the same study, the most popular sport reported for boys was football. For girls, basketball was the leader. Emergency Room Visits

Sports injuries necessitate visits to emergency rooms. In 1981, [36] among organized sports, football was the leading cause of such injuries, with 453.9 visits per 100,000 participants in the 5- to 14-year age group. The greatest number of emergency room visits (906.7/100,000) was related to bicycling.[14] Age

Fear of Crippling Injuries

Age is a factor in the overall incidence of athletic injuries in the pediatric age group. In 1956, the American Medical Association (AMA) published a statement warning against the participation of skeletally immature individuals in organized athletic events.[13] The AMA stated categorically that such participation was unsafe because of the large number of physeal or growth injuries that could occur. Subsequent follow-up studies[32] showed that this fear of so-called crippling injuries was unfounded. In fact, injuries to the physes accounted for less than 5% of all sports injuries. Age-Related Injuries

Injuries are age-related.[53] Among grade school athletes, the injury rate is very low. The injury rates increase steadily with age so that the maximums are seen in the high school age group.[35] In summary, the overall risk of injury to the pediatric athlete is related to the nature of the sporting event, the age of the participant, and the method by which the players are grouped. There appears to be a greater risk of injury in the skeletally immature individual among participants in nonorganized recreational or play activities than in players who are under some type of adult supervision. Physical (Mechanical) Factors

Influence of Physes

The presence of the physeal plates about the shoulder provides matrices of lesser strength than those provided by the adjacent capsules and ligaments, or even in some cases by the periosteum. The physes have an age-related variability in strength. The physis and its perichondrial ring weaken just before maturity.[10] This fact is borne out clinically in the classic study by Peterson and Peterson, [39] who

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found that physeal injuries occurred between 11 and 12 years of age in girls and between 13 and 14 years of age in boys. Influence of the Metaphysis

Weakness of metaphyseal bone results in minimally displaced greenstick-type fractures ( see Fig. 21M2-1 ). The proximal humerus is one of the most common locations for unicameral bone cysts. Because the cortex is weakened by the cyst, fractures can occur in this location with simple throwing activities ( Fig. 21M2-2 ).

Figure 21-M2-2 Pathologic fracture. Fracture through a large unicameral bone cyst. This developmental defect greatly weakens the bone, making it susceptible to pathologic fracture. Specific Sporting Events

Macrotrauma

In 1978, Garrick and Requa[21] surveyed the overall incidence of injuries over a 2-year period in high school sports. They mainly looked at macrotrauma injuries. Predictably, football and wrestling produced the greatest number of injuries overall ( Fig. 21M2-3 ), whereas swimming and tennis had the lowest injury rates.

Figure 21-M2-3 Macrotrauma. Injury rates for macrotrauma for various athletic events in high school sports. (From Garrick JG, Requa RK: Injuries in high school sports. Reproduced by permission of Pediatrics 61:465, 1978.) Football

Rate Increases with Age.

Most injuries to the shoulder in football result in macrotrauma (i.e., fracture of the clavicle or glenohumeral dislocation). The overall injury rate increases with age. In the Little League age group, the rate of football injuries overall was only 7.8% versus 17% in high school players.[22] Shoulder Vulnerable.

When specific body areas are examined, the percentage of football injuries involving the shoulder is fairly consistent, ranging from 8% to 12%. [6] [16] [22] [38] The shoulder ranks second after the knee in overall injuries sustained in football. There appears to be an increased incidence of shoulder injuries in more recent years. Culpepper and Niemann[16] theorized that this was due to the outlawing of spearing, which brought a return of shoulder-body contact to tackling. In one study of recurrent anterior shoulder dislocations requiring surgical correction, 49% of the patients sustained their initial injury in football.[27] In another study of acromioclavicular injuries, 41% of patients sustained their initial injury in football.[15] Bicycling

Although bicycling is usually a recreational activity, it is becoming increasingly popular as an organized sport. Most bicycle injuries among the pediatric age group occur during idle play. Sixty percent of all bicycle injuries occur in children between 5 and 14 years of age.[14] [36] In bicycle injuries, 85% involve the upper extremity.[29] One unique injury is the so-called bicycle shoulder.[24] This occurs when the cyclist is thrown over the front of the

cycle when it is suddenly stopped. Failure to stay with the bicycle causes the cyclist to be thrown forward and to land directly on the shoulder. This forward propulsion over the wheels produces a direct injury to the acromioclavicular area (fracture of the distal clavicle or acromioclavicular separation) ( Fig. 21M2-4A ). Bicycle shoulder injuries can be prevented by teaching the cyclist to maintain a tight grip on the handlebar and to roll with the cycle, allowing the body to absorb some of the forces of the fall ( see Fig. 21M2-4B ).

Figure 21-M2-4 Bicycle shoulder. A, If the bicyclist maintains his grip on the handlebars and is thrown forward, he often lands directly on his shoulder, sustaining a disruption of the acromioclavicular joint. B, The proper way of falling is to stay with the bicycle and roll, so that the pressure is distributed evenly throughout the body.

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Basketball

There are no published data on high school basketball shoulder injuries. In a review of professional players by Henry and colleagues,[25] shoulder injuries accounted for only 3% of all injuries and 1% of games missed. Skiing

Upper Extremity Less Involved.

In a study of skiing injuries by Carr and coworkers,[8] only 25% involved the upper extremity. Forty percent of these involved the hand (specifically, the thumb). The shoulder was next, with dislocations and severe sprains occurring in almost 30% of upper extremity injuries. It was surmised that conditions that increased the speed of the skier (e.g., ability and snow pack) increased the chances that an injury to the upper extremity would be sustained. Snowboarding Increases Risk.

In a recent review of skiing injuries by Kocher and coworkers, [30] it was found that the incidence of shoulder injuries in snowboarding was greater than that among Alpine skiers. This was felt to be due to the aerial maneuvers of the snowboarders. Wrestling

During the average high school season, as many as 75% of participants in wrestling sustain some type of injury.[41] Twenty-nine percent of these injuries involve the upper extremity, of which almost all involve the shoulder. In looking at shoulder injuries

occurring in wrestling specifically, Snook[46] found that almost 78% involved the acromioclavicular joint. Such injuries are probably the result of a direct blow when the shoulder hits the mat. Because the object of wrestling is often to put leverage about the shoulder, one might expect a high incidence of glenohumeral dislocations. The incidence of glenohumeral dislocations, however, is quite low (less than 10% of all shoulder injuries and less than 2% of injuries overall). This fact can probably be explained by the fact that the leverage forces applied to the shoulder are gradual and are strongly resisted by the muscular forces of the opponent. Horseback Riding

Trauma sustained by young horseback riders most frequently involves head and neck injuries. Next to head injuries, however, is skeletal trauma, with two thirds of fractures occurring in the upper extremity.[5] In Sweden, the major cause of fracture of the proximal humerus in girls ( see Fig. 21M2-1 ) is falling off a horse.[31] Baseball

Fractures of the humeral shaft in pediatric baseball players are relatively rare but do occur.[28] [52] Usually, they are related to some inherent defect in the bony structures ( Fig. 21M2-5 ). Ireland and Andrews[28] have described a case in a young pitcher with an acute avulsion of the coracoid epiphysis.

Figure 21-M2-5 Throwing injury. This 12-year-old sustained an acute fracture while simply throwing a baseball during practice. The fracture occurred through a cystic osseous defect in the proximal humeral diaphysis (arrows).

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Microtrauma

Three Categories.

Injuries due to microtrauma are especially prevalent in the shoulder region. Hill[26] divided these microtrauma or overuse forces into three categories. The first is explosive force such as that occurring when a baseball is pitched and is thrown repetitively at maximum force but for relatively short periods. The second or dynamic force is gentler but is sustained for more repetitions and for longer periods. The classic example of this dynamic force is that used in swimming. The third type is a static force in which isometric contractions are maintained across the shoulder for various periods. Examples of this type of force are seen in the weightlifter or gymnast who suspends his or her trunk with the upper extremities.

Sports-Specific Microtrauma

Baseball

Baseball is the sport that produces little macrotrauma but a great deal of microtrauma in the shoulder. Pitching Phases.

Tullos and King[51] divided pitching activity into three phases ( Fig. 21M2-6 ): cocking, acceleration, and follow-through.

Figure 21-M2-6 Phases of pitching. A, Cocking phase. B and C, Acceleration phase. D, Follow-through phase. (Reprinted with permission from Woods GW, Tullos HS, King JW: The throwing arm: Elbow joint injuries. J Sports Med 1[suppl 4]:45, 1973.)

First is the cocking phase, in which the shoulder is markedly externally rotated. This tightens the triceps and biceps as well as both the internal and external rotators across the shoulder. This part of the throwing act in the adolescent pitcher results in increased external and decreased internal rotation arcs in the shoulder. Richardson[42] pointed out that during this phase the internal rotators and adductors are at maximum stretch. If the body or shoulder moves forward too soon, the arm has to catch up by putting an excessive load on these structures, thereby creating an inflammatory tendinitis that is the most common cause of anterior shoulder pain among adolescent pitchers. The second, or acceleration, phase consists of two parts. First, the shoulder is brought forward with the forearm behind. Next, the forearm and hand are whipped forward, owing in large part to forces generated by the pectoralis major and latissimus dorsi. The third, or follow-through, phase involves coordination of the forearm muscles to release the ball at the proper time and with the proper spin. The deceleration forces generated in this phase are unique to baseball and tennis.[42] This phase puts stretch on the posterior capsule and external rotators that can be a source of the posterior shoulder pain syndrome. Richardson[42] found that during this phase there might also be stress on the rhomboids and levator scapular insertions, which produces pain along the medial scapular border. Both Rotational and Compressive Forces.

Tullos and King[51] found that the pitching patterns among adolescents and adults were remarkably similar. The forces generated during pitching are very large, especially when rotation is considered. Gainor and his coworkers[20] pointed out that pitching involves both rotational forces from the internal

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and external rotators of the shoulder and compressive forces from the flexors and extensors of the elbow. They calculated that internal rotational torque is 14,000 inch-pounds just before release of the ball. The kinetic energy produced is 27,000 inch-pounds during the throw. These forces are four times greater than those generated in the lower extremity when an athlete is kicking a ball. In addition, they are greater than the forces required to fracture an isolated cadaver humerus. Shoulder Problems Among Adolescents.

In baseball, however, elbow problems predominate in immature players. Shoulder pain and chronic problems do not develop until adolescents are in their late teens.[2] [3] [26] [44] Some authors have speculated that the late incidence of shoulder problems is related to abnormal pitching patterns due to chronic elbow conditions that have developed during the earlier years.[2] [44] Little Leaguer's Shoulder.

One area of skeletal weakness that can fail with repeated microtrauma is the proximal humeral physeal plate. Failure usually occurs as a stress fracture of the proximal humeral physis. Dotter[18] first described this entity as little leaguer's shoulder in 1953. Since then, numerous cases have been described in the literature.[1] [4] [7] [33] [48] [49] [50] All of these cases occurred in high-performance male pitchers who were 11 to 13 years old. The common radiographic finding is a widening of the proximal humeral physeal plate ( Fig. 21M2-7 ). In the cases presented, all except one responded to rest for the remainder of the season plus a vigorous preseason-conditioning program the following year.[47] In only one case was operative intervention necessary. This was an individual described by Lipscomb[33] in whom a localized avascular necrosis of the epiphysis per se developed, producing a loose body that had to be removed surgically.

Figure 21-M2-7 Baseball shoulder. A, This 13-year-old high-performance Little League pitcher experienced pain while throwing toward the end of the season. This radiograph demonstrates widening of the physis (arrows), which is indicative of a stress fracture through the physis, or baseball shoulder. B, Normal left side for comparison. Other Stresses.

In addition to chronic repetitive rotational and compressive forces across the shoulder, there appear to be other factors that may create microtrauma in young, skeletally immature pitchers. Albright[2] found in an extensive study of Little League pitchers that the incidence of symptoms reflected the form of pitching rather than the age of the pitcher. Those who had poor pitching skills were more likely to become symptomatic. For this reason, Slager [44] advised that the first emphasis of immature pitchers should

be on the development of skills and control; as they mature, emphasis can then be placed on increasing the speed of pitching. Social tensions can also be a factor. Torg and associates[49] found that in comparable age groups, those who performed in a less competitive environment were less likely to develop symptoms in the throwing arm than those who were subjected to high competitive pressures. Swimming

The most common orthopaedic problem among competitive swimmers involves the shoulder and is almost exclusively seen in high-performance swimmers. In Dominquez'[17] study, shoulder problems were rare among athletes younger than age 10 but increased dramatically after that age. Repetitive Forces.

Swimming is a sport that involves a tremendous amount of repetition. It has been calculated that the average male freestyle swimmer performs almost 400,000 strokes per arm per year.[43] Women, who require more strokes to swim the same distance, may perform as many as 660,000 strokes per year. Richardson and colleagues,[43] in their classic review of swimming injuries, found consistent patterns among swimmers who had shoulder problems. Symptoms increased with the caliber of the athlete, were more common among men, and were more frequent in sprint than in long-distance swimmers. Symptoms were more common during the early and middle portions of the season and were often exacerbated by the use of hand paddles during training. Impingement Syndrome.

The major cause of shoulder

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pain in swimming is repeated friction of the humeral head and rotator cuff on the coracoacromial arch during abduction of the shoulder. This produces what Richardson calls an impingement syndrome.[42] [43] The maximum amount of impingement occurs at the beginning of the pull-through phase of the swimming stroke ( Fig. 21M2-8A ). In the backstroke, the greatest stress is on the anterior capsule during the pull-through phase ( see Fig. 21M2-8B ). In addition, backstroke swimmers often stretch the capsule to the point at which they develop anterior subluxation.[43]

Figure 21-M2-8 Swimmer's shoulder. A, During the beginning of the pull-through phase, the humeral head forces the rotator cuff against the acromion (arrows), creating an impingement in this area. B, In the backstroke, with initiation of the pull-through phase, there is a tendency to place tension on the anterior portion of the glenohumeral capsule (arrows).

Gymnastics

Gymnastic events produce unique forces across the shoulder. Rather than performing motions repetitively, the gymnast often has to maintain one position for relatively prolonged periods.[42] Ringman's Shoulder.

Among male gymnasts who perform extensively on the rings, which produces a great deal of stress across the shoulder, a benign cortical hypertrophy often develops at the insertion of the pectoralis major muscle into the proximal humerus. This has been called by Fulton and his coworkers[19] the Ringman's shoulder lesion. Supraspinatus Tendinitis.

In a study of female gymnasts by Snook,[45] the second most common injury was a supraspinatus tendinitis, which emphasizes the great degree of tension and compressive force about the shoulder that occur with gymnastics. Tennis

Most of the injuries among immature tennis players involve only the soft tissues. Similar to Baseball.

The forces placed on the upper extremity in the forearm stroke and the serve are very similar to those characteristic of baseball pitching. Cocking, acceleration, and follow-through phases occur. The only difference is that the racquet, which serves as an extension of the extremity, increases the forces applied to this extremity. In the backhand stroke, there is a reverse mechanism. Here, the internal rotators are the decelerators, and the weaker external rotators must provide the acceleration force. Because of this, many players use a two-handed stroke, which allows the twisting motion of the body to add some power to the stroke.[42] Tennis Shoulder.

Priest and Nagel[40] described a characteristic posture of young tennis players called tennis shoulder. It is a depression or drooping of the shoulder associated with postural scoliosis. They ascribed this to two factors. First, the service motion stretches the elevators of the shoulders (trapezius, levator scapulae, and rhomboids) ( Fig. 21M2-9 ). This stretching makes the player less able to maintain the normal postural elevation of the shoulder. Second, a documented hypertrophy occurs that simply increases the mass of the upper extremity. It was surmised that the downward rotation of the scapula that occurs with the drooping of the shoulder could produce a rotator cuff irritation by decreasing the distance between the acromion and the greater tuberosity. These

authors also described cases of this phenomenon (i.e., shoulder drooping) in adolescent baseball pitchers and shot putters. Treatment consists of selective exercises designed to strengthen the shoulder elevators.

Figure 21-M2-9 Tennis shoulder. This results from stretching of the shoulder elevator muscles during both the acceleration and follow-through phases of overhead serve. (From Priest JD, Nagel DA: Tennis shoulder. Am J Sports Med 4:28-42, 1976.)

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Specific Fracture Patterns

Fractures of the proximal humerus include both pure metaphyseal fractures and fractures involving the physeal

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plate. Because this is the area where growth and remodeling occur, the incidence and patterns of fractures are much different from those in the shaft. Because of the increased remodeling potential, there is more leeway in accepting the position of the fracture fragment. This metaphysis is also the most common location for a unicameral bone cyst. As a result, there is a high incidence of pathologic fracture in this area ( see Fig. 21M2-2 ). Structure

The proximal humerus is composed of the epiphysis, the physeal plate, and the metaphysis, all of which have unique biomechanical properties. These properties contribute to the specific injury patterns seen in this area. A review of the unique structural anatomy of this area will give the reader a better understanding of both the mechanism and the treatment of injuries that occur in the proximal humerus. Epiphysis Development

Two Ossification Centers.

The proximal humeral epiphysis is a hemispherical structure with a cone-shaped physeal plate. The physis is more proximally directed posteriorly, which provides some intrinsic stability ( Fig. 21M2-10 ). The hemispherical epiphysis contains the articular

surface and the greater and lesser tuberosities. The epiphyseal mass is formed by two separate ossification centers, which fuse to form a single center by about 7 years of age and are completely fused to the proximal humerus by 17 or 18 years of age.[64]

Figure 21-M2-10 Epiphyseal structure. A, Line drawings of the proximal epiphysis and physis demonstrating their conical configuration. (From Grant JCB: An Atlas of Anatomy, 5th ed. Baltimore, Williams & Wilkins, 1962.) B, This Salter-Harris type I physeal injury demonstrates this conical configuration as well. Ossification Process.

This serial development of the proximal humeral epiphysis has been studied in great detail by Ogden and his coworkers.[80] The initial contour of the physis is transversely oriented. At birth, there is usually no radiographically discernible ossification center. The first center develops as the capital or articular center at about 2 months of age (Fig. 21M2-11 (Figure Not Available) ). By 7 months of age, a second center develops in the area of the greater tuberosity. By 3 years, these centers have enlarged and matured, and the physis is assuming its conical shape. By 7 years, there is complete fusion of these two centers, and the physis becomes more conical in shape. From 10 to 13 years of age, the greater tuberosity ossification center expands until it completely fills the cartilaginous space on the lateral portion of the epiphysis. Figure 21-M2-11 (Figure Not Available) Epiphyseal maturation. The schematic development of the proximal humeral epiphysis and metaphysis from age 2 months to 14 years. (From Ogden JA, Conlogue GJ, Jensen P: Radiology of postnatal skeletal development: The proximal humerus. Skel Radiol 2:153-160, 1978.) Physeal Closure

By 14 years, the physis begins to close, starting in the center and extending peripherally. Metaphysis Weaker

When the epiphyseal centers fuse, the lateral metaphyseal cortex becomes thicker, composed almost entirely of cortical bone up to the physis, whereas the cortex on the medial metaphysis remains thin with a trabecular structure. This is thought to be one of the reasons why the metaphyseal fragment in the Salter-Harris II fracture occurs medially. As the physis closes, the medial metaphyseal cortex increases in density. Even though the cortex on the medial side is thicker, it has developed some trabecular pattern next to the physis. This produces an inherent weakness on the medial side of the proximal humerus.

The Periosteum

Thinnest Anteriorly.

In laboratory studies on humeri obtained from stillborn infants, Dameron and Reibel[60] found that displacement of the metaphysis was extremely difficult to accomplish. They attributed this to the fact that the periosteum of the metaphysis was considerably thicker posteromedially. Anterior displacement of the metaphysis was relatively easy to achieve because of the thinner periosteum on the anterolateral surface. If it remains intact, the periosteal sleeve can also stabilize an undisplaced fracture. Once the metaphyseal fragment has torn the periosteum, all of its intrinsic stability is lost. Metaphysis Slips Anteriorly.

When the periosteum disrupts, the proximal portion of the metaphysis tends to displace laterally to the intertubercular groove under the long head of the biceps. [77] Muscle Attachments

Epiphyseal Displacement.

The proximal humeral epiphysis has four muscles attached to it. In the greater

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tuberosity posterolaterally are the teres minor, infraspinatus, and supraspinatus ( Fig. 21M2-12A ). The subscapularis inserts into the lesser tuberosity anteriorly. The pectoralis major attaches distally to the anterior metaphysis. When the proximal epiphysis becomes disrupted from the metaphysis, the unopposed action of the muscles on the epiphysis tends to pull this fragment into flexion, abduction, and external rotation ( see Fig. 21M2-12B ).[60]

Figure 21-M2-12 Muscle forces. A, Effect of muscle forces on the proximal humeral epiphysis and metaphysis. (From Dameron TB: Fractures and dislocations of the shoulder. In Rockwood CA Jr, Wilkins KE, King RE [eds]: Fractures in Children, vol 3. Philadelphia, JB Lippincott, 1984.) B, Radiographic representation of the muscle force displacement. The epiphyseal fragment is rotated into flexion abduction and external rotation (white arrow). The metaphyseal fragment is forced cephalad by the pectoralis and deltoid muscles (black arrow). Metaphyseal Displacement.

Because the pectoralis inserts on the metaphyseal fragment, it tends to pull it

anteromedially to the head or epiphysis ( Fig. 21M2-13 ; see also Fig. 21M2-12 ).

Figure 21-M2-13 Metaphyseal-epiphyseal relationships. Salter-Harris type II fracture of the proximal humerus physis. Posteroanterior (A) and transthoracic (B) views. Notice that the metaphyseal fragment (smooth line) is anterolateral to the epiphyseal fragment (dotted line). C, Axillary lateral view confirms that the proximal metaphyseal fragment is anterior to the head. Capsular Attachments

The glenohumeral joint capsule on the medial side attaches distally past the edge of the articular surface to the metaphysis. Thus, the fracture line, when it passes through the medial physeal plate, creates a line that is intra-articular in location (Fig. 21M2-14 (Figure Not Available) ). [61] Figure 21-M2-14 (Figure Not Available) Capsular attachments. The relationship of the physeal plate and the glenohumeral capsular attachment to the proximal humerus. The medial end of the physeal plate extends across an area covered by articular cartilage in the area noted by stippling. This area of metaphysis is intra-articular. (From Dameron TB: Fractures and dislocations of the shoulder. In Rockwood CA Jr, Wilkins KE, King RE [eds]: Fractures in Children, vol 3. Philadelphia, JB Lippincott, 1984.) Blood Supply

With the exception of the suprascapular artery, the blood supply to the shoulder arises from the second and third

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parts of the axillary artery ( Fig. 21M2-15 ). The major supply to the proximal humerus comes from the anterior and posterior circumflex humeral arteries, which arise from the third part of the axillary artery.

Figure 21-M2-15 Blood supply. The arteries of the shoulder region. (From O'Rahilly R: Gardner-Gray-O'Rahilly: Anatomy, 5th ed. Philadelphia, WB Saunders, 1986.) Anterior Source.

Most of the blood supply to the osseous humeral head comes from the anterior ascending branch of the anterior circumflex artery.[67] This artery ascends proximally along the upper end of the bicipital groove and then enters the head by branches that pierce the greater and lesser tuberosities. Once inside the humeral head, this artery assumes a form like that of the lateral epiphyseal artery of the femoral head, that is, it

forms an arcuate system from which branches radiate at right angles to the periphery of the epiphysis. Posterior Source.

A small amount of blood is also supplied from the posterior humeral circumflex artery. This artery enters the epiphysis through a small portion on the posteromedial surface of the humeral head and corresponds to the medial epiphyseal arteries of the femoral head. Muscular Sources.

A part of the blood supply also arises anterolaterally through the rotator cuff into the greater tuberosity. Because much of the blood supply enters through the muscular attachments to the proximal humeral epiphysis, avascular necrosis of the humeral head is extremely rare after a fracture through the proximal humeral physis (see Avascular Necrosis, later). Incidence

It is difficult to determine the true incidence of pure physeal versus metaphyseal fractures of the proximal humerus because many of the reported series list these generically as fractures of the proximal humerus. Female Preponderance in Non-Sports

In Landin's study,[68] fractures of the proximal humerus accounted for only 2.2% of all fractures in children. More

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of these fractures occurred in girls. In his series of children between the ages of 9 and 10 years in Sweden, fully 50% of the fractures resulted from falls that occurred with horseback riding, and almost all of these patients were girls. Even when horseback riding injuries were removed from the overall group, there was still a preponderance of girls. In this same study, Landin found that the incidence of females sustaining fractures of the proximal humerus had increased dramatically since 1970. This large preponderance of girls sustaining fractures of the proximal humerus was also found in another study from Sweden.[62] Male Predominance in Sports

In another study that looked only at fractures of the proximal humerus per se, Kohler and Trillaud[66] found that 22% of 136 fractures occurred during sporting events. In their

series, 60% of patients were males. The peak age incidence was 10 to 14 years of age. Two thirds of the fractures involved the proximal metaphysis, and the other third involved the physeal plate. Bone Cysts

In Kohler and Trillaud's review period covering 20 years of proximal humeral fractures,[66] one fourth of the metaphyseal fractures occurred through unicameral bone cysts ( see Fig. 21M2-2 ). Pure Physeal Injuries

The most recent large review of physeal injuries has been that by Peterson and coworkers in 1994.[82] Their series looked at 951 physeal injuries in Olmsted County, Minnesota, from 1979 to 1988. In this group, only 1.9% involved the proximal humerus, which was less than the range of 2% to 6.7% in four other previous series totaling 3326 cases. [73] [74] [76] [81]

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Salter-Harris I or II

Almost all physeal fractures in this area are either Salter-Harris type I or II. [55] [60] [66] Type I fractures are less common and occur usually in younger children (i.e., younger than the age of 10 years). Almost all fractures among individuals older than age 10 are Salter-Harris type II lesions. [60] [66] Because of the flexibility of the shoulder, forces applied directly against the articular surface or perpendicular to the physis are rarely applied to the proximal humerus. As a result, Salter-Harris type III and IV fracture patterns are almost unheard of. [54] [55] [79] Type V lesions, which involve the development of a humerus varus, are usually the result of injuries that occur during early infancy or childhood and usually do not occur at athletic events. Mechanism of Injury

Metaphyseal FracturesYounger Age Group

Proximal metaphyseal fractures are characteristically predominant in children younger than 10 years of age. The mechanism of the fracture probably is the same as that causing proximal humeral physeal fractures. The combination of a weaker metaphysis and a stronger perichondrial physeal ring probably accounts for the occurrence of the fracture in the metaphysis rather than the physis in this younger age group. Physeal FracturesOlder Age Group

The exact mechanism of proximal humeral physeal injuries is not completely clear.

Physeal fractures are more common among athletes nearing skeletal maturity. Multiple Mechanisms.

One of the first to truly analyze the mechanisms of proximal humeral physeal injuries was Williams in 1981.[88] He did this by examining different displacement patterns of these fractures in his patients. It was determined that four forces could be applied to the proximal physis either singly or in combination. Only six variations of this, however, are likely to occur in the clinical situation. These include: (1) pure extension; (2) pure flexion; (3) forced extension with lateral rotation; (4) forced extension with medial rotation; (5) forced flexion with lateral rotation; and (6) forced flexion with medial rotation. When the mechanism is determined according to the fracture patterns and the position of the patient's upper extremity, it is hoped that a better reduction can be obtained. Displacement Probably Dictated by Local Architecture.

The periosteum is weaker on the anterolateral aspect of the proximal humerus. In fractures involving the humeral

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physis, the distal fragment usually is forced anteriorly and laterally through this weakened area ( see Figs. 21M2-12 and 21M2-13 ). Neer and Horowitz[74] reasoned that this force resulted from a direct blow to the shoulder by a posterolateral shearing force that adducted the humeral shaft and forced it anteriorly. Dameron,[61] on the other hand, believed that the force was directed longitudinally up the upper extremity as it was used to break a fall in a backward direction. The force originating as the hand hits the ground is transmitted proximally through the humeral shaft with the shoulder extended and adducted. This forces the metaphysis anteriorly, laterally, and cephalad. The horizontal alignment of the physis in the anterolateral portion of the proximal humerus facilitates this displacement in an anterolateral direction. The combination of a stronger posteromedial periosteum and compressive posteromedial forces results in the triangular metaphyseal fracture fragment in this area. Classification

In general, there are three types of fractures of the proximal humerus. These include (1) the more common metaphyseal fractures; (2) the less common injuries to the proximal humeral physis; and (3) the very rare avulsion fractures of the lesser tubercle. Metaphyseal Fractures

Cortex Intact.

Ogden[79] classifies metaphyseal fractures into two types. In the first type, the cortex

remains intact. These are usually torus or greenstick fractures ( Fig. 21M2-16A ).

Figure 21-M2-16 Metaphyseal fracture patterns. A, Simple greenstick metaphyseal pattern with minimal angulation. B, Complete metaphyseal pattern with medial translocation of the distal fragment. Loss of Cortical Integrity.

In the other type, there is loss of cortical integrity with either angular or translocation displacement ( see Fig. 21M2-16B ). Physeal Fractures

Proximal humeral physeal fractures can be either acute or chronic. In the acute injuries, there is immediate partial or complete displacement of the physis from the adjacent metaphysis. The chronic type represents a stress injury. Acute Injuries.

Fractures of the proximal humeral physis can be classified by location, degree of displacement, and stability. The degree of stability usually depends on the degree of initial displacement and the magnitude of the injury. The most commonly accepted classification of displacement is that proposed by Neer and Horowitz,[74] who separated the displacement into four grades: Grade Iless than 5 mm; Grade IIup to one-third the width of the physis; Grade IIIup to two-thirds the width of the physis;

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Grade IVgreater than two-thirds the width of the physis, including total displacement.

It should be noted that Neer and Horowitz in their original article used the term width of shaft instead of width of physis to denote the degree of displacement. In their illustrative cases, however, they demonstrated displacement of the physis. Thus, we have taken the license to correct this anatomic inaccuracy because the actual displacement is measured by the amount of physeal displacement, not by the amount of displacement of the proximal shaft (actually the metaphysis).

Chronic Injuries.

Chronic injuries involve chronic repetitive stress forces to the physis. These are usually repeated rotational forces applied to the physis. They are most commonly seen in the immature baseball player (see Little Leaguer's Shoulder). This injury has also been seen in gymnasts[59] and badminton players.[58] Avulsion (Lesser Tubercle) Injuries

Avulsion of the lesser tubercle by the subscapularis tendon is very uncommon in the skeletally immature.[65] [78] [85] [87] If it does occur and is initially unrecognized, it can produce a late exostosis, which can interfere with the activity of a throwing athlete. Signs and Symptoms

Displacement Dictates Swelling

In undisplaced metaphyseal fractures, especially those in which cortical integrity is maintained, there may be only minimal swelling. The tenderness is usually localized over the proximal humerus. In physeal fractures and metaphyseal fractures with displacement, there is usually considerable bleeding into the soft tissues of the deltoid area with marked swelling. The athlete with this type of fracture is usually uncomfortable and holds the extremity adducted to the chest. The weight of the extremity is often supported at the elbow and forearm with the opposite hand. Often the prominence of the proximal metaphyseal fragment can be palpated under the anterolateral deltoid. Check for Ipsilateral Injuries

It is important to assess all the nerves of the upper extremity to rule out a concomitant injury to any of the peripheral nerves of the brachial plexus. The vascular status of the upper extremity needs to be evaluated. Because the force was transmitted from the hand longitudinally, the entire extremity must be checked for the occurrence of less obvious ipsilateral fractures, especially in the distal radial metaphysis. Diagnostic Studies

Usually routine roentgenograms are enough to demonstrate the presence of the fracture. The proximal and lateral displacement of the metaphyseal portion is usually obvious on routine anteroposterior views of the shoulder. It may be necessary to use transthoracic lateral or oblique scapular views to determine the degree of apex in anterior angular

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displacement ( Fig. 21M2-17 ). In some cases in which there may be complex fragment patterns, a computed tomography (CT) scan with horizontal cuts or three-dimensional reconstruction may be helpful in determining the fracture patterns and degree of displacement.

Figure 21-M2-17 Metaphyseal-epiphyseal angulation. A, Anteroposterior view of a swimmer who injured her proximal humeral physis when she fell from a diving board. The anterior angulation cannot be determined from this view. B, An oblique view demonstrates that the metaphyseal (solid line)-epiphyseal (dotted line) alignment is angulated apex anterior at 137 degrees. Treatment

The major emphasis in this section will be on the most common injuries, that is, the metaphyseal and physeal fractures. The less common physeal stress and lesser tuberosity avulsion injuries will be discussed only briefly. Metaphyseal Fractures

Nonoperative Management

Undisplaced Fractures.

Simple metaphyseal fractures that are undisplaced or only minimally angulated usually can be treated quite adequately with a collar and cuff. In the acute stage, added comfort may be achieved by binding the arm to the chest with a circular elastic bandage. Most of these fractures are intrinsically stable; thus shoulder motion can be initiated early. In the pediatric athlete, it is extremely important to regain shoulder motion as soon as possible to achieve maximum rehabilitation. Displaced Fractures.

In the completely displaced metaphyseal fracture, very little abduction of the proximal fragment is usually present because some adduction force is maintained by both the pectoralis major and the latissimus dorsi on the proximal metaphysis ( Fig. 21M2-18 ). As a result, these fractures often develop bayonet apposition. Although shortening occurs because of the longitudinal pull of the triceps, biceps, and deltoid muscles, as in shaft fractures, it is usually not sufficient to cause any functional or cosmetic residua. These fractures usually can be treated quite well using a collar and cuff plus a thoracic elastic bandage. Healing with the bayonet apposition (although it may initially concern the parents) usually results in an acceptable cosmetic and functional result, even in the adolescent patient ( Fig. 21M2-19 ).

Figure 21-M2-18 Metaphyseal muscle forces. A, The distal metaphyseal fragment (M) is displaced (translocated) medially (arrow). The proximal epiphyseal fragment (E) is less rotated than with physeal fractures. B, The pectoralis major is the main deforming force on the distal metaphyseal fragment. The deltoid muscle tends to decrease the rotation on the proximal fragment. (Reproduced with permission from Healey JE Jr, Seybold WD: A Synopsis of Clinical Anatomy. Philadelphia, WB Saunders, 1969.)

Figure 21-M2-19 Bayonet remodeling. A, Injury film of an 8-year-old Little League baseball player who sustained a proximal metaphyseal fracture. The bayonet apposition and shortening were accepted. Initially, he was treated with a simple collar and cuff, supplemented with an Ace bandage. B, Radiograph obtained 4 months after injury shows remarkable remodeling. The shoulder range of motion and strength have since returned to the pre-injury level.

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Operative Indications

Olecranon Traction.

If there is an extremely marked displacement of the proximal metaphysis, and concern exists that the bayonet apposition may restrict shoulder motion, especially in an athlete who performs throwing activity, the patient can be placed in overhead olecranon pin traction to alleviate the shortening. Usually, these fractures stabilize rapidly, and the skeletal traction can be converted to a hanging arm cast or a simple collar and cuff after 10 to 14 days, when callus first appears at the fracture site. Percutaneous Techniques.

In this era, traction, although effective, may not be acceptable either socially or financially. A better alternative would be a manipulative closed reduction performed with the patient under a general anesthesia and stabilization of the fracture with either cross-pins ( Fig. 21M2-20 ) or intramedullary pins ( Fig. 21M2-21 ).[86]

Figure 21-M2-20 Metaphyseal cross-pin. A, Initial radiograph of a female gymnast who sustained this markedly displaced humeral metaphyseal fracture with a very short metaphyseal segment. B, Following the closed reduction, the fracture was very unstable and was stabilized with a percutaneous pin placed cephalocaudad. C, Radiographs taken 3 months after fracture show satisfactory healing and alignment. Clinically, the athlete had regained full abduction.

Figure 21-M2-21 Metaphyseal intramedullary pins. A, Injury radiograph of an 8-year-old female who sustained a contralateral displaced lateral condyle, in addition to this displaced proximal humeral metaphyseal fracture. B, In an effort to facilitate early recovery of both injuries, this fracture was stabilized with retrograde intramedullary pins for a short period of time. Open Reduction.

Other than the rare open fracture, there is probably no indication to perform an open reduction of a proximal humeral metaphyseal fracture. The only possible exception is treatment of an athlete who is approaching skeletal maturity. Physeal Fractures

Proximal Fragment Rotated.

In displaced fractures of the proximal humeral physis, rotation of the proximal fragment often occurs because there is an absence of adductor forces on this fragment. The adductor forces act entirely on the distal metaphyseal fragment ( see Fig. 21M2-12 ). At no other physis in the body is there a larger proportional contribution to longitudinal growth than at the proximal humeral physis. Approximately 80% of the longitudinal growth occurs in this area.[55] [63] [68] Remodeling Capacity.

As a result, the remodeling potential in this area is tremendous. The younger the athlete, the greater is the potential for remodeling. Because of the wide range of motion of the glenohumeral joint, the residual varus that may occur usually does not result in any functional limitation.[55] Shortening of these fractures is also well tolerated because of the independent function and weight-bearing status of the upper extremity. It must be emphasized that there needs to be at least 12 to 18 months of growth remaining in the proximal humeral physis for adequate remodeling to be achieved. Closed Methods

Obtaining a Reduction.

The argument for reduction of the fragments is that it decreases the degree of shortening that can develop if the displacement is allowed to remain. [57] [61] Various closed methods have been advocated to realign the fracture fragments into a more anatomic position. In some cases, a primary closed reduction is performed, either with sedation or under general anesthesia, and then the reduction is maintained by external support. The reduction per se is usually achieved by bringing the distal shaft fragment into flexion and some abduction and external rotation to align it with the flexed, abducted, and externally rotated proximal fragment.[61] The real question concerns whether an anatomic reduction is necessary. Many series [54] [55] [56] [66] [69] [72] [74] [75] have shown that for most individuals, even those who have considerable initial displacement,

simple immobilization often produces satisfactory results. Baxter and Wiley[55] found in their retrospective review that the manipulative process improved the arm's position in only a third of the patients in whom it was attempted. When there was an improvement in position, the final result was no better than that seen in patients in whom the equal displacement had been accepted. These authors questioned whether active manipulation had had any effect on the final outcome. The most recent work to confirm the good results of nonoperative management is the article by Beringer and coworkers.[56] They demonstrated excellent results in their series of 39 patients who were treated nonoperatively. In the 9 patients who were treated operatively, there was a high rate of complications. Maintaining the Reduction

Cast Methods.

If the fracture is stable after the reduction, it can be immobilized alongside the chest. If it is not stable, this position of flexed abduction and external rotation must be maintained with either a shoulder spica cast in the salute position or a commercial splint, neither of which is well tolerated by the athlete or the parents. The Statue of Liberty position with a spica cast should be avoided because of its potential to cause injury to the brachial plexus or to lead to development of vascular compromise to the upper extremity.[79] [83] With the minimally invasive surgical techniques now available coupled with the unreliability of a cast to adequately maintain the reduction achieved, there is almost no use of casts in the treatment of these fractures.

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Traction Methods

Some[75] have used the traction produced by the hanging arm cast to achieve a reduction or to improve the final fracture position. This method may not be effective if the cast is applied after the fracture clot has congealed. Overhead skeletal olecranon traction can be used for patients in whom the usual external immobilization techniques cannot be used. It is a good method of achieving and maintaining a reduction, but it requires expensive and extensive hospitalization and has all the problems associated with the management and care of the skeletal pin or screw. The major indication for this method would be a severely comminuted fracture.

Operative Intervention

The High-Performance Athlete.

It must be remembered, however, that these aforementioned series concerned mainly individuals with normal activity. What about the high-performance athlete? Is there a greater need to achieve a more anatomic reduction in athletes? The only citation in the literature that relates to this is a case described by Dameron and Rockwood, [61] in which a 14-year-old track star sustained a displaced Salter-Harris II fracture of the proximal humerus while pole vaulting. At the time of healing, there was a small proximal lateral spur on the anterolateral aspect of the metaphysis due to proximal migration of the distal fragment. When the patient had fully recovered, he was able to play football but was unable to participate in throwing sports because of a restriction of about 20 degrees in flexion and abduction. This author had experience with a high-performance pitcher who was treated nonoperatively and had a minor residual deformity ( Fig. 21M2-22 ). After the fracture, he had enough residual restriction of motion that he could no longer pitch and had to change to playing the outfield.

Figure 21-M2-22 High-performance athlete. Anteroposterior (A) and lateral (B) injury radiographs of a high-performance 14-year-old baseball pitcher who sustained a displaced proximal humeral physeal fracture. Anteroposterior (C) and lateral (D) radiographs taken 6 months after fracture demonstrate some incongruity of the proximal humerus. Although mild, this injury was severe enough to interfere with his ability to pitch at a high level.

Thus, in the high-performance throwing athlete, a more aggressive approach may be necessary to obtain and maintain an anatomic reduction. Percutaneous Methods.

The major indication for operative stabilization is to maintain as near anatomic reduction as possible in a throwing athlete who needs to regain a full range of shoulder motion. A semiclosed method of operative management involves reducing the fracture by closed methods first, and then stabilizing it with pins placed across the fracture site percutaneously under image intensifier guidance. More recently, cannulated screws have become a popular method of stabilizing the fragments. These techniques have the advantage of maintaining fracture alignment, with the arm in the normal position supported only with a splint or collar and cuff. Because of rapid healing, the pins can be removed within 2 to 3 weeks. Retrograde intramedullary flexible nails also can be used in those fractures requiring that an anatomic reduction be maintained.[86]

Open Reduction

Rarely Indicated.

Primary open operative reduction just to improve the position has almost no role in treatment of this fracture. The major absolute indications are the rare open fractures and fractures with vascular injuries. Other relative indications include comminuted intra-articular Salter-Harris type III and IV injuries or cases in which large amounts of periosteum or the biceps tendon have become interposed in the fracture site ( Fig. 21M2-23 ).

Figure 21-M2-23 Open reduction. A, Image following an attempted closed reduction of an almost skeletally mature male, demonstrating a persistent gap between the proximal metaphyseal and epiphyseal fragments. (The anteroposterior and lateral radiographs were seen as Figures 21M2-13A and B .) The decision had been made that the sporting activities of this athlete required as close to an anatomic reduction as possible. B, At open surgery, the periosteum and biceps tendon were found to be interposed between the fragments. Once this tissue was removed, the fragments were reduced anatomically and secured with cannulated screws. (Photos courtesy Earl A. Stanley, Jr., M.D.) Poor Results.

In general, open reduction of these fractures has produced poor results, worse than the results of comparable fractures managed closed.[72] Nilsson and Svartholm[75] believed that the poor outcomes seen after an open reduction were the result of the surgical intervention and not the fracture per se. This conclusion was echoed 20 years later by Baxter and Wiley,[55] who stated that open reduction improved the displacement in only three of seven patients, inflicting a cosmetically unattractive scar for no obvious advantage. Less Common Proximal Humeral Fractures

Physeal Stress Injuries.

These fractures usually respond well to rest for the remainder of the season plus a vigorous muscle conditioning program. The pitching technique may need to be critically evaluated and any errors corrected. If the player continues to participate by ignoring the pain, a slippage of the proximal physis can occur. [59] Avulsion of the Lesser Tubercle.

If untreated, these avulsions by the subscapularis and shoulder capsule can result in loss of shoulder motion. This can be disabling in a high-performance athlete who uses that upper extremity for throwing. Once the exostosis has developed, it may

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require surgical removal to permit full recovery of the shoulder motion. For this reason, some authors[65] [87] have recommended primary reattachment of the tubercle if recognized acutely in a young athlete. Author's Preferred Method of Treatment

Metaphyseal Fracture

Minimally Displaced.

For undisplaced or minimally displaced fractures of the proximal humeral metaphysis, I use a collar and cuff supplemented with an elastic bandage, and I strap the extremity to the chest wall. Within a few days, the elastic bandage strap is discontinued, and the cuff is gradually lowered until the elbow is at 90 degrees. At this time, circumduction exercises of the shoulder are begun. By 3 weeks after the injury, when early callus has formed, active abduction exercises can be initiated, and usually the arm can then be supported with a simple sling. Usually after 6 weeks, there is sufficient stability to initiate a formal rehabilitation program that includes strengthening all the muscles about the shoulder girdle, in addition to the biceps, triceps, and forearm muscles. In noncollision sports, the athlete can return to participation when muscle strength

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and range of motion in the affected extremity are equal to those in the uninjured extremity. In collision sports, there must additionally be sufficient bony healing to have reestablished good cortical margins at the fracture site. Bayonet Apposition.

In those complete metaphyseal fractures that are in bayonet apposition, I usually accept this position and treat them similarly to the minimally or undisplaced fractures. These fractures usually are slower to recover their range of motion. It usually requires a major degree of explaining to convince the parents that these will completely remodel. I usually keep pictures or radiographs of previous cases handy to convince them. Percutaneous Fixation.

In those patients who are very near skeletal maturity, I usually do a closed reduction and then secure the fragments with percutaneous intramedullary pins.

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I have no experience in performing an open reduction in metaphyseal fractures. Physeal Fractures

Minimally Displaced.

The Neer I or II fracture can usually be treated similarly to the minimally or undisplaced metaphyseal fracture, with simple immobilization and early motion. Significantly Displaced.

In markedly displaced physeal fracture, one must be sure that sufficient reduction exists to ensure uninhibited motion of the glenohumeral joint. This is especially true for those athletes who need full glenohumeral motion for throwing, gymnastics, or swimming activities. In such cases, an anatomic reduction is achieved first by manipulation. This reduction is then stabilized with percutaneous pins ( Fig. 21M2-24 ). Recently, I have found cannulated screws to be more satisfactory for fixation. They allow the patient to start motion almost immediately and do not have risk of infection associated with pins protruding from the skin.

Figure 21-M2-24 Percutaneous pins. A, Displaced proximal humeral physeal injury in the dominant extremity of a 13-year-old high-performance quarterback. B, Anatomic reduction was achieved by closed reduction and was maintained by percutaneous pin fixation. Pins were removed 4 weeks after injury, and shoulder motion was initiated. If the patient is very close to skeletal maturity, fixation with cannulated screws may be a better method.

I have found that external immobilization methods are cumbersome and uncomfortable and are not well accepted by the patient, in addition to being unreliable in maintaining the position of the fragments.

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Open Reduction.

In my experience, I have found very few indications for an open reduction. In these very rare open fractures or fractures with vascular compromise, I would not hesitate to perform an open reduction. In an athlete in whom there is interposed tendon or other tissue, one would have to weigh the risks of surgical damage to the shoulder muscles against the benefits of achieving an anatomic reduction. Once the decision has been made to achieve as anatomic a reduction as possible, an open reduction via a

deltopectoral approach may be the only way to achieve this ( see Fig. 21M2-23 ). Complications

The complications associated with proximal humeral fractures can be divided into either nonskeletal or skeletal. Nonskeletal

Nonskeletal complications are rare with injuries in this area. Baxter and Wiley[55] described one patient with complete disruption of the brachial artery at the lateral border of the axilla. In some patients, they also found severe tenting of the skin, which required operative intervention to prevent skin necrosis. Dameron and Reibel[60] reported one case of brachial plexus paresis in a patient treated in a statue of liberty cast. Transient axillary nerve paralysis has also been described.[79] Usually, however, these problems resolve by the time the athlete is ready to start the recovery or rehabilitation phase. Skeletal

Late Malunion.

Residual varus angulation and shortening, although they do occur, are rarely a problem among athletic individuals.[55] In some adolescents in whom a fracture is not reduced anatomically just before the onset of skeletal maturity, there may be sufficient deformity to produce a disabling loss of motion. In these patients, the surgeon must weigh the benefits of surgical intervention versus the risks of the procedure ( Fig. 21M2-25 ).

Figure 21-M2-25 Malunion. A, Injury film of an adolescent female basketball player who sustained a significantly displaced proximal humeral physeal injury. The proximal spike of the metaphyseal fragment (dotted line) was very prominent (arrow). B, Eighteen months later, she still could not abduct past 120 degrees, which interfered with her basketball skills. The prominence of the metaphyseal spike remained (arrow). C, A valgus osteotomy was performed, which directed the varus of the head and allowed her to assume full abduction. (Photo courtesy Earl A. Stanley, Jr., M.D.) Avascular Necrosis.

Avascular necrosis of the humeral head is not uncommon in comminuted fractures of the proximal humerus in adults. It is extremely rare in the skeletally immature. A recent article by Martin and Parsons[71] described a case of a 14-year-old who had a Neer II physeal injury. The patient was not symptomatic until 7 months after the fracture. One year later, the lesion had healed with no significant deformity. Lipscomb[70] in 1975 described a case of localized avascular necrosis producing a

condition similar to osteochondritis dissecans of the knee that developed in an athlete from a chronic stress injury involving the proximal humeral epiphysis. This resulted in a loose body that needed to be removed surgically.

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Section N Nerve Lesions of the Shoulder Kenneth P. Butters MD Kenneth M. Singer MD Suprascapular Nerve Palsy

Compression or injury of the suprascapular nerve at the scapular notch can result in pain and motor weakness of the supraspinatus and infraspinatus muscles. Atrophy will later result and is often the clue to the clinical diagnosis. A direct blow or forceful scapular protraction may cause traction on the nerve at Erb's point or kinking at the suprascapular or spinoglenoid notch.[64] Suprascapular neuropathy has been reported in many types of athletes.[10] [26] [59] In the sports setting, spontaneous recovery of suprascapular nerve function is the usual course, suggesting that the process is often a nerve injury rather than entrapment neuropathy. Isolated partial infraspinatus palsy may present as painless posterior shoulder atrophy and weakness in throwers, allowing good function. Compression of the infraspinatus branch with a ganglion at the spinoglenoid notch has also been reported,[66] as have bilateral nerve palsies. [30] Anatomy and Biomechanics

The suprascapular nerve arises from C5-C6 at the upper trunk of the brachial plexus, where it passes deep to the trapezius and the omohyoid. It enters the supraspinatus fossa via the suprascapular notch beneath the transverse scapular ligament ( Fig. 21N-1 ). The nerve continues deep to the supraspinatus, innervating it with two branches and sensory branches to the glenohumeral and acromioclavicular joints. There is no cutaneous sensory distribution of the suprascapular nerve. The nerve then reaches the lateral edge of the spine of the scapula and descends through the spinoglenoid notch to enter the infraspinatus fossa. A spinoglenoid ligament is described in 50% to 80% of patients[10] [18] passing from the glenoid neck up to the spine of the scapula and dividing the two spinati muscles. Demirhan and associates[19] found

the spinoglenoid ligament present more commonly in men (64% to 36%). The ligament inserts into the posterior capsule and tightens with cross-body adduction/internal rotation.

Figure 21-N-1 Anatomy of the suprascapular nerve. (Redrawn from Black KP, Lombardo JA: Suprascapular nerve injuries with isolated paralysis of the infraspinatus. J Sports Med 18[3]:225-228, 1990.)

Cummins and colleagues[18] classified two types of spinoglenoid ligament: Type I, a thin fibrous band 60%, and type II, a distinct ligament 20% with 20% absent. Bigliani and coworkers[9] found the average distance from the supraglenoid tubercle to the nerve at the suprascapular notch was 3 cm. The distance from glenoid rim to spinoglenoid notch is 1.8 to 2.1 cm.[9] [73] The suprascapular notch may assume various shapes, as was described by Rengachary and associates.[56] It is most commonly U-shaped and varies from wide open to enclosed with bone. The suprascapular nerve, then, is fixed at its origin in the brachial plexus and at its terminal branches into the infraspinatus. In addition to the suprascapular notch and the lateral edge of the spine of the scapula (spinoglenoid notch), several other possible sites of injury have been suggested in anatomic studies.[59] The width of the transverse scapular ligament parallels the size of the notchthat is, a larger bony notch results in a larger foramen.[56] No translational motion of the suprascapular nerve through the foramen has been seen. The nerve, however, forms an angle at the foramen. Nerve contact with the ligament is accentuated with depression retraction or hyperabduction of the shoulder. The mechanism of nerve injury, then, may well result from this sling effect. [56] The cadaver studies[57] showing that extremes of scapular motion can render the suprascapular nerve taut and kink it present a concept that is supported by Sunderland[65] and Drez.[23] Regarding compression of the suprascapular nerve at the spinoglenoid notch, Ferretti and colleagues[27] suggested a mechanism of nerve compromise by hyperabduction of the shoulder with eccentric contraction of the infraspinatus. Another theory is nerve compression against the lateral margin of the spine of the scapula by supraspinatus and infraspinatus tendons at their point of juncture.[27] Ganglions are thought to form from superior labral tears, with the cyst expanding into this region without overlying muscle or tendon, compressing the infraspinatus branch ( Fig. 21N-2 ).[50] Mallon and coworkers[45] reported suprascapular nerve palsy after resection of the distal clavicle. The nerve is located only 1.4 cm behind the clavicle and within 2 to 3 cm of the joint.

Figure 21-N-2 Magnetic resonance imaging of the right shoulder shows a ganglion at the superior and posterior glenoid, compressing the infraspinatus branch of the suprascapular nerve at the spinoglenoid notch.

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Clinical Evaluation

The athlete may have a history of trauma, but more often, the complaint is vague discomfort or weakness. Pain is usually localized posteriorly. If the infraspinatus alone is involved in the lesion at the spinoglenoid notch distal to the acromioclavicular and glenohumeral branches, the presentation may be one of painless atrophy and external rotation weakness. Diagnosis of suprascapular nerve compression is often difficult. It requires careful shoulder examination, including visual posterior shoulder inspection and testing of external rotation strength, as well as complete neurologic evaluation at the neck and proximal extremity and, most importantly, electrical evaluation. The pain is usually located in the posterior shoulder and radiates to the arm; it may be worse with adduction of the shoulder.[54] Posterior shoulder muscular atrophy, especially in the infraspinatus fossa, is an important finding. Supraspinatus atrophy may be difficult to see, and its weakness is not as easily exposed as that of the infraspinatus. I have not found suprascapular notch tenderness to be consistently helpful, but Post and Mayer[54] noted it in seven of nine patients. There are few data on the incidence of fracture of the scapula with associated nerve palsy. Edeland and Zachrisson described 18 scapular fractures, 7 with clinical involvement of the suprascapular nerve and only 1 with positive electromyographic (EMG) findings.[24] Treatment of suprascapular neuropathy after scapular fracture should probably include early exploration of the nerve with neurolysis and notch resection. A work-up for a patient with suprascapular nerve palsy should include shoulder views and, if necessary, a cervical spine series. A 30-degree cephalic tilt view radiograph to visualize the suprascapular notch is helpful, especially in patients with fractures ( Fig. 21N-3 ). If the differential diagnosis includes suspicion of rotator cuff disease, appropriate evaluation of the rotator cuff is indicated with ultrasound, magnetic resonance imaging (MRI), or arthrogram. MRI is the optimal imaging study for evaluating sites of entrapment by soft tissue lesions most commonly ganglion cysts.[47] I have also used a local anesthetic block in the suprascapular notch area as part of a series of diagnostic injections.

Figure 21-N-3 Radiograph of suprascapular notch fracture with 30-degree cephalic tilt.

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Nerve Studies

Electrical evaluation should include EMG of the entire shoulder girdle, including the paraspinous muscles, and nerve conduction studies from Erb's point to the supraspinatus, then comparison of these values with those of the opposite side. Of course, the supraspinatus may be spared by a lesion at the spinoglenoid notch. Normal latency values in nerve conduction studies are 1.7 to 3.7 msec to the supraspinatus and 2.4 to 4.2 msec to the infraspinatus. Nerve conduction studies should be abnormal to confirm the diagnosis of suprascapular nerve compression. Electromyographic abnormalities occur with brachial neuritis, cervical root compression, and incomplete brachial plexus stretch. Also, some feel that EMG studies may be normal with an obvious clinical suprascapular nerve deficit,[15] [74] confirming the need for the nerve latency examination. Compression with ganglia may involve only one of the three or four suprascapular nerve branches to the infraspinatus, so EMG recordings should be done at more than one location within the muscle. Treatment

Treatment of a patient with closed, acute suprascapular nerve injury is initially conservative, involving follow-up of the problem at frequent intervals, including electrical studies. A patient with a chronic condition (6-12 months) with well-established atrophy requires surgery, as does a patient with suprascapular nerve palsy associated with scapular fracture in the area of the suprascapular notch, or the presence of posterior scapular ganglia that produce pain. When a ganglion is discovered as the cause of suprascapular nerve palsy, arthroscopy should be done to look for labrum lesions commonly needing repair or débridement.[25] In addition, Ianotti [37] described arthroscopic decompression of the cyst, usually seen at the posterior labrum through the anterosuperior portal with the assistance of a knife or probe along the glenoid neck through the posterolateral portal. Aspiration and steroid injection of posterior/superior ganglia is also good initial treatment, with one report of only 1 in 5 cases developing recurrent cyst. In painless infraspinatus muscle palsy, without a cyst, function is usually good with nonoperative care. Also, asymptomatic ganglia without nerve findings may not require treatment.[22] [25] [27] [67] In cases of suprascapular nerve palsy or infraspinatus branch palsy alone with a ganglion, surgical treatment is indicated. Surgical decompression of the suprascapular nerve is done with the patient in the lateral decubitus position, and the incision is made parallel to the spine of the scapula. Subperiosteal removal of the trapezius attachment to the spine exposes the supraspinatus and its superior border. This upper border of the supraspinatus is carefully retracted inferiorly and posteriorly to expose the superior surface of the scapula and the suprascapular notch and ligament. The suprascapular artery crosses above the ligament and the nerve below. Ligament excision should be done, along with appropriate bony resection, with a laminectomy rongeur. Rask reported two cases in which repeat decompression of the nerve with bony resection gave good results; he recommends wide notch resection as primary treatment.[55] Certainly, if there is any question about the nerve being free, notch resection is indicated. In thin individuals, a less extensile trapezius-splitting approach can be used through a strap incision across

the spine of the scapula 2 cm medial to the acromioclavicular joint. The trapezius is split 5 cm in length centered over the skin incision. When decompression of the nerve at the spinoglenoid notch is necessary with excision of ganglia, a surgical approach to the posterior glenoid is taken. This approach is begun with a deltoid split over the glenohumeral joint with limited deltoid detachment laterally from the acromion. The superior edge of the infraspinatus is identified, and at most, the upper one half of that tendon is detached, leaving a humeral side stump for repair.[66] The size of the exposure needed is based on the MRI position of the ganglion and the size of the patient. Sports

Suprascapular nerve injury may present after specific trauma, with chronic onset of pain or weakness, or with insidious painless muscle atrophy. Bateman stated that athletic stress, especially throwing, produces a backward and forward rotation of the scapula, and suprascapular nerve compression at the notch.[5] Jobe and colleagues have stated that in the athlete, the nerve is often injured as it passes around the lateral spine of the scapula, sparing the supraspinatus.[39] It has been their experience that if the nerve lesion is at the suprascapular notch, the condition does not respond well to surgical management. In patients with spinoglenoid notch lesions, if the infraspinatus alone is not completely denervated, a program of therapy can allow the elite pitcher to return to high-level competition. Jobe and colleagues' EMG studies showed that only 30% to 40% of the maximum strength of the infraspinatus is used during throwing, and, with a partial nerve injury, a return to pitching, at least, is possible. [39] Ferretti and associates[26] studied asymptomatic volleyball players and found that 12 of 96 had isolated partial infraspinatus paralysis mostly in a dominant shoulder; some had electrical abnormalities, others had muscle atrophy, and there was a 15% to 30% loss of external rotation power.[26] They suggested that the cause was nerve tension at the spinoglenoid notch when the arm is cocked in maximum stretch and during follow-through. In a longer term study, Ferretti had 35 such patients with isolated infraspinatus atrophy and re-examined 16 at 5.5 years average follow-up. All were still able to play volleyball at a high level with atrophy unchanged. He also found the incidence of subacromial impingement in this series to be no higher than in the general population of volleyball players.[27] Suprascapular neuropathy has been reported with acute shoulder dislocation in a cyclist[78] and with sudden onset after a hard throw from center field in a professional baseball player.[11] The literature is confusing in that it refers to problems with the suprascapular nerve as both compression syndrome and nerve stretch injury.

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The overall good response to conservative management suggests that nerve injury may be the cause. Rest from sports or other inciting causes may be helpful. Return to activity is permitted according to the judgment of the physician, based on factors in the course of follow-up, including the extent of the initial paralysis, electrical studies, symptoms, and improvements in the muscle examination with therapy. Surgical exploration of a well-localized lesion should be performed if conservative management of 3 to 6 months has failed.

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Long Thoracic Nerve Anatomy

Long thoracic nerve palsy causing paralysis of the serratus anterior with winging of the scapula is a rather disabling lesion. The nerve is formed from roots of C5, C6, and C7, which branch shortly after they exit from the intervertebral foramina. Branches of C5 and C6 pass anteriorly through the middle scalene muscle, then fuse and pass over the posterior scalene. A C7 branch joins to form the long thoracic nerve. The nerve courses behind the brachial plexus to perforate the fascia of the proximal serratus anterior. It then passes medial to the coracoid on the frontal view and has an overall length of 30 cm[34] ( Fig. 21N-4 ). The serratus anterior covers much of the lateral thorax and acts with the trapezius to position the scapula for elevation. It arises from the upper nine ribs and attaches at the deep surface of the scapula along the vertebral border. This powerful muscle draws the scapula forward and rotates its inferior angle upward. The serratus anterior also acts as an accessory inspiratory muscle, as is seen in runners who fix their scapulae by holding their thighs to catch their breath after a race.

Figure 21-N-4 The brachial plexus. (Modified from Haymaker W, Wood-hall B: Peripheral Nerve Injuries. Philadelphia, WB Saunders, 1956.) Etiology of Disorders

The long thoracic nerve is often affected by the poorly understood syndrome of brachial neuritis. Long thoracic nerve palsy may occur with prolonged recumbency or intraoperative stretch during thoracic surgery. Serratus anterior weakness following transaxillary first rib resection is not uncommon and has a good prognosis, although complete paralysis has a poor outlook.[39] Other causes of nerve palsy include backpacking and shoveling. Proposed traumatic mechanisms include crushing of the

nerve between the clavicle and the second rib, [36] tetanic scalenus medius muscle contraction, and nerve stretch with head flexion or rotation and lateral tilt with ipsilateral arm elevation or backward arm extension.[34] The outcome of acute traction injuries is good.[36] [56] Because the nerve is deeply located, a direct blow seems unlikely to cause isolated palsy. Serratus anterior rupture has been reported in patients with rheumatoid arthritis.[49] Brachial neuritis is a clinical syndrome of unknown cause and is the most common cause of serratus anterior palsy in the authors' experience. Significant pain lasting a variable timedays to weeksprecedes loss of function in one or more shoulder girdle proximal extremity muscles. Sensory loss does not exclude the syndrome. In the literature, there is a good prognosis for recovery, with 36% of patients recovered by the end of the first year and 75% by the end of the second year.[68] Some improvement may occur after 2 years.[28] Recurrent long thoracic nerve palsy is very rare.[34] Parsonage and Turner coined the term neuralgic amyotrophy (brachial neuritis) in 136 military personnel, 30 of whom had isolated serratus anterior paralysis. They also noted a right-sided predominance. Clinical Evaluation

In the clinical syndrome, paralysis of the serratus anterior causes winging and a lack of scapular stabilization, limiting active shoulder elevation to 110 degrees in patients with complete lesions.[34] Winging of the scapula is usually brought out with resisted active arm elevation or by doing a push-up while leaning against a wall ( Fig. 21N-5 ). A patient with an early palsy may present with subtle changes in the ability to perform his or her sport, along with decreased active range of motion of the shoulder and altered scapulohumeral rhythm. Other causes of winging other than serratus anterior palsy include trapezius palsy, painful shoulder conditions resulting in splinting of the glenohumeral joint, winging associated with multi-directional instability, and voluntary winging. The onset of long thoracic nerve palsy may be painful as in brachial neuritis, or it may be more subtle, involving problems with weight-lifting or the feeling of pressure from a chair against the winging scapula while one is sitting. After an acute injury, several weeks may pass before marked scapular winging is evident. Gregg and colleagues believe that time is needed for the trapezius to stretch out and for scapular winging to become evident.[34]

Figure 21-N-5 Scapular winging is often discovered during weight training as the scapula protrudes with resisted elevation or contacts the flat surface during bench press. If weightlifting is felt to be the cause, resumption of participation should await return of nerve function. Return to sports by patients with long thoracic nerve palsy depends upon the demands placed on the upper extremity by the sport.

Electromyographic studies will confirm the diagnosis of long thoracic nerve palsy. Conduction studies can be

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performed from Erb's point to the serratus anterior muscle on the anterolateral chest wall. The appearance of winging with arm elevation due to serratus anterior palsy differs from that of winging due to trapezius palsy. When the serratus anterior muscle does not function, the inferior tip of the scapula is pulled medially and posteriorly. With trapezius paralysis, the scapular body is held in position, and the medial border merely becomes more prominent, a more subtle deformity. In neither type is the scapula rotated laterally to facilitate arm elevation. Treatment

Cessation of the suspected inciting activity is important. Canvas-reinforced shoulder braces cannot begin to normalize the force coupled on the scapula of the serratus anterior and the trapezius. With serratus winging, braces may prevent the stretching out of the trapezius muscle. Surgically, pectoralis minor transfer[13] [71] to the lateral inferior scapula for dynamic support has been reported. Transfer of the pectoralis major (sternal head) with fascia lata extension to the inferior border of the scapula is the currently favored reconstruction. [46] Fortunately, surgical treatment is seldom needed. Sports

Sports have been implicated as a cause of isolated serratus anterior palsy[28] [34] [40] with traction injurysingle or repetitiveto the long thoracic nerve being the proposed mechanism. In one series, the repetitive trauma of tennis and archery was thought to be the cause of the lesion in 5 of 20 patients. Other sports implicated in this type of injury are basketball, football, golf, gymnastics, and wrestling.[48]

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Accessory Nerve Anatomy

The spinal accessory nerve is a pure motor nerve innervating the trapezius and sternocleidomastoid muscles. The nerve leaves the jugular foramen at the base of the skull, goes through the upper third of the sternocleidomastoid muscle, and crosses the posterior triangle of the neck. It is here that it is superficial and vulnerable to injury. The nerve enters the trapezius and is the predominant motor nerve to that muscle. Root fibers from C3 and C4 also innervate the trapezius and may blend with the accessory nerve; some feel that this C3-C4 contribution is only proprioceptive.[51] The accessory nerve is smallonly 1 to 3 mm in diameter.[70] Scapular stabilization and elevation result from the balance of the forces of the trapezius and serratus anterior. The upper trapezius elevates and tilts the scapula, raising the point of the shoulder and assisting in arm elevation, respectively. The lower trapezius works with the rhomboids to retract the scapula and balance the pull of the serratus anterior. The nerve may be damaged, as it is most commonly, during a posterior triangle node biopsy or by a direct blowfor example, with a hockey stick or in a traction injury with a cross-face maneuver in wrestling.[16] Stretch injury resulting from distal upper extremity distraction and contralateral head rotation has been reported.[44] Clinical Evaluation

The patient complains of a sagging shoulder and incomplete arm elevation with loss of strength ( Fig. 21N-6 ). The symptoms may be quite severe owing to muscle spasm and brachial plexus traction neuritis. Examination does indeed show a drooping of the shoulder or a deepening of the supraclavicular fossa after trapezius atrophy has occurred. Also, winging of the scapula occurs with resisted arm elevation. The levator scapulae is palpable and is seen as a band of muscle in the neck; rhomboid contraction

is also palpable on attempted scapular adduction.

Figure 21-N-6 A, Drooping of the right shoulder when the patient is relaxed. B, There is no voluntary elevation of the shoulder on the right compared with the left. Treatment

Closed injuries should be followed for 6 months before exploration of the nerve is considered, and for 12 months before reconstruction is done. Accessory nerves that are not functioning clinically or electrically at 6 weeks following open posterior triangle surgery should be explored with neurolysis, repair, or graft. The clinical situation may require earlier exploration. When accessory nerve palsy is judged to be permanent and the patient is symptomatic

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with upper extremity drooping, aching, and numbness with incomplete active arm elevation, reconstruction may be indicated. Adjacent scapular muscles cannot substitute for a paralyzed trapezius with muscle strengthening alone. The current operation of choice has been described by Bigliani.[7] The levator scapulae and rhomboids are moved to a more lateral insertion on the scapula to substitute for the upper, middle, and lower trapezius. Other operations described include a scapular suspension with fascial grafts from the vertebral spine to the medial scapula or from the ribs to the scapula, and scapulothoracic fusion.[2] Sports

Cases have been reported of a wrestler and a hockey player[16] with closed accessory nerve palsy, and the authors have seen a rugby player with palsy resulting from a direct blow; all were recovering nerve function with observation. Winging is less obvious and often is less disabling with trapezius palsy than with serratus anterior palsy. Shoulder function in an athlete with accessory nerve palsy may be inadequate for competition.

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Section O Thoracic Outlet Syndrome Karim Abdollahi MD Virchel E. Wood MD History

Thoracic outlet syndrome (TOS) was described by Paget as an effort thrombosis of the subclavian vein in 1875 and was discussed similarly by von Schroetter in 1884.[27] In 1740, Hunauld[12] first described compression of the thoracic outlet secondary to a cervical rib. In 1919, Stopford and Telford showed that the neurovascular structures could be compressed by the first thoracic rib and that surgical removal of this rib would alleviate symptoms of the compression.[31] The first cervical rib removal was performed by Coote[5] in St. Bartholomew's Hospital in 1861. Twenty-nine years later, the second case of a cervical rib was removed. Murphy[15] was the first to remove a normal first thoracic rib for TOS in 1910. TOS has been called by various names ( Table 21O-1 ). TABLE 21-O-1 -- Synonyms for Thoracic Outlet Syndrome Shoulder-hand syndrome Paget-Schroetter syndrome Cervical rib syndrome

First thoracic rib syndrome

Scalenus anterior syndrome

Brachiocephalic syndrome

Scalenus minimus syndrome

Scalenus medius band syndrome

Costoclavicular syndrome

Humeral head syndrome

Hyperabduction syndrome

Nocturnal paresthetic brachialgia

Fractured clavicle syndrome

Cervicobrachial neurovascular compression syndrome

Pneumatic hammer syndrome

Effort vein thrombosis

Rucksack paralysis

Pectoralis minor syndrome

Cervicothoracic outlet syndrome

Subcoracoid syndrome

Syndrome of the scalenus medius band

Naffziger's syndrome

Acroparesthesia

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Anatomy

The thoracic outlet involves the area of the shoulder girdle and thorax in which the subclavian artery and vein exit the chest cavity and combine with the brachial plexus, passing through the scalene triangle over the first rib and under the clavicle to enter the axillary region of the shoulder ( Fig. 21O-1 ). The anatomic boundary of the thoracic outlet consists of the superior surface of the first rib and the anterior scalene muscle and the middle scalene muscle, both of which insert into the first rib. The clavicle overrides the neurovascular structures and applies pressure on the thoracic outlet if it is displaced or positioned posteriorly. Neurovascular compression within the thoracic outlet involves the subclavian artery, the subclavian vein, or the brachial plexus within this area. Compression may involve a cervical rib abnormality or the anterior or middle scalene muscle, or it may occur at the costoclavicular or subclavian tendon junction, at the level of the first rib, or as far laterally as the pectoralis minor insertion into the coracoid process.[16]

Figure 21-O-1 Compression of neurovascular structures may occur at three points. The brachial plexus may be compressed between the anterior and the middle scalene muscles, causing upper thoracic outlet syndrome (A). Most commonly, compression occurs between the clavicle and the first rib (B). The pressure effect between the pectoralis minor and the rib cage is specifically assessed when performing Wright' hyperabduction maneuver (C). a., artery; m., muscle; v., vein.

Anatomic factors include an inadequate intrascalene triangle (which may be due to anterior or middle scalene hypertrophy or spasm), a high first thoracic rib, or descent of the shoulder girdle with age, allowing a sagging effect and compression of the neurovascular structures. Congenital factors, such as a cervical rib, a rudimentary or anomalous first thoracic rib, variant scalene muscles, an elongated transverse process, or adventitial fibrotic bands, may be present.[24] Wood and Marchinski[34] described anomalous muscles such as the axillopectoral muscle (4% to 8%), chondroepitrochlear muscle, and subscapularis-teres-latissimus muscle (5.2%). Further considerations

include traumatic factors, such as fracture of the clavicle, injuries to the cervical vertebrae, dislocation of the head of the humerus, and atherosclerosis of the major arteries at the isthmus of the neck of the humerus.[20] Kofoed[13] emphasized the necessity of ruling out cervical disk herniation in the evaluation of TOS. Differential diagnoses in TOS include any pathology creating pain in the neck, arms, or shoulders ( Table 21O-2 ). TABLE 21-O-2 -- Differential Diagnoses for Thoracic Outlet Syndrome Bursitis Cervical arthritis Glenohumeral joint instability Myositis Fibrositis Brachial plexus neuritis Raynaud's disease Thromboangiitis Neoplasm of the spinal canal Neoplasm of the peripheral nerve Apical pulmonary neoplasm Cervical disk disease Peripheral nerve compression (cubital and carpal tunnels)

Roos[26] observed that 98% of his patients with TOS had anomalous fibrous muscular bands that probably irritated or compressed the brachial plexus. Nine different bands were described. The most frequent one is type 3, which is

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a fibromuscular structure originating on the neck of the first rib and passing horizontally across the thoracic outlet to lie between the T1 root of the plexus and the subclavian artery ( Fig. 21O-2 ). Type 7 is a fibrous cord attaching to the anterior surface of the anterior scalene passing under the subclavian vein to attach to the posterior surface of the sternum ( Fig. 21O-3 ). The other seven types have been described in detail.[26]

Figure 21-O-2 Type 3 is the most frequent type of anomalous band encountered in thoracic outlet syndrome. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome. The results of first rib

resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

Figure 21-O-3 A type 7 band found in thoracic outlet syndrome may cause venous thrombosis. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome. The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

TOS usually involves the lower plexus, but when the upper plexus is involved, other abnormalities may be present. Roos[26] described five types of anomalies that primarily involve the relationship between scalene muscles and the upper brachial plexus. The patient clinically presents with symptoms of median nerve compression. The most frequent upper plexus anomaly is type 3, in which the anterior scalene muscle passes between the roots and trunks of the plexus ( Fig. 21O-4 ).

Figure 21-O-4 In a type 3 anomaly, the anterior scalene muscle passes between the roots and the trunks of the plexus. (From Wood VE, Ellison DW: Results of upper plexus thoracic outlet syndrome operation. Ann Thorac Surg 58:458-461, 1994. Reprinted with permission from the Society of Thoracic Surgeons.)

TOS may be caused by compression in the subcoracoid space, which is immediately posterior to the origin of pectoralis minor from the coracoid process. [19] When performing the Wright hyperabduction maneuver, the neurovascular bundle gets stretched by the coracoid process and compressed by the pectoralis minor in the subcoracoid space and may lead to loss of radial pulse, paresthesias, or both. Effort thrombosis of axillary or subclavian vein seems to be related to overstretching of the venous wall or occluding pressure against the vein by the first rib.

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Symptoms

Although pain, weakness, and neurovascular deficits are associated with TOS, often the symptoms are quite bizarre and may be intermittent. Awareness of the occurrence of TOS and the presence of clinical objective findings are necessary to diagnose this syndrome. Neurologic symptoms consist of weakness, fatigability, numbness, and tingling, particularly in the distribution of posterior and medial cords of the brachial plexus. A pain diagram with a questionnaire can be helpful. Vascular symptoms consist of ischemia, claudication, cold intolerance, swelling with venous congestion, and occasional thromboembolic phenomena with distal arterial occlusion. Symptoms are especially pronounced with arm elevation

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above the level of the shoulder, particularly during throwing, combing the hair, or sleeping with the arm above the head. Half of our patients indicated that a single traumatic event precipitated TOS, such as a motor vehicle accident in which the neck or upper torso was injured.[8] In our cases, the problem with the ulnar nerve alone was the most common symptom,[35] followed by problems of the artery and the median nerve alone in 12%. There were many combinations of symptoms. Two of our patients were admitted to the hospital for a heart attack, and two other patients had Raynaud's phenomenon. Three women had unilateral breast swelling and severe breast pain. Shoulder pain in athletes usually is due to musculoskeletal problems, such as impingement syndrome and glenohumeral instability. Less commonly, the shoulder pain

may be caused by TOS. Repetitive throwing activities in the extended, abducted, externally rotated position of the arm aggravate the symptoms ( Fig. 21O-5 ). Pressure on the brachial plexus and artery, especially during overhead exertions, may result in fatigue, aching, and inability to perform competitive activities such as swimming.[14] The swimmer may present with complaints of inability to keep fingers together during the pull-through phase of the swimming strokes. The water polo athlete may have trouble grabbing, holding, and throwing the ball. These symptoms are due to weakness in the intrinsic muscles of the hand, which suggests compromise of C8 and T1 nerve roots.

Figure 21-O-5 Axillary artery compression by the pectoralis minor muscle at the coracoid process insertion in the throwing athlete.

Effort thrombosis of the subclavian vein (Paget-Schroetter syndrome) has been reported in a competitive swimmer.[33] TOS of vascular origin comprises only 2% of patients; 97% present with neurologic symptoms. Athletes may present with generalized aching, fullness, and swelling of the arm. If acute, swelling may be significant; superficial veins may not drain with arm elevation. The incidence is higher in young, physically active males 15 to 40 years old.[14] Ten of our patients presented with a venous thrombosis, which represented 3% of our patients with TOS. Paget-Schroetter syndrome has been reported in several overhead athletes, including weightlifters ( Fig. 21O-6 ).

Figure 21-O-6 A, This weightlifter developed effort vein thrombosis with swelling and pain in the left arm. B, The venogram shows multiple clots. This was called Paget-Schroetter syndrome in the older literature. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome. The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

Because aquatic athletes are primarily overhead athletes, one may expect a higher incidence of TOS in this population. Swimmers require controlled, repetitive power strokes

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at the extremes of abduction and external rotation of the shoulder.[19] If the athlete complains of tightness and pain about the shoulder at the point the hand enters the water, the physician should be alerted to the possibility of TOS. Water polo also subjects the shoulder to repetitive abduction and external rotation in throwing and in blocking a shot. In upper TOS, athletes may complain of pain in the lower face and ear; headaches; and radiation of the pain to shoulder, thumb, and index and middle fingers.[19] This presentation should be distinguished from swimmer's ear (otitis externa). Patients also may complain of weakness or fatigue in the upper extremity muscles.

Priest and Nagel[17] described tennis shoulder as a depression or drooping of the exercised shoulder that they attributed to stretching of the muscles that elevate the shoulder and hypertrophy of the extremity. Shoulder droop may induce TOS by increasing the pressure at the thoracic outlet. Symptoms may be reduced by strengthening the shoulder-elevating muscles (levator scapulae, rhomboids, and upper trapezius). Rayan [18] reported on two young athletes with TOS resulting from a cervical rib. Their symptoms increased with sporting activities. They responded well to resection of the cervical rib. Four cases of TOS in athletes were reported by Strukel and Garrick.[31] Their patients responded well to conservative treatment. TOS is seen not only in the throwing athlete,[31] but also in heavy muscular athletes, such as weightlifters, football players, and athletes who may sustain traction injuries to the upper arm and chest. Direct trauma that results in rib fractures, transverse process fractures, clavicular fractures, and shoulder dislocations may precipitate thoracic outlet symptoms.[32]

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Physical Examination

The physical examination is the most important aspect of diagnosing TOS. Adequate time must be allowed to perform the initial evaluation. The female athlete should be in a gown with her hair up. The shoulders should be observed for slouching. The physician should note if the breasts are large. The physician should look for any shoulder asymmetry, especially unilateral drooping or hypertrophy, as may be seen in professional tennis players, shot putters, javelin throwers, and other overhead athletes. The physician should note any venous engorgement or arm swelling (vein thrombosis). The physician should palpate the clavicle for deformity and the supraclavicular area for a cervical rib. Muscles and bones around the shoulder should be palpated, and the physician should document areas of tenderness, especially areas where the patient complains of pain. Sensation may be tested by static and moving two-point discrimination. I (K. A.) prefer to use the 10 test, in which I touch the same area in both upper extremities and ask the patient to rate the symptomatic side 0 to 10 with 10 being normal sensation (as felt on the asymptomatic side) and 0 being no sensation at all. By sensory testing, one can attempt to distinguish between lower TOS (ulnar nerve distribution) and upper TOS (median nerve distribution). If pathology at the nerve root level is suspected, the physician should test sensation by dermatomes and note any reflex asymmetry. Motor weakness, such as with intrinsic muscles of the hand, may be subtle. Comparison to the opposite side is essential. The physician should test for distal sites of nerve compression, such as carpal or cubital tunnel syndromes, before doing provocative maneuvers for TOS.[9] This practice helps minimize false-positive findings of peripheral nerve compression that are seen when the brachial plexus is irritated by provocative maneuvers first.

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Provocative Signs

For a test to be positive, either the symptoms must be reproduced, or the radial pulse must shut off. If the pulse

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shuts off, the opposite side also should be tested. Less value is placed on a positive test result if the pulse shuts off on the asymptomatic arm also. The physician should ask the patient if the baseline paresthesia gets worse with the maneuver and returns to baseline after the maneuver. Between tests, the physician should give the patient a few seconds to shake his or her hand and recover from paresthesias caused by the maneuver. Adson's Test.

The physician palpates the radial pulse and abducts the arm slightly ( Fig. 21O-7 ). The physician asks the patient to hyperextend the neck to turn it to the affected side and inhale deeply. Diminution or obliteration of the pulse probably is due to compression of the axillary artery by the anterior scalene muscle. The patient should turn the head to the opposite side (reverse Adson's test) to test compressive effect of the middle scalene.

Figure 21-O-7 Adson's test: Hold patient's arm in slight abduction while palpating the radial pulse. Ask the patient to extend the neck and rotate toward the affected side. Adson's test is positive if the patient reports paresthesias or if the pulse fades away.

Halstead's Maneuver.

The physician has the patient retract the shoulders downward and backward to draw the clavicle closer to the first rib ( Fig. 21O-8 ). The physician palpates the pulse and asks about worsening paresthesias.

Figure 21-O-8 Halstead's maneuver: Ask patient to pull shoulders backward and downward to depress the clavicle against the first rib. Halstead's maneuver is positive if the patient reports paresthesias or if the pulse is diminished. Wright's Hyperabduction Test.

The physician passively abducts the patient's shoulder to 180 degrees and extends it to compress brachial plexus and vessels between the pectoralis minor and the rib cage ( Fig. 21O-9 ). This maneuver also stretches the structures under the coracoid process. The physician should palpate the pulse and ask about worsening paresthesias.

Figure 21-O-9 Wright's hyperabduction maneuver: Passively abduct the affected side to 180 degrees (more than shown here) while palpating the radial pulse. Paresthesias or diminution of the pulse suggests a positive test. Roos' Test.

Both shoulders are abducted 90 degrees and externally rotated 90 degrees ( Fig. 21O-10 ). The patient opens and closes both hands rapidly for 3 minutes. The physician asks the patient if the two hands feel different from each other and if there are any paresthesias or numbness in the involved hand. A cold sensation or rapid fatigue is suggestive of arterial compromise. A patient with

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TOS is unable to keep the arms and hands elevated because of an ischemic, vascular type of pain.

Figure 21-O-10 Roos' test: Ask the patient to abduct and externally rotate the shoulders and open and close both hands simultaneously for up to 3 minutes. Worsening paresthesias on the affected side indicate a positive Roos' test.

Retroclavicular Spurling's Test.

The physician places the thumb flat and deep into the retroclavicular space and attempts to compress the brachial plexus and vascular structures.[30] The physician should ask the patient if he or she has increasing numbness or tingling in the hand. If the answer is yes, the test is performed on the opposite side as a control. Wright,[37] in his series of 150 asymptomatic normal subjects, found that 92.6% had obliteration of the radial pulse in at least one upper extremity tested in the elevated position. In our experience, the best objective test to diagnose TOS is the Roos test.[24] The retroclavicular Spurling's test is our second most reliable objective test. We believe that at least three or four of the aforementioned five signs should be clearly positive to make the diagnosis of TOS.

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Diagnostic Studies

Diagnostic tests consist of routine chest, cervical spine, and shoulder radiographs. Radiographic evaluation for cervical ribs ( Fig. 21O-11 ), anomalous first and second ribs, pathologic clavicular fractures, and space-occupying lesions such as tumor or aneurysm must be ruled out.

Figure 21-O-11 Prominent cervical rib seen on the right can compress the neurovascular structures in the thoracic outlet.

Arteriography documents arterial compression and possible aneurysm formation about the first rib. Venography documents venous compression or occlusion ( see Fig. 21O-6 ). Peripheral vascular studies, including pulses, blood pressure measurements, and Doppler studies, aid in the diagnosis of thoracic outlet compression and occlusion of the arterial supply to the arm. Electromyography and nerve conduction velocity is negative in most cases of TOS. This test still is recommended, however, because it can help diagnose cervical radiculopathy, carpal tunnel, and cubital tunnel syndromes, which can be seen commonly as part of a double-crush phenomenon. [36] These other sites of compression can be treated to decrease symptoms. MRI has been used to evaluate TOS.[10] [28] Using special techniques in an open MRI scanner, patients were imaged at 0 and 90 degrees and compared with normal subjects. A significantly smaller distance between the rib and the clavicle was seen in the patients with TOS. On coronal views, the compression of the brachial plexus often could be visualized in abduction. Gadolinium-enhanced magnetic resonance angiography, in the neutral and the abducted position, is a good screening test for patients suspected of having TOS. There is no single test that is diagnostic for TOS. The diagnosis is based on the history, physical findings, and supportive diagnostic

testing.

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Nonsurgical Treatment

In most cases, nonoperative treatment is the initial form of management when the diagnosis of TOS is suspected. The treatment program includes not only evaluation, but also patient education, behavior modification, and joint mobilization exercises. If successful, this program is followed continually and should not be terminated. Continued evaluation and monitoring of the patient are necessary. Behavior modification consists of altering sleep patterns, working patterns, and driving patterns and taking general precautions for activities that could compromise the thoracic outlet. Faulty posture must be corrected. Shoulder exercises with emphasis on gradual scapular retraction and shoulder range of motion increase joint motion and allow the cervical spine to achieve axial body and extremity extension and open the thoracic outlet space. Diaphragmatic breathing exercises often are indicated to aid in respiration when there is hypertrophy of the accessory muscles of the chest and neck. In particular, elevation of the rib cage by the pectoralis minor and scalene muscles should be eliminated because this tendency decreases the thoracic outlet space. Weak musculature about the neck

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and shoulder should be strengthened, and shoulder posture should be improved. The upper trunk muscles, such as the serratus anterior, middle and lower trapezius, latissimus dorsi, and rhomboids, must be strengthened. Joint mobilization techniques for the sternoclavicular, acromioclavicular, and scapulothoracic joints improve and increase the costoclavicular space. Likewise, mobilization of the occiput on the atlas facilitates axial extension body movements and improves the symptoms of TOS. Specific joint mobilization and therapy programs have been outlined by Smith.[29] Conservative management should produce improvement in symptoms 1 to 3 months after the onset of symptoms. Physical therapy often exacerbates TOS, however, and should not be tried indefinitely.

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Surgical Treatment

When symptoms persist or become worse with conservative management, surgical intervention may be necessary.[2] Patients with severe, intractable pain; disability; arterial or venous compromise, or neurologic compromise fall into this category.[11] Surgery ranges from resection of the scalenus anterior, described by Adson in 1927, [1] to removal of the first thoracic rib, described by Murphy[15] in Australia and Brickner[3] in the United States. Anterior and supraclavicular approaches have been used by these authors for first rib resection. Another approach used by Clagett [4] was a limited posterior thoracotomy incision, and a transaxillary approach was used by Roos.[22] First rib resections now are done most commonly according to the techniques of Roos through a transaxillary approach. In addition to first rib resection, this approach allows the possibility of performing a thoracic sympathectomy at the same time for pain relief. Scalenectomy by itself does not provide predictable relief of TOS symptoms. Strict attention must be paid to the pathology, and when other causes appear to be operative, they must be corrected. Such correction may include cervical rib resection or excision of callus after a fractured clavicle. Vascular changes, particularly aneurysmal dilation or thromboembolism of the intima of the vessel, must be addressed and corrected surgically at the time of thoracic outlet decompression. In certain instances, a combination of supraclavicular and transaxillary approaches has been used for decompression of the thoracic outlet, first rib resection, and vascular reconstruction including brachial plexus exploration as indicated. Edwards and colleagues[7] performed 52 transaxillary first rib resections in 46 patients, and 42 patients (91%) had immediate improvement in symptoms after surgery, but symptoms recurred in 3 patients 6 to 8 months postoperatively. Donaghy and colleagues'[6] surgical treatment of suspected neurogenic TOS relieved pain and sensory disturbance in 90% of patients but was less effective for relieving muscle weakness (50%). Thrombosis of subclavian or axillary vein may require fibrinolytic therapy with intravenous streptokinase.[33] When recannulation at the vein is confirmed by venogram,

after an appropriate period of warfarin treatment (about 4 months), a first rib resection is recommended. The postoperative care is simple. The patient is allowed limited range of motion of the arm for 3 to 4 weeks. Excessive movement immediately postoperatively encourages scar formation. At 4 weeks, if the range of motion of the shoulder is restricted, we send the patient to physical therapy for range of motion and strengthening exercises. By 2 months, the patient should have full use of the operated extremity.

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Criteria for Return to Sports Participation

Resumption of sports depends on return of range of motion, strength, and endurance in the shoulder girdle and upper extremity. A recovery period of 6 months to 1 year usually is required to maximize functional return in competitive athletes. In the case of effort thrombosis of axillary or subclavian vein, retirement from competitive swimming is likely because of the long-lasting effects.[14]

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Authors' Preferred Method of Treatment Conservative Treatment

Conservative treatment of TOS is aimed at reducing inflammation around the brachial plexus; improving the posture of neck, shoulders, and upper back; and treating muscle spasms.[19] Nonsteroidal anti-inflammatory medications and oral steroids should help decrease nerve irritation. Therapists experienced in dealing with TOS can work on improving flexibility of the shoulder to allow more space between the clavicle and the first rib. Correcting posture and improving muscle balance should decrease compression of the neurovascular structures. Most upper extremity sports, such as tennis, baseball, and all water sports, involve repetitive overhead motions. A period of rest from the offending activity should help. The athlete should be advised to avoid sleeping with the arms overhead either prone or supine. Muscle spasm is thought to play a role in causing TOS. Stretching of scalenes, pectoralis major and minor, trapezius, and levator scapulae may help relieve symptoms or prevent symptoms in the future. Success of conservative treatment of TOS is reported to be 50% to 90%.[19] Our experience has shown, however, that many patients cannot tolerate physical therapy and become much worse. A negative response to therapy may be helpful in the decision process as to when surgery should be done. Surgical Technique

Roos[22] [23] [25] described the operative technique for the transaxillary approach in several articles and gave many valuable pointers for success. We briefly describe our current technique, which is modified from that of Roos. The patient is placed on a table (usually covered with

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an air cushion) with the hips in a straight lateral position and the thorax tilted 60 degrees, with sandbags supporting the back for easy manipulation of the arm. The buttocks are taped in a criss-cross fashion for stability, a pillow is placed between the legs, and the legs are strapped to the table. The incision is made transversely in the axilla at the point where the hairline first breaks from the rib cage up to the axilla when the arm and shoulder are elevated properly toward the ceiling. If one gets too high in the axilla, the fat and lymph nodes from axillary fat make dissection impossible. If one gets below the third rib, the hole becomes extremely deep, making dissection difficult. The transverse incision is curved slightly in the shape of a smile so that it lies in the axillary skin lines, becoming almost imperceptible after 6 months. One of the first structures encountered is the intercostal brachial nerve in the midfield coming from the second intercostal space. Although this may be thought to be a blood vessel, it should not be ligated. The intercostal brachial nerve is protected best by dissecting it free along with a bit of fat tissue. The arm position is extremely important. The wrist lock prevents nerve damage and is the only way to get exposure. This procedure is well described by Roos.[22] The surgeon dissects immediately to the chest wall, at which point all of the structures fall away until the first rib becomes visible. Often the superior thoracic artery lies in the field near the first rib. The artery is ligated easily using vascular clamps. We use a Cobb elevator to remove the soft tissues from the anteroinferior surface of the first rib. When the soft tissues are dissected free, the Cobb elevator is directed posteriorly under the first rib to open up the surrounding field. Theoretically, removing the rib subperiosteally invites recurrence. We and others have not found this to be a problem, but resecting it extraperiosteally invites almost certain damage to the pleura. We next take a right-angle clamp and carefully tease all of the structures from the superior surface of the rib, including the scalenus anterior, subclavius, and a bit of the ligament between the first rib and the anterior clavicle (although this is cut more easily with a knife). All of the abnormal muscle structures inserting on the first rib are teased free with the muscle fibers spread carefully and the pleura protected at all times. The scalenus medius muscle is teased from the first rib. The surgeon now can remove the first rib safely; a special rib cutter and a nerve root retractor (designed by Roos) are indispensable at this point. We have modified the rib cutter to one that is smaller and cuts at a 60-degree angle. The rib cutter is placed as far posterior as possible so that the T1 nerve root is visualized away from the tips of the rib cutter. The posterior part of the rib is cut, and using two Kocher clamps, the rib is pulled gently from the rib cage. Particularly in women, the rib can be avulsed by a gentle pull from the sternocostal junction. If it is impossible to remove the rib from the sternocostal junction, it can be cut anteriorly with the rib cutter. With these maneuvers, one can obtain, in most cases, the entire first rib except for the posterior stump. The stump

should be cut and left short so that it lies posterior to the T1 cervical root; the remaining first rib should be less than 2 cm in length. A box rongeur is used to trim the first rib back to the level of the transverse process of the seventh cervical vertebra. If a cervical rib is 2 cm or less, resection usually is not necessary, but the muscles coming from its tip should be removed. At this point, the lung is checked carefully for holes by putting saline into the wound and overinflating the lungs. If a pneumothorax is found, a chest tube is placed into the hole. The skin is reapproximated with a subcutaneous and subcuticular stitch, and the wound is left undrained because there have been few problems with infection. The chest tube usually is removed the following day. Roos[26] suggested that a clinical presentation of upper or lower plexus symptoms is an appropriate criterion to use in selecting the surgical approach for relieving thoracic outlet compression. Because the upper plexus lies beneath the anterior scalene muscles, we recommend an anterior scalenotomy through the superior clavicular approach for upper plexus symptoms as well as a transaxillary resection of the first rib. A first rib resection is recommended for the relief of lower plexus symptoms; scalenectomy and first rib resection are performed easily through the transaxillary approach. If there is any indication that the thoracic outlet is not decompressed thoroughly, one should not hesitate to do a combined approach. Removal of the first rib is a surgical procedure that must be thought out carefully and executed meticulously because it is a procedure often associated with malpractice suits. The TOS operation is not a procedure that lends itself well to teaching, and it is not a procedure easily mastered.[21] The procedure requires at least two assistants.

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Coote H: Exostosis of the left transverse process of the seventh cervical vertebra, surrounded by blood vessels and nerves: Successful removal. Lancet 360, 1861. 5.

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Hunauld FJ: Sur le nombre des cotes, moindre ou plus grand a l'ordinaire. Hist Acad Roy d sc (de Paris), 1740. 12.

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Kofoed H: Thoracic outlet syndrome: Diagnostic evaluation by analgesic cervical disk puncture. Clin Orthop 146:145-148, 1980. 13.

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McMaster WC: Swimming injuries: An overview. Sports Med 22:332-336, 1996.

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Murphy T: Brachial neuritis caused by pressure of first rib. Aust Med J 15:582, 1910.

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Nichols HM: Anatomic structures of the thoracic outlet. Clin Orthop 207:13-20, 1986.

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Priest JD, Nagel DA: Tennis shoulder. Am J Sports Med 4:28-42, 1976.

Rayan GM: Lower trunk brachial plexus compression neuropathy due to cervical rib in young athletes. Am J Sports Med 16:77-79, 1988. 18.

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Richardson AB: Thoracic outlet syndrome in aquatic athletes. Clin Sports Med 18:361-378, 1999.

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Riddell DH: Thoracic outlet syndrome: Thoracic and vascular aspects. Clin Orthop 51:53-64, 1967.

Roeder DK, Mills M, McHale JJ, et al: First rib resection in the treatment of thoracic outlet syndrome: Transaxillary and posterior thoracoplasty approaches. Ann Surg 178:49-52, 1973. 21.

Roos DB: Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 163:354-358, 1966. 22.

Roos DB: Experience with first rib resection for thoracic outlet syndrome. Ann Surg 173:429-442, 1971. 23.

Roos DB: Congenital anomalies associated with thoracic outlet syndrome: Anatomy, symptoms, diagnosis and treatment. Am J Surg 132:771, 1976. 24.

Roos DB: Essentials and safeguards of surgery for thoracic outlet syndrome. Angiology 32:187-197, 1981. 25.

Roos DB: The place for scalenectomy and first-rib resection in thoracic outlet syndrome. Surgery 92:1077-1085, 1982. 26.

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Smedby O, Rostad H, Klaastad O, et al: Functional imaging of the thoracic outlet syndrome in an open MR scanner. Eur Radiol 10:597-600, 2000. 28.

Smith KF: The thoracic outlet syndrome: A protocol of treatment. J Orthop Sports Phys Ther 1:89, 1979. 29.

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Vogel CM, Jensen JE: Effort thrombosis of the subclavian vein in a competitive swimmer. Am J Sports Med 13:269-272, 1985. 33.

Wood VE, Marchinski LJ: Neurovascular abnormalities associated with congenital anomalies. In Rockwood CA (ed): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 142-163. 34.

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Chapter 22 - Arm Section A Soft Tissue Injury and Fractures 1. SOFT TISSUE INJURY AND FRACTURES OF THE ARM IN THE ADULT James B. Bennett MD Thomas L. Mehlhoff MD Anatomy

The arm, exclusive of the glenohumeral joint and the elbow joint, consists of the bony architecture of the humerus, musculotendinous units that originate from the shoulder girdle to insert onto the humerus or pass across the elbow joint, associated neurovascular structures, soft tissue, and skin. This anatomic region is also referred to as the brachium. Skeletal support for the arm is provided by the humerus, which is approximately one fifth the body height in length.[123] The proximal shaft of the humerus at the upper border of the pectoralis major tendon is initially rounded but becomes more prismatic distally in the region of the supracondylar ridges. A medial torsion of approximately 35 degrees occurs in the humerus during growth and is not complete until nearly 20 years of age.[64] The anterolateral surface of the humerus presents a prominent V-shaped roughening approximately at its midlength, the deltoid tuberosity. The anteromedial surface usually presents no conspicuous surface markings. One exception to this is the supracondylar process. A supracondylar process exceeding 3 mm can be found on the anteromedial surface of the distal humerus, 5 to 7 cm proximal to the elbow, in approximately 1% of anatomic specimens.[110] The posterior surface of the humerus is notable for a shallow groove for the radial nerve, passing obliquely in a

lateral and downward direction. Strong intermuscular septa arise from the periosteum of the lateral and medial aspects of the humerus, forming a strong tubular investment that divides the musculature of the brachium into anterior and posterior compartments ( Fig. 22A1-1A ). The anterior compartment includes the preaxial muscles, namely, the coracobrachialis, biceps brachii, and brachialis anticus. The posterior compartment includes the postaxial muscles, namely, the triceps brachii and the anconeus. Interfascial spaces provide for the passage of neurovascular structures, including the radial, ulnar, and median nerves, as well as the brachial artery. The brachial artery is a single vessel throughout the brachium in 80% of cases; however, a proximal bifurcation of the brachial artery in the upper arm may result in a high radial artery in 10% of cases, a high ulnar artery in 3% of cases, and both in 7% of cases.[71] The biceps brachii (musculocutaneous nerve, C5-C6) is a long fusiform muscle with two heads proximally and one tendon distally. The long head of the biceps originates from the supraglenoid tubercle, and the short head originates from the coracoid process; they then join as a common muscle belly. The distal tendon proper inserts into the radial tuberosity but also has a flattened attachment to the lacertus fibrosus[85] ( Fig. 22A1-1B ). One or more accessory heads of the biceps brachii are not uncommon and have been reported in 21% of 130 anatomic dissections.[43] The brachialis anticus (musculocutaneous nerve, C5-C6) arises from the anterior surface of the humerus, as do the medial and lateral intermuscular septa. The brachialis insertion cloaks the capsule of the elbow, the coronoid process, and the ulnar tuberosity distally. The triceps brachii (radial nerve, C7-C8) is composed of three heads. The long head of the triceps originates from the infraglenoid tubercle and with the lateral head forms a common aponeurosis, which inserts along the proximal olecranon. The third head, the medial head, lies deep to the aponeurosis. The cutaneous innervation of the medial aspect of the arm in the axilla is provided by the intercostal brachial nerve (T2). The anterior surface of the arm is supplied by the medial brachial cutaneous nerve (C8, T1) arising from the medial cord of the brachial plexus. The posterior surface of the arm is supplied by the superolateral brachial (branch of the axillary nerve), inferior lateral brachial, and posterior brachial cutaneous nerves, derivatives of the radial nerve. The medial antebrachial cutaneous nerve (C8, T1) follows the basilic vein to supply the medial forearm. The lateral forearm is supplied by the lateral antebrachial cutaneous nerve (C5, C6, C7), continuing from the musculocutaneous nerve ( Fig. 22A1-1C and D ).

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Hypertrophy

Athletic participation in competition produces myriad developmental changes within the upper arm complex. Hypertrophy results from repetitive muscle activity. In an analysis of 50 professional baseball pitchers, King and colleagues [61] demonstrated striking hypertrophy of the entire shoulder girdle, including the latissimus dorsi, pectoralis major, and serratus, as well as of the flexors of the forearm ( Fig. 22A1-2 ). The biceps and triceps are hypertrophied as well. Flexion contracture of the elbow was present in more

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Figure 22-A1-1 A, Muscles, compartments, and intermuscular septa of the arm. B, Neuromuscular anatomy of the upper arm, anterior view. C and D, Cutaneous nerve supply to the arm, anterior and posterior views. E, Neuromuscular anatomy of the upper arm with axillary, radial, and musculocutaneous nerves, lateral view.

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than 50% of the pitchers examined. Almost uniformly, hypertrophy of the humerus was noted, with an increase in both cortical size and density of the humerus.[61] Priest and Nagel[97] reported similar hypertrophy of the humerus in tennis players. Cortical thickness of the humerus on the playing side was 35% greater than that on the nonplaying side in male athletes and 28% greater in female athletes.[61] King and colleagues[61] also reported that along with cortical hypertrophy and muscle hypertrophy, the professional throwing athlete usually demonstrated an increase in external rotation with a concomitant decrease in internal rotation in the shoulder of the pitching arm.

Hypertrophy is a normal response to prolonged heavy arm exercise and should not be misinterpreted as a pathologic condition ( Fig. 22A1-3 ). King and colleagues,[61] in the analysis of the pitching arm of the professional athlete, divided the act of throwing into a cocking phase, an acceleration phase, and a follow-through phase. Each phase of throwing requires a specific interaction of biomechanical forces. The cocking phase is accomplished during the wind-up, when the shoulder is brought into extreme external rotation, abduction, and extension.

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Figure 22-A1-2 Shoulder-upper arm muscle hypertrophy in a professional baseball pitcher.

Repetition of the cocking phase increases external humeral rotation and decreases internal humeral rotation, as noted in professional baseball pitchers. The acceleration phase is a two-stage process. The shoulder is brought

Figure 22-A1-3 Cortical bone thickening and increased bone density in the humerus of a professional athlete.

forward with force while the forearm and hand are left stationary. The elbow is placed in a position of extreme valgus stress as the forces increase in the humeral shaft. The forearm and hand are then rapidly brought forward by the internal rotator of the shoulder. This phase terminates with the release of the ball from the hand. The follow-through phase is the terminal event of the throwing act. It begins with the release of the ball, applies rotation for ball control, and terminates with the force of deceleration of the arm and forearm rotation.[61] Repetitive throwing, muscle imbalance due to hypertrophy or contracture, and fatigue result in pathologic conditions of the arm without a history of specific trauma in the athlete.

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Tendon and Muscle Ruptures

The first report of a tendon rupture is credited to Petit in 1772. [7] Two series of 100 tendon ruptures each were reported by Gilcreest [41] in 1934 and by Haldeman and Soto-Hall[45] in 1935. In each series, the authors noted that tears of the supraspinatus, the long head of the biceps, and the finger extensors (extensor digitorum communis and extensor pollicis longus) were the most common tendon ruptures in the upper extremity. Quadriceps and biceps femoris tendon ruptures were most common in the lower extremity; disruption of the trunk, such as rupture of the rectus abdominis, composed only a small percentage of ruptures. The largest series of tendon injuries was reported in 1959 by Anzel and associates[7] and included lacerations as

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well as ruptures. Of 1014 tendon injuries in 781 patients, 85% occurred in the upper extremity. Of 106 tendon ruptures in the upper extremity, 54.7% involved the supraspinatus tendon, 26.4% the biceps tendon (predominantly the long head), and 1.9% the triceps tendon. Many factors, both local and systemic, may predispose to tendon ruptures. Degenerative changes within tendons near the osseotendinous insertion, sometimes associated with calcification or even bone spurring, have been implicated. [28] Other intrinsic factors leading to tendon rupture have been reported to include intratendinous tumors, such as xanthoma and hemangioendothelioma.[126] Systemic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, hyperparathyroidism, and secondary hyperparathyroidism related to chronic renal failure, have been associated with tendon ruptures.[73] [96] [116] Finally, systemic steroids and local steroids have been

implicated with tendon rupture both clinically and experimentally.[60] [117] The pathophysiologic mechanism of tendon rupture was scientifically investigated and reported by McMaster[75] in 1933. His work demonstrated that a normal tendon will not rupture when the tendon is under stress. In fact, even when a normal tendon had 75% of its fiber sectioned, normal activity did not result in a rupture. Increasing linear tension across the muscle tendon unit caused failure at one of three locations other than within the tendon itself, namely, the muscle belly, the musculotendinous junction, and the tendo-osseous insertion. Most clinical ruptures occur at the tendo-osseous insertion and are more accurately termed avulsions. Rupture of the Pectoralis Major Muscle

Patissier[93] first described the rupture of the pectoralis major muscle from its humeral insertion in 1822. This pectoralis major muscle injury may be incomplete or complete and may occur at the muscle origin from the clavicle or sternum, at the muscle belly, at the musculotendinous junction, or at its insertion into the proximal humerus. This is a relatively uncommon injury but is seen increasingly in sports activities requiring forced contraction against resistance, as in weightlifting, and in those involving forceful adduction and internal rotation against resistance, as in contact sports, football, and wrestling. McEntire and associates[74] reviewed 45 cases in the literature as well as 11 cases from their study in 1972. Currently, there are approximately 100 reported cases in the literature. Clinical Evaluation

The pectoralis major muscle rupture presents clinically as swelling and ecchymosis about the muscle insertion to the humerus and the chest wall. Weakness of internal rotation is present. There is a history of severe searing, burning pain with forceful internal rotation or sudden external rotation against a fixed fulcrum by an adducted, internally rotated forearm. The ecchymosis, which may be delayed, occurs at the site of injury and may be located on the chest wall, at the insertion into the proximal humerus,

Figure 22-A1-4 Left pectoralis major tendon rupture at insertion into humerus. Note ecchymosis at insertion site and enlargement of pectoralis major over chest wall as a result of muscle retraction.

or in the axillary fold ( Fig. 22A1-4 ). The axillary fold is deficient and demonstrates a palpable pectoralis muscle, with a visible defect when the arm is abducted at 90 degrees if insertional avulsion is present. Clinical weakness with adduction and internal rotation is associated with pain and muscle defect. Plain films are normal; however, ultrasound examination and magnetic resonance imaging show pectoralis rupture. Hematoma and pseudocyst formation may be shown as well.

Treatment Options

Conservative treatment is used in pectoralis major muscle sprain or partial rupture. Complete rupture from the chest wall origin and within the muscle substance is also treated conservatively. The hematoma is controlled with cooling, ice, and rest, followed by heat and mobilization to restore shoulder function and pectoralis function. Complete rupture of the pectoralis major muscle in a nonathlete may be treated conservatively as with partial ruptures; however, full strength will not return. The active athlete should be treated with surgical reattachment in cases of tendon avulsion injuries from the proximal humerus for complete restoration of shoulder strength and function. Orava and colleagues[90] and Berson[14] have demonstrated surgical repair of pectoralis major muscles to the humeral insertion lateral to the long head of the biceps brachii tendon. Musculotendinous tears may be sutured directly, but this may be difficult to accomplish owing to the failure of muscle tissue to hold an appropriate suture repair. Park and Espiniella[92] reported excellent results in 90% of their patients repaired surgically compared with approximately 60% of patients treated nonoperatively. Patients treated nonoperatively had varying degrees of weakness in adduction and internal rotation; however, the function of the pectoralis major was well compensated for by the teres major, subscapularis, and latissimus dorsi. Zeman and associates[127] reported similar excellent results in surgically repaired cases and compared them with the residual weakness in the conservatively treated population of patients.

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Postoperative Management and Rehabilitation

The pectoralis major muscle reattachment to the proximal humerus or repairs to the musculotendinous junction are treated initially in a shoulder immobilizer with the arm adducted to the chest wall and internally rotated onto the abdomen, with the elbow flexed at 90 degrees in a neutral position. Immobilization is maintained full-time for 4 weeks; a gentle pendulum and circumduction exercise program is initiated at 2 weeks after repair. After 4 weeks, immobilization is removed, and active and passive range of motion without resistance is continued for an additional 4 weeks. The arm is maintained in a sling at this time, and full range of motion is obtained. Resistive range of motion and strengthening are begun at 8 weeks and continued for 12 weeks. Gentle restricted throwing activities are begun at this time. The entire upper extremity is involved in the rehabilitation process because of disuse atrophy and weakness. Unprotected heavy lifting is restricted for 6 months during the rehabilitation process. Criteria for return to sports participation are maximal functional strength compared with the opposite shoulder and upper arm and full range of motion. Return to sports activities may be at 3 months, with protection against forceful external rotation. Full sports contact

begins at 6 months if strength and range of motion have plateaued and equal those in the opposite extremity. A shoulder harness, a strap to block full external rotation, may be used if the participant is involved in the contact sport of football. Otherwise, full unrestricted activities are allowed at 6 months. Authors' Preferred Method of Treatment

Conservative treatment is used for incomplete tears or tears from the chest at the sternal or clavicular origins. Surgical repair at the musculotendinous junction with nonabsorbable suture and the rehabilitation program are used for high-performance athletes with tears at the musculotendinous junction. In the nonathlete, management is conservative. Tendon avulsions at the insertion of the proximal humerus are reattached to surgically created troughs and drill holes into the humerus with nonabsorbable sutures through cortical bone and are reinforced with appropriate soft tissue and deltoid fascia as outlined in the techniques of Orava and coworkers[90] and Berson.[14] Evacuation of hematoma or pseudocyst with seroma is performed at the same time. Care must be taken to protect the brachial plexus as well as the axillary and brachial vasculature during surgical exposure and reconstruction. The surgical exposure is through a deltopectoral incision, and identification of the tendinous insertion is performed. Mobilization of the pectoralis major muscle from the chest is performed if the muscle is retracted. Repair is lateral to the biceps tendon at the level of the deltoid insertion. In cases of late repair, mobilization is difficult, contraction may be fixed, and reconstruction may be difficult, although Kretzler and Richardson[65] reported repair up to 5 years after injury. Rehabilitation in these cases yields less satisfactory results, with restriction of full functional motion and weakness. For the best outcome, early diagnosis and repair (less than 4 weeks after injury) are recommended. Rupture of the Long Head of the Biceps Brachii Tendon

Ruptures of the long head of the biceps tendon in patients older than 40 years reflect intra-articular impingement and rotator cuff disease. The patient often presents with painless deformity of the biceps that is retracted distally into a ball. This may be associated with relatively minor trauma, such as lifting or pulling activities. The patient has often had shoulder symptoms compatible with impingement. Much less common is rupture or avulsion of the short head of the biceps off the coracoid related to forceful trauma in the young competitive athlete. Neer[83A] reported that in older patients with rotator cuff disease, one third have biceps involvement. Clinical Evaluation

The anterior aspect of the brachium presents with a deformity from the retracted biceps distally as well as localized swelling and ecchymoses. Pain may or may not be a factor and is often minimal in the older age group. In the young adult athlete, the forcefully avulsed short head of the biceps may be painful and swollen. Symptoms may be directed at the rotator cuff and impingement of the shoulder girdle with only secondary

complaints from the biceps rupture. Function is nearly normal with the short head of the biceps intact. Minimal loss of flexion, strength, and supination is detected. Cosmesis is a greater concern to the athlete with this injury. Plain films are normal. Arthrography shows rotator cuff disease in many instances. Magnetic resonance imaging shows the ruptured biceps tendon retracted from the bicipital groove. It may additionally show rotator cuff disease. Treatment Options

Conservative treatment is recommended for the athlete older than 40 years. Return to athletic activities is generally at 2 to 3 months after rupture. Surgical repair for cosmetic correction may be entertained in a patient for whom this appears to be a specific requirement. In the young adult athlete without rotator cuff disease, biceps repair with suture to the bicipital groove may be preferred. Arthroscopic or open anterior acromioplasty should be considered. Avulsion of the short head of the biceps from the coracoid process should be repaired back to the coracoid process. Repair in the bicipital groove uses the technique of Hitchcock [49A] described by Crenshaw and Kilgore.[26A] Gilcreest has recommended repair of the long head back to the coracoid process as a treatment alternative.[41] When rupture of the long head of the biceps is seen late, no appreciable weakness in flexion of the elbow or supination is detected. No indication for surgery in late cases exists other than cosmesis.

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Postoperative Management and Rehabilitation

The long head of the biceps tendon repair associated with anterior acromioplasty and rotator cuff surgery follows a regimen of postoperative management and rehabilitation as outlined for rotator cuff surgery. Isolated biceps tendon repair through either tenodesis in the bicipital groove or reattachment to the coracoid process is protected in a posterior splint and sling at 90 degrees until biceps healing occurs at approximately 6 weeks. A posterior night splint is used for an additional 6 weeks as rehabilitation for range of motion begins along with muscle tone and strengthening exercises. Return to sports activities is restricted to a minimum of 3 months for noncompetitive activities and 6 months for forceful contact in competitive sports.

Authors' Preferred Method of Treatment

Treatment is conservative, with rest, splint, ice, nonsteroidal anti-inflammatories, and gentle range of motion as pain, swelling, and recovery allow. If the short head of the biceps is intact and an isolated rupture of the long head of the biceps exists, return to sports activities is permitted as the patient's symptoms allow. Heavy lifting activities are prevented for approximately 3 months. In the young adult athlete with an isolated rupture of the long head of the biceps, tenodesis or transfer to the coracoid process is performed to improve strength recovery. Cosmetic concerns are addressed in those late cases or in the age group older than 40 years when repair is performed. Midsubstance muscle tear occasionally occurs from direct trauma. These tears are treated conservatively with elbow flexion at 90 degrees in a posterior splint or cast for 4 to 6 weeks and initiation of range of motion and strengthening at 6 weeks to 3 months. Return to sports activities in 3 months is allowed. Distal Biceps Avulsion

Avulsion of the distal biceps tendon at the elbow is an uncommon injury.[7] [10] [31] [36] [69] [77] [80] [87] Gilcreest[41] reported that 97 of 100 biceps ruptures were proximal (long head, 96; short head, 1), whereas only three biceps ruptures occurred at the elbow. The first description of distal biceps avulsion is credited to Starks in 1843.[118] Operative treatment of a distal rupture was first reported by Acquaviva in 1898.[69] [118] In 1941, Dobbie[31] reported a collection of 51 cases from 40 surgeons; most reported an experience of only two or three cases each, emphasizing the rarity of this lesion. Fewer than 200 cases of distal biceps avulsion have been reported in the literature. Clinical Evaluation

Rupture of the distal biceps brachii tendon typically occurs in men between the fourth and sixth decades of life.[36] All cases reported have been in men, with the possible exception of one case.[76] The average age at rupture is 50 years, but in the literature, the ages range from 21 to 70 years. Approximately 80% of the injuries occur in the dominant extremity. [80] Bilateral avulsion is extremely rare, but at least three cases have been reported.[118] Avulsion typically occurs during a heavy lift with the elbow flexed approximately 90 degrees and is the result of a sudden or prolonged contracture of the biceps against high load resistance.[80] In most instances, a single traumatic event is recalled by the patient.[10] [80] [87] Prodromal or prerupture symptoms are uncommon.[69] The tear usually occurs at the tendo-osseous insertion and notably leaves no distal tendon at the tuberosity.[80] [87] The lacertus fibrosus attachment is damaged to a varying degree but is usually left intact.[31] In fact, the distal biceps tendon may rupture in stages, first with avulsion of the distal biceps tendon proper from the radial tuberosity and then by a

second tearing from the lacertus fibrosus.[85] Preexisting degenerative changes within the distal tendon at the radial tuberosity are thought to predispose the tendon to rupture. [94] It is unusual to see radiographic changes in the radial tuberosity before tendon avulsion,[76] but Davis and Yassine[28] did identify degenerative changes at the volar aspect of the radial tuberosity. They postulated that these hypertrophic changes could cause tears in the tendon during pronation and supination of the forearm. When rupture occurs, the patient usually experiences a popping or tearing sensation and presents with acute pain in the antecubital fossa. The patient may not be aware of a flexion or supination loss of strength after rupture. Clinical findings include tenderness, swelling, and mild to moderate ecchymosis in the antecubital fossa.[36] [80] The distal biceps tendon is not palpable after a complete rupture. Deformity may occur as the muscle belly retracts proximally during an attempted contraction. The patient can still flex the elbow because the brachialis is intact and supinate the forearm owing to an intact supinator, but powers of flexion and especially residual supination are decreased.[36] The diagnosis is usually established by the history and physical examination. It is unusual to see radiographic evidence of avulsion fragments from the radial tuberosity. The differential diagnosis of pain in the antecubital fossa includes biceps tendinitis, partial distal biceps avulsion, bicipital bursitis, and the lateral antebrachial cutaneous nerve entrapment syndrome. The absence of a palpable tendon in the antecubital fossa should distinguish a complete rupture from the other entities; however, a correct diagnosis of a partial tendon rupture may be more difficult. Magnetic resonance imaging may be useful when the diagnosis is unclear. Treatment Options

Treatment of the distal biceps tendon rupture is surgical. The goal is to restore supination and flexion power to the elbow and forearm through anatomic repair of the tendon to the radial tuberosity.[10] [17] [31] [77] [80] [87] Although only slight functional deficit follows a disruption of the long head of the biceps (provided that the short head is intact), rupture of the distal tendon results in significant loss of flexion and supination strength and endurance.[10] [23] [77] [80] Meherin and

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Kilgore[77] reported a threefold increase in disability for unrepaired cases. Baker and Bierwagen[10] used Cybex testing to document an 86% decrease in supination endurance in unrepaired cases. Morrey and colleagues[80] reported only 61% flexion strength and 65% supination strength in unrepaired cases. Nonoperative treatment is no longer recommended in the athlete. In patients undergoing anatomic repair, flexion and supination strength and endurance

can be returned to normal. Morrey and colleagues[80] reported 97% flexion strength and 95% supination strength in patients with injuries repaired within 2 weeks after the injury. Late cases (after 4 weeks) with repair of the brachialis resulted in 87% flexion strength but only 43% supination strength. Operative repair for a complete avulsion can be performed through the anterior extensile exposure of Henry using one incision. In these cases, a pullout suture is used over a skin button distally.[69] [87] Most authors, however, advocate the two-incision approach proposed by Boyd and Anderson in 1961.[10] [17] [78] [80] Postoperative Management and Rehabilitation

After repair of the avulsed distal biceps tendon, the elbow is immobilized in 90 degrees of flexion with neutral, moderate, or full supination of the forearm, depending on the tension of the tendon repair. Most authors recommend 8 weeks of protection.[10] [80] [87] For the athletic population, 4 weeks of static immobilization in this position can be followed by 4 weeks of dynamic splinting. [80] A gradual range of motion and strengthening program is initiated 6 to 8 weeks after surgery, followed by a progressive resistance exercise program for 8 to 12 weeks; unprotected heavy lifting should not be allowed for 6 months. Aerobic conditioning should be emphasized to the athlete for maintaining endurance and performance in uninjured extremities while rehabilitating the arm. Criteria for Return to Sports Participation

Return of maximal functional strength occurs at 4 to 6 months. Maximal range of motion is attained by 6 months. Cybex isokinetic testing may be used as an objective test to determine recovery.[10] Return to sports without contact or maximal resistance forces may be allowed at 3 months. Return to full-contact or maximal resistance sports may be allowed at 6 months after surgery if strength and motion of the involved arm have reached a plateau in the rehabilitation program. An elbow brace or strap to prevent full extension or hyperextension may be required in contact sports during the first few months of active participation. Authors' Preferred Method of Treatment

Either the two-incision approach described by Boyd and Anderson [17] or the one-incision anterior approach described by Lintner and Fischer[67A] may be used. The incidence of heterotopic bone and radioulnar synostosis appears to be increased in the two-incision technique. Suture anchors are used in the one-incision technique. Similarly, suture anchors may be used in the two-incision technique; however, the pullout technique may also be used. A limited antecubital fossa incision is made to retrieve the distal biceps tendon. Care must be taken to identify the lateral antebrachial cutaneous nerve so that it will not be injured. A modified Bunnell suture is placed in the distal aspect of the tendon, using a heavy, nonabsorbable suture. A second incision is placed just lateral to the subcutaneous border of the proximal ulna, and an extraperiosteal dissection along the proximal ulna then exposes the radial tuberosity. The forearm must be kept in a

pronated position to minimize risk to the posterior interosseous nerve. The suture in the distal tendon can then be passed through the biceps tunnel with a Kelly clamp so that it can be seen at the second incision. The tuberosity bed is prepared with a bur, and the suture is then passed through drill holes into the bone to secure the tendon ( Fig. 22A1-5 ). The wound is then repaired over a closed Hemovac drainage pump. In cases of late reconstruction for a complete rupture, it is difficult to return the avulsed biceps tendon to the radial tuberosity. Increased risk to the radial nerve is significant. Reconstruction of the biceps tendon may be performed by attaching the tendon to the brachialis muscle or coronoid process of the proximal ulna in repairs done more than 4 weeks after injury[80] ( Fig. 22A1-6 ). This will regain most of the flexion strength. If restoration of supination strength is required, use of a fascial graft extension into the radial tuberosity is necessary. Although the extensile anterior approach of Henry is preferred by some authors, dissection about the radial nerve and recurrent leash vessels is difficult. Radial nerve palsy has been reported with this approach.[17] The use of two incisions avoids dissection of the neurovascular structures. Heterotopic ossification and synostosis of the proximal radioulnar joint have occasionally been reported with use of the two-incision approach, however.[32] [80] To decrease this risk, Morrey and colleagues [80] recommend (1) avoiding

Figure 22-A1-5 Biceps tendon reinsertion technique into the radial tuberosity.

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Figure 22-A1-6 Biceps tendon transfer insertion into the coronoid process with or without fascial slip extension for late reconstruction of distal biceps tendon rupture.

subperiosteal dissection on the ulna, (2) clearing all bone debris from the radial tuberosity after burring, and (3) draining the wound to prevent hematoma. The lateral antebrachial cutaneous nerve and the posterior interosseous nerve can be at risk with either approach. Nielson[85] reported a single case of partial rupture of the distal biceps tendon that resulted in an elongated and redundant biceps and lacertus fibrosus 8 months after injury. The patient presented with weakening of elbow flexion and forearm supination but without significant pain. The tendon was found to be too long and slack. The problem was addressed by shortening the tendon to normal tension by a step-cut Z-plasty and imbrication, resulting in restoration of normal strength and motion 8 to 12 weeks after surgery.

Distal Triceps Avulsions

The triceps tendon avulsion is a rare injury and perhaps the least common of all tendon ruptures.[7] [9] [35] [50] Only four cases of avulsion were reported by Anzel and associates[7] in their review of tendon injuries at the Mayo Clinic. Partridge is credited with the first description of a triceps rupture in 1863.[50] Tarsney[109] described seven patients who had sustained tendo-osseous avulsions during a 16-year period. Aso and Torisu[8] noted 35 cases reported in the English literature; only two of these cases had been ruptures of the muscle belly. They added an additional two cases of muscle belly tears. Farrar and Lippert[35] emphasized the importance of distinguishing between complete and incomplete ruptures of the distal triceps tendon. Nearly 75% of the ruptures reported in the literature occurred in male patients, with a male-to-female ratio of 3:1. [9] Although the mean age at injury was approximately 26 years, case reports have spanned an age range from 7 to 72 years. Dominant and nondominant extremities appear to be injured with equal frequency.[9] Two cases of bilateral avulsion have been reported.[73] Most avulsions of the distal triceps follow trauma. Indirect trauma is the most common cause of injury and usually involves a fall onto the outstretched upper extremity. This imparts a deceleration stress on an already contracted triceps, resulting in distal avulsion at the tendo-osseous insertion. The tendon usually retracts with bone from the proximal olecranon embedded in it.[9] [35] [50] [109] In exceptional cases, midsubstance belly ruptures and musculotendinous junction ruptures have been reported.[41] [78] Some of these injuries may also result from a direct blow to the elbow. In addition, spontaneous avulsion of the distal triceps tendon has been reported in patients with hyperparathyroidism, renal osteodystrophy, osteogenesis imperfecta, Marfan's syndrome, systemic lupus erythematosus, and systemic administration of steroids. [35] [73] [96] [103]

The same mechanism of injury responsible for distal triceps tendon avulsions may result in the less common transverse or oblique avulsion fracture through the proximal olecranon. A high incidence of proximal olecranon avulsion fractures was noted in javelin throwers, and proximal olecranon avulsion fractures have also been reported in baseball pitchers.[105] Such fractures are also not uncommon in children, who are more inclined to have a fracture of the proximal olecranon apophysis than a tendo-osseous avulsion of the triceps mechanism ( Fig. 22A1-7 ). The radiographic vagaries of the proximal olecranon have previously been addressed in the literature and should be referred to by physicians treating pediatric athletes. [104] Clinical Evaluation

The clinical features of triceps tendon avulsion include pain and swelling of the posterior elbow. A palpable depression just proximal to the olecranon may be noted.[35] [109]

Figure 22-A1-7 Proximal olecranon apophysis separation with triceps insufficiency.

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These findings may be difficult to appreciate in the face of severe pain and swelling, especially in a well-muscled athlete with large bulk.[91] [109] Ecchymosis may be marked several days after injury but not immediately. Careful testing of elbow extension strength is important to determine whether the tear is partial or complete. [35] Loss of active extension of the elbow signifies a complete tear of the triceps tendon. Variations in clinical symptoms and signs after incomplete or complete avulsions of the triceps may lead to a delay in correct diagnosis. Rupture of the triceps tendon may present as a cubital tunnel syndrome,[48] snapping elbow,[32] collar stud-shaped olecranon bursitis,[26] or even posterior compartment syndrome.[20] Radiography should be performed in all suspected cases. Avulsed flecks of bone from the olecranon were demonstrated in approximately 83% of cases reported in the literature.[9] [35] [109] The remainder of the upper extremity should be carefully examined for associated fractures. Levy and associates[67] reported their experience with 16 patients who sustained concomitant triceps ruptures in radial head fractures. The triceps rupture may be overlooked if the posterior aspect of the elbow is not specifically examined. An avulsed bone fleck present on the lateral radiograph of the elbow may be the only clue to the correct diagnosis ( Fig. 22A1-8 ). Treatment Options

Complete avulsion of the triceps should be surgically repaired to restore extension strength.[9] [35] [50] [109] The role of surgery in treating partial triceps tendon ruptures is unclear, however. Farrar and Lippert[35] have stated that if full active extension can be demonstrated on the physical examination,

Figure 22-A1-8 Triceps tendon rupture with small avulsion fragment of olecranon.

Figure 22-A1-9 Triceps tendon reinsertion approximating the joint surface after olecranon fracture excision.

these injuries are partial and can be observed closely without surgical repair. For complete tears, the accepted method of repair is reattachment of the avulsed triceps tendon to the olecranon with nonabsorbable sutures through drill holes in bone.[35] [91] [109] If a large fragment (50%) of the olecranon is present and displaced, open reduction and

internal fixation of the olecranon are indicated. Otherwise, excision of the bone fragments and repair of the triceps tendon to the articular surface are indicated. Repair of the triceps to the articular surface is necessary to minimize anterior-posterior instability of the elbow after excision of the proximal olecranon fragment ( Fig. 22A1-9 ). Other methods of triceps repair have been described, including an inverted tongue of triceps used as a turned-down flap, a periosteal flap from the olecranon, and a posterior forearm fascial flap.[6] [50] These techniques may be useful in cases of delayed reconstruction if primary reattachment failed or initial diagnosis was missed and triceps retraction occurred. Complications with operative repair may include skin slough, infection, and rerupture. Pantazopoulos and colleagues[91] reported the development of an olecranon bursitis after wire suture fixation. This resolved after removal of the wire. In general, good extension strength has been restored.[9] [35] Several authors have noted a mild flexion contracture, ranging from 5 to 20 degrees, in perhaps 10% of their series. [67] [109] Postoperative Management and Rehabilitation

The elbow is immobilized postoperatively in extension for a variable time, ranging from 10 days to 6 weeks in the literature.[9] The elbow is generally immobilized at 30 to 45 degrees of flexion for 4 weeks before a graduated

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range of motion and strengthening program is begun. The elbow is immobilized at 30 degrees of flexion for 4 weeks, and then 0 to 45 degrees of range of motion is allowed during the next 2 weeks, after which graduated range of motion and strengthening exercises are begun. An extension night splint is used for the first 3 months after repair. Criteria for Return to Sports Participation

Return to contact sports should be restricted until maximal motion and extension strength have been obtained, generally after 6 months. Active resistive strengthening to achieve equal triceps strength is performed 3 to 6 months after surgery. Five patients in the literature were treated nonoperatively.[9] This treatment has generally been reserved for patients with partial ruptures or muscle belly ruptures that still demonstrated some ability to extend against gravity. Avulsion of the lateral head alone has been stated to result in no significant functional impairment and in fact may be more frequent than has been recognized.[20] Authors' Preferred Method of Treatment

Avulsions are reattached with nonabsorbable heavy suture through drill holes in the

proximal olecranon tip. Mobilization of the triceps tendon may be required, care being taken not to injure the radial nerve with proximal mobilization. Fracture fragments of less than 50% of the olecranon, nonunion of the olecranon apophysis, or fragments that are severely comminuted are excised, and the triceps tendon is reattached to the olecranon adjacent to the articular surface. Large fragments (50% or greater) are reconstructed with open reduction and internal fixation by the AO/ASIF technique of tension band wiring. Delayed or late reconstruction of the triceps is accomplished by triceps mobilization and a turn-down triceps fascia flap or the use of a fascial strip of palmaris longus tendon or tensor fascia lata placed through a drill hole in the olecranon. Triceps midsubstance muscle tears are treated with the elbow in extension. The athlete may be allowed gentle range of motion at 3 to 4 weeks as symptoms allow. The patient is allowed 4 to 6 weeks for muscle healing, but gentle range of motion may be permitted during that period with an elbow extension splint or a cast as the patient's requirements are addressed. Surgical repair of a triceps muscle tear is not indicated.

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Fractures Rotational Stress Fracture of the Proximal Humeral Epiphysis

Rotatory torque stresses to the epiphyseal growth plate of the proximal humerus in adolescent throwers can result in little leaguer's shoulder. Initially described as epiphysitis or osteochondrosis by Adams, [1] this lesion is a fatigue

Figure 22-A1-10 Little leaguer's shoulderproximal humerus epiphyseal stress fracture in the adolescent.

fracture or slip of the proximal humeral epiphyseal plate[21] [113] ( Fig. 22A1-10 ). Cahill [21] described five cases in Little League pitchers aged 11 to 12 years. Pain and inability to perform were the usual presenting complaints. Decreased range of shoulder motion and anterior glenohumeral tenderness were found on physical examination. Radiographs usually revealed widening of the epiphyseal line with a metaphyseal separation. With rest, the stress fractures healed with periosteal new bone formation secondary to periosteal stripping. The recommended treatment is rest for approximately 6 weeks or until the lesion is healed.[113] Considering the large number of participants in Little League baseball, little leaguer's shoulder is uncommon.[112] Resumption of sports activity is allowed when pain is resolved and healing is noted on radiographs. Humeral Shaft Spiral Fractures

Although the most common cause of humeral fractures is blunt trauma, a spiral fracture of the shaft of the humerus resulting from muscle violence has been reported in various throwing sports, including baseball, javelin, and handball, as well as in arm wrestling.[19] [24] [47] [49] [113] [121] This fracture has become a recognized clinical entity ( Fig. 22A1-11 ). One of the first cases of spontaneous fracture of the humerus due to muscle violence was reported in 1947.[19] Herzmark and Klune[49] reported an additional four cases in

prison inmates who were throwing baseballs. They postulated torsional stress as the cause of this spiral fracture. These fractures were also reported in three soldiers throwing hand grenades, and Chao and colleagues[24] reported 129 cases in the Chinese army between 1959 and 1966; their report also included an experimental study that confirmed the role of torsional stress in causing spiral fractures of the

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Figure 22-A1-11 Spiral oblique fracture of the humerus. A, Anteroposterior view. B, Lateral view. C, Muscular rotational and biomechanical forces producing spiral fracture of the humerus.

distal humerus and quantitated the necessary force as 7 foot-pounds of torque. A similar fracture was reported in an arm wrestler in 1962, and Heilbronner and associates [47] reported a series of 28 cases of humeral fractures caused by arm wrestling. Clinical Evaluation

The age of patients sustaining these spiral fractures averages 25 years and ranges from 18 to 38 years. The dominant extremity is fractured in more than 90% of cases, which is not surprising because the stronger arm is usually used for throwing or arm wrestling. These fractures have more frequently been reported in unorganized sporting events. [121] Typically, a spiral fracture of the humerus results, usually in the middle to distal third of the humerus, and is often associated with a butterfly fragment. Chao and colleagues[24] found these fractures in the upper third of the humerus in 1.6% of cases, in the middle third in 3.1% of cases, and in the distal third in 95.3% of cases. No underlying bone disease has ever been documented in these cases.[113]

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Radial nerve injury may accompany these fractures. In a review of 42 cases in the English literature, radial nerve palsy was present in 5, for an incidence of approximately 12%.[47] The radial nerve injury was a neurapraxia in each of these cases, and recovery occurred by 6 months. Only Chao and colleagues[24] reported laceration of the radial nerve, which necessitated repair at 6 months. Many explanations for the spiral fracture have been offered, most being variations on the theme of torsional stress. Powerful internal rotation is applied to the upper shaft of the humerus by the pectoralis major, subscapularis, teres major, and latissimus dorsi while a force across the forearm imparts external rotation to the distal humerus through the ulnotrochlear joint ( see Fig. 22A1-11C ). Only 7 foot-pounds of torque are necessary for this fracture to occur, even without a stress raiser, as shown

experimentally.[24] This degree of force can be attained in the throwing motion during the transition from the cocking phase to the acceleration phase.[113] This force is also easily attained during an arm wrestling match, particularly during a draw or losing match. [121] Treatment Options

The majority of these fractures have been treated successfully with closed management, usually a hanging arm cast.[19] [47] [49] [121] Conservative, nonoperative treatment consists of a coaptation splint followed by functional orthotic bracing with a humeral sleeve. No nonunions or delayed unions have been reported in arm wrestlers with closed treatment.[121] The fractures have generally healed within 6 to 10 weeks. Open treatment has been reported in 16 cases in the literature, usually for failure to obtain reduction. [47] Muscle interposition at the fracture site was noted in a number of these open cases. Heilbronner and associates[47] reserve open reduction and internal fixation for markedly displaced segmental fractures, for fractures associated with elbow articular injuries requiring early mobilization, for fractures associated with vascular injury, when radial nerve palsy is present after a manipulation of the fracture, and with inability to obtain reduction because of soft tissue interposition. Transverse fractures and short oblique fractures are best treated with intramedullary rod fixation. Concern about rotator cuff disease during the insertion and subsequent recovery, however, requires rod removal once healing is complete in the competitive athlete ( Fig. 22A1-12 ). Comminuted displaced fractures and fractures with neurovascular compromise are better treated with open reduction and internal fixation by use of the AO/ASIF 4.5 compression plate. Bone loss or bone defects require bone grafting techniques. The healing of these fractures requires the same time as the nonoperatively treated fractures do; however, the rehabilitation process may be accelerated in regard to proximal and distal joint mobilization, muscle strengthening, and general body conditioning ( Fig. 22A1-13 ). There is no series in the literature that demonstrates superiority of open reduction and internal fixation over closed management of these fractures. These fractures are the result of low-energy trauma, which in most cases preserves the periosteal and muscular envelope of the humerus. With uneventful healing of the humeral fracture at 3 months, a full range of motion should be present, and strengthening exercises from 3 to 6 months are then required. Criteria for Return to Sports Participation

When strength returns, sports are resumed. Contact sports require a functional humeral brace or a protective pad during the first year of competition. Postoperative Management and Rehabilitation

A coaptation splint, hanging arm cast, or humeral sleeve orthosis is used until fracture healing occurs with closed treatment. If open reduction and internal fixation are used, a humeral sleeve orthosis is applied. Authors' Preferred Method of Treatment

We recommend a coaptation splint for 2 weeks, followed by a humeral sleeve orthosis for approximately 6 weeks. These fractures are usually nontender by 8 weeks and demonstrate radiographic callus. A graduated range of motion and strengthening program should be resumed at this time. Particular emphasis should be placed on regaining external rotation, which is important to the throwing athlete. After apparent healing, refracture of the humerus has been reported. [38] [121] [122] Whitaker[121] reported recurrence of fracture in two of five cases. Garth and colleagues [38] reported three recurrent fractures in a baseball pitcher during a 21-month span. Each fracture was in a different location of the humerus; the authors postulated that a nonhealed extension of the spiral fracture acted as a stress raiser for each of the new fractures. Because of this, they recommended tomograms to assess healing in all spiral humeral fractures before any torque-producing activity is resumed. Open reduction and internal fixation are performed for severely displaced fractures that cannot be reduced, combined vascular injuries that require repair, loss of radial nerve function during reduction of fracture fragments, and ipsilateral elbow or forearm fractures. Open reduction and internal fixation are indicated for isolated radial nerve lesions associated with spiral distal displaced fractures, as described by Holstein and Lewis,[51A] particularly if radial nerve loss follows manipulation of the fracture. Ipsilateral elbow or forearm fractures associated with humeral fractures are treated with open reduction and internal fixation. The increased incidence of nonunion is reported by Rodgers and colleagues[98A] to be 33% in those humeral fractures associated with ipsilateral elbow or forearm fractures that are treated conservatively for fracture of the humerus. Supracondylar Process Fracture

A supracondylar process has been noted in approximately 1% of anatomic specimens.[11] [71] [110] Terry[110] noted a

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Figure 22-A1-12 Displaced fracture of the humerus treated with a Polaris intramedullary rod to include proximal and distal screw fixation. A and B, Anteroposterior and lateral oblique views of fracture of the humeral shaft. C and D, Anteroposterior and lateral views of Polaris nail fixation.

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Figure 22-A1-13 Displaced fracture of the humerus treated with open reduction and internal fixation with a 4.5 compression plate. A and B, Anteroposterior and lateral views of comminuted displaced spiral fracture of the humeral shaft. C and D, Anteroposterior and lateral views of 4.5 dynamic compression plate fixation with intrafragment fixation.

supracondylar process exceeding 3 mm in 6 of 515 whites and 1 of 1020 blacks examined. A tendency toward familial occurrence was suspected. A fibrous band, the ligament of Struthers, usually connects the tip of the supracondylar process to the medial epicondyle. The median nerve passes through this arcade, often accompanied by the brachial or radial artery.[11] [71] An anomalous pronator teres frequently attaches to the process, and the process sometimes serves as a distal attachment for the coracobrachialis ( Fig. 22A1-14 ). The supracondylar process can usually be palpated on clinical examination if it is carefully sought. Routine anteroposterior and lateral radiographs may fail to catch the process in profile, and oblique views of the anterior medial aspect of the humerus may be necessary[30] [39] ( Fig. 22A1-15 ). Fracture of the supracondylar process has been reported after a direct blow to the process.[30] [39] [63] In one case, the healing fracture was misinterpreted as an osteochondroma

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Figure 22-A1-14 Supracondylar process and ligament of Struthers with compression entrapment of the median nerve.

Figure 22-A1-15 Supracondylar process of the distal humerus.

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and excised. Conservative management is recommended for these injuries unless persistent pain or median nerve entrapment symptoms mandate excision and nerve exploration.

Rib Fractures in Throwing Athletes

Fracture of the first rib may occur through the subclavian groove between the attachment of the scalenus anticus and the scalenus medius muscles in throwing athletes, particularly baseball pitchers.[113] This occurs on the side contralateral to the pitching arm. Although it has been postulated that the fracture may result from a sudden muscle contraction,[27] most of these fractures are most likely stress fractures.[113] The symptoms of pain are often vague and poorly defined. Technetium bone scanning or tomograms may confirm the diagnosis. The recommended treatment is conservative, and rest is advised until the symptoms subside. Although a high rate of nonunion was reported in one series, the majority of these fractures are painless.[15] Despite the proximity of this injury to the subclavian artery, no neurovascular injury has been reported[95] ( Fig. 22A1-16 ). Similar fractures in the lower three floating ribs have been described in both pitchers and batters.[113] Sudden or repetitive vigorous ipsilateral contraction of the external abdominal oblique muscles, interdigitating with the latissimus dorsi, serratus posterior inferior, and internal abdominal oblique muscles at the tips of the 10th, 11th, and 12th

Figure 22-A1-16 First rib stress fracture in the throwing athlete.

Figure 22-A1-17 Avulsion fractures of the 10th, 11th, and 12th ribs in the throwing athlete.

ribs, can result in stress fractures at the tips of these ribs. Multiple oblique radiographs with rib details or bone scan may be required to confirm the diagnosis. These fractures have also been described in laborers.[52] Conservative treatment is recommended, including rest and modification of training activities. Injection with local anesthetic may be necessary to obtain temporary symptomatic relief ( Fig. 22A1-17 ).

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Myositis Ossificans

Myositis ossificans is a nonmalignant lesion of heterotopic bone localized in the soft tissues and associated with trauma and debilitating illnesses, such as poliomyelitis, paraplegia, and tetanus.[115] The most common cause is trauma, and the lesion occurs particularly in contact sports such as football, rugby, and lacrosse.[111] Although also noted in soft tissues, myositis ossificans has been classified as extraosseous, periosteal, and parosteal.[42] Hait and colleagues [44] related the lesion to trauma of large muscle masses as well as of investing tissues against bone, including avulsion of tendinous origins and fascia from their bony attachments. Related terminology includes heterotopic ossification, myositis ossificans, and ossifying hematoma, all of which appear to be a result of direct trauma, contusion, bleeding, calcification, and subsequent ossification. Heterotopic ossification about the elbow and shoulder joint is well recognized as a sequel to fracture-dislocations of these joints. Myositis ossificans in the muscle of the upper arm is less common than heterotopic ossification about the joints after

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dislocation; likewise, it is less common than myositis ossificans in the lower extremity.[33] Localized myositis ossificans must be distinguished from osteogenic sarcoma. Myositis ossificans is usually situated over the diaphysis, as opposed to the metaphyseal site of osteogenic sarcoma. With myositis ossificans, the pain and mass decrease with time, whereas the opposite is true with osteogenic sarcoma. In myositis ossificans, radiographs demonstrate an intact underlying cortex, whereas the cortex is usually violated with osteogenic sarcoma. Biopsy specimens of myositis ossificans after 2 weeks show a definite zonal pattern with the most differentiated tissue at the periphery of the lesion. With osteogenic sarcoma, the most differentiated tissue occurs in the

central portion of the lesion.[34] Clinical Evaluation

In the typical history, an adolescent football player who has received a direct blow to the upper arm region has persistent swelling and tenderness. A palpable mass may be detected, and a flexion contracture about the elbow or shoulder may occur. The skin may show discoloration or may be normal. Initial radiographs are normal; however, after 2 to 3 weeks, radiologic changes are noted[86] ( Fig. 22A1-18 ).

Figure 22-A1-18 Heterotopic bone (myositis ossificans) within the brachialis muscle.

Figure 22-A1-19 Cortical irregularity (ringman's shoulder) in the proximal humerus of a gymnast. Treatment Options

Rest of the affected extremity, application of protective support such as plaster or foam padding, analgesics, and anti-inflammatory drugs, particularly indomethacin, may be of some benefit. Diamond and McMaster[29] described a form of myositis ossificans traumatica occurring in the area of the lateral humerus in the deltoid insertion in football players, particularly defensive linebackers, and coined the term tackler's exostoses. They described the cause of this lesion as damage to the osseous insertion of the deltoid or the origin of the brachialis, producing a periosteal tear. It may be seen bilaterally and, if treated early with adequate rest and splinting, may undergo spontaneous regression. Huss and Puhl[58] described a triad of pain, hard palpable mass in the muscle, and flexion contracture of the elbow. They noted that 70% of these symptoms significantly improved in less than 3 months with conservative, nonoperative management. Thirty percent of these cases required surgery for a persistent painful mass, which recurred postoperatively in two thirds of the surgical cases, although surgery was delayed until radiologic evidence of maturation was present. Lipscomb and associates[68] likewise recommended conservative treatment consisting of rest, elevation, ice, and immobilization with a compression dressing. They used oral proteolytic enzymes and also recommended aspiration of a fluctuant hematoma mass, if present, under sterile conditions. When all pain and tenderness have subsided and joint motion returns, the athlete is allowed to resume participation in sports with protective padding. If radiographic evidence of residual myositis ossificans persists but no pain or mass is present, no other treatment is recommended. In those cases in which a palpable mass, muscle

atrophy, and

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joint limitation are problems despite conservative treatment and radiographs have revealed mature laminar bone formation within the myositis ossificans traumatic mass, surgical excision is recommended. These masses have been removed at 6 months or later if bone maturation appears to be complete.[56] Bone scans may be used to distinguish active (immature) bone formation from the mature nonactive lesion. The lesion may recur if immature bone is excised. If the lesion is mature, the sedimentation rate and alkaline phosphatase activity should be normal. Although lesions of heterotopic bone in the biceps and at the deltoid insertion appear to be related to direct trauma, Fulton and associates [37] have described cortical, desmoid-like lesions of the proximal humerus in gymnasts (ringman's shoulder lesion). This is described radiologically as a cortical irregularity of the proximal humerus at the insertion of the pectoralis major muscle into the proximal humerus ( Fig. 22A1-19 ). This irregularity may simulate malignancy; however, it is considered a benign reactive lesion secondary to the excessive forces at the pectoralis major insertion. This lesion is unique to gymnasts because of the strength movements involved in the shoulder girdle and pectoralis muscle group. Avulsions, either complete or partial, of the pectoralis major insertion or latissimus dorsi insertion onto the humerus may result in heterotopic bone formation and a painful mass. These have been noted particularly in football players ( Fig. 22A1-20 ). Postoperative Management and Rehabilitation

Padded protective splints are worn for contact sports unless pain persists. Sports are terminated until pain resolves and are then resumed with protective equipment.

Figure 22-A1-20 Pectoralis major muscle avulsion at the insertion with heterotopic bone formation.

If the lesion is excised, Hemovac drainage of the wound is used to prevent hematoma formation. Postoperative indomethacin is administered to reduce the formation of heterotopic bone. Range of motion exercises are begun at 7 to 10 days and are maximized at 3 to 4 weeks to prevent contracture formation. A postoperative extension splint is used at night on the elbow to prevent recurrence of a flexion contracture. Strengthening and resistive exercises are begun at 4 weeks. Criteria for Return to Sports Participation

Painless range of motion and return of strength to a level equal to that in the

nonaffected area are the criteria for return to sports participation. Authors' Preferred Method of Treatment

Small hematomas due to acute direct trauma are treated with ice and cold packs, rest, and nonsteroidal anti-inflammatory drugs. Large, fluctuant hematomas are aspirated in a sterile fashion and wrapped for compression and are then given the same conservative treatment. Painful bruises or hematomas are padded for sports. If heterotopic bone formation is noted on radiographs but the lesion is asymptomatic, sports activity may be continued. Symptomatic heterotopic bone, if it is immature on radiographs and characterized by increased uptake on bone scan and increased sedimentation rate and alkaline phosphatase levels, is treated with padding, cast, and cessation of sports activity if this activity is painful. Mature heterotopic bone that remains symptomatic is surgically excised and splinted until skin and soft tissue healing occurs; a range of motion and strengthening program is then initiated. Nonsteroidal anti-inflammatory drugs, particularly indomethacin, are taken postoperatively for 3 to 6 months to retard new bone formation.

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2. FRACTURES AND SOFT TISSUE INJURY OF THE ARM IN THE CHILD Kaye E. Wilkins MD Incidence

Fractures of the humeral shaft in skeletally immature patients are quite rare. They account for less than 2% of all pediatric fractures. In the pediatric age group, only 10% of all humeral fractures are isolated to the shaft. [15] The largest percentage of fractures of the humeral shaft occurring in patients older than 10 years of age is associated with athletic or recreational activities.

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Types Trauma-Related Fractures

Complete humeral shaft fractures usually are the result of severe indirect or direct trauma. In indirect trauma, the force is rotational and produces a longitudinal or spiral pattern. Fractures due to direct trauma are usually characterized by a transverse fracture pattern. In both types, shortening occurs because of unopposed muscle contractures. Stress Fractures

Humeral shaft fractures can be the result of repetitive microtrauma (e.g., stress fractures). These are usually seen in high-performance athletes who are poorly conditioned. The classical clinical findings of increasing pain with activity and decreasing pain with rest are usually present. Periosteal new bone formation may not become apparent for at least 2 to 3 weeks. In those suspected of having a stress fracture, often a radionucleotide scan for new bone formation becomes positive as early as 5 to 7 days. These fractures usually occur with repeated rotational stresses, such as those experienced by baseball pitchers[1] [26] [29] or players wielding a tennis racquet.[22]

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Anatomic Considerations Bony Structure

The shaft of the humerus both thickens and narrows in diameter at its junctions with the proximal metaphysis. Distally, it becomes more triangular before it widens mediolaterally and narrows in the anteroposterior plane to form a somewhat elliptical shape at the distal metaphysis ( Fig. 22A2-1 ). Because it is thick, the periosteum often remains intact after fracture and provides a good source for remodeling.[5] [6] The head is usually somewhat retroverted in relationship to the distal supracondylar area. Vulnerability of Nerves

Radial Nerve

The radial nerve is usually separated from the posterior aspect of the shaft by varying thicknesses of either the

Figure 22-A2-1 Osseous structure. The cross-sectional architecture of the various areas of the humerus as it changes from a proximal triangular shape to a distal elliptical one. (Reprinted with permission from Gausepohl T, Koebke J, Pennig D, et al: The anatomical base of unilateral external fixation in the upper limb. Injury 31:11-20, 2000.)

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triceps or the brachialis. It is adjacent to the lateral edge of the distal humerus when it passes from posterior to anterior through the lateral intermuscular septum. It must be emphasized that the radial nerve does not lie directly adjacent to the humeral shaft in the posterior spiral groove.[31] Ulnar Nerve

This nerve usually lies medial to the shaft and is held posterior to the intermuscular septum by an arcade and by the medial brachial ligament. In some individuals, the ulnar nerve may be vulnerable to injury because there is very little muscle of the medial head of the triceps lateral to the nerve to protect it from the medial aspect of the distal shaft.[14] Median Nerve

The median nerve is usually well protected from the underlying shaft of the underlying muscle and is rarely injured. Muscle Forces

Displacement Determined by Deltoid

The end of the deltoid tuberosity appears to be the cut-off for determining the displacement produced by various muscle forces. The effect of muscle forces on strictly proximal metaphyseal fractures was discussed in Chapter 21 in relation to fractures of the proximal humerus ( see Fig. 21M1-18 ). Above-Deltoid Insertion.

Between the deltoid tuberosity and the pectoralis insertion, the proximal fragment is shifted medially by the pectoralis (Fig. 22A2-2 (Figure Not Available) ). The deltoid pulls the distal fragment proximally. Below-Deltoid Insertion.

Below the deltoid insertion, the deltoid muscle abducts the proximal fragment. The distal fragment is displaced medially and is shortened by the coracobrachialis, the triceps, and the biceps (Fig. 22A2-3 (Figure Not Available) ).[11] [18] [19]

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Diagnosis Physical Examination

The diagnosis is usually obvious. The arm is shortened, swollen, and very tender. Crepitus and angular motion may be palpable at the fracture site. Although vascular injuries are quite rare with closed humeral shaft fractures, a thorough examination of the function of the vascular system distally is essential. In open injuries, it is crucial to examine the integrity of the vascular system to rule out a forearm compartment syndrome. It is important to check for ipsilateral injuries, especially in the distal forearm. Some of these may be minor, and their symptoms may be greatly overshadowed by the magnitude of the humeral shaft fracture. Figure 22-A2-2 (Figure Not Available) Proximal shaft displacement. In fractures occurring between the deltoid and pectoralis major muscle insertions, the distal fragment is abducted and the proximal fragment is adducted, producing an apex medial angulation. (Reproduced with permission from Healey JE Jr, Seybold WD: A Clinical Synopsis of Anatomy. Philadelphia, WB Saunders, 1969, p 57.) Radiographic Evaluation

Rotation of Patient, Not Extremity

The fracture is usually quite obvious on plain roentgenograms. One word of caution is necessary, however. Two views of the humerus are essential. These views should be obtained by rotating the patient, not the extremity ( Fig. 22A2-4 ). Techniques requiring internal and external rotation of the arm are avoided. The anteroposterior view is usually easy. To obtain a lateral view, it may be necessary to take a transthoracic lateral film. It is also important to be sure that both the glenohumeral and elbow joints are visualized. Osseous Integrity

The prefracture integrity of the bone needs to be determined as well. The fracture site must be carefully evaluated

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Figure 22-A2-3 (Figure Not Available) Distal shaft displacement. A, In fractures occurring distal to the deltoid tuberosity, the proximal fragment is abducted (single arrow) and the distal fragment is pulled medially by the biceps and triceps muscles (double arrow). B, Schematic drawing of the muscle forces acting on the two fragments. (Reproduced with permission from Healey JE Jr, Seybold WD: A Clinical Synopsis of Anatomy. Philadelphia, WB Saunders, 1969, p 57.)

to determine whether some defect such as a bone cyst or nonossifying fibroma may have made the bone more susceptible to fracture ( Fig. 22A2-5 ).

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Treatment

Almost all humeral shaft fractures can be treated nonoperatively. There are very few instances in which operative methods are necessary in treating the pediatric athlete with fracture of the humeral shaft. Nonoperative Techniques

Stress Fractures

Stress fractures must be rested by cessation of the offending process (usually throwing) until there is good, mature callus and the fracture site is nontender. Failure to do so can result in the development of a complete fracture. [1] It is important during this period of rest that a program of muscle strengthening be initiated. Often, stress fractures occur when there is inadequate muscle strength to protect the bone. The mechanics of the throwing process needs to be examined as well because improper pitching techniques can lead to abnormal stress on the bone. Nondisplaced Fractures

In nondisplaced fractures, a simple posterior splint, or a modified Velpeau (so-called Jacksonville) sling,[9] is usually all that is necessary ( Fig. 22A2-6 ). Displaced Fractures

When there is complete displacement, treatment must be directed toward controlling angulation. Shortening usually does not produce any significant clinical or functional effect.[12] In completely displaced fractures, angulation can be controlled by several simple noninvasive external mobilization techniques.

Hanging-Arm Cast.

The hanging-arm cast was once a popular method of treating humeral shaft fractures. Its major advantage is that it can be wedged to the correct angulation ( Fig. 22A2-7 ). Angulation can be corrected by adjusting the attachment to the suspension strap of the cast, as advocated by Pollen.[20] The hanging-arm cast has

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Figure 22-A2-4 Rotational effects. A, Anterior-posterior radiograph of a distal humeral shaft fracture. B, Evaluation of the lateral planes was attempted by rotating only the distal fragment (arrow). The proximal fragment still presents an anterior-posterior profile. This is an incorrect method of obtaining two views of the fractured humerus.

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Figure 22-A2-5 Osseous defect. A, Injury film in an 11-year-old with midshaft fracture. The diseased area is not well defined. B, Six weeks after fracture, the diseased nature is seen, with definition of an area of irregular ossification at the fracture site (arrow) and a better-defined margin (dotted line) of the lytic lesion.

disadvantages in that it may initially be uncomfortable. In addition, the patient may need to sleep sitting up. The weight of the cast may distract the fracture, which can lead to delayed union or even nonunion.[28] Coaptation Splint.

A sugar tong type of coaptation splint is easy to apply. It consists of a U-shaped slab of plaster that encases the arm from the axilla medially to the elbow and laterally to the deltoid ( Fig. 22A2-8 ). The splint is molded to control angulation in the coronal plane. It is usually secured with an elastic bandage wrapped around the arm. The forearm requires some type of sling suspension. If the forearm needs more support, as in fractures in which there is an associated radial nerve paralysis, a second coaptation splint can be placed 90 degrees to the splint around the arm ( Fig. 22A2-9 ). The advantages of the coaptation splint are its ease of application and the early return of elbow motion. Angulation in the coronal plane (varus-valgus) is easy to control. Angulation in the sagittal plane (flexion-extension) may be more difficult to manage.

Braces.

These orthotic devices are usually reserved for the later stages of healing, after some intrinsic stability has been obtained. In older children, the braces designed for ankle injuries can be used ( Fig. 22A2-10 ). They are more effective in the adolescent athlete. Their major advantages are their lightness and the fact that they allow early motion.[2]

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Figure 22-A2-6 This Little League pitcher sustained an undisplaced fracture of the humeral shaft, which was treated with a modified Velpeau (so-called Jacksonville) sling. [ 9] This type of sling both supports the extremity and prevents rotation.

Figure 22-A2-7 A, Injury films of a spiral distal shaft fracture in an 8-year-old gymnast. The fracture was placed in a hanging-arm cast but drifted into varus. B, Varus was corrected by performing a medial opening wedge of the distal portion of the cast (arrows). C, Six weeks after injury, there is good solid callus, and the linear alignment is maintained.

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Figure 22-A2-8 Coaptation splint. A, Injury film. B, As the immobilization material is hardening, the tendency toward varus angulation of the shaft is counteracted by the placement of molds over the apex and the distal medial aspect of the fracture fragments (arrows). C, The forearm is supported with a collar and a cuff. D, Position of the fragments in the coaptation splint.

Figure 22-A2-9 A, Injury films in a 6-year-old boy who was thrown from a horse and sustained a midshaft fracture of the left humerus, along with an associated paralysis of the radial nerve. B, Radiograph of the fracture fragments in the coaptation splint shows satisfactory linear alignment but minimal bayonet apposition. C, Clinical photograph of the coaptation splint with molding around the midshaft. A forearm coaptation splint was added to support the wrist because of the radial nerve paralysis.

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Figure 22-A2-10 Temporary coaptation splint. The fracture can be protected with a commercial ankle splint, after some internal stability has been achieved. Operative Approaches

There are very few indications for operative intervention for humeral shaft fractures in the pediatric athlete. These special indications usually include multiple fractures in an athlete who must be treated in a recumbent position for the other injuries. In the patient with a closed head injury and spastic extremities, internal fixation may be the only means of controlling both angulation and excessive shortening. Associated radial nerve injury is not an indication for primary open reduction. Open fractures per se also are not always indications for internal fixation. The four major methods of operative intervention in order of their invasive ness are traction, external fixation, percutaneous intramedullary rod or pin fixation, and internal fixation with plates. Traction

Skeletal traction applied distally through the olecranon with either a pin or a special screw may be useful in fractures that are severely comminuted. It is especially useful in comminuted distal fractures for which internal or external fixation devices may be difficult to use ( Fig. 22A2-11 ). Traction can be applied in either the overhead or the side-arm mode. It is useful in those who must remain recumbent for treatment of other injuries, but this is an uncommon situation in modern polytrauma management. It is contraindicated in the patient who is thrashing because of an associated head injury. External Fixation

Little Indication in Athletes.

Although it is used occasionally in the trauma patient, external fixation would have

Figure 22-A2-11 A, Injury film of a 15-year-old baseball player who sustained a comminuted fracture of the distal humeral shaft when he slid into home plate. Because of the marked comminution, he was treated with overhead olecranon pin traction for 10 days (B) until some early callus formed; then he was placed in a long-arm cast (C).

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little use in the isolated humeral shaft fractures most often seen as athletic injuries. The simple, isolated, closed fracture of the humeral shaft can usually be managed by other, simpler methods. External fixators are usually reserved for patients with bilateral, ipsilateral, or extensive open injuries or for polytrauma patients.[3] Results in these situations are usually good regarding union and resumption of function.

Central Shaft Ideal.

Fractures proximal to the deltoid tuberosity or distal to the supracondylar area usually are not amenable to external fixation because of the lack of solid bone or the presence of thick, overlying muscle, which causes pin tract irritation ( Fig. 22A2-12 ). [8] Distal Screw Placement.

If very distal placement of a screw is required in a transcondylar area, a smaller guide pin can be placed just distal to the screw across the intercondylar area. This is usually replaced by a larger fixation screw.[23] In some cases, open placement of screws may be necessary to prevent radial nerve injury.[3] Percutaneous Intramedullary Rod or Pin Fixation

In treatment of the pediatric or adolescent athlete, intramedullary fixation is usually performed with small flexible rods or nails. These are usually placed from distal to proximal. The rotator cuff should not be violated. Intramedullary fixation is especially useful in treating obese patients

Figure 22-A2-12 Pin placement. Pins are best placed in those parts of the humerus with little muscle coverage (black sections). The pin penetration should enter into those areas designated by black arrows. (Reprinted with permission from Gausepohl T, Koebke J, Pennig D, et al: The anatomical base of unilateral external fixation in the upper limb. Injury 31:11-20, 2000.)

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Figure 22-A2-13 Intramedullary fixation. A, Injury film. The angulation was difficult to control with a coaptation splint because of some obesity of the patient. B, The fracture was stabilized with intramedullary pins, allowing better control of the angular alignment.

for whom the fracture site tends to drift into the varus because of the massiveness of the adjacent chest. The pins can be inserted posteriorly via a triceps-splitting technique through an entrance site just proximal to the olecranon fossa, as described by Hackethal.[10] Probably, the more commonly used approach is through the medial and lateral epicondyles ( Fig. 22A2-13 ). Problems associated with this technique involve pin backout and distraction at the fracture site. Acutely, some type of external stabilization is usually necessary.

Internal Fixation with Plates

Compressive plate fixation is an effective method of stabilizing shaft fractures. When applied properly, this method is associated with a low rate of complications and a high rate of union.[30] In patients with midshaft fractures, the plate provides the best compressive force when applied to the posterior surface. In proximal and distal fractures, the lateral surface of the shaft may need to be used. The major advantage is the security of fixation, which allows early motion and rehabilitation. A disadvantage is the need for a second operation to remove the plate. Open reduction is usually mandatory in patients with vascular injuries. It may also be necessary if ipsilateral forearm fractures are present. [16] It is especially important to remove the plate in athletes, particularly those participating in collision sports. Thus with this type of treatment, two recovery periods are

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needed. The first occurs after the initial fracture. The second occurs after plate removal because the bone must be protected until it is intrinsically stablethat is, until the defects produced by the screws and plate are completely filled with new bone, a time span that is not exactly predictable. An ideal indication for the use of the lightweight coaptation brace may be during this second recovery period ( see Fig. 22A2-10 ).

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Author's Preferred Method of Treatment

In simple displaced closed fractures, the use of the coaptation splint is ideal for both comfort and adequate stability. As the swelling subsides, the circular wrapping can be tightened. Early in the course of treatment, the patient is started on isometric simultaneous biceps and triceps contractures to preserve muscle function and provide compressive forces across the fracture callus. In the pediatric athlete, there is usually enough internal stability by 4 to 5 weeks to remove the splint. At this point, shoulder motion can be initiated.

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Postoperative Care

Once the fracture is stable, the athlete can progress to a vigorous rehabilitation program that emphasizes muscle strengthening not only of the biceps and triceps but also of the muscles about the shoulder girdle and forearm. The athlete can safely return to full activity, depending on the nature of the sport. Athletes participating in swimming and tennis can return earlier than those involved in collision sports. Return to such sports may be best delayed until the callus has developed a distinct cortex. Added protection in the early stages may be provided by a lightweight coaptation brace ( see Fig. 22A2-10 ).

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Special Fractures Pathologic Fractures

Fractures occurring through benign bone lesions should be allowed to heal. In the nonathlete, unicameral bone cysts may heal, in many cases with saline irrigation and steroid injection techniques. This usually is a prolonged process, but it does stabilize the bone for the stresses of normal activity. In the athlete, however, because rapid and complete reconstitution is desired, curettage and bone grafting are the best methods of restoring the bone to a stable condition to allow a return to activity as soon as possible. Ipsilateral Fractures

If the forearm fracture is complex, it may need to be stabilized internally. The humeral shaft fracture can then often be treated nonoperatively. If a complex humeral fracture or other systemic problem is present, internal fixation of the humerus may be necessary.[16]

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Complications Angular and Rotational Deformities

Cut-off of 10 Degrees

In the adolescent athlete, angulation of up to 10 degrees usually has an insignificant effect on both function and cosmetic appearance. Angulation greater than 10 degrees usually poses a cosmetic problem, especially if the distal fragment is in varus. Any angulation greater than 10 degrees needs to be corrected. Often, this can be done with a delayed manipulation performed 3 to 4 weeks after occurrence of the fracture, when the callus is reasonably stable. Elbow Extension Cast

In some cases, especially if angulation occurs in the sagittal plane, a manipulating cast can be applied with the elbow in extension. The athlete can usually tolerate this for the 2 to 3 weeks necessary for the fracture to become stable enough that all immobilization devices can be removed. Rotation

In complete fractures treated with coaptation splints or hanging-arm casts, the forearm rests against the anterior trunk. This can result in some internal rotation of the distal fragment. Usually, this is no greater than 10 degrees and is not evident clinically.[7] If the extremity is used for throwing, this degree of rotation may be critical. In such patients, the upper extremity may have to be immobilized with the forearm directed anteriorly. This may require incorporating the arm cast into a thoracobrachial type of body cast.

Vascular Injuries

Vascular injuries usually result from severe violence and fortunately are rarely seen in the athletic setting. They most often occur with open injuries. When they do occur, they are surgical emergencies. A temporary vascular shunt may have to be placed to perfuse the extremity while bony repair is undertaken. These injuries require internal fixation to protect the vascular repair. Nerve Injuries

Median Nerve

Only one isolated median nerve injury has been reported in the pediatric age group. [17] This occurred in a patient with an incomplete greenstick midshaft fracture in which the nerve was entrapped in the fracture site.

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Ulnar Nerve

Injuries to the ulnar nerve with humeral shaft fractures have not been reported. Radial Nerve (Most Common)

Middle Third Vulnerable.

The radial nerve is commonly injured in humeral shaft fractures. Twenty-five percent of reported radial nerve injuries have occurred in patients under the age of 20.[21] This injury is more common in fractures of the middle third of the shaft. Whitson[31] demonstrated anatomically that the radial nerve is separated posteriorly from the humeral shaft by a layer of deep triceps muscle and thus is relatively protected in this area. Holstein Fracture.

The radial nerve is juxtaposed to the lateral cortex at the junction of the distal third and the middle third of the shaft, where it passes from posterior to anterior through the lateral intermuscular septum. Because of this, Holstein and Lewis[13] suggested that all fractures in this area have a potential for acute or delayed radial nerve injury and thus should be fixed internally. Recovery Usually Spontaneous.

Subsequent follow-up studies have shown that from 73% to 93% of radial nerve injuries associated with fractures of the humeral shaft recover spontaneously, and there is no advantage to early exploration.[4] [24] [25] Operative Indications

Delayed.

Szalay and Rockwood[27] have outlined the method for estimating waiting time. They measure the distance from the tip of the most proximal spike to the medial epicondyle and then calculate 1 to 2 mm per day for regeneration, plus 30 to 60 days for good measure. If there is no return of either gross muscle activity or electromyographic (EMG) activity after this period, the nerve needs to be explored. They also note that even if the nerve has been lacerated, the results with delayed repair are better than those associated with primary repair. Primary.

The major indication for primary open exploration is an open fracture or poor nerve function in a patient who needs open exploration for vascular repair.

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Nerve Injuries Involving the Shoulder Area

Nerve injuries can be classified as acute, due to tension or blows directly to the nerve, or chronic, due to repeated pressure by the adjacent muscles, tendons, or ligaments. Acute injuries are usually characterized by the sudden onset of pain associated with development of a sensory or motor dysfunction in the distribution of the nerve involved. Chronic injuries often manifest as pain syndromes with rather occult sensory and motor findings. Acute Injuries

Incidence

Stretching vs Direct Blow.

These are usually the result of either acute stretching of the nerve or a direct blow. Bateman[1] described the mechanism of acute nerve injuries in great detail. Initially, the symptoms of an acute traumatic nerve syndrome include complaints by the athlete of burning numbness in the shoulder or distally in the extremity. There may be other sensations such as radiating, shocklike pain as well. Often the athlete is reluctant to move the extremity because of severe pain. One of the most important points of differentiation is whether the pain arises from compression in the area of the cervical spine and brachial plexus, or distally in the shoulder region. High Incidence in Football.

In a recent review of EMG studies by Krivickas and Wilbourn,[9] the highest incidence of nerve injuries was noted to occur in football players, followed by those associated with wrestling, weightlifting, and baseball-softball. In football players, the injury most commonly reported was the burner, which is a C5-C6 radiculopathy caused by forced

lateral flexion or hyperex tension of the neck. Motor Examination Critical.

The initial assessment of motor function is often more helpful than evaluation of the patient for sensory deficits. All of the major muscle groups about the shoulder, elbow, and wrist need to be carefully evaluated. Two muscles that are often overlooked clinically are the trapezius and the serratus anterior. Nerve conduction velocities and EMG studies are helpful at appropriate times. Bateman's Five Categories.

Bateman grouped the mechanisms that cause acute traumatic shoulder neuropathies into five categories, based usually on the mechanism of injury. He emphasized the importance of trying to reconstruct as accurately as possible the position of the player (or players) at the time of body contact or fall. His five categories are as follows: (1) projectile falls, (2) shoulder angle blows, (3) frontal force, (4) axillary injuries, and (5) twisting trauma. Projectile Falls

A projectile fall is one in which the athlete falls directly onto the point of the shoulder. Usually, the head and neck are abducted in the opposite direction. The major nerve damage associated with this type of fall occurs to the supraclavicular portion of the brachial plexus. This usually places most of the stretch on the upper roots and spares the lower roots. Bateman believed that this was the most common traumatic nerve injury in the shoulder. Shoulder Angle Blows

This type of injury involves a direct blow to the area between the shoulder and the neck and usually occurs in such stick-handling sports as hockey and lacrosse, as well as in certain riding and vehicular riding events. Usually, most of the force is applied to the edge of the trapezius and the cephalad margin of the scapula. With this type of blow, the accessory nerve can be injured at the cephalad margin of the trapezius. The major result here is paralysis of the middle and lower portions of the trapezius muscle. If the blow or stretch is more distal, the suprascapular nerve can be injured from either a direct contusion or an acute stretch. Again, the symptoms of weakness of the supraspinatus and infraspinatus muscles may be vague and difficult to elicit in the initial evaluation. Finally, the axillary nerve can be injured as it courses posteriorly around the proximal humerus. This injury occurs very rarely, however,

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because the bulk of the deltoid muscle provides protection against direct blows.

Frontal Force

This injury occurs when the player crouches forward and spreads his or her arms at the shoulder in an abducted and externally rotated position, as in blocking or tackling positions. In this position, the infraclavicular branches of the brachial plexus can be crushed against the head of the humerus by a direct blow from an object such as a player's helmet or knee. The nerves most vulnerable to injury by this mechanism are the axillary and musculocutaneous nerves. Axillary Injuries

Direct blows to the axilla from an inferior direction can crush the posterior cord of the brachial plexus against the upper aspect of the humerus and the glenoid labium. This type of injury occurs in football, hockey, and ice racing sports. Because the posterior cord is accompanied by large venae comitantes, there may be significant hematoma formation with this injury. The deltoid and triceps muscles are often weakened because of injury to the posterior cord. The lower portion of the radial nerve often remains functional. Twisting Trauma

This injury usually occurs in football when a twisting motion is applied to the shoulder. It also can occur with discus throwing. The most common associated injury complex is the injury to the axillary nerve that occurs in conjunction with dislocation of the glenohumeral joint. Most Effects Temporary.

Most of these acute neuropathies represent simple stretching (neurapraxia) of the nerve, and the dysfunction is temporary. In these instances, the extremity needs to be rested and supported until the nerve has recovered. On rare occasions, the nerve may be completely torn (axonotmesis), and surgical exploration and repair may be necessary. Chronic Injuries

Involvement of Three Major Nerves

The three major nerves affected by overuse or impingement syndromes of the shoulder are the axillary nerve in the quadrilateral space, the suprascapular nerve, and the long thoracic nerve. Priest and Nagel[11] reported a rare thoracic outlet syndrome in the depressed shoulder that is associated with the tennis shoulder syndrome. Very little has been written about these syndromes in the pediatric athlete. The orthopaedist who deals with adolescent athletes must be aware of the clinical

manifestations of these syndromes in these often rather physically mature youngsters. Suprascapular Nerve

Anatomic Vulnerability.

The suprascapular nerve is vulnerable to injury because of its anatomic characteristics. It is accompanied by a branch of the suprascapular artery, which originates from the thyrocervical trunk. When these structures reach the superior border of the scapula, they separate briefly. The nerve passes under the suprascapular ligament and the artery passes over it (Fig. 22A2-14 (Figure Not Available) ). At Figure 22-A2-14 (Figure Not Available) Neurologic injuries about the shoulder. The suprascapular nerve is bound down in the suprascapular notch by the transverse scapular ligament (large black arrow). Compression of the suprascapular nerve can also occur as it curves around the base of the acromion process to supply the infraspinatus muscle (double open arrows). The third area of compression is the axillary nerve as it emerges from the quadrangle space (double curved black arrows). (From Anderson TE, Bergfield JA: Common throwing injuries of the shoulder. Mediguide Orthop 4[1], 1982.)

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this point, the nerve is restricted in its motion and is thus vulnerable to traction or to compression injury with extremes of shoulder motion. In the suprascapular fossa, the artery and nerve are joined where the nerve supplies the supraspinatus muscle. The nerve then courses distally to the root of the acromion, where it gives off articular branches to the glenohumeral and acromioclavicular joints. At the root of the acromion, it curves caudad around the spine of the scapula to supply the infraspinatus muscle. Although it supplies most of the sensory and sympathetic innervation to the glenohumeral capsule, it has no cutaneous branches.[5] Chronic Shoulder Pain.

The symptoms of this nerve compression syndrome produce chronic posterior shoulder pain and weakness, which often mimic the symptoms of a torn rotator cuff.[6] Drez[6] described a 16-year-old basketball player who developed weakness and pain after falling directly on his shoulder. Atrophy of the supraspinatus and infraspinatus muscles developed. An electromyogram showed denervation in both muscles. This athlete recovered with only supportive therapy. Drez felt that in this case (and in most other cases), the cause was a neurapraxia of the suprascapular nerve at the point at which it is stretched over the superior margin of the suprascapular notch (see Fig. 22A2-14 (Figure Not Available) ). This injury can occur when the shoulder is acutely depressed. It has also been noted to happen when the shoulder is repeatedly depressed, causing repeated microtrauma to the nerve. Bennett[2] suggested that traction to this nerve occurs in the follow-through phase of baseball throwing.

Surgical Indications.

In cases that fail to respond to rest and rehabilitation, surgical release of the suprascapular ligament is believed to help because it eliminates the point of nerve fixation. Jobe and his coworkers,[8] however, believed that the point of injury in this syndrome is where the nerve crosses the base of the acromion (see Fig. 22A2-14 (Figure Not Available) ). In their cases, which were more chronic, only the infraspinatus muscle was involved, and the supraspinatus was spared. This syndrome often manifests as chronic pain that is misdiagnosed as tendinitis in high-level baseball pitchers. In their experience, the residual infraspinatus muscle could be strengthened with exercises so that the pitcher could return to a competitive level. They did not believe that this type of suprascapular nerve syndrome would respond to surgical decompression. Electrical diagnostic studies may aid in differentiation of involved structures. Axillary Nerve in the Quadrilateral Space

Mechanism.

This injury was originally described in baseball pitchers by Bennett [2] as an injury caused by a traction exostosis that occurred on the inferior border of the glenoid fossa owing to the pull of the long head of the triceps and the posterior glenohumeral capsule. He surmised that this exostosis irritated the axillary nerve as it coursed through the quadrilateral space. Cahill[3] [4] more recently suggested that the nerve may be injured when it is chronically compressed by fibrous bands in the quadrilateral space (see Fig. 22A2-14 (Figure Not Available) ). Diagnostic Measures.

This compressive force usually is greatest during the cocking phase of throwing. As a result of this compression, posterior shoulder pain occurs, which increases when the shoulder is abducted and externally rotated. An arteriogram may be helpful by demonstrating compression of the posterior humeral circumflex artery when the shoulder is abducted and externally rotated. Treatment.

Treatment consists of rest and local steroid injections to decrease the inflammation. If this fails, surgical decompression of the quadrilateral space may be necessary. Necessity for Alertness to These Injuries.

The important aspect of these two chronic nerve syndromes is that the possibility of their presence should always be kept in mind when one is evaluating the athlete who complains of chronic posterior shoulder pain. In athletes with this complaint, the strength

of the supraspinatus, the infraspinatus, and the deltoid muscles must be carefully evaluated. If there is any question about the diagnosis, EMG evaluation of these muscles may be helpful. Long Thoracic Nerve

Injury to this nerve can occur as an idiopathic entity or following a traction injury to the shoulder, such as occurs with bench press or shoulder resistance exercises. It has also been reported in young throwers who experienced no major injury. [7] [11] The usual diagnostic test is to have the athlete push forward against a fixed object such as a wall while the clinician looks for winging of the scapula. This injury usually recovers with rest and prevention of re-injury. It must be remembered, however, that winging of the scapula can also be a manifestation of a C7 root neuropathy. [10]

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References Fractures of the Humeral Shaft 1.

Allen ME: Stress fracture of the humerus: A case study. Am J Sports Med 12:244-245, 1984.

Balfour GW, Mooney V, Asby ME: Diaphyseal fractures of the humerus treated with a ready-made fracture brace. J Bone Joint Surg Am 64:11-13, 1982. 2.

Bennek J: The use of upper limb external fixation in paediatric trauma. Injury Int J Care Injured 31:21-26, 2000. 3.

Bostman O, Bakalim G, Vainionpaa S, et al: Radial palsy in shaft fracture of the humerus. Acta Orthop Scand 57:316-319, 1986. 4.

Curtis RJJ, Dameron TB Jr, Rockwood CA Jr, et al (eds): Fractures in Children, 3rd ed. Philadelphia, JB Lippincott, 1991, pp 829-919. 5.

Dameron TB Jr: Transverse fractures of distal humerus in children. AAOS Instr Course Lect 30:224-235, 1981. 6.

7.

Dameron TB Jr, Grubb SA: Humeral shaft fractures in adults. South Med J 74:1461-1467, 1981.

Gausepohl T, Koebke J, Pennig D, et al: The anatomical base of unilateral external fixation in the upper limb. Injury Int J Care Injured 31:11-20, 2000. 8.

Gilchrist DK: A stockinette Velpeau for immobilization of the shoulder girdle. J Bone Joint Surg Am 49:750-751, 1949. 9.

10.

Hackethal KH: Die Bundel-Nagelung. Berlin, Springer-Verlag, 1961.

11.

Healey JE Jr, Seybold WD: A Clinical Synopsis of Anatomy. Philadelphia, WB Saunders, 1969, p 57.

Hedstrom O: Growth stimulation of long bones after fracture or similar trauma: A clinical and experimental study. Acta Orthop Scand Suppl 122:1-62, 1969. 12.

Holstein A, Lewis GB: Fractures of the humerus with radial nerve paralysis. J Bone Joint Surg Am 45:1382-1396, 1963. 13.

Kane E, Kaplan EB, Spinner M: Observations of the course of the ulnar nerve in the arm. Ann Chir 27:487-496, 1973. 14.

15.

Landin LA: Fracture patterns in children. Acta Orthop Scand Suppl 202:1-109, 1983.

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Lange RH, Foster RJ: Skeletal management of humeral shaft fractures associated with forearm fractures. Clin Orthop 195:173-177, 1985. 16.

MacNicol MF: Roentgenographic evidence of median nerve entrapment in a greenstick humeral fracture. A case report. J Bone Joint Surg Am 60:98-100, 1978. 17.

Martin RF: Fractures of the proximal humerus and humeral shaft. In Letts RM (ed): Management of Pediatric Fractures. New York, Churchill-Livingstone, 1994, pp 37-157. 18.

19.

Ogden JA: Skeletal Injury in the Child. New York, Springer-Verlag, 2000.

20.

Pollen AG: Fractures and Dislocations in Children. Baltimore, Williams & Wilkins, 1973, pp 7-22.

Pollock FH, Drake D, Bovill EG, et al: Treatment of radial neuropathy associated with fractures of the humerus. J Bone Joint Surg Am 63:239-243, 1981. 21.

Rettig AC, Beltz HF: Stress fracture in the humerus in an adolescent tennis tournament player. Am J Sports Med 13:55-58, 1985. 22.

Ruland WO: Is there a place for external fixation in humeral shaft fractures? Injury Int J Care Injured 31:27-34, 2000. 23.

Shah J, Bhatti NA: Radial nerve paralysis associated with fracture of the humerus: A review of 62 cases. Clin Orthop 172:171-176, 1983. 24.

Sonneveld GJ, Patka P, Van Mourick JC, et al: Treatment of fractures of the shaft of the humerus accompanied by paralysis of the radial nerve. Injury 18:404-406, 1987. 25.

Sterling JC, Calvo RD, Holden SC: An unusual stress fracture in a multiple sport athlete. Med Sci Sports Exerc 23:298-303, 1991. 26.

27.

Szalay EA, Rockwood CA Jr: Fractures of the distal shaft of the humerus associated with radial nerve

injury. San Antonio, Texas, The University of Texas Health Science Center of San Antonio, 1981. 28.

Tachdjian M: Pediatric Orthopedics, vol 4, 2nd ed. Philadelphia, WB Saunders, 1990.

Tullos HS, Erwin WD, Woods GW, et al: Unusual lesions of the pitching arm. Clin Orthop 88:169-182, 1972. 29.

Vander Griend R, Tomasin J, Ward EF: Open reduction and internal fixation of humeral shaft fractures. J Bone Joint Surg Am 68:430-433, 1986. 30.

Whitson RO: Relation of the radial nerve to the shaft of the humerus. J Bone Joint Surg Am 36:85-88, 1954. 31.

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References Nerve Injuries 1.

Bateman JE: Nerve injuries about the shoulder in sports. J Bone Joint Surg Am 49:785-792, 1967.

2.

Bennett GE: Elbow and shoulder lesions of baseball players. Am J Surg 98:484-492, 1959.

Cahill BR: Quadrilateral space syndrome. In Omer GE, Spinner O, Spinner M (eds): Management of Peripheral Nerve Problems. Philadelphia, WB Saunders, 1980, pp 599-606. 3.

4.

Cahill BR, Palmer RE: Quadrilateral space syndrome. J Hand Surg 8:65-69, 1983.

De Palma AF: Nerve entrapment syndromes. In DePalma AF (ed): Surgery of the Shoulder. Philadelphia, JB Lippincott, 1983, pp 593-594. 5.

Drez D Jr: Suprascapular neuropathy in the differential diagnosis of rotator cuff injuries. Am J Sports Med 4:43-45, 1976. 6.

Ireland ML, Andrews JR: Shoulder and elbow injuries in the young athlete. Clin Sports Med 7:473-494, 1988. 7.

Jobe FW, Tibone JE, Jobe CM, Kuitne RS: The shoulder in sports. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 961-987. 8.

Krivickas LD, Wilbourn AJ: Sports and peripheral nerve injuries. Report of 190 injuries evaluated in a single electromyographic laboratory. Muscle Nerve 21:1092-1094, 1998. 9.

Makin JG, Brown WF, Ebers GC: C7 Radiculopathy: Importance of scapular winging in clinical diagnosis. J Neurol Neurosurg Psychiatr 49:640-644, 1986. 10.

11.

Priest JD, Nagel DA: Tennis shoulder. Am J Sports Med 4:28-42, 1976.

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Section B Neurovascular Injury of the Arm James B. Bennett MD Thomas L. Mehlhoff MD Neurovascular Injury in the Upper Arm

Neurovascular injuries distal to the glenohumeral joint and proximal to the elbow joint are infrequent and generally related to direct trauma, particularly fracture-dislocations of either the glenohumeral joint or the elbow joint. Spiral oblique fractures of the humerus are well recognized as the cause of neurapraxic injuries to the radial nerve, with predictable recovery in most cases.[89] Axillary nerve neurapraxic injuries with shoulder dislocations, particularly posterior dislocations, are also well documented in the literature.[16] Direct trauma can likewise produce neurapraxic injuries to the axillary nerve as it exits posteriorly at the level of the proximal humerus and enters the deltoid region ( Fig. 22B-1 ) or to the radial nerve as it travels about the spiral groove of the humerus. Motor and sensory deficits are noted in the appropriate nerve distribution. Specific treatment of nerve injuries is addressed elsewhere in this text. The ulnar nerve is less commonly injured in its course along the medial aspect of the arm. The most common site of ulnar nerve injury about the elbow is in the cubital tunnel; this is likewise discussed elsewhere in this text. Median nerve injury in the humerus may be associated with injury to the supracondylar process and ligament of Struthers. Decompression is indicated if clinical and electrodiagnostic studies localize compression to this level. Combined or mixed nerve injuries may be associated with major fractures or dislocations of the glenohumeral joint or the elbow joint. Compression of the musculocutaneous nerve by the coracobrachialis has been described in weightlifters by Braddom and Wolfe[17A] with painless weakness and atrophy of the biceps muscle and dysesthesias in the volar radial forearm. As an isolated sensory component, compression of the musculocutaneous nerve as it exits the biceps

and penetrates the deep brachial fascia above the elbow creates paresthesias in the lateral antebrachial cutaneous nerve of the forearm. Decompression of the musculocutaneous nerve at the coracobrachialis for the combined lesion or as the lateral antebrachial cutaneous nerve exits the biceps and the brachial fascia for isolated sensory deficits is indicated as described by Bassett and Nunley. [12A] Brachial artery injury in the arm is a rare injury. It may, however, be associated with a high-velocity closed fracture of the humerus, a compound fracture, or lacerations or puncture wounds of the medial aspect of the arm. Arteriographic

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Figure 22-B-1 Axillary nerve compression or stretch injury at the posterior aspect of the deltoid muscle.

diagnosis and appropriate surgical repair are indicated. Thrombosis of the brachial artery secondary to trauma is uncommon, but if it is present, a more proximal lesion should be ruled out arteriographically. Cahill and Palmer[22] have described compression of the circumflex humeral artery as a quadrilateral space syndrome. This may also result in compression of the axillary nerve. It is seen in throwing athletes and is produced with forward flexion, abduction, and external rotation of the humerus, aggravating the symptoms of pain, weakness, and fatigability. Documentation is obtained with arteriography that reveals occlusion of the posterior circumflex humeral artery with the arm in abduction and external rotation. Conservative treatment with cessation of throwing activities should relieve the symptoms. If persistent tenderness and pain exist and findings on arteriography are abnormal, surgical decompression through a posterior incision is recommended, with exploration of the quadrilateral space and decompression of the posterior circumflex humeral artery and axillary nerve as indicated by pathologic findings in this region.

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Compartment Syndrome

Compartment syndrome of the upper extremity localized to the upper arm is a rare lesion, as reported by Leguit,[66] Holland and associates,[51] and Brumback.[20] The patient has a massive, swollen, and tense upper arm with severe pain, loss of active and passive motion, and sensory and motor deficits secondary to a history of direct trauma. Holland and associates[51] described a patient with a normal brachial arteriogram but massive swelling and a secondary hematoma displacing the artery, which necessitated immediate operative decompression, evacuation of the hematoma, and secondary wound closure; treatment was successful with return of function and return to sports activities. Because of the soft tissues and muscles, compartmental pressure measurements are somewhat less reliable in this area than in the forearm and hand, with their constrictive fascia. Pressure measurements are recommended, however, as is arteriographic evaluation of the axillary and brachial arteries before surgical intervention for compartment syndrome.[81]

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Venous and Arterial Insufficiency

The swollen arm in the athlete with no history of significant trauma presents a diagnostic dilemma ( Fig. 22B-2 ). Differential diagnosis of upper extremity pain and swelling includes muscle sprains, tears and contusions, edema, bone or soft tissue infection, cellulitis, and venous thromboses. Obviously, a fracture due to direct trauma or a pathologic lesion of bone resulting in fracture must be ruled out. Upper extremity venous insufficiency results from acute axillary or subclavian vein obstruction, which is due to iatrogenic trauma in the form of central venous catheters in 70% to 80% of cases; 10% to 20% of cases are associated with spontaneous thromboses (effort thromboses), and the remaining 5% to 10% are secondary to chronic disorders of the venous system. Not infrequently, patients with upper extremity venous thromboses have complications that include pulmonary embolism,[12] septicemia, and chronic postphlebitic syndrome.[55] Sudden, painless arm swelling in a patient with a central venous line is virtually diagnostic of subclavian vein thrombosis. In the athletic population, spontaneous or effort thrombosis of the axillary vein is more common in men than in women, occurs on the dominant side in the majority of cases, and is most common in the fourth decade of life. Most of these patients have a history of trauma or recent strenuous exertion.[72] The arm is swollen with unilateral nonpitting edema that becomes cyanotic in appearance with continued exercise. Idiopathic chronic venous insufficiency without previous

Figure 22-B-2 Swollen arm-forearm-hand secondary to effort thrombosis of the axillary vein.

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symptoms may occur. Von Schrötter [102] described thrombosis of the axillary vein in 1884 and used the term primary or idiopathic thrombosis of the axillary vein. Venous occlusion may be secondary to thoracic outlet syndrome. Vogel and Jensen[120] described effort thrombosis in the competitive swimmer. A similar lesion has also been described in the throwing athlete, particularly baseball pitchers. Direct trauma in contact sports has produced venous thrombosis of the axillary and subclavian veins. The patient has good arterial flow, but the pathologic process lies in restricted venous outlet flow. In addition to thoracic outlet syndrome, certain congenital and developmental anomalies may predispose a patient to venous insufficiency. Abnormalities in blood coagulation as well as secondary causes, such as malignant neoplasia, congestive heart failure, polycythemia vera, and the previous use of any indwelling catheters about the shoulder region, must be ruled out.[101] Duplex ultrasound scanning of the arterial system may be used to diagnose poststenotic aneurysms and to identify intraluminal lesions as a source of emboli. It can be used in the diagnosis of major venous occlusions. Color Duplex sonography combines direct noninvasive, real-time images of the subclavian vessels with Doppler waveform analysis. Studies can be performed at rest and during provocative maneuvers, allowing a physiologic assessment of arterial and venous compression. Conventional duplex or color Doppler sonography offers significant advantages over arteriographic techniques in that the study is noninvasive and may be performed bilaterally, the artery and vein can be examined in one study, and waveforms can be obtained to analyze flow dynamics.[65A] [68A] Diagnosis is confirmed with venography[2] ( Fig. 22B-3 ). Doppler ultrasonography and plethysmography are less

Figure 22-B-3 Venogram of axillary and subclavian vein occlusion.

reliable in the upper extremity. Venous pressure measurements have been recommended by Veal and Hussey[119] ; arteriography shows a patent arterial tree in these cases. A delayed venous phase on the arteriogram shows dilatation and dysfunction of the venous system. Treatment of patients with minimal symptoms is conservative, with rest and cessation of sports activities. Surgery to reconstitute the vein has not been uniformly successful, and thrombosis tends to recur. Collateral circulation develops in the course of time, and venous decompression results. Historically, anticoagulation with heparin followed by warfarin for 2 to 3 months has been the treatment of choice. [70] More recently, fibrinolytic therapy for the lysis of either intra-arterial or intravenous clots has been successful.[13] Streptokinase or urokinase intravenous injections to lyse the clot may allow restoration of blood flow into the thrombosed segment.[79] Complications are significant with fibrinolytic therapy, and the patient must be monitored closely to detect a bleeding tendency or hemorrhage at other sites within the body, arrhythmias, allergic reaction, or fever secondary to the therapy program. Recanalization of the axillary or subclavian vein, as well as of the collateral circulation, develops during the course of 6

months to 1 year. First rib resection to decompress the thoracic outlet and axillary-subclavian vein complex may be required.[124] Acute arterial thrombosis has been described in the pitching or throwing athlete, involving acute occlusion, vascular ischemia, pain, and development of retrograde thrombosis, which may occlude the proximal carotid and vertebral arteries. [113] Symptoms of severe arm pain, diminished or absent pulse, and a pale extremity suggest acute arterial thrombosis; diagnosis is confirmed through arteriographic studies ( Fig. 22B-4 ). Treatment, depending on the

Figure 22-B-4 Arteriogram with thrombosis of subclavian artery.

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duration of the arterial lesion, may involve surgery, including embolectomy or vascular reconstruction, resolution of the thrombus with fibrinolytic therapy in the form of streptokinase or urokinase, or angioplastic dilatation at the time of catheterization. Laser therapy for intra-arterial lesions is under study. With chronic thrombosis, bypass vascular surgery is recommended to restore circulation in the extremity if the collateral circulation is inadequate and evidence of ischemia with exercise or rest pain is present. If the components of a thoracic outlet syndrome or anomalous cervical rib contribute to venous or arterial insufficiency, removal of the pathologic structure as well as reconstruction of the arterial supply to the upper extremity is recommended. Postoperative Management and Rehabilitation

Medical management may vary from anticoagulation with heparin and warfarin (Coumadin) to low-dose aspirin, depending on the severity of the occlusion, the collateral blood flow in the extremity, and the extent of surgical reconstruction, if required. Rehabilitation requires range of motion and strengthening exercises and medical control of bleeding and clotting factors. Criteria for Return to Sports Participation

Return to sports may not be possible if arterial or venous reconstruction is required. Medically managed vascular occlusive disease should allow return to competition in athletes who have a patent vascular trunk and good collateral circulation into the extremity. Authors' Preferred Method of Treatment

Venous occlusion and arterial thrombosis of the upper extremity are managed by the cardiology and cardiovascular departments with use of the various methods outlined

before. Transcatheter thrombophlebitic therapy with urokinase, streptokinase, or tissue plasminogen activator is recommended. The stenosis and residual thrombosis may be dilated with balloon angioplasty or vascular resection with reconstruction to achieve patency. Anticoagulation therapy with oral warfarin sodium continues for 3 months, and the antithrombolytic profile is monitored by prothrombin and partial thromboplastin times. If patency is not achieved, venous or arterial bypass surgery is recommended to resolve the symptoms of venous occlusion or arterial thrombosis.

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Chapter 23 - Elbow and Forearm Section A Biomechanics of the Elbow and Forearm Bernard F. Morrey MD In this chapter, we discuss the topic of biomechanics of the elbow according to joint motion, stability, and forcestrength. The biomechanical features of the forearm are discussed separately. Joint Surfaces

The elbow is a trochoginglymoid joint; that is, it possesses two degrees of freedom: flexion-extension and forearm rotation.[24] There are certain special features of this articulation that account for the motion attributed to it. The joint surfaces of the humerus, the radius, and the ulna have specific and discrete orientations with regard to the long axis of each. Recognition of these orientations is especially important for proper treatment of some fractures about the elbow. Humerus

The articulation surface of the humerus is rotated anteriorly approximately 30 degrees in reference to the long axis of the humerus, viewed from the lateral projection. Although there is considerable individual variation, a mean of 5 to 7 degrees of valgus tilt of the axis of rotation is thought to be normal. Viewed end-on, the distal humeral articulation is also externally rotated approximately 3 to 5 degrees in reference to the posterior surface

of the medial and lateral supracondylar columns.[18] Articular Surface.

The articular surface of the distal humerus is composed of a trochlea containing medial and lateral elements. Cartilage covers the trochlea through an arc of approximately 300 degrees. The capitellum is an almost perfect geometric hemisphere, with an arc of curvature of approximately 180 degrees in both medial lateral and proximal distal meridians. The orientation of this semicircle is directly anterior. This important fracture allows a fixation plate to be contoured and applied to the posteroin-ferior aspect of the lateral column without violating the articular surface of the capitellum.[2] The more congruous the joint, the thinner the articular surface; the elbow is considered one of the most congruous articular joints in the body. The thickness of the articular cartilage of the distal humerus, hence, is only 2 to 3 mm; as such, it is one of the thinnest articular surfaces of the human body. Ulna

The articular surface of the ulna makes approximately a 5- to 7-degree valgus angulation with regard to the long axis of the shaft when viewed on the anteroposterior projection. Laterally, the articular surfaces are oriented approximately 30 degrees posterior referable to the long axis. As such, it matches well with the anterior rotation of the distal humeral articulation ( Fig. 23A-1 ). This particular articular orientation allows the elbow to be stable when completely extended, an important function for some athletic activities. Articular Surface.

The ulnar articulation is composed of two components. The greater sigmoid fossa (often referred to as the olecranon) consists of the coronoid process distally and the olecranon process proximally. The arc of curvature of this articulation is approximately 185 degrees. The articular surface is thin, measuring 2 to 3 mm. A very important anatomic feature is the lack of articular cartilage at the center of the greater sigmoid fossa.[18] Hence, the contact area consists of the anterior coronoid and posterior olecranon surfaces. When investigating the ulnohumeral joint arthroscopically, one must take care not to interpret this normal variation as articular disease. Exposure by means of osteotomy should also be directed through this portion of the olecranon. On the lateral side of the greater sigmoid fossa, the lesser sigmoid notch, with an arc of curvature of about 70 degrees, accommodates the radial head. Radial Head

The radial head and neck deviate approximately 15 degrees away from the radial tuberosity ( Fig. 23A-2 ). This

Figure 23-A-1 The 30-degree anterior rotation of the distal humerus is matched by the 30-degree opening of the greater sigmoid notch, thus providing stability to the elbow in full extension.

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Figure 23-A-2 The radial head and neck deviate 15 degrees away from the radial tuberosity. This allows a full arc of forearm rotation without translation at the radiohumeral joint. (By permission of the Mayo Foundation.)

angular relationship allows the forearm to undergo an arc of forearm rotation approximating 180 degrees while maintaining a precise and constant orientation in regard to the capitellum. Articular Surface.

The articular surface of the radial head is composed of a disk-shaped impression with an arc of curvature of 40 degrees.[18] The margin of the radial head is covered by hyaline cartilage through an arc of about 240 degrees and articulates with the lesser sigmoid fossa. The remaining 120 degrees constitutes the nonarticular portion of the radial head. This portion is weaker because there is no subchondral bone, which may account for the predilection for shear fractures to occur through this region from falls on the outstretched hand.

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Joint Motion

The three-dimensional motion of the elbow joint has been carefully studied.[14] [24] The carrying angle undergoes a linear change from valgus to varus from extension to flexion ( Fig. 23A-3 ). Furthermore, there is a slight axial rotation of the ulna internally during the initiation of extension and then externally at the completion of extension as a result of the geometric characteristics of the ulnohumeral joint. The subtle axial rotation of the ulna may contribute to the osteophyte that develops on the radial tip of the olecranon in the throwing athlete.[31] Axis of Rotation

The locus of the instant center of rotation of the elbow is less than 3 mm in its widest dimension.[8] Hence, elbow flexion may be considered primarily a spinning motion for all practical purposes. The hinge axis may thus be approximated by a line that pierces the lateral projection of the center of the capitellum and the center of the trochlea ( Fig. 23A-4 ). The axis is located medially at the anteroinferior aspect of the medial epicondyle. Axis of Forearm Rotation

The axis of forearm rotation passes directly through the center of the radial head and thus through the center of the capitellum in both anteroposterior and lateral projections.[17] This axis then traverses the interosseous membrane and emerges through the base of the styloid process of the ulna, at the center of curvature of the distal ulna. Normal Elbow Motion

The normal arc of elbow flexion is 0 to 145 degrees, with considerable individual

variation.[7] Lax-jointed individuals may hyperextend 10 or more degrees, and well-muscled individuals may flex only 130 degrees. Pronation and supination arcs are usually symmetrical. Pronation averages about 80 degrees, about 5 to 10 degrees less than supination, which averages about 85 degrees. Normal average forearm rotation thus is not typically a full arc of 180 degrees but approximately 165 to 170 degrees.[7] Calculation of flexion-extension is one of the easiest joint measurements in the body. Hand-held goniometers are accurate to within 5 degrees. To obtain follow-up information about this function, we have found that motion may be accurately estimated by tracing the silhouette in full flexion and full extension. Goniometric measurements of these tracings are comparable to in vivo measurements. Carrying Angle

The normal valgus orientation of the forearm varies as a function of both age and sex. It is less in children than in adults and averages 3 to 4 degrees greater in females than in males.[6] [16] The carrying angle is formed by the valgus tilt of the axis of rotation (humeral articulation) and the valgus orientation of the ulnar shaft in reference to the olecranon. [32] The normal angle varies greatly and averages approximately 10 degrees in the male and 13 degrees in the female. The proper definition of the carrying angle is the orientation of the forearm in reference to the humerus when the elbow is in full extension. The concept loses its significance as the elbow flexes.[3] Functional Motion

As with many joints, the full available arc of motion is not required for routine daily activities. Our study has shown that activities involving personal hygiene and daily sustenance are accomplished with an arc of 30 to 130 degrees of flexion and with 50 degrees of pronation and 50 degrees of supination.[23] For the athlete, functional motion

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Figure 23-A-3 A, During elbow flexion, the carrying angle changes in a linear fashion from valgus to neutral or varus. B, The ulna undergoes a slight axial rotation during flexion and extension. (By permission of the Mayo Foundation.)

Figure 23-A-4 The axis of rotation of the elbow is approximated by a line running through the middle of the lateral epicondyle and the center of the trochlea, emerging in the anterior inferior aspect of the medial epicondyle.

requirements for various sports have not been addressed. It is known, however, that the thrower frequently develops a flexion contracture of up to 10 degrees; this contracture does not impair function. It has also been shown that pitchers tend to develop an increased carrying angle compared with the opposite side. This condition is also known to affect performance adversely. [31] Greater motion might be anticipated during some athletic activities, such as gymnastics. Less motion, however, is associated with increased muscle mass, as might be seen with body builders.

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Elbow Stability

Three major elements contribute to the stability of any joint: the articular surface, the capsular and ligamentous

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structures, and the muscles. Unlike the shoulder, the dynamic contribution of the musculature to elbow stability under normal circumstances is minimal.[11] The elbow relies on the contributions of the static constraints: the articular surface and the capsular ligamentous complex.[25] Articular Contribution to Stability

An accurate means of measuring the relative contribution of the articular surface to joint stability is still being developed. The Ulnohumeral Joint

Olecranon.

Ignoring the muscular influences, resection of successive portions of the ulnar articulation decreases the stability of that joint in proportion to the amount that has been removed.[4] Hence, a 50% resection of the olecranon causes a 50% reduction in ulnohumeral stability (Fig. 23A-5 (Figure Not Available) ). Coronoid.

Fracture of the tip of the coronoid does not compromise articular stability but indicates that the elbow has undergone dislocation or subluxation. The critical amount of coronoid needed for stability is 50%. This amount may be estimated by a line drawn from the tip of the intact olecranon through the remaining coronoid. If the line converges with the long axis of the ulna distally, the articular stability of the ulnohumeral joint has been lost. If the line converges proximally, the stabilizing effect of the coronoid is probably intact (Fig. 23A-6 (Figure Not Available) ). The clinical implication of these data is extremely important when managing individuals with coronoid fractures because the goals of such treatment are to ensure stability and to provide functional motion. This requirement is not easily resolved and sometimes requires the use of external fixators Figure 23-A-5 (Figure Not Available) With serial removal of the olecranon, a linear decrease in ulnohumeral stability is observed. Note the 50% loss with 50% resected. (By permission of the Mayo Foundation.) Figure 23-A-6 (Figure Not Available) Absence of 50% of the coronoid is estimated by drawing a line from the olecranon tip to the coronoid release. The line is parallel to the shaft at the 50% level. (By permission of the Mayo Foundation.)

and continuous motion machines. Return to high-level competition is, of course, compromised. The Radial Head

Studies of the contribution of the radial head to elbow stability reveal that about 20% to 30% of an applied valgus load is transmitted through, and thus resisted by, the radiohumeral joint.[12] [19] [26A] [29] The role of the radial head in resisting valgus stress must be considered with the associated ligamentous structures.[19] The relative contributions of the radial head and the ligamentous structures are demonstrated by a technique of serial release.[22] These data clearly show that with simulated flexion and extension, the radial head does not resist physiologic valgus stresses in the presence of an intact medial collateral ligament. If the medial collateral ligament has been removed or violated, however, the radial head plays a major role in resisting the

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Figure 23-A-7 (Figure Not Available) Left, Removing the radial head (RH) (1) but leaving the medial collateral ligament (MCL) intact (2) results in no alteration in valgus stability. Right, When the medial collateral ligament is removed first (1), the radial head is observed to provide some resistance to valgus stress. When both constraints are released (2), the elbow is grossly unstable. (By permission of the Mayo Foundation.)

valgus torque. If both the medial collateral ligament and the radial head are removed, the elbow predictably dislocates (Fig. 23A-7 (Figure Not Available) ). Interpretation of these data is best done in a format familiar to the sports medicine

physician when considering the contributions of the meniscus and the anterior cruciate ligament to knee stability. The radial head has a role similar to that of the meniscus, and the role of the medial collateral ligament is analogous to that of the anterior cruciate ligament. The radial head may be considered a secondary stabilizer in valgus elbow instability. Its contribution is seen only if the medial collateral ligament complex is deficient ( Fig. 23A-8 ). Capsuloligamentous Complex

Medial Collateral Ligament

The role of the anterior bundle of the medial collateral ligament in resisting valgus stability has been well

Figure 23-A-8 The radial head provides a secondary constraint to a valgus stress but is unimportant when the medial collateral ligament (MCL) is intact. (By permission of the Mayo Foundation.)

described.[20] Acute rupture of the medial complex may, therefore, be effectively addressed by reconstructing or repairing the anterior bundle of this complex. The anterior element of the medial collateral ligament originates at the site of the axis of rotation for the elbow ( Fig. 23A-9 ). The posterior bundle originates off the axis. Hence, a cam effect is present and the posterior bundle is taut only in flexion. The anterior bundle is taut throughout the arc of motion; the anterior fibers are most taut in extension, and the posterior bundles become tightened in flexion. Hence, the role of the anterior portion of the medial collateral ligament is not unlike that of the anterior cruciate ligament at the knee. These experiments specifically show that the anterior bundle is the essential component of the medial complex. Given this fact, precise restoration of the humeral origin of the ligament must be attained with ligament reconstruction procedures.[15] Lateral Collateral Ligament Complex

A discrete portion of the lateral collateral ligament complex has now been demonstrated to originate from the humerus and to attach on the tubercle crista supinatoris of the ulna.[20] This component of the lateral collateral ligament is thus properly termed the lateral ulnar collateral ligament and should be distinguished from the radial collateral ligament, which attaches to the annular ligament ( Fig. 23A-10 ). The existence of this particular structure explains the maintenance of varus stability after the radial head has been excised. Because the radial collateral ligament becomes lax as the annular ligament loses its tension, resistance to varus stress is provided by the lateral ulnar collateral ligament. It is, therefore, believed that the most appropriate concept of collateral ligament stability of the elbow is that of a medial and a lateral ulnar collateral ligament complex that functions independently in the presence or the absence of a radial head ( Fig. 23A-11 ). This concept is consistent with the anatomic findings as well

as with clinical experience. Deficiencies of the lateral ulnar collateral ligament result in posterior lateral rotatory instability of the elbow.[27] This condition most frequently occurs after elbow dislocation or from release and inadequate reconstitution after surgical procedures involving this structure. Unlike the medial collateral complex, the lateral collateral ligament complex originates in the precise center of the axis of rotation of the elbow joint ( see Fig. 23A-10 ). This anatomic and biomechanical fact is important when a lateral collateral ligament reconstruction is undertaken. Relative Contribution of the Collateral Ligaments

Experimental data may be summarized by stating that the articular surfaces provide approximately 50% of elbow stability, and the collateral ligaments provide the remaining 50%. When the elbow is in full extension, the anterior capsule contributes about 15% of the resistance to varus-valgus stress.[19]

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Forces across the Elbow Joint

Accurate determination of forces across the joint is difficult owing to the many uncontrolled variables. Nonetheless,

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Figure 23-A-9 A, Anatomic distribution of the medial collateral ligament (MCL). B, The origins of the anterior and posterior bundles do not lie along the axis of rotation. Thus, some change in length of these ligaments is seen as they function with changes in elbow flexion angle. (By permission of the Mayo Foundation.)

Figure 23-A-10 A, The medial collateral ligament complex consists of not only the radial collateral ligament (RCL) but also a lateral ulnar collateral ligament. B, With flexion, there is no change in length of the radial collateral ligament complex. This suggests that the origin is at the axis of rotation. (By permission of the Mayo Foundation.)

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Figure 23-A-11 The ulnohumeral joint is stabilized by both medial and lateral constraints, independent of the presence of the radial head. LUCL, lateral ulnar collateral ligament; MUCL, medial ulnar collateral ligament.

a rather accurate estimation of the resultant forces across the joint has been offered. Muscle Contribution

Muscle force is based on three features: cross-sectional area, orientation or line of action, and specific activity during a given function.[2] [5] [9] [13] This information allows one to estimate the resultant force at the elbow in certain positions. The greatest amount of force generated at the elbow occurs with the initiation of flexion. During flexion, the moment arm of the muscles increases, so that less force of contraction is required. Up to three times body weight can theoretically be transmitted to the elbow under maximal loading conditions.[1] [21] The resultant vector with greatest magnitude is directed axially toward the humeral head. Greater strength of flexion is generated with the elbow in 90 degrees of flexion, however, because the mechanical advantage of the elbow flexors has improved from the fully extended position so that less force is actually applied to the joint. The actual force across the elbow is thus less in this position than in full extension, and the resultant force is deviated posterior and superiorly. Calculations suggest that approximately three times body weight may be transmitted across the elbow joint when it is flexed at 90 degrees. It is important to note that the resultant vector undergoes a change in direction depending on whether the elbow is flexing or extending ( Fig. 23A-12 ).[28] Posteriorly Directed Forces

One feature of particular note is the posteriorly directed force component originating from the line of action of biceps, brachialis, and triceps muscles. Hence, there is a tendency for posterior displacement as the elbow flexes and as it extends (Fig. 23A-13 (Figure Not Available) ). These large forces are responsible for the frequently observed loss of fixation of distal humeral fractures, for the tendency toward posterior displacement of the joints after severe ligament injury, and for injury to the ligaments during forceful activities such as pitching.[11]

Figure 23-A-12 With flexion and extension, the resultant force of the elbow undergoes a cyclic change in direction. The order of magnitude can be as much as three times the body weight. Figure 23-A-13 (Figure Not Available) The posteriorly directed force component of the triceps (TR), the biceps (BC), and the brachialis (BR) all tend to displace the forearm posteriorly. ( By permission of the Mayo Foundation.)

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Figure 23-A-14 The distributive forces with the elbow in full extension and an axial load placed at the

wrist show that about 60% of the force goes across the radiohumeral joint and 40% goes across the ulnohumeral joint. This does not change the section of the interosseous membrane. (By permission of the Mayo Foundation.) Radiohumeral Joint

Using a physiologic model of active joint loading in which muscle flexion and extension were simulated, the greatest amount of force across the radiohumeral joint was shown to occur in extension.[21] The maximum amount of force across the radiohumeral articulation, however, approaches but does not exceed body weight.[19] With the elbow in full extension, approximately 40% of the applied force is transmitted across the ulnohumeral joint, and 60% is transmitted across the radial head.[10] Release of the interosseous membrane did not affect the measurements ( Fig. 23A-14 ).[33] Finally, with varus-valgus stress, the load pivots medially and laterally at a point located in the center of the lateral face of the trochlea.

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References Amis AA, Dowson D, Wright V: Elbow joint force predictions for some strenuous isometric actions. J Biomech 13:765-775, 1980. 1.

An KN, Hui FC, Morrey BF, et al: Muscles across the elbow joint: A biomechanical analysis. J Biomech 14:659-669, 1981. 2.

3.

An KN, Morrey BF, Chao EYS: Carrying angle of the human elbow joint. J Orthop Res 1:369-378, 1984.

An KN, Morrey BF, Chao EYS: The effect of partial removal of the proximal ulna on elbow constraint. Clin Orthop 209:270-279, 1986. 4.

Basmajian JV, Latif S: Integrated actions and functions of the chief flexors of the elbow. J Bone Joint Surg Am 39:1106-1118, 1976. 5.

6.

Beals RK: The normal carrying angle of the elbow. Clin Orthop 119:194-196, 1976.

Boone DC, Azen SP: Normal range of motion of joints in male subjects. J Bone Joint Surg Am 61:756-759, 1979. 7.

Fischer G: Handbuch der Anatomie und Mechanik du Gelenke, unter Berucksichtigung der bewegenden Muskeln, vol 2. Jena, G Fisher, 1911. 8.

Funk DA, An KN, Morrey BF, Daube JR: An EMG analysis of muscles controlling elbow motion. J Orthop Res 5:529-538, 1989. 9.

10.

Halls AA, Travill R: Transmission of pressures across the elbow joint. Anat Rec 150:243-248, 1964.

Hamilton CD, Glousman RE, Jobe FW, et al: Dynamic stability of the elbow: Electromyographic analysis of the flexor pronator group and the extensor group in pitchers with valgus instability. J Shoulder 11.

Elbow Surg 5:347-354, 1996. 12.

Hotchkiss RN, Weiland AJ: Valgus stability of the elbow. J Orthop Res 5:372-377, 1987.

Hui FC, Chao EY, An KN: Muscle and joint forces at the elbow during isometric lifting [abstract]. Orthop Trans 2:169, 1978. 13.

Ishizuki M: Functional anatomy of the elbow joint and three-dimensional quantitative motion analysis of the elbow joint. Nippon Seirigaku Zasshi 53:989-996, 1979. 14.

Jobe FW, Fanton GS: Nerve injuries. In Morrey BF (ed): The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985, pp 497-501. 15.

Keats TE, Teeslink R, Diamond AE, Williams JH: Normal axial relationship of the major joints. Radiology 87:904-907, 1966. 16.

17.

London JT: Kinematics of the elbow. J Bone Joint Surg Am 63:529-535, 1981.

Morrey BF: Radial head fracture. In Morrey BF (ed): The Elbow and Its Disorders, 3rd ed. Philadelphia, WB Saunders, 2000. 18.

Morrey BF, An KN: Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med 11:315-319, 1983. 19.

20.

Morrey BF, An KN: Functional anatomy of the ligaments of the elbow. Clin Orthop 201:84-90, 1985.

Morrey BF, An KN, Stormont TJ: Force transmission through the radial head. J Bone Joint Surg Am 70:250-256, 1988. 21.

Morrey BF, An KN, Tanaka S: Valgus stability of the elbow: A definition of primary and secondary constraints. Clin Orthop 265:187-195, 1991. 22.

Morrey BF, Askew LJ, An KN, Chao EY: A biomechanical study of functional elbow motion. J Bone Joint Surg Am 63:872-877, 1981. 23.

24.

Morrey BF, Chao EYS: Passive motion of the elbow joint. J Bone Joint Surg Am 59:501-508, 1976.

25.

Morrey BF: Complex instability of the elbow. J Bone Joint Surg Am 79:460-469, 1997.

Nicol AC, Berme N, Paul JPA: A biomechanical analysis of elbow joint function. In Joint Replacement in the Upper Limb. London, Institute of Mechanical Engineers, 1977, p 45. 26.

26A. Markolf

RL, Lamey D, Yang S, et al: Radio-ulnar load-sharing in the forearm. A study in cadavera. J Bone Joint Surg Am 80: 879-888, 1998. O'Driscoll SW, Bell DF, Morrey BF: Posterolateral rotatory instability of the elbow. Clinical and radiographic features. J Bone Joint Surg Am 73:440-446, 1991. 27.

Pearson JR, McGinley DR, Butzel LM: A dynamic analysis of the upper extremity: Planar motions. Hum Factors 5:59-66, 1963. 28.

29.

Pribyl CR, Kester MA, Cook SD, et al: The effect of the radial head and prosthetic radial head

replacement on resisting valgus stress at the elbow. Orthopedics 9:723-726, 1986. Regan W, Morrey BF: Fractures of the coronoid process of the ulna. J Bone Joint Surg Am 71:1348-1354, 1989. 30.

31.

Tullos HS, Erwin W, Woods GW, et al: Unusual lesions of the throwing arm. Clin Orthop 88:169, 1972.

32.

von Lanz T, Wachsmuth W: Praktische Anatomie. Berlin, Springer-Verlag, 1959.

Walker PS: Human joints and their artificial replacements. Springfield, Ill, Charles C Thomas, 1977, pp 182-183. 33.

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Section B Tendinopathies about the Elbow Bernard F. Morrey MD William D. Regan MD What we refer to today as tennis elbow was originally described in relationship to lawn tennis by Major in 1883.[15] [39] Today, however, the condition of epicondylitis is well known to occur spontaneously or in association with other recreational and occupational pursuits. Demographics

Although 95% of reported cases occur in individuals other than tennis players,[13] [65] it is estimated that 10% to 50% of people who regularly play tennis experience the symptoms of tennis elbow in varying degrees some time during their tennis lives.[41] [48] An analysis of 2500 patients at the Vic Braden Tennis Camp revealed a 50% incidence of tennis elbow.[48] Another study involving 200 tennis players revealed an incidence of 50% in players older than 30 years experiencing symptoms characteristic of tennis elbow for less than 6 months; the remaining 50% had major symptoms of an average duration of 2.5 years. This malady can affect participants of any sport involving the use of the upper extremities. The incidence of tennis elbow is equal among men and women, but among tennis players, it is more common in men. [13] It is rare in blacks, as evidenced by a series of 1000 patients in the southern United States in an area of equal racial distribution in which the occurrence was limited to whites only.[13] Although frequently seen in the age group spanning the fourth to sixth decades, it occurs four times more commonly in the fourth decade, with a peak at age 42 years.[13] [65] It involves the lateral epicondyle approximately seven times more frequently than the medial epicondyle.

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Macroscopic Pathology

Some variation exists in the precise gross pathologic anatomy of this condition. Local inflammation,[5] [23] muscle[5] [53] or ligament strain,[5] [45] synovial fringe inflammation,[19] [20] [23] [54] tendoperiosteal tears, [14] [22] [39] [40] [41] [45] disturbance in local metabolism,[51] degenerative changes in the orbicular ligament,[6] [7] and cervical root irritations[28] have been held responsible for the symptoms. The studies of Coonrad and Hooper[14] confirmed earlier works by Goldie,[23] who demonstrated the essential lesion in tennis elbow to be a tear of the common extensor or flexor origin at or near the respective lateral or medial epicondyle. It was believed that these tears were produced in a degenerating tendon fiber by mechanical overload in sports or at work. Tendon tears were found to range from microscopic to macroscopic. The origins of the extensor carpi radialis brevis and the superficial part of the supinator are blended and inseparable.[25] Both originate from the lateral epicondyle, the elbow joint capsule, and the orbicular ligament. Furthermore, the extensor carpi radialis longus arises from the lateral epicondyle as well as more proximally along the lateral epicondylar ridge. Finally, the extensor digitorum communis takes origin in part from the lateral epicondyle and does indeed contribute to this condition. Careful gross inspection of the extensor carpi radialis brevis tendon reveals a characteristic grayish, gelatinous, and friable immature tissue. In Nirschl's series of patients with tennis elbow,[41] 97% of cases demonstrated various degrees of this pathologic tissue. In his experience, a macroscopic tear of the tendinous origin was found in 35% of cases. In Coonrad and Hooper's work,[14] a tear of the extensor or flexor tendon was demonstrated in 28 of 39 patients, or 72%. In the remaining 11 patients, there was no actual tear, but 9 patients demonstrated excessive scar tissue replacement of the tendinous origin. The macroscopic tears can be superficial or deep; when they are deep, the superficial tendon attachment to bone may completely obscure the pathologic process.

Hence, a macroscopic tear of the extensor carpi radialis brevis tendon, with a possible contribution from the extensor digitorum communis, either superficial or deep, can be defined as the most common pathologic anatomy producing the pain of lateral epicondylitis.[13] [14] [45]

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Microscopic Pathology

Today, less controversy exists about the etiology and histopathology of the clinical entity of lateral epicondylitis. Most authors have placed the macroscopic pathologic process at the extensor carpi radialis brevis origin.[13] [14] [23] [40] [41] The microscopic features now seem well defined as well. Whereas Nirschl described the pathologic lesion as vascular granulation termed angiofibroblastic hyperplasia, the lesion is recognized today as a degenerative, necrotic process. A single-blind, randomized study of specimens from control subjects and patients was conducted at the Mayo Clinic to determine this as definitively as possible.[50] Two questions were addressed: (1) Are there any consistent microscopic pathologic changes? and (2) Is there an objective means of grading the changes? All 11 patients with an unequivocal clinical diagnosis of refractory lateral epicondylitis experienced relief after surgery. Macroscopic pathologic change at the origin of the extensor carpi radialis brevis was observed in all, and 40% were also found to have involvement of the common extensor origin.[50] Twelve unembalmed and radiologically normal cadaveric specimens were employed as a control. Fifteen microscopic pathologic features reported as characteristic of lateral epicondylitis were identified from the literature. All specimens were reviewed, and each histologic feature was graded in a single, randomized blinded manner by a single pathologist. The presence of vascular

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Figure 23-B-1 A, Vascular proliferation is a consistent feature of surgically excised tissue. B, Focal

hyaline degeneration is also present but has infrequently been recognized in the literature.

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Radiographic Studies

Routine anteroposterior and lateral radiographs are usually of little help in the diagnosis; however, according to Coonrad,[13] a gun-sight oblique view of the medial or lateral epicondyle often shows irregularity of punctate calcification ( Fig. 23B-2 ). Nirschl[40] has reported calcification of some degree in 22% of cases in his experience.

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Electromyographic Studies

These studies are of little or no help in the diagnosis of lateral epicondylitis. Even when a concurrent posterior interosseous nerve irritation is present, the electromyogram remains normal.[65]

Figure 23-B-2 The gun-sight oblique view of the lateral epicondyle demonstrates punctate calcification suggestive of lateral epicondylitis. Figure 23-B-3 (Figure Not Available) Arthroscopic view of a full-thickness capsular defect in a patient with chronic lateral epicondylitis. (Reproduced by permission of the Mayo Foundation.)

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Arthroscopy

There is growing interest in and experience with arthroscopy as a therapeutic modality.[34] If intra-articular symptoms are present or predominate in the clinical presentation, arthroscopy is a reasonable diagnostic approach. We have observed a degenerative process in the lateral capsule at the common extensor origin in about 80% of those patients undergoing such investigation (Fig. 23B-3 (Figure Not Available) ).

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Differential Diagnosis

The diagnosis is confused in some instances, such as distal neurologic entrapment, localized interarticular disease such as osteochondritis dissecans, radiocapitellar osteoarthrosis, and bone tumors about the elbow. Subtle instability of the radiocapitellar joint may also be considered. Localized pathologic processes within the elbow joint or localized tumor processes are usually ruled out with a careful history and by routine anteroposterior, lateral, and oblique radiographs of the elbow. A localized cervical root irritation is best diagnosed by a careful history and examination of the cervical spine for point tenderness and a distal neurologic examination for cervical radiculopathy. Subtle instability of the radiocapitellar joint can also be diagnosed by a history of a previous dislocation of the elbow, a severe varus stress, or previous surgery for release of the common extensor origin. Radial nerve compression may occur in 5% of those with lateral epicondylitis.[65] In this condition, the pain is located directly over the point of nerve compression, which is generally 3 or 4 cm distal to the lateral epicondyle. Werner[65] has shown that the most common site of entrapment of the posterior interosseous nerve occurs as the nerve courses through the arcade of Frohse. Other common causes of compression in this area include adhesions of or pressure on the nerve from the vessels at the leash of Henry overlying the nerve, constriction from the extensor carpi radialis muscle as it passes anteromedial to the nerve, and the supinator muscle itself.

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Treatment Options Nonsurgical Treatment

Elimination of provocative activities, such as repetitive pronation-supination motions and occupational lifting of heavy weights, is recommended. With rest and the use of anti-inflammatory medications, most of the pain can often be eliminated. If the pain is persistent, relief of acute inflammation is attempted with physiotherapy, such as ultrasound and galvanic stimulation for 3 minutes daily for a maximum of 5 days. Once the acute inflammatory phase has been relieved, an exercise program is initiated. Two studies have shown ultrasound to be ineffective for this condition, but a carefully controlled exercise program has been shown to be of value.[46] In the athlete, specifically the tennis player, one must first obtain relief of acute pain and then increase the forearm extensor power, flexibility, and endurance. In combination with these efforts, the athlete must attempt to decrease the moment of force placed against the elbow by altering sport mechanics or changing equipment. Proper stroke techniques are emphasized for the club tennis player, particularly for backhand strokes, so that the forearm is not placed in the fully pronated position with this stroke. Avoidance of impact without the proper forward body weight transference is also stressed. For selecting the proper racquet, Nirschl suggests that the distance from the midpalmar crease to the ring finger is helpful in determining handle size ( Fig. 23B-4 ). We have also successfully used this technique in treating patients with this condition. One should also consider reducing racquet string tension, enlarging the grip handle, and avoiding the use of heavy tennis balls.[13] Isotonic eccentric hand exercises with use of graduated weights of usually no more than 5 pounds may also be helpful. Repetitions are increased on a daily basis as the patient is able to perform them. If pain recurs, return to a lower level of exercise is advised in

combination with anti-inflammatory medications or rest. Transverse friction massage is also sometimes used. If this baseline program fails, we prescribe phonophoresis[33] of 10% hydrocortisone cream administered with an ultrasonic beam through the skin. This is done in a continuous fashion at 1.5 to 2 W/cm2 every other day during a course of 10 days. This treatment is not recom mended except in a patient with a chronic, refractory condition, that is, with signs similar to those initiating recommendation of an injectable steroid. If local injections are performed, we do not recommend more than three in a period of a year because the injections themselves can produce tendon necrosis.[60] Both Froimson[17] and Nirschl [40] [41] advocate the use of counterforce braces. These are approximately 5 to 6 cm wide and consist of a band of heavy-duty, nonelastic fabric lined with foam rubber padding to prevent slipping ( Fig. 23B-5 ). Velcro fasteners allow easy application of the band, which encircles the forearm just below the elbow. Tension is adjusted to a comfortable degree with the muscles relaxed. The patient is advised to use the support only during actual play, to avoid excessive tightness, and to remove it during periods of inactivity.

Figure 23-B-4 Nirschl technique for determining proper handle size measured from proximal palmar crease to tip of ring finger. Place measuring rule between ring and long fingers for proper ruler placement on palmar crease. The measurement obtained is the proper handle sizethat is, if this distance is 4.5 inches, the proper grip size is 4.5 inches. (Reproduced by permission of the Mayo Foundation.)

Figure 23-B-5 Lateral elbow counterforce brace. Note that the wide, nonelastic support is curved to fit the conical forearm shape. This concept does not allow full muscle expansion, thereby diminishing intrinsic muscle force on the lateral epicondyle. (From Morrey BF: The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985.)

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It is believed that such bracing provides gentle compression of the muscle-tendon areas and partially decreases muscle expansion at the time of intrinsic muscle contraction. This was investigated by Groppel and Nirschl[24] with electromyographic studies using counterforce bracing. A lateral counterforce brace demonstrated lower muscle activity in the two extensor muscles across all skill levels with the serve and one-handed backhand. Surgical Treatment

Surgery is not usually recommended before symptoms have been present for a year. If the pain is disabling and recurrent in spite of faithful compliance with the nonoperative program, surgical intervention may be initiated sooner than 1 year. The numerous

operations that have been described for tennis elbow may be classified into five basic types: (1) repair of the extensor origin after excision of torn tendon, granulation tissue, and part of the epicondyle ( Fig. 23B-6 )[8] [14] [40] [45] ; (2) relief of tension of the common extensor origin by fasciotomy, direct release of the extensor origin, or lengthening of the extensor carpi radialis brevis tendon distally[19] ; (3) decompression of the radial or posterior interosseous nerves[28] [64] ; (4) intra-articular procedures, such as division of the orbicular ligament[6] [7] and synovectomy[45] ; and (5) arthroscopic inspection and débridement. It is now generally accepted that the macroscopic lesion of tennis elbow is most commonly at the extensor carpi radialis brevis origin. On occasion, synovitis is present with effusion, which can resolve after extensor origin repair. [14] According to Froimson,[17] fasciotomy with complete extensor release done openly or percutaneously has resulted in loss of strength, particularly in skilled tennis players. Because the fasciotomy extends across normal fibers as

Figure 23-B-6 The interval between the extensor digitorum communis and the extensor carpi radialis longus tendon is opened, exposing the degenerative tendon of the extensor carpi radialis brevis beneath.

well as scarred ones, the proper extent of the fasciotomy is unknown. Pain relief obtained by additional resection of a partially torn tendon such as the extensor carpi radialis brevis, by creating a larger defect in the tendon and fascia, seems illogical. Extensor tendon lengthening at the wrist, as described by Garden,[19] appears to relieve pressure from the extensor carpi radialis brevis tendon proximally but does not address the pathologic process directly. Our treatment of choice is to excise the torn, scarred origin of the extensor carpi radialis brevis and extensor digitorum communis, if it is involved, and remove the granulation tissue. The elbow joint capsule is not intentionally violated unless an intra-articular problem coexists. In this instance, arthroscopy is employed. Arthroscopy is increasingly being used. Most of those who now use this method of treatment believe that intra-articular pathologic change is evident in virtually all cases. The débridement is carried out by the percutaneous insertion of the débriding instrument through an anterolateral portal; visualization is obtained from an anteromedial portal (Fig. 23B-7 (Figure Not Available) ).[42] Kuklo and associates[34] have provided data about the safety and efficacy of this technique. Authors' Preferred Operative Technique

Although this operation can be performed under regional anesthesia, we still prefer a general anesthetic. We also use a pneumatic tourniquet to obtain a bloodless field for more precise recognition of the pathologic tissue.

The patient is placed supine, and the affected upper extremity is supported on an armboard with the forearm in a pronated position. A short, oblique incision is made, extending approximately 2 cm proximal to the lateral epicondyle and 4 or 5 cm distal to it. Through this incision, the common extensor origin is exposed after the deep fascia, which lies immediately over the extensor aponeurosis, is excised and gently retracted. The fibers of the common extensor origin beneath the lateral epicondyle and the inferior and superior margins of the epicondyle are then inspected. A tear or scar tissue is occasionally evident. The fibers of the common extensor tendon are separated, and the superficial fibers of the extensor brevis, which usually lie partially covered by the fibers of the extensor longus and the extensor digitorum communis, are observed. If a tear or scar tissue is not identified by observing the superficial fibers of the extensor brevis, the common extensor origin should be elevated more deeply. This is accomplished by splitting the tendon longitudinally and then sharply dissecting it off the lateral epicondyle, approximately 0.5 cm both anteriorly and posteriorly. The tear is typically identified at this time ( see Fig. 23B-6 ). Necrotic and torn tendon fibers are excised along with any granulation tissue in the tendon. The extensor carpi radialis brevis is almost always involved; however, the extensor digitorum communis aponeurosis may also be involved. It is important that the excision of all fibers and granulation tissue be done sharply with a 15-blade knife, dissecting particularly the extensor carpi radialis brevis cleanly from the fibers of the radial collateral ligament and ensuring that this ligament is left in continuity. Complete removal of abnormal granulation tissue generally includes the total origin of the extensor

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Figure 23-B-7 (Figure Not Available) Arthroscopic view of a degenerated lateral capsule (A) treated by arthroscopic débridement (B) with clinical resolution of symptoms. (Reproduced by permission of the Mayo Foundation.)

brevis ( Fig. 23B-8 ). The remaining part of the extensor brevis tendon does not retract because of the closed fascial adherence to the extensor longus muscle. To ensure improved blood supply, the exposed lateral epicondyle is decorticated by a rongeur or by drilling multiple small 2.0-mm drill holes. The interface between the extensor carpi radialis longus and the anterior edge of the extensor aponeurosis is repaired with a running 1-0 resorbable suture. The subcutaneous and skin layers are closed with 2-0 and 3-0 resorbable subcuticular suture and Steri-Strips. A posterior plaster splint is worn for approximately 7 days, with the elbow placed at 90 degrees of flexion and

Figure 23-B-8 The extensor carpi radialis brevis tendon is removed in its entirety with a 15-blade knife, cleanly dissecting this tendon origin from the fibers of the radial collateral ligament and ensuring that this ligament is left in continuity. The remaining part of the extensor brevis tendon does not retract because of the closed fascial adherence to the extensor longus muscle.

the forearm in neutral rotation. After removal of this bulky splint, we continue to protect the elbow in a posterior splint for 2 weeks before range of motion exercises are begun. Once full range of motion is achieved, a gentle, graduated exercise program is initiated. For the first 6 weeks, the patient is encouraged to regain grip strength by use of a hand-held rubber ball. After this, gentle resistive elbow and wrist eccentric loading exercises are performed, using no more than a 5-pound weight. Residual pain is generally treated with decrease in activity, nonsteroidal anti-inflammatory medication, and ultrasound in conjunction with transverse massage performed gently on the affected area. Tennis can usually be resumed gradually at about 12 weeks when adequate strength has returned and little or no pain remains. A counterforce support band should be worn indefinitely.

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Medial Tennis Elbow

Medial epicondylitis develops from repetitive valgus and flexor forearm stress. Sporting activities producing this condition include squash, racquetball, tennis, and golf. Tennis and any racquet strokes most likely to initiate difficulty are the serve and forehand. Symptoms and Signs

Symptoms of aching pain in the flexor musculature at the medial epicondyle are most common. Weakness of grip strength is also common. Patients may have either an acute injury of the common flexor origin or rupture of the medial collateral ligament from a throwing injury. In an acute injury of the common flexor origin, forearm flexor muscle pain or medial tendinitis is enhanced by flexing and pronating the wrist against resistance ( Fig. 23B-9 ). In rupture of the medial collateral ligament, the valgus stress test localizes injury to the ligament ( Fig. 23B-10 ). In either condition, there may be associated symptoms of mild ulnar neuropathy. Although this does not occur in all instances, forearm pain or radicular symptoms must be

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Figure 23-B-9 Medial epicondylitis may be diagnosed clinically from pain localized to the medial epicondyle during wrist flexion and pronation against resistance. Pain is often elicited after a tight fist is made, and grip strength is usually diminished on the affected side. (From Morrey BF: The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985.)

considered if surgical intervention is undertaken. Nirschl[39] found ulnar nerve dysfunction in 60% of patients undergoing surgery for medial epicondylitis. Concomitant osteocartilaginous loose bodies and triceps tendinitis were also found in 1% of his cases. Symptoms are generally mild, intermittent, and primarily sensory, occurring after prolonged use and with heavy forearm activity. Tinel's sign may be present. This is presumably secondary to local inflammation and edema, causing a compressive neuropathy of the ulnar nerve in the region of the cubital tunnel. In the majority of cases, electromyographic conduction study findings are normal. Decompression by release of the flexor carpi ulnaris arcade generally resolves these symptoms.[40] It is important to obtain radiographs before surgery to ensure that there is no evidence of degenerative changes in the posterior medial aspect of the olecranon, mimicking medial epicondylitis. Such changes can be visualized radiologically by simple radiographic assessment.

Figure 23-B-10 Medial joint-line pain elicited by applying a valgus stress to the elbow identifies injury to the ulnar collateral ligament. (From Morrey BF: The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985.) Treatment

Nonsurgical Treatment

The treatment of medial epicondylitis is similar to that of lateral epicondylitis; the principles center on the relief of the acute or chronic inflammatory process. This involves the use of nonsteroidal anti-inflammatory medication in combination with ice and a decrease or modification in the activities that produce the tension overload. Finally, a therapy program aimed at gradually increasing flexibility, power, and endurance is initiated. A counterforce elbow splint has been devised that is similar to the lateral counterforce brace but provides an additional support just distal to the medial epicondyle. Unfortunately, this has not proved to be of much value in our hands. Gradual resumption in play is usually recommended when symptoms have subsided, generally between 6 and 12 weeks after injury. If a corticosteroid injection is administered, one must be careful in performing this injection to remain anterior to the medial epicondyle and to be aware that the ulnar nerve lies just posterior to the injection site. We have sometimes noted that ulnar neuropathy subsides after an injection of the medial epicondyle. We have also observed instances of a subluxing ulnar nerve masquerading as medial epicondylitis, however. Hence, a careful examination must be conducted before injection or surgical intervention.

Operative Treatment

The data regarding surgical management of medial epicondylitis are limited but slowly increasing.[13] [40] Precise localization of the maximal point of tenderness is necessary before surgery. [66] A needle may be used for this purpose, and the medial epicondyle is exposed while the needle is in position. The tendon origin of the pronator teres and a portion of the flexor carpi radialis, often at the interval between these two muscles, are generally the sites of involvement. Torn or scarred tissue is excised, and repair is done in a manner similar to that described for the lateral epicondyle. All normal tissue is left attached to the medial epicondyle for fear that total excision of the common flexor origin may include a portion of the origin of the medial collateral ligament, which may then lead to subtle posteromedial instability. Coonrad[13] identified the ulnar nerve in each case with this exposure, although he does not transpose the ulnar nerve or perform a neurolysis unless evidence of associated neuropathy is present. Management of the ulnar nerve usually involves decompression just distal to the medial epicondylar groove. Decompression by release of the flexor ulnaris arcade generally resolves these symptoms in our experience and in that of others. Indications for anterior ulnar nerve transposition include (1) nerve subluxation or dislocation from the epicondylar groove; (2) cubital valgus, with symptomatic tension neurapraxia, which is common in throwers; and (3) a hostile environment, such as scarring from previous surgery. The elbow is protected for approximately 3 weeks in 90 degrees of flexion and neutral rotation of the forearm. Limbering exercises are performed for 2 weeks, followed by strength and endurance-resistance exercises, including

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isometrics, isotonics, and isokinetics in proper sequence and intensity. These resistance exercises are continued until full strength returns. Nearly full strength returns about 6 months after surgery. Modified sporting technique patterns 6 weeks after surgery and no competitive sports are recommended until full strength returns at approximately 6 months. It appears that there are few complications except a rare loss of extension of about 5 degrees. In our experience, the major problem has been the overall lack of predictability of the procedure when the ulnar nerve is involved. In fact, reports from the Mayo Clinic and other reports reveal that the 90% satisfactory rate is adversely affected by ulnar nerve involvement.[18] [43] [62] Authors' Preferred Method of Treatment

The patient lies supine with the arm abducted and flexed to 90 degrees and resting on an elbow table. A gentle, curved incision is made, beginning just posterior to the medial epicondyle. After excision down to the fascia overlying the medial epicondyle, the ulnar nerve is identified and protected proximally. If there is any sign of compression of the

nerve, or if symptoms have suggested that this is the case, the forearm fascia is split where the nerve enters the forearm between the two heads of origin of the flexor carpi ulnaris. We avoid a detailed dissection of the nerve unless intrinsic disease is found. Specifically, the cubital tunnel retinaculum is not violated unless constriction occurs at this point ( Fig. 23B-11 ). The fibers between the pronator teres and the flexor carpi radialis are then excised longitudinally. The tendinous origin of these muscles is sharply excised from the medial epicondyle in the direction of the joint. The fascia and fleshy muscle fibers are sutured back to the cuff of tissue left on the medial epicondyle; the scarred and degenerative tendon is excised in an elliptical and longitudinal fashion. Little attempt is made to close the defect, but normal tissue, if detached, is repaired. The longitudinal incision made through the common flexor origin is then closed with 2-0 absorbable suture. When the ulnar nerve is extremely irritable or subluxed, or when there is objective clinical or electromyographic evidence of ulnar compromise, this is addressed by a submuscular transposition of the nerve. The entire origin of the medial epicondyle is resected, leaving a cuff of normal tendon ( Fig. 23B-12 ), and the ulnar nerve is transposed submuscularly. The tendinous origin of the common flexors is removed, and the fascia and muscle fibers are then reattached to the cuff of tissue at the origin of the medial epicondyle ( Fig. 23B-13 ). Before reattachment, the degenerative tendinous portions of the common flexor muscle mass are excised, and the medial epicondyle is freshened with a rongeur or a curet. The patient is kept in a bulky arm dressing, which is well padded with the elbow at 90 degrees of flexion in the form of neutral rotation. This is maintained for approximately 3 weeks. Gentle range of motion exercises without resistance are conducted until range of motion has been restored. At the end of 6 weeks, we encourage the restoration of grip strength by having the patient squeeze a rubber ball or by the use of exercise putty. Between 10 and 12 weeks postoperatively, resisted elbow and wrist flexion exercises are initiated with the use of light weights. At the end of 4 to 6 months, patients have usually regained adequate strength to resume light duties or sporting activities. We recommend no return to their level of sport or work until we have evidence by objective testing that they have gained 80% or more strength compared with the opposite extremity. In our experience, this usually takes approximately 6 months. We recommend the use of a forearm support band while working or playing any overhand sports for up to 6 months after surgery.[40] We recognize that this program is more prolonged than that which is often followed. This regimen, however, is based on observation that a number of failed procedures appear to be the result of too early return to sport without restriction.

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Triceps Tendinitis and Rupture Anatomy

The tendon of the triceps brachii muscle consists of two aponeurotic lamellae that join together above the elbow

Figure 23-B-11 Ulnar nerve zones at the cubital tunnel: zone 1, proximal to medial epicondyle; zone 2, at medial epicondyle; zone 3, distal to medial epicondyle. Zone 3 includes penetration of the nerve through the flexor ulnaris arcade and is the most common site of compression neurapraxia of the ulnar nerve. (From Morrey BF: The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985.)

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Figure 23-B-12 The common flexor origin is detached, leaving a cuff of tendon. The degenerative tendon is resected, and the ulnar nerve, if it is involved, is transposed beneath the common flexor origin. Drill holes are placed in the medial epicondyle to enhance blood supply.

and insert into the posterior portion of the dorsal surface of the olecranon. A lateral band extends over the anconeus muscle to attach to the dorsal fascia of the forearm. This has important reconstruction implications. Triceps Tendinitis

Triceps tendinitis is thought most often to be an isolated entity associated with loose

bodies in the posterior compartment of the elbow or with lateral tennis elbow. [53] [55] This condition occurs in baseball players, weightlifters, and those with occupations involving repetitive elbow extension, such as carpenters. The same conservative management program is used for triceps tendinitis as for lateral or medial tennis elbow. We have operated on only a single case of triceps tendinitis and doubt that operative treatment is indicated unless the pathologic process is actually a partial rupture. In cases that have been refractory to all conservative treatment for more than 1 year, Nirschl[40] has elected surgical

Figure 23-B-13 The common flexor origin is sewn back to the cuff of normal tendon origin with the ulnar nerve transposed beneath it.

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excision of a small portion of the triceps insertion. The site of resection coincides with the area of maximal point tenderness, previously eliminated by local lidocaine injection. The technique is essentially that of tennis elbow débridement. Triceps Rupture

A rupture or avulsion of the triceps tendon is a rare injury. In 1868, Partridge [44] reported the first case, which was managed by rest and graduated exercise. The site of disruption was at the tendo-osseous junction. Reported ages affected range from 7 to 72 years. The majority of patients are men, and right and left sides are equally affected. Injury in the skeletally immature is rare.[29] [67] There is no correlation of the side of rupture with the dominant or nondominant side. Anzel and associates[2] reported a 9-year experience of consecutive tendon ruptures in 781 patients involving 1014 tendon ruptures. Eight triceps ruptures represented 1.9% of the tendon injuries. Our experience, discussed in the following, is from a review of 22 patients treated for triceps tendon repair or reconstruction.[26] Mechanism of Injury

The mechanism of injury is either a fall onto an outstretched hand or direct laceration from a direct blow.[57] Disruption of the triceps may occur spontaneously with minimal trauma in individuals who have been compromised by a systemic disease process, such as hyperparathyroidism, [47] and in those receiving steroid treatments for lupus erythematosus.[59] The most common site at the tendo-osseous attachment represents avulsion of the insertion, occasionally with a fleck of bone. Musculotendinous injuries

have also been reported.[3] [52] The association of additional injuries cannot be overlooked. Levy and coworkers[36] [37] described 16 patients who had incurred triceps avulsion in association with radial head fractures. Clayton and Thirupathi[12] found an association with chronic olecranon bursitis. Diagnosis

The most common mechanism of injury is a deceleration stress superimposed on a contracted triceps muscle, with or without a concomitant blow to the posterior aspect of the elbow. The diagnosis is usually evident in patients who present with a characteristic history and a palpable depression just proximal to the olecranon. On examination, pain, swelling, and a palpable depression just proximal to the olecranon and posterior ecchymosis may be present. Because of the expansion of the triceps laterally with the anconeus, however, active extension is still possible in some. Radiographs are particularly helpful, with flecks of osseous tissue visible on the lateral radiograph, but this occurs in less than 20% of patients ( Fig. 23B-14 ).[16] [26] [52] Magnetic resonance imaging and even ultrasonography have more recently proved useful in the diagnosis of subtle cases.[31] [58]

Figure 23-B-14 Anteroposterior and lateral radiograph illustrating the small avulsion fracture off the tip of the olecranon, indicative of a triceps tendon rupture. Treatment

Acute repair is recommended, but a reconstruction procedure is necessary for those with a delayed intervention. At exploration, the tendinous central portion of the triceps may be found to be retracted, sometimes accompanied by a bone avulsion from the olecranon. Delamination due to a partial disruption of the triceps tendon is also seen.[1] [26]

For acute rupture, a nonabsorbable suture placed in drill holes in the olecranon is effective (Fig. 23B-15 (Figure Not Available) ).[26] [36] [37] Stainless steel wire is not recommended because the wire fatigues and fragments. [7] If treatment has been delayed or if the patient has a systemic disease that compromises the quality of tissue and hence the quality of repair, a reconstructive technique may be considered. Farrar and Lippert[16] suggested using a periosteal flap from the olecranon to reinforce the repair. Bennett [4] used a flap of fascia taken from the posterior aspect of the forearm with its base attached to the medial and lateral epicondyles to the humeral anterior olecranon process. Clayton and Thirupathi[12] achieved successful results by splitting the triceps tendon into a partial-thickness flap. We have had excellent success with a rotation flap employing the anconeus; if there is marked tissue deficiency, an Achilles tendon allograft is employed.[26]

Postoperative Rehabilitation

Postoperative immobilization varies from 10 days to 6 weeks, but most patients are generally immobilized for 2 to 3 weeks in a posterior splint at 35 to 40 degrees of elbow flexion. Active range of motion exercises are then begun. In a single report, an Olympic weightlifter began progressive active and active-assisted exercises at 2 Figure 23-B-15 (Figure Not Available) A crisscross suture is secured to the olecranon by a cruciate attachment through drill holes in the olecranon. (Reproduced by permission of the Mayo Foundation.)

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months; by 4 months after the procedure, he had resumed weight training. [3] In our experience, recovery is slow and may even require a full year for complete functional return.[26] Results

In most instances of acute or delayed repair, nearly normal strength and full motion are restored with no pain. Levy and associates[36] [37] noted a 10% to 20% limitation of range of motion in two patients. Anderson and LeCoco[1] and Bennett[4] have noted 5-degree flexion-contraction in two patients. Sherman and colleagues[52] noted that a professional body builder was able to bench-press 370 pounds without difficulty 3 months after repair. Most of these reports are without the benefit of precise objective strength measurements. In our experience with 22 procedures, only 5 occurred from athletics; the 3 with acute repair had slightly better functional results than the 9 with reconstructions. Overall, 21 of the 22 considered the result satisfactory. Authors' Preferred Method of Treatment

The treatment of choice of acute rupture is immediate repair by use of a posterior base incision just lateral to the midline. We prefer 5-0 nonabsorbable sutures. The first is placed in a Bunnell fashion through the proximal torn triceps tendon and then through crossed holes drilled through the olecranon (see Fig. 23B-15 (Figure Not Available) ). A second transverse suture secures the precise site of attachment. The sutures are tied with the elbow at 60 degrees of flexion. This is the same technique that is used to reattach the triceps after elective reconstructive procedures. If repair is not possible or requires additional support, we prefer to mobilize the anconeus and lateral triceps extension and relocate this over the olecranon rather than create free tissue flaps (Fig. 23B-16 (Figure Not Available) ). In those with extensive deficiencies, the Achilles tendon allograft is used. This is attached to the olecranon first, either by screw fixation of the calcaneal portion or by advancement of the Achilles tendon into the bone of the olecranon. The fascial portion is attached to the triceps

muscle with the elbow flexed about 45 degrees (Fig. 23B-17 (Figure Not Available) ). We advocate protected immobilization for 2 to 3 weeks with the arm held in 30 to 40 degrees of flexion. Active-assisted motion is begun at 3 to 4 weeks. Training for avid athletes is not recommended until Cybex testing indicates that 80% strength has returned; this may take 6 months. We allow full participation in all active sporting events and expect 90% to 100% return of strength if the injury has occurred at the site of attachment. We are careful to advise that it takes a full year for complete recovery.

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Olecranon Bursitis

Athletic trauma causing bursitis most frequently occurs at the patellar bursa of the knee and at the olecranon bursa Figure 23-B-16 (Figure Not Available) The anconeus serves as a rotational flap providing continuity with the triceps mechanism. (Reproduced by permission of the Mayo Foundation.)

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Figure 23-B-17 (Figure Not Available) When the anconeus is unavailable and for large defects, an Achilles tendon allograft is employed to reconstruct the extensor mechanism. (Reproduced by permission of the Mayo Foundation.)

of the elbow. Football and ice hockey have been the chief athletic events implicated in the development of olecranon bursitis at the elbow. We are careful to advise that it takes a full year for complete recovery from this problem and that chronic conditions may need resection. Anatomy

The bursae in the olecranon region exist in three locations: (1) the subcutaneous bursa, so commonly seen clinically; (2) an intratendinous bursa, in the substance of the triceps tendon near its insertion; and (3) the subtendinous bursa between the tendon and capsule ( Fig. 23B-18 ), as described by Morrey.[38] Although there have been no recognizable clinically documented presentations concerning the two deep bursae about the olecranon, the intratendinous bursa may indeed be involved with tears of the triceps tendon as described earlier in this chapter.

In the literature, the only subtendinous bursa was described by Vizkelety[63] and was idiopathic in nature. We have not encountered this bursa in our practice. Inflammation of the superficial olecranon bursa is the bursitis of the elbow. The bursitis may be acute or chronic, septic or nonseptic; it is associated most commonly with occupational or sports trauma. It has been called a miner's elbow or student's elbow. In sports injuries, Larson and Osternig [35] have documented that this is a common football injury, almost exclusively associated with artificial turf. In one season, 14 of the 16 cases (87.5%) were sustained on artificial turf. We have encountered this lesion in hockey as often as in football. The relation to artificial turf centers on the construction features of the artificial turf. This turf is composed of an upper layer of durable, synthetic grass, which is applied over a layer of padding of varying thickness and resiliency. These two surfaces are usually applied over a hard surface, such as asphalt. Consequently, artificial turf gives an even and consistent upper playing surface but has a relatively unyielding quality at the base compared with actual grass. Repeated falls on the partially flexed elbow result in trauma to the region, and sometimes an olecranon spur develops ( Fig. 23B-19 ). Such traumatic episodes may produce an acute inflammation and subsequent bursitis. On occasion, with severe trauma, vascular disruption with hemorrhagic distention of the bursal sac may occur. An inflammatory response then ensues. The initial episode is usually one of hemibursitis. After resolution, recurrent episodes develop with less trauma and are not associated with intrabursal hemorrhage. Classification

Olecranon bursitis may be classified as acute, chronic, and suppurative. The acute entity results either from a direct blow or from acute repeated insults to the superficial elbow. Chronic bursitis develops as a sequel to recurrent acute episodes when the trauma is relatively mild. It occurs when the resorptive phase of an acute bursitis is repeatedly interrupted by further trauma. In this situation, the lining of the bursa is replaced by fibrous tissue, which becomes the predominant characteristic. Suppurative bursitis may

Figure 23-B-18 Lateral illustration of the elbow demonstrating the superficial olecranon bursa, the intratendinous bursa found in the substance of the tendon, and the subtendinous bursa lying between the tip of the olecranon and the triceps tendon. (Reproduced by permission of the Mayo Foundation.)

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Figure 23-B-19 Lateral radiograph demonstrating a spur off the tip of the olecranon, indicative of

olecranon bursitis.

also develop from an infective process in an acute or chronic bursitis after contamination through a skin wound or dermatitis. Acute Bursitis

Clinical Presentation

A painless distention of the bursa after a direct blow is the most common presentation. The differential diagnosis includes acute arthritis, ligament injury, and tendinitis if the swelling is diffuse. Otherwise, the diagnosis is easily made; the most important distinction is whether this represents a septic process. Joint motion is usually not limited in patients with olecranon bursitis except when flexion produces skin tension and increased pressure over the tender, distended bursa. This is an important point because septic bursae are painful. Fluctuation of the distended bursa in the absence of true joint findings further localizes the injury to the bursa. Canoso [10] [11] has characterized the clinical features of 30 patients with acute traumatic olecranon bursitis. Repetitive trauma was cited as the most important factor in 14 cases. When symptoms were present more than 14 days, the bursa was discretely swollen; but if symptoms were observed in less than 2 weeks, parabursal edema was present, and swelling was also observed in the arm and forearm in 50% of cases. We have not observed this associated swelling except with septic bursitis. Aspiration of the acute entity shows evidence of recent hemorrhage. The bursal fluid is characterized by a low white blood cell count with a high percentage (80%) of monocytes.[10] Treatment

In the athletic population, olecranon bursitis is most commonly a post-traumatic disorder; but in the older patient, systemic inflammatory processes such as calcium pyrophosphate dihydrate crystal deposition disease[21] must be considered. Once a bursitis has occurred, recurrence becomes more frequent with less trauma, resulting in the need to provide additional protective covering to lessen the forces of impact. In the acute situation, if the bursa is distended and uncomfortable or interferes with use of the joint, aspiration is recommended. This, of course, is done under strictly sterile conditions and is followed by the application of continuous compressive bandages for 48 hours. If the distention is not too severe, there is no need to aspirate the bursa. Compression and cold packs at the first sign of swelling help to minimize bleeding into the sac, which usually reaches a maximum 24 hours after injury. After this, warm packs can be used to hasten absorption of bursal fluid. The bursal fluid often resorbs if it is not subjected to recurrent trauma. If continued trauma occurs, however, accumulation of fluid recurs.

This can result in fibrous tissue formation, which becomes the predominant characteristic and then leads to subacute and chronic bursitis, which may require surgery. Chronic Bursitis

Presentation

This follows recurrent traumatic episodes, and in this situation, the bursal walls have usually become much thickened. Trabeculae and villi form, increasing in number and density and filling the bursal space.[32] The villi that arise represent granulation in the floor of the bursa, consisting of central blood vessels surrounded by fibrous tissue cells. In a mild subacute form, this may be clinically evident as a slight, palpable thickening of the bursa; in the chronic form, a large rubbery mass containing numerous hard movable bodies occurs in the subcutaneous tissues ( Fig. 23B-20 ). The causal factor in the development of a chronic bursitis is frequently not sports but the patient's occupation. Occurrences have been so common in certain occupations that they have been given names such as miner's elbow for chronic olecranon bursitis. By far the largest number of cases of chronic olecranon bursitis develop from an acute traumatic episode, such as a football injury. In such cases, the acute injury is superimposed on a chronic or recurrent bursitis. Definitive measures are usually required in this situation. Operative Intervention

Surgery is indicated if the process is refractory to nonoperative intervention and bothers the athlete to the point that

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Figure 23-B-20 Trabeculae and villi fill the bursal sac to produce a scarred, thickened bursa. This is excised through an incision centered lateral to the midline.

he or she cannot participate in the sport of choice or if a septic episode has been imposed on the chronic process. A longitudinal incision just medial to the midline[30] or centered directly over the olecranon bursa[9] has been recommended. The bursa is carefully dissected without opening it if at all possible ( Fig. 23B-21 ). On occasion, a bursa must be removed piecemeal; if this is necessary, all pieces

Figure 23-B-21 The olecranon bursa is resected without opening the bursal sac.

of the bursal sac should be carefully removed. Freeing the bursa from the skin can devitalize the skin over the olecranon process or cause problems with healing. We recommend a compressive dressing with the elbow held in less than 45 degrees of flexion. [38] [56] Breck and Higinbotham[9] have suggested placing mattress sutures on either side of the incision centered over the appropriate half of the dead space under the skin flaps. These sutures are passed down through the skin and then into the underlying deep tissues of the muscle and fascia of the triceps. The suture is then brought back up to the skin and snugly tied over a button. This brings the skin into firm contact with the underlying structures and tends to prevent the formation of a hematoma and recurrence of a bursa or skin breakdown. Quayle and Robinson[49] have avoided the problem of wound healing secondary to the subdermal dissection of the bursa by simply reflecting the skin with the bursal tissue from a medial to a lateral direction. The tip of the olecranon is obliquely osteotomized, leaving the bursal tissue intact. The subcutaneous tissue plus bursa is then reflected over the olecranon, and the wound is closed with a drain. Results

In a series of 11 patients described by Quayle and Robinson,[49] there have been no recurrences. Experience with 16 non-rheumatoid arthritis patients at the Mayo Clinic revealed 15 without recurrence an average of 5 years after surgery. [56] Authors' Preferred Method of Treatment

We prefer a skin incision over the lateral aspect of the olecranon. [56] The skin and subcutaneous tissue are carefully incised, exposing the bursal sac. If possible, the bursal sac is enucleated in total, without violating its contents. The minimal amount of subdermal dissection required to accomplish this is performed equidistant on the medial and lateral aspects of the olecranon. Any olecranon spur or prominence is removed. The tourniquet is deflated to assess the viability of the skin, and meticulous hemostasis is attained. Closure is accomplished with absorbable sutures placed in the medial and lateral skin flaps and sewn down to the deep fascia. In this way, the dead space is obliterated, and the chance of subdermal hematoma is minimized. The wound is then closed in the usual fashion, and the elbow is immobilized in 0 to 45 degrees of flexion to prevent further recurrence. A compressive dressing is maintained for 2 to 3 weeks. Normal elbow motion is easily attained. Septic Bursitis

A large number of patients with a septic bursa give a history of previous idiopathic or traumatic bursitis. The presentation varies widely and includes the acute onset of localized cellulitis, a generalized cellulitis involving the forearm, a low-grade subacute process of 10 to 14 days in duration, or a fulminating process with systemic symptoms.

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In general, the patient with septic bursitis is not likely to be febrile, but unlike in the patient with an aseptic process, pain is present over the olecranon bursa and with motion. The infected bursa is often tender to palpation, and there is sometimes an abrasion or a skin lesion. These findings are not diagnostic of infection, however; some nonseptic cases also show these features. In addition, their absence does not rule out an infected bursa. In all cases of a painful bursa, the diagnosis is made by needle aspiration of the bursal contents. With aspiration, a cell count, crystal determination, and Gram stain should be done in all cases. Crystals are determined because gout may coexist with or even predispose the patient to olecranon bursitis.[21] The drawn septic fluid generally appears purulent as either frank or bloody pus.[9] [10] Bursal fluid analysis in septic cases shows a predominance of polymorphonuclear cells, and nonseptic fluids have a predominance of mononuclear cells. Gram stain smears of bursal fluid demonstrated organisms in all 10 septic cases reported by Ho and Tice.[27] The most common organism was Staphylococcus aureus in 94% of cases in their series[27] ; this is in agreement with our experience. After an accurate diagnosis, initial treatment includes adequate drainage coupled with antibiotic therapy. Intravenous antibiotics are required. Treatment with parenteral antibiotics continues for 1 to 3 weeks. Oral antibiotics are continued an additional 2 weeks. Authors' Preferred Method of Treatment

All painful bursae are aspirated. If the aspirate is purulent or cloudy or if the patient is febrile, we inject 0.5 g of methicillin in 10 mL of saline into the bursa after it has been lavaged. Oral antibiotics effective against S. aureus are started. If the process recurs, a second aspiration is performed. The elbow is elevated and splinted in 45 degrees of flexion with an anterior splint. There is no reason for an incision in most cases. If a septic bursa occurs or if the septic process has followed a course of recurrent aseptic bursitis, the bursa is excised only after the septic process has resolved. Special protective efforts are employed for contact sports, and the antibiotic is continued at a prophylactic dose if repeated trauma is anticipated.

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Section C Throwing Injuries 1. THROWING INJURIES IN THE ADULT Jeffrey R. Dugas MD James R. Andrews MD Introduction and Basic Science

Although the most widely studied sport involving overhead throwing is baseball, several other sporting activities require the same type of motion. Some such sports include football, volleyball, handball, javelin, softball, racquetball, squash, and tennis (the serve).[7] [24] [37] [38] [70] [75] [79] The overhead throwing motion can be broken down into several discrete steps, which include the wind-up, early cocking, late cocking, acceleration, deceleration, and follow-through phases. The process of overhead throwing, regardless of specific sport, involves the generation of potential energy and the subsequent transfer of that potential energy to kinetic energy, which is imparted to the object being thrown. In total, the overhead throwing motion takes approximately 2 seconds to complete, with nearly 75% of that time taken up by the pre-acceleration phases.[22] [28] [29] [68] The first phase of throwing, the wind-up, is when the body readies itself by raising the center of gravity and the shoulder is placed in slight abduction and internal rotation. During this phase, virtually no stress is placed upon the upper extremity.[30] [33] [43] [46] The early cocking phase is when the arm is placed into the abducted, externally rotated position. In addition, the arm rotates behind the body axis approximately 15 degrees. This phase ends at the top of the motion just before the beginning of forward arm and body motion. Early in this phase the deltoid is active as it abducts the arm, followed by later activity in the rotator cuff musculature to cock the arm into a more externally rotated position. The third, late cocking, phase begins as the lead leg contacts the ground and ends when the arm reaches maximal external rotation of nearly 180

degrees ( Fig. 23C1-1A and B ). During this phase, the scapula retracts in order to provide a stable glenoid surface for the humeral head to compress against. The upper arm is maintained in 90 to 100 degrees of abduction and the elbow moves even with the plane of the torso. As the humerus progresses into external rotation, the humeral head translates posteriorly on the glenoid owing to increasing tightness in the anterior structures. The external rotators

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Figure 23-C1-1 Adult male pitcher at the beginning (A) and end (B) of the late cocking phase of the throwing motion. This phase begins as the foot contacts the ground and ends as the arm reaches maximum external rotation.

(infraspinatus and teres minor) are active early in this phase, as are the supraspinatus and deltoid. The subscapularis is active toward the end of this phase as the internal rotation of the arm begins. During this phase, the rotator cuff musculature generates a compression force of 650 N.[28] The acceleration phase begins as the arm initiates its internal rotation and ends at ball release. During this phase, the arm rotates at an angular velocity greater than 7000 deg/sec. [22] [28] Despite this tremendous movement, little stress is noted in the shoulder musculature during this phase.[43] The arm is maintained in the same abduction as in the late cocking phase. Other important muscles that are active during this phase are the triceps early on, followed by the pectoralis major and latissimus dorsi later.[43] [68] The deceleration phase begins just after the ball is released and ends when humeral internal rotation ceases. This phase is heralded by tremendous loads generated by the rotator cuff muscles, as the rapidly rotating arm is slowed to a halt.[22] [28] The scapula protracts while maintaining a stable glenoid surface for the humeral head. In essence, the deceleration phase is where the energy not imparted to the ball is dissipated. Eccentric loads are seen in the posterior cuff musculature as compressive joint loads exceed 1000 N.[43] [68] Shear forces are also significant posteriorly and inferiorly. Finally, the follow-through phase concludes the throwing motion as the body regains balance and stability. During this phase, muscle firing ceases and joint compression loads drop to 400 N.[22] [28] Shear loads also diminish during this phase. Stresses across the elbow joint have been measured during the overhead throwing motion. Maximum elbow velocity reaches over 2300 degrees per second during the acceleration phase.[91] Just before reaching maximal external humeral rotation in the late cocking phase, valgus torque at the elbow has been measured at 64 N-m.[28] Cadaveric studies have demonstrated the tensile strength of the ulnar collateral ligament (UCL) to be approximately 32 Nm.[23] The UCL provides the most static stability against a valgus stress, taking up nearly 55% of the valgus stress at 90 degrees of elbow flexion. [60] [87] Because 55% of 64 Nm is greater than the 32 Nm tensile strength of the intact UCL, contributions from the bony architecture and surrounding soft tissues are needed to assist the UCL in providing medial elbow stability during the overhead throw. These contributions come mainly from the flexor carpi radialis and the pronator teres.[33] [35]

When the medial soft tissues fatigue, more stress is placed upon the lateral radiocapitellar articulation as well as upon the UCL. With increased compression through the radiocapitellar articulation, avascular necrosis, osteochondritis dissecans, and loose body formation may occur.[9] [93] Regardless, the UCL remains the primary stabilizer to the medial side of the elbow during throwing. As one can see, the throwing athlete's upper extremity experiences tremendous stresses each time a throw is made. With the repetitive application of such stresses, several adaptive changes are apparent within the normal thrower's shoulder and elbow. A knowledge of these normal adaptations is necessary when evaluating the throwing athlete. In comparison with nonthrowers, the humeral head and glenoid of the thrower are in a more retroverted position, allowing more external rotation.[20] Throwers have been shown to have no significant difference in total range of shoulder rotation, but the arc of motion is spun back with increased external rotation and decreased internal rotation.[20] [47] The soft tissues about the shoulder are affected similarly with laxity of the anterior structures to allow for the increased external rotation, and contracture of the posterior capsule preventing normal internal rotation. The thrower's elbow may have an increased carrying angle (more valgus) as well as a loss of extension and hypertrophy of the flexor pronator muscle group.[47] Up to 50% of throwers without symptoms have some degree of extension loss.[47] In most cases the motion loss is due to contracture

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of the soft tissues anteriorly, but in some, the cause is posterior bony apposition caused by osseous overgrowth. Increased laxity is present in the UCL in the throwing elbow versus the nonthrowing elbow in pitchers.[26]

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Evaluation

The most important aspect of the evaluation of the throwing athlete is the history and physical examination. The history should include a precise chronologic description of the symptoms, with particular attention to the phase of the throwing motion that causes the symptoms. The individual's pitching mechanics should be reviewed. Albright demonstrated that there is an increased risk of medial elbow injury in pitchers who throw with a sidearm delivery.[1] Also, any changes in the routine training regimen to which the thrower had been accustomed may provide useful information to the clinician. Along with clinical symptoms, throwing symptomatology such as decreased velocity, loss of control, and early fatigue are important parts of the history. Any previous treatment that has been rendered including rest, anti-inflammatory medications, injections, physical therapy, and surgical procedures should be documented. Any changes in the sensory function in the hand and arm should be carefully noted. Tingling or discoloration in the fingers may be the first and only signs of a vascular or neurologic abnormality related to throwing. Reviewing the entire physical examination of the shoulder and elbow is beyond the scope of this chapter. Several examination tests are highlighted as part of the routine evaluation in the throwing athlete. In the shoulder, a precise range of motion should be documented for both shoulders. A careful examination for normal laxity versus instability should be performed with specific attention to discomfort experienced by the patient as the humeral head is translated anteriorly and posteriorly. The internal impingement test is done with the patient supine and the arm abducted. The arm is forced into maximal external rotation ( Fig. 23C1-2A and B ). [55] [56] Pain in the region of the infraspinatus insertion is considered a positive test, indicating possible injury to the undersurface of the posterior rotator cuff. Internal and external rotation strength is of particular importance in the thrower.[92] Impingement testing is a routine part of the thrower's evaluation owing to the high incidence of rotator cuff disorders. Palpation and inspection of the posterior shoulder with particular attention to the infraspinatus fossa and the posterior deltoid are of particular importance in the thrower's evaluation. Infraspinatus wasting may be the only clinical indication of a suprascapular nerve entrapment,

whereas pain to palpation posteriorly in the quadrilateral space or posterior deltoid wasting may be indicative of axillary nerve compression or impingement within the quadrilateral space.[14] The active compression test (O'Brien's test) or other provocative test is performed to determine if there is any labral disorder ( Fig. 23C1-3 ). [65] O'Brien's test, as with other tests for labral injury, is very sensitive but limited in its specificity. Owing to the location of the labrum and the difficulty in performing direct examination, O'Brien's test seems to be the most helpful in our hands. At the elbow, special attention should again be paid to the range of motion of the throwing elbow with comparison to the opposite side. Test for valgus stability should be performed with the patient supine and the arm abducted and externally rotated in order to limit scapular motion ( Fig. 23C1-4 ). The elbow is flexed 20 degrees, and a valgus stress is applied. Pain in the region of the UCL or increased laxity with a soft end point may be indicative of UCL disorder. The test for valgus extension overload is done by repeatedly forcing the elbow into hyperextension while a valgus force is applied. This test attempts to recreate the stress across the elbow with throwing. Pain in the posteromedial aspect of the elbow is considered a positive

Figure 23-C1-2 A and B, Test for internal impingment. The arm is placed in the plane of the scapula and in maximal external rotation. Impingement of the undersurface of the rotator cuff between the humeral head and the posterosuperior glenoid and the labrum occurs in this position. The patient will experience pain in the posterior aspect of the shoulder at the level of the glenohumeral joint if internal impingement is present.

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Figure 23-C1-3 O'Brien's Active Compression Test (ACT). This maneuver attempts to entrap the anterosuperior labrum between the humeral head and the glenoid. The patient is asked to place the arm in 90 degrees of forward elevation and 20 degrees of cross-body abduction. The arm is maximally internally rotated with the elbow straight. The patient is then asked to resist a downward force placed on the forearm. The occurrence of pain in the anterosuperior shoulder that re-creates the symptoms is considered a positive test result.

test, and may indicate bony or soft tissue impingement in the area of the pain. Once the history and physical examination are completed, additional tests for diagnostic purposes may be obtained. The first radiographic studies should include plain radiographs in the anteroposterior, lateral, oblique,[2] and axial planes for the elbow, and anteroposterior-internal

Figure 23-C1-4 The test for valgus stability at the elbow. The arm is abducted and externally rotated as a valgus stress is placed across the elbow. Any appreciable increase in valgus opening or pain with

valgus stress is considered a positive test result, indicative of possible ulnar collateral ligament rupture.

rotation, anteroposterior-external rotation, Stryker notch, axillary, and supraspinatus outlet views for the shoulder. [54] At the elbow, the above standard views will demonstrate bony osteophytes on the posteromedial olecranon tip as well as general joint space integrity and bony alignment. In some cases plain radiographs may detect loose bodies within the elbow. Stress anteroposterior radiographs of the elbow can be obtained using a stress device to determine if increased medial laxity exists when compared with the nonaffected side. After plain radiography, magnetic resonance imaging (MRI) is the study of choice for both the shoulder and elbow. * With the exception of stress fractures and other rare bony abnormalities, MRI is best for demonstrating soft tissue architecture and disorders at both locations. Contrast is particularly important at the elbow when looking for UCL injury, since any contrast seen leaking through the ligament indicates a full-thickness injury, versus contrast within the ligament indicating a partial thickness injury. If stress fracture of the olecranon or other fracture or osteochondral injury is suspected, CT scan or bone scan may also be obtained to assist in the diagnosis and subsequent management.

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Shoulder Disorders in Throwers

As a result of the extreme forces generated by the throwing motion, the soft tissues and bony architecture about the shoulder are susceptible to injury caused by repetitive overuse or acute trauma. The two most common types of pathologic process seen in the throwers are injuries to the rotator cuff and the labrum. Other types of shoulder disease seen include osteochondral lesions of the humeral head or glenoid, osteoarthritic changes, loose body formation, gross instability, nerve entrapment syndromes, and neurovascular injuries. The following pages discuss the diagnosis and treatment of these conditions as well as the unique aspects of the throwing athlete that make the care of these injuries challenging. Rotator Cuff Injuries

As noted earlier, the rotator cuff musculature is active during various stages of the throwing motion. Owing to the high stresses experienced by the cuff, a spectrum of disorders is possible. Disorders within the rotator cuff tendons range from mild tendinitis to full-thickness tears of the cuff. Debate still exists as to the mechanism of cuff injuries. Certainly tension is a possible and even probable mode of failure as the cuff tendons decelerate the arm in the deceleration and follow-through phases of the throwing motion.[46] Jobe and colleagues demonstrated eccentric contraction of the infraspinatus and supraspinatus during the follow-through phase of throwing.[46] Compression has also been demonstrated when the arm is in maximal external rotation. In this position, the infraspinatus has been found to be compressed or pinched between the posterior superior *See references

[ 13] [ 19] [ 27] [ 34] [ 39] [ 48] [ 49] [ 53] [ 57] [ 58] [ 61] [ 62] [ 66] [ 67] [ 72] [ 86] [ 87]

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and [ 97] .

glenoid rim and the humeral head. This situation was termed internal impingement by Walsh and coworkers.[90] External impingement occurs when the bursal side of the rotator cuff is pinched or abutted by some structure. Such offending structures as a thickened coracoacromial ligament, an acromial spur, or thickened bursa may cause significant impingement pain and dysfunction. Tendinitis

Tendinitis is, by definition, inflammation of a tendon. In many cases of tendinitis, it is the tendon sheath that is actually inflamed rather than the tendon itself. In the case of the rotator cuff, the term tendinitis is frequently used when a patient has shoulder pain with activity but no obvious detachment of the cuff. In these cases, tendon inflammation is likely not present, but rather inflammation in the subacromial bursa, which is termed bursitis. Tendinosis implies true intratendinous disease, such as intrasubstance degeneration or tearing. The careless use of these terms is not insignificant in the case of a thrower because of the potential for catastrophic failure of the cuff, which may disable the player completely. The hallmarks of tendinitis or tendinosis of the rotator cuff are pain with overhead activity and weakness secondary to the pain. In the thrower, the symptoms are pain at the top of the motion when the arm is in maximal external rotation or pain after ball release as the cuff is trying to slow the arm down. Weakness of the supraspinatus and/or infraspinatus is a frequent finding. In most cases the athlete will not recall a specific throw when the shoulder became sore. Rather, many will notice the pain as they try to warm up and then are unable to get rid of the pain as they progress to full speed. In almost all cases, tendinitis in the thrower represents an overuse injury rather than an acute trauma. For this reason, the first act of the treating physician is to rest the player. For mild tendinitis, short-term rest (3 to 5 days) along with oral anti-inflammatory medication and a rehabilitation program designed to strengthen the cuff muscles is enough to eliminate the symptoms. With more severe or recurrent tendinitis, more prolonged rest from throwing along with extended cuff rehabilitation may be necessary. In refractory cases, subacromial injection of corticosteroid may be considered, although this should be the last conservative option. Partial-Thickness Tears

The normal rotator cuff inserts over the entire greater tuberosity. In addition, the normal tendons may reach a thickness of 10 mm or greater. Partial-thickness tears generally occur on the articular side of the rotator cuff, although bursal-sided tears have been seen. In the cases of internal impingement, the deepest fibers of the infraspinatus become entrapped between the glenoid rim and the humeral head as the arm moves into hyperexternal rotation. This impingement causes fraying of these deep fibers, leading to recurrent pain at the top of the throwing motion. [21] [32] [40] [41] [51] [90] Players will report pain in the back of their shoulder as opposed to pain on the top of their shoulder with this condition. Partial-thickness tears of the supraspinatus are also seen in throwing athletes, and these patients will tend to complain of pain on top of their shoulder. In treating partial-thickness tears, it is important to determine, as accurately as possible, the extent of the tear. As noted earlier, MRI with or without contrast is the study of choice in these cases. Although there are no absolute guidelines as to the surgical

indications for throwers with partial thickness tears, it is always wise to begin with conservative management. If MRI fails to demonstrate a full-thickness tear, rest and rehabilitation along with modalities and anti-inflammatory medications should be initiated. If the player fails to improve or return to throwing after a 6- to 12-week period, arthroscopy should be entertained. At the time of arthroscopy, a better determination regarding the thickness of the rotator cuff injury should be made. If the tear is less than 75% of the thickness of the cuff, débridement of the torn tissue should be carried out. In nonthrowers, success rates of 80% to 90% have been reported with simple débridement of partial-thickness lesions.[12] [31] [81] [95] If more than 75% of the thickness of the tendon is torn, however, open or arthroscopic repair is indicated following débridement. The decision between open and arthroscopic repair is an individual one. Certainly as experience with arthroscopic techniques increases and more confidence is gained, the decreased morbidity associated with these techniques may be preferred to traditional open methods. In cases of internal impingement and/or labral fraying, débridement of the frayed tissue is usually enough to eliminate symptoms in nonthrowers, as noted earlier. Simple débridement, however, will not address the rotational instability that most throwers with shoulder disease possess. The results of shoulder arthroscopy with débridement alone in the throwing population have been met with lesser rates of success. In Andrews and associates' initial report of 73 pitchers, 76% had an excellent result, but follow-up was limited to only 13 months. [5] A later study by Payne with longer follow-up demonstrated less than 50% return to competition in a similar population with associated instability.[69] Therefore, in most cases of internal impingement and labral disorders, arthroscopic stabilization using thermal capsular shrinkage or capsular plication is carried out in the anterior, posterior, and inferior aspects of the joint capsule as indicated. Treatment of instability in the throwing athlete is a delicate matter owing to the balance that must be maintained between motion and stability. Throwers have increased external rotation owing to both bony and soft tissue factors mentioned previously. Some throwers, however, develop pathologic instability that leads to increased stress upon the capsule and rotator cuff tissues without frank dislocation. This subtle increase in instability can be demonstrated by an increase in humeral translation on the glenoid in either the anteroposterior or the inferior direction. Regardless of the direction, the instability must be addressed in order to correct the underlying pathologic process. Although open stabilization procedures certainly accomplish the goal of obtaining stability, the subsequent rate of return to competitive throwing is significantly decreased when compared with arthroscopic means of regaining stability.[42] [76] Early results with thermal capsular shrinkage have yielded very encouraging results. In patients who undergo débridement and thermal shrinkage, the average player returns to competitive throwing at 7.4 months, with 93% of players obtaining return to competition, and

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86% still playing at the same or higher level at 2 years after surgery.[50] The addition of labral repair to surgical treatment of throwing athletes delays the return to competition to just over 11 months, with 73% of athletes still competing at 2 years after surgery. Interestingly, in the study by Levitz and associates, the percentage of throwers

competing after thermal shrinkage increased in the interval from 16 to 24 months after surgery.[50] This indicates that the results in the throwing athlete after thermal shrinkage may continue to improve with increasing interval from surgery. Although different types of shrinkage devices are available and variations in technique have been reported, no data are currently available to demonstrate any difference between equipment or technique with regard to clinical outcome. The postoperative treatment of throwing athletes is just as important as the procedure itself. In general the first 4 to 6 weeks following surgery are spent regaining motion, after which strength in the rotator cuff is regained. By 3 to 4 months after the procedure, the athletes are ready to begin an interval throwing program under supervision by a trainer or therapist. Once the interval throwing program is completed, the player is ready to return to competition. The time for return to competition varies with pathologic process and procedure as well as from individual to individual. Full-Thickness Tears

Full-thickness rotator cuff injuries are rare in the throwing population. In some cases, the injury occurs as a result of a nonthrowing trauma to the throwing arm. Regardless of the mechanism, full-thickness rotator cuff tear is an absolute indication for surgery. Traditionally, shoulder arthroscopy with or without subacromial decompression is followed by a limited open approach to the rotator cuff with strong fixation back to the greater tuberosity. In a study by Tibone and coworkers, only 55% of overhead athletes requiring open rotator cuff repair were able to return to their previous level of competition.[83] With the advent of and increasing experience with arthroscopic repair as well as the decreased morbidity associated with arthroscopic techniques, fewer and fewer open procedures are being performed on these athletes. It is imperative at the time of repair to achieve as strong a repair as possible, and to ensure that there is no impingement upon the cuff by the acromion, coracoacromial ligament, or distal clavicle. The postoperative course for these patients is very much the same as with the partial-thickness injuries and the thermal shrinkage procedures. The early portion of the rehabilitation is spent regaining motion, followed by strength gains, followed by return to throwing via an interval throwing program. Labrum Injuries

The labrum is a fibrocartilaginous ring around the bony glenoid rim that not only deepens the socket but also serves as the attachment site for the glenohumeral ligaments and biceps tendon. Although compression of the labrum against the glenoid by the humeral head certainly occurs, it is more likely in throwers that the disorders seen in the labrum are due to failure in tension related to the biceps tendon and glenohumeral ligaments. Morgan and Burkhart described the peel-back phenomenon, during which the biceps tendon rotates behind the axis of the humeral head, leading to a tensile stress on the biceps anchor and superior labrum.[59] Posterior labral fraying is common in throwers, likely due to compression as is seen in internal impingement of the infraspinatus tendon, discussed earlier. Complete disruption of the posterior labrum

away from the glenoid rim, however, is less common than its anterior counterpart. As noted earlier, the physical examination tests for labral disorders are less specific than they are sensitive. We prefer the active compression test (O'Brien's test) for physical diagnostic purposes along with confirmation by contrast-enhanced MRI. In the absence of MRI findings, conservative management is usually initiated. If symptoms persist after adequate rest and rehabilitation, shoulder arthroscopy may be indicated. At the time of arthroscopy, examination under anesthesia should also be performed in order to gauge the laxity in the soft tissues. The labrum should be inspected and probed thoroughly along its entire course around the glenoid rim. Several normal anatomic variants have been described, particularly involving the anterior labrum. Knowledge of these variants is mandatory in order to avoid overconstraining the shoulder by repairing a normal structure. Among the more common anatomic variants is the sublabral foramen. This hole beneath the labrum is most commonly seen at the anterior labrum just below the biceps anchor. No true labral detachment is present, with no evidence of trauma or labral detachment. No increased laxity is attributed to this condition, and the sublabral foramen should not be closed. If a true labral detachment is noted, arthroscopic repair is the procedure of choice, inasmuch as débridement alone has led to disappointing results.[3] [17] [52] [88] Obviously anterior lesions can be treated through the standard anterior portal; however, superior lesions are more difficult to repair through the anterior cannula. This is due to the angle of insertion for the anchor or other fixation device that is used. For this reason, we routinely utilize a small permanent anchor placed through a 4-mm trochar via a direct lateral stab incision. By doing this, the smallest possible defect is made in the rotator cuff without compromising the arthroscopic repair and fixation. Regardless of which device or approach is used, arthroscopic fixation should be as firm as possible. Before placing any anchor or tack, débridement of the glenoid rim down to bleeding bone should be undertaken. The fixation should be at the articular margin, not recessed on the glenoid neck. Fixation on the glenoid neck as opposed to the correct periarticular location may lead to instability and subsequent re-injury. Careful inspection of the superior labrum should be carried out before repair in order to ensure that the attachment is in fact detached. The normal superior labrum may be recessed or meniscoid, with its fibers attaching medial to the articular surface. This condition should not be mistaken for a true labral tear. Fraying of the biceps tendon is also seen at the time of arthroscopy in the throwing population. The mechanism of

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injury to the biceps tendon is not entirely clear at this time. The frayed tissue should be débrided during arthroscopy with caution so as not to completely amputate the tendon. Synovitis in the anterior recess of the shoulder can also be débrided. As with internal impingement, thermal capsular shrinkage is carried out in the majority of

throwers with labral detachments. Levitz and Andrews demonstrated a significant increase in the rate of return to competition with the use of concomitant shrinkage at the time of labral repair versus labral repair alone.[50] In their series, only 50% of throwers treated without thermal shrinkage were competing at 2 years, whereas 73% of those whose treatment included thermal shrinkage were still competing at the same interval. Following surgery, the same postoperative protocol is used as with the internal impingement patients. The first 6 weeks are spent regaining range of motion along with dynamic stability. The next 6 weeks are used to regain strength and proprioception, along with initiating plyometric exercise. By 3 to 4 months, the interval throwing program is initiated. If thermal shrinkage alone is performed, return to competition can be expected by 7.5 months. [50] If labral repair is performed in addition to the shrinkage, the average return time is 11.2 months. True traumatic dislocation is rare in the throwing shoulder. In most cases of frank dislocation, the injury occurred as the result of a nonthrowing action. Regardless of mechanism, it is of paramount importance to regain the stability and strength necessary to throw. For the overhead thrower with a dislocation history, it is possible to regain full function using conservative treatment, as would be the case for many simple shoulder dislocations. Many, however, will require operative fixation of the detached structures that are usually the anterior labrum and capsule. With increasing frequency, these procedures are performed arthroscopically, although no clinical data are currently available in the throwing population. Certainly it is reasonable to expect less difficulty with postsurgical scarring and range of motion with arthroscopic techniques than with traditional open techniques in this patient population. This remains, however, to be proven clinically. Other Shoulder Disorders

Suprascapular Nerve Entrapment

In some cases, wasting of the infraspinatus may be noted when compared with the nonthrowing shoulder. In these cases, suprascapular nerve entrapment or injury must be suspected. Although this represents a pathologic condition, many throwers with infraspinatus wasting are completely asymptomatic and do not warrant any intervention. If, on the other hand, the patient has symptoms of nerve entrapment such as pain, weakness, or decreased ability to perform, it is reasonable to perform open decompression of the suprascapular nerve. Arthroscopic decompression has been advocated but not widely accepted as safe or effective. MRI should be obtained before surgery to determine if there is any cyst or other structure of articular origin that may be causing the compression. In either case, shoulder arthroscopy should be carried out at the time of nerve decompression in order to be certain that no perilabral cyst exists. If a cyst is present, it should be removed. Otherwise, simple decompression of the suprascapular nerve via spinoglenoid notchplasty is generally sufficient to relieve symptoms.[77]

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DeLee: DeLee and Drez's Orthopaedic Sports Medicine, 2nd ed., Copyright © 2003 Elsevier

Elbow Disorders in Throwers

As with the shoulder, tremendous forces are generated at the elbow during the overhead throwing motion. The soft tissues about the elbow along with the bony articulations provide stability to this complex joint. The UCL, specifically the anterior band, provides the most static stability at the elbow joint to oppose a valgus stress.[60] The discrepancy between the tensile strength of the UCL and the forces imparted to the ligament during the throwing motion demonstrates the importance of the dynamic muscular stabilizers as well as the bony contributions to the resistance to valgus stress. Not surprisingly, flexor tendinitis as well as partial- and full-thickness injuries to the UCL are very common in throwers. Also, bony disease is seen particularly in the radiocapitellar articulation and at the posteromedial aspect of the olecranon. Although some players will not recall any specific throw that initiated their symptoms, an equal number will be able to pinpoint exactly when symptoms began. Players may complain of numbness or tingling in the ulnar nerve distribution with medial elbow injuries owing to the proximity of the nerve. Also, any increase in valgus opening at the elbow increases the stress placed on the nerve, which can cause paresthesias. Tendinitis

Tendon injuries about the elbow range from minor inflammation to complete rupture of the flexor musculature.[11] [63] [80] [94] Flexor tendinitis and tendinosis are common in throwers owing to the dynamic function inherent to the muscles. In such cases, patients will have pain to palpation of the flexor-pronator mass as well as pain with a valgus stress. Careful attention to the location of pain will likely distinguish tendinitis from UCL injury. Resisted pronation of the forearm and wrist volar flexion will also elicit pain in the region with tendinitis, but rarely in cases of UCL damage. Triceps tendinitis is also seen in throwers owing to the rapid extension required during the acceleration phase. In these cases, the pain is easily traced to the distal triceps tendon and insertion onto the

olecranon. In addition, resisted elbow extension should elicit symptoms. As with other locations of tendinitis, the treatment of tendinitis about the elbow begins with rest from throwing along with anti-inflammatory medication and a flexibility and strengthening program. Therapeutic modalities and corticosteroid injection have also demonstrated some beneficial effect. In general, corticosteroid injection is reserved for the recurrent or recalcitrant tendinitis cases. With aggressive flexibility and strengthening, most players will return to competition following 1 to 3 weeks of treatment. In more chronic or recurrent cases, the required period of

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rest and treatment may be prolonged. In very few cases that fail conservative measures, operative débridement of the medial flexor tendon origin or triceps insertion can be performed through an open approach. Similarly, in cases of chronic resistant tendinoses, we prefer open débridement and repair of the flexor pronator mass. In these cases we prefer to reattach the flexor tendon to the medial epicondyle using a suture anchor. Although the results of operative treatment are excellent, most will not require this type of management. Ulnar Collateral Ligament Injuries

The UCL is the most commonly injured ligamentous structure in the thrower's elbow for the reasons described earlier. The spectrum of UCL injury ranges from minimal fraying to complete ligament disruption and frank instability. [1] [16] [44] [45] [85] The distinction between partial-thickness and full-thickness injuries is difficult to make on clinical examination in the awake patient. In cases of complete ligament disruption with frank elbow instability or dislocation, the diagnosis of UCL injury may be easier on clinical examination. Unfortunately, most throwers do not fall into this category. Significant clinical history along with appropriate physical findings and supporting radiographic studies will usually be sufficient to make the correct diagnosis. It is also important to note that not all full-thickness injuries require reconstruction, and not all partial injuries will be treated successfully without surgery. The symptomatology as well as the clinical history are the most important facets of the decision-making process for the clinician. Partial-thickness injury of the undersurface of the UCL and intrasubstance degeneration occur in the throwing population.[85] Certainly it is reasonable to suspect that these lesions are precursors to full-thickness injury. In the thrower who has no frank instability or increased medial opening with a valgus stress but has clinical symptoms of a UCL injury, MRI with contrast is the diagnostic study of choice. Partial-thickness injury or edema within ligament are easily detected with MRI.[78] In such cases, short-term active rest (3 to 6 weeks) followed by a supervised return to throwing in an interval throwing program is the treatment of choice. Anti-inflammatory medications as well as other modalities may be used during this time. If the player cannot return to throwing without pain after an adequate rest period and throwing program, prolonged rest (3 to 6 months) may be indicated. In professional athletes as well as many amateur and college level

athletes, these periods of prolonged rest are not well tolerated owing to the rigorous schedules imposed upon such players. In players who have recurring bouts of difficulty with partial-thickness injury or who fail to improve with adequate conservative management, UCL reconstruction may be considered. If, on the other hand, the diagnosis of full-thickness injury is made, it is less likely that conservative management will lead to favorable results in the throwing athlete. UCL reconstruction may be considered in these players without the need for prolonged rest and rehabilitation in an attempt to heal the ligament injury. It is important to note at this point that the UCL is important for the purpose of throwing in athletics. Rarely is it necessary to reconstruct the nondominant UCL or to perform reconstruction in those who wish to discontinue their throwing activities. Once the decision is made to proceed with ligament reconstruction, the choice of graft site must be made. In general, we prefer the ipsilateral palmaris longus tendon if present. In the general population, 85% of people have a palmaris longus. It is imperative at the time of physical examination and preoperative counseling that the presence or absence of a palmaris longus tendon is documented on either the operative or the nonoperative side. Reconfirmation just before induction of anesthesia is a routine part of our practice in order to avoid any graft-related complications. Nearly 15% of the normal population has no palmaris longus tendons. In these cases, a gracilis tendon is harvested from the opposite leg. Other graft choices include the plantaris tendon, lesser toe extensor tendon, a portion of the Achilles tendon, or allograft tendon. Techniques

If the diagnosis of UCL rupture is unclear after complete clinical and radiographic evaluation, elbow diagnostic arthroscopy should be performed in order to document the status of the ligament. At arthroscopy, a standard anterolateral portal is established after insufflation of the joint with saline solution.[6] The anterior compartment is visualized and inspected for loose bodies, chondral injuries, and capsular integrity. The elbow is then placed in 70 degrees of flexion and a valgus stress is applied. The normal UCL will not permit more than 1 mm of medial opening in this position.[84] [85] If the medial ulnohumeral joint space opens more than 1 mm, the UCL is considered injured and not providing adequate medial stability. Following this arthroscopic stress test, arthroscopy is abandoned, and UCL reconstruction can proceed. Jobe first described the technique for UCL reconstruction.[45] Since that time, several modifications have been made to his original methods; however, the basic tenets of the procedure remain the same.[16] For UCL reconstruction, the patient is positioned supine with the arm on a hand table. A nonsterile tourniquet is inflated for the case. The incision is made extending from 4 cm above the medial epicondyle to 6 cm distal to it. The medial antebrachial cutaneous nerve is identified and protected during the case. The ulnar nerve is isolated above and below the medial epicondyle. The medial intermuscular septum should be resected. Next, the flexor-pronator mass is elevated off the UCL until the UCL can be completely visualized. The native ligament is split longitudinally in line with its fibers to expose the underlying ulnohumeral joint. The torn or degenerative ligament tissue can be débrided. A 9/64 drill bit is then used to drill two

connecting holes in the proximal ulna, one from medial to lateral, and one from anterior to posterior. Curved curets can be used to connect the two holes if necessary. The same drill is used to drill two converging holes in the medial epicondyle, one from proximal to distal, and one from medial to distal. These two holes should converge to exit the epicondyle at the origin of the UCL. Straight curets can be used to connect these holes if necessary. Suture passers are then used to pull suture loops through these tunnels. The native ligament is

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repaired side to side using nonabsorbable suture, leaving the proximal most ligament unrepaired. By closing the native ligament, the joint surfaces are covered, protecting the graft from abrasion. The proximal ligament is left without repair in order to visualize the entrance to the epicondylar tunnels. If the native ligament was torn away from either insertion, sutures can be placed in the leading edges of the ligament for the purpose of repair through the tunnels for the graft. The graft of choice is then harvested. The minimum graft length is 12 cm. Nonabsorbable braided sutures are placed in each end of the graft tissue in Bunnell or Krakow fashion. The graft is then passed through the tunnels using suture passers and sewn to itself. We routinely perform subcutaneous transposition of the ulnar nerve at the time of UCL reconstruction. Recently, a docking technique for UCL reconstruction has been described in which the graft is passed through the ulna in the same fashion as described earlier; however, the medial epicondyle is reamed from distal to proximal using a 3-mm round bur without violating the proximal aspect of the medial epicondyle.[2] A small dental drill is then used to make two small holes in the epicondyle connecting to the larger bur hole. The sutures from the graft are brought through these two drill holes through the tunnel and tied on the outer surface of the epicondyle. This technique does not typically include ulnar nerve transposition and has been noted to involve less soft tissue dissection than the standard technique as first described by Jobe. No head-to-head studies have been undertaken to determine if one technique leads to superior results. The UCL originates on the distal aspect of the medial epicondyle and inserts onto the sublime tubercle of the medial proximal ulna. Many adult throwers have either a bony extension from the sublime tubercle directed proximally along the course of the ligament or one or more small ossicles of bone within the ligament ( Fig. 23C1-5 ). In most cases, the bony ossicles represent old avulsion fractures, likely occurring during the childhood or adolescent years. The same may be true of the development of a bony extension from the sublime tubercle, although the exact cause of this finding is uncertain. These bony findings are critical in the treatment of elbow instability in the throwers. Since bone is stronger in compression than in tension, these bony abnormalities will create a weak link in the medial stabilizing tissues. Both the ossicles and the bony extension are actually within the substance of the UCL. In the case of the bony projection from the ulna, the terminal distal fibers of the UCL actually insert onto the prominence. The presence of these types of bony disease may make the decision to proceed with UCL reconstruction somewhat less difficult. If the decision is made to perform UCL reconstruction in these type patients, a larger graft should be used if possible. This is

necessary because of the tissue deficiency that will result from débridement of the bony disease from within the native ligament. In the absence of such a deficiency, the native ligament can be left in place or reattached at the site of rupture along with ligament reconstruction, creating significant tissue thickness at the UCL site. In fact, the native ligament is usually placed beneath the graft tissue in order to protect the graft from abrasion by the joint surfaces. If the native ligament cannot be retained or if it is insufficient, a larger thickness

Figure 23-C1-5 Magnetic resonance imaging scan with contrast of the elbow demonstrating bony osteophyte of the medial proximal ulna. In such cases, the ulnar collateral ligament attaches to the tip of the osteophyte. The bone is acting in a tension mode, which places it at risk for failure. If the ulnar collateral ligament is reconstructed in people with osteophytes such as the one pictured here (arrow), it is important to obtain a graft that can replace the native ligament because the distal ligament is deficient after removal of the bony prominence.

graft should be used to make up for the missing tissue. We prefer the gracilis tendon in such cases. Results

In Jobe's original report, 10 of 16 (63%) throwing athletes were able to return to their previous level of competition.[45] In Conway's group of 70 patients, only 50% of the athletes who underwent repair of the ligament returned to competition, versus 68% (45 of 56) of those who underwent UCL reconstruction.[16] Later, Andrews reported on 72 professional baseball players with elbow disorders, 14 of whom underwent UCL reconstruction, with 12 of those (86%) returning to previous level of competition. [8] Most recently, Azar and Andrews reported on 67 patients with 81% (48 of 59) of those undergoing UCL reconstruction returning to the same or higher level of play.[10] Valgus Extension Overload/Loose Bodies

UCL injury is not the only cause of medial elbow pain in the throwing athlete. Valgus extension overload (VEO) is a condition most commonly seen in throwers in which the valgus stress across the elbow causes impingement of the posteromedial olecranon tip against the medial wall of the olecranon fossa. With repeated impingement, a bony osteophyte may grow on the olecranon at the site of impingement. Bony growth within the olecranon fossa has

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also been seen. In addition, soft tissue including the synovium of the elbow joint may become hypertrophied with repeated impingement at the same location leading to additional symptoms and swelling. With VEO, throwers will typically complain of posteromedial elbow pain at the initiation of the acceleratio