Clinical Sports Medicine

MOSBY ELSEVIER

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

CLINICAL SPORTS MEDICINE ISBN-13: 978-0-323-02588-1 ISBN-IO: 0-323-02588-9 Copyright © 2006 by Mosby, Inc., an affiliate of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier's Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 2152393805, e-mail: [email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com).by selecting "Customer Support" and then "Obtaining Permissions."

Notice Knowledge and best practice in Medicine are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book.

ISBN-13: 978-0-323-02588-1 ISBN-IO: 0-323-02588-9

To my girls—Donna, Lindsay, Hailey, Kiley, and Jaycie. I can’t wait for your next soccer game. —SDM To my patients, medical students, residents, fellows, athletic trainers, physical therapists, and colleagues for all they have taught me; they have made this profession an honor and a privilege to be a part of. With love to my wife Nancy, son Brandon, and daughters Kelsey and Lauren for making my life complete. —DLJ

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Contributors J. Winslow Alford MD West Bay Orthopaedics, Warwick, RI. Rotator Cuff Disorders Answorth A. Allen MD Hospital for Special Surgery, New York, NY. Knee: Graft Choices in Ligament Surgery David R. Anderson MD Orthopedic Surgeon, Minnesota Sports Medicine, Minneapolis, MN. Superior Labrum Anterior to Posterior Lesions Robert B. Anderson MD Chief, Foot and Ankle Service, Department of Orthopaedic Surgery, Carolinas Medical Center; Co-Director, Foot and Ankle Fellowship OrthoCarolina, Charlotte, NC. Ankle Ligament Injury and Instability Thomas D. Armsey MD Associate Professor; Director Sports Medicine Fellowship, Palmetto Health Family Practice Center, Columbia, SC. On-Field Emergencies and Preparedness Bernard R. Bach, Jr. MD The Claude Lambert-Susan Thomson Professor of Orthopedic Surgery; Rush University Medical Center, Chicago, IL. Complex Issues in Anterior Cruciate Ligament Reconstruction Champ L. Baker, Jr. MD Clinical Assistant Professor, Department of Orthopaedics, Medical College of Georgia, Augusta; Chair, Sports Medicine Fellowship Program, The Hughston Clinic, Columbus, GA. Elbow: Physical Examination and Evaluation George K. Bal MD, FACS Assistant Professor, Sports Medicine and Shoulder Reconstructive Surgery, Department of Orthopaedics, West Virginia University, Morgantown, WV. Clavicle Fractures and Sternoclavicular Injuries R. Shane Barton MD Assistant Professor, Department of Orthopaedic Surgery, Louisiana State University Health Sciences Center; Medical Director, Sports Medicine, Willis Knighton Hospital System, Shreveport, LA. Shoulder: Nerve Injuries Carl J. Basamania MD, FACS Division of Orthopaedic Surgery, Duke University Medical Center, Durham, NC. Clavicle Fractures and Sternoclavicular Injuries Frank H. Bassett III MD Sports Medicine Service, Duke University Medical Center, Durham, NC. The Role of the Team Physician Todd C. Battaglia MD, MS Clinical Instructor, Department of Orthopaedics, Tufts University School of Medicine; Fellow, Sports Medicine and Arthroscopic Surgery, New England Baptist Hospital, Boston, MA. Posterior Cruciate Ligament Nathalee S. Belser MPA Department of Orthopaedic Surgery, University of Louisville School of Medicine, Louisville, KY. Pediatric Knee

Philip E. Blazar MD Assistant Professor of Orthopaedic Surgery, Harvard Medical School; Assistant Professor of Orthopaedic Surgery, Brigham and Women’s Hospital, Boston, MA. Wrist Soft-Tissue Injuries Michael R. Boland MBChB, FRCS, FRACS Assistant Professor, University of Kentucky; Chief, Orthopaedic Hand and Upper Extremity Surgery, University of Kentucky Medical Center, Veterans Administration Hospital, Lexington, KY. Wrist and Hand: Physical Examination and Evaluation Craig R. Bottoni LTC, MD Chief, Sports Medicine, Orthopaedic Surgery Service, Tripler Army Medical Center; Assistant Clinical Professor, Department of Surgery, John A. Burns School of Medicine, University of Hawaii, Honolulu HI; Assistant Professor of Surgery, Department of Surgery, F. E. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD. Shoulder: Anterior Instability Jeff C. Brand, Jr. MD Alexandria Orthopaedics and Sports Medicine, Alexandria, MN. Knee: Tendon Ruptures Stephen F. Brockmeier MD Chief Resident, Department of Orthopaedics, Georgetown University, Washington, DC. Knee: Overuse Injuries Amy Bullens-Borrow MD Georgia Sports Orthopedic Specialists, Gainesville, GA. Elbow: Instability and Arthroscopy J.W. Thomas Byrd MD Nashville Sports Medicine and Orthopaedic Center, Nashville, TN. Hip Joint E. Lyle Cain, Jr. MD Fellowship Director, American Sports Medicine Institute; Orthopaedic Surgeon, Alabama Sports Medicine and Orthopaedic Center, Birmingham, AL. Internal Impingement Kenneth Cayce IV Cincinnati Sports Medicine and Orthopaedics Center, Cincinnati, OH. The Preparticipation Physical Examination Constantine Charoglu MD Southern Bone and Joint Specialists, PA, Hattiesburg, MS. Hand and Wrist Rehabilitation

Adam C. Crowl MD Attending Physician, Orthopedic Spine Surgery, Advanced Orthopedic Centers, Richmond, VA. Cervical Spine Lisa T. DeGnore MD Volunteer Faculty, Department of Orthopaedic Surgery, University of Kentucky, Lexington, KY. Forefoot and Toes Christopher C. Dodson MD Resident, Department of Orthopaedic Surgery, Hospital for Special Surgery, New York, NY. Traumatic Shoulder Muscle Ruptures Jeffrey R. Dugas MD Fellowship Director, American Sports Medicine Institute, Birmingham, AL. Elbow: Instability and Arthroscopy R. Matthew Dumigan MD Fellow, Steadman-Hawkins Clinic, Vail, CO. Ankle Intra-articular Injury T. Bradley Edwards MD Clinical Instructor, Department of Orthopedic Surgery, University of Texas at Houston; Shoulder Surgeon, Fondren Orthopedic Group, Texas Orthopedic Hospital, Houston, TX. Pediatric Shoulder Hussein Elkousy MD Volunteer Faculty, University of Texas Health Sciences Center, Houston, TX. Principles of Shoulder Arthroscopy Ivan Encalada-Diaz MD Associate Clinical Professor of Orthopedic Surgery, National Autonomous University of Mexico; Attending Orthopedic Surgeon, Arthroscopy and Sports Medicine Service, Institute of Orthopedics, National Center for Rehabilitation, Mexico City, Mexico. Meniscal Injury Kyle R. Flik MD Attending Surgeon, Sports Medicine, Northeast Orthopaedics, LLP, Albany, NY. Knee: Articular Cartilage Philip C. Forno Orthopaedic Resident, University of South Cardina, Columbia, SC. Shoulder: Overuse Injuries Stephen French MD Big Thunder Orthopedics, Thunder Bay, Ontario, Canada. Knee: Arthritis in the Athlete

Kevin Charron MD Chief Resident, Department of Orthopaedic Surgery, Boston University Medical Center, Boston, MA. Patellofemoral Instability

Freddie H. Fu MD Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine; Chief, Department of Orthopaedic Surgery, UPMC Presbyterian Hospitals, Pittsburgh, PA. Anterior Cruciate Ligament

Michael J. Coen MD Department of Orthopaedic Surgery, Loma Linda University, East Campus, Loma Linda, CA. Thigh and Leg

James R. Gardiner MD Pacific Sports Medicine at Multicare, Tacoma, WA. Multiligament Knee Injuries

Brian J. Cole MD Associate Professor, Department of Orthopaedic Surgery, Section Head, Cartilage Restoration Center, Rush University Medical Center, Chicago, IL. Knee: Articular Cartilage

Gary Gartsman MD Clinical Professor, Department of Orthopaedics, University of Texas Health Sciences Center; Texas Orthopedic Hospital, Houston, TX. Principles of Shoulder Arthroscopy

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Contributors

C. David Geier, Jr. MD Assistant Professor, Orthopaedic Surgery; Chief, Sports Medicine Service, Medical University of South Carolina, Charleston, SC. Pediatric Elbow

James D. Kang MD Associate Professor of Orthopaedic and Neurological Surgery, University of Pittsburgh School of Medicine; University of Pittsburgh Medical Center, Pittsburgh, PA. Cervical Spine

Walter R. Lowe MD Associate Professor, Baylor College of Medicine; Chief, Sports Medicine Section, Department of Orthopedic Surgery, Baylor College of Medicine, Houston, TX. Superior Labrum Anterior to Posterior Lesions

Thomas J. Gill MD Assistant Professor of Orthopaedic Surgery, Harvard Medical School; Sports Medicine Service, Department of Orthopedic Surgery, Massachusetts General Hospital, Boston, MA. Shoulder: Nerve Injuries

Richard W. Kang BS Research Coordinator, Rush University Medical Center, Chicago, IL. Knee: Articular Cartilage

Scott D. Mair MD Associate Professor, Department of Orthopaedic Surgery; University of Kentucky, Lexington, KY. Shoulder: Posterior Instability

Spero G. Karas MD Assistant Professor of Orthopaedic Surgery, Emory University School of Medicine, Atlanta, GA. Shoulder: Multidirectional Instability

Terry Malone PT, EdD, ATC Professor of Physical Therapy, University of Kentucky, Lexington, KY. Knee Rehabilitation

James Kercher MD Department of Orthopaedics, Emory University School of Medicine, Atlanta, GA. The Female Athlete

Todd C. Malvey DO, CAQSM Physician, Moncrief Army Community Hospital, Fort Jackson, SC. On-Field Emergencies and Preparedness

John J. Klimkiewicz MD Assistant Professor, Department of Orthopedic Surgery, Georgetown University Hospital– MEDSTAR Health; Head Team Physician, Georgetown Hoyas, Washington, DC. Knee: Overuse Injuries

Bert R. Mandelbaum MD Santa Monica Orthopaedic Surgery and Sports Medicine Group, Orange, CA. Abdomen and Pelvis

Jennifer A. Graham MD Resident, Harvard Combined Orthopaedic Surgery Program, Boston, MA. Wrist Soft-Tissue Injuries Letha Y. Griffin MD, PhD Team Physician, Adjunct Professor, Department of Kinesiology and Health, Georgia State University; Partner, Peachtree Orthopaedic Clinic, Atlanta, GA. The Female Athlete Kevin M. Guskiewicz PhD, ATC Professor and Chair, Department of Exercise and Sport Science; Professor, Department of Orthopaedics, University of North Carolina, Chapel Hill, NC. Head Injuries Jeffrey A. Guy MD Assistant Professor, Director, Sports Medicine Center, Medical Director, University of South Carolina; Orthopedic Surgeon, Palmetto Health Richland, Columbia, SC. Shoulder: Overuse Injuries Christopher D. Harner MD Blue Cross of Western Pennsylvania Professor, University of Pittsburgh; Medical Director, UPMC Center for Sports Medicine, Pittsburgh, PA. Safety Issues for Musculoskeletal Allografts; The Stiff Knee Richard J. Hawkins MD Attending Physician, Steadman-Hawkins Clinic of the Carolinas, Spartanburg, SC. Shoulder: Physical Examination and Evaluation Robert Hosey MD Associate Professor, Department of Family Medicine and Orthopaedics, Director, Primary Care Sports Medicine Fellowship, University of Kentucky, Lexington, KY. The Preparticipation Physical Examination Joel Hurt MD Orthopedic Surgeon, Texas Bone and Joint Sports Medicine Institute, Austin, TX. Ankle and Foot: Physical Examination and Evaluation Peter Indelicato MD Professor, Shands Healthcare, University of Florida, Gainesville, FL. Knee: Medial Collateral Ligament William M. Isbell MD Raleigh Orthopaedic Clinic, Raleigh, NC. Elbow: Tendon Ruptures Darren L. Johnson MD Professor and Chair, Department of Orthopaedic Surgery; Director of Sports Medicine, University of Kentucky School of Medicine, Lexington, KY. Multiligament Knee Injuries Grant L. Jones MD Assistant Professor, Department of Orthopaedic Surgery, Ohio State University College of Medicine; Vice Chair, Department of Orthopaedics, Ohio State University Medical Center, Main Campus; Ohio State University Hospital East, Columbus, OH. Elbow: Physical Examination and Evaluation

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Mininder Kocher MD, MPH Assistant Professor, Department of Orthopaedic Surgery, Harvard Medical School; Associate Director, Division of Sports Medicine, Children’s Hospital, Boston, MA. The Pediatric Athlete Sumant G. Krishnan MD Clinical Assistant Professor, Department of Orthopaedic Surgery, University of Texas Southwestern; Attending Orthopedic Surgeon, Shoulder and Elbow Service, The Carrell Clinic, Dallas, TX. Shoulder: Physical Examination and Evaluation John E. Kuhn MS, MD Associate Professor, Department of Orthopaedics and Rehabilitation, Vanderbilt University Medical School; Chief of Shoulder Surgery, Team Physician, Vanderbilt University and Nashville Sounds Baseball Club, Vanderbilt Sports Medicine, Nashville, TN. Scapulothoracic Disorders Laurence Laudicina MD Orthopaedic Surgeon, Steadmans-Hawkins Fellow, Florida Sports Medicine Institute, St. Augustine, FL. Elbow: Overuse Injuries, Tendinosis, and Nerve Compression Steven J. Lawrence MD Head, Foot and Ankle Section, University of Kentucky; Associate Professor of Orthopedics, A.B. Chandler Medical Center, University of Kentucky, Lexington, KY. Midfoot and Hindfoot Jeffrey N. Lawton MD Hand and Upper Extremity Surgeon, Department of Orthopaedic Surgery, Cleveland Clinic Foundation, Cleveland, OH. Carpal Fractures Paul Lewis MS Rush University Medical Center, Chicago, IL. Knee: Articular Cartilage Robert Litchfield MD, FRCS(C) Associate Professor, Department of Surgery, Fowler Kennedy Sports Medicine Center, University of Western Ontario, London, Ontario, Canada. Knee: Arthritis in the Athlete Daniel S. Lorenz PT, ATC, CSCS Department of Sports Medicine, Duke University, Durham, NC. Knee: Posterolateral Corner

Steven D. Maschke MD Department of Orthopaedic Surgery, Cleveland Clinic Foundation, Cleveland, OH. Carpal Fractures Elizabeth G. Matzkin MD Foundry Sports Medicine, Providence, RI. Clavicle Fractures and Sternoclavicular Injuries Craig S. Mauro MD Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Safety Issues for Musculoskeletal Allografts; The Stiff Knee David Mayman MD Department of Orthopedic Surgery, Hospital for Special Surgery, New York, NY. Shoulder: Nerve Injuries L. Pearce McCarty III MD Sports and Orthopaedic Specialists, P.A., Edina, MN. Complex Issues in Anterior Cruciate Ligament Reconstruction Ryan C. Meis MD Center for Neurosciences, Orthopaedics, and Spine, Dakota Dunes, SD. Internal Impingement William C. Meyers MD Professor and Chairman, Department of Surgery; Senior Associate Dean for Clinical Affairs, Drexel University College of Medicine, Philadelphia, PA. Abdomen and Pelvis Mark D. Miller MD Professor of Orthopedic Surgery, Head of Division of Sports Medicine, University of Virginia, Charlottesville; Team Physician, James Madison University, Harrisonburg, VA. Posterior Cruciate Ligament Peter J. Millet MD Steadman-Hawkins Clinic, Vail, CO. Shoulder: Nerve Injuries Amir R. Moinfar MD Chesapeake Orthopedics, Glen Burnie, MD. Knee: Posterolateral Corner Claude T. Moorman III MD Associate Professor, Department of Orthopaedic Surgery; Director, Sports Medicine, Duke Medical Center; Head Team Physician, Duke Athletics; Durham, NC. The Role of the Team Physician; Knee: Posterolateral Corner

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Contributors

Steve A. Mora MD Active Staff, Orthopedic Department, St. Joseph Hospital, Orange, CA. Abdomen and Pelvis Kevin J. Mulhall MB, MCh, FRCSI Consultant Orthopaedic Surgeon, Department of Orthopaedic Surgery, Dublin, Ireland. Posterior Cruciate Ligament Gregory Nicholson MD Department of Orthopedics, Division of Shoulder and Sports Medicine, Rush University, Chicago, IL. Rotator Cuff Disorders Thomas Noonan MD Partner, Steadman-Hawkins Clinic–Denver, Greenwood Village; Medical Director, Colorado Rockies Baseball Club, Denver, CO. Elbow: Overuse Injuries, Tendinosis, and Nerve Compression James Nunley MD J. Leonard Goldner Professor of Surgery; Chief of Orthopedics, Duke University Medical Center, Durham, NC. Ankle Tendon Disorders and Ruptures John Nyland EdD, PT, SCS, ATC, CSCS, FACSM Assistant Professor, Department of Orthopaedic Sugery, Division of Sports Medicine, University of Louisville; Consultant, Sports Health Program, Norton Hospital, Louisville, KY. Foot and Ankle Rehabilitation Adam C. Olsen MPT, ATC Rehabilitation Coordinator, St. Louis Cardinals, St. Louis, MO. Principles of Rehabilitation George A. Paletta, Jr. MD Orthopedic Center of St. Louis, St. Louis, MO. Pediatric Elbow Kyle Parish MD Assistant Professor, Departments of Family and Community Medicine and Sports Medicine, University of Kentucky, Lexington, KY. Environmental Stressors Andrew D. Pearle MD Instructor of Orthopedic Surgery, Cornell University New York Hospital; Assistant Attending Orthopedic Surgeon, Hospital for Special Surgery, New York, NY. Knee: Graft Choices in Ligament Surgery George C. Phillips MD Clinical Assistant Professor of Pediatrics, Children’s Hospital of Iowa, University of Iowa Carver College of Medicine, Iowa City, IA. Medications, Supplements, and Ergogenic Drugs James C. Puffer MD Professor, Department of Family and Community Medicine, University of Kentucky School of Medicine; President and Chief Executive Office, American Board of Family Medicine, Lexington, KY. Cardiac Problems and Sudden Death

Arthur C. Rettig MD Clinical Instructor, Orthopedic Surgery, Wishard Memorial Hospital; Clinical Assistant Professor, Orthopedic Surgery, Indiana University Medical Center; Adjunct Professor, Butler University, Indianapolis; Adjunct Professor, Purdue University, West Lafayette; Orthopedic Surgeon and Partner, Methodist Sports Medicine Center, Indianapolis, IN. Hand Injuries

Dale S. Snead MD Partner, Methodist Sports Medicine Center, Indianapolis, IN. Hand Injuries

Lance A. Rettig MD Volunteer Clinical Assistant Professor of Orthopedics, Indiana University; Staff Orthopedic Surgeon, Methodist Sports Medicine Center, Indianapolis, IN. Hand Injuries

Tracy Spigelman Med, ATC Doctoral Student and Graduate Assistant, University of Kentucky, Lexington, KY. Shoulder Rehabilitation

John C. Richmond MD Professor, Orthopedic Surgery, Tufts University School of Medicine; Chair, Department of Orthopaedic Surgery, New England Baptist Hospital, Boston, MA. Meniscal Injury Jeffrey A. Rihn MD Resident Physician, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Safety Issues for Musculoskeletal Allografts Craig S. Roberts MD Professor, Residency Program Director, Department of Orthopaedic Surgery, School of Medicine, University of Louisville, Louisville, KY. Pediatric Knee Richard Rodenberg MD Assistant Professor, Department of Family Medicine, Program Director, Sports Medicine Fellowship, Grant Medical Center, Columbus, OH; Assistant Professor, Department of Family Medicine, Lexington, KY. Environmental Stressors Mark W. Rodosky MD Center for Sports Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA. Biceps Tendon Disorders Anthony R. Romeo MD Department of Orthopedics, Division of Shoulder and Sports Medicine, Rush University, Chicago, IL. Rotator Cuff Disorders Greg Sassmannshausen MD Clinical Faculty, Fort Wayne Medical Education Program Fort Wayne, IN. The Older Athlete Anthony Schepsis MD Professor, Department of Orthopaedic Surgery; Director, Department of Sports Medicine, Boston University Medical Center, Boston, MA. Patellofemoral Instability

Jeffrey T. Spang MD Chief Resident, Department of Orthopaedics, University of North Carolina, Chapel Hill, NC. Shoulder: Multidirectional Instability

J. Richard Steadman MD Steadman-Hawkins Clinic; Steadman-Hawkins Research Foundation, Vail, CO. Psychological Aspects of Healing the Injured Athlete William I. Sterett MD Steadman-Hawkins Clinic; Steadman-Hawkins Research Foundation, Vail, CO. Ankle Intra-articular Injury Steven J. Svoboda MD Orthopedic Surgery Service, Brooke Army Medical Center, Fort Sam Houston, TX. Muscle Injuries Dean C. Taylor MD Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, MN. Muscle Injuries John M. Tokish MD, USAF MC Head Team Physician, U.S. Airforce Academy, Colorado Springs, CO. Physical Examination and Evaluation Rachael Tucker MBChB, BHB Research Assistant, Clinical Effectiveness Unit, Children’s Hospital, Boston, MA. The Pediatric Athlete Tim Uhl PhD, ATC, PTC Associate Professor, Department of Rehabilitation Sciences, Division of Athletic Training; Director of Musculoskeletal Laboratory, University of Kentucky, Lexington, KY. Shoulder Rehabilitation William P. Urban MD Clinical Associate Professor; Chair, Orthopaedics and Rehabilitation, SUNY Downstate Medical Center, Brooklyn, NY. Principles of Knee Arthroscopy Armando F. Vidal MD Blue Sky Orthopedics and Sports Medicine, Brighton, CO. Anterior Cruciate Ligament K. Mathew Warnock MD Fondren Orthopedic Group; Texas Orthopedic Hospital, Houston, TX. Pediatric Shoulder

Theodore F. Schlegel MD Assistant Professor, Department of Orthopedic Surgery, University of Colorado–Denver; Team Physician, Denver Broncos and Colorado Rockies; Consultant, Steadman-Hawkins Clinic–Denver, Denver CO. Disorders of the Acromioclavicular Joint

Robert G. Watkins MD Professor of Clinical Orthopaedic Surgery, University of Southern California; Orthopaedic Surgeon; Los Angeles Spine Surgery Institute at St. Vincent Medical Center, Los Angeles, CA. Lumbar Spine

Fred Reifsteck MD Clinical Assistant Professor, Medical College of Georgia, Augusta; Head Team Physician, University of Georgia, Athens, GA. The Female Athlete

Jeffrey B. Selby MD University of Kentucky; VA Medical Center, Lexington, KY. Ankle Fractures and Syndesmosis Injuries

Daniel E. Weiland MD Orthopaedic and Sports Medicine Center, Trumball, CT. Biceps Tendon Disorders

Michael M. Reinold PT, DPT Adjunct Faculty, Department of Physical Therapy, Northeastern University; Assistant Athletic Trainer, Boston Red Sox, Boston, MA. Principles of Rehabilitation

Patrick Siparsky BS University of Colorado Health Sciences Center, Denver, CO. Disorders of the Acromioclavicular Joint; The Pediatric Athlete

Kevin E. Wilk PT, DPT Clinical Director, Champion Sports Medicine and Rehabilitation Center; Vice President of Education, Benchmark Medical, Birmingham, AL. Principles of Rehabilitation

Matthew Alan Rappé MD Resident Physician, University of Florida, Gainesville, FL. Knee: Medial Collateral Ligament

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Contributors

Jeffrey D. Willers MD Staff, Orthopaedic Surgery, Baptist Hospital and St. Thomas Hospital, Nashville, TN. Ankle Ligament Injury and Instability Riley J. Williams III MD Associate Professor, Weill Cornell Medical College; Attending Orthopaedic Surgeon, Hospital for Special Surgery, New York, NY. Traumatic Shoulder Muscle Ruptures

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Sharrona Williams MD Southern Orthopaedic Specialists, Atlanta, GA. Ankle Tendon Disorders and Ruptures Timothy C. Wilson MD Central Kentucky Orthopaedics, Georgetown, KY. Knee: Physical Examination and Evaluation

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Preface “It’s what you learn after you know it all that counts.”— John Wooden Sports medicine is an ever-expanding and changing field, but the primary goal remains the same as it was decades ago— to allow the injured athlete to return safely to participation and perform to the best of his or her ability. Clinical Sports Medicine presents, in a concise manner, the latest techniques for achieving this goal. Emphasis is placed on summary boxes, illustrations, and algorithms in order to provide an easy reference to commonly seen medical problems and injuries. All chapters are written with the treatment of the athlete in mind. The resultant text is a useful reference to all members of the sports medicine team—trainers, therapists, physicians, and even coaches and parents. The authors were selected based on their specific areas of expertise, and were asked to cover essential material and pearls based on their personal experience. The first 15 chapters cover general principles and medical issues. The remainder of the book is divided by anatomic areas. Emphasis is placed on physical examination and evaluation of the injured athlete because the key to proper treatment almost always starts with an accurate diagnosis. Also emphasized is appropriate rehabilitation, with five chapters devoted solely to this topic, and further mention made in each chapter addressing specific types of injuries. Surgery is addressed, not with the

goal of presenting step-by-step instructions, but rather the rationale for surgical intervention, general principles, and tips based on experiences, good and bad. Athletes seem to be getting both younger and older at the same time. As children strive to become the next Michael Jordan or Mia Hamm, the number of pediatric injuries (particularly those related to overuse) has risen dramatically. Four chapters are devoted to prevention and treatment of pediatric injuries. On the other end of the spectrum, “weekend warriors” participate into their retirement years, and chapters addressing the older athlete and arthritis in the athlete are included. Chapters are organized for easy reference. Each starts with a section titled “In This Chapter” to emphasize what is covered. This is followed by an introductory summary box of the most important concepts. The general outline follows with clinical features and evaluation, relevant anatomy, treatment options, surgery, rehabilitation, criteria for return to sports, results and outcomes, and potential complications. We hope that the text is an easy-to-read reference that helps those who treat athletes to achieve the preceding goals. We wish to thank all of the authors for all of their work in organizing the material in a concise and interesting format. Scott D. Mair Darren L. Johnson

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Foreword It has been several years since a comprehensive book on the medical aspects of clinical sports medicine has been published. In the early 1990s, books by The Hughston Clinic, Drs. Fu and Stone, and Drs. Drez and DeLee made important contributions to the sports medicine literature. Since that time, the sports medicine subspecialty has come a long way. The American Board of Orthopaedic Surgery has recognized sports medicine as a clinical subspecialty. A test leading to a certificate of subspecialization in sports medicine is presently being written and will be offered in 2007. Indeed, we have come a long way from the old concept of “orthopaedics for people with numbers.” Clinical Sports Medicine is an excellent representation of where sports medicine is in the early 21st century. Chapters dealing with the role of the team physician; preparticipation physicals; on-field emergencies and preparedness; as well as specialized chapters on the pediatric, female, and older athlete, ensure full coverage of the ever-widening spectrum of sports medicine. There is even a chapter on the psychology of the injured athlete that deals with how injury affects the athlete’s well-being.

The remainder of the book is broken down into sections dealing with various anatomic regions. Each chapter is written by an expert in the field, often with assistance from their younger partners. Each chapter has a well-identified introduction. Tables throughout the book are easily readable and are quite helpful as short, quick studies for the chapter. The authors are orthopaedic surgeons, family physicians, internists, physical therapists, and athletic trainers. Their combined experience is overwhelming, and their writing style is very compatible. Sports medicine has a separate specialized core curriculum, and this book encompasses the aspects of that curriculum. It should be included in the library of all residency and fellowship programs and should be valued as a reference for practicing orthopaedists regardless of their training level or expertise. Drs. Johnson and Mair should be commended for their success in gathering together so many well-respected physicians to share their knowledge in this exciting book on sports medicine. Congratulations to you both. Champ L. Baker, Jr., MD

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CHAPTER

1

The Role of the Team Physician Claude T. Moorman III and Frank H. Bassett III

In This Chapter Responsibilities of the team physician Preparticipation clearance In-season coverage Game coverage

INTRODUCTION • The defining role for physicians in sports medicine is to serve as team physician. • The role of the physician in a sports medicine environment may at times require responsibility for the surgical, medical, emotional, and even spiritual well-being of the athlete. • Specific responsibilities for the team physician can be broken down into roles that evolve over the course of the athlete’s season. At different times in the year, the physician will be responsible for preparticipation clearance, practice and game injury evaluation, treatment of practice and game injuries, coordination and implementation of postseason medical and surgical treatment, and the continuing education of both himor herself and the rest of the health care team.

RESPONSIBILITIES OF THE TEAM PHYSICIAN The responsibilities facing the team physician are considerable, and all of them have ethical and legal ramifications. This creates some potential conflicts that need to be resolved in order to care safely and effectively for the athlete. The intention of this chapter is to outline the specific roles and responsibilities of the team physician. We also discuss potential sociopolitical conflicts and strategies for managing these conflicts.1 Several of the great team physicians of the past generation are featured in an attempt to further understand the role of the team physician and the many subtleties that exemplify a successful sports medicine team.

Preparticipation Clearance The team physician is responsible for the overall process through which athletes are cleared to play. This requires coordination of the various subspecialists who often assist in these evaluations as well as determining the setting and facility requirements to implement this important portion of the athlete’s evaluation (Box 1-1).2 At different levels of participation, the requirements vary, as does the sophistication of the testing measures instituted. In the high school environment, the evaluations are often carried out in the school gymnasium, usually with a relatively

minimal number of subspecialty providers available. The various different governing bodies in sports medicine, including the American Orthopaedic Society for Sports Medicine (AOSSM), the American Academy of Family Physicians, the American Academy of Pediatrics, the American College of Sports Medicine, the American Medical Society for Sports Medicine, and the American Osteopathic Academy of Sports Medicine have come together with a consensus document for what is required for preparticipation physical examinations (John Bergfeld, personal communication, 1996). At the collegiate and professional levels, oftentimes more sophisticated measures and a more comprehensive array of consulting physicians are available to assist with the screening. In many scenarios, electrocardiograms and echocardiograms are a common part of the screening. The goal is to rule out conditions such as hypertrophic cardiomyopathy, which may predispose the participating athlete to significant risk or even death. The team physician’s responsibility to the athlete generally begins with this preparticipation clearance. (Please see Chapter 2 for additional detail.)

In-Season Coverage During the athlete’s season, the physician’s role varies considerably depending on the sport and the setting. The majority of team physicians are involved, at some point in time, in coverage of contact sports, particularly football. The majority of the following discussion centers on football with the realization that lower risk sports will generally require less frequent on-site presence of the team physician. In the majority of situations, the physicians are involved in game coverage with a more limited role in the practice setting. At our institution, the standard has been to cover both home and away games, with training room presence of the attending team physician at the heavy contact practice during the week as well. In the collegiate environment, Tuesday practice tends to be the heaviest contact day, and this is the day that we have selected as the most important for physician presence. In our setting, this translates into the physician arriving toward the end of the practice setting with involvement in running a clinic in the training room following that practice. We have found this to be the highest yield in terms of determining the significant injuries that require physician attention. It is also important to make a distinction between a true team physician and the “office arthroscopist.”3 With the increasing financial pressures in the health care market today, there is increasing pressure for the team physician to play a decreasing role in the true environment of the athlete. This represents a substantive threat to the team physician’s persona as it has been reflected through the ages. Now more than ever before, the team physician needs to recognize work in the training room as

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Section 1 Overview

Box 1-1 Preparticipation Clearance • Requires coordination of various subspecialists • Sophistication may vary with level of participation • Consensus document of various societies outlines requirements

a true “labor of love” as there is seldom any opportunity to financially benefit from this activity. There is clearly a large distinction between the physicians who are willing to make the sacrifices to become an integral part of the athletic environment and those who simply manage an office practice with a very limited on-site role for the athlete. This distinction, while obvious, has important ramifications for the quality of care that we deliver to the athlete. There is no question that a physician who is familiar with the athlete and his or her environment and who takes the time to get to know the players, managers, trainers, and administrators involved in the milieu that makes up the athlete’s world, will be a much more effective physician when called on to manage injury and illness. The physicians highlighted in the next section have all demonstrated an excellent understanding of this concept. There is no way that the labor of love that is required to be effective in this role can ever be justified on a financial basis. Few physicians even at the professional level are financially rewarded for their role.

Game Coverage The team physician needs to be present on the game day for contact sports such as football. There are several different logistical arrangements, depending on the level (Box 1-2). At our institution, the team physician arrives 90 minutes prior to the posted kick-off time. Final evaluations are made at this time and any concerns addressed. Under some circumstances, it may be appropriate for athletes with soft-tissue injuries to receive intramuscular ketorolac (Toradol) injections 1 hour prior to the kickoff, which may help to minimize their pain. Additionally, it is occasionally appropriate to consider a local anesthetic injection for a limited number of conditions. In our practice, it has been safe and effective to consider Marcaine injections for grade 1 acromiodavicular (AC) separations, hip pointers, and bruised ribs. These are the only three conditions for which pregame local anesthetics are considered to be both safe and effective. We do discourage the use of local anesthetics for any joint, muscular, and/or bony lesion that does not fall into these three categories. While the skill and expertise of the individual physician may allow for additional indications, this intervention must be very carefully balanced with risks and carefully agreed to by the athlete with full informed consent. Few areas of the physicianathlete relationship generate more controversy or concern on the part of the general public. It is important for the physician to understand the subtleties of game flow to position him- or herself effectively on the sideline. In most scenarios, this requires the physician to be on the sideline on the end of the field in which the ball is in play. This Box 1-2 Game Coverage • • • •

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Pregame injections considered only for certain conditions Trainers make initial on-field evaluations Detailed evaluation done on the sideline Postgame checks in the training room

will allow ready access to injured players while staying out of the way of the coaches and players as they orchestrate the game. Each staff member must determine the appropriateness of the initial on-field evaluations. At our institution, the trainers make the initial evaluations; they call for the physician, should this be necessary. In the majority of cases, the trainers evaluate the players on the field and escort them off without the physician needing to be involved directly until the player reaches the sideline. We do have an examination table set up on the sideline for evaluations. In most scenarios, it is best to get the player off of the field as soon as it is safely possible following an injury and to do the more detailed evaluations on the sideline. This allows the game to continue and minimizes the crowd’s focus on management of the athlete’s injury. Obviously, when a player has a significant cervical spine or head injury, this scenario is considerably different (see Chapter 15 on cervical spine injury). For injuries that may represent fracture or significant joint injury, radiographs are oftentimes appropriate. It is important to have a scenario whereby imaging studies can be obtained when necessary. At our institution, we have a radiology technician on the sideline and imaging apparatus within 100 yards of the playing field. Many institutions and stadiums have portable fluoroscopy machines available that may serve the same purpose. Additional personnel who can be quite helpful are a paramedic or emergency medical team with medical evacuation equipment if transfer of the athlete is necessary. Some health care teams have anesthesiologists and neurosurgeons available depending on the sport and the setting. Postgame evaluations are done in the training room with careful attention to any injuries that may require further evaluation. A true team approach with trainers, primary care team physicians, and orthopaedic surgeons is helpful to provide a comprehensive approach to the myriad of injuries from muscle strains to concussions that are seen in contact athletics. Neuropsychological testing is used at our institution for mild traumatic brain injuries; the testing is performed following the game with comparison to baseline testing performed during the preparticipation examinations. An injury clinic is commonly held on the day following the game. This allows further identification of potential and real injury problems that may not have been obvious to the athlete or physician on the day of the game. It has also been our experience that following a victory, many of the athletes who actually have seemingly smaller injuries do not report for postgame evaluation and are better assessed on the day following the game. This provides a less harried environment after the excitement of the game has passed to get a true handle on the extent of injuries and to provide a plan for timely imaging and other treatments. This training room clinic generally sets the tone for the week to come and prepares the coaches and players for the availability or lack thereof of key players.

LIABILITY Team physicians have come under increasing scrutiny in recent years, an extension of what has become commonplace in the medicolegal environment in the rest of medicine. As recently as 2003, there were 18 active lawsuits against National Football League team physicians. This is reflective of the general attitude in society of persons seeking financial compensation through the legal system in the case of injury. In many environments, it is common for professional athletes who have not been able to fit into the plans of the various franchises to seek remu-

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neration through the medicolegal pathway. This creates additional strain on the doctor-patient relationship for team physicians and exposes the team physicians to significant financial risk. While there is no way to eliminate this concern completely, there are some steps that can be taken to attempt to minimize the risk. First, the physician needs to maintain the tradition of honor, service, integrity, and dedication required in our role of protecting the well-being of the athlete. Second, the team physician should maintain a very active pursuit of continuing medical education to stay up with modern techniques and treatment options so that the athletes receive the very best care possible. Third, it is imperative that the team physician be a true on-site provider with good relationships with the coaches, trainers, and players rather than serving in a remote setting as an “office arthroscopist.” Fourth, it is important for the team physician to understand his or her options in relation to his or her role in a professional sports setting. Oftentimes, the physician can be indemnified as a member of the organization and, therefore, at decreased risk. Another option is to consider additional riders on malpractice policies to cover the potentially exorbitant awards that may be made in the setting of a perceived medicolegal injury. Fifth, it is imperative to review very carefully the service contract as it relates to high school and collegiate relationships. It is not uncommon for some institutional malpractice coverage to contain exclusions for community service. The unsuspecting team physician may be caught in a bind if these matters are not carefully analyzed ahead of time. While these measures will not prevent exposure from an egregious plaintiff ’s bar, they may well head off many of the problems that increase liability exposure.

REPRESENTATIVE TEAM PHYSICIANS While it is possible to summarize the tasks that a team physician carries out, simple descriptions cannot adequately portray the passion involved in truly caring for athletes. With this in mind, a summary of the careers of five pioneers in the field of sports medicine provide the best definition of what it means to be a team physician.

Dr. Jack Hughston The recent passing of Dr. Jack Hughston has been difficult for many of us who believe that he was the consummate team physician. Dr. Hughston, a brilliant man with many attributes that placed him way ahead of his time, is often considered to be the “father of sports medicine.”4 He started the Hughston Clinic, P.C., in Columbus, GA, more than 50 years ago as a site not only for elite athletes but also for the “young boy or girl playing school or neighborhood sports, the weekend golf or tennis player, and the employee in the work place or industrial setting.”5 Dr. Hughston received his undergraduate education at Auburn University and did his orthopaedic residency at Duke University. Dr. Hughston was active in the care of recreational, high school, collegiate, and professional athletes. He seldom missed a game of his beloved Auburn Tigers (Fig. 1-1). He emphasized the truly multidisciplinary team approach among health care professionals including physicians, physical therapists, athletic trainers, and administrators and insisted that each work toward the common goal of serving the athlete.5 Dr. Hughston was also an innovator in the field of education and started one of the first sports medicine fellowship programs in 1970 to train orthopedic residents in the subtleties of sports

Figure 1-1 Dr. Jack Hughston as many of us remember him—in his role as a dedicated team physician for the Auburn Tigers.

medicine, preparing them for service at the highest level. He was a founding member of the AOSSM in the early 1970s and also served a term as society president. He founded the American Journal of Sports Medicine, which he edited until 1990. Many of us consider the American Journal of Sports Medicine to be his most important contribution, because the Journal serves today as the most important vehicle for disseminating new information in the field. For his many accomplishments, he was named Mr. Sports Medicine by the AOSSM and inducted into its Hall of Fame. He has also received the distinguished Southern Orthopaedist Award and many other honors too numerous to mention (see Fig. 1-1).

Dr. John Bergfeld Dr. Bergfeld distinguished himself on the playing fields and developed his love of sports medicine while an offensive lineman at Bucknell University. He did his internship and residency at the Cleveland Clinic Foundation and subsequently served as the team physician at the Naval Academy where he honed his skills along with another well-known sports medicine team physician, Dr. Bill Clancy. He subsequently served for more than 25 years as the Cleveland Browns team physician (Fig. 1-2) and was very active in helping set up the medical staff for the Baltimore Ravens during the mid-1990s. He has been one of the top mentors for young orthopedists in the history of the AOSSM. For these efforts and general excellence in the field of sports medicine education, he received the George D. Rovere Award in 1996. His fellowship group, The Warthog Society, is perhaps the most active alumni group of any of the fellowship programs in North America. Dr. Bergfeld, known to many of us as “Bergie,” is a beloved figure as an educator, researcher, and team physician. He has had a particular interest in the posterior cruciate ligament and has been responsible for the popularity of the inlay technique and for better understanding which injuries may be managed nonoperatively. Perhaps his greatest contribution has been the integration of the primary care sports medicine team physicians into the active care of the athletes. He has worked hard to break down the sociopolitical barriers and “turf ” concerns that had impeded this progress previously. His only concern has been that the athlete is cared for and is the focus of a truly multidisciplinary approach. His many colorful aphorisms have been widely quoted throughout his alumni group and

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A

B Figure 1-2 A and B, Dr. John Bergfeld served as the head team physician for the Cleveland Browns for more than 25 years.

those of us who have been directly and indirectly influenced by him. His insistence that you “do what you do best” has been a mantra for young physicians confused over particular techniques of management. For many years, Dr. Bergfeld has also been an innovator in running the safety committee of the National Football League Team Physician Society. He has been a trusted confidant of both management council and the National Football League Players Association in traversing very difficult sociopolitical issues related to the care of the professional athlete. He has been responsible for distributing millions of dollars of grant funding for National Football League charities and has never lost sight of the big picture as it relates to integrity and dedication in the care of the athlete at every level (see Fig. 1-2).

Dr. James Andrews Dr. Andrews is perhaps the best known of all the sports medicine team physicians in our era. Dr. Andrews graduated from Louisiana State University in 1963 where he was a southeastern conference indoor and outdoor pole vault champion. He did his orthopedic residency at Tulane Medical School and had sports medicine fellowships at the University of Virginia and at the University of Lyon, France. He joined the staff at the Hughston Clinic where he served for many years prior to starting the

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Figure 1-3 Dr. James Andrews is perhaps best known for his care of professional athletes in many sports. He also has a love for participation in collegiate and high school sports as well. Here he is seen attending to a local high school athlete in Birmingham.

Alabama Sports Medicine and Orthopaedic Center in Birmingham in 1986. He has been involved in the care of athletes at all levels from high schools in the Birmingham area (Fig. 1-3) and management of Division I-AA programs such as Troy State, to Auburn, AL, and many of the professional teams, including the Washington Redskins. Dr. Andrews has also been a tremendous gentleman in terms of helping young physicians to become successful in their practice. He developed one of the top fellowship programs in the world, and many of his fellows have become high-level team physicians, many with careers in academic sports medicine. He has also been a true favorite among the agents caring for the athletes due to his tremendous technical skills and capability in managing the sociopolitical aspects and his considerable attention to detail. In spite of his schedule, which is tremendously busy, he has also maintained a role as an excellent communicator and facilitator of information in consultation with other physicians in the care of their athletes. Dr. Andrews’s specific contributions are many, and he has been a leader in both the AOSSM and the Arthroscopy Association of North America, having served on the board of directors of both societies. He is known for his marked technical proficiency and has built one of the most impressive surgical setups in the world at the American Sports Medicine Institute. He is also known for his colorful aphorisms and his insistence that the team physician be careful to avoid being the one to make the “big statement.” He is referring to the tendency for some of us to state that the athlete will “never play again” or that he will be ready to play by a “certain date” or other ways in which we box ourselves in with statements that may come back to haunt us and perhaps to have a negative impact on the athlete’s situation. His wisdom and mentorship are evidenced by the fact that his fellowship has trained the largest number of fellows of any of the major programs over the past decade (see Fig. 1-3).

Dr. Russell F. Warren Many consider Dr. Russell F. Warren to be the epitome of the physician/scientist. Few if any physicians have achieved the same balance of scientific innovation and true clinical excellence

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as Dr. Warren. Dr. Warren was a standout running back at Columbia in the early 1960s. He had a tryout and made it to the last cut with the New York Giants as a professional player. He subsequently did his orthopedic training at the Hospital for Special Surgery and initially went into private practice in Lynchburg, VA, for 4 years before going back to do a shoulder fellowship at Columbia. He subsequently joined the staff at the Hospital for Special Surgery where he served as surgeon-in-chief until July 2004. He has served as the head team physician for the New York Giants since 1984 (Fig. 1-4). Dr. Warren is perhaps the most decorated academic surgeon in history having won the O’Donoghue Award for the outstanding clinical contribution to the AOSSM three times and also having won the Neer Award three times for making the most outstanding contribution in shoulder surgery. He was named Mr. Sports Medicine by the AOSSM in 2003 and has a list of scientific publications that is perhaps unsurpassed in the history of academic sports medicine. Dr. Warren is known to have a completely open mind and is willing to learn from anyone around him. This is in contrast to the majority of us who, over the ages, become narrower in our focus and less willing to learn from others. His fellowship training program has been very heavy in basic science, and he has led the field in innovations regarding cellular level research. Dr. Warren has also been very altruistic in the use of funding as it comes from his innovations. In many instances, he has directed the royalties from product innovations in the laboratory to support general orthopedic sports medicine research. This research has not only led to many innovations but has also had a substantive impact on education of the next generation of leaders in the field of orthopedic sports medicine. Dr. Warren’s fellowship alumni group occupies more team physician positions at the professional level than any other institution. He has also been a tremendous innovator in operative technique and has helped to create many of the techniques and approaches that we use in both shoulder and knee surgery today. He has further created an environment at the Hospital for Special Surgery where fellowship training can and does involve active basic science research with a rigorous clinic exposure. He has created a fellowship program that has provided many of the innovators who represent our generation’s best physicians.

Figure 1-4 Dr. Russell F. Warren on the sidelines with author Dr. C. T. Moorman III prior to the Giants-Ravens game in the Super Bowl XXXV. Dr. Warren has been the Giants team physician for more than 20 years.

In spite of his capabilities in the laboratory and in the operating room, he is perhaps best known for his familiarity on the sideline and in the training rooms with the New York Giants. During my (CTM III) fellowship with Dr. Warren, his happiest moments were on the Wednesday afternoons when we were headed out to the Giants training room at the Meadowlands or on the sidelines at Giants games on Sundays. His relationship with Ronnie Barnes, the head athletic trainer for the New York Giants, has been legendary and a model for those of us who aspire to develop a quality interdisciplinary sports medicine team (see Fig. 1-4).

Dr. Frank H. Bassett III To those of us who trained in the Duke program, the ultimate example of the team physician has always been Dr. Frank H. Bassett III. Dr. Bassett played for Coach Paul “Bear” Bryant at the University of Kentucky before being drafted into the military and serving in the Korean conflict. He was the first infantry soldier to try out the new body armor and this ultimately saved his life when he was shot but sustained only bruises rather than a through and through gunshot wound that would have occurred without the protective body armor. He was awarded the Purple Heart for this incident. He subsequently did his training at Duke under Lenox Baker and became the head team physician at Duke University in 1966. Dr. Bassett cared for the athletic teams at Duke for over 30 years and was the epitome of the true team physician (Fig. 1-5). In his honor, the Bassett Society has been created to provide scholarship support for Duke lettermen who enter medical and dental school. In addition to his role as a professor in orthopedics, he was also a faculty member in the Department of Anatomy. Many of his research papers focused on identification of new structures and a further delineation of the pathoanatomy of orthopedic entities. Dr. Bassett has also served as a mentor for many physicians who have pursued careers in sports medicine. He has been the “godfather” for the AOSSM Traveling Fellowship and has received many research honors including the O’Donoghue Award. He has been president of the AOSSM and has been

Figure 1-5 Dr. Frank H. Bassett III (right center [with hat]), in his familiar surroundings on the sidelines of a Duke football game. He is standing by Dr. William E. Garrett, Jr., at the time a Duke orthopedic resident. Dr. Garrett is immediate past president of the American Orthopaedic Society for Sports Medicine and has a career in the care of collegiate, Olympic, and professional soccer athletes.

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honored as Mr. Sports Medicine and also named to the AOSSM Hall of Fame. Dr. Bassett’s greatest contributions have been in caring for the athletes and mentoring the next generation of sports medicine physicians. He has been particularly innovative in furthering the art of sideline and training room management of the athlete. His love for Duke University has more recently placed him in a position to successfully build endowment support for the athletic department and a considerable upgrade to the facilities. He has been one of the favorites among the coaches to assist in recruiting athletes, particularly those interested in a career in medicine (see Fig. 1-5).

FUTURE OF THE TEAM PHYSICIAN’S ROLE In spite of the many challenges, particularly involving financial and liability pressures, we do believe that the future is bright for the team physician. The blessings that come from caring for the athlete at all levels will continue to be tremendously rewarding for the team physician and motivate the next generation of physicians to continue to serve in this role. It will be increasingly important to “dot the Is and cross the Ts” regarding contracts and to be increasingly vigilant regarding the pitfalls of the liability situation. Furthermore, we believe that it will be very important for the physician to run counter to some of the financial pressures that may limit our involvement in the training room and to play an active role in on-site management of our athletes. This will be increasingly important to maintain good relationships with the coaches, administration, and the training staff as well as the athletes themselves. It is important for the team physician to remember that this is a “labor of love.” The additional burden of the regulatory process as it relates to resident and fellow involvement in the care of athletes also needs careful attention. The Accreditation Council for Graduate Medical Education (ACGME) and other governing bodies

are placing additional administrative demands on the supervising team physicians in terms of understanding the role of supervision in the training process. This requires additional documentation and in some instances a restructuring in terms of making sure that supervision requirements are met. This requires considerable case-by-case evaluation. These requirements need to be carefully reviewed and the contractual side of those attended to in order to avoid pitfalls in these areas. At our institution, contractual agreements are required with each of the high schools and collegiate relationships that we serve. We believe that today’s team physician is better educated and more likely to be part of a coordinated multidisciplinary relationship that allows the best care of our athletes than ever before. We must be mindful of the liability and confidentiality issues that face us today that were not present in the past. Though the team physician’s role has evolved in these areas, we do think that it will always be a tremendous honor to serve in what we consider to be the defining role for the sports medicine doctor, that of the team physician.

CONCLUSIONS As a result of the dedication and excellence of the team physicians who have gone before us, some of whom are highlighted in this chapter, we believe that today’s team physician is better educated and more likely to be skilled in managing the issues that athletes of all levels face. It is imperative that we always keep care of the athlete as a central focus of our efforts. We must be mindful of the liability and confidentiality issues that face us today but not allow this to interfere in a negative way with our relationship with the athletes for whom we care. The team physician’s role and responsibilities will continue to evolve. We should never lose sight of what a tremendous honor that it is to serve in the defining role for the sports medicine doctor, that of team physician.

REFERENCES 1. Rubin A: Team physician or athlete’s doctor? Physician Sportsmedicine 1998;26:27–29. 2. Madden CC, Walsh WM, Mellion MB: The team physician: The preparticipation examination and on-field emergencies. In DeLee JD, Drez DD, Miller MM (eds): Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, Saunders, 2003, pp 737–768. 3. American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, American Medical Society

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for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Academy of Sports Medicine: Preparticipation Physical Evaluation, 3rd ed. Overland Park, KS, American Medical Society for Sports Medicine, 2005, pp 93–98. 4. Jacobson KE: Jack C. Hughston, MD—Orthopaedist and pioneer of sports medicine. Am J Sports Med 2004;32:1816–1817. 5. Johnston L: From orthopaedics to sports medicine—One man’s vision. M.D. News, Western Georgia Edition 2003;3:6–10.

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The Preparticipation Physical Examination Robert Hosey and Kenneth Cayce IV

In This Chapter Timing and frequency Methods of conducting preparticipation exams History Physical exam The special-needs athlete Determination of clearance Future of the preparticipation exam

Society of Sports Medicine, American College of Sports Medicine, American Orthopaedic Society for Sports Medicine, and American Osteopathic Academy of Sports Medicine has evaluated and updated the preparticipation sports examination.6 The resulting monograph, published in 2004, was designed to help physicians identify specific and relative contraindications to participate in certain sports and to attempt to produce a standardized preparticipation examination.

TIMING AND FREQUENCY INTRODUCTION • The preparticipation sports examination is a tool to detect medical and orthopedic conditions that may be problematic for safe participation in athletics. • The origins of the preparticipation examination date back about 35 years when the American Medical Association Committee on Medical Aspects of Sports drafted the first guidelines for a preparticipation examination.1 Since then, there have been many alterations and changes to the way in which physicians complete the examination. • It is now an annual event that sports medicine physicians conduct to clear athletes to participate in sports.

In 1992, the first standardized preparticipation examination form was introduced to the sports medicine community.2 Despite the availability of standardized examination forms, there has not been widespread use of a common form. Ninetyseven percent of colleges and universities require the preparticipation examination process, and all 50 states and the District of Columbia require a preparticipation examination to be completed for high school athletes.3,4 When preparticipation examinations are used in colleges and universities, only 51% required it to be done annually. These examinations have often been performed by various health care providers, including athletic trainers and nurse practitioners.5 The primary objectives of the preparticipation examination are to screen for conditions that may be life threatening or disabling or that may predispose to injury or illness and to meet administrative requirements. Secondary objectives include determining general health, serving as an entry point to the health care system for adolescents, and providing opportunity to discuss health-related topics.6 Recently, a consensus panel made up of practitioners from the American Academy of Family Physicians, American Academy of Pediatrics, American Medical

The preparticipation examination should be done at least 6 weeks prior to beginning the sport season to allow time for rehabilitation of old injuries, improvement of flexibility and strength, and further evaluation of any illness or injury that may restrict participation. A complete preparticipation examination should be done upon entry to junior high, high school, and college. Screening history and blood pressure monitoring should be done in subsequent years. In addition, a more detailed examination on identified areas of illness and injury that occurred during the previous year should also be performed. This is the process that is endorsed by the National Collegiate Athletic Association, but few states have seen fit to follow.7 For those athletes older than the age of 35, the American Heart Association recommends exercise testing in men older than 40 years of age and women older than 50 who have one or more cardiac risk factors and/or symptoms of chest pain, palpitations, or syncope. Athletes who are 65 years or older and athletes with a history of coronary artery disease with or without symptoms should have an exercise stress test regardless of risk factors.8 When athletes are not allowed to participate in their sport, recommendations should be made for activity that is appropriate.

METHODS OF CONDUCTING PREPARTICIPATION EXAMINATIONS Preparticipation examinations may be performed in the office or at a mass screening venue. An office examination gives the physician and the athlete time to build rapport and discuss health issues at length. When a mass screening format is employed, a station-based preparticipation examination is often used. In this setting, a single physician may do the entire medical portion of the examination or it may be divided among a number of physicians. In the station-based examination, information gathering is typically divided between several different stations. An example of a station format for a preparticipation examination is outlined in Table 2-1. Additional stations for evaluation of body composition, flexibility, nutrition, strength, speed, agility,

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Table 2-1 Representative Stations for a Mass Screening Preparticipation Examination

answer affirmatively any portion of the history, then detailed evaluation of these areas in the physical examination is necessary.

PHYSICAL EXAMINATION 1. Fill out history form 2. Sign in, height, and weight 3. Visual acuity 4. Blood pressure screening 5. Medical examination 6. Orthopedic examination 7. Checkout (review forms, determination of clearance)

power, endurance, and balance may also be incorporated. With the use of these formats, an excellent preparticipation examination can be completed in 30 to 60 minutes.

HISTORY A complete and accurate medical history is the cornerstone of a good preparticipation examination. Approximately 75% of problems can be discovered by history alone in the preparticipation examination.9 In younger athletes, emphasis is placed on fitness evaluation, obesity, maturity assessment, and identification of medical, orthopedic, and psychosocial situations.10 In older athletes, emphasis is placed on the detection of previous injuries and ongoing problems. In both age groups, one should ask about any recent illnesses, allergic reactions, cardiac/ pulmonary complications, previous head injuries or other neurologic deficits, skin problems, loss of organs, history of heat illness, medications and substance/supplement abuse, bloodborne pathogens, and immunizations.7 In a recent study, female athlete participation had grown to 1 in 2.5 of high school athletes and 43% of all college athletes in the United States.11 Recent findings of six medical societies have found that questions relating to eating, amenorrhea, and osteopenia/osteoporosis need to be emphasized. The combination of all three symptoms has been termed the female athlete triad.12 Some things that should be screened for include dry skin and mucous membranes, history of fractures, menstrual history, and hair loss. Most of the history and physical examination is dedicated to the cardiovascular and musculoskeletal portions. A thorough cardiovascular history should include questions to determine 1. prior occurrence of exertional chest pain/discomfort or syncope/near-syncope as well as excessive, unexpected, and unexplained shortness of breath or fatigue associated with exercise 2. previous detection of a heart murmur or increased systemic blood pressure 3. family history of premature death or significant disability from cardiovascular disease in close relatives younger than 50 years old or specific knowledge of the occurrence of certain conditions (cardiomyopathy, Marfan syndrome, arrhythmia). Screening for medications or drug abuse is also important due to the potential side effect of arrhythmia.8 If the athletes

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The physical examination should include measurement of height and weight. Significant, unexpected changes should warn physicians of the potential of eating disorder or steroid use. General assessment of the head, ears, eyes, nose, and throat is performed. If the athlete has corrected vision less than 20/40, one eye, or history of eye trauma or surgery, then eye protection is required. Anisocoria, astigmatism, strabismus, refractive errors, and poor visual acuity should also be evaluated in athletes and noted in the chart for possible assessment of head injuries in the future.7 For the physical examination of the cardiovascular system, the American Heart Association recommends checking blood pressure, auscultating for murmurs, palpating peripheral pulses to determine for coarctation, and assessing for Marfan syndrome.9 The heart should be auscultated with the athlete in the standing and supine positions. Murmurs that need further evaluation by a cardiologist include 3/6 or higher systolic murmur, any diastolic murmur, and any murmur that increases with standing or with Valsalva maneuver. Sudden cardiac death is the most common cause of nontraumatic death in young athletes and occurs in approximately one in 200,000 with a few cases each year.9 Many cases occur in individuals with pre-existing heart disease.4 In the United States, most cases are due to hypertrophic cardiomyopathy (26.4%), followed by commotio cordis (19.9%), and coronary artery anomalies (13.7%).13 The American Heart Association and 26th Bethesda Conference have developed various guidelines and recommendations for athletic screening and participation14 (Table 2-2). Abnormal cardiovascular examinations are uncommon in athletes younger than the age of 35. In one study of high school athletes, it was found that 0.37% of the participants had either severe hypertension or syncope that prompted further evaluation.15 Many studies have been conducted on the effectiveness and cost efficiency of electrocardiography in risk stratifying athletes who need further evaluation by a cardiologist. Today, there is no consensus on the use of electrocardiography in the preparticipation examination. Another tool for sports medicine physicians to evaluate athletes at risk for sudden cardiac death is echocardiography. It has been proposed, because of its low positive predictive value and cost, that echocardiography should only be used as a follow-up examination in selected patients and not as a primary screening tool.10 Noninvasive screening tests may be developed in the future to help sports medicine physicians diagnose athletes who are at significant risk of cardiac sudden death. This may potentially include a portable echocardiography machine and genetic screening for coronary disease.10 The athlete must be further evaluated if chest tightness, shortness of breath, cough, or wheezing within the first 10 minutes after exercise is noted. The lungs should be auscultated for any wheezes, crackles, or rubs. If the athlete is found to have any of the features, they must be suspected of having exerciseinduced bronchospasm, especially if the athlete has a history of asthma.7 It is now recommended that all elite athletes in swimming, cycling, rowing, snow skiing, cross-country skiing, scuba diving, and figure skating have a bronchial provocation test prior to competition to exclude exercise-induced bronchospasm.16 The eucapnic voluntary hyperpnea challenge test is recom-

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Table 2-2 26th Bethesda Conference Guidelines for Athletic Participation for Selected Cardiovascular Abnormalities Hypertrophic cardiomyopathy

Exclusion from most competitive/noncompetitive sports, with possible exception of low-intensity sports, regardless of medical treatment, absence of symptoms, or implantation of defibrillator.

Coronary artery abnormalities

Exclusion from all competitive sports. Participation may be considered 6 months after surgical correction and after exercise stress testing.

ARVD

Exclusion from all competitive sports.

Mitral valve prolapse

Exclusion if history of syncope is associated with arrhythmia, family history of mitral valve prolapse and sudden death, documented arrhythmia, or moderate to severe mitral regurgitation.

Ebstein’s anomaly

Severe disease precludes participation in all sports. After surgical repair, low-intensity sports are permitted if tricuspid regurgitation is absent or mild, heart size is normal, and no arrhythmias are present on Holter monitoring and stress testing.

Marfan syndrome

Exclusion from contact sports. Patients with aortic regurgitation and marked dilation of aorta are excluded from all competitive sports. Others may participate in low-intensity sports, with biannual echocardiography.

Long QT syndrome

Exclusion from all competitive sports.

Myocarditis

Athletes with history of myocarditis in previous 6 months are excluded from all competitive sports.

Wolff-ParkinsonWhite syndrome

Patients with normal exercise testing ± electrophysiologic study may be eligible for participation in all sports.

Coronary artery disease

Individual risk assessment based on ejection fraction, exercise tolerance, presence of inducible ischemia or arrhythmias, and presence of hemodynamically significant coronary stenoses on angiography.

ARVD, arrhythmogenic right ventricular dysplasia. Reprinted from American College of Sports Medicine and American College of Cardiology: 26th Bethesda Conference. Recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Med Sci Sport Exerc 1994;26:5223–5283, with permission from the American College of Cardiology Foundation.

mended by the International Olympic Committee (IOC) for elite athletes. This test has two different protocols: stepped and single stepped. The stepped protocol is indicated for athletes with severe or unstable airway disease and involves increasing the athlete’s ventilation over three stages. The single-stepped protocol is indicated for athletes with asthma or exerciseinduced bronchospasm and involves a single level of ventilation for 6 minutes. Each protocol measures lung function and a decrease of more than 10% from baseline indicates exerciseinduced bronchospasm.17 The type of test to perform for confirmation of exercise-induced bronchospasm is determined by what is most readily available. For the abdominal examination, one should pay particular attention to abdominal distention and tenderness, organomegaly, rigidity, or masses. A hernia by itself is not a disqualifying factor but needs further evaluation and possible treatment prior to play. Female athletes should be questioned about the possibility of pregnancy. If there is a possibility of pregnancy, pain, or enlargement of the abdomen, a pelvic examination should be performed in a private setting prior to participation.7 In the past, physicians have provided a male testicular examination during the preparticipation examination. Today, the evidence has shown that counseling, describing the examination, and having athletes do the examination at home allows the athlete to learn more about testicular cancer and its symptoms.17 The sports medicine physician should ask about history of undescended testes, masses, loss of a testicle, and inguinal hernias, and, if positive, then a testicular examination may be warranted. Tanner staging is no longer recommended as part of the preparticipation examination. Its use is mainly for evaluating musculoskeletal injuries in the physically immature. The musculoskeletal examination should be done in an orderly manner with attention to identifying potential abnormalities in musculature and bone structure. An example that is evidence based is the 14-point examination6 (Table 2-3; Figs.

2-1 through 2-3), as outlined in the consensus monograph, with additions to measure supraspinatus strength and a dynamic strength test (balancing on one foot).18 This examination is good for most athletes, but a more detailed examination should be performed for certain populations (e.g., professional athletes).19 If an athlete has a history of an injury (e.g., fracture, joint pain) or answers yes to any musculoskeletal question in the original history form, then that athlete should be evaluated further with a detailed examination of that bone or joint. A major goal of the orthopedic examination is that full rehabilitation of injuries is accomplished prior to participation in the sport. Some sports medicine physicians have included measurements of endurance, strength, and flexibility with the preparticipation examination, but these measurements add significant time to the overall process. Neurologic examination should be done while performing the musculoskeletal examination. Any neurologic deficits (e.g., loss of strength, paresthesias) should be explored, as should a history of stingers/burners or head injury. The athlete must be without signs or symptoms of neurologic deficit prior to starting sports. The preparticipation examination may give the sports medicine physician the opportunity to assess baseline neuropsychological function. This can be a helpful tool for guiding return to play decisions in the concussed athlete.20 Any skin problems (e.g., rashes, infections, abrasions, blisters) should be assessed during the examination. By addressing these skin reactions early and prior to the start of the season, the athlete can be treated and participate in sports. Skin infections need to be treated prior to participating in sports involving body contact.

THE SPECIAL-NEEDS ATHLETE Special-needs athletes include athletes with cerebral palsy, blindness, paralysis, mental retardation, amputation, arthritis,

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Table 2-3 The 14-Point Musculoskeletal Screening Examination6 Examination

Assessment

1. Inspection, athlete standing, facing examiner

Symmetry of trunk, upper extremities

2. Forward flexion, extension, rotation, lateral flexion of neck

Cervical spine range of motion

3. Resisted shoulder shrug

Trapezius strength

4. Resisted shoulder abduction

Deltoid strength

5. Internal and external rotation of shoulder

Glenohumeral joint range of motion

6. Extension and flexion of elbow

Elbow range of motion

7. Pronation and supination of forearm

Wrist range of motion

8. Clench fist, spread fingers

Hand and fingers range of motion

9. Inspection, athlete facing away from examiner

Symmetry of truck, upper extremities

10. Back extension, knees straight

Spondylolysis, spondylolisthesis

11. Back flexion with knees straight (see Fig. 2-1)

Spine range of motion, scoliosis, hamstring flexibility

12. Inspection of lower extremities, quadriceps contraction

Alignment, symmetry

13. “Duck walk” four steps (see Fig. 2-2)

Hip, knee, ankle motion, strength/balance

14. Standing on toes, then heels (see Fig. 2-3)

Symmetry, calf strength, balance

Figure 2-2 “Duck walk” to assess range of motion, strength, and balance. Figure 2-1 Assessment of back flexion with knees straight.

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Table 2-4 Sample History Questions for the Special-Needs Athlete Does the athlete have any history of any of the following: Seizures Hearing loss Vision loss Cardiopulmonary disease Renal disease or a unilateral kidney Atlantoaxial instability Pressure sores or ulcers Heat stroke or heat exhaustion Fractures or dislocations Autonomic dysreflexia Are seizures controlled and with what medications? What prosthetic devices or special equipment are required? Is there an indwelling urinary catheter or requirement of intermittent catheterization? What levels has the athlete participated in previously? What is the level of independence? Is a special diet required?

Figure 2-3 Standing on toes.

muscular dystrophy, and multiple sclerosis. The benefits of exercise for the special-needs athlete are the same as those for other athletes. Additionally, special-needs athletes have fewer pressure ulcers, fewer infections, improved proprioception, increased proficiency using prosthetic devices, and decreased hospitalizations. The Special Olympics and the United States Paralympics require a preparticipation examination to be done within 12 months of competition. An office-based examination is preferred for these athletes. Questions on which the physician should focus are listed in Table 2-4. These questions should be asked and appropriate consultations made if needed. Special attention should be given to the vision, cardiovascular, neurologic, dermatologic, genitourinary, and musculoskeletal portions of the examination. The functional assessment with sportspecific tasks should be done on all athletes with special needs. Diagnostic imaging should be done on all athletes at risk of atlantoaxial instability, including athletes with Down syndrome wanting to compete in judo, equestrian sports, gymnastics, diving, pentathlon, swimming (butterfly stroke and diving starts), high jump, Alpine skiing, snowboarding, squat lift, and soccer.21

DETERMINATION OF CLEARANCE Clearance for the athlete is the most important decision to be made at the completion of the preparticipation examination. Fortunately, only approximately 11.9% of athletes who have a preparticipation examination will require further evaluation and about 1.9% are not allowed to participate in their sport.22

The American Academy of Pediatrics Committee on Sports Medicine and Fitness has developed a guideline for clearance for athletes23 (Table 2-5). For each athlete, one must determine whether participation in that sport will put the athlete, teammate, or competitors at risk of injury. It must be determined whether there is treatment for the athlete, such as medicines or protective gear, that will allow the athlete to compete safely. The answers to these questions make it easier for the sports medicine physician to decide whether the athlete is cleared without restriction, cleared after completing further evaluation, cleared after completing rehabilitation for a particular injury/ illness, or not cleared for participation.2 These decisions should be discussed with the athlete, parents, trainer, and coach. Many medical conditions must be evaluated prior to starting any type of sport. In some cases, an athlete is not allowed to participate in one sport but may be allowed to participate in a less strenuous type of activity. The American Academy of Pediatrics Committee on Sports Medicine and Fitness has classified individual sports based on the amount of contact and strenuousness23 (Tables 2-6 and 2-7). Although there are many guidelines that assist the sports medicine physician in determining eligibility, each athlete should be considered individually. It should be noted that only a few athletes are not allowed to participate after completion of the preparticipation examination. If there is any disagreement between the athlete and the physician, it may be wise for the physician to obtain written consent or a legal waiver signed by the athlete and the parent. A second opinion may also be obtained. If there is still disagreement between the athlete and the physician, legal counsel may be useful in providing information regarding issues related to athletic participation or disqualification.2

FUTURE OF THE PREPARTICIPATION EXAMINATION The future of the preparticipation examination is headed to the computer age. Today, there are institutions that use electronic

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Table 2-5 Medical Conditions and Sports Participation* Condition

May Participate

Atlantoaxial instability (instability of the joint between cervical vertebrae 1 and 2) Explanation: Athlete needs evaluation to assess risk of spinal cord injury during sports participation.

Qualified yes

Bleeding disorder† Explanation: Athlete needs evaluation.

Qualified yes

Cardiovascular disease Carditis (inflammation of the heart) Explanation: Carditis may result in sudden death with exertion.

No

Hypertension (high blood pressure) Explanation: Those with significant essential (unexplained) hypertension should avoid weight and power lifting, body building, and strength training. Those with secondary hypertension (hypertension caused by a previously identified disease) or severe essential hypertension need evaluation. The National High Blood Pressure Education Working group defined significant and severe hypertension.

Qualified yes

Congenital heart disease (structural heart defects present at birth) Explanation: Those with mild forms may participate fully; those with moderate or severe forms or who have undergone surgery need evaluation. The 26th Bethesda Conference defined mild, moderate, and severe disease for common cardiac lesions.

Qualified yes

Dysrhythmia (irregular heart rhythm) Explanation: Those with symptoms (chest pain, syncope, dizziness, shortness of breath, or other symptoms of possible dysrhythmia) or evidence of mitral regurgitation (leaking) on physical examination need evaluation. All others may participate fully.

Qualified yes

Heart murmur Explanation: If the murmur is innocent (does not indicate heart disease), full participation is permitted. Otherwise, the athlete needs evaluation (see “Congenital heart disease” above).

Qualified yes

Cerebral palsy† Explanation: Athlete needs evaluation.

Qualified yes

Diabetes mellitus Explanation: All sports can be played with proper attention to diet, blood glucose concentration, hydration, and insulin therapy. Blood glucose concentration should be monitored every 30 minutes during continuous exercise and 15 minutes after completion of exercise.

Yes

Diarrhea Explanation: Unless disease is mild, no participation is permitted because diarrhea may increase the risk of dehydration and heat illness. See “Fever” below.

Qualified no

Eating disorders Anorexia nervosa, bulimia nervosa Explanation: Patients with these disorders need medical and psychiatric assessment before participation.

Qualified yes

Eyes Functionally one-eyed athlete, loss of an eye, detached retina, previous eye surgery, or serious eye injury Qualified yes Explanation: A functionally one-eyed athlete has a best-corrected visual acuity of less than 20/40 in the eye with worse acuity. These athletes would suffer significant disability if the better eye were seriously injured, as would those with loss of an eye. Some athletes who previously have undergone eye surgery or had a serious eye injury may have an increased risk of injury because of weakened eye tissue. Availability of eye guards approved by the American Society for Testing and Materials and other protective equipment may allow participation in most sports, but this must be judged on an individual basis. Fever Explanation: Fever can increase cardiopulmonary effort, reduce maximum exercise capacity, make heat illness more likely, and increase orthostatic hypertension during exercise. Fever may rarely accompany myocarditis or other infections that may make exercise dangerous. Heat illness, history of Explanation: Because of the increased likelihood of recurrence, the athlete needs individual assessment to determine the presence of predisposing conditions and to arrange a prevention strategy.

Qualified yes

Hepatitis Explanation: Because of the apparent minimal risk to others, all sports may be played that the athlete’s state of health allows. In all athletes, skin lesions should be covered properly, and athletic personnel should use universal precautions when handling blood or body fluids with visible blood.

Yes

Human immunodeficiency virus infection Explanation: Because of the apparent minimal risk to others, all sports may be played that the athlete’s state of health allows. In all athletes, skin lesions should be covered properly, and athletic personnel should use universal precautions when handling blood or body fluids with visible blood.

Yes

Kidney, absence of one Explanation: Athlete needs individual assessment for contact, collision, and limited-contact sports.

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No

Qualified yes

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Condition

May Participate

Liver, enlarged Explanation: If the liver is acutely enlarged, participation should be avoided because of risk of rupture. If the liver is enlarged, individual assessment is needed before collision, contact, or limited-contact sports are played.

Qualified yes

Malignant neoplasm† Explanation: Athlete needs individual assessment.

Qualified yes

Musculoskeletal disorders Explanation: Athlete needs individual assessment.

Qualified yes

Neurologic disorders History of serious head or spinal trauma, severe or repeated concussions, or craniotomy Explanation: Athlete needs individual assessment for collision, contact, or limited-contact sports and also for noncontact sports if deficits in judgment or cognition are present. Research supports a conservative approach to management of concussion. Seizure disorder, well controlled Explanation: Risk of seizure during participation is minimal. Seizure disorder, poorly controlled Explanation: Athlete needs individual assessment for collision, contact, or limited-contact sports. The following noncontact sports should be avoided: archery, riflery, swimming, weight or power lifting, strength training, or sports involving heights. In these sports, occurrence of a seizure may pose a risk to self or others.

Qualified yes

Yes Qualified yes

Obesity Explanation: Because of the risk of heat illness, obese persons need careful acclimatization and hydration.

Qualified yes

Organ transplant recipient† Explanation: Athlete needs individual assessment.

Qualified yes

Ovary, absence of one Explanation: Risk of severe injury to the remaining ovary is minimal. Respiratory conditions Pulmonary compromise, including cystic fibrosis Explanation: Athlete needs individual assessment, but generally, all sports may be played if oxygenation remains satisfactory during a graded exercise test. Patients with cystic fibrosis need acclimatization and good hydration to reduce the risk of heat illness. Asthma Explanation: With proper medication and education, only athletes with the most severe asthma will need to modify their participation.

Yes

Qualified yes

Yes

Acute upper respiratory infection Explanation: Upper respiratory obstruction may affect pulmonary function. Athlete needs individual assessment for all but mild disease. See “Fever.”

Qualified yes

Sickle cell disease Explanation: Athlete needs individual assessment. In general, if status of the illness permits, all but high exertion, collision, and contact sports may be played. Overheating, dehydration, and chilling must be avoided.

Qualified yes

Sickle cell trait Explanation: It is unlikely that persons with sickle cell trait have an increased risk of sudden death or other medical problems during athletic participation, except under the most extreme conditions of heat, humidity, and, possibly, increased altitude. These persons, like all athletes, should be carefully conditioned, acclimatized, and hydrated to reduce any possible risk.

Yes

Skin disorders (boils, herpes simplex, impetigo, scabies, molluscum contagiosum) Explanation: While the patient is contagious, participation in gymnastics with mats, martial arts, wrestling, or other collision, contact, or limited-contact sports is not allowed.

Qualified yes

Spleen, enlarged Explanation: A patient with an acutely enlarged spleen should avoid all sports because of risk of rupture. A patient with a chronically enlarged spleen needs individual assessment before playing collision, contact, or limited-contact sports.

Qualified yes

Testicle, undescended or absence of one Explanation: Certain sports may require a protective cup.

Yes

*This table is designed for use by medical and nonmedical personnel. “Needs evaluation” means that a physician with appropriate knowledge and experience should assess the safety of a given sport for an athlete with the listed medical condition. † Not discussed in the text of the monograph. Reproduced with permission from American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 2001;107:1205–1209.

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Table 2-6 Classification of Sports by Contact Contact or Collision

Limited Contact

Noncontact

Basketball Boxing* Diving Field hockey Football, tackle Ice hockey† Lacrosse Martial arts Rodeo Rugby Ski jumping Soccer Team handball Water polo Wrestling

Baseball Bicycling Cheerleading Canoeing or kayaking (white water) Fencing Field events High jump Pole vault Floor hockey Football, flag Gymnastics Handball Horseback riding Racquetball Skating Ice In-line Roller Skiing Cross-country Downhill Water Skateboarding Snowboarding‡ Softball Squash Ultimate frisbee Volleyball Windsurfing or surfing

Archery Badminton Body building Bowling Canoeing or kayaking (flat water) Crew or rowing Curling Dancing§ Ballet Modern Jazz Field events Discus Javelin Shot put Golf Orienteering¶ Power lifting Race walking Riflery Rope jumping Running Sailing Scuba diving Swimming Table tennis Tennis Track Weight lifting

*Participation not recommended by the American Academy of Pediatrics. † The American Academy of Pediatrics recommends limiting the amount of body checking allowed for hockey players 15 years and younger to reduce injuries. ‡ Snowboarding has been added since previous statement was published. § Dancing has been further classified into ballet, modern, and jazz since the previous monograph was published. ¶ A race in which competitors use a map and compass to find their way through unfamiliar territory. Reproduced with permission from American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 2001;107:1205–1209.

medical records as a tool for obtaining a history and physical examination to screen athletes for participation in sports. In addition, a Web-based preparticipation examination questionnaire has been used. The questionnaire is provided to athletes and answered prior to the physical examination. When the athlete comes for his or her physical examination, the physician is provided with the history. In 1998, Stanford University

Table 2-7 Classification of Sports by Strenuousness High to Moderate Intensity High to Moderate Dynamic and Static Demands

High to Moderate Dynamic and Low Static Demands

High to Moderate Static and Low Dynamic Demands

Boxing* Crew or rowing Cross-country skiing Cycling Downhill skiing Fencing Football Ice Hockey Rugby Running (sprint) Speed skating Water polo Wrestling

Badminton Baseball Basketball Field hockey Lacrosse Orienteering Race walking Racquetball Soccer Squash Swimming Table tennis Tennis Volleyball

Archery Auto racing Diving Horseback riding (jumping) Field events (throwing) Gymnastics Karate or judo Motorcycling Rodeo Sailing Ski jumping Waterskiing Weight lifting

Low Intensity Low Dynamic and Low Static Demands Bowling Cricket Curling Golf Riflery *Participation not recommended by the American Academy of Pediatrics. Reproduced with permission from American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 2001;107:1205–1209.

started using the Web-based preparticipation examination history. They posted the questionnaire on a Web site, which allowed access for the athletes to answer questions about their history prior to the physical examination. The sports medicine physicians reported that they were allowed more time to spend with the athlete to counsel athletes on health issues. The Webbased preparticipation examination was found to be 97% sensitive in detecting medical issues that needed further evaluation. Athletes reported that the Web-based preparticipation examination was easy to use and allowed the overall time for the examination to be reduced.24 There are many variations of the preparticipation examination, which in some cases tailor the examination and screening tests to specific populations (e.g., females, adolescents). The use of an electronic medical record or the Web-based preparticipation examination will perhaps aid sports medicine physicians come to a consensus on a common preparticipation examination for athletes of all sports.1

REFERENCES 1. Best TM: The preparticipation evaluation, an opportunity for change and consensus. Clin J Sport Med 2004;14:107–108. 2. Armsey TD, Hosey RG: Medical aspects of sports: Epidemiology of injuries, preparticipation physical examination, and drugs in sports. Clin Sports Med 2004;23:255–279. 3. Glover DW, Maron BJ: Profile of preparticipation cardiovascular screening for high school athletes. JAMA 1998;279:1817–1819.

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4. Gomez JE, Lantry BR, Saathoff KN: Current use of adequate preparticipation examination history forms for heart disease screening of high school athletes. Arch Pediatr Adolesc Med 1999;153:723– 726. 5. Pfister GC, Puffer JC, Maron BJ. Preparticipation cardiovascular screening for US collegiate of student athletes. JAMA 2000;283: 1597–1599.

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6. American Academy of Family Physicians, American Academy of Pediatrics, American Medical Society of Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Academy of Sports Medicine: Preparticipation Physical Examination, 3rd ed. Minneapolis, The Physician and Sportsmedicine, 2004. 7. Madden CC, Walsh MW, Mellion MB: The Team Physician: The Preparticipation Examination and On-Field Emergencies. Orthopaedic Sports Medicine, Principals and Practice, 2nd ed. Philadelphia, WB Saunders, 2003. 8. Beckerman J, Wang P, Hlatky M: Cardiovascular screening of athletes. Clin J Sport Med 2004;14:127–132. 9. Maron BJ, Thompson PD, Puffer JC, et al: Cardiovascular preparticipation screening of competitive athletes. Circulation 1996;94:850– 856. 10. Wingfield K, Matheson GO, Meeuwisse WH: Preparticipation evaluation, an evidence based review. Clin J Sport Med 2004;14:109–122. 11. The National Coalition for Women and Girls in Education: Title XI at 30: Report card on gender equity. Washington, DC, 2002. Available at www.scwge.org/ 12. Otis CL, Drinkwater B, Johnson M, et al: American College of Sports Medicine position stand: The female athlete triad. Med Sci Sports Exerc 1997;29:i–ix. 13. Maron BJ, Araujo CG, Thompson PD, et al: Recommendations for pre-participation screening and the assessment of cardiovascular disease in masters athletics: An advisory for healthcare professionals for the working groups of the World Heart Federation, the International Federation of Sports Medicine, and the American Heart Association on exercise, cardiac rehabilitation and prevention. Circulation 2001;103: 327–334.

14. American College of Sports Medicine, American College of Cardiology: 26th Bethesda Conference. Recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Med Sci Sport Exerc 1994;26:5223–5283. 15. Smith J, Laskowski ER: The Preparticipation physical examination: Mayo Clinic experience with 2,739 examinations. Mayo Clin Proc 1998;5:419–429. 16. Holzer K, Brukner P: Screening of athletes for exercise-induced bronchoconstriction. Clin J Sports Med 2004;14:134–137. 17. United States Preventative Services Task Force (USPSTF) Web site: Available at www.ahcpr.gov/clinic/uspstfix.htm/ 18. Gomez JE, Landry GL, Bernhardt DT: Critical evaluation of the 2minute orthopaedic screening examination. Sports Med 1993;147: 1109–1113. 19. Garrick JG: Preparticipation orthopedic screening evaluation. Clin J Sport Med 2004;14:123–126. 20. McCrory P: Preparticipation assessment for head injury. Clin J Sports Med 2004;14:139–144. 21. Boyajian-O’Neill, Cardone D, Dexter W, et al: The preparticipation examination for the athlete with special needs. Physician Sportsmedicine 2004;32:13–19. 22. Corrado D, Basso C, Schiavon M, et al: Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998;339:364–369. 23. American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 1994;94:757–760. 24. Peltz JE, Haskell WL, Matheson GO: A comprehensive and cost-effective preparticipation exam implemented on the World Wide Web. Med Sci Sports Exerc 1999;31:1727–1740.

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On-Field Emergencies and Preparedness Todd C. Malvey and Thomas D. Armsey

In This Chapter Head and spinal cord injury Athletes with a helmet and face mask Lightning safety Preparedness Preseason planning Emergency planning Game-day planning Medical bag Sideline medical supplies

INTRODUCTION • Life-threatening emergencies in athletics are rare, but the potential causes of an on-field emergency are numerous. • Adequate preparation and management of an on-field emergency is key to a successful outcome. • Initial management of an on-field emergency includes a primary survey using the ABCDE (airway, breathing, circulation, disability/neurologic status, exposure) method and cervical immobilization. When appropriate, immediate use of cardiopulmonary resuscitation, an automated external defibrillator, and artificial ventilation improves the chances of survival. • Special considerations must be followed when caring for an athlete with a suspected head or spinal cord injury as well as an athlete wearing a helmet and face mask. • A major goal of the sports medicine team’s preseason planning is to develop and implement an emergency response plan. • By maintaining a sideline “medical bag” and emergency equipment, the sports medicine team can provide rapid and appropriate treatment to an athlete in an emergency situation.

Emergencies at sporting events are usually caused by trauma, aggravation of a known medical problem, presentation of a previously unknown medical problem, or an environmental cause/catastrophe. The list of potential causes of on-field emergencies is numerous and still expanding (Table 3-1). Some of the potential causes of on-field emergencies are immediately life threatening (cardiac arrhythmia, airway compromise), while others may rapidly become life threatening if medical care is not administered quickly (cervical spine injury, traumatic brain injury). The team physician and other medical personnel should be able to acutely assess, manage, and triage both traumatic injuries and numerous medical conditions.

When reaching an athlete that is injured, a primary survey should be made using the ABCDE method (airway, breathing, circulation, disability/neurologic status, exposure). Cervical immobilization should be started immediately, especially if the athlete has neurologic deficits, pain, or altered mental status. Immobilization of the cervical spine should be maintained until spinal cord and brain injury is ruled out. Evidence of airway compromise includes labored and/or unequal breath sounds. Noisy respirations may be an indication of a partial airway obstruction, and clearing the airway of the obstruction should be attempted by sweeping a gloved finger into the oropharynx and/or by suction. The athlete’s circulatory status can be affirmed by palpation of a carotid artery pulse. Any bleeding should be identified and controlled by applying a pressure dressing. If spontaneous respirations and/or a pulse are absent, then cardiopulmonary resuscitation should be started immediately. The athlete is artificially ventilated with either mouth-to-mouth, mouth-to-mask, bag-valve mask, or oropharyngeal airway (unconscious athletes only) respirations, cricothyrotomy, or endotracheal intubation. Chest compressions should be started, and an automated external defibrillator should be attached to the athlete as soon as possible. It has been shown that early defibrillation helps to save lives by converting ventricular fibrillation, the most common lethal arrhythmia, to a normal rhythm.

HEAD AND SPINAL CORD INJURY One of the more common emergency conditions encountered during coverage of athletic events are head and neck injuries. Any athlete that has altered mental status, neck pain, or neurologic complaints should be considered to have a spinal cord or brain injury. By properly managing head and neck injuries, the medical team can lessen the chance of complications and expedite emergency transportation. The first step in managing a cervical spinal injury is cervical immobilization. This immobilization should be maintained until a spinal cord or brain injury is ruled out by a thorough examination and/or radiographic studies at an emergency facility. Cervical immobilization is typically achieved by one of the responders. Care needs to be taken to keep the head in a neutral position in line with the spine and to avoid flexion and extension of the cervical spine. If the athlete is lying prone, the log roll maneuver is used to turn the athlete to the supine position. Once the athlete has been placed in a cervical collar and attached to a spine board, he or she is transported by paramedics to a previously determined emergency facility for a more detailed evaluation.

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TABLE 3-1 Potential Causes of On-Field Emergencies in the Athlete5,6 Trauma

Medical

Head injury Spinal cord injury Flail chest Hemothorax Tension pneumothorax Laryngeal fracture Cardiac tamponade Cardiac contusion Commotio cordis Ruptured viscus Multiple fractures, e.g., femur, pelvis Blood loss Pulmonary contusion

Coronary artery disease Arrhythmia Congenital abnormality Hypertrophic cardiomyopathy Hyperthermia Hypothermia Cerebrovascular accident Hypoglycemia Hyponatremia Asthma Spontaneous pnuemothorax Pulmonary embolism Allergic anaphylaxis Drugs, e.g., cocaine, morphine Other, e.g., vasovagal, postural hypotension Blood pooling postexercise, hyperventilation, hysteria Lightning

Athletes with a Helmet and Face Mask Particular attention needs to be given to emergency conditions occurring in the athlete wearing a helmet and face mask. 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 or neck injury.1 The helmet and shoulder pads hold the cervical spine in relative alignment, and removal of them would cause movement of the cervical spine that could trigger neurologic complications. Table 3-2 lists the only exceptions to the guideline of never removing the helmet in the prehospital setting. Leaving the helmet in place does not inhibit assessment of the athlete’s airway, breathing, circulatory, and neurologic status. Prior to transport, care should be given to stabilizing the head and neck to the spine board by strapping, taping, and/or using lightweight bolsters. Once at an emergency care facility, satisfactory radiographs can usually be obtained with the helmet in place.1

TABLE 3-2 Only Exceptions to Guideline of Never Removing Helmet of an Athlete with a Suspected Head or Neck Injury in the Prehospital Setting1 1. Helmet does not hold the head securely, such that immobilization of the helmet does not immobilize the head. 2. Even after removal of the face mask, the airway cannot be controlled or ventilation provided. 3. After a reasonable period of time, the face mask cannot be removed. 4. Helmet prevents immobilization for transportation in an appropriate position.

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TABLE 3-3 Protocol for Helmet Removal2 1. Manually stabilize the head, neck, and helmet throughout the procedure. 2. Cut the chin strap. 3. Remove the cheek pads by slipping the flat blade of a screwdriver or bandage scissor under the pad snaps and above the inner surface of the shell. 4. If an air cell padding system is present, deflate it by releasing the air at the external port with an inflation needle or large-gauge hypodermic needle. 5. Rotate the helmet slightly forward; it should now slide off the occiput. 6. Slight traction can be applied to the helmet as it is carefully rocked anteriorly and posteriorly without moving the head/neck unit. 7. Do not spread apart the helmet by the ear holes because this will tighten the helmet on the forehead and occiput regions.

While in most circumstances the helmet should not be removed, the face mask should be taken off soon after the primary survey. The face mask should be removed to monitor breathing, care for facial injury, or prior to transport regardless of respiratory status.1 This can be done by unscrewing or cutting the loops that attach the mask to the helmet. A PVC pipe cutter, garden shears, screwdriver, or pocketknife will all work. It is essential that the medical team readily have the proper tools for face mask removal and should practice face mask removal prior to the season.2 If the helmet needs to be removed to initiate life-saving treatment, ensure cervical immobilization, or obtain special radiographic studies, a specific protocol needs to be followed (Table 3-3).1 Both on-field medical personnel and medical staff in emergency care facilities should be trained to remove athletic helmets in a safe and efficient manner. All staff who participate in a helmet removal should perform the maneuver with caution and coordination of every move in the protocol.1

LIGHTNING SAFETY Nature itself can cause an emergency situation on an athletic field. Lightning is the most common weather hazard that affects athletics.3 The National Severe Storms Laboratory estimates that 100 fatalities and 400 to 500 injuries requiring medical treatment occur from lightning strikes in the United States each year.1 A lightning strike should be considered a life-threatening emergency situation. While the probability of being struck by lightning is extremely low, the odds are significantly greater when a storm is in the area and proper safety precautions are not followed.1 The National Collegiate Athletic Association and National Severe Storms Laboratory have developed lightning safety guidelines to diminish the lightning hazard at an athletic event (Table 3-4).1 The most important aspect to monitor is how far away the lightning is occurring and how fast the storm is approaching, relative to the distance of shelter.1 The flash-to-bang method is the easiest and most convenient way to estimate how far away lightning is occurring.1 To use the flash-to-bang method, count the seconds from the time the lightning is sighted to when the clap of thunder is heard. Divide this number by five to obtain how

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TABLE 3-4 Lightning Safety Guidelines Developed by the National Collegiate Athletic Association and National Severe Storms Laboratory1 1. Designate a chain of command as to who monitors the weather and who makes the decision to remove a team or individuals from an athletic site or event. 2. Obtain a weather report each day before a practice or event. 3. It does not have to be raining for lightning to strike. 4. Be aware of National Weather Service–issued thunderstorm “watches” and “warnings” and the signs of thunderstorms developing nearby. 5. By the time a monitor obtains a flash-to-bang count of 30 seconds (equivalent to 6 miles), all individuals should have left the athletic site and reached a safe structure or location. 6. Know where the closest safe structure or location is and how long it takes to get there. A safe structure or location is defined as: (a) Any building normally occupied or frequently used by people. Avoid using shower facilities for shelter and do not use showers or plumbing facilities during a thunderstorm. (b) Any vehicle with a hard metal roof and rolled-up windows. Do not touch the sides of the vehicle. 7. If no safe structure or location is within a reasonable distance, find a thick grove of trees surrounded by taller trees or a dry ditch. Assume a crouched position on the ground with only the balls of the feet touching the ground, wrap your arms around your knees, and lower your head. Minimize contact with the ground and do not lie flat. Stay away from the tallest trees or objects, individual trees, standing pools of water, and open fields. Avoid being the highest object in a field. 8. A person who feels his or her hair stand on end or skin tingle should immediately crouch as described above. 9. Avoid using the telephone, except in emergency situations. A cellular phone or portable remote phone is a safe alternative if the person and antenna are located within a safe structure or location. 10. Athletic activity can be resumed after waiting for 30 minutes after the last flash of lightning or sound of thunder. 11. People who have been struck by lightning do not carry an electrical charge, and cardiopulmonary resuscitation is safe for the responder. If possible, the injured person should be moved to a safer location before starting cardiopulmonary resuscitation.

far away (in miles) the lightning is occurring. When the flashto-bang count is less than 30 seconds (6 miles), all individuals should leave the athletic field and move to shelter.1 Everyone can return to the athletic field 30 minutes after the last flash of lightning or sound of thunder.1

PREPAREDNESS The key to managing on-field emergencies is thorough preparation. To accomplish this goal, the sports medicine physician should assist in developing an integrated medical system that includes extensive preparation and evaluation in the off-season, as well as game-day planning.4

Preseason Planning Preseason planning is the most important facet of sideline preparedness. It should promote safety and minimize routine prob-

lems associated with athletic participation as well as emergency situations. All personnel who have the potential to be involved with the medical care of athletes (e.g., athletic trainers, coaches) should use this time to maintain their training in cardiopulmonary resuscitation and basic first aid as a minimum requirement. Additional training in advanced cardiac life support and advanced trauma life support is strongly recommended for team physicians. The goals of the sports medicine team’s preseason planning should include the following 2: • All athletes complete a preparticipation evaluation by a licensed physician • Development of a chain of command that establishes and defines the responsibilities of all parties involved • Establishment of an emergency response plan for practice and competition • Compliance with Occupational Safety and Health Administration standards relevant to the medical care of the athlete • Establishment of a policy to assess environmental concerns and playing conditions for modification or suspension of practice or competition • Compliance with all local, state, and federal regulations regarding storing and dispensing pharmaceuticals • Establishment of a plan to provide for proper documentation and medical record keeping • Regular rehearsal of the emergency response plan • Establishment of a network with other health care providers, including medical specialists, athletic trainers, and allied health professionals • Establishment of a policy that includes the team physician in the dissemination of any information regarding the athlete’s health • Preparation of a letter of understanding between the team physician and the administration that defines the obligations and responsibilities of the team physician

Emergency Planning A major objective of the sports medicine team’s preseason planning is to develop and implement an emergency plan. Professional and legal requirements mandate that organizations or institutions sponsoring athletic activities have a written emergency plan.5 Limb-threatening or life-threatening emergencies on the athletic field are unpredictable and therefore have the potential to cause chaos and an ineffective response if medical personnel are not well prepared for these situations. A welldesigned and rehearsed emergency plan can provide the medical team with an organized approach to handle an emergency. Preparation for response to emergencies includes education and training, maintenance of emergency equipment and supplies, appropriate use of personnel, and the formation and implementation of an emergency plan.3 In addition, medical personnel have a legal duty to provide high-quality care to athletic participants and failure to have an emergency response plan could be considered negligence.3 Table 3-5 highlights some recommended guidelines to use when establishing an emergency response plan. For an emergency response plan to be effective, careful planning and organization should be given to personnel, equipment, communication, transportation, the referring emergency care facility, and documentation. All personnel associated with practices, competitions, skills instruction, and strength and conditioning activities should have training in automatic external defibrillation and current certification in cardiopulmonary resus-

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TABLE 3-5 Recommendations to Establish an Effective Emergency Response Plan3,4 1. Each institution or organization that sponsors athletic activities must have a written emergency plan that is comprehensive, practical, and flexible. 2. It should be distributed to athletic trainers, team physicians, institutional and organizational safety personnel and administrators, and coaches. 3. It should be developed with local emergency receiving facility and emergency medical services personnel. 4. It must identify the personnel involved in carrying out the emergency plan and outline the qualifications of those executing the plan. 5. Sports medicine professionals, officials, and coaches should be trained in automatic external defibrillation, cardiopulmonary resuscitation, first aid, and prevention of disease transmission. 6. It should specify the equipment needed and the location of the emergency equipment. 7. It should establish a clear mechanism for communication to appropriate emergency care service providers and identify the mode of transportation for the injured participant. 8. The plan should be specific to the activity venue. 9. Emergency receiving facilities should be notified in advance of scheduled events and contests. 10. It should include an inclement weather policy with specific provisions for decision making and evacuation plans. 11. It should identify who is responsible for documenting actions taken during the emergency, evaluation of the emergency response, and institutional personnel training. 12. The plan should be reviewed and rehearsed at least annually. 13. The plan should be reviewed by the administration and legal counsel of the sponsoring organization or institution.

citation, first aid, and the prevention of disease transmission.3,4 The emergency plan should also specifically name who is responsible for summoning help and clearing the noninjured athletes from the field. It is recommended that an emergency plan follow the most recent American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. The American Heart Association guidelines state that defibrillation is considered a component of basic life support and call for the availability and use of automated external defibrillators.3 Also, the guidelines emphasize the use of a bag-valve mask, oxygen, and advanced airways in emergency care.3 Therefore, all personnel on the medical team should receive appropriate training for these devices. All necessary supplemental equipment should be at the site of the athletic event and quickly accessible. In addition, all equipment should be checked on a regular basis to ensure that it is in proper working order. The medical team has numerous communication options including land-line phones, cell phones, or walkie-talkies as their primary communication system in the emergency plan. However, access to a working telephone, whether fixed or mobile, should always be ensured.3 Verifying that the communication system is operational prior to each practice or competition is essential. A list of emergency numbers should be prominently posted as well as the street address and directions to the athletic venue.

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In an emergency situation, the athlete should be transported by ambulance to the most appropriate receiving facility.3 When determining on-site medical coverage of athletic events, it is important to consider emergency medical services response time and the level of transportation service that is available.3 It is recommended to have an ambulance on-site at high-risk events (Table 3-6).3,4 When an ambulance is on-site, a location should be designated with rapid access to the site and a cleared route for entering and exiting the venue.5 Access to an emergency care facility is part of the emergency plan. When choosing an emergency care facility, consideration should be given to its location with respect to the athletic venue and the level of service available.3 This will help to ensure rapid and effective care of athletes. Also, steps should be taken to notify the emergency care facility in advance of athletic events. The facilities administration and medical staff should review the emergency response plan to address any care issues from their perspective. The primary documentation will be the written emergency response plan itself. The emergency plan will be separate and specific to each athletic venue. Each emergency plan should name a person or group to be responsible for documenting the events of the emergency situation.3 Also, documentation of regular rehearsal of the emergency plan, personnel training, and equip-

TABLE 3-6 National Collegiate Athlete Association Guidelines for Recommended On-Site Medical Coverage of Sport Activities4 Minimum qualifications: certification in cardiopulmonary resuscitation, first aid, and prevention of disease transmission High-risk sports: certified athletic trainer physically present during all practices and competitions Basketball (men) Football Skiing Gymnastics Ice hockey Wrestling Moderate-risk sports: certified athletic trainer (ATC), or other designated person with the minimal qualifications physically present, or ATC must be able to respond within 4 minutes Basketball (women) Diving Soccer Indoor track Lacrosse Volleyball Field hockey Low-risk sports: Any individual who possesses the minimum qualifications Baseball Outdoor track Water polo Golf Tennis Fencing Swimming Cross country Crew Softball Strength/conditioning, individual skill sessions, and voluntary summer workouts

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ment maintenance is recommended to ensure high-quality medical care.3 Once the emergency response plan has been developed, the plan must be implemented. The first step to implement the emergency response plan is to have the plan committed to writing to provide a clear response mechanism and to allow for continuity among emergency team members.3 Typically, this is accomplished by using a flow sheet or organizational chart. Table 3-7 shows an example for a venue-specific emergency response plan. The written plan will need to have the ability to be mod-

TABLE 3-7 Sample Venue–Specific Emergency Protocol3 University Sports Medicine Football Emergency Protocol 1. Call 911 or other emergency number consistent with organizational policies. 2. Instruct emergency medical services (EMS) personnel to “report to __________ and meet __________ at __________ as we have an injured student athlete in need of emergency medical treatment.” University Football Practice Complex: __________ Street entrance (gate across street from __________) cross street: __________ Street University Stadium: Gate __________ entrance off __________ Road 3. Provide necessary information to EMS personnel: a. Name, address, telephone number of caller b. Number of victims, condition of victims c. First-aid treatment initiated d. Specific directions as needed to locate scene e. Other information as requested by dispatcher 4. Provide appropriate emergency care until arrival of EMS personnel; on arrival of EMS personnel, provide pertinent information (method of injury, vital signs, treatment rendered, medical history) and assist with emergency care as needed.

ified depending on the athletic venue and for practices versus games. The second step in implementing an emergency response plan is educating the members of the medical team.3 All personnel should be given a written copy of the emergency response plan to review. The emergency plan should provide team members with a description of their roles and responsibilities during an emergency situation. Also, a copy of the emergency response plan specific to each venue should be posted in a prominent area, such as by an available telephone.3 The third and final step to ensure proper implementation of the emergency response plan is rehearsal.3 By rehearsing the emergency plan and procedures, the medical team can continue to improve their emergency skills. In addition, this allows medical and emergency medical services personnel to communicate and modify the plan if needed. A minimum of an annual in-service meeting/rehearsal is recommended to achieve these goals. The sports medicine team should strive to provide improved medical care to its athletes each season. The team physician should coordinate a postseason meeting with appropriate team personnel and administration to review the injuries and illnesses that occurred during the season.2 This postseason meeting would be a good time to review and modify the existing medical and administrative protocols as well as implement new strategies to improve sideline preparedness for the upcoming season. Postseason evaluation of the sports medicine team’s sideline coverage will promote improvement of medical services for future seasons and optimize the medical care of injured or ill athletes.4

GAME-DAY PLANNING Game-day planning will optimize the medical care for an athlete on the day of the event. The duties of the team physician on a game day are numerous and were covered in Chapter 1. However, essential duties of the team physician on game day to prevent, prepare for, or manage an emergency situation are shown in Box 3-1.2

Note 1. Sports medicine staff member should accompany student athlete to hospital. 2. Notify other sports medicine staff immediately. 3. Parents should be contacted by sports medicine staff. 4. Inform coach(es) and administration. 5. Obtain medical history and insurance information. 6. Appropriate injury reports should be completed. Emergency Telephone Numbers __________ Hospital

__________-__________

__________ Emergency department

__________-__________

University Health Center

__________-__________

Campus Police

__________-__________

Emergency Signals Physician: arm extended overhead with clenched fist Paramedics: point to location in end zone by home locker room and wave onto field Spine board: arms held horizontally Stretcher: supinated hands in front of body or waist level Splints: hand to lower leg or thigh

Box 3-1 Game-day Planning • Determination of final clearance or return-to-play status of injured or ill athletes • Preparation of sideline “medical bag” (Table 3-8) and check of sideline medical equipment (Table 3-9) to ensure all is in working order • Close observation of the game from an appropriate location • Assessment of environmental concerns and playing conditions • Presence of medical personnel at the competition site with sufficient time for all pregame preparations • Planning with the medical staff of the opposing team for medical care of the athletes • Introductions of the medical team to game officials • Review of the emergency medical response plan with all personnel who are responsible for carrying out the plan • Checking and confirming communication equipment • Identification of examination and treatment sites

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TABLE 3-8 Description of What to Include in Sideline “Medical Bag”2,5,6 • Alcohol swabs and providone iodine swabs • Bandage scissors • Bandages, sterile/nonsterile, Band-Aids • 50% dextrose water solution • Disinfectant • Gloves, sterile/nonsterile • Large-bore Angiocath for tension pneumothorax (14–16 gauge)

MEDICAL BAG The team physician needs to be prepared to treat a wide variety of traumatic and medical conditions. By maintaining a sideline “medical bag,” the team physician can provide rapid and appropriate treatment to an athlete, especially in an emergency situation. Table 3-8 provides a list of suggested items to carry in the team physician’s bag for contact/collision and high-risk sports. The contents of this bag may vary somewhat depending on the type of sport, the availability of medical supplies provided by the athletic trainer or event site, and the physician’s own preferences.2,5,6

• Local anesthetic/syringes/needles

Sideline Medical Supplies

• Sharps box and red bag

There are several sideline medical supplies that may be needed in an emergency situation (Table 3-9). Many of these items are too bulky to be carried in the team physician’s bag, so care should be taken to ensure that these supplies are provided by the athletic trainer, athletic venue, or on-site paramedics.2,5,6 The most essential of these supplies would be items used for cardiopulmonary resuscitation and airway management, such as an automated external defibrillator, advanced cardiac life support drugs, and a bag-valve mask with an oxygen supply. Once again, the type of sport, level of competition, and available medical resources must all be considered when determining the on-site sideline medical supplies.

• Suture set/Steri-Strips • Wound irrigation materials (e.g., sterile normal saline, 10–50 mL syringe) • Oral airway • Blood pressure cuff • Cricothyrotomy kit • Epinephrine, 1 : 1000 in a prepackaged unit • Mouth-to-mouth mask • Short-acting beta agonist inhaler • Stethoscope • Dental kit (e.g., cyanoacrylate, Hank’s solution) • Eye kit (e.g., blue light, fluorescein stain strips, eye patch pads, cotton tip applicators, ocular anesthetic and antibiotics, contact remover, mirror) • Flashlight • Pin or other sharp object for sensory testing

TABLE 3-9 Recommended Sideline Medical Supplies2,5,6

• Reflex hammer • Rectal thermometer • Benzoin • Blister care materials • Contact lens case and solution • 30% ferric subsulfate solution (e.g., Monsel’s solution) • Injury and illness care instruction sheets for the patient • List of emergency phone numbers • Nail clippers • Nasal packing material • Oto-ophthalmoscope • Paper bags for treatment of hyperventilation • Prescription pad • Razor and shaving cream • Scalpel • Skin lubricant • Skin staple applicator • Small mirror • Supplemental and parenteral • Tongue depressors • Topical antibiotics

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• Automated external defibrillator • Advanced cardiac life support drugs and equipment (crash cart) • IV fluids and administration set • Tourniquet • Access to a phone • Extremity splints • Ice • Oral fluid replacement • Plastic bags • Sling • Blanket • Crutches • Mouth guards • Sling psychrometer and temperature/humidity activity risk chart • Tape cutter • Sideline concussion assessment protocol • Face mask removal tool • Semirigid cervical collar • Spine board and attachments

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REFERENCES 1. Klossner D, Schluep C, Allen B (eds): NCAA Sports Medicine Handbook, 16th ed. Indianapolis, National Collegiate Athletic Association, 2003. 2. The American Academy of Family Physicians, American Academy of Orthopedic Surgeons, American College of Sports Medicine, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Society for Sports Medicine. Sideline preparedness for the team physician: A consensus statement, 2000. Available at: www.amssm.org/SidelinePrepare.html. 3. Anderson JC, Courson RW, Kleiner DM, et al: National Athletic Trainers’ Association position statement: Emergency planning in athletics. J Athletic Train 2002;37:99–104.

4. The National Athletic Trainers’ Association Recommendations and Guidelines for Appropriate Medical Coverage of Intercollegiate Athletics, 2003. Available at: www.nata.org/publicinformation/files/amciarecsandguidesrevised.pdf. 5. Brukner P, Khan K: Clinical Sports Medicine, 2nd ed. New York, McGraw-Hill, 2002, pp 713–725. 6. Delee JC, Drez D, Miller MD: Orthopaedic Sports Medicine Principles and Practice, 2nd ed. Philadelphia, Elsevier, 2003, pp 737–768.

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CHAPTER

4

Cardiac Problems and Sudden Death James C. Puffer

In This Chapter

ETIOLOGY

Epidemiology Athletic heart Specific causes of sudden deat Hypertrophic cardiomyopathy Coronary artery abnormalities Arrythmogenic right ventricular cardiomyopathy Screening

Sudden death in young athletes is usually associated with physical exertion, and unsuspected congenital cardiac abnormalities are usually found postmortem in young athletes. For the purposes of this chapter, we limit our discussion of SCD to the younger athlete (those younger than 35 years of age), since in the older athlete, this issue is relatively straightforward; the overwhelming majority of sudden deaths are caused by atherosclerotic coronary artery disease. The etiology of SCD in young athletes has been well documented. Maron et al1 analyzed 158 sudden deaths in athletes in the United States from 1985 to 1995. Eighty-five percent of deaths were cardiovascular in nature, and hypertrophic cardiomyopathy (HCM) and congenital coronary artery abnormalities were the most common causes of sudden death. Basketball and football players accounted for 68% of deaths, this in large part due to the greater number of athletes participating in these two sports at all levels. The common causes of SCD in young athletes are listed in Table 4-1.

INTRODUCTION • Sudden cardiac death (SCD) in young athletes occurs infrequently, but most occurrences are highly publicized and renew questions about screening and prevention. • Approximately 85% of deaths in young athletes are cardiovascular in nature. • Hypertrophic cardiomyopathy and congenital coronary artery abnormalities are the most common causes of SCD. • The rate of SCD has been estimated between 0.46 and 1.6 per 100,000 athletes annually. • Premonitory symptoms in athletes, such as syncope and chest pain, deserve aggressive investigation. • The current American Heart Association recommendation for screening of athletes is a careful history and physical examination with specific attention to 13 recommended items.

Perhaps nothing is more sobering than to pick up the newspaper and learn of the sudden and tragic death of a promising young athlete. While many of these unfortunate events are traumatic in nature, some are due to structural or acquired heart disease. Even though sudden death due to cardiac disease is a relatively infrequent event in athletes, a single occurrence is almost always highly publicized and renews questions about the screening of young athletes and the ability of such screening to prevent these rare, but highly visible events. In this chapter, we explore the common causes of SCD in athletes and review the clinical assessment of these disorders. We contrast these pathologic conditions with the normal physiologic changes that occur in the heart in response to athletic training. Finally, we critically assess the utility of the cardiac preparticipation examination as a screening tool and the extent to which it can prevent SCD in athletes.

EPIDEMIOLOGY SCD occurs infrequently in young athletes. Using mandatory catastrophic insurance program data for high school athletes in Minnesota, Maron et al2 calculated prevalence rates of SCD during the 12-year period from 1985 to 1997 for athletes in grades 10 through 12. A total of 651,695 athletes competed in 27 sports for a total of 1,453,280 overall participations. Three deaths occurred, one from anomalous origin of the left main coronary artery from the right sinus of Valsalva, one from congenital aortic stenosis, and one from myocarditis. The calculated risk of sudden death was 1 per 500,000 participations. The annual rate of sudden death was 0.46 per 100,000 participants. Somewhat similar findings have been reported by Waller et al.3 Using data over 6 years from 44,481 necropsies in Marion County, they found that 18 athletic deaths had occurred for an overall incidence of 0.04%. Eighty-eight percent of deaths were cardiac in origin. As would be expected, the incidence of SCD varied annually, ranging from a low of 0% in 1989 to a high of .09% in 1988. It might be instructive to look at the epidemiologic aspects of SCD in a country where aggressive screening strategies are mandated by law for comparison. Thiene et al4 assessed the prevalence of sudden death in young athletes in the Veneto region of Italy and found an annual SCD rate of 0.75 per 100,000 in nonathletes compared to an annual rate of 1.6 per 100,000 athletes. Unlike the United States, arrhythmogenic right ventricular cardiomyopathy (ARVC) was found to be the

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Table 4-1 Causes of Sudden Cardiac Death in Young Athletes

Possible hypertrophic cardiomyopathy Coronary artery abnormalities Ruptured aortic aneurysm Myocarditis

No. of athletes

Hypertrophic cardiomyopathy

200

100

Aortic stenosis Arrhythmogenic right ventricular dysplasia

leading cause of death, followed by atherosclerotic coronary artery disease and coronary artery abnormalities as the second and third leading causes, respectively.

ATHLETIC HEART Before reviewing in detail the specific causes of sudden cardiac death in athletes, it is important to review the normal adaptations that occur in the athlete’s heart in response to training. These adaptations result in changes in heart morphology, increased parasympathetic activity, and down-regulation of sympathetic drive, with characteristic findings on the electrocardiogram (ECG) and echocardiogram. Collectively, this constellation of findings has been described as the athletic heart syndrome; it has been well described in the medical literature.5 It is important to contrast these normal physiologic adaptations to training with the pathologic conditions that are described later in this chapter, and for purposes of discussion in this chapter, we focus primarily on the morphologic changes that occur in the heart in response to athletic training.

Historical Perspective For more than a century, it has been well known that athletes benefit from hearts that are larger. Indeed, Sir William Osler appropriately recognized the importance of both genetic endowment and physical training in creating a heart that conferred advantage in athletic competition when he opined in 1892: “In the process of training, the getting of wind as it is called, is largely a gradual increase in the capability of the heart . . . . The large heart of athletes may be due to the prolonged use of their muscles, but no man becomes a great runner or oarsman who has not naturally a capable if not large heart.” Unfortunately, at the turn of the past century, many believed that the cardiac changes that resulted from vigorous exercise were potentially deleterious to the athlete’s health. These misconceptions were eventually dispelled, and work in the early 20th century by Deutsch and Kauf6 helped ground our understanding of the athletic heart. They systematically studied the radiographic dimensions of thousands of hearts of athletes of all ages at the Vienna Heart Station by measuring the transverse diameter of the hearts of male and female competitors in 16 sports and compared them to published norms. Not surprisingly, the average heart size for male competitors exceeded norms by 30% to 40%, and the average heart size for female competitors exceeded norms by 4% to 12%. Older athletes and those who had trained longer had the largest transverse diameters.

Changes in Cardiac Morphology Grasping a few basic concepts of cardiac physiology will help explain the changes in cardiac dimensions that occur in specific

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0 55 mm) and diminished in HCM (55, lower risk of cardiovascular complications Less expensive Can lower plasma volume, cardiac output, peripheral vascular resistance Banned in elite athletes

b-Blockers

Decrease cardiac output May decrease exercise tolerance Can cause hypoglycemia Banned in some Olympic sports

ACE inhibitors

Can decrease heart rate and total peripheral resistance Prevent kidney remodeling effects of chronic hypertension Often cause cough Risk of hyperkalemia

Calcium channel blockers

Result in generalized vasodilation Concerns regarding side effects and cardiovascular risks

ACE, angiotensin-converting enzyme.

effects on exercise parameters by decreasing cardiac output. bBlockers have been suggested to increase perceived effort with exercise, which may lead to decreased exercise tolerance. bBlockers may also cause hypoglycemia after exercise due to inhibition of glycolysis and glycogenolysis.6 The use of combination a- and b-blockers has been proposed in hopes of limiting the impairment of skeletal blood flow and oxygen uptake due to the b-blocker effects of decreased cardiac output.4 However, there are concerns for a-blockers, discussed later, which may preclude the use of such combination agents. More recently, abnormal recovery of heart rate after exercise has been linked with increased risk of cardiovascular and allcause mortality. The negative chronotropic effects of b-blockers can decrease heart rate recovery following exercise, and the risk of using this medication in an already at-risk population with hypertension is unclear. Desai et al7 argue that heart rate recovery is not a separate variable but a reflection of a patient’s chronotropic response to exercise. However, this does not remove the potential risk associated with the negative chronotropic effects of b-blockers, and this risk must be weighed against the benefit of blood pressure control on an individual basis. b-Blockers have also been shown to increase the likelihood that an exercise treadmill test will be nondiagnostic. While a negative exercise treadmill test did not lose predictive value in the face of b-blocker use, as many as 20% of patients on bblockers with a nondiagnostic exercise treadmill test were subsequently found to have significant coronary artery disease.8 Following a myocardial infarction, patients on long-acting bblockers for 3 months experienced increased exercise capacity. This finding runs counter to the general association of decreased exercise tolerance with b-blockers, as mentioned previously. In patients who have had a heart attack, this difference in longacting b-blocker effects may be explained by improved left ventricular filling during diastole with improved subendocardial perfusion and subsequently less ischemia.9

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b-Blockers are banned in certain Olympic sports, although this is more for their calming or anxiolytic effect. In fact, bblockers are generally accepted as ergolytic with regard to endurance activities.5 Angiotensin-Converting Enzyme Inhibitors ACEIs can cause slight decreases in heart rate and total peripheral resistance along with an increase in stroke volume. ACEIs have not been shown to impair energy metabolism, maximal oxygen uptake, or training capacity.4 ACEIs have special utility in preventing kidney remodeling effects due to chronic hypertension. As this utility especially applies to African-American patients and patients with diabetes mellitus, ACEIs may be superior to b-blockers for these patients.10 It has also been suggested that ACEIs are most effective in combination with diuretics and that the renoprotective effect of ACEIs counterbalances the increase in creatinine that can be seen with diuretic use. The antihypertensive effects of ACEIs may be blocked by use of nonsteroidal anti-inflammatory drugs (NSAIDs).11 ACEIs are notorious for causing significant cough. For patients who experience cough, consideration may be given to switch to an angiotensin-receptor blocker. Angiotensin-receptor blockers also prevent proteinuria, which is beneficial for diabetic patients with renal disease.11 As compared to b-blockers, angiotensin-receptor blockers improve the risk of stroke and equally protect against high blood pressure and all-cause mortality.12 Also among the medications affecting the reninangiotensin-aldosterone axis are aldosterone-receptor antagonists. These medications are relatively new and do not have large amount of study data to support effects on morbidity and mortality. They also carry significant risks of hyperkalemia and interaction with medications metabolized by cytochrome P-450.2 The general utility of aldosterone-receptor antagonists remains unclear. Calcium Channel Blockers Calcium channel blockers (CCBs) result in generalized vasodilation, but they do not have effects on energy metabolism or oxygen uptake.4 While previously popular, newer evidence based on side effect profiles and cardiovascular risks discourages early use of short-acting calcium channel blockers, with consideration for the use of other CCBs only if ACEIs or b-blockers are ineffective.13 a-Blockers a-Blockers decrease systemic vascular resistance without changes in heart rate or cardiac output, and they do not change energy metabolism or oxygen uptake. Their use may also result in centrally mediated side effects such as dry mouth, drowsiness, and decreased sexual function.4 The use of a-blockers was discontinued in the ALLHAT study due to an associated increased risk of congestive heart failure and stroke.14

Hypercholesterolemia Statins Hypercholesterolemia contributes significantly to overall cardiovascular morbidity and mortality. Statins are the number one class of anticholesterol medications. They are well known for side effects of gastrointestinal disturbance, headache, and rash. For athletes, myalgias and, rarely, rhabdomyolysis are possible complications of significant import. Baseline creatine kinase levels prior to onset of statin therapy may be useful in case these complications arise.15 Most changes in creatine kinase levels with statin use and/or exercise are asymptomatic. Rhabdomyolysis

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appears to be more likely to occur due to a combination of statin use, exercise, and another medication metabolized by cytochrome P-450.16 In an experimental trial of over-thecounter use of statins, 17% of users experienced a drug-related adverse event, and 12% of users discontinued statin therapy due to an adverse event.17 Most studies of statins and exercise involve patients with some form of vascular disease. In patients with claudication due to peripheral artery disease, statin use improved total treadmill time and walking distance.18,19 In patients with significant coronary artery disease, statin use significantly decreased myocardial ischemia due to exercise without affecting peak heart rate, systolic blood pressure, or diastolic blood pressure.20

Exercise-Induced Asthma The prevalence of exercise-induced asthma ranges from 9% to 50%, depending on the sport cited.21 The acute release of bronchoconstricting agents and the chronic inflammatory airway changes, both of which are complexly intertwined, suggest two pathways to target for prevention of exercise-induced asthma attacks. A recent Cochrane review confirms that albuterol, a short-acting beta agonist, is the number one treatment for exercise-induced asthma episodes. The bronchodilating effects of albuterol are superior in the acute setting to the anti-inflammatory effects of cromolyn (a mast cell stabilizer) or the anticholinergic effects of ipratropium.22 Appropriate use of albuterol must consider tolerance, timing of use, and ergogenic effects. Beta Agonists Daily use of short-acting beta agonists has been linked with increased frequency of bronchoconstriction during exercise and suboptimal efficacy of rescue.23 While no ergogenic effects of short-acting beta agonists have been demonstrated at therapeutic doses, increased use among Olympic athletes has been documented.24 Long-acting beta agonists are equally effective, can have similarly quick time to onset, and often result in longer periods of protection.25,26 Long-acting beta agonists have also not been shown to possess ergogenic benefits.27 Anti-inflammatory Medications Inhaled corticosteroids are standard therapy for patients with persistent asthma. While not well studied in exercise, the pulmonary delivery of inhaled corticosteroids has not shown any evidence of ergogenic or anabolic effects, and they are approved by the International Olympic Committee (IOC) via medical waiver for athletes with asthma.21 Leukotriene inhibitors are a new class of oral anti-inflammatory medications for asthmatics. While considered to be less effective than inhaled corticosteroids, the oral delivery of leukotriene inhibitors may provide better compliance for some asthmatics. They can prevent acute episodes of exercise-induced asthma,28–30 but optimal protection requires them to be used 12 hours prior to exercise.28 Studies in children and adults have shown protective benefits after a brief period of 5 to 7 days of use.29,30 Minimal studies in adults have shown no change in time to anaerobic threshold with leukotriene inhibitor use, but there was a decrease in ratings of perceived exertion.30 Further studies of potential ergogenic effects of leukotriene inhibitors would be helpful.

Psychiatric Conditions Antidepressants and Anxiolytics Primary care physicians commonly treat patients with depression and anxiety, and athletes with these conditions compete at

all skill levels. However, very little research exists studying the interaction of medications for these conditions and exercise. In a study of patients with major depressive disorder, decreases in isokinetic quadriceps and hamstring strength were shown to improve significantly after 3 months of treatment with a selective serotonin reuptake inhibitor.31 However, selective serotonin reuptake inhibitors have also been linked with significant weight gain after 6 to 12 months of use32 and possible episodes of heatrelated illness and hyponatremia.33,34 In a small trial of patients, use of loprazolam, a benzodiazepine that can be used for anxiety, did not affect hand-eye coordination, 30-m sprint time, V·O2max, or time to exhaustion. However, use of loprazolam was associated with prolonged reaction time and a significant hangover effect.35 In a smaller study with midazolam, subjects experienced significant changes in heart rate variability and had significant orthostatic changes in blood pressure.36 No large, double-blind, randomized, controlled trials exist for either class of medication. Accordingly, no contraindications exist for the appropriate treatment of depression or anxiety. The only performance concerns might relate to a possible advantage from the anxiolytic effects of these medications (especially benzodiazepines) in shooting events such as the biathlon. Stimulant Therapy for Attention Deficit Disorder Attention-deficit disorder (ADD) affects an estimated 5% of the school-age population,37 with a growing trend toward the identification of impairment due to ADD among adults. Methylphenidate is the standard treatment for ADD with either hyperactive, inattentive, or mixed predominance of symptoms. Methylphenidate is also a stimulant with properties and side effects similar to those of other drugs in the amphetamine class, including an ergogenic effect mediated by delayed fatigue. Methylphenidate is banned by the IOC and the National Collegiate Athletic Association. However, the National Collegiate Athletic Association has recognized the utility of methylphenidate in helping student athletes with ADD to succeed academically. Therefore, a therapeutic use exemption exists for National Collegiate Athletic Association athletes with documented ADD and appropriate methylphenidate therapy.38 ADD is known to affect athletic participation in a number of ways, including lessened motivation to participate, impaired motor skills, and decreased performance success.39,40 Methylphenidate has been shown to improve the attention of youths with ADD during baseball games, as reflected in higher rates of on-task behavior while on the field and better knowledge of their current game-specific situation.41 Methylphenidate has also been demonstrated to improve visual tracking by athletes with ADD during table tennis by maintaining their gaze on the ball in flight for significantly longer periods of time.42 Athletes with ADD who use methylphenidate should be aware of a possible increased risk of heat-related illness due to the stimulant’s cardiovascular properties. However, methylphenidate may not only help athletes with ADD to succeed at work or school, but it may help them to more fully participate in athletics, thereby receiving a boost in self-esteem that many patients with ADD need.

Pain Relievers/Osteoarthritis Acetaminophen Acetaminophen is a well-known pain reliever, yet it is often thought of as secondary to NSAIDs because it is thought to not possess anti-inflammatory effects (Table 5-2). However, acetaminophen has been shown to affect prostaglandin production in

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Table 5-2 Pain Relievers/Osteoarthritis Medications Medication

Characteristics

Acetaminophen

Better side effect profile, especially for gastrointestinal effects No anti-inflammatory effects? Less pain relief?

NSAIDs

Analgesic, anti-inflammatory Impaired healing of muscle, tendon, and bone?

COX-2 inhibitors

Decreased gastrointestinal side effects Increased risk of thrombotic events?

Glucosamine

Good safety profile Efficacy less proven?

COX, cyclooxygenase; NSAIDs, nonsteroidal anti-inflammatory drugs.

exercised muscle, which may be linked to decreasing the building of new muscle after exercise.43 In low back pain, acetaminophen has been shown to be equally beneficial as compared to NSAIDs.44 Acetaminophen also has a role in first-line pharmaceutical management of osteoarthritis,45 with studies suggesting benefit equal to that of NSAIDs in pain relief with a better side effect profile, especially for gastrointestinal effects.46 More recent research has suggested that acetaminophen provides less pain relief without side effect benefits as compared to cyclooxygenase (COX)-2 inhibitors such as celecoxib.47 Yet given the newer concerns for COX-2 inhibitors and their prothrombotic potential, acetaminophen remains for most patients a more appropriate first-line choice for analgesia based on side effect profiles. Nonsteroidal Anti-inflammatory Drugs NSAIDs make up a popular class of over-the-counter and prescription pain relievers. Advertisements for NSAIDs are often targeted at athletes of all levels for their anti-inflammatory effects, which differentiate this class from other pain relievers such as acetaminophen. Such directed marketing is apparently effective, as one study found that at least 20% of high school football players surveyed used NSAIDs on a daily basis in season. These athletes used NSAIDs with expectations of improved athletic performance and prevention of pain that might occur during practice or competition.48 NSAIDs are not thought to have stand-alone ergogenic properties. Their analgesic effect may allow increased training and/or performance, but the masking of pain by use of NSAIDs interrupts a natural defense mechanism for preventing further injury. Additionally, as inflammation is a part of the healing process for most injuries, the antiinflammatory effect of NSAIDs may be detrimental to recovery from injury. Several studies, using animal and human models, have examined the impact of various NSAIDs on the healing of injuries to soft tissue and bone. In the case of muscle injury, NSAIDs may provide an initial protective effect in the first several days, but over time their use has been associated with impaired rates of healing in both macrotrauma and microtrauma.49,50 One human subject study showed that naproxen did improve recovery from delayed-onset muscle soreness, but the study did not examine the drug’s effects on muscle structure or objective strength.51 In animal studies of medial collateral ligament injuries, use of NSAIDs was again associated with a brief initial improvement,52

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yet no benefit to ligament strength was shown 3 to 4 weeks after the injury.52,53 In human subject testing, the Kapooka Ankle Sprain Study is perhaps the best investigation of the effects of NSAIDs on ligamentous injury. Following treatment with piroxicam, the military recruits in the study noted better pain relief and a faster return to physical training compared to placebo. However, the authors noted “some evidence of local abnormalities such as instability and reduced range of movement” with NSAID therapy.54 For tendon injuries, a review of nine studies of treatment with NSAIDs documented significant pain relief compared to placebo in only five of the studies.55 In a separate study of Achilles’ tendon injury, no benefit to either range of motion or strength was seen following piroxicam therapy.56 It should be noted that none of these studies involved biopsy of the tendons involved, possibly reflecting the different characteristics of tendonopathy versus tendonitis. For injuries to bone, use of NSAIDs is of concern for two reasons. NSAIDs likely inhibit the production of prostaglandin E2, a prostaglandin with a known role in bone healing. NSAIDs also inhibit pain, which is a useful marker in recovery from injury, especially stress fracture. One study from the United Kingdom showed that regular use of NSAIDs was associated with a 47% increase in the rate of nonvertebral fractures.57 In comparison with acetaminophen, a Cochrane review demonstrated no evidence that NSAIDs are more effective for low back pain.44 A recent meta-analysis of studies involving patients with osteoarthritis showed NSAIDs were superior to acetaminophen in terms of pain relief, but the better analgesia came at the cost of a significant increase in side effects, with gastrointestinal effects being most common.58 Therefore, NSAIDs may benefit minor muscle injury, but they appear equivocal at best for ligament and tendon injuries and may hinder healing of more severe muscle and bone injuries. While effective at pain relief, the analgesia of NSAIDs may block an important defense mechanism to further injury and be accompanied by significant side effects. Cyclooxygenase-2 Inhibitors The cyclooxygenase-2 (COX-2) enzyme mediates production of prostaglandins involved in tissue inflammation, while prostaglandins that protect the mucosal lining of the gastrointestinal tract are made via COX-1 pathways. NSAIDs are nonspecific in their inhibition of COX-1 and COX-2. Therefore, a new class of medication, COX-2 inhibitors, was designed to specifically target the COX-2 enzyme and improve the side effect profile of earlier NSAIDs. Two studies of ankle sprains in human subjects showed no difference between the COX-2 inhibitor celecoxib and ibuprofen or naproxen with regard to reports of pain or activity levels; celecoxib did outperform placebo therapy. As expected, the gastrointestinal side effects were significantly reduced with COX-2 inhibitor therapy.59,60 COX-2 inhibitors have been more prominent in the news in recent months due to an associated risk of thrombotic events with use of rofecoxib. In reviewing the data surrounding this controversy, it is important to remember that COX-2 inhibitors were initially designed for use in patients with rheumatoid arthritis and that studies reflect their use in that population. It has yet to be determined whether the results are generalizable to younger athletes or how this association might affect adults without rheumatoid arthritis but who have significant cardiovascular risk factors and attempt to exercise regularly.

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The Vioxx Gastrointestinal Outcomes Research study compared treatment with rofecoxib versus naproxen in patients with rheumatoid arthritis. Rofecoxib successfully decreased serious gastrointestinal events by one half (4% incidence to 2%). However, the incidence of myocardial infarction in users of rofecoxib was 500% higher than among naproxen users.61 It was initially argued that the difference seen might be attributed to the relatively small number of cardiac events and/or a possible protective effect of naproxen, as COX-1 inhibition can prevent platelet aggregation. More recently, the APPROVe (Adenomatous Polyp Prevention on Vioxx) study was stopped early because an 84% increase in heart attacks and a 390% increase in serious thrombotic events were observed among rofecoxib users.62 Some researchers believe that this association is due to the inhibition of prostaglandin I2, which normally blocks platelet aggregation and protects the endothelial surface of blood vessels. Prostaglandin I2 production was previously believed to be mediated by COX-1, but new research has determined that prostaglandin I2 is regulated by COX-2. Also concerning was the fact that the APPROVe study was not aimed at patients with rheumatoid arthritis, but was rather a more general study of adult patients. Therefore, this prothrombotic effect may be more generalizable than previously believed, as well as a class effect of COX-2 inhibitors and not specific to rofecoxib. The Celecoxib Long Term Arthritis Safety study published data showing no increase in cardiovascular risks after 6 months of celecoxib therapy. However, after 12 months of use, a trend toward increased risk of thrombotic events was noted, although the study was not specifically designed to detect this specific risk. Additionally, celecoxib appeared to lose its effectiveness in preventing gastrointestinal side effects in those patients on daily aspirin therapy.62 Therefore, COX-2 inhibitors possess similar analgesic properties as compared to general NSAIDs, and the improvement in side effect profile of the COX-2 inhibitors seems tenuous when the prothrombotic risks associated with rofecoxib are considered. Glucosamine Glucosamine is a popular over-the-counter supplement for osteoarthritis. Most studies support glucosamine as effective in both symptom improvement and prevention of joint space loss.63–65 One additional study suggests no improvement compared with placebo, but this was an Internet-based survey using only subjective measures of symptoms and function.66 All the studies cited agree on the relative safety of glucosamine use, at least in the short term. Little can be said for long-term effectiveness or safety of glucosamine beyond 3 years of use. Interestingly, there is some evidence that glucosamine may not prevent flare-ups of osteoarthritis symptoms even after previous improvement with glucosamine.67 These differences between studies, as well as differences between patients, may exist based on rates of cartilage turnover. Research exists suggesting that high rates of cartilage turnover support a favorable response to glucosamine therapy.68 Overall, glucosamine appears safe and effective for many with osteoarthritis, and based on population studies, it is considered cost-effective for improving the quality of life of these patients.69

SUPPLEMENTS Dietary supplements grew in popularity in the late 20th century out of a confluence of various motivations, including nutritional improvement, weight control, and performance enhancement.

Many dietary supplements contained ingredients found in other foods and/or medications, yet their production alone or in certain combinations placed them outside of both of these wellregulated categories. In 1994, the U.S. Congress passed the Dietary Supplement Health and Education Act, creating separate regulatory control for the multibillion dollar industry of dietary supplement manufacturing. Unfortunately, as evidenced by the 7-year process that culminated in the 2004 ban on products containing ephedra, the Dietary Supplement Health and Education Act lacks effective means for enforcing production standards and protecting consumers’ health.70 Nevertheless, dietary supplements remain immensely popular among athletes of all ages and skill levels. Physicians should actively inquire as to the use of supplements by their patients and provide appropriate counseling for informed decision making.

Creatine Creatine is one of the most common nutritional supplements employed for possible ergogenic benefits. The Metzl et al71 survey of high school students reported use by as many as 44% of high school senior athletes, which parallels estimates of collegiate use. Creatine has become generally accepted to provide benefit in short, maximally anaerobic events, likely through enhancement of adenosine triphosphate regeneration.72 There is also some evidence suggesting a possible direct effect of creatine on muscle development through increased expression of mRNA and growth factors specific to muscle.73 Whether by direct effect or through increased capacity for resistance training, creatine has been linked with increases in muscle mass, including by direct measurements such as ultrasonography.74 As to the effects of creatine on actual strength and sports performance, the supplement has had mixed results at best. Some authors have demonstrated improvement in shortduration events like repeated sprints,75 although this has not been reproduced in other trials.76 Other investigators have shown improvement in specific soccer drills,77 but again this has not held for studies with athletes from other sports such as rugby or softball.78,79 Kilduff et al80 noted that subjects with the largest increases in body mass had the greatest increases in strength, suggesting that there are some athletes who are “responders” to creatine while others are not. Overall, creatine may have some benefit for short-term bursts of exercise, yet this benefit is highly variable and may not apply to all athletes. Creatine has been linked anecdotally to reports of heat-related illness and renal dysfunction. However, with the brief use of 6 to 12 weeks documented in most trials, creatine has appeared to be relatively safe. With its popularity among young athletes, concern should be given to the possible effects of increased muscle mass on open growth plates, as well as the lack of studies involving long-term use among children and adolescents.

Prohormones Prohormones such as DHEA (dehydroepiandrosterone) and androstenedione reached a peak in popularity during the 1990s as their use by high-profile athletes became common knowledge. In a survey conducted by the Department of Health and Human Services in 2002, an estimated 2% to 2.5% of high school students reported using androstenedione.81 Unfortunately, the perceived success of athletes known to use these products has been interpreted by many youths as a cause-and-effect relationship, when medical evidence runs to the contrary.

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In his review of the literature, Ahrendt82 found no published studies that reported ergogenic benefits of DHEA use. In one study, DHEA did increase androgen levels, but there were no increases in strength or lean body mass measurements following resistance training.83 Similarly, Tokish et al72 reviewed the literature and found no evidence of ergogenic benefits of androstenedione. In fact, there may be an increased risk of cardiovascular disease with androstenedione use due to decreased high-density lipoprotein levels. Other studies have demonstrated no effect of androstenedione on testosterone levels while increasing estrogen levels in males.84,85 Conversely, androstenedione has also been linked to elevating testosterone levels in females,86 suggesting a gender-specific metabolism of these products. Based on the clear estrogenic and androgenic effects of these products in the absence of any reasonable benefits, the U.S. Food and Drug Administration in 2004 issued a summary of the negative effects of androstenedione and a warning to its manufacturers that such products are in violation of the 1994 Dietary Supplement Health and Education Act, and that their production and marketing should cease.81,87

Beta-hydroxy-beta-methylbutyrate Beta-hydroxy-beta-methylbutyrate (HMB) is a relatively new product marketed as an “anti-catabolic” compound. Use of HMB has been associated with increased lean muscle mass and decreased CPK levels after exercise, but the mechanism of these effects is unclear.72 In a separate study, brief use of HMB did not prevent common effects of exercise such as muscle soreness or swelling.88 Other studies have shown HMB does not have an androgenic effect nor does it have a significant impact beyond resistance training alone on strength and body composition among athletes.89–91 Used either alone or with creatine, HMB has not shown ergogenic effects on either aerobic or anaerobic exercise, although one isolated study did demonstrate an increased time to peak lactate production with its use.92,93 Again, no clear mechanism exists to explain this effect. No major risks have been associated with HMB use. In fact, HMB may impart favorable cardiovascular effects via lipid metabolism.94 In summary, no clear performance advantage or positive health benefit has been attributed to HMB.

Alpha Agonists Phenylpropanolamine and pseudoephedrine, both alpha agonists, are commonly found in over-the-counter medications and known for their stimulant effects. In fact, since the U.S. Food and Drug Administration banned dietary supplements containing ephedrine, many manufacturers have replaced ephedrine with a variety of alpha agonist compounds. Numerous studies of the effects of phenylpropanolamine and pseudoephedrine on aerobic and anaerobic exercise have failed to show ergogenic benefits, with no significant benefits to power, work, V·O2max, or perceived exhaustion.95–100 These studies have tended to demonstrate a relatively safe cardiovascular profile, which would parallel the safety of these compounds in over-the-counter medications.96,98 However, one study has suggested increased heart rate at submaximal exercise levels and prolonged time to heart rate recovery with a common nonprescription dose of pseudoephedrine.100 An older trial also demonstrated an increased incidence of sinus arrhythmias without complication at maximal over-the-counter dose of pseudoephedrine.101 Cardiovascular side effects at supratherapeutic doses have not been studied, although these risks persist in theory. However, even at thera-

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peutic doses, phenylpropanolamine and pseudoephedrine are easily detected with blood and urine testing.99

Caffeine Caffeine is perhaps the most popular stimulant used by the general population. Prior to the U.S. Food and Drug Administration ban on products containing ephedrine, products combining caffeine and ephedrine were among the most purchased dietary supplements and weight-control compounds. Accordingly, much of the research into the ergogenic properties of caffeine actually studies combinations of caffeine and ephedrine. With regard to caffeine alone, caffeine is thought to be most beneficial for performance in endurance events, perhaps to enable the “kick” at the end of such an event.102 The metaanalysis of Doherty and Smith103 demonstrated caffeine’s ergogenic benefits, primarily in studies of endurance exercise and time-to-exhaustion measurements. The IOC threshold for caffeine, the equivalent of five to six cups of coffee, recognizes that dietary caffeine intake is ubiquitous. A commonly studied dose of 5 mg/kg 1 to 2 hours before exercise falls well below the IOC threshold for caffeine.102 However, that dose has been shown to decrease ratings of perceived exertion, increase power, and increase time to exhaustion.104–107 Effects appear to last for as long as 6 hours, but the effects are not enhanced by a second dose.105 The ergogenic effects are more pronounced in those who do not normally use caffeine,106 and similar results have been reproduced following as short as 6 days of abstinence from caffeine.107 Users should consider a recent study suggesting that heavy coffee consumption increased the short-term risk of heart attack and sudden cardiac death regardless of other cardiovascular risk factors.108 Yet at appropriate doses, caffeine appears to be a relatively safe ergogenic aid for endurance events.

ERGOGENIC DRUGS Clearly, athletes employ the supplements discussed previously in hopes of gaining an ergogenic benefit. However, this section focuses on drugs with clear ergogenic effects, as well as some that may result in ergolytic effects with long-term use. These drugs are banned by most sports-governing bodies, and most are illegal to obtain except for specific therapeutic purposes. However, these drugs remain relatively easy to procure, they pose significant health risks, and their use jeopardizes fair competition in sports.

Anabolic-Androgenic Steroids Anabolic-androgenic steroids (AASs) have well-known ergogenic effects, resulting in increased muscle mass and strength. Estimated gains in strength with AAS use range from 5% to 20%, but the doses of AAS used in studies may not match doses of abuse.109 More recent research has focused on the side effects of AAS use as well as strategies to prevent the use and abuse of AASs, especially among adolescents. AAS use is known to affect multiple organ systems. Negative effects on lipid profiles, especially decreases in high-density lipoprotein, have been known since the mid-1980s.110 While cardiac hypertrophy is commonly associated with steroid use, a recent review of the literature provided mixed results regarding this relationship.111 However, other research suggests that steroids may also cause abnormal left ventricular wall motion in an additive effect to resistance exercise.112 Steroids also affect red blood cell mass via erythropoietin production, as well as

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bone metabolism.109 Research has also explored the effects of AAS use on mental health. While AAS use has been linked with increased levels of aggression and manic behavior, these effects appear to vary greatly among individuals at controlled doses of AASs.113 In their survey published in 1998, Faigenbaum et al114 estimated that nearly 3% of junior high school students had used AASs, with the average user participating in three to four sports.114 With the frightening thought of the long-term repercussions of AAS use prior to or during puberty, research explored avenues of preventing AAS use among adolescents. The ATLAS study demonstrated rates of AAS use among high school students at 4% to 12%. During the intervention phase, adolescents were less likely to use or intend to use AASs. However, one year after the intervention, rates of actual use did not decline, demonstrating the difficulties in diverting adolescents from using “performance enhancers” such as AASs.115 The effects of AASs appear to be dose dependent as well as proportional to the duration of use.72 Therefore, testing not only plays a role in maintaining fair competition, but it also plays a preventive health role for these athletes. Traditional testing has analyzed the testosterone-to-epitestosterone ratio, with the cutoff ratio of 6 being two to six times greater than normal.72 However, the emergence of compounds such as tetrahydrogestrinone illustrates the sophistication of doping in sports. Tetrahydrogestrinone was identified thanks to the provision of a sample by a U.S. track coach in 2003. Tetrahydrogestrinone was a completely new compound, as opposed to an older steroid or veterinary medication.116 In vitro testing showed tetrahydrogestrinone to be highly androgenic but with no estrogenic activity.117 Tetrahydrogestrinone is a prime example of the need for cooperation among athletes, coaches, and medical professionals to not only police sport but to protect the health of athletes as well.

Human Growth Hormone Human growth hormone (HGH) has been approved for treatment of persons with endogenous HGH deficiency or short stature secondary to chronic renal failure. Additionally, HGH is used off label for patients with Turner’s syndrome and children born small for gestational age who have not had sufficient catchup growth.118 However, because of its success in treating these conditions, the abuse of HGH as an ergogenic aid has become widespread as well. In a survey of high school sophomores, Rickert et al119 found 5% of respondents had used HGH, with a significant association with AAS use as well. HGH is known to increase uptake of glucose and amino acids by skeletal muscle, increase protein synthesis, increase lipid breakdown, and increase rate of bone growth. At therapeutic doses of HGH, no studies have reported improvement in exercise performance parameters, including work capacity and strength.118 However, athletes abusing HGH are likely to use doses that surpass the therapeutic range. Known side effects of excess HGH include acromegaly, in which skeletal muscles are weaker. This myopathic effect likely explains the lack of performance enhancement at therapeutic doses. Other side effects of HGH abuse include insulin resistance and cardiomyopathy.72 Healy et al120 studied the use of HGH at doses similar to those in anecdotal reports of HGH abusers. While some “positive” effects such as increased protein synthesis and increased lean body mass were demonstrated, adverse effects were also found, including increased fasting insulin levels and increased insulin resistance. Additionally, no changes in body fat or performance parameters were seen after 4 weeks of HGH use.

In addition to the negative health effects of HGH abuse by athletes, Conrad and Potter121 excellently summarize the ethical dilemma of HGH use for purported antiaging effects and for idiopathic short stature. Consider the potential impact of using HGH for otherwise healthy pediatric patients at the third percentile for growth, resulting in a vicious cycle as the third percentile would then shift higher and higher with time. Equally disturbing would be the treatment of the 5 foot 10 inch high school basketball player in the hopes of reaching 6 feet and the perceived benefits of that difference. These possibilities highlight the need for testing for HGH abuse. Although difficulties in direct testing may exist due to similarities between endogenous and exogenous HGH, research has shown dose-dependent changes in markers of bone turnover that may be used for detection of HGH abuse.122 Sports-governing bodies must support further efforts to protect the health of their athletes as well as the integrity of their sport.

Erythropoietin Aerobic performance obviously requires oxygen delivery, and athletes have employed many methods to enhance oxygen delivery. Training at high altitudes to increase oxygen carrying capacity has become commonplace for elite athletes. Blood doping using autologous transfusions is a common illegal practice that continues to be employed, although it is more easily discovered with testing techniques for red blood cell age and requires equipment for storage, processing, and reinfusion.123 Erythropoietin (EPO) is the hormone responsible for red blood cell production in the human body. In the late 1980s, recombinant EPO (rEPO) was developed for patients with anemia secondary to chronic renal failure. Subsequently, the use of rEPO has been expanded to include patients with cancer and patients with human immunodeficiency virus.123 rEPO has been shown to increase hematocrit concentration in as little as 4 weeks, accompanied by significant increases in V·O2max124,125 and time to exhaustion.126 However, the mechanism of rEPO’s benefits relies on polycythemia with the potential for hyperviscosity.127 Therefore, the potential side effects of rEPO abuse include heart attack, stroke, and pulmonary embolus. While not linked conclusively, rEPO has been implicated in the deaths of several elite athletes. Testing for rEPO abuse initially focused on testing serum hematocrit levels, as well as levels of other blood cells that may reflect rEPO use.128 While generally effective, this method can be avoided by serum dilution with saline infusion. rEPO can be detected by urine or blood electrophoresis, but only if the testing occurs within a few days of rEPO administration.129 New research suggests that increases in the levels of soluble transferrin receptor occur with rEPO abuse and that this may be used for testing purposes.124

Alcohol Alcohol is the most popular mind-altering substance used. Athletes may use alcohol for an ergogenic benefit, believing that its anxiolytic effects can enhance self-confidence and thereby improve athletic performance.130 For certain sports, this anxiolytic effect may improve performance by decreasing tremor. Accordingly, the IOC has banned alcohol for fencing and shooting sports. Beyond these sports, however, alcohol tends to have negative impacts on performance, otherwise known as ergolytic effects. The American College of Sports Medicine released a position statement on alcohol use in 1982 citing detrimental psychomotor effects, no benefit to the work of skeletal muscle,

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decreased ability to control body temperature in cold temperatures, and no positive benefits to cardiopulmonary variables including V·O2max.131 Since then, further studies have shown actual declines in performance due to acute alcohol ingestion as measured by decreased time to exhaustion,132 slower distance run times,133 and slower times on short and middle distance run.134 The hangover effect of alcohol has also been estimated to decrease aerobic performance by 11%.135 Long-term concerns for alcohol use by athletes have centered on the profile of athletes as risk takers. Rates of alcohol abuse by athletes in one survey were 21%, and alcohol abuse was correlated with depression and other mental health symptoms. In a separate survey, drinking to cope with stress had the strongest link with negative consequences of alcohol use, including repercussions on athletes’ education, health, legal problems, and involvement in violent acts.136 A European survey showed that young adults who drank alcohol had a significantly higher risk of sports injury compared to nondrinkers.137

Marijuana Marijuana is the number one illegal drug used in the United States. Its legal status remains controversial, with viewpoints polarized between critics who view marijuana as a possible gateway drug and advocates for its medicinal use for patients undergoing chemotherapy or with acquired immunodeficiency syndrome.138 For athletes, concern again rises for possible marijuana use among a population of risk takers. In a survey of U.S. high school students, Ewing139 found that male athletes used marijuana more than their nonathlete peers, but that female athletes used marijuana less than their nonathlete peers. Interestingly, a French study suggests that elite athletic participation by adolescents and young adults has a protective effect against marijuana use.140 Marijuana might provide a performance benefit at low doses through relaxation and a possible improvement in auditory and visual perception.130 However, persistent use of marijuana, which is often accompanied by increased use or abuse due to tolerance, has definite ergolytic effects. THC (delta-9-tetrahydrocannabinol), the active compound in marijuana, causes significant increases in heart rate with either no change or a reduction in stroke volume, as well as an inappropriate chronotropic response to exercise.141 Decreases in V·O2max and maximal exercise tolerance have also been demonstrated with long-term marijuana use.142 Long-term use or abuse of marijuana can lead to an “amotivational syndrome,”130 from which loss of ambition, poor academic performance, and impaired social relationships can negatively affect athletic, academic, and professional success for athletes at all levels.

Cocaine Reaching its peak in popularity during the 1980s, the use of cocaine declined during the 1990s. The cardiac risks of cocaine

use are well-known, especially following the sudden deaths of high-profile athletes. Yet cocaine continues to be used by an estimated 2% of young adults.130 While cocaine enhances a sense of euphoria, it has been shown to be definitively ergolytic in animal studies. Cocaine use leads to faster depletion of muscle glycogen stores and lactate accumulation, along with decreased time to exhaustion.143 Interestingly, South Americans who routinely chew coca leaves were found to have increased plasma levels of free fatty acids, which might allow longer periods of submaximal exercise. However, these persons did not have any increase in maximal exercise capacity or efficiency with chewing coca leaves.144 Chronic use of crack cocaine has been linked in nonathletes with decreased aerobic capacity and decreased maximal heart rate.145

Methamphetamine Methamphetamine may have replaced cocaine in popularity as an illegal stimulant and euphoric. Methamphetamine is the number one controlled substance produced clandestinely since 1997. Methamphetamine should be considered ergogenic in the same manner as the class of amphetamines and other stimulants, with delayed time to exhaustion and improved ratings of perceived exertion. Its short-term effects include decreased appetite and increased energy, along with increases in heart rate and body temperature. However, long-term use of methamphetamine is directly linked with poor nutrition, fatigue, mental health disturbance, and lasting impairment in cognitive function. As mentioned before with alcohol, use of methamphetamine is also linked to coping with various stressors. Women tend to use methamphetamine for issues such as family/social dysfunction, emotional problems, and weight control. For men, parental use of methamphetamine or other drugs appears to have the strongest gender-specific influence on personal use. Most importantly, methamphetamine’s ease of acquisition is the number one factor in its use by all abusers.146 Athletes should be educated about the long-term debilitating effects of methamphetamine, and drug testing in sports should continue to include screening for amphetamine abuse.

CONCLUSIONS The lines between treating illness, maximizing health, and sports performance enhancement have been blurred by well-intentioned medical advances and societal pressures that lead athletes of all levels to seek a competitive edge. Unfortunately, for many athletes the inappropriate use of medications, supplements, and other drugs not only damage the image of their sport but also cause significant health consequences that extend well beyond the field of competition. Sports medicine professionals must remain educated regarding the impact of medications, supplements, and ergogenic drugs on both sport performance and, more importantly, the health of the patients whom they serve.

REFERENCES 1. Lively MW: Preparticipation physical examinations: A collegiate experience. Clin J Sport Med 1999;9:3–8. 2. Magill MK, Gunning K, Saffel-Shrier S, Gay C: New developments in the management of hypertension. Am Fam Physician 2003;68: 853–858. 3. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial: Major outcomes in high-risk hyperten-

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sive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2002;288:2981–2997. [Published errata in JAMA 2003;289: 178 and JAMA 2004;291:2196.] 4. Niedfeldt MW: Managing hypertension in athletes and physically active patients. Am Fam Physician 2002;66:445–452, 457– 458.

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5. Knopp WD, Wang TW, Bach BR Jr: Ergogenic drugs in sports. Clin Sports Med 1997;16:375–392. 6. Chick TW, Halperin AK, Gacek EM: The effect of antihypertensive medications on exercise performance: A review. Med Sci Sports Exerc 1988;20:447–454. 7. Desai MY, De la Pena-Almaguer E, Mannting F: Abnormal heart rate recovery after exercise as a reflection of an abnormal chronotropic response. Am J Cardiol 2001;87:1164–1169. 8. Diercks DB, Kirk JD, Turnipseed SD, Amsterdam EA: Utility of immediate exercise treadmill testing in patients taking beta blockers or calcium channel blockers. Am J Cardiol 2002;90:882– 885. 9. Poulsen SH, Jensen SE, Egstrup K: Improvement of exercise capacity and left ventricular diastolic function with metoprolol XL after acute myocardial infarction. Am Heart J 2000;140:6–11. 10. Wright JT Jr, Bakris G, Greene T, et al, for the African American Study of Kidney Disease and Hypertension Study Group: Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: Results from the AASK trial. JAMA 2002;288:2421–2431. 11. Thurman JM, Schrier RW: Comparative effects of angiotensinconverting enzyme inhibitors and angiotensin receptor blockers on blood pressure and the kidney. Am J Med 2003;114:588–598. 12. Dahlof B, Devereux RB, Kjeldsen SE, et al: Cardiovascular morbidity and mortality in the Losartan Intervention for Endpoint reduction in hypertension study (LIFE): A randomised trial against atenolol. Lancet 2002;359:995–1003. 13. Opie LH, Schall R. Evidence-based evaluation of calcium channel blockers for hypertension: Equality of mortality and cardiovascular risk relative to conventional therapy. J Am Coll Cardiol 2002;39:315–322. [Published erratum in J Am Coll Cardiol 2002;39:1409–1410.] 14. ALLHAT Collaborative Research Group: Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2000;283:1967–1975. [Published erratum in JAMA 2002;288:2976.] 15. Safeer RS, Lacivita CL: Choosing drug therapy for patients with hyperlipidemia. Am Fam Physician 2000;61:3371–3382. 16. Durstine JL, Thompson PD: Exercise in the treatment of lipid disorders. Cardiol Clin 2001;19:471–488. 17. Melin JM, Struble WE, Tipping RW, et al: A Consumer Use Study of Over-the-Counter Lovastatin (CUSTOM). Am J Cardiol 2004;94: 1243–1248. 18. Aronow WS, Nayak D, Woodworth S, Ahn C: Effect of simvastatin versus placebo on treadmill exercise time until the onset of intermittent claudication in older patients with peripheral arterial disease at six months and at one year after treatment. Am J Cardiol 2003;92: 711–712. 19. Mondillo S, Ballo P, Barbati R, et al: Effects of simvastatin on walking performance and symptoms of intermittent claudication in hypercholesterolemic patients with peripheral vascular disease. Am J Med 2003;114:359–364. 20. Ramires JAF, Sposito AC, Mansur AP, et al: Cholesterol lowering with statins reduces exercise-induced myocardial ischemia in hypercholesterolemic patients with coronary artery disease. Am J Cardiol 2001;88:1134–1138. 21. Storms WW: Review of exercise-induced asthma. Med Sci Sports Exerc 2003;35:1464–1470. 22. Spooner CH, Spooner GR, Rowe BH: Mast-cell stabilising agents to prevent exercise-induced bronchoconstriction. Cochrane Database of Systematic Reviews 2003;4:CD002307. 23. Hancox RJ, Subbarao P, Kamada D, et al: b2-agonist tolerance and exercise-induced bronchospasm. Am J Respir Crit Care Med 2002;165:1068–1070. 24. McKenzie DC, Stewart IB, Fitch KD: The asthmatic athlete, inhaled beta agonists, and performance. Clin J Sport Med 2002;12:225– 228. 25. Shapiro GS, Yegen U, Xiang J, et al: A randomized, double-blind, single-dose, crossover clinical trial of the onset and duration of pro-

26.

27.

28.

29.

30.

31.

32. 33.

34. 35.

36.

37.

38.

39. 40.

41.

42.

43.

44. 45. 46.

47.

tection from exercise-induced bronchoconstriction by formoterol and albuterol. Clin Ther 2002;24:2077–2087. Richter K, Janicki S, Jorres RA, Magnussen H: Acute protection against exercise-induced bronchoconstriction by formoterol, salmeterol, and terbutaline. Eur Respir J 2002;19:865–871. Stewart IB, Labreche JM, McKenzie DC: Acute formoterol administration has no ergogenic effect in nonasthmatic athletes. Med Sci Sports Exerc 2002;34:213–217. Peroni DG, Piacentini GL, Ress M, et al: Time efficacy of a single dose of montelukast on exercise-induced asthma in children. Pediatr Allergy Immunol 2002;13:434–437. Melo RE, Sole D, Naspitz CK: Exercise-induced bronchoconstriction in children: Montelukast attenuates the immediate-phase and latephase responses. J Allergy Clin Immunol 2003;111:301–307. Steinshamm S, Sandsund M, Sue-Chu M, Bjermer L: Effects of montelukast on physical performance and exercise economy in adult asthmatics with exercise-induced bronchoconstriction. Scand J Med Sci Sports 2002;12:211–217. Bilici M, Koroglu MA, Cakirbay H, et al: Isokinetic muscle performance in major depressive disorder: Alterations by antidepressant therapy. Int J Neurosci 2001;109:149–164. Masand PS: Weight gain associated with psychotropic drugs. Expert Opin Pharmacother 2000;1:377–389. Coris EE, Ramirez AM, Van Durme DJ: Heat illness in athletes: The dangerous combination of heat, humidity, and exercise. Sports Med 2004;34:9–16. Palmer BF, Gates JR, Lader M: Causes and management of hyponatremia. Ann Pharmacother 2003;37:1694–1702. Grobler LA, Schwellnus MP, Trichard C, et al: Comparative effects of zopiclone and loprazolam on psychomotor and physical performance in active individuals. Clin J Sport Med 2000;10:123–128. Lindqvist A, Jalonen J, Laitinen LA, et al: The effects of midazolam and ephedrine on post-exercise autonomic chronotropic control of the heart in normal subjects. Clin Auton Res 1996;6:343–349. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC, American Psychiatric Association, 1994. Mazur AF: ADHD exception available. The NCAA News April 12, 2004. Available at www.ncaa.org/news/2004/20040412/active/4108n36. html/. Pascual-Castroviejo I: Attention deficit hyperactivity syndrome and the capacity to practice sports. Rev Neurol 2004;38:1001–1005. Karatekin C, Markiewicz SW, Siegel MA: A preliminary study of motor problems in children with attention-deficit/hyperactivity disorder. Percept Mot Skills 2003;97:1267–1280. Pelham WE Jr, McBurnett K, Harper GW, et al: Methylphenidate and baseball playing in ADHD children: Who’s on first? J Consult Clin Psychol 1990;58:130–133. Vickers JN, Rodrigues ST, Brown LN: Gaze pursuit and arm control of adolescent males diagnosed with attention deficit hyperactivity disorder (ADHD) and normal controls: Evidence of a dissociation in processing visual information of short and long duration. J Sports Sci 2002;20:201–216. Trappe TA, Fluckey JD, White F, et al: Skeletal muscle PGF2a and PGE2 in response to eccentric resistance exercise: Influence of ibuprofen and acetaminophen. J Clin Endocrinol Metab 2001;86:5067–5070. Harwood MI, Chang SI: Clinical inquiries. What is the most effective treatment for acute low back pain? J Fam Pract 2002;51:118. Brandt KD: The role of analgesics in the management of osteoarthritis pain. Am J Ther 2000;7:75–90. Bradley JD, Brandt KD, Katz BP, et al: Comparison of an antiinflammatory dose of ibuprofen, an analgesic dose of ibuprofen, and acetaminophen in the treatment of patients with osteoarthritis of the knee. N Engl J Med 1991;325:87–91. Pincus T, Koch G, Lei H, et al: Patient Preference for Placebo, Acetaminophen (Paracetamol) or Celecoxib Efficacy Studies (PACES): Two randomised, double blind, placebo controlled, crossover clinical trials in patients with knee or hip osteoarthritis. Ann Rheum Dis 2004;63: 931–939.

43

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48. Warner DC, Schnepf G, Barrett MS, et al: Prevalence, attitudes, and behaviors related to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in student athletes. J Adolesc Health 2002;30:150– 153. 49. Almekinders LC, Gilbert JA: Healing of experimental muscle strains and the effects of nonsteroidal antiinflammatory medication. Am J Sports Med 1986;14:303–308. 50. Mishra DK, Friden J, Schmitz MC, Lieber RL: Anti-inflammatory medication after muscle injury. A treatment resulting in short-term improvement but subsequent loss of muscle function. J Bone Joint Surg Am 1995;77:1510–1519. 51. Dudley GA, Czerkawski J, Meinrod A, et al: Efficacy of naproxen sodium for exercise-induced dysfunction muscle injury and soreness. Clin J Sport Med 1997;7:3–10. 52. Dahners LE, Gilbert JA, Lester GE, et al: The effect of a nonsteroidal antiinflammatory drug on the healing of ligaments. Am J Sports Med 1988;16:641–646. 53. Moorman CT III, Kukreti U, Fenton DC, Belkoff SM: The early effect of ibuprofen on the mechanical properties of healing medial collateral ligament. Am J Sports Med 1999;27:738–741. 54. Slatyer MA, Hensley MJ, Lopert R: A randomized controlled trial of piroxicam in the management of acute ankle sprain in Australian Regular Army recruits. The Kapooka Ankle Sprain Study. Am J Sports Med 1997;25:544–553. 55. Almekinders LC, Temple JD: Etiology, diagnosis, and treatment of tendonitis: An analysis of the literature. Med Sci Sports Exerc 1998;30:1183–1190. 56. Astrom M, Westlin N: No effect of piroxicam on Achilles tendinopathy. A randomized study of 70 patients. Acta Orthop Scand 1992;63:631–634. 57. van Staa TP, Leufkens HG, Cooper C: Use of nonsteroidal antiinflammatory drugs and risk of fractures. Bone 2000;27:563–568. 58. Zhang W, Jones A, Doherty M: Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A meta-analysis of randomised controlled trials. Ann Rheum Dis 2004;63:901–907. 59. Ekman EF, Fiechtner JJ, Levy S, Fort JG: Efficacy of celecoxib versus ibuprofen in the treatment of acute pain: A multicenter, double-blind, randomized controlled trial in acute ankle sprain. Am J Orthop 2002;31:445–451. 60. Petrella R, Ekman EF, Schuller R, Fort JG: Efficacy of celecoxib, a COX-2-specific inhibitor, and naproxen in the management of acute ankle sprain: Results of a double-blind, randomized controlled trial. Clin J Sport Med 2004;14:225–231. 61. Bombardier C, Laine L, Reicin A, et al: Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group. N Engl J Med 2000; 343:1520–1528. 62. Fitzgerald GA: Coxibs and cardiovascular disease. N Engl J Med 2004;351:1709–1711. 63. Reginster JY, Deroisy R, Rovati LC, et al: Long-term effects of glucosamine sulphate on osteoarthritis progression: A randomised, placebo-controlled clinical trial. Lancet 2001;357:251–256. 64. Pavelka K, Gatterova J, Olejarova M, et al: Glucosamine sulfate use and delay of progression of knee osteoarthritis: A 3-year, randomized, placebo-controlled, double-blind study. Arch Intern Med 2002;162: 2113–2123. 65. Bruyere O, Pavelka K, Rovati LC, et al: Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: Evidence from two 3-year studies. Menopause 2004;11:138–143. 66. McAlindon T, Formica M, LaValley M, et al: Effectiveness of glucosamine for symptoms of knee osteoarthritis: Results from an Internet-based randomized double-blind controlled trial. Am J Med 2004;117:643–649. 67. Cibere J, Kopec JA, Thorne A, et al: Randomized, double-blind, placebo-controlled glucosamine discontinuation trial in knee osteoarthritis. Arthritis Rheum 2004;51:738–745. 68. Christgau S, Henrotin Y, Tanko LB, et al: Osteoarthritic patients with high cartilage turnover show increased responsiveness to the cartilage

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69. 70.

71. 72.

73.

74.

75.

76.

77. 78.

79.

80.

81.

82. 83.

84.

85.

86.

87.

88.

89.

90.

protecting effects of glucosamine sulphate. Clin Exp Rheumatol 2004;22:36–42. Segal L, Day SE, Chapman AB, Osborne RH: Can we reduce disease burden from osteoarthritis? Med J Aust 2004;180:S11–S17. Phillips GC: Medicolegal issues and ergogenic AIDS: Trade, tragedy, and public safety, the example of ephedra and the dietary supplement health and education act. Curr Sports Med Rep 2004;3:224–228. Metzl JD, Small E, Levine SR, Gershel JC: Creatine use among young athletes. Pediatrics 2001;108:421–425. Tokish JM, Kocher MS, Hawkins RJ: Ergogenic aids: A review of basic science, performance, side effects, and status in sports. Am J Sports Med 2004;32:1543–1553. Willoughby DS, Rosene JM: Effects of oral creatine and resistance training on myogenic regulatory factor expression. Med Sci Sports Exerc 2003;35:923–929. Chilibeck PD, Stride D, Farthing JP, Burke DG: Effect of creatine ingestion after exercise on muscle thickness in males and females. Med Sci Sports Exerc 2004;36:1781–1788. Mujika I, Padilla S, Ibanez J, et al: Creatine supplementation and sprint performance in soccer players. Med Sci Sports Exerc 2000;32:518–525. Redondo DR, Dowling EA, Graham BL, et al: The effect of oral creatine monohydrate supplementation on running velocity. Int J Sport Nutr 1996;6:213–221. Ostojic SM: Creatine supplementation in young soccer players. Int J Sport Nutr Exerc Metab 2004;14:95–103. Ahmun RP, Tong RJ, Grimshaw PN: The effects of acute creatine supplementation on multiple sprint cycling and running performance in rugby players. J Strength Cond Res 2005;19:92–97. Ayoama R, Hiruma E, Sasaki H: Effects of creatine loading on muscular strength and endurance of female softball players. J Sports Med Phys Fitness 2003;43:481–487. Kilduff LP, Pitsiladis YP, Tasker L, et al: Effects of creatine on body composition and strength gains after 4 weeks of resistance training in previously nonresistance-trained humans. Int J Sport Nutr Exerc Metab 2003;13:504–520. HHS launches crackdown on products containing andro: FDA warns manufacturers to stop distributing such products. U.S. Dept. of Health and Human Services, March 11, 2004. Available at www.fda.gov/bbs/topics/news/2004/hhs_031104.html/. Ahrendt DM: Ergogenic aids: Counseling the athlete. Am Fam Physician 2001;63:913–922. Brown GA, Vukovich MD, Sharp RL, et al: Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. J Appl Physiol 1999;87:2274–2283. King DS, Sharp RL, Vukovich MD, et al: Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: A randomized controlled trial. JAMA 1999;281: 2020–2028. Leder BZ, Longcope C, Catlin DH, et al: Oral androstenedione administration and serum testosterone concentrations in young men. JAMA 2000;283:779–782. Leder BZ, Leblanc KM, Longcope C, et al: Effects of oral androstenedione administration on serum testosterone and estradiol levels in postmenopausal women. J Clin Endocrinol Metab 2002;87:5449– 5454. FDA White Paper: Health Effects of Androstenedione. U.S. Food and Drug Administration, March 11, 2004. Available at www.fda.gov/oc/ whitepapers/andro.html/. Paddon-Jones D, Keech A, Jenkins D: Short-term beta-hydroxybeta-methylbutyrate supplementation does not reduce symptoms of eccentric muscle damage. Int J Sport Nutr Exerc Metab 2001;11:442–450. Slater GJ, Logan PA, Boston T, et al: Beta-hydroxy beta-methylbutyrate (HMB) supplementation does not influence the urinary testosterone: Epitestosterone ratio in healthy males. J Sci Med Sport 2000;3:79–83. Ransone J, Neighbors K, Lefavi R, Chromiak J: The effect of betahydroxy beta-methylbutyrate on muscular strength and body composition in collegiate football players. J Strength Cond Res 2003;17:34–39.

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91. Slater G, Jenkins D, Logan P, et al: Beta-hydroxy-beta-methylbutyrate (HMB) supplementation does not affect changes in strength or body composition during resistance training in trained men. Int J Sport Nutr Exerc Metab 2001;11:384–396. 92. O’Connor DM, Crowe MJ: Effects of beta-hydroxy-beta-methylbutyrate and creatine monohydrate supplementation on the aerobic and anaerobic capacity of highly trained athletes. J Sports Med Phys Fitness 2003;43:64–68. 93. Vukovich MD, Dreifort GD: Effect of beta-hydroxy beta-methylbutyrate on the onset of blood lactate accumulation and VO2 peak in endurance-trained cyclists. J Strength Cond Res 2001;15:491–497. 94. Nissen S, Sharp RL, Panton L, et al: b-Hydroxy-b-methylbutyrate (HMB) supplementation in humans is safe and may decrease cardiovascular risk factors. J Nutr 2000;130:1937–1945. 95. Hodges AN, Lynn BM, Bula JE, et al: Effects of pseudoephedrine on maximal cycling power and submaximal cycling efficiency. Med Sci Sports Exerc 2003;35:1316–1319. 96. Chester N, Reilly T, Mottram DR: Physiological, subjective and performance effects of pseudoephedrine and phenylpropanolamine during endurance running exercise. Int J Sports Med 2003;24:3–8. 97. Chu KS, Doherty TJ, Parise G, et al: A moderate dose of pseudoephedrine does not alter muscle contraction strength or anaerobic power. Clin J Sport Med 2002;12:387–390. 98. Swain RA, Harsha DM, Baenziger J, Saywell RM Jr: Do pseudoephedrine or phenylpropanolamine improve maximum oxygen uptake and time to exhaustion? Clin J Sport Med 1997;7:168–173. 99. Gillies H, Derman WE, Noakes TD, et al:. Pseudoephedrine is without ergogenic effects during prolonged exercise. J Appl Physiol 1996;81: 2611–2617. 100. Clemons JM, Crosby SL: Cardiopulmonary and subjective effects of a 60 mg dose of pseudoephedrine on graded treadmill exercise. J Sports Med Phys Fitness 1993;33:405–412. 101. Bright TP, Sandage BW Jr, Fletcher HP: Selected cardiac and metabolic responses to pseudoephedrine with exercise. Clin Pharmacol 1981;21:488–492. 102. Schwenk TL, Costley CD: When food becomes a drug: Nonanabolic nutritional supplement use in athletes. Am J Sports Med 2002;30: 907–916. 103. Doherty M, Smith PM: Effects of caffeine ingestion on exercise testing: A meta-analysis. Int J Sport Nutr Exerc Metab 2004;14: 626–646. 104. Doherty M, Smith P, Hughes M, Davison R: Caffeine lowers perceptual response and increases power output during high-intensity cycling. J Sports Sci 2004;22:637–643. 105. Bell DG, McLellan TM: Effect of repeated caffeine ingestion on repeated exhaustive exercise endurance. Med Sci Sports Exerc 2003;35:1348–1354. 106. Bell DG, McLellan TM: Exercise endurance 1, 3, and 6 h after caffeine ingestion in caffeine users and nonusers. J Appl Physiol 2002;93:1227–1234. 107. Doherty M, Smith PM, Davison RC, Hughes MG: Caffeine is ergogenic after supplementation of oral creatine monohydrate. Med Sci Sports Exerc 2002;34:1785–1792. 108. Happonen P, Voutilainen S, Salonen JT: Coffee drinking is dosedependently related to the risk of acute coronary events in middleaged men. J Nutr 2004;134:2381–2386. 109. Hartgens F, Kuipers H: Effects of androgenic-anabolic steroids in athletes. Sports Med 2004;34:513–554. 110. Hurley BF, Seals DR, Hagberg JM, et al: High-density-lipoprotein cholesterol in bodybuilders v powerlifters. Negative effects of androgen use. JAMA 1984;252:507–513. 111. Joyner MJ: Designer doping. Exerc Sport Sci Rev 2004;32:81–82. 112. Climstein M, O’Shea P, Adams KJ, DeBeliso M: The effects of anabolic-androgenic steroids upon resting and peak exercise left ventricular heart wall motion kinetics in male strength and power athletes. J Sci Med Sport 2003;6:387–397. 113. Pope HG Jr, Kouri EM, Hudson JI: Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: A randomized controlled trial. Arch Gen Psychiatry 2000;57:133–140.

114. Faigenbaum AD, Zaichkowsky LD, Gardner DE, Micheli LJ: Anabolic steroid use by male and female middle school students. Pediatrics 1998;101:E6. 115. Goldberg L, MacKinnon DP, Elliot DL, et al: The adolescents training and learning to avoid steroids program: Preventing drug use and promoting health behaviors. Arch Pediatr Adolesc Med 2000;154:332– 338. 116. Catlin DH, Sekera MH, Ahrens BD, et al: Tetrahydrogestrinone: Discovery, synthesis, and detection in urine. Rapid Commun Mass Spectrom 2004;18:1245–1249. 117. Death AK, McGrath KC, Kazlauskas R, Handelsman DJ: Tetrahydrogestrinone is a potent androgen and progestin. J Clin Endocrinol Metab 2004;89:2498–2500. 118. Stacy JJ, Terrell TR, Armsey TD: Ergogenic AIDS: Human growth hormone. Curr Sports Med Rep 2004;3:229–233. 119. Rickert VI, Pawlak-Morello C, Sheppard V, Jay MS: Human growth hormone: A new substance of abuse among adolescents? Clin Pediatr (Phila) 1992;31:723–726. 120. Healy ML, Gibney J, Russell-Jones DL, et al: High dose growth hormone exerts an anabolic effect at rest and during exercise in endurance-trained athletes. J Clin Endocrinol Metab 2003;88:5221–5226. 121. Conrad P, Potter D: Human growth hormone and the temptations of biomedical enhancement. Soc Health Illn 2004;26:184–215. 122. Longobardi S, Keay N, Ehrnborg C, et al: Growth hormone (GH) effects on bone and collagen turnover in healthy adults and its potential as a marker of GH abuse in sports: A double blind, placebocontrolled study. The GH-2000 Study Group. J Clin Endocrinol Metab 2000;85:1505–1512. 123. Scott J, Phillips GC: Erythropoietin in sports: A new look at an old problem. Curr Sports Med Rep 2005;4:224–226. 124. Birkeland KI, Stray-Gundersen J, Hemmersbach P, et al: Effect of rhEPO administration on serum levels of sTfR and cycling performance. Med Sci Sports Exerc 2000;32:1238–1243. 125. Lundin AP, Akerman MJ, Chesler RM, et al: Exercise in hemodialysis patients after treatment with recombinant human erythropoietin. Nephron 1991;58:315–319. 126. Ekblom B, Berglund B: Effect of erythropoietin administration on maximal aerobic power. Scand J Med Sci Sports 1991;1:88–93. 127. Denker B: Erythropoietin: From bench to bedside. Nephrol Rounds 2004;2.3 www.nephrologyrounds.org/ 128. Pascual JA, Belalcazar V, de Bolos C, et al: Recombinant erythropoietin and analogues: A challenge for doping control. Ther Drug Monit 2004;26:175–179. 129. Wide L, Bengtsson C, Berglund B, Ekblom B: Detection in blood and urine of recombinant erythropoietin administered to healthy men. Med Sci Sports Exerc 1995;27:1569–1576. 130. Iven VG: Recreational drugs. Clin Sports Med 1998;17:245–259. 131. The use of alcohol in sports. American College of Sports Medicine Position Stand. Med Sci Sports Exerc 1982;14:ix–xi. 132. Bond V, Franks BD, Howley ET: Effects of small and moderate doses of alcohol on submaximal cardiorespiratory function, perceived exertion and endurance performance in abstainers and moderate drinkers. J Sports Med Phys Fitness 1983;23:221–228. 133. Houmard JA, Langenfeld ME, Wiley RL, Siefert J: Effects of the acute ingestion of small amounts of alcohol upon 5-mile run times. J Sports Med Phys Fitness 1987;27:253–257. 134. McNaughton L, Preece D: Alcohol and its effects on sprint and middle distance running. Br J Sports Med 1986;20:56–59. 135. O’Brien CP: Alcohol and sport. Impact of social drinking on recreational and competitive sports performance. Sports Med 1993;15:71– 77. 136. Martens MP, Cox RH, Beck NC: Negative consequences of intercollegiate athlete drinking: The role of drinking motives. J Stud Alcohol 2003;64:825–828. 137. O’Brien CP, Lyons F: Alcohol and the athlete. Sports Med 2000;29:295–300. 138. Campos DR, Yonamine M, de Moraes Moreau RL: Marijuana as doping in sports. Sports Med 2003;33:395–399.

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139. Ewing BT: High school athletes and marijuana use. J Drug Educ 1998;28:147–157. 140. Peretti-Watel P, Guagliardo V, Verger P, et al: Sporting activity and drug use: Alcohol, cigarette and cannabis use among elite student athletes. Addiction 2003;98:1249–1256. 141. Sidney S: Cardiovascular consequences of marijuana use. J Clin Pharmacol 2002;42(11 suppl):64S–70S. 142. Renaud AM, Cormier Y: Acute effects of marihuana smoking on maximal exercise performance. Med Sci Sports Exerc 1986;18:685– 689. 143. Braiden RW, Fellingham GW, Conlee RK: Effects of cocaine on glycogen metabolism and endurance during high intensity exercise. Med Sci Sports Exerc 1994;26:695–700.

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144. Spielvogel H, Caceres E, Koubi H, et al: Effects of coca chewing on metabolic and hormonal changes during graded incremental exercise to maximum. J Appl Physiol 1996;80:643–649. 145. Marques-Magallanes JA, Koyal SN, Cooper CB, et al: Impact of habitual cocaine smoking on the physiologic response to maximum exercise. Chest 1997;112:1008–1016. 146. Cretzmeyer M, Sarrazin MV, Huber DL, et al: Treatment of methamphetamine abuse: Research findings and clinical directions. J Subst Abuse Treat 2003;24:267–277.

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Environmental Stressors Richard Rodenberg and Kyle Parish

In This Chapter Heat illness Hypothermia Frostbite Nonfreezing injuries High-altitude illness

INTRODUCTION • As the new breed of endurance athletes and adventure seekers push the limits of human endurance in extreme environments and competitions, health care professionals must strive to better understand the demands placed on human physiology by these extreme conditions. • Early recognition and treatment of heatstroke is imperative. • The best treatment for heat illness is prevention. • Hypothermia may be treated with passive or active rewarming. • Recommendation for rewarming of frostbite injury is a water bath at 40∞ to 42oC. • High-altitude illnesses include acute mountain sickness, highaltitude pulmonary edema, and high-altitude cerebral edema.

HEAT ILLNESS Every summer the topic of heat illness gains increased press in the news headlines. Much of this press is related to the fact that heatstroke is the third most common cause of exercise-related death in U.S. high schools, following head injuries and cardiac disorders.1 With the increasing popularity of endurance and ultraendurance competitions (marathons, ultra-marathons, and triathlons), our understanding of exercise-associated collapse (EAC) falls into question. No longer can an athlete who collapses during endurance competitions, in heat-related conditions, be simply diagnosed as a casualty of heat-related exertion. The mechanisms of collapse can be very different when comparing this new endurance athlete and the classic high school or collegiate competitor. Treatment of athletic populations that exercise in heat-related conditions requires medical personnel to have a thorough understanding of thermoregulatory physiology, dehydration in athletics, populations at risk of heat illness,

and treatment of the various heat-related illnesses. At the same time, one must be able to keenly and astutely recognize and treat the athlete affected by other conditions surrounding EAC.2 Thermoregulation is normally a highly efficient process. Normal core body temperature, as regulated by the hypothalamus, varies based on environmental climate and internal metabolic function associated with work-related activity. It is estimated that there is only a 1°C change in core temperature for every 25° to 30°C change in ambient temperature.3,4 It is thought that for every 0.6°C increase in core temperature, there is a 10% elevation in the basal metabolic rate.3 Muscle contraction is an inefficient process, allowing only 20% to 25% of the energy sources converted to muscle activity to be converted into work.1,5 The hypothalamus regulates the parasympathetic nervous system, which controls sweating, and the sympathetic nervous system, which regulates skin blood flow and vasodilatation for heat dissipation.3,4 There are many conditions, including chronic disease states and pre-existing conditions, medications, and poor physical conditioning, that can impair the body’s normal mechanisms for dissipating ambient temperature (Table 6-1). Ambient temperature is related to environmental factors such as clothing, temperature, and humidity.3 In addition to the previously mentioned conditions for impaired heat dissipation, there are known differences in heat dissipation between children, adults, and elderly and between females and males. It is known that children are at a greater disadvantage when exercising in the heat compared to adults secondary to the following factors: (1) children produce more heat relative to body mass for the same exercise,1,3,5,6 (2) children are less efficient in dissipating heat secondary to a larger body surface area,1,3,5,6 (3) children have a lower sweating rate,1,5,6 (4) the sweating threshold is increased in children,6 (5) composition of sweat is different in children compared to adolescents,6 (6) children develop higher body temperatures with the same amount of dehydration,1,3,5,6 and (7) overall cardiac output per unit of oxygen uptake is lower in children.6 The practical implication is that children have a slower rate of acclimation to heat (2 weeks in children compared to 1 week in young adults).1,3,5,6 Transition to an adult pattern of sweating and sweat composition occurs in early puberty.6 It is also known that elderly individuals, like children, have a lower sweat rate compared to young adults.7 Elderly individuals are afflicted with more chronic medical conditions that impair the body’s ability to dissipate heat. These chronic medical conditions are often also treated with many of the medications that decrease the body’s ability to dissipate heat.3 There are four mechanisms by which the body regulates excessive heat accumulation. These same four mechanisms of heat dispersion are at work during activity in the cold environ-

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Table 6-1 Predisposing Conditions and Medications for Heat Illness Conditions Recent or current illness Febrile state Chronic illnesses DM, CHF, CF, sweating inefficiency syndromes Mental retardation Anorexia/Bulemia Previous episode of heat illness Poorly conditioned athlete Certain medications Age Medications Sympathomimetics Amphetamines Epinephrine Ephedrine Cocaine Norepinephrine Anticholinergics Atropine sulfate Scopolamine Bentropine Belladona and synthetic alkaloids Antihistamines Diuretics Furosemide Hydrochlorothiazide Bumetanide Phenothiazines Prochloroperazine Chlorpromazine Promethazine Butyrophenones Haloperidol Cyclic antidepressants Amitriptyline Imipramine Nortriptyline Protriptyline Monoamine oxidase inhibitors Phenelzine Tranlcypromine sulfate Alcohol Lysergic acid diethlamide Lithium Multiple supplement medications (i.e., herbal)

ment. The mechanisms consist of conduction (heat transfer by direct contact), convection (heat transfer by movement such as air current over the body), radiation/infrared dissipation (heat transfer to the environment), and evaporation (heat transfer through the loss of water vapor from the skin and airway).3,8 Evaporation plays the major role in the body’s ability to dissipate heat when the ambient temperature is above 20°C (68°F).3

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Dehydration interferes with the evaporative process, resulting in decreased blood volume, stroke volume, and cardiac output. The body responds to this assault with protective mechanisms. The body’s first response is with vasoconstriction, preferentially shunting blood to vital organs and away from the muscles (where it picks up heat), skin, and sweat glands (where it is dissipated by the previously mentioned mechanisms). The body is then overwhelmed with decreased sweat production in the face of a rising body temperature.9 This adaptive response is particularly applicable when explaining the contribution dehydration makes in at-risk and/or unacclimated populations. However, some researchers believe that evidence-based medicine does not support the assumption that dehydration is the sole underlying cause of heat illness or EAC in acclimated and endurance trained athletes. The study of Wyndham and Strydom10 in 1969 forced the athletic community to recognize the dangers of dehydration, but may have led to the popular belief that everyone who collapses in heat, during exercise, must have dehydration-induced heat illness.9–11 Noakes points out that dehydration is just one factor contributing to increased body temperature; metabolic rate is the major determinant during exercise in endurance athletes.9,11 Through his own research, Noakes stresses that no published data show that an acclimated endurance athlete afflicted with heat illness is more dehydrated than those who complete the same race with normal body temperature.11 In a study looking at impaired highintensity cycling performance time at low levels of dehydration, Walsh et al12 were able to show that fluid ingestion may enhance performance time to exhaustion by changes in unexplained psychological factors, as opposed to measurable differences in physiologic factors (rectal or skin temperature, heart rate, oxygen consumption, plasma electrolyte concentrations, plasma volume changes, sweat rate, or leg muscle power). Also, dehydration was not found to affect leg muscle power, correlating with previous studies documenting dehydration causing up to a 7% decrease in body mass does not impair strength or muscular force generation. This study supports replacement of fluid losses, in exercise lasting longer than 60 minutes, to prevent impairment of exercise performance, not prevention of heat illness in endurance athletes.12 Heat cramps are painful muscle spasms that commonly affect abdominal or calf muscles.2,3 Historically, it has been thought that since this condition is usually associated with physically fit individuals exercising in excessive heat, the condition was secondary to severe dehydration, large sodium chloride losses, and muscle fatigue.2,11 There are few data to support the belief that heat cramps are caused by dehydration or excessive electrolyte losses during exercise. In fact, cramps can occur at rest or during or after exercise in a variety of environmental conditions.11 Clinicians have advocated many methods for treating and preventing heat cramps including salt replacement, IV fluid administration, muscle massage and stretching, and even use of IV benzodiazepines. Keep in mind that most of the information on preventing heat cramps is more anecdotal than scientific and based on the experience of individual practitioners.2,13 Until further research distinguishes the inherent mechanism of muscle cramping during exercise, recommendations for prevention of cramps include stretching, adequate hydration, and maintaining a high level of physical fitness.2 The classic definition of heat exhaustion is a core body temperature greater than 38°C (100.4°F) but below the cutoff for heatstroke (40°C or 104°F), associated with tachycardia and

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postural hypotension. Signs and symptoms of heat exhaustion include nausea/vomiting, headache, malaise, myalgia, lightheadedness, irritability, or confusion. Many believe that heat exhaustion is a more mild form or precursor to heatstroke, which mani-fests as the core body temperature elevates above 40°C (104°F) with more severe manifestations of shock and cognitive dysfunction (delirium, obtundation, coma, or seizures). Popular thought has upheld the notion that heat exhaustion can precede heatstroke.2,3,11,13 As in heat cramps, dehydration has been traditionally reported as the underlying mechanism for the development of heat exhaustion and heatstroke. However, studies have shown that rectal temperatures are not abnormally elevated in all individuals with symptoms of heat exhaustion, nor is there published evidence supporting the notion that individuals with heat exhaustion will progress to heatstroke if left untreated. Based on experience in treating collapsed athletes in endurance running events, there has been no evidence that collapsed athletes are more dehydrated or hyperthermic compared to their well counterparts.2,11,14,15 In fact, rectal temperatures in excess of 40°C (104°F) are commonly found in asymptomatic subjects performing exercise of moderate to high intensity.15 Based on the preceding discrepancies, the term heat exhaustion has been called into question. The term heat exhaustion and the traditional association with dehydration and hyperthermia may be more appropriately applied to unacclimated individuals, children, elderly, and individuals with pre-existing medical conditions that may predispose themselves to heat illness. A more appropriate term, when discussing the new breed of endurance athlete, would be EAC. EAC does not include cardiovascular collapse, chest pain, insulin reaction/hypoglycemia, seizures, or other readily identifiable medical conditions.2,16 EAC is not a diagnosis but instead describes a main complaint characterized by the inability to stand or walk unaided as a result of lightheadedness, faintness, dizziness, or syncope in association with a constellation of symptoms such as exhaustion, nausea, cramps, and normal, low, or high body temperatures.2,15,17 The cause of EAC has yet to be determined. Recent thought points to postural blood pressure changes as the main cause of EAC. Cessation of exercise causes inactivation of the muscle pump resulting in pooling of large amounts of blood volume in the lower extremities and pelvis leading to circulatory collapse and syncope.15 A number of other factors, such as a lack of a readily available energy source, temporary dysfunction of the central nervous system or temperature-regulating system, excessive racing effort, mild dehydration, and training-induced reduction in the vasoconstrictor response to any hypotensive stress may contribute to EAC.2,15,16 It is important to recognize the two categories of heatstroke: classic and exertional. Classic heatstroke affects individuals at the extremes of age or with chronic medical conditions in hot conditions. The triad of classic heatstroke consists of hyperpyrexia, anhidrosis, and mental status changes. Classic heatstroke is the result of an exogenous heat load overwhelming the body’s ability to cope with it. In exertional heatstroke, which affects laborers and athletes, the exogenous heat load combined with the endogenous heat load, overwhelms the body’s ability to dissipate heat. The key difference between classic and exertional heatstroke is the lack of anhidrosis. In exertional heatstroke, the majority of people will continue to sweat.2,3,18 There are no data that endurance athletes afflicted with exertional heatstroke are more dehydrated than those athletes who complete a race with normal body temperature. Many athletes dehydrate during endurance competitions but do not col-

lapse.11,19 Because of the rarity of heatstroke in endurance and ultra-endurance events, it has been proposed that there could be an acquired, genetic condition triggered by intense exercise such as malignant hyperthermia, which predisposes individuals to heatstroke.11,19 Clinical in vitro testing of people at risk of malignant hyperthermia is not practical secondary to cost and low specificity; making it difficult to confirm this theory. More study is required to confirm the genetic correlate between theses two disease processes.20 It is imperative that heatstroke be recognized and treated promptly, as morbidity is directly proportional to peak core temperature and length of time spent in the hyperthermic state.2,17,18 With prompt and proper treatment, the survival rate has increased significantly.2,3,18 Persistent hyperthermia can lead to cellular damage and end organ failure in the form of cardiac myocyte damage, hepatic necrosis, rhabdomyolysis, disseminated intravascular coagulation, adult respiratory distress syndrome, renal failure, and seizures.18 Immediate cooling to 38°C should be instituted when an athlete with an elevated temperature and mental status changes is encountered. Rapid reduction in body temperature reverses peripheral vasodilatation and restores central circulation, with a decrease in heart rate and increases in central volume, stroke volume, and blood pressure, thereby improving the prognosis.17,21 The most effective cooling method proven in endurance athletes with heatstroke consists of immersing the athlete in an ice bath for 5 to 10 minutes. This method induces cooling at a rate of 1°C/min (1.8°F/min). It is imperative to watch for hypothermia. Because rectal temperatures lag behind esophageal (core) temperature, cooling should be terminated before the rectal temperature reaches normal body temperature. Shivering is an indication that the core temperature has decreased to 37°C (98.6°F).17,21 The sidelines of high school or collegiate sports are not always comparative to the medical tents at endurance events and ice baths are not always available. The medical provider should first evaluate the ABCs (airway, breathing, circulation) and immediately move the athlete to a cool environment. As much as possible, the athlete’s clothing should be removed and ice packs placed in areas of high heat dissipation (neck, axilla, and groin). Emergency medical services should be contacted and the athlete sprayed with cool water, while fanning to promote evaporative heat loss.3,18 For a comprehensive management plan for dealing with the collapsed athlete, the reader is referred to the proposal of Holzthausen and Noakes17 for dealing with the collapsed athlete based on years of experience in managing competitive ultraendurance events in South Africa. Their approach applies an evidence-based, rapid, and comprehensive means of assessing and treating athletes for common conditions who collapse during and after endurance events. The approach highlights pitfalls, such as knee jerk administration of IV fluids, which could exacerbate symptomatic hyponatremia in these athletes. As discussed earlier, with the emergence of the new breed of endurance athlete, the clinician needs to be aware of his or her patient population. The concerns in high school or collegiate athletes may not be the same as in the endurance athlete. The younger and less acclimated athlete is more apt to suffer from dehydration and hyperthermia. The best treatment for heat illness is prevention. Because high humidity reduces the rate of evaporation and heat dissipation, exercise in hot and humid environments should be avoided based on using available objective measures of heat stress, the Wet Bulb Globe Temperature Index and Heat Index Chart. The Heat Index Chart takes into account air

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temperature and relative humidity and is the most economical means for assessing heat stress. 1,3,18 A copy of this chart can easily be obtained through the National Weather Service (www.weather.noaa.gov/). Prevention may require practicing/ competing in the early morning or later in the evening when heat and humidity have decreased. Athletes should be acclimated to a warm environment and wear attire appropriate for exercise in heat. Any pre-existing condition should be treated prior to beginning any exercise program in the heat. There should be liberal use of fluids during practice and competition at regular intervals and when the athlete is thirsty.1,3,18 Fluid hydration begins prior to exercising by incorporating a balanced diet into a healthy lifestyle and adequately hydrating.1,22 Ingested fluids should be cooler than ambient temperature (15° to 22°C [59° to 72°F]). Flavoring the fluid can enhance palatability.22 For endurance events lasting longer than 1 hour, it may be appropriate to add carbohydrates (4% to 8%) and electrolytes to fluidreplacement solutions.22 There are few studies documenting strategies for an athlete to return to competition following an episode of heat illness. Our best information comes from military studies involving soldiers collapsing from exertional heat illness. One study advocates exercise tolerance testing in soldiers 6 to 8 weeks after an initial event.20 Another study showed weak and inconsistent associations between initial episodes of exertional heat illness and future hospitalization or recurrence of heat illness.23

HYPOTHERMIA The classic definition of hypothermia is a decrease in core body temperature to less than 35oC (95oF). This develops when the rate of heat loss in an individual exceeds the rate at which the body can produce heat24 and when the ambient temperature is less than the body’s core temperature.8 Classification is based on both cause and clinical severity. Primary, or accidental, hypothermia is what occurs in an otherwise healthy individual and is simply due to environmental exposure. Secondary hypothermia occurs in the face of a specific systemic disease or condition that may predispose one to heat loss.25–27 Other classifications include acute versus chronic and immersion versus nonimmersion. It is difficult to determine the exact worldwide incidence of hypothermia since it can be both a symptom as well as a disease entity. Deaths from secondary hypothermia are often considered as a natural complication of the underlying disease and often underreported. From the epidemiologic data that are available, the average annual incidence of fatal hypothermia in the United States during a 16-year period following 1979 was less than 750, and over half of these occurrences were in people older than the age of 65 years.26 Mortality depends on the severity of hypothermia. An average 1.8% increase in mortality rate for every 1oC (1.8°F) drop in temperature has been reported and overall mortality is around 17%.25 In the world of sports, the athletes most at risk tend to participate in outdoor or aquatic activities, such as skiing, mountaineering, snowmobiling, river rafting, and swimming. The same four mechanisms of heat dispersion are at work during activity in cold environment as were discussed in the section on heat exposure. When the body cannot maintain heat production to match these four mechanisms, an individual is at risk of hypothermia.8 Hypothermia has an effect on multiple body systems including the central nervous, cardiovascular, renal, endocrine, respiratory, gastrointestinal, hematologic, and muscular.28 This is due to a progressive metabolic depression in each system.27 The clin-

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ical presentation and associated pathology therefore vary based on the severity of the core temperature reduction. Based on that fact, hypothermia can be further classified into mild, moderate, and severe. Mild hypothermia is defined as core temperature between 32oC (90oF) and 35oC (95oF). Patients in this temperature range generally exhibit pale, cool skin due to maximal vasoconstriction of the peripheral vessels. Uncontrollable shivering and varying degrees of alterations of mental status, such as confusion, amnesia, apathy, and impaired judgment, are usually present.25,27,29 Tachycardia and hypertension may be present, but generally the cardiovascular system is stable.25,28 A “cold diuresis” usually occurs at this stage of hypothermia. It is due to several mechanisms, including a defect in distal tubular sodium and water reabsorption, an increase in catecholamines, coldinduced glucosuria, and increases in glomerular filtration rate from the increase in cardiac output.27,28 Neuromuscular effects include hypertonicity, ataxia, dysarthria, and deterioration of fine motor skills.25,27 More serious and life threatening, moderate hypothermia occurs when the core body temperature of an individual falls between 28oC (82oF) and 32oC (90oF). Within this temperature range, the body loses its ability to generate heat, becoming poikilothermic.25 Reflexive shivering ceases and muscles become rigid. The central nervous system function declines precipitously. Pupillary dilation, decline in the level of consciousness to stupor or coma, hyporeflexia, paradoxical undressing, and hallucinations may all be present. Vital signs are also profoundly affected. Cardiovascularly, the cardiac cycle slows with prolongation of PR, QRS, and QT intervals.8,25,27 On electrocardiography, the pathognomonic Osborn or J wave may also be present. These are thought to be due to a disturbance in ion fluxes that results in a late depolarization or an early repolarization of the left ventricle.26 The result of all these effects is bradycardia and hypotension from a decrease in cardiac output.9,27 The myocardium also becomes sensitive to minor insults and, as a result, is more susceptible to atrial or ventricular arrhythmias.27,29 The respiratory system slows its normal function. Hypoventilation leads to respiratory acidosis and hypoxemia. The ability to adequately protect the airway is also compromised, increasing the risk of aspiration.27,28 Renal function is relatively stable at this stage. Blood flow remains high despite the decrease in cardiac output, predominantly due to central vasodilatation.27 Hyperkalemia, hyperglycemia, and lactic acidosis can be seen with the increase in load metabolic by-products and cellular injury.28 Severe hypothermia occurs when the core body temperature falls below 28oC (82oF). At this point, victims may appear dead. Decline in cerebral perfusion leads to a profound coma.27 Pupils become unresponsive and extremities are rigid and areflexic.25,29 Blood pressure is generally unobtainable and cardiac rhythm ranges from various degrees of heart block to pulseless electrical activity.25,28 Respirations become slow and shallow and may progress to apnea. Oxygen consumption decreases to approximately 75% of baseline. Renal blood flow and thus renal function decrease in conjunction with the decrease in cardiac output.27 Because of the clinical presentation of these victims, no patient should be pronounced dead until the core temperature has been raised to 30oC (84.2oF).25 The obvious goal of treatment for hypothermia is to rewarm the victim to a normal physiologic temperature range. That goal can be achieved through passive external, active external, and active core rewarming. The choice of method depends on the

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degree of hypothermia and on the setting where the treatment is taking place. Passive external rewarming is the easiest and most readily available method. It involves moving the victim into a warm, sheltered environment, removing all wet clothing, and covering with dry blankets.8,29 It works best for the otherwise healthy individual with mild hypothermia. The rate of rewarming using this technique is usually in the range of 0.5o to 2oC (0.9°F–3.6°F) per hour.28 The active methods of rewarming both involve the application of an exogenous source of heat.29 Active external rewarming methods include the use of warmed blankets, hot packs, radiant heat lamps, and partial warm water (40oC; 104°F) immersion. Total warm water immersion is not advised because it makes monitoring difficult and is associated with more frequent complications, including “after drop” and rewarming shock.28,29 The phenomenon of “after drop” occurs when the victim’s core temperature actually decreases due to rapid vasodilation in the extremities and the circulation of cool blood to the core.27,28 Rewarming shock is also a result of rapid peripheral dilation and leads to relative hypotension and hypovolemia.29 This method is required for any individual with moderate to severe hypothermia and should not be initiated until in a controlled environment (e.g., a tertiary care center). The rate of rewarming varies with each method.29 Active internal or core rewarming can be further differentiated as simple or invasive. Simple techniques include administration of warmed, humidified oxygen via mask or endotracheal tube and warmed intravenous fluid.8,29 Initiation can be immediate, and the rate of rewarming is usually 1o to 2oC (1.8°F–3.6°F) per hour.28 Invasive techniques include peritoneal dialysis and hemodialysis, extracorporeal circulation, venovenous circulation, and pleural and peritoneal lavage. Lavage of hollow viscous is no longer advised due to the potential for major electrolyte imbalances that may ensue.8,27,29 All the fluids used for core rewarming should be in the range of 40o to 45oC (104o–113oF).25 The rate of invasive core rewarming varies based on technique but can be as high as 1o to 2oC (1.8°F–3.6°F) per 5 minutes.28 Some experts suggest that this rate is too rapid, and in order to avoid potential cardiovascular instability, a goal for rewarming rate should be 1o to 2oC (1.8°F–3.6°F) per hour.8 Core warming methods are reserved for the victim with moderate to severe hypothermia and should be performed only when the victim has been transported to the appropriate facility.28,29

Frostbite Frostbite is a localized lesion of the skin, predominantly of the periphery, caused by the direct effects of cold exposure. Enough heat is lost from the area that ice crystals are allowed to form in the tissues.29 Most commonly affected are the feet and lower extremities, accounting for 57% of injuries. Also common are injuries of the hands (46%) and exposed areas of the face such as the nose, ears, and cheeks (17%).30 Historically, frostbite has had its highest prevalence during military campaigns. Today, those most at risk are mountain climbers and cold-weather endurance athletes.29 Frostbite occurs with exposure to an ambient temperature of 0oC (32oF) or less for a moderate to long length of time.29,30 Other factors that play a role in determining the time required to develop the lesion and the extent of injury include the windchill index, the humidity, and the wetness of the environment. As the cold exposure causes the skin temperature to drop, vasoconstriction occurs through stimulation by the sympathetic adrenergic nerve fibers.31 At a skin temperature of 10oC (50oF),

peripheral vessels are maximally vasoconstricted.25 Every 5 to 10 minutes, a period of vasodilation replaces maximal vasoconstriction. This is known as cold induced vasodilation or the “hunting response.” There is considerable variability based on acclimatization and genetic factors, explaining differences in susceptibility to frostbite injury based on race and ethnicity.25,31 Also, any factor, endogenous or exogenous, that affects peripheral circulation can predispose individuals to frostbite injury.30,31 Pathophysiologically, frostbite has four distinct phases. The first is the prefreeze phase. This occurs when the tissue temperature is in the range of 3o to 10oC (37o to 50oF). Sensation is generally absent. No ice crystal formation is present, but vasospasticity and cellular membrane instability cause plasma leakage and clinically obvious edema.29,31 Tissue enters the freeze-thaw phase when it cools to the range of -15o to -6oC (5o to 21oF). Actual ice crystals begin to form. When cooling takes place slowly, extracellular crystals form and cause a movement of free water into the extracellular space. As the cells dehydrate and shrink, a toxic concentration of electrolytes build up.25,31 With rapid cooling, ice crystals can form intracellularly, which is more damaging. Tissues most susceptible to injury include endothelial, bone marrow, and nerve tissue. The vascular stasis phase is a result of continued plasma leakage and ice crystal formation.29,31 The blood vessels begin to spasm and dilate leading to stasis coagulation and shunting.29,31 The last phase is the late ischemic phase. Progression to thrombosis formation and continued shunting of blood lead to tissue ischemia, gangrene, and autonomic dysfunction.29–31 Clinically, frostbite can be classified either by degree or by depth of injury. First- and second-degree injuries are considered superficial, whereas third- and fourth-degree injuries are considered deep.29 At initial presentation, it is difficult to determine the true extent of injury and an accurate clinical classification of the injury may not be completely clear until days after rewarming.30 First-degree injury presents with a firm, pale yellow to white plaque over the injured area. There is associated edema, erythema, and initial numbness followed by significant pain during rewarming. Ultimately little to no tissue loss is involved.29,31 Second-degree injury also involves initial numbness, erythema, and edema, but rather than a plaque, vesicles filled with a clear to milky fluid form over the area.31 Thirddegree injury develops vesicles as well, but they characteristically contain a darker, purple fluid indicating that the injury is deeper, involving the vascularity of the dermis.25,31 Fourthdegree injury remains cold and mottled after rewarming and eschar and mummification of the tissue develops in the area with involvement of muscle and bone.31

Treatment The basic principle, regardless of clinical class, is rapid rewarming of the injured area. Before any attempt is made at rewarming, it is important to have the victim in an environment where there is little to no possibility that the involved tissue will have a chance to refreeze. A thaw-refreeze cycle carries with it significantly higher morbidity than does a period of extended freezing.29 The first step in treatment is removal of all wet and binding clothing, replacing them with dry, loose wraps. This can be performed while in transit to a local medical facility as there is little risk of thawing-refreezing. On arrival, treatment begins immediately. Core body temperature should be initially measured, and if the temperature is less than 34oC (93oF), therapy should first be directed at treating hypothermia.29,31 When core body

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temperature has been corrected, treatment is directed at rapid tissue rewarming. The most generally accepted method used is immersion of the injured area into a water bath warmed to between 40o and 42oC (104o and 108oF) for 15 to 30 minutes or until the involved skin becomes pliable.25,28,31 It is important the water remain in such a narrow range for two reasons. If allowed to fall to a lower temperature, there is less benefit to potential tissue survival. On the other hand, if the temperature is allowed to go above the range, there is risk of compounding the injury with a thermal burn. Also, the higher the temperature, the less comfortable it is for the victim.31 Following the initial thawing phase, treatment is focused on preventing the progressive phase of the injury. A protocol designed by McCauley et al31 has been shown to decrease tissue loss, lower amputation rate, and decrease the hospital stay of victims (Table 6-2). The focus of this protocol is to inhibit the action of prostaglandins and thromboxanes that act locally to potentiate tissue damage.29,31 Surgery has little role in the acute treatment of frostbite. Deep injuries often require surgical treatment to remove nonviable or gangrenous tissue, but this is delayed at least 3 weeks and preferably later to allow the tissue to demarcate. Technetium bone scanning has shown some promise as a way to detect the line of demarcation earlier, but most experts still advise delayed amputation. Early postoperative prosthetics are advocated for the best fit.25,30,31 Long-term sequelae relate to the severity of the initial injury. Common problems include hyperhidrosis, increased sensitivity to cold exposure, skin color change, decreased sensation, and joint pain and stiffness.25,31 Skeletally immature victims may develop premature epiphyseal closure in the area of injury, resulting in bone shortening or angular deformity.31

Nonfreezing Injuries Immersion or “trench” foot is a significant cause of morbidity, particularly during military operations. Its name was first coined during World War I, after troops who stood in water-filled trenches for days developed this injury. It occurs in ambient temperatures of 0o to 10oC (32o to 50oF) and is caused by a prolonged exposure to cold water.29,32 The exact pathophysiology remains somewhat controversial, but it is widely believed that the prolonged vasoconstriction causes an ischemic injury leading to demyelination of nerve fibers, muscle atrophy, skin atrophy, and decreased compliance of the small vessels.24,25,32 On presentation, the affected limb appears mottled, pale, and cool to the touch. Sensation is impaired, and the victim will often describe the feeling as “walking on cotton wool.” After rewarming, the involved area becomes warm, dry, erythematous, and excruciatingly painful. This may last several weeks. Long-term sequelae include cold sensitivity, hyperhidrosis, paresthesias, and chronic neuropathic pain.32 Treatment of choice is removing the victim from the environment, elevating the affected extremity, and allowing passive rewarming.24,32 Although less severe, chilblains and pernio are also caused by prolonged exposure to a cold and wet environment. The ambient temperature is usually between 0o and 15oC (32o and 60oF) for these injuries to occur.25,32 Chilblains are subcutaneous vesicles that appear after 3 to 6 hours of exposure. They are usually painless and resolve with no long-term sequelae. As length of exposure reaches 12 hours or more, partial thickness eschars and deep pain can develop. The eschars slough without scarring; however, the pain may persist and is termed pernio.32 The major

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Table 6-2 Protocol for Rapid Rewarming 1. Admit frostbite patients to a specialized unit if possible. 2. Do not discharge or transfer to another facility victims of acute frostbite requiring hospitalization unless it is necessary for specialized care. Transfer arrangements must protect the victim from cold exposure. 3. On admission, rapidly rewarm the affected areas in warm water at 40° to 42°C (104° to 108°F), usually for 15 to 30 minutes or until thawing is complete. 4. On completion of rewarming, treat the affected parts as follows: a. Débride white blisters and institute topical treatment with aloe vera (Dermaide aloe) every 6 hours. b. Leave hemorrhagic blisters intact and administer topical aloe vera (Dermaide aloe) every 6 hours. c. Elevate the affected part(s) with splinting as indicated. d. Administer antitetanus prophylaxis. e. For analgesia, administer morphine or meperidine (Demerol) intravenously or intramuscularly as indicated. f. Administer ibuprofen 400 mg orally every 12 hours. g. Administer penicillin G 500,000 U intravenously every 6 hours for 48 to 72 hours. h. Perform hydrotherapy daily for 30 to 45 minutes at 40°C (104°F). The solution should meet the following specifications: 1. Large tank capacity: 425 gallons Fill level estimate: 285 gallons Sodium chloride: 9.7 kg Calcium hypochlorite solution: 95 mL 2. Medium tank capacity: 270 gallons Fill level estimate: 108 gallons Sodium chloride: 3.7 kg Calcium hypochlorite solution: 36 mL 3. Small tank capacity: 95 gallons Fill level estimate: 72 gallons Sodium chloride: 2.5 kg Potassium chloride: 71 g Calcium hypochlorite solution: 24 mL 5. For documentation, obtain photographs on admission, at 24 hours, and serially every 2 to 3 days until discharge. 6. Discharge patients with specific instructions for protection of the injured areas to avoid reinjury and follow up weekly until wounds are stable. If the patient is being discharged with no open lesions, instruct him or her to use wool socks, wear a hat, and use mittens instead of gloves to decrease the loss of heat between the fingers. Explain to patients that they are more susceptible to refreezing, so they should avoid exposure to cold and should wear warm clothing and shoes or boots if going outside is necessary. Give similar instructions to patients who are discharged with open lesions. Also instruct these patients to keep the affected extremity elevated and to take ibuprofen 400 mg orally every 12 hours. Aloe vera should be applied to the involved areas or scarlet red ointment used if the open areas are small. From McCauley RL, Smith DJ, Robson MC, Heggers JP: Frostbite. In Auerbach PS (ed): Wilderness Medicine, 4th ed. St. Louis, Mosby, 2001, p. 188.

long-term complication associated with pernio is increased cold sensitivity. The pathology of these conditions is thought to be just like that of trench foot. The treatment is supportive, allowing passive rewarming.29,33 In addition to directly causing injury, the cold environment can stimulate other conditions in susceptible individuals. Cold urticaria with or without angioedema is produced by the degranulation of mast cells that are stimulated by the cold. Symptoms are generally mild and self-limited and may be relieved with the

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use of antihistamines.25,29 Bronchospasm may also be induced, particularly with hyperventilation of cold air. Cold-induced asthma is considered a variant of exercise-induced asthma. The cold air causes a drying of the mucosa due to evaporative loss and local irritation of the mucosa leading to a cascade of immune response and ultimately to smooth muscle contraction in the bronchial tree. Preactivity use of inhaled b2-agonist is the mainstay of treatment.25,29,34 Raynaud’s disease is a condition caused by intermittent vasospasm of the digital vessels and is often exacerbated by cold. It may be associated with an underlying medical condition but is mainly idiopathic. With exposure, the digits become pale and numb. After rewarming, redness, swelling, and throbbing pain are seen. The primary treatment is avoidance of cold exposure.25,29 Cold air exposure of the nasal mucosa can stimulate an increase in mucous production resulting in rhinitis or “skier’s nose.” It causes no long-term problems and can be treated with nasal atropine sulfate.29

High-Altitude Illness High altitude has captivated athletes and adventure seekers for years. Athletes subject themselves to living high and training low in the hopes of achieving that small edge to push them past their competitors. Extreme athletes traverse harsh and dangerous terrain, pushing the limits of human physiology in search of excitement and adventure. In recent years, the adventure travel industry has boomed by providing quick and rapid excursions for individuals who may not be prepared emotionally or physically to tackle the potential medical complications encountered at such extremes of altitude.33 It is generally agreed that high altitude ranges from 1500 to 3500 m (4921 to 11,483 feet). At this altitude, there is minor impairment of oxygen saturation (SaO2 >90%). Manifestations of mountain sickness are common with rapid ascent above 2500 m (8202 feet). Very high altitude ranges from 3500 to 5500 m (11,483 to 18,045 feet) with maximum arterial oxygen saturation falling below 90% with concomitant decrease in PaO2 to below 20 mm Hg. Hypoxemia is normally mild at this range, but severe altitude illness may present during exercise and sleep. Extreme altitude is marked by elevations over 5500 m (18,045 feet).35,36 At this altitude, the benefits of acclimatization are overwhelmed by marked hypoxemia and physiologic decline,35 making permanent human habitation impossible.35,36 High-altitude illness is a spectrum of conditions caused by a body’s physiologic response to the hypobaric hypoxia environment of elevated altitude.36 Because the same general pathologic mechanisms are at work in all these conditions, there is considerable overlap with no clear delineation between the different forms of illness.33,35 Also, individuals presenting with altitude illness often have more than one of these conditions. The spectrum of diseases includes acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema. Acute mountain sickness (AMS) is the most common and most benign of the high altitude–induced illnesses. Typically symptoms will develop in an unacclimatized individual within 6 to 10 hours of arrival at an area of high altitude, usually at or above 2500 m (8202 feet).36,37 The diagnosis of AMS is a clinical one based on setting and symptoms and exclusion of other illnesses.36 There are no reliable findings on physical examination or from other diagnostic modalities to confirm or rule out the diagnosis.38 Therefore, in 1991 (with revision in 1993), a group called the Lake Louise Consensus Committee proposed a definition of AMS as headache with at least one of the following symptoms: gastrointestinal upset (anorexia, nausea, and/or

vomiting), fatigue or weakness, dizziness or lightheadedness, and difficulty sleeping associated with an ascent in altitude.37,39 The headache of victims of AMS is usually described as bitemporal or occipital, throbbing, worse with bending over or Valsalva maneuvers, and worse at night or on awakening.35,40 The severity of the symptoms is based primarily on the rate of ascent and the ultimate altitude achieved. If no further ascent is attempted, symptoms usually resolve completely in 24 to 72 hours as acclimatization is achieved.37,40 With continued ascent or when a very high altitude is achieved initially, symptoms may progress rapidly to one of the more life-threatening forms of highaltitude illness. Treatment depends on severity of symptoms. Proceeding to higher altitudes is absolutely contraindicated until the victim is symptom free.39 Small descents of 500 m (1640 feet) or more often yield dramatic improvement and is the initial treatment of choice.35–37 Acetazolamide (125 to 250 mg twice daily), a potent carbonic anhydrase inhibitor, improves symptoms and speeds acclimatization by producing a bicarbonate diuresis.36,37,41 It can also be used as a prophylactic measure if started 24 to 48 hours prior to ascent and continued for 2 days at maximum altitude.36,37 Dexamethasone (4 mg every 6 hours), a potent synthetic glucocorticoid, has a mechanism of action in AMS that is not entirely clear. Its proposed mechanism is a decrease in the permeability of the intracranial capillaries.37 Effects may be additive when used with acetazolamide.35 Unlike acetazolamide, it has no effect on acclimatization and there is a significant risk of rebound effects when discontinued.35,37 If descent is not possible or the condition is deteriorating, low flow oxygen (0.5 to 4 L/min) may be useful in preventing further decompensation.36,37 Portable hyperbaric chambers are also an option and have been shown to be as effective as oxygen in controlling symptoms while facilitating descent or other definitive treatment.42 AMS, as well as the other high-altitude illnesses, is preventable. Acetazolamide can be used but is generally reserved for individuals with a history of AMS or other illness. The mainstays of prevention are proper acclimatization and a slow, graded ascent limiting gains to 300 to 800 m per 24-hour period.35,41 High-altitude pulmonary edema (HAPE) is the second most common form of high-altitude illness and is the most common cause of altitude-related death.35,36,43 Just as with AMS, it is rarely seen in individuals below an altitude of 2500 m (8202 feet). The overall incidence depends greatly on individual susceptibility and rate of ascent, but has been estimated to be from 0.1 to 15% in those who ascend rapidly.8 About 5% to 10% of those diagnosed with AMS will develop HAPE, and 50% of those with HAPE will also have symptoms of AMS.33,36 Overall, mortality is estimated to be around 11% but can be more than 40% without proper treatment.33,40 HAPE is a noncardiogenic form of pulmonary edema that usually presents on the second night at altitude. Early symptoms are mild and include exertional dyspnea, cough, and decreased exercise performance.44,45 The Lake Louise Consensus diagnostic criteria for HAPE are at least two of the following symptoms: dyspnea at rest, cough, chest tightness or congestion, or weakness/decreased exertional performance. Also, the victim must have two of the following signs: rales or wheezing, central cyanosis, tachycardia, or tachypnea37,40 The rales start localized to the area over the right middle lobe and as symptoms progress become more diffuse.36 Symptoms are generally worse at night and may progress to include irrational behavior, orthopnea, and temperature elevated generally not higher than 38.5oC (101.3oF).33,36 When available, a chest radiograph will show a patchy, peripheral infiltrate with

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normal cardiac size.43,44 Electrocardiography shows a pattern of right ventricular strain.43 The first priority in treatment is descent. When this is not immediately available, or while this is being planned, efforts must concentrate on improving oxygenation. This can be achieved directly by oxygen administration or indirectly by use of a portable hyperbaric chamber. The goal of therapy is to maintain oxygen saturation of at least 90%.35,37,44 The calcium channel blocker nifedipine, given at a dose of 10 mg initially and then 30 mg in extended-release form every 12 hours, is a vasodilator that reduces pulmonary vascular resistance without causing hypotension.35–37 Because of potential side effects, other medications are of little use until descent is achieved.36 Measures taken to prevent HAPE, such as graded ascent and proper acclimatization, are especially important to those with a history of the illness because the recurrence rate has been estimated to be as high as 66%.8,33 Because it shares both clinical and pathophysiologic features with AMS, high-altitude cerebral edema (HACE) is considered by most experts to be an extension of the illness.46 Therefore, HACE generally presents several hours to days after the first symptoms of AMS.33,37 It is seen at the same altitudes at which both AMS and HAPE are seen, but it is far less common. Often victims will suffer from both HAPE and HACE. Case reports show that 13% to 20% of individuals treated for HAPE also had signs and symptoms of HACE, and an even higher percentage of HACE patients also had HAPE.46 The hallmark features are varying degrees of confusion, altered consciousness, and ataxia, in addition to the symptoms common to AMS.36,37,46 Victims may initially exhibit irrational behavior that progresses to severe lassitude, lethargy, obtundation, and ultimately coma over a period of hours to days.33,35,37 The ataxia is nearly always truncal and affects tandem gait testing (no effect on the finger-to-nose test).37,40 Because HACE is a global encephalopathy, focal neurologic signs are rarely present. Imaging studies are not necessary for the diagnosis, but one would expect to see evidence of edema in the white matter, specifically the corpus callosum, with no gray matter edema.46 Treatment is essentially the same as for AMS, with more emphasis on descent as quickly as possible with other modalities used before and during transport.36,37 The overall mortality of HACE is 13%, and for those who progress to coma, it is closer to 60%.8 Because it is such a lifethreatening illness and can have similar signs and symptoms of other serious illnesses, all but those with very mild cases who have a rapid and complete recovery on descent should be hospitalized for a full workup and observation.46 Prevention is the same as for all the other altitude illnesses, particularly AMS.36,37,46 The high-altitude environment can pose other potential medical concerns. High-altitude retinopathy is a generally benign, asymptomatic condition that is relatively common, especially above 5000 m (16,000 feet). Blindness or scotomas may be present when the macula is involved, but these usually resolve with descent and cause no permanent sequelae.35,40 Peripheral edema in the absence of any of the acute altitude illness is also common, especially in women, and can be treated with low-dose diuretics. It too will resolve on descent.35,36 High-altitude pharyngitis and bronchitis can cause significant morbidity due to persistent coughing spasms. It is thought to be more related to the inspiration of large volumes of cold, dry air leading to a

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drying of the mucosa and is treated by staying well hydrated, using lozenges, and breathing through a scarf or cloth.37,38 Susceptibility to bacterial infection is increased because of a mild reduction in T-lymphocyte function.36 Dehydration, relative inactivity, polycythemia, and constrictive clothing increase the risk of thrombotic events.35,36 Low temperatures increase the risk of hypothermia and frostbite.35 Ultraviolet radiation is increased at altitude and usually enhanced when reflected off snow that is usually present. This increases the risk of ultraviolet keratitis (snow blindness) and significant sunburn.35 In order for an individual to reduce and/or avoid the symptoms associated with mountain sickness, a period of acclimatization to the environment at high altitude must be accomplished. The slow and gradual exposure to hypoxia through staged ascent maximizes oxygen delivery for a given altitude, thereby enhancing survival and performance.8,36 This process involves a complex series of physiologic adjustments including hyperventilation and hypoxic ventilatory drive, circulation, and most importantly increased erythropoiesis resulting in increased hematocrit.33,35,36 Acclimatization is an individual process. Study of populations who live at high altitudes suggest a possible genetic component. The severity of the hypoxic stress, rate of onset, and individual physiology determine whether the body successfully acclimatizes or is overwhelmed.36 The role of staged ascent cannot be overemphasized. Guidelines for staging ascent are well published. A plan for acclimatization should be discussed with a trained medical professional knowledgeable in high-altitude medicine, taking into account altitude profile, the type of ascent, the performance capacity, the history of previous high-altitude illness, and the medical support available on the climb.47 Pharmacologic prophylaxis with medication such as acetazolamide is a consideration for individuals who cannot stage their ascent or are at risk of high-altitude illness.8 The most important method for avoiding high-altitude illness is careful preparation and education concerning proper climbing etiquette, signs and symptoms of AMS, and reaction if acute mountain illness is encountered by yourself or a fellow climber.8,47 Athletes and coaches alike have strived to achieve a performance edge by trying to harness the beneficial effects of intermittent hypoxic training as it affects the physiology of human adaptation to high altitude. The strategies of intermittent hypoxic training revolve around providing hypoxia at rest (living high/training low) or providing hypoxia during exercise (living low/training high).48 Living high/training low has been shown to increase performance at sea level.36,48,49 The benefit arises from increases in erythropoietin leading to increased red cell mass,36,48,49 submaximal exercise efficiency,36,50 and running performance.36,48–50 Adequate iron stores are needed secondary to increased red cell mass production.36 There have been no data supporting the benefit of training at altitudes above 2400 m (7874 feet). Training between 1500 to 2000 m (4921 to 6562 feet) maximizes the benefits of training in a hypoxic environment without substantial detriment.36 These benefits can be quickly obtained (within 10 days of initiation of training)36 and quickly diminish (within 3 weeks) with cessation of intermittent hypoxic training.50 Athletes competing at high altitude will require a period of acclimatization. The duration and extent of acclimatization depend on the altitude of residence, the altitude of the athletic event, and the duration of the event.

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REFERENCES 1. Martin TD: Special issues and concerns for the high school and college aged athletes. Pediatric Clin North Am 2002;49:533–552. 2. Vigil DV: Heat illness. In Puffer JC (ed): 20 Common Problems Sports Medicine. New York, McGraw Hill, 2002, pp 303–322. 3. Wexler R: Evaluation and treatment of heat-related illnesses. Am Fam Physician 2002;65:2307–2314. 4. Blows WT: Crowd physiology: The ‘penguin effect.’ Accid Emerg Nurs 1998;6:126–129. 5. Coyle EF: Thermoregulation. In Andenson SJ, Sullivan JA (eds): Care of the Young Athlete. Chicago, American Academy of Pediatrics and The American Academy of Orthopaedic Surgeons, 2001, pp 65– 80. 6. Bar-Or O: Children’s responses to exercise in hot climates: Implications for performance and health. Gatorade Sports Science Exchange 1994;7: No. 2. 7. Bar-Or O: Effects of age and gender on sweating pattern during exercise. Int J Sports Med 1998;19:S106–S107. 8. Tom PA, Garmel GM, Auerbach PS, et al: Environment dependent sports emergencies. Med Clin North Am 1994;78:305–325. 9. Noakes TD: Dehydration during exercise: What are the real dangers? Clin J Sport Med 1995;5:123–128. 10. Wyndham CH, Strydom NB: The danger of an inadequate water intake during marathon running. S Afr Med J 1969;43:893–896. 11. Noakes TD: Fluid and electrolyte disturbances in heat illness. Int J Sports Med 1998;19:S146–S149. 12. Walsh RM, Noakes TD, Hawley JA, Dennis SC: Impaired highintensity cycling performance time at low levels of dehydration. Int J Sports Med 1994;15:392–398. 13. Eichner ER: Treatment of suspected heat illness. Int J Sports Med 1998;19:S150–S153. 14. Roberts WO: A 12 year profile of medical injury and illness for the Twin Cities Marathon. Med Sci Sports Exer 2000;32:1549–1555. 15. Holtzhausen LM, Noakes TD, Kronig B, et al: Clinical and biochemical characteristics of collapsed ultramarathon runners. Med Sci Sports Exerc 1994;26:1095–1101. 16. Roberts WO: Exercise-associated collapse in endurance events: A classification system. Phys Sport Med 1989;17:49–55. 17. Holtzhausen LM, Noakes TD: Collapsed ultraendurance athlete: Proposed mechanism and an approach to management. Clin J Sport Med 1997;7:292–301. 18. Sandor RP: Heat illness. On site diagnosis and cooling. Phys Sport Med 1997;25:35–41. 19. Bowden L, Canini F: On the nature of the link between malignant hyperthermia and exertional heat stroke. Med Hypoth 1995;45:268–270. 20. Porter AMW: Collapse from exertional heat illness: Implications and subsequent decisions. Mil Med 2003;168:76–81. 21. Armstrong CE, Crago AF, Adams R, et al: Whole-body cooling of hyperthermic runner: Comparison of two field therapies. Am J Emerg Med 1996;14:355–358. 22. American College of Sports Medicine: Position stand on exercise and fluid replacement. Med Sci Sports Exerc 1996;28:i–vii. 23. Phinney LT, Gardner JW, Kark JA, Wenger CB: Long-term follow-up after exertional heat illness during recruit training. Med Sci Sports Exerc 2001;33:1443–1448. 24. Lloyd EL: ABC of sports medicine: Temperature and performance I: Cold. BMJ 1994;309:531–534.

25. Hixson EG: Cold injury. In DeLee JC, Drez D (eds): Orthopaedic Sports Medicine Principles and Practice. Philadelphia, Elsevier Science, 2003, pp 305–325. 26. Danzl DF: Accidental hypothermia. In Auerbach PS (ed): Wilderness Medicine. St. Louis, Mosby, 2001, pp 135–177. 27. Danzl DF, Pozos RS: Accidental hypothermia. N Engl J Med 1994;331:1756–1760. 28. Bien J, Koehncke N, Dosman J: Out of the cold: Management of hypothermia and frostbite. CMAJ 2003;168:305–311. 29. Sallis R, Chassay CM: Recognizing and treating common cold-induced injury in outdoor sports. Med Sci Sports Exerc 1999;31:1367–1373. 30. Foray J: Mountain frostbite. Int J Sports Med 1992;13:S193–S196. 31. McCauley RL, Smith DJ, Robson MC, Heggers JP: Frostbite. In Auerbach PS (ed): Wilderness Medicine. St. Louis, Mosby, 2001, pp 178–196. 32. Hamlet MP: Nonfreezing cold injuries. In Auerbach PS (ed): Wilderness Medicine. St. Louis, Mosby, 2001, pp 129–134. 33. Bezruchka S: High altitude medicine. Med Clin North Am 1992;76:1481–1497. 34. Regnard J: Cold and the airways. Int J Sports Med 1992;13:S191–S193. 35. Zafren K, Honigman B: High-altitude medicine. Emerg Med Clin North Am 1997;15:191–222. 36. Hacket PH, Roach RC: High-altitude medicine. In Auerbach PS (ed): Wilderness Medicine. St. Louis, Mosby, 2001, pp 2–32. 37. Gallagher SA, Hacket PH: High-altitude illness. Emerg Med Clin North Am 2004;22:329–355. 38. Hacket PH, Roach RC: High-altitude illness. N Engl J Med 2001;345:107–114. 39. Bärtsch P, Bailey DM, Berger MM, et al: Acute mountain sickness: Controversies and advances. High Alt Med Biol 2004;5:110–124. 40. Harris MD, Terrio J, Miser WF, Yetter JF: High-altitude medicine. Am Fam Physician 1998;57:1907–1914. 41. Coote JH: Medicine and mechanism in altitude sickness. Sports Med 1995;20:148–159. 42. Bärtsch P, Merki B, Hofstetter D, et al: Treatment of acute mountain sickness by simulated descent: A randomized controlled trial. BMJ 1993;306:1098–1101. 43. Adelman DC, Spector SL: Acute respiratory emergencies in emergency treatment of the injured athlete. Clin Sports Med 1989;8:71–79. 44. Bärtsch P: High altitude pulmonary edema. Med Sci Sports Exerc 1999;31:S23–S27. 45. Bärtsch P: High altitude pulmonary edema. Respiration 1997;64: 435–443. 46. Hackett PH, Roach RC: High altitude cerebral edema. High Alt Med Biol 2004;5:136–145. 47. Bärtsch P, Grunig E, Hoenhaus E, Dehnart C: Assessment of high altitude tolerance in healthy individuals. High Alt Med Biol 2001;2:287–296. 48. Levine BD: Intermittent hypoxic training: Fact and fancy. High Alt Med Biol 2002;3:177–193. 49. Levine BD, Stray-Gundersen J: A practical approach to altitude training: Where to live and train for optimal performance enhancement. Int J Sports Med 1992;13:S209–S212. 50. Katayama K, Matsuo H, Ishida K, et al: Intermittent hypoxia improves endurance performance and submaximal exercise efficiency. High Alt Med Biol 2003;4:291–304.

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Psychological Aspects of Healing the Injured Athlete J. Richard Steadman

In This Chapter Establishing reasonable goals Stages of injury and recovery Preinjury Immediate postinjury Treatment decision and implementation Early postoperative rehabilitation Late postoperative rehabilitation Specificity Return to sport

INTRODUCTION • It is well-known that the psychological impact of serious injury on both the professional and amateur athlete must be dealt with if the patient is to achieve optimal healing and a timely return to sports. • There are three types of rehabilitation: psychological, physiologic (aerobic conditioning, overall strength, and flexibility), and rehabilitation specific to the injured area. • The athlete should be given a complete and honest explanation of the injury and rehabilitation process, allowing him or her to feel like a part of the team guiding the recovery.

sports injuries to professionals or amateurs require the same degree of dedication to the correct use of three types of postinjury rehabilitation.

ESTABLISHING REASONABLE GOALS Being goal oriented, both types of athletes are highly motivated to improve the skills and speeds that lead to better scores. This focus on goal achievement can be harnessed in rehabilitation if the physician, sports medicine therapist, and athlete work together and are creative in their approach to the healing process. Goals give the athlete something concrete to work toward and require his or her active engagement in the rehabilitation process. It is important that these goals be achievable. For example, in the early postoperative period, a goal of full motion may be unrealistic, yet the athlete may be able to achieve at least partial motion. Setting a goal that the athlete can reach helps to reestablish self-esteem and allows the patient to begin charting a course toward recovery. In general, early rehabilitation stages should focus on short-term goals, although long-term goals can be helpful in mental training techniques, such as visualization. As recovery progresses toward the specificity period, goals related to return to competition and athletic performance can be brought into progressively sharper focus.

• An understanding of the seven stages of injury and recovery is crucial in guiding the athlete toward a return to sport.

STAGES OF INJURY AND RECOVERY

• The establishment of realistic, yet demanding goals helps the athlete to focus on each stage.

When planning a rehabilitation program, the rehabilitation team will find it helpful to identify and observe the relationship between specific time periods beginning with preinjury and ending with the athlete’s return to sport. The stages of this process are shown in Figure 7-1. During each of these periods, there is intense psychological pressure on the patient. A treatment approach that addresses the key psychological issues of each stage will optimize the outcomes of surgery and rehabilitation. The treatment approach for injuries requiring surgery is similar to that employed for severe injuries that do not require surgery. With relatively minor injuries, rehabilitation moves more directly from treatment design and implementation toward the specificity period and return to play.

• The appropriate application of psychological precepts is critical to the successful treatment of the injured athlete. In fact, ignoring this facet of the rehabilitation process makes it less likely that the patient will make a full recovery.

In modern society, the pursuit of fitness, good health, and longevity is important to people of all ages who participate in many types of physical activity to reach these goals. Their identities are strongly tied to the sports they enjoy, and they are just as serious about them as professional athletes are about their careers. The dedicated amateur’s eagerness to achieve full recovery and his or her previous activity level parallels that of the elite professional whose very livelihood depends on performance. Although there are greater psychological pressures on the pro who can lose his job if he or she returns to the game with diminished speed and skill, the injured amateur takes his or her performance level no less seriously. Thus, successful outcomes after

PREINJURY STAGE Several studies have indicated that injury is often not purely accidental but is caused by a combination of factors, including loss of concentration, the pressures of performance, and fatigue. It is helpful for the practitioner to examine factors in the envi-

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Preinjury

Immediate postinjury

Treatment decision/implementation

Early postoperative rehabilitation

Late postoperative rehabilitation

Specificity

Return to sport Figure 7-1 Stages of rehabilitation for the injured athlete.

ronment that may have affected the occurrence of the injury. If identified, preinjury factors may be addressed through psychological counseling during the course of treatment and rehabilitation.

IMMEDIATE POSTINJURY STAGE This stage is characterized by fear and denial, which accompanies the immediate pain and disability caused by the injury. At this point, the patient will need an accurate diagnosis that is thoroughly explained to him or her, a proposed course of treatment, and an estimate of the duration of treatment. This estimate will be approximate, but it will give the athlete an idea of what to expect. Most athletes, particularly successful ones, realize that injury is often a part of athletics. It is a mistake, however, for clinicians to assume that athletes know much about injury, treatment, and rehabilitation. A patient’s denial and fear can deter healing, though this can be countered by a plan that explains the severity of the injury, the duration of disability, and the expected recovery level. Such a plan gives the patient a measure of control and encourages active participation as an important part of the recovery team.

TREATMENT DECISION AND IMPLEMENTATION Choosing treatment options is easier if the first two stages are managed satisfactorily, that is, if the patient has accepted the reality of the injury and is psychologically prepared to assume an analytical role in helping to choose the appropriate treatment. Treatment may be easily decided on in some cases, but when many issues are involved, the decision can be difficult to make. For instance, treatments may affect a patient’s career or a team’s performance and the physician should be aware of such

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factors, which necessarily affect the final decision on a treatment course. In some cases, injury at a critical point in a career may force an athlete to make a decision that may endanger his or her future physical well-being. This seemingly irresponsible decision may nonetheless be a good one for the athlete, especially one who feels strongly that an additional year’s salary or other benefits may provide irresistible financial stability. Also, some athletes may view the psychological gratification gained from playing one more game or one more year as worth any risk. In cases like these, it is necessary for the athlete, agent, team management, and family to understand the hazards involved before a treatment course is chosen or rejected. The patient’s input can only be truly effective if he or she has been fully apprised of the choices available and understands the risks involved with any course of action.

EARLY POSTOPERATIVE REHABILITATION STAGE In the immediate postoperative phase, the rehabilitation team must consider more than the surgical event and its sequelae. The patient is affected in varying degrees by important psychological factors that can influence the final outcome of treatment. If surgery is performed, the athlete is transformed from an athletic person (with the healthy self-image associated with physical activity) to a bedridden, disabled patient. To counteract the negative aspects of this stage (from both a physical and psychological standpoint), it is necessary to initiate a program of rehabilitation goals. Providing an athlete with well-leg aerobic workouts following knee surgery encourages a goal-seeking attitude and helps the athlete maintain aerobic conditioning. In addition, setting appropriate goals for the injured area, for example, achieving a certain range of motion or level of exer-cise intensity, permits the patient to take an active part in treatment and assume a level of control over the postoperative environment.

LATE POSTOPERATIVE REHABILITATION STAGE During this phase, the drudgery of rehabilitation takes its toll. The physician must help the patient and the sports medicine therapist continue on a direct course to recovery. Continued goal orientation, provided by steadily increasing levels of activity, allows sustained patient input, and helps the patient to feel in control throughout rehabilitation. This emphasis on setting and achieving goals parallels the patient’s preinjury mind set. For example, the athlete’s preinjury goal may have been to run 5 miles in 30 minutes, and if he or she achieved this, confidence was increased. During rehabilitation, it is necessary to focus on different goals; for example, the completion of three sets of onethird knee bends becomes the mark of achievement. If goals are met, the patient feels empowered and enjoys a definite sense of accomplishment. Achieving rehabilitation goals requires several elements. First, the milestones should be challenging but realistic and should be designed by the physician, sports medicine therapist, and patient working together. Second, goals should stretch the limits of what the injured area can tolerate (without causing deformation or further injury) but should not extend beyond these limits. This requires a thorough understanding of the physiology and biomechanics of the injured area. Third, the patient should strengthen uninjured parts of the body in aerobic training, which

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helps prevent reinjury while providing more goal orientation. In the case of a leg injury, this training can include well-leg biking or swimming with or without a float. The positive psychological effects of aerobic training are an important aspect of treatment during this period.

SPECIFICITY STAGE This period is less challenging psychologically because, at this point, recovery is in sight. Exercise should become more specific for the sport, which entails a greater emphasis on patterns and muscle recruitment mimicking those used in the sport. During this period, the athlete needs reassurance that he or she will return to sport and once again achieve success. The patient may fear that success will not occur and thus may need psychological reinforcement, which can be readily supplied by continued emphasis on reaching achievable goals. Psychological counseling may be required if the athlete’s subconscious fears of failure are severe and seem obsessive.

RETURN TO SPORT STAGE This period may require psychological counseling for several reasons. First, the athlete’s lengthy absence from sport can produce fears, especially if success has not been reinforced in the earlier stages of rehabilitation. Second, the athlete may feel that peers have passed him or her by. Third, even though the rehabilitation program has been designed to return the athlete to a preinjury level, the absence of regular participation in a sport can create other realistic concerns. If the road to recovery has been successfully navigated and the team (athlete, sports medicine therapist, physician, and psychologist) has provided appropriate standards for achievement at each level of rehabilitation, the experience will have served a useful psychological purpose. The athlete’s ability to overcome the obstacles of injury and to gain a level of performance equal to or higher than preinjury levels can raise confidence that will enhance performance. It is unlikely that this success can be achieved, however, unless each stage of the rehabilitation program has been effectively followed.

CONCLUSIONS This approach represents a physician’s clinical perspective on the psychology of injury rehabilitation. The opportunities I have had to observe numerous world-class and dedicated recreational athletes have reinforced my appreciation for the role of psycholo-

gical factors in active rehabilitation. In some cases, patients intuitively apply the principles mentioned here. This ability to structure their rehabilitation effectively is probably a reflection of the way in which they achieved their preinjury success. In treating many athletes, I have observed quite a number who have returned to their sports at higher levels than they had achieved at the time of injury. This can be partially explained by the possibility that they were in an ascending curve of performance at the time of the accident, but this cannot be the entire explanation. Nor can good surgery and rehabilitation account for such successful recoveries. A multifaceted approach to rehabilitation provides a learning opportunity and helps create the psychological momentum that accompanies the athlete beyond rehabilitation and back to competition. The psychological rehabilitation program is summarized in Box 7-1. Although this program seems simple, it requires careful judgment calls by the rehabilitation team at each treatment stage. This approach to treatment is based on over 25 years of clinical experience with most of the major world-class competitive sports as well as work with many recreational athletes. The careful use of standardized treatment methods along with personal attention to the athlete’s needs during his or her different rehabilitation stages have proven effective. Our treatment team has contributed to some outstanding postinjury success stories. The return of several of our patients to top world-class performance levels after career threatening accidents is eloquent testimony to the validity of this approach as well as to the intensity of the athletes’ motivation.

Box 7-1 Rehabilitation Program Summary The patient’s psychological rehabilitation includes the following steps: 1. Complete understanding of the injury, the treatment, and the stages of treatment. This allows the patient to feel like a real part of the team guiding the recovery process. 2. Establishment of attainable goals at each stage in rehabilitation. These are realistic but demanding goals that provide an immediate focus but do not look too far ahead. 3. Prompt initiation of an aerobic program to help avoid the depression associated with the immediate postinjury period. In addition, the aerobic program counters other stress-related psychological changes that occur due to the abrupt transition from intense physical activity to no activity at all. 4. Psychological counseling, when necessary, to help the patient deal with his or her altered status as an athlete, especially during extended periods of inactivity.

SUGGESTED READINGS Hardy CJ, Crace RK: Dealing with injury. Sport Psychol Train Bull 1990;1:1–8. Heil J (ed): Psychology of Sports Injury. Champaign, IL, Human Kinetics Publishers, 1993. McGowan RW, Pierce EF, Williams M, et al: Athletic injury and self diminution. J Sports Med Phys Fitness 1994;34:299–304.

Pearson L, Jones G: Emotional effects of sports injuries: Implications for physiotherapists. Physiotherapy 1992;78:762–770. Smith AM: Psychological impact of injuries in athletes. Sports Med 1996;22:391–405. Smith AM, Scott SG, Wiese DM: The psychological effects of sports injuries. Coping. Sports Med 1990;9:352–369.

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8

The Female Athlete Letha Y. Griffin, James Kercher, and Fred Reifsteck

In This Chapter Scoliosis Shoulder instability Anterior knee pain Anterior cruciate ligament (ACL) injuries Forefoot pain Female athlete triad Anemia Psychological issues

INTRODUCTION • With the recent explosion of participation in women’s sports has come an understanding of musculoskeletal problems seen more commonly in the female athlete. • The rate of noncontact ACL injuries has been found to be higher for women in numerous sports, and strategies for injury prevention have gained popularity. • The medical issue of greatest concern in women has been termed the female athlete triad: disordered eating, amenorrhea, and osteoporosis.

The past 30 years has witnessed a tremendous growth in the participation of women in sports at all levels of play (middle school, high school, collegiate, professional, and recreational levels). According to U.S. government statistics, women’s sport participation increased by 700% during the 1980s. In the 2003 to 2004 academic year, 2,865,299 girls participated in high school sports (National Federation of State High School Associations NFHS 2003 to 2004 High School Athletics Participation Survey, unpublished data, 2004). At the 2000 Olympic Games, 38% of the approximately 10,000 athletes were women, a far cry from the two dozen who competed in the 1928 games. Not only has the number of female athletes increased, but the level and intensity of play have also increased for most women’s sports. Although many of the musculoskeletal problems seen in women are similar to those seen in men, a few injuries and conditions appear to occur with greater frequency. These include scoliosis, shoulder laxity issues, patellofemoral problems (acute patellar instability and chronic overuse injuries), ACL injuries, and overuse problems of the forefoot. Medical issues of note include anemia, disordered eating, and poor nutrition, the latter of which can result in osteopenia or even osteoporosis and can predispose the athlete to stress frac-

tures. Psychological stresses that can arise when young girls “grow out of their sport” is another area of concern that merits discussion as does sport burnout and overtraining syndrome. These topics are the focus of this chapter.

MUSCULOSKELETAL CONCERNS Scoliosis Knowledge of common spinal deformities and the effects strenuous sporting activities have on the developing spine is especially pertinent to diagnosis, outcomes, and level of participation in the female. Scoliosis is defined as the lateral and rotational curvature of the spine. Idiopathic scoliosis refers to the presence of curvature in the absence of congenital or neurologic abnormalities. Idiopathic scoliosis is the most prevalent form of scoliosis, accounting for approximately 70% of all cases. The adolescent form of this disease is most common and is of particular concern for the female athlete due to the female-to-male ratio approaching 6:1. This is further compounded by the more aggressive progression pattern within the female gender. The prevalence of adolescent idiopathic scoliosis is reported as 2% to 3% in the general population.1 However, in certain female dominated sports such as gymnastics, ballet, and swimming, the prevalence has been found to be much higher. In a study involving Junior Olympic swimmers, Becker2 reported a 6.9% incidence of idiopathic scoliosis and a 16% incidence of mild functional curves. It was of particular importance that these curves were toward the swimmers’ dominant hand side. This implicates muscle imbalance as a possible contributor to scoliosis. It has been postulated that the inequity of forces in these specific training regimens produces asymmetrical development of paraspinal musculature, thus creating a potential risk of the progression of spinal deformity. Many athletes begin vigorous training in early childhood. It is thought that rapid growth makes immature bone more susceptible to intense training. Hellstrom et al3 reviewed radiographs of competitive athletes and found abnormalities in the vertebral ring apophyses in gymnasts. In a study by Wojtys et al,4 the authors correlated the amount of exposure to intense athletic training and the development of spinal curvatures in the immature spine. They found that increased spinal curvature was associated to cumulative hours spent in training; hence, biomechanical stresses may play a role in the progression. In previous studies on ballet dancers, Warren et al5 found the incidence of idiopathic scoliosis to be 24%. This was correlated to small body habitus and delayed menarche. It was found that dancers with scoliosis had a slightly higher prevalence of secondary amenorrhea. This suggests hypoestrogenism from

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delayed menarche and prolonged intervals of amenorrhea may predispose ballet dancers to scoliosis. Tanchev et al6 found a 10fold higher incidence of scoliosis in rhythmic gymnastic trainees, which they related to asymmetrical loading, delayed menarche, and ligamentous laxity. Similar to the male athlete, the diagnosis of adolescent idiopathic scoliosis is made only after a thorough history, physical examination, and appropriate radiographs. The spine should be examined with particular attention given to the neurologic examination. Secondary sex characteristics should be assessed and the skin should be examined for café-au-lait spots, suggesting neurofibromatosis. The Adams forward bend test is one of the most common screening tests used (Fig. 8-1). The patient bends forward as if to touch the toes. This enhances the spinal curve and demonstrates imbalances in the rib cage. This test is most sensitive to curves in the thoracic region. Concern that significant deformity is present during screening justifies radiographic evaluation, typically a long anteroposterior and lateral radiograph of the torso that includes the thoracic and lumbar spines on one film and also includes the iliac crest. In addition to curve evaluation, radiographs are also useful for determining skeletal maturity. Additional tests such as a magnetic resonance imaging are indicated in patients with idiopathic scoliosis in the presence of neurologic abnormalities7 or if the presenting complaint is back pain that does not respond to several weeks of conservative care (rest from activity, back exercises, and anti-inflammatory drugs). It is generally accepted that scoliosis is normally a painless condition.1 The presence of pain may indicate an underlying condition such as fracture, tumor, spondylolysis, or disk herniation and therefore warrants investigation. Routine magnetic resonance imaging evaluation of all patients with adolescent idiopathic scoliosis is not recommended.

In the past, athletes identified with scoliosis were largely restricted from athletic participation. This philosophy was grandfathered from traditional teachings and based on studies demonstrating exercise was of no benefit in preventing progression. Experience and increasing understanding of scoliosis have begun to reverse this trend. Becker2 believed that exercise and cross-training might help counteract overloading forces secondary to sport-specific training. Mooney et al8 discuss this in a report on the effect of measured strength training in adolescent idiopathic scoliosis. These authors found measured strength differences between sides ranging from 12% to 47% and describe a benefit to rotary torso strengthening. Encouraging adolescents with scoliosis to participate in sports is now generally accepted as it is now thought that activity can help maintain endurance and flexibility, minimizing the asymmetrical forces on the spine. The use of bracing has been shown in several studies to halt progression. Bracing is generally recommended in those whose curve is greater than 20 to 25 degrees. With the development of newer materials and evidence of the efficacy of nighttime brace wear, athletes now can participate both in and out of brace, depending on their unique situation (e.g., degree of curve, sport). Discussion of specific indications and therapeutic options for athletes with progressive or severe curves is beyond the scope of this chapter. In deciding treatment, the type of sport and level of performance should be considered in combination with the severity of the deformity.9 Much controversy exists over athletic participation after surgical intervention. Rubery and Bradford10 polled members of the Scoliosis Research Society on athletic activity following spine surgery and presented the opinions of 261 surgeons active in treating spinal deformities. They discovered that the most common time to resume low-impact, noncontact sports was 6 months and that contact sports were generally allowed after 12 months. However, athletes were encouraged not to participate in collision sports. In summary, increasing numbers of female athletes with idiopathic scoliosis are participating in sports. It is prudent for the treating physician to identify sport-specific risks associated with spinal deformity. Care for these athletes should be individualized. Increased knowledge and improvements in bracing protocols and surgical techniques have enhanced the quality of life for female athletes with scoliosis by allowing continued involvement in their athletic endeavors.

Shoulder Instability

Figure 8-1 The Adams forward bend test.

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Shoulder laxity has been traditionally associated with the female athlete. Hormonal factors such as progesterone, estrogen, and relaxin11 as well as decreased upper extremity muscle mass12 have all been implicated. Yet there has been much debate as to whether these gender-specific differences contribute to injury patterns. The shoulder is a complex, highly mobile structure. In order to accommodate for extremes in motion, there is a delicate dynamic between normal and pathologic. The glenohumeral joint is inherently unstable. Relative to the glenoid, the humeral head is very large, providing only a small contact surface area for bony support. Thus, the joint relies heavily on balanced contraction of rotator cuff musculature, coordinated scapulothoracic motion, and the integrity of the soft tissues. It has been proposed that the female athlete is predisposed to atraumatic or multidirectional shoulder instability due to laxity of capsuloligamentous constraints. McFarland et al13 and Borsa et al14 investigated these issues and found shoulders to be appreciably

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more lax in females than males. However, it must be noted that the terms laxity and instability should not be interchanged. While laxity describes the physiologic motions of the glenohumeral joint, it is not itself pathologic.15 The term instability should be reserved for painful motion resulting in subluxation or dislocation.11 In 1980, Neer and Foster12 recognized multidirectional instability as a specific entity. While the essential lesion was initially thought to be capsular redundancy, operative findings of capsular tears and labral avulsions (Bankart lesions) have shown that the etiology is multifactorial.11,16–18 It is thought that direct trauma or repetitive microtrauma, such as that found in overhead-throwing athletes, superimposed on a lax shoulder might result in instability.18 The physical examination is important in differentiating these two entities. The patient may present with vague complaints of pain, apprehension, and shoulder fatigue with or without voluntary subluxation. The shoulder should be assessed for rangeof-motion deficits, rotator cuff weakness, and asymmetry of scapular motion. Excessive anterior and posterior motion of the humeral head and inferior translation with downward traction on the humerus (sulcus sign) can help identify laxity (Fig. 8-2). Many provocative tests such as the load and shift test, the apprehension relocation test, and the release test, described in the shoulder section of this book, can be used to elicit instability. In general, pain or apprehension while placing the shoulder in the abduction external rotation position is suggestive of instability. Initial treatment for multidirectional instability should be conservative. With the assistance of a physical therapist, a program of mobilization, flexibility, and strengthening should be initiated. Graduated resistance training using elastic bands or weights through internal and external rotation motions are

useful for strengthening the rotator cuff, thereby improving dynamic stability of the joint (Fig. 8-3). Scapular stabilizing muscles (trapezius, serratus anterior, rhomboids, and levator scapulae) must also be strengthened. Scapulothoracic motion is vital to overhead activity; in order to abduct the arm, the scapula must tilt and elevate. Failure of this motion can result in impingement on the underlying structures. To address this, activities such as pull backs, shoulder shrugs, and knee and wall push-ups, which emphasize protraction of the scapula as well as the correction of poor posture, are typically prescribed (Fig. 84). In addition, athletes should be enrolled in sport-specific training to enhance muscular control and proprioception. Surgical treatment should be offered if the patient has not responded within 6 to 9 months of rehabilitation. The original surgical procedure was the open inferior capsular shift, aimed to reduce capsular redundancy.12 Many authors report improvements in stability and return to preinjury activity level with this procedure or variations of open stabilization techniques.17,19,20 Arthroscopic stabilization has been introduced as an alternative to established open procedures. The advantages include better identification of underlying intra-articular pathology,16 less morbidity, and improved cosmesis. With the development of improved arthroscopic techniques, several clinical trials have reported excellent results for the treatment of multidirectional instability. Arthroscopic repair has also been shown to withstand the stress of sports activities.21,22 Mazzocca et al22 examined the results of arthroscopic anterior shoulder stabilization in collision and contact athletes. They reported 100% return to organized sports and believe that participation in collision and contact athletics was not a contraindication for arthroscopic repair. No gender-specific trials on the fate of patients treated operatively or nonoperatively are available. Arthroscopic thermal capsulorrhaphy, which uses heat to shrink capsular volume, has been introduced in recent years. However, several authors have reported high failure rates and increased incidences of postoperative complications,23,24 making this a less favored procedure.

Anterior Knee Pain

Figure 8-2 Sulcus sign. Note displacement of the humeral head inferiorly when traction is applied to the extremity.

Difficulties with patellofemoral tracking can result in acute injuries (patellar subluxation or dislocation) or overuse problems (patellofemoral stress syndrome or anterior knee pain). Patellar subluxation and dislocation are discussed in detail in Chapter 57 and are not covered in this section. Patellofemoral stress syndrome is a name given to the syndrome of anterior knee pain or patellofemoral pain associated with diffuse anterior knee pain that increases with such activities as squatting, kneeling, running, walking down steps, or walking downhill and is common in women athletes, especially young women. The diagnosis of patellofemoral stress is based on history and clinical examination (Table 8-1). Squats and lunges (i.e., those activities that increase patellofemoral forces) frequently enhance symptoms. Swelling is rarely present. Other symptoms of this syndrome include popping, catching, and snapping. Athletes may experience acute episodes of the knee giving out or giving way. Occasionally, crepitus may be present, although in general, this symptom more typically occurs in those with true softening and fraying of the retropatellar surfaces (chondromalacia) rather than the overuse problem of patellofemoral irritability, anterior knee pain, or patellofemoral stress syndrome. Athletes will frequently report that they have a change in their exercise activity prior to the onset of symptoms with either

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Table 8-1 Diagnosis of Patellofemoral Stress Syndrome Frequent Symptoms Locking Catching Giving out Increased pain with flexion-extension movements (e.g., kicking, running) Pain while squatting, kneeling, prolonged sitting, sitting cross-legged style, and climbing stairs Physical Examination Features Increased hip varus Increased knee valgus Vastus laterals > vastus medials Foot pronation Increased lumbar lordosis Weak core strength Increased tightness (apparent or real) of the hamstrings, iliotibial band and/or quadriceps

A

B Figure 8-3 Exercises to strengthen the rotator cuff. A, External rotation: Stand with elbow at side and gently rotate arm out as illustrated. B, Internal rotation: Rotate arm across front of body as illustrated.

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an increase in running-type activities or an increase in squats and lunges or knee extension exercises. They may report completing the same number of knee extensions but with a higher weight than what they would normally lift. Occasionally, and particularly in recreational athletes, the inciting factor may be related to job or home activities, for example, using a clutch car, moving to an upstairs apartment, or sitting more at work, even though the pain is elicited with sport. The onset of pain in women is often during the mid-to-late teenage years at the time of transition from the narrower pelvis of adolescence into the wider pelvis of womanhood. College may bring a dramatic change in lifestyle to young women resulting in more seated study time and less active sport play or exercise, resulting in persistent patellofemoral forces from the bent knee position of studying and less vastus medialis obliquus strength. The patella is guided in the trochlear groove by the bony anatomy of both the patella and the trochlear groove, by the surrounding quadriceps muscle and by the complex ligamentous structures that surround the patella, including the lateral patellofemoral ligament. If, during adolescence, the four heads of the quadriceps do not all develop symmetrically, the asymmetrical pull of the quadriceps can create abnormal patellofemoral forces or at least uneven patellofemoral forces.25–27 On physical examination, alignment and flexibility of the extremity should be carefully assessed. Hip varus, knee valgus, and foot pronation are frequently, but not always, present. The athlete may stand with her knees “locked” in hyperextension, a posture that is thought to be associated with increased patellofemoral forces. Tightness of the hamstring and quadriceps muscle groups can add to the abnormal mechanics about the knee and the increase or unequally distributed patellofemoral forces.28 The normal progression of patellofemoral contact areas during knee flexion is illustrated in Figure 8-5.29 As the knee

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45°

A 30°

B

D C Figure 8-4 Exercises to strengthen the scapular stabilizers. A, Pull backs; B, shoulder shrugs; C, wall push-ups; D, knee push-ups.

flexes, the contact area on the patella moves proximally as the contact area on the femur moves inferiorly. At no time is the entire surface of the patella in contact with the trochlear groove of the femur. Symptomatic athletes will generally have pain to palpation around and behind the patella. Infrequently they have apprehension with lateral deviation of the patella (i.e., a positive apprehension test). They do, however, have pain with slight downward pressure of the patella in the femoral groove. This sign can be enhanced by asking the patient to actively contract the quadriceps muscle while the examiner places an inferiorly directed force on the patella (Fig. 8-6). Typically, no effusion is present. The range of motion of the knee is full. One theory of the cause of patellofemoral pain is based on the premise that abnormal patellofemoral mechanics can cause increased retropatellar forces that overwhelm the articular surface’s ability to absorb the increased stress, resulting in increased pressure on the bone beneath. Dye,30 who has done a great deal of research in this area, stresses the need to stay within one’s “envelope of function.” The envelope is determined

not only by one’s own personal anatomy but also can be influenced by exercise, braces, and orthotics, that is, by altering patellofemoral forces favorably, one can increase the envelope of function. Radiographs can also be helpful as they may demonstrate an asymmetrical position of the patella in the trochlear groove (Fig. 8-7). Many different radiographic views have been used to describe the relationship of the patella to the trochlear groove. However, the degree of quadriceps contraction at the time the radiograph is taken can markedly change the patella’s position in the trochlear groove.31 Therefore, care must be taken in interpreting these views. Skyline views of the patella are helpful, however, to provide indirect evidence of the thickness of the patellofemoral articular cartilage. With chondromalacia of the patella, this space may be diminished, but in the overuse syndrome of anterior knee pain or patellofemoral stress, the thickness of the patellofemoral articular cartilage should be normal, indicating a reversible situation (Fig. 8-8). The progression of patellofemoral stress syndrome to chondromalacia is not well known. Most young people

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Figure 8-7 Note asymmetrical position of the patella in the trochlear groove.

Figure 8-5 Normal progression of patellofemoral contact forces. A, Method of applying force to patellofemoral joint; B, 20 degrees of flexion; C, 60 degrees of flexion; D, 90 degrees of flexion; E, 120 degrees of flexion; F, 135 degrees of flexion. (Adapted from Ficat and Hungerford.29)

Figure 8-6 Patients with patellofemoral stress syndrome generally will have pain with downward pressure of the patella in the femoral groove.

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with the overuse problem of anterior knee pain do not develop pathologic softening of the retropatellar surface (chondromalacia). More studies on the natural history of anterior knee pain are needed. The treatment of athletes with patellofemoral pain centers on altering patellofemoral forces by altering the patella’s position in the femoral groove (Table 8-2). Quadriceps strengthening, typically focused on the vastus medialis muscle, is combined with exercises to strengthen muscles of the hip and trunk. Exercise routines can employ machines, rubber tubing, or free weights. Athletes should incorporate flexibility exercises for all muscles of the lower extremity and trunk into their program. A hyperextended lumbar spine (i.e., increased lumbar lordosis) can result in apparent shortening of hip external rotators including the iliotibial band and hamstrings and hence influence patellofemoral mechanics. A strong core (i.e., trunk muscles) to absorb impact force on landing may minimize increased stresses to the knee and foot. A good example to use for athletes is to explain that they need to land as “light as a feather” like the ballerina does when she lands en pointe. Braces or tape are used to shift the patella’s position to a more favorable one in the femoral groove.32,33 Some patients prefer braces with a lateral pad; other patients prefer braces that have a pad about the entire patella. Others prefer an open patellar brace; some like merely an infrapatellar strap that lifts the patella superiorly in the groove or at least attempts to decrease pressure on the patellofemoral surface by elevating the patella (Fig. 8-9). A trial-and-error method in selecting a brace is often used as it may be difficult to predict which type of brace will be most helpful to the athlete. Orthotics to decrease foot pronation may be used to better align the patella as foot pronation can result in an increase in apparent knee valgus and hence lateral displacement of the patella in the groove.34 Oral nonsteroidal anti-inflammatory drugs can be used at a time of marked increased symptoms, but athletes must understand that these drugs do not alter the course of the overuse syndrome, but merely temporarily decrease symptoms caused by the inflammatory reaction. Therefore, it is essential to participate in an exercise program and incorporate other conservative measures into their routine. Activity modification, even if

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A

B

Figure 8-8 Skyline view of the patellofemoral joint. A, Note the width of the cartilage space (arrow) in a young knee with patellofemoral stress syndrome and no loss of articular cartilage space. B, Note the reduced width of the cartilage space (arrrow) in the knee of a patient with significant chondromalacia.

only temporary, may be needed to decrease irritability until patellofemoral forces can be altered advantageously.

Anterior Cruciate Ligament Injuries The rate of noncontact ACL injuries in high-risk sports such as soccer and basketball is greater in female than in male athletes.35–37 The young appear to be most at risk, with the vast majority of ACL injuries occurring in those 15 to 45 years of age.38 In one study, the average age of those who sustained an ACL injury was 26 years.39 Neither risk factors nor the mechanism of injury is well defined for ACL noncontact injuries. Proposed risk factors include shoe-surface interactions and other environmental concerns; anatomic factors such as hip varus, knee valgus, foot pronation, femoral notch size, and size of the ACL; hormonal factors (levels of estrogen, progesterone, relaxin, and others); and neuromuscular factors such as upright posture, landing a jump and cutting on a straight knee, leg dominance, and poor hamstring strength relative to quadriceps strength (quadriceps dominance).40,41 Landing a jump, cutting, pivoting, or changing directions accounts for 80% to 85% of all noncontact ACL injuries. Often

Table 8-2 Overview of Treatment for Patellofemoral Stress Syndrome Strengthen

Quadriceps, particularly vastus medialis obliques and core

Increase flexibility

Trunk and lower extremities

Braces

To support, lift, or move the patella medially

Shoe orthotics

To decrease foot pronation

Activity modification

Decreased flexion/extension activities until acute symptoms subside

Nonsteroidal If no stomach irritability and no history of anti-inflammatory drugs allergies to these medications

the athlete recalls that just prior to making a planned move, someone cut in front of her, bumped her, or in some similar way made her accommodate quickly to the change in direction of movement or landing.42 Men have less hip varus and knee valgus than women, and they appear to land a jump with their hips and knees more flexed than women.43 Unlike women, men’s strength is relatively equal in both lower extremities, and they fire their hamstrings more rapidly and prior to their quadriceps with an anteriorly directed tibial force, both appropriate responses to protect the ACL.40,44 The diagnosis and management of ACL injuries in women are similar to those in men, as discussed in Chapter 51. Although at one time it was theorized that women would fare less well than men following ACL reconstruction, studies have not found this to be true. ACL reconstruction using autologous bonepatellar tendon-bone is as functionally stable in females as in males, and Tegner and Lysholm’s scores after reconstruction are similar.45,46 Although Barrett et al47 reported increased laxity scores in women following ACL reconstruction with autologous quadruple hamstring tendon, others have reported equivalent results in males and females.48–50 During rehabilitation following ACL reconstruction, the therapist should emphasize avoidance of abnormal mechanics leading to ACL injury, substituting instead proper landing and cutting skills and agility skills minimizing dominant leg characteristics if such exist. Moreover, these same principles should be highlighted as a part of preseason conditioning programs. Drills to enhance balance and agility, incorporating plyometrics with an emphasis on proper landing techniques (i.e., landing light as a feather by contracting core muscles and with more hip and knee flexion and with the body balanced over the lower extremity) should be practiced. In fact, a six-part preseason and in-season prevention program has been proposed by some and includes recognition of injury mechanics, flexibility and strengthening exercises, aerobic conditioning, plyometrics, and agility drills (Table 8-3).51 These exercises should be incorporated into normal sport conditioning programs. Programs using these strategies or even those merely

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A

B

D C Figure 8-9 Braces/taping are frequently used as part of the treatment for patellofemoral stress. A, Brace with lateral pad; B, brace with a doughnut pad around patella; C, infrapatellar strap; D, patellar taping. The tape “pulls” the patella medially.

Table 8-3 Six-Part Alternative Warm-up Program for Anterior Cruciate Ligament Injury Prevention Enhance recognition of injury mechanics Increase flexibility of core and lower extremity muscles Increase strength of core and lower extremity muscles Aerobic conditioning Incorporate plyometrics Perform agility drills

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incorporating simple balance drills into preseason and in-season condition routines have been reported to decrease the incidence of ACL noncontact injuries (Table 8-4).41,52 Some investigators have also proposed that those girls found to have poor landing skills and significant deficits in hamstring strength may benefit from participating in an intense therapy program prior to the beginning of the season or even during the season, in addition to performing an alternative in the field conditioning program.53 More data from randomized, controlled trials with numbers sufficient to have adequate power from which to draw reliable conclusions are needed. However, early reports from trials of existing programs are very encouraging.

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Forefoot Pain It has been reported that 8% of all females wear shoes smaller than their feet and that this trend starts with adolescence. Girls also engage in more “foot abusive” sports than men. Although women spend more than men on athletic shoewear ($5.4 billion versus $5.3 billion), many shoe manufacturers do not make a last sized to a female’s foot but merely scale down their male last. This results in a shoe with an inappropriate forefoot widthto-length ratio, predisposing female athletes to develop corns, calluses, bunions, bunionettes, and hammertoes. Treatment of these forefoot abnormalities is generally symptomatic conservative care with pads, creams, moleskin, exercises, and shoe modification. Surgery should be approached with great caution as secondary biomechanical problems can result. Figure 8-10 is a radiograph of a young cross-country runner who had bunion surgery and then developed stress fractures in the second and thirds metatarsals from altered mechanical forces resulting from a shorter first metatarsal. Stress fractures of the metatarsals are also frequent in dancers as well as runners and gymnasts. Bone is a dynamic tissue constantly repairing damage to its structure caused by activity. Stress fractures or microfractures of the bone occur when the rate of bone repair falls behind the rate of bone formation. This can occur if the athlete does too much too fast without proper conditioning or the repair processes are slowed secondary to one of several factors including inadequate sleep, a poor diet, or lack of adequate estrogen (as discussed in the section on the female athlete triad). Clinically, the athlete with a forefoot stress fracture will complain of pain and swelling in the midfoot just behind the metatarsal heads. The swelling and pain increase with activity and improve with rest. They are better in the morning after a night’s sleep. Initial radiographs may not demonstrate the early stress reaction, but if the athlete continues to participate in her sport despite pain, the increased insult to the bone results in a fracture line, which can be seen radiographically. If rest is instituted early when pain first begins, radiographs may never show a fracture line but instead may reveal an area of increased bone density indicative of healing. Because foot mobility is needed for performance by many female athletes (e.g., the gymnast, runner, and dancer), these athletes cannot perform in a hard-soled shoe, as might a football lineman, and will lose from 4 to 10 weeks from sport until their fracture heals. Preventing stress fractures by proper conditioning, adequate sleep, and appropriate diet and footwear is essential.

Figure 8-11 Schematic diagram of the compression of the interdigital nerve by adjacent metatarsal heads.

Interdigital neuroma or Morton’s neuroma is a painful condition of the forefoot resulting from entrapment and perineural fibrosis of the interdigital nerve as it traverses the web space between the metatarsal heads (Fig. 8-11). This condition, which is eight times more prevalent in women than men, occurs most commonly between the second and third metatarsal heads but can also occur between the third and fourth metatarsal heads. The term neuroma, which is often used to describe this condition, is incorrect. The condition arises from entrapment and perineural fibrosis rather than a proliferation of neuronal tissue. Patients will report paresthesias in the adjacent two toes as well as a vague pain relieved by removing the shoe and massaging the foot. On physical examination, swelling may be present between the metatarsal heads at the involved interspace, and pain can be reproduced by transverse pressure on the metatarsal heads while simultaneously placing upward pressure on the plantar surface of the foot at the site of discomfort (Fig. 8-12). Radiographs are normal but may show close proximity of the metatarsal heads at the involved site. Conservative treatment includes the use of a wide toe box shoe, metatarsal pads, foot and toe exercises, and consideration of a steroid injection. If these measures fail to relieve symptoms, the most common surgical procedure is resection of the nerve in the intermetatarsal area, which can achieve satisfactory results.54,55 Once again, caution should be exerted before surgery is undertaken as scar secondary to surgical intervention may alter performance in a female athlete who depends on mobility of the foot for her sport.

MEDICAL CONCERNS Figure 8-10 Runner who sustained a stress fracture of the second metatarsal after bunionectomy. Note shortening of the first metatarsal increasing stress to the second.

The Female Athlete Triad The term the female athlete triad was selected by a 1992 consensus conference called by the Task Force on Women’s Issues

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Table 8-4 Prevention Programs No. Author

Sport

No.

Sex

Random

Equipment

Strength

Flexibility Agility

Plyometrics

1

Griffis et al (1989) S

Basketball

Not 8 yr reported 2 teams

Duration

F

No

Jump box, balance

No

No

Yes

No, landing technique

2

Ettinger et al (1995)

Alpine skiing

T: 4000 C: ?

1 yr with 2 yr of historic controls

M/F

No

Video clips of No skiers sustaining ACL injuries and those who avoided injury in very similar falls

No

No

No

3

Caraffa et al (1996)

Soccer

T: 300 C: 300

3 seasons

M

No, Balance boards prospective

PNF Yes facilitation exercises

No

No

4

Hewett et al (1999) A

Basketball, 1263 volleyball, soccer

1 yr

M/F

Yes

Jump box, balance

Yes

No

No

Yes

5

Heidt et al (2000) A, S

Soccer

300

1 yr F intervention (7-wk period)

No

Sports cord, box jump

Yes

No

Yes

Yes

6

Söderman et al (2000) S

Soccer

T: 121 C: 100

1 season F (Apr–Oct)

Yes

Balance board in addition to regular training

No

No

No

No

7

Myklebust et al (2003)

Team handball

900

3 yr

F

No

Wobble board, balance foam mats

No

Yes

Planting NM control

No, landing technique

8

Wedderkopp et al (2003) A, S

Team handball

236

10 mo

F

Yes, cluster RCT

Balance board No (proprioceptive) in 4 levels

No

Yes

Yes

9

Gilchrist et al (2004)

Soccer

561

1 yr

F

Yes

Cones, soccer ball

Yes, Yes glut med. abd, ext, hamstring, core

Deceleration, sport specific

No, landing technique, multiplanar

10

Pfeiffer et al (2004)

Soccer

1439

9 wk

F

No

No

No

Cut, NM control

No, landing technique

11

Mandelbaum et al (2005)

Soccer

T: 1041 C: 844

2 yr

F

No, Cones, soccer voluntary ball enrollment

Hamstring, Yes core

Soccer specific with dec tech

No, landing technique, multiplanar

12

Olsen et al (2005) A

Team handball

1837

1 yr

M/F

Yes, cluster RCT

Yes

Cut, NM control

No, landing technique

Wobble board, balance foam mats

Yes

Yes

A, Anterior cruciate ligament (ACL) injuries not specifically assessed; M, male; F, female; RCT, randomized controlled trial; S, sample size relatively small (power inadequate?). From Griffin LY, Albohm MJ, Arendt EA, et al.41

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Proprioception

Program/Study Strengths

Yes, deceleration pattern (3-step shuffle)

Changing deceleration and Not randomized, unpublished landing technique (encouraged knee and hip flexion)

Program/Study Weaknesses

Outcome

No

Nonrandomized, controlled interventional study. Large number of injuries

Not randomized. Not all potential Severe knee sprains were reduced by 62% participants trained. Historic controls. among trained skiers (patrollers and Exact diagnosis of knee sprain not instructors) compared to unperturbed group always available. Exact exposure to who had no improvement during the study risk not precisely determined period

Yes, balance board activities, multilevel

Mechanoreceptor/ proprioception training

Additional equipment; not costeffective on large-scale basis

Yes

Decrease peak landing forces 1-on-1 program in sports facility, not and valgus/varus perturbations, feasible to implement across large increase vertical leap, increase cohort hamstring strength and decrease time to contraction

Yes

Increased strength, lower overall injury rates

Not statistically significant, 7 wk 61.2% injuries in knee/ankle, 2.4% injury rate insufficient for NM education to occur in intervention vs 3.1 in control at mechanoreceptor level

Yes, balance

Randomized

Small number, low overall injury Intervention did not reduce risk of primary incidence. 37% dropout rate, not all traumatic injuries to lower extremities; 4 of 5 subjects received same amount of ACL injuries in total sample occurred training. Unknown whether additional in intervention group training was controlled

Balance activities on mats and boards

Compliance to program monitored; instructional video

Not randomized

In elite team division, risk of injury was reduced among those who completed program (odds ratio: 0.06 [0.01–0.54]) compared with control, overall reduction of ACL injury

Balance training with ankle disks

RCT

Injury types not specified. Description of ankle disk training not provided. Intervention group also did warm-up exercises but not specified. Compliance not assessed

Ankle injuries were significantly greater in control group (2.4 vs 0.2). Unspecified knee injuries were not significantly less in trained group (0.9 vs 0.6). Five knee sprains and 1 knee subluxation in control group vs 1 knee sprain in trained group

Strength on field perturbation on grass

Instructional video, Web site, compliance monitored (random site visits)

1 yr intervention, began at day 1 of season

Overall 72% reduction in ACL injury, 100% reduction in practice contact and noncontact ACL injury, 100% reduction in contact and noncontact ACL injury in last 6 wk of season

No

Compliance monitored; significant reduction in F & RFD in intervention

No decrease in injury, intervention 6 noncontact ACL injuries: 3 in treatment and performed at end of training, possible 3 in control = no direct effact fatigue phenomenon

Strength on field perturbation on grass

Instructional video, Web site, compliance monitored

Not randomized, inherent selection bias

Injury rates: yr 1: 88% reduction in noncontact ACL injury; yr 2: 74% reduction in noncontact ACL injury

Balance activity on mats and boards

Randomized, compliance monitored, reduction of injury

Efficacious component(s) of intervention not known

129 acute knee & ankle injuries overall, 81 in control (0.9 overall, 0.3 train, 5.3 match) vs 48 injuries in intervention (0.5 overall, 0.2 train, 2.5 match)

89% decrease in noncontact ACL injury

87% decrease in noncontact ACL injury, 1.15 rate reduced to 0.15/1000 AE Female injury rates 0.43–0.12 (male = 0.9) over 6-wk program. Untrained group 3.6–4.8 higher rates of ACL injury

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Table 8-5 Types of Eating Disorders Anorexia nervosa Restricting type Binge eating/purging type Bulimia nervosa Purging type Nonpurging type Eating disorder not otherwise specified

Figure 8-12 The pain from a Morton’s neuroma can be elicited with upward pressure on the plantar aspect of the foot between the metatarsal heads simultaneously with transverse compression across the metatarsal heads.

of the American College of Sports Medicine to refer to the association of disordered eating, amenorrhea (lack of normal periods for three consecutive months), and osteoporosis (low bone mineral density), three conditions seen with increasing prevalence over the past several decades in female athletes, which individually, and certainly together, can result in impaired health and athletic performance. Disordered eating can result in inadequate nutrition or energy, which can lead to abnormal menstrual function; abnormal menstrual function can result in low estrogen amenorrhea, which can result in osteopenia (minimally decrease bone mineral density) or even osteoporosis (more severe loss of bone mineral density). Stress fractures may be the consequence of the latter. Bone mass is influenced by estrogen, calcium, and exercise. Peak bone mineral density is achieved by age 25 after which premenopausal women lose 0.3% of their skeleton per year and postmenopausal women or those without periods (e.g., amenorrheic athletes) lose 2% of their bone mass per year. Therefore, concern has been raised that either inadequate calcium intake and/or inadequate estrogen from amenorrhea during the years of maximal bone mineral storage (young teens through 25) may lead to significant osteoporosis during the postmenopausal years. More recently, amenorrhea has been linked to cardiovascular disease and disordered eating to poor function of the immune system. Athletes most at risk of developing the triad are young women involved in sports in which the lean look is thought to be advantageous (e.g., gymnastics, figure skating, dance, diving, and cheerleading), sports in which weight categories exists (e.g., rowing), and endurance sports (e.g., swimming and crosscountry running).56 Disordered eating refers to a continuum of abnormal eating behaviors of which three categories have been recognized: anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified (Tables 8-5 through 8-8). The athlete with disordered eating has abnormal eating behaviors that may involve the quantity of food ingested; abnormal eating patterns (e.g., eating excessively and vomiting following eating); or inappropriate use of laxatives, diuretics, or other medical substances.

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The prevalence of disordered eating is higher for athletes than nonathletes; female athletes are more affected than male athletes. Studies have reported a 62% occurrence rate in female collegiate gymnasts, a 47% occurrence in long-distance female runners, and a 15.4% occurrence rate in elite female swimmers.57,58 Overall, 32% to 64% of all female athletes have been reported to display some type of disordered eating.59 Recognition of the athlete with disordered eating is frequently difficult. Coaches may report a decrease in performance. Abnormal behavior during meals or a preoccupation with food may provide clues to the diagnosis. Once the diagnosis is made, treatment is provided through a team approach with a sports medicine physician, sports nutritionist, and mental health provider, preferably an eating disorder specialist. Amenorrhea is defined as 3 or more months of missed menstrual cycles and has been associated with heavy physical training. Primary amenorrhea has been redefined by the American Society of Reproductive Medicine as the absence of menstrual cycles in a girl who has not menstruated by age 15. Secondary amenorrhea is cessation of menses after the first menstrual cycle.60 Prevalence of amenorrhea has been documented as high as 65% in long-distance runners and 44% in dancers compared to 2% to 5% in nonathletic collegiate women.60 Amenorrhea was

Table 8-6 Diagnostic Criteria for Anorexia Nervosa Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g., weight loss leading to maintenance of body weight less than 85% of that expected or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected). Intense fear of gaining weight or becoming fat, even though underweight. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight. In postmenarcheal females, amenorrhea, i.e., the absence of at least three consecutive menstrual cycles. (A woman is considered to have amenorrhea if her periods occur only following hormone, e.g., estrogen, administration.) Restricting type: During the current episode of anorexia nervosa, the person has not regularly engaged in binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas) Binge eating/purging type: During the current episode of anorexia nervosa, the person has regularly engaged in binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas) American Psychiatric Association.70

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Table 8-7 Diagnostic Criteria for Bulimia Nervosa Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating). Recurrent inappropriate compensatory behavior to prevent weight gain, such as self-induced vomiting; misuse of laxative, diuretics, enemas, or other medications; fasting; or excessive exercise. The binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for 3 months. Self-evaluation is unduly influenced by body shape and weight. The disturbance does not occur exclusively during episodes of anorexia nervosa. Purging type: During the current episode of bulimia nervosa, the person has regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas. Nonpurging type: During the current episode of bulimia nervosa, the person has used other inappropriate compensatory behaviors, such as fasting or excessive exercise, but has not regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas. American Psychiatric Association.70

initially thought to result from low body weight and low body fat. More recently, its onset is thought to be more related to energy deficit. The energy deficit may be caused by inadequate energy intake (disordered eating). Once thought to be a benign, reversible condition that many athletes considered a benefit for athletic participation, pro-

Table 8-8 Eating Disorder Not Otherwise Specified This category is for those eating disorders that do not meet the criteria for any specific eating disorder. Examples include the following: For females, all the criteria for anorexia nervosa are met except that the individual has regular menses. All the criteria for anorexia nervosa are met except that, despite significant weight loss, the individual’s current weight is in the normal range. All the criteria for bulimia nervosa are met except that the binge eating and inappropriate compensatory mechanisms occur at a frequency of less than twice a week or for a duration of less than 3 months. The regular use of inappropriate compensatory behavior by an individual of normal body weight after eating small amounts of food (e.g., self-induced vomiting after the consumption of two cookies). Repeatedly chewing and spitting out, but not swallowing, a large amount of food. Binge eating disorder: Recurrent episodes of binge eating in the absence of the regular use of inappropriate compensatory behaviors characteristic of bulimia nervosa. American Psychiatric Association.70

longed amenorrhea is now thought to be a serious medical problem linked to diminished estrogen and a resultant loss of normal bone mineral density as well as to cardiovascular disease as occurs in postmenopausal women. Therefore, recognition and treatment are essential. Treatment consists of correcting the disordered eating and energy deficit, a major challenge in most of the athletes with this disorder. Osteoporosis, the third component of the female athlete triad, is defined as decreased bone mass with disruption of the normal microarchitecture of bone. Bone is a living tissue and is continually undergoing remodeling and repair. Discrepancies that occur when the rate of bone resorption exceeds the rate of formation lead to the onset of diminished bone mineral density. The degree of loss of bone mass has been defined by the World Health Organization based on the amount of bone mineral density detected by bone densitometry. Bone densitometry measurements are most commonly done by dual-energy x-ray absorptiometry. In this technique, an aerial section of the spine or hip is analyzed for mineralized tissue. The results are compared with peers and against a young healthy adult population known to have peak bone mass, resulting in a value termed a T score (Fig. 8-13). Individuals found to be between 1 and 2.4 standard deviations below peak bone mass are considered to have osteopenia or low bone mineral density, and those with values greater than 2.5 standard deviations below peak bone mass are thought to have osteoporosis or severe loss of bone mineral density (Table 8-9). Recently, Khan et al61 have suggested replacing the term osteoporosis in the triad with osteopenia, a far more common entity than osteoporosis among athletes and one that lends itself to early recognition and lifestyle changes to avoid further bone loss. The International Society for Clinical Densitometry has recommended that the bone density of young women (adolescents and premenopausal women) be compared to that of women of their own age group. This is known as the Z score.60 Values are interpreted according to the same scale as the T scores. A loss of 1 standard deviation of bone mineral density results in a 1.9 increased risk of spine fracture or a 2.4 increased risk of hip fracture in the elderly.62 Such data are not available for young athletes, but inferences can be drawn. As in the discussions on disordered eating and amenorrhea, detection of athletes with the female athlete triad is difficult. Screening athletes for menstrual, diet, and exercise history may be helpful (Table 8-10); however, frequently athletes with this disorder do not wish to be detected and will supply inaccurate answers. The sports medicine specialist must be alert to indirect signs of this disorder such as alteration in performance and secretive eating behaviors. A stress fracture in a lean female athlete should prompt further investigation into menstrual and dietary habits. Consideration of bone mineral density studies should be given to those following an initial stress fracture and indeed for those who have recurrent stress fractures. Treatment intervention in the athlete diagnosed with the triad is frequently difficult and requires a multidisciplinary approach typically involving the physician, athletic trainer, physical therapist, coach, nutritionist, and sport psychologist. Improving the energy deficit through increasing caloric intake will help to establish regular periods and hence increase estrogen to improve bone health. A reasonable goal should be smaller amounts of food throughout the day to avoid the sensation of “overeating” or “being too full.” Women athletes are not unique compared to men in needing to maintain a good nutritional state, but they are unique in regard to many medical conditions linked

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Dual femur bone density

1

Region Reference: neck

3

1.10

1

0.98

0

0.86

–1 Osteopenia

–2

0.62 0.38

–3

1 Change (%)

2

0.50

2

YA T-score

BMD (g/cm2)

4 Normal

1.22

0.74

2,7

Young adult (%) T-score

3

Age-matched (%) Z-score

Trend: neck mean

1.46 1.34

BMD (g/cm2)

0

–1

–4

Osteoporosis

–5

20 30 40 50 60 70 80 90 100

–2 50.0

Age (years)

51.0

Neck Left Right Mean Difference Total Left Right Mean Difference

Age (years)

Comments:

0.594 0.626 0.610 0.032

61 64 62 3

–3.2 –3.0 –3.1 0.3

54 56 55 3

–4.3 –4.0 –4.2 0.3

0.628 0.655 0.642 0.027

63 65 64 3

–3.1 –2.9 –3.0 0.2

55 57 56 2

–4.4 –4.1 –4.2 0.2

Trend: neck mean 1

Measured date

Age (yrs)

BMD (g/cm2)

Change (%)

Change (% per yr)

08/16/2002

50.0

0.610

Baseline

Baseline

Figure 8-13 An example of a dual energy x-ray absorptiometry scan of a female athlete.

to poor nutritional or energy states. Athletes are frequently resistant to increasing calories for health reasons but frequently understand the need to improve energy for improved performance. (The analogy of a car being unable to go far without adequate fuel is often used.) Along with an increase in calories, athletes must also look at the quality of food ingested. A balance of protein, fats, and carbohydrates is needed, and adequate calcium is required, 1200 to 1500 mg daily (Tables 8-11 and 812), along with 400 to 800 IU of vitamin D. Controversy surrounds the use of oral contraceptives in the treatment of athletes with the triad. One study reported an increase in the lumbar spine and total bone mineral density following their use,60 while other studies have not shown an

Table 8-9 Definition of Normal Bone Mineral Density, Osteopenia, and Osteoporosis Normal

BMD £1 SD below the mean peak bone mass in normal women

Osteopenia

BMD >1 but 120 degrees pain-free active knee motion; equal thigh girth bilaterally

Full active range of motion; full squat; pain free in all activities; wear thigh girdle with thick pad 3–6 mo for all contact sports

Mild and moderate, treat daily; severe, treat twice daily. From Ryan JB, Wheeler JH, Hopkinson WJ, et al: Quadriceps contusions. West Point update. Am J Sports Med 1991;19:299–304.

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As in the treatment of muscle strain injury, the use of NSAIDs is controversial. The West Point series used no medications in the treatment of quadriceps contusions and experienced no loss to activity return.38 There are no other large clinical series from which to draw inferences about NSAID use, although there is some animal research in this area. NSAIDs have been found to decrease the catabolic loss of protein in the early postinjury period as well as the degree of inflammatory response, but this has also led to a decrease in tensile muscle strength in the long term.35 Thus, the beneficial effect in the short term may be overshadowed by the longer term inhibition of the normal muscle regeneration cascade.36 While no firm evidence supports this application, at our institution, we currently begin a course of NSAIDs 2 days after injury to limit formation of myositis ossificans.

surgery for this problem. The incidence of compartment syndrome in the thigh after contusion is not well described, but in rare instances may occur and must then be treated with fasciotomy. Most authors advocate a high clinical suspicion for compartment syndrome in limbs where thigh girth fails to stabilize after contusion and recommend compartment pressure monitoring; however, no report of anterior thigh compartment release for contusion related compartment syndrome has demonstrated muscle injury at the time of surgery.39 None of the major series describing treatment of quadriceps contusions report any cases of compartment syndrome or the completion of thigh fasciotomies.38–40 In cases in which arterial injury is suspected, fasciotomy should still be considered as a treatment option. Arteriography is a useful study in this unlikely scenario.

Surgery The operative treatment of contusions is controversial. Anecdotal descriptions exist of large hematomas being evacuated after contusions,35 and in the face of large spatial defect within a contused muscle, direct suturing of muscle may be indicated, but more work is needed to make a generalization about

Criteria for Return to Sports Noncontact sports participation may be resumed once the patient advances to the functional rehabilitation portion of his or her treatment. Once full strength, motion, and endurance are achieved, contact sports may be resumed. For individuals playing

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contact sports, a football thigh girdle is worn for 3 to 6 months during contact sports.

Results and Outcomes In the series of 117 quadriceps contusions treated in West Point cadets, all returned to full activity to include performing as well or better on their Army Physical Fitness Test (2-mile run, 2 minutes of sit-ups, 2 minutes of push-ups) and Indoor Obstacle Course Test. For the 71 mild contusions, average disability time was 13 days. For the 38 moderate contusions, the average disability time was 19 days, and for the eight severe contusions, it was 21 days. The disability time was defined as the amount of time a cadet was unable to participate fully in the cadet activity schedule due to injury. The disability times for the moderate and severe contusions seen in this later study are much shorter than those noted in the first series (56 and 72 days, respectively). This has been attributed to the change in the initial position of immobilization from unstretched (knee extended) to stretched (knee flexed). Subjectively, two cadets had subjective weakness, two complained of endurance issues, and one complained of numbness in the area of the contusion after 5 miles of jogging.

Complications The most significant, yet uncommon, complication associated with muscle contusion is myositis ossificans, also referred to as myositis ossificans traumatica or post-traumatic ectopic calcification.41 Myositis Ossificans Risk Factors Five factors have been described for the development of myositis ossificans after contusion by Ryan et al.38 These authors determined that range of motion less than 120 degrees at classification, participation in football, history of a contusion injury to the same site, sympathetic knee effusion, and delayed treatment for 3 or more days were associated with the occurrence of myositis ossificans. By themselves, each risk factor was not significant; however, cadets with myositis ossificans averaged 3.3 risk factors, while cadets in whom myositis ossificans did not develop averaged only 1.6. The application of aggressive, passive stretching past the pain-free region of motion should be strictly avoided as this also has been linked to the onset of myositis ossificans. Incidence Myositis ossificans developed in 11 of 117 (9%) of the cadets sustaining quadriceps contusions in the most recent West Point study.38 This occurred in 18% of moderate contusions and 13% of severe contusions, but only 4% of mild contusions. Myositis ossificans developed in none of the cadets with more than 120 degrees of knee range of motion at presentation, and it should be noted that the 4% of cadets with mild contusions in whom myositis ossificans developed had knee range of motion between 90 and 120 degrees. The primary location of myositis ossificans correlates with the most common sites of contusion, namely, the anterior thigh followed by the brachialis.38,40,41 Etiology Intramuscular hematoma, most commonly occurring with muscle contusion injury, is the major etiology of myositis ossificans.41 The pathway for this at the molecular level is

unknown.42 Enchondral bone formation is the predominant mechanism of osteoid production and, in its early stages, may be mistaken for extraosseous osteosarcoma. A key distinguishing factor between osteosarcoma and myositis ossificans is the pattern of ossification seen both radiographically and histopathologically; it is characterized by maturation from the outside to inside in myositis ossificans and maturation from inside to outside in osteosarcoma.18 Clinical Features and Evaluation The most common presentation is after a severe contusion and, while it is developing, persistent swelling is the norm with the thigh becoming increasingly tender and warm.40 Radiographic evidence of myositis ossificans can be noted between 2 and 4 weeks after injury. Radiographs reveal three forms of myositis ossificans: a stalk type, a periosteal type in which all ectopic bone is in continuity with underlying bone, and a broad-based type transitional between the first two types.18,40 It has been suggested that the stalk type and broad-based type may present symptomatically due to the increased risk of a mechanical block to gliding within the affected muscle.41 The utility of bone scan in the evaluation of myositis ossificans is equivocal, but MRI can be useful to localize the affected muscle in the acute phase. It has also been suggested that the erythrocyte sedimentation rate and serum alkaline phosphatase activity are increased in the early process of myositis ossificans.18 Treatment Options Early treatment of injuries suspicious for myositis ossificans is similar to the initial treatment of contusions including rest, ice, compression, and elevation. Use of indomethacin has been advocated to reduce heterotopic calcification after total hip replacement and acetabular fracture open reduction and internal fixation. It may be effective in preventing myositis ossificans after contusion injuries. It is unclear whether indomethacin’s increased efficacy over other drugs in its class is due to increased potency or having a different specific action.41 Surgery Surgery is indicated only for lesions associated with significant activity limiting pain and loss of function due to muscle tethering. It should never be done in the acute phase because, postoperatively, the lesion is likely to recur. A bone scan should be performed to determine whether the lesion is mature. Resection of mature lesions should be performed with meticulous hemostasis and suction drainage with the goal of limiting the amount of postoperative hematoma formation. No clear objective guidance, other than the application of bone scan, has been published to facilitate the evaluation of this ectopic bone in order to characterize it as mature. Criteria for Return to Sports The criteria for return to sport are the same as for muscle contusion. Return of full motion and activity does not depend on reabsorption or excision of the ectopic bone.18 Results and Outcomes Resection of the symptomatic, mature myositis ossificans lesion should result in adequate return of function, assuming no postoperative recurrence of the lesion. No series documenting outcomes after resection of myositis ossificans have been published.

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REFERENCES 1. Garrett WE, Best TM: Anatomy, physiology, and mechanics of skeletal muscle. In Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science, 2nd ed. Chicago, American Academy of Orthopaedic Surgeons, 2000, p 683. 2. Best TM: Soft-tissue injuries and muscle tears. Clin Sports Med 1997;16:419–434. 3. Noonan TJ, Garrett WE Jr: Muscle strain injury: Diagnosis and treatment. J Am Acad Orthop Surg 1999;7:262–269. 4. Tidball JG: Inflammatory cell response to acute muscle injury. Med Sci Sports Exerc 1995;27:1022–1032. 5. Noonan TJ, Garrett WE Jr: Injuries at the myotendinous junction. Clin Sports Med 1992;11:783–806. 6. Lieber RL, Friden J: Morphologic and mechanical basis of delayed-onset muscle soreness. J Am Acad Orthop Surg 2002;10:67–73. 7. Cheung K, Hume P, Maxwell L: Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Med 2003;33: 145–164. 8. Foley JM, Jayaraman RC, Prior BM, et al: MR measurements of muscle damage and adaptation after eccentric exercise. J Appl Physiol 1999;87:2311–2318. 9. Garrett WE Jr, Nikolaou PK, Ribbeck BM, et al: The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension. Am J Sports Med 1988;16:7–12. 10. Garrett WE Jr: Muscle strain injuries. Am J Sports Med 1996;24: S2–S8. 11. Garrett WE Jr, Safran MR, Seaber AV, et al: Biomechanical comparison of stimulated and nonstimulated skeletal muscle pulled to failure. Am J Sports Med 1987;15:448–454. 12. Nikolaou PK, Macdonald BL, Glisson RR, et al: Biomechanical and histological evaluation of muscle after controlled strain injury. Am J Sports Med 1987;15:9–14. 13. Obremsky WT, Seaber AV, Ribbeck BM, et al: Biomechanical and histologic assessment of a controlled muscle strain injury treated with piroxicam. Am J Sports Med 1994;22:558–561. 14. Garrett WE Jr: Muscle strain injuries: Clinical and basic aspects. Med Sci Sports Exerc 1990;22:436–443. 15. Speer KP, Lohnes J, Garrett WE Jr: Radiographic imaging of muscle strain injury. Am J Sports Med 1993;21:89–95. 16. Hughes CT, Hasselman CT, Best TM, et al: Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med 1995;23:500–506. 17. Hasselman CT, Best TM, Hughes CT, et al: An explanation for various rectus femoris strain injuries using previously undescribed muscle architecture. Am J Sports Med 1995;23:493–499. 18. Arrington ED, Miller MD: Skeletal muscle injuries. Orthop Clin North Am 1995;26:411–419. 19. Mair SD, Seaber AV, Glisson RR, et al: The role of fatigue in susceptibility to acute muscle strain injury. Am J Sports Med 1996;24:137–143. 20. Taylor DC, Dalton JD Jr, Seaber AV, et al: Viscoelastic properties of muscle-tendon units. The biomechanical effects of stretching. Am J Sports Med 1990;18:300–309.

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21. Black JD, Stevens ED: Passive stretching does not protect against acute contraction-induced injury in mouse EDL muscle. J Muscle Res Cell Motil 2001;22:301–310. 22. Safran MR, Garrett WE Jr, Seaber AV, et al: The role of warmup in muscular injury prevention. Am J Sports Med 1988;16:123–129. 23. Noonan TJ, Best TM, Seaber AV, et al: Thermal effects on skeletal muscle tensile behavior. Am J Sports Med 1993;21:517–522. 24. Sallay PI, Friedman RL, Coogan PG, et al: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 1996;24:130–136. 25. Cross TM, Gibbs N, Houang MT, et al: Acute quadriceps muscle strains: Magnetic resonance imaging features and prognosis. Am J Sports Med 2004;32:710–719. 26. Standard Nomenclature of Athletic Injuries. Chicago, American Medical Association, 1968. 27. Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237–248. 28. Kujala UM, Orava S, Jarvinen M: Hamstring injuries. Current trends in treatment and prevention. Sports Med 1997;23:397–404. 29. Taylor DC, Dalton JD Jr, Seaber AV, et al: Experimental muscle strain injury. Early functional and structural deficits and the increased risk for reinjury. Am J Sports Med 1993;21:190–194. 30. Johnson AE, Granville RR, DeBerardino TM: Avulsion of the common hamstring tendon origin in an active duty airman. Mil Med 2003;168: 40–42. 31. Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 2002;30:742–747. 32. Kragh JF Jr, Basamania CJ: Surgical repair of acute traumatic closed transection of the biceps brachii. J Bone Joint Surg Am 2002;84:992–998. 33. Kragh JF Jr, Svoboda SJ, Wenke JC, et al: The role of epimysium in suturing skeletal muscle lacerations. J Am Coll Surg 2005;200:38–44. 34. Kragh JF Jr, Svoboda SJ, Wenke JC, et al: Passive biomechanical properties of sutured mammalian muscle lacerations. J Invest Surg 2005;18:19–23. 35. Beiner JM, Jokl P: Muscle contusion injuries: Current treatment options. J Am Acad Orthop Surg 2001;9:227–237. 36. Beiner JM, Jokl P: Muscle contusion injury and myositis ossificans traumatica. Clin Orthop 2002;S110–S119. 37. Walton M, Rothwell AG: Reactions of thigh tissues of sheep to blunt trauma. Clin Orthop 1983;(176):273–278. 38. Ryan JB, Wheeler JH, Hopkinson WJ, et al: Quadriceps contusions. West Point update. Am J Sports Med 1991;19:299–304. 39. Diaz JA, Fischer DA, Rettig AC, et al: Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med 2003;31:289–293. 40. Jackson DW, Feagin JA: Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am 1973;55:95–105. 41. King JB: Post-traumatic ectopic calcification in the muscles of athletes: A review. Br J Sports Med 1998;32:287–290. 42. Kaplan FS, Glaser DL, Hebela N, et al: Heterotopic ossification. J Am Acad Orthop Surg 2004;12:116–125.

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14

Head Injuries Kevin M. Guskiewicz

In This Chapter Concussion Cerebral contusion Cerebral hematoma Second impact syndrome Immediate management Return to sports

INTRODUCTION • Signs and symptoms of significant head injury include loss of consciousness (LOC), cranial nerve deficit, mental status deterioration, and worsening symptoms. • The most common head injury is a cerebral concussion. • Serial assessment is critical in classification and management of concussion. • Grading of head injury is done only after symptoms have resolved. • No athlete should return to participation while still experiencing symptoms of a head injury. • Decisions about return to play follow established guidelines but are made on an individual basis. The immediate management of the head-injured athlete depends on the nature and severity of the injury. It is therefore important for the sports medicine clinician to be skilled in the early detection and follow-up evaluation procedures of these injuries.1 Several terms are used to describe the injury, the most global being traumatic brain injury, which can be classified into two types: focal and diffuse. Focal or post-traumatic intracranial mass lesions include subdural hematomas, epidural hematomas, cerebral contusions, and intracerebral hemorrhages and hematomas. These are considered uncommon in sport but are serious injuries; the sports medicine clinician must be able to detect signs of clinical deterioration or worsening symptoms during serial assessments in order to classify the injury and manage it appropriately. Signs and symptoms of these focal vascular emergencies can include LOC, cranial nerve deficits, mental status deterioration, and worsening symptoms. Concern for a significant focal injury should also be raised if the signs or symptoms occur after an initial lucid period in which the athlete seemed normal.1 Diffuse brain injuries can result in widespread or global disruption of neurologic function and are not usually associated with

macroscopically visible brain lesions except in the most severe cases. Most diffuse injuries involve an acceleration/deceleration motion, in a linear plane, a rotational direction, or both. In these cases, lesions are caused by the brain being shaken within the skull.2,3 The brain is suspended within the skull in cerebrospinal fluid (CSF) and has several dural attachments to bony ridges that make up the inner contours of the skull. With a linear acceleration/deceleration mechanism (side to side or front to back), the brain experiences a sudden momentum change that can result in tissue damage. The key elements of injury mechanism are the velocity of the head before impact, the time over which the force is applied, and the magnitude of the force.2,3 Rotational acceleration/deceleration injuries are believed to be the primary injury mechanism for the most severe diffuse brain injuries. Structural diffuse brain injury (diffuse axonal injury) is the most severe type of diffuse injury because axonal disruption occurs, typically resulting in disturbance of cognitive functions, such as concentration and memory. In its most severe form, diffuse axonal injury can disrupt the brain stem centers responsible for breathing, heart rate, and wakefulness.2,3

CEREBRAL CONCUSSION The most common type of head injury sustained by athletes is a cerebral concussion. Cerebral concussion can best be classified as a mild diffuse injury and is often referred to as mild traumatic brain injury. The injury involves an acceleration/deceleration mechanism in which a blow to the head or the head striking an object results in one or more of the following conditions: headache, nausea, vomiting, dizziness, balance problems, feeling “slowed down,” fatigue, trouble sleeping, drowsiness, sensitivity to light or noise, LOC, blurred vision, difficulty remembering, or difficulty concentrating.4 It is often reported that there is no universal agreement on the standard definition or nature of concussion; however, agreement does exist on several features that incorporate clinical, pathologic, and biomechanical injury constructs associated with head injury: 1. Concussion may be caused by a direct blow to the head or elsewhere on the body from an “impulsive” force transmitted to the head. 2. Concussion may cause an immediate and short-lived impairment of neurologic function. 3. Concussion may cause neuropathologic changes; however, the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury. 4. Concussion may cause a gradient of clinical syndromes that may or may not involve LOC. Resolution of the clinical and cognitive symptoms typically follows a sequential course.

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5. Concussion is most often associated with normal results on conventional neuroimaging studies.5

Classification of Cerebral Concussion Occasionally, players sustain a blow to the head resulting in a stunned confusional state that resolves within minutes. The colloquial term “ding” is often used to describe this initial state. However, the use of this term is not recommended because this stunned confusional state is still considered a concussion resulting in symptoms, although only very short in duration, which should not be dismissed in a cavalier fashion.1 It is essential that this injury be reevaluated frequently to determine whether a more serious injury has occurred because often the evolving signs and symptoms of a concussion are not evident until several minutes to hours later. Although it is important for the sports medicine clinician to recognize and eventually classify the concussive injury, it is equally important for the athlete to understand the signs and symptoms of a concussion, as well as the potential negative consequences (e.g., second-impact syndrome, predisposition to future concussions) of not reporting a concussive injury. Once the athlete has a better understanding of the injury, he or she can provide a more accurate report of the concussion history.1

Several grading scales have been proposed for classifying and managing cerebral concussions.4,6–14 None of the scales have been universally accepted or followed with any consistency by the sports medicine community. Some of the scales are more conservative than others; however, most of them are believed to be useful in the management of concussion. It is recommended that athletic trainers and team physicians working together choose one scale, while ensuring consistent use of that scale. Although most scales are based primarily on level of consciousness and amnesia, it is very important to consider other signs and symptoms associated with concussion because the majority of concussions will not involve LOC or observable amnesia. It is reported that only 8.9% involve LOC and only 27.7% involve amnesia.15 Regardless of the grade of injury, clinicians should focus on the duration of any and all symptoms associated with the injury. Table 14-1 contains a list of signs and symptoms associated with cerebral concussion, which can be checked off or graded for severity on an hourly or daily basis following an injury. The graded symptom checklist is best used in conjunction with the Cantu evidence-based grading system for concussion6 (Table 14-2), which very appropriately emphasizes signs and symptoms other than LOC and amnesia in the grading of the injury. It is also important to grade the concussion only after the athlete’s symptoms have resolved, as the duration of symptoms are believed to be a good indicator of overall outcome.6,16

Table 14-1 Graded Symptom Checklist for Concussion Symptom

Time of Injury

2–3 Hr Postinjury

24 Hr Postinjury

48 Hr Postinjury

72 Hr Postinjury

Blurred vision Dizziness Drowsiness Fatigue Feel “in a fog” Feel “slowed down” Headache Irritability Loss of consciousness Memory problems Nausea Poor balance/coordination Poor concentration Ringing in ears Sadness Sensitivity to light Sensitivity to noise Sleep disturbance Vomiting A postconcussion signs and symptoms checklist is used not only for the initial evaluation but for each subsequent follow-up assessment, which is periodically repeated until all postconcussion signs and symptoms have returned to baseline or cleared at rest and during physical exertion.

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Table 14-2 Cantu Evidence-based Grading System for Concussion6 Grade 1 (mild)

No LOC, PTA 3.5 mm

= 20 – (–2) = 22

} = 20 – (–4) = 24 } > 11 ∞

B Figure 15-2 Radiographic assessment of cervical spine alignment. A, The anterior vertebral line, posterior vertebral line, spinolaminar line, and spinous process line should be smooth and continuous without step-off. B, Sagittal displacement greater than 3.5 mm or angular deformity greater than 11 degrees indicates an unstable injury of the cervical spine.

The definition of stenosis has generated considerable debate. Originally, stenosis was diagnosed from measurements of the transverse spinal canal diameter on plain radiographs.20 Wolfe et al21 and Penning22 recognized the relations between radiographic measurements and myelopathy as early as 1956 and 1962, respectively. Gore et al13 understood that technique factors in obtaining plain radiographs could cause significant discrepancies in absolute measurements obtained from them. Torg and Pavlov in 1987 put forth the Pavlov ratio as a method to avoid problems of magnification when evaluating for possible stenosis.23 This is the ratio of the spinal canal to the vertebral

body. A Pavlov ratio of less than 0.85 qualified as stenosis and a ratio of more than 0.8 was reported to place athletes at risk of catastrophic neurologic injury. Herzog et al24 recognized that football players generally have larger vertebral bodies and that even if these athletes had normal canal measurements, the Pavlov ratio could be less than 0.8, a false-positive result that may prevent an asymptomatic athlete from participating in contact sports. Computed tomography and MRI have been subsequently used to determine ranges of “normal” canal diameter. The average spinal cord diameter ranges from 5.0 to 11.5 mm (mean, 10 mm).20 The average canal diameter from C3–C7 is 15 to 25 mm (mean, 17 mm).25,26 A canal diameter less than 13 mm is considered stenotic and absolute stenosis considered to be less than 10 mm.27,28 Blackley et al29 showed a poor correlation between Pavlov’s ratio and computed tomography scan measurements of canal diameter. Prasad et al30 demonstrated that Pavlov’s ratio correlated poorly with MRI measurements of the space available for the cord. Matsuura et al31 demonstrated that the anteroposterior diameter of the spinal canal on computed tomography was less in patients with spinal cord injury than in controls. Of importance in this topic is that the overall space available for the cord is dependent on the sagittal and transverse diameters of the canal. Cantu,32 expounding Burrows’33 ideas, proposed the concept of “functional stenosis.” This concept takes into account the variability in anatomy of the canal and cord among athletes and states that the more important factor is whether there is enough spinal fluid surrounding the cord to protect it from injury. Functional stenosis must be determined on a case-by-case basis, as the predictability of absolute measurements and ratios is moderate at best. Stenosis may be either acquired, congenital, or a combination of both. Acquired causes include disk pathology, osteophytes, degenerative subluxation, hypertrophic ligamentum flavum, fracture, or ossification of the posterior longitudinal ligament. Congenital causes may vary from shortened pedicles, KlippelFeil syndrome, or other congenital anomalies. Previously, stenosis alone was thought to be a contraindication to contact sports, but more recent literature has suggested a revision of that doctrine.4,34 Currently, the use of Pavlov’s ratio should not be used as a screen for prediction of spinal cord injury given its low positive predictive value (0.2%). A ratio of less than 0.8 has, however, been demonstrated to have reasonable predictive value for a recurrent episode of either transient neurapraxia or burner syndrome but not catastrophic injury.35,36 Kang et al37 demonstrated that the canal diameter at the time of injury was positively correlated to the severity of the neurologic injury sustained. Higher energy injuries were associated with smaller canal diameters and more severe neurologic injuries. This study raises concern for athletes with severe stenosis who wish to participate in collision sports.37 Some authors continue to recommend that asymptomatic athletes with stenosis not participate in contact sports.38 A proven screening tool for prediction of catastrophic injury remains elusive. In the existing literature, quadriplegia has been more closely associated with axial loading from poor tackling techniques, such as spearing, that lead to catastrophic vertebral body fracture than to stenosis.39

TRANSIENT QUADRIPARESIS Temporary paralysis after a collision in sports with rapid and complete resolution of symptoms within 10 to 48 hours after injury has been termed transient quadriparesis or cervical cord

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neurapraxia.23 The incidence in collegiate football players has been estimated to be 7.3 in 10,000 athletes. The mechanism of injury is usually axially loading of the cervical spine in flexion or extension. Penning22 described the pathoanatomy of the “pincer mechanism” of hyperextension on the cervical cord. Taylor reported that infolding of the ligamentum flavum can reduce canal diameter up to 30%. The cervical spinal cord gets pinched between the inferior aspect of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the inferior adjacent vertebra. Similarly, with hyperflexion the cervical cord gets pinched between the anterosuperior aspect of the spinolaminar line of the superior vertebrae and the posterior superior aspect of the vertebral body of the inferior vertebrae.22,40 Although the precise etiology of transient quadriparesis remains elusive, Torg has postulated that cord function is disrupted because of local cord anoxia and the increased concentration of intracellular calcium.41 Zwimpfer and Bernstein42 described a “postconcussive state” of the spinal cord after brief conduction block causing axon dysfunction. Transient quadriparesis encompasses a spectrum of neurologic dysfunction. Motor dysfunction ranges from bilateral upper and lower extremity weakness to complete paralysis. Sensory dysfunction ranges from dysesthesias to complete absence of sensation. Deficits may resolve in as little as 10 minutes but may persist for up to 48 hours. Deficits lasting longer than 48 hours are not due to transient quadriparesis.43 Radiographic evaluation of patients with transient quadriparesis or an abnormal neurologic examination includes plain radiographs and MRI. Imaging is negative for fractures but may reveal congenital anomalies (Klippel-Feil), congenital stenosis (canal diameter 100% displacement of CC interspace. Deltotrapezial fascia often disrupted.

AC ligament: ruptured CC ligament: ruptured Inferior displacement of clavicle beneath coracoid. Likely mechanism is severe hyperadduction with external rotation.

AC, acromioclavicular; CC, coracoclavicular.

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with type III AC separations and found that the majority had acceptable results.14 Patients were not given a specific treatment regimen other than rest, ice, and the use of nonsteroidal antiinflammatory drugs. Patients demonstrated no limitation in range of motion or loss in rotational strength. However, there was, on average, a 17% deficit in bench press strength compared to the uninvolved extremity. Twenty percent believed their results were suboptimal, but none were severe enough to warrant surgery. Of these individuals, the perceived disability was fatigue with maximal overhead activities, such as lifting and climbing. There is still considerable controversy regarding the management of high-grade AC separations in overhead athletes. There are very few studies in the literature that address this topic, particularly for the high-level thrower. Lemos15 suggested operative management for high-level pitchers after a retrospective review of patients. McFarland et al16 surveyed 42 orthopedic surgeons participating in the care of 28 professional baseball teams; 31% recommended immediate operative treatment. However, this same group of surgeons estimated that normal function and significant pain relief were achieved in 80% of their athletes with nonoperative management. We recently completed a retrospective review of National Football League quarterbacks with complete grade III AC separations. When the injury involved the dominant extremity, nonoperative management had variable success. If the player was treated in a Kenny-Howard sling full time for at least 3 weeks, missing an average of eight games, all were able to eventually return to play without problems. When the player was treated with a sling for comfort and early motion, the average time lost was only five games. However, a high percentage of these quarterbacks eventually underwent surgical reconstruction in the off season. In quarterbacks who had early surgery, all of them missed the remainder of the season but were able to return the following year without problems. From this review, it has been our opinion that if a quarterback has an injury to his dominant extremity early in the season, then a trial of nonoperative management is warranted. If he fails this treatment or if the injury occurs late in the season, then surgical reconstruction can be expected to result in a good outcome.

pathology. In 1941, Gurd27 and Mumford28 independently described their results of excision of the distal end of the clavicle. Mumford recommended this operation for AC instability, particularly in those with arthritis of the joint.28 Gurd27 recommended his procedure in symptomatic type III AC separations. Technically speaking, excision of the distal end of the clavicle is referred to as the Mumford or Gurd operation only when this procedure is used for excision of the clavicle with associated instability. Nowadays, the distal clavicle excision is more routinely used for patients with arthritis. Patients with true AC instability are typically managed with a reconstructive procedure (described later in this chapter). The operation is usually performed in the beach chair position. The arm is prepped and draped free. When this procedure is being done for isolated AC arthritis, a vertical incision approximately 2.5 to 3 cm in length is placed directly over the distal end of the clavicle (Fig. 26-7). An incision is made through the skin and dissection is carried out through the subcutaneous tissue. On incising the capsule by sharp dissection, a degenerative disk will often be identified along with articular cartilage changes on the distal end of the clavicle. After removing the disk and/or hypertrophic synovium, a subperiosteal dissection is then performed to expose the distal end of the clavicle. An attempt to preserve a thick fascial sleeve will be helpful at the time of closure. A large Darrach retractor is placed underneath the clavicle to protect the underlying neurovascular structures. A sagittal saw is then used to make a perpendicular cut in order to remove approximately 1 to 1.5 cm of the distal clavicle (Fig. 26-8). Care Deltoid trapezius fascia

Nonoperative Treatment for Traumatic Acromioclavicular Separations In all cases, patients are treated with ice, analgesics, and nonsteroidal anti-inflammatory drugs for acute pain control. Options for immobilization for these injuries include sling,17,18 brace and harness,19–21 adhesive straps,22,23 figure-eight straps,24 and a sling strap.25 Of these, the most popular is the Kenny-Howard sling. This consists of a sling with a strap over the distal end of the clavicle, which is tightened to manually reduce the distal end of the clavicle in relationship to the acromion. However, for effective reduction, the patient is required to wear the sling continuously for the first 3 to 4 weeks. Removal of the strap leads to loss of joint reduction. The sling can also be problematic because the pressure of the strap can cause necrosis of the skin over the distal clavicle. One case of posterior interosseous nerve palsy caused by the sling has been reported in the literature.26

SURGERY Open Distal Clavicle Resection Traditionally, distal clavicle excisions have been performed using open techniques. These have been done in isolation for AC arthritis, as well as with concomitant surgeries for rotator cuff

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A Deltoid

B Figure 26-7 Open distal clavicle resection. A, A vertical incision approximately 2.5 to 3 cm in length is placed directly over the distal end of the clavicle. B, A large Darrach retractor is placed underneath the clavicle to protect the underlying neurovascular structures. (Adapted from Hawkins RJ, Bell SB, Lippitt LH: Atlas of Shoulder Surgery. Philadelphia, Mosby, 1996.)

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Figure 26-8 With a distal clavicle resection, approximately 1 to 1.5 cm of the distal clavicle is removed. (Adapted from Hawkins RJ, Bell SB, Lippitt LH: Atlas of Shoulder Surgery. Philadelphia, Mosby, 1996.)

should be taken to avoid excessive resection of the distal clavicle, as this will often lead to instability if the CC ligaments are disrupted. The completion of the cut can be done using osteotomes. Following the resection, a gloved finger should be able to remain between the clavicle and the acromion as the arm is brought into maximal adduction. This serves as a method to determine whether the distal clavicle has been sufficiently excised. It is not uncommon to find that more of the anterior portion of the clavicle has been removed, leaving more of the posterior clavicle, which can create pain from ongoing contact of the distal end of the clavicle with acromion (Fig. 26-9). After thorough irrigation, the deltotrapezial fascia is reapproximated using no. 1 Vicryl sutures. The deep subcutaneous tissue is closed with interrupted 3-0 absorbable sutures. The skin is either closed with a running nylon suture or staples. Postoperatively, the patient is placed into a sling for comfort, passive range of motion is started between 0 and 2 weeks, active motion between 2 and 4 weeks, and a light strengthening program can begin at 4 weeks.

capsule identifying the distal end of the clavicle. As noted with the open technique, there will often be a degenerative disk and/or degenerative changes of the articular cartilage overlying the clavicle. Eventually, the working instruments will be brought to the anterior portal site to allow resection of the capsule and then bone. Synovial shavers are initially used to resect the soft tissue and then a round 4-0 bur is employed. As opposed to the open technique, the arthroscopic resection often will remove no more than a centimeter. This can be done by removing bone on both acromial and clavicular sides. Once an adequate amount of resection of the bone has been performed, the scope should be taken out of the posterior viewing portal and placed into the anterior portal. This will then allow visualization of the posterior aspect of the AC joint. A spinal needle is then used to identify the location for a direct posterior portal site, and once this is confirmed, a no. 11 scalpel blade can be used to make a skin incision. Blunt dissection is carried out to bring the shavers and bur into the posterior aspect of the AC joint. This is helpful to resect the bone posteriorly. It is equally as problematic when using an arthroscopic technique as in the open technique if adequate posterior clavicle resection is not achieved. The other pitfall with the arthroscopic technique is often not taking enough of the soft tissue prior to bony resection, making assessment of the superior bone inadequate. This can be remedied by using an electric cautery wand to identify the end of the bone and the overlying capsule, particularly superiorly. Once an adequate resection has been performed, it is then possible to remove the scope from the anterior portal and place it in the direct posterior portal site to view the amount of anterior resection. An instrument such as an arthroscopic osteotome or probe can then be used to confirm an adequate amount of bony resection. Care is taken to preserve the

Supraspinatus

Arthroscopic Distal Clavicle Resection With an increasing number of shoulder procedures being done completely arthroscopically, it is important for physicians treating these problems to have a method of addressing the degenerative AC joint using an all-arthroscopic technique. After performing a thorough diagnostic arthroscopy of the shoulder and addressing the associated pathology, preparations are made for distal clavicle excision. The distal clavicle resection usually begins with the arthroscope in the posterior portal, using the lateral accessory portal for the working instruments. This procedure is often done in conjunction with a subacromial decompression. In most cases, the bursa has been excised and the acromion has been converted to a type I morphology. This allows visualization of the AC joint. The joint can be identified either by pushing on the end of the distal clavicle and looking for movement or by placing a spinal needle in the AC joint to identify the exact location. At this point, a shaver can be used to remove the underlying joint

Figure 26-9 Contact between the distal end of clavicle and the acromion may cause pain. (Adapted from Hawkins RJ, Bell SB, Lippitt LH: Atlas of Shoulder Surgery. Philadelphia, Mosby, 1996.)

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dorsal AC ligaments. This is one of the advantages of the arthroscopic technique. It is often thought to result in an earlier recovery. In cases of osteolysis, there is rarely a need to resect any bone since this disorder leads to bone loss. In this pathologic entity, the joint usually has an inflammatory process that is best treated by resection of the inflamed joint tissue. Postoperative care involves the use of a sling for comfort. Cryotherapy is also undertaken. Patients are able to work through the active and passive range-of-motion program more quickly than what is traditionally seen with an open procedure. Once pain subsides, progressive resisted exercises are initiated. In our experience, the greatest advantage of the arthroscopic resection is that time lost can be reduced by nearly 4 weeks. By preserving the AC joint capsule and ligaments, the recovery time can be expected to be as short as 8 weeks.

Acromioclavicular ligament

Coracoacromial ligament

Coracoclavicular ligament

A

Acromioclavicular Reconstruction Indications for early surgery include a grossly unstable highriding distal clavicle, fixed deformities, and occasionally in the overhead throwing athlete. Traditionally, these are addressed by performing a primary autogenous repair of the disrupted AC and CC ligaments. This is then supplemented with an absorbable no. 9 braided polydiaxone monofilament suture strand that is passed around the base of the coracoid and then through a drill hole in the anterior aspect of the clavicle, as described by Warren29 (Fig. 26-10). This creates a strong absorbable construct lasting approximately 6 to 8 weeks, which is long enough to hold the clavicle in position while the autogenous tissue heals. In acute cases, the distal end of the clavicle may be preserved if there is a normal intra-articular disk and no evidence of arthritis. Delayed AC reconstructions are recommended in patients who have a high-riding unstable dislocation that has failed nonoperative treatment. Because of the difficulty in maintaining the

B Figure 26-11 A and B, The reconstruction is performed using existing ligaments and supplemented with absorbable polydiaxone monofilament suture. (A, Adapted from Hawkins RJ, Bell SB, Lippitt LH: Atlas of Shoulder Surgery. Philadelphia, Mosby, 1996.)

Figure 26-10 Acromioclavicular reconstruction. A vertical drill hole (arrow) is made through the anterior aspect of the clavicle. (Adapted from Hawkins RJ, Bell SB, Lippitt LH: Atlas of Shoulder Surgery. Philadelphia, Mosby, 1996.)

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reduction in these situations, we have described a “three-in-one” repair (Fig. 26-11).30 This technique employs a modified Weaver-Dunn reconstruction supplemented with either a palmaris or hamstring tendon as an autogenous graft. In chronic cases, we always resect approximately 1.5 cm of the distal end of the clavicle. This eliminates the possibility of postoperative pain in cases of degenerative arthritis or when there is partial loss of reduction of the distal clavicle. The coracoacromial ligament is then transferred into the medullary canal of the clavicle as part of the modified Weaver-Dunn reconstruction. A 3/8-inch drill is used to make a hole in the anterior aspect of the clavicle at the level of the coracoid to eventually pass a polydiaxone monofilament suture strand and palmaris/hamstring graft. It is important to keep the drill hole anterior so to better position the clavicle in relationship to the acromion as these structures are secured. If the drill hole is placed too posteriorly, it will have a tendency to pull the clavicle anteriorly in relationship to the acromion. Once these structures are around the coracoid, they are passed through the drill hole in the clavicle creating a figure-eight construct for both the polydiaxone

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monofilament suture and palmaris graft. With the clavicle reduced, it is now possible to maintain the reduction by tying the palmaris/hamstring graft using a surgeon’s knot. This has been proved to be the strongest method to secure the autogenous tissue.31 As with the acute surgeries, we protect the reconstruction with an absorbable suture strand. In the past, we used to braid the suture but found this extremely difficult to handle and tie this construct. We have now modified this braided technique after being shown a new method that we have nicknamed the Skyler Scroll after Dr. Skyler DeJong from West Point. This method creates a polydiaxone monofilament suture rope by taking three individual strands of polydiaxone monofilament suture and securing them at one end while rotating the group 30 times in a clockwise manner. After each of the three strands is created, the entire group is then rotated 40 times in a counterclockwise manner. Once the AC joint is reduced, the deltotrapezial fascial flaps are reapproximated as part of the repair. The skin is then closed with a running nylon stitch. Postoperatively these patients are protected in a sling for a total of 4 weeks without any motion. We have learned that accelerated rehabilitation programs often lead to loss of reduction. At the 4-week mark, passive range of motion is employed for 2 weeks. An active range-of-motion program with terminal stretching then follows this for 2 weeks. At the 8-week mark, a light resisted strengthening program can be instituted, with return to the weight room at 3 months. The patient is released to all activities without restriction at 4 months.

CRITERIA FOR RETURN TO SPORTS In general, patients are restricted from unlimited activities until they have a full pain-free range of motion with normal strength. With nonoperative treatment of acute AC separations, the time lost from participation depends on the grade of injury and the sport. On average, those with grade I injuries miss 1 week, those with grade II are out 2 to 4 weeks, and those with grade III AC separations can be expected to miss up to 6 weeks. It has been our experience that in the athletic patient population, time lost can be significantly reduced when a corticosteroid injection is used acutely as an adjunct to the nonoperative program, immediately after these injuries occur (Fig. 26-12). We

have had experience with this form of treatment in the professional football player population.32 With higher grade AC separations, time lost was dramatically reduced when the nonoperative program was augmented with injection. When an athlete returns to contact sports, an AC pad is helpful to limit recurrent injuries. In this select group, we have found the injections to be safe and have had no complications such as infection or progression to higher grade AC separations.

RESULTS AND OUTCOMES The success rate of nonoperative treatment in grade I and II AC separations and chronic disorders is high. For this reason, it is critical to exhaust all options before recommending surgery. If surgery is necessary, a distal clavicle resection performed using either open or arthroscopic techniques can lead to good results. With open surgery, Cook and Heiner33 and Tibone et al34 reported a 95% success rate in an athletic population with a painful joint secondary to degenerative arthritis or as a result of traumatic arthritis from a first- or second-degree AC separation. The only complaint following treatment was that patients often were unable to regain maximal bench press strength. Recent studies evaluating the success of arthroscopic distal clavicle resection have demonstrated equally successful outcomes.35–37 Kay et al37 reported good and excellent long-term results in 100% of their patients. Martin et al36 found no significant strength differences of the involved shoulder but did report that a small percentage of athletes had mild pain with strenuous overhead activities. Although the literature is scant on the subject, we have also found that arthroscopic débridement for osteolysis has a very high success rate. For grade III AC separation, we have reported success in the majority of patients treated nonoperatively.38 If an AC reconstruction is necessary, as is the case with higher grade injuries, good results have been achieved in 93% of the patients undergoing a Weaver-Dunn reconstruction.39 In this series, the outcome was not affected by whether this was done acutely or in chronic injuries.40

COMPLICATIONS The most frequent complication following distal clavicle resection is excess bone removal, which ultimately compromises the CC ligaments. In these situations, there is often a cosmetic deformity and pain. Although the case of pain is not fully understood, it is thought to be secondary to medial translation of the scapula in relation to the clavicle. With AC reconstruction, loss of reduction is the most common problem. Although this leads to a deformity, it has been our experience that some of these patients still have a good functional outcome.

CONCLUSIONS

Figure 26-12 Corticosteroid injection into the acromioclavicular joint.

Successful treatment of AC disorders relies on an accurate diagnosis obtained through a detailed history, thorough physical examination, and a complete radiographic evaluation. The radiographic findings of degenerative arthritis alone are not enough to warrant treatment since this is commonly seen after the age of 40. The painful joint that is unresponsive to nonoperative management including injection will be expected to have a good outcome following a distal clavicle excision.

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In traumatic AC separations, the majority of these injuries will respond to a nonoperative treatment regimen. In grade III AC separations including overhead throwers, we have recommended a trial of nonoperative management. For those with grade III separations who fail nonoperative treatment, along with high-grade AC separations (grades IV to VI), we have had success employing a “three-in-one” operative technique. The

postoperative program should curtail any motion for the first 4 weeks to enhance the likelihood of maintaining the position of the distal clavicle in relationship to the acromion. Return to sports is allowed when the player has pain-free range of motion with good strength. In lower grade AC separations, this can occur within several weeks after the injury but will ultimately take as long as 4 months following surgery.

REFERENCES 1. Fukuda K, Craig EV, An KN, et al: Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 1986;68:434–440. 2. Petersson CJ: Degeneration of the acromioclavicular joint. A morphological study. Acta Orthop Scand 1983;54:434–438. 3. Petersson CJ, Redlund-Johnell I: Radiographic joint space in normal acromioclavicular joints. Acta Orthop Scand 1983;54:431–433. 4. Cahill BR: Osteolysis of the distal part of the clavicle in male athletes. J Bone Joint Surg Am 1982;64:1053–1058. 5. Zanca P: Shoulder pain: Involvement of the acromioclavicular joint. (Analysis of 1,000 cases). Am J Roentgenol 1971;112:493–506. 6. Bossart PJ, Joyce SM, Manaster BJ, et al: Lack of efficacy of ‘weighted’ radiographs in diagnosing acute acromioclavicular separation. Ann Emerg Med 1988;17:20–24. 7. Tossy JD, Mead NC, Sigmond HM: Acromioclavicular separations: Useful and practical classification for treatment. Clin Orthop 1963; 28:111–119. 8. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Matsen FA (ed): The Shoulder. Philadelphia, WB Saunders, 1990, pp 413–476. 9. Bergfeld JA, Andrish J, Clancy WG: Evaluation of the acromioclavicular joint following first- and second-degree sprains. Am J Sports Med 1978;6:153–159. 10. Kennedy DC, Cameron J: Dislocations of the acromioclavicular joint. J Bone Joint Surg Am 1954;36:202–208. 11. Warren-Smith CD, Ward MW: Operation for acromioclavicular dislocation. A review of 29 cases treated by one method. J Bone Joint Surg Am 1987;69:715–718. 12. Kennedy JC: Complete dislocation of the acromioclavicular joint: 14 years later. J Trauma 1968;8:311–318. 13. Imatani RJ, Hanlon JJ, Cady GW: Acute, complete acromioclavicular separation. J Bone Joint Surg Am 1975;57:328–332. 14. Schlegel TF, Burks RT, Marcus RL, et al: A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med 2001;29:699–703. 15. Lemos MJ: The evaluation and treatment of the injured acromioclavicular joint in athletes. Am J Sports Med 1998;26:137–144. 16. McFarland EG, Blivin SJ, Doehring CB, et al: Treatment of grade III acromioclavicular separations in professional throwing athletes: Results of a survey. Am J Orthop 1997;26:771–774. 17. Jones R: Injuries of Joints. London, Hoddard & Stoughton, 1917. 18. Watson-Jones R: Fractures and Joint Injuries. New York, Churchill Livingstone, 1982. 19. Currie DI: An apparatus for dislocation of the acromial end of the clavicle. BMJ 1924;(570). 20. Warner AH: A harness for the use of treatment of acromioclavicular separations. J Bone Joint Surg 1937;19:1132–1133. 21. Giannestras, NJ: A method of immobilization of acute acromioclavicular separations. J Bone Joint Surg 1944;26:597–599. 22. Rawlings G: Acromial dislocations and fractures of the clavicle. A simple method of support. Lancet 1939;2:789.

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23. Thorndyke AG, Quigley TB: Injuries to the acromioclavicular joint: A plea for conservative treatment. Am J Surg 1942;55:250–261. 24. Usadel G: Zur Behandlung ter Luxatio Claviculae Supraacromialis. Arch Klin Chir 1940;200:621–626. 25. Howard NJ: Acromioclavicular and sternoclavicular joint injuries. Am J Surg 1939;46:284–291. 26. O’Neill DB, Zarins B, Gelberman RH, et al: Compression of the anterior interosseous nerve after use of a sling for dislocation of the acromioclavicular joint. A report of two cases. J Bone Joint Surg Am 1990;72: 1100–1102. 27. Gurd FB: The treatment of complete dislocation of the outer end of the clavicle: A hitherto undescribed operation. Ann Surg 1941;113: 1094–1098. 28. Mumford EB: Acromioclavicular dislocation. J Bone Joint Surg 1941; 23:799–802. 29. Warren LF, Field LD: Acromioclavicular joint separations. In Hawkins RJ, Misamore GW (eds): Shoulder Injuries in the Athlete: Surgical Repair and Rehabilitation. New York, Churchill Livingstone, 1996, pp 201–217. 30. Schlegel TF, Boublik M, Hawkins RJ: An Updated Approach to Acromioclavicular Injuries. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2002. 31. Lee SJ, Nicholas SJ, Akizuki KH, et al: Reconstruction of the coracoclavicular ligaments with tendon grafts: A comparative biomechanical study. Am J Sports Med 2003;31:648–655. 32. Schlegel TF, Martin L, Keller J, et al: The use of corticosteroid injections for acute acromioclavicular separations. AOSSM Annual Meeting, 2005, Keystone, CO. 33. Cook DA, Heiner JP: Acromioclavicular joint injuries. Orthop Rev 1990;19:510–506. 34. Tibone J, Sellers R, Tonino P: Strength testing after thirddegree acromioclavicular dislocations. Am J Sports Med 1992;20: 328–331. 35. Snyder SJ, Banas MP, Karzel RP: The arthroscopic Mumford procedure: An analysis of results. Arthroscopy 1995;11:157–164. 36. Martin SD, Baumgarten TE, Andrews JR: Arthroscopic resection of the distal aspect of the clavicle with concomitant subacromial decompression. J Bone Joint Surg Am 2001;83:328–335. 37. Kay SP, Dragoo JL, Lee R: Long-term results of arthroscopic resection of the distal clavicle with concomitant subacromial decompression. Arthroscopy 2003;19:805–809. 38. Schlegel TF, Boublik M, Hawkins RJ: Grade III AC separations in NFL quarterbacks. Paper presented at the AOSSM Annual Meeting, 2005, Keystone, CO. 39. Weaver JK, Dunn HK: Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg Am 1972;54:1187–1194. 40. Weinstein DM, McCann PD, McIlveen SJ, et al: Surgical treatment of complete acromioclavicular dislocations. Am J Sports Med 1995;23:324–331.

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Clavicle Fractures and Sternoclavicular Injuries Carl J. Basamania, Elizabeth G. Matzkin, and George K. Bal

In This Chapter Clavicle fractures Nonoperative management Surgery Plate fixation Intramedullary fixation Sternoclavicular joint disorders Degenerative conditions Atraumatic subluxation/dislocation Traumatic injury/dislocation Surgery—sternoclavicular (S-C) reconstruction

INTRODUCTION • Clavicle fractures account for 1 of every 20 fractures1 and most occur in men and women younger than the age of 25. Most commonly they are secondary to participation in contact or collision sports. • Eighty percent of these fractures occur in the middle one third, 12% to 15% in the lateral one third, and 5% to 6% in the medial one third of the clavicle.2 • Most fractures of the clavicle unite by various treatment methods including benign neglect, sling, sling and swathe, figure-eight, Velpeau dressing, collar and cuff, external fixation, and open reduction and internal fixation with plates, screws, or intramedullary pins. • Each treatment option has been shown to allow for fracture healing, nearly normal function, cosmesis, activity level, and satisfaction, but more recent studies have suggested that the satisfaction that patients achieve after fractures of the clavicle may not be as high as previously thought.3–5 • Many patients are left with some residual deformity and shortening. The ultimate goal of treatment is to restore the anatomy and allow rapid and safe return of the athlete to sports participation.

CLAVICLE Clinical Features and Evaluation Displaced fractures of the clavicle are easily diagnosed if the patient is seen soon after injury. Patients usually present with an obvious clinical deformity and a consistent history of some form of direct or indirect injury to the shoulder. The proximal frag-

ment is commonly displaced upward and backward and may be tenting the skin. Mobilization of the extremity elicits pain, and therefore the patient prefers to splint the involved extremity at the side in a forward and downward position due to the weight of the arm and pull of the pectoralis minor muscle. This position may accentuate the posterosuperior angulation seen in most clavicle fractures. The acute swelling and hemorrhage may hide the initial injury and deformity. In a fracture in close proximity to the acromioclavicular or sternoclavicular joints, the deformity may mimic a purely ligamentous injury. Examination reveals tenderness to palpation over the fracture site and pain with any attempts at movement. There may be a significant amount of bruising over the fracture site, especially with severely displaced fractures. This indicates a tearing of the underlying soft tissues. Some patients may present with their heads tilted toward the injury, relaxing the pull of the trapezius. Alternatively, some may tilt their chin to the opposite side to decrease the pull of the sternocleidomastoid. A complete and thorough examination should rule out any associated injuries to the entire extremity, lungs, scapula, chest wall, and neurovascular structures. Nondisplaced fractures or isolated fractures of the articular surfaces may not cause deformity and may be overlooked unless they are specifically sought for radiographically. If the diagnosis is in doubt, special radiographs or a repeat radiograph of the clavicle in 7 to 10 days may be indicated.

Radiographic Evaluation In most cases, the diagnosis of a clavicular fracture is fairly obvious with the clinical deformity and confirmatory radiographs. Unfortunately, many physicians obtain only an anteroposterior radiograph of the shoulder when a clavicle fracture is suspected. Due to the unusual shape and orientation of the clavicle, it is difficult to adequately determine displacement and angulation on a single anteroposterior radiograph. This is due to the fact that the plane of the fracture is not perpendicular to the plane of the x-ray beam. The clavicle not only shortens, but it also becomes angulated inferiorly and rotated medially; therefore, the deformity is truly in three planes. It is extremely difficult, if not impossible, to characterize the true deformity with radiographs. For the most accurate radiographic evaluation of the fractured clavicle possible, at least two projections of the clavicle should be obtained: an anteroposterior view and a 45degree cephalic tilt view. In the anteroposterior view, the proximal fragment is characteristically displaced upward and the distal fragment downward (Fig. 27-1A). In the cephalic tilt, the tube is directed from inferior, projecting upward. This view more accurately reveals the anteroposterior relationship of the two fragments and hence is the best view for assessment of

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A

to the overlying skin and after injury may result in painful neuroma. Below the clavicle lie the important neurovascular structures: the subclavian vessels and brachial plexus. These are protected by the clavipectoral fascia within the costoclavicular space. The medial cord of the brachial plexus (ulnar nerve) is located in the smallest portion of the costoclavicular space and can be compromised by fracture or healing callus.8 Behind the medial clavicle and the sternoclavicular joint, the internal jugular and subclavian veins join to form the innominate vein. Medially, the omohyoid fascia covers the internal jugular and subclavian veins. The myofascial layer also protects the subclavian and axillary veins at the middle and medial thirds behind the clavicle.9

Treatment Options

B Figure 27-1 A, Preoperative anteroposterior radiograph of a patient with a middle third clavicle fracture. B, Preoperative 45-degree cephalic tilt radiograph of same patient.

displacement (see Fig. 27-1B).6 An axillary view with the beam angled slightly cephalad can also help determine fracture displacement and can be useful in assessing possible nonunions. Rowe7 has recommended that with an anteroposterior radiograph, the film should include the upper third of the humerus, the shoulder girdle, and the upper lung fields to rule out any associated injuries. The fracture personality is also important to assess because it may give a clue to the presence of associated injuries. Normally the clavicular shaft fracture in the adult is slightly oblique; however, if there is significant comminution, this is indicative of significant force and neurovascular and pulmonary injuries must be ruled out.

Relevant Anatomy The clavicle is the first bone in the body to ossify, around the fifth fetal week, but the medial physis does not fuse until young adulthood at ages 22 to 25. This is important in order to distinguish medial clavicle physeal injuries from fractures in this age group. The clavicle is an S-shaped bone that is anchored by strong ligamentous attachments on both its medial and lateral ends. Muscular attachments to the clavicle include the sternocleidomastoid, pectoralis major, and subclavius muscles proximally and the deltoid and trapezius muscles distally. There are no muscular or ligamentous attachments on the middle section of the clavicle, and this supports the fact that most fractures occur in this area. There is thin coverage of the superior aspect of the clavicle by the platysma muscle. The supraclavicular nerves lie just below the platysma muscle, which give sensory innervation

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The concept of nonoperative treatment historically has consisted of bracing the shoulder girdle to raise the outer fragment upward, outward, and backward; depressing the inner fragment; maintaining the reduction; and enabling the ipsilateral elbow and hand to be used so that associated problems with immobilization can be avoided. Review of the literature indicates that immobilization of a clavicle fracture is virtually impossible to accomplish and shortening and deformity are often the results. Historically, clavicle shortening appeared to be inconsequential; however, more recent data indicate that this is one of the most significant predictors of an unsatisfactory outcome.10,11 There are numerous methods to attempt to immobilize the clavicle, ranging from long-term recumbency,12,13 various types of ambulatory treatment,14 and numerous internal fixation methods.15–25 Partial immobilization can be performed by numerous bandaging methods such as a sling, sling and swathe, Velpeau dressing, figure-eight, or cuff and collar. These options are used to treat many middle third or shaft fractures. It is important to understand that the injury radiographs are predictive of the fracture healing results, and a completely displaced or shortened fracture is more likely to stay in this position regardless of the immobilization method used. A reduction maneuver may be performed and if crepitus between the two fractured ends of the clavicle are felt, then it may be more likely that the fracture will go on to union. If there is no crepitus felt, then soft tissue may be interposed and this may contribute to fracture nonunion.25 Operative treatment of clavicle fractures (external fixation or open reduction internal fixation) should be considered in the following cases: 1. Open fractures requiring débridement. 2. Neurovascular compromise that is progressive or nonresponsive to reduction maneuvers. 3. Displacement (angulation and comminution) that tents the skin. 4. Polytrauma patients that may need to use upper extremities for mobilization purposes. 5. The “floating shoulder” injury (clavicle and unstable scapular fracture with compromised acromioclavicular and coracoacromial ligaments). 6. Type II distal clavicular fractures. 7. Factors that render the patient unable to tolerate closed immobilization, such as with neurologic problems.25 8. Patients for whom the cosmetic lump over the healed clavicle is intolerable. 9. Relative indications are shortening of more than 15 to 20 mm and displacement greater than the width of the clavicle.

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Medial clavicle fractures and physeal injuries are easily and best treated by nonoperative measures. One must also rule out sternoclavicular injuries in these cases, which may require additional treatment. Middle third clavicle fractures, which are the most common, can also be managed nonoperatively. The most concerning fractures of the midshaft of the clavicle are generally those that have absorbed the greatest energy. In the senior author’s experience, these higher energy fractures tend to have a remarkably consistent pattern: shortened and comminuted with an anterior/inferior butterfly fragment. Soft-tissue injury and stripping are significant, leading to greater instability, all of which increase the risk of nonunion. It is our belief that these fractures are best treated with open reduction and internal fixation. Distal clavicle fractures, if nondisplaced, can be treated nonoperatively. If displaced, one must determine the integrity of the coracoclavicular ligaments. If the coracoclavicular ligaments or some portion of them remain attached to the medial clavicular fragment, then the coracoclavicular interval will be maintained and prevent further displacement of the fracture ends. If the coracoclavicular ligaments are not attached, then the medial fragment can displace, with an increased risk of nonunion. In unstable cases, operative stabilization of the coracoclavicular interval may be indicated.

Techniques Open reduction and internal fixation can be performed by intramedullary devices or plate fixation. Plate fixation can be performed with a six- to eight-hole low-contact dynamic compression or reconstruction plate. Semitubular plates are less rigid and have a high risk of failure. The patient may be placed in a beach chair position. The fracture is exposed through a curvilinear incision. The platysma muscle is incised in line with its fibers, and care is taken to protect the branches of the supraclavicular nerve. The periosteum is sparingly stripped off the superior surface of the clavicle for plate application. Care must be taken when drilling and placing screws to avoid injury to the underlying subclavian vessels and thoracic cavity. A malleable retractor may be placed beneath the clavicle to protect the drill from unintentionally entering the thorax. The screw-plate fixation is performed using standard AO techniques. The plate does have the disadvantage of requiring a second operation to remove the hardware if its prominent position irritates the skin after healing. Also, the screw holes weaken the bone and protection is needed after hardware removal. At our institution, intramedullary fixation is used for most of these fractures with a modified Hagie pin (Depuy Orthopaedics). We prefer this method for several reasons. First, the exposure for an intramedullary pin is much smaller than what is necessary for a formal open reduction and internal fixation with plates and screws. This preserves what remains of the soft-tissue envelope. The intramedullary pin allows for compression at the fracture site and load sharing, which has been shown to be advantageous in the healing of other long bone fractures. The intramedullary pins come in different sizes to allow for proper canal fill and can easily be removed under local anesthesia. Last, unlike plate and screw fixation, placement of the intramedullary pin allows us to avoid drilling in the direction of the lungs and neurovascular structures. The patient is placed in a beach chair position on the operating table. A radiolucent shoulder-positioning device optimizes clavicle and shoulder visibility and an image intensifier or a C arm facilitates pin placement. A 2- to 3-cm incision in Langer’s lines over the distal end of the medial fragment is made. Care

Figure 27-2 Incision over distal end of medial fragment. Splitting platysma muscle in line with its fibers.

is taken to prevent injury to the thin platysma muscle, which can be divided in line with its fibers using scissors (Fig. 27-2). The middle branch of the supraclavicular nerve, which is usually found directly beneath the platysma muscle near the midclavicle, should be identified and protected. The proximal end of the medial clavicle is elevated through the incision using a towel clip, elevator, or bone-holding forceps. Once the appropriate sized drill is attached to the ratchet T handle or a power drill, the intramedullary canal is reamed and then tapped without penetrating the anterior cortex. Proper sizing is important. If the fit is too loose, the fixation will not be adequate, and if the fit is too tight, this may compromise the integrity of the bone. The C arm is used to assess the orientation of the drill (Fig. 27-3).

Figure 27-3 Drill positioned in medial fragment.

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The lateral fragment is then elevated through the incision. The arm may be placed in external rotation to facilitate positioning of the lateral fragment canal. The same size drill used in the medial fragment is used to drill the intramedullary canal of the lateral fragment followed by the appropriate tap. Under Carm guidance, the drill is advanced out through the posterolateral cortex of the clavicle, usually at the level of the coracoid. While holding the distal fragment with a bone clamp, the nuts from the pin assembly are removed and the smaller trocar end of the DePuy clavicle pin are passed into the medullary canal of the lateral fragment. The pin should exit through the previously drilled hole in the posterolateral cortex. The pin tip can be felt subcutaneously, and a small incision is created over this area. The Jacobs chuck and T handle is attached to the end of the pin protruding laterally, and the pin is pulled in a retrograde fashion into the lateral fragment. The shoulder and lateral fragment may be elevated by pushing up on the bent elbow to facilitate fracture reduction. The pin is then advanced into the medial fragment and the fracture reduced, ensuring that all threads of the pin are across the fracture site. Pin position and fracture reduction are then verified by the C arm or by obtaining a radiograph. The medial nut is then placed on the pin, followed by the smaller lateral nut. The two nuts are cold-welded together. The T-handle wrench is then placed on the medial nut and the pin backed out until the lateral nut is seen at the skin surface. A double-action pin cutter is used to cut the pin flush with the lateral nut. The pin is then advanced back in the medial fragment using the lateral wrench. The pin can generate considerable compression force, and care must be taken not to overreduce the fracture. The common butterfly fragment may be cerclaged into a reduced position using no. 1 polydiaxone monofilament suture passed beneath the fragment and protected with a Crego elevator. The periosteum, platysma muscle, and skin are then reapproximated. Postoperative radiographs confirm reduction (Fig. 27-4).

Postoperative Rehabilitation The patient is placed in a sling for comfort postoperatively but may remove it when comfort allows. The patient is allowed to resume daily living activities as soon as tolerated but is instructed to avoid strenuous activities such as pulling, lifting, or pushing and arm elevation higher than face level for 4 to 6 weeks. Sutures are removed at 7 to 10 days. Radiographs are

obtained at the 4- to 6-week postoperative clinic visit. If the fracture appears clinically healed (nontender, palpable callus), the patient can advance to daily activities as tolerated. The patient should be seen at 8 to 12 weeks postoperatively. Once radiographs (anteroposterior and 45-degree cephalic tilt anteroposterior radiographs) show healing of the fracture, the pin is removed. The pin can be removed in the office or in an ambulatory surgery setting. We typically use local anesthesia, which may be supplemented with IV sedation. Following pin removal, patients may resume activities of daily living as tolerated but are asked to refrain from strenuous or competitive sports for 6 weeks. If open reduction and internal fixation with plate and screws are performed, hardware removal is not routine, unless the plate and screws are prominent or are causing patient discomfort after evidence of fracture healing. This must be done through the initial incision in the operating room. Protection after plate removal is warranted for an extended period of time to avoid refracture.

Complications and Results Complications of both plate and pin fixation include infection, hardware breakage, neurovascular compromise, refracture, malunion, and nonunion.11,26–32 Shen et al27 treated 251 middle third clavicle fractures with a 3.5-mm reconstruction plate. Average time to union was 10 weeks with 7 nonunions, 14 malunions, and 5 infections; 28 had residual skin numbness and 171 eventually required plate removal. Overall, 94% were satisfied with the end result. Bostman et al26 treated 103 middle third clavicle fractures with plate fixation and 24 (23%) had 1 or more complications, including infection, plate breakage, nonunion, and refracture after plate removal. Results of plate fixation have been favorable for both malunions and nonunions with or without bone grafting.11,28 Prior to the introduction of a specifically designed clavicle pin, the use of intramedullary devices has historically been fraught with complications, mostly secondary to pin migration.29,30 More recently, intramedullary pin fixation using a specifically designed clavicle pin has had excellent results.31,33 Boehme et al33 treated 21 patients with a clavicle nonunion with a modified Hagie pin and bone grafting and showed healing in 20 of 21 of them. Wu et al32 compared plate and intramedullary nail fixation with bone grafting in 33 patients with a middle third clavicular nonunion and noted a higher union rate and lower complication rate in the intramedullary group. Complications of the clavicle pin, in our experience, have been potential posterior skin breakdown from a prominent pin, possible skin numbness in the supraclavicular nerve distribution, and rarely nonunion.

Conclusions

Figure 27-4 Postoperative reduction anteroposterior radiograph.

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Clavicle fractures are common and treatment historically has been conservative. The ultimate goal of treatment is to achieve bone healing with minimal morbidity while avoiding loss of function and residual deformity. Nonoperative immobilization of the clavicle is nearly impossible and shortening is customary, resulting in altered biomechanics of the shoulder girdle. Recent studies indicate that displaced midshaft clavicle fractures have a higher nonunion rate (15% to 25%)10,34 than previously thought, and as many as half of patients are symptomatic as long as 10 years after injury.10 In view of this, we recommend operative intervention for displaced and shortened midshaft clavicle fractures, particularly in highdemand individuals and athletes. The clavicle pin offers an easy

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and safe method of treatment for most clavicle fractures with excellent results both cosmetically and functionally.

secondary to injury/chronic instability. Other degenerative conditions include rheumatoid arthritis, gout, Reiter’s syndrome, condensing osteitis, sternoclavicular hyperostosis, and psoriasis.37

Sternoclavicular Joint Atraumatic Subluxation/Dislocation Relevant Anatomy The S-C joint is the isolated articulating point for the upper extremity to the axial skeleton. The blood supply to the joint arises from the clavicular branch of the thoracoacromial arch, with contributions from the internal mammary and suprascapular arteries. The innervation of the S-C joint is from both the nerve to the subclavius and the medial suprascapular nerve. The joint ends are flattened, with poor congruity, and relatively little innate stability. The joint surface of the medial end of the clavicle is much larger than the corresponding joint surface of the sternum.35 The superior portion of the clavicle is easily palpable in the sternal notch. A thick intra-articular disk is present, which improves the articular congruity. The disk is attached to the first rib and sternum inferiorly and superiorly to the superior border of the clavicle. The major ligaments supporting the joint are the anterior and posterior S-C ligaments. The costoclavicular ligaments run from the superior surface of the first rib to the inferior surface of the medial clavicle. The interclavicular ligament runs between the medial ends of both clavicles, attaching to the anterior surface of the sternum (Fig. 27-5). The epiphysis on the medial end of the clavicle is the last to ossify, at 18 to 20 years, and the last to close, at age 23 to 25.

Range of Motion Motion of the S-C joint is directly linked to upper extremity motion. Fusion of the S-C joint has been shown to severely limit shoulder abduction. The sternum remains fixed as the clavicle moves in rotation, elevation, and levers anterior to posterior with upper extremity motion. The main resistance to rotation comes from the anterior and posterior S-C ligaments. The intraarticular disk resists superior translation of the medial end of the clavicle. The anterior capsule resists anterior translation. The posterior capsule is the most important restraint to posterior translation of the S-C joint.36 The subclavius muscle functions as a dynamic stabilizer during activity.

Pathology Degenerative Conditions Osteoarthritis is the most common degenerative condition occurring in the S-C joint. It may occur as a primary process or

Spontaneous instability of the S-C joint has been well described.38 It most commonly occurs in young patients and is associated with ligamentous laxity in other joints. The patient is typically able to displace the medial end of the clavicle anteriorly with abduction or overhead motion. The condition is rarely symptomatic, and conservative treatment is usually acceptable. Attempting to operatively stabilize the joint in these patients is generally unsuccessful and should be avoided.

Trauma Mechanisms of injury to the S-C joint can be viewed in two ways: direct blows and indirect force applied to the shoulder or upper back. As previously described, the medial epiphysis of the clavicle can persist into the mid-20s. Injuries to the epiphysis can mimic S-C joint injuries. Sprains and subluxations to the SC joint can also be seen. These typically present as isolated pain and swelling. A spectrum of injuries can be grouped into three categories: type I (sprain), type II (subluxation), and type III (dislocation).39 Recurrent subluxations can occur and should be treated similarly to the methods described in the following for traumatic dislocations. The two primary directions of dislocation are anterior and posterior. Anterior dislocations occur more frequently than posterior. The most common mechanism is sports-related injuries. A compressive force is applied to the anterolateral shoulder, whether by a direct blow or traction, and the medial clavicle dislocates anteriorly. The injury presents with pain and swelling over the medial end of the clavicle. The patient will usually support the affected arm in internal rotation and resist any shoulder motion. The medial end of the clavicle can be palpated anterior to the sternum. Posterior dislocations typically result from a direct blow to the medial end of the clavicle or compressive force applied to the posterolateral shoulder. This is seen most commonly in motor vehicle accidents and sports and crush injuries. There may be swelling over the S-C joint and a palpable defect where the medial clavicle would normally be felt. The patient will again resist any motion of the involved shoulder. More concerning symptoms can manifest with posterior dislocations because of pressure on the vital structures posterior to the joint. Shortness

Anterior sternoclavicular ligament

Interclavicular ligament

Figure 27-5 Anatomy of the sternoclavicular joint.

Subclavius muscle and tendon

Costoclavicular ligament

Intra-articular disk

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of breath, hoarseness, or difficulty swallowing can be seen. Venous congestion of the involved arm or neck may also be present.

Radiographic Evaluation The S-C joint is difficult to visualize on plain chest or shoulder radiographs. The shadows from surrounding structures overlap the outlines of the joint. Several radiographic views have been described in a specific attempt to better visualize the S-C joint. The most familiar is the serendipity view, initially described by Rockwood and Wirth.39 The view is obtained by placing the patient supine, with the x-ray cassette placed under the upper shoulders and neck. The x-ray beam is centered on the upper chest and tilted 40 degrees off of vertical. Plain tomography was originally described as the preferred way to visualize S-C joint injuries. When available, tomograms can be a simple, inexpensive way to evaluate the joint. Computed tomography is now recognized as the most reliable way to identify abnormalities of the S-C joint. Fine-cut sections (1 to 2 mm) through the joint can easily define medial clavicle fractures, dislocations, or degenerative changes. Computed tomography should be performed to visualize any acute injury to the S-C joint. For posterior dislocations, compression of structures behind the medial end of the clavicle can be well seen on computed tomography. Efforts have been made to visualize structures of the S-C joint with magnetic resonance imaging. While not as well accepted as computed tomography for trauma, magnetic resonance imaging has been found to reliably identify damage to the intra-articular disk and supporting ligamentous structures.40

figure-eight wrap can be used to assist. These limitations should be followed for 6 to 8 weeks before activities progress. Acute posterior dislocations need extremely careful evaluation. Associated intrathoracic injuries are commonly seen. Hoarseness or difficulty swallowing can indicate pressure on the trachea or esophagus. Venous congestion in the affected arm or jugular distention can indicate pressure on the great vessels. If these symptoms are present, a general or thoracic surgeon should be consulted. Computed tomography is indicated, possibly combined with arterial contrast, to evaluate the position of the medial clavicle and vascular structures. Attempted closed reduction should only be performed after careful preparation. Most authors agree that the reduction should be done in an operating room under general anesthesia. The positioning is the same as described for the reduction of anterior dislocations. Traction is then placed on the affected extremity, and the arm gradually extended. If the clavicle does not reduce easily, the skin over the area is cleaned, and the medial end of the clavicle grasped with a sharp towel clamp. Once the reduction is obtained, it is usually stable. Postreduction care is similar to that used for anterior dislocations, except that adduction of the affected extremity is the motion that should be avoided. This can be facilitated with a figure-eight harness. If a closed reduction cannot be obtained, an operative reduction should be performed. An unreduced posterior dislocation can cause late intrathoracic complications from the posteriorly displaced medial clavicle.43 The operative technique involves a curved incision over the S-C joint. Every effort should be made to preserve the intact anterior ligaments. The assistance of a thoracic surgeon should be considered if significant posterior displacement is present. Stabilization of the joint with pins or wires should be avoided, secondary to concerns of late migration.

Treatment Options Sprains (type I injuries) and subluxations (type II injuries) should be treated with ice and rest initially. A sling to prevent painful motion is useful. Persistent subluxations may require reduction by retracting the shoulders. Mild sprains should be protected for 1 to 2 weeks and then may gradually return to regular activity. More significant sprains or subluxations should be protected for 4 to 6 weeks. Occasionally, the subluxation may progress to chronic instability. Treatment for this eventuality is addressed in that section. Medial clavicle epiphysis displacement must be considered when evaluating injuries to the S-C area in young patients. Most injuries can be treated conservatively, with the expectation that some remodeling of the deformity will occur. Symptomatic posterior deformities should be reduced. If the closed reduction is unsuccessful, an open reduction and possible internal fixation should be performed.41 The treatment of traumatic anterior dislocations is not clearly defined. There are reports of good outcomes with conservative management.42 However, an initial attempt at closed reduction may reduce the deformity. Closed reduction usually requires IV sedation or general anesthesia. The patient is placed supine, with a towel or pad between the shoulders. The affected shoulder is pushed posterior, while manual pressure is used to reduce the medial end of the clavicle. The medial end of the clavicle is frequently unstable after the reduction. If a closed reduction cannot be maintained, conservative management is the best course. Operative stabilization is not recommended for the initial treatment of unstable anterior dislocations. If the reduction remains stable, the arm should be placed in a sling. Retraction and elevation of the shoulder should be avoided. A

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Recurrent Instability Recurrent instability or chronic dislocation of the S-C joint may result in persistent symptoms that require surgical treatment. The goals of the surgical reconstruction are the same as those for instability or persistent dislocation: to remove the degenerative, or damaged, end of the clavicular joint surface and stabilize the medial end of the clavicle. There were several procedures initially described for stabilization of the medial clavicle. These included subclavius tendon transfer, free fascia lata, and osteotomy of the medial clavicle. Arthrodesis of the S-C joint should not be performed because of the associated loss of motion. A recent biomechanical comparison suggests that a figure-eight free tendon graft reconstruction is stronger than using the intra-articular ligament or subclavius tendon.44 The senior author advocates one of two reconstructive methods for S-C joint instability: free tendon transfer or transfer of the intraarticular ligament, as originally described by Rockwood et al.45

Surgical Technique A curvilinear incision is made, based over the medial end of the clavicle and onto the sternum (Fig. 27-6). The attachment of the sternocleidomastoid muscle should be preserved and retracted medially. The anterior capsule is incised carefully to preserve the anterior capsular ligaments and intra-articular disk. The periosteal sleeve is elevated off of the medial clavicle, taking care to preserve it for later repair (Fig. 27-7). On exposure of the joint, care should also be used to preserve the inferior attachments of the intra-articular disk. Using a side-cutting bur, the medial end of the clavicle is resected, using caution to protect underlying structures (Fig. 27-8). Care should also be

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Chapter 27 Clavicle Fractures and Sternoclavicular Injuries

Figure 27-6 Incision for sternoclavicular joint reconstruction.

Figure 27-7 Preservation of periosteal sleeve.

Figure 27-8 Resection of medial clavicle with side-cutting bur.

taken to avoid resecting too much bone and thus injuring the inferior costoclavicular ligaments and further destabilizing the medial clavicle. When using the intra-articular disk for reconstruction, the end of the clavicle must be hollowed with a bur (Fig. 27-9). Nonabsorbable sutures are woven into the ligament/disk and pulled into the medial clavicle, out through dorsal drill holes, and tied over a bone bridge (Fig. 27-10). If a free tendon graft (palmaris longus, semitendinosis, or allograft) is to

be used, drill holes are placed in the sternum and medial clavicle. The tendon is passed through these tunnels, tensioned, and sewn into place (Fig. 27-11). At the completion of either reconstruction, the periosteal sleeve is closed carefully over the repair.

Postoperative Care Initial postoperative swelling and pain can be severe. The extremity should remain protected in a sling for 6 to 8 weeks.

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Figure 27-9 Preparation of medial clavicle for ligament transfer.

Figure 27-10 A–C, Intra-articular disk reconstruction. (From Spencer EE, Kuhn JE: Biomechanical analysis of reconstructions for sternoclavicular joint instability. J Bone Joint Surg [Am] 2004;86:98–105.)

A

B

C

Figure 27-11 A–C, Sternoclavicular joint reconstruction with free soft-tissue graft. (From Spencer EE, Kuhn JE: Biomechanical analysis of reconstructions for sternoclavicular joint instability. J Bone Joint Surg [Am] 2004;86:98–105.)

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Chapter 27 Clavicle Fractures and Sternoclavicular Injuries

Range-of-motion and strengthening exercises are slowly progressed. Activity restrictions should be enforced for 4 to 6 months. Recurrent instability can occur if activity is resumed too early.

Treatment for Arthritis Symptomatic degenerative changes of the S-C joint are not usually associated with instability. Operative management should

only be considered for persistently painful arthritis that is otherwise unresponsive. The goal of surgical treatment is to achieve pain relief by removing the degenerative end of the medial clavicle. The surgical technique is essentially the same as described previously, with the exception that no ligamentous reconstruction is necessary.46 Postoperatively, for arthritic resections, a gradual return to full activity may begin after 8 weeks.

REFERENCES 1. Neer CS: Fractures of the clavicle. In DP RCaG (ed): Fractures in Adults. Philadelphia, JB Lippincott, 1984, pp 707–713. 2. Basamania C: Clavicle Fractures. In Delee J, Drez D (eds): Orthopaedic Sports Medicine, vol. 1. Philadelphia, Saunders, 2003, pp 958–969. 3. Eskola A, Vainionpaa S, Myllynen P, et al: Outcome of clavicular fracture in 89 patients. Arch Orthop Trauma Surg 1986;105:337–338. 4. Hicks J: Rigid fixation as a treatment for hypertrophic nonunion. Injury 1976;8:199–205. 5. McCandless DN, Mowbray MA: Treatment of displaced fractures of the clavicle. Sling versus figure-of-eight bandage. Practitioner 1979;223: 266–267. 6. Widner LA, Riddervold HO: The value of the lordotic view in diagnosis of fractures of the clavicle. Rev Interam Radiol 1980;5:69–70. 7. Rowe CR: An atlas of anatomy and treatment of midclavicular fractures. Clin Orthop 1968;58:29–42. 8. Kay SP, Eckardt JJ: Brachial plexus palsy secondary to clavicular nonunion. Case report and literature survey. Clin Orthop 1986:219–222. 9. Abbott LC, Lucas DB: The function of the clavicle; its surgical significance. Ann Surg 1954;140:583–599. 10. Hill JM, McGuire MH, Crosby LA: Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J Bone Joint Surg Br 1997;79:537–539. 11. McKee MD, Wild LM, Schemitsch EH: Midshaft malunions of the clavicle. J Bone Joint Surg Am 2003;85:790–797. 12. Bateman J: The Shoulder and Neck. Philadelphia, WB Saunders, 1978. 13. Quigley T: The management of simple fractures of the clavicle in adults. N Engl J Med 1950;243:286–290. 14. Conwell H: Fractures of the clavicle. JAMA 1928;90:838–839. 15. Breck LW: Partially threaded round pins with oversized threads for intramedullary fixation of the clavicle and the forearm bones. Clin Orthop 1958;4:227–229. 16. Jablon M, Sutker A, Post M: Irreducible fracture of the middle third of the clavicle. Report of a case. J Bone Joint Surg Am 1979;61:296–298. 17. Katznelson A, Nerubay J, Oliver S: Dynamic fixation of the avulsed clavicle. J Trauma 1976;16:841–844. 18. Lee H: Treatment of fracture of the clavicle by internal nail fixation. N Engl J Med 1946;234:222–224. 19. Lengua F, Nuss JM, Lechner R, et al: Treatment of fractures of the clavicle by closed pinning inside-out without back-and-forth. Rev Chir Orthop Reparatrice Appar Mot 1987;73:377–380. 20. Moore TO: Internal pin fixation for fracture of the clavicle. Am Surg 1951;17:580–583. 21. Murray G: A method of fixation for fracture of the clavicle. J Bone Joint Surg 1940;22:616–620. 22. Neviaser RJ, Neviaser JS, Neviaser TJ: A simple technique for internal fixation of the clavicle. A long term evaluation. Clin Orthop 1975;109: 103–107. 23. Paffen PJ, Jansen EW: Surgical treatment of clavicular fractures with Kirschner wires: A comparative study. Arch Chir Neerl 1978;30: 43–53. 24. Rush LV, Rush HL: Technique of longitudinal pin fixation in fractures of the clavicle and jaw. Mississippi Doctor 1949;27:332. 25. Zenni EJ Jr, Krieg JK, Rosen MJ: Open reduction and internal fixation of clavicular fractures. J Bone Joint Surg Am 1981;63:147–151.

26. Bostman O, Manninen M, Pihlajamaki H: Complications of plate fixation in fresh displaced midclavicular fractures. J Trauma 1997;43:778–783. 27. Shen WJ, Liu TJ, Shen YS: Plate fixation of fresh displaced midshaft clavicle fractures. Injury 1999;30:497–500. 28. Olsen BS, Vaesel MT, Sojbjerg JO: Treatment of midshaft clavicular nonunion with plate fixation and autologous bone grafting. J Shoulder Elbow Surg 1995;4:337–344. 29. Leppilahti J, Jalovaara P: Migration of Kirschner wires following fixation of the clavicle—A report of 2 cases. Acta Orthop Scand 1999; 70:517–519. 30. Nordback I, Markkula H: Migration of Kirschner pin from clavicle into ascending aorta. Acta Chir Scand 1985;151:177–179. 31. Boehme D, Curtis RJ Jr, DeHaan JT, et al: The treatment of nonunion fractures of the midshaft of the clavicle with an intramedullary Hagie pin and autogenous bone graft. Instr Course Lect 1993;42:283–290. 32. Wu CC, Shih CH, Chen WJ, Tai CL: Treatment of clavicular aseptic nonunion: Comparison of plating and intramedullary nailing techniques. J Trauma 1998;45:512–516. 33. Boehme D, Curtis RJ Jr, DeHaan JT, et al: Non-union of fractures of the mid-shaft of the clavicle. Treatment with a modified Hagie intramedullary pin and autogenous bone-grafting. J Bone Joint Surg Am 1991;73:1219–1226. 34. Eskola A, Vainionpaa S, Myllynen P, et al: Surgery for ununited clavicular fracture. Acta Orthop Scand 1986;57:366–367. 35. Soames RW: Skeletal system. In Williams PL, Bannister LH, Berry MM, et al (eds): Gray’s Anatomy, 38th ed. New York, Churchill Livingstone, 1995, pp 725–736. 36. Spencer EE, Kuhn JE, Huston LJ: Ligament restraints in anterior and posterior translation of the sternoclavicular joint. J Shoulder Elbow Surg 2002;11:43–47. 37. Ross JJ, Shamsuddin H: Sternoclavicular septic arthritis: Review of 180 cases. Medicine 2004;83:139–148. 38. Rockwood CA, Odor JM: Spontaneous atraumatic anterior subluxations of the sternoclavicular joint in young adults. Report of 37 cases. Orthop Trans 1988;12:557. 39. Rockwood CA, Wirth MA: Disorders of the sternoclavicular joint. In Rockwood CA, Matsen FA, Wirth MA, et al (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 2004, pp 597–653. 40. Benitez CL, Mintz DN, Potter HG: MR imaging of the sternoclavicular joint following trauma. Clin Imaging 2004;28:59–63. 41. Gobert R, Meuli M, Altermatt S, et al: Medial clavicular epiphysiolysis in children: The so-called sterno-clavicular dislocation. Emerg Radiol 2004;10:252–255. 42. Bicos J, Nicholson GP: Treatment and results of sternoclavicular joint injuries. Clin Sports Med 2003;22:359–370. 43. Noda M, Shiraishi H, Mizuno K: Chronic posterior sternoclavicular dislocation causing compression of a subclavian artery. J Shoulder Elbow Surg 1997;6:564–569. 44. Spencer EE, Kuhn JE: Biomechanical analysis of reconstructions for sternoclavicular joint instability. J Bone Joint Surg (Am) 2004;86:98–105. 45. Rockwood CA, Groh GI, Wirth MA, et al: Resection arthroplasty of the sternoclavicular joint. J Bone Joint Surg (Am) 1997;79:387–393. 46. Noble JS: Degenerative sternoclavicular arthritis and hyperostosis. Clin Sports Med 2003;22:407–422.

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CHAPTER

28

Scapulothoracic Disorders John E. Kuhn

In This Chapter Scapular winging Scapulothoracic crepitus Surgery—superomedial border resection Scapulothoracic bursitis Surgery—endoscopic bursectomy Scapulothoracic dyskinesis

While at rest, the scapula is anteriorly rotated relative to the trunk approximately 30 degrees.1,2 At rest, the medial border of the scapula is also rotated with the inferior pole diverging away from the spine approximately 3 degrees. When viewed from the side, the scapula is tilted forward about 20 degrees in the sagittal plane.1 Deviations in this normal alignment conceivably could contribute to glenohumeral instability3 and impingement4–6 and likely contribute to scapulothoracic crepitus and bursitis. Interestingly, the resting scapular position may change with aging.7

INTRODUCTION • The scapulothoracic articulation is an important, yet relatively unstudied component of upper extremity function, particularly in athletics. • A variety of disorders have been described that affect the scapula directly. In addition, observations have been made in which the scapula functions abnormally in athletes with shoulder pain. • For many of these observations, it is not known whether the scapulothoracic problem preceded the glenohumeral joint problem or vice versa, yet treating the scapulothoracic component of these disorders seems to be an important part of treating the athlete.

RELEVANT ANATOMY Scapulothoracic Articulation Seventeen muscles have their origin or insertion on the scapula (Table 28-1; Fig. 28-1) making it the command center for coordinated upper extremity activity. A number of muscles secure the scapula to the thorax, including 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 (supraspinatus, infraspinatus, subscapularis, and teres minor) provide dynamic stability and help to control activities of the glenohumeral articulation. Disorders of these muscles are common in athletes and are covered in other sections of this text. The series of muscles that join the humerus to the scapula 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. Nearly every functional upper extremity movement has components of scapulothoracic and glenohumeral motion.

Scapular Bursae The location and orientation of the bursae about the scapulothoracic articulation have been known since Codman’s time. Two major or anatomic bursae and four minor or adventitial bursae have been described (Table 28-2; Fig. 28-2). The major bursae are easily found,8,9 whereas the adventitial bursae are not. These two major bursae are found in the space between the serratus anterior muscle and the chest wall and in the space between the subscapularis and the serratus anterior muscles.8,10 The superomedial angle and the inferior angle of the scapula are the most common anatomic regions involved in patients with scapulothoracic bursitis. When inflamed and symptomatic, the bursae are easily found; however, these bursae may be adventitious as they are not found reliably in cadavers.8,11–13 When scapulothoracic bursitis affects the inferior angle of the scapula, the inflamed bursa will be found between the chest wall and the serratus anterior muscle.14–16 This bursa has been called the infraserratus bursa14 and the bursa mucosa serrata.16,17 The second and more common site of scapulothoracic bursitis occurs at the superomedial angle of the scapula. Codman14 described the superomedial angle bursa as an infraserratus bursa lying between the upper and anterior portion of the scapula and the back of the first three ribs. O’Donoghue18 agreed with Codman and described this bursa as a problem in athletes with pain and crepitus. Von Gruber,17 on the other hand, described the bursa mucosa angulae superioris scapulae lying between the subscapularis and the serratus anticus muscles. A third major bursa, the scapulotrapezial bursa, was recognized by Williams et al,9 lying between the superomedial scapula and the trapezius muscle. This bursa is not thought to be a source of scapulothoracic crepitus or bursitis and contains the spinal accessory nerve. Codman14 also recognized a third minor or adventitial bursa called the trapezoid bursa found over the triangular surface at the medial base of the spine of the scapula under the trapezius muscle, which he believed was another site of painful crepitus in scapulothoracic crepitus. Some believe that these minor bursae are not anatomic major bursae and develop in response to abnormal pathomechanics of the scapulothoracic

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articulation.8,11,13 This may help explain the variety of bursae and their different locations as described in these series.

Table 28-1 Muscles with Origins or Insertions on the Scapula

WINGING OF THE SCAPULA

Scapulohumeral Muscles

Winging of the scapula is one of the most common scapulothoracic disorders encountered in athletes. Winging can be divided into primary, secondary, and voluntary types. Primary scapular winging results from identifiable anatomic disorders that directly affect the scapulothoracic articulation. Secondary scapular winging usually is associated with some form of glenohumeral pathology. This type of winging will resolve as the glenohumeral pathology is addressed. Voluntary winging is quite rare and may have an underlying secondary gain concern or psychological cause. Primary winging is most commonly due to nerve injuries in athletes and is the focus of this review.

Long head of biceps Short head of biceps Deltoid Coracobrachialis Teres major Long head of triceps Scapulothoracic Muscles Levator scapulae Omohyoid Rhomboid major

Serratus Anterior Palsy

Rhomboid minor

Pathophysiology The long thoracic nerve is the motor source for the serratus anterior muscle. It is found beneath the brachial plexus and clavicle and over the first rib. It then travels superficially along the lateral aspect of the chest wall, which makes the nerve susceptible to injury (Fig. 28-3). Blunt trauma or stretching of this nerve is particularly common in athletics and has been observed in tennis players, golfers, swimmers, gymnasts, soccer players, bowlers, weight lifters, ice hockey players, wrestlers, archers, basketball players, and football players.19–22

Serratus anterior Trapezius Pectoralis minor Rotator Cuff Muscles Supraspinatus Infrapinatus Subscapularis Teres minor 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.

Conjoined tendon of coracobrachialis and biceps

Trapezius muscle Omohyoid muscle Superior angle Levator scapular muscle

Evaluation Patients with serratus anterior palsy will complain of pain as the other periscapular muscles fatigue as they are used to

Pectoralis minor muscle

Coracoid

Scapular notch Omohyoid muscle Acromion Deltoid muscle Glenoid fossa

Supraspinatus muscle Rhomboid minor muscle

Scapula neck Triceps (long head)

Infraspinatus muscle Teres minor muscle Medial border

Serratus anterior muscle

Subscapularis muscle

Lateral border

Rhomboid major muscle

Teres major muscle Inferior angle Latissimus dorsi muscle Figure 28-1 Muscles with origins or insertions on the scapula. Anterior and posterior 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.)

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Chapter 28 Scapulothoracic Disorders

Table 28-2 Bursae around the Scapula Major/Anatomic Bursae Infraserratus bursae: Between the serratus anterior and chest wall Supraserratus bursae: Between the subscapularis and serratus anterior muscles Minor/Adventitial Bursae Scapulotrapezial bursae: Between the superomedial scapula and the trapezius Superomedial angle of the scapula Infraserratus bursae: Between the serratus anterior and chest wall Supraserratus bursae: Between the subscapularis and serratus anterior Inferior angle of the scapula Infraserratus bursae: Between the serratus anterior and chest wall Spine of the scapula Trapezoid bursae: Between the 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.

compensate for the lost function. With a serratus anterior palsy, the scapula assumes a position of superior elevation and medial translation, and the inferior pole is rotated medially (Fig. 28-4). The patient will have difficulty with arm elevation above 120 degrees, which will magnify the degree of winging.23,24 Electromyography is recommended to confirm the diagnosis and follow the recovery of the injured long thoracic nerve. Because the majority of long thoracic nerve palsies will recover spontaneously, regular electromyographic examinations at 3month intervals have been recommended to follow nerve recovery.25,26

Figure 28-3 Location of the long thoracic nerve. Its superficial location along the chest wall makes it susceptible to injury. (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.)

Treatment Nonoperative treatment with shoulder range-of-motion exercises is begun immediately after diagnosis in order to prevent glenohumeral stiffness. Many types of braces and orthotics have been developed, but their use is of questionable benefit.22,25 In general, these braces attempt to hold the scapula against the

Figure 28-2 Bursae of the scapula. The location 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.)

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Figure 28-4 Resting location of the scapula with palsy of the serratus anterior, and trapezius palsy. (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, LippincottRaven, 1997, pp 357–375.)

chest wall and may have some role if they provide symptom relief, despite their cumbersome nature.24,26–28 Most long thoracic nerve injuries recover spontaneously within 1 year20,23,24,26,27,29–38; however some may take as long as 2 years.23,39,40 Certainly, a trend for nerve recovery would be noted by at least 1 year. There are few data in the literature regarding the results of neurolysis, nerve grafting, or repair of an injured long thoracic nerve.41 Nevertheless, penetrating injuries should undergo nerve exploration and early repair. Neurorrhaphy may be indicated when the lesion can be localized.26 Many patients with persistent impairment of the serratus anterior are able to compensate and not elect to have a surgical reconstruction.26 In patients with

symptomatic serratus winging that persists for more than 1 year, surgical intervention may alleviate pain and improve function. While a number of procedures have been described for refractory serratus anterior palsy, transferring the sternocostal head of the pectoralis major with a fascia lata or hamstring graft extension has become the most popular25,26,31,32,42–46 (Fig. 28-5). While this surgery has been shown to be very helpful for patients with permanent palsy of the serratus anterior, there are no data in athletes, and it is highly unlikely that athletes who require the use of their upper extremity would return to their previous level of competition following this surgery. Fortunately, most athletic injuries to the long thoracic nerve are neuropraxic and recover spontaneously.

Figure 28-5 Pectoralis major transfer for scapular winging. As described by Marmor and Bechtol,114 the sternocostal head of the pectoralis major is sutured to a tubularized fascia lata graft and woven through a foramen made in the inferior angle 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.)

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Figure 28-6 Location of the spinal accessory nerve. Its location in the posterior cervical triangle makes it susceptible to injury during surgical procedures in this area. (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.)

Semispinalis capitis muscle

Splenius capitis muscle Levator scapulae muscle Sternocleidomastoid muscle

Spinal accessory nerve

Anterior scalenus muscle Omohyoid muscle (inferior belly)

Posterior and medial scalenus muscle

Clavicle

Trapezius Winging Pathophysiology The spinal accessory nerve, the only nerve to the large trapezius muscle, is superficial, lying in the subcutaneous tissue on the floor of the posterior cervical triangle. Its superficial location makes it susceptible to injury47,48 (Fig. 28-6). Injury to this nerve results in painfully disabling alterations in scapulothoracic function as well as significant deformity.47–55 This nerve can be injured by blunt trauma,55–57 stretching of the nerve,55 and penetrating trauma that includes surgical biopsy of lymph nodes in the posterior cervical triangle50,53,54 and radical neck dissection.58–60 In athletes, stretching and blunt trauma injuries are most common,56 particularly in contact sports like wrestling. Evaluation Patients will attempt to compensate for a palsy of the trapezius by straining other muscles of the shoulder girdle, including the levator scapulae and the rhomboid muscles which can lead to disabling pain and spasm.57 Patients can also develop pain from a stiff shoulder, shoulder subacromial impingement, and radiculitis from traction on the brachial plexus as the shoulder girdle droops. Upon examination, patients will have difficulty when attempting to shrug their shoulder and will have weakness in forward elevation and abduction of the arm. The patient will assume a position with the shoulder depressed and the scapula translated laterally with the inferior angle rotated laterally (see Fig. 28-4). The diagnosis is confirmed by electromyography. Treatment The initial treatment for patients with trapezius winging is nonoperative. The arm can be placed in a sling to rest the other periscapular muscles. Physical therapy is helpful to maintain glenohumeral motion, preventing shoulder stiffness.61 In cases

caused by blunt trauma, serial electromyographic analysis should be performed at 1- to 3-month intervals to follow the returning function of the nerve. In cases caused by penetrating trauma or when there is no evidence of nerve function on electromyographic analysis, neurolysis and/or nerve grafting can be performed.50,54,62–64 The results of these procedures have been variable; however, the success rate seems to be improved if neurolysis is performed before 6 months.57 Patients who have had symptoms in excess of 1 year are unlikely to benefit from continued nonoperative treatment,53 and surgery can be offered. Historically, a variety of procedures have been described for the treatment of trapezius winging,49,65,66 but the Eden-Lange procedure67–69 is the most popular. In this procedure, the levator scapulae, rhomboideus minor, and rhomboideus major muscles are transferred laterally (Fig. 28-7). The levator scapulae substitutes for the upper third of the trapezius; the rhomboid major substitutes for the middle third of the trapezius; and the rhomboid minor substitutes for the lower third of the trapezius. By moving these muscle insertions laterally, their mechanical advantage is improved and winging is eliminated. Bigliani et al57 recently reported their results using this procedure in 23 patients with trapezius scapular winging, with excellent and good results in 87%. Significant improvement in pain was seen in 91% of these patients, and 87% had significant improvement in function.57 This procedure, while effective at improving function for activities of daily living, would be unlikely to return a competitive athlete back to a high level of performance.

SCAPULOTHORACIC CREPITUS Pathophysiology Symptomatic scapulothoracic crepitus has been described by a number of different authors and has been called the snapping

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Levator scapula muscle Rhomboideus muscle Rhomboideus major muscle

Figure 28-8 Osteochondroma of the scapula causing scapulothoracic crepitus. Note the increased signal in the bursa surrounding this osteochondroma of the scapula. (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.) Figure 28-7 Eden-Lange procedure for trapezius palsy. In this procedure, the levator scapulae is transferred laterally to function as the upper trapezius, while advancement of the rhomboid major and minor compensates for the loss of the middle and lower trapezius. (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.)

Table 28-3 Causes of Scapulothoracic Crepitus Interposed Tissue Muscle Atrophy15 Fibrosis15,17,76 Anatomic variation77 Bone Rib osteochondroma78 Scapular osteochondroma76,79,80 Rib fracture15,76 Scapular fracture81 Hooked superomedial angle of the scapula79,82 Luschka’s tubercle15,81,83 Reactive bone spurs from muscle avulsion67,84,85 Other soft tissue Bursitis86,87 Tuberculosis15 Syphilitic lues15 Abnormalities in Scapulothoracic Congruence Scoliosis88,89 Thoracic kyphosis11 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.

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scapula,15 the grating scapula,43 the rolling scapula,11 the washboard syndrome,70 the scapulothoracic syndrome,71 and the scapulocostal syndrome.72 Boinet73 was the first to describe this disorder in 1867. Mauclaire,74 some 37 years later, classified scapulothoracic crepitus into three groups: froissement was considered physiologic and was described as a gentle friction sound, frottement was a louder sound with grating and was usually pathologic, and craquement was a loud snapping sound and was always pathologic. These noises are thought to occur from two sources, from either anatomic changes in the tissue interposed between the scapula and the chest wall or incongruence in the scapulothoracic articulation (Table 28-3). In reviewing Milch,15 frottement (the lower volume crepitus) may suggest soft-tissue pathology or bursitis while craquement may suggest bony pathology as the source of symptomatic scapulothoracic crepitus. Codman14 writes that he 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 will amplify these noises, acting like a resonance chamber of a string instrument.75 A number of pathologic conditions that could lead to crepitus that affect the muscle in the scapulothoracic articulation include atrophied muscle,15 fibrotic muscle,15,17,76 and anomalous muscle insertions.77 With regard to bony pathology, the most common source of scapulothoracic crepitus is an osteochondroma, arising from either the ribs78 or the scapula76,79,80 (Fig. 28-8). Malunited fractures of the ribs or scapula are also capable of creating painful crepitus.15,76,81 Abnormalities of the superomedial angle of the scapula, including a hooked superomedial angle79,82 and a Luschka’s tubercle (which originally was described as an osteochondroma but has subsequently come to mean a prominence of bone at the superomedial angle15,81,83), have also been implicated as sources for scapulothoracic crepitus. Others67,84,85 implicate reactive spurs of bone that are created by repeated small periscapular muscle avulsions. Any bony pathology that causes scapulothoracic crepitus is capable of forming a reactive bursa around the area of pathology.86,87 In fact, at the time of resection of bony pathology, a

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bursa is frequently seen. Bursae can become inflamed and painful in the absence of bony pathology 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,15 which are exceedingly rare in athletes. However, it is not uncommon for athletes to have abnormalities in congruence of the scapulothoracic articulation that could lead to scapulothoracic crepitus. Both thoracic kyphosis11 and scoliosis,88,89 have been identified as sources of scapulothoracic crepitus. In many sports, particularly swimming, thoracic kyphosis is common90,91 and may be the most likely source of scapulothoracic crepitus.

Evaluation When evaluating the athlete, it is important to know the primary sport and training in which the athlete participates. Athletes who participate in sports that require repetitive overhead activity are commonly affected by scapulothoracic crepitus.13 There may be a familial tendency toward developing symptoms.11 Patients may relate a history of mild trauma that precipitates symptoms,92 and scapulothoracic crepitus may be bilateral in some patients.10 If scapular winging or fullness is identified on inspection of the resting scapula, the examiner should consider a space-occupying lesion, such as an osteochondroma. It is helpful to ask the patient with symptomatic scapulothoracic crepitus to point to the location of the pain. He or she will generally point to the superomedial angle or the inferior angle. Palpation or auscultation while the patient moves the shoulder may help to identify the source and location of the periscapular crepitus.10,93 Supplemental radiographs, which include tangential views of the lateral scapula, computed tomography, or magnetic resonance imaging may be helpful in identifying bony pathology.

Treatment It is important to recognize that scapulothoracic crepitus is not necessarily a pathologic condition. Up to 35% of normal asymptomatic people can demonstrate scapulothoracic crepitus,94 including Codman.14 Therefore, scapular crepitus could potentially be used for secondary gain in patients with hidden agendas or psychiatric conditions. However, if the athlete presents with pain, winging, or other disorders of the scapulothoracic articulation, the scapulothoracic crepitus is considered to be pathologic. Most athletes with scapulothoracic crepitus can successfully be treated nonoperatively, particularly if the crepitus is related to soft-tissue abnormalities, altered posture, or scapulothoracic dyskinesia.10,15 Nonoperative treatment includes postural exercises designed to prevent sloping of the shoulders.10,95 A figureeight clavicle fracture brace may be a useful tool to remind patients to maintain upright posture. Exercises to strengthen periscapular muscles are also important.10,13,15 Oral nonsteroidal anti-inflammatory drugs as well as local modalities such as heat, massage, phonophoresis, ultrasound, and the application of ethyl chloride to trigger points may also prove useful.10,13,15 Injectable local anesthetics and corticosteroids into the painful area have also been recommended.11,13,15,42,92 Caution must be used, as there is a risk of creating a pneumothorax.92 Using these means, most athletes are expected to improve significantly.13,42 However, for those who fail, a number of operations have been described. Athletes with clearly defined bony pathology such as an osteochondroma generally require surgical treatment.15

Resection of the bony pathology is usually necessary to alleviate symptoms with a high likelihood of success.13,76,96 Historically, some authors have used muscle plasty operations to treat scapulothoracic crepitus.74,92 This is thought to be inadequate, however, because the muscle flap may atrophy with time and symptoms could return.15 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 scapula97 and more commonly on the superomedial angle.11,15,82,85,93,98,99

Surgery The surgical technique for the resection of the superomedial angle of the scapula begins with the patient in the prone position (Fig. 28-9). An incision following Langer’s lines is made slightly lateral to the medial border of the scapula, from the superior angle to the scapular spine. The subcutaneous tissue is undermined, exposing the spine of the scapula. Following the spine of the scapula, the periosteum is incised and a plane is developed between the superficial trapezius and the underlying scapula and supraspinatus. Next a plane is developed between the supraspinatus and the rhomboids and 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 and to the subscapularis fossa, elevating the serratus and subscapularis with the rhomboids and levator. The superomedial angle of the scapula is resected with an oscillating saw. It is important to avoid progressing too far laterally as the scapular notch is at risk with the potential for injury to the dorsal scapular artery and the suprascapular nerve. After resecting the bone, the reflected muscles fall back into place, and the medial border of the supraspinatus is repaired to the rhomboid/levator flap with permanent no. 2 polyester suture. Inferiorly, the periosteum is repaired back to the spine of the scapula using suture passed through drill holes. Postoperatively, the patient is placed in a sling and begins passive motion immediately. Active motion is begun at 6 weeks, and resistance exercises follow at 8 to 12 weeks. Complications associated with partial scapulectomy include postoperative hematoma, pneumothorax, and mild residual winging. In younger patients, bone may try to form again, but this rarely produces symptoms. The exposure and potential for complications have led some to perform this procedure arthroscopically.100 The reported results for this procedure are generally good.11,15,82,98 However, it must be remembered that athletes typically do not require surgical intervention; as such, 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 and avoid a partial scapulectomy.16,101,102

SCAPULOTHORACIC BURSITIS When scapulothoracic crepitus is accompanied by pain, an inflamed scapulothoracic bursa is typically found. It is important to realize that, while these two conditions are frequently found

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A Figure 28-9 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, LippincottRaven, 1997, pp 357–375.)

B

C together, an athlete may have crepitus without pain and another may have scapulothoracic bursitis without crepitus. As described previously, symptomatic scapulothoracic bursitis seems to affect two areas of the scapula: the superomedial angle and the inferior angle. These bursae, when inflamed, are thought to be adventitious.8,11,13

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Evaluation Patients with scapulothoracic bursitis 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 pathology. Periscapular fullness is

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frequently appreciated in thinner athletes. This may become significant enough to produce subtle scapular winging. Scapular winging has been identified in 50% of patients with a snapping scapula and no bony abnormalities.13 Infrequently, patients may describe minor trauma as a predisposing event,93,101 but most have a history of repetitive overhead activities in work or athletics.16,42,101 The repetitive motion may irritate soft tissues until inflammation occurs and chronic bursitis develops. The bursa may undergo scarring and fibrosis, which may be the source of crepitus. Scapulothoracic bursitis in athletes may have its roots in postural abnormalities and scapulothoracic dyskinesia. In the evaluation of athletes with scapulothoracic crepitus, local anesthetic injected into the bursa may relieve pain and serve as a diagnostic aid.18

Treatment Nonoperative measures (rest, analgesics, and nonsteroidal antiinflammatory drugs) are the mainstay of treatment for scapulothoracic bursitis. Physical therapy to improve posture, heat, and local steroid injections has also been recommended.16,42 Efforts to strengthen periscapular muscles and stretching are frequently added.16,42 For patients who continue to have symptoms despite conservative treatment, surgery may be considered. As recognized by Sisto and Jobe,16 baseball pitchers may be at risk of bursitis at the inferior angle of the scapula. They described an open procedure for resecting a bursa at the inferior angle of the scapula in four pitchers. Pitchers with this problem have difficulty pitching and tend to have pain during the early and late cocking phases as well as during acceleration (Fig. 28-10). While all pitchers had a palpable bursal sac ranging in size from 1 to 2 cm, best seen with the arm abducted to 60 degrees and elevated forward 30 degrees, only one of the four patients presented with scapulothoracic crepitus. 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, and then the latissimus dorsi muscle, were reflected medially, 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, stressing motion, was begun after 1 week and progressed to allow gentle throwing at 6 weeks with progression to full speed pitching as symptoms allowed. After this procedure, all were able to return to their former level of pitching. Open excision of symptomatic superomedial scapulothoracic bursae have been described by many authors.42,101–103 In most of these reports, dissection is carried out until a plane is developed between the serratus anterior and the chest wall. The thickened bursa is resected and any bony projections removed. With this technique, more than 80% of patients with symptomatic scapulothoracic bursitis had good or excellent results. Resection of the symptomatic scapulothoracic bursa has been performed endoscopically as well.8,10,104–107 Ciullo and Jones10 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 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, limiting the assembly line use of vibrating tools.10 Matthews et al106 have described the technique for scapulothoracic endoscopy. Patients can be placed in the prone or lateral position; however, the lateral position is preferred, as it allows 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, improving access to the bursae. Three portals are used, 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 three finger breadths medial to the medial border of the scapula to avoid

Figure 28-10 Bursa at the inferior angle of the scapula in throwers. This is an infraserratus bursa, which has been described in baseball pitchers, where 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.)

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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 three finger breadths medial to the vertebral border of the scapula just below the spine will penetrate the interval between the rhomboideus major and 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 chest wall, landmarks are generally absent except the ribs. 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 completing the bursectomy, 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. Early results suggest this condition can be treated successfully using the arthroscope with minimal risk.10,103,107

Evaluation Patients with scapulothoracic dyskinesis will not typically direct the physician toward the scapula and will commonly complain of pain in the glenohumeral joint. Inspection of the scapulae from the back will demonstrate asymmetry at rest, with the affected shoulder frequently depressed, the scapula protracted and tilted forward. Mild scapular winging may be present with the posterior angle and the medial border of the scapula prominent. Patients will frequently have pain to palpation at the medial coracoid, the insertion of the pectoralis minor. Asking the patient to elevate the arm in the frontal plane and in the scapular plane will reveal asymmetry of scapulothoracic motion. In the presence of rotator cuff pathology, this may be related to decreased firing of the middle and lower trapezius.111

Treatment Treatment of scapulothoracic dyskinesis is with exercises and modalities of physical therapy. Kinetic chain–based rehabilitation programs have been recommended,112,113 as many of the patients with scapulothoracic kinematic abnormalities will have weakness in the core stabilizers of the trunk. This work is currently in its infancy. Clearly much more work is needed to clearly define pathologic scapulothoracic kinematics and their effect on other shoulder pathologies.

CONCLUSIONS SCAPULOTHORACIC DYSKINESIS Abnormalities in scapulothoracic motion are now receiving much more attention in the literature. Burkhart et al108 recently described a condition known as the SICK scapula. The acronym SICK stands for scapula malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement. The scapula assumes an abnormal position at rest characterized by a position that is inferior, protracted, and tilted anteriorly. Tenderness is typically found on the medial edge of the coracoid, and the pectoralis minor is thought to be in spasm. The authors recognized this pattern in throwing athletes with shoulder pain. Myers et al109 studied this concept by measuring scapulothoracic motion in a population of throwing athletes and compared this to scapulothoracic motion in a control population. They showed that throwing athletes demonstrated significantly increased upward rotation, internal rotation, and retraction of the scapula during humeral elevation, implying that throwing athletes may develop these adaptations for more efficient performance of the throwing motion. Su et al110 have demonstrated that scapular kinematics may be altered in symptomatic swimmers, an effect that is magnified with fatigue associated with a practice.

A variety of scapulothoracic conditions can affect the athlete’s shoulder. These include winging of a variety of forms, crepitus and bursitis, and dyskinesia of the scapulothoracic articulation. Scapular winging in athletes most commonly results from a long thoracic nerve neuropraxic injury and will recover spontaneously. Scapulothoracic crepitus and scapulothoracic bursitis are two related conditions but 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 shoulders10,95 and periscapular muscle strengthening.10,13,15 A figure-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.10,11,13,15,42,92 In athletes with refractory symptoms, surgical correction may be considered; however, there are only a few reports in the literature for this select population and thus it is difficult to predict outcomes with regard to returning to sport. Scapular dyskinesia is only now under study as a source of shoulder pathology, and early results suggest the effects of scapular dyskinesia may be of critical importance. Clearly more work is needed to gain a complete understanding of scapulothoracic problems in the athlete.

REFERENCES 1. Laumann U: Kinesiology of the shoulder joint. In Kolbel R, Helbig B, Blauth W, et al (eds): Shoulder Replacement. Berlin, Springer-Verlag, 1987, pp 23–31. 2. Steindler A: Kinesiology of the Human Body under Normal and Pathological Conditions. Springfield, IL, Charles C Thomas, 1955. 3. von Eisenhart-Rothe R, Matsen FA 3rd, Eckstein F, et al: Pathomechanics in atraumatic shoulder instability: Scapular positioning correlates with humeral head centering. Clin Orthop 2005;433:82–89. 4. Endo K, Ikata T, Katoh S, Takeda Y: Radiographic assessment of scapular rotational tilt in chronic shoulder impingement syndrome. J Orthop Sci 2001;6:3–10.

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5. Hebert LJ, Moffet H, McFadyen BJ, Dionne CE: Scapular behavior in shoulder impingement syndrome. Arch Phys Med Rehabil 2002;83:60– 69. 6. Lewis JS, Wright C, Green A: Subacromial impingement syndrome: The effect of changing posture on shoulder range of movement. J Orthop Sports Phys Ther 2005;35:72–87. 7. Endo K, Yukata K, Yasui N: Influence of age on scapulo-thoracic orientation. Clin Biomech (Bristol, Avon) 2004;19:1009–1013. 8. Kolodychuk LB, Regan WD: Visualization of the scapulothoracic articulation using an arthroscope: A proposed technique. Orthop Trans 1993–1994;17:1142.

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9. Williams GR Jr, Shakil M, Klimkiewicz J, Ianotti JP: The anatomy of the scapulothoracic articulation. Clin Orthop 1999;357:237–246. 10. Ciullo JV, Jones E: Subscapular bursitis: Conservative and endoscopic treatment of “snapping scapula” or “washboard syndrome.” Orthop Trans 1992–1993;16:740. 11. Cobey MC: The rolling scapula. Clin Orthop 1968;60:193–194. 12. Colas F, Nevoux J, Gagey O: The subscapular and subcoracoid bursae: Descriptive and functional anatomy. J Shoulder Elbow Surg 2004; 13:454–458. 13. Percy EL, Birbrager D, Pitt MJ: Snapping scapula: A review of the literature and presentation of 14 patients. Can J Surg 1988;31:248– 250. 14. Codman EA: The anatomy of the human shoulder. In Codman EA (ed): The Shoulder, Supplemental Edition. Malabar, FL, Kreiger Publishing, 1984, pp 1–31. 15. Milch H: Snapping scapula. Clin Orthop 1961;20:139–150. 16. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 1986;14:192– 194. 17. Von Gruber W: Die Bursae mucosae der Inneren Aschselwand. Arch Anat Physiol Wissenschaft Med 1864;358–366. 18. O’Donoghue DH: Treatment of Injuries to Athletes. Philadelphia, WB Saunders, 1962, pp 14–144. 19. Fiddian NJ, King RJ: The winged scapula. Clin Orthop 1984; 185:228–236. 20. Gregg JR, Labosky D, Harty M: Serratus anterior paralysis in the young athlete. J Bone Joint Surg Am 1979;61:825–832. 21. Leffert RD: Pectoralis major transfers for serratus anterior paralysis. Orthop Trans 1992–1993;16:761. 22. Vastamaki M, Kauppila LI: Etiologic factors in isolated paralysis of the serratus anterior muscle: A report of 197 cases. J Shoulder Elbow Surg 1993;2:240–243. 23. Foo CL, Swann M: Isolated paralysis of the serratus anterior. J Bone Joint Surg Br 1983;65:552–556. 24. Johnson JTH, Kendall HO: Isolated paralysis of the serratus anterior muscle. J Bone Joint Surg Am 1955;37:563–574. 25. Iceton J, Harris WR: Results of pectoralis major transfer for winged scapula. J Bone Joint Surg Br 1987;69:108–110. 26. Leffert RD: Nerve injuries about the shoulder. In: Rowe CR (ed): The Shoulder. New York, Churchill Livingstone, 1988, pp 435–454. 27. Foucar HO: The “clover leaf ” sling in paralysis of the serratus magnus. BMJ 1933;2:865–866. 28. Wolfe J: The conservative treatment of serratus palsy. J Bone Joint Surg Am 1941;23:959–961. 29. Berkheiser EJ, Shapiro F: Alar scapula. Traumatic palsy of the serratus magnus. JAMA 1937;108:1790–1793. 30. Duncan MA, Lotze MT, Gerber LH, Rosenberg SA: Incidence, recovery, and management of serratus anterior muscle palsy after axillary node dissection. Phys Ther 1983;63:1243–1247. 31. Fery A: Results of treatment of anterior serratus paralysis. In Post M, Morrey BF, Hawkins RJ (eds): Sugery of the Shoulder. St. Louis, CV Mosby, 1990, pp 325–329. 32. Gozna ER, Harris WR: Traumatic winging of the scapula. J Bone Joint Surg Am 1979;61:1230–1233. 33. Hauser CU, Martin WF: Two additional causes of traumatic winged scapula occurring in the armed forces. JAMA 1943;121:667–668. 34. Horowitz MT, Tocantins LM: An anatomic study of the role of the long thoracic nerve and the related scapular bursae in the pathogenesis of local paralysis of the serratus anterior muscle. Anat Rec 1938;71: 375–385. 35. Ilfeld FW, Holder HG: Winged scapula: Case occurring in soldier from knapsack. JAMA 1942;120:448–449. 36. Overpeck DO, Ghormley RK: Paralysis of the serratus magnus muscle caused by lesions of the long thoracic nerve. JAMA 1940;114: 1994–1996. 37. Potts CS: Isolated paralysis of the serratus magnus: Report of a case. Arch Neurol Psychiatry 1928;20:184–186. 38. Prescott MU, Zollinger RW: Alar scapula an unusual surgical complication. Am J Surg 1944;65:98–103.

39. Goodman CE, Kenrick MM, Blum MV: Long thoracic nerve palsy: A follow-up study. Arch Phys Med Rehabil 1975;56:352–355. 40. Leffert RD: Neurological problems. In Rockwood CA, Matsen FA (eds): The Shoulder, vol 2. Philadelphia, WB Saunders, 1990, pp 750–773. 41. Skillern PG: Serratus magnus palsy with proposal of a new operation for intractable cases. Ann Surg 1913;57:909–915. 42. 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. 43. Neer CS II: Less frequent procedures. In Neer CS II (ed): Shoulder Reconstruction. Philadelphia, WB Saunders, 1990, pp 421–485. 44. Noerdlinger MA, Cole BJ, Stewart M, Post M: Results of pectoralis major transfer with fascia lata autograft augmentation for scapula winging. J Shoulder Elbow Surg 2002;11:345–350. 45. Post M: Pectoralis major transfer for winging of the scapula. J Shoulder Elbow Surg 1995;4:1–9. 46. Steinmann SP, Wood MB: Pectoralis major transfer for serratus anterior paralysis. J Shoulder Elbow Surg 2003;12:555–560. 47. Kauppila LI: Iatrogenic serratus anterior paralysis. Long term outcome in 26 patients. Chest 1996;109:31–34. 48. Kauppila LI: The long thoracic nerve: Possible mechanisms of injury based on autopsy study. J Shoulder Elbow Surg 1993;2:244– 248. 49. Dewar FP, Harris RI: Restoration of function of the shoulder following paralysis of the trapezius by fascial sling fixation and transplantation of the levator scapulae. Ann Surg 1950;132:1111–1115. 50. Dunn AW: Trapezius paralysis after minor surgical procedures in the posterior cervical triangle. South Med J 1974;67:312–315. 51. Hoaglund FT, Duthie RB: Surgical reconstruction for shoulder pain after radical neck dissection. Am J Surg 1966;112:522–526. 52. Langenskiold A, Ryoppy S: Treatment of paralysis of the trapezius muscle by the Eden-Lange operation. Acta Orthop Scand 1973;44: 383–388. 53. Olarte M, Adams D: Accessory nerve palsy. J Neurol Neruosurg Psychiatry 1977;40:1113–1116. 54. Woodhall B: Trapezius paralysis following minor surgical procedures in the posterior cervical triangle. Results following cranial nerve suture. Ann Surg 1952;136:375–380. 55. Wright YA: Accessory spinal nerve injury. Clin Orthop 1975;108: 15–18. 56. Hirasawa Y, Sakakida K: Sports and peripheral nerve injury. Am J Sports Med 1983;11:420–426. 57. Bigliani LU, Perez-Sanz JR, Wolfe IN: Treatment of trapezius paralysis. J Bone Joint Surg Am 1985;67:871–877. 58. Bocca E, Pignataro O: A conservation technique in radical neck surgery. Ann Otol Rhinol Laryngol 1967;76:975–978. 59. Roy PH, Bearhs OH: Spinal accessory nerve in radical neck dissections. Am J Surg 1969;118:800–804. 60. Spira E: The treatment of the dropped shoulder. A new operative technique. J Bone Joint Surg Am 1948;30:229–233. 61. Pianka G, Hershman EB: Neurovascular injuries. In Nicholas JA, Hershman EB (eds): The Upper Extremity in Sports Medicine. St. Louis, CV Mosby, 1990, pp 691–722. 62. Anderson R, Flowers RS: Free grafts of the spinal accessory nerve during radical neck dissection. Am J Surg 1969;118:769–799. 63. Harris HH, Dickey JR: Nerve grafting to restore function of the trapezius muscle after radical neck dissection. (A preliminary report). Ann Otol Rhinol Laryngol 1965;74:880–886. 64. Norden A: Peripheral injuries to the spinal accessory nerve. Acta Chir Scand 1946;94:515–532. 65. Hawkins RJ, Willis RB, Litchfield RB: Scapulothoracic arthrodesis for scapular winging. In Post M, Morrey BF, Hawkins RJ (eds): Surgery of the Shoulder. St. Louis, CV Mosby, 1990, pp 356–359. 66. Ketenjian AY: Scapulocostal stabilization for scapular winging in fascioscapulohumeral muscular dystrophy. J Bone Joint Surg Am 1978;60:476–480. 67. Eden R: Zur Behandlung der Trapeziuslahmung mittelst Muskelplastick. Dtsch Z Chir 1924;184:387–389.

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68. Lange M: Die Behandlung der Irrepairablem Trapeziuslahmung. Langenbecks Arch Klin Chir 1951;270:437–439. 69. Lange M: Die Operative Behandlung der Irrepairablem Trapeziuslahmung. Tip Fakult Mecmausi 1959;22:137–141. 70. Cohen JA: Multiple congenital anomalies. The association of seven defects including multiple exostoses, Von Willebrand’s disease, and bilateral winged scapula. Arch Int Med 1972;129:972–974. 71. Moseley HF: Shoulder Lesions, 2nd ed. New York, Hocher Publishing, 1933. 72. Shull JR: Scapulocostal syndrome: Clinical aspects. South Med J 1969;62:956–959. 73. Boinet W: Societe Imperiale de Chirurge (2nd series) 1867;8:458. 74. Mauclaire M: Craquements sous-scapulaires pathologiques traites par l’interposition musculaire interscapulo-thoracique. Bull Mem Soc Chir Paris 1904;30:164–168. 75. Bateman JE: The Shoulder and Neck, 2nd ed. Philadelphia, WB Saunders, 1978. 76. Milch H: Partial scapulectomy for snapping scapula. J Bone Joint Surg Am 1950;32:561–566. 77. Ssoson-Jaroschewitsch JA: Uber Skapularkrachen. Arch Klin Chir 1923;123:378. 78. DeMarquay J: Exostosis of Rib. In Dictionaire de Medicine et de Chirugie Pratique, 1868. 79. Milch H, Burman MS: Snapping scapula and humerus varus: Report of six cases. Arch Surg 1933;26:570–588. 80. Parsons TA: The snapping scapula and subscapular exostoses. J Bone Joint Surg Br 1973;55:345–349. 81. Steindler A: Traumatic Deformities and Disabilities of the Upper Extremity. Springfield, IL, Charles C Thomas, 1946, pp 112–118. 82. Richards RR, McKee MD: Treatment of painful scapulothoracic crepitus by resection of the superomedial angle of the scapula. Clin Orthop 1989;247:111–116. 83. Von Luschka H: Uber ein Costo-scaplular-gelenk des Menschen. Vierteljahrshefte Prakt Heilk 1870;107:51–57. 84. Roldan R, Warren D: Abduction deformity of the shoulder secondary to fibrosis of the central portion of the deltoid muscle. (Proceedings of the American Academy of Orthopaedic Surgeons). J Bone Joint Surg Am 1972;54:1332. 85. Strizak AM, Cowen MH: The snapping scapula syndrome. J Bone Joint Surg Am 1982;64:941–942. 86. Cuomo F, Blank K, Zuckerman JD, Present DA: Scapular osteochondroma presenting with exostosis bursata. Bull Hosp Jt Dis 1993; 52:55–58. 87. Shogry ME, Armstrong P: Case Report 630: Reactive bursa formation surrounding an osteochondroma. Skel Radiol 1990;19:465–467. 88. Gorres H: Ein Fall von Schmerzhaften Skapularkrachen durch Operation Geheilt. Dtsch Med Wochenschr 1921;472:897–898. 89. Volkmann J: Uber Sogenannte Skapularkrachen. Klin Wochenschr 1922;37:1838–1839. 90. Hellstrom M, Jacobsson B, Sward L, et al: Radiologic abnormalities of the thoraco-lumbar spine in athletes. Acta Radiol 1990;31:127–132. 91. 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 2000;28:490–498. 92. Butters KP: The scapula. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 335–366.

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93. Arntz CT, Matsen FA III: Partial scapulectomy for disabling scapulothoracic snapping. Orthop Trans 1990;14:252. 94. Grunfeld G: Beitrag zur Genese des Skapularkrachens und der Skapulargerausche. 95. Michele A, Davies JJ, Krueger FJ, Lichtor JM: Scapulocostal syndrome (fatigue-postural paradox). NY J Med 1950;50:1353–1356. 96. Morse BJ, Ebrahem NA, Jackson WT: Partial scapulectomy for snapping scapula syndrome. Orthop Rev 1993;22:1141–1144. 97. Cameron HU: Snapping scapulae. A report of three cases. Eur J Rheumatol Inflamm 1984;7:66–67. 98. Kouvalchouk JF: Subscapular crepitus. Orthop Trans 1985;9:587– 588. 99. Wood VE, Marchinski L: Congenital anomalies of the shoulder. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 98–148. 100. Harper GD, McIlroy S, Bayley JI, Calvert PT: Arthroscopic partial resection of the scapula for snapping scapula: A new technique. J Shoulder Elbow Surg 1999;8:53–57. 101. McCluskey GM III, Bigliani LU: Surgical management of refractory scapulothoracic bursitis. Orthop Trans 1991;15:801. 102. Nicholson GP, Duckworth MA: Scapulothoracic bursectomy for snapping scapula syndrome. J Shoulder Elbow Surg 2002;11:80–85. 103. Lehtinen JT, Macy JC, Cassinelli E, Warner JJ: The painful scapulothoracic articulation: Surgical management. Clin Orthop 2004; 423:99–105. 104. Bizousky DT, Gillogly SD: Evaluation of the scapulothoracic articulation with arthroscopy. Orthop Trans 1992–1993;16:822. 105. Gillogly SD, Bizouski DT: Arthroscopic evaluation of the scapulothoracic articulation. Orthop Trans 1992–1993;16:196. 106. 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. 107. Pavlik A, Ang K, Coghlan J, Bell S: Arthroscopic treatment of painful snapping of the scapula by using a new superior portal. Arthroscopy 2003;19:608–612. 108. Burkhart SS, Morgan CD, Ben Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 2003;19:641–661. 109. Myers JB, Laudner KG, Pasquale MR, et al: Scapular position and orientation in throwing athletes. Am J Sports Med 2005;33:263–271. 110. Su KP, Johnson MP, Gracely EJ, Karduna AR: Scapular rotation in swimmers with and without impingement syndrome: Practice effects. Med Sci Sports Exerc 2004;36:1117–1123. 111. Cools AM, Witvrouw EE, Declercq GA, et al: Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms. Am J Sports Med 2003;31:542–549. 112. Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 2003;11:142–151. 113. Rubin BD, Kibler WB: Fundamental principles of shoulder rehabilitation: Conservative to postoperative management. Arthroscopy 2002;18(9 Suppl 2):29–39. 114. Marmor L, Bechtol CO: Paralysis of the serratus anterior due to electrical shock relieved by transplantation of the pectoralis major muscle. A case report. J Bone Joint Surg Am 1983;45:156–160.

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Nerve Injuries R. Shane Barton, David Mayman, Peter J. Millett, and Thomas J. Gill

In This Chapter Peripheral nerve injury Burner/stinger syndrome Suprascapular nerve entrapment Surgery—suprascapular nerve decompression Axillary nerve injury Long thoracic nerve injury Spinal accessory nerve injury Musculocutaneous nerve injury

INTRODUCTION • An increased awareness of peripheral nerve injuries about the shoulder and their effect on athletic function is reflected in the growing body of published reports on the subject. • These injuries have a varied presentation, with associated acute trauma demanding on-field decision making or athletes with chronic symptoms presenting in the clinic after failure of previous diagnostic attempts.

Axonotmesis involves loss of continuity of the axon, with varying degrees of injury to the endoneurium and perineurium. Prognosis for recovery varies greatly due to varying degrees of nerve tissue injury. Wallerian degeneration takes place, and the nerve must regenerate from the site of injury at the rate of 1 mm/day, with recovery of end-organ function possibly taking months. Neurotmesis involves complete disruption of the nerve, including the axon, endoneurium, perineurium, and epineurium, although the outermost nerve sheath may or may not be intact. The prognosis for recovery is very poor, and nerve repair or grafting may be indicated. The differential diagnosis of peripheral nerve injury about the shoulder includes cervical spine instability, cervical spine fracture, herniated cervical disk, cord concussion/contusion, transient quadriplegia, acute brachial plexitis (Parsonage-Turner syndrome), rotator cuff tear or tendonitis, clavicular fracture, acromioclavicular joint injury, glenohumeral subluxation/ dislocation, glenohumeral arthritis, adhesive capsulitis, thoracic outlet syndrome, scapular fracture, and proximal humerus fracture. Each of these must be considered in the evaluation of the athlete with shoulder-related complaints.

• These injuries present a significant challenge to medical personnel attempting to provide athletes with full and safe participation in competitive activities.

TRANSIENT BRACHIAL PLEXOPATHY (BURNER/STINGER SYNDROME)

• In this chapter, we discuss the presentation, diagnosis, and management of commonly encountered nerve injuries about the shoulder. These include the burner/stinger syndrome, suprascapular nerve entrapment and surgical techniques used in its treatment, and axillary, long thoracic, spinal accessory, and musculocutaneous nerve injuries.

Clinical Features and Evaluation

• Less commonly encountered conditions, such as the Parsonage-Turner and thoracic outlet syndromes, are beyond the scope of this chapter but are mentioned in the context of a complete diagnostic workup.

PERIPHERAL NERVE INJURY The pathophysiology of peripheral nerve injury has been studied in great detail. Seddon1 developed the classification system most commonly used today, defining three progressive patterns of injury severity. This has been further modified by Sunderland2 to include five levels of injury. The mildest form, neurapraxia, involves an interruption of axonal function without frank disruption of the axon. The prognosis for recovery is favorable, with complete functional return expected within weeks to months.

The “burner” or “stinger” is one of the most frequently encountered conditions evaluated by athletic team medical personnel. The majority of these injuries occur in American football, in which as many as 65% of collegiate squad members have reported one or more episodes during a 4-year career.3,4 The syndrome is so frequently encountered by and familiar to athletes that it may often go unreported to team staff. An athlete with a burner usually presents after a traumatic event with a complaint of pain, numbness, burning, tingling, or stinging pain radiating from the shoulder down the arm, possibly into the hand, most often unilaterally. The athlete may also complain of weakness in the shoulder, elbow, or hand of the affected upper extremity. He or she may be holding the affected extremity by his or her side or be noticed to shake the hand or arm as if it is “asleep” or “dead.” More ominous signs may include holding the neck in a flexed position to alleviate pressure on the cervical nerve roots or a complaint of bilateral or lower extremity symptoms. This may suggest the possibility of spinal cord involvement instead of nerve root or plexus injury. Pain localized to the trapezius may be present, but neck pain is usually not a complaint, and its presence, especially if severe, requires medical personnel to initiate spinal precautions and to perform a detailed workup for spinal injury.

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less common in athletic injuries,5 to peripheral nerve injury, as described previously. The injury level likely is a function of the position of the neck, arm, and shoulder at the time of impact. It is thought to result from a compression or traction (pinchstretch) injury to either the cervical nerve root or the brachial plexus, most frequently the upper trunk.6 There are three commonly described mechanisms of injury in burner syndrome, occurring in isolation or combination. Forceful neck extension and lateral bending can cause neural foraminal narrowing, leading to compression of the cervical nerve roots.6,7 A traction injury may occur from forceful depression of the ipsilateral shoulder, as occurs in blocking, tackling, or wrestling, with the nerve roots fixed proximally.3 This injury mechanism may be enhanced with lateral bending of the neck to the contralateral side. A third mechanism may be a direct blow to the anterolateral neck at Erb’s point (Fig. 29-1), located superior and deep to the clavicle, lateral to the sternocleidomastoid. At this point, the brachial plexus is most superficial and susceptible to injury. The relationship of cervical stenosis to burner syndrome has been extensively reviewed. The Torg ratio is determined by measuring the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line and dividing this value by the anteroposterior diameter of the vertebral body on a lateral radiograph.8 Meyer et al6 concluded that there was a relationship between cervical stenosis, defined as a Torg ratio less than 0.8, and the occurrence of stingers or nonparalyzing extension/compression injuries, although the clinical significance of the Torg ratio continues to be debated.9

The physical examination should focus on the spine and affected extremity of the athlete. Careful attention to the results will help differentiate a relatively benign condition from a more severe injury. Most athletes will have a normal physical examination by the time they arrive on the sideline. Clinical observation of the athlete is followed by palpation for tenderness and deformity along the spine, shoulder, and extremity, facilitated by removal of clothing and protective gear as needed. Spinal examination should then test active flexion, extension, lateral bending, and rotation and, if normal, may include provocative tests such as Spurling’s compression maneuver or axial manual traction. The shoulder/extremity examination should concentrate on sensation, motor testing, and reflexes. The upper trunk of the brachial plexus, most often involved in burner syndrome, is evaluated by sensory examination of the C5 and C6 dermatomes, and strength testing of the deltoid, biceps, and rotator cuff. Weak shoulder abduction may be present, even after pain cessation. Deep tendon reflex testing of the biceps (C5), brachioradialis (C6), and triceps (C7) should then be performed. The lower trunk is less frequently involved. Sensory examination is performed with attention to the C7, C8, and T1 dermatomes, and motor testing should concentrate on the intrinsic muscles of the hand, including grip strength and finger abduction.

Relevant Anatomy and Pathophysiology The exact mechanism of burner syndrome is debated and likely represents varying levels of injury location and severity. The injury location can vary from nerve root, which is thought to be

C4 C5 Dorsal scapular nerve (Rhomboid minor and major) C5–C6 Suprascapular nerve (Supraspinatus infraspinatus)

K UN TR

RD

OR D

CO

LC

C6

C7 Phrenic nerve (diaphragm) C8

T1 Long thoracic nerve (Serratus anterior)

PO

ST

ER IO R

LA TE

LO W ER

LE

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to rve us Ne clavi b K su UN TR

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Median nerve C6–T1 (C7–T1)

To longus and scalene muscle

R PE UP

C5–C6 Upper subscapular nerve (Subscapularis) C5–C6 Lower subscapular nerve (Subscapularis teres major)

C5–C6 Musculocutaneous nerve (Coracobrachialis biceps brachialis) C5–C6 Axillary nerve (Deltoid teres minor)

C5

D

OR

C AL

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Lateral pectoral nerve (Pectoralis major)

E

M

Medial pectoral nerve (Pectoralis major and minor) Thoraco dorsal nerve (Latissimus dorsi) (C6–C8)

Medial brachial cutaneous Medial antebrachial cutaneous Ulnar nerve Radial nerve (C6–T1)

No motors

Figure 29-1 Diagram of the brachial plexus demonstrating the location of Erb’s point (arrow). Brachial plexus stretch injuries may result from traction 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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Criteria for Return to Sports If the athlete’s sensory and motor symptoms resolve within seconds or minutes and there is no associated neck pain, rangeof-motion limitation, or findings consistent with other more significant injuries to the neck or shoulder, then the player may safely return to competition. Full motor strength is an absolute requirement for return to sports. Paresthesias usually resolve within seconds to minutes and motor symptoms within 24 hours. Persistence of symptoms, including paresthesias, weakness, limited range of motion of the neck or extremity, or pain, requires removal from participation and further evaluation. Persistent or recurrent episodes require complete neurologic workup, including cervical spine radiographs and possibly magnetic resonance imaging (MRI) or computed tomography myelography to assess for cord or root compression. If symptoms persist for more than 2 to 3 weeks, electromyography (EMG) may be useful in determining the extent of injury. However, electromyographic changes may persist for several years after injury and should not be used as a criterion for return to sports. Abnormal findings on these studies require a case-by-case evaluation for return to sports. A physical rehabilitation program that emphasizes neck and trunk strengthening should be instituted on return to competition. The use of a neck roll, collar, or molded thermoplastic neck-shoulder-chest orthosis,4 in conjunction with well-fitted shoulder pads, has been shown to decrease the recurrence and severity of episodes in athletes with a history of stingers.

SUPRASCAPULAR NERVE ENTRAPMENT Clinical Features and Evaluation Injury to the suprascapular nerve has been associated with multiple sports, including baseball, football, tennis, swimming, volleyball, and weight lifting.10 Direct trauma to the neck or scapula may cause injury to the suprascapular nerve, and crutch use has been implicated,11 as has heavy labor. The athlete with suprascapular nerve palsy may present with an often vague range of symptoms or even be asymptomatic.12 Pain over the posterolateral shoulder or easy fatigability with overhead activities may be reported, or painless weakness of external rotation with or without spinati muscle atrophy may be noted. Compression of the nerve at the suprascapular or spinoglenoid notch is a commonly reported mechanism of injury in the athlete and is discussed in detail. The physical examination plays a critical role in discerning the site of suprascapular nerve injury. Clinical observation of the athlete’s shoulder girdle is important. More proximal injury, as seen with suprascapular notch compression, may result in atrophy of both the supraspinatus and infraspinatus, whereas more distal compression at the spinoglenoid notch will result in isolated infraspinatus weakness and atrophy (Fig. 29-2). Tenderness over the course of the nerve may be present but is often difficult to localize. Weakness of shoulder abduction or external rotation with vague posterolateral shoulder pain may be the only significant examination finding, although a decreased range of motion, specifically adduction, may be noted due to pain. Plain radiographs of the shoulder are routinely negative. EMG and nerve conduction velocity (NCV) studies play a particularly useful role in the diagnosis and localization of a suspected suprascapular nerve injury. As with most nerve injuries, these studies are generally more useful if obtained in the subacute phase of injury, at least 3 to 4 weeks after onset of symptoms. However, careful clinical correlation with study results

Figure 29-2 Suprascapular neuropathy resulting in infraspinatus atrophy. (From Jobe FW: Operative Techniques in Upper Extremity Sports Injuries. St. Louis, Mosby, 1996.)

must be used, as both false-negative and false-positive nerve findings have been described.13 MRI may be useful in demonstrating atrophic muscle degeneration of the spinatii or to reveal the presence of a compressive lesion along the course of the nerve. Most commonly, this will be a ganglion cyst, often seen in association with a superior labral tear (Fig. 29-3).

Relevant Anatomy and Pathophysiology At Erb’s point, the suprascapular nerve branches from the upper trunk of the brachial plexus, with contributions from C5 and C6. The nerve then travels below the transverse scapular

Figure 29-3 Magnetic resonance imaging of the right shoulder demonstrating a ganglion in the spinoglenoid notch compressing the infraspinatus branch of the suprascapular nerve.

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used to evaluate for a compressive lesion. If a compressive lesion or cyst is noted on imaging, the patient can be observed for 2 to 3 months, followed by surgical decompression if symptoms continue (see “Surgery”). An athlete with symptoms associated with repetitive overhead activity, as seen with volleyball, tennis, or baseball players, should be followed for 6 to 12 months with observation, activity restriction, and periscapular therapy, after confirming the absence of a compressive lesion. Periodic EMG/NCV studies can follow the electrophysiologic nerve recovery. Surgical intervention with this overuse mechanism of injury has demonstrated variable results at best,17 and function usually returns by 12 months. As with other painful nerve injuries about the shoulder, Parsonage-Turner syndrome (acute brachial neuritis) must be considered and, if present, should be managed conservatively with pain control, observation, and therapy.

Surgery The suprascapular nerve can be approached either with an open technique or arthroscopic technique. If the lesion is proximal and both the supraspinatus and infraspinatus are involved, then the entire nerve should be released, but most importantly the transverse scapular ligament must be released. If only the infraspinatus is involved or if there is a structural lesion in the spinoglenoid notch such as a paralabral cyst, then the nerve may be simply decompressed at the spinoglenoid notch. Associated labral tears should be repaired using standard techniques. Figure 29-4 Anatomy of the suprascapular nerve. (From Jobe FW: Operative Techniques in Upper Extremity Sports Injuries. St. Louis, Mosby, 1996.)

ligament as it crosses the suprascapular notch to enter the supraspinatus fossa (Fig. 29-4), while the suprascapular artery usually travels above the ligament. The nerve traverses the supraspinatus fossa, giving motor branches to the supraspinatus, with variable minor sensory contributions to the glenohumeral and acromioclavicular joints and occasionally to the skin.14 The nerve then angles around the spine of the scapula at the spinoglenoid notch, traveling with the artery under the spinoglenoid ligament.15 The motor branches to the supraspinatus are approximately 3 cm from the origin of the long head of the biceps, while the motor branches to the infraspinatus average 2 cm from the posterior glenoid rim.16 Like other nerves, the suprascapular nerve is susceptible to injury from compression, traction, or direct trauma. Vascular microtrauma has also been postulated to cause nerve dysfunction. The most commonly reported mechanism of injury is compression by a ganglion cyst, usually at the suprascapular or spinoglenoid notch. A thickened or calcified ligament may also compress the nerve. A ganglion cyst is often associated with a tear in the glenohumeral joint capsule or labrum, with fluid being forced through the tear and then being trapped outside the joint.

Treatment Options Treatment of the acute injury to the suprascapular nerve is similar to that for most nerve injuries about the shoulder. Relative rest and pain control are followed with progressive range-of-motion and strengthening exercises as tolerated. More chronic cases are managed depending on the duration of symptoms and the mechanism of injury, although the exact duration of symptoms is frequently difficult to determine. MRI can be

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Open Decompression The suprascapular nerve can be approached either by the direct approach, splitting the trapezius, or by an extensile approach, elevating the trapezius from the spine of the scapula. The transverse scapular ligament is found 2.5 to 3 cm medial to the acromioclavicular joint at the medial border of the coracoid process. With a direct superior approach, the skin is incised in line with Langer’s lines medial to the acromioclavicular joint in a typical Saber style. The trapezius muscle is split in line with its fibers for approximately 5 cm. The supraspinatus muscle is retracted posteriorly, and the suprascapular notch and transverse ligament are palpated. The suprascapular artery can either be retracted out of the way or ligated and the transverse scapular ligament is then released. A neurolysis can then be performed. If the ligament is ossified, which can be seen on computed tomography scan, then a small rongeur can be used to remove the bone and decompress the nerve. This approach is cosmetic but limits access to the posterior course of the nerve at the spinoglenoid notch. For open suprascapular nerve decompression, the authors prefer to use the extensile approach. This allows access to the entire nerve if necessary. An incision is made along the spine of the scapula and the trapezius is elevated and reflected anteriorly. This gives access to the entire supraspinatus fossa. The supraspinatus muscle is retracted posteriorly and the transverse scapular ligament is palpated, visualized, and released as described. By working on either side of the supraspinatus muscle belly, the suprascapular nerve can be visualized over most of its course and can be followed to the spinoglenoid notch. By extending the incision inferiorly and splitting the posterior deltoid, the suprascapular nerve can be traced to its terminal arborization into the motor branches that supply the infraspinatus muscle. The suprascapular nerve runs just at the base of the scapular spine in the spinoglenoid notch. Often there is a thickened band of connective tissue called the spinoglenoid ligament

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that can tether the nerve in this region. If present, this should be released as well. Since this approach uses extensile, internervous planes, closure is simply done by repairing the trapezius back to the spine of the scapula using nonabsorbable sutures. Arthroscopic Decompression An arthroscopic approach is a more sophisticated way of addressing the suprascapular nerve and is our preference when there is an associated intra-articular lesion, such as a SLAP (superior labrum anterior to posterior) tear or labral tear. It is our preferred method for treating spinoglenoid neuropathy due to paralabral cysts, and, furthermore, it is becoming our preferred method for decompressing the nerve at the suprascapular and spinoglenoid notches. It does require advanced arthroscopic skills but offers a less invasive and more cosmetic approach with better overall visualization and access. Moreover, concomitant intra-articular pathology can be addressed easily. Arthroscopic Release at the Suprascapular Notch We prefer to use the beach chair position. The arthroscope is placed in an anterolateral portal and accessory anterior and posterior portals are used. The view is initially into the subacromial space. The coracoid process must be visualized and the dissection is then carried medially. Arthroscopic retractors are helpful to retract the supraspinatus muscle belly posteriorly. The dissection is carried along the posterior aspect of the coracoid process. The coracohumeral and coracoclavicular ligaments are identified and at the base of the coracoid the suprascapular notch is identified. The artery is cauterized using radiofrequency ablation, and the ligament is released using hand-held arthroscopic tissue punches (Fig. 29-5). The nerve can be probed to ensure there is no compression. It can be seen passing deep to the supraspinatus.

Figure 29-6 Arthroscopic view of right shoulder spinoglenoid notch cyst immediately following perforation (arrow) and decompression. The suprascapular nerve is deep and medial to the cyst wall.

Arthroscopic Release at Spinoglenoid Notch or Cyst Decompression This is our preferred technique for treating paralabral cysts. Again the beach chair position is used. Standard anterior and posterior portals are created. A transrotator cuff portal as used

for SLAP repairs is created. The arthroscope is placed laterally through the transcuff portal. This gives excellent visualization. If there is a labral tear, it is repaired with suture anchors using standard technique. Some have advocated working through the labral tear to access the cyst, but we have found this to be quite difficult and furthermore it is virtually impossible to visualize the suprascapular nerve. Therefore, we have gone to performing a capsulotomy, releasing the posterosuperior capsule at the periphery of the labrum until the fibers of the supraspinatus are identified. The supraspinatus muscle is then elevated superiorly using a retractor, which is placed from our anterior portal. With careful and meticulous dissection, the cyst itself can invariably be demonstrated and resected. The typical ganglion cyst fluid is seen when the cyst is perforated (Fig. 29-6). The suprascapular nerve runs 2.5 to 3 cm medial to the superior aspect of the glenoid at the base of the supraspinatus fossa (Fig. 29-7). It can be traced posteriorly from there until it passes through the

Figure 29-5 Arthroscopic view of right shoulder suprascapular notch demonstrating the transverse scapular ligament (large arrow) traveling over the suprascapular nerve (small arrow). The suprascapular artery above the ligament has been coagulated.

Figure 29-7 Arthroscopic view of right shoulder spinoglenoid notch demonstrating the infraspinatus branch of the suprascapular nerve (arrow) after débridement of the compressive cyst.

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spinoglenoid notch. Using hand-held basket punches and arthroscopic probes, a careful neurolysis can be performed.

Results and Outcomes The results of both operative and nonoperative treatment of suprascapular nerve injuries are not easily interpreted. The duration of symptoms is often difficult to assess, and the diagnosis may be incorrect or incomplete with respect to associated intraarticular pathology. Several studies have reported on the results of both operative and nonoperative treatment.10,13,17 In a recent meta-analysis of the literature, Zehetgruber et al18 found suprascapular nerve entrapment to be rare, occurring mainly in patients younger than 40 years of age. Isolated infraspinatus atrophy was most often associated with a ganglion cyst, whereas a history of trauma was usually associated with ligamentous compression of the nerve. Surgical treatment seems to give reliable pain relief, with persistent atrophy of the spinatii muscle, a common but well-tolerated finding.

Postoperative Rehabilitation Postoperatively patients are immobilized in a sling for comfort. Early motion is encouraged. If a labral tear was repaired, then the athlete is protected for 4 weeks before resuming active motion. Strengthening begins at 6 weeks. Throwing and overhead activities generally commence at 4 to 5 months postoperatively.

Criteria for Return to Sports While the athlete remains symptomatic, full athletic function should be avoided, especially when the injury mechanism is one of overuse. Patients undergoing surgical intervention for persistent symptoms demonstrate excellent pain relief, and although the spinatii often demonstrate persistent atrophy, return to full competitive activity can still be expected.19

AXILLARY NERVE INJURY Clinical Features and Evaluation Axillary nerve injury is a relatively common peripheral nerve injury in the athlete, particularly in contact sports.20 Shoulder dislocation or direct trauma to the deltoid muscle can result in axillary nerve injury and subsequent deltoid or teres minor muscle paralysis. When injury does occur, the athlete often presents not with an obvious motor deficit, but rather may complain of easy fatigability of the shoulder with overhead activity or resisted shoulder abduction.21 However, the athlete may note weakness of shoulder external rotation, forward flexion, or abduction. Sensation over the lateral aspect of the shoulder may or may not be intact, even in the face of motor weakness. The quadrilateral space of the shoulder may be a site of compression of the axillary nerve22 and posterior humeral circumflex vessels, with subsequent injury and dysfunction (Fig. 29-8). The athlete may complain of a vague, poorly localized ache over the lateral or posterior shoulder, often aggravated by activity, especially forward flexion, abduction, and external rotation, as seen in overhead sports such as throwing. A history of unsuccessful shoulder surgery for the pain is not uncommon. The physical examination should, as stated previously, concentrate on the cervical spine, shoulder, and extremity involved. Observation of the shoulder girdle may demonstrate deltoid and/or teres minor atrophy if the injury is long-standing. A detailed neurovascular examination should always be performed, with special attention paid to sensation to light touch

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Figure 29-8 The boundaries of the quadrilateral space as viewed from behind. (From Jobe FW: Operative Techniques in Upper Extremity Sports Injuries. St. Louis, Mosby, 1996.)

over the lateral shoulder. Point tenderness is often present over the quadrilateral space22 if neurovascular compression is present, and this may be accentuated by testing in the FABER (forward flexion, abduction, and external rotation) position.22 Weakness of external rotation due to teres minor involvement may be present, and deltoid dysfunction may be noted in testing shoulder abduction, forward flexion, or extension. With respect to diagnostic testing, plain radiographs of the shoulder are a necessity to rule out associated bony injury, especially in the traumatic injury setting. Cervical spine radiographs may also be indicated. EMG and NCV studies are useful to confirm the diagnosis and determine the severity of injury but will likely not be positive until 3 or more weeks after injury. The intermittent compression of quadrilateral space syndrome may result in normal EMG and NCV studies. Magnetic resonance imaging may demonstrate muscle substance changes in chronic cases. With regard to quadrilateral space syndrome, associated arterial occlusion of the posterior humeral circumflex artery can be diagnosed with arteriography.22 Historically, the study will be normal with the affected shoulder in adduction but will demonstrate a filling defect with the shoulder in the FABER position (Fig. 29-9). However, magnetic resonance arthrography has demonstrated positive findings in asymptomatic patients, and its value is unclear.23

Relevant Anatomy and Pathophysiology The axillary nerve originates from the posterior cord of the brachial plexus, directly behind the coracoid process and conjoined tendon, with contribution from the C5 and C6 cervical nerve roots. It courses along the anterior inferolateral border of the subscapularis tendon and then passes near the inferior shoulder capsule,24 receiving a sensory branch from the anterior capsule. The nerve then passes with the posterior humeral circumflex artery through the quadrilateral (quadrangular) space, formed by the long head of the triceps medially, the humeral

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Figure 29-9 An angiogram of a patient with quadrilateral space syndrome. A, Digital subtraction angiogram with arm in adduction reveals patent posterior humeral circumflex artery. B, Angiogram of same patient with the arm in abduction reveals complete occlusion of the posterior humeral circumflex artery (arrow), confirming the diagnosis. (From Safran MR: Nerve injury about the shoulder. Am J Sports Med 2004;32:803–819, 1063–1076.)

shaft laterally, the teres minor superiorly, and the teres major inferiorly. At this point, it branches into an anterior and posterior branch along the posterior humeral surgical neck. The anterior branch innervates the middle and anterior deltoid, traveling an average of 6 cm distal to the lateral edge of the acromion.5 The posterior branch divides into the upper lateral brachial cutaneous sensory branch and the nerve to teres minor. The posterior deltoid is variably innervated by the anterior, or less frequently, the posterior branch.5 The axillary nerve is relatively fixed at the posterior cord and the deltoid, thus leaving it susceptible to traction injury in anterior shoulder dislocation or proximal humeral fracture. The proximity to the shoulder capsule also makes the nerve susceptible to injury during arthroscopic or open shoulder surgery. Direct injury to the nerve from impact to the anterolateral shoulder has also been reported.21 The factors that may increase the likelihood of axillary nerve injury with shoulder dislocation include age older than 40 years, unreduced dislocation longer than 12 hours, or higher energy mechanisms of injury.20

may be indicated. This may include decompression of the quadrilateral space in the presence of a positive arteriogram, neurolysis, or nerve grafting and results in more predictable functional return if undertaken within the first year after injury. Tendon transfer may also be considered for refractory cases, but return to competitive activity may not be possible.

Criteria for Return to Sports As with other injuries about the shoulder, maintenance of motion is key during the recovery period. Passive, activeassisted, and active range-of-motion exercises should be instituted early. Sport-specific rehabilitation begins when symptoms allow. Residual weakness of the deltoid and teres minor is often well tolerated but may result in easy fatigability of the shoulder. Therefore, a maintenance program of posterior capsular stretching and rotator cuff and periscapular strengthening should be instituted.

LONG THORACIC NERVE INJURY (MEDIAL SCAPULAR WINGING)

Treatment Options The treatment of an axillary nerve injury is a function of the mechanism of injury. Timely shoulder reduction and management of bony injury must be addressed when present, and the athlete should be reassured that the prognosis for recovery of function is good. Even with persistent weakness of the deltoid, return to competitive sports can be expected,20 although athletes with significant overhead demands may note decreased function. Nonoperative treatment is the mainstay of management of these injuries, particularly in the first 3 to 6 months after injury.25

Surgery In the symptomatic athlete with incomplete clinical or EMG/NCV evidence of recovery after 3 to 6 months, surgery

Clinical Features and Evaluation Although relatively uncommon, traction injury to the long thoracic nerve has been recognized in athletes participating in numerous sports. Some of the activities previously associated with this injury include archery, backpacking, baseball, basketball, bowling, football, golf, gymnastics, hockey, rifle sports, shoveling, soccer, tennis, volleyball, weight lifting, and wrestling.26 The athlete may present with medial winging of the scapula during shoulder forward flexion but more often may note only vague shoulder pain or easy fatigability, especially with overhead activity. Onset of symptoms is often insidious but may be associated with trauma, often a result of depression of the shoulder girdle from a direct blow to the top of the shoulder or a traction injury to the arm.27 Symptom onset may follow the

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trauma by several weeks. Acute brachial neuritis should be considered when significant pain precedes the onset of dysfunction, as the long thoracic nerve is often involved in Parsonage-Turner syndrome. As with any complaint of shoulder pain or dysfunction, the physical examination should include evaluation of the cervical spine, shoulder, and extremity involved. Observation of the shoulder girdle may demonstrate medial winging of the scapula at rest. This involves medial and posterior translation of the inferior angle of the scapula (Fig. 29-10), which can be accentuated with resisted forward flexion of the shoulder, as demonstrated by the wall push-up. Forward flexion may be weak, and serratus anterior muscle atrophy may be noted in the thin, muscular patient. Scapular dyskinesia will be evident,28 with possible associated impingement symptoms. Relief of the impingement symptoms may be noted with stabilization of the medial scapular border by the examiner while testing forward flexion and abduction. Complete serratus anterior paralysis may limit forward flexion to 110 degrees.29 Confirmation of the diagnosis with EMG and NCV studies may useful to determine the severity of injury.

Relevant Anatomy and Pathophysiology The long thoracic nerve originates from the ventral rami of the C5, C6, and C7 cervical nerve roots. There are variable contributions from the intercostal nerves and, less frequently, the C8 cervical nerve root. The individual contributing roots variably pass through or between the middle and anterior scalene muscles, before joining and traveling anterior to the posterior scalene muscle. The nerve then travels deep to the clavicle and variably the first or second rib before exiting the thoracic wall in the midaxillary line. The nerve innervates the serratus anterior muscle slips. The serratus anterior muscle arises from the anterolateral surface of the first eight ribs and inserts into the medial scapular border, functioning to stabilize and protract the scapula during abduction or forward flexion of the shoulder. In sports, repetitive stretching of the nerve, as may occur in overhead activity, has been implicated in the dysfunction of the serratus anterior muscle.29 As with brachial plexus injuries, shoulder depression and contralateral neck bending may further contribute to neurapraxia of the long thoracic nerve. Compression from multiple locations along the nerve as well as direct trauma to the anterolateral chest wall may also contribute to injury.

Treatment Options As with many sports-related nerve injuries about the shoulder, conservative treatment should be the mainstay. The aggravating activity must be curtailed to allow recovery, which can be expected usually within 9 months.29 Application of a canvas brace may stabilize the scapula enough to prevent stretching of the serratus anterior during recovery but it is insufficient to allow full return to activity.30

Surgery

A

Surgical treatment of isolated long thoracic nerve injury is rarely necessary and is aimed at restoring scapular stability. For severe dysfunction of 6 months’ duration or longer, neurolysis may play a role.31 For refractory cases of longer than 12 to 24 months’ duration, transfer of the sternal head of the pectoralis major to the scapula has been shown to provide excellent restoration of scapular function.32 Scapulothoracic fusion may stabilize the scapula but has been shown to result in significantly decreased function.33

Criteria for Return to Sports Exercises to maintain range of motion should be instituted early, followed by progressive strengthening of the rotator cuff and periscapular muscles. Maintenance of motion is vital during the recovery period, with passive, active-assisted, and active rangeof-motion exercises playing a key role. Sport-specific rehabilitation begins when symptoms allow, usually within 6 months of injury. A maintenance program of rotator cuff and periscapular strengthening should be instituted, as with other shoulder injuries.

SPINAL ACCESSORY NERVE INJURY (LATERAL SCAPULAR WINGING) Clinical Features and Evaluation

B Figure 29-10 Photographs of patient with right long thoracic neuropathy demonstrating medial scapular winging, as seen from behind (A) and laterally (B).

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The diagnosis of an injury to the spinal accessory nerve in the athlete is often missed due to its rarity, thus potentially delaying its treatment.34 A history of surgery in the area of the posterior neck, such as a cervical lymph node biopsy, or of penetrating trauma may lead to consideration of the diagnosis.

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Blunt trauma to the posterior neck or traction may also result in injury to the accessory spinal nerve.35 The most common presentation is a painful shoulder or neck, especially with activities that involve using the involved extremity above eye level. Loss of motion or early fatigue may be a secondary complaint. The athlete may note shoulder asymmetry, and rotator cuff impingement symptoms are often present. Examination of the athlete with a spinal accessory nerve injury will reveal a depressed, or sagging, shoulder on the involved side. The supraclavicular recess may be relatively deepened due to trapezius atrophy. Lateral winging of the scapula, involving lateral rotation of the inferior scapular angle, may be elicited with resisted forward flexion but will not be as dramatic as the medial winging of long thoracic nerve palsy. Inability to elevate the acromion with a shoulder shrug may also indicate trapezius dysfunction. This may result in examination findings of rotator cuff tendonopathy. The levator scapulae and rhomboids may be prominent and palpable due to spasm in their effort to compensate for the weak trapezius. As with many nerve injuries about the shoulder, EMG and NCV studies may be useful in confirming the diagnosis and determining the severity of injury after 4 to 6 weeks of observation.

Relevant Anatomy and Pathophysiology The spinal accessory, or 11th cranial, nerve exits the skull through the jugular foramen, innervating the sternocleidomastoid and traveling across the posterior cervical triangle to innervate the trapezius. The trapezius arises from the ligamentum nuchae to the lower thoracic vertebrae and inserts into the lateral clavicle, the acromion, and the scapular spine. It functions to stabilize, elevate, and retract the scapula. The trapezius receives innervation not only from the spinal accessory nerve but also the ventral rami of the C2, C3, and C4 spinal nerve roots, possibly preventing complete denervation atrophy after accessory nerve injury. Scapulohumeral dyskinesia may result in depression of the acromion, with resultant subacromial impingement symptoms.

in patients with heavy demands on the shoulder. Prognosis for return to competitive athletic activity is very poor, however.

Criteria for Return to Sports Full functional return of trapezius strength is a prerequisite for return to vigorous overhead athletic activity. Many patients may be able to compensate for mild to moderate weakness of the nondominant shoulder, allowing adequate daily activity function and return to less demanding athletic activity. Although shoulder range of motion and strengthening exercises can maximize available function, it is unlikely that the other periscapular muscles can compensate for significant trapezius paralysis, especially if the dominant extremity is involved. Shoulder function may not be sufficient to allow return to competitive activity with persistent trapezius weakness, even after reconstructive surgery.36

MUSCULOCUTANEOUS NERVE INJURY Clinical Features and Evaluation Isolated musculocutaneous nerve injury in the athlete is rare. It has been reported in weight lifters37 and rowers38 and has been associated with strenuous, sustained physical activity. The athlete presents with paresthesias of the lateral forearm, with or without painless weakness of the biceps. The history may often reveal recent surgery to the anterior shoulder, or a direct blow to the anterior chest in the area of the coracoid. Rarely, history of a recent anterior glenohumeral dislocation may be elicited. The examination must differentiate between isolated musculocutaneous nerve dysfunction and injury to the brachial plexus or C5 or C6 nerve roots. Observation may reveal an atrophied or flaccid biceps, and reflex testing should demonstrate an absent biceps reflex with an intact brachioradialis reflex. The sensory changes will be isolated to the lateral and radial forearm, with sparing of the C6 dermatome of the radial hand. Relative weakness of elbow flexion and forearm supination may also be present.

Treatment Options The treatment of spinal accessory nerve injury depends on the mechanism history. A closed injury, either from a direct blow or trauma, can be observed for a minimum of 6 months. If the patient remains symptomatic with continued pain, sagging of the shoulder, or weakness on forward flexion, surgical exploration with neurolysis, direct repair, or nerve grafting can be considered, especially if EMG/NCV findings confirm dysfunction. In the face of penetrating or operative trauma to the nerve, consideration of surgical exploration should be given after 6 weeks, with the best results reported for surgical intervention within 6 months.34 It is imperative that shoulder range of motion be maintained during the observation period.

Surgery As stated previously, local surgical exploration may be beneficial with associated “open” trauma. When symptomatic trapezius weakness continues for more than 12 months, regardless of the injury mechanism, reconstructive surgical intervention should be considered. Tendon transfer procedures, most notably the EdenLange procedure with transfer of the levator scapulae and rhomboids, have a good prognosis for return of functional activities of daily living.36 Prognosis for return to sports, however, is less favorable. Scapulothoracic fusion is an acceptable salvage procedure and may be considered the primary reconstructive option

Relevant Anatomy and Pathophysiology The musculocutaneous nerve arises from the posterior cord of the brachial plexus, with contributions from the C5 and C6 nerve roots. It enters the coracobrachialis approximately 5 cm distal to the coracoid,13 although smaller branches may enter earlier. It then exits the tendon approximately 7 cm distal to the coracoid before entering the biceps and brachialis muscles, providing motor innervation to these.39 The nerve leaves the brachialis and enters the deep brachial fascia above the elbow crease to continue as the lateral antebrachial cutaneous nerve, providing sensory innervation to the anterolateral forearm. The most common mechanism of injury is associated with anterior shoulder surgery, usually due to vigorous medial retraction of the conjoined tendon near the coracoid, although anterior arthroscopic portal placement may also injure the nerve.40 This combined motor-sensory dysfunction may be differentiated from the isolated dysesthesias in the lateral forearm that may occur with compression of the musculocutaneous nerve as it enters the deep brachial fascial compartment at the elbow.

Treatment Options Since most injuries are related to stretching of the nerve, observation of the athlete for a period of 4 to 6 weeks usually results in evidence of recovery. However, continued weakness or

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paresthesias after 4 weeks can be further evaluated with EMG/NCV studies to determine the level and severity of injury.

specific activity, modification of the athlete’s mechanics may be necessary to prevent recurrence.

Surgery If clinical and/or electrophysiologic recovery is not noted, surgical exploration within the first 6 months after injury may be indicated. Surgical treatment may include decompression, neurolysis, and nerve grafting or may include nerve transfer using branches of the proximal ulnar nerve. For cases evaluated more than 1 year after injury, tendon transfer procedures may be indicated to supplement weak elbow flexion.

Criteria for Return to Sports Return to sports-related activity should be customized to the individual athlete. The prognosis for return of full function after postsurgical traction injury or direct blow trauma to the nerve is good, and athletic participation can be allowed. However, if the nerve injury is associated with repetitive or sustained sport-

CONCLUSIONS An athlete presenting with pain about the shoulder can pose a significant diagnostic challenge to the athletic medical staff. The etiologies of the symptoms vary from minor to career ending. The examination of the athlete includes a detailed examination of the spine, shoulder, and upper extremity, and nerve injuries must be considered in the wide differential diagnosis. A thorough understanding of the presentation, anatomy, and pathophysiology of nerve injuries about the shoulder of the athlete is imperative for accurate and timely diagnosis and treatment. Prompt management of both bony and soft-tissue injuries may prevent or minimize the long-term impact of these injuries on the athlete.

REFERENCES 1. Seddon JH: Surgical Disorders of the Peripheral Nerves. Baltimore, Williams & Wilkins, 1972. 2. Sunderland S: The anatomy and physiology of nerve injury. Muscle Nerve 1990;13:771–784. 3. Clancy WG Jr, Brand RL, Bergfield JA: Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 1977;5:209–216. 4. Markey KL, Di Benedetto M, Curl WW: Upper trunk brachial plexopathy. The stinger syndrome. Am J Sports Med 1993;21:650– 655. 5. Bateman JE: Nerve injuries about the shoulder in sports. J Bone Joint Surg Am 1967;49:785–792. 6. Meyer SA, Schulte KR, Callaghan JJ, et al: Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 1994;22: 158–166. 7. Levitz CL, Reilly PJ, Torg JS: The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am J Sports Med 1997;25:73–76. 8. Torg JS, Naranja RJ Jr, Palov H, et al: The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. J Bone Joint Surg Am 1996;78:1308–1314. 9. Brigham CD, Warren R: Head to head on spear tackler’s spine: Criteria and implications for return to play. J Bone Joint Surg Am 2003;85:381–383. 10. Martin SD, Warren RF, Martin TL, et al: Suprascapular neuropathy. Results of non-operative treatment. J Bone Joint Surg Am 1997;79: 1159–1165. 11. Shabas D, Scheiber M: Suprascapular neuropathy related to the use of crutches. Am J Phys Med 1986;65:298–300. 12. Holzgraefe M, Kukowski B, Eggert S: Prevalence of latent and manifest suprascapular neuropathy in high-performance volleyball players. Br J Sports Med 1994;28:177–179. 13. Post M: Diagnosis and treatment of suprascapular nerve entrapment. Clin Orthop 1999;368:92–100. 14. Ajmani ML: The cutaneous branch of the human suprascapular nerve. J Anat 1994;185:439–442. 15. Plancher KD, Peterson RK, Johnston JC, et al: The spinoglenoid ligament. Anatomy, morphology, and histological findings. J Bone Joint Surg Am 2005;87:361–365. 16. Warner JP, Krushell RJ, Masquelet A, et al: Anatomy and relationships of the suprascapular nerve: Anatomical constraints to mobilization of the supraspinatus and infraspinatus muscles in the management of massive rotator-cuff tears. J Bone Joint Surg Am 1992;74:36–45.

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17. Antoniou J, Tae SK, Williams GR, et al: Suprascapular neuropathy. Variability in the diagnosis, treatment, and outcome. Clin Orthop 2001;386:131–138. 18. Zehetgruber H, Noske H, Lang T, et al: Suprascapular nerve entrapment. A meta-analysis. Int Orthop 2002;26:339–343. 19. Ringel SP, Treihaft M, Carry M, et al: Suprascapular neuropathy in pitchers. Am J Sports Med 1990;18:80–86. 20. Perlmutter GS, Apruzzese W: Axillary nerve injuries in contact sports: Recommendations for treatment and rehabilitation. Sports Med 1998; 26:351–361. 21. Perlmutter GS, Leffert RD, Zarins B: Direct injury to the axillary nerve in athletes playing contact sports. Am J Sports Med 1997;25:65– 68. 22. Cahill BR, Palmer RE: Quadrilateral space syndrome. J Hand Surg [Am] 1983;8:65–69. 23. Mochizuki T, Isoda H, Masui T, et al: Occlusion of the posterior humeral circumflex artery: Detection with MR angiography in healthy volunteers and in a patient with quadrilateral space syndrome. AJR Am J Roentgenol 1994;163:625–627. 24. Price MR, Tillett ED, Acland RD, et al: Determining the relationship of the axillary nerve to the shoulder joint capsule from an arthroscopic perspective. J Bone Joint Surg Am 2004;86:2135–2142. 25. Lester B, Jeong GK, Weiland AJ, et al: Quadrilateral space syndrome: Diagnosis, pathology, and treatment. Am J Orthop 1999;28:718–722, 725. 26. Mendoza FX, Main WK: Peripheral nerve injuries of the shoulder in the athlete. Clin Sports Med 1990;9:331–342. 27. Warner JJ, Navarro RA: Serratus anterior dysfunction. Recognition and treatment. Clin Orthop 1998;349:139–148. 28. Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 2003;11:142–151. 29. Gregg JR, Labosky D, Harty M, et al: Serratus anterior paralysis in the young athlete. J Bone Joint Surg Am 1979;61:825–832. 30. Marin R: Scapula winger’s brace: A case series on the management of long thoracic nerve palsy. Arch Phys Med Rehabil 1998;79:1226– 1230. 31. Disa JJ, Wang B, Dellon AL: Correction of scapular winging by supraclavicular neurolysis of the long thoracic nerve. J Reconstr Microsurg 2001;17:79–84. 32. Connor PM, Yamaguchi K, Manifold SG, et al: Split pectoralis major transfer for serratus anterior palsy. Clin Orthop 1997;341:134–142. 33. Bunch WH, Siegel IM: Scapulothoracic arthrodesis in facioscapulohumeral muscular dystrophy. Review of seventeen procedures with

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three to twenty-one-year follow-up. J Bone Joint Surg Am 1993; 75:372–376. 34. Kretschmer T, Antoniadis G, Braun V, et al: Evaluation of iatrogenic lesions in 722 surgically treated cases of peripheral nerve trauma. J Neurosurg 2001;94:905–912. 35. Cohn BT, Brahms MA, Cohn M: Injury to the eleventh cranial nerve in a high school wrestler. Orthop Rev 1986;15:590–595. 36. Bigliani LU, Compito CA, Duralde XA, et al: Transfer of the levator scapulae, rhomboid major, and rhomboid minor for paralysis of the trapezius. J Bone Joint Surg Am 1996;78:1534–1540.

37. Braddom RL, Wolfe C: Musculocutaneous nerve injury after heavy exercise. Arch Phys Med Rehabil 1978;59:290–293. 38. Mastaglia FL: Musculocutaneous neuropathy after strenuous physical activity. Med J Aust 1986;145:153–154. 39. Flatow EL, Bigliani LU, April EW: An anatomic study of the musculocutaneous nerve and its relationship to the coracoid process. Clin Orthop 1989;244:166–171. 40. Speer KP, Bassett FH 3rd: The prolonged burner syndrome. Am J Sports Med 1990;18:591–594.

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Traumatic Shoulder Muscle Ruptures Christopher C. Dodson and Riley J. Williams III

In This Chapter Pectoralis major rupture Surgery—pectoralis repair Subcapularis rupture Surgery—subscapularis repair

INTRODUCTION • Traumatic muscle ruptures about the shoulder girdle are rare. However, these injuries do occur and are typically avulsion injuries to either the pectoralis major or rotator cuff muscles. • Rupture of one of these muscles can lead to substantial functional disability. • Pectoralis major ruptures most commonly occur during weight-lifting activities and in response to external trauma, such as during high-impact contact sports. • Isolated subscapularis tendon tears are relatively rare and usually occur in conjunction with other injuries about the shoulder. • The purpose of this chapter is to review the relevant anatomy, presentation, and management of traumatic muscle injuries of the pectoralis major and subscapularis muscles.

RUPTURE OF THE PECTORALIS MAJOR Relevant Anatomy The pectoralis major is a triangle-shaped muscle that arises from the clavicle, sternum, ribs, and external oblique fascia (Fig. 301). The muscle has two heads: clavicular and sternal. As these various origins converge to their insertion at the lateral aspect of the bicipital groove, the muscle twists. Ultimately, the superior fibers insert distally and the inferior fibers insert proximally. These fibers terminate in a flat tendon that is approximately 4 to 5 cm wide. This tendon consists of two laminae, one anterior to the other. The main function of the pectoralis major is to adduct and internally rotate the humerus. The pectoralis major is innervated by the medial (C8–T1) and lateral (C5–C7) pectoral nerves; the muscle receives its blood supply from the pectoral branch of the axillary artery.

Clinical Features and Evaluation Rupture of the pectoralis major is a relatively rare injury; approximately 200 case outcomes have been described in the

literature.1–3 Few of these reports have more than 20 patients, and to date, there have been no prospective studies that have examined clinical outcomes following surgical repair. The first case report dates back to 1822 and was described by Patissier.4 Most patients sustain a rupture of the pectoralis major while participating in sports. Weight lifting is the most common activity associated with acute pectoralis tendon rupture. Other sports, including football, rugby, wrestling, rodeo riding, and windsurfing have also been reported to have caused pectoralis tendon injury.5 The injury usually occurs in skeletally mature males in the third, fourth, and fifth decades of life; there have been no cases reported in a female. Pectoralis major ruptures are classified as complete or incomplete and usually involve the humeral attachment of either the sternal or clavicular head. Most cases reports describe a complete rupture in an individual participating in athletics. Incomplete tears or complete tears involving the musculotendinous junction or muscle belly have also been reported.6 Patients with an acute tear of the pectoralis major often present with some inciting event, whether it be weight lifting or a direct blow to the chest. Many patients will report an audible pop and pain that is described as tearing or burning in nature. In most cases, an immediate disability is noted. As most reported cases are associated with bench pressing, the mechanism of injury is thought to be indirect. A forceful eccentric muscle contraction of the pectoralis major muscle in response to a large, acutely applied load results in the muscle injury. Incomplete or complete tears that involve the muscle belly or musculotendinous junction can also be caused by eccentric muscle contraction, but can also occur following direct trauma to the chest wall. Avulsion injuries of the clavicular and sternal heads may also occur in older individuals.7

Physical Examination A complete physical examination is essential in evaluating patients who are suspected of having a pectoralis major rupture. The patient is examined with a bare chest; symmetry between the two pectoralis muscle bellies is assessed. Patients will often present with a splinted ipsilateral upper extremity often supported by the opposite hand. Ecchymosis may be present in the axilla on the affected side. Physical examination usually demonstrates an obvious defect in the anterior axillary border. Acutely, it can be very difficult to distinguish between complete and incomplete tears because of the local swelling, edema, and ecchymosis in the upper thorax and axillary area. In subacute or chronic injuries, complete tears will often have a bulge where the muscle belly has retracted, a characteristic webbed appearance of the axillary fold, and obvious cosmetic deformity (Fig. 30-2). These findings can be accentuated by having the

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Figure 30-3 Magnetic resonance image demonstrating avulsion of the pectoralis muscle tendon off the humeral insertion (arrow).

Figure 30-1 Anatomic drawing of the pectoralis major muscle demonstrating its origins from the clavicle and sternum and its insertion onto the humerus.

patient actively contract the muscle by placing both arms in the forward flexed position and having the patient press his or her palms together in front of the abdomen. A great deal of discomfort with minimal movement about the shoulder is present and weakness is noted when the patient tries to adduct and internally rotate the shoulder.

Treatment Options

Radiographs of the chest (posteroanterior, lateral) and shoulder (anteroposterior, axillary) should be obtained as bony avulsion

Distinguishing between incomplete and complete tears, as well as the location of the tear, is crucial. Most authors agree that partial ruptures of the pectoralis major tendon and intramuscular strain or crush injuries can be successfully treated without surgery. These injuries typically have less pain, swelling, and

Figure 30-2 A patient with an acute pectoralis major muscle rupture. Notice the webbed appearance of the axillary fold on the right side.

Figure 30-4 Axial magnetic resonance image demonstrating avulsion of the pectoralis muscle tendon off the humeral insertion (hatch marks).

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type fractures involving the proximal humerus can occur. Typically, radiographs are without significant findings. Magnetic resonance imaging is the gold standard diagnostic imaging modality in detecting pectoralis muscle injury. Connell et al8 found magnetic resonance imaging to be optimal in evaluating the location, size, and degree of the tear Acute injuries often show a high signal intensity near the humeral cortex, due to periosteal stripping off the humerus as the tendon is avulsed from its insertion9 (Figs. 30-3 and 30-4). Chronic injuries are more associated with muscle retraction and dense scarring at the lateral border of the pectoralis major.

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ecchymosis and lack the physical examination characteristics that were previously outlined. Initial management should consist of rest, cryotherapy, and sling wear; activity is increased according to patient tolerance. For the most part, these injuries heal without a significant strength loss. It is important to stress the idea of gradual rehabilitation and patients often will not return to heavy lifting for at least 8 to 12 weeks. Both surgical and nonsurgical approaches have been described in the literature for the treatment of complete rupture of the pectoralis major. Nonsurgical management of complete tears is usually applied in those cases in which an intramuscular injury has occurred. Complete tears of the pectoralis tendon are generally managed operatively. Park and Espiniella10 reviewed 29 patients and found that only 58% of patients with rupture of the pectoralis major tendon treated by nonoperative means had good results, while nearly 90% in the same series had good to excellent results after surgery. Other studies have also shown poor results after nonoperative management.11 The goal of surgery is to restore strength, function, and cosmesis. The authors recommend operative repair of the pectoralis major for the active patient who wishes to return to his or her previous level of function; this includes participation in sport. It is clear that the clinical results after surgery are significantly better than those that follow nonoperative treatment. We also recommend surgery for patients who are not satisfied with their function despite extensive rehabilitation.

Surgical Technique: Pectoralis Tendon Repair Patients indicated for pectoralis tendon repair are positioned in the supine position, with the torso flexed to approximately 45 degrees. Regional anesthesia (interscalene block) is used and should be supplemented with local anesthetic injections at the inferior-most portion of the wound. Following a full prepping and sterile draping of the operative arm, a deltopectoral approach is used. The cephalic vein should be identified and spared if possible. A deep retractor is placed beneath the distal deltoid to facilitate visualization of the humeral insertion of the pectoralis major. The lateral free tendon end is identified and retracted. The muscle belly should be mobilized and freed from any adhesions or residual hematoma. The humeral insertion of the pectoralis lies just lateral to the biceps tendon. The authors’ preferred approach uses suture anchors for fixation of the damaged tendon to the humerus. Alternatively, a bone trough can be fashioned and used to reinsert the torn pectoral tendon (Figs. 30-5 through 30-7). Pectoralis repair is preferable in the acute setting, but repair up to 2 years following injury has been described. Chronic cases occasionally require tendon reconstruction with autograft or allograft tissue. This tissue is woven into the distal muscle and sutured in place, and repair to bone is accomplished as described previously, with suture anchors or a bone trough.

Postoperative Rehabilitation Patients are kept in a sling for approximately 6 weeks. Passive range-of-motion exercises, including pendulum and Codman exercises, are started immediately. Patients are encouraged to begin active elbow, wrist, and hand exercises immediately following the surgical repair. Isometric abduction and external rotation exercises are employed during this early phase. At 6 weeks after surgery, active, active-assisted, and terminal end range stretch passive range-of-motion exercises are begun. At this point, the patient may start to use the extremity for activities of daily living. A weight limit of 20 pounds is suggested for

the operative extremity through the first 12 weeks following surgery. Progressive upper extremity strengthening begins in earnest at 6 weeks postoperatively. In general, most patients are cleared for noncontact sports at 4 months; avid weight lifters and contact athletes are held from full participation for 6 months.

Results and Outcomes In general, because pectoralis major ruptures typically occur in young athletic patients, most surgeons advocate surgical repair in order to regain strength and optimal function. Several studies have shown the advantages of surgical intervention. Wolfe et al12 found that surgically treated patients showed comparable torque and work measurements, while conservatively treated individuals demonstrated a marked deficit in both peak torque and work repetition. Schepsis et al13 retrospectively reviewed 17 patients with distal pectoralis major rupture to compare acute and chronic injuries as well as conservative versus operative management. Both subjective and objective results were better in the acute group versus the chronic group, and these patients fared significantly better than patients treated nonoperatively.

RUPTURE OF THE SUBSCAPULARIS TENDON Relevant Anatomy The subscapularis arises from the deep surface of the scapula anteriorly and its broad tendon inserts onto the lesser tuberosity of the humeral head (Fig. 30-8). It also acts as a dynamic stabilizer of the shoulder. It is one of the four rotator cuff muscles and is the only one that is an internal rotator of the shoulder. The subscapularis forms the upper border of the quadrangular space, which contains the axillary nerve and posterior humeral circumflex artery.

Clinical Features and Evaluation Isolated subscapularis muscle tears are uncommon. However, these are significant injuries because they are often difficult to diagnose and can lead to prolonged disability. These injuries typically occur in an older population, although younger patients are more commonly affected in the traumatic setting. The exact mechanism of injury is poorly described in the literature, but it is thought that the typically affected patient falls on an outstretched arm or experiences a traumatic external rotation of an adducted arm. Deutsch et al14 described a series of 14 shoulders in 13 patients with surgically confirmed isolated subscapularis tears and found that the injuries were a result of violent, traumatic events such as falls, direct blows, or forceful boxing punches. Traumatic hyperextension or external rotation accounted for 11 of the 14 injuries. Most patients will present with pain, swelling, and disability about the affected shoulder joint. It is important to do a thorough physical examination, looking for other injuries because, as described previously, these injuries are rarely isolated. Weakness of internal rotation along with increased passive external rotation is present. There are a number of tests that are applicable in both diagnosing isolated tears as well as other associated injuries. Gerber et al15 described a “lift-off ” test that is performed by bringing the arm passively behind the body into maximum internal rotation away from the small of the back. If the patient is able to maintain the internal rotation, the test is negative for subscapularis rupture. If the patient cannot maintain maximal internal rotation and the hand drops straight back,

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Figure 30-5 A–C, The classic pectoralis tendon repair technique. The tendon is mobilized and tagged with several nonabsorbable sutures that are then used to attach the ruptured tendon to the humerus, using a bone trough medially and drill holes laterally.

A

B

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Figure 30-6 A–C, The authors’ preferred technique of pectoralis tendon repair. This method requires a preparation of a bony bed at the humeral insertion using a bur followed by tendon attachment to bone using double-loaded suture anchors.

A

B

C

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Figure 30-7 Intraoperative photograph demonstrating mobilization of the ruptured pectoralis tendon.

then the test is considered positive. If the resistance is weak and the hand drops back more than 5 degrees but not all the way to the spine, it is called a weak test. In the study by Gerber et al15 of 16 patients, 13 tests were positive and three were weak. In the same report, they also describe a “belly press test” for instances in which the patient cannot get the hand behind the back to perform the lift-off test. In the belly press test, the patient sits upright and presses the abdomen with the hand flat and attempts to keep the arm in maximum internal rotation. If active internal rotation is strong, the elbow stays in front of the trunk (Fig. 30-9A). If the function of the

A

B Figure 30-9 A, Belly press test as described by Gerber et al.15 The patient in this figure has a negative test. Active internal rotation by the subscapularis is intact; thus, the elbow remains anterior to the patient’s torso during the test. B, Positive belly press test. The injured subscapularis cannot internally rotate the humerus during the maneuver; thus, the elbow falls posterior to the torso.

Figure 30-8 Anatomy drawing of the subscapularis muscle demonstrating its origin and insertion.

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subscapularis is impaired, then, the elbow falls behind the trunk (Fig. 30-9B). The patient exerts pressure on the abdomen by extension of the shoulder. This test was positive for all eight patients with complete subscapularis tears for whom the study was performed.

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Figure 30-10 Axial magnetic resonance imaging demonstrating an acute subscapularis tear.

Lesions of the biceps tendon have been reported in the traumatic setting of subscapularis tears. The Speed test and Yergason test may be helpful in diagnosing bicipital subluxation or dislocation in the setting of a subscapularis tear. Anterior instability can also be associated with subscapularis tears and can be diagnosed clinically by the apprehension test. Most reported cases of subscapularis tears are associated with supraspinatus tears. We cannot overemphasize the importance of a complete physical examination of the shoulder, even when a diagnosis seems apparent. Plain radiographs including anteroposterior, lateral, and axillary views of the shoulder will usually not be helpful in diagnosing isolated subscapularis tears. However, they can be crucial in diagnosing avulsion fractures of the lesser tuberosity, subacromial pathology, and dislocation when present. Magnetic resonance imaging is the gold-standard imaging modality in confirming this diagnosis. Deutsch et al14 emphasized the importance of high-contrast axial plane images that permit visualization of the subscapularis tendon as it inserts onto the lesser tuberosity, as well as the appearance of the long head of the biceps tendon in the bicipital groove. When the biceps tendon is dislocated medially out of its groove, this is nearly pathognomonic for subscapularis injury. Axial magnetic resonance imaging of the shoulder demonstrating an acute subscapularis tear is shown in Figure 30-10. The normal insertion onto the lesser tuberosity is completely disrupted.

block) is used and should be supplemented with local anesthetic injections at the inferior-most portion of the wound. An arm holder is used for upper extremity positioning. Following a full prepping and sterile draping of the operative arm, a deltopectoral approach is used. The cephalic vein should be identified and retracted. A deep retractor is placed beneath the deltoid laterally and the pectoralis tendon medially to facilitate visualization of the anterior shoulder. The subdeltoid bursa and hematoma are removed. The ruptured lateral free edger of the subscapularis tendon should be within the field of view. If the tendon is not immediately visualized, the surgeon should carefully dissect medially along the glenoid neck, posterior to the conjoined tendon and inferior to the coracoid process. Once the tendon has been identified and tagged, the muscle is mobilized to ensure that the lateral tendon edge reaches the lesser tuberosity of the humerus (Fig. 30-11). The lesser tuberosity is gently prepared using a bur; suture anchors are used to reattach the free subscapularis tendon to the lesser tuberosity. The rotator interval should also be closed using nonabsorbable sutures. Alternatively, subscapularis repair can be performed arthroscopically. The method is similar. Suture anchors are placed in the lesser tuberosity, the tendon is mobilized, the sutures are passed through the tendon, and arthroscopic knots are tied.

Postoperative Rehabilitation Patients are kept in a sling for approximately 6 weeks. Passive range-of-motion exercises, including pendulum and Codman’s exercises are started immediately. Patients are encouraged to begin active elbow, wrist, and hand exercises immediately following the surgical repair. Isometric abduction and external rotation exercises are employed during this early phase. While passive internal rotation can also be started immediately, no active range-of-motion exercises are started until 6 weeks following surgery. At 6 weeks after surgery, active, active-assisted, and terminal end range stretch passive range-of-motion exercises are begun. At this point, the patient may start to use the extremity for activities of daily living. A weight limit of 20 pounds is suggested for the operative extremity through the first 12 weeks following surgery. Progressive upper extremity strengthening begins in earnest at 6 weeks postoperatively.

Treatment Options When diagnosing a subscapularis tear, it is important to distinguish between isolated tears and tears associated with other injuries. When tears occur in conjunction with anterior instability, the subscapularis should be repaired during anterior stabilization. Tears associated with lesser tuberosity avulsions, biceps tendon subluxation or dislocation, and other injuries to the rotator cuff also require treatment of all injured structures. There are no reports describing conservative management of symptomatic isolated tears. We recommend primary repair of all isolated injuries.

Surgical Technique: Subscapularis Repair Patients indicated for subscapularis tendon repair are positioned in the beach chair position. Regional anesthesia (interscalene

Figure 30-11 Intraoperative photograph demonstrating mobilization of the subscapularis before reinsertion on the lesser tuberosity.

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Results and Outcomes The management of isolated traumatic subscapularis tears has only been addressed in a few studies, most of which are limited by the number of patients. Gerber et al15 reported on 16 patients treated surgically and found that 82% of the patients assessed their postoperative functional shoulder score as good and that the capacity of the patients to work in their original occupation had increased from 59% preoperatively to 95% postoperatively.

In the study by Deutsch et al,14 with an average follow-up of 2 years, an improvement in preoperative symptoms, including pain with activities of daily living, pain with attempted sports activities, and weakness of the extremity was reported in 100% of the shoulders tested. All patients returned to their previous employment, and 12 of 13 patients returned to their previous sports activities. Other authors have also reported favorable results after operative treatment.16–18

REFERENCES 1. Bak K, Cameron EA, Henderson IJ: Rupture of the pectoralis major: A meta-analysis of 112 cases. Knee Surg Sports Traumatol Arthrosc 2000;8:113–119. 2. Kretzler HH, Richardson AB: Rupture of the pectoralis major muscle. Am J Sports Med 1989;17:453–458. 3. McEntire JE, Hess WE, Coleman SS: Rupture of the pectoralis major muscle. J Bone Joint Surg (Am) 1972;54:1040–1046. 4. Patissier P: Traite des Maladies des Artisans. Paris, 1822, pp 162–165. 5. Dunkelman NR, Collier F, Rook JL, et al: Pectoralis major muscle rupture in windsurfing. Arch Phys Med Rehabil 1994;75:819–821. 6. Zeman SC, Rosenfeld RT, Lipscomb PR: Tears of the pectoralis major muscle. Am J Sports Med 1979;7:343–347. 7. Berson BL: Surgical repair of pectoralis major rupture in an athlete. Am J Sports Med 1979;7:348–351. 8. Connell DA, Potter HG, Sherman MF, et al: Injuries of the pectoralis major muscle: Evaluation with MR imaging. Radiology 1999;210: 785–791. 9. Shubin Stein BE, Potter HG, Wickiewicz TL: Repair of chronic pectoralis major ruptures. Tech Shoulder Elbow Surg 2002;3:174–179. 10. Park JY, Espiniella JL: Rupture of pectoralis major muscle: A case report and review of the literature. J Bone Joint Surg (Am) 1970;52:577–581.

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11. Liu J, Wu JJ, Chang Cy, et al: Avulsion of the pectoralis major tendon. Am J Sports Med 1992;20:366–368. 12. Wolfe SW, Wickiewicz TL, Cavanaugh JT: Ruptures of the pectoralis major muscle: An anatomic and clinical analysis. Am J Sports Med 1992;20:587–593. 13. Schepsis AA, Grafe MW, Jones HP, et al: Rupture of the pectoralis major muscle: Outcome after repair of acute and chronic injuries. Am J Sports Med 2000;28:9–15. 14. Deutsch A, Altchek DW, Veltri DM, et al: Traumatic tears of the subscapularis tendon: Clinical diagnosis, MRI findings, and operative treatment. Am J Sports Med 1997;25:13–22. 15. Gerber C, Hersche O, Farron A: Isolated rupture of the subscapularis tendon: Results of operative repair. J Bone Joint Surg Am 1996;78: 1015–1023. 16. Gerber C, Krushell RJ: Isolated ruptures of the tendon of the subscapularis muscle. J Bone Joint Surg Br 1991;73:389–394. 17. McAuliffe TB, Dowd GS: Avulsion of the subscapularis tendon: A case report. J Bone Joint Surg 1987;69:1454–1455. 18. Edwards TB, Walch G, Sirraux F, et al: Repair of tears of the subscapularis. J Bone Joint Surg Am 2005; 87:725–730.

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Pediatric Shoulder T. Bradley Edwards and K. Mathew Warnock

In This Chapter Clavicle fracture Proximal humerus fracture Glenohumeral dislocation/instability Acromioclavicular (AC) and sternoclavicular (SC) dislocation/instability Little leaguer’s shoulder Internal impingement Scapular winging

INTRODUCTION • Although once considered rare, increasing participation of children in sports has increased the frequency of pediatric shoulder injuries. • The majority of pediatric shoulder injuries involve fractures of the shoulder girdle, both physeal and extraphyseal. • The increasing level of competition within organized pediatric athletics, however, has led to a rise in the occurrence of overuse-type injuries. • Most pediatric shoulder problems, whether traumatic or related to overuse, can be successfully treated nonoperatively.

RELEVANT ANATOMY AND PHYSIOLOGY The principal anatomic factor differentiating pediatric shoulder injuries from adult shoulder injuries is the presence of open physes. The proximal humerus is formed by the coalescence of three ossification centers (humeral head, greater tuberosity, lesser tuberosity) occurring between 5 and 7 years of age. The remaining proximal humeral physis between the epiphysis and metaphysis contributes 80% of the longitudinal growth to the humerus and completely closes between 19 and 22 years of age.1 The proximal humeral physis is commonly involved in both traumatic and overuse pediatric shoulder injuries. The clavicle, one of the most frequently fractured bones in childhood, forms via intramembranous ossification. The medial physis of the clavicle is the last to fuse in the body between 22 and 27 years of age and provides 80% of the longitudinal growth of the clavicle.1 The scapula is similarly formed by intramembranous ossification and is largely protected from injury during sports participation by its close proximity to the thorax and protective muscular covering. Physeal biomechanics play a role in the type of injuries observed in pediatric athletes. In early childhood, the cartilagi-

nous nature of the physis protects the ossified portions of the bone by helping absorb forces. When this absorptive capacity is overcome, residual forces are transmitted to the metaphysis resulting in a torus type fracture. In later childhood, the resiliency of the physis is reduced, and, by virtue of its relative biomechanical weakness, the physis becomes the most likely site of fracture.1 The physis is susceptible to not only acute fracture, but also stress fracture from overuse. The soft tissues of the shoulder girdle are grossly identical to those observed in adults. In our experience, we have noted, however, that the amount of physiologic laxity present in children exceeds that observed in adults. This observation becomes important when evaluating a patient for glenohumeral instability, particularly when evaluating pediatric patients with multidirectional hyperlaxity. As these patients complete adolescence, much of this hyperlaxity will resolve, in many cases resulting in resolution of shoulder symptoms.

RELEVANT BIOMECHANICS The biomechanics of throwing are well described and have been divided into wind-up, cocking, acceleration, and followthrough.2 Large forces are generated during throwing with peak angular velocity rates exceeding 7000 degrees per second occurring during the acceleration phase.3 The forces generated during throwing have unique implications in the immature athlete. The effects of competitive throwing on a skeletally immature proximal humerus are usually adaptive and protective but in some cases become pathologic. As the arm enters late cocking and transitions to early acceleration, a large external rotation torsional moment is placed on the arm. As the soft tissues of the shoulder (rotator cuff, capsuloligamentous structures) reach maximal limits of external rotation, the remaining forces are transmitted to the humerus. These torsional forces preferentially affect the weaker physis. With repetitive throwing, these forces result in an adaptive and protective remodeling of the proximal humerus. Previously, throwers were thought to have increased external rotation and decreased internal rotation in their dominant shoulder as a result of lax anterior soft tissue and a tight posterior capsule. More recently, however, it has been recognized that osseous change in the form of increased humeral retroversion is largely responsible for this phenomenon.4 The torsional forces occurring with repetitive throwing introduce remodeling of the proximal humerus through the open physis resulting in more humeral retroversion (Fig. 31-1). This remodeling provides two benefits. First, increased external rotation is advantageous to pitching mechanics, allowing for greater throwing velocity. Second, increased humeral retroversion effectively moves the

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FRACTURES, DISLOCATIONS, AND INSTABILITY Clavicle Fractures Clavicle fractures are among the most common injuries observed in childhood sports. These injuries usually result from a fall onto the shoulder during activity. These fractures most often occur in the midshaft of the clavicle but may also be observed at the terminal portions of the bone. Clinical Features and Evaluation Pain, swelling, and deformity are the common presenting features of a clavicle fracture. Physical examination of the shoulder girdle is usually limited by pain in the acute setting. Particular attention is paid to skin and soft tissues overlying the area of injury to ensure that fracture fragments do not jeopardize these structures. Additionally, a thorough neurovascular examination is performed to evaluate for compromise caused by displaced fracture fragments. Physical examination is always followed by radiographic examination of the clavicle. In cases with midshaft deformity, a simple anterior posterior radiograph of the clavicle is sufficient. In cases with lateral deformity, a 20-degree cephalic tilt acromioclavicular joint view is added.1 In cases with medial deformity, a sternoclavicular joint view is added (serendipity view).1 Fractures of the medial and lateral clavicle most commonly occur through the physis and may appear radiographically as a dislocation of the sternoclavicular or acromioclavicular joints. In cases of medial clavicle fractures presenting with signs of neurovascular compromise, difficulties breathing or swallowing, or posterior displacement on plain radiography, computed tomography should be performed as part of the evaluation. Figure 31-1 The torsional forces occurring with repetitive throwing introduce remodeling of the proximal humerus through the open physis resulting in more humeral retroversion.

greater tuberosity further away from the posterior superior glenoid rim, minimizing the mechanical contact now referred to as internal impingement (Fig. 31-2). Unrestricted throwing by skeletally immature patients may create a pathologic effect. The repetitive forces acting on the physis may cause what is effectively a stress fracture. This phenomenon has been well described and tagged with the moniker “little leaguer’s shoulder.”5

Figure 31-2 Increased humeral retroversion effectively moves the greater tuberosity further away from the posterior superior glenoid rim minimizing the mechanical contact now referred to as internal impingement.

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Treatment and Results Treatment of clavicle fractures in pediatric patients is largely nonoperative. Clavicle fractures generally do not require reduction because of the remarkable ability to remodel in the pediatric and adolescent age group. Children up to age 17 years have shown the ability to remodel clavicle fractures with as much as 90 degrees of angulation and as much as 4 cm of overlap.6 The vast majority of middle third clavicle fractures are best treated nonoperatively. Nonoperative treatment of clavicle fractures in the pediatric age group is sling immobilization. Reduction maneuvers are seldom necessary or helpful. Figure-eight strapping is often uncomfortable and unnecessary. Shortening and malunion generally do not occur in children, and the clinical results are usually excellent, with most fractures healing successfully with nonoperative treatment (Fig. 31-3). In the skeletally immature patient, operative management is indicated in open fractures or when the clavicle impinges on the subclavian vessels or brachial plexus causing neurologic or vascular compromise. “Floating shoulder,” a concomitant fracture of the clavicle and scapula, is a relative indication for operative management; however, this severe injury is very rare in childhood athletics, only occurring with severe trauma such as might be seen in junior motor cross. Occasionally, in adolescents who are approaching or who have reached skeletal maturity, operative management is indicated. These patients often have comminuted fractures or large butterfly fragments, and many have considerable shortening of the clavicle. Highly competitive athletes nearing skeletal maturity, especially those who use their arm for overhead sports or throwing, may benefit from open reduction and internal fixation.

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Generally, results of treatment of clavicle fractures in children are excellent without residual dysfunction.

Proximal Humerus Fractures Proximal humeral fractures in children are relatively common and may involve the growth plate or be strictly metaphyseal. Most of these fractures occur as a result of a fall during activity, although rarely insignificant trauma will cause a proximal humeral fracture through a preexisting benign bone cyst. Physeal fractures with varus displacement have been reported in skeletally immature gymnasts.7 Proximal humeral physeal fractures have tremendous remodeling potential. This fact combined with a wide arc of shoulder motion allows for good shoulder function despite significant fracture displacement.

A

B Figure 31-3 A, Displaced midshaft clavicle fracture in a skeletally immature patient. B, Complete healing of the fracture 6 weeks later.

Medial clavicle fractures are usually physeal injuries that successfully remodel in pediatric patients. The best treatment for these injuries is nonoperative. Patients with a posteriorly displaced medial clavicle fracture who have difficulty swallowing or breathing or signs of neurovascular compromise may require operative reduction. Operative reduction is performed under general anesthesia in the operating room with a thoracic surgeon available in case of vascular complications. The distal clavicle, like the medial clavicle, has tremendous potential for remodeling. Most pediatric distal clavicle fractures can be treated nonoperatively. Some distal clavicle injuries in children are, however, actually periosteal sleeve avulsion injuries.1 In these injuries, the lateral clavicle rips through the thick periosteal sleeve that surrounds the distal clavicle. The acromioclavicular and coracoclavicular ligaments are strongly attached to the periosteum of the distal clavicle. In cases of severe displacement, management involves operative reduction, placing the clavicle back into the thick periosteal sleeve, and repairing the periosteum with sutures. Rehabilitation after clavicle fracture should begin as soon as pain permits. Initially, pendulum exercises are begun followed by isometric exercises of the triceps, biceps, deltoid, and rotator cuff muscles. Normal activities of daily living are permitted, and active range of shoulder motion is begun 4 to 6 weeks after injury. Strengthening begins when there is radiographic evidence of healing and the patient has regained full range of shoulder motion. When strength has returned to normal, a return to noncontact sports is permitted. Contact sports are permitted when there is adequate radiographic and clinical evidence of healing and sufficient remodeling, usually around 3 months after injury.

Clinical Features and Evaluation Proximal humerus fractures generally present with pain and deformity. The deformity is often obvious with the arm held in internal rotation. Physical examination consists of palpation, which causes pain at the fracture site, and neurovascular examination. Further examination is usually limited by pain. Radiographs are always obtained including perpendicular views of the proximal humerus and of the entire humerus. Fractures are usually obvious on radiographs; however, certain nondisplaced physeal fractures may have normal-appearing radiographs. In this circumstance, diagnosis of nondisplaced physeal fracture is largely clinical. Treatment and Results Most proximal humeral fractures can be treated nonoperatively. Metaphyseal and physeal fractures that are nondisplaced or minimally angulated are generally stable and heal quite well with immobilization followed by early pendulum exercises. Displaced fractures often have a bayonet apposition with shortening. These fractures generally heal with minimal residual deformity, especially in younger children. Patients who are approaching skeletal maturity with more limited remodeling potential may require closed reduction with or without internal fixation. Dameron and Rockwood8 have proposed guidelines for managing pediatric proximal humeral fractures. Nonoperative treatment is indicated in patients younger than 5 years of age with less than 70 degrees of angulation and as much as 100% displacement and in patients 5 to 12 years of age with less than 40 degrees of angulation and 50% displacement. Patients older than 12 years of age have more limited remodeling potential and should be treated more aggressively in cases of moderate to severe angulation and displacement. Nonoperative treatment consists of early pendulum exercises as soon as the fracture is stable. Formal rehabilitation is generally begun 3 to 4 weeks after the initial injury when the fracture shows early signs of consolidation. Early passive motion exercises are followed by active range of motion exercises. Subsequent physical therapy focuses on strengthening of the rotator cuff, trapezius, and deltoid muscles. Full return to sports is usually allowed between 3 and 6 months. In patients approaching skeletal maturity with moderate to severely displaced proximal humeral fractures, reduction should be performed to avoid potential deformity and functional limitation. Specifically, high-level athletes involved with overhead sports or throwing may require operative treatment. These patients require a near anatomic reduction in order to regain full shoulder motion and return to their same level of play. We emphasize, however, that operative treatment should gen-

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erally be reserved for patients with little or no growth remaining who are unlikely to remodel significantly displaced fractures. Reduction of proximal humeral fractures is generally carried out with the patient under anesthesia. A reduction of maneuver of longitudinal traction, abduction, and external rotation will

A

usually reduce the fracture. Fluoroscopic examination is helpful to assess adequacy of reduction and stability. If the fracture is unstable, percutaneous fixation with Kirschner wires is used (Fig. 31-4). The wires can be left protruding externally allowing for removal in clinic at about 4 weeks postoperatively. Rarely,

B

Figure 31-4 A, Displaced proximal humeral physeal fracture in a 14-year-old patient after a fall while snowboarding. B, Radiograph after closed reduction and percutaneous pinning. C, Radiograph at 1 year after injury. The patient has full function and no complaints.

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closed reduction is not possible because of soft-tissue incarceration. In this scenario, open reduction is necessary. After surgery, rehabilitation consists of the same regimen used for nonoperative treatment of proximal humerus fractures with full return to sports expected between 3 and 6 months postoperative.

Glenohumeral Dislocations/Instability Traumatic dislocations of the shoulder in young skeletally immature patients are rare. However, traumatic dislocations are seen in adolescents, and recurrent instability in these patients is a common problem. Anterior dislocations are far more common than posterior and inferior dislocations. Clinical Features and Evaluation Anterior shoulder dislocations present with pain, swelling, and deformity. The acromion often appears prominent, and the posterolateral portion of the shoulder may appear flattened. The arm is generally supported and held in an abducted and externally rotated position. Pain is present with movement of the shoulder. The humeral head is usually palpable anterior to the glenoid. Posterior shoulder dislocations present with the arm at the side and the forearm internally rotated. A painful loss of external rotation and inability to supinate the forearm is commonly seen in posterior dislocations. In athletic events, posterior dislocations are often associated with posteriorly directed force acting on the outstretched arm. Inferior shoulder dislocations present with the arm abducted, the elbow flexed, and the hand above the head and may result from a hyperabduction force acting on the arm. Evaluation of the neurologic and vascular status of the arm is an essential part of the physical examination both initially and after reduction. The remainder of the physical examination is limited in acute dislocations. In patients with initial or recurrent glenohumeral instability presenting in the subacute phase, complete physical examination including stability examination is usually possible (details of shoulder examination for instability are covered in Chapter 16). With acute shoulder dislocation, two perpendicular radiographic views of the shoulder are obtained. These are used to identify the presence of any fractures as well as the direction of the dislocation. Postreduction radiographs confirm the reduction and help identify any associated injuries. In the subacute setting, we use an anteroposterior radiograph and a glenoid profile radiograph, as described by Bernageau et al9,10 to identify osseous abnormalities consistent with instability. In patients with suspected instability (no clear history of dislocation) and normal radiographs, we obtain secondary imaging with magnetic resonance arthrography to confirm the presence of instability lesions, that is, labral injury. Treatment and Results The treatment of acute shoulder dislocations includes sedation or an intra-articular lidocaine injection followed by reduction using one of the standard reduction techniques. Care must be used during the reduction maneuver to prevent a proximal humerus fracture. Considerable debate exists over proper management of adolescent first-time shoulder dislocations. While some authors recommend surgical stabilization after an initial instability episode to prevent recurrence, new research suggests that a brief period of immobilization in external rotation after reduction of a traumatic anterior dislocation reduces the incidence of recurrent instability.11,12

In the absence of early immobilization in external rotation, the incidence of recurrent shoulder instability after an acute traumatic shoulder dislocation in young patients is extremely high. These patients may benefit from surgery after a traumatic first-time shoulder dislocation. Details of operative treatment of recurrent shoulder instability are detailed in preceding chapters.

Atraumatic Shoulder Instability Atraumatic shoulder instability is the most common type of instability seen in skeletally immature patients. Rehabilitation should be the mainstay of treatment for nearly all these cases. The goal of treatment is to increase the dynamic stabilization force of the shoulder joint by strengthening the rotator cuff musculature. Second, the scapular stabilizers should be strengthened to maintain proper positioning of the glenoid in relation to the humeral head. Neuromuscular control should also be emphasized during rehabilitation to improve shoulder proprioception. A minimum of 12 months of aggressive rehabilitation and avoidance of provocative maneuvers should be achieved before surgical management should be considered. Most patients will eventually improve with the passage of time. Voluntary dislocators comprise a unique group that should almost universally be treated nonoperatively.13

Acromioclavicular and Sternoclavicular Dislocations/Instability Since the joint capsule and ligaments in a child are much stronger than the physis, sternoclavicular and acromioclavicular dislocations are extremely rare in the pediatric population. Acromioclavicular separations are generally not seen until adolescence at which time they can be treated like adult injuries (see Chapter 26). Skeletally immature patients may appear to have an acromioclavicular separation, but most of these injuries are actually physeal fractures. Injuries to the lateral clavicle and acromioclavicular joint are different in children compared to adults. The pediatric distal clavicle has a thick periosteal tube that is continuous with the acromioclavicular joint. The acromioclavicular joint is rarely dislocated in children because the weak link is the physis, not the ligamentous attachments. The acromioclavicular and coracoclavicular ligaments are tightly connected to the periosteum encasing the distal clavicle. Injuries to this area most commonly result in physeal fractures with the distal clavicle splitting out of the periosteal sleeve. True dislocations of the sternoclavicular joint in children and adolescents are very rare. Medial clavicular injuries usually affect the medial physis of the clavicle.

OVERUSE INJURIES Proximal Humeral Epiphyseolysis Proximal humeral epiphyseolysis, more commonly known as little leaguer’s shoulder, is an overuse injury occurring exclusively in skeletally immature throwing athletes and almost exclusively in baseball pitchers.5,14 During repetitive throwing, torsional forces act on the arm, externally rotating the humerus distally, while the proximal portion is secured at the glenohumeral joint via the capsuloligamentous structures. These forces result in remodeling of the proximal humerus through the weakest osseous point, the proximal humeral physis. When throwing becomes excessive, this remodeling phenomenon may become pathologic resulting in a stress fracture through the proximal humeral physis.

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Clinical Features and Evaluation Individuals presenting with proximal humeral epiphyseolysis are nearly always high level little league baseball pitchers between 10 and 14 years of age.14 They report progressive onset of pain that occurs only with throwing activities. They also commonly report loss of velocity and/or control of their pitches. They usually are able to participate in hitting activities without exacerbation of symptoms. Physical examination findings may demonstrate mild tenderness over the proximal humeral physis with deep palpation. A provocative maneuver of abduction, external rotation, and extension may produce pain in the dominant shoulder. Alternatively, examination may not reveal any pathologic findings. Mobility examination usually demonstrates greater external rotation and less internal rotation of the dominant shoulder compared to the nondominant shoulder. This discrepancy in the arc of motion between the two shoulders is a result of physiologic remodeling and is a nonspecific finding in pitchers.4 Radiographic examination serves to confirm the diagnosis of proximal humeral epiphyseolysis, which is suspected initially largely based on the history. Proximal humeral radiographs demonstrate widening of the physis, usually most readily apparent on the anteroposterior view. Comparative radiographs of the contralateral proximal humerus are helpful in confirming the pathologic condition of the physis (Fig. 31-5). Treatment and Results Treatment of proximal humeral epiphyseolysis involves a period of selective rest and activity modification. After diagnosis of proximal humeral epiphyseolysis, repetitive throwing activities are halted for a period of 3 months. During this time, painless activities such as hitting are allowed. Often pitchers are allowed to play first base, enabling continuation of hitting while minimizing throwing activities. After 3 months of activity restrictions, gradual resumption of throwing is allowed, preferably using a progressive throwing program under the supervision of a qualified athletic trainer or physical therapist. Provided symptoms do not recur, full return to pitching is usually possible within 6 months of initiation of treatment. Recurrence of pain with throwing is treated with prolongation of throwing restrictions until symptoms subside. Appropriate treatment of proximal humeral epiphyseolysis nearly always results in successful return to throwing activities. Rarely, a patient may have continued symptoms preventing pitching until reaching a more skeletally mature age. We have never observed a case of permanent physeal damage or early physeal closure caused by proximal humeral epiphyseolysis.

A

B Figure 31-5 A, Radiograph showing physeal widening (arrows) of the throwing shoulder of a 12 year old. B, Contralateral normal physis.

Internal Impingement Internal impingement, or posterosuperior glenoid impingement, is the contact that occurs between the greater tuberosity and the posterosuperior aspect of the glenoid rim during abduction, external rotation, and extension of the arm (Fig. 31-6).15,16 This contact is physiologic, occurring in nearly all individuals including the skeletally immature. In the throwing athlete, the repetitive nature of this contact can result in pathologic glenohumeral lesions including partial thickness rotator cuff tears and/or superior labral tears. In the skeletally immature throwing athlete, symptomatic internal impingement is uncommon with proximal humeral epiphyseolysis predominating as the cause of pain. When symptomatic internal impingement occurs in pediatric athletes, it usually results from poor pitching mechanics. Davidson et al17

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Figure 31-6 Mechanism of internal impingement.

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A

B Figure 31-7 A, Hyperangulation occurs from the arm being in excessive extension and/or the scapula being in excessive protraction during late cocking and early acceleration and may result in symptomatic internal impingement. B, Throwing with the arm in the plane of the scapula prevents hyperangulation and minimizes internal impingement.

usually lack rotator cuff pathology associated with internal impingement. Poor control of the scapula as evidenced by scapular winging during glenohumeral elevation is usually present in skeletally immature individuals with symptomatic internal impingement. This type of scapular winging results from fatigued or poorly conditioned scapular retractors and not from neurologic deficit. Additionally, individuals will have increased external rotation and decreased internal rotation of the dominant shoulder compared to the nondominant shoulder as a result of physiologic remodeling.3 Walch et al16 described a variety of findings in individuals with symptomatic internal impingement using various imaging modalities and diagnostic arthroscopy in a skeletally mature population. Plain radiography demonstrates changes (sclerosis, geodes, cysts) on the greater tuberosity in 67% of patients and lesions of the posterosuperior glenoid in 33% of patients (Fig. 31-8). Computed tomography demonstrates posterosuperior glenoid changes in 70% of patients. Arthrography demonstrates partial thickness tearing of the supraspinatus and/or infraspinatus in 50% of adult patients, although this probably occurs much less frequently in pediatric patients. Magnetic resonance imaging shows an abnormal signal at the insertion of the rotator cuff in 95% of adult patients. Labral pathology has been identified in most adult patients with symptomatic internal impingement undergoing arthroscopy including a torn or frayed posterior superior labrum in 83% and frank labral disinsertion in 72%. The arthroscopic hallmark of the diagnosis is the “kissing lesion.” During arthroscopy, the arm is positioned in abduction, external rotation, and extension, incurring contact in the area of the labral and rotator cuff lesions (Fig. 31-9). In our practice, we obtain radiographs on all pediatric patients presenting with shoulder pain at the time of initial evaluation including an anteroposterior view and a glenoid profile view as described by Bernageau et al.9 We only obtain secondary imaging with magnetic resonance arthrography in patients with suspected symptomatic internal impingement who have failed all reasonable nonoperative treatment to evaluate them

reported the role of hyperangulation of the arm during throwing in the development of symptomatic internal impingement. This hyperangulation can occur from the arm being in excessive extension and/or the scapula being in excessive protraction during late cocking and early acceleration (Fig. 31-7). Although some authors maintain that underlying anterior glenohumeral instability is the etiology of symptomatic internal impingement, this has not been scientifically substantiated in the pediatric or adult population as most of these patients lack evidence of anterior capsulolabral injury on imaging studies or during arthroscopy.16 Clinical Features and Evaluation Symptomatic internal impingement occurs only in throwing athletes including participants in baseball, tennis, volleyball, team handball, and javelin. The athlete’s chief complaint is typically shoulder pain during throwing activities that is usually relieved by rest. Pitchers commonly report loss of velocity and/or control of their pitches. Nonthrowing activities are usually unaffected. Frequently, symptoms begin after an increase in frequency of throwing activities. Physical examination demonstrates pain with abduction, external rotation, and extension of the involved shoulder; no apprehension occurs with this maneuver. The pain is relieved by eliminating the extension component of the maneuver. Rotator cuff testing is usually unremarkable in pediatric patients as they

Figure 31-8 Posterior glenoid changes (arrows) in an adolescent pitcher with symptomatic internal impingement. This same individual also has physeal changes consistent with proximal humeral epiphyseolysis.

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injury pattern occurs in the pediatric population, it is quite rare; more commonly, scapular winging in skeletally immature athletes is caused by overuse and/or poor conditioning of the scapular retractors (trapezius, rhomboids, levator scapulae). Scapular winging leads to hyperangulation (excessive extension angle occurring between the humerus and scapula), which in turn leads to symptomatic internal impingement. The athletes most commonly presenting with scapular winging are those participating in baseball pitching and swimming.

Figure 31-9 Arthroscopic view (looking from the anterior portal) of the contact that occurs between the posterior superior glenoid labrum and the supraspinatus tendon. This patient has a partial thickness supraspinatus tear (arrows) as a result.

for mechanical lesions (labral tears, partial thickness rotator cuff tears). Treatment and Results In the pediatric population, almost all cases of symptomatic internal impingement can be treated successfully with nonoperative interventions. A period of relative rest combined with a specific physical therapy regimen addressing the pathomechanics of internal impingement is employed. This physical therapy regimen attempts to minimize hyperangulation by strengthening the scapular retractors (trapezius, rhomboids, levator scapulae), controlling scapular protraction, strengthening the subscapularis, and controlling external rotation and extension during throwing activities. Posterior capsular stretching is used to address any posterior capsular tightness. Therapeutic modalities and nonsteroidal anti-inflammatory medications are used as indicated. As symptoms subside, a progressive throwing program, preferably under the supervision of a qualified athletic trainer or physical therapist, is initiated. Attempts are made to correct mechanical deficiencies in the throwing motion to avoid recurrence of symptoms. Successful return to throwing activities may be possible in as little as 6 weeks in mild cases but may take up to 6 to 9 months in more severe cases. Operative treatment is rarely indicated in the skeletally immature patient with symptomatic internal impingement. In select individuals with symptomatic labral tears from internal impingement with persistent pain after appropriate nonoperative treatment and correction of faulty pitching mechanics, arthroscopic labral repair can be considered with or without an associated anterior capsulorrhaphy to control hyperangulation. Although this arthroscopic treatment has been reported successful in as many as 85% of adult patients, results in the pediatric population are unknown.18

Scapular Winging Traditionally, scapular winging is related to an injury of the long thoracic nerve resulting in serratus anterior paralysis. While this

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Clinical Features and Evaluation Most athletes with scapular winging present with findings of internal impingement as described previously caused by overuse and/or poor conditioning of the scapulothoracic musculature. Symptoms, generally shoulder pain, occur almost exclusively with overhead and throwing activities. Rarely, athletes with scapular winging report a direct blow to the thorax just beneath the axilla resulting from a fall onto an object (commonly a piece of equipment in gymnasts) or during contact sports. In this second scenario, blunt injury to the long thoracic nerve causes paralysis of the serratus anterior muscle with resultant scapular winging. Scapular winging is observed on clinical examination by the examiner standing behind the patient as he or she actively forward flexes the shoulder. Subtle scapular winging may be observed only as asymmetry of the scapula during forward flexion. Having the patient push against a fixed object (wall or closed door) will also demonstrate scapular winging. Plain radiography is performed and may reveal findings consistent with internal impingement as described previously in patients with scapular winging emanating from overuse/ poor conditioning. Additionally, magnetic resonance arthrography may show labral tears and/or partial thickness rotator cuff tears in these patients. In patients with scapular winging resulting from an injury to the long thoracic nerve, imaging studies are usually normal. Electromyography and nerve conduction studies will usually demonstrate decreased potentials in the serratus anterior muscle in this second group of patients. Treatment and Results Nonoperative treatment is initially indicated in all pediatric patients presenting with scapular winging. Physical therapy concentrating on strengthening of the periscapular and trunk musculature is nearly always successful. Surgical treatment of patients with long thoracic nerve palsy has been reported (nerve exploration, pectoralis major transfer), although we have no experience with this in the pediatric population. Even in cases of electromyographically proven long thoracic nerve palsy, physical therapy and observation usually result in resolution of symptoms in children, although complete resolution may take an average of 9 months.19

CONCLUSIONS The presence of an open proximal humeral physis leads to some clinical problems unique to the pediatric shoulder. The majority of these injuries result from overuse, and they are becoming more common as children more frequently concentrate on one or two sports and spend increased time participating in them, with fewer seasonal breaks. Most of these problems can be successfully treated nonoperatively.

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REFERENCES 1. Curtis RJ Jr, Dameron TB Jr, Rockwood CA Jr: Fractures and dislocation of the shoulder in children. In Rockwood CA Jr, Wilkins KE, King RE (eds): Fractures in Children, 3rd ed. Philadelphia, Lippincott, 1991, pp 829–919. 2. Tullos HS, King JW: Lesions of the pitching arm in adolescents. JAMA 1972;220:264–271. 3. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 1993;18:402–408. 4. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 2002;30:20–26. 5. Dotter WE: Little leaguer’s shoulder: A fracture of the proximal humeral epiphyseal cartilage of the humerus due to baseball pitching. Guthrie Clinic Bull 1953;23:68–72. 6. Wilkes JA, Hoffer MM: Clavicle fractures in head-injured children. J Orthop Trauma 1987;1:55–58. 7. Dalldorf PG, Bryan WJ: Displaced Salter-Harris type I injury in a gymnast: A slipped capital humeral epiphysis? Orthop Rev 1994;23: 538–541. 8. Dameron TB Jr, Rockwood CA Jr: Fractures and dislocation of the shoulder. In Rockwood CA Jr, Wilkins KE, King RE (eds): Fractures in Children. Philadelphia, Lippincott, 1984, pp 589–607. 9. Bernageau J, Patte D, Bebeyre J, et al: Intérêt du profil glénoïdien dans les luxations récidivantes de l’épaule. Rev Chir Orthop 1976;62(Suppl II):142–147. 10. Edwards TB, Boulahia A, Walch G: Radiographic analysis of bone defects in chronic anterior shoulder instability. Arthroscopy 2003;19: 732–739.

11. DeBerardino TM, Arciero RA, Taylor DC, et al: Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes: Two- to five-year follow-up. Am J Sports Med 2001;29:586–592. 12. Itoi E, Hatakeyama Y, Kido T, et al: A new method of immobilization after traumatic anterior dislocation of the shoulder: A preliminary study. J Shoulder Elbow Surg 2003;12:413–415. 13. Huber H, Gerber C: Voluntary subluxation of the shoulder in children: A long term follow-up study of 36 shoulders. J Bone Joint Surg Br 1994;76:188–122. 14. Carson WG Jr, Gasser SI: Little leaguer’s shoulder: A report of 23 cases. Am J Sports Med 1998;26:575–580. 15. Jobe CM, Sidles J: Evidence for a superior glenoid impingement upon the rotator cuff. J Shoulder Elbow Surg 1993;2:S19. 16. Walch G, Boileau P, Noel E, et al: Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1992;1:238–245. 17. Davidson PA, Elattrache NS, Jobe CM, et al: Rotator cuff and posterior-superior glenoid labrum injury associated with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 1995;4:384–390. 18. Levitz CL, Dugas J, Andrews JR: The use of arthroscopic capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy 2001;17:573–577. 19. Gregg JR, Labosky D, Harty M, et al: Serratus anterior paralysis in the young athlete. J Bone Joint Surg Am 1979;61:825–832.

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CHAPTER

32

Shoulder Rehabilitation Tracy Spigelman and Tim Uhl

In This Chapter Adjacent joints Pain control Restoring range of motion Dynamic stability Neuromuscular control Strengthening Interval training

INTRODUCTION • The shoulder is a complex system and is second only to the knee to being commonly injured in athletic endeavors. • Shoulder rehabilitation is often carried out by a licensed therapist or certified athletic trainer, but the physician often oversees the process and makes recommendations of progression. • Rehabilitation progression depends on the severity and nature of the injury determined by the physical examination or surgical procedures. • The rehabilitation process is typically laid out in three primary phases. • The underlying principles of shoulder rehabilitation drive the intervention undertaken (Table 32-1).

The first principle of appropriate rehabilitation is that a complete and accurate diagnosis must be made that identifies not only the problem but the cause of the problem as well. This is particularly critical in the shoulder as there are several microtraumatic injuries from high demand tasks such as throwing.1–3 It is critical that the clinician considers the entire body in the examination of all shoulder injuries, particularly in an activity such as throwing, because the shoulder can be the victim of another dysfunctioning component of the kinetic chain.4 If the rehabilitation program only addresses shoulder symptoms, the precipitating issue will not be identified and treated adequately. Understanding of this complex anatomic and biomechanical system is critical to making the correct diagnosis and properly rehabilitating the shoulder. The nature of many sports medicine rehabilitation programs is that the goal of the program is to return the athlete to the exact same event that caused the injury. Therefore, a comprehensive understanding of the sport’s biomechanical demands and pathomechanics that can lead to a microtraumatic injury must be addressed to get the athlete back to the sport activity when designing a rehabilitation program.5

The rate at which the return can take place depends on respecting the physiologic healing restraints and the tissue state of irritability. After an acute traumatic event or surgical intervention, the physiologic healing restraints of the injured tissue must be considered when prescribing rehabilitation activities.5 The exercise progression must be adequate to facilitate healing but not overload a tissue. Overloading tissue can produce pain and substitution patterns that are difficult to resolve later in the rehabilitation process. Often the demands of the total exercise program prescribed are not completely appreciated until the day after. Providing the patient with variations of an exercise and considering the total volume of exercises prescribed can help prevent flare-ups. The final, and probably most important, principle to any rehabilitation program is open and honest communication between all parties, particularly between the patient, physician, and rehabilitation specialists. The exchange of concerns and findings will enhance the process of recovery. Nothing is more frustrating to a patient than to get conflicting information from caregivers. In those patients undergoing surgical rehabilitation, the operating surgeon has the best information as to quality of tissue and repair, which will dictate the rehabilitation program. Once the complete and accurate diagnosis has been made and the recommendation from the physician to start rehabilitation is given, the patient needs to enter into the appropriate phase of the rehabilitation program. There are three basic phases of rehabilitation: acute, prefunctional, and functional (Table 32-2). The primary goals of the acute phase are to decrease pain and increase motion. Restoration of upper extremity neuromuscular control and dynamic stability of the glenohumeral joint is the primary goal during the prefunctional phase. In the functional phase, the goal is to regain full endurance and power in order to return the athlete to sport participation.2 The nature of the injury, deficits found, and the goals of the individual patient will determine which phase is most appropriate for the patient. It is not uncommon for athletes with chronic overuse problems, which are typically degenerative and not inflammatory conditions,6 to focus on the functional phases during their rehabilitation.

ACUTE PHASE During the acute phase, rehabilitation focuses on decreasing the multiple components of inflammation and restoring normal motion, while protecting the injured area from further damage.5 The patient is often requested to go through a relative rest period to minimize inflammation and in some cases may actually be immobilized for a short period of time. It is critical that maintenance of strength, endurance, and mobility of the rest of the body is addressed along with cardiovascular conditioning during this period.2,5

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Table 32-1 Principles of Rehabilitation 1. Complete an accurate diagnosis with appreciation of etiology 2. Understand anatomic and biomechanical concepts of the shoulder complex 3. Respect physiologic healing of injured tissue 4. Maintain open communication lines among the sports medicine team members

Adjacent Joints To minimize loss of function and maintain conditioning, exercising the noninvolved extremities is essential. This benefits the immobilized tissues by cross-education training, which helps maintain muscular strength on the untrained limb.7 Surgical patients with an immobilized shoulder are commonly prescribed active range of motion (ROM) exercise of the hand, wrist, and elbow to minimize distal swelling, facilitate venous return, and prevent stiffness.8 In addition, proximal joints of the scapula, cervical, thoracic, and lumbar spine should be exercised along with the lower extremity.4 The neuromuscular system uses the proximal trunk as a base of support for distal motion.9 Initiating a core strengthening and stretching program will activate the normal neuromuscular system and potentially minimize losses due to the relative rest period.10 Loss of muscular strength can occur as soon as 3 days in a trained individual and significant cardiovascular decreases have been noted within 14 days.11

Pain Control Medical management of this phase is typically carried out with nonsteroidal anti-inflammatory agents, although some concerns exist that this may delay healing.12 Physical therapy modalities

such as electrical stimulation and ultrasound are often recommended to control inflammation.8 However, only cryotherapy and compression have been demonstrated with good scientific evidence to be effective in controlling inflammation.13 Cryotherapy continuously for 3 days after arthroscopic surgery of the shoulder has been found to decrease the use of pain medication.14 Positioning of the injured extremity is critical to facilitate healing and minimize discomfort. After injury to a rotator cuff tendon or surgical intervention, a resting position of neutral rotation, 20 to 40 degrees of abduction, and 20 to 30 degrees of flexion minimize the load of the rotator cuff tendon and facilitates blood flow through the poorly vascularized rotator cuff tendon.15 A reclined position of 30 to 45 degrees with the elbow supported to prevent shoulder extension is recommended to address the common complaint of patients who are unable to find a comfortable sleep position.15,16 Historically, traumatic shoulder dislocations were immobilized in a sling and swathe with the arm internally rotated.16 Protzman17 suggests that time of immobilization did not have a significant bearing on redislocation rate. Recently, a position of external rotation at 45 degrees for 3 weeks has been advocated by some to diminish redislocation rates and promote labral compression onto the glenoid by the tension of the subscapularis.18 Diminishing pain and swelling minimizes the inhibitory effect on the neuromuscular system.19 The dynamic neuromuscular system is critical to the stability of the shoulder2,20 and is primarily supplied by the rotator cuff and periscapular musculature. Without adequate pain control, muscular re-education will be delayed and normal movement patterns will be difficult to reestablish in this acute phase.19,21 Exercises or activities that elicit pain should be modified to reduce the negative and inhibitory effects.

Functional Phase

1. Control pain 2. Increase motion 3. Protect healing structures

1. Re-establish neuromuscular control 2. Encourage tissue remodeling along lines of functional stress 3. Restore normal motion

1. Expose tissue to loads specific to sport demands 2. Interval return to sport activities

Immobilization (relative rest) Cryotherapy Electrical stimulation Manual therapy

Heat/cold modalities Ultrasound Electrical stimulation Massage Biofeedback

Heat/cold modalities Massage

PROM AAROM Isometrics Neuromuscular training Adjacent joint motion Cardiovascular exercises

AROM Proprioceptive neuromuscular facilitation Manual therapy Closed chain kinetics Mirroring sports motions Cardiovascular exercise

Overload resistive exercises Sport-specific drills Isokinetic exercises Plyometrics Power exercises Interval programs

Full AROM with minimal pain and coordinated scapulohumeral rhythm 70%–80% of opposite side’s strength

Completes interval program without symptoms Strength, endurance, and power of the upper extremity can withstand the demands of the sport activity

Time

AAROM, active assisted range of motion; AROM, active range of motion; PROM, passive range of motion.

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Criteria to Progress

AROM to at least 90 degrees with minimal pain and without scapular substitution 75% of PROM reestablished

Therapeutic Exercise

Prefunctional Phase

Modalities

Acute Phase

Goals

Healing Progression

Table 32-2 Outline of the Three Healing Phases and Suggested Rehabilitation Interventions That Are Appropriate for Each Level

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Figure 32-3 Arm sliding along elevated surface to allow a greater range of motion while minimizing the load of the arm.

Figure 32-1 Illustration of forward bow exercise with hand stabilized and the body moving away from the stable hand.

Therapeutic Exercise Passive ROM is often the initial exercise routine after significant shoulder injury or surgery. Passive ROM is prescribed during the inflammatory phase of healing to increase joint surface nutrition, prevent adhesions from forming, minimize stress to healing tissue, and decrease pain.8 Passive ROM is an exercise that takes the joints through a partial or complete ROM by some external source. This source can be from another individual, use of the healthy arm, or through a machine. Theoretically, passive ROM involves no volition of the dynamic system, but electromyographic studies indicate low to minimal activity present in the involved shoulder musculature.22 This low demand of muscle activity may place gentle stress on healing tissue collagen fibers to help with alignment, strength, and blood flow but not overload healing tissues.5 Passive exercises such as pendulum, supine passive elevation, and standing forward bow (Fig. 32-1) have all been found to activate the rotator cuff musculature by less than 10% of maximal voluntary isometric contraction, a common reference used to standardize electromyographic studies.22

Exercises are progressed from passive to active assisted ROM exercises to incrementally increase tissue demand and engage the neuromuscular system. In some cases, patients can start in this phase if minimal tissue protection is appropriate. Our goal is to start with low-demand and progress to high-demand activities. A common mistake made by rehabilitation specialists is to rush through this exercise level because it seems “too easy” for the patient. This is a critical step in the rehabilitation program to reestablish neuromuscular control of the shoulder girdle and to prevent substitution patterns from developing.1 If an exercise is too stressful, the motivated patient will focus on the goal of lifting the arm overhead 30 times and develop a substitution pattern of his or her upper trapezius, which may lead to further problems in the later phases.4 Active assisted ROM exercise is defined as movement through a partial or complete range that involves voluntary effort of the involved limb but is performed with external assistance.23 There are several examples of external assistance exercises from which to choose. Based on our electromyographic research, we have found assistive elevation tasks that minimize gravitational loads on the arm such as table slides (Fig. 32-2) and side-lying elevation (Fig. 32-3) are less demanding than exercises performed against gravity, such as rope and pulley– or stick-assisted elevation exercises.24 These active assisted ROM exercises indicate greater electromyographic activity than passive ROM but typically less than active ROM exercises.22 Therefore, active assisted ROM can be initiated before active and resistive exercises, without taxing new tissue. The goal is to engage the neuromotor system to facilitate the reestablishment of normal patterns of upper limb motion.

Criteria to Progress Once patients demonstrate good neuromuscular control of active assisted ROM, they typically are ready to progress to the next phase of the program. A general guideline for this is active elevation to at least 90 degrees in the plane of the scapula with no substitution and minimal pain. Passive ROM should be well established and have at least reached 140 degrees of elevation and external rotation of 30 degrees in most cases.2,5

PREFUNCTIONAL PHASE Figure 32-2 Arm sliding along horizontal surface with a towel under the hand to diminish friction and load on the upper extremity while activating the shoulder musculature.

The initial inflammatory phase has typically resolved, and the proliferative phase of healing is ongoing as patients enter this

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phase of rehabilitation. The tissue is less irritable and is now ready for more demanding activity. Reestablishing dynamic control of the shoulder girdle by activating both feedforward (voluntary motor program) and feedback (sensorimotor reflexive responses) neuromotor systems is a goal of this phase and important in prevention of future injuries.20 Exercises during this phase will certainly strengthen the shoulder musculature but also will emphasize activities to compress and centralize the humeral head on the glenoid.10

Restoring Full Range of Motion Normal motion is an important component of the prefunctional phase because most overhead sports require excessive external rotation to perform successfully at high levels. Restoring full ROM requires movement through the terminal ranges of motion.3 This is achieved through voluntary or active movement (active ROM) with static passive overpressure, which may result in increased joint compression along with stimulation of afferent joint and muscle receptors.6,25 Stimulation of these receptors may produce protective guarding but is necessary to reestablish afferent input. Care should be taken, however, not to damage the newly arranged collagen fiber. By applying these stresses, the collagen tissue will adapt to the stresses that they will be subjected to in the future.26 Joint mobilization techniques and static stretching techniques are effective measures to regain complete passive and active ROM.

Restoring Dynamic Stability Restoring dynamic stability of the glenohumeral joint primarily involves increased joint concavity/compression27 by engaging the periscapular muscles to stabilize and control scapular motion while allowing the rotator cuff to compress the humeral head into the glenoid. Closed kinetic chain exercises can facilitate dynamic stability by increasing glenohumeral congruency and stimulate joint receptors through functional ranges of motion. These types of exercises can stimulate motor activation20,28 and improve joint position sense,29,30 which enhances dynamic stability. Dynamic stability is also enhanced by progressive resistive strengthening exercises. Incorporation of light resistive elastic bands or dumbbells that target rotator cuff and scapular musculature has been demonstrated to increase shoulder strength.31 Gradual progression to higher resistive exercises such as prone horizontal abduction (Fig. 32-4) or rows places higher demands

Figure 32-5 Kinetic chain step-up with arm elevation.

on the trapezius and rhomboid muscles to regain the scapular strength and endurance necessary in overhead sports.32 Incorporation of greater loads through this phase with closed kinetic chain exercises, such as rhythmic stabilization with a ball, facilitates more demand on the shoulder musculature while simulating sports such as football and wrestling.20 Incorporating sport-specific tasks involving the entire body facilitates dynamic stability and helps recreate normal neuromuscular control of the upper extremity.

Restoring Neuromuscular Control

Figure 32-4 Prone horizontal abduction, found to place large demands on lower and mid-trapezius musculature.

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Neuromuscular control of a joint entails two components, a feedforward and feedback motor response. Feedforward motor programs are associated with voluntary movements that occur without afferent input. These motor programs have been found to incorporate not simply the prime movers of the limb but actually incorporate the entire body.9,33 This is necessary to provide a stable base for the distal limb to move on. As we are trying to return the athlete to normal motor patterns, we attempt to recreate these movement patterns during the rehabilitation of the athlete. This is accomplished by activating proximal trunk and hip extensor musculature just before activating the prime arm elevation musculature in order to retrain normal arm elevation movement patterns (Fig. 32-5). This technique is a primary principle of proprioceptive neuromuscular facilitation techniques that are commonly used in this rehabilitation phase.

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The feedback component is necessary to stabilize the joint to unexpected perturbations. Athletes often have to stabilize the shoulder complex in response to an unexpected external stimulus, such as catching themselves from a fall or attempting to grasp an opponent who is trying to evade them. These types of exercises, called rhythmic stabilization, are often incorporated into the closed chain dynamic stability exercises described previously, by placing the hand on an unstable surface and disturbing the surface. This requires the athlete to contract shoulder girdle musculature and stabilize the joint and his or her body to prevent losing his or her balance (Fig. 32-6). Development of full strength and endurance of the rotator cuff and scapular muscles is the key to maintaining dynamic stability and regaining neuromuscular control in the shoulder.25

Criteria to Progress Progression into the final phase should depend on physiology of healing and the individual functional response during the prefunctional phase. Certainly, we should expect nearly full active and passive ROM for most patients. No observable substitution patterns should be present with active ROM and sport-specific motions. Strength should be approaching 70% to 80% of the opposite side by isometric or dynamic testing.

FUNCTIONAL PHASE The functional phase of rehabilitation focuses on return to play. Rehabilitation exercises introduced in this phase should continue to stress the static and dynamic restraints by increasing velocity and torque demands. Emphasis on ballistic sportspecific exercises that incorporate eccentric and plyometric activities are recommend during the functional phase.4,32 These types of exercises prepare the shoulder for the demands required to return to full sport participation.34 The athlete should also begin an interval training program to gradually reintroduce proper biomechanics and demands of the sport to the body. During interval training, the coach should be involved in evaluating and providing feedback to the athlete about proper mechanics of the skill being performed.2,4 Progressive resistive open kinetic chain exercises incorporating heavier dumbbells or requiring performance at a faster rate increase demands at the shoulder joint because the distal segment is not fixed. These exercises add to the eccentric forces placed on the rotator cuff musculature. Another way to increase the stress on the static and dynamic stabilizers is with plyometric exercises.2 The objective of plyometrics is to use elastic properties of the muscle to increase concentric power, prestretching the tissue with an eccentric action followed quickly with a concentric action. The shorter the period is between eccentric and concentric phases, the better.35 Weighted ball overhead plyometric activities simulate demands of the act of throwing and are a good indicator that the athlete is able to progress to interval sport activities.34

Interval Training Program

A

Return to any overhead sport requires that the athlete is gradually exposed to the sport demands. Much of the functional phases is focused on sport-specific activities that are created for the individual’s needs. Incorporating the coach and a certified athletic trainer is very helpful at this point to ensure that proper biomechanics of the task are being met. The goal is to return the athlete to play with correct mechanics, thus preventing recurrence of the same injury. There are several excellent resources for a variety of sports interval training programs available in the literature 2,36

Return to Play Criteria

B Figure 32-6 A and B, Rhythmic stabilization with ball perturbation.

The final, and often most difficult, task of the physician is to determine when it is safe to return an athlete to sport. Return to play criteria should include objective physical parameters specific to the sport demands. Nothing replaces experience in making this decision, but we have attempted to give some general suggestions of minimal requirements for most overhead athletic activities in Table 32-3.

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Table 32-3 Suggested Minimal Requirements for Most Overhead Athletic Activities Criteria

Assessment

Range of motion

Full active arm elevation in both frontal and sagittal planes. External rotation equal or greater than opposite arm for dominant arms. Internal rotation should be within 10% of opposite arm internal rotation.

Strength

Normal (5/5) with manual muscle testing of the rotator cuff, deltoid, and scapular musculature. If isokinetic testing is available, assessment at a safe position of 45 degrees abduction in the plane of the scapula is suggested for internal (25% of body weight) and external rotation (15% of body weight) with an external-to-internal rotation ratio of 66%.

Endurance

Completion of interval program; isokinetic testing at 300 degrees/sec; limited fatigue

Quality of pain

Athlete describes only minimal “fatigue” after exercises but no sharp pain, night pain, or increase in pain the following day.

Quality of motion

Coordinated scapular-thoracic motion; no substitutions; no hesitation

Quality of attitude

Confident without hesitation; positive; eager to return to play

REFERENCES 1. Pink M, Jobe FW: Shoulder injuries in athletes. Clin Manag 1991;1:39–47. 2. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 2002;30:136–151. 3. Bigliani LU, Codd TP, Conner P, et al: Shoulder motion and laxity in the professional baseball player. Am J Sports Med 1997;25:609–613. 4. Pappas AM, Zawacki RM, McCarthy CF: Rehabilitation of the pitching shoulder. Am J Sports Med 1985;13:223–235. 5. Uhl TL: Rehabilitation after shoulder injury and surgery. In Baker CL, Flandry F, Henderson JM (eds): Hughston Clinic Sports Medicine. Baltimore, Williams & Wilkins, 1995, pp 291–298. 6. Almekinders LC, Temple JD. Etiology, diagnosis, and treatment of tendonitis: An analysis of the literature. Med Sci Sports Exerc 1998;30:1183–1190. 7. Yue G, Cole KJ: Strength increases from the motor program: Comparison of training with maximal voluntary and imagined muscle contractions. J Neurophysiol 1992;67:1114–1123. 8. Prentice WE: Therapeutic Modalities in Sports Medicine, 3rd ed. St. Louis, Mosby, 1994. 9. Cordo PJ, Nashner LM: Properties of postural adjustments associated with rapid arm movements. J Neurophysiol 1982;47:287–308. 10. Borsa PA, Livingston B, Kocher MS, Lephart SP: Functional assessment and rehabilitation of shoulder proprioception for glenohumeral instability. J Sport Rehabil 1994;3:84–104. 11. Convertino VA, Bloomfield SA, Greenleaf JE: An overview of the issues: Physiological effects of bed rest and restricted physical activity. Med Sci Sports Exerc 1997;29:187–190. 12. Prisk V, Huard J: Muscle injuries and repair: The role of prostaglandins and inflammation. Histol Histopathol 2003;18:1243–1256. 13. Merrick MA, Knight KL, Ingersol CD, Potteiger JA: The effects of ice and compression wraps on intramuscular temperature at various depths. J Athl Train 1993;28:241–245. 14. Speer KP, Warren RF, Horowitz L: The efficacy of cryotherapy in the postoperative shoulder. J Shoulder Elbow Surg 1996;5:62–68. 15. Itoi E, Tabata S: Conservative treatment of rotator cuff tears. Clin Orthop 1992;275:165–173. 16. Bankart AS, Cantab MC: Recurrent or habitual dislocation of the shoulder-joint. Clin Orthop 1993;291:3–6. 17. Protzman RB: Anterior instability of the shoulder. J Bone Joint Surg Am 1980;62:909–918. 18. Itoi E, Hatakeyama Y, Kido T, et al: A new method of immobilization after traumatic anterior dislocation of the shoulder: A preliminary study. J Shoulder Elbow Surg 2003;12:413–415. 19. Roe C, Brox J, Bohmer A, Vollestad N: Muscle activation after supervised exercises in patients with rotator tendinosis. Arch Phys Med Rehabil 2000;81:67–72. 20. Lephart SM, Pincivero DM, Giraldo JL, Fu FH: The role of proprio-

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21.

22.

23.

24.

25. 26.

27.

28.

29.

30.

31.

32.

33.

34.

35. 36.

ception in the management and rehabilitation of athletic injuries. Am J Sports Med 1997;25:130–137. Wilk KE, Arrigo CA, Andrews JR: Current concepts: The stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther 1997;25:364–379. McCann PD, Wootten ME, Kadaba MP, Bigliani LU: A kinematic and electromyographic study of shoulder rehabilitation exercises. Clin Orthop 1993;288:179–188. Kisner K, Colby L: Introduction to therapeutic exercise. In: Therapeutic Exercise—Foundations and Techniques, 3rd ed. Philadelphia, FA Davis, 1996, pp 3–23. Gaunt B, Uhl TL, Humphrey L, et al: Electromyography of shoulder and scapular musculature during exercise strengthening progression. J Orthop Sports Phys Ther 2006 (in review). Riemann BL, Lephart SM: The sensorimotor system, part I: The physiological basis of functional joint stability. J Athl Train 2002;37:71–79. Woo SL-Y, Gomez MA, Siters TJ, et al: The biomechanical and morphological changes in the medial collateral ligament of the rabbit after immobilization and remobilization. J Bone Joint Surg Am 1987;69:1200–1211. Lippitt SB, Vanderhooft JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quantitative analysis. J Shoulder Elbow Surg 1993;2:27–35. Uhl TL, Carver TJ, Mattacola CG, et al: Shoulder musculature activation during upper extremity weight-bearing exercise. J Orthop Sports Phys Ther 2003;33:109–117. Ubinger ME, Prentice WE, Guskiewicz KM: Effect of closed kinetic chain training on neuromuscular control in the upper extremity. J Sport Rehabil 1999;8:184–194. Rogol IM, Ernst G, Perrin DH: Open and closed kinetic chain exercises improve shoulder joint reposition sense equally in healthy subjects. J Athl Train 1998;33:315–318. Wang C-H, McCure P, Pratt N, Nobilini R: Stretching and strengthening exercises: Their effects on three-dimensional scapular kinematics. Arch Phys Med Rehabil 1999;80:923–929. Swanik KA, Swanik CB, Lephart SM, Huxel K: The effect of functional training on the incidence of shoulder pain and strength in intercollegiate swimmers. J Sport Rehabil 2002;11:140–154. Zattara M, Bouisset S: Posturo-kinetic organisation during the early phase of voluntary upper limb movement. 1. Normal subjects. J Neurol Neurosurg Psychiatry 1988;51:956–965. Cordasco F, Wolfe IN, Wootten ME, Bigliani LU: An electromyographic analysis of the shoulder during a medicine ball rehabilitation program. Am J Sports Med 1996;24:386–392. Stone JA, Partin NB, Lueken JS, et al: Upper extremity proprioceptive training. J Athl Train 1994;29:15–18. Axe MJ, Konin J: Distance based criteria interval throwing program. J Sport Rehabil 1992;1:326–336.

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33

Physical Examination and Evaluation Grant L. Jones and Champ L. Baker, Jr.

In This Chapter History Inspection/palpation Range of motion Strength testing Stability testing Provocative and special tests Imaging

INTRODUCTION • The keys to diagnosing elbow injury are a comprehensive history and physical examination of the elbow and the surrounding anatomy, such as the shoulder, wrist, hand, and cervical spine, to rule out possible causes of referred pain. • A detailed history can help to narrow the differential diagnosis. • Many specialized tests exist for confirming the diagnosis of specific pathologic entities about the elbow. • Diagnostic tests, such as radiography, computed tomography (CT), and magnetic resonance imaging (MRI) can help in making a diagnosis or ruling out potential disorders.

HISTORY Taking a comprehensive history helps the physician to develop a differential diagnosis. The examiner should determine whether a single traumatic event or repetitive traumatic episodes caused the symptoms. Acute injuries to be considered include ulnar collateral ligament (UCL) rupture, medial epicondyle avulsion, biceps rupture, loose-body formation, acute wrist extensor or flexor origin muscle strain or tendon rupture, and acute subluxation of the ulnar nerve. Chronic injuries include UCL strain or rupture, valgus extension overload, musculotendinous strains, tendonopathies, and osteochondral defects that can progress to degenerative changes.1,2 The examiner should inquire about the location of the pain. Dividing the elbow into four anatomic regions (lateral, medial, anterior, and posterior) helps to narrow the range of differential diagnoses.1–7 Symptoms in the lateral region of the elbow indicate radiocapitellar chondromalacia, osteochondral loose bodies, radial head fractures, osteochondritis dissecans lesions, or posterior interosseous nerve entrapment. Symptoms in

the medial region can indicate UCL sprain or rupture, a medial epicondyle avulsion fracture, ulnar neuritis, ulnar nerve subluxation, medial epicondylitis, osteochondral loose bodies, valgus extension overload syndrome, or pronator teres syndrome. The differential diagnoses for symptoms of the anterior region include anterior capsular sprain, distal biceps tendon strain or rupture, brachialis muscle strain, and coronoid osteophyte formation. Finally, symptoms in the posterior region can indicate valgus extension overload, posterior osteophytes with impingement, triceps tendonitis, triceps tendon avulsion, olecranon stress fracture, osteochondral loose bodies, or olecranon bursitis.1,2 The examiner should ask the patient about the presence and character of the pain, swelling, and locking and catching episodes. Sharp pain radiating down the medial portion of the forearm with paresthesia in the fifth and the ulnar-innervated half of the fourth digit indicates ulnar neuritis or cubital tunnel syndrome. When these symptoms are associated with a snapping or popping sensation, ulnar nerve subluxation might be the underlying cause. Pain that occurs in the posteromedial portion of the elbow with intense throwing and is associated with localized crepitation might indicate valgus extension overload syndrome.8,9 Pain localized in the posterior region of the elbow at the triceps tendon insertion or poorly localized, deep, aching pain in the posterior region of the elbow at the triceps insertion can signal triceps tendonitis. Poorly localized, deep, aching pain in the posterior region of the elbow can also be associated with an olecranon stress fracture.1,2,10 Sharp pain in the lateral region associated with locking or catching can be the result of loose bodies in the radiocapitellar joint from a radial head fracture or osteochondritis dissecans lesions of the capitellum.11,12 Acute, sharp pain in the anterior region of the elbow can be caused by an acute rupture of the biceps tendon. Persistent, aching pain in the anterior region can indicate inflammation involving the anterior capsule. A patient whose symptoms are related to throwing or to an occupational stress should be asked to reproduce the position that causes the symptoms. Pain during the early cocking phase of throwing might be the result of biceps or triceps tendonitis. Pain during the late cocking phase caused by valgus stresses on the medial region of the elbow can indicate UCL incompetency or ulnar neuritis. A thrower who reports pain in the posterior region of the elbow during the late cocking and acceleration phases and reports an inability to “let the ball go” might have valgus extension overload syndrome. Pain during the late acceleration or follow-through phases may signal a flexorpronator tendonopathy due to forceful wrist flexion and forearm pronation during these phases. In the skeletally immature patient, pain in the lateral region of the elbow during the late

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acceleration and follow-through phases often indicates radiocapitellar joint injuries, such as osteochondritis dissecans lesions.

PHYSICAL EXAMINATION Inspection Careful inspection of the elbow joint and surrounding areas is the next step in evaluating the elbow. First, the examiner should note atrophy or hypertrophy of muscle groups of the arm or forearm and should obtain girth measurements. Hypertrophy of the forearm musculature often is present in the dominant extremity of the throwing athlete and should be considered a normal variant. Atrophy of arm and forearm musculature, however, could be the result of an underlying neurologic disorder. Next, the examiner should measure the carrying angle of the elbow with the arm extended and the forearm supinated (Fig. 33-1). The normal carrying angle is 11 degrees in men and 13 degrees in women.13 An increase in the carrying angle is termed cubitus valgus. Often, this angle increases from 10 to 15 degrees in throwing athletes because of adaptive remodeling from repetitive valgus bony stress.9,14 A progressive cubitus valgus deformity can also be caused by a nonunited lateral condylar fracture, which can lead to a tardy ulnar nerve palsy.15 Cubitus varus, a decrease in the carrying angle, can be the result of a malunited supracondylar humeral fracture or a previous growth plate disturbance caused by trauma or inflammation. Inspection of the four mentioned elbow regions should be performed next.16 First, on the lateral aspect, the soft spot, a

Figure 33-2 Palpate the lateral “soft spot” for swelling from a joint effusion or synovial proliferation.

triangular region defined by the lateral epicondyle, olecranon, and the radial head, is evaluated. Swelling or fullness in this region can indicate joint effusion, synovitis, or bony deformity (Fig. 33-2). Next, inspection of the posterior region is performed. Swelling or a prominence in this region may indicate an olecranon bursitis, an olecranon traction spur, or nodules from gout or rheumatoid arthritis. The olecranon may also appear prominent as a result of a defect in the distal triceps tendon when there is a distal triceps tendon rupture. Swelling or fullness medially may indicate an avulsion fracture of the medial epicondyle, a UCL injury, a subluxated ulnar nerve, or, in the more chronic situation, an enthesophyte in the wrist flexorpronator origin on the medial epicondyle. The anterior region should be inspected for any deformity. A more proximal position of the distal end of the biceps muscle belly compared with that of the contralateral muscle may be indicative of a distal biceps tendon rupture. A deformity in the more proximal portion of the lateral biceps muscle (“Popeye” deformity) is indicative of a rupture of the long head of the tendon proximally, whereas a medial deformity in the proximal portion of the muscle belly suggests a rupture of the short head.17,18 Finally, the skin should be inspected for erythema, which can be a sign of an infectious or inflammatory process.

Palpation

Figure 33-1 Observe the carrying angle of the elbow with the arm extended and forearm supinated.

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The examiner palpates the medial and lateral epicondyles and views them from a posterior angle. When the elbow is in full extension, these landmarks normally form a straight line (Fig. 33-3). With the elbow in 90 degrees of flexion, however, they form an equilateral triangle. Any alignment abnormality can indicate fracture, malunion, unreduced dislocation, or growth disturbances involving the distal end of the humerus.19 The examiner should palpate all four regions of the elbow (anterior, medial, posterior, and lateral) in an orderly fashion. Beginning with the anterior structures, the distal biceps tendon is palpated anteromedially in the antecubital fossa with the patient’s

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A

lacertus fibrosus, which can be confused with the biceps tendon. Deep, poorly localized tenderness can be caused by anterior capsulitis or coronoid hypertrophy due to hyperextension injuries or repetitive hyperextension stress.6 Next, the examiner should feel the brachial artery pulse deep to the lacertus fibrosus, which is just medial to the biceps tendon. Finally, one should conduct Tinel’s test in the area of the lacertus fibrosus, which is a common site of median nerve compression.21 A positive Tinel sign can indicate pronator syndrome. Next, the clinician should palpate the structures in the medial region of the elbow, beginning with the supracondylar ridge. If a congenital medial supracondylar process is present in this area, it gives rise to a fibrous band (ligament of Struthers) that inserts on the medial epicondyle. This band can compress the brachial artery and median nerve and result in neurovascular symptoms with strenuous use of the extremity. The examiner should palpate the medial epicondyle and flexor-pronator mass. Tenderness at the origin of the flexor-pronator mass on the epicondyle suggests an avulsion fracture in adolescents or medial epicondylitis in adults. Flexor-pronator strains produce pain anterior and distal to the medial epicondyle. The UCL also is present in this area as it courses from the anteroinferior surface of the medial epicondyle to insert on the medial aspect of the coronoid at the sublime tubercle (Fig. 33-4).22 Palpation of the ligament can be facilitated by using the “milking maneuver.”23,24 During this maneuver, the patient grasps the thumb of the affected arm with the opposite hand. With the injured elbow flexed to greater than 90 degrees, a valgus stress is applied to the elbow by pulling on the thumb. This hyperflexion isolates the anterior bundle of the UCL, and the valgus stress places the anterior bundle under stretch. This elbow position facilitates the location and palpation of the tensioned ligament under the mass of the flexor-pronator origin. This position alone can elicit pain

B Figure 33-3 A, The medial and lateral epicondyles and olecranon form a straight line with the elbow in full extension. B, When the elbow is flexed to 90 degrees, these landmarks form an equilateral triangle.

forearm in supination and elbow in active flexion.1 Tenderness in this area without a defect could indicate biceps tendonitis or a partial biceps tendon rupture.20 Tenderness with a defect or decreased tension in the biceps tendon is consistent with a complete rupture. To avoid missing a distal biceps tendon rupture, it is imperative to make sure that one is not palpating an intact

Figure 33-4 The examiner flexes the patient’s elbow to 100 degrees to facilitate palpation of the ulnar collateral ligament (UCL) and to uncover the distal insertion of the anterior oblique portion of the UCL.

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over the medial elbow as the anterior bundle is placed on stretch. In the posteromedial area of the elbow, the ulnar nerve is easily palpable in the ulnar groove. An inflamed ulnar nerve is tender and can have a doughy consistency. The examiner should conduct Tinel’s test in three areas: proximal to the cubital tunnel (zone I), at the level of the cubital tunnel where the fascial aponeurosis joins the two heads of the flexor carpi ulnaris (zone II), and distal to the cubital tunnel where the ulnar nerve descends to the forearm through the muscle bellies of the flexor carpi ulnaris (zone III).25 A positive test produces paresthesia in the fifth digit and ulnar-innervated half of the fourth digit and suggests a diagnosis of ulnar neuritis due to entrapment, trauma, or subluxation. The clinician also should test the nerve for hypermobility. The examiner brings the patient’s elbow from extension to terminal flexion as he or she palpates the nerve to determine whether it subluxates or completely dislocates over the medial epicondyle (Fig. 33-5).26 In the posterior region of the elbow, the clinician evaluates the olecranon bursa for swelling or fluctuation, which would indicate olecranon bursitis. One should also palpate this region for any palpable osteophytes on the subcutaneous border of the olecranon that could contribute to the overlying bursitis. The medial subcutaneous border is then palpated for tenderness that could be caused by a stress fracture in a throwing athlete.27 Next, the triceps insertion is examined (Fig. 33-6); tenderness here indicates triceps tendonitis or an avulsion injury if there is an associated defect. Finally, the clinician palpates the posterior,

Figure 33-6 Tenderness over the triceps tendon insertion on the olecranon might indicate triceps tendonitis or triceps avulsion injury.

medial, and lateral aspects of the olecranon in varying degrees of flexion to detect osteophytes or loose bodies. Palpation of the posteromedial olecranon can reveal an osteophyte and swelling, which are present in the throwing athlete with valgus extension overload syndrome.8 Examination of the lateral region of the elbow begins with palpation of the lateral epicondyle. Tenderness directly over the lateral epicondyle is typical of lateral epicondylitis (Fig. 33-7). Tenderness approximately 4 cm distal to the lateral epicondyle over the wrist extensor muscle mass is present in a patient with radial tunnel syndrome, which is a compressive neuropathy of the radial nerve as it travels from the radial head to the supinator muscle.25 Finally, tenderness distal to the location of the radial tunnel can be due to compression of the posterior interosseous nerve as it descends beneath the arcade of Frohse and the supinator muscle. The radial head and radiocapitellar joint distal to the lateral epicondyle are palpated next. Pronation and supination of the forearm enhance this evaluation. Tenderness or crepitation in this area could indicate fracture or dislocation of the radial head, osteochondritis dissecans, or Panner’s disease in the adolescent athlete, or articular fragmentation and bony overgrowth with possible progression to loose-body formation in the young adult athlete.1,28 Finally, palpation of the lateral recess, or soft spot, is performed to evaluate elbow joint effusion.

Range of Motion Figure 33-5 As the patient’s elbow is brought from extension to flexion, the examiner might feel the ulnar nerve subluxate or dislocate anteriorly over the medial epicondyle as in this subject who has a hypermobile nerve.

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Range of motion of the elbow occurs about two axes: (1) flexion and extension and (2) pronation and supination. The normal arc of flexion and extension ranges from 0 to 140 degrees of flexion,29 but the functional arc about which most activities of daily living are performed ranges from 30 to 130 degrees (Fig.

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33-8).30,31 The examiner must compare the range of motion to that of the contralateral extremity to account for normal individual variance. An athlete who has pitched many innings may have a flexion contracture on the dominant side that increases as the season progresses and can decrease between seasons. Injuries that cause loss of extension include capsular strain, flexor muscle strain, intra-articular loose bodies, and an intraarticular fracture. In a recent study, lack of full extension in an acute situation was found to be 97% sensitive in diagnosing a significant bone or joint injury; therefore, if a patient has full extension of the elbow after an acute injury, there is a very low likelihood of a significant bone or joint injury.32 Injuries that cause abnormal lack of flexion include loose bodies, capsular tightness, triceps strain, anterior osteophytes, and coronoid hypertrophy. To measure pronation and supination, the examiner has the patient flex the elbows to 90 degrees while holding pencils in each hand (Fig. 33-9). The examiner must immobilize the humerus in a vertical position when evaluating forearm rotation because patients tend to adduct or abduct the shoulder to compensate for loss of forearm pronation or supination. Acceptable norms for full pronation and supination are 70 and 85 degrees, respectively.19 The functional arc of motion is 50 degrees for both pronation and supination.19 Loss of pronation or supination can be caused by loose bodies, radiocapitellar osteochondritis, radial head subluxation, radial head fractures, or motor nerve entrapment lesions resulting in weakness of the biceps, pronator teres, pronator quadratus, or supinator muscles.1 The examiner also should assess the wrist because wrist injury can cause loss of forearm rotation. When testing range of motion, the examiner also should note the presence or absence of crepitus. He or she must test both

A

B Figure 33-8 The normal arc of extension (A) and flexion (B).

active and passive range of motion because crepitus might not be present on passive range of motion and might be unveiled only through active range of motion. In addition, the clinician should compare active and passive range of motion; if motion is full on passive testing but limited on active testing, pain or paresis might be the limiting factor rather than a mechanical block. Finally, the quality of the endpoint should be noted. Firm endpoints often mean that there is a bony block to motion such as loose bodies, osteophytes, or other joint incongruities. Soft endpoints, on the other hand, most likely are a result of softtissue contractures, such as flexion contractures seen in baseball pitchers.

Strength Testing

Figure 33-7 Lateral epicondylitis causes tenderness over the lateral epicondyle.

It is important to examine the strength of elbow, wrist, and hand muscle groups when evaluating an elbow disorder to assess for a neurologic problem or tendon injury. Biceps brachii muscle strength testing is best conducted against resistance with the forearm supinated and the shoulder flexed from 45 to 50 degrees (Fig. 33-10). Triceps strength testing, on the other hand, is best performed with the shoulder flexed to 90 degrees and

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Figure 33-10 Biceps muscle strength is assessed with the forearm supinated and the shoulder flexed from 45 to 50 degrees. The examiner applies resistance to flexion.

B Figure 33-9 While the patient holds pencils in each hand and flexes the elbows to 90 degrees, measure pronation (A) and supination (B). Due to a previous fracture in the distal radius, this patient demonstrates a slight loss of pronation in the left extremity compared with the right extremity.

the elbow flexed from 45 to 90 degrees (Fig. 33-11).1 Elbow extension strength is normally 70% of flexion strength.29 Pronation, supination, and grip strength are best studied with the elbow in 90 degrees of flexion and the forearm in neutral rotation. Supination strength is approximately 15% greater than pronation strength, and the dominant extremity is from 5% to 10% stronger than the nondominant extremity.29 Finally, the examiner tests the forearm musculature and hand intrinsic strength. The extensor carpi radialis longus musculotendinous unit is best studied with the elbow flexed to 30 degrees and resistance applied to wrist extension.1 However, the extensor carpi radialis brevis musculotendinous unit is best isolated by providing resistance to wrist extension with the elbow in full flexion. The clinician studies the extensor carpi ulnaris muscle by resisted ulnar deviation of the wrist. Weakness in the wrist, finger, and thumb extensors may indicate a posterior interosseous nerve palsy. Weakness of the flexor pollicis longus and flexor digitorum profundus muscles of the index finger is present in an entrapment palsy of the anterior interosseous nerve, which branches from the median nerve approximately 5

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Figure 33-11 Triceps muscle strength is best tested with the shoulder flexed to 90 degrees and the elbow flexed from 45 to 90 degrees.

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cm distal to the medial epicondyle.33 Finally, weakness in the hand intrinsics can indicate ulnar nerve entrapment at the cubital tunnel.

Reflexes Reflexes are evaluated to rule out potential sources of referred pain, such as cervical radiculopathy. An increased response to stimulation can indicate an upper motor neuron lesion, whereas a decreased response can signify a lower motor lesion. The examiner tests the C5 nerve root by the biceps reflex, the C6 nerve root by the brachioradialis reflex, and C7 nerve root by the triceps reflex.

Sensory Examination Next, the examiner should conduct a comprehensive sensory examination to assess for a cervical radiculopathy or a peripheral neuropathy. Light touch and pinprick sensation are both assessed. Diminished sensation in the fifth and ulnar-innervated half of the fourth digits can signify an ulnar neuropathy. However, many entrapment neuropathies of the elbow and forearm, such as anterior interosseous neuropathy, pronator syndrome, posterior interosseous neuropathy, and radial tunnel syndrome, do not have abnormal objective sensory examinations.

A

Stability Testing Either an acute traumatic event or a chronic overload syndrome can result in valgus instability of the elbow. Attenuation or rupture of the anterior oblique bundle of the UCL causes this pattern of instability.1,2 The elbow is examined with patient in either the seated or supine position and the shoulder in maximal external rotation.2 The manual valgus stress test is performed with the elbow flexed 20 to 30 degrees to unlock the olecranon tip from the olecranon fossa while stabilizing the humerus (Fig. 33-12). Valgus stress is then applied to the elbow with the forearm in maximal pronation. Any increased opening or reproduction of the patient’s pain with valgus stress may be indicative of injury to the UCL.2 Often only pain can be elicited without any detectable opening when performing this test when the patient is awake due to patient guarding and the fact that even with complete sectioning of the anterior bundle of the UCL in cadaveric studies, there is only minimal valgus opening that may not be clinically detectable.34

Figure 33-12 Valgus stress testing is accomplished with the patient’s elbow flexed from 20 to 30 degrees and his or her arm secured between the examiner’s arm and trunk.

B Figure 33-13 The lateral pivot-shift test. The examiner supinates the elbow, applies a valgus moment and axial compression, and moves the elbow from full extension (A) to flexion (B).

Posterolateral rotatory instability is essentially a rotational displacement of the ulna and radius on the humerus that causes the ulna to supinate away from the trochlea.35 O’Driscoll35 describes four principal physical examination tests to diagnose this form of instability. The most sensitive is the lateral pivotshift apprehension test. The patient is placed in the supine position with the affected extremity overhead, and the patient’s wrist and elbow are grasped as the ankle and knee are held when examining a knee. The elbow is supinated with a mild force at the wrist, and a valgus moment and compressive force are applied to the elbow during flexion (Fig. 33-13). This results in an apprehension response with reproduction of the patient’s symptoms akin to the anterior apprehension test of the shoulder. The next test is the lateral pivot-shift test or posterolateral rotatory instability test, which reproduces the actual subluxation and the clunk that occurs with reduction. This can usually be accomplished only with the patient under general anesthesia or occasionally after injecting local anesthetic into the elbow. The pivot-shift maneuver causes posterolateral subluxation or dislocation of the radius and ulna off the humerus that reaches a maximum at 40 degrees of flexion, creating a posterolateral prominence over the dislocated radial head and a dimple between the radius and capitellum. As the elbow is flexed past

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extended can also cause discomfort as it stretches the extensor tendons. Finally, the “chair test” can also aid in the diagnosis.36,37 In this test, the patient raises the back of a chair with the elbow in full extension, the forearm pronated, and the wrist dorsiflexed (Fig. 33-16). As the patient attempts to lift the chair, he or she exhibits apprehension in anticipation of pain. The most sensitive test for radial tunnel syndrome is resisted supination with the supinator and extensor carpi radialis brevis muscles in the stretched position (pronation and wrist flexion), which produces pain approximately 4 to 5 cm distal to the lateral epicondyle.38 Resisted third-digit extension can also cause pain in this area in patients with radial tunnel syndrome; however, this maneuver also causes similar pain in patients with lateral epicondylitis. Another indicator of radial tunnel syndrome is the pronator-supinator sign.39 The test is positive if direct tenderness over the radius at 5 cm distal to the lateral epicondyle is markedly greater in full supination than in pronation due to the fact that the radial nerve is located in this position in full supination but moves medially and distally with pronation. Passive pronation of the forearm to its end range with elbow extension also can recreate the symptoms of radial tunnel syndrome by causing a tightening of the origin of the extensor carpi radialis brevis muscles over the nerve.40 Recently, a neural tension test has been described to aid in the diagnosis of radial tunnel syndrome.41 In this test, the radial nerve is placed under tension, which causes pain distal to the lateral epicondyle if the patient has radial tunnel syndrome. This nerve tension is created with shoulder girdle depression, forearm pronation, elbow extension, wrist and finger flexion, and shoulder abduction while the patient is in the supine position. Finally, the clinician tests for damage to the articular surface of the radiocapitellar joint. With the patient’s elbow extended,

Figure 33-14 A, A positive test for posterolateral rotatory subluxation of the elbow. The posterolateral dislocation of the radiohumeral joint produces an osseous prominence and an obvious dimple in the skin just proximal to the dislocated radial head. B, Lateral radiograph made simultaneously with the photograph. The radiohumeral joint is dislocated posterolaterally, and there is rotatory subluxation of the ulnohumeral joint. The semilunar notch of the ulna is rotated away from the trochlea. (From Hyman J, Breazeale NM, Altchek DW: Valgus instability of the elbow in athletes. Clin Sports Med 2001;20:25–45.)

40 degrees, reduction of the ulna and radius together on the humerus occurs suddenly and produces a palpable and visible snap (Fig. 33-14). The third test is the posterolateral drawer test, which is a rotatory version of the Lachman test of the knee. During the test, the lateral side of the forearm subluxates away from the humerus, pivoting around the medial collateral ligament. The final test is the “stand-up test” in which the patient’s symptoms are reproduced as he or she attempts to stand up from the sitting position by pushing on the seat with the hand at the side and the elbow fully supinated.

Provocative and Special Tests Lateral Stress to the extensor carpi radialis longus and brevis muscles reproduces the discomfort associated with lateral epicondylitis. To create this stress, the patient fully extends the elbow and resists active wrist and finger extension (Fig. 33-15). Pain at the lateral epicondyle with this maneuver indicates lateral epicondylitis. This is the most sensitive provocative maneuver for this disorder. Passive flexion of the wrist with the elbow

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Figure 33-15 Test for lateral epicondylitis. Stress to the origin of extensor carpi radialis brevis and longus tendons, which is created by resisting active wrist extension with the elbow fully extended, elicits pain at the lateral epicondyle.

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Figure 33-16 The “chair test.” While holding the elbow in full extension, pronating the forearm, and dorsiflexing the wrist, the patient lifts the back of a chair. The test elicits apprehension in patients with lateral epicondylitis.

the examiner applies an axial load to the joint while supinating and pronating the forearm repeatedly. Pain with this maneuver is a positive radiocapitellar compression test. Medial The most sensitive indirect maneuver for the diagnosis of medial epicondylitis is resisted forearm pronation, which is positive in 90% of patients with this disorder (Fig. 33-17).39 A positive test

Figure 33-17 Resisted forearm pronation elicits pain at the medial epicondyle in patients who have medial epicondylitis.

Figure 33-18 Elbow flexion test for ulnar nerve compression. With the patient’s wrist neutral and forearm supinated, the examiner flexes the patient’s elbow to 135 degrees as he or she applies digital pressure over the cubital tunnel.

elicits pain at the flexor-pronator muscle mass origin on the medial epicondyle. The second most sensitive maneuver is resisted palmar flexion, which is positive in 70% of patients.39 Passive extension of the wrist and fingers also can elicit pain at the medial epicondyle in these patients. The most sensitive and specific provocative test maneuver for diagnosing ulnar nerve compression at the elbow is the elbow flexion test conducted with direct pressure over the cubital tunnel.33 With the patient’s wrist in neutral and forearm supinated, the examiner flexes the elbow to 135 degrees and applies digital pressure over the cubital tunnel for a period of 3 minutes or until the symptoms are elicited (Fig. 33-18).42 A positive test results in paresthesia or dysesthesia in the fifth and ulnar-innervated half of the fourth digit. A simple nerve compression test and Tinel’s test also are used to aid in making the diagnosis. Positive findings with these tests without the use of electrodiagnostic studies have been shown to accurately predict the success rate of an ulnar nerve transposition procedure.43 Anterior Vague anterior elbow or proximal forearm pain can be caused by entrapment of the median nerve at many sites. First, as discussed previously, the median nerve can become compressed under the ligament of Struthers. In this case, resisted flexion of the elbow between 120 and 135 degrees of flexion elicits the symptoms.25 Active elbow flexion with the forearm in pronation, which tightens the lacertus fibrosus, causes symptoms in patients with compression of the nerve by the lacertus fibrosus.25

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If resisted pronation of the forearm combined with flexion of the wrist reproduces the symptoms, the nerve may be compressed as it passes through the pronator teres muscle.25 Finally, if resisted flexion of the superficialis muscle of the third digit results in pain in this area, the nerve may be entrapped in the superficialis arch.25 Anterior elbow pain also can be due to biceps or brachialis tendonitis. These diagnoses are suggested when resisted forearm supination and elbow flexion produce increased pain. The clinician should also assess for the tension on the distal biceps tendon with resisted flexion and supination because decreased tension could be the result of a distal biceps tendon tear. Finally, a new clinical test has been described for the diagnosis of complete distal biceps tendon ruptures, the passive pronation-supination test (Warren Harding, MD, personal communication, 2004). With an intact biceps tendon, the biceps’ muscle belly rises visibly and palpably in the arm with passive supination, returns to a normal position with return to the neutral position, and then flattens and moves to a more distal position with pronation. In an unpublished study of patients with MRI-documented complete biceps tendon avulsions, Harding found that the muscle belly did not rise and fall with passive supination and pronation of the forearm. Posterior The valgus extension overload test and valgus extension snap maneuver consistently produce discomfort in patients with valgus extension overload syndrome.1 With the patient in the seated position, the examiner applies a moderate amount of valgus stress to the elbow as he or she moves the elbow from 30 degrees of flexion to full extension. This maneuver simulates posteromedial olecranon impingement and recreates the pain that the athlete experiences during the late acceleration phase of throwing. A modified Thompson test has been described to help diagnose a complete distal triceps tendon tear.44 This test is performed with the elbow flexed to 90 degrees and the arm abducted to eliminate the effect of gravity on elbow extension. The examiner squeezes the triceps muscle belly and observes the elbow for extension motion. If there is no motion, a complete tear is present.

Figure 33-19 Anteroposterior radiographic view.

humerus, and the olecranon and coronoid processes. Fat pad signs are visualized on the lateral view and indicate capsular distention or joint effusion, and, if present, intra-articular abnormalities should be suspected. The presence of the anterior fat pad sign sometimes is normal, whereas the presence of the posterior fat pad sign is always abnormal. If an injury to the radiocapitellar joint is suspected, the clinician should order a radiocapitellar view, which is obtained with the elbow positioned as for a lateral projection, but with the beam angled 45 degrees anteriorly (Fig. 33-21). This provides an unobstructed view of the proximal radius and capitellum and is useful in making the diagnosis of osteochondral fractures of the capitellum or injuries to the radial head and neck.

Imaging Studies Plain Radiography Plain radiographs may be ordered to supplement the information obtained during the history and physical examination. They enable the clinician to gather formative information on bone, joint positioning, and the presence or absence of soft-tissue swelling, loose bodies, ectopic ossification, and foreign bodies. Standard radiographic views include anteroposterior and lateral projections, which can be supplemented by oblique and axial views as necessary.45 An anteroposterior view is taken with the arm in full extension and the forearm supinated (Fig. 33-19). This position allows good visualization of the medial and lateral epicondyles, the radiocapitellar joint, and the trochlear articulation with the medial condyle. The lateral radiographic view should be taken with the elbow flexed to 90 degrees and the forearm in neutral rotation and the beam should be reflected distally to account for the normal valgus position of the elbow (Fig. 33-20). The lateral projection provides visualization of the radiocapitellar and ulnotrochlear articulations, the distal

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Figure 33-20 Lateral radiographic view.

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Figure 33-21 Radial head radiographic view.

The axial view is often helpful in evaluating injury in the throwing athlete. For this view, the elbow is flexed to 110 degrees with the forearm flat on the cassette, and the beam is directed perpendicular to the cassette (Fig. 33-22). This allows visualization of the posterior compartment, specifically visualization of the articulation of the posterior olecranon and the humerus. The clinician should closely evaluate this view for a posteromedial osteophyte, which occurs with valgus extension overload syndrome. The reverse axial projection, which provides better visualization of the olecranon and trochlea, is taken with the elbow in maximal flexion and the arm flat on the cassette.45 Stress Radiography Stress views can be obtained in patients with suspected ligament disruption or elbow instability. The examiner applies varus or valgus stress to the elbow during radiography and assesses the films for any asymmetrical widening of the joint. A gravity stress view is obtained with the patient supine and the arm abducted to 90 degrees from the body; the beam is centered on the elbow. With maximal supination of the forearm, a valgus stress is applied to the elbow. Static views that demonstrate an increase in joint space of more than 2 mm are considered abnormal.45

Cain et al2 suggest obtaining anteroposterior views with 0, 5, 10, and 15 N of valgus stress applied to each elbow at 25 degrees. An increase in opening with increasing stress compared with the contralateral uninjured side is indicative of UCL injury. Dynamic evaluation under fluoroscopy can be helpful in identifying subtle abnormalities; however, instability is often not well visualized with these dynamic views. Computed Tomography CT provides excellent osseous detail and can be used to evaluate the elbow for loose bodies not evident on plain films, osteochondral defects, articular congruity, trabecular irregularities, and fractures for displacement (Fig. 33-23).45 Images are acquired in 1-mm intervals and can be reformatted into coronal, sagittal, or three-dimensional images to help with surgical planning. CT arthrography may be indicated to detect intra-articular loose bodies, to evaluate capsular topography in patients with capsular contractures or tears, and to evaluate the articularbearing surfaces.45 It may be the diagnostic modality of choice to examine these entities in patients in which an MRI is contraindicated (e.g., patients with loose metal fragments in

Figure 33-22 Axial radiographic view.

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B Figure 33-23 This 34-year-old woman had a traumatic elbow dislocation. After reduction, sagittal computed tomography scan reconstruction (A) shows a small coronoid fracture and posterior olecranon fossa intra-articular bone fragment, also seen in axial image (B).

their eye orbits or perispinal region or in those with pacemakers). Timmerman et al46 compared CT arthrography with nonenhanced MRI in 25 baseball players for the ability to correctly diagnose UCL injuries and discovered that CT arthrography had a sensitivity of 86% and specificity of 91% compared to nonenhanced MRI, which had sensitivity of 57% and specificity of 100%. Both techniques were 100% sensitive for complete tears; however, partial tears were more accurately diagnosed by CT arthrogram. Magnetic Resonance Imaging MRI is the modality of choice for the evaluation of soft-tissue structures, such as ligaments, tendons, and muscles, and has largely replaced arthrography as the study of choice for intraand periarticular soft-tissue structures. MRI is used to evaluate capsuloligamentous or musculotendinous disruption as well as intra-articular abnormalities, such as epiphyseal fractures or chondral defects (Fig. 33-24). Images are obtained in 1- to 3-mm intervals with formats in sagittal, coronal, and axial planes. Nonenhanced MRI can be used to evaluate tendons such as the biceps and triceps when physical examination is equivocal. MRI may be helpful to evaluate for partial-thickness distal biceps tendon ruptures (Fig. 33-25) when physical examination reveals an intact tendon but a patient has pain in the distal biceps tendon area with associated weakness.20 T1-weighted images demonstrate a replacement of the normal low signal intensity in the distal biceps tendon with intermediate signal intensity, and T2-weighted images reveal high signal edema surrounding the distal biceps tendon and its insertion. MRI can also aid in the diagnosis of tendonopathy and partial tears involving the wrist extensor and pronator-wrist flexor tendon origins seen in patients with lateral and medial epicondylitis, respectively. The changes that accompany tendinosis manifest as either intermediate to low signal intensity on T1-weighted images in cases of fibroblastic proliferation or high signal intensity in cases of

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fibroblastic proliferation with mucoid degeneration.47 Attrition on both T1- and T2-weighted images with high signal intensity is consistent with a partial tear of the tendon’s origin. Discontinuity on both T1- and T2-weighted images with high signal intensity of the free ends is indicative of a complete tear (Fig. 33-26). Saline-enhanced MRI direct arthrogram has been shown to be the most accurate study to evaluate UCL injuries (Fig. 3327).48 Schwartz et al48 reported 92% sensitivity and 100% specificity with diagnosing UCL injury using this modality. Sensitivity was higher for complete tears (95%) than for partial tears (86%). Saline is injected through the lateral soft spot into the joint, and saline extravasation through the UCL indicates a full-thickness tear. MRI can also be used to identify disorders associated with UCL injury, such as posteromedial impingement changes. A recent study, however, cautions against diagnosing UCL injuries and associated disorders based solely on MRI findings.49 Sixteen asymptomatic professional baseball players with no history of injury to their elbows underwent MRI. UCL abnormalities (thickening, signal heterogeneity, or discontinuity) were present on 87% of players’ dominant elbows, and findings consistent with posteromedial impingement were present in 13 of 16 subjects.49 Finally, MRI can also be used to evaluate for subtle avulsion fractures or stress fractures that may not be evident on plain radiographs (Fig. 33-28). Using a combination of radiographs and MRI scans, Salvo et al50 were able to identify eight avulsion fractures of the sublime tubercle of the ulna in 33 consecutive patients treated for UCL injuries. Regarding stress injury to bone, Schickendantz et al27 reported on a series of seven professional baseball players with proximal ulnar osseous stress injury detected on MRI with normal plain radiographs. Poorly defined, patchy areas of low signal intensity in the proximal posteromedial olecranon continuous with the cortex were seen on all of the T1-weighted images. All short tau inversion recovery

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Figure 33-24 A, Magnetic resonance imaging (MRI) arthrogram in a 54-year-old man with previous football injuries and limited motion. Sagittal section shows loose body in anterior aspect of the elbow joint (arrow). Anteroposterior radiographic view (B) and coronal MRI (C) in a 20-year-old pitcher with elbow pain show osteochondritis dissecans of the capitellum. Arrow indicates chondral defect.

C

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A Figure 33-26 Coronal magnetic resonance image shows traumatic combined proximal ulnar collateral ligament disruption and common flexor origin disruption in a 17-year-old wrestler after a second elbow dislocation.

B Figure 33-25 Sagittal (A) and axial (B) images show a complete distal biceps tendon avulsion off the radius.

Figure 33-27 Contrast coronal magnetic resonance image reveals complete ulnar collateral ligament disruption. Arrow indicates positive capsular T sign.

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A

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Figure 33-28 Lateral radiographic view (A) and lateral magnetic resonance image (B) show posterior olecranon stress fracture in a teenage pitcher with posteromedial impingement. Arrows indicate area of stress.

images showed areas of high signal intensity in the posteromedial olecranon.

CONCLUSIONS A comprehensive history and physical examination of the elbow and surrounding joints are the most important part of the evalu-

ation of elbow disorders. The examiner can use additional diagnostic tests, such as plain radiographs, CT, and MRI, to confirm the diagnosis or further narrow the scope of potential diagnoses. Because the elbow is a very complex joint with multiple different potential disorders, it is imperative to perform a very thorough examination and to conduct every portion of the examination to avoid missing a diagnosis.

REFERENCES 1. Andrews JR, Whiteside JN, Buettner CM: Clinical evaluation of the elbow in throwers. Oper Tech Sports Med 1996;4:77–83. 2. Cain EL, Dugas JR, Wolf RS, et al: Elbow injuries in throwing athletes: A current concepts review. Am J Sports Med 2003;31:621–635. 3. Slocumb DB: Classification of elbow injuries from baseball pitching. Tex Med 1968;64:48–53. 4. Jobe FW, Nuber GN: Throwing injuries of the elbow. Clin Sports Med 1986;5:621–635. 5. Dehaven KE, Evarts CM: Throwing injuries of the elbow in athletes. Orthop Clin North Am 1973;4:801–808. 6. Barnes DA, Tullos HS: An analysis of 100 symptomatic baseball players. Am J Sports Med 1978;6:62–67. 7. Bennett GE: Elbow and shoulder lesions of baseball players. Am J Surg 1959;98:484–492. 8. Wilson FD, Andrews JR, Blackburn TA, et al: Valgus extension overload in the pitching elbow. Am J Sports Med 1983;11:83–87. 9. King JW, Brelsford HJ, Tullos HS: Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop 1969;67:116–123. 10. Parr TJ, Burns TC: Overuse injuries of the olecranon in adolescents. Orthopedics 2003;26:1143–1146. 11. Kobayashi K, Burton KJ, Rodner C, et al: Lateral compression injuries in the pediatric elbow: Panner’s disease and osteochondritis dissecans of the capitellum. J Am Acad Orthop Surg 2004;12:246–254. 12. Yadao MA, Field LD, Savoie FH 3rd: Osteochondritis dissecans of the elbow. Instr Course Lect 2004;53:599–606. 13. Beals RK: The normal carrying angle of the elbow. Clin Orthop 1976;19:194–196.

14. Andrews JR, Wilks KE, Satterwhite YE, et al: Physical examination of the thrower’s elbow. J Orthop Sports Phys Ther 1993;17:296–304. 15. Flynn JC, Richards JF, Saltzman RI: Prevention and treatment of non-union of slightly displaced fractures of the humeral condyle in children. An end-result study. J Bone Joint Surg Am 1975;57:1087– 1092. 16. Coleman WW, Strauch RJ: Physical examination of the elbow. Orthop Clin N Am 1999;30:15–20. 17. Shah AK, Pruzansky ME: Ruptured biceps brachii short head muscle belly: A case report. J Shoulder Elbow Surg 2004;13:562–565. 18. Cope MR, Ali A, Bayliss NC: Biceps rupture in bodybuilders: Three case reports of rupture of the long head of the biceps at the tendon-labrum junction. J Shoulder Elbow Surg 2004;13:580–582. 19. Volz RE, Morrey BF: The physical examination of the elbow. In Morrey BF (ed): The Elbow and Its Disorders. Philadelphia, WB Saunders, 1985, pp 62–72. 20. Vardakas DG, Musgrave DS, Varitimidis SE, et al: Partial rupture of the distal biceps tendon. J Shoulder Elbow Surg 2001;10:377–379. 21. Gessini L, Jandolo B, Pietrangeli A: Entrapment neuropathies of the median nerve at and above the elbow. Surg Neurol 1983;19:112–116. 22. O’Driscoll SW, Jaloszynski R, Morrey BF, et al: Origin of the medial collateral ligament. J Hand Surg [Am] 1992;17:164–168. 23. Veltri DM, O’Brien SJ, Field LD, et al: The milking maneuver: A new test to evaluate the MCL of the elbow in the throwing athlete [Abstract]. J Shoulder Elbow Surg 1995;4:S10. 24. Hyman J, Breazeale NM, Altchek DW: Valgus instability of the elbow in athletes. Clin Sports Med 2001;20:25–45.

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25. Eversmann WW: Entrapment and compressive neuropathies. In Green DP (ed): Operative Hand Surgery. New York, Churchill Livingstone, 1993, pp 1341–1385. 26. Childress HM: Recurrent ulnar-nerve dislocation at the elbow. Clin Orthop 1975;108:168–173. 27. Schickendantz MS, Ho CP, Koh J: Stress injury of the proximal ulna in professional baseball players. Am J Sports Med 2002;30:737–741. 28. Birk GT, DeLee JC: Osteochondral injuries: Clinical findings. Clin Sports Med 2001;20:279–286. 29. Boone DC, Azen SP: Normal range of motion of joints in male subject. J Bone Joint Surg Am 1979;61:756–759. 30. Morrey BF, Askew LJ, An K-N, et al: A biomechanical study of normal functional elbow motion. J Bone Joint Surg Am 1981;63:872– 877. 31. Askew LJ, An K-N, Morrey BF, et al: Functional evaluation of the elbow: Normal motion requirements and strength determinations. Orthop Trans 1981;5:304–305. 32. Docherty MA, Schwab RA, Ma OJ: Can elbow extension be used as a test of clinically significant injury? South Med J 2002;95:539– 541. 33. Wright TW: Nerve injuries and neuropathies about the elbow. In Norris TR (ed): Orthopaedic Knowledge Update: Shoulder and Elbow. Rosemont, IL, American Association of Orthopedic Surgeons, 1997, pp 369–377. 34. Callaway GH, Field LD, O’Brien SJ, et al: The contribution of medial collateral ligaments to valgus stability of the elbow: A biomechanical study [Abstract]. J Shoulder Elbow Surg 1995;4:S58. 35. O’Driscoll SW: Classification and evaluation of recurrent instability of the elbow. Clin Orthop 2000;370:34–43. 36. Plancher KD, Halbrecht J, Lourie GM: Medial and lateral epicondylitis in the in the athlete. Clin Sports Med 1996;15:283–305. 37. Gardner RC: Tennis elbow: Diagnosis, pathology, and treatment: Nine severe cases treated with a new reconstructive operation. Clin Orthop 1970;72:248–253.

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38. Lister GD, Belsole RB, Kleinert HE: The radial tunnel syndrome. J Hand Surg [Am] 1979;4:52–59. 39. Gabel GT, Morrey BF: Tennis elbow. Instr Course Lect 1998;47: 165–172. 40. Portilla Molina AE, Bour C, Oberlin C, et al: The posterior interosseous nerve and the radial tunnel syndrome: An anatomical study. Int Orthop 1998;22:102–106. 41. Ekstrom RA, Holden K: Examination of and intervention for a patient with chronic lateral elbow pain with signs of nerve entrapment. Phys Ther 2002;11:1077–1086. 42. Buehler MJ, Thayer DT: The elbow flexion test. A clinical test for cubital tunnel syndrome. Clin Orthop 1988;233:213–216. 43. Greenwald D, Moffitt M, Cooper B: Effective surgical treatment of cubital tunnel syndrome based on provocative clinical testing without electrodiagnostics. Plast Reconstr Surg 1999;104:215–218. 44. Viegas SF: Avulsion of the triceps tendon. Orthop Rev 1990;19: 533–536. 45. Chen AL, Youm T, Ong BC, et al: Imaging of the elbow in the overhead throwing athlete. Am J Sports Med 2003;31:466–473. 46. Timmerman LA, Schwartz ML, Andrews JR: Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography. Evaluation in 25 baseball players with surgical confirmation. Am J Sports Med 1994;22:26–32. 47. Miller TT: Imaging of elbow disorders. Orthop Clin North Am 1999; 30:21–36. 48. Schwartz ML, Al-Zahrani S, Morwessel RM, et al: Ulnar collateral ligament injury in the throwing athlete: Evaluation with saline-enhanced MR arthrography. Radiology 1995;197:297–299. 49. Kooima CL, Anderson K, Craig JV, et al: Evidence of subclinical medial collateral ligament injury and posteromedial impingement in professional baseball players. Am J Sports Med 2004;32:1602–1606. 50. Salvo JP, Rizio L, Zvijac JE, et al: Avulsion fracture of the ulnar sublime tubercle in overhead throwing athletes. Am J Sports Med 2002;30: 426–431.

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34

Instability and Arthroscopy Jeffrey R. Dugas and Amy Bullens-Borrow

In This Chapter Acute dislocation Ulnar collateral ligament (UCL) injury Nonoperative management Surgery—UCL reconstruction Posterolateral rotatory instability Elbow arthroscopy

INTRODUCTION • The incidence of overuse elbow injuries is increasing at an alarming rate, particularly in the young overhead athlete population. • With increasing frequency, injuries that were once limited to the elite professional are now being treated in the young adolescent. Awareness of these trends on the part of the treating physicians, trainers, therapists, and parents is crucial to injury prevention. • This chapter is designed to review the injuries that occur to the elbow that cause instability, along with the evaluation and treatment of these injuries. As a related topic, elbow arthroscopy techniques and indications are reviewed.

ELBOW INSTABILITY Relevant Anatomy The elbow articulation allows two major motions: flexionextension through the ulnohumeral and radiocapitellar joints and pronation-supination through the proximal radioulnar joint. The osseous configuration confers up to 50% of the stability of the joint when in full extension, but stability is increasingly reliant on soft tissues with increasing flexion. Disruption of the bony architecture as a result of fractures or dysplasias can affect the stability of the elbow and subsequently alter the motion and stresses placed on the soft-tissue supports. As an example, some fractures of the coronoid process can lead to significant elbow instability and increased stress on the radial head. The radial head is an important secondary restraint to valgus load that becomes the primary restraint with injury to the UCL. Thus, if the radial head is fractured, it is important to check the UCL for injury. The soft-tissue stabilizers are the joint capsule, ligaments, and musculotendinous units.1 The major ligaments of the elbow are the UCL (ulnar collateral ligament) and the lateral collateral

ligament (LCL) complex (Fig. 34-1). The UCL has two clinically important bundles: the anterior bundle and the posterior bundle. The LCL complex is the primary restraint to varus and posterolateral rotatory stress. The lateral UCL, connecting the lateral epicondyle of the humerus to the supinator crest of the lateral side of the ulna, is the most important stabilizer for posterolateral rotatory instability. The annular ligament stabilizes the proximal radioulnar joint1 and functions as a secondary restraint to posterolateral rotatory stress along with the common extensor origin, anterior and posterior capsules, and the radial collateral ligament, which is the portion of the LCL between the lateral epicondyle and the annular ligament.2

Epidemiology The elbow is the second most common joint that is dislocated in adults, with most dislocations occurring in the posterolateral direction.3 The annual incidence is 6 to 8 dislocations per 100,000 people. Elbow dislocations account for 11% to 28% of elbow injuries.1 Although simple elbow dislocations are typically managed with closed reduction and early range of motion, a small percentage of patients continue to have instability symptoms, many of these due to posterolateral rotatory instability. The exact percentage is not known. Medial instability can occur secondary to an elbow dislocation that was traumatic or can be secondary to chronic overuse. Although medial instability is rarely symptomatic in the nonoverhead athlete, it can be problematic in activities of daily living or recreation and warrants investigation in such individuals. In the overhead athletic population, UCL injury is rarely the result of a frank dislocation but rather due to chronic overuse. Acute medial elbow instability can occur in overhead athletes but occurs more commonly in contact or tumbling sports. In football, UCL injuries can be an acute injury, but, as documented in a report by Kenter et al,4 even in the National Football League, UCL injuries that are acute rarely require operative intervention even in overhead athletes (e.g., the quarterback). It is similarly believed that an acute UCL injury to a baseball thrower also can be treated nonoperatively if it is secondary to trauma and the player has not previously had medial-side elbow pain. Chronic injuries are becoming an increasingly concerning problem, even in the high school baseball athlete, as we have seen a significant increase in the number of high school athletes seeking medical attention for medial-side elbow pain, secondary to UCL tears.

Acute Dislocation Elbow dislocation usually occurs from a fall on an outstretched hand. It is theorized that valgus and axial load occur while the forearm is in supination (Hildebrand) and the elbow may be

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A

B Figure 34-1 A, The medial ligamentous structures of the elbow. Note the anterior band of the ulnar collateral ligament, which is the main stabilizer to a valgus stress. B, The lateral collateral ligament complex. (From Agur AMR, Lee MJ: Grant’s Atlas of Anatomy, 10th ed. Philadelphia, Lippincott, Williams & Wilkins, 1999.)

slightly flexed or hyperextended. Elbow dislocations are classified by direction of dislocation as posterior, lateral, anterior, or divergent and also as simple or complex, depending on whether fractures are also present. Posterior or posterolateral dislocations are most common.

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Elbow dislocations occur during a variety of sporting activities, both contact and noncontact. The effect of the injury on the athlete’s return to play depends on the sport and position as well as associated injuries. Some sports are more commonly associated with elbow dislocations. A recent study highlighted

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the increase in elbow dislocations associated with winter sporting activities since snowboarding has become more popular. Snowboarders had 17 elbow dislocations (simple or complex) of 64 elbow injuries compared to 8 elbow dislocations of 152 elbow injuries in skiers.5 Treatment of acute simple elbow dislocations begins with a good history and examination of the affected extremity. While obtaining the history, the mechanism of injury, previous injury to the affected extremity, symptoms of numbness, paresthesias, weakness, and excessive pain should be sought. Physical examination should involve inspection, palpation (elbow, forearm, shoulder, wrist, and hand) as well as a thorough neurologic and vascular examination of the affected extremity and comparison to the unaffected extremity before reduction. Reduction should be performed with adequate sedation and should be followed by a postreduction radiograph showing concentric reduction. There are many techniques to reduce posterior elbow dislocations, but the most common method is by longitudinal traction of the forearm with the elbow held in about 30 degrees of flexion while an assistant is holding countertraction on the upper arm. If any medial or lateral translation is present, it is corrected first, then the olecranon is pushed distally with the thumb of the person performing the reduction. Once the elbow is reduced, it is fully flexed. Prior to splinting, the elbow should be taken through a range of motion to determine the stable arc of motion. Checking for instability of the UCL should be performed and the forearm should be pronated and supinated while the elbow is flexed and extended. If there is isolated damage to the UCL, then the elbow will be more stable with the forearm in supination. If the LCL complex is damaged without damage to the UCL being present, then the elbow will be more stable with the forearm in pronation. If both ligaments are damaged, then the elbow is best splinted with the forearm in neutral.1 The elbow should be splinted, and then an early range-of-motion program begun as early as 3 days postreduction. In some cases, a hinged brace can be employed with increasing degrees of extension allowed as the healing process progresses.1 It is rare for a simple elbow dislocation to be irreducible by closed means or for immediate surgical repair or reconstruction of the ligaments to be required. There has been a recent trend to shortening the immobilization period even further. In a study performed at the Naval Academy, 20 posterior elbow dislocations were treated on postreduction day 1 with an active range-of-motion protocol. They were seen on nearly a daily basis for a supervised rangeof-motion program and supplemental modalities such as cryotherapy, electrical stimulation, and compression bandages to reduce swelling for 2 weeks. These patients achieved their final range of motion in 19 days. All patients achieved range of motion within 5 degrees of the unaffected elbow. Only 15% had heterotopic ossification on follow-up radiographs, none of which were clinically significant. No early redislocations occurred. One patient had a redislocation 15 months later in a contact injury and was treated with the same protocol without further incident. No other cases of instability occurred.6 Common sequelae of acute simple elbow dislocations include loss of motion of the affected elbow, heterotopic ossification, and recurrent instability. Loss of motion is the most frequent complaint, with loss of 10 to 20 degrees of extension not uncommon.3 Heterotopic ossification can occur in as many as 55% of patients.1 Degenerative changes were also found after dislocation in some patients.3 Neurovascular injuries can occur in simple dislocations and must be identified in the initial assess-

ment in order to avoid potentially disastrous complications. The brachial artery can become entrapped as can the median or ulnar nerves. Treatment is exploration of the affected structures immediately upon discovery of the problem. Return to play is based on sport-specific and position-specific requirements. In the early postdislocation period, a noncontact athlete may be able to perform at competition level with a hinged brace for protection. In contact sports, even a hinged brace may not be enough protection. Certain minimal goals should be achieved before return to play in any sport. These include return of range of motion, normal neurovascular examination, and relative stability through the functional range of motion for the sport. Soft-tissue healing is generally adequate to begin ligament-stressing exercise by 6 weeks after the injury. Return to contact sports with a brace can be considered after stability is restored but should be individually based. As a general rule, we do not like to remove a protective brace from an athlete during a competition season. If an athlete suffers an elbow dislocation and we begin bracing for sport activity, we continue the brace until the end of the season. If the elbow is stable after the season is over, bracing is not required for further participation in subsequent seasons.

MEDIAL INSTABILITY Medial elbow pain in the overhead athlete should be taken seriously by both the player and health care team. Medial instability secondary to UCL injury should be suspected and ruled out. Chronic medial instability can be caused by chronic overuse due to repetitive intrinsic stress such as muscular contraction or extrinsic stress due to tensile overload.7 This can lead to microtears in the UCL that, if not given appropriate time to heal, can lead to attenuation and medial instability.

Relevant Anatomy The UCL is the primary restraint to valgus stress, with the radial head being a secondary restraint. The UCL has two components: the anterior bundle and the posterior bundle. The anterior bundle is the primary restraint to valgus stress to the elbow when it is at 30, 60, or 90 degrees of flexion.8 Its origin is the anteroinferior aspect of the medial epicondyle of the humerus and its insertion is the medial portion of the coronoid process, an area called the sublime tubercle.9 Its mean length is 27.1 ± 4.3 mm and mean width, in one study, is 4.7 ± 1.2 mm.8 An unpublished study done at our institution, regarding the anterior bundle of the UCL, showed that the mean proximal width of the ligament is 6.8 ± 1.4 mm and mean distal width is 9.2 ± 1.6 mm. Also noted in this cadaveric study was a mean distance of 2.8 mm from the proximal edge of insertion of the ligament into the ulna to the ulnar articular cartilage edge.10

Biomechanics of the Ulnar Collateral Ligament and Pitching The majority of stress present in the UCL occurs during the late cocking and early acceleration phases of throwing.11–13 The baseball pitch occurs with the elbow flexed from 90 to 120 degrees during the acceleration phase of throwing, after which the elbow rapidly extends.14 The elbow is then subjected to distraction stress during extension in the release phase. The UCL accounts for 54% of the valgus stability during elbow flexion of 90 degrees and resists 78% of distraction during the release phase.15 The static torque experienced by the UCL in the course of overhead throwing is nearly the same as the ultimate strength of the lig-

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ament itself.12 Tensile stress occurs in the medial compartment subjecting the UCL, flexor-pronator mass, ulnar nerve, and medial epicondyle apophysis in the skeletally immature athlete to tremendous stress. Shear stress occurs in the posterior compartment subjecting the olecranon and olecranon fossa/trochlea to injury. Compression laterally occurs during throwing, which subjects the radiocapitellar joint to injury. Thus, if the medial elbow is chronically unstable, other areas of the elbow can have clinical findings as well, such as chondromalacia and osteophyte formation as a result of microinstability. Subtle laxity may present with symptoms of ulnar neuritis or flexor-pronator tendonitis. All cases of elbow pain in the throwing athlete should be checked for UCL laxity as an underlying cause.13

History Overhead athletes presenting with medial elbow pain need a very detailed history taken for diagnostic as well as educational purposes. Information on onset of symptoms, the phase of throwing in which the symptoms occur, training changes, previous injuries to the elbow or shoulder, changes in velocity and accuracy, which types of pitches are painful, the number of innings pitched in recent seasons, and associated symptoms such as nerve and vascular symptoms should all be collected.7,13,16 Eighty-five percent of patients have pain in the acceleration phase and less than 25% have any pain in the deceleration phase.13,17 In some patients, the offending pitch can be identified as causing an acute rupture of the UCL, but more often the pain comes on gradually and becomes more persistent and painful over time. Ulnar nerve symptoms such as paresthesias in the fourth and fifth digits are present in nearly one fourth of patients; some authors have found ulnar neuritis in as many as 40%.7,11 Nineteen percent have accompanying posterior elbow pain as noted in one study.11 Any history of previous treatment such as therapy, injections, and surgery is essential to interpreting current signs and symptoms as well as radiographic studies.

Physical Examination Physical examination should begin with an inspection of the elbow for any deformity, limitation of motion, swelling, or bruising. Carrying angle averages 11 degrees in men and 13 degrees in women. Some asymptomatic professional throwers can have carrying angles exceeding 15 degrees. Elbow flexion contractures are seen in 50% of professional throwers as well. Neither finding is necessarily indicative of an injury but is important to note nonetheless.13,18 Palpation of the elbow should include all bony prominences as well as the UCL, flexor-pronator origin, ulnar nerve, and other soft-tissue structures. The UCL is best palpated with the elbow in 50 to 70 degrees of flexion.13 Point tenderness is most common 1 to 2 cm distal to the medial epicondyle.7 Palpation of the ulnar nerve for tenderness, subluxation, and Tinel’s sign as well as distal motor and sensory examination should be performed to evaluate for ulnar neuritis or neuropathy.13 Palpation of pulses should also be performed. Testing the elbow for medial laxity is best performed with the elbow flexed at 30 degrees, forearm pronated, and the wrist passively flexed (Fig. 34-2). The patient can also be placed supine with the arm abducted and the shoulder maximally external rotated. This position provides the examiner with the easiest position to hold the patient’s arm and prevents shoulder rotation from clouding the examination. The pronation and wrist flexion, when done passively, relax the flexor-pronator mass and make the medial aspect of the elbow easier to palpate for joint

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Figure 34-2 Clinical evaluation of the ulnar collateral ligament. The elbow is placed in 30 degrees of flexion and full pronation with the wrist passively flexed. The examiner places a valgus stress and assesses the end feel, the amount of valgus opening, and any pain elicited.

opening. This also decreases any potential dynamic stabilization that occurs.13 Andrews tests the laxity in the position described with the patient seated, then tests the stability also with the patient supine, the forearm supinated, and elbow flexed at 30 degrees. The test is then repeated with the patient prone with the elbow flexed 30 degrees and the forearm pronated. The Milking maneuver is also performed by grasping the patient’s thumb and flexing the elbow to 90 degrees using the thumb to provide valgus stress. This was originally described with the patient grasping his or her own thumb with the opposite hand, but not all patients can perform this maneuver and the examiner needs to be able to simulate it in those patients who cannot. Valgus extension overload can be tested by repeatedly forcefully extending the elbow while placing a valgus stress on it. A positive test occurs when the patient has pain at the posteromedial olecranon tip as the elbow reaches full extension.7,13,19

Radiographic Studies Radiographic studies are necessary in the evaluation of a throwing athlete with medial elbow pain. Anteroposterior, lateral, two oblique, an oblique axial with the elbow in 110 degrees of flexion, and stress views of both the affected and the unaffected extremity comprise a thorough radiographic examination.13 The oblique axial view is helpful for visualizing posteromedial osteophytes. The standard anteroposterior, lateral and two oblique views may appear normal or may show signs of chronic injury to the medial elbow such as medial osteophytes or calcifications within the ligament.8 Stress radiographs should be obtained bilaterally to compare the patient’s overall ligamentous laxity. A difference of 2 mm is considered diagnostic of medial elbow instability.8 In the past, computed tomography arthrography was used frequently to check for UCL tears. Its sensitivity is 86% and specificity is 91%. Saline-enhanced magnetic resonance imaging is now the gold standard, with sensitivity of 92% and specificity of 100% (Fig. 34-3).20 Magnetic resonance imaging also has the added benefit of diagnosing other potential injuries such as injuries to the flexor-pronator origin. It was previously believed that the T sign of dye on a contrast study was diagnostic of UCL injury. Recent data suggest that the proximal fibers of the UCL insertion onto the sublime tubercle and the capsular fibers may

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has not met with favorable results in overhead athletes, all the currently employed reconstruction techniques have enjoyed significant clinical success with high rate of return in elite athletes. Our preference is to use a modification of Jobe’s original technique, including ulnar nerve transposition to a subcutaneous location beneath a leash of flexor-pronator fascia. This preference is born out of nearly 2 decades of experience at our institution with predictably good results. It is not, however, considered by us to be the only way to achieve the expected goal. This is simply the technique with which we are most acquainted and comfortable.

Author’s Preferred Surgical Technique

Figure 34-3 Contrast-enhanced magnetic resonance imaging of the elbow. Note the contrast extravasated distal to the elbow joint on the medial side. The ulnar collateral ligament is noted to have a tear in its midsubstance.

insert up to 3 mm distal to the articular surface, making the T sign a less-than-perfect diagnostic finding.10

Treatment Options Once the diagnosis of UCL injury is made, the decision regarding treatment is made with careful consideration of the athlete’s demands on the injured area (sport and position played), previous treatment of the injury (rest and rehabilitation done appropriately), and the degree of ligament injury. The vast majority of partial ligament injuries should be treated initially with conservative treatment. Complete injuries in nonthrowing athletes or low-demand throwing athletes may also be treated with a trial of conservative care. Nonoperative treatment consists of a period of rest, anti-inflammatory medi-cation, and therapy modalities such as cryotherapy to decrease pain. Range-ofmotion exercises of the elbow and strengthening exercises of the flexor-pronator muscles should be performed during the rest period. Bracing may be used if necessary. In throwing athletes, shoulder strengthening should also be performed to prevent any shoulder injury from occurring when returning to throwing. After a period of “active rest,” a throwing program should be instituted. Generally, the program takes about 3 months to complete if done properly.13,14 Some authors recommend a brace be worn at night in the “active rest” period and a hyperextension brace be worn in the throwing program. With this protocol, one study shows that 42% of players will return to play at the same level in 24 to 25 weeks. In the patients with an acute injury, 44% returned without the need for surgical treatment.14 It is very important to note that nonoperative treatment does not include any injections into the ligament or elsewhere in the elbow.13 Operative treatment is reserved for the overhead athlete with a complete tear or a partial tear that has failed nonoperative treatment. Select other athletes (e.g., gymnasts, wrestlers) may also be unable to return to their sports of choice and may also be considered for reconstruction. There are several different methods of reconstructing the UCL. These include the docking technique, the muscle-splitting approach using bone tunnels, and a suture anchor technique. Although UCL repair

The patient is placed supine on the operating table and general anesthesia is used. The elbow is examined under anesthesia and then placed on an arm board. We use a tourniquet inflated to 250 mm Hg. Until 3 years ago, we performed elbow arthroscopy through an anterolateral portal prior to beginning the UCL reconstruction. We abandoned performing the elbow arthroscopy because we did not change anything in our surgical technique based on the findings during the arthroscopy. The procedure begins with a medial incision centered over the medial epicondyle approximately 10 cm in length. Identification of the medial antebrachial cutaneous nerve is performed, and it is protected using a vessel loop for retraction. The ulnar nerve is then dissected from the cubital tunnel and release of the nerve is taken proximally to the arcade of Struthers and distally into the flexor carpi ulnaris muscle mass (Fig. 34-4). The medial intermuscular septum is excised distally to prevent tenting of the nerve after transposition. The anterior band of the UCL is exposed by elevating the flexor muscle mass from the ligament at its attachment to the sublime tubercle (Fig. 34-5). The ligament is then incised longitudinally, from the apex of the sublime tubercle toward its origin on the medial epicondyle in line with the fibers (Fig. 34-6). This splitting of the native ligament allows direct visualization of the origin and insertion of the ligament, as well as excision of any bony osteophytes or previously avulsed bony fragments. If valgus extension overload is also present, we perform a vertical incision in the posterior capsule proximal to the fibers of

Figure 34-4 Surgical exposure of the medial elbow, including isolation of the ulnar nerve. Note the preservation of the motor branch to the flexor musculature. At the time of ulnar nerve dissection, the medial intermuscular septum is excised.

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Figure 34-5 The flexor-pronator mass is elevated off the underlying ulnar collateral ligament. This allows visualization of the entire length of the anterior band of the ligament. Note also the tear in the proximal portion of the ligament.

Figure 34-7 The palmaris longus graft is harvested using two small incisions at the distal forearm and one incision at the level of the muscle-tendon junction.

the posterior band. This exposes the olecranon tip for inspection and removal of any offending osteophytes. The osteophytes are removed with a small osteotome and a high-speed bur. The capsule is then closed with absorbable suture. Graft harvest is then performed. We prefer the ipsilateral palmaris longus tendon if it is present and of sufficient size (Fig. 34-7). If it is not, then the contralateral gracilis tendon is our next choice. The palmaris is harvested with three small transverse incisions in the volar forearm with the most distal incision at the proximal wrist crease. Care should be taken to avoid harvesting the flexor carpi radialis or median nerve, which are in close proximity. Next, the ulnar tunnels are drilled using a 9/64-inch drill bit (palmaris graft) or 5/32-inch drill bit (gracilis graft). The ulnar tunnels are drilled 3 to 4 mm distal to the articular surface. The first tunnel begins just at the posterior aspect of the sublime

tubercle and is directed laterally and slightly posteriorly. The second tunnel begins at the anterior aspect of the sublime tubercle and is directed posteriorly. The two tunnels are connected to each other with curved curets and irrigated. Two tunnels are then drilled in the medial epicondyle of the humerus, converging at the origin of the native UCL. The first tunnel is drilled proximally to distally, and the second medially to distally with a 1-cm bridge between the two tunnels. The tunnels are then curetted and irrigated. Suture loops are then passed through the three tunnels. The distal portion of the native ligament is closed with nonabsorbable suture to enhance the stability, leaving the proximal portion of the native ligament open to allow graft passage. The graft is brought on the table, and a tendongathering stitch is placed in each end of the graft in order to allow tensioning. One of the graft ends is passed through the ulnar tunnel using a suture loop. The ends of the graft are then passed in a figure-eight fashion through the humeral tunnels, and the proximal portion of the native ligament is closed (Fig. 34-8).

Figure 34-6 The ulnar collateral ligament is split longitudinally to expose the underlying lateral elbow articulation. This allows the surgeon exposure of the undersurface of the ligament, which is the location of most pathology. Also, the visualization facilitates drilling of the humeral and ulnar tunnels.

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Figure 34-8 The graft is passed in figure-eight fashion through the ulnar and humeral tunnels.

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Figure 34-9 The graft is tensioned with the elbow in 30 degrees of flexion and neutral rotation. The limbs of the graft are then tied to one another above the medial epicondyle of the humerus.

Figure 34-11 The ulnar nerve is transposed beneath a leash of flexor fascia in a subcutaneous fashion. After transposition, the cubital tunnel is closed to prevent the ulnar nerve from returning to its previous location.

The graft is tensioned with the elbow in 30 degrees of flexion and the valgus stress on the elbow removed. While holding this position and holding the tension on the graft ends, which are crossed above the medial epicondyle, the graft is sutured to itself with multiple nonabsorbable sutures (Fig. 34-9). The limbs of the graft spanning the humeral-ulnar course of the ligament are then sutured to one another using permanent suture to add more tension to the graft (Fig. 34-10). The ulnar nerve is transposed anteriorly using a fascial sling from the flexor-pronator muscle mass (Fig. 34-11). The cubital tunnel is closed and the split in the flexor carpi ulnaris fascia is closed distally with one stitch to prevent propagation of the split and herniation of the muscle. The skin is closed and the elbow placed in a well-padded posterior splint flexed to 90 degrees for 5 to 7 days. The patient then is placed in a hinged range-ofmotion brace and follows a supervised rehabilitation program. The patient will begin a throwing program at 16 weeks, and will be able to return to competition at an average of nearly 9 months.

Results After nonoperative treatment of UCL injuries in overhead athletes, the return to play rate is 42%.14 UCL repair may have a better return to play rate (50% to 63%) than nonoperative treatment, but it does not approach the rate of return of reconstructive treatment.17,21 This decreased chance to return to play is especially true for the attenuated and partial ligament tears, which are not amenable to repair but could theoretically be imbricated. UCL reconstruction fares much better with reported return to play rates being 80% to 92%.11,12,22 The rate of return to play at the same or higher level is not as good for high school baseball players, averaging 74%. The reason for the lower rate of return to play in the high school athlete may be only secondary to other issues with adolescents such as loss of interest in the sport or decreased opportunity to play at the next level (e.g., a senior high school player being injured and not being recruited for college or drafted).23

POSTEROLATERAL ROTATORY INSTABILITY Posterolateral rotatory instability was a phrase coined by O’Driscoll et al24 in 1991 after describing the clinical entity as we know it today. Since then, interest and knowledge of the topic has grown. It is thought that this condition usually arises after traumatic dislocation of the elbow and clinically presents along a wide spectrum of instability. The affected structure is the LCL complex of the elbow, with specific injury to the lateral UCL. The degree of injury to the lateral side of the elbow that is necessary to cause instability is currently still under investigation. As stated earlier in this chapter, elbow dislocations are relatively common injuries and yet this type of instability was only recognized in the past 2 decades. It is still unknown how common this condition is and what the predisposing factors are that cause instability after elbow dislocation. The percentage of elbow dislocations that later have posterolateral rotatory instability is still unknown.

Relevant Anatomy Figure 34-10 The graft is sewn to itself and the underlying native ulnar collateral ligament. This provides additional tension to the graft.

As noted at the beginning of the chapter, the elbow joint is a very congruous joint with bony anatomy accounting for the

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majority of the stability of the elbow. The LCL complex is thought to have four major components: lateral UCL, radial collateral ligament (RCL), annular ligament, and accessory LCL. It appears to have a Y-shaped configuration.25 Proximally, the complex originates as a broad band from the lateral humeral epicondyle.26 Some authors refer to this as the superior band.25 Distally, the ligament may continue as one band or split into two bands, the anterior band being the radial collateral ligament and the posterior band being the lateral UCL.25,26 The annular ligament stabilizes the proximal radioulnar joint and the accessory collateral ligament is a band from the ulna to the annular ligament.26 The insertion point of the lateral UCL is the supinator crest of the ulna. Cadaveric studies have shown that the entire LCL complex provides stability to the elbow. Sectioning of the radial collateral ligament does cause an increase in external rotation when the elbow is passively flexed and extended and causes an increase in varus laxity with the elbow ranged from 10 to 120 degrees. However, subluxation did not occur when the radial collateral ligament was sectioned because the lateral UCL and the coronoid prevented subluxation in those situations. When the lateral UCL was sectioned, gross instability with joint subluxation occurred to rotation.25 The common extensor origin also provides some dynamic stability to the lateral side of the elbow. Maintenance of the integrity of the proximal radioulnar joint is also necessary for posterolateral rotatory instability to occur as both the radial head and the ulna rotate and subluxate. If the proximal radioulnar joint is disrupted, then the ulna will not subluxate with the radial head, causing solely radial head instability.24,26,27 O’Driscoll et al also believe that the posterolateral capsule provides some stability.2,24 A study of 62 elbow dislocations and fracture-dislocations showed that 52% of injuries to the lateral UCL complex occurred as a proximal soft-tissue avulsion off the lateral humeral epicondyle. Twenty-nine percent sustained a midsubstance rupture. Eight percent had a proximal bony avulsion that was large enough to repair by osteosynthesis and 2% had a similar injury off the ulna. Only 5% had distal soft-tissue avulsion off the ulna.2 Concomitant rupture of the common extensor origin was seen in 62% of fracture-dislocations and 80% of pure dislocations.2 Though these injuries were more severe than the average elbow injuries because they required treatment secondary to inability to obtain or maintain closed reduction, a study of elbow dislocations that were able to be reduced found that 14 of 18 elbows where the lateral side was explored showed injury to the common extensor origin.28 It is O’Driscoll’s opinion that damage to the supporting structures on the lateral side of the elbow (RCL, common extensor origin, anterior and posterior capsules) may cause posterolateral rotatory instability in the situation where the lateral UCL is torn.

History Most patients present to the office complaining of lateral elbow pain or discomfort combined with sensation of snapping, catching, or locking. They may be able to express the feeling that the elbow is slipping out of place with the forearm in supination and the elbow slightly flexed. Some more severe cases may present with the history of multiple dislocation episodes. Seventy-five percent of patients younger than 20 years old will have a history of traumatic dislocation. Older patients may have a history of varus/extension stress. Still others may have other history such

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as lateral epicondylar release or cubitus varus deformity from childhood trauma.7,26,29

Physical Examination Primarily, the elbow should be palpated for tenderness and inspected for deformity and range-of-motion deficits. Testing for other types of instability including valgus instability should be performed. The pivot-shift maneuver should be done by standing at the head of the patient with the patient lying supine and the arm extended above his or her head. The forearm should be maximally supinated, the elbow should begin extended, then the axial load is applied, and the elbow is slowly flexed. Many patients will have pain or apprehension with this maneuver but may not have noticeable subluxation in the office. Often the subluxation is only felt with the patient under general anesthesia.26,29,30 Other provocative maneuvers include having the patient push up from a prone or wall position with the forearms in maximal pronation, then repeat with forearms maximally supinated. The patient will have symptoms with maximal supination. Another method is to have the patient push up from a seated position in a chair with the arm maximally supinated.26

Radiographic Studies Standard practice is to obtain anteroposterior and lateral radiographs to look for evidence of previous trauma (e.g., heterotopic ossification, fracture deformity). Usually these radiographs are normal. Stress views can be obtained with the arm held in the pivot-shift position if the patient can tolerate it. Magnetic resonance imaging and computed tomography are of very limited value.7,26

Arthroscopy Diagnostic arthroscopy can show evidence of posterolateral rotatory instability with two signs. First, the radial head can be demonstrated to subluxate when a pivot-shift maneuver is performed. Second, a drive-through sign can be seen by driving from the lateral gutter from the posterolateral portal and going into the ulnohumeral joint (i.e., driving through the radiocapitellar joint).26

Treatment The first line of treatment is prevention of the problem. Although it is unknown how many elbow dislocations will later develop posterolateral rotatory instability, recognition of damage to lateral structures in a dislocated elbow and treating it accordingly are the first steps in prevention. If an elbow dislocation has evidence of damage to the lateral structures, then stabilizing the elbow with the forearm in pronation is helpful to prevent future lateral instability problems.27,31 Unfortunately, elbows with significant medial instability as well may not be stable in pronation. Once chronic posterolateral rotatory instability is diagnosed, there are no conservative measures that appear to treat this condition. Surgical reconstruction of the LCL complex is the only treatment with known clinical success. The method of surgical treatment in chronic cases is usually ligament reconstruction with a tendon graft obtained from palmaris longus or a piece of triceps tendon.26,29,30 Occasionally, the ligament is only attenuated and can be imbricated.26,29 The reconstruction of the ligament complex can be performed via bone tunnels similar to the method of UCL reconstruction described earlier in the chapter or with anchors and bone tunnels.29,30 Recently arthroscopic

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capsular plication and ligament imbrication has been performed in some centers with some success.26

Rehabilitation and Results The rehabilitation protocols are still evolving for this condition. Different surgeons are still using slightly different recommendations. Postoperatively, the elbow is immobilized at 70 to 90 degrees of flexion in full pronation from 2 to 6 weeks, depending on the surgeon. Full range of motion is begun from 3 to 6 weeks. Some surgeons require that the patient wear a hinged elbow brace until 3 months postoperatively for protection of the reconstruction. Return to play is allowed at 6 to 9 months postoperatively.26,29,30 Complications of the procedure that have been reported include recurrent instability, loss of motion, and injury to the lateral antebrachial cutaneous nerve.7,30 A potential risk to the posterior interosseous nerve is present, especially with the arthroscopic technique. There are very few studies with longterm follow-up or a significant patient sample size from which to report results. O’Driscoll et al24 found 90% satisfactory outcomes in the patients without significant degenerative changes. Olsen and Sojbjerg30 had 89% good to excellent results using their technique with suture anchors and bony trough in the ulna and a triceps graft; 83% returned to preinjury activity level and 94% were satisfied with the outcome. It is important to note that the natural history of posterolateral rotatory instability is not known.7 If a patient is symptomatic but not surgically reconstructed, it is unknown whether degenerative changes or worsening of the symptoms will result.

ELBOW ARTHROSCOPY Elbow arthroscopy is becoming a more common procedure as surgeons become more familiar with the techniques of arthroscopy and the indications for the use of arthroscopy in elbow surgery expand. The equipment necessary to perform elbow arthroscopy is similar to that of other arthroscopic procedures. A 4.0-mm, 30-degree arthroscope and a 2.7-mm shortbarreled arthroscope are necessary to perform a thorough procedure. Standard 3.5- and 4.5-mm shavers and burs and graspers are often needed. A gravity or inflow pump and, depending on positioning, a bean bag, a traction setup, and a post are needed. In some cases, osteotomes and mallets may be used as well. Generally, an experienced arthroscopist has all these tools available. Indications for performing elbow arthroscopy are constantly evolving. Well-accepted indications include diagnostic arthroscopy, removal of loose bodies, excision of osteophytes, synovectomy in patients with inflammatory arthropathies, treatment of osteochondritis desiccans of the capitellum, radial head excision, treatment of lateral epicondylitis, treatment of arthrofibrosis, septic arthritis, resection of plica, and assisting in fracture reduction.32 A newer indication includes treatment of posterolateral rotatory instability.26 Contraindications to elbow arthroscopy are significant distortion of normal anatomy, bony ankylosis, and severe fibrous ankylosis. Caution should be used in cases of previous ulnar nerve transposition, as anterior medial portals and some posterior portals place this structure at risk. Positioning in the operating room is mostly surgeon preference. There are three main ways in which a patient may be positioned: supine with the arm on a table or suspended from a boom, prone with the arm over a post, or lateral decubitus with

the arm over a post. Supine positioning has the advantage of ease of transitioning to an open procedure. The disadvantage to supine positioning is that the surgeon is often working with the instruments directed upward, which can be awkward, and the arm may swing back and forth while working. The advantages to prone positioning are the ease of working in the posterior compartment, the ease of manipulating the joint, and the improved scope mobility. Disadvantages to the prone position are the lack of flexion that can be obtained in that position, difficulty in working in the anterior compartment, and difficulty in repositioning the patient for a subsequent open procedure. Advantages to the lateral position are the relative ease to convert to supine, good posterior visualization, and other benefits similar to those of prone positioning. A disadvantage to the lateral position is some difficulty in accessing the anterior compartment. The procedure starts with elevation of the extremity and inflation of the tourniquet. Ten to 15 milliliters of sterile fluid is injected into the elbow from the “soft spot” in the lateral elbow (between the lateral epicondyle, radial head, and olecranon). There are several portals that can be used in elbow arthroscopy. The anterolateral portal can be used as the initial portal. The location of the portal is 2 to 3 cm distal and 1 cm anterior to the lateral epicondyle.33 The structure that is most at risk with this portal placement is the radial nerve, which is 2 to 10 mm away from the portal.34 The proximal lateral portal is also used as the initial portal by some because it is farther away from the neurovascular structures. The proximal lateral portal is located approximately 2 cm proximal to the lateral epicondyle along the anterior surface of the distal humerus.34 The posterior antebrachial cutaneous nerve may be the closest structure to the portal at 0 to 14 mm away and the radial nerve is on average 10 mm away.34 The anteromedial portal is generally made under direct visualization. The location is 2 cm distal and 2 cm anterior to the medial epicondyle.33 The most at-risk major structure there is the median nerve, which is 5 to 13 mm away (lateral) from the cannula.34 The proximal medial portal is thought to be safer than the anteromedial portal and is located 2 cm proximal to the medial epicondyle and just anterior to the intermuscular septum.35 Again, the median nerve is at risk but is farther away at 7 to 20 mm.34 The ulnar nerve is not at risk except for possible subluxating ulnar nerve or history of transposition. The direct lateral portal is located between the lateral epicondyle, radial head, and olecranon, in the soft spot.33 This is a safe portal. If work is going to be performed in the lateral compartment of the elbow, two portals need to be made laterally. One should be about 1 cm distal so there is enough room to work in this space. The posterolateral portal is placed under direct visualization with the elbow in 30 to 45 degrees of flexion. The portal should be 3 cm proximal to the olecranon tip at the lateral edge of the triceps tendon.33 This portal has relatively low risk. The direct posterior portal is placed under spinal needle localization. It may be placed either directly through the triceps tendon or just medial to it, 3 cm proximal to the olecranon tip. The ulnar nerve is at risk if the portal is placed medial to the tendon. Care must be taken to cut away from the nerve and use the nick-and-spread technique.33

Results and Outcomes An early study of results following elbow arthroscopy showed that the best results followed loose body removal, with up to 89% of patients significantly improved, and the results for treatment of chondromalacia were less favorable.33,36 A followup study by Andrews et al37 confirmed that the best results

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occurred after treatment of mechanical problems such as loose bodies. Treatment of capitellar OCD has also been found to have good short-term results with 13 of 16 adolescent athletes returning to their sports after surgery.38 Treatment of osteophytes with posterior elbow impingement showed 100% good to excellent results in one study of 21 patients at nearly 3 years of follow-up.39 Treatment of arthrofibrosis, while beneficial, shows moderately impressive results with 79% rated as good to excellent; although the average flexion contracture was still more than 10 degrees postoperatively, the average gain of extension was 18 degrees.40 The results of arthrofibrosis surgery are good overall, but it is more risky to perform.

Complications Reported complications of elbow arthroscopy include compartment syndrome, septic arthritis, superficial infection, drainage from portal sites, and neurovascular injuries. In one study, the most common immediate complication was transient nerve palsy; it occurred in 12 of 473 patients. Four were superficial radial nerve, five ulnar nerve, one posterior interosseous nerve, one anterior interosseous nerve, and one medial antebrachial cutaneous nerve palsies. All palsies resolved within 6 weeks except one, which resolved in 6 months. Factors that were found to increase risk included rheumatoid arthritis, contractures, and capsular releases. No permanent nerve injuries were found in 473 procedures. No compartment syndromes or hematomas

occurred. The most common delayed complication was prolonged drainage from the portal site (defined as drainage for longer than 5 days), which occurred in 5% of patients. Increased risk factors for this drainage included not suturing the portals or using simple stitches. The anterolateral and direct lateral portals were the most common portals affected. Superficial infections occurred in 2% of patients. Septic arthritis occurred in nearly 1% of patients. This was increased in patients who had steroids injected into the elbow at the end of the procedure. Seven of 473 procedures had persistent loss of motion between 5 and 15 degrees.32 Reported severe nerve injuries include posterior interosseous nerve transection during capsulectomy, and complete transection of the median and radial nerves in a patient with posttraumatic elbow contracture.41,42 Kim also reported two transient median nerve palsies.43 Risk factors for neurovascular injuries include rheumatoid arthritis and arthrofibrosis. Rheumatoid arthritis increases the risk of injury secondary to the thin and friable capsule and loss of normal intra-articular landmarks. Arthrofibrosis increases risk secondary to decreased capsular distention and the process of capsular release as well as the increased complexity of the procedure. Kelly et al32 believe that the use of retractors in the anterior part of the elbow while performing capsular release and arthroscopic identification of the nerves decrease the risk of serious nerve injury.

REFERENCES 1. Hildebrand KA, Patterson SD, King GJW: Acute elbow dislocations: Simple and complex. Orthop Clin North Am 1999;30:63–79. 2. McKee MD, Schemitsch EH, Sala MJ, O’Driscoll SW: The pathoanatomy of lateral ligamentous disruption in complex elbow instability. J Shoulder Elbow Surg 2003;12:391–396. 3. Eygendaal D, Verdegaal SHM, Rosing PM et al: Posterolateral dislocation of the elbow joint: Relationship to medial instability. J Bone Joint Surg Am 2000;82:555–560. 4. Kenter K, Behr CT, Warren RF, et al: Acute elbow injuries in the National Football League. J Shoulder Elbow Surg 2000;9:1–5. 5. Takagi M, Sasaki K, Kiyoshige Y: Fracture and dislocation of snowboarder’s elbow. J Trauma 1999;47:77–81. 6. Ross G, McDevitt ER, Chronister R, Ove PN: Treatment of simple elbow dislocation using an immediate motion protocol. Am J Sports Med 1999;27:308–311. 7. Lee ML, Rosenwasser MP: Chronic elbow instability. Orthop Clin North Am 1999;30:81–89. 8. Hyman J, Breazeale NM, Altchek DW: Valgus instability of the elbow in athletes. Clin Sports Med 2001;20:25–45. 9. Salvo JP, Rizio L, Zvijac JE, et al: Avulsion fracture of the ulnar sublime tubercle in overhead throwing athletes. Am J Sports Med 2002;30:426–431. 10. Ostrander R, Dugas J, Kingsley D: Anatomy of the anterior bundle of the ulnar collateral ligament (unpublished data, 2006). 11. Thompson WH, Jobe FW, Yocum LA, et al: Ulnar collateral ligament reconstruction in athletes: Muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg 2001;10:152–157. 12. Rohrbough JT, Altchek DW, Hyman J, et al: Medial collateral ligament reconstruction of the elbow using the docking technique. Am J Sports Med 2002;30:541–548. 13. Cain EL, Dugas JR, Wolf RS, Andrews JR: Elbow injuries in throwing athletes: A current concepts review. Am J Sports Med 2003;31: 621–635. 14. Rettig AC, Sherrill C, Snead DS, et al: Nonoperative treatment of ulnar collateral ligament injuries in throwing athletes. Am J Sports Med 2001;21:15–17.

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15. Andrews JR, Heggland EJH, Fleisig GS, Zheng N: Relationship of ulnar collateral ligament strain to amount of medial olecranon osteotomy. Am J Sports Med 2001;29:716–721. 16. Dugas JR, Weiland AJ: Vascular pathology in the throwing athlete. Hand Clin 2000;16:477–485. 17. Conway JE, Jobe FW, Glousan RE, et al: Medial instability of the elbow in throwing athletes: Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am 1992;74:67–83. 18. King JW, Brelsford HJ, Tullos HS: Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop 1969;67:116–123. 19. Wilson FD, Andrews JR, Blackburn TA, et al: Valgus extension overload in the pitching elbow. Am J Sports Med 1983;11:83–88. 20. Schwartz ML, Al-Zahrani S, Morwessel RM, et al: Ulnar collateral ligament injury in the throwing athlete: Evaluation with saline-enhanced MR arthrography. Radiology 1995;197:297–299. 21. Azar FM, Andrews JR, Wilk KE, Groh D: Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med 2000;28:16–23. 22. Andrews JR, Timmerman LA: Outcome of elbow surgery in professional baseball players. Am J Sports Med 1995;23:407–413. 23. Petty DH, Andrews JR, Fleisig GS, Cain EL: Ulnar collateral ligament reconstruction in high school baseball players: Clinical results and injury risk factors. Am J Sports Med 2004;32:1158–1164. 24. O’Driscoll SW, Bell DF, Morrey BF: Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991;73:440–446. 25. Seki A, Olsen BS, Jensen SL, et al: Functional anatomy of the lateral collateral ligament complex of the elbow: Configuration of Y and its role. J Shoulder Elbow Surg 2002;11:53–59. 26. Yadao MA, Savoie FH, Field LD: Posterolateral rotatory instability of the elbow. Instructional Course Lecture 2004;53:607–614. 27. O’Driscoll SW: Elbow dislocations. In Morrey BF (ed): The Elbow and Its Disorders, 3rd ed. Philadelphia, WB Saunders, 2000, pp 409–420. 28. Josefsson PO, Johnsell O, Wendeberg B: Ligamentous injuries in dislocations of the elbow joint. Clin Orthop 1987;221:221–225.

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29. Lee BPH, Teo LHY: Surgical reconstruction for posterolateral rotatory instability of the elbow. J Shoulder Elbow Surg 2003;12:476–479. 30. Olsen BS, Sojbjerg JO: The treatment of recurrent posterolateral instability of the elbow. J Bone Joint Surg Br 2003;85:342–346. 31. Cohen MS, Hastings H: II. Acute elbow dislocation: Evaluation and management. J Am Acad Orthop Surg 1998;6:15–33. 32. Kelly EW, Morrey BF, O’Driscoll SW: Complications of elbow arthroscopy. J Bone Joint Surg Am 2001;83:25–34. 33. Andrews JR, Carson WG: Arthroscopy of the elbow. Arthroscopy 1985;1:97–107. 34. Stothers K, Day B, Regan WR: Arthroscopy of the elbow: Anatomy, portal sites, and a description of the proximal lateral portal. Arthroscopy 1995;11:449–457. 35. Poehling GG, Whipple TL, Sisco L, Goldman MS: Elbow arthroscopy: A new technique. Arthroscopy 1989;5:22–24. 36. Ogilvie-Harris DJ, Schemitsch E: Arthroscopy of the elbow for removal of loose bodies. Arthroscopy 1993;9:5–8.

37. Andrews JR, St Pierre RK, Carson WG Jr: Arthroscopy of the elbow. Clin Sports Med 1986;5:653–662. 38. Baumgarten TE, Andrews JR, Satterwhite YE: The arthroscopic classification and treatment of osteochondritis dissecans of the capitellum. Am J Sports Med 1998;26:520–523. 39. Ogilvie-Harris DJ, Gordon R, MacKay M: Arthroscopic treatment for posterior impingement in degenerative arthritis of the elbow. Arthroscopy 1995;11:437–443. 40. Timmerman LA, Andrews JR: Arthroscopic treatment of posttraumatic elbow pain and stiffness. Am J Sports Med 1994;22:230–235. 41. Jones GS, Savoie FH: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 1993;9:277–283. 42. Haapaniemi T, Berggren M, Adolfsson L: Complete transection of the median and radial nerves during an arthroscopic release of posttraumatic elbow contracture. Arthroscopy 1999;15:784–787. 43. Kim SJ, Kim HK, Lee JW: Arthroscopy for limitation of motion of the elbow. Arthroscopy 1995;11:680–683.

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Overuse Injuries, Tendonosis, and Nerve Compression Laurence Laudicina and Thomas Noonan

In This Chapter Lateral tendonosis (tennis elbow) Medial tendonosis (golfer’s elbow) Olecranon bursitis Olecranon stress fracture Valgus extension overload Nerve compression syndromes

INTRODUCTION • Overuse injuries of the elbow are best diagnosed by a thorough history and physical examination. • Most overuse injuries of the elbow can be treated with conservative means. • Some conditions may prove recalcitrant to such treatment. • Less invasive surgical techniques have evolved. • Avoidance of iatrogenic injury caused by surgical intervention, especially for nerve compression disorders, remains paramount.

LATERAL TENDONOSIS/EPICONDYLITIS (TENNIS ELBOW) Clinical Features and Evaluation Lateral epicondylitis or tendonosis is usually an overuse injury, although it may be precipitated by minor elbow trauma. The condition is typically due to repetitive flexion/extension or pronation/supination with the elbow near extension. It generally presents as lateral-side elbow pain and tenderness directly over the lateral epicondyle (at the extensor origin), and just distal to it. Pain is elicited at the lateral epicondyle extensor insertion with passive wrist flexion and with resisted wrist and digital extension. The elbow is extended for both provocative maneuvers.1

Relevant Anatomy Lateral epicondylitis (tennis elbow) occurs secondary to repetitive microtrauma involving extensor carpi radialis brevis, sometimes also involving the extensor carpi radialis longus and extensor carpi ulnaris (Fig. 35-1). Microscopic changes in the extensor carpi radialis brevis have been described as angiofibroblastic hyperplasia and hyaline degeneration (Fig. 35-2).2

Treatment Options The mainstay of treatment is nonoperative and can include activity modification, nonsteroidal anti-inflammatory drugs, counterforce brace, physical therapy with stretching and strengthening, ultrasound therapy, ionto-/phonophoresis3,4 as well as activity modification and sport technique refinement such as modifying racquet grip size and string tension. Limited corticosteroid injections may also be considered. Trephination of tissue and bone in conjunction with percutaneous injection has provided anecdotal relief. Laser therapy and extracorporeal shock wave therapy have recently been suggested as treatments, although significant benefit has yet to be demonstrated.5–7 Corticosteroid injections have demonstrated short-term benefit, while physical therapy has demonstrated long-term benefit.8 Surgery Surgery is generally reserved for cases not relieved by conservative means and persisting for longer than 6 months. Several techniques have been described (Figs. 35-3 and 35-4). Generally, open excision of the torn abnormal origin and granulation tissue with repair of the extensor carpi radialis and extensor digitorum communis is performed. Decortication of the lateral epicondyle with a rongeur, bur, or pick is typically preferable to lateral epicondylectomy.9,10 Arthroscopy has been recently described to delineate concurrent intra-articular pathology. The undersurface of the lateral pathology is débrided via an anterolateral portal and visualized through an anteromedial portal.11 Percutaneous release has also been described.12 Complications of surgical treatment can include residual pain, posterolateral instability, and posterior interosseous nerve injury. Postoperative Rehabilitation A postoperative posterior splint at 90 degrees of elbow flexion and neutral rotation is removed within 2 weeks. Progressive range-of-motion exercises are followed by progressive resistance exercises once full range of motion is achieved. Residual or recurrent pain is treated with decreased activities, antiinflammatory drugs, scar massage, ultrasound therapy, and cryotherapy.

Criteria for Return to Sports Little or no residual pain, full range of motion, full strength, and ability to tolerate activities in a progressive manner are appropriate return to activity criteria. Initially, a counterforce brace should be used during activities.

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Extensor carpi radialis longus muscle

Supracondylar ridge

Extensor carpi radialis brevis muscle

Site of common extensor origin tear

Lateral epicondyle

Figure 35-1 Lateral elbow anatomy with common extensor origin. (From Froimson A: Tennis elbow. In Green DP, Hotchkiss RN, Pederson WC [eds]: Green’s Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999, p 684.)

Common digital extensors

Figure 35-2 A, Angiofibroblastic hyperplasia demonstrating vascular proliferation. B, Focal hyaline degeneration. (From Morrey B, Regan W: Elbow and forearm: Section B: Tendinopathies about the elbow. In DeLee J, Drez D, Miller, MD [eds]: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 2003, p 1222.)

A

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Extensor carpi radialis brevis

B A

D

Extensor carpi radialis brevis

Lateral epicondyle

Cut bone surface

E C Figure 35-3 Lateral elbow extensor tendon débridement and repair. A, Longitudinal incision directly over extensor insertion at the lateral epicondyle. B, Common extensor tendon longitudinally incised. C, Necrotic, degenerative tendon and granulation tissue excised. D, Lateral epicondyle decorticated with osteotome, rongeur, bur, or pick. E, Common extensor tendon reapproximated over lateral epicondyle. (From Froimson A: Tennis elbow. In Green DP, Hotchkiss RN, Pederson WC [eds]: Green’s Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999, p 686.)

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ECRB

ECRL

A

C

ERCB tendon

Capitellum

B

D Figure 35-4 A, Proximal lateral (1) and direct lateral (2) portals. B, An arthroscopic shaver is used to débride the extensor carpi radialis brevis (ECRB) tendon at the insertion. C, Fatty degenerative changes (arrow) in the extensor carpi radialis brevis tendon overlying the extensor carpi radialis longus (ECRL). D, A hooded bur is used to decorticate the lateral epicondyle. (From Murphy K, Lehman R: Arthroscopic management of lateral epicondylitis. In Miller M, Cole B [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 355–357.)

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MEDIAL EPICONDYLITIS/TENDONOSIS (GOLFER’S ELBOW)

antebrachial cutaneous nerve branches. Avoid medial epicondylectomy and consider nerve transposition if significant preoperative neuropathy exists.9

Clinical Features and Evaluation Medial epicondylitis is usually an overuse injury, although it may be precipitated by minor elbow trauma. Repetitive pronation and valgus with the elbow near extension is the typical mechanism. It presents with medial elbow pain, pain with active wrist flexion, and weakness of grip with tenderness over the medial epicondyle at the flexor-pronator origin. Provocative maneuvers include pain with passive wrist extension and elbow extension and pain with resisted wrist and digital flexion and forearm pronation.

Postoperative Rehabilitation Postoperative care is slower than that of lateral epicondylitis and may require as long as 6 months. A posterior elbow splint is placed in 90 degrees of elbow flexion and neutral forearm rotation for 3 weeks. Range of motion is progressively increased followed by progressive strength and endurance exercises at approximately 6 weeks.

Criteria for Return to Sport Relevant Anatomy The flexor-pronator mass inserts at the medial epicondyle (Fig. 35-5). Ulnar collateral ligament injury is differentiated by valgus stress testing with pain localized to the ligament. Mild ulnar neuropathy may also be concurrent with medial epicondylitis.

Treatment Options The mainstay of treatment is nonoperative and involves nonsteroidal anti-inflammatory drugs, counterforce brace, physical therapy with stretching and strengthening, ultrasound therapy, ionto-/phonophoresis, and activity modification and sport technique refinement. Injections may be considered; however, care should be taken and multiple injections are to be avoided due to the proximity of the ulnar nerve and ulnar collateral ligament. Injections should remain anterior to the medial epicondyle to avoid the ulnar nerve.1 Surgery Surgical intervention is reserved for refractory cases with symptoms persisting longer than 6 months to 1 year despite persistent conservative management. Precise localization of the maximal point of tenderness preoperatively is important (Fig. 35-6). The origin of the pronator teres and flexor carpi radialis are exposed. Torn, scarred, and abnormal tissue is excised. Normal tissue is left intact to avoid iatrogenic injury to the ulnar collateral ligament. Care must be taken to protect the medial

Figure 35-5 Medial elbow anatomy demonstrating the common flexor insertion and ulnar nerve. (From Froimson A: Tennis elbow. In Green DP, Hotchkiss RN, Pederson WC [eds]: Green’s Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999, p 685.)

Little or no residual pain, full range of motion, full strength (within 85% of the contralateral side), and ability to tolerate activities in a progressive manner are appropriate return to activity criteria. A counterforce brace should be used during initial sporting activities.

Complications Persistent ulnar neuropathy, ulnar nerve injury, iatrogenic medial instability, and elbow stiffness are recognized complications. All are fortunately rare.13

OLECRANON BURSITIS (MINER’S OR STUDENT’S ELBOW) Clinical Features and Evaluation Olecranon bursitis involves inflammation of the superficial olecranon bursa and may be considered acute, chronic, or septic. It has been termed miner’s or student’s elbow. Nonseptic bursitis is most commonly seen in football and hockey and other contact sports that may involve a direct fall onto a partially flexed elbow. Painless swelling of the bursa after a direct blow is the most common presentation. Recurrent episodes may be the result of less trauma than the initial insult. Septic bursitis is more commonly seen in mat sports such as wrestling or gymnastics, and clinical suspicion should leave a low threshold for aspiration and analysis of warm, erythematous or painful bursitis. The most common organism is Staphylococcus aureus. Chronic cases may replace the bursa with fibrous tissue and

Ulnar nerve Common flexor origin

Medial epicondyle

Medial collateral ligament

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A

B

Figure 35-6 Medial epicondylitis operative débridement. A, Excision of the frayed, degenerative common flexor origin. B, Normal tissue of the flexor pronator origin left intact. C, Reapproximation of the flexor pronator origin following decortication. (From Dlabach JA, Baker CL: Lateral and medial epicondylitis in the overhead athlete. Op Tech Orthop 2001;11:52.)

C can prove difficult to resolve by conservative means (Fig. 35-7).

Relevant Anatomy The subcutaneous bursa is most often involved in olecranon bursitis. Intratendinous and subtendinous bursae have been described but are rarely involved. With recurrent episodes, trabeculae and villiform and fibrous masses may be palpable in the subcutaneous bursa. An olecranon bone spur may be present in chronic recurrent cases.

Treatment Options Compression and cryotherapy can help minimize swelling following traumatic acute olecranon bursitis. Protective covering and doughnut padding are important to prevent recurrent trauma and subsequent swelling, fibrous tissue formation, and progression to chronic bursitis. Aspiration may be considered for severe bursa distension interfering with elbow function and is recommended if there is suspicion of infection. Cell count, crystal analysis, and Gram stain should be performed. A purulent aspiration may be lavaged and injected with 0.5 g methicillin in 10 mL saline. Aspiration is performed with sterile technique and followed by compressive dressing for 36 to 48 hours.1

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Figure 35-7 Olecranon bursitis clinical appearance. (From Baker CL, Cummings PD: Arthroscopic management of miscellaneous elbow disorders. Op Tech Sports Med 1998;6:16–21.)

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Figure 35-8 The thickened, scarred olecranon bursa is excised through an incision centered lateral to the midline. (From Morrey B, Regan W: Elbow and forearm: Section B: Tendinopathies about the elbow. In DeLee J, Drez D, Miller, MD [eds]: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 2003, p 1234.)

Surgery Surgical intervention is considered for cases that do not respond to nonoperative therapy or prevent function and performance (Fig. 35-8). Septic bursitis that does not respond to aspiration and antibiotics should undergo open incision and drainage. A longitudinal incision directly over the midline or slightly lateral (to avoid the ulnar nerve) is performed, carefully dissecting the bursa in its entirety (Fig. 35-9). Meticulous skin handling and closure followed by compressive dressing and 7 to 10 days of elbow splinting help prevent wound-healing problems and recurrence. Protective padding should be used for return to activities. Endoscopic débridement has also been described.

Figure 35-9 Portal placement for olecranon bursectomy. The arthroscope is in the proximal central portal; the shaver is in the lateral portal. (From Baker CL, Cummings PD: Arthroscopic management of miscellaneous elbow disorders. Op Tech Sports Med 1998;6:16–21.)

partial, may be concurrent with olecranon stress fracture. Epiphyseal injury should also be considered in the skeletally immature gymnast, wrestler, or weight lifter.14

Treatment Options

OLECRANON STRESS FRACTURE Clinical Features and Evaluation The insidious onset of posterior elbow pain during the acceleration phase of throwing and point tenderness over the olecranon or pain with valgus stress should raise suspicion for an olecranon stress fracture (Fig. 35-10). Repetitive impaction of the olecranon against the olecranon fossa as in valgus extension overload or triceps traction during the deceleration phase of throwing may cause stress reaction. Plain radiographs may show the stress fracture, but computed tomography, bone scan, and magnetic resonance imaging may be more definitive studies.

Relevant Anatomy Transverse olecranon stress fractures are due to triceps traction and extension forces, while oblique fractures are due to olecranon impaction on the medial wall of the olecranon fossa due to valgus extension overload. Ulnar collateral ligament injury, often

Initial nonoperative treatment involves rest from throwing with lifting restrictions and may require as long as 6 months. Once point tenderness resolves and radiographic union is present, reconditioning may commence. Gradual progression through rotator cuff, scapulothoracic, biceps, and triceps exercises; plyometrics; and eventually an interval throwing program is appropriate. Surgery Should symptoms fail to resolve with nonoperative means or if lengthy healing times cannot be tolerated, operative intervention is indicated. A single large cannulated screw across the fracture site placed percutaneously through the triceps tendon is most appropriate (Fig. 35-11). The screw only needs to be removed if local soft-tissue irritation persists after the fracture is well healed. A titanium screw may cause less artifact should magnetic resonance imaging be required at some point in the postoperative course.15,16

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A B

C

D

Figure 35-10 Radiographic appearance of olecranon stress fracture. A, Plain film lateral view. B, Bone scan. C, Computed tomography scan. D, Magnetic resonance imaging. (From Jones R, Miller R: Bony overuse injuries about the elbow. Op Tech Orthop 2001;11:58.)

VALGUS EXTENSION OVERLOAD/POSTERIOR MEDIAL OSTEOPHYTE Valgus extension overload can occur during the acceleration phase of throwing (Fig. 35-12). Posterior elbow pain during acceleration is characteristic. Flexion contracture, pain with forced extension, and tenderness of the posterior joint line is typical. A posterior medial osteophyte results from repetitive stress to this area. The osteophyte can be excised through open or arthroscopic techniques (Figs. 35-13 and 35-14). Evaluation for medial instability is also important clinically, under anesthesia and arthroscopically, as posteromedial bone resection may unmask underlying medial instability. Care should be taken not to create iatrogenic medial instability by overzealous resection of the posteromedial olecranon.17

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NERVE COMPRESSION SYNDROMES Ulnar Nerve Compression Clinical Features and Evaluation The ulnar nerve is most commonly compressed at the elbow. Medial elbow pain with radiating paresthesias to the small and ring fingers is a common presentation in these patients. Examination may reveal decreased ulnar sensation, a positive Tinel’s sign at the cubital tunnel, reproduction of symptoms with prolonged elbow flexion, and, in severe cases, weakness of the ulnar intrinsics (flexor carpi ulnaris, interossei, adductor). Subluxation of the ulnar nerve can also occur.1 Segmental nerve conduction velocity may prove more sensitive than standard motor conduction velocity testing.18

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A B

Figure 35-11 Percutaneous screw fixation of an olecranon stress fracture. (From Morrey B, Regan W: Elbow and forearm: Section B: Tendinopathies about the elbow. In DeLee J, Drez D, Miller, MD [eds]: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 2003, p 1246.)

Relevant Anatomy The ulnar nerve passes through the cubital tunnel at the medial elbow. Several potential sites of compression include the aponeurosis of the flexor carpi ulnaris, arcade of Struthers, or cubital tunnel retinaculum (Fig. 35-15). Ulnar neuropathy may be the result of mechanical irritation due to medial collateral ligament deficiency in an athlete. Treatment Options Nonsurgical Typical nonoperative treatment involves cessation of aggravating activities, elbow padding, elbow extension splints at night, and evaluation for valgus overload.

C Figure 35-13 Osteophytes are excised from the olecranon with two osteotomies: transverse (A) and oblique (B). (From Miller M, Howard R, Plancher K: Surgical Atlas of Sports Medicine, Saunders 2003, p 439.) B

D Compression

Traction

A

Figure 35-12 Biomechanical forces on the elbow during throwing. Traction on the medial collateral ligament (A); posteromedial olecranon stress (B); olecranon fossa stress (C); compression stress on the radiocapitellar joint (D). (From Morrey B, Regan W: Elbow and forearm: Section B: Tendinopathies about the elbow. In DeLee J, Drez D, Miller, MD [eds]: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 2003, p 1272.)

Surgery Surgical techniques for ulnar nerve compression include decompression as well as submuscular, subcutaneous, and intramuscular transposition techniques. Submuscular techniques have generally achieved better results.19,20

Posterior Interosseous and Radial Nerve Clinical Features and Evaluation Posterior interosseous compression syndrome can present with vague elbow pain, weakness of the wrist and finger extensors, and lack of sensory changes. Radial tunnel syndrome presents with dorsal lateral forearm pain at night. Passive pronation with wrist flexion and resisted

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Figure 35-14 Osteophytes are débrided from the olecranon fossa. (From Miller M, Howard R, Plancher K: Surgical Atlas of Sports Medicine. Philadelphia, WB Saunders, 2003, p 439.)

Figure 35-15 Potential ulnar nerve compression sites. (From Posner M: Compressive ulnar neuropathies at the elbow. I. Etiology and diagnosis. J Am Acad Orthop Surg 1998;6:283.)

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Radial nerve

Figure 35-16 Potential radial nerve compression sites. ecrb, extensor carpi radialis brevis; ecrl, extensor carpi radialis longus. (From Spinner M: Injuries to the Major Branches of the Forearm, 2nd ed. Philadelphia, WB Saunders, 1978.)

Posterior interosseous nerve Arcade of Frohse Extensor digitorum communis

forearm supination with wrist extension aggravate symptoms. Pain with resisted middle finger extension during elbow extension (Maudsley’s test) can distinguish radial tunnel syndrome from lateral epicondylitis.21

Relevant Anatomy The radial nerve divides proximal to the elbow joint into the posterior interosseous nerve and superficial radial nerve. The supinator muscle’s two heads can compress the posterior interosseous nerve as it passes distally (Fig. 35-16). Nerve conduction velocity studies are generally diagnostic.

Treatment Options For posterior interosseous nerve compression, cessation of aggravating activities and conservative means should provide relief. Surgical decompression may be considered for recalcitrant cases. For radial tunnel syndrome, injection of the radial tunnel should eliminate pain and produce a temporary wrist drop. If rest and nonsteroidal anti-inflammatory drugs do not relieve symptoms, surgical decompression may be considered.22

Median Nerve (Pronator Syndrome) Clinical Features and Evaluation Repetitive pronation/supination activities can aggravate symptoms. Symptoms are similar to carpal tunnel syndrome with paresthesias of the radial digits and weakness or atrophy of the thenar muscles. However, Phalen’s test is negative and percussion at the volar elbow and forearm reproduces symptoms. Anterior interosseous nerve compression can result in vague anterior forearm pain and the loss of thumb to finger pinch. Bilateral anterior interosseous nerve compression present for at least 3 months is known as Parsonage-Andrew-Turner syndrome. Relevant Anatomy Pronator syndrome involves compression of the median nerve at the elbow by the bicipital aponeurosis, pronator teres, flexor digitorum superficialis, medial supracondylar process, and/or ligament of Struthers (Fig. 35-17). Treatment Options If rest and nonsteroidal anti-inflammatory drugs do not relieve symptoms, surgical decompression may be considered if debilitating symptoms persist despite extended conservative management.14

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Brachial artery Median nerve Median nerve Reflected humeral head, pronator teres

Pronator teres Bicipital aponeurosis

Radial artery Radial artery FDS arch Ulnar head, pronator teres Pronator teres insertion

B A

Reflected humeral head, pronator teres Median nerve Radial artery

Reflected ulnar head, pronator teres

Reflected FDS arch

Anterior interosseous nerve

C

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Figure 35-17 Potential sites of median nerve compression. A, The bicipital aponeurosis may compress the flexor muscle in pronation and is divided. B, The reflected humeral head of pronator teres exposes the flexor digitorum superficialis (FDS) arch and ulnar head of the pronator teres. C, The radial origin of the FDS is elevated to expose the deep volar compartment and anterior interosseous nerve. (From Szabo R: Entrapment and compression neuropathies. In Green’s Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999, p 1420.)

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REFERENCES 1. Morrey B, Regan W: Elbow and forearm: Section B: Tendinopathies about the elbow. In DeLee J, Drez D, Miller, MD (eds): DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 2003, pp 1221–1235. 2. Kraushaar B, Nirschl R: Current concepts review—tendonosis of the elbow. Clinical features and findings of histological immunohistochemical and electron microscopy studies. J Bone Joint Surg (Am) 1999;81:259–278. 3. Nirschl R, Rodin D, Ochiai D, et al: Iontophoretic administration of sodium dexamethasone phosphate for acute epicondylitis: A randomized, double-blind, placebo controlled study. Am J Sports Med 2003;31:189–195. 4. Runeson L, Haker E: Iontophoresis with cortisone in the treatment of lateral epicondylalgia (tennis elbow): A double-blind study. Scand J Med Sci Sports 2002;12:136–142. 5. Simunovic Z, Trobonjaca T, Trobonjaca Z: Treatment of medial and lateral epicondylitis—tennis and golfer’s elbow—with low level laser therapy: A multicenter double-blind, placebo-controlled clinical study on 324 patients. J Clin Laser Med Surg 1998;16:145–151. 6. Haake M, Konig I, Decker T, et al: Extracorporeal shock wave therapy in the treatment of lateral epicondylitis: A randomized multicenter trial. J Bone Joint Surg Am 2002;84:1982–1991. 7. Speed C, Nichols D, Richards C, et al: Extracorporeal shock wave therapy for lateral epicondylitis: A double blind randomized controlled trial. J Orthop Res 2002;20:895–898. 8. Smidt N, van der Windt D, Assendelft W, et al: Corticosteroid injections, physiotherapy, or a wait and see policy for lateral epicondylitis: A randomized controlled trial. Lancet 2002;359:657–662. 9. Teitz C, Garrett W, Miniaci A, et al: Tendon problems in athletic individuals. Instructional course lecture. J Bone Joint Surg Am 1997; 79:138–152. 10. Jobe F, Ciccotti M: Lateral and medial epicondylitis of the elbow. J Am Acad Orthop Surg 1994;2:1–8. 11. Baker C, Murphy K, Gottlob C, et al: Arthroscopic classification and treatment of lateral epicondylitis: Two-year clinical results. J Shoulder Elbow Surg 2000;9:475–482.

12. Grundberg A, Dobson J: Percutaneous release of the common extensor origin for tennis elbow. Clin Orthop 2000;376:137–140. 13. Dlabach JA, Baker CL: Lateral and medial epicondylitis in the overhead athlete. Op Tech Orthop 2001;11:46–54. 14. Garrick J: Sports Medicine 3 Orthopaedic Knowledge Update. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2004. 15. Nuber G, Diment M: Olecranon stress fractures in throwers: A report of two cases and review of the literature. Clin Orthop 1992;278:58– 61. 16. Schickendantz M, Ho C, Koh J: Stress injury of the proximal ulna in professional baseball players. Am J Sports Med 2002;30:737–741. 17. Azar F, Andrews J, Wilke K, et al: Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med 2000;28:16–23. 18. Azreili Y, Weimer L, Lovelace R, et al: The utility of segmental nerve conduction studies in ulnar mono-neuropathy at the elbow. Muscle Nerve 2003;27:46–50. 19. Posner M: Compressive ulnar neuropathies at the elbow. I. Etiology and diagnosis. J Am Acad Orthop Surg 1998;6:289–297. 20. Nikitins M, Ch’ng S, Rice N: A dynamic anatomical study of ulnar nerve motion after anterior transposition for cubital tunnel syndrome. Hand Surg 2002;7:177–182. 21. Fairbank S, Corelett R: The role of the extensor digitorum communis muscle in lateral epicondylitis. J Hand Surg (Br) 2002;27:405–409. 22. Lorei M, Hershman E: Peripheral nerve injuries in athletes: Treatment and prevention. Sports Med 1993;16:130–147.

SUGGESTED READING Gabel G: Acute and chronic tendinopathies at the elbow. Curr Opin Rheumatol 1999;11:138–143. Miller M, Cole B: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004. Miller M, Cooper D, Warner J: Review of Sports Medicine and Arthroscopy, 2nd ed. Philadelphia, WB Saunders, 2002.

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36

Tendon Ruptures William M. Isbell

In This Chapter

BICEPS RUPTURE

Distal biceps tendon rupture Surgery—biceps tendon repair Triceps tendon rupture Surgery—triceps tendon repair

Clinical Features and Evaluation

INTRODUCTION • Distal biceps tendon ruptures are more common than triceps ruptures. • In athletes, triceps tendon ruptures are most commonly seen in professional football players, particularly linemen. • Nonoperative treatment of a complete distal biceps tear results in significant loss of supination strength, while nonoperative treatment of a complete triceps tendon tear results in loss of elbow extension strength. • Partial tears of both biceps and triceps ruptures can be treated nonoperatively. If pain and/or weakness persist, surgical repair is undertaken.

Ruptures of the tendons of the elbow joint are relatively rare. Rupture of the distal biceps tendon accounts for most of these injuries. The distal biceps tendon is ruptured most commonly in the dominant extremity of patients in their 40s to 60s and is more common in men than women.1 The mechanism of injury is thought to occur from traumatic extension of a flexed elbow with a maximally contracted biceps. Degradation or degeneration of the tendon may play some role in its rupture. Other theories that have been advanced for the cause of biceps rupture have included hypovascularity of the tendon, mechanical failure of the tendon, and impingement of the surrounding structures on the tendon leading to its failure.2 Compared to the number of patients presenting with biceps rupture, the number of patients with triceps rupture is small. The largest number of triceps tendon ruptures has been reported in professional football players.3 The mechanism of injury involves an eccentric load to a contracting triceps. Several risk factors have been identified for this injury including anabolic steroids, renal dialysis, lupus, and hyperparathyroidism.4–8 Tendinosis of the triceps tendon is thought to play some role, with the weakened tendon often progressing from a partial tear to a complete rupture.

Patients who present to the orthopedic clinic after sustaining a rupture of the biceps tendon often complain of feeling a sudden pop at the elbow. Frequently, there is the onset of significant swelling and pain, followed by a reduction in pain and increasing ecchymosis. These patients may or may not have a palpable defect at the elbow. There is detectable weakness with resisted supination and flexion of the elbow. In some patients, with resisted elbow flexion, the muscle belly may be seen retracting proximally forming a mass in the arm much larger than that of the contralateral biceps (Fig. 36-1). Plain radiographs are usually obtained but have a limited role in making the diagnosis. MRI is helpful to determine the location of the tear as well as the degree to which the tendon is torn. It is also useful to evaluate for tendinosis and the quality of the ruptured tissue.

Relevant Anatomy The biceps muscle lies in the anterior compartment of the arm. Its proximal origin of the short head is at the coracoid, and its proximal origin of the long head is intra-articular at the glenoid. The distal biceps tendon attaches at the radial tuberosity, the most common site of its rupture. It is innervated by the musculocutaneous nerve, which originates at cervical roots 5, 6, and 7. The biceps is the strongest supinator of the forearm. This supination force increases as the elbow is flexed. With the brachialis, the biceps acts as an elbow flexor as well. When the elbow is flexed with a supinated forearm, the biceps is more active than when the forearm is in a pronated position.9

Treatment Options Treatment of injuries of the distal biceps tendon depends on the degree to which the tendon is torn and whether it is acutely or chronically ruptured. There is no universally established treatment for partial ruptures of the biceps tendon. If some tendon remains attached, frequently the initial treatment is conservative. In the initial phase, reducing swelling and re-establishing range of motion are paramount. The patient gradually progresses to strengthening once the pain has subsided and motion has been regained. If there is persistent pain and weakness, the partially ruptured tendon is débrided and reattached anatomically to the radial tuberosity. Simple débridement of the tendon has not been shown to effectively reduce pain following partial ruptures.10 The results of surgical repair of acute, complete ruptures of the biceps are far more favorable than those of chronic repairs, as one might expect. However, not all patients require repair of a completely ruptured tendon. Low demand and elderly patients

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Figure 36-1 Patient flexing the elbows after right distal biceps tendon rupture, showing retraction of the affected muscle belly into arm.

without significant pain are often treated conservatively for these ruptures, especially if it involves the nondominant arm. However, in most patient populations, the benefit of greater strength and function make acute repair the best choice. The primary reason to fix these complete tears is the restoration of supination strength. Many techniques have been described for the repair of distal biceps ruptures using a single or a double incision. The most commonly used technique is that of Boyd and Anderson, using two incisions for the anatomic repair. Single-incision techniques have been shown to have higher incidences of posterior interosseous nerve complications, but newer techniques using suture anchors have shown some promise in reducing these complications.11

Surgery Biceps Tendon Repair (Modified Boyd-Anderson12) In the case of an acute rupture, a transverse incision is made over the flexion crease of the elbow. Dissection is carried down to the level of the ruptured tendon. Careful attention is made to retract the lateral antebrachial cutaneous nerve laterally. The ruptured tendon is bluntly freed from any adhesions or scar. Its end is tagged with two nonabsorbable locking stitches (Fig. 36-2). A tunnel is created between the radius and ulna with blunt dissection. A curved clamp can aid in this dissection. With the curve of the clamp going medially around the radius, a small posterolateral incision is made at the tip of the clamp. Through this incision, the radial neck and tuberosity are exposed while keeping the forearm in maximal pronation, thereby protecting the posterior interosseous nerve. Once the radial tuberosity is exposed, a trough is created in the tuberosity with a bur. Three holes are drilled in the radius adjacent to the trough. The tagged tendon is then passed through the interval between the radius and ulna once again with a curved clamp pointing away from the ulna and following the curve of the radius (Fig. 36-3). The suture limbs are then passed through the trough and out the holes in the radius and tied over the top of the bony bridge. The incisions are then closed in two layers, and the elbow is placed into a well-padded posterior splint.

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Figure 36-2 Tendon of ruptured distal biceps taken out through a transverse incision in the flexion crease of the elbow.

Chronically ruptured biceps tendons may be repaired directly, provided that the tendon of the biceps has not retracted significantly or that the muscle itself has not shortened significantly. It is recommended that these repairs be performed through two incisions to reduce the risk of injury to the radial nerve. If the native tendon is significantly retracted or if the quality of the chronically ruptured tendon is poor, the repair may be augmented with either autograft or allograft tendon. The semitendinosus is a good choice for this augmentation because of its similarity in size to that of a native biceps tendon.

Postoperative Rehabilitation The patient’s arm is immobilized in 90 degrees of flexion for 2 weeks. At the time of suture removal, the patient is placed into a hinged elbow brace. Range of motion is progressed to full over the next 4 weeks. At 6 to 8 weeks postoperatively, gentle strengthening of the biceps is begun. Any aggressive strengthening is avoided until at least 12 weeks postoperatively. The patient is allowed to return to competitive activities when full

Figure 36-3 Posterolateral incision with tagged biceps tendon pulled into position to be anchored into the radial tuberosity.

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range of motion is obtained and strength is close to that of the opposite side, somewhere around 4 to 6 months postoperatively.

Results The results of nonoperative treatment of distal biceps ruptures have been shown to result in a loss of as much as 50% of supination strength at the elbow. Morrey et al have shown a return of 97% of flexion strength and 95% of supination strength in patients who had repairs of distal biceps ruptures.13 D’Alessandro et al14 showed similar excellent results in a group of 10 athletes who underwent distal biceps repair. All the athletes in this group returned to full unlimited activity, with the only deficit seen being a decrease in endurance of 20% compared with the opposite side in functional testing. The repair of chronic ruptures has shown less favorable results. Weakness following chronic repair has been reported as high as 50%15 (similar to that of nonoperative repair) and as little as 13% in other cases.16

TRICEPS RUPTURE Clinical Features and Evaluation Patients with distal triceps tendon ruptures often present with a history of a direct blow to the elbow or forced elbow flexion while the triceps was contracted. Oftentimes, these patients have a history of corticosteroid injections for presumed olecranon bursitis.4 There are usually pain and swelling at the elbow with some limitation of range of motion and weakness with resisted extension. In patients with a complete rupture, there is usually a palpable defect in the distal triceps. Using a modification of the T. Campbell Thompson Test for Achilles tendon ruptures, the elbow may be flexed over the examination table and the triceps muscle belly squeezed, resulting in no elbow extension when the triceps tendon is torn.17 Lateral radiographs of the elbow may show a small piece of bone pulled off with the triceps tendon. Occasionally there is a large piece of bone similar to that of an olecranon fracture. Magnetic resonance imaging is useful to delineate between partial and complete tears as well as to localize the tear itself (Fig. 36-4).

Figure 36-4 Magnetic resonance imaging showing a rupture of the triceps tendon off the olecranon.

Relevant Anatomy The triceps is named for its three heads. The origin of the lateral head is the posterolateral aspect of the humerus, the origin of the long head is the infraglenoid tubercle of the scapula, and the medial head originates from the spiral groove of the humerus. The insertion of the triceps is the olecranon. The function of the triceps is to extend the elbow, and the long head aids in shoulder adduction and arm extension. The innervation of the triceps is the radial nerve, which originates at cervical roots 6, 7, and 8.

Treatment Options There is no consensus regarding what percentage of the triceps tendon must be torn before repair is warranted. In general, most partial tears of the tendon may initially be treated conservatively. Treatment focuses on swelling reduction, pain relief, and restoration of range of motion. Contact athletes may return to play after partial tears in a hinged brace with an extension block. However, there are reported cases of complete ruptures of partial tears following a return to contact sports.3 Complete ruptures of the triceps tendon have been shown to cause significant disability, not only in athletes, but also in chronically ill patients in whom the triceps is very important for transfers and mobilization.5 There have been reports of repairs of both acute and chronic ruptures of the triceps tendon. The cornerstone of the surgical treatment of these ruptures is repair of the tendon to the bone of the olecranon. Occasionally large bony avulsions of the triceps are treated like an olecranon fracture with screw or tension band fixation.

Surgery Triceps Tendon Repair The repair is accomplished through a posterior approach to the elbow with a direct midline incision, curving around the tip of the olecranon. Dissection is carried through the subcutaneous tissue to the triceps muscle and tendon below (Fig. 36-5). The dissection medially is done carefully to prevent injury to the ulnar nerve (in chronic cases, the nerve may be encapsulated in scar requiring decompression and transposition). Once the torn tendon is dissected free, a nonabsorbable suture is placed through the tendon with a locking stitch. Two bone tunnels are drilled in the olecranon. These may be placed parallel to or crossing each other. The sutures are then tied down through these bone tunnels while the elbow is in extension (Fig. 36-6). Particular attention is made not to place the knot medially

Figure 36-5 A complete rupture of the distal triceps mobilized for repair.

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strength is similar to that of the opposite side. Additional protection for contact athletes may be provided by a hinged elbow brace.

Results

Figure 36-6 Distal triceps rupture being repaired through drill holes in the olecranon.

(adjacent to the ulnar nerve) to prevent irritation or too superficially, which will cause pain when resting the elbow on a hard surface. The incision is closed in two layers. The elbow is immobilized in a well-padded posterior splint in 45 degrees of flexion.

Postoperative Rehabilitation After repair of a distal triceps rupture, the arm is immobilized in 45 degrees of flexion for 2 weeks. At the time of suture removal, the elbow is put into a hinged elbow brace and active and passive range-of-motion exercises are begun. At 6 weeks postoperatively, gentle strengthening is begun. Aggressive resistive strengthening is avoided until 3 months postoperatively. Athletes may return to competitive play between 4 and 6 months postoperatively if range of motion has returned and

Excellent results have been reported with both early and delayed repairs of complete ruptures of the triceps. In the largest series reported, 10 of 11 professional football lineman who had early repair of a complete rupture of the triceps returned to play at least 1 year of football following repair. All the players were found to have full range of motion, no pain, and no discernible weakness 1 year following repair. Ten players with partial tears were identified. The tears of one of these players progressed to a complete tear when he returned to play. The remaining nine players were able to finish out their season with a partial tear. Six of these players healed their partial tears and required no further intervention, and three players underwent repair of partial tears in the off season.3

CONCLUSIONS Ruptures of the tendons about the elbow may be uncommon injuries, but they will be encountered in a sports medicine practice. Complete ruptures of both the distal biceps tendon and the triceps tendon are best treated with early anatomic repair followed by early restoration of range of motion and delayed strengthening. Partial ruptures of either of these tendons may be initially treated conservatively with pain and swelling reduction and restoration of motion. However, in highly active patients, these partial tears may continue to be symptomatic or progress to complete tears, requiring repair.

REFERENCES 1. Friedmann E: Rupture of the distal biceps brachii tendon: Report on 13 cases. JAMA 1963;184:60–63. 2. Siler JG III, Parker LM, Chamberland PD, et al: The distal biceps tendon: Two potential mechanisms involved in its rupture—Arterial supply and mechanical impingement. J Shoulder Elbow Surg 1995; 4:149–156. 3. Mair SD, Isbell WM, Gill TJ, et al: Triceps tendon ruptures in professional football players. Am J Sports Med 2004;32:431–434. 4. Lambert MI, St. Clair Gibson A, Noakes TD: Rupture of the triceps tendon associated with steroid injections. Am J Sports Med 1995;23:778. 5. Mankin HJ: Rickets, osteomalacia, and renal osteodystrophy. J Bone Joint Surg Am 1974;56:101, 352–386. 6. Martin JR, Wilson CL, Matthews WH: Bilateral rupture of ligament patellae in case of disseminated lupus erythematosus. Arthritis Rheum 1958;6:548–552. 7. Preston FS, Adicaff A: Hyper parathyroidism with avulsion of three major tendons: Report of a case. N Engl J Med 1962;266:968–971. 8. Sallender JL, Ryan GM, Borden GA: Triceps tendon rupture in weight lifters. J Shoulder Elbow Surg 1984;7:151–153. 9. Basmajian JV, Latif A: Integrated actions and functions of the chief flexors of the elbow: A detailed electromyographic analysis. J Bone Joint Surg Am 1957;39:1106–1118.

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10. Bourne MH, Morrey BF: Partial rupture of the distal biceps tendon. Clin Orthop 1985;193:189–194. 11. Ozyurekoglu T, Tsai TM: Ruptures of the distal biceps brachii tendon: Results of three surgical techniques. Hand Surg 2003;8:65–73. 12. Boyd HD, Anderson LD: A method for reinsertion of the distal biceps brachii tendon. J Bone Joint Surg Am 1961;43:1041–1043. 13. Morrey BG, Askew LJ, An KN, Dobyns JH: Rupture of the distal tendon of the biceps brachii: A biomechanical study. J Bone Joint Surg Am 1985;67:418–421. 14. D’Alessandro DF, Shields CL Jr, Tibone JE, Chandler RW: Repair of distal biceps tendon ruptures in athletes. Am J Sports Med 1993;21:114–119. 15. Boucher PR, Morton KS: Rupture of the distal biceps brachii tendon. J Trauma 1967;7:626–632. 16. Hang DW, Bach BR Jr, Bojchuk J: Repair of chronic distal biceps brachii tendon rupture using free autogenous semitendinosis tendon. Clin Orthop 1996;323:188–191. 17. Viegas SF: Avulsion of the triceps tendon. Orthop Rev 1990; 19:533–536.

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Pediatric Elbow C. David Geier, Jr. and George A. Paletta, Jr.

In This Chapter Little leaguer’s elbow Medial epicondylar apophysitis Medial epicondyle avulsion fracture Ulnar collateral ligament injury Olecranon injury Lateral epicondylar apophysitis Panner’s disease Osteochondritis dissecans

INTRODUCTION • The widespread participation in organized sports among skeletally immature athletes has led to an increase in elbow injuries among this population in recent years. Children and adolescents are competing at earlier ages, and single-sport specialization often requires these athletes to participate throughout the year. • As the frequency and intensity of these athletes’ participation have increased, the cause of elbow injuries has shifted from macrotrauma, including fractures and dislocations, to repetitive microtrauma. • Athletic elbow injuries are seen in both overhead sports, such as baseball and tennis, and sports requiring the elbow to serve as a weight-bearing joint, as in gymnastics. • Treatment of elbow injuries in these athletes requires a thorough knowledge of the anatomy and bony development of the adolescent elbow, an understanding of the natural history of its disorders, and a grasp of the expected outcomes with conservative and operative management.

RELEVANT ANATOMY The growth and development of the human skeleton can be divided into three general stages. The first, childhood, ends with the appearance of the secondary centers of ossification. Adolescence ends with the fusion of the secondary ossification centers to their respective long bones. Finally, young adulthood terminates with the completion of all bone growth and the achievement of the final adult musculoskeletal form.1 Characteristic patterns of elbow injury occur during each stage of elbow growth and development. The injury patterns are influenced greatly by the sport played and the resulting forces applied to the athlete’s upper extremity. In each stage of development,

the elbow has a characteristic weak link that is susceptible to injury. Skeletal growth and development of the male and female elbow occur at characteristic times.1–4 At birth, the distal humerus is a single epiphysis comprised of both condyles and epicondyles with one physis. Over the course of the first decade, the epiphysis differentiates into two epiphyses (the capitellum and trochlea) and two apophyses (the medial and lateral epicondyles). The radial head and olecranon epiphyses also develop secondary growth centers during this period. The appearance of the secondary centers of ossification follows a characteristic pattern. The capitellum appears at age 1 to 2. At roughly 2-year intervals, the other centers appear. The appearance of the radial head at age 3 is followed by the medial epicondyle at age 5, the trochlea at age 7, the olecranon at age 9, and the lateral epicondyle at age 10 in females and age 11 in males. Fusion of these secondary ossification centers occurs in a sequential, agedependent order in the early teens in girls and mid-teens in boys. The capitellum, trochlea, and olecranon close at approximately age 14, while the medial epicondyle closes at 15, and the radial head and lateral epicondyle fuse at 16 years of age.

LITTLE LEAGUER’S ELBOW The term little leaguer’s elbow refers to a group of elbow problems in the young throwing athlete.4–7 The injuries include medial epicondyle fragmentation and avulsion, delayed or accelerated apophyseal growth of the medial epicondyle, delayed closure of the medial epicondylar apophysis, osteochondrosis and osteochondritis of the capitellum, osteochondrosis and osteochondritis of the radial head, hypertrophy of the ulna, olecranon apophysitis, and delayed closure of the olecranon apophysis. Repetitive overuse injuries in the adolescent elbow can be categorized based on the pattern of applied forces. These categories include medial tension, lateral compression, and posterior shear or traction injuries. Medial epicondyle apophysitis, medial epicondyle avulsion fractures, and ulnar collateral ligament injuries comprise medial tension overload injuries. Lateral compression injuries include Panner’s disease and osteochondritis dissecans (OCD) of the capitellum. Olecranon apophyseal injury and avulsion of the olecranon fall within the realm of posterior shear or traction injuries.

CLINICAL FEATURES AND EVALUATION A thorough clinical history and physical examination along with routine radiography are critical for the diagnosis of adolescent elbow pathology.2,4 Necessary historical information includes the

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age, handedness, sport, and position of the athlete as well as the level of competition and the amount of practice and playing time per week. The onset, duration, quality, and anatomic location of elbow symptoms must be elicited. Whether sports participation affects the symptoms is critical to address. The specific motions and positions that precipitate the elbow complaints, such as medial pain in the late cocking and acceleration phases of throwing, should be sought. Previous treatments should be noted. The duration of symptoms and the acute or chronic nature of the injury are important for making the diagnosis. A single traumatic episode suggests an acute traumatic condition such as an avulsion fracture of the medial epicondyle, while an insidious onset of chronic pain implies an overuse syndrome such as medial epicondylar apophysitis. The physical examination includes inspection and palpation of the elbow, motion assessment, stability testing, and neurologic and vascular evaluation. Bony hypertrophy, flexion contracture, and carrying angle are important to note. The presence of tenderness at the epicondyles, olecranon, radial head, and collateral ligaments should be recorded. Any ulnar nerve subluxation should be recorded. The ulnar collateral ligament is tested with valgus stress and external rotation of the arm, while the lateral ligaments are stressed with varus and internal rotation. Basic imaging includes at least anteroposterior and lateral radiographs. Often oblique views and stress films are helpful. Common lateral elbow radiographic findings include lucent areas in the capitellum or loose bodies in the anterior or lateral compartments that suggest OCD of the capitellum or radial head. Enlargement, beaking, and fragmentation of the medial epicondyle or an avulsion of the epicondyle are common observations on the medial side of immature elbows. Posterior findings, including osteophytes or loose bodies, are often seen with repetitive impingement of the olecranon. It is critical to evaluate comparison views of the opposite elbow when assessing equivocal radiographic findings of the symptomatic elbow. Magnetic resonance imaging is becoming more popular for evaluation of pediatric elbow injuries. Young patients often have difficulty cooperating sufficiently to obtain a magnetic resonance imaging, but in older adolescents, it can be helpful for defining developing apophyses and epiphyses, joint capsules, ligaments, and soft tissues that are not well seen on plain radiographs.

MEDIAL EPICONDYLAR APOPHYSITIS Repetitive tensile stress from the flexor-pronator mass and the ulnar collateral ligament on the medial epicondyle can lead to medial epicondylar apophysitis and ultimately a stress fracture of the medial epicondylar apophysis.1,3,8 Throwing athletes with this disorder will often complain of progressively worsening medial elbow pain with activity. The characteristic triad includes medial epicondyle pain, a decrease in throwing distance or velocity, and a decrease in throwing effectiveness.1,4 The valgus stress placed on the elbow in the late cocking or early acceleration phases causes an exacerbation of the pain with repetitive throwing. Physical examination reveals tenderness at the medial epicondyle. Valgus stress often reveals pain, but obvious instability is not present. Radiographs often appear normal. A comparison with the opposite elbow will sometimes demonstrate widening of the apophysis. Occasionally fragmentation or hypertrophy of the medial epicondyle is present.

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Conservative management of medial epicondylar apophysitis usually results in complete resolution of symptoms with no lasting functional deficit. Eliminating repetitive valgus stress on the elbow by stopping all throwing activities, often for at least 6 weeks, as well as ice and nonsteroidal anti-inflammatory medications will usually provide symptomatic relief. Physical therapy focusing on range of motion, muscle stretching, and strengthening can be helpful. Evidence of radiographic healing is not necessary to allow a return to activity, as long as the athlete gradually increases his throwing in a supervised program that emphasizes proper mechanics.

MEDIAL EPICONDYLE AVULSION FRACTURES Medial epicondyle avulsions are acute injuries that usually result from a single tensile force applied to the medial elbow of adolescent athletes.1–4,6,9,10 Failure of the medial epicondylar apophysis results from an acute valgus stress coupled with a violent contraction of the flexor-pronator muscle mass. The player will present with acute onset of medial pain after a throw. The pain is severe enough to prevent him or her from returning to play. It usually occurs in the late cocking or early acceleration phases of throwing, and the athlete will often feel or hear a pop. Ulnar nerve paresthesias may occur after the injury. Chronic medial elbow symptoms occasionally precede the event. Physical examination reveals discrete tenderness to palpation at the medial epicondyle, edema, and occasionally ecchymosis. The last 15 degrees of elbow extension are limited due to pain, which can make stability testing difficult. Ulnar collateral ligament injury is possible in this setting, although it is less likely given the fact that the physis of the medial epicondyle is the weak link in the developing elbow. Coexisting ulnar collateral ligament rupture and medial epicondyle avulsion is unusual. The occurrence of a spontaneously reduced elbow fracturedislocation should be kept in mind. Radiographs will usually show a minimally displaced avulsion fracture (Fig. 37-1). Findings are often subtle, requiring comparison elbow views or stress radiographs. While rare, the avulsed fragment can be displaced by the flexor-pronator mass, sometimes into the elbow joint, as often seen in elbow dislocations. The appropriate treatment for these fractures is a matter of some debate. Stress fractures and nondisplaced fractures are usually treated nonoperatively, while fractures in which the fragment is displaced or incarcerated in the joint are treated operatively if the fragment cannot be reduced by closed manipulation. Ulnar nerve dysfunction often mandates exploration along with open reduction and internal fixation of the fracture. Nonoperative management of minimally displaced medial epicondyle fractures is based on the observation that fractures displaced less than 3 to 5 mm will develop an asymptomatic fibrous union. Ulnar nerve symptoms and valgus instability must be absent. Whether this approach is adequate for the young throwing athlete is not fully understood. If a nonoperative approach is chosen, the elbow should be immobilized in 90 degrees of flexion and moderate pronation in a long-arm splint for as long as 2 to 3 weeks.2,3,8,11 A hinged elbow brace can then be used to regain range of motion. When the fracture site is nontender and there is radiographic evidence of healing, flexor-pronator strengthening is started, and a gradual return to

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B C Figure 37-1 A 15-year-old male pitcher with long history of pain at the medial epicondyle who showed no improvement with conservative management. A, Magnetic resonance arthrography demonstrates edema in the medial epicondyle, consistent with a nondisplaced avulsion injury. B and C, Anteroposterior and lateral postoperative radiographs showing two cancellous screws across the fracture.

throwing is initiated in a supervised program when the athlete is asymptomatic.2,3 Many authors advocate an operative treatment of these fractures, especially with more than 2 mm of displacement, rotation or incarceration of the fragment, valgus instability, or ulnar nerve symptoms.3,10,12,13 Young overhead throwing athletes may be prone to developing radiocapitellar degenerative changes if displaced fractures are treated nonoperatively,12 so accepting less displacement may be indicated in these patients. Surgical management consists of open reduction and internal fixation using one or two cancellous screws (see Fig. 37-1B and C). Valgus stability is determined intraoperatively after fixation is achieved, with exploration and possible repair of the ulnar collateral ligament necessary if instability still exists. If the

fragment is too small for adequate fixation, it should be excised, and the ulnar collateral ligament and possibly the flexor-pronator muscles primarily repaired.2,3,10 Postoperatively, the elbow is placed in a hinged-elbow orthosis for 6 weeks, with early rangeof-motion and strengthening exercises started immediately if the fixation is adequate. When radiographs show fracture union and the athlete is asymptomatic, a gradual return to activity is allowed.

ULNAR COLLATERAL LIGAMENT INJURIES Ulnar collateral ligament injuries, especially the chronic attritional tears seen in the skeletally mature, are uncommon in the

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juvenile and adolescent thrower.12 If a rupture is present, it most likely is the result of an acute event.9,14 The thrower will complain of the acute onset of pain and inability to continue throwing. The physical examination will reveal tenderness to palpation distal to the medial epicondyle. Jobe’s valgus stress test may demonstrate pain and instability. Radiographs are needed to rule out the presence of a medial epicondyle fracture. Stress films are often helpful to demonstrate instability. Greater than 2 mm of medial opening compared to the uninjured side is strongly suggestive of a tear. Magnetic resonance arthrography with gadolinium contrast can also help demonstrate the presence of an ulnar collateral ligament tear.15 The treatment for an ulnar collateral ligament tear in the juvenile or adolescent thrower begins with conservative measures before proceeding to operative intervention, if necessary. A brief period of immobilization, nonsteroidal anti-inflammatory medications, and ice are used to control the initial pain. Physical therapy to regain motion and maintain strength and a hinged elbow brace to prevent valgus stress on the elbow are used for approximately 6 weeks. At this point, stability of the elbow is reassessed. If a complete tear and instability are present in a young thrower who wants to continue throwing sports, surgical treatment is advised. Athletes who do not demonstrate a complete tear or instability but continue to have medial elbow pain with activity for at least 3 months are also offered surgery. If an avulsion of the ligament is observed, direct repair may be possible. Reconstruction using autograft tendon such as the palmaris longus, as is commonly performed in adults, is more commonly the procedure of choice. Premature closure of the medial epicondylar apophysis is possible, but this is not significant clinically, as the longitudinal growth of the distal humerus is not affected.

LATERAL EPICONDYLAR APOPHYSITIS

An avulsion fracture of the tip of the olecranon results from an acute overload failure of the olecranon apophysis. It occurs more commonly in older adolescents than in juvenile or young adolescent throwers. The injury occurs in the acceleration or followthrough phases of throwing. The athlete will note an acute onset of severe pain at the olecranon. Physical examination will reveal tenderness to palpation at the tip of the olecranon and pain with active extension. Full active extension of the elbow is often not present. Radiographs will demonstrate avulsion of the tip of the olecranon. This diagnosis may be difficult in younger throwers in whom the secondary ossification center of the olecranon is not visible. If more than 2 mm of displacement of the fracture exists, open reduction and internal fixation using a tension band or cannulated screw technique is recommended.

Lateral epicondylitis in the adolescent is similar to the analogous disorder in adults. It is more commonly seen in the athlete who participates in racquet sports due to repetitive wrist extension. While medial epicondylitis is more common in the throwing athlete, lateral symptoms can occur due to the eccentric activity of the wrist extensors and traction forces applied to the lateral apophysis during the follow-through phase of throwing.2 Improper technique or equipment can exacerbate the microtrauma to the apophysis.9 The athlete will give a history of pain at the lateral epicondyle or the extensor muscle origin that is aggravated by activity. On examination, pain may be reproduced with resisted wrist and finger extension. If the symptoms are attributable to an apophysitis, point tenderness will be present at the lateral epicondyle rather than the muscle origin, as in a tendonitis. Radiographs are usually normal but can show widening or fragmentation of the lateral epicondylar apophysis. In the vast majority of cases, successful treatment can be achieved with nonsurgical measures. Ice, nonsteroidal antiinflammatory drugs, and activity modification should decrease symptoms. When the athlete is more comfortable, physical therapy for stretching and strengthening are instituted. Correcting improper techniques and poorly fitting equipment is essential. A counterforce brace can be used to try to alter the pull of the extensor muscles on the apophysis. Surgical treatment is rarely indicated.

OLECRANON APOPHYSEAL INJURY

PANNER’S DISEASE

Repetitive throwing places stress on the olecranon apophysis due to powerful contraction of the triceps during the acceleration phase of throwing. The resulting tensile stress can lead to olecranon apophyseal injury.2,8,11,12 A traction apophysitis, similar to that which occurs at the medial epicondyle, occurs as a result of the traction force applied by the triceps. Throwers often complain of acute or chronic pain at the posterior tip of the elbow, swelling, and decreased range of motion. Tenderness to palpation at the olecranon tip and pain with resisted extension are seen on physical examination. Radiographs will show widening, fragmentation, or sclerosis of the olecranon physis compared to

Panner’s disease is a focal lesion or osteochondrosis of the subchondral bone and overlying articular cartilage of the capitellum that begins as degeneration or necrosis followed by regeneration or recalcification of the capitellar ossification center.2,3,8,14,16,17 It is the most common cause of lateral elbow pain in young children, characteristically occurring in children younger than 10 years old. In the vast majority of cases, it is a benign, self-limiting process. The appearance, size, and contour of the capitellum and the overlying cartilage are usually restored. Collapse of the subchondral bone is rare.17–19 The distinction between Panner’s disease and osteochondritis dissecans is important because they

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the uninvolved elbow. Normal radiographs, however, do not rule out the presence of this disorder, so a high index of suspicion must be maintained when appropriate signs and symptoms exist. Comparison views of the opposite elbow are important to differentiate this entity from a stress fracture of the olecranon, which can be seen in the older adolescent athlete whose olecranon apophysis has already closed. Treatment of olecranon apophyseal injury depends on the duration and severity of symptoms, as well as the degree of separation of the apophysis. The initial management consists of conservative measures to decrease the athlete’s symptoms, such as ice, nonsteroidal anti-inflammatory drugs, activity modification, and physical therapy. Good results are usually seen in 4 to 6 weeks. The persistence of symptoms or failure of the olecranon apophysis to close as seen on radiographs within 3 to 6 months of conservative treatment implies the need to consider operative management. Fixation can be achieved with a single cancellous screw (Fig. 37-2A and B). A short period of immobilization followed by physical therapy to resume active flexion and passive extension begins postoperatively. Active extension should be restricted for 6 weeks.

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B

Figure 37-2 A 16-year-old male high school pitcher with posterior elbow pain with throwing and persistence of the olecranon apophysis. Lateral (A) and anteroposterior (B) postoperative radiographs show closure of the apophysis 6 months after single cancellous screw fixation.

have markedly different natural histories and therefore, different treatment options. Children with Panner’s disease complain of dull, aching pain of the lateral elbow that is increased with activity and relieved with rest. They may complain of joint stiffness or loss of motion. Physical examination may reveal tenderness at the radiocapitellar joint, a flexion contracture of 20 degrees or less, and crepitus. Radiographs often show an irregular capitellum that appears smaller than that on the opposite side. Areas of fissuring or fragmentation can be seen. Involvement can be found in the anterior capitellum or in the entire ossific center.3,20 Conservative management of Panner’s disease, including activity modification, avoidance of valgus stress to the elbow, ice, nonsteroidal anti-inflammatory drugs, and exercises to maintain range of motion, is usually sufficient. Arthroscopic treatment for this disorder has been described,16 but surgical treatment is rarely necessary. Symptoms may persist for many months, but the long-term prognosis is excellent.3,20

OSTEOCHONDRITIS DISSECANS OCD of the capitellum is a condition in which a focal injury to the subchondral bone causes a loss in structural support for the overlying articular cartilage. The articular cartilage and subchondral bone then undergo degeneration and fragmentation, often resulting in alteration of the capitellar articular surface

congruency and even the development of loose bodies. Although the term OCD implies an inflammation of the osteochondral articular surface, a true inflammatory process has not been proven to exist.3,20 The exact cause of OCD is unknown, but it is commonly thought to be related to a combination of repetitive microtrauma in the face of a tenuous blood supply to the capitellum.2,3,21,22 Unlike Panner’s disease, which affects children younger than 10 years old, OCD usually causes lateral elbow pain in adolescents between ages 11 and 16. It is seen in the elbows of throwing athletes, which sustain repetitive valgus stress and lateral compression and in those of gymnasts whose elbows function as weight-bearing joints and thus are subjected to repetitive compressive loads and shear forces.23 The athlete will present complaining of poorly localized, progressive lateral elbow pain. Pain is often exacerbated with activity and relieved with rest. Mechanical symptoms such as locking, clicking, and catching can occur if a fragment has become unstable or a loose body is present. Physical examination often reveals tenderness to palpation in the anterolateral elbow, swelling, and crepitus. Loss of extension and forearm rotation can be seen. The active radiocapitellar compression test, consisting of pronation and supination with the elbow in full extension, often provokes symptoms.3 Radiographs classically demonstrate radiolucency or rarefaction of the capitellum with flattening and irregularity of the articular surface (Fig. 37-3A). The lesion will often be seen as a

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B

A

C

Figure 37-3 A 13-year-old female gymnast with lateral elbow pain but no mechanical symptoms. A, Anteroposterior radiograph demonstrates the osteochondritis dissecans (OCD) lesion in the capitellum. B and C, T1- and T2-weighted magnetic resonance images showing marrow edema and disruption of the subchondral plate. The fluid deep to the base of the lesion suggests that this is an unstable lesion.

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D

E

F

G

H

I

Figure 37-3—Cont’d D, Arthroscopy demonstrates the nondisplaced, unstable OCD lesion in the capitellum. E, A probe placed in the fissure on the medial side of the lesion proves this to be unstable. F, The crater of the lesion is seen after the unstable flap of cartilage has been detached. G, The cartilaginous piece is manually removed with an arthroscopic grasper. H, A microfracture awl is directed into the base of the lesion. I, Bleeding is demonstrated from the multiple microfracture sites after the tourniquet has been deflated.

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focal sclerotic rim surrounding a radiolucent crater. Anteroposterior radiographs with the elbow in 45 degrees of flexion can be helpful.24 In advanced OCD, collapse of the articular surface, loose bodies, enlargement of the radial head, subchondral cysts, and osteophyte formation can be seen. However, plain radiographs are often nondiagnostic in this condition, especially in the early stages of the disease. Magnetic resonance imaging can be useful in diagnosing OCD in its earlier stages and assessing the status of the articular cartilage.25,26 Low signal changes on T1-weighted images in the capitellum can suggest early OCD lesions.24 Fluid between a fragment and the capitellum seen on T2-weighted images indicates a detached fragment (Fig. 37-3B and C). The natural history of a capitellar osteochondritis dissecans lesion is hard to predict. There are no reliable criteria to predict which lesions will heal and which will collapse and cause later joint incongruity. If healing is to occur, it will occur by the time that the physes close. If the lesion is left untreated and the elbow continues to experience repetitive microtrauma, the subchondral bone may eventually collapse. The joint incongruity can cause articular cartilage damage, loose body formation, and degenerative joint changes.1–3,27 Therefore, appropriate treatment of OCD lesions in the young athlete is not only critical for return to competition but also for long-term acceptable elbow function with normal everyday activities. A useful classification of capitellar OCD is based on the stability of the subchondral bone and its overlying articular cartilage. The combination of clinical, radiographic, and arthroscopic findings can be used to classify lesions into three types.17 Type Ia lesions have intact articular cartilage and no loss of subchondral bone stability. Type Ib lesions are intact but unstable, having intact articular cartilage but unstable subchondral bone potentially at risk of collapse. The treatment of these type I lesions is initially nonsurgical, emphasizing rest, ice, nonsteroidal antiinflammatory drugs, and early range-of-motion exercises. Activity should be modified until radiographs demonstrate evidence of revascularization and healing.1 Radiographic changes in OCD often persist for several years, so the decision to return an athlete to sports is based on resolution of symptoms. Conservative treatment of OCD of the capitellum is not always successful.14,26,28 Surgical indications for type I lesions include radiographic evidence of lesion progression, such as capitellar collapse, or failure of nonsurgical management to relieve symptoms after a 6-month period. The preferred surgical treatment involves arthroscopic evaluation; débridement, if necessary; and drilling or microfracture of the lesion. Type II lesions are open and unstable, with cartilage fracture and collapse or partial displacement of the subchondral bone. These are often flap lesions that should be treated surgically, usually with débridement and drilling the bed of the lesion.18,27,29 If the fragment is large and has adequate subchondral bone backing, open reduction and internal fixation can be attempted.30 Type III lesions are completely detached loose bodies within the elbow joint. The most accepted surgical treatment involves arthroscopy or arthrotomy with excision of the loose bodies, débridement, and drilling the bed of the lesion.1,18,31,32 Type IV lesions have accompanying radial head involvement. These

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“bipolar” lesions often lead to severe degenerative changes with likely poor long-term outcomes. Few long-term studies of OCD lesions have been published. Ruch et al32 presented the results of 12 adolescents who had undergone arthroscopic débridement. They noted that at an average follow-up of 3.2 years 92% of the patients were highly satisfied with minimal symptoms.32 McManama et al18 reviewed the results of 14 athletes who underwent arthrotomy, excision of loose bodies, and curettage of the lesion beds. Of those 14 athletes, 12 returned to competitive activity without restrictions. Many authors believe that the beneficial short-term results will deteriorate over time if repetitive loads are continually placed on incongruous joints. Jackson et al31 observed that in gymnasts with OCD lesions that required surgery, return to competition was unlikely. Bauer et al25 showed that at an average follow-up of 23 years, radiographic evidence of degenerative changes and reduced range of motion were present in more than half of the elbows studied. While pain and limited motion were the most common complaints, little functional impairment resulted.

SURGERY For arthroscopic treatment of OCD lesions, we prefer to place the patient in the prone position with the elbow draped over a padded arm board. Portals are carefully made in standard fashion to avoid neurovascular injury. We base our decision regarding portal placement on the pathology observed and the angle at which the appropriate instruments can approach the lesion. We use anteromedial and anterolateral portals to visualize the anterior compartment, followed by proximal posterolateral, direct posterior, and direct lateral or anconeus portals for work in the posterior compartment. The OCD lesion is visualized and probed in order to plan treatment. Loose bodies observed in the assessment of each elbow compartment are removed. The articular cartilage is probed for fissures and flaps, and the stability of the underlying subchondral bone is assessed. If a ballotable area without an unstable flap is noted, drilling with a Kirschner wire is performed. Areas of cartilage surface fraying can be débrided with a shaver if necessary. If an unstable flap of cartilage is lifted with the probe, inspection for attached subchondral bone is necessary. If sufficient subchondral bone is seen on the base of the lesion, internal fixation using cannulated screws can be attempted. In our experience, subchondral bone is rarely found on the flap of cartilage. If no subchondral bone is seen attached to the lesion, fixation efforts are unlikely to be successful. The articular surface is débrided back to a stable rim of cartilage. Microfracture of the subchondral bone in the lesion bed is performed. The tourniquet is deflated to ensure adequate bleeding from the microfracture sites (Fig. 37-3D through I). The portal incisions are closed with a nylon suture. A sterile soft dressing is applied, and the patient’s upper extremity is placed in a standard sling for comfort. Early range-of-motion exercises are begun in the immediate postoperative period. Strengthening is delayed until approximately 12 weeks postoperatively. Return to sports such as baseball or gymnastics is not permitted for at least 6 to 12 months.

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REFERENCES 1. Pappas AM: Elbow problems associated with baseball during childhood and adolescence. Clin Orthop 1982;164:30–41. 2. DeFelice GS, Meunier MJ, Paletta GA: Elbow injuries in children and adolescents. In Altchek DW, Andrews JR (eds): The Athlete’s Elbow. New York, Lippincott Williams & Wilkins, 2001, pp 231–248. 3. Rudzki JR, Paletta GA: Juvenile and adolescent elbow injuries in sports. Clin Sports Med 2004;23:581–608. 4. Bradley JP, Petrie RS: Elbow injuries in children and adolescents. In DeLee JC, Drez D, Miller MD (eds): DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, Saunders, 2003, pp 1249–1264. 5. Augustine SJ, McCluskey GM, Miranda-Torres L: Little league elbow. In Baker CL, Plancher KD (eds): Operative Treatment of Elbow Injuries. New York, Springer, 2002, pp 69–77. 6. Gugenheim JJ, Stanley RF, Woods GW, et al: Little league survey: The Houston study. Am J Sports Med 1976;4:189–200. 7. Larson RL, Singer KM, Bergstrom R, et al: Little league survey: The Eugene study. Am J Sports Med 1976;4:201–209. 8. DaSilva MF, Williams JS, Fadale PD, et al: Pediatric throwing injuries about the elbow. Am J Orthop 1998;27:90–96. 9. Jobe FW, Nuber G: Throwing injuries of the elbow. Clin Sports Med 1986;5:621–636. 10. Woods GW, Tullos HS: Elbow instability and medial epicondyle fractures. Am J Sports Med 1977;5:23–30. 11. Gill TJ, Micheli LJ: The immature athlete. Common injuries and overuse syndromes of the elbow and wrist. Clin Sports Med 1996;15:401–423. 12. Ireland ML, Andrews JR: Shoulder and elbow injuries in the young athlete. Clin Sports Med 1988;7:473–494. 13. Case SL, Hennrikus WL: Surgical treatment of displaced medial epicondyle fractures in adolescent athletes. Am J Sports Med 1997;25:682–686. 14. Norwood LA, Shook JA, Andrews JR: Acute medial elbow rupture. Am J Sports Med 1981;9:16–19. 15. Chen AL, Youm T, Ong BC, et al: Imaging of the elbow in the overhead throwing athlete. Am J Sports Med 2003;31:466–473. 16. Ruch DS, Poehling GG: Arthroscopic treatment of Panner’s disease. Clin Sports Med 1991;10:629–636. 17. Petrie RS, Bradley JP: Osteochondritis dissecans of the humeral capitellum. In DeLee JC, Drez D, Miller MD (eds): DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1284–1293.

18. McManama GB, Micheli LJ, Berry MV, et al: The surgical treatment of osteochondritis of the capitellum. Am J Sports Med 1985;13:11– 21. 19. Baumgarten TE, Andrews JR, Satterwhite YE: The arthroscopic classification and treatment of osteochondritis dissecans of the capitellum. Am J Sports Med 1998;26:520–523. 20. Kobayashi K, Burton KJ, Rodner C, et al: Lateral compression injuries in the pediatric elbow: Panner’s disease and osteochondritis dissecans of the capitellum. J Am Acad Orthop Surg 2004;12:246–254. 21. Cain EL, Dugas JR, Wolf RS, et al: Elbow injuries in throwing athletes: A current concepts review. Am J Sports Med 2003;31:621–635. 22. Schenck RC, Athanasiou KA, Constantinides G, et al: A biomechanical analysis of articular cartilage of the human elbow and a potential relationship to osteochondritis dissecans. Clin Orthop 1994;299:305– 312. 23. Peterson RK, Savoie FH, Field LD: Osteochondritis dissecans of the elbow. Instr Course Lect 1999;48:393–398. 24. Takahara M, Shundo M, Kondo M, et al: Early detection of osteochondritis dissecans of the capitellum in young baseball players. Report of three cases. J Bone Joint Surg Am 1998;80:892–897. 25. Bauer M, Jonsson K, Josefsson PO, et al: Osteochondritis dissecans of the elbow. A long-term follow-up study. Clin Orthop 1992;284: 152–160. 26. Takahara M, Ogino T, Sasaki I, et al: Long term outcome of osteochondritis dissecans of the humeral capitellum. Clin Orthop 1999;363: 108–115. 27. Schenck RC, Goodnight JM: Osteochondritis dissecans. J Bone Joint Surg Am 1996;78:439–456. 28. Takahara M, Ogino T, Fukushima S, et al: Nonoperative treatment of osteochondritis dissecans of the humeral capitellum. Am J Sports Med 1999;27:728–732. 29. Byrd JW, Jones KS: Arthroscopic surgery for isolated capitellar osteochondritis dissecans in adolescent baseball players: Minimum three-year follow-up. Am J Sports Med 2002;30:474–478. 30. Harada M, Ogino T, Takahara M, et al: Fragment fixation with a bone graft and dynamic staples for osteochondritis dissecans of the humeral capitellum. J Shoulder Elbow Surg 2002;11:368–372. 31. Jackson DW, Silvino N, Reiman P: Osteochondritis in the female gymnast’s elbow. Arthroscopy 1989;5:129–136. 32. Ruch DS, Cory JW, Poehling GG: The arthroscopic management of osteochondritis dissecans of the adolescent elbow. Arthroscopy 1998;14:797–803.

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38

Physical Examination and Evaluation Michael R. Boland

In This Chapter History Wrist pain Radial Dorsal Ulnar Palmar Wrist instability and impaction Wrist tendonitis Hand injuries Imaging

INTRODUCTION • The history is important in directing the examination of the wrist and hand. • When inspecting or examining the wrist, it is best to divide the wrist into four basic areas for assessment: radial, dorsal, ulnar, and palmar. • Special examination tests are available to test for wrist instability and impaction syndromes. • Plain radiographs are the mainstay of diagnostic imaging of the wrist and hand. • Specific radiographic views are available for many wrist problems. • Computed tomography and magnetic resonance imaging scans are often used when further studies are necessary.

Injuries to the wrist and hand are common in all sports. About 10% of all athletic injuries involve the wrist and hand.1 The incidence of wrist problems is much higher in contact sports and is seen in as many as 85% of participants in gymnastics.2 The function of the wrist in athletic endeavors is twofold. The primary motion is from a position of radial deviation/extension to ulnar deviation/flexion. This motion assists in the power of throwing activities where the wrist is cocked into radial deviation/extension, accelerates through a neutral position into ulnar deviation/flexion, and then recovers back to a neutral position. For example, basketball free-throw shooting involves an extensionflexion arc of about 120 degrees in the shooting hand.1 In baseball, the arc of motion is approximately 94 degrees.3 The second function of the wrist is to position the hand in space, along with positioning the forearm in various degrees of pronation and

supination. The function of the hand in sports is to grasp objects such as rackets, balls, or clubs. Wrist anatomy is complex, but functionally the extensor carpi radialis longus and extensor carpi radialis brevis are the cocking muscles of the wrist, with flexor carpi ulnaris the primary accelerator. The flexor carpi radialis and extensor carpi ulnaris are primarily dynamic stabilizers of the wrist. These four primary motors of the wrist (extensor carpi radialis longus and extensor carpi radialis brevis act together) sit at four corners of a quadrilateral pulling the wrist into the distal radius like a hot air balloon is held against the ground by guide ropes. The true collateral ligaments of the wrist assist in holding the carpus against the radius. These include the radioscaphocapitate ligament on the volar side and the dorsal radiocarpal ligament on the dorsal side, the former coming from a relatively radial volar position and the latter coming from a dorsal ulnar direction. The hand and carpus are slung up to the distal radius. At the distal radioulnar joint, the ulnar head holds up the distal radius during pronation and supination of the wrist. The distal radius is held against the distal ulna by the ligaments within the triangular fibrocartilage. The ligaments from the ulna to the carpus are relatively loose. Joint anatomy within the hand is relatively uniform. Each interphalangeal and metacarpophalangeal joint contains a volar plate to prevent translation of the joint, two collateral ligaments, and a flimsy dorsal capsule. Injuries to the wrist and hand can be summarized as being either traumatic in nature or from overuse. Overuse injuries occur due to either compression or stretch tension when the wrist is moved outside its primary range of motion. An example is ulnar-side wrist pain in tennis players who use a western grip, which places the wrist into extreme ulnar deviation. These athletes are prone to tendonitis of the first and second dorsal compartments due to stress and compression problems of the triangular fibrocartilage. Traumatic injuries include fractures, dislocations, and ligament tears, all of which are common in collision or contact sports.

CLINICAL FEATURES AND EVALUATION Evaluation of the hand and wrist in athletes requires a careful history followed by a specific examination. Many radiographic techniques have been described to assist in the visualization of the wrist and hand, and these should be obtained when looking for specific problems. Table 38-1 shows the radiographic views that are available and summarizes when they should be used. The history should begin with an evaluation of the specific sport and level at which the patient participates. This often directly affects the management of the wrist or hand problem.

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Table 38-1 Summary of Radiologic Views Radiograph

When to Use

Reasons for Use

Posteroanterior

Routine view

Standard radiograph looking at contours of distal radius and ulna for fractures; alignment of proximal and distal rows

Oblique wrist

Routine view

Helpful in looking at distal radius fractures with displacement in ulnar columns

Lateral

Routine view

Important for proper carpal alignment looking for dorsal and volar intercollating instability deformities

Radial deviation

Instability series

Scaphoid should flex and thus the ring sign should be present; look for scapholunate widening

Ulnar deviation

Instability series

Also for scapholunate widening, ulnar impaction, and instability; increases relative ulnar variance, important in ulnar impaction syndromes

Clenched fist

Impaction and stability series

Can increase the scapholunate and lunotriquetral gap when there is ligament injury

Posteroanterior in pronation

Impaction series

Increased ulnar plus impaction

Scaphoid view

Special view

Look for scaphoid fractures

Carpal tunnel view

Special view

Look for hamate and scaphoid tubercle fractures

Pisotriquetral view

Special view

Shows pisotriquetral osteoarthritis and hamate fractures

For example, a lineman in football can often play wearing a cast, but a quarterback needs a nearly complete range of wrist motion. The history important in decision making is how the problem started, how the problem is affecting the patient’s sporting endeavor currently, what the general health of the patient is with particular reference to joint-related diseases, previous upper extremity injury, and what treatment the patient has had prior to presentation. After obtaining a general sports history, the first question should be how did this problem begin? A differential should be obtained between traumatic and spontaneous origin of onset. A specific history of the mechanism of injury should be obtained when there has been a traumatic event. The most common event causing wrist injury in athletes is a direct fall onto an outstretched hand. Finger injuries and fractures are often caused by a direct blow to the end of the finger, or getting the finger caught in another object such as an opponent’s jersey. Sudden flexion of the distal interphalangeal joint will cause a mallet finger, whereas sudden extension creates a flexor digitorum profundus tendon avulsion (jersey finger) or avulsion fracture. A radial deviation injury to the thumb may result in an ulnar collateral ligament tear. With injuries of insidious onset, overuse is usually the pertinent factor. With these injuries, a description of technique can be helpful in elucidating the origin of the problem. With wrist injuries, pain is the usual presenting factor. Table 38-2 gives a differential diagnosis of wrist pain. This differential diagnosis is very helpful when assessing wrist problems. The patient will generally point to the location of pain as either being radial, dorsal central, ulnar, or palmar wrist pain. As with any pain, aggravating and relieving factors are important, particularly the specific position that the wrist is in when pain occurs. The presence of a click or catch is uncommon but helpful when considering mechanical problems within the wrist joint itself or secondary to instability. Following wrist or hand injuries, specific tingling and/or numbness can occur. Postural changes occur in the cervical spine and shoulder region causing compression of the thoracic outlet

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leading to an escalation in pain and often nonspecific tingling or numbness below the elbow region. Pain associated with this problem is often generalized, involving the entire upper extremity. The specific site of numbness and tingling can be indicative of carpal or cubital tunnel syndrome. Patients with cubital Table 38-2 Wrist Pain: Differential Diagnoses Radial

Intersection syndrome de Quervain’s tenosynovitis Wartenberg’s radial neuritis Radial styloid/scaphoid impingement Scaphoid fracture STT problems Thumb CMC joint problems

Dorsal central

Scapholunate ligament tear Carpal boss Ganglion Lunotriquetral ligament tear Kienböck’s disease CMC joint instability (other than thumb) Tendonitis of the second to fifth extensor compartments Distal radius fracture

Ulnar

Distal radioulnar joint osteoarthritis Distal radioulnar joint instability Triangular fibrocartilage tear Extensor carpi ulnaris tendonitis Triquetral avulsion fracture Ulnar lunate impaction Ulnar triquetral impaction Cubital tunnel syndrome

Palmar

Carpal tunnel syndrome Hook of hamate fracture Wrist flexor tenosynovitis STT problems Scaphoid tubercle fracture

CMC, carpometacarpal; STT, scaphotrapeziotrapezoid.

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tunnel syndrome often present with ulnar-side wrist pain and clumsiness of the hand. When looking specifically at the hand, the site of pain and swelling is important, as is any deformity. Examples include abnormal radial or ulnar deviation in a proximal interphalangeal dislocation, or the presence of a boutonniere or mallet deformity when the central slip or common distal tendon of the extensor mechanism has been injured. The site and quality of wrist pain can help direct the differential diagnosis. Pain secondary to instability occurs with weight bearing, such as lifting a heavy object or pushing oneself up from a chair. Pain because of impingement or impaction occurs in certain positions. Post-traumatic arthritic pain increases with activity and is often greatest after activity.

PHYSICAL EXAMINATION While history taking is very important in the evaluation of wrist and hand problems, physical examination is the cornerstone of diagnosis. It should be directed toward the type of injury suspected. Physical examination should follow a methodical and reproducible pattern. Examination should begin with the patient sitting directly opposite the examiner with the patient undressed from the midhumerus down and the hands placed upon a small examination table, directly in front of the examiner. Visual inspection should be performed, assessing for deformity and swelling. Swelling of an interphalangeal joint can be easily seen with direct inspection in comparison with other interphalangeal joints and in particular the opposite extremity. Visual inspection of the fingers for a mallet or a boutonniere deformity is performed. Hand fractures will cause radial and ulnar deviation deformities and swelling. The examiner particularly needs to look for abnormal rotation of the affected digit. The more proximal a fracture, the less angulation or displacement is acceptable. Visual inspection of the wrist and distal radioulnar joint may show swelling of the radiocarpal or snuff box regions, a prominence of the distal ulna, or swelling around the distal radioulnar joint with ulnar-side wrist problems. When inspecting or examining the wrist, it is best to divide the wrist into four basic areas for assessment: radial, dorsal, ulnar, and palmar. Physical examination should then follow this regional approach.4 The differential diagnosis listed in Table 38-2 is very helpful in looking for and ruling out specific wrist conditions. If physical examination is the mainstay of diagnosis in the wrist and hand, then palpation of specific tenderness and in particular the maximum site of tenderness is the key to a diagnosis. Structures of the wrist and hand are readily palpated.5 The joint to be palpated will be directed by the history of injury and by the presence of deformity and swelling. Palpation of a thumb or finger joint needs to include palpation of radial collateral ligament origin and insertion, ulnar collateral ligament origin and insertion, insertion of tendons in the region of the joints (such as the central slip of the extensor tendon), and palpation over the volar aspect, in particular the volar plate. The metacarpophalangeal joint of the thumb requires specific palpation of the preceding structures and the volar sesamoid bones on the radial and ulnar aspects.

pain, palpation should begin proximally with tapping over the radial nerve for radial neuritis as it passes beneath the brachioradialis. This is over the radial border of the radius at the junction between the middle and distal thirds of the radius. As one moves distally, there is a prominence over the dorsal and radial aspect of the radius approximately 8 cm from the radial styloid. This is where the long tendons to the thumb cross the wrist extensors, the site of intersection syndrome. All extensor tendons pass through a fibrous tunnel and can be subject to tenosynovitis. Tenosynovitis in the first dorsal compartment is known as de Quervain’s disease. Swelling over the first dorsal compartment and tenderness associated with it is an indicator of this problem. Next, one should palpate the radiocarpal joint and over the radial styloid. Tenderness here is an indicator of styloid scaphoid impingement. Classic scaphoid fracture tenderness is in the anatomic snuff box, but tubercle scaphoid fractures are tender more volarly over the scaphoid. Problems of the scaphotrapeziotrapezoid joint and thumb carpometacarpal joint, such as chondromalacia and occasionally carpometacarpal instability, cause tenderness specifically over these joints and are best felt on the volar aspect. The scaphotrapeziotrapezoid joint is palpated by feeling the scaphoid tubercle and rolling the examining digit into the crevice just distal to that tubercle. Carpometacarpal tenderness is best palpated by providing longitudinal traction to the thumb and palpating down the metacarpal distally until a crevice is felt over the joint. Dorsal Side If the wrist pain is dorsal and central, then one needs to palpate over the second to fifth dorsal compartments looking for tendonitis. The soft spot bordered by extensor digitorum communis, extensor carpi radialis brevis, and extensor pollicis longus on the dorsum of the wrist is the site of most dorsal wrist ganglions and tenderness over this point is indicative of a ganglion or a scapholunate ligament tear (Fig. 38-1). Dorsal wrist ganglions are usually associated with grade I to II dorsal scapholunate ligament disruption. The distal radius should be palpated, and tenderness may represent a distal radius fracture. Ulnar Side Ulnar-side wrist pain has been called the back pain of the upper extremity. However, as with examination of other regions of the wrist, a methodical examination can usually determine the cause of ulnar-side wrist pain. This should begin with palpation of the distal radioulnar joint proper, the region where the ulnar head meets the sigmoid notch of the radius. Tenderness at this point is often indicative of post-traumatic osteoarthritis and distal radioulnar instability. A tear of the triangular fibrocartilage complex is tender more distally at the region of the ulnar carpal joint. The sixth dorsal compartment (the compartment for the extensor carpi ulnaris) should be palpated proximally to distally, and swelling or tenderness in this region is an indication of tendonitis of the extensor carpi ulnaris. Impaction syndromes occur between the ulna and lunate, resulting in tenderness more in the region of ulnar carpal joint. Ulnar styloid triquetral impaction is felt more medially, directly over the ulnar styloid (Fig. 38-2). It should be noted that patients with ulnar-side wrist problems often have cubital tunnel syndrome and Tinel’s sign should be part of a routine examination of the ulnar side of the wrist.

Wrist Radial Side The best way to palpate the wrist for tenderness is to work regionally, proximally to distally. If there is radial-side wrist

Palmar Side If the patient has palmar-side wrist pain, the patient is likely to have one of the following conditions: carpal tunnel syndrome,

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imal volar forearm and work distally toward the wrist. Often Tinel’s sign is in the distal third of the forearm, not just over the carpal tunnel itself. Specific tenderness over the hook of the hamate or the scaphoid tubercle can be indicative of fractures in this region.

Range of Motion

Figure 38-1 Magnetic resonance imaging showing an acute tear of the scapholunate ligament (arrow).

hook of hamate fracture, flexor tenosynovitis, a scaphoid tubercle fracture, or scaphotrapeziotrapezoid joint problems. Direct compression of the median nerve with a flexed wrist (Phalen’s compression test), which reproduces the tingling in the hand, is a reliable sign for carpal tunnel syndrome. When looking for Tinel’s sign over the median nerve, one should start in the prox-

Figure 38-2 Radiograph of a patient with ulnar styloid triquetral impaction. Note the length of the ulna in relation to the radius (ulnar positive variance). Arrow indicates prominent ulnar styloid.

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Once a thorough inspection and palpation has taken place, the patient should be asked to put the forearm, wrist, and hand joints through a range of motion. Usually this can be done quickly by asking the patient to place the palm of the hand up toward the ceiling to look for supination, then the palms downward for full pronation. Full wrist dorsiflexion can be examined by placing the entire volar surfaces of the hands against one another as in a religious prayer position and then asking the patient to elevate both elbows. Wrist palmar flexion is evaluated with the reverse prayer position by placing the dorsal aspect of each hand against its opposite and lowering the elbows toward the floor. Next one should assess active radial and ulnar deviation. Then the patient is asked to do a full power grip, followed by full-spanning finger and thumb extension. Finally, the range of motion of the thumb is examined by asking the patient to touch the base of the volar aspect of the small finger. The patient should be able to at least touch the metacarpophalangeal crease at the base of the small finger for full thumb range of motion. Any lack of range of motion is measured with a goniometer and documented. Obviously, a lack of motion in any direction is indicative of stiffness of wrist or hand joints. Lack of range of motion is a major cause of morbidity in athletes. Certain sports require a full range of wrist motion, such as the shooting hand in basketball. The supporting nonshooting hand can have a markedly reduced range of motion and the basketball player may still be functional.

Wrist Instability and Impaction Specific tests are available for assessing wrist stability. This should start at the distal radioulnar joint. Anteroposterior translational force is placed on the distal radioulnar joint in full pronation, in neutral, and in full supination. If scapholunate ligament instability is suspected, then one should perform the Watson shift test. This is done by placing a thumb over the scaphoid tubercle and moving the hand from radial to ulnar deviation. The test is positive when the scaphoid tubercle does not become prominent or flex during radial deviation.6 If the Watson test is painful, this is likely due to scaphotrapeziotrapezoid joint pathology and is indicative of a positive grind test due to the scaphoid moving in relation to the trapezoid and trapezium. Lunotriquetral instability is assessed by performing a Ballottement test, whereby one holds the pisiform and triquetrum in a pinch grasp with one hand and the scaphoid and lunate in a pinched grasp of the opposite. An anteroposterior force is then placed between the two. Mid-carpal instability is assessed by grasping the proximal row of the wrist with one hand and the distal with another and then placing an anteroposterior force. An associated clunk is indicative of mid-carpal instability. Ulnar impaction syndromes are assessed by ulnarly deviating the wrist and then rotating the forearm. Pain with this maneuver indicates ulnar impaction and is often associated with a triangular fibrocartilage tear. Painful radial deviation of the wrist is an indicator of a possible radioscaphoid impaction syndrome.

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Wrist Tendonitis Tendonitis of the wrist occurs due to excessive tension involving any of the wrist compartments. The most common of these is tendonitis of the first dorsal compartment (de Quervain’s disease). This is examined by placing tension on the tendons within the first compartment. These tendons are extensor pollicis brevis and abductor pollicis longus. Finkelstein’s test is performed by asking the patient to grasp a fully flexed thumb, followed by application of a radial deviation force. The patient should have significant pain over the radial aspect of the wrist for a positive test. This test can be positive for extensor pollicis longus tendonitis if the pain is caused during ulnar deviation and with wrist flexion. Forced radial deviation with wrist flexion creates tension in the extensor carpi ulnaris tendon, and if the patient gets significant ulnar-side wrist pain in this position, then extensor carpi ulnaris tendonitis may be present.

Hand Injuries If a metacarpophalangeal or interphalangeal joint injury is suspected, then that particular joint should be placed into radial and ulnar deviation and hyperextension. This evaluates collateral ligament and volar plate injury, respectively. The most important collateral ligament injury in the hand is a Stener lesion, with an ulnar collateral ligament tear of the metacarpophalangeal joint of the thumb. The importance of this is that if it is not surgically corrected, then permanent instability will result. A Stener lesion occurs when the ulnar collateral ligament avulses from the proximal phalanx and gets caught on the superficial side of the adductor aponeurosis (Fig. 38-3). The hand examination is completed by examining the long tendons. Extensor pollicis longus and flexor pollicis longus are examined by actively flexing and extending the interphalangeal joint of the thumb, but if the extensor pollicis longus injury is more proximal than the dorsal thumb extensor hood, then this

A

B

is examined by placing the palm of the hand on a flat tabletop and asking the patient to lift the thumb off the tabletop. The extensor pollicis longus tendon can be palpated to assess its potency. The long flexor tendons to the fingers are examined as follows: the flexor digitorum profundus is examined by grasping the proximal interphalangeal joint and holding it in extension. The patient is then asked to flex the distal interphalangeal joint. Because the profundus tendon is essentially a mass action muscle, by holding all fingers in full extension (except for the digit to be examined), the intact superficialis tendon should still be able to flex that finger.

IMAGING Plain Radiographs Plain radiographs are essential in the evaluation of any sportsrelated wrist and hand injury. Three standard radiographs of the involved part should be obtained. For example, if the proximal interphalangeal joint is involved, then anteroposterior, oblique, and true lateral views should be obtained. The radiograph is centered over the involved part. When evaluating the radiograph, it should be noted that the radiograph taken is centered on the involved or injured part. Specific radiographs of the wrist are summarized in Table 381. For all wrist problems, a routine series of posteroanterior, lateral, and oblique radiographs should be taken. In the posteroanterior view, the ring sign (Fig. 38-4) at the distal scaphoid should not be present and there should be easily defined carpal arches at the radiocarpal and mid-carpal joints. When specifically looking at the lunate, cystic change can occur in ulnar lunate impaction syndrome and sclerosis or collapse in Kienböck’s disease. The normal finding on a posteroanterior radiograph is that the ulna is slightly shorter than the radius, there is a slight ulnar negative variance, and the slope of the distal radius relative to the shaft of the radius is about 14 degrees volar. On a lateral radiograph, the first step is to look at overall carpal alignment where the radius, lunate, capitate, and third

C

Figure 38-3 A complete tear of the ulnar collateral ligament of the thumb can result in a Stener lesion. A, The ulnar collateral ligament is normally covered by the adductor aponeurosis. B, With significant radial deviation, the ulnar collateral ligament tears distally and is displaced outside the aponeurosis. C, After the stress is released, the torn ulnar collateral ligament remains outside the aponeurosis in a position far from its insertion. This cannot heal and requires surgery to restore stability.

Figure 38-4 Scaphoid ring sign (arrow). The distal scaphoid is seen on end, due to abnormal flexion of the bone in a volar direction, as a result of chronic scapholunate instability.

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A

the scaphoid is best appreciated by finding the distal pole and tubercle and following them in a proximal and dorsal direction. In dorsal intercollating segment instability, a line drawn through the midpole of the lunate will point distally in a dorsal direction, and the angle between the midpole of the scaphoid and the lunate will be greater than 65 degrees (Fig. 38-5). In volar intercollating segment instability, the lunate scaphoid angle will be less than 30 degrees. A dorsal intercollating segment instability deformity indicates probable scapholunate instability, and volar intercollating segment instability indicates probable lunotriquetral instability. In looking for impaction or instability problems, ulnar deviation, radial deviation, clenched fist, and posteroanterior clenched fist views can be helpful (see Table 38-1). Special scaphoid, carpal tunnel, or pisotriquetral views are useful when considering other specific conditions. Other imaging including radioisotope scanning, ultrasonography, and wrist arthrography have now been generally superseded by computed tomography and magnetic resonance imaging, and the author rarely uses these in his practice. Computed tomography is very useful when looking for occult fractures of the carpal bones or a carpometacarpal fracture dislocation. Magnetic resonance imaging is useful in looking for a wrist ganglion, ligament tears, triangular fibrocartilage tears, Kienböck’s disease, and occult scaphoid fractures.

CONCLUSIONS

B Figure 38-5 A, Lateral radiograph of a patient with chronic scapholunate instability, resulting in a dorsal intercollating segment instability deformity. The angle between the scaphoid and lunate is greater than 65 degrees. B, Magnetic resonance imaging in a patient with chronic scapholunate instability with the lunate (arrow) angulated.

metacarpal are generally in a straight line. This line will be broken in a perilunate dislocation, with the lunate sitting anterior to the capitate. A true lateral radiograph aligns the tubercle of the scaphoid and pisiform. With this alignment, the radius and ulna should be overlapping totally; if they are not, consider distal radioulnar joint subluxation or dislocation. The outline of

Wrist and hand problems are common in the sporting arena. Evaluation of these problems requires a careful history with particular attention to the initiating factor, be it traumatic or spontaneous. Attention should be paid to how the injury is affecting the athlete at the time of presentation. The specific site and associated factors of pain will help guide the examiner to the site of specific pathology. With hand and digital injuries, the site of pathology is usually obvious. With the wrist, the site of pathology should be divided into radial, dorsal, ulnar, and palmar aspects. Specific examination of the anatomic part involved should then be performed. An exposed upper extremity should then be inspected. Palpation should be specific to the region involved. Tests for range of motion, instability, and impaction should then be done. Plain radiographs are still the mainstay of imaging in the wrist and hand. When further studies are needed, magnetic resonance imaging and computed tomography are most commonly used. After careful evaluation of the wrist or hand problem, the clinician should be able to come to a specific diagnosis. This allows for decision making with regard to treatment options; observation, bracing or splinting, hand therapy, or open or arthroscopic surgery can be tailored to the specific diagnosis. Details of such management are provided in subsequent chapters of this text.

REFERENCES 1. Rettig AC: Athletic injuries of the wrist and hand: Part 1, traumatic injuries of the wrist. Am J Sports Med 1998;31:1038–1048. 2. Buterbaugh JA, Brown TR, Horn PC: Ulnar sided wrist pain in athletes. Clin Sports Med 1998;17:567–583. 3. Pappas AM, Morgan WJ, Schulz LA, et al: Wrist kinematics during pitching—A preliminary report. Am J Sports Med 1995;23:312–315. 4. Cooney WP, Bishop AT, Linscheid RL: Physical examination of the wrist.

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In Cooney WP, Linscheid RL, Dobyns JH (eds): Wrist Diagnosis and Operative Treatment. St. Louis, Mosby Year-Book, 1998, pp 236–261. 5. Linscheid RL, Dobyns JH: Physical examinations of the wrist. In Linscheid RL, Dobyns JA (eds): Physical Examinations of the Musculoskeletal System. Chicago, Yearbook Medical Publishers, 1987, pp 80–94. 6. Watson HK, Ashmead D, Makhlof V: Examination of the scaphoid. J Hand Surg [Am] 1988;13:657–660.

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Carpal Fractures Steven D. Maschke and Jeffrey N. Lawton

In This Chapter Scaphoid fracture Nonoperative management Surgery—scaphoid fixation Hook of the hamate fracture Triquetral fracture

INTRODUCTION • Hand and wrist injuries account for 3% to 9% of all athletic injuries; these are being seen more frequently as recreational and competitive sports participation increases.1,2 • The human wrist consists of eight carpal bones arranged in two rows, stabilized by numerous volar and dorsal ligaments that function synergistically to provide stability and pain-free range of motion. • Most athletic activities involve the extremes of wrist range of motion. Therefore, physicians must identify carpal injuries early in order to prevent long-term functional decline and select operative procedures, when appropriate, that do not limit the required sport-specific wrist range of motion. • Carpal fractures are often misdiagnosed as “wrist sprains” leading to delays in diagnosis and treatment. These delays may limit the options for both conservative and operative interventions leading to (1) longer treatment protocols, (2) more significant operative procedures, (3) extended loss of sports participation, and (4) permanent functional decline with decreased athletic performance. • Scaphoid fractures account for the majority of carpal fractures. Hook of the hamate fractures occur with increased frequency in stick-handling sports. Appropriate diagnosis requires a high index of suspicion for each fracture type with expeditious treatment optimizing long-term outcomes. Newer percutaneous and arthroscopically assisted procedures allow improved outcomes and early return to play due to less operative morbidity.

SCAPHOID Relevant Anatomy The unique anatomy of the scaphoid leads to a predisposition for significant functional sequelae of malunited fractures while increasing the risks for fracture nonunion and avascular

necrosis. First, the scaphoid is positioned anatomically as a link between the proximal and distal carpal rows. Fracture leads to uncoupling of the distal and proximal fragments, resulting in altered load distribution and abnormal wrist kinematics. The distal fragment flexes and the proximal fragment extends leading to the commonly described “humpback” deformity. The resultant scaphoid shortening and/or angular malunion or nonunion often progresses to carpal collapse resulting in significant functional disability and wrist degeneration.3 Second, the scaphoid has a precarious vascular supply. Branches from the radial artery enter the dorsal ridge of the scaphoid either at or distal to the anatomic waist of the bone. These dorsal branches provide 70% to 80% of the entire intraosseous blood supply and 100% of the vascularity to the proximal pole.4 This retrograde blood supply accounts for the direct correlation between proximal fractures and the increasing risk of delayed healing, nonunion, and avascular necrosis. Thus, successful management of scaphoid fractures demands restoring precise anatomy and choosing appropriate treatments based on fracture location and configuration.

Clinical Features and Evaluation Scaphoid fractures account for 60% to 70% of all carpal fractures.1,2 Athletes are at increased risk due to the extremes of wrist positions and forces at injury. The annual incidence of scaphoid fractures in collegiate football players is estimated to be as high as 1%.5 The mechanism of injury is most often a fall on the outstretched hand, placing the wrist in extreme dorsiflexion and radial deviation.6 Athletes present with pain localized to the radial side of the wrist either following an acute trauma or, not uncommonly, at the conclusion of the athletic season. Often, the athlete provides a history of recurrent, nagging “wrist sprains.” Clinical and radiographic evaluation must be systematically performed to identify the presence of a scaphoid fracture and define the parameters known to guide appropriate treatment and affect long-term outcomes. Paramount to this endeavor is a high index of suspicion for scaphoid fracture in any athlete presenting with radial-side wrist pain. History centers on (1) the acute event, with emphasis placed on the timing and energy of injury and (2) history of upper extremity trauma or wrist pain/swelling. Time from injury to presentation has significant implications with regard to success of treatment and length of time to fracture union. Several studies have documented substantially increased risk of delayed healing and nonunion in fractures where treatment is initiated later than 4 weeks after injury.1,2,6,7 Defining the energy of injury, documenting previous wrist pain/swelling, and correlating these with radiographic findings allow the differentiation of an acute fracture versus an exacerbation of a

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previous scaphoid nonunion. It is critical that these two diagnoses remain separate with appropriate treatment initiated for each specific diagnosis. Physical examination of the entire upper extremity is undertaken to diagnose concomitant upper extremity injuries and establish the clinical suspicion for a scaphoid fracture. The athlete will often demonstrate painful wrist motion, radial-side swelling, and decreased grip strength. Focused examination of the involved wrist helps the athlete define the location and quality of the pain and allows the examiner to grade the current functional impact of the injury with respect to wrist strength and range of motion. Tenderness localized to the anatomic snuff box and pain with wrist dorsiflexion/radial deviation increase the clinical suspicion for a scaphoid fracture. Radiographic evaluation confirms the diagnosis and defines the fracture configuration and geometry. Routine radiographs of the wrist include posteroanterior, true lateral, and scaphoid (30 degrees of supination and ulnar deviation) views.6,8 These initial images identify established fracture nonunions, displaced/angulated fractures, and concomitant wrist injuries. However, plain radiographs are notorious for missing acute nondisplaced scaphoid fractures and are often the cause for delay in diagnosis and treatment (Fig. 39-1). Seven percent of patients with clinical evidence of scaphoid injury and negative plain radiographs will have a scaphoid fracture.9 Therefore, further imaging is often required to establish the diagnosis. Bone scintigraphy has been the gold standard for evaluating patients with clinical suspicion of fracture and no radiographic evidence of injury.8,9 All fractures should have increased tracer uptake at 3 days after injury and most are apparent within the initial 24 hours.8 However, false positives are expected given this modality’s high sensitivity but relatively low specificity.9 Therefore, magnetic resonance imaging is gaining favor as a first-line imaging modality in the diagnosis of occult scaphoid fractures.9 Studies have shown equivalent sensitivity with superior specificity compared to bone scintigraphy.9 Magnetic resonance imaging has the additional advantages of (1) excellent soft-tissue evaluation including the scapholunate ligament,8 (2) ability to assess proximal pole vascularity, (3) identification of fracture location and configuration, (4) no radiation exposure, and (5) speed of examination.9 Radiographs further establish fracture location (distal third, waist, or proximal third) and define stability based on

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Figure 39-1 A, Occult scaphoid fracture: Initial presentation. B, Scaphoid waist fracture: Two-week follow-up (arrow).

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radiographic evidence of fracture displacement and/or angulation. Computed tomography is used when fracture displacement remains uncertain given its superior definition of cortical integrity and bony anatomy.6,8 By definition, displaced scaphoid fractures have at least 1 mm of cortical offset and an increased intrascaphoid angle greater than 30 degrees.1,2,6 Therefore, a high index of clinical suspicion, thorough history and physical examination, and appropriate imaging allow early identification of scaphoid injuries and accurate determination of fracture location, geometry, and time from injury to presentation.

Treatment Options Management of acute scaphoid fractures is guided by fracture location, displacement, and time from injury to presentation.1,2,6 Athletes require additional consideration as to sport and position as well as the athlete’s specific wishes regarding return to play. Restoring precise anatomy and achieving solid fracture union are the primary goals of any treatment. The importance of restoring precise anatomy cannot be overstated. Displacement is the hallmark of unstable fractures. Several studies evaluating closed treatment of fractures with greater than 1 mm of cortical offset have revealed nonunion rates ranging from 46% to 92%.10 Fracture nonunion and/or malunion often lead to painful wrist instability and debilitating degenerative arthritis.3 Therefore, we perform open reduction and internal fixation on all acute displaced scaphoid fractures. Alternatively, arthroscopic reduction with percutaneous fixation may be employed.11 The treatment of nondisplaced scaphoid fractures is more controversial. Historically, cast immobilization was initiated for all nondisplaced fractures, with 6 weeks in a long-arm cast followed by an additional 6 weeks or longer in a short-arm thumb spica cast.7,12,13 The prolonged periods of immobilization coupled with the continued risk of fracture nonunion spurred the development of more aggressive treatment regimens. Today, the selection of an appropriate treatment algorithm is guided by fracture location and individualized to the patient’s vocational, recreational, and athletic demands. Distal third fractures of the scaphoid occur infrequently and involve the tuberosity in isolation or the entire distal third of the bone. Fractures occurring in this location maintain an adequate blood supply and have a high propensity to heal.1,7 Successful union is most often achieved with 6 weeks of immobilization in a short-arm thumb spica cast.7 Proximal third fractures account for 20% of scaphoid fractures and are plagued by higher rates of nonunion and avascular necrosis. Casting has been the standard of care, often requiring as long as 6 months of strict immobilization to achieve successful healing.1,13 Considerable disagreement as to the appropriate type and duration of immobilization continues.6,14 Current recommendations consist of 6 weeks in a long-arm thumb spica cast followed by immobilization in a short-arm thumb spica cast until clinical and radiographic fracture union.2 Few patients can afford such lengthy periods of immobilization. Prolonged casting often leads to significant muscle atrophy, stiffness, and contractures requiring extended periods of rehabilitation prior to return to work or sport.1 Therefore, we recommend consideration of early operative intervention for all proximal scaphoid fractures occurring in active individuals. We use a dorsal approach and perform our fixation either open or percutaneously based on the need for fracture reduction. The vast majority of scaphoid fractures (70% to 80%) are nondisplaced fractures through the anatomic waist.1 Treatment

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options include (1) cast immobilization until radiographic union, (2) cast treatment plus application of playing splints, or (3) immediate internal fixation. Cast immobilization is an effective and appropriate treatment when initiated early for nondisplaced scaphoid waist fractures. Studies have shown 95% rates of union following 8 to10 weeks of cast immobilization initiated within 4 weeks of injury.12,15 Fractures showing no radiographic evidence of healing after 6 to 8 weeks of appropriate immobilization should be considered for internal fixation to minimize the risks of both prolonged casting and fracture nonunion.1,16 Athletes must be appropriately counseled regarding the anticipated 3 months out of competition prior to initiating cast immobilization. Few athletes are willing to undergo this prolonged regimen, and, thus, alternatives have been sought for nondisplaced scaphoid waist fractures in the athletic population. Cast immobilization with the application of a playing splint and immediate return to competition have been described.2 The specific athletic event and the level of competition determine whether playing casts/splints are permitted. Review of this treatment regimen has revealed increased rates of fracture nonunion and subsequent operative intervention.2 Athletes must be informed of the increased risks with this treatment protocol, and we currently do not implement this as a preference in our practice. Advances in surgical technique and internal fixation have revolutionized the operative repair of scaphoid fractures. Absolute indications for immediate internal fixation include displaced fractures, nonunions, and fractures associated with carpal instability.1 Relative indications include delayed presentation (greater than 4 weeks), proximal pole fractures, and malunions.1 Immediate internal fixation for nondisplaced fractures of the scaphoid waist remains controversial, but this approach is gaining more widespread acceptance.1,2,6,13,16 Recent studies comparing immediate operative repair versus cast immobilization reveal equivalent rates of fracture healing with dramatically reduced times to return to work and sport.1,2,6,13,16 We advise our athletes about the risks and benefits of all treatment regimens and advocate immediate internal fixation of nondisplaced scaphoid waist fractures in those desiring an expeditious return to competition.

Surgery Operative fixation of scaphoid fractures is increasing in popularity with advances in intraoperative imaging, surgical approaches/instrumentation, and trends toward less invasive surgical procedures. Currently, acute scaphoid fractures can be repaired via open volar or dorsal approaches, percutaneous techniques, or arthroscopically assisted procedures.1,6,11 Fracture location and geometry as well as surgeon skill and experience guide the appropriate selection for operative repair. Common to all operative techniques is the use of biplanar fluoroscopy to confirm fracture reduction and appropriate guidewire/screw insertion as well as the use of headless compression screws specifically designed for scaphoid fixation. Precise restoration of anatomy and compression of the fracture surfaces are paramount to achieving successful healing. Appropriate screw placement requires critical evaluation. Biomechanical and clinical studies have shown superior loads to failure, stiffness, and strength with central screw placement resulting in decreased times to fracture union.16 Ideally, contact sport athletes are immobilized postoperatively in a short-arm thumb spica cast until radiographic confirmation of bony union, while noncontact athletes may be placed in a removable splint,

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Figure 39-2 Dorsal, percutaneous, scaphoid stabilization. A, Placement of guidewire. B, Fluoroscopic image of starting point for insertion. C, Final guidewire placement.

allowing immediate range-of-motion exercises and potentially earlier return to competition. Minimally invasive techniques have been developed to reduce operative morbidity and expedite fracture healing and rehabilitation (Figs. 39-2 and 39-3). Both percutaneous and arthroscopic procedures are currently in practice.1,6,11,13 Cannulated, headless compression screws allow insertion via minimal incisions, and biplanar fluoroscopy confirms accurate, central screw placement. Both techniques are best suited for nondisplaced or minimally displaced scaphoid fractures.1,6 Athletes are immobilized in a postoperative cast and may immediately return to competition if permitted; alternatively, some must delay return until confirmed fracture healing and cast removal. Taras et al13 reported return to athletics averaging 5.4 weeks with successful union achieved in all patients undergoing percutaneous scaphoid fixation. These techniques are best reserved for surgeons experienced in wrist arthroscopy and operative scaphoid repair. Compromising accurate reduction and central screw placement, for the sake of a percutaneous approach, must be avoided. Open reduction and internal fixation remains the treatment of choice for displaced, unstable scaphoid fractures.6 The operative approach is determined by fracture location. The volar approach preserves the vital dorsal blood supply and allows easy access to middle and distal third fractures. The dorsal approach provides exposure of proximal third fracture and is reserved for this indication as the vascular leash is maintained. Direct visualization of fracture reduction and guidewire placement is correlated with biplanar imaging to confirm anatomic reduction and central screw placement.

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Figure 39-3 Volar, percutaneous, scaphoid stabilization. A, Placement of guidewire. B, Fluoroscopic image of volar starting point.

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Technique: Volar Open Reduction/Internal Fixation The volar approach to the wrist begins with a 4- to 5-cm curvilinear incision extending from the scaphoid tuberosity along the radial border of the flexor carpi radialis tendon. The flexor carpi radialis tendon sheath is exposed and longitudinally incised allowing ulnar retraction of the tendon. Commonly, the superficial palmar branch of the radial artery is encountered, requiring ligation. The volar capsule is obliquely incised exposing the radioscaphocapitate and long radiolunate ligaments. These ligaments are critical to wrist stability and are either partially divided or completely transected and tagged for later repair. The fracture is visualized and cleared of clot and debris. Preliminary reduction, usually by wrist extension, is achieved and fluoroscopic imaging obtained to confirm reduction and correction of the “humpback” deformity. Careful scrutiny of the scapholunate angle on lateral fluoroscopy is critical. The scaphotrapezial joint is entered and 2 to 3 mm of volar trapezium excised to allow accurate guidewire and screw placement. A compression jig or free-hand technique is used to centrally place the guidewire. Biplanar imaging confirms accurate wire placement and a second Kirschner wire may be inserted to control rotation and displacement during drilling, tapping, and screw insertion. Screw placement/length and fracture reduction and stability are confirmed with biplanar imaging and both Kirschner wires removed (Fig. 39-4). The volar radiocarpal ligaments and capsule are reapproximated and repaired using 3-0 permanent figure-eight sutures. The wound is closed in layers and a sterile dressing is applied. A short-arm volar thumb spica splint is applied. The patient is seen at 1 week postoperatively for splint removal and application of a short-arm thumb spica cast.

Postoperative Rehabilitation Immobilization is continued until radiographic confirmation of fracture healing. Computed tomography is the gold standard for defining fracture union and can be obtained on patients prior to discontinuation of immobilization. The average time to fracture union following operative repair ranges from 5 to 7 weeks.12,13 Therapy is instituted immediately following cast removal with emphasis on wrist and digital range of motion followed by strengthening.

Criteria for Return to Play The athlete’s return to play is individualized, dependent on progress in healing, sport, position, and level of competition. All

scaphoid fractures must be protected with a cast or splint until radiographic confirmation of fracture healing.6 The goal of splint/cast immobilization is to limit wrist hyperextension upon potential impact. Noncontact sport athletes can immediately return to competition following stable internal fixation with a short-arm thumb spica cast/splint. Contact athletes and those undergoing conservative management should remain out of competition until confirmed fracture union. Athletes must demonstrate painless, full wrist range of motion and near normal strength prior to allowing unprotected athletic participation.

Results and Outcomes Cast immobilization of a nondisplaced scaphoid fracture initiated within 4 weeks of injury has a greater than 90% chance of achieving fracture union.15 Conservative treatment of fractures with 1 mm or greater displacement is complicated by nonunion rates ranging from 46% to 92%.10 Immediate operative repair for both displaced/unstable fractures as well as nondisplaced scaphoid waist and proximal third fractures leads to fracture union rates exceeding 90%.2,12 Early diagnosis and treatment with anatomic reduction and appropriate immobilization optimize long-term results.

Complications Scaphoid fracture nonunions and malunions alter carpal kinematics potentially leading to radiocarpal and midcarpal osteoarthritis.4 These degenerative changes often lead to chronic pain, limited motion, and diminished function.1,2,4,6 Athletes with symptomatic malunions and nonunions require thorough evaluation and consideration of scaphoid reconstruction. Athletes with an incidental finding of a scaphoid fracture nonunion and/or malunion present a treatment dilemma. The patient must understand the natural history of these clinical entities with either observation or operative intervention instituted at the conclusion of the season on an individualized basis.

HOOK OF THE HAMATE Anatomy The hamulus, or hook of the hamate, protrudes into the palm surrounded by critical soft-tissue structures. The hook serves as the origin of the flexor and opponens digiti minimi muscles and forms the ulnar border of the carpal tunnel and radial border of Guyon’s canal.1 The deep motor branch of the ulnar nerve courses around the base of the hook with the superficial sensory branch remaining in close contact with the tip. The hook also functions as a pulley for the superficial and deep flexor tendons to the small and ring fingers, especially during ulnar deviation involved with power grip. Therefore, fracture and/or fracture nonunion of the hook of the hamate jeopardize injury to any or all of the previously mentioned structures. The vascular anatomy of the hamate hook has been extensively evaluated.17 Vessels penetrate the radial base as well as the ulnar tip with relatively poor vascular anastomoses between the two.7,17 This resultant vascular watershed predisposes even nondisplaced hook fractures to nonunion.1,17,18

Clinical Features and Evaluation

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Figure 39-4 Postoperative radiographs: Percutaneous scaphoid stabilization. A, Scaphoid view. B, Oblique view.

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Hook of the hamate fractures account for only 2% to 4% of all carpal fractures.1 Athletes participating in stick-handling sports account for the vast majority of these injuries and are most at risk of long-term complications secondary to missed or delayed diagnosis.1,2,19,20 The mechanism of injury is either (1) direct

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impact via the handle of a club, racquet, or bat or (2) shearing forces arising from the hypothenar muscles as well as the flexor tendons to the ring and small fingers. The nondominant hand is most commonly involved in golf and baseball, whereas the dominant hand is more common in tennis and racquetball.1 Early diagnosis is critical to successful management of hook of the hamate fractures. The majority of these injuries will proceed to nonunion if left untreated.20 Fracture nonunion predisposes the athlete to (1) chronic ulnar-side wrist pain, (2) ulnar nerve paresthesias/motor weakness, and/or (3) flexor tenosynovitis with potential flexor tendon rupture. Diagnosis begins with a detailed history focusing on the mechanism and timing of injury. Ulnar wrist pain occurring during stick-handling sports is almost pathognomonic for hook fracture. Athletes with symptoms directed at the carpal tunnel, Guyon’s canal, or ulnarside digital flexors require critical evaluation for established nonunion of the hamate’s hook. Tenderness to palpation over the hook, painful grip, pain with resisted small/ring finger flexion, and a high index of suspicion further aid in the diagnosis. Radiographic evaluation confirms suspected diagnoses. Routine anteroposterior, lateral, and oblique wrist radiographs often do not reveal the fracture.1,17,21 Subtle radiographic signs on anteroposterior projections include (1) absence of the hook, (2) lack of cortical density, and (3) sclerosis.1 Special projections can be useful in establishing the diagnosis. The carpal tunnel view may allow imaging of the hamate hook but requires wrist dorsiflexion often unattainable in patients with wrist injuries (Fig. 39-5).17 Computed tomography is the gold standard for confirming the presence of hook of the hamate fracture and should be obtained in any athlete with ulnar-side wrist pain and negative plain radiographs (see Fig. 39-5).1,2,17 A high index of suspicion for fracture and appropriate radiographic evaluation allow prompt diagnosis, early management, and avoidance of long-term complications.

Treatment Options Appropriate management of hook of the hamate fractures aims to eliminate the risk of long-term complications and return the athlete to his or her preinjury level of play. Treatment options include cast immobilization, fragment excision, and open reduction and internal fixation.1,17 The choice of management is guided by time from injury to presentation, displacement, and accompanying nerve/tendon pathology.1,17 Athletes must be appropriately counseled regarding the potential complications arising from untreated fractures and fracture nonunions. Displaced fractures compromise the intricate anatomy and encroach on the vital soft-tissue structures adjacent to the hamate’s hook. Neurovascular and tendinous structures are at risk and must be preserved.1,19,20,22 Therefore, all displaced fractures require immediate fragment excision.

Nondisplaced fractures are treated based on the timing from injury to presentation. Acute fractures are defined as those diagnosed and treated within 7 days of injury. Whalen et al23 managed six acute fractures in short-arm casts incorporating the fourth and fifth metacarpophalangeal joints. Successful union was achieved in all acute injuries, with healing times averaging 8 to 12 weeks. Other studies document high rates of nonunion following cast immobilization that is initiated greater than 7 days from injury.10,17,24 Thus, cast immobilization is a viable treatment option only for fractures diagnosed and immobilized within 7 days of injury.1,23 Athletes must be informed of the 3 to 4 months out of competition required for successful conservative management. Fractures presenting more than 7 days from injury require operative intervention. Operative management consists of fragment excision versus open reduction and internal fixation. Indications for surgery include (1) displaced fractures, (2) fractures accompanied by ulnar nerve paresthesias or tendinous pathology, (3) fractures diagnosed later than 7 days from injury, and (4) athletes unwilling to undergo prolonged immobilization of acute injuries.1,17,24 Open reduction and internal fixation have been described. The small size of the fragment and precarious vascular supply adds complexity and uncertainty to this procedure.1,10 Thus, excising the fractured hook remains the gold standard among operative procedures.1,24,25 A volar approach is used, with care to identify and protect the surrounding neurovascular and tendinous structures. The fragment is subperiosteally excised, and the bone edges smoothed to prevent ulnar nerve irritation or tendon fraying. The wrist is immobilized postoperatively to protect the operative wound.

Postoperative Rehabilitation Following fragment excision, the wrist is immobilized for 10 to 14 days to protect wound healing. Athletes undergoing prolonged immobilization require hand therapy following cast removal to regain full, painless wrist range of motion.

Criteria for Return to Play Stable fracture healing and painless full wrist range of motion are required following cast immobilization or open reduction and internal fixation prior to return to play. Athletes undergoing fragment excision may return to competition as tolerated following successful wound healing. The majority of athletes prefer to wear well-padded gloves for several months after treatment to protect the hypothenar eminence from irritation inflicted by their racquet, club, or bat.1,21

Results and Outcomes The vast majority of athletes return to their previous level of sports participation following hook of the hamate excision.10,19,24 The time to return to full athletics averages 8 weeks with nearly normal grip strength regained within 3 months of fragment excision.2,20 Associated nerve or tendon injury prolongs the time course for return to athletics and complicates the surgical repair and postoperative rehabilitation.22

Complications

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Figure 39-5 Hook of the hamate. A, Carpal tunnel view: hook (arrow). B, Computed tomography image: hook fracture (arrow).

The surrounding soft-tissue structures can be irritated and damaged by the fractured hamate hook or callous from a hypertrophic nonunion. Ulnar nerve compression is common and presents as paresthesias extending into the ring and small fingers.21 The flexor tendons to the small and ring fingers can be abraded by the fractured hook, developing painful

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tenosynovitis.19,22 Untreated, these tendons are at risk of rupture.19,22 All complications must be promptly identified and treated appropriately along with fragment excision. Early diagnosis is critical in avoiding the late sequelae of hook fracture and nonunion.

OTHER CARPAL FRACTURES Significant forces transmitted through the wrist from a fall or collision can potentially fracture any of the eight carpal bones. Unlike the previously discussed injuries, the remaining carpal fractures are more straightforward with regards to diagnosis and treatment. Athletes presenting with significant wrist pain, swelling, or deformity require a precise physical examination with palpation of each carpal bone followed by appropriate radiographs. Subtle fractures may be difficult to identify on plain radiographs. Computed tomography can significantly aid in the diagnosis of occult fractures occurring in the setting of wrist pain/swelling and negative plain radiographs. Dorsal triquetral fractures require specific mention as they are the second most common carpal fracture in athletes.1 These

injuries arise from either bony impaction occurring with extreme wrist dorsiflexion and ulnar deviation or from bony avulsion via the strong dorsal capsular ligaments.1,10 Plain radiographs demonstrate the injury on the lateral film. Immobilization for 4 weeks with protected athletic participation leads to excellent clinical results and early return to play.1,10 Fractures of the other carpal bones are rare and most often occur in high-energy trauma. These injuries require immobilization and referral to a hand surgery specialist. Excellent outcomes and return to play are expected following appropriate treatment.

CONCLUSIONS Early diagnosis is critical in the appropriate diagnosis of carpal fractures. Scaphoid fractures are most common, and plain radiographs may not reveal the acute fracture. Magnetic resonance imaging or computed tomography is often required. Treatment of scaphoid fractures has evolved, and operative intervention is commonly employed. This generally allows for earlier return to sports. When diagnosed acutely and treated appropriately, a good outcome is usually achieved.

REFERENCES 1. Geissler WB: Carpal fractures in athletes. Clin Sports Med 2001; 20:167–188. 2. Rettig AC: Athletic injuries of the wrist and hand—part 1: Traumatic injuries of the wrist. Am J Sports Med 2003;31:1038–1048. 3. Mack GR, Bosse MJ, Gelberman RH, et al: The natural history of scaphoid non-union. J Bone Joint Surg Am 1984;66:504–509. 4. Gelberman RH, Menon J: The vascularity of the scaphoid bone. J Hand Surg 1980;5:508–513. 5. Zemel NP, Stark HH: Fractures and dislocations of the carpal bones. Clin Sports Med 1986;5:709–724. 6. Cooney WP: Scaphoid fractures: Current treatment and techniques. Instr Course Lect 2003;52:197–208. 7. Burge P: Closed cast treatment of scaphoid fractures. Hand Clin 2001;17:541–552. 8. Plancher KD: Methods of imaging the scaphoid. Hand Clin 2001; 17:703–721. 9. Fowler C, Sullivan B, Williams L, et al: A comparison of bone scintigraphy and MRI in the early diagnosis of occult scaphoid waist fracture. Skeletal Radiol 1998;27:683–687. 10. Melone CP: Fractures of the wrist. In Nicholas JA, Hershman EB (eds): The Upper Extremity in Sports Medicine, 2nd ed. St. Louis, Mosby, 1995, pp 401–448. 11. Slade JF, Geissler WB, Gutow AP, et al: Percutaneous internal fixation of selected scaphoid non-unions with an arthroscopically assisted dorsal approach. J Bone Joint Surg Am 2003;85:20–31. 12. Saeden B, Tornkvist H, Ponzer S, et al: Fracture of the carpal scaphoid: A prospective, randomized 12 year follow up comparing operative and conservative treatment. J Bone Joint Surg Br 2001;83: 230–234. 13. Taras JS, Sweet S, Shum W, et al: Percutaneous and arthroscopic screw fixation. Hand Clin 1999;15:467–473.

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14. McAdams TR, Spisak S, Beaulieu CF, et al: The effects of pronation and supination on the minimally displaced scaphoid fracture. Clin Orthop 2003;411:255–259. 15. Cooney WP, Dobyns JH, Linscheid RL: Non-union of the scaphoid: Analysis of the results from bone grafting. J Hand Surg Am 1980;5:343–354. 16. Chan KW, McAdams TR: Central screw placement in percutaneous screw scaphoid fixation: A cadaveric comparison of proximal and distal techniques. J Hand Surg Am 2004;29:74–79. 17. Walsh JJ, Bishop AT: Diagnosis and management of hamate hook fractures. Hand Clin 2000;16:397–403. 18. Failla JM: Hook of the hamate vascularity: Vulnerability to osteonecrosis and non-union. J Hand Surg Am 1993;18:1075–1079. 19. Stamos BD, Leddy JP: Closed flexor tendon disruption in athletes. Hand Clin 2000;16:359–365. 20. David TS, Zemel NP, Mathews PV: Symptomatic, partial union of the hook of the hamate fracture in athletes. Am J Sports Med 2003;31:106–111. 21. Murray PM, Cooney WP: Golf-induced injuries of the wrist. Clin Sports Med 1996;15:85–108. 22. Milek MA, Boulas HJ: Flexor tendon ruptures secondary to hamate hook fractures. J Hand Surg Am 1990;15:740–744. 23. Whalen JL, Bishop AT, Linscheid RL: Non-operative treatment of acute hamate hook fractures. J Hand Surg Am 1992;17:507–511. 24. Stark HH, Chao E, Zemel NP, et al: Fracture of the hook of the hamate. J Bone Joint Surg Am 1989;71:1202–1207. 25. Aldridge JM, Mallon WJ: Hook of the hamate fractures in competitive golfers: Results of treatment by excision of the fractures hook of the hamate. Orthopedics 2003;26:717–719.

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Wrist Soft-Tissue Injuries Philip E. Blazar and Jennifer A. Graham

In This Chapter Triangular fibrocartilage complex (TFCC) injury Nonoperative management Surgery—wrist arthroscopy Scapholunate instability Tendonitis de Quervain’s disease Intersection syndrome

INTRODUCTION • Athletic soft-tissue injuries of the wrist may be acute or degenerative in nature. • Injuries of the TFCC are a frequent source of ulnar side wrist pain. • Wrist arthroscopy is often employed to repair or débride TFCC tears. • The preferred treatment of acute disruption of the scapholunate ligament is open repair. • Chronic scapholunate injuries are more difficult to treat and often require a salvage procedure. • Other wrist soft-tissue problems include tendonitis, de Quervain’s disease, and intersection syndrome.

TRIANGULAR FIBROCARTILAGE COMPLEX INJURIES Clinical Features and Evaluation One of the most common complaints about the wrist is ulnar side wrist pain. Injuries to the TFCC usually occur as the result of a hyperextension, ulnar deviation, and axially loading force and can also be found in association with distal radius fractures. However, not all disruptions of the TFCC are traumatic in nature, as inflammatory and degenerative conditions can also lead to TFCC pathology. Patients presenting with TFCC injuries may report ulnar side wrist pain, occasional clicking, loss of grip strength, and pain with pronation and supination. The mechanical symptoms may improve with rest and are worsened with loading. A complete history including any history of trauma or repetitive use injury should be taken and a complete examination of the wrist should be performed. Traumatic injuries may present with a pop and immediate pain and swelling, and chronic

injuries may be indolent in nature. On inspection of the injured wrist, prominence of the distal ulna may indicate distal radial ulnar joint (DRUJ) instability or a significant TFCC injury. On physical examination, the TFCC may be palpated midway between the extensor carpi ulnaris (ECU) and flexor carpi ulnaris (FCU) tendons, in the soft recess just distal to the ulnar styloid. The piano key test is performed by balloting the distal ulna in an anteroposterior direction indicating a DRUJ or TFCC injury. Findings are always compared to the contralateral wrist and should be compared on multiple positions of forearm rotation. Comparison between wrists is important because (in young women in particular) physiologic laxity may exist. Additional ulnar side structures to be examined include the lunotriquetral interval, which is located between the fourth and fifth extensor compartments, one fingerbreadth distal to the DRUJ, with the wrist in 30 degrees of flexion. The ECU tendon must also be examined for subluxation or tendonitis along the distal ulna and its insertion into the base of the fifth metacarpal. Tenderness may be elicited with the TFCC grind or compression test, which can be performed by ulnar deviation of the wrist while applying an axial load and rotating the forearm. The differential diagnosis of ulnar side wrist pain includes ECU subluxation, lunotriquetral ligament injury, pisotriquetral arthritis, hook of the hamate fracture, ulnar artery thrombosis, ulnar neuropathy, and ulnar impaction. Radiographic imaging for TFCC injuries should begin with posteroanterior and lateral views of the wrist, but plain films are usually normal. Arthrography was the previous gold standard but has been replaced in many centers by magnetic resonance imaging or magnetic resonance arthrography. On a T2-weighted magnetic resonance image, the synovial fluid will have a bright signal that outlines a TFCC tear, while a normal TFCC should be homogeneously dark throughout. The Palmer classification1 of TFCC injuries divides injuries into types I (traumatic) and II (degenerative; Fig. 40-1). Type I injuries are subclassified into type A, B, C, and D depending on the location of the lesion. A type IA lesion is a tear in the horizontal portion of the TFCC near the attachment to the radius. A type IB lesion is a traumatic avulsion of the TFCC off its attachment to the distal ulna and may be associated with a fracture of the ulnar styloid. This lesion may be associated with DRUJ instability since the TFCC is the major stabilizer of the DRUJ. It may also be associated with ECU subluxation. A type IC lesion involves a peripheral avulsion from the insertions of the ulnolunate and ulnotriquetral ligaments. A type ID injury is a traumatic avulsion of the TFCC from its radial attachment at the distal aspect of the sigmoid notch. Degenerative lesions of the TFCC are a result of chronic loading to the TFCC (i.e., ulnar impaction syndrome) and are

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Type IA

Type IB

T

T

R

L

S

L

S

R

U

Type IC

U

Type ID

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S

L

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U

A Figure 40-1 Palmer classification of triangular fibrocartilage complex (TFCC) injuries. A, Type I injuries are traumatic in nature. A type IA lesion involves a perforation near the radius. A type IB lesion is an avulsion of the TFCC from the ulnar attachment. A type IC lesion is an avulsion of the ulnar ligaments. A type ID lesion is an avulsion from the distal radius.

subclassified A, B, C, D, and E. Ulnar impaction syndrome is a degenerative condition usually associated with a length imbalance between the distal radius and ulna (i.e., the ulna is longer than the radius). This syndrome can present in a wide age range depending on the predisposing condition. Conditions that predispose to this syndrome include Madelung’s deformity, premature closure of the radial physis secondary to trauma, naturally positive ulnar variance, malunions of distal radius fractures leading to shortening of the distal radius, or excision of the radial head with distal forearm instability (i.e., Essex-Lopresti injury). On physical examination, symptoms can be reproduced with an axial load applied to an ulnar deviated wrist and extremes of pronation and supination. A posteroanterior radiograph of the affected wrist will typically reveal a positive ulnar variance or ulnar styloid index. The ulnar styloid index is equal to the ulnar styloid length minus the ulnar variance divided by the ulnar head width. An index greater than 0.22 is considered elevated. Radiographs may also reveal sclerotic or cystic changes between the lunate and ulnar styloid. Magnetic resonance imaging of the wrist may reveal edema on the ulnar side of the lunate. This can be confused with Kienböck’s disease, but findings on the ulnar aspect of the lunate are not characteristic of Kienböck’s disease.

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Arthroscopy may reveal a TFCC tear or a lunotriquetral ligament tear. TFCC tears secondary to degenerative change are classified according to the presence or absence of a TFCC tear and/or chondromalacia. Type IIA lesions involve wear of the horizontal portion of the TFCC without perforation. Type IIB involves wear of the TFCC plus lunate or ulna chondromalacia. Type IIC involves perforation of the TFCC and chondromalacia. Type IID lesions are TFCC perforation, chondromalacia, and lunotriquetral ligament perforation. Type IIE lesions are the final stage of ulnar impaction syndrome including TFCC perforation, chondromalacia, lunotriquetral ligament perforation, and ulnocarpal arthritis.

Relevant Anatomy The TFCC has three major functions: First, it is considered the primary stabilizer of the DRUJ; second, it transmits approximately 20% of the load across the wrist; and third, it supports the ulnar carpus. Palmer and Werner2 described the TFCC as the triangular fibrocartilage proper, the palmar and dorsal radioulnar ligaments, the ulna collateral ligament, the subsheath of the ECU tendon and the ulnolunate and ulnotriquetral ligaments (Fig. 40-2). Volar and dorsal branches of the anterior

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Type IIA

Type IIB

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T

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Type IIC

U

Type IID

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B Figure 40-1—cont’d B, A type II lesion is a degenerative lesion. A type IIA lesion is TFCC wear without perforation. A type IIB lesion involves TFCC wear and lunate or ulnar chondromalacia. A type IIC lesion involves TFCC perforation. A type IID lesion involves TFCC perforation, chondromalacia, and lunotriquetral ligament perforation. L, lunate; R, radius; S, schaphoid; T, triquetrum; U, ulna. (From Palmer AK, Werner FW: The triangular fibrocartilage complex of the wrist—Anatomy and function. J Hand Surg [Am] 1981;6:153–162.)

interosseous artery supply the TFCC. The central portion of the TFCC is relatively avascular, while the peripheral portion is well vascularized. This pattern is analogous to the knee menisci and explains why central tears are débrided and peripheral tears may by repaired. The relationship between the distal radius and distal ulna is important in the transmission of forces across the wrist. When the variance is neutral, 80% of a load will be transmitted through the radius and 20% through the ulna. A positive ulnar variance leads to increased load sharing by the ulna and the opposite is also true; decreased ulnar variance leads to decreased load sharing across the ulna. Ulnar variance is measured on a posteroanterior neutral rotation radiograph of the wrist and is equal to the difference between a line drawn across the lunate fossa of the distal radius and another line drawn across the top of the ulnar head.

Treatment Options Initial treatment of acute TFCC injuries is immobilization for 6 to 8 weeks. Significant instability of the DRUJ and ECU sub-

luxation should be ruled out. Peripheral tears are expected to heal because of their vascularity, and central tears may become asymptomatic despite not healing. Indications for wrist arthroscopy include a proven or suspected TFCC injury with ulnar wrist symptoms that interfere with activities. Patients should have failed 3 to 4 months of conservative management including rest, immobilization, and anti-inflammatory medications.

Surgery Wrist arthroscopy has gained a prominent role in the diagnosis and treatment of wrist disorders. It may used in the débridement and repair of TFCC tears, débridement of intercarpal ligament tears, visualization of scaphoid and distal radius fractures, removal of loose bodies, débridement of articular injuries, excision of ganglion cysts, radial and ulnar styloidectomy, synovectomy, and débridement of septic joints. The Palmer classification of TFCC injuries serves as a guide to surgical treatment. Type IA lesions, isolated central tears of the TFCC, can be treated with limited arthroscopic débridement of the tear. It has been

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T A S

B

L

C U R

D E

Figure 40-2 Anatomy of the triangular fibrocartilage complex (TFCC). Ulnolunate ligament (A); ulnotriquetral ligament (B); palmar radioulnar ligament (C); ECU sheath (D); triangular fibrocartilage proper (E); dorsal radioulnar ligament (F). L, lunate, R, radius; S, scaphoid; T, triquetrum; U, ulna.

F

reported that 80% to 85% of patients have had a good result with limited débridement. Type IB lesions, a peripheral detachment from the ulnar styloid, are often diagnosed by a diagnostic arthroscopy. The pathognomic sign is the “trampoline” sign, which is the loss of the normal tautness of the TFCC when probed. Type IB lesions can be associated with ECU subluxation, which, if present, requires an open repair of the ECU subsheath in addition to an arthroscopic or open repair of the TFCC. In the acute setting of DRUJ instability associated with an ulnar styloid fracture, an open repair of the fracture may be required. This scenario is often associated with displaced distal radius fractures. After repair, 85% to 90% of patients have good to excellent results.3 A type IC lesion, a distal avulsion of the ulnolunate and ulnotriquetral ligaments, theoretically can be repaired because it is peripheral and well vascularized. A type ID lesion, avulsion of the TFCC from the sigmoid notch, is most commonly associated with a distal radius fracture and may be repaired by open or arthroscopic techniques. The preferred treatment for type ID lesions remains controversial. Degenerative tears of the TFCC are related to chronic overloading of the ulnar side of the wrist. These lesions are the result of ulnar impaction. Diagnostic arthroscopy is the best method to stage the ulnar impaction lesion. The primary goal in treating ulnar impaction is unloading the ulnar head. This is usually done by an ulnar shortening procedure such as a shortening osteotomy, partial ulnar head resection, or ulnar salvage procedures. Arthroscopy will reveal TFCC wear and chondromalacia associated with type IIA and IIB lesions. They can be treated with TFCC débridement arthroscopically, followed by an open or arthroscopic Feldon ulnar shortening procedure (distal ulnar head resection)4 or an ulnar shortening procedure proximal to the wrist. Type IIC lesions, including TFCC perforation and chondromalacia, are treated with arthroscopic débridement of the TFCC and/or an ulnar shortening procedure. Type IID and

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IIE lesions are the end stage of ulnar impaction syndrome. Arthroscopic débridement of the TFCC and ulnar shortening may be performed. The assessment of the integrity of the lunotriquetral ligament is the primary indication for arthroscopy. If the lunotriquetral ligament is unstable after ulnar shortening osteotomy, the lunotriquetral joint can be pinned or a lunotriquetral fusion can be performed. Lesions with ulnocarpal arthritis are treated with a Bower’s distal ulna resection5 or Suave-Kapandji procedure,6 if the surgeon thinks that a distal ulnar resection will be sufficient.

Surgical Technique: Wrist Arthroscopy Regional anesthesia is generally used and a tourniquet is placed. After the patient has been placed under anesthesia, an examination of the wrist should be performed. The patient is placed supine and the wrist is then placed under 10 to 15 pounds of distraction force. Distraction towers are available commercially for this purpose. Arthroscopes are between 2 and 3 mm and a 30-degree arthroscope is the most commonly used. Arthroscopic portals are named in relation to the extensor tendon compartments. There are five radiocarpal portals, two midcarpal portals, one STT (scapho-trapezio-trapezoid) portal, and two DRUJ portals. Portals are named for their relationship to the extensor compartments. The 3-4 portals are the primarily visualization portals, the 4-5 portals are work portals, and the 6-R and 6-U portals are used as outflow portals or working portals for the ulnar wrist. The portals can be used interchangeably. Portals used depend on the pathology present. Following the 12-degree volar tilt of the radius, an 18-gauge needle is introduced into the third to fourth interval, distal to Lister’s tubercle, and the joint is injected with 5 to 7 mL of normal saline. A skin incision is made and a blunt trocar is introduced into the joint (Fig. 40-3). From the 3-4 portal, 70% of the joint can be examined including the radial styloid, scaphoid, scapholunate ligament, radial

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Figure 40-4 Trampoline sign. A probe is inserted to test the tautness of the triangular fibrocartilage complex (TFCC). The TFCC is relatively firm when probed. If it is not firm, the TFCC should be closely examined for a perforation.

can be examined. After wrist arthroscopy has been completed, the wrist should be re-examined and clicks present secondary to TFCC injury should not be present. The portals are closed with a nylon suture. The wrist is placed in a splint for 1 week to support the extensor tendons and then intermittently for 3 weeks with restrictions on grasping and repetitive activities.

B Figure 40-3 A, Arthroscopic setup. B, Portals. Cannula is placed in 3-4 portal. Midcarpal portal is marked 1 cm distal to 3-4 portal.

attachment of the TFCC, extrinsic ligaments, and tautness of the TFCC. An ulnar portal such as the 6-R or 4-5 is made when needed to improve visualization. A shaver can be introduced to remove synovitis that is present. A probe is inserted to test for a flap tear, the tautness of the TFCC (trampoline sign), and the integrity of the intercarpal ligaments (Fig. 40-4). From the ulnar portal, the lunate, triquetrum, lunotriquetral ligament, TFCC, ulnolunate ligament, and ulnotriquetral ligament can be examined if the arthroscopic portal is switched. For resection of an unstable flap, a punch is used and the edges can be débrided with a shaver. Alternatively, a bipolar or monopolar electrocautery can débride the tissue. Only unstable portions are débrided. If chondromalacia is present indicating a type II lesion, a distal ulna resection can be performed arthroscopically using a bur. Once the radiocarpal joint has been examined from the radiocarpal and ulnar portals, the midcarpal joint must be examined. The radial midcarpal portal is 1 cm distal to portal 3/4. From this portal, the scapholunate and lunotriquetral articulations, distal scaphoid, proximal capitate, and proximal hamate

Postoperative Rehabilitation For TFCC lesions in which only a débridement is performed, the wrist is placed in a splint for 1 week and then used intermittently as needed for the next 3 weeks. At 1 week, range-ofmotion exercises are started with restrictions on lifting and repetitive motions. Repaired TFCC lesions should be immobilized in either a splint or cast for 4 to 6 weeks and then rangeof-motion exercises are begun with restrictions on lifting and repetitive motion.

Return to Sports Patients may return to athletics once they have demonstrated progress in strength and range of motion of the affected extremity. For débridement, this is typically at 4 to 6 weeks. Three months is typically the minimum after a repair. One to 3 months of a supervised physical therapy program is normally required. A protective splint should be worn while participating in athletic activities. The protective splint may be discontinued once full strength and range of motion have been obtained.

Complications Complications of wrist arthroscopy involve injury to superficial nerves during portal placement. The dorsal cutaneous branch of the ulnar nerve can be injured during the placement of the 6-U portal. The superficial radial and lateral antebrachial cutaneous nerves may be injured during placement of the 1-2 portal.

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SCAPHOLUNATE INSTABILITY Clinical Features and Evaluation Scapholunate instability is the most common carpal instability pattern, either alone or in conjunction with another instability pattern or distal radius fracture. The most common mechanism of injury is a fall on an outstretched wrist with hyperextension, ulnar deviation, and supination of the wrist. Patients will often have pain and swelling with acute injuries. Those presenting with chronic injuries may report pain and popping with loading of the wrist. Patients may also complain of weak grip, limited motion, and point tenderness over the dorsal aspect of the scapholunate interval. Diagnosis is often delayed because the injury is thought only to be a sprained wrist. On physical examination, patients will have tenderness located over the anatomic snuffbox and dorsally over the scapholunate interval. The Watson scaphoid shift test is the provocative maneuver for scapholunate ligament injury (Fig. 40-5). The examiner places his or her thumb over the distal pole of the scaphoid and the other hand moves the wrist in an ulnar to radial direction, which elicits pain or a palpable clunk. Imaging consists of posteroanterior and lateral radiographs of the injured wrist. Injuries may be static or dynamic. Static injuries will be seen on radiographs. On the posteroanterior wrist, the scapholunate interval may be greater than 3 mm (positive Terry Thomas sign), the scaphoid will appear shortened (positive cortical ring sign), and the lunate will be extended (Fig. 40-6). On the lateral film, the normal scapholunate angle is 30 to 60 degrees. A scapholunate angle greater than 70 degrees suggests scapholunate instability7 (Fig. 40-7). In cases of dynamic instability a load must be applied to generate abnormal findings. A clenched-fist anteroposterior radiograph of the wrist can be obtained to accentuate the scapholunate diastasis. Magnetic resonance imaging is a noninvasive modality that can be used to evaluate wrist ligaments, although it is thought to be technique and interpreter dependent. Arthroscopy can also be used to diagnose scapholunate injury. Geissler et al,8 devised a classification system to standardize arthroscopic observation of injury to the intercarpal ligaments. Grade I lesions involve attenuation or hemorrhage of the involved ligament. Grade II lesions involve attenuation or hemorrhage of the interosseous ligament with intercarpal step-off and a slight gap is present between carpal bones. Grade III lesions involve a step-off in carpal alignment and a probe may be passed between carpal bones. Grade IV lesions involve a stepoff in carpal alignment and there is gross instability in which the arthroscope may be passed between carpal bones. During a diagnostic arthroscopy, a positive “drive through” sign is a grade IV lesion in which the arthroscope can be passed through the scapholunate interval into the midcarpal joint.

Relevant Anatomy The interosseous scapholunate ligament, the dorsal scapholunate ligament, and the palmar radioscaphoid ligament are involved in scapholunate instability. Isolated transection of the interosseous scapholunate ligament has been shown not to reproduce instability in cadavers. Scapholunate disassociation results from injury to the scapholunate interosseous ligament and the palmar radioscaphoid ligament.9

Treatment Options Treatment of scapholunate instability depends on when the injury is diagnosed. Partial tears of the interosseous scapholunate ligament can be treated with cast immobilization for 6 to

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10 weeks to allow healing. Patients with partial tears that remain symptomatic after immobilization may undergo arthroscopic débridement of the tear with some relief of symptoms. Complete tears of the scapholunate ligament should be treated surgically.

Acute Scapholunate Injuries Injuries of the scapholunate ligament usually involve an avulsion of the ligament off the scaphoid. Closed reduction and cast immobilization are no longer used in the treatment of complete scapholunate ligament tears because there are no data supporting the success of this method. Even when an anatomic reduction could be achieved, it was rarely maintained. Closed reduction and percutaneous pinning of the scapholunate ligament have also been abandoned because of inability to maintain reduction. The preferred treatment of acute scapholunate ligament injuries is open reduction and direct repair of the scapholunate ligament. Through a dorsal approach, the joint is reduced and the scapholunate ligament is directly repaired using sutures through bone tunnels or suture anchors. Some authors also advocate reinforcement of the repair with dorsal capsulodesis (Blatt procedure). After open reduction and internal fixation of the scapholunate ligament, the wrist is kept in a thumb spica cast for 2 to 3 months, followed by 1 month in a short arm cast, followed by a protective splint and physical therapy.

Return to Sports Patients may return to athletics once they have demonstrated progress in strength and range of motion of the affected extremity. One to 3 months of a supervised physical therapy program is normally required after cast removal. A protective splint should be worn while participating in athletic activities. The protective splint may be discontinued once full strength and range of motion have been obtained.

Treatment of Chronic Injuries without Degenerative Changes Chronic instability is defined as a scapholunate ligament injury that has been present for more than 3 months. These injuries are more difficult to deal with. Over time, the scapholunate ligament becomes scarred and the edges contract so a direct repair is no longer feasible. Subacute injuries that do not have cartilage wear secondary to the injury have a joint that remains reducible, but as time progresses and fibrosis develops, the joint becomes irreducible and this influences the chosen treatment. When the scapholunate joint remains reducible, a soft-tissue reconstruction (Blatt procedure) may be performed to prevent rotatory subluxation of the scaphoid. The Blatt procedure10 involves a proximally based flap of dorsal capsule off the ulnar side of the distal radius, approximately 1 cm wide, which serves as a checkrein to volar rotation of the scaphoid. The scaphoid then is reduced and held in place by a Kirschner wire. The flap is inserted into the distal pole of the scaphoid. The flap of tissue is then secured by a pullout wire over a button on the volar surface of the wrist or with a suture anchor. The wrist is kept in a thumb spica for 2 months, followed by active range-ofmotion exercises. The Kirschner wire is removed at 3 months and intercarpal motion is allowed. Other options for treatment of reducible injuries include free tendon grafts, bone-ligamentbone grafts, or other types of capsulodesis using dorsal wrist capsule. Normal intercarpal mechanics cannot be restored when the scapholunate joint cannot be reduced; therefore, treatment of

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A

B

Trapezium Scaphoid (extended) Trapezium Scaphoid (flexed)

C

D

Figure 40-5 Watson’s scaphoid shift test. A and B, Clinical photographs of Watson’s scaphoid shift test. C and D, Diagram of Watson’s scaphoid shift test. (From Cooney WP, Linscheid RL, Dobyns JH: The Wrist. St. Louis, Mosby, 1997, p 258.) Figure continues

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E Figure 40-5—cont’d E, Diagram of a positive test.

30°–60°

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>60°

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Figure 40-7 Radiographic findings of scapholunate injury on lateral radiograph. A, Normal scapholunate angle is 30 to 60 degrees. This angle can be measured by a line bisecting the lunate and a line following the longitudinal axis of the scaphoid. B, A scapholunate angle greater than 60 degrees suggests injury to the scapholunate ligament. Figure 40-6 Radiographic findings of scapholunate injury on a posteroanterior radiograph. Scapholunate interval of 3 mm or greater (white arrow). Flexed scaphoid appears as a cortical ring (black arrows).

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the injury focuses on salvage procedures. The STT arthrodesis, also known as the triscaphoid arthrodesis, has commonly been used in the treatment of irreducible chronic scapholunate instability. The goal is to realign the radioscaphoid joint to minimize future degenerative change. Unfortunately, cases of joint deterioration after a lengthy reduced level of symptoms do occur and the incidence is unclear. Both range of motion and grip strength are lost after fusion. A meta-analysis of STT arthrodesis reported in the literature revealed nonunion rates of approximately 13%.11 Although scapholunate arthrodesis seems like the

A

most logical treatment for this injury, nonunion rates are as high as 50%.11

Treatment of Chronic Instability with Arthritic Change Patients with long-standing scapholunate instability who have developed arthritis will not have relief of symptoms with the previously mentioned procedures. The most common type of wrist arthritis is the SLAC (scapholunate advanced collapse) pattern described by Watson and Ballet12 (Fig. 40-8). Stage I

B

Figure 40-8 Stages of SLAC (scapholunate advanced collapse) wrist. A, Stage I begins with degenerative change at the radial styloid. B, Stage II reveals change along the entire radioscaphoid joint. C, Stage III reveals changes at the capitate-lunate articulation and proximal migration of the capitate.

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begins with degenerative change between the radial styloid and distal pole of the scaphoid. Stage II reveals change along the entire radioscaphoid joint. Stage III reveals arthritic change of the capitate-lunate joint and proximal migration of the capitate. As the capitate continues to migrate proximally, pancarpal arthrosis develops. Patients will often present with decreased grip strength and stiffness with extension and radial deviation. In stage I disease, radial styloidectomy will decrease symptoms associated with impingement of the scaphoid on the radial styloid, but the underlying instability will lead to further deterioration. If the joint is reducible, a dorsal capsulodesis can be performed. If the joint is not reducible, an STT or scaphocapitate (SC) fusion can be performed in addition to the radial styloidectomy. In stage II disease, the arthritic radioscaphoid joint must be eliminated. This can be accomplished with either a proximal row carpectomy or a scaphoid excision and fourcorner fusion (lunate-capitate-hamate-triquetrum), which is also known as the SLAC procedure. A proximal row carpectomy is considered by many to be contraindicated if arthritic change is present on the proximal capitate. Both the SLAC procedure and proximal row carpectomy will lead to decreased grip strength and range of motion compared to the normal wrist. After proximal row carpectomy, patients retain approximately 52% of motion and 67% of grip strength compared to the normal wrist.13 Although stage II disease may be treated with a variety of procedures, proximal row carpectomy was found to retain the most motion.14 Patients with stage III disease may be treated with either the SLAC procedure or total wrist arthrodesis. A proximal row carpectomy is contraindicated if arthritic change is present on the proximal capitate. The ideal position for wrist arthrodesis is 10 degrees of extension and neutral or slight ulnar deviation.

TENDONITIS Tendonitis is a common wrist problem dealt with by physicians. Patients may present with pain and swelling of the involved tendons. History often reveals overuse as the inciting event, and patients report that the pain worsens with use of the inflamed tendon. Physical examination often reveals swelling and tenderness of the involved tendon. Radiographs are most often negative.

Figure 40-9 Finkelstein’s test. The thumb is fully adducted and the wrist is ulnar deviated, which will reproduce the patient’s symptoms.

tion syndrome report pain 4 cm proximal to the wrist joint. Patients with carpometacarpal arthritis may have evidence of arthritis on radiographs. Patients are treated conservatively with a combination of splinting, anti-inflammatory medications, and avoidance of the inciting activity. Corticosteroid injections can be used with 50% to 80% success. It has been shown that patients receiving an injection did not receive any additional benefit from splinting after the injection.15 The first dorsal compartment can be injected with 0.5 mL 1% lidocaine and 1 mL dexamethasone. When conservative measures fail, surgical release of the first dorsal compartment may be performed. A dorsal release of the compartment is performed. The abductor pollicis longus can often have multiple slips, and the extensor pollicis brevis may sometimes have its own subsheath so care must be taken to release all slips and subsheaths. Some authors report that surgical cases have an increased incidence of these minor anatomic differences. Care must be taken not to injure the radial sensory nerve. The patients are placed in a soft dressing for 10 to 14 days and then strengthening and range-ofmotion exercises are begun.

de Quervain’s Disease de Quervain’s disease involves a stenosing tenosynovitis of the first dorsal wrist compartment, which contains the abductor pollicis longus and the extensor pollicis brevis. Patients often present with radial side wrist pain that is worsened with movement of the thumb. It is more common in the fourth and fifth decades and in females. Patients often report a history of repetitive activities involving thumb abduction and ulnar deviation of the wrist. On physical examination, Finkelstein’s test will be positive (Fig. 40-9). This test is performed by fully adducting the thumb and then the wrist, which will reproduce the patient’s pain. The differential diagnosis includes intersection syndrome and carpometacarpal arthritis. Patients with intersec-

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Intersection Syndrome Intersection syndrome is a stenosing tenosynovitis of the second extensor compartment. Patients often report radial side wrist pain 4 cm proximal to the wrist joint. This syndrome is often found in lifting and rowing athletes. On physical examination, an audible squeak may be heard and there may be palpable crepitus. Conservative management includes modifying activities, splinting in extension, anti-inflammatory medication, and corticosteroid injection of the second dorsal compartment. In cases that fail conservative management, surgical release of the second dorsal compartment can be performed, but this is rarely necessary.

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REFERENCES 1. Palmer AK: Triangular fibrocartilage complex lesions: A classification. J Hand Surg [Am] 1989;14:594–606. 2. Palmer AK, Werner FW: The triangular fibrocartilage complex of the wrist—Anatomy and function. J Hand Surg [Am] 1981;6:153– 162. 3. Zachee B, De Smet L, Fabry G: Arthroscopic suturing of TFCC lesions. Arthroscopy 1993;9:242–243. 4. Feldon P, Terrono AL, Belsky MR: Wafer distal ulnar resection for triangular fibrocartilage tears and/or ulna impaction syndrome. J Hand Surg [Am] 1992;17:731–737. 5. Bowers WH: Distal radioulnar joint hemiarthroplasty, the hemiresection technique. J Hand Surg [Am] 1985;10:169–178. 6. Nakamura R, Tsunoda K, Wantanabe K, et al: The Suave-Kapandji procedure for chronic dislocation of the distal radial ulnar joint with destruction of the articular surface. J Hand Surg [Br] 1992;17: 127–132. 7. Dobyns JH, Linscheid RL, Chao EYS, et al: Traumatic instability of the wrist. Intr Course Lect 1975;24:182–199.

8. Geissler WB, Freeland AE, Savoie FH, et al: Intercarpal soft tissue lesions associated with an intraarticular fracture of the distal end of the radius. J Bone Joint Surg [Am] 1996;78:357–365. 9. Mayfield JK: Mechanism of carpal injuries. Clin Orthop 1980;149: 45–59. 10. Blatt G: Capsulodesis in reconstructive hand surgery: Dorsal capsulodesis for unstable scaphoid and volar capsulodesis following excision of the distal ulna. Hand Clinics 1987;3:81–101. 11. Seigal JM, Ruby LK: A critical look at intercarpal arthrodesis: Review of literature. J Hand Surg [Am] 1996;21:717–723. 12. Watson HK, Ballet FL: The SLAC wrist: Scapholunate advanced collapse pattern of degenerative arthritis. J Hand Surg [Am] 1984;9:358–365. 13. Culp RW, McGulgan FX, Turner MA, et al: Proximal row carpectomy: A multicenter study. J Hand Surg [Am] 1993;1A:19–25. 14. Krakauer JD, Bishop AT, Cooney WP: Surgical treatment of scapholunate advances collapse. J Hand Surg [Am] 1994;19:751–759. 15. Weiss AP, Akelman E: Treatment of de Quervain’s disease. J Hand Surg [Am] 1994;19:595–598.

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Hand Injuries Arthur C. Rettig, Dale S. Snead, and Lance A. Rettig

In This Chapter Metacarpal fracture Phalangeal fracture Thumb ligament injury Surgery—ulnar collateral ligament (UCL) repair Proximal interphalangeal (PIP) joint ligament injury PIP joint dislocation Distal interphalangeal (DIP) joint injury Closed tendon injury Pulley injury

INTRODUCTION • The energy transmitted to the hand that causes injuries in athletics is often relatively low; thus, the fracture patterns are generally simple and minimal soft-tissue injury is involved. • The goal of treating hand fractures is to allow the athlete to participate in a safe fashion but to prevent the development of malunion, nonunion, joint stiffness, and tendon adhesions. • Treatment is determined by the sport, position played, and timing of the injury in relationship to the season. • The high demand on the upper extremity in sports makes the hand very susceptible to a variety of injuries.1 • Fractures of the metacarpals and phalanges frequently result in the loss of playing time and altered performance. Sportsrelated activities are the most common cause of phalangeal fractures in 10- to 49-year-olds. • There are a variety of ways to treat fractures of the metacarpals and phalanges. In many cases, treatment can allow the athlete to return to competition safely and quickly.

EPIDEMIOLOGY Injuries to the fingers or hand can occur from a direct blow, a crush injury, or a laceration. A direct blow causes most phalangeal and metacarpal fractures. This typically results in a transverse fracture. Spiral fractures occur secondary to a torsional type injury. Intra-articular fractures occur secondary to an axial load. These are the most common fracture patterns seen in the hand. Basketball players injure the PIP joint more frequently. Baseball players are more likely to sustain an injury of the distal phalangeal joint and distal phalanx. Football players usually sustain

a crush injury resulting in a metacarpal or proximal phalanx fracture. A study performed at the Cleveland Clinic evaluated 113 hand and wrist injuries; 96 of these injuries were fractures and 97 of the injuries occurred in football, with metacarpal fractures being most common at 40% (38 fractures). DeHaven and Lintner2 described hand injuries based on 3431 cases treated at the University of Rochester. Hand injuries represented 5% (171 cases) of those treated, again the most common injury to the hand involved fracture. There were 102 fractures in this study representing 60% of the hand injuries, with the majority occurring in football. Of the 102 fractures, 72 were of the phalanx and 27 involved the metacarpals. A study by Dawson and Pullos3 looked at baseball and softball injuries in a suburban 150-bed hospital over a 3.5-month period. There were 153 injuries and fractures represented 6% of the injuries. Interestingly, a greater percentage of injuries occurred when a larger softball was used. The number of people seen for hand injuries represented 2.2% of the emergency department visits. Stein and Ellasser4 reported on significant hand injuries that occurred in a professional football team over a 15-year period. There were 46 major injuries, almost equally split among offense and defense. Fingers were the most commonly injured area of the body. Rettig5 performed a study over a 1-year period noting 213 injuries in 207 athletes. These 207 patients represented approximately 3% of the new patient visits seen at the center during this time period. Of these injuries, 125 were fractures. The greatest number of hand injuries occurred during football, and the majority of injuries occurred during competition.

CLINICAL FEATURES AND EVALUATION Metacarpal and phalangeal fractures often present with swelling, ecchymosis, and gross deformity. Passive flexion can falsely create a normal-appearing alignment of the digits. Having the patient actively flex each digit allows a more accurate check of rotation. This is a crucial part of the evaluation despite the discomfort that it may cause the athlete. A missed rotational deformity can be devastating.6 It is useful to compare the injured extremity with the unaffected side when evaluating for a rotational deformity. At full flexion, all digits should point toward the tubercle of the scaphoid.

Radiography Many fractures of the hand are overlooked or misinterpreted because of failure to obtain appropriate radiographs. Short spiral fractures may appear relatively nondisplaced on an anteroposterior view, yet are significantly displaced on an oblique view. Fractures of the hand must be evaluated with appropriate

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Radiograph

Radiograph

Radiograph

Figure 41-1 Axial relationships of metacarpals illustrating that a lateral radiograph of the hand requires slight pronation and slight supination for independent visualization of index and small metacarpals. (From Hastings, Rettig, Strickland: Management of Extra-articular Fractures of the Phalanges and Metacarpals. Philadelphia, Elsevier, 1992.)

Lateral radiograph

For index, pronate

radiographs and include at a minimum posteroanterior, lateral, and oblique views. It is important to know that a true lateral radiograph is a lateral view of the third metacarpal only and an oblique view of the other digits. The hand must be rolled into 30 degrees of supination to obtain a lateral view of the index metacarpal and 20 to 30 degrees of pronation to obtain a lateral view of the ring and small fingers (Fig. 41-1). A Brewerton view is helpful for evaluation of fractures at the base of the proximal phalanx.7

METACARPAL FRACTURES Metacarpal Neck Fractures Metacarpal neck fractures account for as many as 36% of all fractures of the hand.8 Metacarpals are weakest at the metacarpal neck and are often fractured by a direct blow, torsion, or bending load applied to the digit distally. Most metacarpal neck fractures affect the ring and little fingers. The most famous of these is the Boxer’s fracture (although rarely seen in boxers), a fracture of the fifth metacarpal neck. Fractures at this level occur secondary to the instability of the ulnar digits and because the metacarpal head is already in 15 degrees of flexion. Treatment of these injuries is usually splinting and early range of motion (ROM). If angulation is greater than 50 degrees, closed reduction and casting or operative fixation may be necessary.9,10 A prospective study by Lowdon11 found no relationship between residual angulation and the presence of symptoms.

Metacarpal Shaft Fractures Metacarpal fractures are the most commonly seen hand fractures.12 Due to the low forces involved in athletic activities, com-

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For small, supinate

pared to motor vehicle accidents, most fractures are stable. Metacarpals are connected to one another via the transverse intermetacarpal ligament (Fig. 41-2). This is important when there is a fracture of a single metacarpal. Fractures of the middle and ring metacarpals are more stable because there are two transverse intermetacarpal ligaments supporting these bones. Rotational and shortening deformities are more likely to be seen in the index and small finger fractures. The more distal the fracture is, the greater amount of angulation that can be accepted (Fig. 41-3). The ulnar aspect of the hand is more susceptible to fractures due to its greater mobility when compared to the radial aspect of the hand, and for the same reason, more angulation can be tolerated in the ulnar digits. Between 30 and 40 degrees of angulation can be accepted in the ring and small fingers.13 Carpometacarpal motion at the index and long fingers is minimal; therefore, the amount of angulation that is tolerated by these digits is less. The amount of angulation that can be accepted in the index and long fingers is 15 degrees.13 Dorsal angulation of these fractures affects the biomechanics of the digit. This angulation weakens the intrinsic muscles, resulting in metacarpal phalangeal joint hyperextension and weakness of the central slip as it extends the PIP joint. A closed reduction maneuver, as described by Jahss,14 is performed by first disimpacting the fracture by longitudinal traction. The metacarpophalangeal (MCP) and PIP joints are then fully flexed, and a dorsally directed pressure is applied to the proximal phalanx through the flexed PIP joint. The digit should not be immobilized in the Jahss position, but in the safe position (metacarpal phalangeal joints flexed, fingers extended), using an ulnar or radial gutter splint. This allows the extensor

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Figure 41-2 A spiral fracture of the metacarpal tends to be more unstable in the border digits, where only one side of the metacarpal is supported by a deep intermetacarpal ligament. (From Hastings, Rettig, Strickland: Management of Extra-articular Fractures of the Phalanges and Metacarpals. Philadelphia, Elsevier, 1992.)

mechanism to act as a tension band. The splint is continued for 10 to 14 days, and the affected finger is buddy taped to an adjacent finger. It is important to repeat radiographs early in the treatment to prevent any unrecoverable displacement. When treating metacarpal fractures the patient is told to expect that (1) the knuckle contour may be lost permanently, (2) there will be some residual deformity of the digit, (3) if the finger heals in a more flexed position, there is a greater likelihood of refracture with less trauma, and (4) there may be a residual bump on the dorsum of the hand. Nondisplaced fractures of the index and long fingers and minimally displaced fractures of the ring and small fingers can usually be treated by external immobilization alone. If crepitus is present, a cast is used for the first 2 weeks. Splinting for a total of 4 to 6 weeks is sufficient to heal most fractures.

Figure 41-4 Radiograph of a displaced metacarpal fracture.

Surgery Various methods can be used to treat failed closed reductions or comminuted fractures in which a closed reduction would not be possible (e.g., intra-articular fractures). Open reduction internal fixation is often necessary if there is entrapment of soft tissues, irreducibility of the fracture, or the fracture is a result of highenergy trauma.15 It is important to rule out any rotational deformity because a slight misalignment at the base is greatly magnified at the tip of the finger. Rotational deformity is an indication for surgery. Dorsal angulation greater than 10 to 15 degrees in the index and long fingers or 30 to 40 degrees in the ring and small fingers or greater than 5 mm of shortening (Fig. 41-4) are other parameters of fractures of metacarpals that call for surgical treatment. Intra-articular extension of a fracture is also generally treated operatively.

Figure 41-3 Effect of fracture level on metacarpal head displacement. (From Hastings, Rettig, Strickland: Management of Extraarticular Fractures of the Phalanges and Metacarpals. Philadelphia, Elsevier, 1992.)

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Figure 41-5 A, Radiograph of a midshaft metacarpal fracture. B, Radiograph after closed reduction percutaneous pinning of metacarpal fracture.

A

B

Many arrangements of Kirschner (K)-wire fixation have been described.16–18 This can consist of crossed K wires, intramedullary wires, or transverse K wires16–18 (Fig. 41-5). The downside of using K wires is that it does not allow for immediate ROM. The use of a single dorsal plate provides the greatest stability and will allow early ROM.19,20 Interfragmentary screws alone may be chosen when the fracture is greater than twice the diameter of the shaft.21 Incisions should not be made directly over the metacarpal in order to minimize adhesions. The average return to sports is approximately 14 days in football for metacarpal injuries and is independent of nonoperative or operative fixation. This time frame is very sport specific and position dependent. For example, a football lineman will be able to return more quickly than a receiver. However, the receiver will return sooner than a person involved in a racquet sport.

Fractures of the Metacarpal Base There are certain fractures of the first and fifth metacarpal that deserve to be mentioned. There are essentially two types of intra-articular fractures involving the thumb: a Bennett fracture and a Rolando fracture. A Bennett fracture involves a portion of the base of the first metacarpal that is displaced by the pull of the abductor pollicis longus tendon (Fig. 41-6). Rolando fractures are more comminuted and affect both sides of the first metacarpal base. Treatment of both of these fractures consists of operative fixation, either closed reduction and percutaneous fixation22,23 or

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open reduction and screw fixation.15 With either treatment, return to sports can be as rapid as 1 week, if return to play in a cast is possible. Complete recovery from this type of injury takes 4 to 6 weeks. A similar fracture is also seen in the fifth metacarpal (Fig. 417). This is the so-called baby Bennett fracture, which becomes displaced by the pull of the extensor carpi ulnaris tendon.24 Treatment and return to play are similar for fractures at the base of the first metacarpal.

PHALANGEAL FRACTURES Phalangeal fractures are usually stable due to the adhering softtissue envelope. The diaphysis is thicker on the radial and ulnar borders than on the anterior/posterior borders. This thickening is continued laterally by osteocutaneous ligaments called Cleland’s and Grayson’s ligaments. These ligaments anchor the bone at the mid-portion of the diaphysis and stabilize the bony shaft to the envelope. Occasionally these structures can become trapped in the fracture site and prevent reduction of the fracture. The flexor and extensor tendons provide both stability and induce deforming forces. The flexor tendons are stronger and can cause a dorsal angulation of the fracture. Healing in this position can result in the extensor tendons being weakened and functioning with an extensor lag. The extensor tendons can also

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A

Figure 41-6 Radiograph of a first metacarpal fracture (Bennett fracture).

cause a volar angulation of the bone, which will limit flexion of the digit. It is important to remember that fractures of the proximal phalanx displace with volar angulation. The proximal fragment is flexed by the bony insertion of the interossei into the base of proximal phalanx. The distal fragment is pulled into hyperextension by the central slip through the PIP joint.

Base of the Proximal Phalanx Fractures Fractures at the base of the proximal phalanx usually occur in a transverse direction with dorsal impaction and apex volar angulation. This fracture is seen more commonly in teenagers. It can usually be treated with an orthosis in the safe position; however, fracture instability can occur. Burkhalter25 described an immobilization method whereby the MCP joint is flexed and active motion of the PIP joint is allowed. For unstable fractures, the use of closed reduction percutaneous pinning, open reduction with internal fixation with screws or a plate and screws or external fixation is often used. In displaced fractures, the finger will rest in the position of abduction.26 Of surgical importance, it is often difficult to place pins in the proximal phalanx from a distal to proximal direction. However, it is much easier to place the pins from a proximal to distal direction through the dorsal portion of the metacarpal head into the proximal phalanx fracture.13 This aids in maintaining the metacarpal phalangeal joint in the safe position (30 to 40 degrees of flexion). Immediate

B Figure 41-7 A, Radiograph of a fifth metacarpal fracture (baby Bennett fracture). B, Radiograph after reduction.

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thus creating “ice cream on the tip of a cone” effect. Intraarticular fractures that are nondisplaced (2 mm of abnormal symphysis) Neurologic: Referred pain from lumbar spine, peripheral nerve entrapment (obturator nerve entrapment, and ilioinguinal nerve) Nonmusculoskeletal conditions: gynecologic disease (endometriosis, ovarian cysts, tumors), true hernias, rectal cancer, and urologic disease (cystitis, ureteral stones)

round ligament. Several of the latter patients had pelvic endometriosis and no grossly detectable round ligament implant. In one case, active endometriosis was identified histologically within the round ligament specimen. In our experience, nonendometriosis ovarian cystic disease is the second most common gynecologic problem mimicking athletic pubalgia. We have also seen a wide variety of genitourinary problems mimicking the pain in both males and females. Overall, the most common urologic problem has been bladder or ureteral stones. It is particularly important to mention that we have also seen several testicular and other tumors. One interesting tumor resided within a seminal vesicle. In that case, the patient’s pain occurred with ejaculation. Still, a wide variety of other problems have caused enough lower abdominal, pelvic, or inguinal pain in athletes to be referred to us. Some of the more interesting other problems that we have seen associated with exertional pain include herpes disease, true spigelian hernias, pelvic inflammatory disease, and arterial insufficiency. We have also seen a chronically perforated hepatoma, a bile leak after laparoscopic cholecystectomy, and an incarcerated femoral hernia.

PELVIS AND HIP FRACTURES caused by our folding the lateral edge of the rectus muscle down to support the pubic joint. We identified and repaired the latter problem via laparoscopy. Exertional pain was not a factor in any of these three cases. On the other hand, there is nothing about being an athlete that should prevent the occurrence of standard direct or inguinal hernias. We have taken care of a number of such athletes and repaired the hernias by either laparoscopic (pre- or intraperitoneal) or open techniques. The general incidence of hernia development does not seem to be particularly increased compared with nonathletes, nor does it seem to be associated with much exertional pain. Therefore, inguinal hernias do need to be considered in the differential diagnosis of most of these athletes, but rarely remain considerations after a good history and physical examination. We now turn to some other problems that we have seen. Interestingly, in both males and females, one of the most common considerations with respect to exertional pain in this area of the body in athletes is inflammatory bowel disease. Usually, a careful history detects this possibility. The patient elicits that he or she has either had years of gastrointestinal problems or a recent change in bowel habits. In most of the cases that we have seen, there has been at least one thickened bowel loop within the pelvis. Therefore, it seems likely that the exertion caused this loop to irritate the pelvic parietal peritoneum. Sometimes the pain can go down into the thigh. Psoas signs of inflammation may also accompany the irritation. A wide variety of other gastrointestinal problems can also mimic the musculoskeletal problems of athletes. We have now seen two patients with rectal cancer. One had resectable disease and is a long-term survivor. The other had locally metastatic disease at the time of presentation and did not do well in the long term. We have also seen one case of chronic perforated appendicitis. Beyond a doubt, in females, there are many gynecologic problems that can mimic the athletic pubalgia pain patterns. The most common problem is endometriosis. An endometriosis implant can also occur directly within the round ligament. We suspect that several successes after pelvic floor repair in young women in our series were related to our routinely dividing the

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General Fractures of the pelvis and sacrum are usually pathologic due to stress or fatigue. Those fractures due to falls or high-velocity impact are uncommon and are not the focus of this section. Many stress fractures of the pelvis go undiagnosed because the prudent patient may end up self-treating with self-imposed rest until the symptoms ameliorate and activity is once again possible. When they occur, stress injuries occur at the sacrum, sacroiliac joint, pubic rami, and femoral neck. Classically, a pelvis or sacral stress fracture occurs following a recent increase in mileage or intensity. For example, stress fractures of the pubic rami are the most common in the pelvis and usually occur in long-distance runners (Fig. 44-1). Although these fractures are common, in general, the most common stress fracture is in the tibia. Stress fractures may be simplified as (1) primary osseous failure—insufficiency fracture due to inherent weakness such as osteopenia or osteoporosis, and (2) a fatigue fracture from excessive overloading of normal bone. The situation, in most cases, may be a combination of these factors. The stress fracture should also be observed as part of a spectrum of disease. On one end is a stress reaction and on the other end is a frank fracture with a distinct fracture line. Stress fracture cause is also thought to be varied. The current most widely accepted theory is that of repetitive stress causing a periosteal resorption that surpasses the rate of bone remodeling, weakening the cortex and resulting in a stress fracture. The high-intensity female athlete is at risk of stress fractures as a consequence of high-intensity training, catabolic state, poor diet, and low body mass along with menstrual problems. Risk factors for multiple stress fractures include a high longitudinal arch of the foot, leg length inequality, and excessive forefoot varus, female patients with menstrual irregularities, and high weekly training mileage.4 The pain pattern of a stress fracture is typically described as a “crescendo” effect beginning as a tolerable dull ache that quickly transforms into an intense pain, making the lightest exercise activity not possible. The symptoms of a stress injury are worsened with any pounding-type of weight-bearing activities. The key to the diagnosis is in the history and physical examination. The point of maximal tenderness should be identified so

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Figure 44-1 Magnetic resonance imaging of the pelvis depicts a fracture through the right parasymphyseal inferior pubic ramus in a 48-year-old sheriff reservist. The fracture occurred insidiously during endurance training. The patient presented with anterior hip flexor pain and tenderness. The plain radiographs remained negative for 4 weeks. This fracture was successfully treated with activity modification including nonimpact athletic activities and physical therapy. Despite union after 8 weeks, this patient experienced residual symptoms associated with adductor tightness.

that imaging studies may be focused to this area. Plain radiographs are usually negative because of the lack of callus formation in the early stages and sometimes when a fracture line does not form. When a fracture is thought to be occult or difficult to characterize, an MRI is considered more sensitive than a bone scan. The ideal MRI sequence for femoral neck fractures is the “fat saturation T2” (high TR and TE >60) or short tau inversion recovery (STIR) sequences, which are easier and quicker to perform than other sequences. The treatment for pelvis stress fractures, except femoral neck, is fairly straightforward. Most resolve with 4 to 6 weeks of relative rest and progressive reintroduction of activities. When the patient is pain free, then progressive sporting activities may be initiated. Due to their potential for major disability, femoral neck stress fractures require special consideration. This includes having increased awareness so that a timely diagnosis is made and specific treatment implemented. In general, these injuries are seen in two distinct populations: (1) young, healthy, active individuals such as runners or military recruits and (2) the elderly who have osteoporosis. In the high performance athlete, a devastating problem may occur when a seemingly simple nondisplaced femoral neck fracture becomes displaced. A delay in the correct diagnosis may be highly problematic and therefore a high index of suspicion is important.5 The early clinical presentation of a femoral stress fracture may mimic other more common conditions. The pain is usually around the anterior groin region similar to a hip flexor strain or pull. To a lesser degree, the pain may

also be nonspecific, ill defined, or atypical around the gluteal region. Refraining from the offensive repetitive activity or excessive loading will eventually improve the symptoms and allow union. The complication rate for femoral neck fractures is partly related to the specific type and the promptness of treatment. In an effort to efficiently guide the treatment, these fractures have been classified based on their plain radiographic and MRI appearance. The tension-type fracture involving the lateral cortex is considered more unstable and should be treated with weight-bearing protection and then expeditious surgical stabilization using a plate and screw device. The reasoning behind surgical treatment of these fractures stems from the potential for malunion and osteonecrosis if they become displaced. The compression-type fracture involving the medial side is biomechanically more stable and can usually be treated conservatively with serial radiographs, protected weight bearing, and activity modification (Fig. 44-2). In view of the fact that these fractures have potential for major disability, it behooves the clinician to order an MRI study sooner in performance athletes, especially females, to both obtain an expeditious diagnosis and avoid potential litigation. Although extremely uncommon, there have been reports of compression-type fractures also becoming displaced, and, as a consequence, some authors have recommended internal fixation if a compression type of neck fracture involves more than 50% of the cortex.6 All patients with femoral neck fractures should be educated about potential problems with their hip joint. The surgical risks include chondrolysis, nonunion, malunion, osteonecrosis, and subtrochanteric iatrogenic fractures. An appropriate period of toe-touch weight bearing should

Figure 44-2 Magnetic resonance imaging (MRI) of the pelvis depicts a stable compression type of femoral neck fracture. These fractures are typically stable and can be treated with close observation, serial radiographs, protected weight bearing, and physical therapy. In an athlete with groin pain, the consideration for an early MRI should be made in order to avoid potential complications.

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follow surgical fixation. Radiographic healing and signs of osteonecrosis are monitored with periodic plain radiographs. Even in cases of appropriate treatment, many patients may have persistent long-term disabling complaints. The results of surgical treatment may be influenced by the amount of fracture displacement and the quality of the fracture reduction. The incidence of osteonecrosis in nondisplaced fractures is approximately 15%.7 Fractures that develop osteonecrosis may require a prosthetic replacement or other secondary procedure. MRI following fixation of a femoral neck fracture is usually of poor quality due to the artifactual signal from the metal screws. Routine removal of the hip fixation device is not recommended unless the hardware has failed or when a future MRI is anticipated. Hip arthroscopy after a healed femoral neck fracture has not been evaluated well in the literature. Young patients who develop symptomatic osteonecrosis may benefit from a referral to a specialist experienced in core decompression, bone grafting, and vascularized fibula transfers. Unfortunately, many patients will continue to experience differing levels of symptoms at long-term follow-up following femoral neck fractures.8

Abdominal muscles

Adductor muscles

OSTEITIS PUBIS Osteitis pubis in the athlete is an inflammatory condition of the pubic symphysis and surrounding structures. Due to the ubiquitous nature of this disease, it is imperative that all factors, such as infection, urologic, gynecologic, and rheumatologic issues are taken into consideration for the accurate diagnosis and treatment. The pathogenesis of this disorder remains obscure. It can occur secondary to vertical instability or as a primary condition. It may also coexist with other conditions including athletic pubalgia. Among athletes, primary osteitis pubis is thought to be caused by repetitive microtrauma, chronic overuse injury, and muscle imbalance. The abdominal and adductor muscles have a central point of attachment on the symphysis pubis or the “pivot point,” but these muscles act antagonistically to each other, predisposing the pubic symphysis to opposing forces. These forces become critical in the kicking activities associated with sports such as soccer, Australian rules football, and North American football (Fig. 44-3). When an athlete kicks, the kicking limb is hyperextended at the hip while the trunk is rotated laterally in the opposite direction. Greater than 2 mm of vertical motion is seen in cases that are associated with pubic symphysis instability. The clinical findings include tenderness at and around the pubis symphysis area. The examination should focus on carefully defining the pathoanatomic zones. The “groin” is not sufficiently descriptive, and therefore the clinician should further define this region into the different anatomic areas including pubic, suprapubic, abdominal, anterior hip capsule, proximal thigh, inguinal ring, and perineal. A digital direct and indirect hernia examination is important to evaluate the superficial inguinal ring, spermatic cord, conjoined tendon, and deep inguinal ring. Coventry and William9 described two provocative maneuvers: (1) the rocking cross-leg test in which examiner bears down on the crossed knee while holding down the opposite iliac crest and (2) the lateral pelvis compression test done with the patient on his or her side and the examiner pressing the presenting wing. The examiner may also glean diagnostic information by palpating the tender areas while the patient does a sit-up maneuver. Careful digital examination of the scrotum, spermatic cord, inguinal ring,

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Figure 44-3 The pubis pivot point in a soccer player.

and conjoined tendon of the abdominal wall should be performed to evaluate for abdominal wall injuries (athletic pubalgia) and true hernias. If the pain is difficult to characterize or if it is of a radiating nature, the clinician should consider remote causes for the pain such as referred spinal pain or peripheral nerve entrapment. Sometimes a referral is necessary to evaluate for gynecologic, urologic, rheumatologic, or general surgery problems. Imaging studies for osteitis pubis begins with plain radiographs as well as single-leg standing “flamingo” views to document vertical instability (abnormal if >2-mm difference in height exists). MRI may be helpful in identifying a tear of the anterior abdominal wall musculature (external oblique aponeurosis, superficial inguinal ring, conjoined tendon); however, it is frequently negative. MRI is also beneficial for nonorthopedic conditions that may be coincidentally diagnosed. A technetium 99m triple phase bone scan is useful for identifying ambiguous areas of pain caused by stress reactions or fractures. Most of the time, nonoperative treatment will lead to resolution of symptoms. Core strengthening and flexibility, as well as an active program, are encouraged.10–12 The patient should be educated regarding the drawn-out clinical course and to the fact that, on average, symptoms will last

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Figure 44-4 Pubic symphysis arthrodesis.

6 to 9 months. The full spectrum of conservative measures includes cessation of offending physical activity, physical therapy, ultrasonography, nonsteroidal anti-inflammatory drugs, oral glucocorticoids, radiation therapy, anticoagulation, intravenous pamidronate, and corticosteroid pubic symphysis injections. For patients who remain symptomatic, a fluoroscopically guided steroid injection may be performed in the office. If the patient does not experience immediate pain relief, then other causes, such as athletic pubalgia, need to be considered. Rarely do patients require surgical treatment. There are a few case reports showing limited success after a proximal adductor release and drilling of the pubic bone in soccer players. Most of the literature regarding surgical management of osteitis pubis has focused exclusively on bony procedures. The procedures that have been described are either a pubic symphysis trapezoidal wedge resection or an arthrodesis with or without a compression plate (Fig. 44-4). Wedge resection of the symphysis pubis is useful as a first-line surgical procedure because of its short operative time, reliability, and low complication risk.13 However, there is a risk of late anterior pelvis instability due to anterior pelvis disruption. Alternatively, some authors have successfully used pubic symphysis bone grafting and compression plating in athletes with documented pelvic instability.14 There is a risk of stress fracture of the arthrodesis site if a plate is not employed. Although the surgery seems to be aggressive, there have been excellent results with low complication rates. Additionally, the issue of late instability is ameliorated.

groin pain with restricted range of motion and inability to bear weight will follow. Transient meralgia paresthetica may be seen due to the swelling around the lateral femoral cutaneous nerve. A displaced apophysis is usually apparent on plain radiographs, but if the clinician is not keen to the injury, a subtle opacity may be missed. An astute clinician may make the presumptive diagnosis despite “negative” radiographs. In cases of anterior inferior iliac spine avulsions, an oblique plain radiograph projection may be necessary to appreciate a subtle displacement. Despite the occasional delay in diagnosis, there is usually no major problem from wrongly receiving acute treatment for a strain instead of a fracture. On the other hand, a robust formation of callus may lead to inadvertent overtreatment due to the concern for Ewing’s tumor or osteomyelitis. The treatment of most avulsion fractures is nonoperative. The treatment can include rest and protected weight bearing with crutches followed by a supervised rehabilitation and a home exercise program. Most authors have reported excellent results following nonoperative treatment.16 Without adequate protection, a symptomatic nonunion is possible; therefore, nonweight bearing or protected weight bearing for up to 3 weeks is a prudent decision. Despite the massive callus that frequently forms, an excellent result is likely. The most common complication of nonoperative treatment is a tender exostosis-like formation at the fracture site. Rarely will these exostosis-like lesions require surgical removal. Surgery may be considered in the case of a severely displaced fracture in a high-level athlete. A displaced fracture may create a shortened muscle and as a consequence a theoretical decrease in muscular power. Indications for open treatment and internal fixation are not well defined. Open treatment and internal fixation may be considered in a high-level athlete with displaced (>3 cm) fractures or in cases associated with hip dislocations. Reports on surgical fixation are few, and no improvement in outcome has been proven. When surgery is chosen, the apophysis is reduced and fixated using wiring and/or screw fixation.17 Potential complications are the same as those associated with adult fracture treatment including cutaneous nerve injury, misguided hardware, hemorrhage, infection, and hip joint damage. Complete recovery, return to sports, and no long-term sequelae may be anticipated following most apophyseal fractures, regardless of the type of treatment chosen.

APOPHYSEAL AVULSION INJURIES ATHLETIC PUBALGIA An apophyseal avulsion fracture of the pelvis is a fracture through the physis of a secondary center of ossification. These commonly involve the anterior superior iliac spine, anterior inferior iliac spine, and ischial tuberosity apophysis. These fractures occur almost exclusively in 11- to 17-year-old patients. They are most commonly seen in soccer, track, football, and baseball. In most cases, these fractures occur during fast running, hurdling, pitching, or sprinting.15 These injuries usually do not occur due to direct trauma. They may occur as a consequence to a hip dislocation. Fractures of the anterior superior iliac spine result from the pull of the sartorius and the tensor fascia lata muscles. Fractures through the anterior inferior iliac spine result from pull of the straight head of the rectus femoris muscle. A forceful sprint or a swing of a baseball bat will typically avulse the anterior superior iliac spine. The injured athlete will frequently recall an associated “pop” at the moment of injury. Then acute lower extremity, hip, and

We have recently written overviews of our current understanding of the anatomic and pathophysiologic bases for this set of syndromes.1,3 Briefly, this set of syndromes accounts for most of the surgical problems that we see in athletes. Athletes create tremendous torque that occurs at the level of the pelvis. The anterior pelvis takes much of the brunt of these forces. The attachments to the anterior pelvis play the most important roles with respect to the direct and opposing forces that are involved in this torque. However, the posterior, lateral, and medial compartments are usually also involved and need to be considered in planning therapy. From an anatomic perspective, it is important to understand fully the pelvic anatomy that is involved. Basically, one thinks of the pubic symphysis as the fulcrum around which the forces occur. Then one thinks of the injuries as a combination of acute or chronic weakening and compensatory overuse of various

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insertions or attachments. In many of these injuries, one thinks in terms of an “unstable pubic joint.” Pathophysiologically, one then can think in terms of which attachments to the joint are involved either directly in the injury or conversely as compensatory mechanisms. In addition to the attachments, one may also think in terms of there being a variety of “strap muscles” or “compensatory compartments.” An example of a strap muscle might be the psoas tendon, which does not insert directly into the pubis. Nonetheless, the psoas muscle and tendon do provide considerable pubic joint stability. While the anterior compartment is the most common one involved in injury, the other compartments may also be directly involved, in which case the nondirectly involved compartments become “compensatory.” One must figure out the mechanisms of the primary injuries and then determine the method of repair. The most common injury is a weakening of the rectus abdominis muscle as it inserts on the pubis, associated with compensatory overuse of the other side, the adductor longus, adductor brevis, and/or pectineus. In total, we have described more than 18 syndromes that occur relatively commonly. One should also remember that there are other parts of these muscles or attachments that can be injured in different locations. For example, the rectus abdominis muscles can fray anywhere within the anterior abdominal wall or can also cause a subluxation syndrome of the lowermost ribs or cartilages. We have seen the latter syndromes in fighters, rowers, women tennis players, and bull riders. We classify the pathology seen at surgery associated with the preceding syndromes as grade 1, single or multiple small tears; grade 2, partial avulsion or avulsions; and grade 3, complete avulsion or avulsions or a complete avulsion associated with another partial avulsion. There are some other “confusors.” As suggested by the previous discussion, proper diagnosis of these injuries can be tricky. At this point, we just mention some of the considerations that can be confusing. Four of the confusors are (1) identification of patients who need surgery, (2) the type of surgery, (3) the timing of surgery, and (4) the duration of rehabilitation. Briefly, surgery is indicated when joint instability is clearly demonstrated after the acute effects of injury, for example, hematoma, have resolved and physical therapy does not seem appropriate. Surgery involves a combination of tightening, loosening, or other procedures that focus on preventing persistence of pain. The specific surgery depends greatly on understanding precisely the direct and compensatory parts of the injury as well as the principal

causes of the pain. Timing of surgery depends on various medical, social, and business factors such as the proper identification of the specific injury, the degree of debility that the injury causes, the possible negative consequences of playing with the injury, and the relative risks in relation to such things as the importance of upcoming games, the player’s contract, the team’s interests in the player, and confidence that performance will not hurt the player’s overall value. Duration of rehabilitation is a particularly tricky consideration. We get most players back within 6 weeks of the injury, depending, of course, on the type of injury. There is evidence that we could get the players back even earlier, but long-term success possibly could be negatively associated with returning too quickly. Finally, we mention two more confusors. One is that the psoas “snapping hip” syndrome can be, but does not have to be, associated with athletic pubalgia or a labral tear. Because the iliopsoas tendon glides by the hip joint so closely, one has to consider that the patient can have one, two, or three syndromes at the same time. To make things even more confusing, one can at the same time demonstrate a clear labral tear by MRI or arthroscopy, but the tear still may be totally asymptomatic. A second confusor is the consideration of osteitis pubis. It is important that we realize that most athlete patients with this radiographic diagnosis have a secondary type of osteitis that responds favorably to treatment of the underlying joint instability. However, there still is a “primary” type of osteitis pubis that can affect athletes. The primary form of this problem involves continuous and debilitating pain that may be aggravated or ameliorated by exertion. The pain and tenderness often involve multiple bony sites in the pelvis. The primary type of osteitis pubis is difficult to treat. Fortunately, from an athletic standpoint, the primary osteitis pubis occurs much more in nonathletes. The problem is nonetheless, of course, very unfortunate for the patients involved because it is so difficult to treat. On the other hand, the syndrome does seem usually to be time limited.

SUMMARY Abdomen and pelvis injuries due to sports are usually a consequence of repetitive trauma and instability. These problems can become chronic problems and possibly negatively affect the athlete’s performance. Due to the rising popularity of kicking sports, these types of problems are more common and are becoming better understood.

REFERENCES 1. Meyers WC, Greenleaf R, Saad A: Anatomic basis for evaluation of abdominal and groin pain in athletes. Op Tech Sports Med 2005;13:55–61. 2. Meyers WC, Foley DP, Garrett WE: Management of severe lower abdominal or inguinal pain in high-performance athletes. Am J Sports Med 2000;28:2–8. 3. Meyers WC et al: Am J Sports Med in press. 4. Korpelainen R, Orava S, et al: Risk factors for recurrent stress fractures in athletes. Am J Sports Med 2001;29:304–310. 5. Johansson C, Ekenman I, et al: Stress fractures of the femoral neck in athletes. Am J Sports Med 1990;18:524–528. 6. Shin AY, Morin WD, Gorman JD, et al: The superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med 1996;24:168–176.

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7. Haidukewych GJ, Rothwell WS, et al: Operative treatment of femoral neck fractures in patients between the ages of fifteen and fifty years. J Bone Joint Dis Am 2004;86:1711–1716. 8. Weistroffer JK, Muldoon MP, Duncan DD, et al: Femoral neck stress fractures: Outcome analysis at minimum five-year follow-up. J Orthop Trauma 2003;17:34–37. 9. Coventry MB, William MC: Osteitis pubis: Observations based on a study of 45 patients. JAMA 1961;178:898–905. 10. Fricker P, Taunton J, Ammann W: Osteitis pubis in athletes: Infection, inflammatory or injury. Sports Med 1991;12:266–279. 11. Holt MA, Keene JS, Graf BK, Helwig DC: Treatment of osteitis pubis in athletes. Results of corticosteroid injections. Am J Sports Med 1995;23:601–606. 12. Harris NH, Murray RG: Lesions of the symphysis pubis in athletes. In

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Proceedings of the British Orthopaedic Association. J Bone Joint Surg Br 1974;56:563–564. 13. Grace JN, Sim FH, Shives TC, Coventry MB: Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am 1989;71:358–364. 14. Williams PR, Thomas DP, Downes EM: Osteitis pubis and instability of the pubic symphysis. When nonoperative measures fail. Am J Sports Med 2000;28:350–255.

15. Metzmaker J, Pappas A: Avulsion fractures of the pelvis. Am J Sports Med 1985;13:349–358. 16. Sundar M, Carty H: Avulsion fractures of the pelvis in children: A report of 32 fractures and their outcome. Skeletal Radiol 1994;23:85–90. 17. Meyer NJ, Orton D: Traumatic unilateral avulsion of the anterior superior and inferior iliac spines with anterior dislocation of the hip: A case report. J Orthop Trauma 2001;15:137–140.

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CHAPTER

45

Hip Joint J.W. Thomas Byrd

In This Chapter History and physical examination Imaging Surgery—hip arthroscopy Loose bodies Labral tears Articular cartilage injury Ligamentum teres injury Synovial disease Impinging osteophytes Instability

INTRODUCTION • Sports-related injuries to the hip joint have received relatively little attention. • This trend is changing, but, until recently, there have been few publications in peer-reviewed journals and the topic has rarely been presented at scientific meetings. This is due to three reasons. • First, perhaps hip injuries are less common than in other joints. • Second, investigative skills, including clinical assessment and imaging studies, for the hip have been less sophisticated. • Third, there have been few interventional methods, including surgical techniques and conservative modalities, available to treat the hip and thus there has been little impetus to delve into this unrecognized area. • Arthroscopy has revealed a plethora of intra-articular disorders that previously went undiagnosed and largely untreated. Uncovering the existence of these disorders has led to improved clinical assessment skills and improved imaging technology. Thus, more forms of pathology are being recognized and there are now more methods available to treat these injuries.

The indications for hip arthroscopy fall into two broad categories. In one, arthroscopy offers an alternative to traditional open techniques previously employed for recognized forms of hip pathology such as loose bodies or impinging osteophytes. In the other, arthroscopy offers a method of treatment for disorders that previously went unrecognized including labral tears, chondral injuries, and disruption of the ligamentum teres. Most athletic injuries fall into this latter category. In the past, athletes

were simply resigned to living within the constraints of their symptoms, often ending their competitive careers, being diagnosed as having a chronic groin injury. Based on the results of arthroscopy among athletes, it is likely that many of these careers could have been rejuvenated with arthroscopic intervention.1 In a study of athletes undergoing arthroscopy, in 60% of the cases, the hip was not recognized as the source of symptoms at the time of initial treatment, and these patients were managed for an average of 7 months before the hip was considered as a potential contributing source.1 The most common preliminary diagnoses were various types of musculotendinous strains. Thus, it is prudent to consider the possibility of intra-articular pathology in the differential diagnosis when managing a strain around the hip joint. However, the incidence of intra-articular pathology is probably quite small relative to other extra-articular injuries, and thus it is best to temper the interest in an extensive intra-articular workup for every hip flexor or adductor strain. What is important is thoughtful follow-up and reassessment of injuries, especially when they do not seem to be responding as expected.

CLINICAL FEATURES AND EVALUATION The evaluation of a patient with hip pain focuses on whether the source of symptoms is intra-articular and thus potentially amenable to arthroscopy.2 Characteristic features of hip joint pathology are summarized in Table 45-1. In general, a history of a specific traumatic event is a better prognostic indicator than a patient who simply develops insidious onset of hip pain. Onset of symptoms in the absence of injury implies a degenerative process or predisposition to damage that is less likely to be corrected by arthroscopic intervention. Mechanical symptoms such as sharp stabbing pain, locking, or catching are also better prognostic indicators of a potentially correctable problem. Common examination findings are summarized in Table 45-2. Although the hip receives innervation from branches of L2 to S1 of the lumbosacral plexus, its principal innervation is the L3 nerve root. This explains why irritation of the joint may result in anterior groin and radiating medial thigh pain that follows the L3 dermatome. Posterior pain is rarely indicative of an intraarticular process but, if clinically suspected, can be confirmed with a fluoroscopically guided intra-articular injection of anesthetic, which should provide temporary alleviation of the pain. The C sign is very characteristic of hip joint pathology. The patient cups the hand above the greater trochanter with the thumb over the posterior aspect and gripping the fingers into the groin. It may appear as if the patient is describing a lateral

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Table 45-1 Characteristic Features of Hip Joint Pathology Straight plane activity relatively well tolerated Torsional/twisting activities problematic Prolonged hip flexion (sitting) uncomfortable Pain/catching going from flexion to extension (rising from seated position) Inclines/stairs more difficult than level surfaces

problem such as the iliotibial band or trochanteric bursitis, but this maneuver is actually performed to describe deep interior joint pain. The log roll test is the most specific test for intra-articular pathology. Gently rolling the thigh internally and externally rotates only the femoral head in relation to the acetabulum and capsule, not stressing any of the surrounding extra-articular structures. More sensitive maneuvers include forced flexion combined with internal rotation (also referred to as the impingement test) and abduction combined with external rotation. These maneuvers normally cause some discomfort and must be compared to the unaffected hip. However, more important is whether the maneuver recreates the type of pain that the patient experiences with activities. An accompanying click or pop may be elicited, but this can occur for various reasons, and, again, most important is whether it recreates the patient’s symptoms. Intra-articular lesions are usually easily differentiated from extra-articular causes of a snapping hip. Snapping of the iliopsoas tendon is a common condition that may need to be differentiated from an intra-articular problem. The tendon snaps across the anterior joint and pectineal eminence as the hip is brought from a flexed abducted externally rotated position into extension with internal rotation.3 Iliopsoas bursography and ultrasonography are helpful in substantiating this condition. Radiographs are an integral part of the assessment but are unreliable at detecting most lesions amenable to arthroscopy. Careful attention should be given to early signs of degenerative arthritis, which is a poorer prognostic indicator of arthroscopic outcomes. High-resolution magnetic resonance imaging is showing more promise at detecting intra-articular pathology but requires a 1.5-T magnet and surface coil with small field of view images of the involved hip.4 The most reliable indicators are often indirect

findings including effusion, paralabral cysts, and subchondral cysts. Gadolinium arthrography combined with magnetic resonance imaging (magnetic resonance angiography) demonstrates superior sensitivity at detecting numerous intra-articular lesions, but the specificity is less certain with some reports of increased false-positive interpretation. In general, these studies are best for showing labral pathology and poor for demonstrating lesions of the articular surface. The intra-articular contrast injection should include long-acting anesthetic (bupivacaine) as part of the diluent. Whether the patient’s symptoms are temporarily alleviated by the intra-articular anesthetic is the most reliable indicator of the joint being the source of their problem. Following the injection, it is important that the patient be instructed to perform activities that normally create symptoms in order to assess their response.

TECHNICAL OVERVIEW The hip joint has an intra-articular and peripheral compartment. Most hip pathology is found within the intra-articular region, and distraction is necessary to achieve arthroscopic access. The patient can be placed in the supine or lateral decubitus position for performing the procedure.5,6 Both techniques are equally effective, and the choice is simply dependent on the surgeon’s preference. An advantage of the supine approach is its simplicity in patient positioning while the lateral approach may be preferable for severely obese patients. Performing hip arthroscopy without traction has not been popular because it does not allow access to the intra-articular region. However, it is now recognized that this method can be a useful adjunct to the traction technique.7,8 Hip flexion relaxes the capsule and allows access to the peripheral compartment, which is intracapsular but extra-articular. Numerous lesions are encountered in this area that are overlooked with traction alone. Synovial disease often covers the capsular surface, and free-floating loose bodies can hide in the peripheral recesses. This also allows generous access to the capsule for capsulorrhaphy and is essential for addressing impingement lesions of the proximal femur.

SURGERY: HIP ARTHROSCOPY The technique illustrated is with the patient in the supine position. The important principles for performing safe, effective, reproducible arthroscopy are the same whether the patient is in the lateral decubitus or supine orientation. Portal placements, relationship of the extra-articular structures, and arthroscopic anatomy are all the same regardless of positioning.

Equipment Table 45-2 Examination Findings Groin, anterior, and medial thigh pain C-sign characteristic of interior hip pain: hand gripped above greater trochanter Log rolling of leg back and forth: most specific indicator of intraarticular pathology Forced flexion/internal rotation or abduction/external rotation: more sensitive measure of hip joint pain; reproduces symptoms that patient experiences with activities

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A standard fracture table or custom distraction device is needed to achieve effective joint space separation. A tensiometer can be helpful to monitor the traction forces intraoperatively. The C arm is important for precise placement of the instrumentation within the joint. Extra-length arthroscopy instruments are also available to accommodate the dense surrounding soft tissue.

Anesthesia The procedure is commonly performed under general anesthesia. It can be performed under epidural anesthesia but requires

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an adequate motor block to ensure optimal distractibility of the joint.

Intra-articular (Central) Compartment Setup The perineal post is heavily padded and lateralized against the medial thigh of the operative hip (Fig. 45-1). This aids in achieving the optimal traction vector (Fig. 45-2) and reduces pressure directly on the perineum, lessening the risk of neurapraxia of the pudendal nerve. Neutral rotation achieves a constant relationship between the topographic landmarks and the joint. Slight flexion may relax the capsule, but excessive flexion should be avoided as this places undue tension on the sciatic nerve and may block access for the anterior portal. Typically, about 50 pounds of force is needed to distract the joint. In general, the goal is to use the minimal force necessary to achieve adequate distraction and keep traction time as brief as possible. Two hours is usually recognized as a reasonable limit for traction. Portals Three standard portals are used for this portion of the procedure (Figs. 45-3 and 45-4). Two of these (anterolateral and posterolateral) are placed laterally over the superior margin of the greater trochanter at its anterior and posterior borders. The anterior portal is placed at the site of intersection of a sagittal line drawn distally from the anterior superior iliac spine and a transverse line across the tip of the greater trochanter. With careful orientation to the landmarks in relation to the joint, these portals are a safe distance from the surrounding major neurovascular structures (Figs. 45-5 to 45-7; Table 45-3).9

Pressure Perineal post Distraction vector

Traction Figure 45-2 The optimal vector for distraction is oblique relative to the axis of the body and more closely coincides with the axis of the femoral neck than the femoral shaft. This oblique vector is partially created by abduction of the hip and partially accentuated by a small transverse component to the vector created by lateralizing the perineal post. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

Diagnostic Procedure After applying traction, a spinal needle is placed from the anterolateral position and the joint is distended with fluid. The anterolateral portal is then established under fluoroscopic control for introduction of the arthroscope (Fig. 45-8). Careful

Figure 45-1 The patient is positioned on the fracture table so that the perineal post is placed as far laterally as possible toward the operative hip resting against the medial thigh. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

Figure 45-3 The site of the anterior portal coincides with 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 direction of this portal courses approximately 45 degrees cephalad and 30 degrees toward the midline. The anterolateral and posterolateral portals are positioned directly over the superior aspect of the trochanter at its anterior and posterior borders. (From Byrd JWT: Hip arthroscopy utilizing the supine position. Arthroscopy 1994;10:275–280.)

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Lateral femoral cutaneous nerve Femoral artery and nerve Figure 45-4 The relationship of the major neurovascular structures to the three standard portals is demonstrated. The femoral artery and nerve lie well medial to the anterior portal. The sciatic nerve lies posterior to the posterolateral portal. Small branches of the lateral femoral cutaneous nerve lie close to the anterior portal. Injury to these is avoided by using proper technique in portal placement. The anterolateral portal is established first since it lies most centrally in the safe zone for arthroscopy. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

Sciatic nerve

Superior gluteal nerve

Femoral nerve Lateral femoral cutaneous nerve

Portal pathway Sartorius muscle

Ascending branch, lateral circumflex femoral artery Rectus femoris muscle Figure 45-5 Anterior portal pathway. The portal penetrates the sartorius and rectus femoris before entering the anterior capsule. Its course is almost tangential to the axis of the femoral nerve, lying only slightly closer at the level of the capsule. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

Gluteus medius muscle

Portal pathway

Figure 45-6 Anterolateral portal pathway. The portal penetrates the gluteus medius, entering the lateral capsule at its anterior margin. The superior gluteal nerve lies well cephalad to this site. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

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Table 45-3 Distance from Portal to Anatomic Structures Based on an Anatomic Dissection of Portal Placements in Eight Fresh Cadaver Specimens Piriformis tendon Sciatic nerve

Gluteus minimus muscle

Gluteus medius muscle

Piriformis tendon

Portals

Anatomic Structure

Anterior

Anterior superior iliac spine Lateral femoral cutaneous nerve* Femoral nerve Level of Sartorius† Level of rectus femoris Level of capsule Ascending branch of lateral circumflex femoral artery Terminal branch‡

Portal pathway

Figure 45-7 Posterolateral portal pathway. The portal penetrates the gluteus and minimus, entering the lateral capsule at its posterior margin. Its course is superior and anterior to the piriformis tendon and is closest to the sciatic nerve at the level of the capsule. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

attention is necessary to avoid perforating the labrum or scuffing the articular surface.10 Using the 70-degree scope, the anterior and posterolateral portals are then placed under direct arthroscopic view as well as fluoroscopy for precise entry into the joint. Diagnostic and operative arthroscopy is then achieved by interchanging the arthroscope and instruments between the three established portals. Use of both the 70- and 30-degree scopes provides optimal viewing despite limitations of maneuverability within the joint (Figs. 45-9 to 45-12).

Peripheral Compartment Positioning After completing arthroscopy of the intra-articular compartment, the instruments are removed, the traction released, and the hip flexed approximately 45 degrees (Fig. 45-13).

Average (cm)

Range (cm)

6.3 0.3

6.0–7.0 0.2–1.0

4.3 3.8 3.7 3.7

3.8–5.0 2.7–5.0 2.9–5.0 1.0–6.0

0.3

0.2–0.4

Anterolateral

Superior gluteal nerve

4.4

3.2–5.5

Posterolateral

Sciatic nerve

2.9

2.0–4.3

*Nerve had divided into three or more branches, and measurement was made to the closest branch. † Measurement made at superficial branch of Sartorius, rectus femoris, and capsule. ‡ Small terminal branch of ascending branch of lateral circumflex femoral artery identified in three specimens. From Byrd JWT, Pappas JN, Pedley MJ: Hip arthroscopy: An anatomic study of portal placement and relationship to the extraarticular structures. Arthroscopy 1995;11:418–423.

This relaxes the capsule, providing access to the peripheral compartment. Portal Placement Two portals are routinely used to access the peripheral compartment. These include the anterolateral portal and an ancillary portal established 4 to 5 cm distally. Diagnostic Procedure The anterolateral portal is redirected onto the anterior neck of the femur (Fig. 45-14). The ancillary portal is then established distally under direct arthroscopic and fluoroscopic guidance (Fig. 45-15). The arthroscope and instruments are interchanged, also using the 30- and 70-degree scopes for inspection (Figs. 4516 and 45-17).

Figure 45-8 The arthroscope cannula is passed over a guidewire that was inserted through a pre-positioned spinal needle. Fluoroscopy aids in avoiding contact with the femoral head or perforating the acetabular labrum. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

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Anterior wall

Anterior labrum Lateral labrum

Femoral head

Lateral wall

Femoral head

Greater trochanter

Anterior portal (camera)

A Anterolateral portal (camera)

A

B B Figure 45-9 A, Arthroscopic view of a right hip from the anterolateral portal. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.) B, Demonstrated are the anterior acetabular wall (AW) and the anterior labrum (AL). The anterior cannula is seen entering underneath the labrum and the femoral head (FH) is on the right. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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Figure 45-10 A, Arthroscopic view from the anterior portal. B, Demonstrated are the lateral aspect of the labrum (L) and its relationship to the lateral two portals. (A, Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

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Posterior wall

Femoral head Ligamentum teres

Femoral head

Posterior labrum Ligamentum teres

Femoral head

A A

Posterolateral portal (camera)

Femoral head

Posterolateral portal (camera)

B B Figure 45-11 A, Arthroscopic view from the posterolateral portal. B, Demonstrated are the posterior acetabular wall (PW), posterior labrum (PL), and the femoral head (FH). (A, Courtesy of Smith & Nephew Endoscopy, Andover, MA. B, Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

Figure 45-12 A, The acetabular fossa can be inspected from all three portals. B, The ligamentum teres (LT), with its accompanying vessels, has a serpentine course from its acetabular to its femoral attachment. (A, Courtesy of Smith & Nephew Endoscopy, Andover, MA. B, Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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Figure 45-13 The operative area remains covered in sterile drapes while the traction is then released and the hip flexed 45 degrees. Inset: Illustrates position of the hip without the overlying drape. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

Figure 45-14 From the anterolateral entry site, the arthroscope cannula is redirected over the guidewire through the anterior capsule, onto the neck of the femur. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

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Figure 45-15 With the arthroscope in place, prepositioning is performed with a spinal needle for placement of an ancillary portal distally. (Courtesy of Smith & Nephew Endoscopy, Andover, MA.)

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A A

B B Figure 45-16 A, Peripheral compartment viewing superiorly. B, Demonstrated is the anterior portion of the joint including the articular surface of the femoral head (FH), anterior labrum (AL), and the capsular reflection (CR). (A, Courtesy of Smith & Nephew Endoscopy, Andover, MA. B, Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

Figure 45-17 A, Peripheral compartment viewing medially. B, Demonstrated are the femoral neck (FN), medial synovial fold (MSF), and the zona orbicularis (ZO). (A, Courtesy of Smith & Nephew Endoscopy, Andover, MA. B, Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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Iliopsoas Bursoscopy Positioning Flexion is slightly less (15 to 20 degrees) than that used to view the peripheral compartment. The hip is also externally rotated, which moves the lesser trochanter more anterior and accessible to the portals. Portals Two portals are needed for viewing and instrumentation within the bursa (Fig. 45-18). These portals are distal to those used for the peripheral compartment and require fluoroscopy for precise positioning. These portals may be slightly more anterior to completely access the area of the lesser trochanter.

Loose Bodies Removal of symptomatic loose bodies is not the most common indication for hip arthroscopy, but it is the clearest indication. Loose bodies can be extracted and arthroscopy offers an excellent alternative to arthrotomy, previously indicated for this condition (Fig. 45-19).11–13 Most problematic loose bodies reside in the intra-articular compartment and are addressed with standard arthroscopic methods. However, many may remain hidden in the peripheral compartment and later become troublesome.

Figure 45-18 The arthroscope and shaver are positioned within the iliopsoas bursa directly over the lesser trochanter, identifying the fibers of the iliopsoas tendon (IT) at its insertion site. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

A

B

Figure 45-19 A 20-year-old male with a 3-month history of acute left hip pain. A, Anteroposterior radiograph demonstrates findings consistent with old Legg-Calvé-Perthes disease. B, Lateral view defines the presence of intra-articular loose bodies (arrows).

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D

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F

Figure 45-19—Cont’d C, Computed tomography substantiates the intraarticular location of the fragments (arrows). D, Arthroscopic view medially demonstrates the loose bodies. E, Viewing anteriorly, the anterior capsular incision is enlarged with an arthroscopic knife to facilitate removal of the fragments. F, One of the fragments is being retrieved. G, Loose bodies are removed whole. (From Byrd JWT: Indications and contraindications. In Byrd JWT [ed]: Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 6–35.)

G

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Thus, arthroscopy to address symptomatic fragments must include both the intra-articular and peripheral joint.7,8 Many can be débrided with shavers or flushed through large-diameter cannulas. Large ones can sometimes be morselized and removed piecemeal. However, often fragments may be too large to be removed through a cannula system and must be removed free hand with sturdy graspers. Once a portal tract has been developed, these larger graspers can be passed along the remaining tract into the joint in a free-hand fashion. Make sure to enlarge the capsular incision with an arthroscopic knife and the skin incision so that as the fragment is retrieved, it will not be lost in the tissues, either at the capsule or subcutaneous level.

pathology, but poor at identifying associated articular damage present in a significant portion of cases. These studies may also overinterpret pathology with lesions reported among asymptomatic volunteers, and among elite athletes, some damage may accrue simply as a consequence of the cumulative effect of their sport (Fig. 45-20). Traumatic labral tears may respond remarkably well to arthroscopic débridement (Fig. 45-21).14–18 However, at arthroscopy, be especially cognizant of any underlying degeneration that may have predisposed to the acute tear. There will often be accompanying articular damage, and the extent of this may be a significant determinant on the eventual response to débridement (Fig. 45-22). Also, with the evolving understanding of femoroacetabular impingement and its role in the development of labral and chondral damage, it is important to make a careful radiographic assessment of accompanying bony lesions of the anterior acetabulum or femoral head that may require reshaping (Fig. 45-23).19

Labral Tears Labral lesions represent the most common indication for hip arthroscopy among athletes. Magnetic resonance imaging and magnetic resonance angiography are best at detecting labral

A

B

Figure 45-20 Three National Hockey League players were referred, each with a 2-week history of hip pain following an injury on the ice. Each case demonstrated evidence on magnetic resonance imaging of labral pathology (arrows). These cases were treated with 2 weeks of rest followed by a 2-week period of gradually resuming activities. Each of these athletes was able to return to competition and have continued to play for several seasons without needing surgery. A, Coronal image of a left hip demonstrates a lateral labral tear (arrow). B, Coronal image of a right hip demonstrates a lateral labral tear (arrow). C, Sagittal image of a left hip demonstrates an anterior labral tear with associated paralabral cyst (arrow). (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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A Figure 45-21 A 25-year-old top-ranked professional tennis player sustained a twisting injury to his right hip. A, Coronal magnetic resonance imaging demonstrates evidence of labral pathology (arrow). B, Arthroscopy reveals extensive tearing of the anterior labrum (asterisk) as well as an adjoining area of grade III articular fragmentation (arrows). C, The labral tear has been resected to a stable rim (arrows) and chondroplasty of the grade III articular damage (asterisk) is being performed. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

Labral tears can be adequately accessed through the three standard portals. Similar to a meniscus in the knee, the task is to remove unstable and diseased labrum, creating a stable transition to retained healthy tissue. The most difficult aspect is creating the stable transition zone. Thermal devices have been quite useful at ablating unstable tissue adjacent to the healthy portion of the labrum. Caution is necessary because of the concerns regarding depth of heat penetration, but with judicious use, these devices have been exceptionally useful for precise labral débridement despite the constraints created by the architecture of the joint. The natural evolution in arthroscopic management of labral pathology is from débridement to repair. Current methods of acetabular labral repair are in their infancy. A few have been attempted with mixed results. Reliable techniques remain to be developed but are probably not far off. In addition to technical advancements, there is much that remains regarding our understanding of labral morphology and pathophysiology. There is considerable variation in the normal appearance of the labrum including a labral cleft at the articular labral junction that can

C be quite large.14 It is important to distinguish this from a traumatic detachment, which can also occur. Additionally, many labral tears, even in the presence of a significant history of injury, seem to occur due to some underlying predisposition or degeneration. Under these circumstances, even with reliable techniques, repair of a degenerated or morphologically vulnerable labrum would unlikely be successful.

Articular Cartilage Injury A propensity for acute articular injury has been identified among athletes associated with a direct blow to the trochanter (Fig. 4524).20 Chondroplasty can be effectively performed for lesions of both the acetabular and femoral surfaces. Curved shaver blades are helpful for negotiating the constraints created by the convex surface of the femoral head. Due to limitations of maneuverability, thermal devices have again been especially helpful in ablating unstable fragments. However, cautious and judicious use around articular surface is even more important because of potential injury to surviving chondrocytes.

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D

Figure 45-22 A 23-year-old elite professional tennis player sustained an injury to his right hip. A, Coronal magnetic resonance imaging demonstrates evidence of labral pathology (arrow). B, Arthroscopy reveals the labral tear (arrows), but also an area of adjoining grade IV articular loss (asterisk). C, Microfracture of the exposed subchondral bone is performed. D, Occluding the inflow of fluid confirms vascular access through the areas of perforation. The athlete was maintained on a protected weight-bearing status emphasizing range of motion for 10 weeks with return to competition at 31/2 months. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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C

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D

Figure 45-23 A 16-year-old high school football player develops acute onset of right hip pain doing squats. A, Sagittal view magnetic resonance arthrogram demonstrates a macerated anterior labrum (arrows). B, Viewing from the anterolateral portal, a macerated tear of the anterior labrum is probed along with articular delamination at its junction with the labrum. C, The damaged anterior labrum has been excised, revealing an overhanging lip (arrows) of impinging bone from the anterior acetabulum. D, Excision of the impinging portion of the acetabulum (acetabuloplasty) is performed with a bur. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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A

B C Figure 45-24 A, Fall results in direct blow to the greater trochanter, and, in absence of fracture, the force generated is transferred unchecked to the hip joint. B, Arthroscopic view of the left hip of a 20-year-old collegiate basketball player demonstrates an acute grade IV articular injury (asterisk) to the medial aspect of the femoral head. C, Arthroscopic view of the left hip of a 19-year-old male who sustained a direct lateral blow to the hip, subsequently developing osteocartilaginous fragments (asterisks) within the superomedial aspect of the acetabulum. (From Byrd JWT: Lateral impact injury: A source of occult hip pathology. Clin Sports Med 2001;20:801–816.)

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Microfracture of select grade IV articular lesions has been beneficial (see Fig. 45-22).18 As with other joints, it is best indicated for focal lesions with healthy surrounding articular surface. The lesion most amenable to this process is encountered in the lateral aspect of the acetabulum. This is followed by 8 to 10 weeks of protected weight bearing to neutralize the forces across the hip joint while emphasizing range of motion. Using this protocol, among a cohort of 24 patients, 86% demonstrated a successful outcome at 2- to 5-year follow-up.21

Ligamentum Teres Injury Injury to the ligamentum teres is increasingly recognized as a source of hip pain in athletes (Fig. 45-25).1 The disrupted fibers catch within the joint and can be quite symptomatic. This disruption may be the result of trauma, degeneration, or a combination of both.22 The tear may be partial or complete with the goal of treatment being to débride the entrapping, disrupted fibers. Our recent report documented excellent success in the arthroscopic management of traumatic lesions of the ligamentum teres. The average improvement was 47 points (100-point

modified Harris hip score system), with 93% showing marked (>20 points) improvement.23 The acetabular attachment of the ligamentum teres is situated posteriorly at the inferior margin of the acetabular fossa and attaches on the femoral head at the fovea capitis. The disrupted portion of the ligament is avascular, but the fat pad and synovium contained in the superior portion of the fossa can be quite vascular. Débridement is facilitated by a complement of curved shaver blades and a thermal device. The disrupted portion of the ligament is unstable and delivered by suction into the shaver. A thermal device can also ablate tissue while maintaining hemostasis within the vascular pulvinar. Access to this inferomedial portion of the joint is best accomplished from the anterior portal. External rotation of the hip also helps in delivering the ligament to the shaver brought in anteriorly. The most posterior portion of the fossa and the acetabular attachment of the ligament may be best accessed from the posterolateral portal. Indiscriminate débridement of the ligamentum teres should be avoided because of its potential contribution to the vascularity of the femoral head.

* A

B

Figure 45-25 A 16-year-old cheerleader has a 2-year history of catching and locking of the left hip following a twisting injury. A, Arthroscopic view from the anterolateral portal reveals disruption of the ligamentum teres (asterisk). B, Débridement is begun with a synovial resector introduced from the anterior portal. C, The acetabular attachment of the ligamentum teres in the posterior aspect of the fossa is addressed from the posterolateral portal. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

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Synovial Disease

arthroscopically. Ultimately, with a well-performed procedure, the response to treatment will be mostly dictated by the extent of pathology, much of which cannot be reversed.24–27

Primary synovial disease may be encountered in athletes, but more often synovial proliferation occurs in response to other intra-articular pathology. Synovitis may be diffuse, encompassing the lining of the joint capsule, or focal, emanating from the pulvinar of the acetabular fossa. Focal lesions within the fossa may be dense and fibrotic or exhibit proliferative villous characteristics. Presumably, because of entrapment within the joint, these lesions can be quite painful and respond remarkably well to simple débridement. While a complete synovectomy cannot be performed, a generous subtotal synovectomy can be carried out. Enlarging the capsular incisions with an arthroscopic knife improves maneuverability within the intra-articular portion of the joint. For most synovial disease, arthroscopy of the peripheral compartment is necessary in order to adequately resect the diseased tissue.7,8,19 In the presence of arthritis, there will be arthroscopic evidence of various pathology including free fragments, labral tearing, articular damage, and synovial disease. With a meticulous systematic approach, each component can be addressed

Impinging Osteophytes Post-traumatic impinging bone fragments, occasionally encountered in an active athletic population, may respond well to arthroscopic excision.28,29 Degenerative osteophytes rarely benefit from arthroscopic excision as the symptoms are usually more associated with the extent of joint deterioration and not simply the radiographically evident osteophytes that secondarily form. However, the post-traumatic type may impinge on the joint, causing pain and blocking motion. These fragments are often extracapsular and require a capsulotomy, extending the dissection outside the joint for excision (Fig. 45-26). This necessitates thorough knowledge and careful orientation of the extraarticular anatomy and excellent visualization at all times during the procedure. In general, the dissection should stay directly on the bone fragments and avoid straying into the surrounding soft tissues. Various techniques aid in maintaining optimal visualiza-

A B

Figure 45-26 An 18-year-old high school football player sustained an avulsion fracture of the left anterior inferior iliac spine. A, Threedimensional computed tomography illustrates the avulsed fragment (arrow), which ossified, creating an impinging painful block to flexion and internal rotation. B, Viewing from the anterolateral portal, a capsular window is created, exposing the osteophyte (asterisk) anterior to the acetabulum (A). C, The anterior capsule (C) has been completely released allowing resection of the fragment along the anterior column of the pelvis (P). Postoperatively, the patient regained full range of motion with resolution of his pain. (From Byrd JWT: Arthroscopy of select hip lesions. In Byrd JWT [ed]: Operative Hip Arthroscopy. New York, Thieme, 1998, pp 153–170.)

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Figure 45-27 A 19-year-old female had undergone two previous arthroscopic procedures on her right hip for reported lesions of the ligamentum teres. Following each procedure, she developed recurrent symptoms of “giving way.” A, Radiographs revealed normal joint geometry. B, She was noted to have severe diffuse physiologic laxity best characterized by a markedly positive sulcus sign. C, With objective evidence of laxity and subjective symptoms of instability, an arthroscopic thermal capsulorrhaphy was performed, accessing the redundant anterior capsule from the peripheral compartment. Modulation of the capsular response was controlled by a hip spica brace for 8 weeks postoperatively with a successful outcome. (Courtesy of J.W. Thomas Byrd, MD, Nashville, TN.)

C tion. A high-flow pump is especially helpful, maintaining a high flow rate without excessive pressure, which would worsen extravasation. Hypotensive anesthesia, placing epinephrine in the arthroscopic fluid, and electrocautery or other thermal device for hemostasis all aid in visualization for effectively performing the excision.

Instability Hip instability can occur but is much less common than seen in the shoulder. There are several reasons, but, most principally, it is due to the inherent stability provided by the constrained balland-socket bony architecture of the joint. Also, the labrum is not as critical to stability of the hip as it is in the shoulder as there is no true capsulolabral complex. On the acetabular side,

the capsule attaches directly to the bone, separate from the acetabular labrum.30 An entrapped labrum has been reported as a cause of an irreducible posterior dislocation and a Bankart type detachment of the posterior labrum has been identified as the cause of recurrent posterior instability.31,32 These circumstances have only rarely been reported but may be recognized with increasing frequency as our understanding of and intervention in hip injuries evolves. Instability may occur simply due to an incompetent capsule. This is seen in hyperlaxity states and less often encountered in athletics. The most common cause is a collagen vascular disorder such as Ehlers-Danlos syndrome. With normal joint geometry, thermal capsular shrinkage has continued to meet with successful results (Fig. 45-27). If subluxation or symptomatic

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instability is due to a dysplastic joint, it is likely that bony correction for containment is necessary to achieve stability. Based on this author’s observations, posterior instability has been found to be associated with macrotrauma. This is due to the characteristic mechanisms of injury, including dashboard injuries and axial loading of the flexed hip encountered in collision sports. Atraumatic instability or instability due to repetitive microtrauma is anterior and develops when the normally occurring anterior translation of the femoral head exceeds the physiologic threshold and becomes pathologic. Symptoms may be due to primary instability, secondary intra-articular damage, or a combination of both.

COMPLICATIONS The reported complication rate associated with large hip arthroscopy series ranges from 1.3% to 6.4%.33–35 Most of these are minor or transient, but a few major complications have been reported. Traction neuropraxia is usually associated with prolonged procedures and excessive traction but can occur even when staying within established guidelines. With normal precautions, it is expected that the condition should be transient and recovery complete. Direct trauma to the major neurovascular structures should be avoidable with thoughtful orientation to the landmarks and careful technique in portal placement. The consequences of these types of injuries are generally devastating. Small branches of the lateral femoral cutaneous nerve invariably lie around the anterior portal. Even with careful technique, there is a 0.5% chance of incurring a small patch of reduced sensation in the lateral thigh due to instrumentation around one of these branches. Potentially life-threatening intra-abdominal extravasation of fluid has been reported.36 This is generally attributed to fresh acetabular fractures, extra-articular procedures, and prolonged operating times.34 It is imperative that the surgeon be cognizant of the balance of ingress and egress of fluid throughout the operative procedure.

It is likely that the most common complication, which goes largely unreported, is iatrogenic intra-articular damage. Even with careful attention to the details of the procedure, this cannot be entirely avoided. However, it can be minimized and emphasizes the importance of meticulous technique in performing the procedure.

CONCLUSIONS Hip joint injuries in athletes may go unrecognized for a protracted period of time, most commonly diagnosed as a strain. With an increase in awareness of intra-articular disorders, these problems are now being diagnosed earlier. However, much remains to be understood regarding the pathogenesis and natural history of many of these lesions that may influence the results of both surgical and conservative management. Nonetheless, arthroscopy has defined numerous sources of intra-articular hip pathology. In many cases, operative arthroscopy has met with significant success. For some, arthroscopy offers a distinct advantage over traditional open techniques, but for many, arthroscopy offers a method of treatment where none existed before. With this procedure, there are three important principles that must be thoroughly considered. First, a successful outcome is dependent on proper patient selection. A technically well-performed procedure will fail when performed for the wrong reason, which may include failure of the procedure to meet the patient’s expectations. Second, the patient must be properly positioned for the procedure to go well. Poor positioning will ensure a difficult procedure. Third, simply gaining access to the hip joint is not an outstanding technical accomplishment. The paramount issue is that the joint must be accessed in as atraumatic a fashion as possible. Because of its constrained architecture and dense soft-tissue envelope, the potential for inadvertent iatrogenic scope trauma is significant and, perhaps to some extent, unavoidable. Thus, every reasonable step should be taken to keep this concern to a minimum by performing the procedure as carefully as possible and being certain that it is performed for the right reasons.

REFERENCES 1. Byrd JWT, Jones KS: Hip arthroscopy in athletes. Clin Sports Med 2001;20:749–762. 2. Byrd JWT: Physical examination. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 36–50. 3. Allen WC, Cope R: Coxa saltans: The snapping hip revisited. J Am Acad Orthop Surg 1995;3:303–308. 4. Byrd JWT, Jones KS: Diagnostic accuracy of clinical assessment, MRI, gadolinium MRI, and intraarticular injection in hip arthroscopy patients. Am J Sports Med 2004;32:1668–1674. 5. Byrd JWT: The supine approach. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 145–169. 6. Sampson TG: The lateral approach. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 129–144. 7. Dienst M, Godde S, Seil R, et al: Hip arthroscopy without traction: In vivo anatomy of the peripheral hip joint cavity. Arthroscopy 2001;17:924–931. 8. Dienst M: Hip arthroscopy without traction. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 170–188. 9. Byrd JWT, Pappas JN, Pedley MJ: Hip arthroscopy: An anatomic study of portal placement and relationship to the extraarticular structures. Arthroscopy 1995;11:418–423. 10. Byrd JWT: Avoiding the labrum in hip arthroscopy. Arthroscopy 2000;16:770–773.

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11. Byrd JWT: Hip arthroscopy for post-traumatic loose fragments in the young active adult: Three case reports. Clin J Sport Med 1996;6:129– 134. 12. McCarthy JC, Bono JV, Wardell S: Is there a treatment for synovial chondromatosis of the hip joint? Arthroscopy 1997;13:409– 410. 13. Medlock V, Rathjen KE, Montgomery JB: Hip arthroscopy for late sequelae of Perthes disease. Arthroscopy 1999;15:552–553. 14. Byrd JWT: Labral lesions: An elusive source of hip pain: Case reports and review of the literature. Arthroscopy 1996;12:603–612. 15. Lage LA, Patel JV, Villar RN: The acetabular labral tear; an arthroscopic classification. Arthroscopy 1996;12:269–272. 16. Farjo LA, Glick JM, Sampson TG: Hip arthroscopy for acetabular labrum tears. Arthroscopy 1997;13:409–410. 17. Santori N, Villar RN: Acetabular labral tears: Result of arthroscopic partial limbectomy. Arthroscopy 2000;16:11–15. 18. Byrd JWT, Jones KS: Inverted acetabular labrum and secondary osteoarthritis: Radiographic diagnosis and arthroscopic treatment. Arthroscopy 2000;16:417. 19. Byrd JWT: Hip arthroscopy: Evolving frontiers. Op Tech Sports Med 2004;14:58–67. 20. Byrd JWT: Lateral impact injury: A source of occult hip pathology. Clin Sports Med 2001;20:801–816.

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21. Byrd JWT, Jones KS: Microfracture for grade IV chondral lesions of the hip. Arthroscopy 2004;20(SS-89):41. 22. Gray AJR, Villar RN: The ligamentum teres of the hip: An arthroscopic classification of its pathology. Arthroscopy 1997;13:575–578. 23. Byrd JWT, Jones KS: Traumatic rupture of the ligamentum teres as a source of hip pain. Arthroscopy 2004;20:385–391. 24. Farjo LA, Glick JM, Sampson TG: Hip arthroscopy for degenerative joint disease. Arthroscopy 1998;14:435. 25. Villar RN: Arthroscopic debridement of the hip: A minimally invasive approach to osteoarthritis. J Bone Joint Surg Br 1991;73(Suppl II):170–171. 26. Santori N, Villar RN: Arthroscopic findings in the initial stages of hip osteoarthritis. Orthopedics 1999;22:405–409. 27. Byrd JWT, Jones KS: Prospective analysis of hip arthroscopy with five year follow up. Paper presented at the AAOS 69th Annual Meeting, February 14, 2002, Dallas, TX. 28. Byrd JWT: Indications and contraindications. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 6–35. 29. Byrd JWT: Arthroscopy of select hip lesions. In Byrd JWT (ed): Operative Hip Arthroscopy. New York, Thieme, 1998, pp 153–170.

30. Seldes RM, Tan V, Hunt J, et al: Anatomy, histologic features, and vascularity of the adult acetabular labrum. Clin Orthop 2001;382:32– 40. 31. Paterson I: The torn acetabular labrum: A block to reduction of a dislocated hip. J Bone Joint Surg Br 1957;39:306–309. 32. Dameron TB: Bucket-handle tear of acetabular labrum accompanying posterior dislocation of the hip. J Bone Joint Surg Am 1959;41: 131–134. 33. Clarke MT, Arora A, Villar RN: Hip arthroscopy: Complications in 1054 cases. Clin Orthop 2003;406:84–88. 34. Sampson TG: Complications of hip arthroscopy. Clin Sports Med 2001:20;831–835. 35. Byrd JWT: Complications associated with hip arthroscopy. In Byrd JWT (ed): Operative Hip Arthroscopy, 2nd ed. New York, Springer, 2005, pp 229–235. 36. Bartlett CS, DiFelice GS, Buly RL, et al: Cardiac arrest as a result of intraabdominal extravasation of fluid during arthroscopic removal of a loose body from the hip joint of a patient with an acetabular fracture. J Orthop Trauma 1998;12:294–300.

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Physical Examination and Evaluation Timothy C. Wilson

In This Chapter Examination of specific ligaments Patellofemoral exam Meniscus exam Multiligamentous knee injuries

INTRODUCTION • The physical examination of the knee has been described as an art and a science.1 • The purpose of the examination is to arrive at the correct diagnosis. • A complete patient history must be combined with a thorough physical examination in order to direct treatment. • Additional tests such as radiographs, magnetic resonance imaging, bone scans, and angiography are sometimes used to provide information in the evaluation of a knee injury.

HISTORY The clinical examination of the knee begins with a thorough history that focuses on the presenting symptoms and mechanism of injury. Questions should be asked regarding the onset and duration of symptoms. The location and quality of pain should be ascertained as well as the presence of any previous injuries or history of surgery. It is important to document the presence of swelling, mechanical symptoms, and instability. Mechanical symptoms may include locking and catching. Giving way may be the patient’s description of instability. Many patients who experience a “pop” in their knee at the time of injury will have an anterior cruciate ligament (ACL) tear. In many cases, the history itself will direct the examiner toward the correct diagnosis. The mechanism of injury provides useful information with regards to the direction and degree of injury. Ligament injuries are the result of forces from the opposite direction. For example, an anterior blow to the knee may cause a posterior knee dislocation. This injury pattern is commonly seen in “dashboard knee.” Anterior dislocations commonly occur from extreme knee hyperextension. This happens when an anterior force occurs to the tibia against a fixed foot, and the femur is forced posterior to the tibia. Medial and lateral ligament injuries are most likely to occur from valgus and varus forces, respectively.2 Knowledge of each patient’s mechanism of injury will be useful in determining which structures may be injured and the potential risk of associated injuries. In summary, the history can

lead the examiner to a specific area to inspect and improve the ability to correctly diagnose.

PHYSICAL EXAMINATION A thorough examination of the knee involves a systematic approach. Having the patient relax is of utmost importance. The best physical examination can sometimes be obtained immediately after the injury before significant swelling and pain preclude a relaxed examination. It is helpful to examine the uninjured knee first not only to serve as a baseline, but also to gain the confidence of the patient. The least painful tests should be performed before progressing to the more painful examination techniques. The patient’s gait pattern should be inspected. An antalgic gait is demonstrated by a shortened stance phase and will confirm the involved extremity. During the stance phase the presence of a varus thrust should be noted if present. A short leg gait may be observed, and this can be noted by measuring for a leg length discrepancy. The clinical alignment of the limb should be observed for genu varus or valgus. This is measured by placing a goniometer on the patella and measuring the angular alignment of the femur in relation to the tibia. This measurement differs from the radiographic measurement of the mechanical axis. The physical examination of the knee includes an inspection for any soft-tissue swelling or joint effusion (Fig. 46-1). It is important to distinguish between these two types of fluid accumulation. Fluid that is intra-articular signifies an injury to the joint itself. Common causes of an effusion include an ACL tear, patellar dislocation, or osteochondral injury. The finding of a ballotable patella is a sign of an effusion. Another sign of an effusion is the loss of the normal skin dimple that is visible just distal to the vastus medialis obliquus insertion on the patella. Prepatella swelling may be from a bursitis. Other soft-tissue swelling may be associated with extra-articular ligament tears and sprains. For example, a medial collateral ligament sprain may present with medial soft-tissue swelling. The ability to distinguish an effusion from soft-tissue swelling is an important aspect of the physical examination. The range of motion of the knee should be measured. A goniometer can be used to measure the amount of knee flexion and extension. The knee should be evaluated for hyperextension as well. Both knees should always be measured as asymmetry may be a sign of injury. A locked knee is a knee with the inability to fully extend because of a mechanical block such as from a bucket handle meniscus tear or a loose body. Measurements should be taken of the girth of the quadriceps muscle. Quadriceps atrophy is commonly seen after surgery or

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capsule. It is important to specifically examine each of the four elements carefully. Magnetic resonance imaging should not be extensively relied on because the accuracy of that test is diminished without clinical correlation.

Anterior Cruciate Ligament

Figure 46-1 Right knee effusion after a patellar dislocation.

a chronic injury. The measurement is taken at a set distance from either the patella or joint line and the two knees are compared to one another. Subsequent measurements can be made to follow a patient’s progress with rehabilitation. Palpation is an essential part of all examinations. The bony landmarks should be assessed for tenderness. Joint line tenderness is sensitive for the diagnosis of a meniscus tear. Sometimes a meniscal cyst may be visible and palpable in the joint line. A medial patellofemoral plica can be palpable medially, just above the joint line, and is sometimes tender as it is compressed between the examiner’s fingers and the medial femoral condyle. The inferior pole of the patella, patellar tendon, and tibia tubercle are common areas of tenderness in athletes with anterior knee pain. Lateral patellofemoral compression may be associated with tenderness of the lateral patellar facet. Other common areas of tenderness include the iliotibial band, pes anserine bursa, and quadriceps. Crepitation of the knee joint as it goes through a range of motion is a common sign of patellofemoral chondromalacia. The knee should be assessed for warmth. A normal knee should always feel cooler to the touch than the surrounding musculature. The back of the examiner’s hand may be used to detect subtle temperature differences. Synovitis is a common cause of a subtle increase in temperature of the knee.

The ACL serves as the primary restraint to anterior translation of the tibia in relation to the femur. It provides 86% of the resistance to anterior translation.3 The ACL also serves as a secondary stabilizer to varus, valgus, and rotational stresses about the knee.4 The most reliable and sensitive test for assessing ACL deficiency is the Lachman test (Fig. 46-2). To perform the test, the examiner stabilizes the femur with one hand and performs an anterior drawer with the other hand on the tibia. The knee is held in 20 to 30 degrees of flexion with neutral rotation. The Lachman test measures laxity, and the examiner should appreciate the quality of an endpoint. Any increased translation is a positive result and is graded I, II, and III. A grade I is 0 to 5 mm of translation. A grade II is 6 to 10 mm, and a grade III is greater than 10 mm and lacks a firm endpoint. In multiple-ligament injured knees, this test is more difficult to perform. For example, PCLdeficient knees can mislead the examiner because of the abnormal translation. Also, a complete MCL disruption can give a false-positive result on the Lachman test if care is not taken to perform the test in neutral rotation. This results from the anteromedial rotational instability secondary to MCL disruption. The ACL does more than just prevent anterior translation of the tibia on the femur. It also serves as the principal restraint to anterolateral rotatory instability. Tests that are designed to examine this elicit the pivot-shift phenomenon. These tests include Slocum’s anterior rotatory drawer test, the HughstonLosee jerk test, and the MacIntosh lateral pivot shift test. All these tests are performed with a valgus force during flexion and extension of the knee to elicit subluxation or reduction of the tibia on the femur. In an ACL-deficient knee, as the knee goes from flexion to extension, the iliotibial band is anterior to the center of rotation of the knee and subluxates the tibia anteriorly. The tibia is reduced as the knee goes back into flexion. These tests are difficult to perform in the acute setting because of pain and guarding.

EXAMINATION OF SPECIFIC LIGAMENTS In the acute setting, swelling and pain often prevent a detailed ligament examination. However, the best possible assessment should be obtained. Gross instability to varus or valgus testing in extension suggests injury to one or both cruciate ligaments, the joint capsule, and the associated collateral ligament. If the joint capsule has been disrupted, there may not be an effusion. Flexion is often not possible because of pain. This precludes anterior and posterior drawer testing. The information obtained from the physical examination should be correlated with the history and mechanism of injury. The four main ligamentous structures include the ACL, posterior cruciate ligament (PCL), medial collateral ligament (MCL) with the posteromedial capsule, and the posterolateral corner (PLC). The PLC is composed of the lateral collateral ligament, popliteus tendon, popliteofibular ligament, arcuate ligament, fabellofibular ligament, and the posterolateral joint

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Figure 46-2 Lachman test for anterior cruciate ligament laxity. The left hand stabilizes the femur with the knee in 30 degrees of flexion. The left hand applies an anterior load and the amount of anterior translation of the tibia in relation to the femur is assessed.

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The flexion rotation test combines elements of the Lachman and the pivot-shift tests. The patient is supine with the knee in neutral rotation. The leg is lifted up and the tibia subluxates anteriorly with the femur posteriorly and externally rotated. The knee is then flexed with a valgus stress and anterior force on the proximal tibia. This results in the tibia moving posteriorly as the femur internally rotates, which reduces the tibia.5 The examiner should become proficient in the Lachman test and at least one of the pivot-shift tests.

Posterior Cruciate Ligament Injuries to the PCL are sometimes subtle, and careful attention should be paid to a complete knee ligament examination. The PCL serves as the primary restraint to posterior translation of the tibia.3 The physical examination of the PCL includes the posterior drawer test, posterior sag sign, and quadriceps active test. The most sensitive test is the posterior drawer test (Fig. 46-3). The posterior drawer test is performed with the knee in 90 degrees of flexion. The examiner’s thumbs are placed on the joint line and a posterior drawer is applied. The anterior tibiofemoral step-off is important to note when performing this test. Normal step-off is 8 to 10 mm (tibia anterior to the femur with the knee flexed 90 degrees). This test is graded according to the amount of translation with a posteriorly directed force. A positive test has increased translation. With a grade I, the tibia remains anterior to the femoral condyles. A grade II results in the tibia being equal to the femoral condyles, and with a grade III, the tibia can be subluxated posterior to the femoral condyles and lacks a firm endpoint. Grade III laxity on the posterior drawer test is suggestive of a clinically significant injury and usually involves injury to the secondary restraints as well.

Medial Collateral Ligament The MCL is the primary restraint to a valgus knee stress at 20 to 30 degrees of flexion. It is also a secondary restraint to ante-

Figure 46-4 Valgus stress to right knee in full extension. The knee opened up in full extension, which signifies significant injury to the medial collateral ligament and posteromedial capsule.

rior translation. Testing is performed by applying a valgus stress at 20 to 30 degrees flexion. This test is graded according to the amount of joint line opening in millimeters and the presence of an endpoint. Grade I is less than 5 mm of opening, grade II is 6 to 10 mm, and a grade III is greater than 10 mm. The knee is also tested in full extension. Opening to valgus testing in full extension implies damage to the posteromedial capsule in addition to the superficial medial collateral ligament6 (Fig. 46-4). The posteromedial capsule is part of the deep MCL and may need to be repaired or reconstructed in some cases. For patients with medial collateral ligament injuries, it is important to document the precise location of the tenderness. This can help differentiate the location and severity of the injury. Although most medial collateral ligaments may do well with nonoperative treatment, a subset of MCL injuries with complete disruption off the tibia may have an indication for a direct anatomic repair. Patients with a complete disruption of the MCL off the tibia have been shown to have tenderness over the tibia as opposed to the femoral side of the MCL.7

Posterolateral Corner

Figure 46-3 Posterior drawer test. The knee is placed in 90 degrees of flexion. A posterior force is applied to the femur. The amount of posterior displacement is assessed.

The posterolateral corner resists varus and rotational forces to the knee. The anatomic structures of the PLC can be divided into three layers. Layer 1 is composed of the iliotibial band and the biceps femoris tendon. Layer 2 consists of the lateral retinaculum and lateral patellofemoral ligaments. Layer 3 is the deepest and contains the lateral collateral ligament or fibular collateral ligament, the fabellofibular ligament, the popliteus, the arcuate complex, and the important popliteofibular ligament. Testing of the PLC consists of varus stress to the knee at 0 and 30 degrees. Increased external rotation of the tibia at 30 and 90 degrees is tested and compared to the contralateral knee. Increased external rotation at 30 degrees that decreases at 90 degrees suggests an isolated injury of the posterolateral corner. If the external rotation does not decrease at 90 degrees, then

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there may also be an injury to the PCL. Other tests include the posterolateral drawer test, external rotation drawer test (dial test), and reverse pivot-shift test. The posterolateral drawer test is performed with an anterior drawer at 90 degrees of knee flexion. If the posterolateral structures are torn, then the knee will have increased translation with internal rotation as compared to neutral rotation. The dial test is performed with the hips and knees flexed. Both lower extremities are evaluated by externally rotating the feet of the patient. Increased external rotation signifies injury of the posterolateral complex. A variant of this test is the external rotation recurvatum test. In this test, the examiner holds both feet by the toes and if the relaxed knee falls into recurvatum, it is a positive test result. The reverse pivot-shift test begins with the knee flexed and the tibia externally rotated. The knee is then passively extended, and when posterolateral laxity is present, a sudden shift will occur at 20 to 30 degrees of flexion as the posteriorly subluxated lateral side of the tibia abruptly reduces. Increased opening to varus stress at 30 degrees without opening at 0 degrees or other signs of a PLC injury suggests an isolated tear of the fibular collateral ligament.8 Failure to diagnose and treat an injury of the posterolateral corner of the knee in a patient who has a tear of the ACL or PCL can result in failure of the reconstructed ligament.

PATELLOFEMORAL EXAMINATION The patellofemoral joint has many examination tests specific to evaluate for patellofemoral disorders. The tracking of the patella as the knee goes from a flexed to an extended position may take the form of an upside down letter J. The positive J sign suggests a tight lateral retinaculum. As previously described, the quadriceps angle or Q angle should be measured along with the lower extremity alignment. The examiner should also assess for crepitus, patellar apprehension, and specific areas of tenderness. A maneuver has been described that can detect patella instability, with the knee flexed 30 degrees and applying a distal lateral force. Increased patellar translation with a softer endpoint compared with a normal contralateral knee may suggest disruption of the medial patellofemoral ligament.9

dislocations present with obvious deformity, most multipleligament knee injuries spontaneously reduce. One must have a high index of suspicion for these injuries. The patient’s history provides essential information regarding the mechanism of injury and potential associated injuries. The direction of the force to the knee and the position of the leg are important variables. Contact versus noncontact injury is worth documenting. A high-energy motor vehicle accident is important to differentiate from a sports-related dislocation because of the greater incidence of severe soft-tissue injury and associated injuries.11,12 Vascular injuries, open dislocations, irreducible dislocations, and compartment syndromes require prompt diagnosis and immediate treatment. Open dislocations must be reduced with subsequent irrigation and débridement in the operating room and be treated with intravenous antibiotics for 48 hours. Softtissue wounds should be evaluated for problems with closure because plastic surgery consultation is sometimes necessary. Posterolateral knee dislocations may present as an irreducible dislocation (Fig. 46-5). The medial femoral condyle may become buttonholed through the medial retinaculum and present with the dimple sign.13 This particular type of dislocation may require open reduction. Prolonged dislocation in this position has been associated with skin necrosis. Compartment syndrome must always be ruled out and emergent fasciotomies are required when this condition exists or is impending. A detailed neurovascular examination follows the visual inspection. The initial assessment of a multiligamentous knee injury must include a thorough and expedient physical examination with particular attention directed to the vascularity of the extremity. Vascular injuries should be ruled out immediately. Vascular injuries can occur with all types of dislocations. The risk of arte-

MENISCUS EXAMINATION There are many different tests used to assess for meniscus tears. The most sensitive test is joint line tenderness.10 Other tests attempt to produce the symptoms of a torn meniscus such as McMurray’s test, Apley’s grind test, and others. McMurray’s test is performed with passive motion from flexion to extension with internal and external rotation. A palpable click on the joint line is a positive test. Apley’s grind test is performed with the patient prone and the knee flexed 90 degrees. Compression of the tibiofemoral joint will elicit pain, whereas distraction of the joint will cause diminished pain in a positive result of the Apley test. A bucket handle tear that is displaced may present with true locking of the knee. True locking of the knee is the inability of the patient to be able to fully extend the knee because of a mechanical block.

EXAMINATION OF MULTILIGAMENTOUS KNEE INJURIES The initial diagnosis of a knee dislocation or multiple-ligament knee injury is an orthopedic emergency. Although some knee

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Figure 46-5 “Dimple sign” on the medial side of a right knee with an irreducible posterolateral knee dislocation.

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rial injury with a knee dislocation is between 10% and 64%.14 Green and Allen15 reported rupture of the artery to be as high as 44% with posterior dislocations. Anterior dislocations are associated with arterial injury in as many as 39%, and the incidence with medial is reported at 25% and lateral at 6%. The dorsalis pedis and posterior tibialis pulses should both be palpated. Never assume that a decreased pulse is normal and the result of spasm. Ankle brachial indices are assessed and a decrease of 0.15 or greater indicates a significant vascular injury.16 The importance of early recognition of vascular injury cannot be overstated because a missed or delayed diagnosis may result in a below-knee amputation if the leg is not reperfused within 6 to 8 hours. All patients with a normal vascular examination must have serial pulse examinations or undergo arteriography because intimal tears may be present. Intimal tears of the artery may present in a delayed fashion and are more difficult to diagnose. The initial physical examination may be completely normal in a knee with an intimal tear. Intimal tears can lead to a gradual thrombosis, which may propagate to complete arterial occlusion.

NERVE INJURIES The neurologic examination, particularly of the peroneal nerve, should be documented. The patient is asked to actively dorsiflex the foot and to activate the extensor hallucis longus tendon. These specific tests assess the peroneal nerve function. Sensation in all the nerve distributions, as well as motor function of the tibial nerve should be examined. The incidence of nerve injury with knee dislocation is between 16% and 40%.17–19 The peroneal nerve is most commonly injured, but injuries to the tibial nerve have occurred.20 Injuries to the lateral corner and PLC of the knee place the peroneal nerve at increased risk because of its superficial location as it curves around the fibular head. Posterior dislocations have a high incidence of nerve injuries. The prognosis of peroneal nerve injuries is poor. Complete nerve injuries only recover about 50% of the time. Nerve injuries are generally followed conservatively for 3 months. Of these injuries, about one third will recover, one third will have minor deficits, and one third will have a complete palsy.19 A detailed examination of the knee ligaments is performed on the ACL, PCL, MCL, and posterolateral anatomic structures. Initial and postreduction radiographs require thorough evaluation to assess for periarticular fractures, direction of dislocation, and adequacy of reduction. Magnetic resonance imaging will provide detailed information about the ligaments, bone or subchondral bone, menisci, and articular cartilage.21 The physical

Box 46-1 Pearls 1. In most cases, the history itself will lead the examiner to the correct diagnosis. 2. Always examine the uninjured knee for a comparison. 3. The Lachman test should be performed in neutral rotation. External rotation may cause a false-positive result in a knee with a medial collateral ligament injury. 4. Laxity of the knee joint with varus or valgus stress in full extension is a sign of a multiligamentous injury.

examination must be correlated with the magnetic resonance imaging findings for preoperative planning.

CONCLUSIONS The purpose of the physical examination is to obtain the correct diagnosis. A complete patient history must be combined with a thorough physical examination in order to direct treatment of the knee injury. Additional tests such as radiographs, magnetic resonance imaging, bone scans, and angiography are sometimes used to provide information in the evaluation of a knee injury. The initial diagnosis of a knee dislocation or multiple-ligament knee injury is an orthopedic emergency. A vascular injury must be assumed until it can be ruled out. After the vascular status has been addressed, radiographs followed by a magnetic resonance imaging scan should be obtained. A complete ligament examination will help correlate the magnetic resonance imaging findings, and a preoperative plan can be established (Boxes 461 and 46-2).

Box 46-2 Pitfalls 1. Failure to examine the hip and spine in conjunction with the knee can result in a misdiagnosis (e.g., knee pain in a young adolescent can be the result of a slipped capital femoral epiphysis at the hip). 2. Do not assume that all knee swelling is an effusion. 3. A missed posterolateral corner injury is a common cause of anterior cruciate ligament reconstruction failure.

REFERENCES 1. Feagin JA: Physical examination of the knee. In Garrett WE, Speer KP, Kirkendall DT (eds): Principles and Practice of Orthopaedic Sports Medicine. New York, Lippincott Williams & Wilkins, 2000, pp 613–622. 2. Kennedy J: Complete dislocation of the knee joint. J Bone Joint Surg Am 1963;45:889–904. 3. Butler DL, Noyes FR, Grood ES: Ligamentous restraints to anteriorposterior drawer in the human knee: A biomechanical study. J Bone Joint Surg (Am) 1980;62:259–270. 4. Wilson SA, Vigorta VJ, Scott WN: Anatomy. In Scott WN (ed): The Knee. St. Louis, Mosby, 1994, pp 15–54. 5. Fanelli GC, Maish DR: Knee ligament injuries: Epidemiology, mechanism, diagnosis, and natural history. In Fitzgerald RH, Kaufer H, Malkani AL (eds): Orthopaedics. St. Louis, Mosby, 2002, pp 619–636.

6. Tria AJ: Clinical examination of the knee. In Insall JN (ed): Surgery of the Knee. New York, Churchill Livingstone, 2001, pp 161–174. 7. Wilson TC, Satterfield WH, Johnson DL: Medial collateral ligament “tibial” injuries: Indication for acute repair. Orthopedics 2004;27: 389–393. 8. Covey DC: Injuries of the posterolateral corner of the knee. J Bone Joint Surg Am 2001;83:106–118. 9. Tanner SM, Garth WP, Soileau R, Lemons JE: A modified test for patellar instability: The biomechanical basis. Clin J Sport Med 2003;13:327–338. 10. Eren OT: The accuracy of joint line tenderness by physical examination in the diagnosis of meniscus tears. Arthroscopy 2003;19:850– 854.

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11. Wascher DC: High-velocity knee dislocation with vascular injury treatment principles. Clin Sports Med 2000;19:457–477. 12. Shelbourne KD, Porter DA, Clingman JA, et al: Low velocity knee dislocation. Orthop Rev 1991;20:995–1004. 13. Quinlan A: Irreducible posterolateral dislocation of the knee with button-holing of the medial femoral condyle. J Bone Joint Surg Am 1966;48:1619–1621. 14. Cole BJ, Harner CD: The multi-ligament injured knee. Clin Sports Med 1999;18:241–262. 15. Green NE, Allen BL: Vascular injuries associated with dislocation of the knee. J Bone Joint Surg Am 1977;59:236–239. 16. Kendall RW, Taylor DC, Salvain AJ, et al: The role of arteriography in assessing vascular injuries associated with dislocations of the knee. J Trauma 1993;35:875–878.

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17. Kennedy J: Complete dislocation of the knee joint. J Bone Joint Surg (Am) 1963;45:889–904. 18. Taft TW, Almenkinders LC: The dislocated knee. In Fu F (ed): Knee Surgery. Baltimore, Williams and Wilkins, 1994, pp 837–857. 19. Borden PS, Johnson DL: Initial assessment of the acute and chronic multiple-ligament injured knee. Sports Med Arthrosc Rev 2001;9: 178–184. 20. Welling R, Kakkasseril J, Cranley J: Complete dislocations of the knee with popliteal vascular injury. J Trauma 1981;21:450–453. 21. Wilson TC, Johnson DL: Initial evaluation of the multiple-ligament injured knee. Oper Tech Sports Med 2003;11:187–192.

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Principles of Knee Arthroscopy William P. Urban

INTRODUCTION • Knee arthroscopy is the most common procedure in orthopedic surgery. • Originally developed as a diagnostic tool, the ability to directly visualize anatomic structures within the knee joint allows surgeons to perform intra-articular surgery through minimal incisions. • While improvements in modern-day magnetic resonance imaging has decreased its usefulness as a diagnostic tool, advances in arthroscopic equipment and techniques have led to an increase in the number and complexity of arthroscopic procedures (Table 47-1). • Current indications include the treatment of meniscal pathology, articular lesions, loose or foreign bodies, cruciate ligament reconstruction, patella malalignment, and intra-articular fractures. More than 600,000 knee arthroscopies are performed annually.1

EQUIPMENT Knee arthroscopy requires the use of basic instrumentation for all procedures. The arthroscope is a small telescopic device that is used to visualize structures within the knee joint. While a 30degree arthroscope is typical, a 70-degree scope is sometimes used. The remainder of the video capture equipment includes a light source, camera head, and video system. Pictures can be saved as video or computer files or printed to paper depending on the equipment. A motorized shaver system and handheld instruments are the basic implements for performing surgery, although a wide array of equipment has been developed for specific procedures. Electrothermal devices or lasers should be considered an adjunct to the basic shaver and handheld instruments. Knee arthroscopy is performed in a fluid environment using saline. A fluid management system or infusion pump is used to maintain fluid in the joint, distend the capsule, and lavage blood or other fluids that may obscure visualization. Current systems allow the surgeon to maintain a selected intra-articular pressure and flow rate.

ANESTHESIA Arthroscopic surgery can be performed under local, regional, or general anesthesia. Factors to be considered include the length

of the procedure, tourniquet use, and postoperative pain control as well as patient and surgeon preference. Local anesthesia has become more popular with the increasing use of ambulatory surgery centers. Local anesthesia is typically used for simple cases with limited operative time. Local anesthesia is a poor choice for cases requiring additional portals or incisions. Since local anesthesia will be inadequate in 1% to 15% of cases,2 monitored anesthesia care can be used to provide supplemental sedation in order to increase patient acceptance. An intra-articular anesthetic with epinephrine should be injected 20 minutes before surgery3 to maximize analgesia and decrease bleeding. The skin and portals are injected prior to the incision. The use of a long-lasting anesthetic should be considered for postoperative pain control. When additional portals or incisions are used, and hemostasis using a tourniquet is desired, regional anesthesia should be considered. Regional anesthesia, such as spinal or epidural blocks using a combination of analgesics and fentanyl, also allows manipulation and stressing of the knee to improve visualization and access to intra-articular structures. Spinal and epidural regional blocks can also be used for postoperative pain control through the use of a long-acting anesthetic or patient-controlled analgesia. Peripheral nerve blocks can be used to increase analgesia in conjunction with local anesthesia, to decrease anesthesia requirements with general anesthetics, or as a method of postoperative pain control. General anesthesia is typically reserved for cases in which regional or local anesthesia would be inappropriate or contraindicated. Examples include long, complicated cases that require complete relaxation, cases involving infection or coagulopathy, and cases in which the patient is unable or unwilling to remain awake during surgery.

SURGICAL TECHNIQUE Preparation The surgical sight should be marked by the surgeon before leaving the holding area in compliance with current patient safety protocols.4 Patients are given preoperative antibiotics 20 minutes before surgery using a broad-spectrum antibiotic covering Staphylococcus and Streptococcus organisms. This protocol can be modified when specific antibiotic coverage is needed for a known or suspected organism. Before positioning, an examination under anesthesia is performed. This examination, when the patient is pain free and relaxed (if under general anesthesia), is used to corroborate preoperative planning, the office examination, and radiographic studies. The repetitive performance of an examination under anesthesia before all surgical cases to deduce subtle findings is also an important technique for the

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Table 47-1 Arthroscopic Procedure Lavage Removal of loose/foreign body Plica resection/débridement Synovectomy Chondroplasty Microfracture/abrasion arthroplasty Lysis of adhesions Lateral release/capsular imbrication

The foot of the table is dropped, and the operative leg is typically placed in an arthroscopic leg holder (Fig. 47-1). A leg holder allows the knee joint to be stressed and manipulated in order to help visualize the intra-articular compartments. Alternatively, a lateral post can be used to provide a valgus stress and the leg can be brought into a figure-four position to provide a varus stress. The nonoperative leg is placed in a leg holder to move it out of the way, allowing adequate access to the surgical extremity. With the increasing complexity of modern arthroscopic procedures resulting in increasing operative times, ensuring that the well-leg holder is appropriately padded to avoid abnormal pressure that could result in compartment syndrome or neurologic injury is critical.

Meniscectomy Meniscal repair Cruciate ligament reconstruction Arthroscopically assisted fracture open reduction/internal fixation Osteochondral autograft transplantation

beginning arthroscopist to hone his or her physical examination skills.

Positioning The patient is placed supine on a standard operating table with a tourniquet placed around the thigh. A wide, well-padded tourniquet should be used to decrease neurologic complications. The tourniquet should be kept as proximal as possible on the thigh to avoid the possibility of encroaching on the operative site. The decision to use a tourniquet is based on the operative procedure and surgeon’s preference. New fluid management systems and high-flow cannulas, which control knee pressure and flow, make the performance of basic arthroscopic procedures without a tourniquet possible. Studies have shown that the use of a tourniquet increases postoperative quadriceps inhibition,5 and the surgeon should weigh this against the benefits of using a tourniquet, primarily decreased bleeding, and faster operative time. Procedures requiring additional incisions and bony work should entail the use of a tourniquet. Regardless, a tourniquet is applied in case its unexpected use is necessitated.

Figure 47-1 Patient positioning for arthroscopy of the right knee.

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Landmarks Anatomic landmarks and incision sights should be clearly marked out before starting the case (Fig. 47-2). The use of standard landmarks that can be used consistently for most arthroscopic knee cases improves efficiency and prevents the need for determining new landmarks during unforeseen circumstances, after the knee has been distended and the anatomy altered. Standard landmarks should include the inferior pole of the patella, the medial and lateral edges of the patellar tendon, and the tibial tubercle. The medial and lateral joint line should also be marked in case posterior portals are required. The anterolateral and anteromedial portals are then marked. The anterolateral portal is created just below the level of the inferior pole of the patella, approximately 1 cm above the joint line. The incision is placed just lateral to the patellar tendon. While the center of the “soft spot” more laterally has been advocated, this position makes accessing the posterior notch and the posterior compartment difficult in patients with a large Q angle.

Figure 47-2 Standard landmarks include the inferior pole of the patella (inf), lateral joint line (lj), lateral portal (lp), medial joint line (mj), medial portal (mp), edges of the patella tendon (pt), and tibial tubercle (tt).

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The anteromedial portal is considered the working portal for arthroscopic surgery. This portal is approximately 5 mm lower than the lateral portal or 5 mm superior to the joint line. Again, the placement of this portal close to the patellar tendon allows access to the back of the notch and posterior compartments. Some fluid management systems require the use of a superomedial or superolateral portal. These portals are also used to remove loose/foreign bodies from the retinacular gutters or to provide direct access to the opposite side of the patellofemoral joint when a lateral release, capsular plication, or patellar microfracture is performed. The superolateral and superomedial patella portals are best created intraoperatively under direct visualization using a spinal needle for localization. Similarly, when access to the posterior compartment is required, the posterior portals are created intraoperatively using the previously marked joint lines and transillumination with the arthroscope. A transpatellar portal through the patella tendon has also been described, but because of concerns involving the violation of the extensor mechanism, it is rarely used. During the case, new portals can be easily created along the previously markedout joint line if specific structures need to be accessed. Using transillumination, the joint line is confirmed and then palpated under arthroscopic visualization. Once the best position is determined, a spinal needle is simply placed through the skin. If the surgeon is satisfied with the position, a small stab incision is created using a no. 11 blade. The use of additional portals is preferable to struggling with poor access during the surgery or causing iatrogenic injury by forcing the instruments.

Incision After the patient is positioned and prepped, the anterolateral portal is established. Using a no. 11 blade, a vertical incision directed into the notch is made through the skin large enough to accommodate the arthroscope. The incision is then carried down through the capsular tissue with the blade facing up to avoid accidentally cutting the meniscus. The capsule and underlying fat pad should be cut by dropping the hand, lowering the handle, and raising the cutting edge of the blade. This results in a funnel-shaped portal, wider in the joint than superficially. This geometry allows the scope to be more easily passed around the joint than with a simple stab incision (Fig. 47-3). The stab inci-

Figure 47-4 The ligamentum mucosum (arrow), viewed from above, obscures the cruciate ligaments.

sion results in a tunnel-shaped incision in which the fat pad and retinacular tissue can hinder movement of the scope or, if wide enough, allows fluid to leak out around the arthroscope. Care should be taken not to overextend the skin incision as this will lead to flow from the portal during the procedure. If this does occur, a surgical sponge is simply hung around the scope at the level of the incision to redirect the leaking fluid into the arthroscopy bag. Using a blunt obturator, the arthroscopic cannula is then inserted directly into the notch with the knee hanging in a flexed position. The scope should enter easily, and if resistance is encountered, the cannula should be removed and the capsular incision lengthened. The cannula is then passed behind the patellar tendon into the space anterior to the medial meniscus to ensure that it has completely passed through the fat pad and ligamentum mucosa, which attaches the fat pad to the intercondylar notch (Fig. 47-4). The knee is then brought into full extension, and the scope is directed under the patella into the suprapatellar pouch. The cannula should slip easily into the patellofemoral joint. If difficulty is encountered directing the scope superiorly, the capsular incision should be extended. The obturator is then removed, and the knee is copiously irrigated until clear in order to avoid delays caused by poor visualization. Only then is a 30-degree arthroscope inserted through the cannula. With the arthroscope inserted at a medial angle into the joint through the lateral portal, the lens should be directed laterally. The combined vectors result in a view, which is approximately straightforward (Fig. 47-5). This should be considered the standard arthroscopic position. Manipulation of the arthroscope around the joint requires smooth, mildly arcing motions because of the angle of the lens. Beginning arthroscopists mistakenly push or pull the scope straight back or forward when intending to move anteriorly or posteriorly in the knee joint.

Patellofemoral Compartment

Figure 47-3 A generous capsular incision facilitates manipulation of the arthroscope with the joint.

Once in the suprapatellar pouch, the patella and trochlea should be inspected for any changes. The location and degree of any articular cartilage damage should be consistently graded should the operative report need to be reviewed without access to the intraoperative pictures. The knee should be flexed 45 degrees

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Figure 47-7 A thick fibrous plica (thin arrow) and wear of the femoral condyle (arrowhead). Figure 47-5 Standard arthroscopic position with the 30-degree arthroscope in the lateral portal and the lens rotated laterally.

to visualize the capture of the patella into the trochlear grove (Fig. 47-6). Subluxation and tilt of the patella should be noted. While the importance of a patella that is not anatomically situated in the groove at 45 degrees of flexion during arthroscopy has been debated,6 the technique provides general information that should be considered in conjunction with the physical examination, radiographic studies, and clinical history. With the knee extended, the arthroscope should be directed superiorly and laterally into the lateral gutter, which is inspected for loose bodies or synovial plica. The lens should be rotated downward to visualize the gutter. The arthroscope is then directed medially into the medial gutter to visualize any loose

Figure 47-6 The patella is congruent in the trochlea at 45 degrees of flexion.

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bodies. As the knee is brought into flexion, the lens is rotated medially and inferiorly to check for plica and any resulting damage to the femoral condyle (Fig. 47-7). As the scope continues around the curve of the condyle, the meniscocapsular junction will come into view. At this point, a valgus stress is applied to open up the medial compartment, and the arthroscope is directed into the medial compartment.

Medial Compartment With the arthroscope in the standard position, the medial compartment is assessed for chondral and meniscal pathology (Fig. 47-8). The posterior horn should be visible, and the lens is then rotated downward to view the anterior horn as it runs off the

Figure 47-8 View of the medial compartment.

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anterior tibial plateau. With the lens again facing laterally, the arthroscope is directed into the intercondylar notch.

Intercondylar Notch Unless obscured by the ligamentum mucosum, the anterior cruciate ligament should be visible. If the ligamentum mucosum prevents the scope from being directed laterally, the tip of the arthroscope should be brought superiorly, tracing the outline of the notch. The scope is then directed downward along the lateral margin, posterior to the fat pad, to visualize the cruciate ligaments. If the ligamentum remains a hindrance, a medial portal should be established and the ligamentum resected with a shaver. A no. 11 blade is used to create a stab incision at the previously marked location. The blade can be visualized with the arthroscope as it is directed into the notch. The blade is removed, and the blunt obturator is inserted through the portal into the notch. After the anterior cruciate ligament is visualized, a probe should be inserted into the medial portal (Fig. 47-9). The tension on the anterior cruciate ligament should be assessed with a probe, and it should be visualized as an anterior drawer is performed. The posterior cruciate ligament in most knees will not be visualized, but its synovial covering is apparent. The arthroscope is then brought to the anterior medial corner of the lateral plateau with the knee in flexion. With the arthroscope held in this location, a varus stress is created by bringing the leg into a figure-four position. As the compartment is distracted, the arthroscope is directed into the lateral compartment.

Lateral Compartment The articular cartilage and the meniscus are assessed and noted (Fig. 47-10). The lens should be rotated in order to give a complete view of the meniscus starting with the posterior horn. As the meniscus is examined, the popliteus tendon should be visible as it travels through the hiatus in the posterior horn of the lateral meniscus. As the lens is rotated downward and then medially around the anterior periphery, the anterior horn is visualized anterior to the lateral tibial spine, which separates it from the posterior horn.

Figure 47-9 A probe is used to test the competency of the anterior cruciate ligament.

Figure 47-10 A view of the lateral compartment as the arthroscope is inserted.

Posterior Compartment Occasionally, the posterior compartment must be inspected. In order to visualize the posterior compartment, the scope is brought anteriorly along the joint line of the medial compartment with the knee in flexion. The camera is removed and replaced with the blunt obturator. The cannula is swept laterally across the anterior joint line by moving the base of the scope medially. The tip of the cannula remains in contact with the joint line until it falls into the notch. Remaining in contact with the lateral aspect of the medial condyle, the arthroscope is advanced posteromedially. As it is directed between the anterior cruciate ligament and the lateral aspect of the medial femoral condyle, tension will be felt as it passes the posterior cruciate ligament. As this occurs, the handle of the cannula is raised and it is advanced posteriorly and inferiorly. A sudden release in tension is felt as the obturator passes the posterior cruciate ligament and enters the compartment. The obturator is then removed and the 30-degree scope is reinserted. In order to visualize the posterior aspect of the posterior horn of the medial meniscus and the posterior joint line, a 70-degree arthroscope should be introduced. The wedging of the arthroscope between the wall of the notch and the cruciate ligaments makes moving the arthroscope difficult. The compartment is visualized by rotating the 70-degree lens. The reverse techniques can be used to reposition the scope into the lateral notch, viewing the posterior aspect of the lateral joint. In certain cases, such as posterior cruciate ligament reconstruction, a posterior working portal is necessary. The posteromedial portal places the saphenous nerve at risk, while the posterolateral portal places the peroneal nerve at risk. To avoid possible neurovascular complications, the arthroscope in the posterior compartment is used to transilluminate the posterior joint line. Palpation is used to verify the placement, and a spinal needle is inserted into the joint under arthroscopic visualization. A superficial skin incision is then created, and the tissues are bluntly dissected down to the capsule using a clamp. The capsule is then incised, and a cannula is placed into the joint to avoid having to reestablish the portal every time an instrument is removed.

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Treatment During diagnostic arthroscopy, a probe should be used through the medial portal to test the stability and consistency of any abnormal structures. As pathology is encountered, it should be addressed using instruments through the working portals. Inserting an appropriate arthroscopic grasper through the medial portal can be used to perform the simple removal of loose or foreign bodies. If there is difficulty holding the fragment, a spinal needle inserted into the knee joint through the capsule can pin the fragment in place to allow the surgeon to grasp it without the fragment slipping away. Objects located in the gutters, suprapatellar pouch, or posterior compartment may require the use of the superior patellar or posterior portals. Soft-tissue pathology requiring resection can usually be accomplished using an arthroscopic biter or the motorized shaver. Shavers are usually available in 3.5-, 4.5-, or 5.5-mm diameters. Care should be taken to avoid using a large shaver in a small space where it will damage normal structures. The shaver blade rotates forward or reverse or oscillates based on the settings. The speed can also be controlled, with higher speeds being used to resect bone. Typically, for plica resection or arthroscopic meniscectomy, a full radius shaver is used. Other shavers can be used based on the surgeon’s preference and experience. Soft-tissue resection should be performed with the shaver on oscillate. Suction is used to draw the tissue into the shaver. Bony resection is commonly performed with the shaver on forward or reverse rather than oscillate. While a full-radius shaver can be used, depending on the size of the resection and bone quality, burrs and specialized bone shavers are sometimes utilized.

CLOSURE After the procedure is completed, the knee should be irrigated and drained of fluid. The skin portals may be closed with subcutaneous or simple sutures, although some surgeons opt to use Steri-Strips or leave the portals open. For basic arthroscopy, a sterile dressing should be applied that will not interfere with motion of the knee. If cryotherapy is used for postoperative pain control, the thickness of the dressing should be kept to a minimum. Cryotherapy can decrease pain, improve patient satisfaction, and decrease narcotic requirements.7 Postoperative pain control can also be improved using a combination of analgesics or narcotics as an intra-articular injection.8 The use of peripheral nerve blocks has also been advocated.

COMPLICATIONS Due to the use of limited incisions, short operative times, and the relative lack of neurovascular structures in proximity to the standard portals, surgical complications are uncommon,9 especially after basic arthroscopic procedures. The unexpected nature of these complications makes their occurrence more problematic (Table 47-2). Since complications are rare, their presence may be overlooked and a diagnosis may not be made in an expeditious fashion. It is important to remain vigilant after all cases, especially after complex arthroscopic procedures where the use of additional incisions and increased operative time makes them more common. Intraoperatively, iatrogenic cartilaginous and soft-tissue injuries can arise from trying to maneuver instruments in tight spaces. Appropriately sized instruments should always be used, especially in tight spaces, and constant visualization of the instruments is critical. Neurovascular injuries are uncommon but have been reported even after simple arthroscopy. While the incidence of neurovascular injuries would be expected to increase as the complexity of the case increases and posterior portals are used, popliteal artery occlusion and pseudoaneurysm have been described after arthroscopic meniscectomy.10 During meniscal repairs or simple cruciate ligament reconstructions in which instruments are used to pass sutures or wires posteriorly, visualization is more difficult, and neurovascular structures in closer proximity are more dangerous. Using a methodologic approach throughout the procedure, having a thorough understanding of the anatomy, and using direct visualization whenever possible will decrease these complications. Compressive neurologic injuries caused by positioning, the leg holder, and tourniquet have also been reported.11 Neurovascular injury to the nonoperative leg is possible during prolonged surgical times associated with advanced arthroscopic cases. Care should be taken to ensure that areas in contact with superficial neurovascular structures are padded. A neurovascular examination should be performed immediately postoperatively after all cases and any indication that a problem exists should be immediately investigated. Postoperative complications after arthroscopic surgery include deep vein thrombosis, compartment syndrome, and infection. The short operative time, small incisions, and use of lavage fluid make infection after arthroscopic surgery extremely uncommon. Hemarthrosis after soft-tissue procedures (e.g., lateral release, synovectomy) and drilling bone (e.g., in anterior

REHABILITATION Postoperative pain management using a multimodal approach with opioids and nonsteroidal anti-inflammatory drugs in conjunction with local anesthetics or analgesics will facilitate rehabilitation after knee arthroscopy. Early rehabilitation after basic arthroscopy should focus on decreasing the patient’s postoperative effusion, reversing quadriceps inhibition, and preventing stiffness. Typical postoperative rehabilitation regimens include quadriceps exercises, range of motion, local modalities, and cryotherapy. As inflammation and pain decrease, therapy should advance to incorporate strengthening regimens, endurance exercises, and proprioceptive training followed by functional rehabilitation programs and plyometrics.

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Table 47-2 Complications Intraoperative Anesthesia Neurovascular injury Iatrogenic cartilage or ligament injury Compartment syndrome Hardware/equipment failure Postoperative Deep venous thrombosis Pulmonary embolus Infection Hemarthrosis

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cruciate ligament reconstruction) can lead to increased pain and swelling, inhibiting postoperative rehabilitation. The ambulatory nature of most arthroscopic procedures should decrease the rate of deep vein thrombosis, but it is important for the surgeon to have a high level of suspicion, as the incidence of deep vein thrombosis may be higher than expected.12 When the postoperative course is complicated by unexpected swelling and pain, deep vein thrombosis should be suspected and a vascular study should be performed. Compartment syndromes can occur in the operative or nonoperative leg. Compartment syndrome of the operative leg can be caused by overdistending the joint with the infusion pump.13 The risk is greater during arthroscopically assisted treatment of fractures, where the integrity of the joint has been disrupted, or after a knee dislocation in which the posterior capsule is torn and fluid escapes into the leg. Diagnosis can be complicated by the use of regional anesthesia. Care should be taken to ensure

that the proper pressure and flow are maintained in the knee. Compartment syndrome of the nonoperative leg is a devastating complication if undiagnosed. Recognition of this complication and treatment with emergent fasciotomies are essential.

CONCLUSIONS Arthroscopic surgery is a well-established, well-excepted method of addressing intra-articular pathologic conditions of the knee. The use of arthroscopic surgery to perform increasingly more complex procedures has been a natural progression as our techniques and equipment have improved. The use of arthroscopic techniques has led to improved visualization of pathologic structures, decreased postoperative pain, decreased soft-tissue trauma, decreased complications, faster rehabilitation, and decreased hospital costs.

REFERENCES 1. Rutkow IM: Surgical operations in the United States. Then (1983) and now (1994). Arch Surg 1997;132:983–990. 2. Horlocker TT, Hebl JR: Anesthesia for outpatient knee arthroscopy: Is there an optimal technique? Regional Anesth Pain Med 2003;28: 58–63. 3. Hultin J, Hamberg P, Stenstrom A: Knee arthroscopy using local anesthesia. Arthroscopy 1992;8:239–241. 4. Wong DA: Surgical site marking comes of age. AAOS Bull 2004; 52:30. 5. Saunders KC, Louis DL, Weingarden SI, et al: Effect of tourniquet time on postoperative quadriceps function. Clin Orthop 1979;143: 194–199. 6. Sojbjerg JO, Lauritzen J, Hvid I, et al: Arthroscopic determination of patellofemoral malalignment. Clin Orthop 1987;215:243–247. 7. Lessard LA, Scudds RA, Amendola A, et al: The efficacy of cryotherapy following arthroscopic knee surgery. J Orthop Sports Phys Ther 1997;26:14–22.

8. Goodwin RC, Amjadi F, Parker RD: Short-term analgesic effects of intra-articular injections after knee arthroscopy. Arthroscopy 2005;21: 307–312. 9. Small NC: Complications in arthroscopic surgery of the knee and shoulder. Orthopedics 1993;16:985–988. 10. Kiss H, Drekonja T, Grethen C, et al: Postoperative aneurysm of the popliteal artery after arthroscopic meniscectomy. Arthroscopy 2001;17: 203–205. 11. Kieser C: A review of the complications of arthroscopic knee surgery. Arthroscopy 1992;8:79–83. 12. Michot M, Conen D, Holtz D, et al: Prevention of deep-vein thrombosis in ambulatory arthroscopic knee surgery: A randomized trial of prophylaxis with low–molecular weight heparin. Arthroscopy 2002;18: 257–263. 13. Bomberg BC, Hurley PE, Clark CA, et al: Complications associated with the use of an infusion pump during knee arthroscopy. Arthroscopy 1992;8:224–228.

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48

Meniscal Injury John C. Richmond and Ivan Encalada-Diaz

In This Chapter Classification Nonoperative management Surgery Partial menisectomy Meniscal repair

INTRODUCTION • The mechanisms of meniscal damage are myriad and include twisting and rotational noncontact injuries, often associated with ligament injuries. • Medial meniscus injury is more common than lateral. • Meniscal injuries may be difficult to diagnose since symptoms and physical findings are often nonspecific. • Nonoperative treatment is often appropriate for less active patients and for those patients with minor symptoms. • The tenet of surgical treatment is to preserve as much functioning meniscal tissue as possible through repair or minimal meniscectomy.

CLINICAL FEATURES AND EVALUATION Meniscal injuries are a common source of knee pain, disability, limitation of function, and interference with athletic and recreational pursuits.1 The most frequent mechanism is a noncontact injury resulting from deceleration or acceleration coupled with the athlete changing direction; they also may occur from a contact stress or, in the older athlete, from a degenerative process with little or no trauma. In running/cutting sports, such as soccer and football, meniscal tears can occur with cutting maneuvers. In sports involving jumping, such as basketball and volleyball, the angular momentum coupled with femoral tibial rotation that occurs with landing can cause a meniscal tear. Meniscal injuries also can result from events with a violent varus, valgus, or hyperextension force coupled with femoral tibial rotation. One of the more common events leading to meniscal tearing is an anterior cruciate ligament (ACL) tear or a buckling event from ACL insufficiency The most frequent symptoms of a meniscal tear are pain, swelling, giving way, and locking.1 The onset of pain is often immediate and localized to either the medial or lateral side of the knee. Because of concomitant collateral ligament sprains, the

pain may not be confined to the joint line. With degenerative tears, the onset of pain and swelling may be gradual and is frequently delayed until the next day. Patients with traumatic tears usually can ambulate after an acute injury and frequently may be able to continue to participate in athletics. In some cases, large unstable fragments of meniscal tissue can become incarcerated in the intercondylar notch, leading to a “locked knee” (Fig. 48-1). More commonly, the symptoms are localized pain, with swelling and mechanical symptoms: catching, clicking, or buckling. It is theorized that displaced or nondisplaced tears alter meniscal mobility with resultant traction on the richly innervated capsule and synovium, resulting in knee pain; this pain is localized to the medial or lateral joint line, particularly with twisting or squatting activities. A torn meniscus also can alter the instant center of rotation of the knee, changing the contact area, to cause mechanical symptoms; this may lead to secondary articular cartilage lesions.2 The extent and timing of the effusion relating to a meniscal tear are variable. Young patients who have traumatic tears that disrupt the peripheral blood supply typically present with an early, large effusion or hemarthrosis. In degenerative tears or tears that involve the avascular central body of the meniscus, effusions are typically delayed in onset following the tear and exceedingly variable in size. Sometimes motion is limited by the feeling of tightness in the knee secondary to the effusion. Softtissue swelling should be distinguished from a true effusion of the knee by the finding of either a fluid wave or ballottable patella. Effusions that occur within hours of the injury are due to bleeding within the joint and often indicate rupture of the ACL or an osteochondral fracture. Although the typical effusion following the meniscal lesion develops gradually over 12 to 24 hours or more, a tear at the vascular periphery of the meniscus may cause an acute hemarthrosis. Degenerative meniscal tears are being encountered with increasing frequency as more people over 40 years old are becoming or staying active in sports activities. Older patients with a degenerative tear may have a history of minimal or no trauma, but the diagnosis should be suspected in an older individual with a history of pain, effusions, or mechanical knee symptoms. In this older population, it is difficult to separate the symptoms of meniscal injury from articular surface damage. Meniscal tears in young patients are most commonly longitudinal (vertical) tears that result from acute flexion or rotational injury. By contrast, degenerative tears are frequently complex, showing both radial and horizontal cleavage components (Fig. 48-2). The diagnosis of a meniscal tear can be made by history, physical examination, and appropriate diagnostic tests. The most common finding on physical examination is tenderness over the

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Figure 48-1 Medial meniscus bucket-handle tear locked in the notch of this right knee.

medial or lateral joint line. Knee motion may be limited secondary to pain or an effusion. More than 20 meniscal tests have been described to diagnose meniscal tears; joint line tenderness and McMurray and Apley tests are the most commonly used.1 During provocative testing, forced flexion and circumduction (internal and external rotation of the foot) frequently elicit pain on the side of the knee with the meniscal tear. Putting together a thorough history and physical examination with plain radiographs, the overall clinical evaluation had sensitivity of 95%, specificity of 72%, and positive predictive value of 85% for the medial meniscus tears and sensitivity of 88%, specificity of 92%, and positive predictive value of 58% for lateral meniscus tears.3 Plain radiographs should include posteroanterior weight-bearing views at 45 degrees of flexion with the x-ray beam angled 10 degrees caudad, so-called Rosenberg views, to evaluate not only

Figure 48-2 Complex degenerative tear of the medial meniscus.

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Figure 48-3 Magnetic resonance imaging demonstrating a horizontal tear of the posterior horn of the medial meniscus.

potential bony pathology, but also to assess the tibiofemoral joint spaces.4 Magnetic resonance imaging is the best noninvasive diagnostic tool to assess the menisci, having the potential of analysis in multiple planes and the capacity to evaluate other structures in the knee. The accuracy of magnetic resonance imaging in assessing the menisci is now believed to be 95% or better (Fig. 48-3).5 Its limitations are the relatively high cost and the potential of misinterpretation because of technical inadequacies of the study or variability in interpretation.

Relevant Anatomy Sutton6 first described the meniscus as “the functionless remnants of intra-articular leg muscles.” Clearly, this is not borne out by the significant long-term degenerative issues that result from meniscectomy. The menisci are semilunar-shaped fibrocartilaginous structures located at the periphery of the knee joint between the tibia and femoral surfaces. The anterior and posterior horns are directly attached to bone, and the periphery of the meniscus is attached to the adjacent capsule via the coronary ligaments, also called the meniscofemoral and meniscotibial ligaments. The medial meniscus is more C shaped and has a wider diameter than the lateral meniscus, which is more circular. In addition, the lateral meniscus is free of capsular attachment at the popliteal hiatus. The blood supply to the meniscus is via vessels from the perimeniscal capsular and synovial tissues; penetration into the meniscus is 10% to 30% of the width of the medial meniscus and 10% to 25% of the width of the lateral meniscus.7,8 The inner 66% to 75% of the meniscus is essentially avascular and receives nutrition through diffusion and mechanical pumping. Meniscal lesions are often classified by the location of the tear relative to the blood supply of the meniscus. The so-called “redred” tear has a functional blood supply on both the capsular and meniscal side of the lesion and therefore has the best potential for healing. The “red-white” tear has an active peripheral blood supply, whereas the central surface of the lesion is devoid of

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vessels. These lesions should have sufficient vascularity to heal by fibrovascular proliferation. The “white-white” tears, located centrally in the meniscus, are without blood supply and have a limited healing potential.

Treatment Options The appropriate treatment of meniscal injuries depends on understanding the basic science, the normal anatomy, and vascularity in order to determine the appropriateness of resection versus repair or nontreatment. Meniscal tears occur in virtually all age groups, and the nonoperative or operative approach to the problem must take into consideration factors such as patient age, activity level, associated injury of the knee, potential for soft tissue healing, and judicious and expeditious return to work, sports, and other recreational pursuits. Patients involved in athletics or work endeavors that place high demands on the knee will almost always require surgery to treat a significant meniscal tear; therefore nonsurgical treatment is rarely indicated in this population. For those patients with less strenuous lifestyles, meniscal tears may be treated symptomatically. Following acute injury, protected weight bearing, ice, nonsteroidal anti-inflammatory drugs, and activity modifications are used. The athlete should avoid athletic stresses temporarily and begin a comprehensive progressive resistance exercise program until the strength deficit is within 20% to 30% of the contralateral side.9 Resolution of the signs and symptoms suggestive of meniscal tear suggests a favorable response, and gradual resumption of preinjury activity is begun. Further evaluation is considered and offered if the patient remains symptomatic despite these nonoperative measures.

SURGERY Historically, the surgical treatment of meniscal tears has evolved from open total meniscectomy to arthroscopic partial meniscectomy and subsequently to meniscal repair via open, arthroscopically assisted, and finally all arthroscopic means. This evolution has taken place secondary to a better understanding of the function, vascularity, and healing potential of the menisci as well as clinical studies documenting the adverse effects of removing meniscal tissue.10–15 Arthroscopic treatment of meniscal injuries has become one of the most common orthopedic surgical procedures in the United States; in many centers, it constitutes 10% to 20% of all surgeries.1 Rarely is immediate surgical intervention necessary for the treatment of an isolated meniscal tear. A patient who presents with a locked knee should be operated on acutely to restore knee motion. In this situation, a displaced bucket-handle tear is usually present and should be addressed with early surgery, since a delay may result in secondary damage to the meniscus or the articular surface. When the history and examination of a young athlete suggest a meniscal tear, immediate surgery may be indicated. This is especially true if transient locking has occurred. In this situation, it is possible that recurrent catching or transient locking may cause further damage to the torn meniscus, rendering it more difficult or even impossible to repair. In addition, a delay of more than 8 weeks from the time of injury to repair may diminish the eventual healing rate.16,17 Magnetic resonance imaging has become the diagnostic modality of choice to confirm the presence of a meniscal tear and can be very helpful in assessing the potential for repair versus resection as the treatment of choice.5 In spite of our goal to retain meniscal tissue

through repair, more often than not partial meniscectomy is the most appropriate treatment.18,19

Partial Meniscectomy Arthroscopic partial meniscectomy is currently considered state of the art in most cases of meniscal tearing not suitable for repair. The principle is to remove the torn and unstable portions of the meniscus and to retain as much functioning meniscus as possible, while leaving a well-contoured, stable meniscal remnant.20 Metcalf et al21 have provided general guidelines that apply for arthroscopic meniscectomy (Table 48-1). Following these guidelines for most tears not amenable to repair will preserve functioning meniscal tissue and have a low probability of residual symptoms from the retained meniscal remnant. The meniscal tear should be defined and the extent of the tear palpated with a probe. Certain tears do not require treatment; these include partial-thickness tears, relatively asymptomatic degenerative tears, and stable tears, defined clinically as those tears with less than 3 to 5 mm of movement on arthroscopic probing and those longitudinal tears less than 1 cm in length.18 Horizontal tears less than 7 mm and radial tears less than 5 mm also do not require resection.20,22,23 In order to provide more detail, several types of tear configuration are used here to provide examples of the steps in arthroscopic meniscectomy. Vertical Longitudinal Tear This is commonly seen with chronic ACL injuries and certainly may be encountered in a stable knee. In general, a longitudinal tear needs to extend for at least two thirds the circumference of the meniscus in order to produce an unstable fragment that can lock into the joint. Bucket-handle tears are three times more common in the medial than in the lateral meniscus. In most instances, displaced tears should first be reduced with the probe prior to resection. Determination as to optimal treatment is made based on proximity to the vascular supply, quality of the unstable segment, and concomitant procedures (e.g., ACL reconstruction, which improves healing rates) prior to proceeding with partial meniscectomy (Fig. 48-4). The classic cut-andavulse technique begins with a nearly complete cut at the posterior axilla of the tear, leaving a small tissue bridge to serve as tether.18,24 This keeps the fragment from floating free and obscuring the view of the anterior cut. The anterior axilla of the tear is then identified and cut. This can be best performed with the cutting instrument in the ipsilateral portal for those tears that end in the posterior 60% of the meniscus. Bringing the

Table 48-1 General Guidelines for Arthroscopic Partial Meniscectomy21 1. Remove all mobile fragments of meniscus. 2. There should be no sudden changes in the contour of the rim of meniscus. 3. It is not necessary to obtain a perfectly smooth rim following partial meniscectomy. 4. Use a probe often. 5. Protect the meniscocapsular junction. 6. Use hand and motorized instruments alternatively. 7. Whenever unsure, leave more meniscus than less.

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tissue should be resected. It is not essential to remove all the meniscus involved in the cleavage tear; only the unstable tissue should be resected; any hypermobile portion off superior or inferior leaflets is trimmed. Oftentimes partial resection of the inner margin of the inferior leaflet back to the end of the horizontal cleavage is the easiest and most appropriate treatment. If the tissue is of good quality, the remaining leaflet may be left in place to provide a continuous meniscal rim; in this situation, care must be taken by probing of the intact side, looking for a dimpling effect when probe pressure is applied, indicating inadequate durability of the remnant, an indication for additional resection. If the meniscus requires a partial resection of the more intact leaf to prevent recurrent tearing and the cleavage plane is deep, then a partial resection of both the superior and inferior leaves should be performed, with removal of any unstable segments, while a small cleavage between them may be left (Fig. 48-5).

Meniscal Repair Figure 48-4 Medial meniscal tear, illustrating the most appropriate site to cut for removal.

cutting instrument in from the contralateral portal and visualizing from the ipsilateral site will facilitate balancing the remnant if the anterior axilla is in the anterior 40% of the meniscus. The free anterior edge is then grasped and the fragment is removed, avulsing the small posterior tether. Twisting of the grasper in a circular motion several times helps detach the remaining portion of the posterior horn. By this technique, the torn fragment is removed without leaving significant remnants behind. Loose edges can be smoothed with the motorized shaver.20 Radial Tear These tears are most commonly located in the mid one third of the lateral meniscus, although they are also not uncommon in the posterior horn of the medial meniscus. If longer than 5 mm, then removal of the potentially unstable meniscal tissue anterior and posterior to the radial component is best achieved with the use of a manual instrument from the contralateral portal for lateral tears. Tissue anterior and posterior to the radial tear is removed so that a smooth transition to the depth of the tear is achieved without abrupt changes in the meniscal contour. The partial meniscectomy should remove the anterior and posterior lips of the tears only as deeply as the apex tear extends. Then, the remnant should be contoured as previously described. For posterior medial tears, resection is best accomplished with ipsilateral instrumentation. A radial tear of less than 5 mm in length in the mid-portion of the lateral meniscus is often an incidental finding and typically does not cause symptoms. A tear of this size and configuration may judiciously be left untreated. Radial tears of the lateral meniscus in the mid and anterior thirds of the meniscus may lead to the formation of a parameniscal cyst, often times called cystic lateral meniscus. The cyst results from extrusion of joint fluid through the meniscus. Horizontal Cleavage Tear The usual cleavage plane is central or slightly inferior, leaving two distinct leaves of tissue. Often the superior and inferior surfaces of the meniscus are relatively well preserved, and the cleavage plane extends a variable distance into the meniscus. The extension of this plane determines how much meniscal

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Although many specific techniques for meniscal repair have been developed over the past two decades and new techniques continue to evolve, they can be classified into four types: three arthroscopic techniques, including inside-out, outside-in, and all-inside methods and open repair. One should regard a symptomatic, potentially reparable meniscal tear as the soft-tissue equivalent of an atrophic nonunion in bone. For any surgical treatment to be successful, the intervening soft tissue with limited biologic potential should be removed by rasping both the body of the meniscus and the peripheral rim. Additionally, improved healing can be induced by thoroughly rasping the parameniscal synovium on the meniscofemoral and meniscotibial regions to stimulate both the formation of a local clot and neovascularization or potentially considering the addition of an exogenous clot.16,25 No single study offers direct comparison of the four different techniques. In general, most authors have concluded that all techniques achieve comparable results.17,25–28 When considering meniscal repair, the surgeon must weigh the many factors that may affect its result29 (Table 48-2). These include the extent, type, chronicity, and location of the tear; the

Figure 48-5 Lateral meniscus following minimal partial meniscectomy, retaining torn but stable posterior horn.

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Table 48-2 Indications for Meniscal Repair Peripheral tear Longitudinal in orientation Young patient Within the red-red or red-white zone Stable or stabilizable knee

age of the patient; and the presence of associated injuries such as an ACL tear undergoing concomitant treatment. It is known that the success of a meniscal repair depends on adequate stability and coaptation of the tear site as well as the biologic healing capacity of the meniscus. The addition of an autologous clot to the repair site, when the repair is done without ACL reconstruction, also improves healing rates. This can be done by the traditional removal of venous blood and reinsertion of the clot to the repair site or potentially through microfracture in the intercondylar notch. The indications for meniscal repair are based on an understanding of meniscal function and biology based on both basic science and clinical research. Optimally, a reparable tear would be recent and traumatic, in a young patient, localized near the capsular margin, preferably a single longitudinal tear, and in a stable or to be stabilized knee. Relative contraindications to repair include tears with significant meniscal degeneration, localized in the middle or inner third of the meniscus; oblique, radial or complex tears; or a noncompliant patient. Outside-In Technique This technique is considered the most simple. The instrumentation used includes 18-gauge spinal needles, a probe, and a loop curet, which is beneficial for placing countertraction on the meniscus for needle penetration. The meniscus is visualized and palpated to determine the suitability for repairs on the basis of the previous criteria. The mobility of the tear is the assessed and the segments reduced; the potential for approximation is observed. Both sides of the tear are débrided. Special care must be taken if using the rasp for abrasion to avoid injury to the articular surface. The external entry site for the needle is located on the outside of the joint by finger palpation while visualizing inside the joint. The pressure of the surgeon’s finger will indent the capsule, which will be seen with the arthroscope and progressively moved to the anticipated site of insertion. Using this technique, the preferred site for needle placement is selected and the meniscus is impaled (Fig. 48-6). The needle should easily enter the joint and be visualized. A small skin incision is then made adjacent to the first needle and connecting with this needle. The needle must be free in the incision; this is confirmed by moving the hub of the needle to see that it is free of the skin. Next a hemostat is used to spread the small incision down to the capsule. This provides an opening for placement of the second needle; subsequent ligature can then be tied over the capsule and not the subcutaneous fat. This maneuver also moves small veins, cutaneous nerves, and tendons to the side of the portal. The second needle is passed through the skin opening and into the joint in such a position that subsequently inserted sutures will secure the meniscus (Fig. 48-7). Proper placement of both needles creates the route of suture placement through the tissues. This can be vertical, horizontal, or oblique. There are several techniques to accomplish transfer of the suture inside

Figure 48-6 Outside-in technique for repair of posterior horn, stabilizing the body with a ring curet.

the joint. In one, a loop of wire cable is passed through the needle from the outside to the inside. The wire loop is compressed during passage through the needle and is constructed to expand upon emergence into the joint; a free 2-0 monofilament nonabsorbable suture is placed through the second needle, passage of the suture through the loop is confirmed while watching inside the joint (Fig. 48-8), and the loop is pulled out of the joint, thereby completing the loop of suture through the tear. The needles are removed, and the suture is tied outside the capsule, while watching the repair via the arthroscope. Sequential tying of the sutures helps maintain the meniscus properly reduced for subsequent needle passage. These steps are repeated at approximately 4-mm intervals until the entire tear is stabilized as confirmed both by visualization and by probing. On the basis of this inspection, sutures are removed, replaced, or added. The repair should be mechanically stable and externally secured to the joint capsule.

Figure 48-7 Side-by-side spinal needle passage for outside-in technique.

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Figure 48-8 Retrieval of passed suture in outside-in technique.

Figure 48-9 Joint distractor for meniscal repair.

Inside-Out Technique The medial meniscus is repaired with the knee in relative extension (20 to 30 degrees of flexion), approximating the capsular tissues and meniscus to facilitate repair and avoid posterior capsular plication. The lateral meniscus, in contrast, should be repaired with the knee flexed at 50 to 70 degrees, allowing the peroneal nerve to drop back posteriorly. Posteromedial or posterolateral extracapsular exposure should be obtained to facilitate retrieval of needles as they pass through the capsule, while protecting the neurovascular structures.30 Medially a 3-cm incision is made posterior to the medial collateral ligament, centered at the joint line. The sartorius fascia and sartorial branch of the saphenous nerve are retracted posteriorly along with the gracilis and semitendinous tendons. The exposure is completed by placing a spoon-type retractor anterior to the medial gastrocnemius tendon. The lateral incision is made behind the posterior margin of the lateral collateral ligament, extending from the back of the iliotibial band to the biceps tendon. The dissection is done between the anterior border of the biceps and the posterior margin of the iliotibial band. Blunt dissection is completed between the arcuate complex and capsule anteriorly and the lateral gastrocnemius muscle posteriorly, and a protective retractor is placed between the muscle belly of the gastrocnemius and the capsule. It is important to remember that the peroneal nerve lies medial to the biceps and is not protected by retraction of the biceps alone. Rather, it is the gastrocnemius muscle and the retractor that protect the peroneal nerve. We often employ a joint distractor when the involved compartment is tight, and it is difficult to obtain adequate exposure to protect the articular surfaces through manual traction alone25 (Fig. 48-9). This is applied by inserting threaded pins 3 to 4 cm above and below the joint line into the femur and tibia through small stab incisions, as one would do in applying an external fixator. The distractor is progressively opened to take advantage of the stress relaxation of the collateral ligament (Fig. 48-10). Various single- and double-lumen cannula systems are available to pass the sutures arthroscopically across the tear from the inside out. The number and configuration of the sutures depend

on the type of tear and the clinical judgment of the surgeon. Typically, we recommend use of vertical mattress sutures due to improved coaptation and holding strength, placed at 3- to 4-mm intervals. Horizontal mattress sutures, although easier to place, have less holding strength. Sutures should be sequentially placed from both the upper and lower surfaces of the meniscus to oppose both margins of the tear. The sutures should be placed 3 to 4 mm from the margin of the tear to avoid cutting out of the sutures while also avoiding excess puckering of the meniscus. Care should be taken to avoid short tissue bridges between the arms of the mattress sutures. Posterior horn tears are repaired via the ipsilateral portal, while mid-third tears are often most easily performed from the contralateral portal while viewing from the portal ipsilateral to the tear. For far anterior tears (extending into the anterior third

Figure 48-10 Application of a joint distractor facilitates exposure for meniscal repairs in tight joints.

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Figure 48-11 Multiple vertical mattress sutures in a lateral meniscal tear.

of the meniscus), we revert to an outside-in technique for suture passage. Using the appropriate cannula, the flexible needle of a double-arm suture is advanced. The needle-cannula unit is then advanced to “harpoon” and subsequently reduce the unstable portion of the meniscus. The needle is then advanced across the tear into the stable rim. Posteriorly, the tip of the cannula should be directed away from the midline neurovascular structures. The needle is advanced 1 to 1.5 cm, until the assistant, viewing through the posterior exposure, visualizes and grasps the needle with a needle holder. The needle, with attached suture is then delivered out of the incision. The companion needle is then passed, repeating these steps in either a vertical, horizontal, or oblique configuration (Fig. 48-11). It is our preference to tie the sutures when retrieved to simplify suture management. Soft tissue should be cleared from the suture loops, which are then tied with the knee in the position noted previously for medial or lateral tears. Securing the sutures when retrieved also facilitates the alternating passage of sutures above and below the meniscus, since a suture on the superior surface, when tied, tends to lift the meniscus and improve exposure of the inferior surface. It is important to probe the meniscus after securing each suture to assess the stability and approximation of the repair. All-Inside Techniques The basic principle of these techniques is avoiding the need for another incision and is the most recently developed of the four methods. This was first reported by Morgan31 in 1991 and required a specialized set up, including the placement of a 70degree arthroscope through the notch into the posteromedial or posterolateral compartment of the knee, the creation of posteromedial or posterolateral working portals, and the use of curved cannulated suture-passing hooks as well as arthroscopic knot-tying techniques. This technique is technically demanding and has never seen widespread use. As biomaterial technology has improved, meniscal fixation devices have been developed that eliminate the need for additional incisions, leading to a simpler, safer procedure, with reduced risk of neurovascular

injury. In the United States, the U.S. Food and Drug Administration approved the use of the BionX meniscal arrow in 1996. Since then, many companies have been quick to follow the arrow with a series of new fixators. All fixators are not the same; these devices can be divided into headless or headed, cannulated or noncannulated, and rigid or suture based, often referred to as second-generation fixators. They are made of different materials with different properties including strength, stiffness, and degradation times. Pull-out strength of these devices has been studied in cadaveric bovine and human menisci; the strength of the fixators is less than that of the gold-standard vertical mattress suture.32–36 Most of the experience with these fixators has been with the first-generation implants, some headed and some headless. Experience has raised concerns about the increased potential with headed fixators to contact and damage the overlying femoral articular cartilage. For the all-inside techniques, we have moved to the exclusive use of suture-based implants like the Rapid Loc (DePuyMitek, Raynham, MA) and the FasT-Fix (Smith & Nephew, Andover, MA). This latest generation of meniscal repair devices has the advantage of the earlier all-inside implants, including easy intra-articular handling and short operating time, with superior biomechanical properties and the flexibility of suture material. The FasT-Fix device consists of two 5-mm polymer suture anchors connected via a nonabsorbable braided polyester suture with a pretied, sliding, self-locking knot. After the first anchor is inserted through the meniscal body and rim to be deployed outside the capsule, the insertion needle is removed from the meniscus, the second anchor is advanced, and the meniscus is again impaled a few millimeters away. The second anchor is then deployed and the inserter removed from the joint. The sliding, self-locking knot is then pushed down, fixing the meniscus in a reduced position (Fig. 48-12). As with traditional suturing methods, different sutures should be placed with 3 to 4 mm of separation. The Rapid Loc device consists of a polyactic acid (PLA) or PDS “backstop” soft-tissue anchor, a connecting suture (absorbable Panacryl or permanent Ethibond), and a PLA or poly-

Figure 48-12 Hybrid meniscal repair, with classic inside-out sutures posteriorly, with FasT-Fix (Smith & Nephew, Andover, MA) in the foreground.

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the healing collagen prior to cutting, jumping, or twisting sports. If an ACL reconstruction has been performed simultaneously, the basic ACL rehabilitation protocol is then followed with the additional restrictions noted previously. In isolated meniscal repairs isometric quadriceps and hamstring exercises are begun immediately. Progression varies with the individual, but once adequate strength is obtained along with full range of motion without pain or effusion, the athlete may begin jogging and halfspeed running, cycling, and swimming; this occurs at about 3 months. By 4 to 6 months, the athlete is usually ready to return to full activities.

CRITERIA FOR RETURN TO SPORTS There is no consensus on when an athlete is ready to return to competition following meniscal repair, but the ability to singleleg hop, demonstration of 80% strength of the contralateral quadriceps, and return to full, painless range of motion with no effusion are useful guidelines. The use of a brace is controversial; its main role is to aid in proprioception and comfort. Therefore, a neoprene or elastic knee sleeve provides adequate bracing. Figure 48-13 Lateral meniscal tear stabilized with a Rapid Loc (DePuyMitek, Raynham, MA) implant.

diaxone monofilament suture “top hat” with a pretied slidinglocking knot for meniscal apposition. After the soft-tissue anchor is deployed outside the capsule, the top hat is advanced along with the pretied knot to maintain reduction of the tear (Fig. 48-13). Care must be maintained to be sure that the entry site of the needle inserter is far enough from the free border of the meniscus (and hence close to the tear) to ensure adequate thickness of the meniscus to protect from having the top hat be proud and injure the femoral articular cartilage. This should be about 3 to 4 mm from the tear in most cases.

POSTOPERATIVE REHABILITATION For arthroscopic partial meniscectomy, weight bearing is allowed as tolerated, after any intra-articular local anesthesia has worn off. We encourage protected weight bearing with crutches until the patient can ambulate without a limp. Compression and cold therapy can be employed to minimize postoperative swelling. Range-of-motion and isometric quadriceps exercises can be started immediately. Within the first week isotonic, closed kinetic chain exercises are begun. Usually, the patient regains a full range of motion within the first 2 weeks. Once adequate strength is regained and there is little pain and swelling, the athlete may resume full activities. This is usually by 3 to 4 weeks after surgery for medial tears and 1 or 2 weeks longer for lateral tears. There is significant controversy on the postoperative rehabilitation following meniscal repair; the major controversies are in weight bearing, immobilization, and range of motion. Specific timing in the maturation of the meniscal healing process remains unclear. However, it is widely accepted that it is necessary to protect the meniscal repair during the early healing phase (4 to 6 weeks). It is our preference to limit flexion to 90 degrees and to only allow weight bearing in a brace locked in extension for the first 4 weeks after meniscal repair. The knee is protected from vigorous activity for 4 months to allow for maturation of

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RESULTS AND OUTCOMES Results of arthroscopic meniscal resection tend to deteriorate over time.10,12 In 1995, Jaureguito et al13 compared early and long-term follow-up of 47 patients who had undergone arthroscopic lateral partial meniscectomy for isolated tears. They noted that although 92% of patients had good to excellent results at the time of maximal improvement according to the Lysholm II score, only 62% of patients had good to excellent results at an average of 8 years; 85% were able to return to their preinjury level, but only 42% had maintained that activity level at the most recent follow-up. It appears that the results are somewhat dependent on the amount of meniscal tissue resected.11,37 Clinically, results are better after partial meniscectomy than total meniscectomy.10 The advantage of arthroscopic meniscectomy is the ability to identify specific tear patterns, which permits greater precision on resection of meniscal tissue compared with open techniques. Because neither open nor arthroscopic techniques leave normal meniscus, the results of both methods appear to deteriorate over time38; however, follow-up is longer for the open technique. Apart from the amount of meniscal tissue resection, other factors that influence the outcomes of meniscal resection are listed in Table 48-3. Probably most

Table 48-3 Factors Influencing Results of Meniscal Resection Articular degenerative changes Malalignment Type of meniscal tears Lateral versus medial meniscal tear Instability Age Gender

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significant are the degree of arthritic change, type of meniscal tear, limb alignment, ligament instability and lateral versus medial meniscectomy; less significant are patient age and gender.14 The long-term success (more than 2 years follow-up) of meniscal repair reported in the literature varies between 67% and 92%,16,19 depending on the type or location of the tear and the means of outcome measurement. Factors that have been documented to significantly influence success rates include rim width, ACL laxity and concomitant ACL reconstruction, tear length, whether the tear is acute or chronic, and whether the medial or lateral meniscus is involved. Cannon and Morgan30 documented a 90% success rate for tears with rim widths of less than 2 mm; this success rate decreased to 74% for tears with rim widths of 2 to 3.9 mm and to 50% for tears with rim widths of 4 to 5 mm. Concomitant ACL laxity is also an important factor in meniscal healing; DeHaven16 documented a 46% of failure rate for meniscal repairs in ACL-deficient knees; the success rate of meniscal repair has also been found higher when ACL reconstruction is performed at the same time. Other factors that were found to influence meniscal healing favorably were time from injury to surgery of less than 8 weeks, tear length less than 2.5 cm, and tear of the lateral meniscus. Factors that do not seem to affect the healing rates include age and repair technique. The ability of successfully healed menisci to remain healed over time can be judged by the results in long-term clinical studies; Eggli et al39 reported a 73% survival rate at 7.5-year follow-up of isolated repairs in ACL stable knees. DeHaven reported a 79% survival rate with a minimum of 10 years after repair.2,16,17 In the future, long-term studies are needed to fully evaluate these new all-inside implants in order to confirm better results of the meniscal repair.

COMPLICATIONS Complications in arthroscopic meniscectomy can be categorized into either errors of judgment or technique. Errors of judgment are poor clinical decisions that can affect the short- and longterm outcome. Technical errors are violations of standard operative procedures and include retained meniscal tissue, articular surface iatrogenic damage, and broken instruments. For the different meniscal repair techniques, the complications are divided into two groups: one group consists of general complications such as infection, deep venous thrombosis, arthrofibrosis, and complex regional pain syndrome and the other group is related to the specific technique or implant used for the repair such as nerve injuries, popliteal vessel injuries, synovitis, articular cartilage damage, implant migration, and extra-articular cyst formation.26,40–50

CONCLUSIONS • The goal of partial meniscectomy is to retain as much functional meniscal tissue as possible. • Meniscal tears with 3 mm or less of rim width can be repaired with a high success rate. • When a meniscal tear is treated in association with an ACL reconstruction, one should stretch the indications for repair due to improved healing rates and the documented adverse outcomes of meniscectomy in this population. • Lateral repairs do better than medial repairs. Lateral meniscectomies fare worse than medial.

REFERENCES 1. Greis PE, Bardana DD, Holmstrom MC, Burks RT: Meniscal injury: I. Basic science and evaluation. J Am Acad Orthop Surg 2002;10:168–176. 2. DeHaven KE, Bronstein RD: Arthroscopic medial meniscal repair in the athlete. Clin Sports Med 1997;16:69–86. 3. Terry GC, Tagert BE, Young MJ: Reliability of the clinical assessment in predicting the cause of internal derangements of the knee. Arthroscopy 1995;11:568–576. 4. Rosenberg TD, Paulos LE, Parker RD, et al: The 45° posteroanterior flexion weight-bearing radiograph of the knee. J Bone Joint Surg Am 1988;70:1479–1483. 5. Muellner T, Weinstabl R, Schabus R, et al: The diagnosis of meniscal tears in athletes: A comparison of clinical and magnetic resonance imaging investigations. Am J Sports Med 1997;25:7–12. 6. Sutton JB (ed): Ligaments, Their Nature and Morphology. London, HK Lewis, 1897. 7. Arnoczky SP, Warren RF: Microvasculature of the human meniscus. Am J Sports Med 1982;10:90–95. 8. Renstrom P, Johnson RJ: Anatomy and biomechanics of the menisci. Clin Sports Med 1990;9:523–538. 9. Shelbourne KD, Patel DV, Adsit WS, Porter DA: Rehabilitation after meniscal repair. Clin Sports Med 1996;15:595–612. 10. Andersson-Molina H, Karlsson H, Rockborn P: Arthroscopic partial and total meniscectomy: A long-term follow-up study with matched controls. Arthroscopy 2002;18:183–189. 11. Bonneux I, Vandekerckhove B: Arthroscopic partial lateral meniscectomy long-term results in athletes. Acta Orthop Belg 2002;68:356–361. 12. Fairbanks T: Knee joint changes after meniscectomy. J Bone Joint Surg Br 1948;30:164–170. 13. Jaureguito J, Elliot J, Lietner T, et al: The effects of arthroscopic partial lateral meniscectomy in an otherwise normal knee: A retrospective

14. 15.

16. 17. 18.

19. 20. 21.

22. 23.

24.

review of functional, clinical and radiographic results. Arthroscopy 1995;11:29–36. Rangger C, Klestil T, Gloetzer W, et al: Osteoarthritis after arthroscopic partial meniscectomy. Am J Sports Med 1995;23:240–244. Wu WH, Hackett T, Richmond JC: Effects of meniscal and articular surface status on knee stability, function, and symptoms after anterior cruciate ligament reconstruction: A long-term prospective study. Am J Sports Med 2002;30:845–850. DeHaven KE: Current concepts: Meniscus repair. Am J Sports Med 1999;27:242–250. DeHaven KE, Sebastianelli WJ: Open meniscus repair. Indications, technique, and results. Clin Sports Med 1990;9:577–587. Klimkiewicz JJ, Shaffer B: Meniscal surgery 2002 update: Indications and techniques for resection, repair, regeneration, and replacement. Arthroscopy 2002;18(9 Suppl 2):14–25. Rath E, Richmond JC: The menisci: Basic science and advances in treatment. Br J Sports Med 2000;34:252–257. Rosenberg TD, Metcalf RW, Gurley WD: Arthroscopic meniscectomy. Instr Course Lect 1988;37:203–208. Metcalf RW, Burks RT, Metcalf RS: Arthroscopic meniscectomy. In McGuinty JB, Jackson RW (eds): Operative Arthroscopy. Philadelphia, Lippincott-Raven, 1996, pp 263–297. Lysholm J, Gillquist J: Arthroscopic meniscectomy in athletes. Am J Sports Med 1983;11:436–438. Northmore-Ball MD, Dandy DJ, Jackson RW: Arthroscopic, open partial, and total meniscectomy. A comparative study. J Bone Joint Surg Br 1983;65:400–404. Easley ME, Cushner FD, Scott WN: Arthroscopic meniscal resection. In Insall JN, Scott WN (eds): Surgery of the Knee. Philadelphia, Churchill Livingstone, 2001, pp 473–520.

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25. Henning CE, Lynch MA, Yearout KM, et al: Arthroscopic meniscal repair using an exogenous fibrin clot. Clin Orthop 1990;252:64–72. 26. Al-Othman AA: Biodegradable arrows for arthroscopic repair of meniscal tears. Int Orthop 2002;26:247–249. 27. Shelbourne KD, Porter DA: Meniscal repair. Description of a surgical technique. Am J Sports Med 1993;21:870–873. 28. Warren RF: Meniscectomy and repair in the anterior cruciate ligamentdeficient patient. Clin Orthop 1990;252:55–63. 29. Rispoli DM, Miller MD: Options in meniscal repair. Clin Sports Med 1999;18:77–91. 30. Cannon WD Jr, Morgan CD: Meniscal repair: Arthroscopic repair techniques. Instr Course Lect 1994;43:77–96. 31. Morgan CD: The “all-inside” meniscus repair. Arthroscopy 1991;7:120. 32. Barber FA, Herbert MA, Richards DP: Load to failure testing of new meniscal repair devices. Arthroscopy 2004;20:45–50. 33. Farng E, Sherman O: Meniscal repair devices: A clinical and biomechanical literature review. Arthroscopy 2004;20:273–286. 34. McDermott D, Richards W, Hallam P, et al: A biomechanical study of four different meniscal repair systems, comparing pull-out strengths and gapping under cyclic loading. Knee Surg Sports Traumatol Arthrosc 2003;11:23–29. 35. Miller MD, Kline AJ, Jepsen KG: “All-inside” meniscal repair devices: An experimental study in the goat model. Am J Sports Med 2004;32:858–862. 36. Rankin CC, Lintner DM, Noble PC, et al: A biomechanical analysis of meniscal repair techniques. Am J Sports Med 2002;30:492–497. 37. Schimmer RC, Brulhart KB, Duff C, Glinz W: Arthroscopic partial meniscectomy: A 12-year follow-up and two-step evaluation of the longterm course. Arthroscopy 1998;14:136–142. 38. Rockborn P, Messner K: Long-term results of meniscus repair and meniscectomy: A 13-year functional and radiographic follow-up study. Knee Surg Sports Traumatol Arthrosc 2000;8:2–10.

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39. Eggli S, Wegmuller H, Kosina J: Long-term results of arthroscopic meniscal repair. An analysis of isolated tears. Am J Sports Med 1995;23:715–720. 40. Anderson K, Marx RG, Hannafin J, Warren RF: Chondral injury following meniscal repair with a biodegradable implant. Arthroscopy 2000;16:749–753. 41. Calder SJ, Myers PT: Broken arrow: A complication of meniscal repair. Arthroscopy 1999;15:651–652. 42. Ganko A, Engebretsen L: Subcutaneous migration of meniscal arrows after failed meniscus repair. A report of two cases. Am J Sports Med 2000;28:252–253. 43. Hartley RC, Leung YL: Meniscal arrow migration into the popliteal fossa following attempted meniscal repair: A report of two cases. Knee 2002;9:69–71. 44. Kumar A, Malhan K, Roberts SN: Chondral injury from bioabsorbable screws after meniscal repair. Arthroscopy 2001;17:34. 45. Lombardo S, Eberly V: Meniscal cyst formation after all-inside meniscal repair. Am J Sports Med 1999;27:666–667. 46. Menche DS, Phillips GI, Pitman MI, Steiner GC: Inflammatory foreignbody reaction to an arthroscopic bioabsorbable meniscal arrow repair. Arthroscopy 1999;15:770–772. 47. Menetrey J, Seil R, Rupp S, Fritschy D: Chondral damage after meniscal repair with the use of a bioabsorbable implant. Am J Sports Med 2002;30:896–899. 48. Otte S, Klinger HM, Beyer J, Baums MH: Complications after meniscal repair with bioabsorbable arrows: Two cases and analysis of literature. Knee Surg Sports Traumatol Arthrosc 2002;10:250– 253. 49. Ross G, Grabill J, McDevitt E: Chondral injury after meniscal repair with bioabsorbable arrows. Arthroscopy 2000;16:754–756. 50. Song EK, Lee KB, Yoon TR: Aseptic synovitis after meniscal repair using the biodegradable meniscus arrow. Arthroscopy 2001;17:77–80.

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Articular Cartilage Kyle R. Flik, Paul Lewis, Richard W. Kang, and Brian J. Cole

In This Chapter Nonoperative management Treatment algorithm Surgery Microfracture Osteochondral autograft (OAT) Osteochondral allograft Autologous chondrocyte implantation (ACI)

INTRODUCTION • Cartilage injuries are increasingly recognized due to dramatic increases in sports participation at all ages and improvements in musculoskeletal imaging. • Pain and symptoms from articular cartilage lesions are variable. Similar-appearing articular cartilage lesions in the knee may be asymptomatic or may cause disabling pain, swelling, or mechanical symptoms. • The decision of how to treat articular cartilage lesions is dependent on lesion characteristics such as location, size, and depth coupled with patient factors such as symptom intensity, age, activity level, and the presence of concomitant pathology. • A variety of methods are available to treat articular cartilage lesions, including microfracture, autologous osteochondral transplant, allograft osteochondral transplant, and ACI. • The success following surgery for a focal chondral or osteochondral defect is dependent on concomitant treatment of additional knee pathology and equally dependent on patient commitment to and diligence in the postoperative physical therapy regimen.

CLINICAL FEATURES AND EVALUATION Complete evaluation of the patient with an articular cartilage injury of the knee includes a thorough history, physical examination, specific radiographs, and review of previous surgical notes or arthroscopic images. The initial step in the workup is the history. This should include mechanism of injury, time course and quality of symptoms, and review of previous treatments and the effects of those treatments. Patients will often report pain and swelling with weight bearing and increased activity. Direct communication with previous surgeons may be required to have a more com-

plete understanding of the surgical history and pathoanatomy within the patient’s knee. The mechanism of injury, if determined, is a valuable source of information and should be noted. Damage to articular cartilage can be caused by an acute injury yielding a focal chondral or osteochondral defect, can be the result of a chronic development such as osteochondritis dissecans (typically in younger patients), or simply present insidiously due to focal or diffuse degeneration related to mechanical (e.g., malalignment or instability) or genetic factors. During the physical examination, the surgeon should be careful not to assume that the articular cartilage lesion is responsible for all symptoms. Often concomitant pathology exists and can play a role in the symptoms that the patient may be experiencing. It is important to also assess gait and alignment carefully as well as range of motion and patellofemoral tracking. Evaluation for effusion, ligamentous integrity, and areas of point tenderness or crepitus are additionally valuable in considering concomitant pathologies of the knee. Required radiographs include standing anteroposterior, lateral, patellar skyline (or Merchant), a 45-degree flexion posteroanterior weight-bearing view, and full-length alignment film. The posteroanterior flexion view is crucial for adequate assessment of the posterior femoral condyles where significant wear may not be recognized on a standard weight-bearing anteroposterior view. Full-length alignment films should be obtained to assess the mechanical axis. No cartilage restoration procedure should be performed in the setting of malalignment; therefore, if the mechanical axis bisects the affected compartment, a corrective osteotomy should be strongly considered as a concomitant or staged procedure. Other important information can come from imaging of the knee with magnetic resonance imaging. The quality of magnetic resonance imaging technology continues to improve dramatically. In fact, magnetic resonance has established a niche in evaluating articular cartilage irregularities and the degree of cartilage pathology, while also providing information regarding ligament injury. With high-resolution fast spin echo sequencing techniques in the sagittal, coronal, and axial planes, articular cartilage surfaces can be well imaged.1,2 Computed tomography scanning may be necessary to assess the subchondral bone for anatomic considerations including defect geometry and depth in the presence of osteochondral defects that may require bone grafting in addition to an articular cartilage restorative procedure. An examination under anesthesia is required to better assess the knee for instability. This is performed routinely prior to every knee arthroscopy. The first operation after the diagnosis of an articular cartilage defect is often not the definitive proce-

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dure. At times, arthroscopy is performed initially as a diagnostic tool to assess the lesion, the surrounding articular surfaces in the uninvolved compartments, and the state of the menisci and to determine the presence or absence of additional pathology. If one is considering definitive treatment with ACI, a biopsy should be performed at this time. Similarly, if a significant subchondral defect exists, primary bone grafting can be performed at the index operation. Finally, in the setting of mechanical axis malalignment, preoperative discussions might include performing an osteotomy at the index procedure, especially in slightly older patients who might have articular disease patterns considered more marginal for cartilage restoration. Most importantly, however, the initial arthroscopy should be used to define the lesion fully in terms of its location, geography, surface area, and depth. Careful attention to alternative sources of pain and the condition of opposing surfaces is also important. Lesions are most often graded based on direct visualization using the system of Outerbridge3 or the International Cartilage Repair Society, which established a grading system to help surgeons communicate clearly about cartilage lesions.4 The two systems are nearly identical and grade the degree of cartilage damage on a scale from 0 to 4, with a 0 indicating normal cartilage and a 4 indicating injury that penetrates the subchondral bone. A grade of 2 indicates nearly normal cartilage with minor softening or superficial fissures. Grade 3 reflects fissuring to the level of, but not violating, the subchondral bone. Regardless of the system used, always classify lesions with a written and diagrammatic description including the delineation of how the defect contacts opposing surfaces in varying degrees of flexion. In establishing a surgical plan at the time of initial arthroscopy, consider the status of the menisci for the possible inclusion of a meniscal transplant as well as the standing mechanical axis for consideration of a concomitant osteotomy.

RELEVANT ANATOMY AND BASIC SCIENCE Chondrocytes of mesenchymal origin are responsible for the production and maintenance of the extracellular matrix of collagen. This matrix is composed mainly of type II collagen but also includes types V, VI, IX, X, XI, XII, and XIV to a lesser degree. The combination of this collagen network and water affords the viscoelastic properties that resist compressive and shear forces experienced between the articulating surfaces. Articular cartilage provides a smooth, nearly frictionless surface that protects the subchondral bone through shock absorption and wear resistance. While highly specialized and multifunctional, this tissue ironically maintains itself with little contribution from systemic sources and is in fact avascular. As a consequence, hyaline cartilage has trouble repairing itself when damaged. Should the defect penetrate the subchondral bone (i.e., full thickness), the defect may fill with fibrocartilage repair tissue. This replacement may be sufficient in some instances to render patients less symptomatic but is typically inferior in ultrastructure and function compared to native hyaline cartilage. At this juncture, healthy articular cartilage has properties that are unmatched by any man-made substance.

TREATMENT OPTIONS The spectrum of articular cartilage injury is broad and varies principally in terms of location, size, and depth. A diligent eval-

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uation of these characteristics as well as considerations for patient age, activity level, concomitant pathology, and symptomatology is crucial to making appropriate treatment decisions. It is important to recognize that not all chondral lesions cause symptoms. Conversely, not all symptoms are related to the chondral or osteochondral defect. The first step in management of articular cartilage lesions is usually conservative, nonsurgical treatment. Common methods include weight loss, shoe modification, bracing, cane use, and various pharmacologic interventions. Physical therapy may also play a role by improving strength and flexibility; however, this and the previously mentioned treatment are often ineffective in reducing the symptoms associated with an articular cartilage lesion. Medications and nutritional supplements that should be considered are nonsteroidal anti-inflammatory drugs, acetaminophen, or glucosamine and chondroitin sulfate. Intra-articular injections of corticosteroid and hyaluronic acid can be helpful for symptom control but are generally reserved for the older population. If the preceding conservative treatments prove ineffective, both the patient and clinician need to consider surgical options. The specific surgical technique, or techniques, chosen will depend first on the general state of the knee with regard to mechanical alignment, meniscus status, and compartment involvement. Any clinically significant malalignment must be corrected before or concurrently with the cartilage restoration procedure or the restoration will likely fail because the affected compartment will continue to suffer unnecessarily high loads. In a demand-match approach, the senior author (B.J.C.) routinely performs a medial opening wedge high tibial osteotomy for the patient with a medial compartment lesion and varus alignment, a distal femoral osteotomy for the knee with valgus alignment and a lateral compartment lesion, or an anteromedialization of the tibial tubercle for most patellofemoral defects. Given this generality, it is important to note the medial shift in patellofemoral pressures as a result of anteromedialization.5 For example, in cases of superomedial patellar disease, no anteromedialization is performed because the procedure would overload the repaired defect. In addition to mechanical malalignment, any untreated ligament insufficiency or significant meniscus deficiency is a contraindication to articular cartilage restoration alone. While most comorbidities can be corrected simultaneously with cartilage restoration; staging of procedures is an acceptable alternative. For all surgical candidates, it is necessary that a comprehensive plan be formed and this plan be discussed with each patient so he or she understands the procedure and complies with postoperative instructions. Whenever possible, the initial treatment of an articular cartilage lesion should allow for further treatment if unsuccessful. Despite the availability of several techniques, judicial use of each remains challenging. There are relatively few convincing data on the superiority of one technique over another for some lesions. In fact, every articular cartilage lesion is different and requires its own, unique evaluation. Part of the difficulty in treatment decision making is the fact that the natural history of asymptomatic lesions is unclear and unpredictable. However, it is widely believed that if left untreated, a symptomatic cartilage lesion is likely to persist or worsen.6,7 The risk of a lesion being symptomatic likely depends on its location, size, depth, patient activity level, and any associated knee pathology. Pre-existing instability, meniscal damage, or malalignment provides an inhospitable environment for any articular cartilage lesion and predisposes it to progressive degeneration.

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D+L

MST

ACI

cedure should theoretically allow additional opportunity for cartilage restoration should the initial treatment fail.

OCG

Palliative Reparative Restorative Figure 49-1 Treatment options for articular cartilage lesions overlap and range from palliative to reparative to restorative procedures. Maximal clinical utility for each should be recognized within its range. ACI, autologous chondrocyte implantation; D + L, dèbridement and lavage; MST, marrow stimulation techniques; OCG, osteochondral grafting.

Surgery There are essentially four distinct surgical procedures used to treat chondral or osteochondral lesions in the knee. These include microfracture, osteochondral autograft, osteochondral allograft, and ACI. We conceptualize the treatment possibilities in categories depending on the clinical scenario. The categories range from palliative (débridement/lavage), intended to reduce mechanical irritation and inflammatory mediators, to reparative (microfracture, a marrow stimulation technique), designed to release pluripotential cells from the bone marrow that proliferate as fibrocartilage repair cells in the defect, to restorative (osteochondral grafting, either autograft or allograft), which replaces the articular cartilage and its subchondral bone. ACI bridges the boundary between a reparative technique and a restorative one (Fig. 49-1). The common goal to each of these procedures is to provide the patient with symptom reduction and a return to a high level of function while postponing, if not eliminating, the need for arthroplasty. Each recommended pro-

Treatment Algorithm Surgical treatment of a focal chondral defect is based on the characteristics of the lesion, local comorbidities, and the age and activity level of the patient. Important characteristics of the lesion include its size and depth, degree of containment, and location. For patellofemoral lesions, an anteromedialization osteotomy of the tibial tubercle is generally recommended to unload the repaired defect. For femoral condyle lesions, an intact meniscus and a mechanical axis that does not pass through the affected compartment will provide the ideal environment for healing and the greatest chance for symptom relief. Typically, arthroscopic débridement with marrow stimulation is a reasonable first-line treatment, especially if performed during the initial evaluation of a defect. The intention is to reduce symptoms and provide long-term relief without eliminating options for further restorative or reparative procedures if needed. Secondary treatment for smaller lesions (i.e., 2 to 4 cm2) includes revision with osteochondral autograft transplantation. Larger lesions may be amenable to ACI as ACI is best used in younger patients with contained shallow lesions that are 2 to 10 cm2. Deeper lesions that are larger may be best treated with fresh osteochondral allograft transplantation. Figure 49-2 illustrates a typical treatment algorithm that considers lesion location, size, and the patient’s level of physical demand.8

Surgical Techniques Microfracture Microfracture is a marrow-stimulating technique designed to allow fibrocartilage reparative tissue to form in a contained articular chondral lesion. This technique, performed arthroscopically,

Lesion

Femoral condyle

Considerations 1. Malalignment 2. Meniscal deficiency 3. Ligament insufficiency

Considerations 1. Rehabilitation 2. Patellofemoral alignment

Size

Size

1° Microfracture OC autograft ACI OC allograft

++ ++

2° OC autograft ACI OC allograft

++ +/–

≥ 2–3 cm2 +/– +/– ++ ++ ++ ++

< 2–3 cm2

Low demand

< 2–3 cm2

Microfracture ACI/AMZ OC autograft/AMZ OC allograft/AMZ

++ +/–

High demand or failed 1°

Figure 49-2 Treatment algorithm for focal chondral defects of the femoral condyle or patellofemoral joint. For femoral condyle lesions, assessment must first be made regarding malalignment, meniscus status, and ligamentous stability as these comorbidities must be corrected. For trochlear and patellar lesions, patellofemoral alignment must be assessed and anteromedialization considered. High-demand individuals are more likely to require a secondary line of treatment. ACI, autologous chondrocyte implantation; AMZ, anteromedialization; OC, osteochondral.

Patellofemoral

ACI/AMZ OC autograft/AMZ OC allograft/AMZ

++ + +

≥ 2–3 cm2

++ +/– + ++ ++

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involves the creation of perforations through the subchondral bone that allow the release of blood and mesenchymal cells that form a clot in the lesion and proliferate and differentiate into a fibrocartilage repair tissue.9 The optimal patient for microfracture is the young, compliant patient with a focal grade III or IV articular cartilage lesion surrounded by normal cartilage without bone loss. Contraindications include significant bone loss, malalignment, or an opposing “kissing” lesion. The main advantages of this procedure are its low cost and relatively low technical difficulty. In addition, it is a procedure that does not “burn bridges” for future treatment options (i.e., it does not preclude subsequent restorative techniques if necessary). The major drawback of the procedure is that the repair tissue that forms is composed primarily of type I collagen, which is a fibrocartilage that has inferior biomechanical properties to normal hyaline cartilage and may not withstand prolonged high levels of activity with excessive biomechanical forces across a surface with reparative tissue. The first step in microfracture is to prepare the lesion by removing all damaged cartilage, leaving a perpendicular edge of healthy articular cartilage that results in a “well-shouldered” lesion to contain the clot and reduce shear and compression of the lesion. The calcified layer of bone should then be removed with a curet. An awl is used to create holes in the lesion 2 to 3 mm apart and approximately 2 to 4 mm deep.10 Begin by placing holes in the periphery of the lesion and work centrally until the entire surface of the lesion has been uniformly covered (Fig. 493). It is important to avoid subchondral bone collapse that can result from the creation of converging holes or holes placed too close together. The final step is to clamp the arthroscopy fluid inflow and confirm that blood and fat droplets emerge from each hole (Fig. 49-4). This ensures that the microfracture awl penetrated the underlying cancellous bone and that a clot is likely to form in the defect. Osteochondral Autograft During an osteochondral autograft procedure, a healthy intact osteochondral plug is transferred from a low weight-bearing area to the damaged lesion that is removed as a plug of matching size. Mosaicplasty is the term for this technique when multiple small plugs are used to fill a larger area. Osteochondral autograft refers

Figure 49-3 Arthroscopy image showing prepared lesion with microfracture holes placed uniformly throughout lesion 3 to 4 mm apart.

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Figure 49-4 Arthroscopy image depicting adequate penetration into bleeding subchondral bone.

to the osteochondral articular transfer system devised and marketed by Arthrex Inc. (Naples, FL). This technique is limited by the amount of donor tissue that can be used. The ideal lesion for this technique is a symptomatic distal femoral condyle defect in a knee with intact menisci and normal alignment. The senior author has the best success with lesions that are 1 to 2 cm in diameter, although larger lesions can also be treated. One disadvantage of the technique is the donor site morbidity, which increases as the size of the lesion treated increases. The major advantage of this procedure over osteochondral allograft is that the donor plug is the patient’s own, so there is no infectious or immunologic risk from the transplant. The entire procedure can be performed arthroscopically or through a small arthrotomy, depending on the size and location of the defect. The senior author uses the osteochondral autograft system (Arthrex Inc.); however, there are many commercially available systems. The first step is to use a sizer to determine the number and size of grafts that will be required to fill the area of the lesion. The graft harvester of appropriate size is then introduced perpendicular to the donor site typically through a small parapatellar arthrotomy. The typical donor sites include the femoral intercondylar notch and the periphery of the lateral femur just proximal to the sulcus terminalis (Fig. 495). The harvester is then tapped into the bone to a depth of 12 to 15 mm, twisted sharply 90 degrees clockwise and counterclockwise, and removed with a parallel pull. The donor plug is removed from the harvester with a plunger that will push the donor plug into the recipient hole once this has been prepared. The recipient hole is prepared to an equal depth and extracted in an identical manner. A constant knee flexion angle is required during this portion of the procedure, so that the donor plug can be placed at the same angle. The donor harvester with plug is placed over the recipient site and advanced into the defect while maintaining perpendicular orientation and a constant angle. The donor harvester has a tendency to “back off ” the articular surface and should be held securely as the donor plug is advanced. Once the donor plug has been fully released from the harvester, the plug will typically rest a few millimeters proud. The final seating of the plug is performed with an oversized tamp using a gentle tapping technique to minimize damage

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Figure 49-5 Typical harvest site for osteochondral autografts (OATS).

to the articular cartilage. The plug should be seated flush with the surrounding cartilage. If a mosaicplasty technique is being performed, all plugs (size and depth) should be carefully planned before placing the first one. The difficulty in using multiple smaller plugs is in creating a convexity to match the surrounding articular surface. In addition, the senior author has seen a number of patients whose smaller plugs have delaminated over relatively short periods of time postoperatively and therefore chooses to use the smallest number of larger diameter plugs possible (i.e., 10-mm diameter). Osteochondral Allograft This technique is employed to treat larger lesions or lesions with significant bone loss. As a salvage restorative technique, osteochondral allografts have the advantage of providing fully formed articular cartilage without limitation on size and without donor harvest morbidity. Unfortunately, a small but not negligible risk still remains with allograft tissue with respect to disease transmission and immunogenicity. In addition, the problem of cell viability at the time of implantation remains. Currently, most osteochondral allografts are transplanted as prolonged-fresh grafts stored at 4oC for between 14 and 28 days to maximally preserve cell viability, which directly correlates with the success of implantation.11 A parapatellar mini-arthrotomy is performed on the side of the lesion. The lesion is carefully evaluated to determine the graft shape required to best fit the defect. We use an instrumentation system (Arthrex Inc.) to size and harvest a cylindrical plug from the allograft. After matching the defect diameter to the sizing cylinder that best covers the defect, the osteochondral allograft plug is obtained. The sizing cylinder is placed perpendicular to the defect and a guide pin is drilled in the center of the lesion to a depth of 20 to 30 mm. The appropriately sized cannulated counter bore is drilled over the pin to create a cylindrical defect to a depth of 8 to 10 mm (Fig. 49-6). A small drill or Kirschner wire is then used to make multiple small perforations in the bottom of the prepared defect in order to create vascular access channels. The depth of 6 to 8 mm is a compromise between having sufficient bone to achieve a press fit and minimizing the amount of immunogenic bone implanted. The 12-o’clock position of the defect is marked with a sterile

Figure 49-6 Boring the defect to create cylinder recipient site for osteochondral allograft.

marking pen to help with orientation of the donor plug. Each of the quadrants in the defect is measured with a depth gauge and used to tailor the exact depth of final cut of the donor allograft plug. Attention is then turned to the allograft preparation. A flat surface must be cut first in the allograft, which makes securing the graft in the workstation easier (Fig. 49-7). The bushing on the workstation is then secured over the allograft so that the harvested plug will have a contour that best matches the defect site. With smaller defects (3.0 mrad) are effective for sterilizing the tissue but cause structural weakening of the collagen. Lower dose irradiation does not reliably kill viruses. Chemical sterilization agents such as ethylene oxide leave behind a residue that can cause chronic synovitis. Allografts are commonly preserved by deep freezing, cryopreservation, or freeze-drying. Deep freezing is the most common method of storage and involves an antibiotic soak prior to packaging without solution and freezing to -80∞C. It can then be stored for 3 to 5 years. This process destroys all the cells in the tissue and is thought to decrease the host immune response. Cryopreservation involves controlled-rate freezing with extraction of cellular water in an effort to preserve cellular viability. Freeze-drying involves a lyophilization process to ensure residual moisture of less than 5%; the graft can then be stored at room temperature for 3 to 5 years. The freeze-dried graft requires rehydration for 30 minutes prior to implantation. Freeze-drying destroys cells in the tissue and reduces the immunogenicity of the tissue, but the strength of the graft is altered by the process. The preferred processing method for knee ligament allograft surgery remains deep freezing. A primary concern with the use of allograft is the risk of viral and bacterial disease transmission. Hepatitis and human immunodeficiency virus can be transmitted through these tissues and bacterial infections are also a possibility; Buck et al39 calculated the risk of human immunodeficiency virus transmission in properly screened and tested donors to be 1: 1,600,000. A full review of the risk of disease transmission in allograft tissue is presented in Chapter 12, entitled “Safety Issues for Musculoskeletal Allografts.” Unlike organ transplants, allografts are at minimal risk of tissue rejection by the host due to the minimal protein antigen in the processed allografts. Collagen, the major constituent of

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Chapter 50 Graft Choices in Ligament Surgery

the grafts, has minimal antigenicity, and frank rejection of an allograft ligament is rare. However, a low-grade immune response may occur; Harner et al40 demonstrated a mild humoral response to allograft ligament transplantation in a majority of patients at 6 months after surgery. The clinical significance of this type of immune response is unknown. Like autografts, allografts are thought to function as a biologic scaffold and undergo cellular repopulation, revascularization, and collagen remodeling. Initial repopulation may proceed quickly, as replacement of the graft by host cells has been evident at 4 weeks postoperatively.41 However, the overall ligamentization process is thought to proceed more slowly for allografts compared to autografts, presumably due to a prolonged remodeling phase. Animal studies have investigated the biomechanical properties of allografts versus autografts after ligament reconstruction. In a goat model, Jackson et al42 demonstrated that allograft patellar tendon ACL reconstruction resulted in increased anteroposterior laxity, decreased ultimate tensile load, and diminished biologic incorporation compared to autograft at 6 months after surgery. However, Nikolaou et al43 demonstrated nearly identical ligament strength between ACL allograft and autograft reconstructions in a dog model at 9 months after surgery. It has been estimated that allograft incorporation takes up to 1.5 times as long as the incorporation of autograft tissue. Though the remodeling phase may be prolonged with allografts, once it is complete, allograft ligament tissue appears histologically and functionally similar to autograft tissue. Comparative studies of allograft and autograft ACL reconstruction have failed to demonstrate consistent differences in objective or subjective outcomes.44–47 There remains some concern about long-term allograft function; however, there has been no clinical difference between allograft and autograft function at 3- and 5-year follow-up.44,45

SYNTHETIC GRAFTS Synthetic grafts remain an appealing alternative to biologic grafts but have a long history of failure. The ideal synthetic graft would mimic the characteristics of a normal ACL graft in terms of strength, compliance, elasticity, and durability without side effects.

In the 1990s, Gore-Tex grafts (Gore and Co., Flagstaff, AZ) were used but failed dramatically. These grafts were knitted cable with eyelets on each end that allowed for fixation to the bone outside the tunnels. Repeated cycling led to fragmentation of the grafts with shedding of particulate debris that led to persistent effusions and graft failure. Dacron and carbon fiber grafts had a similar history of failure. More recently, the Kennedy Ligament Augmentation Device (3M, St. Paul, MN) was used to supplement ACL grafts. The purpose of this device was to protect the graft reconstruction until healing occurred. Unfortunately, the ligament augmentation device was too stiff and shielded the graft from normal stresses, delaying maturation of the graft. These devices are no longer used for ACL reconstruction. Currently, there are no prosthetic ligaments in the United States approved by the U.S. Food and Drug Administration, although several are currently being used in Europe.

CONCLUSIONS Graft selection in knee ligament surgery remains a contentious topic among orthopedic surgeons. No single graft has been shown to be clearly superior in terms of overall patient outcome. In choosing the appropriate graft for the individual patient, surgeons must be versed in each graft’s biomechanical characteristics, fixation and incorporation properties, donor site morbidities, and contraindications. In addition, graft selection is mitigated by the surgeon’s comfort level with the surgical techniques required for use of the grafts. At our institution, BPTB grafts are routinely used for ACL reconstruction in young, competitive athletes. Hamstrings grafts are commonly used in patients with pre-existing patellofemoral abnormalities such as chondrosis or arthrosis and in patients whose job requires kneeling such as firefighters or wrestlers. Achilles tendon allografts are commonly used for revision ACL surgery, primary PCL reconstruction, and multiligament knee reconstruction. Increasingly, we are using Achilles tendon allografts for primary ACL reconstruction, particularly in patients older than 30 and in recreational athletes. We have found that matching individual patients with grafts that are tailored to their needs has resulted in more targeted and appropriate graft selection.

REFERENCES 1. Butler DL: Anterior cruciate ligament: Its normal response and replacement. J Orthop Res 1989;7:910–921. 2. Fu FH, Jackson DW, Jamison J, et al: Allograft reconstruction of the anterior cruciate ligament. In Jackson DW, Arnoczky SP, Woo SL-Y, et al (eds): Anterior Cruciate Ligament. Current and Future Concepts. New York, Raven Press, 1993, pp 325–338. 3. McFarland EG, Morrey BF, An KN, et al: The relationship of vascularity and water content to tensile strength in a patellar tendon replacement of the anterior cruciate in dogs. Am J Sports Med 1986;14: 436–448. 4. Ballock RT, Woo SL, Lyon RM, et al: Use of patellar tendon autograft for anterior cruciate ligament reconstruction in the rabbit: A long-term histologic and biomechanical study. J Orthop Res 1989;7:474–485. 5. Ng GY, Oakes BW, Deacon OW, et al: Biomechanics of patellar tendon autograft for reconstruction of the anterior cruciate ligament in the goat: Three-year study. J Orthop Res 1995;13:602–608. 6. Oakes BW: Collagen ultrastructure in the normal ACL and in ACL graft. In Jackson DW, Arnoczky SP, Woo SL, et al (eds): Anterior Cruciate

7.

8. 9.

10. 11.

12.

Ligament. Current and Future Concepts, New York, Raven Press, 1993, pp 209–217. Rodeo SA, Arnoczky SP, Torzilli PA, et al: Tendon-healing in a bone tunnel. A biomechanical and histological study in the dog. J Bone Joint Surg Am 1993;75:1795–1803. Jomha NM, Raso VJ, Leung P: Effect of varying angles on the pullout strength of interference screw fixation. Arthroscopy 1993;9:580–583. Kohn D, Rose C: Primary stability of interference screw fixation. Influence of screw diameter and insertion torque. Am J Sports Med 1994;22:334–338. Matthews LS, Lawrence SJ, Yahiro MA, et al: Fixation strengths of patellar tendon-bone grafts. Arthroscopy 1993;9:76–81. Cooper DE, Deng XH, Burstein AL, et al: The strength of the central third patellar tendon graft. A biomechanical study. Am J Sports Med 1993;21:818–824. Johnson DL, Isbell WM, Atay OA: Grafts. In Miller MD, Cole BJ (eds): Textbook of Arthroscopy. Philadelphia, Saunders, 2004, pp 39– 45.

521

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13. Yoshiya S, Nagano M, Kurosaka M, et al: Graft healing in the bone tunnel in anterior cruciate ligament reconstruction. Clin Orthop 2000;376:278–286. 14. Bach BR Jr, Levy ME, Bojchuk J, et al: Single-incision endoscopic anterior cruciate ligament reconstruction using patellar tendon autograft. Minimum two-year follow-up evaluation. Am J Sports Med 1998;26: 30–40. 15. Bach BR Jr, Tradonsky S, Bojchuk J, et al: Arthroscopically assisted anterior cruciate ligament reconstruction using patellar tendon autograft. Five- to nine-year follow-up evaluation. Am J Sports Med 1998;26: 20–29. 16. O’Brien SJ, Warren RF, Pavlov H, et al: Reconstruction of the chronically insufficient anterior cruciate ligament with the central third of the patellar ligament. J Bone Joint Surg Am 1991;73:278–286. 17. Spindler KP, Kuhn JE, Freedman KB, et al: Anterior cruciate ligament reconstruction autograft choice: Bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med 2004;32:1986–1995. 18. Bynum EB, Barrack RL, Alexander AH: Open versus closed chain kinetic exercises after anterior cruciate ligament reconstruction. A prospective randomized study. Am J Sports Med 1995;23:401–406. 19. Buss DD, Warren RF, Wickiewicz TL, et al: Arthroscopically assisted reconstruction of the anterior cruciate ligament with use of autogenous patellar-ligament grafts. Results after twenty-four to forty-two months. J Bone Joint Surg Am 1993;75:1346–1355. 20. Shelbourne KD, Gray T: Anterior cruciate ligament reconstruction with autogenous patellar tendon graft followed by accelerated rehabilitation. A two- to nine-year followup. Am J Sports Med 1997;25:786– 795. 21. Aglietti P, Buzzi R, Menchetti PM, et al: Arthroscopically assisted semitendinosus and gracilis tendon graft in reconstruction for acute anterior cruciate ligament injuries in athletes. Am J Sports Med 1996;24: 726–731. 22. Aglietti P, Buzzi R, Zaccherotti G, et al: Patellar tendon versus doubled semitendinosus and gracilis tendons for anterior cruciate ligament reconstruction. Am J Sports Med 1994;22:211–218. 23. Aglietti P, Giron F, Buzzi R, et al: Anterior cruciate ligament reconstruction: Bone-patellar tendon-bone compared with double semitendinosus and gracilis tendon grafts. A prospective, randomized clinical trial. J Bone Joint Surg Am 2004;86:2143–2155. 24. Barber FA: Tripled semitendinosus-cancellous bone anterior cruciate ligament reconstruction with bioscrew fixation. Arthroscopy 1999;15: 360–367. 25. Giron F, Aglietti P, Cuomo P, et al: Anterior cruciate ligament reconstruction with double-looped semitendinosus and gracilis tendon graft directly fixed to cortical bone: 5-year results. Knee Surg Sports Traumatol Arthrosc 2005;13:81–91. 26. Maeda A, Shino K, Horibe S, et al: Anterior cruciate ligament reconstruction with multistranded autogenous semitendinosus tendon. Am J Sports Med 1996;24:504–509. 27. Wallace MP, Howell SM, Hull ML: In vivo tensile behavior of a fourbundle hamstring graft as a replacement for the anterior cruciate ligament. J Orthop Res 1997;15:539–545. 28. Hamner DL, Brown CH Jr, Steiner ME, et al: Hamstring tendon grafts for reconstruction of the anterior cruciate ligament: biomechanical evaluation of the use of multiple strands and tensioning techniques. J Bone Joint Surg Am 1999;81:549–557. 29. Marder RA, Raskind JR, Carroll M: Prospective evaluation of arthroscopically assisted anterior cruciate ligament reconstruction. Patellar

522

30.

31.

32.

33.

34. 35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46. 47.

tendon versus semitendinosus and gracilis tendons. Am J Sports Med 1991;19:478–484. Clancy WG Jr, Narechania RG, Rosenberg TD, et al: Anterior and posterior cruciate ligament reconstruction in rhesus monkeys. J Bone Joint Surg Am 1981;63:1270–1284. Grana WA, Egle DM, Mahnken R, et al: An analysis of autograft fixation after anterior cruciate ligament reconstruction in a rabbit model. Am J Sports Med 1994;22:344–351. Williams RJ 3rd, Hyman J, Petrigliano F, et al: Anterior cruciate ligament reconstruction with a four-strand hamstring tendon autograft. J Bone Joint Surg Am 2004;86:225–232. Freedman KB, D’Amato MJ, Nedeff DD, et al: Arthroscopic anterior cruciate ligament reconstruction: A metaanalysis comparing patellar tendon and hamstring tendon autografts. Am J Sports Med 2003;31:2–11. Fulkerson JP, Langeland R: An alternative cruciate reconstruction graft: The central quadriceps tendon. Arthroscopy 1995;11:252–254. Lee S, Seong SC, Jo H, et al: Outcome of anterior cruciate ligament reconstruction using quadriceps tendon autograft. Arthroscopy 2004; 20:795–802. Theut PC, Fulkerson JP, Armour EF, et al: Anterior cruciate ligament reconstruction utilizing central quadriceps free tendon. Orthop Clin North Am 2003;34:31–39. Staubli HU, Schatzmann L, Brunner P, et al: Quadriceps tendon and patellar ligament: Cryosectional anatomy and structural properties in young adults. Knee Surg Sports Traumatol Arthrosc 1996;4:100– 110. Chen CH, Chen WJ, Shih CH: Arthroscopic anterior cruciate ligament reconstruction with quadriceps tendon-patellar bone autograft. J Trauma 1999;46:678–682. Buck BE, Malinin TI, Brown MD: Bone transplantation and human immunodeficiency virus. An estimate of risk of acquired immunodeficiency syndrome (AIDS). Clin Orthop 1989;240:129–136. Harner CD, Thompson W, Jamison J, et al: The immunologic response of fresh frozen patellar tendon allograft ACL reconstruction. Paper presented at American Academy of Orthopaedic Surgeons, 1995, New Orleans, LA. Jackson DW, Simon TM, Kurzweil PR, et al: Survival of cells after intraarticular transplantation of fresh allografts of the patellar and anterior cruciate ligaments. DNA-probe analysis in a goat model. J Bone Joint Surg Am 1992;74:112–118. Jackson DW, Grood ES, Goldstein JD, et al: A comparison of patellar tendon autograft and allograft used for anterior cruciate ligament reconstruction in the goat model. Am J Sports Med 1993;21:176– 185. Nikolaou PK, Seaber AV, Glisson RR, et al: Anterior cruciate ligament allograft transplantation. Long-term function, histology, revascularization, and operative technique. Am J Sports Med 1986;14:348–360. Harner CD, Olson E, Irrgang JJ, et al: Allograft versus autograft anterior cruciate ligament reconstruction: 3- to 5-year outcome. Clin Orthop 1996;324:134–144. Peterson RK, Shelton WR, Bomboy AL: Allograft versus autograft patellar tendon anterior cruciate ligament reconstruction: A 5-year followup. Arthroscopy 2001;17:9–13. Shelton WR, Papendick L, Dukes AD: Autograft versus allograft anterior cruciate ligament reconstruction. Arthroscopy 1997;13:446–449. Shino K, Nakata K, Horibe S, et al: Quantitative evaluation after arthroscopic anterior cruciate ligament reconstruction. Allograft versus autograft. Am J Sports Med 1993;21:609–616.

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Anterior Cruciate Ligament Armando F. Vidal and Freddie H. Fu

In This Chapter Nonoperative management Surgery—anterior cruciate ligament (ACL) reconstruction Graft harvest Tunnel preparation

INTRODUCTION • ACL injuries are common, occurring in approximately one in 3000 people in the United States annually. • ACL injuries are most commonly the result of a noncontact athletic injury; however. they can result from various forms of trauma. • The diagnosis of an ACL tear can typically be made from a thorough history and physical examination. Imaging studies, specifically magnetic resonance imaging (MRI), can be a valuable aid in making the diagnosis and identifying associated injuries. • Nonoperative management of ACL tears in young, active patients often fails, resulting in persistent instability, and meniscal damage. However, nonoperative management in older, more sedentary patients has been associated with good outcomes. • Arthroscopic ACL reconstruction has been a generally successful operation at restoring knee stability and returning patients to a high level of sporting activity. • Reconstruction can be performed with a variety of graft choices and fixation options. Overall outcomes, regardless of graft choice, have been favorable.

CLINICAL FEATURES AND EVALUATION Isolated ACL injuries account for up to half of all ligamentous injuries to the knee and have been reported to occur in an estimated one in 3000 people in the general population.1,2 The incidence of knee ligament injuries, overall, has increased in the past few decades secondary to the escalating activity level of the population in general. ACL ruptures are most often the result of athletic injuries, but may occur from various different types of trauma. A noncontact mechanism is the most common cause; however, they can also occur from direct contact. Contact injuries are commonly created by a direct lateral blow to the knee, imparting a valgus force. This often produces combined

ACL/medial cruciate ligament injuries. Alternatively, a direct anterior force may cause a hyperextension moment to the knee also resulting in an injury to the ACL. Noncontact injuries typically occur from acute deceleration or change-of-direction maneuvers. Patients often describe a mechanism in which they “pivot” on a fixed, planted foot. They will often report a sensation of buckling and will very commonly describe a “pop” or “tearing” sensation in the knee. Most athletes will be unable to continue with the athletic endeavor secondary to pain and giving way. A large hemarthrosis will usually develop within hours of the injury producing the characteristically large effusion that follows acute ACL injury. The presence of any acute hemarthrosis in a patient with a knee injury should raise considerable suspicion for an ACL disruption. However, hemarthrosis can be seen with meniscal tears, osteochondral fractures, and patellar dislocations as well.3,4

PHYSICAL EXAMINATION A thorough physical examination of the knee, as described in Chapter 46, is the cornerstone of diagnosing an ACL injury. On first inspection, the presence of a sizable effusion can typically be detected in acute injuries. The absence of a large effusion, however, does not preclude the diagnosis of an acute ACL tear and is typical in chronically ACL-deficient knees. Palpation of the periarticular structures such as the collateral ligaments and the medial and lateral joint lines is a critical part of the examination and provides important information regarding potential injury to other intra-/periarticular structures. Range of motion is often limited in the acute setting secondary to pain and effusion. Limited motion, however, should raise suspicion of a mechanical block resulting from displaced bucket-handle meniscal tears, displaced ACL stump remnants, or osteochondral fragments. Stability testing of the knee should include a thorough ligamentous examination which includes anterior/posterior, varus/valgus and rotational stability testing. Acute ACL injuries often occur with other combined ligamentous injuries and these should be identified by physical examination. Unidentified associated ligamentous instability is a common cause of failure following reconstruction, and this should be detected prior to surgical planning.5 There are three components of the physical examination that are specific to the diagnosis of an ACL injury: the Lachman, pivot-shift, and anterior drawer tests. The Lachman test is the most sensitive of the three maneuvers6 (Fig. 51-1). It is performed with the knee in neutral rotation at 20 to 30 degrees of flexion. An anterior translation force is imparted to the tibia with one hand while stabilizing the femur with the other hand.

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Figure 51-1 The Lachman test. With the knee in 20 to 30 degrees of flexion, the examiner stabilizes the femur with one hand while imparting an anterior force to the tibia with the other hand. Assessment of translation and endpoint is recorded. Translation is recorded as follows: I = 0 to 5 mm, II = 6 to 10 mm, III = >10 mm; A = firm endpoint, B = soft endpoint.

Degree of translation and presence or absence of an endpoint is assessed. The degree of laxity is graded as a comparison with the contralateral, uninvolved knee. The absence of a firm endpoint is indicative of ACL deficiency. Muscle splinting, effusion,

and rotation of the leg may interfere with accurate Lachman testing. The anterior drawer is performed with the knee in neutral rotation and flexed to 90 degrees. The foot is stabilized with the examiner’s thigh and an anterior stress is applied to the tibia. This test is not considered as sensitive for ACL deficiency as the Lachman.6 Last, the pivot-shift is used to determine the rotational competency of the ACL. A positive pivot-shift is considered pathognomonic of ACL deficiency. In the ACL-deficient knee, the tibia sits in an anteriorly subluxed and internally rotated position. An axial load and a valgus torque is applied to the knee as it is brought into flexion. When the knee reaches a position of 15 to 20 degrees of flexion, the tibia reduces, thus producing the pivot shift. This phenomenon is graded as a grade 1 (spin), grade 2 (jump), and grade 3 (transient lock) based on the degree of the reduction. The sensitivity of this maneuver is poor in the awake patient, but it is very sensitive and specific when performed in a patient under anesthesia6,7 (Fig. 51-2). In addition to a thorough ligamentous and meniscal evaluation as described in Chapter 46, attention should also be paid to the patella. A patient with an acute patellar dislocation may present in a similar fashion and with a painful, swollen knee with a large hemarthrosis. This diagnosis must be considered when evaluating a patient with an injury suspected of being an ACL tear. Plain radiographs are the first-line imaging modality for any acutely injured knee and should be obtained if there is any suspicion of an ACL injury. Standard posteroanterior flexion, lateral, and Merchant views should be obtained. Radiographs should be assessed for possible fractures. Occasionally, a small lateral capsular avulsion fracture of the tibial plateau can be visualized on plain films. This finding is termed a Segond fracture and has been said to be pathognomonic of an ACL injury (Fig. 51-3). Additionally, tibial spine avulsion fractures may be seen in skeletally immature and middle-aged patients with clinical examinations that are suspicious for ACL injury. In the chronic setting, intercondylar notch osteophytes, blunting of the intercondylar eminence, and accentuation of the sulcus terminalis may be observed. This accentuation of the sulcus terminalis has been termed the lateral notch sign (Fig. 51-4). Plain radiographs are also useful for assessment of overall limb alignment and degree of degenerative changes, if present. MRI remains the gold-standard imaging modality for ACL injury. The reported sensitivity of MRI for detecting ACL injury is in excess of 90% to 95%.8,9 Fiber discontinuity, ligament edema, and hemorrhage can be readily detected by MRI and are characteristic of an acute ACL tear (Fig. 51-5). In addition, the MRI scan often demonstrates a characteristic bone bruise pattern in the posterolateral tibial plateau and anterolateral femoral condyle with acute ACL injury. These bruises have been reported in approximately 80% of acute injuries.10,11 The significance and long-term prognostic implications of these “bone bruises” on the natural history of the ACL-deficient knee are unknown at this time11 (Fig. 51-6). MRI is also very useful for detecting associated meniscal, chondral, and ligamentous injuries, which are important to surgical planning.

RELEVANT ANATOMY AND BIOMECHANICS Figure 51-2 The pivot-shift is performed with the hip in slight abduction and with a valgus force applied to the extended knee. The knee is brought into flexion (from full extension) and the tibia reduces. The severity of the reduction (spin, jump, locked out) is graded.

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Understanding ACL anatomy is important for interpreting imaging studies and planning surgical reconstruction. The ACL is approximately 31 to 38 mm in total length and has a midsubstance cross-sectional area of 44 mm2.12,13 It courses from the

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Figure 51-4 Lateral radiograph in a chronically anterior cruciate ligament–deficient patient demonstrating accentuation of the sulcus terminalis (arrow) termed the lateral notch sign. Figure 51-3 Posteroanterior flexion radiograph of an acutely injured knee revealing a classic lateral capsular avulsion (arrow), termed a Segond fracture. This patient underwent magnetic resonance imaging, which confirmed an anterior cruciate ligament tear, and underwent reconstruction.

Distended capsule 2° to effusion

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Figure 51-5 Sagittal magnetic resonance imaging demonstrating an intact (A) and ruptured (B) anterior cruciate ligament. Note the fiber discontinuity, hemorrhage, and sizable effusion present in the injured knee. Arrows indicated normal (A) and abnormal (B) joint capsule position.

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reconstruction. Most patients with isolated ACL injury do well with activities of daily living. They typically can participate in limited sporting activities, but will have difficulty with vigorous activity. Daniel et al4 divided various sports and occupations into tiered levels based on the intensity of the activity. Sports that require jumping, pivoting, and hard cutting such as basketball, football, and soccer are considered level I sports. Sports such as baseball, racket sports, and skiing require lateral motion but less jumping and hard cutting than level I sports and are considered level II. Sporting activities that do not require cutting, pivoting or lateral motion such as jogging, running, and swimming are considered level III. Additionally, Daniel et al4 expanded this classification to include occupations that similarly require cutting and pivoting type maneuvers. The challenge to the surgeon is to decide which patients will benefit from operative or nonoperative management. Generally, patients who participate heavily in level I or II sports/occupations are considered candidates for reconstruction. Age is an important consideration in the management of the ACL-injured knee. Patient age and activity level, however, are often coupled. Noyes et al20 reviewed the results of nonoperaFigure 51-6 Magnetic resonance imaging demonstrating typical bone bruise pattern encountered with acute anterior cruciate ligament injury: posterolateral tibial plateau and anterolateral femoral condyle. Arrows indicate increased signal on MRI in areas of bone bruise on femoral condyle and tibial plateau.

posteromedial surface of the lateral femoral condyle in the intercondylar notch to its tibial attachment approximately 15 mm behind the anterior border of the tibial articular surface, just medial to the anterior horn of the lateral meniscus. At both insertion sites, the ligament attaches over a broad, flattened area that is more than three times the cross-sectional area of the midsubstance ligament.14 Additionally, the ACL has been described as being composed of two distinct anatomic and functional structures: the anteromedial and posterolateral bundles. Each bundle contributes to approximately half of the overall size of the ACL14 (Fig. 51-7). The ligament has an ultimate tensile load of 2160 N and a stiffness of 242 N/mm and can tolerate a strain of 20% prior to failure. The forces in the intact ACL range from 100 N during passive knee extension to about 400 N with walking, and up to 1700 N with cutting and acceleration-deceleration activities.15,16 The individual bundles have been reported to have different biomechanical characteristics and tensioning patterns. Tension in the anteromedial bundle increases with flexion angles greater than 30 degrees, whereas the posterolateral bundle is more taut in extension.17 Additionally, the role of the posterolateral bundle in resisting coupled rotatory loads is being investigated.18

A

TREATMENT OPTIONS The natural history of ACL deficiency is not completely understood, and comparison of operative and nonoperative management in the literature is often difficult.19 Numerous variables influence the decision-making process for nonsurgical or surgical management of these injuries. Patient age, activity level, and associated injuries all play a role in the choice of management. The activity level of the patient, as described by Daniel et al4 is probably the most predictive factor regarding the need for

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B Figure 51-7 A, Arthroscopic picture of intact anterior cruciate ligament (ACL) demonstrating wide tibial footprint. B, Anteromedial (AM) bundle of the ACL is retracted, exposing the posterolateral (PL) bundle.

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tive management of ACL deficiency in a group of 103 patients, with an average age of 26. In their study, a significant number of their patients progressed to have persistent instability, further meniscal damage, and ultimately joint arthroses. Only a small subset could return to turning- or twisting-type activities. Similarly, Hawkins et al21 demonstrated that the results of nonoperative management in an active group of young patients with an average age of 22 were poor. In their cohort, 86% of the patients experienced persistent giving way, and overall 87.5% of these patients rated their knee as fair or poor. Conversely, Ciccotti et al22 reviewed the results of nonoperative management in middle-aged patients between the ages of 40 and 60. They observed that over 80% of patients in this age group did well with nonoperative management consisting of a supervised physical therapy protocol. Patients in this age group who participated in a guided rehabilitation program and modified their activities had a satisfactory outcome without surgery. However, patients who wished to resume competitive sports requiring level I activities (e.g., pivoting) were dissatisfied with nonoperative management and required reconstruction. Overall, ACL reconstructions in the older population are less common. However, in older patients who wish to continue with vigorous or high-level activities, ACL reconstruction has been shown to be a successful option with results similar to those in younger patients.23,24 In individuals who are older and relatively sedentary, nonoperative management of ACL has been shown to yield satisfactory results, provided the patients are willing to accept a modest amount of instability and a slight risk of meniscal injury.25

Nonoperative Management The goal of nonoperative management of ACL injury is to return functional stability to the knee and prevent further injury and degeneration. Activity modification and physical therapy are the cornerstones of nonoperative management. Physical therapy initially is centered on regaining pain-free motion. Once motion is regained, rehabilitation should focus on closed-chain strengthening of both the quadriceps and hamstrings. Once sporting activities are resumed, they need to be modified to avoid highrisk, level I type behaviors. Additionally, functional bracing should be considered. The role of bracing, overall, is controversial. Its use may be helpful in managing subluxation episodes during activities that have infrequent high-risk maneuvers. However, the prevention of further subluxation episodes and injury to the articular cartilage or menisci cannot be ensured.25,26

Operative Management Surgical management of ACL injury has been the subject of intense scrutiny for the past 30 years. Techniques have evolved from repair and extra-articular reconstructions to minimally invasive arthroscopic techniques with various graft choices, sophisticated fixation options, and advanced rehabilitation protocols. There are various issues surrounding ACL surgery that are critical to the success of the reconstruction. Proper surgical technique and graft placement are paramount. However, the timing of surgery, the choice of graft and fixation device, and postoperative rehabilitation also play very important roles. ACL reconstruction in the acute period immediately following injury has been associated with an increased incidence of arthrofibrosis and knee stiffness.27,28 Surgery should be deferred until the acute inflammatory period has passed, range of motion has returned, and strong quadriceps activation is present. This process requires preoperative rehabilitation and modalities such

Figure 51-8 Comparison of advantages and disadvantages for commonly used anterior cruciate ligament graft material.

as cryotherapy, compression, and anti-inflammatory medications. Although some authors have recommended a waiting period of 3 to 4 weeks prior to surgery, there is no true time frame and the overall condition of the knee with regard to motion and quadriceps activation should be the guide. Numerous graft choices and fixation options have been advocated for ACL reconstruction over the years. The selection of a graft is based on various patient factors as well as surgeon philosophy and training. Current alternatives include various autograft and allograft options. At present, the most common autograft choices include autogenous hamstring and patellar tendon grafts. Allografts have gained significant popularity recently, especially in the older patient population, and include Achilles tendon, patellar tendon, and tibialis anterior/posterior tendon. Many factors including patient age, activity level, comorbidities, and surgeon preference play a role in graft selection. Each graft choice has advantages and disadvantages (Fig. 51-8). The biomechanical properties of the graft, ease of harvest, fixation strength, donor site morbidity, and return-to-play guidelines differ with each graft choice and should be considered for each individual patient. Overall, recent prospective controlled studies and meta-analyses have failed to demonstrate a significant difference in clinical outcome between hamstring and patellar tendon autograft reconstructions.29,30 Additionally, the overall clinical success rates of primary allograft reconstruction have been comparable to those of autograft.31,32 An informed discussion between the surgeon and patient of the advantages and disadvantages of each graft should guide the ultimate decision.

Surgery Prior to surgical reconstruction of the ACL, a thorough examination under anesthesia should be performed by the operating surgeon. Depending on the certainty of the diagnosis and surgeon preference, one may either proceed directly to graft harvest or diagnostic arthroscopy. In the case of allograft reconstruction, graft preparation may be performed prior to the initiation of surgery (Fig. 51-9). Graft Harvest: Patellar Tendon An 8 cm long incision is made just medial to the midline centered over the patellar tendon and carried down to just below the tibial tubercle. The incision is carried down to layer 1 of the knee, and full-thickness flaps are developed to expose the patel-

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Figure 51-9 Diagnostic arthroscopy depicting acute complete anterior cruciate ligament disruption.

lar tendon in its entirety. The medial and lateral borders of the patellar tendon are identified and the width of the tendon is measured. The central 10 mm of tendon (which generally corresponds with the central one third) is marked out using a sterile marking pen. The tendon is then incised along these lines longitudinally. These incisions are extended along the periosteum of the patella and tibial tubercle for an additional 2.5 cm in each direction. This serves as the guide for osteotomizing the bone plugs. An oscillating saw is used to create the bone plugs. A trapezoidal bone plug is harvested from the tibial tubercle and a triangular bone plug is harvested from the patella. The bone plugs are then measured and contoured, and drill holes and sutures are passed through the plugs for graft passage (Fig. 51-10). Graft Harvest: Hamstring Tendon A 3- to 4-cm incision is made longitudinally along the anteromedial tibial crest, centered over the pes anserine tendons (Fig. 51-11A). Alternatively, transverse and oblique incisions have been described. This incision is typically approximately three finger breadths below the joint line at the level of the apex of the tibial tubercle and centered equally between the tubercle and the posteromedial aspect of the tibia. The sartorius fascia is identified, and the gracilis and semitendinosis tendon are easily palpable. If visualized, any branches of the infrapatellar branch of the saphenous nerve are preserved. At our institution, we prefer to release the tendons off their insertion on the tibia and use a closed tendon stripper for harvesting. Alternatively, the insertion site can be initially preserved and an open stripper used (Fig. 51-11B). Once the tendons are identified, an incision is made in the sartorial fascia between the two tendons. The tendons are dissected down to the periosteum of the tibia and then reflected as one sleeve, maximizing length. Each tendon is then identified and tagged with a no. 2 nonabsorbable suture. The gracilis is harvested first. All fascial slips are released and the tendon is harvested with the closed tendon stripper. In a similar fashion, the semitendinosis is harvested. The semitendinosis often has multiple fascial connections to the medial gastrocnemius, and these must be released prior to using the tendon stripper in order to avoid premature graft amputation.33

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Figure 51-10 Completed bone-patellar tendon-bone graft with drill holes and sutures for graft passage.

Muscle remnants on the tendon grafts are removed. Final graft preparation is dependent on the fixation device. Typically, a no. 2 nonabsorbable suture whipstitch is placed in each free end and each graft is doubled over to produce a quadruplestrand construct (Fig. 51-12). Numerous fixation devices exist for both femoral and tibial fixation and are a matter of surgeon preference. Tunnel Preparation Diagnostic arthroscopy is performed and any intra-articular pathology is addressed. The ACL stump is débrided with a combination of a motorized shaver and electrocautery device. We leave the tibial footprint of the ACL intact for its proprioceptive and vascular contributions. The intercondylar notch is then prepared with the use of a motorized bur or shaver. We prefer to perform a limited notchplasty, taking just enough bone to expose the “over-the-top” position. The tibial tunnel is prepared first. Tunnel placement is based on the anatomy of the intact ACL. The tibial attachment is adjacent to the anterior horn of the lateral meniscus. Numerous commercially available guide systems can be used. The tip of the guide is placed in the center of the ACL footprint on the tibia and angled about 30 degrees off the midline. The incision used for harvest of either the patellar tendon autograft or hamstring autograft can be used for the tunnel. If an allograft is used, a separate incision is made centered over the anteromedial aspect of the tibia similar to the incision described for the hamstring

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Figure 51-12 Quadruple hamstring graft being prepared for EndoButton (Smith & Nephew, Andover, MA) CL fixation.

A

A

B Figure 51-11 A, Incision site for harvest of autogenous hamstring graft. B, Isolation of gracilis and semitendinosis tendons. A closed tendon stripper is then used to complete the individual tendon harvest.

harvest. A provisional pin is advanced into the ACL footprint using the guide. The aiming guide is then removed and the pin is overreamed with a cannulated reamer of appropriate size (Fig. 51-13A). Any remaining bone fragments are then removed with the use of a motorized shaver. The femoral tunnel can then be

B Figure 51-13 A, Tibial guide pin positioned in the center of the anterior cruciate ligament footprint. B, Femoral tunnel in 2-o’clock position with approximately 1 to 2 mm of remaining posterior wall.

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addressed. The femoral tunnel can be drilled with the use of commercially available offset guides through a transtibial technique. Alternatively, a medial portal technique can be used, in which the femoral tunnel is drilled from the medial portal.34 An offset aimer guide, typically either 6 or 7 mm, is placed in the “over-the-top” position oriented toward the 10- to 11-o’clock (right knee) or 1- to 2-o’clock (left knee) position with the knee in 90 degrees of flexion. A guide pin is then advanced approximately 3 cm and overreamed with an acorn reamer of appropriate size to a depth of about 35 mm. A 1- to 2-mm cortical wall should remain posterior to the tunnel (Fig. 51-13B). Femoral fixation is dependent on graft choice and surgeon preference. We generally use metal interference screw fixation for bone plugs and EndoButton (Smith & Nephew, Andover, MA) fixation for soft-tissue grafts. For bone plug fixation, a Beeth pin is advanced using a transtibial technique through the femoral tunnel and out the lateral aspect of the femur. It is retrieved laterally and used to pull the sutures on the graft through the femoral tunnel. The bone-patellar tendon-bone graft is then advanced through the tibial tunnel and into the femoral tunnel. A guide pin for the interference screw is then placed between the bone plug and the tunnel. A 7 ¥ 25-mm cannulated metal interference screw is then placed over the guidewire. With this technique, the cortical edge of the bone plug is placed posteriorly and the cancellous surface faces anteriorly. In the case of soft-tissue grafts, after the femoral tunnel is drilled, the far cortex is breached with a 4.5-mm EndoButton drill and the depth gauge is used to assess the distance to the far cortex. Similarly, a Beeth pin is advanced through the EndoButton drill hole using a transtibial technique. It is retrieved laterally and used to pull the graft through the femoral tunnel. An appropriate length EndoButton loop is selected. Ideally between 30 and 35 mm of graft should ultimately reside within the tunnel. When EndoButton fixation is desired, the tunnel depth needs to be deep enough to accommodate the intended graft length plus an additional 8 mm for flipping the button. The quadruple-strand graft is placed in the closed loop EndoButton and sutured together using a no. 2-0 bioabsorbable stitch. Pulling sutures (using no. 2 nonabsorbable braided suture) are placed in

the peripheral holes of the EndoButton, and these are advanced into the femoral tunnel using the Beeth pin. The graft is passed in a routine fashion, and the EndoButton loop is flipped to establish femoral fixation. Once femoral fixation is achieved, the knee is cycled through a full range of motion and graft impingement is assessed. Tension is applied to the graft, and tibial fixation is performed in approximately 10 to 20 degrees of knee flexion. Bone-patellar tendonbone grafts are secured with metal interference screw, whereas soft-tissue grafts can be secured with numerous fixation implants. Currently, we use interference fixation with a bioabsorbable screw or an Intrafix (Mitek, Innovasive Devices, Mitek, Westwood, MA) device on the tibial side for soft-tissue grafts (Fig. 51-14).

POSTOPERATIVE REHABILITATION The goal after surgical reconstruction is to return the patient to his or her preinjury level of function without injuring the graft. In the early postoperative period, the patient is placed in a hinged knee brace locked in extension. Intermittent quadriceps sets, straight leg raises, heel slides, and continuous passive motion is encouraged during this period. The patient is allowed to be weight bearing as tolerated during this period. For the first 6 weeks, the patient is maintained in a brace and with two crutches. Quadriceps isometrics and range-of-motion exercises are emphasized. At about 6 to 8 weeks, when the inflammation has subsided and the patient exhibits full extension, at least 90 degrees of flexion, and an adequate quadriceps set, he or she can advance to a stationary bike, closed-chain terminal extension exercises, and hamstring strengthening. Crutches and the brace can be discontinued when the patient has full extension, can perform a straight leg raise without an extension lag, and exhibits a nonantalgic gait pattern. Progressive strength, flexibility, and proprioception exercises are advanced over the course of 6 months. Functional activities and sport-specific drills are initiated between 6 and 9 months.

CRITERIA FOR RETURN TO SPORT Multiple criteria including functional testing, clinical evaluation, and subjective assessment should be used to determine the eligibility of a patient to return to full athletic activity. A full range of motion and satisfactory return of muscle strength and endurance are necessary before return to sport is allowed. In general, a minimum of 5 to 6 months after surgery is required to attain these goals. On average, 6 to 9 months is considered a reasonable time frame for return to sport. There is considerable controversy and individual preference in regards to the timing of return to sport.35 Additionally, the use of a functional brace is recommended by some authors for the first 1 to 2 years after surgery. We generally recommend functional bracing for the first postoperative year and allow the patient to make a decision regarding future brace wear.

RESULTS AND OUTCOMES

Figure 51-14 Final appearance of autogenous hamstring anterior cruciate ligament reconstruction.

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Arthroscopic ACL reconstruction has proven to be a successful and reliable technique for restoring knee stability and function. Recent reports analyzing the results of patellar tendon and hamstring autograft reconstruction have demonstrated that patient

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such as double-bundle reconstruction, and the introduction of improved fixation alternatives and biologics may ultimately improve on these already excellent results37 (Fig. 51-15).

COMPLICATIONS

Figure 51-15 Arthroscopic image of a double-bundle anterior cruciate ligament reconstruction using tibialis anterior allograft. This reconstructive construct is a relatively new, experimental concept that attempts to improve on knee kinematics following reconstruction. AM, anteromedial; PL, posterolateral.

Complications following ACL reconstruction are rare. Graft failure is uncommon and occurs in approximately 2% to 5% of patients. Postoperative stiffness and arthrofibrosis can be a very disabling complication and is reported to occur in 2% to 10% of patients undergoing ACL reconstruction. However, significant, persistent motion loss greater than 5 degrees of the contralateral side is rare and is estimated at between 1% and 2%. Infection is rare, occurring in approximately 0.5% of patients undergoing reconstruction. By far, the most common complication is the presence of anterior knee pain, which occurs in approximately 10% to 20% of patients. This complication can occur in both patients undergoing bone-patellar tendon-bone and hamstring ACL reconstruction, but appears to be more common in patients undergoing bone-patellar tendon-bone reconstruction.38

CONCLUSIONS satisfaction following ACL reconstruction has been very high. Approximately 90% to 95% of patients are satisfied with their knee following ACL reconstruction and would have the procedure performed on their contralateral knee if it were injured. Objectively, approximately 75% to 90% of patients will have restoration of knee stability as assessed by pivot-shift testing and KT-1000 measurements. Additionally, approximately 65% of patients undergoing reconstruction return to their previous level of performance.30,36 Although, these numbers are encouraging, there still remains room for improvement. Innovations in surgical techniques,

Injuries to the ACL are very common and often result in symptomatic knee instability and dysfunction. Both nonoperative and operative management of ACL insufficiency can be successful in appropriately selected patients. Techniques of ACL reconstruction have advanced significantly in recent years, allowing a majority of patients to return to high-level athletics without pain and instability. Attention to surgical technique and adherence to postoperative rehabilitation protocols are the cornerstones of a successful outcome. Continued advances and improved surgical techniques and implants can be expected in the future.

REFERENCES 1. Miyasaka K, Daniel D, Stone M: The incidence of knee ligament injuries in the general population. Am J Knee Surg 1991;4:3–8. 2. Fu FH, Bennett CH, Lattermann C, et al: Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med 1999;27:6 821–830. 3. Butler JC, Andrews JR: The role of arthroscopic surgery in the evaluation of acute traumatic hemarthrosis of the knee. Clin Orthop 1988;228:150–152. 4. Daniel DM, Stone ML, Dobson BE, et al: Fate of the ACL-injured patient. A prospective outcome study. Am J Sports Med 1994;22: 632–644. 5. Carson EW, Anisko EM, Restrepo C, et al: Revision anterior cruciate ligament reconstruction: Etiology of failures and clinical results. J Knee Surg 2004;17:127–132. 6. Malanga GA, Andrus S, Nadler SF, et al: Physical examination of the knee: A review of the original test description and scientific validity of common orthopedic tests. Arch Phys Med Rehabil 2003;84:592– 603. 7. Bach BR Jr, Warren RF, Wickiewicz TL: The pivot shift phenomenon: Results and description of a modified clinical test for anterior cruciate ligament insufficiency. Am J Sports Med 1988;16:571–576. 8. Larson RL, Tailon M: Anterior cruciate ligament insufficiency: Principles of treatment. J Am Acad Orthop Surg 1994;2:26–35.

9. Munshi M, Davidson M, MacDonald PB, et al: The efficacy of magnetic resonance imaging in acute knee injuries. Clin J Sport Med 2000; 10:34–49. 10. Speer KP, Spritzer CE, Bassett FH 3rd, et al: Osseous injury associated with acute tears of the anterior cruciate ligament. Am J Sports Med 1992;20:382–389. 11. Faber KJ, Dill JR, Amendola A, et al: Occult osteochondral lesions after anterior cruciate ligament rupture. Six-year magnetic resonance imaging follow-up study. Am J Sports Med 1999;27:489–494. 12. Arnoczky SP: Anatomy of the anterior cruciate ligament. Clin Orthop 1983;172:19–25. 13. Girgis FG, Marshall JL, Monajem A: The cruciate ligaments of the knee joint. Anatomical, functional and experimental analysis. Clin Orthop 1975;106 216–231. 14. Harner CD, Baek GH, Vogrin TM, et al: Quantitative analysis of human cruciate ligament insertions. Arthroscopy 1999;15:741–749. 15. Markolf KL, Burchfield DM, Shapiro MM, et al: Biomechanical consequences of replacement of the anterior cruciate ligament with a patellar ligament allograft. Part II: Forces in the graft compared with forces in the intact ligament. J Bone Joint Surg Am 1996;78:1728–1734. 16. Woo SL, Hollis JM, Adams DJ, et al: Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med 1991;19:217–225.

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17. Sakane M, Fox RJ, Woo SL, et al: In situ forces in the anterior cruciate ligament and its bundles in response to anterior tibial loads. J Orthop Res 1997;15:285–293. 18. Gabriel MT, Wong EK, Woo SL, et al: Distribution of in situ forces in the anterior cruciate ligament in response to rotatory loads. J Orthop Res 2004;22:85–89. 19. Fithian DC, Paxton LW, Goltz DH: Fate of the anterior cruciate ligament-injured knee. Orthop Clin North Am 2002;33:621–636. 20. Noyes FR, Mooar PA, Matthews DS, et al: The symptomatic anterior cruciate-deficient knee. Part I: The long-term functional disability in athletically active individuals. J Bone Joint Surg Am 1983;65:154– 162. 21. Hawkins RJ, Misamore GW, Merritt TR: Followup of the acute nonoperated isolated anterior cruciate ligament tear. Am J Sports Med 1986;14:205–210. 22. Ciccotti MG, Lombardo SJ, Nonweiler B, et al: Non-operative treatment of ruptures of the anterior cruciate ligament in middle-aged patients. Results after long-term follow-up. J Bone Joint Surg Am 1994;76:1315–1321. 23. Barber FA, Elrod BF, McGuire DA, et al: Is an anterior cruciate ligament reconstruction outcome age dependent? Arthroscopy 1996;12: 720–725. 24. Plancher KD, Steadman JR, Briggs KK, et al: Reconstruction of the anterior cruciate ligament in patients who are at least forty years old. A long-term follow-up and outcome study. J Bone Joint Surg Am 1998;80:184–197. 25. Buss DD, Min R, Skyhar M, et al: Nonoperative treatment of acute anterior cruciate ligament injuries in a selected group of patients. Am J Sports Med 1995;23:160–165. 26. Fithian DC, Paxton EW, Stone ML, et al: Prospective trial of a treatment algorithm for the management of the anterior cruciate ligamentinjured knee. Am J Sports Med 2005;33:335–346. 27. Harner CD, Irrgang JJ, Paul J, et al: Loss of motion after anterior cruciate ligament reconstruction. Am J Sports Med 1992;20:499–506.

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28. Shelbourne KD, Foulk DA: Timing of surgery in acute anterior cruciate ligament tears on the return of quadriceps muscle strength after reconstruction using an autogenous patellar tendon graft. Am J Sports Med 1995;23:686–689. 29. Jansson KA, Linko E, Sandelin J, et al: A prospective randomized study of patellar versus hamstring tendon autografts for anterior cruciate ligament reconstruction. Am J Sports Med 2003;31:12–18. 30. Freedman KB, D’Amato MJ, Nedeff DD, et al: Arthroscopic anterior cruciate ligament reconstruction: A metaanalysis comparing patellar tendon and hamstring tendon autografts. Am J Sports Med 2003;31: 2–11. 31. Harner CD, Olson E, Irrgang JJ, et al: Allograft versus autograft anterior cruciate ligament reconstruction: 3- to 5-year outcome. Clin Orthop 1996;324:134–144. 32. Strickland SM, MacGillivray JD, Warren RF: Anterior cruciate ligament reconstruction with allograft tendons. Orthop Clin North Am 2003; 34:41–47. 33. Pagnani MJ, Warner JJ, O’Brien SJ, et al: Anatomic considerations in harvesting the semitendinosus and gracilis tendons and a technique of harvest. Am J Sports Med 1993;21:565–571. 34. Cha PS, Chabra A, Harner CD: Single-bundle anterior cruciate ligament reconstruction using the medial portal technique. Oper Tech Orthop 2005;15:89–95. 35. Cascio BM, Culp L, Cosgarea AJ: Return to play after anterior cruciate ligament reconstruction. Clin Sports Med 2004;23:395–408. 36. Spindler KP, Kuhn JE, Freedman KB, et al: Anterior cruciate ligament reconstruction autograft choice: Bone-tendon-bone versus hamstring: Does it really matter? A systematic review. Am J Sports Med 2004;32:1986–1995. 37. Vidal AF, Brucker PU, Fu FH: Anatomic double-bundle anterior cruciate ligament reconstruction using tibialis anterior tendon allografts. Oper Tech Orthop 2005;15:140–145. 38. Phillips BB, Haynes DE: Complications of anterior cruciate ligament reconstruction. Instr Course Lect 2002;51:329–333.

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In This Chapter

standing of the etiology behind the failure such that the appropriate corrective measures can be taken.

Revision anterior cruciate ligament (ACL) reconstruction Arthritis and ACL insufficiency Skeletal immaturity

CAUSE OF FAILURE

INTRODUCTION • ACL injury occurs with an estimated incidence of one in 3000 among the general United States population.1 In the majority of these cases, ACL reconstruction has proven to be a reliable and durable procedure for restoring stability, and more than 100,000 of these procedures are performed annually.2 • Good to excellent results in terms of patient satisfaction, stability, and return to play are observed in between 75% and 90% of these cases.3 Clinical failure, however, remains a problem, with rates as high as 10% to 15% at short- and intermediate-term follow-up.4 • Despite improvements in graft fixation and a better understanding of ACL anatomy and biomechanics, this failure rate seems to be holding relatively constant, resulting in higher absolute numbers of clinical failure as the number of reconstructions performed annually continues to rise.5 • There are a number of complex scenarios surrounding ACL injury that require special consideration and can contribute to suboptimal clinical outcomes. Among these are revision of a failed reconstruction, ligament injury in the skeletally immature, treatment of ACL injury in the context of concomitant chondral injury, and treatment of the chronically ACL-deficient arthritic knee.

REVISION ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION Clinical failure following ACL reconstruction can be defined as recurrent knee instability, pain, stiffness, or any combination thereof that prevents a patient from undertaking a desired set of activities.6 Depending on the age and particular demands of the patient, these activities may range from high-level athletic competition to simple tasks of daily living. There is, therefore, a significant subjective element in the definition of clinical failure, and the treating surgeon must remain attuned to the individual needs of each patient. Once the diagnosis of clinical failure has been made, one must develop a thorough under-

Failure following ACL reconstruction typically falls into one or more of four broad categories: (1) graft failure (recurrent or persistent instability), (2) secondary degenerative joint disease, (3) loss of motion, and (4) dysfunction of the extensor mechanism (Fig. 52-1).3 These categories are not mutually exclusive, but rather the variables in each category are often interdependent. Graft failure and loss of motion are the most commonly encountered causes and most often necessitate revision of the index reconstruction.

Graft Failure Failure of the intra-articular portion of the graft most often presents as recurrent or persistent instability. Technical errors during primary reconstruction most commonly cause graft failure, and it is estimated that malpositioned tunnels are responsible for 70% to 80% of these cases.3,4 The most common mistake in tunnel placement has traditionally been thought to be anteriorization of the femoral tunnel, which results in loss of knee flexion, excessive tension on the graft, and early failure through cyclic loading (Fig. 52-2). This sequence of events is easily understood if one considers two anatomic and procedural factors: one, the shape of the distal femur causes the knee joint to function as a cam and two, the graft is first fixed on the femoral side and subsequently tensioned in varying degrees of extension. As the femoral tunnel is anteriorized and the knee brought into extension, the intra-articular portion of the graft progressively shortens. Tensioning and tibial-side fixation of the graft in extension then secure this shortened intra-articular graft, effectively “capturing” the knee in extension (Fig. 52-3).1 Knee flexion then puts excessive force across the graft and potentiates graft attenuation and failure. There also appears to be a trend toward more vertical placement of the femoral tunnel. A centralized graft may control pure anterior translation of the tibia on the femur, thereby eliminating the patient’s Lachman test, but will fail to control tibial rotation resulting in a postoperative pivot-shift and persistent instability.4 Tibial tunnel anteriorization can also result in significant dysfunction, with both loss of extension through notch impingement and loss of flexion via a mechanism analogous to that of an anteriorized femoral tunnel. However, with current endoscopic techniques, posteriorized tibial tunnels are encountered more commonly than anteriorized tibial tunnels and can cause loss of flexion through impingement against the posterior cruciate ligament (PCL). Although these may be the most com-

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Tunnel placement Graft failure (recurrent or persistent instability)

Failure to address secondary stabilizers Graft fixation New traumatic failure Impingement (cyclops lesion, notch)

Loss of motion Clinical failure

“Captured knee” (tunnel malposition) Capsulitis/scarring (arthrofibrosis) Anterior knee pain

Dysfunction of extensor mechanism

Quadriceps weakness Patellar fracture Isolated chondral defect

Secondary degenerative joint disease

Unicompartmental arthritis

Figure 52-2 Lateral radiograph demonstrating anterior malposition of the femoral tunnel.

Tricompartmental arthritis Figure 52-1 Flowchart summarizing potential causes of clinical failure following anterior cruciate ligament reconstruction.

monly encountered types of tunnel malposition, any combination of tibial and femoral tunnel may be observed. Types of tunnel malposition and their effects on knee motion are summarized in Table 52-1. Failure to recognize and treat combined instability patterns represents another significant cause of graft failure, thought to account for as many as 15% of cases.7 Injury to secondary stabilizers of the knee such as the medial collateral ligament, posterolateral corner, and the posterior horn of the medial meniscus can occur during the initial trauma or can become damaged over time, placing additional stress on the graft and potentiating early failure. Posterolateral instability has been reported to accompany as many as 15% of chronic ACL injuries.3 Unrecognized angular malalignment conditions, such as the double varus and triple varus knee (explained later in this chapter) can also lead to excessive graft strain and early failure.8 Catastrophic failure of graft fixation is uncommon but has been reported.9 Certain technical errors are known to contribute to failure of fixation, including interference screw divergence and graft-tunnel mismatch.4,10 In cases of screw divergence, the path taken by the interference screw diverges with that of the graft, decreasing contact area between the screw and the graft and weakening fixation strength.4 This is more problematic with the dual-incision technique than the endoscopic technique,

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although more common with the endoscopic technique. On the femoral side, with the endoscopic technique, screw divergence may still provide a “wedge” or “doorstop,” despite suboptimal contact between the interference screw and bone block. This is not the case with femoral-side fixation using the dual-incision technique, as a result of placement of the interference screw from outside-in.

C

B

A

C B

A

Figure 52-3 The shape of the distal femur results in a cam mechanism that puts excessive tension on grafts whose femoral point of fixation has been anteriorized. Graft A has a femoral tunnel in the desired posterior position and approximates isometry during flexion. Grafts B and C have progressively anteriorized femoral points of fixation and experience excessive strain with knee flexion as the posterior condyles engage.

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Table 52-1 Tunnel Position

Femur

Tibia

Anatomic Position

Tunnel Malposition

Cause

Effect on Graft

Patient Complaint

Sagittal: 1–2 mm anterior to posterior femoral cortex in notch

Anterior

Failure to identify true posterior margin of notch; “resident’s ridge”

Excessive tension in flexion

Loss of flexion; recurrent instability with graft attenuation

Coronal: 1 o’clock (left knee) or 11 o’clock (right knee) position

Central (vertical)

Placement of graft centrally in the notch

Inability to control rotatory forces

Persistent rotatory instability without elimination of pivot shift

Posterior

Nonanatomic technique with graft fixation in “over-the-top” position

Excessive tension in extension

Loss of extension; recurrent instability with graft attenuation

Sagittal: at point of intersection between posterior aspect of anterior horn of lateral meniscus and medial tibial spine; 1–2 mm anterior to leading edge of PCL

Anterior

Excessively large angle on tibial guide/tunnel; failure to adequately débride ACL stump and identify tibial landmarks

Excessive tension in flexion; notch impingement in extension

Loss of flexion; loss of extension with notch impingement; morning stiffness; recurrent instability with graft attenuation

Coronal: midpoint of upslope of medial tibial spine

Posterior

Excessively small angle on tibial guide/tunnel

Impingement on PCL in flexion

Loss of extension; loss of flexion; recurrent instability with graft attenuation

Lateral

Failure to identify tibial footprint of ACL

Impingement on lateral femoral condyle in flexion

Loss of flexion; catching sensation

Medial

Failure to identify tibial footprint of ACL

Impingement on PCL in flexion

Loss of flexion

ACL, Anterior cruciate ligament; PCL, posterior cruciate ligament.

If the length of a bone-tendon-bone graft does not match the composite length of the recipient tibial tunnel + intra-articular + femoral tunnel lengths, then a graft-tunnel mismatch exists. The surface area of bone block in the tibial tunnel for interference screw fixation is therefore reduced, again weakening fixation strength.11 This may lead to micromotion and graft attenuation in the early postoperative period. Several strategies have been advocated for graft tunnel mismatches, including conversion to a dual-incision technique if recognized prior to femoral tunnel creation, recessing the femoral bone plug, rotating the graft 540 degrees to shorten the construct, or removing the bone block to create a free bone block modification. Traumatic tear of a well-functioning reconstruction is also a possible mode of failure, particularly within a population of high-level athletes.

Loss of Motion Loss of motion can arise from multiple causes. Specific causes include presence of a cyclops lesion and notch impingement secondary to inadequate notchplasty or tunnel malposition. A cyclops lesion refers to the presence of a mass of scar tissue lying anterior to the tibial tunnel that impinges against the notch as the knee comes into extension. Patients typically present several months into the postoperative period with complaints ranging from a subtle click to a painless mechanical “clunk” as the knee extends. Inadequate débridement of the ACL stump is thought to be one source of this lesion, which is reported to occur in between 2% and 4% of ACL reconstructions. More general causes of motion loss include scarring of the capsule, scarring of the patellar tendon (patella infera), and contracture of a variety of other soft-tissue structures leading to a

condition known as arthrofibrosis and producing a stiff knee following an otherwise sound reconstruction procedure. Factors associated with the development of arthrofibrosis include poor preoperative range of motion, inability to achieve full extension early in the postoperative period, tunnel malpositioning, inappropriate graft tensioning, concomitant meniscal repair or medial cruciate ligament reconstruction, and male gender.3

CLINICAL FEATURES AND EVALUATION History Complaints of pain versus those of instability should be clearly delineated. A patient with a chief complaint of pain following ACL reconstruction may be treated in a markedly different fashion than one whose chief complaint is recurrent or persistent instability. ACL revision is much more successful in addressing an unstable knee in which pain is not a significant component than those in which pain is the chief complaint. Additionally, infection and complex regional pain syndrome should be considered in those patients complaining primarily of disproportional pain. The degree to which a patient was able to return to normal activity, that is, whether the patient feels stability was ever restored to their knee, should be assessed. Persistent instability suggests failure to identify and treat a complex instability pattern in which secondary knee stabilizers have been injured. Early, abrupt, recurrent instability can be caused by failure of graft fixation. Early, gradual, recurrent instability may result from graft attenuation via tunnel malposition. Late recurrent instability following a period of return to normal activity most often results from traumatic retear.

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Previous operative reports should be obtained to facilitate understanding what was done during the index procedure and to identify the manufacturer of the fixation device so that the appropriate tools for hardware removal can be made available.

Physical Examination Skin condition and configuration of previous incisions should be inspected. Presence or absence of an effusion should be noted. Clinical varus or valgus alignment should be evaluated. Range of motion should be carefully documented and the presence and degree of flexion contracture recorded. Prone heel heights in flexion and extension can be used to assess knee flexion and extension contractures. Varus and valgus laxity should be tested at 0 and 30 degrees of flexion to evaluate collateral ligament integrity. Anterior drawer, Lachman, and pivot-shift testing should be performed and results compared to those of the contralateral, normal knee to identify the degree of instability present. Posterior drawer testing should be conducted to rule out concomitant posterior cruciate ligament injury, and the dial test should be performed at 30 and 90 degrees of flexion to rule out injury to the posterolateral corner. Patellar mobility and the presence of patellofemoral crepitation should be assessed. Finally, the patient’s gait should be observed carefully.

Imaging A standard series of plain radiographs consisting of a standing anteroposterior, Rosenberg (weight bearing posteroanterior in 45 degrees of flexion), and Merchant views of both knees, as well as a lateral of the affected side should be examined for tunnel position, tunnel enlargement, and failure of fixation (see Fig. 523). Clinical evidence of angular malalignment should be further evaluated with standing, long-cassette views of both lower extremities. The presence of significant tunnel enlargement

Figure 52-4 Magnetic resonance imaging of a failed anterior cruciate ligament reconstruction using Achilles tendon allograft reveals marked enlargement of the tibial tunnel that required staged treatment with tunnel débridement and grafting followed by reconstruction.

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on a plain radiograph may require evaluation with computed tomography or magnetic resonance imaging (MRI) to determine whether a single or staged procedure should be undertaken (Fig. 52-4).12 Furthermore, MRI can be useful in identifying intraarticular pathology that may require attention at the time of a revision procedure, such as chondral defects, meniscal tears, and presence of a cyclops lesion. Because instability can exist in the presence of a radiographically intact graft, however, MRI should be relied on to confirm or rule out graft failure. Failure is a clinical, not radiographic, diagnosis.

SURGERY Preoperative Planning Once a diagnosis of failed reconstruction has been made, a plan should be formulated to address the identified mode of failure. Not all scenarios mandate ACL graft revision. For example, presence of an isolated cyclops lesion generating loss of motion in an otherwise stable knee without tunnel malposition can be treated effectively with arthroscopic débridement. The majority of clinical failures, however, do involve index graft revision. Although a trial of functional bracing may be considered for those patients willing to make significant lifestyle modifications and accept the possibility of meniscal injury with its incumbent risk of accelerated arthrosis, most cases necessitate operative treatment. The patient should be counseled that the results of revision reconstruction are not equivalent to those of index procedures.13 Nevertheless, proper planning and execution should result in a stable construct, and if patient expectations are appropriate, the chance of overall success remains high. Following careful clinical evaluation as previously outlined, a preoperative checklist (Table 52-2) of key variables can be formulated to help with planning. Graft selection for revision reconstruction remains a controversial issue, and success has been reported with a variety of different allograft and autograft constructs. Consensus does exist, however, that synthetic graft materials are not recommended for either primary or revision ACL reconstruction. The most commonly reported grafts selected for revision reconstruction are bone-patellar tendonbone (BPTB) autograft, and fresh-frozen BPTB allograft.4 Autograft offers more rapid graft tunnel incorporation and avoids risk of disease transmission but may not be available in a revision setting and carries with it the risk of donor site morbidity. Use of allograft, on the other hand, eliminates donor site morbidity. An additional advantage of allograft use is that accompanying bone blocks are often large, a useful feature when attempting to achieve rigid fixation in the context of tunnel dilatation (Fig. 525). Some patients, however, may be unwilling to accept the small, but finite risk of disease transmission with the use of allografts. Commercial tissue banks often use doses of gamma irradiation between 1.5 and 2.5 mrad to treat harvested tissue. While doses in this range are considered to be bactericidal, Smith et al14 showed that active viral replication of human immunodeficiency virus type 1 persisted in culture after doses as high as 5.0 mrad. Such high doses of gamma irradiation, however, may render allograft tissue mechanically unfit for implantation. Fideler et al15 clearly demonstrated a dosedependent decrease in the biomechanical properties of BPTB allograft following gamma irradiation. With use of 2.0 mrad of gamma irradiation, they observed a 15% reduction in initial biomechanical strength when compared to nonirradiated freshfrozen controls. This reduction increased to as high as 46% when

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Table 52-2 Anterior Cruciate Ligament Revision Preoperative Checklist Preoperative Checklist

Comments

Mode of failure of index procedure Type of hardware used in index procedure

A selection of screwdrivers and other extraction devices when indicated should be available for hardware removal

Presence of tunnel enlargement

Marked enlargement (>15 mm) may require a staged procedure

Presence of concomitant intra-articular pathology

Meniscal tears or focal chondral defects should be addressed at the time of the revision procedure

Presence of angular malalignment

Significant angular malalignment can contribute to index graft failure and should be addressed at the time of the revision procedure

Integrity of secondary stabilizers

Posterolateral corner reconstruction may be required at the time of revision

Revision graft selection

Allograft vs. autograft; irradiated vs. nonirradiated; availability must be confirmed

Revision graft fixation

At least two means (primary and back up) of secure fixation should be available and the surgeon should be facile with each (e.g., interference screw, EndoButton)

Revision tunnel placement

The means of establishing anatomic tunnel position should be decided (e.g., overlapping tunnels, diverging tunnels, two-incision technique)

grafts were exposed to a 4-mrad dose. Use of irradiated versus nonirradiated allograft remains controversial, as does the optimal dose of gamma irradiation in the case of irradiated tissue. Current molecular screening tests, such as reverse-transcriptase polymerase chain reaction and other techniques are highly sensitive, and the surgeon and patient must make a joint, informed decision when it comes to autograft versus allograft and irradiated versus nonirradiated. Another consideration when using allografts for revision work is the amount of tissue that will be necessary given the size of the patient. When ordering a BPTB allograft, inclusion of the patient’s height may help avoid mismatch between the size of graft received and the amount of tissue needed for reconstruction. Finally, quadruple hamstring and quadriceps tendon grafts (allo- and auto-) are also possibilities for revision reconstruction, but experience with these graft selections in the setting of revision surgery is less extensive than that with BPTB grafts.

Figure 52-5 Intraoperative image of a standard bone-patellar tendonbone allograft after the portion to be used for the reconstruction has been harvested. Ample bone stock remains in the allograft, permitting femoral and tibial bone blocks to be fashioned larger as needed and providing substrate for grafting of bony defects.

Surgical Technique with Bone-Patellar TendonBone Allograft Examination of the patient under anesthesia should confirm preoperative diagnosis of graft failure and rule out the presence of a complex instability pattern. The sequence of operative steps is in general the same as that used for primary ACL reconstruction: diagnostic arthroscopy and débridement of failed graft, tibial followed by femoral tunnel preparation, allograft preparation (alternatively, depending on anticipated needs, graft preparation can take place as the initial step or simultaneous to other steps), passage, cycling, and fixation of the graft. Most revision reconstructions can be accomplished via an endoscopic, single-incision technique. The patient is placed in a supine position with the operative extremity held in standard ring-type leg holder. The nonoperative leg is flexed at both the knee and hip and secured in a padded gynecologic leg holder. The waist of the table is flexed and the foot is dropped, permitting easy access to both medial and lateral aspects of the knee. If the need for extensive bone grafting of widened tunnels is anticipated, then the ipsilateral iliac crest can be prepped and draped into the field. Standard arthroscopic portals are established, and a general diagnostic arthroscopy is performed. Status of the medial, lateral, and patellofemoral compartment articular cartilage as well as the menisci is evaluated and recorded. Residual ACL tissue is débrided, taking particular care to débride the tibial ACL footprint such that the medial tibial spine, the leading edge of the posterior cruciate ligament, and the posterior aspect of the anterior horn of the lateral meniscus can be identified as landmarks for accurate tibial tunnel placement. The exit point of the previous tibial tunnel and the entry point of the previous femoral tunnel are defined carefully with a shaver and arthroscopic electrocautery, and a final plan is formulated for revision tunnel preparation. Removal of previously placed interference screws can be challenging and, if not done carefully, can lead to cortical violation of the tibia and/or femur, including posterior wall blowout. Although not routinely necessary, use of intraoperative image intensification can facilitate removal and permits evaluation of

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cortical integrity. A number of strategies can aid in the safe removal of a femoral interference screw. A spinal needle should be used to triangulate and establish the proper angle for removal, and at times the screw can be accessed via the tibial tunnel. Tunnels in acceptable position are redrilled and cleared of all fibrous tissue, and the bone blocks of the allograft sized appropriately to fill the tunnels. Passage of the arthroscope through the tibial and/or femoral tunnel permits confirmation of the adequacy of débridement and maintenance of osseous integrity. Old tunnels that are malpositioned by more than one diameter can be bypassed, as the new tunnels can be placed in anatomic position without overlap (Fig. 52-6) and may not require hardware removal. However, for cases in which preexisting hardware interferes with new tunnel placement, hardware removal and, where indicated, bone grafting of a subsequent defect should be done prior to drilling the new tibial or femoral tunnel. A clear arthroscopic cannula placed through the standard or an accessory inferomedial portal can be useful for packing allograft chips into the femoral tunnel. A solid block of allograft bone fashioned from the excess that accompanies a standard BPTB allograft can be also be used to fill bony defects in either the femoral or tibial tunnels (Fig. 52-7). The degree of tunnel enlargement present at the time of reconstruction may require special attention. Tunnel enlargement that compromises attempts at revision graft fixation must be staged. In the first stage, the failed graft is excised, tunnels are débrided of all soft tissue, and allograft chips, autograft (e.g., iliac crest), or a mixture of both is used to fill all bony defects (Fig. 52-8). The patient is then treated with protected weight bearing for 8 to 12 weeks until bone graft incorporation is complete and new tunnels can be prepared through restored bone

A

B

C

Figure 52-6 Drawing illustrating nonoverlapping tunnels. The anterior position of the existing femoral tunnel (1) allows drilling of the revision tunnel posteriorly (2) as in a primary case. (From Bach BR Jr, Mazzocca A, Fox JA: Revision anterior cruciate ligament surgery. In Grana WA [ed]: Orthopaedic Knowledge Online. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2003.)

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Figure 52-7 Series of intraoperative arthroscopic photos demonstrating revision of a malpositioned femoral tunnel. A, Removal of interference screw from original reconstruction. B, Bone grafting of original femoral tunnel. C, Drilling of revision femoral tunnel in isometric position.

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Figure 52-8 Drawing illustrating bone grafting of an enlarged tibial tunnel. (From Bach BR Jr, Mazzocca A, Fox JA: Revision anterior cruciate ligament surgery. In Grana WA [ed]: Orthopaedic Knowledge Online. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2003.)

stock. For cases of mild tunnel enlargement in which a single interference screw is judged to be inadequate, techniques such as using large bone blocks on the allograft, bone grafting at the time of the reconstruction, or stacking interference screws in which a second screw is placed parallel to and alongside the first screw can enhance fixation strength. As in index reconstruction, the tibial tunnel is prepared first. An elbow-type aiming guide is typically recommended. The tendinous portion of the graft is measured and the “n + 10” rule used to determine the appropriate guide setting. It can be helpful to leave the tibial-side bone block intentionally long to compensate for possible graft-tunnel mismatch. Excess bone block can later be trimmed as needed. In some instances, the posterior wall of the femoral tunnel is found to be “blown out” or is violated during attempts to bypass an old anterior femoral tunnel at the time of revision surgery. Interference screw fixation is compromised in these situations because an intact osseous tube is required for interference fit. Cases of posterior wall blow out can be approached using the “divergent tunnel” concept, which refers to the fact that both the femoral and tibial tunnels can have a variety of different orientations without changing the intra-articular orientation of the graft. Arthroscopic two-incision technique permits rigid interference screw fixation through outside-in screw placement in cases in which the posterior cortex is blown out (Fig. 52-9). Alternatively, an EndoButton (Smith & Nephew, Andover, MA) technique can be used, eliminating the need for posterior wall integrity. Following placement of new tunnels and bone grafting where needed, the graft is passed in standard fashion. Femoral-side fixation is achieved as described; and the graft is cycled in order to pre-tension the graft and evaluate isometry. The graft should translate no more than 1 to 2 mm in the tibial tunnel as the knee comes into full extension if tunnel placement is correct. Tibialside fixation is then achieved with the knee in full extension and axially loaded. Some surgeons prefer to achieve tibial-side fixation with the knee held in a reverse Lachman position, but this maneuver raises concern about overconstraining the knee. Interference screw fixation can be reinforced using a screw and washer construct or staples if bone is deficient or osteopenic or if fixation is simply judged to be inadequate. Restoration of

Figure 52-9 Illustration of the “divergent tunnel” concept, in this case demonstrating a revision femoral tunnel (2) drilled from outside in using a two-incision technique. (From Bach BR Jr, Mazzocca A, Fox JA: Revision anterior cruciate ligament surgery. In Grana WA [ed]: Orthopaedic Knowledge Online. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2003.)

stability is assessed with Lachman and pivot-shift testing intraoperatively.

POSTOPERATIVE REHABILITATION Expectations regarding return to play and knee “normalcy” following revision ACL reconstruction should be tempered by the reality that reported results are less encouraging than those following primary reconstruction.13 Fox et al observed a 28% failure rate (defined as presence of a pivot-shift or KT-1000 manual maximal side-to-side difference greater than 5 mm) in their series of 32 ACL revision reconstructions using nonirradiated, fresh-frozen BPTB allograft in which a standard, accelerated rehabilitation protocol was implemented. The exact effect of the rehabilitation variable in this series is unknown, but it is possible that a less aggressive protocol could have led to less graft attenuation. Nevertheless, the goals of postoperative rehabilitation following revision ACL reconstruction are in general the same as those following an index procedure, and it should be noted that in the Fox et al series no cases of arthrofibrosis were encountered. The patient is protected in a hinged rehabilitation brace postoperatively and is permitted immediate range of motion as tolerated. Typically, weight bearing is also permitted as tolerated in

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the immediate postoperative period as long as the brace is locked in full extension. Weight-bearing restrictions may be indicated, however, if bone grafting was required. Phases of rehabilitation proceed in standard fashion. Focus is initially on regaining quadriceps control and obtaining full active extension. Gait is protected with crutch use during this period. Once quadriceps control and full extension have been regained, typically at 4 to 6 weeks postoperatively, crutch and brace use is discontinued and focus shifts to obtaining full flexion and strengthening with closed-chain exercises. Once full range of motion and appropriate strength have been regained, typically at 3 months postoperatively, jogging straight ahead without cutting or pivoting is initiated. As strength and flexibility return, cutting, pivoting, plyometric, and sport-specific drills are gradually introduced. By 6 months postoperatively, the patient is generally allowed return to unrestricted activity with use of a custom ACL orthosis from 6 months to 1 year postoperatively.

accompany as many as 80% of all acute ACL tears. The majority of bone bruises, termed reticular in nature, are seen on MRI as hemorrhage and edema in medullary bone without involvement of the subchondral plate and typically resolve by 6 to 12 months without known long-term sequelae. A minority of bone bruises, however, termed geographic, demonstrate on MRI signal change contiguous with subchondral bone and have a high likelihood of resulting in osteochondral sequelae.19 At the time of reconstruction, arthroscopic evaluation of the joint may reveal a focal, full-thickness chondral defect, requiring one of a variety of strategies to salvage the articular surface. If the defect involves an osteochondral fragment, the surgeon may attempt reduction and fixation using a variety of techniques. Well-defined, geographic lesions may be amenable to marrow stimulation techniques such as microfracture or osteochondral autograft transfer (Fig. 52-10). Larger lesions may demand osteochondral allograft transfer or autologous chondrocyte implantation. In addition to adding complexity to the ACL reconstruction, cartilage repair procedures require alterations in postoperative rehabilitation protocols, often with restrictions on the patient’s weight-bearing status.

ARTHRITIS AND ANTERIOR CRUCIATE LIGAMENT DEFICIENCY Although acute meniscal and chondral injuries can occur at the time of ACL rupture, injury to articular cartilage commonly presents in the context of chronic ACL deficiency. It is well accepted that the natural history of ACL deficiency in the knee of an active individual is one of repeated episodes of instability, recurrent trauma to the menisci and articular cartilage, and accelerated arthrosis. Wear patterns in the chronically ACL-deficient knee tend to be predominantly posteromedial, with a higher relative frequency of medial meniscus and medial femoral condyle articular cartilage injury than lateral.16–18

Chronically Anterior Cruciate Ligament–Deficient Knee When addressing concomitant injury to articular cartilage in the context of the chronically ACL deficient knee, several very important points must be weighed: (1) the extent of damage to articular cartilage, (2) the status of the menisci, and (3) evidence of angular malalignment. Accurate determination of extent of articular involvement in the painful, unstable knee is perhaps of paramount importance. Significant involvement of two or more compartments may preclude attempts at joint salvage. Unicompartmental arthritis in the ACL-deficient knee, however, can be approached with ACL reconstruction and unloading osteotomy and/or meniscal transplantation where indicated.20 In select ACL-deficient patients without angular malalignment, isolated ACL reconstruction can be considered. Shelbourne et al18 reported significant and durable pain relief (5.5 years mean follow-up) in a group of 58 patients with a chroni-

Articular Cartilage Injury at Time of Anterior Cruciate Ligament Rupture The forces that result in a tear of the ACL produce high tibiofemoral shear forces that can cause focal injury to articular cartilage.19 Evidence of the energy transmitted to articular cartilage when the ACL is torn are the “bone bruises” of the lateral femoral condyle and posterolateral tibial plateau, recognized to

A

B

Figure 52-10 Arthroscopic images depicting microfracture of a large, full-thickness, focal, chondral lesion in a patient undergoing anterior cruciate ligament reconstruction. A, The lesion has been debrided down to a clean base without violation of the subchondral plate. B, Microfracture has been performed to stimulate fibrocartilage formation.

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cally ACL-deficient knee (mean time from injury to surgery, 8.2 years) in whom an isolated ACL reconstruction was performed with BPTB autograft. Interestingly, all patients in this series had obtained temporary relief from both pain and instability with preoperative bracing using an off-the-shelf functional brace designed for ACL insufficiency. The biomechanical importance of the meniscus is well known, and interest in meniscal transplantation has increased in recent years (Fig. 52-11). In the context of the ACL-deficient knee, the medial meniscus in particular has an important function. In addition to its role in minimizing point contact pressures via a hoop stress mechanism, the posterior horn of the medial meniscus functions as a secondary stabilizer against anterior translation of the tibia on the femur.21 The status of the menisci at the time of reconstruction can be an important factor in determining the success of ACL reconstruction. Shelbourne et al17 showed a significant difference in both subjective and objective measures (KT-1000 maximal manual difference) between patients who underwent ACL reconstruction with intact menisci and those status post complete or subtotal medial or medial and

A

lateral meniscectomies. Meniscal transplantation in combination with both primary and revision ACL reconstruction has been shown to be successful in terms of both subjective measures and objective measures of stability.22 Although not compared prospectively against a nontransplanted cohort, Sekiya et al22 reported impressive results in a population of patients (average age, 35 years) having undergone meniscal transplantation along with either primary or revision ACL reconstruction. In their study, 96% of patients did not have pain with activities of daily living, and 71% of patients participated in moderate or strenuous sports without discomfort. Their indications for combined meniscal transplantation and ACL reconstruction included history of meniscectomy, ACL injury with symptomatic instability, joint line pain and no more than 2 mm of joint space narrowing on a weight-bearing in 45 degrees of flexion posteroanterior radiograph. Evidence of extensive grade III or IV chondrosis discovered at the time of arthroscopy precluded meniscal transplantation. Additionally, all patients were evaluated for mechanical malalignment, and two patients in their series underwent lateral closing wedge osteotomy as an added procedure. In a select group of patients with meniscal deficiency and ACL injury, meniscal transplantation at the time of ACL reconstruction should be considered as a viable option for optimizing outcome. Mechanical alignment is also an extremely important consideration. Noyes et al8 have described a mechanical progression that can be seen in individuals with chronic ACL deficiency and baseline varus alignment. This group of patients progress from what the authors term “single” varus to “double” varus, and finally to “triple” varus if the process is not identified and corrected. The single varus knee is one in which the tibiofemoral articulation falls into varus alignment secondary to baseline osseous geometry and degeneration of the medial meniscus and medial compartment articular surfaces. The lateral structures in this case, however, continue to tether against further varus collapse. Once the lateral structures attenuate and the knee falls further into varus, developing a lateral condylar lift off or thrust with activity, the knee is said to have developed double varus. Finally, as the posterolateral structures fail, the tibia falls into external rotation and the knee into recurvatum, resulting in the triple varus knee (Fig. 52-12). Correction of this process can require ACL reconstruction, osteotomy, and meniscal transplant where indicated.

ANTERIOR CRUCIATE LIGAMENT INJURY IN THE SKELETALLY IMMATURE

B Figure 52-11 A, Medial meniscal allograft prepared for transplantation using double bone plug technique. B, Passage of medial meniscal allograft into medial compartment. A Henning retractor has been placed adjacent to the posteromedial joint capsule through a standard posteromedial approach for retrieval of inside-out meniscal sutures.

ACL injury in the skeletally immature patient represents another set of complex issues in ACL reconstruction. Intrasubstance tears of the ACL have been reported with increasing frequency as more children participate in high-level athletic activities.23 As many as 65% of acute pediatric knee injuries (children ages 13 to 18 years) accompanied by hemarthrosis involve injury to the ACL.24 The predicament presented by pediatric ACL injury is a difficult one. On the one hand, neglect of a complete tear of the ACL can, as in adults, lead to repeated episodes of instability, meniscal injury, and accelerated arthrosis.25–27 On the other hand, ACL reconstruction carries the theoretical risk of limb shortening or angular deformity resulting either from direct mechanical disruption of the physis or according to the Hueter-Volkmann principle from increased mechanical loads across the physis.28,29 With the distal femoral and proximal tibial physes together accounting for approximately

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WBL = 33% With or without medial compartment narrowing

Lateral compartment opening

WBL = 20%

WBL = 5%

Lateral compartment opening

Hyperextension and external tibial rotation Primary varus • Tibiofemoral geometry

Double varus • Tibiofemoral geometry • Separation of lateral compartment

Triple varus • Tibiofemoral geometry • Separation of lateral compartment • Varus recurvatum

Figure 52-12 Illustration of the concept of Noyes et al of single, double, and triple varus knee deformity.

65% of total leg length, there exists the potential for significant deformity. This scenario plays itself out most commonly in an adolescent population. Retrospective reviews of large numbers of pediatric patients suggest that intrasubstance tears of the ACL are extremely rare in young children (younger than 12 years old).30,31 More than 80% of ligament injuries involve tibial spine avulsion rather than intrasubstance tear in children younger than 12 years of age.30 Tibial spine avulsions invoke an algorithm different than that of intrasubstance tears, with consensus dictating that displaced fractures should be reduced and fixed anatomically. Complete tear of the ACL without concomitant meniscal or chondral injury in a slightly older, adolescent population represents perhaps the most difficult scenario with respect to decision making. These patients are often 24 to 36 months away from skeletal maturity, at which time definitive, transphyseal reconstruction of the ACL could be performed without concern for iatrogenic injury to the growth plate. This also, however, tends to be a very active population that may not easily accept the necessity of stringent activity modification for these 2 to 3 years, followed by another 3 to 6 months of postoperative rehabilitation prior to returning to preinjury level of competition.

Pathophysiology Several animal studies have looked at growth disturbance as a function of physeal drilling, bridging with soft-tissue grafts and application of tensile force. Stadelmaier et al32 reported that four of four canines who underwent simple transphyseal drilling without soft-tissue graft interposition went on to at least partial

542

epiphysiodesis, where as canines with soft-tissue graft interposition following drilling did not. Of note, the grafts placed in this study were not tensioned. Makela et al33 drilled transphyseal tunnels in a rabbit model and observed no disturbance when the cross-sectional area of the defect was less than 3% of the total physeal area. Osseous bridging was, however, demonstrated when the size of the defect was 7% or more of the total physeal cross-sectional area. Edwards et al34 performed ACL reconstruction using a transphyseal, tensioned soft-tissue graft with extraphyseal fixation in a canine model. They found significant femoral valgus deformity and significant tibial varus deformity without physeal bar formation. A single degree of graft tensioning was used for all subject animals. It is somewhat difficult to interpret how this might translate to ACL reconstruction in the skeletally immature human. Furthermore, without an extraphyseal, tensioned graft control group, it is difficult to sort out the effects of transphyseal drilling versus graft tensioning on the growth disturbance observed. Behr et al35 conducted an anatomic study to determine the relationship between the “over-the-top” position and the distal femoral physis. They found that the femoral attachment of the ACL was at an average of 3 mm from the level of the physis and that the “over-the-top” position was at the level of the physis. All these studies have technical ramifications when contemplating ACL reconstruction in a skeletally immature population. The findings of Stadelmaier et al suggest that soft-tissue grafts such as quadruple hamstring autograft are relatively safe from the standpoint of generating physeal disturbance. The study of Makela et al indicates that more vertically oriented transphyseal

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tunnels, which disturb a smaller cross-sectional area of the physis, are preferred. The relationship between the “over-thetop” position and the distal femoral physis of Behr et al cautions against reconstructive techniques that involve dissection or fixation at or near the “over-the-top” position. Finally, the findings of Edwards et al recommend against overtensioning of the graft, although it is difficult to quantify this recommendation.

ACL and occurrence of medial meniscus injury in a skeletally immature population. This retrospective study did not, as did that of Woods and O’Connor, include a group treated with a specific nonoperative strategy of patient education and activity modification. These studies underscore the absolute necessity of education and strict activity modification if nonoperative treatment of complete tears of the ACL in skeletally immature patients is to be successful.

Clinical Features and Evaluation Physical examination of the pediatric knee follows the same general guidelines as that of the adult. Observation should document any skin injury and should record the presence and relative size of an effusion. Active and passive range of motion should be recorded. Stability should be evaluated with anterior and posterior drawer, Lachman, pivot-shift, and dial tests and varus/valgus stress at 0 and 30 degrees. A complete neurovascular examination should be performed. Imaging studies should include a plain radiographic series to identify the occasional tibial spine fracture presenting as an intrasubstance ACL injury. Varus or valgus stress radiographs may be useful, as femoral physeal fractures can mimic ligamentous injuries to the knee. MRI has been criticized for high falsepositive and false-negative rates in pediatric populations, but with modern techniques, MRI can be valuable in confirming a clinical diagnosis of ACL rupture, identifying osteochondral injury, and diagnosing concomitant meniscal pathology.23,36 The most important part of the pediatric workup is determination of skeletal maturity. Multiple methods can be used, including Tanner staging, radiographic bone age using the radiographic atlas of Greulich and Pyle, and determination peak height velocity.29,37,38 Additionally, onset of menses is an important historical component when treating adolescent females, as it heralds an end to skeletal growth. As no single method is 100% accurate, it may be best prudent to use more than one technique prior to making establishing a definitive treatment plan.

Nonoperative Treatment Nonoperative treatment in the context of a complete ACL tear should be reserved only for those patients willing to accept the significant degree of activity modification necessary to avoid the further meniscal and chondral injury that can lead to accelerated arthrosis. Woods and O’Connor12 reported on a small group of adolescents with complete ACL tears managed successfully with activity modification when compared to a group who underwent early reconstruction. Their study, however, may have been underpowered to detect any real differences between the groups, making it difficult to draw any firm conclusions from their data. Kocher et al39 reported a 31% rate of ACL reconstruction resulting from recurrent instability and reinjury in a group of predominantly skeletally immature patients with incomplete tears of the ACL treated nonoperatively. Following a course of limited weight bearing, progressive mobilization in a hinged knee brace, and supervised physical therapy, return to sports was permitted at 3 months after injury in all cases. All episodes of instability and reinjury occurred during athletic activity. Multivariate analysis identified partial tears of the posterolateral bundle of the ACL and tears measuring more than 50% of the ligament diameter (judged arthroscopically) to be independent predictors of subsequent reconstruction. Millet et al26 found a statistically significant correlation between time to reconstruction following complete tear of the

Surgery Primary Repair Isolated primary repair of complete intrasubstance ACL tears has not been successful in reestablishing stability to the knee and is not recommended. Extraphyseal and Partial Transphyseal Reconstruction Extraphyseal reconstruction, in which either the femoral- or tibial-side attachments of the graft, or both, are routed around rather than through the physis is reserved only for those patients having a significant amount of growth remaining. These reconstructions are nonanatomic and nonisometric and tend to be less durable than standard transphyseal reconstructions, possibly necessitating revision at a later age. Multiple techniques have been reported with varying results. Andrews et al40 described a partial transphyseal technique in which a soft-tissue graft is routed through a 6- to 7-mm central, transphyseal tibial tunnel and subsequently into the “over-the-top” position on the femur. Both the femoral and tibial sides of the graft are secured in an extraphyseal fashion with posts. The authors reported on the use of this technique in a group of eight patients, ages 10 to 15 years, whom they followed through skeletal maturity with scanograms to identify any leg length discrepancy. No significant discrepancy or angular deformity was detected. All patients returned to athletic activity and KT-1000 arthrometer readings at the time of final follow-up were less than 3-mm displacement in four patients and less than 5 mm in the remaining four. Transphyseal Reconstruction Reconstruction with hamstring autograft is the procedure of choice for most skeletally immature patients undergoing ACL reconstruction.41 By minimizing tunnel diameter and orienting the tunnels vertically through the physes, one reduces the crosssectional area of physis disrupted by tunnel placement. The EndoButton (Smith and Nephew) or other extraphyseal means of fixation is used for the femoral side, and a standard post is used for tibial-side fixation. Additionally, one should avoid subperiosteal dissection around the femoral metaphysis, as this can lead to cortical bridging across the physis. The graft is tensioned with the knee in full extension. Use of hamstring autograft versus BPTB autograft avoids the disruption of the tibial tubercle apophysis that occurs with harvest of the latter and also avoids placement of bone blocks across the physis. Nevertheless, Shelbourne et al42 reported excellent results, without gross growth disturbance, following BPTB autograft reconstruction of Tanner stage 3 or 4 patients with “clearly” open physes. In this study, the authors altered standard BPTB technique, using a shortened tibial bone block and drilling the femoral tunnel such that the graft seated in a more proximal position than normal, resulting in both the femoral and tibial bone blocks resting proximal to their respec-

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Table 52-3 Recommended Method of Anterior Cruciate Ligament Reconstruction by Skeletal Age Skeletal Age

Gender

Graft

Femoral

Tibial

12

Male/female

HS

OTT

Transepiphyseal

13

Male/female

HS

OTT

Transphyseal tunnel with extraphyseal fixation

14

Male

HS

OTT

Transphyseal tunnel with extraphyseal fixation

Female

HS/BTB

FT

Transphyseal tunnel

Male

HS

OTT/FT

Transphyseal tunnel with extraphyseal fixation

Female

HS/BTB

FT

Transphyseal tunnel

Male/female

HS/BTB

FT

Transphyseal tunnel

15

16

BTB, Bone-tendon bone; FT, femoral tunnel; HS, hamstring; OTT, over the top. From Pavlovich R, Goldberg SH, Bach BR: Adolescent ACL injury. J Knee Surg 2004;17:79–93.

tive physes. This technique requires meticulous attention to graft and tunnel lengths to avoid crossing the physis with a bony block. An algorithm of recommended reconstructive procedures based on skeletal age is presented in Table 52-3.

CONCLUSIONS In the vast majority of cases, ligament reconstruction following complete tear of the ACL predictably restores stability to the injured knee and permits return to activity. Nevertheless, a number of difficult scenarios can complicate reconstruction, producing suboptimal results. Revision of a failed ACL reconstruction requires diligent preoperative planning, including clear identification of the mode of failure, as well as the technical ability to correct tunnel malposition and achieve secure graft fixation using multiple strategies. Chondral injury in the context of ACL injury, whether acute or in the context of the chronically ACL-deficient knee, presents a particularly challenging problem. In addition to ligament reconstruction, the surgeon may need to perform a corrective osteotomy or one of several biologic resurfacing procedures either at the time of ACL reconstruction or in a staged fashion. Finally, treatment of ACL injury in the skeletally immature requires careful evaluation of the patient’s remaining growth potential and demands a shared decision-making process that involves the patient and patient’s parents. The surgeon and family must weigh the risk of further intra-articular injury incumbent with nonoperative treatment versus reconstruction and the possibility of iatrogenic physeal injury with resultant length or angular deformity.

REFERENCES 1. Bealle D, Johnson DL: Technical pitfalls of anterior cruciate ligament surgery. Clin Sports Med 1999;18:831–845. 2. Brown CH Jr, Carson EW: Revision anterior cruciate ligament surgery. Clin Sports Med 1999;18:109–171. 3. Allen CR, Giffin JR, Harner CD: Revision anterior cruciate ligament reconstruction. Orthop Clin North Am 2003;34:79–98. 4. Bach BR Jr: Revision anterior cruciate ligament surgery. Arthroscopy 2003;19(Suppl 1):14–29. 5. Uribe JW, Hectman KS, Zuijac JE, et al: Revision anterior cruciate ligament surgery: Experience from Miami. Clin Orthop 1996;325: 91–99. 6. Johnson DL, Fu FH: Anterior cruciate ligament reconstruction: Why do failures occur? Instr Course Lect 1995;44:391–406. 7. Getelman MH, Friedman MJ: Revision anterior cruciate ligament reconstruction surgery. J Am Acad Orthop Surg 1999;7:189–198. 8. Noyes FR, Barber-Westin SD, Hewett TE: High tibial osteotomy and ligament reconstruction for varus angulated anterior cruciate ligamentdeficient knees. Am J Sports Med 2000;28:282–296. 9. Bush-Joseph CA, Bach BR Jr: Migration of femoral interference screw after anterior cruciate ligament reconstruction. Am J Knee Surg 1998;11:32–34. 10. Dworsky BD, Jewell BF, Bach BR Jr: Interference screw divergence in endoscopic anterior cruciate ligament reconstruction. Arthroscopy 1996;12:45–49. 11. Novak PJ, Wexler GM, Williams JS Jr., et al: Comparison of screw post fixation and free bone block interference fixation for anterior cruciate ligament soft tissue grafts: Biomechanical considerations. Arthroscopy 1996;12:470–473. 12. Woods GW, O’Connor PD: Delayed anterior cruciate ligament reconstruction in adolescents with open physes. Am J Sports Med 2004;32:201–210. 13. Fox JA, Pierce M, Bojchuk J, et al: Revision anterior cruciate ligament reconstruction with nonirradiated fresh-frozen patellar tendon allograft. Arthroscopy 2004;20:787–794.

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14. Smith RA, Ingels J, Lochemes JJ, et al: Gamma irradiation of HIV-1. J Orthop Res 2001;19:815–819. 15. Fideler BM, Vangsness CT Jr., Lu B, et al: Gamma irradiation: Effects on biomechanical properties of human bone-patellar tendon-bone allografts. Am J Sports Med 1995;23:643–646. 16. Murrell GA, Maddali S, Horovitz L, et al: The effects of time course after anterior cruciate ligament injury in correlation with meniscal and cartilage loss. Am J Sports Med 2001;29:9–14. 17. Shelbourne KD, Gray T: Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the time of surgery. Five- to fifteen-year evaluations. Am J Sports Med 2000;28:446–452. 18. Shelbourne KD, Stube KC: Anterior cruciate ligament (ACL)-deficient knee with degenerative arthrosis: Treatment with an isolated autogenous patellar tendon ACL reconstruction. Knee Surg Sports Traumatol Arthrosc 1997;5:150–156. 19. Levy AS, Meier SW: Approach to cartilage injury in the anterior cruciate ligament-deficient knee. Orthop Clin North Am 2003;34:149–167. 20. Williams RJ 3rd, Wickiewicz TL, Warren RF: Management of unicompartmental arthritis in the anterior cruciate ligament-deficient knee. Am J Sports Med 2000;28:749–760. 21. Cole BJ, Carter TR, Rodeo SA: Allograft meniscal transplantation: Background, techniques, and results. Instr Course Lect 2003;52:383– 396. 22. Sekiya JK, Giffin JR, Irrgang JJ, et al: Clinical outcomes after combined meniscal allograft transplantation and anterior cruciate ligament reconstruction. Am J Sports Med 2003;31:896–906. 23. Dorizas JA, Stanitski CL: Anterior cruciate ligament injury in the skeletally immature. Orthop Clin North Am 2003;34:355–363. 24. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop 1993;13:506–510. 25. Kannus P, Jarvinen M: Knee ligament injuries in adolescents. Eight year follow-up of conservative management. J Bone Joint Surg Br 1988;70:772–776.

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26. Millett PJ, Willis AA, Warren RF: Associated injuries in pediatric and adolescent anterior cruciate ligament tears: Does a delay in treatment increase the risk of meniscal tear? Arthroscopy 2002;18:955–959. 27. Mizuta H, Kubota K, Shiraishi M, et al: The conservative treatment of complete tears of the anterior cruciate ligament in skeletally immature patients. J Bone Joint Surg Br 1995;77:890–894. 28. Koman JD, Sanders JO: Valgus deformity after reconstruction of the anterior cruciate ligament in a skeletally immature patient. A case report. J Bone Joint Surg Am 1999;81:711–715. 29. Paletta GA Jr: Special considerations. Anterior cruciate ligament reconstruction in the skeletally immature. Orthop Clin North Am 2003;34:65–77. 30. Kellenberger R. von Laer L: Nonosseous lesions of the anterior cruciate ligaments in childhood and adolescence. Prog Pediatr Surg 1990;25:123–131. 31. Wessel LM, Scholz S, Rusch M, et al: Hemarthrosis after trauma to the pediatric knee joint: What is the value of magnetic resonance imaging in the diagnostic algorithm? J Pediatr Orthop 2001;21:338–342. 32. Stadelmaier DM, Arnoczky SP, Dodds J, Ross H: The effect of drilling and soft tissue grafting across open growth plates. A histologic study. Am J Sports Med 1995;23:431–435. 33. Makela EA, Vainionpaa S, Vihtonen K, et al: The effect of trauma to the lower femoral epiphyseal plate. An experimental study in rabbits. J Bone Joint Surg Br 1988;70:187–191. 34. Edwards TB, Greene CC, Baratta RV, et al: The effect of placing a tensioned graft across open growth plates. A gross and histologic analysis. J Bone Joint Surg Am 2001;83:725–734.

35. Behr CT, Potter HG, Paletta GA Jr: The relationship of the femoral origin of the anterior cruciate ligament and the distal femoral physeal plate in the skeletally immature knee. An anatomic study. Am J Sports Med 2001;29:781–787. 36. Lee K, Siegel MJ, Lau DM, et al: Anterior cruciate ligament tears: MR imaging-based diagnosis in a pediatric population. Radiology 1999;213:697–704. 37. Greulich WW, Pyle SI: Radiographic Atlas of Skeletal Development of the Hand and Wrist. Stanford, CA, Stanford University Press, 1950. 38. Guzzanti V, Falciglia F, Stanitski CL: Preoperative evaluation and anterior cruciate ligament reconstruction technique for skeletally immature patients in Tanner stages 2 and 3. Am J Sports Med 2003;31:941–948. 39. Kocher MS, Micheli LJ, Zurakowski D, Luke A: Partial tears of the anterior cruciate ligament in children and adolescents. Am J Sports Med 2002;30:697–703. 40. Andrews M, Noyes FR, Barber-Westin SD: Anterior cruciate ligament allograft reconstruction in the skeletally immature athlete. Am J Sports Med 1994;22:48–54. 41. Larson RV, Ulmer T: Ligament injuries in children. Instr Course Lect 2003;52:677–681. 42. Shelbourne KD, Gray T, Wiley BV: Results of transphyseal anterior cruciate ligament reconstruction using patellar tendon autograft in tanner stage 3 or 4 adolescents with clearly open growth plates. Am J Sports Med 2004;32:1218–1222.

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53

Posterior Cruciate Ligament Todd C. Battaglia, Kevin J. Mulhall, and Mark D. Miller

In This Chapter Classification Natural history Nonoperative management Surgery—posterior cruciate ligament (PCL) reconstruction

INTRODUCTION • PCL injury is less common than injury to the anterior cruciate ligament (ACL). • Information concerning PCL anatomy and biomechanics as well as the natural history of PCL deficiency and outcomes of surgical reconstruction is rapidly increasing. • PCL injuries usually occur in athletic or high-energy trauma situations as a result of a posteriorly applied force to the anterior tibia. • Most isolated, low-grade injuries are managed nonoperatively through an aggressive rehabilitation program. High-grade injuries, avulsions, and those combined with other ligamentous injuries are often treated with surgical reconstruction. Numerous surgical techniques have been described. • Although most isolated PCL injuries are treated conservatively, some studies suggest that chronic PCL deficiency may lead to progressive joint degeneration and arthritis.

RELEVANT ANATOMY The PCL originates in an irregular, elliptical attachment on the posterolateral border of the medial femoral condyle where the roof of the notch joins the wall, 2 to 3 mm from the articular surface1–3 (Fig. 53-1). It extends posteriorly, inferiorly, and slightly laterally to insert in a depression between the medial and lateral tibial plateaus termed the PCL facet or fovea. This depression is located 1 to 1.5 cm below the posterior tibial rim and joint line3 (Fig. 53-2). The PCL is an intra-articular but extracapsular (and therefore extrasynovial) structure, and reflected synovium from the posterior capsule surrounds the medial, lateral, and anterior borders of the ligament.4–6 The ligament is in close proximity to the posterior neurovascular bundle throughout its length.1 The PCL is composed primarily of type I collagen, although the mean fibril diameter varies with location and decreases proximally to distally.6 The major blood supply is via the middle

geniculate artery. The average ligament length is 30 to 38 mm, and the width averages 13 mm.1,5,6 The cross-sectional area is approximately 30 mm2 at mid-substance; this is 1.5 times that of ACL.5 The insertion sites are even larger, with cross-sectional areas three times larger than that in the midsubstance.2,5 Overall, the PCL is the strongest ligament crossing the knee and may be as much as twice as strong as the ACL. Multiple models have been used to describe intrinsic PCL anatomy, including models containing three and four bundle divisions as well as a continuum of fiber orientation. In a simplified model, however, there are three main components to the PCL complex: the anterolateral (AL) bundle, the posteromedial (PM) bundle, and meniscofemoral ligaments. The PCL proper is composed of the AL and PM bundles, of which the former is the larger and stronger. These distinctions are more functional than anatomic, as the AL and PM portions are difficult to separate macroscopically or microscopically.7 Although the insertion sites of the two bundles are relatively equal in size, the AL bundle has approximately two to three times the cross section of the PM and may be as much as five times stronger than the PM bundle.2–4,8 The AL bundle begins more anteriorly on the intercondylar surface of the medial femoral condyle, runs laterally, and inserts posteriorly on the lateral aspect of the tibial fovea. The PL bundle begins more posteriorly on the intercondylar femoral surface and inserts on the medial aspect of the fovea.7 Very few fibers of the PCL are truly isometric during the knee flexion arc.4,5 The AL band is tighter and thus more important in knee flexion, while the PM band tightens in extension (Fig. 53-3). During a knee flexion cycle, tension in the bundles appears to develop in a reciprocal fashion.1,9 The PCL is considered the primary restraint to posterior tibial translation, especially when the knee is flexed more than 30 degrees. In PCL-deficient knees, translation is minimal when the knee is in full extension and maximal at 90 degrees.9 The ligament is also a secondary restraint to varus and valgus force and to external tibial rotation, aiding the posterolateral corner complex (PLCC).3 Since it lies near the central axis of the knee, however, the PCL has a relatively small moment arm about the knee axis of rotation.7,8 Biomechanically, the PCL has an ultimate load of approximately 1600 N and a stiffness of 200 N/mm. Forces in response to given anterior tibial load increase as much as fourfold as the knee moves from full extension to 90 degrees of flexion.2 Two variable meniscofemoral ligaments originate from posterior horn of the lateral meniscus and run alongside and contribute fibers to the PCL. The ligament of Humphry passes anterior to the PCL and attaches distally, while the ligament of Wrisberg passes posteriorly and attaches proximally (Fig. 53-4).

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B A

23 mm

19 mm

Level of adductor tubercle

A′

B

A

A′ B′

B′

Figure 53-3 The posteromedial bundle of the posterior cruciate ligament (A-A¢) is taut in extension and lax in flexion, while the anterolateral bundle (B-B¢) is reciprocally tight in flexion and lax in extension. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

32 mm

9 mm

Figure 53-1 The origin of the posterior cruciate ligament forms an ellipse on the posterior portion of the medial femoral condyle. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

At least one ligament is present in more than 90% of specimens and both are found more commonly in younger patients, suggesting that they may degenerate with age.8,10 These meniscofemoral ligaments are believed to provide significant anatomic and biomechanical stability to the lateral meniscus, although their precise role is not currently well defined.9 The ligament of

Anterior cruciate

ETIOLOGY OF INJURY

Posterior cruciate

13 mm

Figure 53-2 The posterior cruciate ligament inserts in a central depression called the tibial fovea located 1 to 1.5 cm below the tibial joint line. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

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Humphry is usually smaller than the ligament of Wrisberg, but the strength of each is comparable to that of each other and to that of the PM band of the PCL.8 These ligaments may act as secondary restraints to posterior tibial translation, especially when the knee is flexed. Meniscofemoral ligaments may sometimes be preserved in the PCL-injured knee, making posterior laxity less dramatic.2 Other ligaments about the knee, the lateral collateral ligament, medial collateral ligament (MCL), and especially the PLCC, are secondary stabilizers to posterior tibial translation, playing a minimal role if the PCL is intact but become important if the PCL is deficient.1 In cadaveric studies, if only the PCL is sectioned, an average posterior tibial translation of 11 to 15 mm results; however, if the PLCC is also disrupted, posterior translation approaches 30 mm.1,2 Muscle forces about the knee also affect in situ forces on the PCL. Specifically, popliteus and quadriceps contraction can reduce PCL load, whereas hamstring and gastrocnemius contraction increase it.9

Historically, PCL injuries have been underdiagnosed. Recent studies describe PCL tears as accounting for 3% to 20% or more of all knee ligament tears, although still occurring less frequently than injuries of the ACL, MCL, and lateral collateral ligament.1,7,11–13 It is reported that dedicated arthroscopists and orthopedic sports physicians may perform only one tenth the number of PCL reconstructions as ACL reconstructions annually.14 The average age for PCL injury is approximately 30 years old. Athletic injuries account for as many as two thirds of all injuries, with high-energy trauma, especially motor vehicle accidents, accounting for much of the remainder.14 The most common sports in which PCL injury occurs involve high-contact forces, such as rugby and football. Injury occurs less frequently in the cutting and pivoting activities classically associated with ACL injury, such as basketball and soccer. Sporting injuries more fre-

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Figure 53-4 The meniscofemoral ligaments arise from the lateral meniscus and run alongside of the posterior cruciate ligament. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

Anterior cruciate ligament Anterior meniscofemoral ligament (ligament of Humphry) Posterior horn of lateral meniscus

quently involve isolated PCL tears, while some authors report that as many as 90% of emergency department trauma patients with PCL disruptions have combined ligamentous injuries. Typically, these are higher grade PCL disruptions and are associated with injury involving the PLCC structures.3,5 Regardless of the circumstances, the most common mechanism of injury involves a posteriorly directed force to the proximal tibia of a flexed knee (Fig. 53-5).This may occur in contact sports when a tackle causes a direct blow to the anterior tibia but also may occur when a player falls forward onto the knee, especially if the foot is in plantar flexion, which allows the

Posterior meniscofemoral ligament (ligament of Wrisberg) Posterior cruciate ligament

ground force vector to intersect the proximal tibia. When the foot is dorsiflexed, the ground force vector contacts the patella and distal femur, avoiding undue stress across the knee ligaments. In motor vehicle trauma, the classic mechanism involves a dashboard injury in which the knee and proximal tibia of a front seat rider strikes the dashboard.1 Forced hyperflexion with or without tibial load is a less common but well-reported mechanism of injury. Indirect methods of injury include twisting and hyperextension and often lead to combined ligament injuries.1,7 Significant varus or valgus force usually only disrupts the PCL after rupture of the appropriate collateral ligament.13

CLINICAL FEATURES AND EVALUATION

Figure 53-5 The most common mechanism of posterior cruciate ligament injury involves a direct force to the front of a flexed knee. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

The first step in determining appropriate management is accurate diagnosis. Isolated PCL tears are commonly overlooked during the initial evaluation, as history is often vague and physical examination findings are subtle. Partial, or even complete, isolated tears usually present with relatively benign symptoms.1 A thorough history should be obtained with special emphasis on the mechanism of injury, as this may give important information regarding injury severity and possible associated injuries. Unfortunately, awareness of ligamentous injury at the moment of PCL disruption is infrequent and many patients are unable to describe precisely how the injury occurred. Some patients may describe a “pop” or tearing sensation at the moment of injury but be unable to describe the exact biomechanical forces that occurred. Location and timing of pain, sensation of instability, and performance-related impairment are important complaints to elicit. During the acute phase of injury, patients may complain of a mild or moderate effusion and posterior knee pain or pain with kneeling. Instability in isolated PCL injury is an infrequent complaint and should lead the physician to suspect associated injuries. In subacute or chronic PCL injury, complaints may include vague anterior knee pain or pain with deceleration or stair descent. Commonly in chronic injury, patients may describe dull, aching pain localized to the patellofemoral and medial compartments.5 On physical examination, observe the patient’s gait and static weight-bearing alignment of the extremity. Varus thrust, where the knee shifts into varus during foot strike, is common in chronic posterolateral deficiency.1,2 In acute injury, the skin

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should be observed for any signs of trauma, especially over proximal tibia, and bruising may be found in the popliteal fossa from posterior capsular rupture. There are a number of specific maneuvers described to evaluate the PCL and its associated structures. Of these, the posterior drawer test is considered the most accurate (Box 53-1).

to cases in which the plateau can be displaced posterior to the condyle (10- to 15-mm displacement)15 (Fig. 53-7). One should also assess the endpoint when performing the posterior drawer test. Most acute injuries have an altered endpoint, although this may return to normal in chronic injuries in as quickly as a few weeks.4 If the tibia displaces more than 10 mm (grade III laxity), a combined injury, most commonly involving the PLCC, should be suspected. Careful examination of the ACL, collateral ligaments, and PLCC is crucial. PCL injury typically allows maximal posterior translation at 90 degrees of knee flexion, which is why the posterior drawer test is performed in this position. Maximal translation at 30 degrees, which decreases at 90 degrees, may indicate isolated PLCC injury.13 It is also critical to recognize that PCL incompetence may cause the tibia to rest in a posteriorly subluxed position, causing a false-positive Lachman test. In fact, it has been reported that 15% of patients surgically treated for isolated PCL injuries have previously undergone unnecessary ACL reconstruction as result of misdiagnosis (Box 53-2).5

Posterior Drawer Test

Posterior Sag (Godfrey) Test

Box 53-1 Clinical Diagnosis of Posterior Cruciate Ligament Injuries • • • • • • •

Posterior drawer test Posterior sag (Godfrey) test Quadriceps active test Dynamic posterior shift test Reverse pivot-shift test Dial (external rotation) test Whipple test

In this maneuver, the patient is supine with the feet on the table, the hip flexed 45 degrees and the knee flexed 80 to 90 degrees. Because the posterior drawer test is based on the relationship between the medial femoral condyle and the medial tibial plateau, comparison to the contralateral side is important in interpretation. First, the examiner must evaluate the tibial starting point. Normally, the tibial plateau step-off is approximately 1 cm anterior to the femoral condyle (Fig. 53-6). If a normal step-off is not palpated, PCL injury should be suspected. Next, a posteriorly directed force is applied to the anterior tibia. In a grade I injury, a palpable but diminished step-off is present, in which the tibial plateau remains anterior to the medial condyle (0- to 5-mm tibial displacement). In grade II injury, the plateau is palpated flush (5- to 10-mm displacement) but cannot be displaced behind the medial femoral condyle, and grade III refers

Here, the patient is also supine with the knee flexed 90 degrees. The examiner looks for abnormal contour or sag at the proximal tibia compared to the contralateral side. This subluxation may be accentuated by passive elevation of the heels.1,6

Quadriceps Active Test Again, the patient is supine with the knee flexed 60 to 90 degrees and the foot secured on the table. In an intact knee, voluntary quadriceps activation will result in slight posterior tibial translation. In PCL injury, however, with resisted knee extension and quadriceps contraction, the posteriorly subluxated tibia reduces anteriorly. This test may be useful in assessing relative anterior and posterior instability in patients with combined ACL and PCL deficiency.2 (Fig. 53-8).

Dynamic Posterior Shift With the hip and knee flexed 90 degrees, the knee is slowly extended. As the knee reaches full extension, the subluxed tibia reduces, often occurring with a palpable clunk.2

Reverse Pivot Shift With the patient supine and the knee flexed 90 degrees, the foot is externally rotated and the knee extended with an applied

Box 53-2 Classification of Posterior Cruciate Ligament Injuries16

Figure 53-6 Tibial step-off is assessed during the posterior drawer test. The examiner’s finger is used to palpate the relationship of the medial tibial plateau to the medial femoral condyle. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

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• Time frame Acute (8 weeks) • Instability Level 1: Posterior drawer £ grade II Level 2: Posterior drawer ≥ grade II; stable to varus and valgus stress at 0 degrees Level 3: Posterior drawer ≥ grade II; unstable to varus and valgus stress at 0 degrees or pathologic hyperextension Level 4: Knee dislocation

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1 cm Grade I (palpable step-off)

Normal

Figure 53-7 Classification of posterior cruciate ligament injury, as assessed with the posterior drawer test. In a normal knee, the anterior edge of the medial tibial plateau is palpated 1 to 1.5 cm anterior to the medial femoral condyle. In grade I injury, 0 to 5 mm of posterior tibial displacement is possible. In grade II injury, the tibia can be displaced flush with the femur (5 to 10 mm of displacement), and in grade III injury (>10 mm), the tibia can be displaced posterior to the condyle. (From Petrie RS, Harner CD: Evaluation and management of the posterior cruciate injured knee. Oper Tech Sports Med 1999;7:93–103.)

90°

90°

Dial (Tibia External Rotation) Test This is considered the most important test for posterolateral instability and is most easily performed with the patient prone.

90°

Grade III (reverse step-off– rule out posterolateral corner injury)

Grade II (palpable step-off eliminated)

valgus stress. A positive test occurs with palpable reduction of the displaced tibia at 20 to 30 degrees of knee flexion. It is important to examine the opposite knee, as a positive reverse pivot can be a normal variant in some patients.1

.5 cm

90°

The tibiae are externally rotated, and the thigh-foot angle measured and compared between sides. A pathologic examination is indicated by more than 10 to 15 degrees of asymmetry. The test should be performed with the knees at both 30 and 90 degrees of flexion. If asymmetry exists only at 30 degrees, this most likely indicates an isolated PLCC injury, but if asymmetry exists at both 30 and 90 degrees, combined PLCC and PCL injury should be suspected.

Figure 53-8 In the quadriceps active test, quadriceps contraction will reduce the posteriorly displaced tibia. (From Giffin JR, Annunziata CC, Harner CD: Posterior cruciate ligament injuries in the adult. In DeLee JC, Drez D Jr, Miller MD [eds]: Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 2083–2106.)

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Whipple (Prone Drawer) Test With the patient prone, the knee is flexed to 70 degrees. PCL insufficiency is tested by grasping the lower leg with one hand and posteriorly displacing the tibia with the other by pushing on the tibial tubercle. Although similar to the posterior drawer test, the prone position theoretically avoids quadriceps contraction, which could interfere with the examination.5,6

Radiography Any knee trauma should have a complete radiographic evaluation, including anteroposterior, lateral, sunrise, and tunnel views. Avulsion injuries (of the PCL, Gerdy’s tubercle, or fibular head), Segond fractures, posterior tibial sag, and lateral joint space widening should be noted (Fig. 53-9). Oblique radiographs may be necessary to evaluate for tibial plateau fractures. Flexion weight-bearing views are useful in chronic cases to assess limb alignment and medial compartment degeneration. Stress radiographs and contralateral comparison views may be useful in difficult cases; a lateral film with posterior tibial force will allow direct measure of posterior translation. A modified Laurin radiograph with or without weights (a sunrise view taken with the knee flexed 70 degrees) may demonstrate increased distance between the anterior femoral condyles and the anterior tibial edge, indicative of posterior tibial subluxation.6 With appropriate techniques and criteria, the sensitivity and specificity of magnetic resonance imaging in the diagnosis of complete PCL tears are thought to approach 100%. On magnetic resonance imaging, the normal PCL appears as a uniform band of low signal intensity. On sagittal images with the knee extended, the PCL is usually seen on one to two contiguous slices with an arcuate shape, whereas on coronal images, it appears as a vertically oblique band (Fig. 53-10). The meniscofemoral ligaments are seen on only 60% of magnetic resonance

Figure 53-9 Posterior tibial subluxation in a posterior cruciate ligament–deficient knee. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

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Figure 53-10 Sagittal magnetic resonance image of a normal posterior cruciate ligament. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

imaging studies, running in an oblique course adjacent to the anterior and posterior margins of the PCL.3 On magnetic resonance imaging, PCL injury typically appears as tearing of a portion, or the entire bulk, of PCL fibers; this is best evaluated on T2-weighted images with fat saturation (Fig. 53-11). Partial intrasubstance tears will be seen as thickening of the ligament with edema and hemorrhage causing fiber separation and associated increases in signal intensity.1,3 Isolated tears most frequently involve the midsubstance or anterior genu and

Figure 53-11 Magnetic resonance image of a complete posterior cruciate ligament tear. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

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less commonly the ligament attachments, although insertions are frequently disrupted in cases of knee dislocation or combined ligament injuries. Because there is some evidence that PCL tears can heal in an elongated fashion, chronic tears (especially grades I and II) may look normal on magnetic resonance imaging. If healed with fibrosis, the ligament may demonstrate abnormal low signal along its length.1,3 Meniscal tears and bone bruises are less commonly associated with isolated PCL tears than with ACL tears. In injuries due to posterior tibial displacement in a flexed knee, any associated bone bruising typically occurs along the anterior tibial articular surfaces and posterolateral femoral condyles. In acute hyperextension injuries, bone bruising may be seen at the anterior tibia and anterior femoral condyles.3,4 Finally, posterior tibial sag may create an illusion of ACL laxity and lead to false diagnoses of ACL injury.1

Diagnostic Arthroscopy Although the diagnosis should be clear before surgery, anesthesia will allow full examination of all structures, and numerous arthroscopic signs of PCL injury have been described. These include partial or complete disruption of fibers, insertion site avulsions, hemorrhage, and decreased ligament tension. Indirect evidence includes ACL pseudolaxity resulting from posterior tibial displacement, altered contact points between the tibia and femur, and degenerative patellofemoral and medial compartment changes.2,6 The PCL can usually be seen in its entirety using a 70-degree scope placed through the notch; if the tibial insertion is not visualized, a posteromedial portal will allow access. Because the PCL lies extrasynovially, it may appear normal unless the synovium is débrided.

NATURAL HISTORY It is widely agreed that when PCL injury occurs in combination with other major knee ligament injuries or when it occurs via bony avulsion, outcomes with nonoperative treatment are much poorer than with surgical intervention. The management of isolated PCL injuries is more controversial, however, because the natural history of isolated PCL injuries continues to be debated. Most series that report the results of nonoperative treatment of PCL tears include patients with mixed injury patterns and severities. While many authors believe that the PCL has some potential for intrinsic healing, this healing phenomena does not necessarily restore normal functional status.1,11,16 Regardless, in some studies, as many as 80% of patients with isolated PCL injuries managed nonoperatively with quadriceps and hamstring strengthening were satisfied with their outcome, and most returned to preinjury levels of activity.17 Furthermore, many high-caliber athletes may function well with PCL-deficient knees because as many as 2% of high-caliber college football players have been found to have a chronic PCL-deficient knee. The outcome of nonoperative treatment may depend on the patient’s ability to maintain quadriceps strength, as patients with better functional results appear to be those with greater quadriceps strength in the affected extremity.17 Many of these individuals have residual translation on posterior drawer testing, but this laxity does not appear to increase over time.12 Conversely, other authors suggest that even after isolated PCL injuries, many patients have frequent pain and occasional instability and giving way.1 In one study, although 88% of com-

petitive rugby players with isolated PCL injuries were able to return to preinjury levels of play, some patients took as long as 7 months to recover and nearly all reported subjective sensations of impaired ability, most commonly manifesting in highspeed running (slower acceleration and delayed response) and while turning.18 Long-term follow-ups have found that as many as 90% of patients with isolated PCL injuries may have persistent pain while walking, 45% report episodic instability, 65% report limitations of activity, and more than 50% demonstrate evidence of degenerative changes.4,7 Increasing literature points to a significant incidence of knee pain, patellofemoral symptoms, and medial compartment degeneration in the PCL-deficient knee. This is likely due to altered knee kinematics, with increased quadriceps activity, altered articular contact pressures (especially patellofemoral) and abnormal tibial translation and rotation noted under complex muscle loads in the PCL-deficient knee.19 Overall, although there currently exists a lack of conclusive scientific and clinical information, nonoperative management of isolated PCL tears is probably not as benign as previously believed. Whereas the outcome of conservative treatment of isolated mild injuries is likely acceptable, conservative treatment of more severe isolated injuries or of combined injuries leads to a worse outcome.15 Whether the PCL-deficient knee is at great risk of the development of significant degenerative changes is not clear, although it appears that progressive changes may occur in some affected knees.

TREATMENT OPTIONS AND RECOMMENDATIONS Traditionally, nonoperative treatment of isolated PCL injuries has been favored, especially with lower grade injuries. This is based on both the capacity of the ligament to heal and some outcome studies demonstrating excellent results in these patients. It appears that individuals are often able to compensate for PCL insufficiency via agonistic muscle function developed through a well-designed therapy program. Nonoperative management is currently recommended for isolated, asymptomatic PCL injuries with minimal or mild laxity.6,10 If posterior translation is less than 10 mm (i.e., grade I or II injuries), as it is in majority of isolated injuries, aggressive rehabilitation is instituted. This may also be used in cases with small tibial avulsion fractures and translation less than 5 to 10 mm. Rehabilitation for these injuries usually consists of 2 to 4 weeks of immobilization with the knee in full extension, often with protected weight bearing. This results in tibial reduction and prevents any posterior sag. Quadriceps strengthening is encouraged, while hamstring loading is prohibited to prevent posterior tibial subluxation. After 4 weeks, active-assisted range of motion and progressive weight bearing are begun.9 Patients can usually be expected to return to sports 1 to 3 months after injury.5 Rehabilitation focuses on closed-chain exercises, with the goal to regain 90% of quadriceps and hamstring strength (compared with the contralateral side). PCL braces have not been found helpful in low-grade chronic injuries. It is recommended that patients treated conservatively be followed yearly for any symptoms or signs of progressive instability or degenerative joint changes.5,14 Treatment of acute grade III injuries (displacement greater than 10 to 15 mm) is more controversial. Historically, these injuries have been treated similarly to lower grade tears, but

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most authors now recommend surgical intervention for all acute injuries resulting in severe tibial subluxation and for combined multiligamentous injuries.1,6,10 Surgery is also recommended for avulsion injuries with translation greater than 10 mm. If the fragments are small, the PCL should be reconstructed, but if the fragments are sufficiently large, internal fixation may be attempted. Combined injuries are best treated within 2 weeks, after which capsular scarring develops and direct repair of collateral and posterolateral corner structures is usually not possible.9 ACL reconstruction may be delayed, however, in order to regain knee motion and allow capsular healing. Multiple surgical options exist for ligament reconstruction, including choice of graft, single- versus double-bundle techniques, and tibial tunnel versus tibial inlay techniques. These are discussed in more detail in the next section. The treatment of chronic instability should be based on the degree of instability, presence or absence of degenerative changes, and response of symptoms to nonoperative management. Nonoperative treatment, including physical therapy and activity modification, is successful for the majority of patients with chronic PCL instability. Surgery may be recommended if posterior displacement is greater than 10 mm and nonoperative modalities have failed to relieve symptoms. In addition, progressively increasing activity on bone scan, indicative of increased metabolic activity due to altered knee biomechanics and progressive degeneration, may be a useful evaluative factor. In the presence of medial compartment wear, valgus osteotomy with or without PCL reconstruction may be considered. One should rarely, if ever, attempt to reconstruct the PCL in patients with a fixed (irreducible) posterior drawer, and direct repair instead of reconstruction of a chronic PCL injury is also strongly discouraged.

SURGERY Several techniques of reconstruction have been developed (Box 53-3). Current literature does not clearly indicate which is superior. Primary repair is attempted only with bony avulsions, in which fragments are fixed with a screw and washer if large enough or suture if the fragment is small. Primary repair of interstitial ligament tears has not been successful. The goals of surgery are to reproduce the normal anterior tibial step-off and restore the native restraint to posterior tibial displacement. Regardless of the chosen technique, a diagnostic arthroscopy is performed in nearly all cases, and any meniscal or osteochondral injuries are addressed. Débridement of the torn PCL, requiring complete visualization of the tibial insertion, may require a 70degree arthroscope placed through the anterolateral portal and notch. A posteromedial portal may then be opened under direct visualization.

Single-Bundle versus Double-Bundle Techniques The femoral side is almost always addressed arthroscopically, although two major techniques, the single bundle and the double bundle, are possible. Early reconstructive techniques, which focused on placing a single femoral tunnel in the “isometric” region of the native PCL, were found to produce abnormal knee kinematics, especially when the knee flexed more than 45 degrees.20 Only 5% to 15% of the femoral footprint is truly isometric, and therefore current single-bundle methods have been modified to place the femoral tunnel in the anterior aspect of the footprint to reproduce only the structurally superior anterolateral bundle. With the patient supine, a 2-cm incision over the anterior knee is necessary and should be placed just medial to the articular edge of the trochlear groove and distal to the vastus medialis obliquus. The retinaculum is incised in line with the skin incision. The proximal portion of the femoral tunnel guide is positioned midway between the patella and medial epicondyle, at least 1 cm from the patellofemoral articular edge to ensure that the joint is not violated. The tip of the drill guide is placed through the medial portal onto the anterior half of the femoral PCL footprint, 8 to 9 mm above the articular surface. The guide pin should be driven with the knee in 70 to 90 degrees of flexion and exit high in the notch at the 11- or 1-o’clock position (for left or right knees, respectively) within the anterior half of the anatomic footprint.10,16 The tunnel is then created by drilling over the wire. Most authors drill the femoral tunnel outside-in in this manner, although an inside-out technique has also been described using an accessory anterolateral portal. It is suggested that this latter method may lead to a more acute, and therefore less favorable, angle between the intra-articular graft and bony tunnel, resulting in fraying and graft wear if the tunnel entrance is not carefully chamfered21 (Fig. 53-12). Because the PCL exhibits a very small zone of isometric fibers, only anatomic reconstructions can accurately restore native function.21 Reconstruction of only the AL bundle may over time allow graft elongation secondary to nonuniform distribution of forces across the graft. To improve the success of reconstruction, some surgeons have added a second bundle to better replicate the native PCL orientation and provide a more uniform load distribution.20 Theoretically, a two-bundle technique offers a biomechanical advantage and is superior to single-

Box 53-3 Principles of Posterior Cruciate Ligament Reconstruction2 • • • • • •

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Identification and treatment of all pathology Protection of neurovascular structures Accurate tunnel placement Recreation of anatomic insertion sites Appropriate graft tension and fixation Structured postoperative rehabilitation

Figure 53-12 Postoperative radiographs of a single-bundle posterior cruciate ligament reconstruction. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

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AL

PM

Figure 53-13 Anatomic position of femoral tunnels for single-bundle (anterolateral [AL] only) or double-bundle (AL and posteromedial [PM]) posterior cruciate ligament reconstruction. (From Allen CR, Rihn JA, Harner CD: Posterior cruciate ligament: Diagnosis and decision making. In Miller MD, Cole BJ [eds]: Textbook of Arthroscopy. Philadelphia, WB Saunders, 2004, pp 687–702.)

bundle methods because it replaces both major portions of the native PCL. As each bundle is tensioned at the appropriate degree of flexion, this technique may decrease posterior laxity and better restore normal knee biomechanics through a greater range of knee motion.14,22 Proper placement of this second bundle is critical, however, as position greatly affects the tension of the AL bundle. A middle or distal second bundle allows cooperative load sharing and decreases anterior bundle tension, but proximal placement of the second bundle may not alter peak anterior bundle tension.20 Clinical studies have not yet consistently demonstrated improved resistance to posterior translation or improved in vivo joint kinematics between the two techniques.5,14 Although technically more challenging, the two-bundle method is similar to the single tunnel except for the fact that two femoral tunnels are drilled, one for the AL bundle in the anterior half of the femoral footprint and a smaller tunnel posteriorly (Fig. 53-13). Both grafts are routed through same tibial tunnel or can originate from the same tibial bone block. Again, the tunnel for the AL band is centered at the 1-o’clock position (for right knee), 2 to 3 mm behind the condylar articular margin, while the tunnel for the PM band is centered on the footprint at about 3:30-o’clock position.

tubercle through a longitudinal 2- to 3-cm incision. This results in a trajectory of 50 to 60 degrees to the long axis of the tibia, creating a graft orientation at the posterior tibia of approximately 45 degrees. This reduces the effects of the “killer turn,” a term referring to the sudden bend that the graft must take as it passes from the tunnel into the knee joint.10 The anterior skin incision can also be placed lateral to the tubercle, which may further reduce graft angulation.21 It has been recommended that one make a 2-cm safety incision posteromedially, which will allow access for the surgeon’s finger to directly protect the neurovascular structures and monitor any instruments placed in posterior knee10 (Fig. 53-14). A guidewire is drilled under arthroscopic visualization, and a 10- to 12-mm tunnel then drilled over the wire, taking care to protect the neurovascular structures at all times because, even with the knee flexed 90 degrees, the distance between the popliteal artery and posterior tibia is less than 1 cm. (Because of this, the inlay technique should be avoided in patients who have had recent or remote vascular repairs, which causes increased scarring and altered anatomy in the posterior knee.) The posteromedial portal and fluoroscopy may be used for direct observation during this step. The final drilling of the posterior cortex should also be completed by hand. The edge of the tibial tunnel must be chamfered to avoid excessive graft wear at the turn (Fig. 53-15).

A

Transtibial versus Tibial Inlay Techniques Two disparate methods for tibial fixation also exist. In the transtibial technique, the tibial tunnel and fixation are performed completely arthroscopically. With the patient supine, the tibial tunnel is drilled from front to back. First, any posterior adhesions are lysed and the posterior capsule separated from the tibial ridge. A PCL drill guide is passed through the intercondylar notch and positioned slightly lateral and distal to the anatomic tibial footprint.7 The anterior portion of the drill guide is placed on the anteromedial tibia 1 to 2 cm below the tibial

B Figure 53-14 A, Posterior cruciate ligament guide positioned for tibial tunnel guidewire placement. B, Position for femoral tunnel guidewire placement. (From Johnson DH, Fanelli GC, Miller MD: PCL 2002: Indications, double-bundle versus inlay technique and revision surgery. Arthroscopy 2002;18:40–52.)

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It is sometimes difficult to pass a graft around the sharp angle at the back of tibial tunnel, and this bend poses several potential long-term disadvantages: tibial tunnel erosion may occur, excessive bending may increase graft strain and wear, and the abrasive ridge may lead to elongation, fraying, or failure.23 Drilling of the tibial tunnel also risks neurovascular injury. Furthermore, the tibial tunnel technique requires a longer graft (usually at least 40 mm), which may be a problem, especially when using bone-patellar tendon-bone grafts. The tibial inlay method is an alternate technique that uses direct exposure and visualization for tibial fixation, eliminating the acute turn because the graft is fixed directly to a trough on the posterior tibia via a bone block. This is theoretically more secure, allows use of a bone-tendon or bone-tendon-bone allograft with boneto-bone healing and may improve isometry. However, patient positioning is more difficult, as is hardware removal if necessary, and revision is more challenging and dangerous due to scarring in posterior knee. Recent studies have debated whether any differences exist in the outcome between inlay and tunnel techniques, and some authors reserve inlay methods for revision or osteopenic bone.5,21 For inlay procedures, the patient is placed in the lateral decubitus position, from which the hip can be externally rotated for arthroscopy. After arthroscopic débridement and preparation of the femoral tunnel(s), a horizontal incision is made in the knee flexion crease, exposing the interval between the semimembranosus and the medial head of the gastrocnemius. A hockey stick incision may also be used, with the inferior arm overlying the medial gastrocnemius. This muscle is then retracted laterally along with the neurovascular structures, allowing the posterior capsule to be incised vertically and the PCL insertion to be visu-

A

B

C

Figure 53-16 Posterior cruciate ligament reconstruction using the tibial inlay technique. After creation of the posterior tibial trough (A), the graft is secured with staple or screw (B), and passed through the femoral tunnel (C). (From Miller MD, Gordon WT: Posterior cruciate ligament reconstruction: Tibial inlay techniques—principles and procedures. Oper Tech Sports Med 1999;7:127–133.)

alized. Pins or sharp-tipped 90-degree retractors can be placed in the posterior tibial cortex to assist with exposure. The hamstrings, if required for a multiligament reconstruction, can also be harvested through this approach. The posterior tibial plateau is exposed and prepared by fashioning a unicortical window to fit the bone block of the graft. A vertically oriented rectangular trough is made in the tibia with an osteotome. This should match the dimensions of the graft bone plug. The upper end of the slot should lie within the tibial anatomic footprint, above the transverse ridge where the posterior capsule inserts. After the graft is impacted into the slot, graft fixation is completed with screws and washers (Fig. 5316).

Graft Passage and Tensioning

Figure 53-15 Posterior cruciate ligament reconstruction using a transtibial tunnel and a double-bundle femoral technique. (From Petrie RS, Harner CD: Double bundle posterior cruciate ligament reconstruction technique: University of Pittsburgh approach. Oper Tech Sports Med 1999;7:118–126.)

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Graft passage and tensioning will depend on the exact techniques chosen on the tibial and femoral sides. If using tibial and single femoral tunnels, a looped 18-gauge wire or tunnel smoother is passed through tibial tunnel, grasped under arthroscopic visualization, redirected through femoral tunnel, and delivered externally. The graft is then pulled anterograde through the femoral tunnel and into tibial tunnel. The tibial tunnel may be oversized by 1 mm to assist with graft passage around the killer turn. The femoral side is usually secured first with an interference screw, and the graft then tensioned with the knee in 70 to 90 degrees of flexion with an anterior drawer force performed to eliminate any posterior sag. Any tension beyond that needed to reestablish normal step-off is excessive. It is critical to tension with the knee in flexion, after which the tibial side may be secured with an interference screw or with a screw and spiked washer. Many authors prefer double fixation on both sides.10 If using a tibial inlay technique, the graft will typically first be fixed to the tibial trough, passed retrograde through the femoral tunnel, and tensioned and fixed as just described. If using a double-bundle technique, the graft limbs will also be passed retrograde (if using a single bone block on the tibial side) or may be passed anterograde if using two separate grafts. Regardless, to reproduce the normal PCL biomechanics, the AL bundle should be tensioned and fixed with the knee flexed 90 degrees, and the PM bundle tensioned and fixed at or near full extension.

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Box 53-4 Considerations for Posterior Cruciate Ligament Reconstruction • • • • • •

Arthroscopic versus open Tibial tunnel or tibial inlay Single bundle or double bundle Graft choice Graft fixation technique Postoperative rehabilitation/weight bearing

Graft Selection Although the perfect PCL graft does not exist, graft selection is an essential part of surgery. Ideally, a graft would have structural properties similar to those of the intact PCL, with minimal harvest site morbidity, easy passage, secure fixation, and fast incorporation.24 One must also consider requirements for additional graft materials, if there are multiple injured ligaments. Autograft options include bone-patellar bone-bone, quadriceps tendon, and hamstring. Bone-patellar bone-bone usually consists of a 10- to 12-mm strip of patellar tendon with 20- to 25-mm bone blocks at each end. Incorporation through bone-to-bone healing is believed to occur within 4 to 6 weeks. Quadriceps grafts consist of a 10- to 12-mm strip of quadriceps tendon with a distal patellar bone block. Quadriceps is typically thicker than patellar tendon, although this does not translate to greater strength. The bone block can be used on the tibial or femoral side, while the other end of the graft requires tendon-to-bone healing. Quadriceps grafts may also be used as split grafts for double-bundle techniques. Hamstrings are usually used as quadruple-stranded grafts or as two double strands for a twotunnel technique. Hamstrings are associated with less graft site morbidity, but fixation appears inferior to that of bone-patellar bone-bone, as it requires tendon-to-bone healing on both ends. All these grafts appear to possess in vitro strength and stiffness greater than those of the native PCL, with quadrupled hamstring having the greatest stiffness and strength and quadriceps tendon the least.24 Allograft choices include all the previously cited tissues in cadaveric form, as well as allograft Achilles, tibialis anterior, and tibialis posterior tendons. Allografts may especially be necessary if multiple ligaments are being reconstructed. Advantages of allografts include the absence of donor site morbidity and reduced operative time. Some allografts (e.g., Achilles tendon) also provide thicker tendons and larger amounts of collagen, which can completely fill larger tunnels.9 Availability, price, risk of disease transmission, tissue quality, and graft incorporation are concerns. Synthetic grafts are not recommended because of high complication rates, including generation of wear debris, cystic changes in bone tunnels, and graft failures (Box 53-4).6

POSTOPERATIVE REHABILITATION Rehabilitation after surgical reconstruction focuses on restoring knee range of motion while simultaneously avoiding excessive graft stress until healing has occurred. Specific protocols are highly variable depending on the authors consulted. Most surgeons brace the knee in full extension from a few weeks to 2 months, and most allow early partial or full weight bearing using crutches with the knee in full extension. Range-of-motion (often

using a continuous passive motion device) and quadriceps exercises are begun within the first 1 to 4 weeks.1,13,14 In this period, efforts are concentrated on unweighted knee extension exercises and straight leg raises. At 4 to 6 weeks after surgery, the brace is unlocked and closed-chain exercises including biking and leg presses are started, followed by treadmill walking or pool jogging at 3 months. Running is allowed at 5 to 6 months and agility drills at 6 to 7 months. A return to regular sporting activities is anticipated at about 9 months, although some patients may take significantly longer. Return to sports is allowed only after the recovery of normal (90% of contralateral side) quadriceps strength is achieved. Loss of motion may be a problem, and some authors report that as many as 20% of patients require a manipulation under anesthesia 6 to 8 weeks after reconstruction to regain full flexion.9

SURGICAL COMPLICATIONS AND OUTCOMES Successful PCL reconstruction is technically more difficult than ACL reconstruction. Factors contributing to this include the fact that the PCL has a complex fiber pattern that is impossible to duplicate precisely, as its broad femoral footprint causes wider variation of fiber tension during knee motion than that of the ACL. In addition, PCL reconstruction is more commonly performed in the setting of combined ligamentous injuries. The most common intraoperative complications concern neurovascular injury, particularly involving the popliteal artery. Techniques to reduce this are discussed in the preceding section and are especially important during procedures using a transtibial approach. Hematoma formation and drainage from a posterior arthrotomy may occur as a result of gravity drainage or bleeding from inferior geniculate vessels. Because of this, some authors recommend routine ligation of the inferior medial geniculate vessels.16 Postoperatively, residual laxity, loss of motion or arthrofibrosis, infection, painful hardware, and anterior knee pain are the most common complications. Reconstructed PCL knees may be slow to regain full flexion; this may be worsened by poor tunnel placement.6 As importantly, patient age, severity of trauma, and ability to actively rehabilitate are important factors often beyond the surgeon’s control. Results comparing different reconstruction techniques are somewhat inconsistent. Choice of autograft versus allograft has not been proven to play a significant role in outcome.16 Theoretically, use of a transtibial approach may decrease accuracy of tunnel placement, and the acute posterior turn of the graft may lead to tunnel erosion, higher graft stresses, and graft elongation. Some authors believe that tibial inlay techniques allow greater initial stability due to avoidance of the killer turn, and, indeed, some recent evidence indicates that tibial inlay techniques may result in less graft laxity. In addition, two-bundle techniques may afford improved stability in both flexion and extension when compared to single-bundle reconstructions.2,3 To date, however, there is no consensus regarding the superiority of one technique over another. Overall, good to excellent results can be expected regardless of the specific operative technique used, with normal or near-normal posterior drawer test results found in more than 95% of postoperative patients. Most knees with grade III laxity before surgery are reduced to grade I, and nearly all are reduced to at least grade II.4–6 In addition, statistically significant improvements in posterior tibial displacement on stress radiographs and KT-1000 testing have been documented after multiple reconstructive techniques.10

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Box 53-5 Causes of Failed Primary Posterior Cruciate Ligament Surgery16 • Biologic Poor graft incorporation or remodeling, tunnel erosion, tunnel expansion • Technical Failure of fixation (bone plug breakage, loss of interference fixation, graft creep or slippage) High internal graft stress (nonisometric placement of anterolateral bundle, internal stress at tunnel edges) • Surgical decision making Failure to treat associated injuries, primary repair versus delayed reconstruction • Inappropriate rehabilitation Early aggressive range-of-motion or hamstring resistance exercises, early weight bearing in combined injuries

It is important to note, however, that PCL reconstruction may not consistently correct abnormal patellofemoral contact pressures or altered knee kinematics.19 This may be related, at least in part, to difficulties with anatomic tunnel placement. To date, there have been no long-term studies providing conclusive proof that operative intervention decreases the risks of longterm degenerative changes. With identification of the PCL reconstruction that most accurately restores knee kinematics and joint contact pressures, one might expect to demonstrate decreases in late-onset arthritis (Box 53-5).

SPECIAL CONSIDERATIONS Pediatric PCL injuries are uncommon. The usual injury pattern described in children involves periosteal stripping of the femoral attachment or a bony avulsion from the tibia. For the former, a suture technique used to reattach the ligament through drill holes in the femur is recommended, while for the latter, bony reattachment similar to that performed in adults is the treatment of choice.25 Revision PCL cases are also fairly uncommon, comprising only 10% or fewer of all PCL reconstructions.14 When evaluat-

ing potential surgical failures, it is important to remember that the reference position of the anterior tibial plateau with respect to medial femoral condyle can be significantly altered after PCL reconstruction. This can, therefore, markedly affect subsequent evaluation and interpretation of posterior tibial translation.15 If clinical and radiographic examination leads to the diagnosis of surgical failure, special consideration must be given to prior surgical scarring, potential loss of bone stock from tunnel enlargement, interference from previous tunnel positions, and location of hardware. As a rule, final stability in revision cases is usually worse that that obtained in primary procedures.10 Finally, although covered in detail in another chapter, multiligament injuries have relatively poor outcomes if treated nonoperatively. Most commonly, these occur as grade III PCL injury combined with posterolateral corner insufficiency, resulting in additive laxity in the posterior and external rotation vectors. For acute injuries, attempts to repair all damaged structures are warranted. The posterolateral corner especially will scar and obliterate normal anatomy if not addressed within 2 to 3 weeks of injury. Combined ACL and PCL injuries often represent an unrecognized knee dislocation. Some authors recommend acute repair or reconstruction, while others initiate early range-of-motion exercises and delay surgery for fear of arthrofibrosis.1 Treatment of combined PCL and MCL injuries may depend on the degree of MCL laxity. Low-grade MCL tears may heal with bracing and protection, while high-grade MCL injuries will have marked valgus instability and typically require acute repair.

CONCLUSION PCL injuries, although less common than ACL injuries, may be seen in variety of clinical settings. These can usually be diagnosed by the skilled physician through a thorough physical examination and confirmatory radiographic studies. Low-grade, isolated PCL injuries are usually treated nonoperatively with acceptable outcomes. Recent studies, however, suggest that chronic PCL deficiency may lead to progressive joint degeneration and arthritis. Multiple surgical options exist for reconstruction of the PCL, although there is little evidence to date demonstrating that PCL reconstruction significantly alters this natural history. Further research is needed to evaluate surgical techniques and treatment controversies.

REFERENCES 1. Cosgarea AJ, Jay PR: Posterior cruciate ligament injuries: Evaluation and management. J Am Acad Orthop Surg 2001;9:297–307. 2. Miller MD, Cooper DE, Fanelli GC, et al: Posterior cruciate ligament: Current concepts. Instr Course Lect 2002;51:347–351. 3. White LM, Miniaci A: Cruciate and posterolateral corner injuries in the athlete: Clinical and magnetic resonance imaging features. Semin Musculoskelet Radiol 2004;8:111–131. 4. Dowd GSE: Reconstruction of the posterior cruciate ligament: Indications and results. J Bone Joint Surg Br 2004;86:480–491. 5. Margheritini F, Rihn J, Musahl A, et al: Posterior cruciate ligament injuries in the athlete: An anatomical, biomechanical and clinical review. Sports Med 2002;32:393–408. 6. St. Pierre P, Miller MD: Posterior cruciate ligament injuries. Clin Sports Med 1999;18:199–221. 7. Schulte KR, Chu ET, Fu FH: Arthroscopic posterior cruciate ligament reconstruction. Clin Sports Med 1997;16:145–156.

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8. Amis AA, Bull AMJ, Gupte CM, et al: Biomechanics of the PCL and related structures: Posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc 2003;11:271– 281. 9. Harner CD, Honer J: Evaluation and treatment of posterior cruciate ligament injuries. Am J Sports Med 1998;26:471–482. 10. Johnson DH, Fanelli GC, Miller MD: PCL 2002: Indications, doublebundle versus inlay technique and revision surgery. Arthroscopy 2002;18:40–52. 11. Shelbourne KD, Carr DR: Combined anterior and posterior cruciate and medial collateral ligament injury: Nonsurgical and delayed surgical treatment. Instr Course Lect 2003;52:413–418. 12. Shelbourne KD, Gray T: Natural history of acute posterior cruciate ligament tears. J Knee Surg 2002;15:103–107. 13. Veltri DM, Warren RF: Isolated and combined posterior cruciate ligament injuries. J Am Acad Orthop Surg 1993;1:67–75.

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14. Harner CD, Fu FH, Irrgang JJ, et al: Anterior and posterior cruciate ligament reconstruction in the new millennium: A global perspective. Knee Surg Sports Traumatol Arthrosc 2001;9:330–336. 15. Ma CB, Kanamori A, Vogrin TM, et al: Measurement of posterior tibial translation in the posterior cruciate ligament-reconstructed knee. Am J Sports Med 2003;31:843–848. 16. Cooper DE, Stewart D: Posterior cruciate ligament reconstruction using single-bundle patella tendon graft with tibial inlay fixation. Am J Sports Med 2004;32:346–360. 17. Parolie JM, Bergfeld JA: Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 1986;14:35–38. 18. Toritsuka Y, Horibe S, Hiro-oka A, et al: Conservative treatment for rugby football players with acute isolated posterior cruciate ligament injury. Knee Surg Sports Traumatol Arthrosc 2004;12:110–114. 19. Gill TJ, DeFrate LE, Wang C, et al: The effect of posterior cruciate ligament reconstruction on patellofemoral contact pressures in the knee joint under simulated muscle loads. Am J Sports Med 2004;32:109–115.

20. Shearn JT, Grood ES, Noyes FR, et al: Two-bundle posterior cruciate ligament reconstruction: How bundle tension depends on femoral placement. J Bone Joint Surg Am 2004;86:1262–1270. 21. Christel P: Basic principles for surgical reconstruction of the PCL in chronic posterior knee instability. Knee Surg Sports Traumatol Arthrosc 2003;11:289–296. 22. Giffin JR, Haemmerle MJ, Vogrin TM, et al: Single- versus doublebundle PCL reconstruction: A biomechanical analysis. J Knee Surg 2002;15:114–120. 23. Margheritini F, Mauro CS, Rihn JA, et al: Biomechanical comparison of tibial inlay versus transtibial techniques for posterior cruciate ligament reconstruction: Analysis of knee kinematics and graft in situ forces. Am J Sports Med 2004;32:587–593. 24. Hoher J, Scheffler S, Weiler A: Graft choices and graft fixation in PCL reconstruction. Knee Surg Sports Traumatol Arthrosc 2003;11: 297–306. 25. Larson RV, Ulmer T: Ligament injuries in children. Instr Course Lect 2003;52:677–680.

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54

Medial Collateral Ligament Matthew Alan Rappé and Peter Indelicato

In This Chapter Classification Management of acute injury Nonoperative management Surgery Medial collateral ligament (MCL) repair Chronic MCL reconstruction

INTRODUCTION • The management of MCL injuries has evolved over the past 30 years. • Whereas most isolated anterior cruciate ligament (ACL) injuries are treated surgically, there remains a place for nonoperative management of isolated MCL injuries. • In combined lesions with other ligaments, surgical repair/reconstruction of the MCL may be indicated. • Whereas the knee has little tolerance for ACL laxity, as an isolated entity, it copes much better with residual MCL laxity even in athletes who perform high-level sports.

CLINICAL FEATURES AND EVALUATION The management of MCL tears continues to evolve as our understanding of the functional anatomy, biomechanics, and physiologic healing of this important extracapsular structure increases. The majority of patients who injure their MCL do so via a twisting or external rotation injury to the knee (during activities such as snow skiing). Another common mechanism in athletics involves a valgus blow to the lower thigh or upper leg (Fig. 54-1). Isolated MCL injuries, irrespective of the mechanism of injury, are not necessarily very painful. In fact, the more severe isolated tears are generally less painful than other injuries that occur about the knee. The key to a successful knee examination is relaxation of the thigh. We have found that gentle stress is more revealing than forceful stress. In order to isolate the superficial MCL and test its integrity, the knee must be flexed to 30 degrees and a valgus stress applied (Fig. 54-2).1,2 The amount of medial opening detected with the knee in 30 degrees of flexion compared with the uninjured knee is a direct reflection of the damage to the MCL. Just like in performing the Lachman test for suspected ACL damage, the quality of the endpoint must also be considered. When a complete MCL injury is present, an absent endpoint is discovered where one is expected. Further valgus load

will eventually elicit one and that endpoint may, in fact, be the intact ACL. To evaluate for associated ligamentous injuries, a valgus stress to the knee while in extension is performed. Asymmetrical medial joint space opening to a valgus stress occurring in full extension is strongly suggestive of combined MCL and posterior oblique ligament (POL) damage and should caution the examiner to suspect associated ACL and/or posterior cruciate ligament involvement. In addition, one should illicit tenderness along the course of the MCL. If the patient is seen acutely, the location is generally related to the mechanism of injury. Twisting, noncontact injuries usually demonstrate proximal tenderness. Valgus contact injuries usually demonstrate distal tenderness. Any asymmetry of opening greater than 4 mm compared to opposite side, especially coupled with a “soft” endpoint, is strongly indicative of a complete disruption of the superficial MCL and underlying medial capsular ligament.1 The gold standard for radiographic evaluation of an MCL injury is magnetic resonance imaging. Magnetic resonance imaging is highly sensitive in identifying injury or detachment of the MCL as well as other associated ligamentous or meniscal injuries about the knee3 (Figs. 54-3 and 54-4). For skeletally immature patients with suspected MCL injuries, it is of paramount importance to perform stress radiographs to rule out the possibility of physeal plate injury (Fig. 54-5). Diagnostic arthroscopy is rarely helpful in deciding to what extent the medial supporting structures of the knee joint have been damaged.

RELEVANT ANATOMY It is important to understand knee anatomy in order to fully comprehend the principles of both nonoperative and operative treatment of MCL injuries. The MCL is composed of both a superficial and deep portion. The MCL’s position about the medial knee is best described by Warren and Marshall4 who introduced the three-layer description of this anatomy. These authors defined layer 1 as that which involves the sartorius and sartorius fascia. Layer 2 includes the superficial MCL, POL, and the semimembranosus. Layer 3 includes the deep MCL and the posteromedial capsule. Layers 1 and 2 blend anteriorly, while layers 2 and 3 blend posteriorly. The proximal attachment site of the superficial MCL is somewhat circular and located on the medial femoral epicondyle. Its distal attachment is much larger and located 4 or 5 cm below the joint on the medial metaphyseal area of the tibia. It is divided from the deep MCL by a bursa. The deep MCL inserts directly into the edge of the tibial plateau and medial meniscus

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Figure 54-1 Valgus contact resulting in medial collateral ligament tear.

Figure 54-4 Magnetic resonance imaging of the knee demonstrating a proximal tear of the medial collateral ligament.

Figure 54-2 Valgus stress in 30 degrees of flexion isolating the superficial medial collateral ligament.

Figure 54-5 Distal femoral physeal injury.

Figure 54-3 Magnetic resonance imaging of the knee demonstrating a distal tear of the medial collateral ligament.

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via its two divisions: the meniscotibial and meniscofemoral attachments. Biomechanical studies have shown that the MCL is the prime medial stabilizer of the knee, which resists valgus loading.1,2 Due to the parallel arrangement of the collagen that composes the MCL, only a relatively small increase of laxity (approximately 5 to 8 mm) is indicative of a complete failure of the ligament. Another point to remember is that the deep capsular ligament (layer 3) is an important anchoring location for the medial meniscus. Therefore, although damage to this layer can extend into the substance of the meniscus, true substance tears of the medial meniscus are seldom seen in conjunction with complete disruption of the MCL. The location of the proximal attachment site of the MCL places it near the knee’s center of rotation. An intact MCL is fan shaped, and, as a result, some aspect of its structure is always under tension during knee flexion. As the knee goes into flexion, the anterior fibers of the MCL remain tight, whereas the posterior fibers slacken. The POL blends in with the posterior edge of the MCL and helps prevent medial opening with valgus loading with the knee in full extension. In a flexed position, the anterior aspect of the POL actually lies underneath the MCL. The bursa that separates the superficial from the deep MCL allows for the 1- to 2-cm anteroposterior excursion that must occur to the MCL during flexion/extension of the knee. While surgically repairing damage to the area, this relationship must be kept in mind. Suturing the anterior aspect of the POL to the posterior fibers of the MCL with the knee in more than 30 degrees of flexion could limit the necessary excursion of the MCL and lead to a significant flexion contracture postoperatively. The complexity of the medial structures of the knee have led some authors to focus on the specific structures injured as opposed to grouping them as simply an injury to the MCL. Specifically in the work of Hughston and Eilers,5 Hughston,6 and Muller,7 the importance of the posteromedial corner of the knee as a dynamic and static stabilizer has been emphasized. These anatomic structures include the posterior horn of the medial meniscus, the POL, semimembranosus, meniscotibial attachments, and oblique popliteal ligament and serve as a restraint to anteromedial rotatory instability.7,8 In a series of 93 knees treated operatively for medial-side knee injuries by Sims and Jacobson8 of the Hughston Clinic and Tulane, 99% of the knees were found to have injury of the POL ligament and 70% had semimembranosus capsular attachment injuries.

TREATMENT The treatment of the MCL continues to evolve. Historically, predictably good or excellent results were achieved with primary repair of the torn MCL and POL.5,9–13 In O’Donoghue’s series14 from 1950, he strongly advocated suture repair immediately after injury. Furthermore, Hughston and Barrett15 supported immediate primary repair of MCL and posterior oblique tears. In their series, they emphasized anterior advancement of the POL in order to restore medial stability. The nonoperative approach to management of complete tears of the MCL was first advocated by Ellsasser et al.16 Fetto and Marshall17 also reported excellent results following complete isolated MCL tears, irrespective of whether they were treated with an open or closed surgical technique. In 1983, the senior author published the results of a series of isolated MCL tears of the knee treated nonoperatively.18 He found no advantage

to direct suture repair when compared with a nonoperative approach that involved a structured rehabilitation program. In a subsequent article, the senior author and colleagues19 showed that this conservative approach was successful, even for the highly competitive athlete who returned to contact sports. In 1993, Reider et al20 reported excellent results in 35 athletes who had undergone conservative management of MCL tears with functional rehabilitation and been monitored for more than 5 years. In patients with combined MCL and ACL injuries, many authors favor nonoperative management of the MCL after reconstruction of the ACL. Shelbourne and Porter21 claim that excellent subjective and objective results can be achieved with proper reconstruction of the ACL and nonoperative management of the MCL, even in the elite athlete. In most cases of combined injuries, Noyes and Barber-Westin22 also favor nonoperative management of the MCL. They state that after reconstruction of the ACL, high-demand athletes with extensive medial joint space laxity may require operative repair of the medial structures.22 More recent work at other centers continues to support nonoperative management of concomitant ACL and MCL injuries. Millett et al23 showed patients with 19 combined ACL tears and minimum grade II MCL tears. These patients underwent early reconstruction of the ACL and nonoperative treatment of the MCL. Serial clinical examinations demonstrated good functional outcomes, range of motion, and strength. No patient experienced ACL graft failure or valgus instability or required subsequent surgery for chondral or meniscal damage at 2 years.23

Acute Medial Collateral Ligament Tear Management For the treatment of incomplete tears, we recommend minimal immobilization for 1 to 3 weeks followed by physical therapy focusing on quadriceps- and hamstring-strengthening exercises. The senior author’s management of grade III acute MCL injuries has evolved over the past 20 years. His initial recommendations were to immobilize all knees with MCL tears in a cast brace in 30 degrees of flexion for 2 weeks, which limited range of motion from 30 to 90 degrees of flexion as well as weight bearing for 6 weeks.18 Now, for complete proximal isolated tears of the MCL, the senior author prefers to place the knee in a commercially available splint in full extension for 2 weeks. A concern with these lesions is the possibility of excessive stiffness developing in the knee early in the healing process; therefore, immobilization should be minimized in any degree of flexion. For distal-based tears of the MCL, we immobilize the knee (splint versus cylinder cast) for 2 weeks in 30 degrees of flexion. Irrespective of the location of the tear, after 2 weeks of immobilization has passed, we begin to mobilize the knee throughout a comfortable range of motion without any set limitations. Weight bearing as tolerated is encouraged. We focus on quadriceps- and hamstringstrengthening exercises similar to those used in an incomplete MCL tear rehabilitation program. Once isokinetic studies show that the extremity has recovered at least 80% of its strength, power, and endurance, then an on-the-field agility program is begun. For contact sports, we recommend a double upright knee orthosis for the first season. After that, the use of an orthosis is left to the patient’s discretion. Since writing the original article in 1983, the senior author does not know of any patient who has developed functional laxity as a result of being treated in this fashion.

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Indications for Primary Repair Indications for primary repair both for isolated and combined ligament injuries of the knee remain somewhat controversial. Most surgeons still choose not to operate on isolated complete tears, especially those that demonstrate no laxity to valgus stress in full extension. When asymmetrical laxity occurs in full extension, some surgeons may choose to perform primary repair of the MCL and posterior capsule. Wilson et al24 reported that in their series distal tears healed less reliably, leading to the need for late reconstructions. This led them to advocate acute surgical repair for distal tears in athletic populations.24 At our institution, we seldom perform acute MCL repair when there is a concomitant anterior and/or posterior cruciate ligament tear(s). In this clinical situation, we immobilize the knee for 3 to 4 weeks to allow early primary healing of the MCL. Following this, patients are started on a rehabilitation program in order to recover most of their motion. This may take up to 6 to 8 weeks, especially if the lesion is proximal. Once most motion and quadriceps control of the leg has been recovered, an ACL reconstruction is performed. Intraoperatively, following the ACL reconstruction, the knee is reexamined for medial laxity, both in 30 degrees of flexion and in full extension. Using this approach, the senior author seldom has needed to perform an MCL repair and/or reconstruction. If the knee remains grossly unstable, particularly in full extension, a small posteromedial incision is made and the POL is tightened by advancing it as advocated by Hughston.5,6 Care is taken to avoid significant anterior advancement or reefing of this ligament because of the risk of developing a flexion contracture, as discussed earlier. Surgical Technique If an acute MCL repair is deemed necessary, it is performed using a straight medial incision extending from the medial epicondyle to 5 cm distal to the medial joint line. The sartorius fascia is divided and the sartorius retracted distally. Flexing the knee further retracts the sartorius and the pes anserinus components, giving visualization of the superficial MCL. If the MCL is torn distally, it is important to reflect it proximally, exposing the deep meniscocapsular ligaments. If these are torn, and they frequently are, they are repaired with simple interrupted suture. The sequence of repair thus proceeds from deep to superficial. If the posterior capsule is torn mid-substance, it is approximated with interrupted sutures. If the posterior capsule is torn from the femoral or tibial attachment, it is advanced and reattached to either the femur or the tibia, respectively, with suture anchors. Once this is accomplished, repair of the superficial MCL is addressed. Reapproximation of mid-substance tears is performed using Bunnell-Kessler suture configuration. Proximal or distal tears are advanced and reattached with anchors or over a post depending on tissue quality. If tissues are deemed inadequate, we commonly will augment this repair with Achilles tendon allograft secured via interference screws. Irrespective of open or closed treatment of a complete MCL tear, normal medial tightness is almost never completely achieved. Despite this fact, the senior author rarely has seen this result in a functionally unstable knee unless there was coexisting laxity in other structures (Figs. 54-6 through 54-10). Rehabilitation for Primary Repair Following surgery, the knee is immobilized in full extension for the first 3 weeks. The focus of the early rehabilitation program

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Figure 54-6 Surgical approach for repair of acute proximal medial collateral ligament tear.

is quadriceps-strengthening exercises in order to minimize muscle atrophy. It is critical to avoid any loss of full extension, particularly if the MCL lesion is more proximal. Hip and ankle exercises also should be included throughout the entire program.

Chronic Medial Collateral Ligament Reconstruction In cases in which the patient is first seen 3 weeks or more after the injury, it is probably too late to treat grade III MCL injuries successfully with either open primary repair or closed conservative management. In reviewing the literature, there are multiple ways to attempt to reconstruct the MCL. This usually means that there is no one procedure available that is always successful. In past years, the senior author reconstructed the MCL mainly by detaching its proximal end and either advancing it or countersinking it in an attempt to “retension” the

Figure 54-7 Higher magnification demonstrating a torn posterior capsule.

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Figure 54-8 Surgical repair of the posterior capsule with interrupted suture.

ligament. In addition, he would advance the posteromedial capsule anteriorly in an attempt to reestablish stability in full extension. Recently, the senior author has used Achilles tendon allograft to reconstruct the MCL (Fig. 54-11). The allograft dimensions are similar to the MCL with the ACL length being greater. The femoral attachment site receives the calcaneal bone (10- to 12-

Figure 54-10 Repair of medial collateral ligament using Bunnell-Kessler suture configuration.

mm plug) with interference screw. The tibial attachment site is sutured over a post and/or biodegradable interference screws are used to achieve fixation via a transtibial tunnel (Fig. 54-12). In addition, a posteromedial capsular advancement is performed, but care is taken following each suture to ensure the ability to achieve full extension, thus preventing a situation in which the advancement “captures” the knee.

Figure 54-11 Achilles tendon allograft.

Figure 54-9 Higher magnification demonstrating torn medial collateral ligament.

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Medial Collateral Ligament Reconstruction Rehabilitation Just as in primary repair, we immobilize the knee for the first 3 weeks in full extension. Following that time, the rehabilitation program is identical to that for ACL reconstruction.

Combined Medial and Posterior Collateral Ligament Injury Associated posterior collateral ligament (PCL) and MCL damage usually implies posterior capsule involvement, and the knee, therefore, will demonstrate some laxity in full extension to valgus stress. As a result, the senior author routinely performs either a primary repair (acutely) or a reconstruction (chronically) of the MCL in this situation. In mild to moderate PCL laxity, the senior author awaits any functional deficit that may develop prior to performing a PCL reconstruction. In severe PCL laxity, he performs a combined PCL and MCL repair/reconstruction at the same time.

CONCLUSIONS

Figure 54-12 Postoperative radiograph demonstrating femoral and tibial fixation of Achilles tendon allograft used for reconstruction of a chronic medial collateral ligament–deficient knee.

The management of MCL injuries continues to evolve. When injuries are isolated to the MCL, most orthopedic surgeons prefer conservative management. In combined lesions of the MCL and ACL, surgical repair of the ACL may be all that is necessary for treatment. If the knee continues to demonstrate medial laxity, repair or reconstruction of the MCL is indicated.

REFERENCES 1. Grood E, Noyes F, Butler D, Suntay W: Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human cadaveric knees. J Bone Joint Surg Am 1981;63:1257–1269. 2. Warren L, Marshall J, Girgis F: The prime stabilizer of the medial side of the knee. J Bone Joint Surg Am 1974;56:665–674. 3. Mandelbaum B, Finerman G, Reicher M, et al: Magnetic resonance imaging as a tool for evaluation of traumatic knee injuries: Anatomic and pathoanatomical correlations. Am J Sports Med 1986;14:361–370. 4. Warren F, Marshall J: The supporting structures and layers on the medial side of the knee: An anatomical analysis. J Bone Joint Surg Am 1979;61:56–62. 5. Hughston J, Eilers A: The role of the posterior oblique ligament in tears of acute medial (collateral) ligament tears of the knee. J Bone Joint Surg Am 1973;55:923–940. 6. Hughston J: 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 1994;76:1328–1344. 7. Muller W: The Knee: Form, Function, and Ligament Reconstruction. Berlin, Springer-Verlag, 1983. 8. Sims F, Jacobson K: The posteromedial corner of the knee: Medial-sided injury patterns revisited. Am J Sports Med 2004;32:337–345. 9. Hughston J, Andrews J, Cross M, Moschi A: Classification of knee ligament instabilities. Part I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am 1976;58:159–172. 10. Abbott L, Saunders J: Injuries to the ligaments of the knee joint. J Bone Joint Surg Am 1944;26:503–521. 11. England R: Repair of the ligaments about the knee. Orthop Clin North Am 1976;7:195–205. 12. Marshall J, Fetto J, Botero P: Knee ligament injuries. A standardized evaluation method. Clin Orthop 1977;123:115–129. 13. Quigley T: The treatment of avulsion of the collateral ligaments of the knee. Am J Surg 1949;78:574–581.

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14. O’Donoghue D: Surgical treatment of fresh injuries to the major ligaments of the knee. J Bone Joint Surg Am 1950;32:721–738. 15. Hughston J, Barrett G: Acute anteromedial rotatory instability. Longterm results of surgical repair. J Bone Joint Surg Am 1983;65:145– 153. 16. Ellsasser J, Reynolds F, Omohundro J: The non-operative treatment of collateral ligament injuries of the knee in professional football players: An analysis of seventy-four injuries treated non-operatively and twentyfour injuries treated surgically. J Bone Joint Surg Am 1974;56:1185–1190. 17. Fetto J, Marshall J: Medial collateral ligament injuries of the knee: A rationale for treatment. Clin Orthop 1978;132:206–218. 18. Indelicato P: Non-operative treatment of complete tears of the medial collateral ligament of the knee. J Bone Joint Surg Am 1983;65:323– 329. 19. Indelicato P, Hermansdorfer J, Huegel M: Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop 1990;256:174–177. 20. Reider B, Sathy M, Talkington J, et al: Treatment of isolated medial collateral ligament injuries in athletes with early functional rehabilitation. A five-year follow-up study. Am J Sports Med 1994;22: 470–477. 21. Shelbourne K, Porter D: Anterior cruciate ligament-medial collateral ligament injury: Nonoperative management of medial collateral ligament tears with anterior cruciate ligament reconstruction: A preliminary report. Am J Sports Med 1992;20:283–286. 22. Noyes F, Barber-Westin S: The treatment of acute combined ruptures of the anterior cruciate and medial ligaments of the knee. Am J Sports Med 1995;23:380–389. 23. Millett P, Pennock A, Sterett W, Steadman J: Early ACL reconstruction in combined ACL-MCL injuries. J Knee Surg 2004;17:94–98. 24. Wilson T, Satterfield W, Johnson D: Medial collateral ligament “tibial” injuries: Indication for acute repair. Orthopedics 2004;27:389–393.

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55

Posterolateral Corner Amir R. Moinfar, Daniel S. Lorenz, and Claude T. Moorman III

In This Chapter Anatomy and biomechanics Nonoperative management Surgery Posterolateral repair Posterolateral reconstruction

INTRODUCTION • The posterolateral corner (PLC) of the knee has been misunderstood and poorly described. In fact, it has been termed the “dark side” of the knee.1 It was defined as a clinical entity as recently as 1976, and there continues to be considerable debate over the proper nomenclature for this region of the knee. • To illustrate, Covey2 reported that the popliteofibular ligament has been termed the short external lateral ligament, popliteofibular fascicles, fibular origin of the popliteus, and the popliteofibular fiber. • There has been no clear algorithm or surgical technique that has been established as a gold standard for either acute or chronic instability.3 • Examination findings have been poorly described and confusing. Complicating this even more, structures in the PLC oftentimes are not well visualized by magnetic resonance imaging, making certain diagnoses challenging.4 • The PLC has received attention in recent years due to its role in the stabilization of the knee joint, especially in the success or failure of concomitant cruciate ligament repair.5

RELEVANT ANATOMY The PLC of the knee has classically been described to include the lateral collateral ligament (LCL), popliteofibular ligament, popliteus tendon, and the arcuate ligament complex. Some authors have included the iliotibial band2,5 and the fabellofibular ligament5,6 in this group. Seebacher et al7 divided the lateral aspect of the knee into three layers: (1) lateral fascia, iliotibial tract, and biceps femoris tendon; (2) patellar retinaculum and patellofemoral ligament; and (3) joint capsule, LCL, arcuate ligament, fabellofibular ligament, and popliteus tendon. It is this third layer that is the focus of this discussion.

The LCL arises from the lateral femoral condyle and attaches on the fibular head. It begins 2 cm above the joint line,5 slightly proximal and posterior to the lateral epicondyle, and then proceeds distally and posteriorly to the posterior aspect of the fibular head.5 The functions of each ligamentous structure in the knee are highlighted in Table 55-1. The popliteus muscle originates on the anterior aspect of the lateral condyle of the femur, courses inferomedially, and inserts on the posterior tibia, proximal to the soleal line.8 It also has attachments to the posterior and middle segments of the lateral meniscus (popliteomeniscal fascicle) and the apex of the fibula (popliteofibular fascicle).5 The popliteus tendon itself lies in the lateral one third of the popliteal fossa, and it is anterior to the LCL femoral attachment.9 The arcuate ligament complex is intimately associated with the popliteus. The arcuate ligament is a Y-shaped ligament arising from the posterior part of the joint capsule. It tapers down to the insertion of the posterior aspect of the fibular head, running over the popliteus muscle.5 The lateral limb of the arcuate ligament blends with the lateral gastrocnemius near its condylar insertion and the oblique popliteal ligament joins the semimembranosus tendon.4 Because of its association with the arcuate ligament complex, the popliteus muscle is both intra-articular and extraarticular. The popliteus tendon passes under the LCL in the popliteal hiatus and then goes under the arcuate ligament before becoming extra-articular and joining the muscle belly of the popliteus.4 Despite its connection with the popliteus, the arcuate ligament complex is often not included in the PLC literature because it is not consistently present in all knees. Researchers have found it to be present in 24%10 to 80%7 of knees. The popliteofibular ligament is the ligamentous scaffolding attaching the popliteus tendon and the fibular head. Researchers9 have shown that it has an anterior division and a posterior division. The anterior division attaches proximal to the musculotendinous junction of the popliteus muscle and distally to the anteromedial fibula, while the posterior division attaches to the posteromedial fibula. Much like the arcuate ligament, there is some debate over the prevalence of the popliteofibular ligament. Maynard et al3 reported it in 100% of cadaver specimens, while Watanabe et al11 reported it in 93% of knees and Sudasna and Harnsiriwattanagit10 in 98% of knees. The fabellofibular ligament is often not referred to in the PLC literature because the fabella is not present in all knees. The fabella is a sesamoid bone in the lateral head of the gastrocnemius at its proximal attachment to the femur. The fabellofibular ligament runs parallel to the LCL from the fabella to the fibula, inserting posterior to the insertion of the biceps tendon on the fibular head.5 The fabellofibular ligament is found to be tight in extension and lax with increasing flexion.12

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Table 55-1 Function of Knee Ligaments Posterior Cruciate Ligament

Lateral Collateral Ligament

Anterior Cruciate Ligament

Posterolateral Corner

Primary restraint

Posterior translation of tibia, IR of tibia

Varus at 30 degrees of knee flexion and 0 degrees of knee extension

Anterior translation of tibia, IR of tibia

ER of tibia

Secondary restraint

Valgus and varus forces

ER of tibia

Valgus and varus forces

Varus at 0 degrees and 30 degrees of knee extension

ER, External rotation; IR, internal rotation.

The iliotibial band, while often not discussed as being part of the PLC, is worth noting as it is important in preventing varus opening of the knee.12 It inserts on Gerdy’s tubercle on the anterolateral aspect of the tibial eminence. Through its origin on the gluteus maximus, it functionally helps to decelerate internal rotation of the tibia during gait. More recent terminology has simplified the posterolateral anatomy into two surgically important structures: the LCL and the popliteus/popliteofibular ligament. Current reconstruction techniques thus focus on restoring stability to these two structures.

Blood Supply and Innervation The popliteal artery and its genicular branches supply blood to the PLC.2 The popliteal artery is a continuation of the femoral artery as it passes through the adductor hiatus. Innervation to the PLC is from multiple sources. The common peroneal nerve arises from the tibial nerve, just distal to the adductor hiatus, and courses inferolaterally posterior to the fibular head. The posterior tibial nerve, which is the distal continuation of the tibial nerve, and branches of the obturator nerve innervate the posterolateral capsule and lateral meniscus. A branch of the common peroneal nerve provides nervous fibers to the inferior/lateral capsule and the LCL. The popliteus is innervated by the tibial nerve, L4-S1.8

rotates internally. Likewise, with a posterior force, the tibia rotates externally.14 Therefore, it is apparent that the PLC and the cruciates are intimately related in the function of the knee. Brunnstrom15 noted that the popliteus complements the PCL by preventing forward slide of the condyles in flexed knees, while also unlocking the lateral aspect of the knee in flexion. The roles of the various parts of the ligamentous and capsular components have been elucidated in studies whereby each structure was selectively sectioned and the resulting biomechanical implications were analyzed. Davies et al5 recently have summarized what is currently known from the literature (Box 55-1; Table 55-2). Collectively, these studies show that sectioning of the posterolateral structures resulted in increased primary posterior translation, primary varus rotation, primary external rotation, and coupled external rotation. LaPrade et al measured forces on anterior cruciate ligament16 and PCL grafts17 following sectioning of posterolateral structures. In both grafts, forces on these grafts increased with varus load at 0 and 30 degrees of knee flexion and was even greater with coupled varus and external rotation than with an intact PLC. In the anterior cruciate ligament graft, coupled varus and internal rotation at 0 and 30 degrees increased graft force beyond that with varus alone. In PCL grafts17, force on the graft was higher with the posterolateral structures transected during varus load at 30, 60, and 90

BIOMECHANICS Much like the anatomy of the PLC, the biomechanics of this region and its resulting clinical implications are becoming better understood. The PLC helps to prevent posterior tibial translation, varus, and external rotation of the tibia.3 Isolated PLC injury is uncommon and is often associated with concomitant cruciate ligament injury. DeLee et al13 reported that in 735 knees treated for knee injury, only 12 (1.6%) had acute isolated PLC injury. Prior to exploring the complex nature of the biomechanics, it is noteworthy that there are coupled motions that occur in the knee joint. With the foot fixed on the ground and the knee fully extended, as a person begins to flex the knee (as in sitting on a chair), the femur rolls posteriorly on the tibia, but glides anteriorly. The initial 10 degrees of knee flexion actually involves a medial rotation of the tibia to “unlock” the knee. Likewise, as the knee is extended with a closed kinetic chain, the femur rolls forward, glides posteriorly, and the tibia externally rotates for the last 10 degrees of extension. The last 10 degrees of external rotation is known as the screw home mechanism. The posterior cruciate ligament (PCL) helps to resist the posterior translation of the tibia, and the PLC resists the rotational forces. When an anterior force is applied to an intact knee, the tibia

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Box 55-1 Biomechanics of Posterolateral Rotary Instability • If the lateral collateral ligament or posterolateral corner is cut individually, there is no change in the posterior translation at all angles of knee flexion. Lateral collateral ligament sectioning resulted in greater varus angulation than with posterolateral corner sectioning. • If the lateral collateral ligament and posterolateral corner are cut together, there is increased posterior translation at all angles of knee flexion, and an increase in coupled external rotation and posterior forces. Additionally, there was increased varus, maximal at 30 degrees of knee flexion. Combined lateral collateral ligament/ posterolateral corner sectioning revealed increased varus, greater than if the lateral collateral ligament alone is cut. • If the posterior cruciate ligament alone is sectioned, there is increased posterior translation at all angles of flexion, increasing as the knee flexes from 0 to 90 degrees. Also, there is a cessation of coupled external rotation with posterior force. • If the posterior cruciate ligament, lateral collateral ligament, and posterolateral corner complex are all cut, there is much greater posterior translation at all angles of flexion, increased varus rotation in response to varus forces, which is maximal at 60 degrees of flexion. Finally, there is an increase in primary external rotation.

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Table 55-2 Motions Restricted by Ligamentous Structures in the Knee Posterior Cruciate Ligament ER of tibia

Lateral Collateral Ligament

÷

Varus at 30 degrees of flexion Posterior translation

Anterior Cruciate Ligament

Posterolateral Corner

÷

÷

At 90 degrees of flexion

÷

Anterior translation ÷

ER and posterior translation ÷

Varus, ER, posterior translation Varus at 0 degrees of extension

÷

Possibly

All angles of flexion

Possibly

IR of tibia

÷

÷ ÷

÷ ÷

Possibly ÷

÷

ER, External rotation; IR, internal rotation.

degrees of knee flexion than with the posterolateral structures intact. In addition, coupled external rotation with a posterior force increased graft force at 30, 60, and 90 degrees compared to that with the posterolateral structures intact. Veltri et al14 studied the rotational contributions of the LCL, popliteofibular ligament, and popliteus tendon attachments. The popliteofibular ligament and the popliteus tendon were found to be crucial in the resisting of posterior translation, varus, external rotation, and coupled external rotation. In addition, they found that isolated sectioning of the anterior cruciate ligament and PCL resulted in increased primary anterior and posterior translation, respectively, and increased coupled external rotation and posterior force, increased varus, and increased primary internal rotation. Finally, at all angles of knee flexion, PCL and PLC sectioning resulted in increased primary posterior translation, increased primary external rotation, and increased varus. These increases were greater at 90 degrees of knee flexion compared to isolated posterior cruciate sectioning. Maynard et al3 demonstrated that after simulation of a varus load, the LCL fails first, followed by the popliteofibular ligament, then the muscle belly of the popliteus. From these studies, one can conclude that in order to differentiate posterior cruciate from PLC involvement, external rotation must be evaluated at both 30 and at 90 degrees of knee flexion. If there is greater external rotation at 30 degrees of flexion but not at 90 degrees of flexion, isolated PLC pathology is likely.

CLINICAL FEATURES AND EVALUATION Posterolateral corner injuries occur from a blow to the anteromedial aspect of the knee, contact and noncontact hyperextension injuries, and varus contact of a flexed knee. There has been some speculation as to certain predisposing factors such as genu varum, pre-existing excess external tibial rotation, ligamentous laxity, recurvatum, and epiphyseal dysplasia. Patients having suffered an acute injury of the PLC describe a traumatic event and report pain over the posterolateral aspect of the knee. Patients may also complain of lower extremity weakness or numbness secondary to peroneal nerve injury. Patients also may report gait difficulties and instability, particularly complaining of hyperextension during toe off. Physical examination that specifically isolates the structures of the posterolateral aspect of the knee is critical. Hughston and Norwood18 described two tests, the posterolateral drawer test

and the external rotational recurvatum test, as key in detecting posterolateral rotatory instability. The posterolateral drawer test is performed to assess posterolateral rotation with the knee at 90 degrees of flexion. The foot is placed in 15 degrees of external rotation, and knee rotation is assessed while a posterolateral force is applied. An increase in rotation compared to the contralateral side typically reflects injury to the popliteus complex.12 The external rotation recurvatum examination is performed by lifting both lower extremities by the hallux with the patient in the supine position. A positive test refers to increased hyperextension and resultant external rotation.19 The reverse pivot shift is performed by slowly extending the knee from 45 degrees of flexion while applying a valgus and external rotational force to the knee. Reduction of the subluxated knee with extension connotes a positive result. Varus testing should be performed at both 0 and 30 degrees of flexion. Varus opening at 0 degrees is likely indicative of severe combined ligamentous injury, while opening at 30 degrees reflects incompetence of the LCL and possibly of other posterolateral structures.18 The posterolateral rotation test, also referred to as the dial test, is performed at both 30 and 90 degrees of knee flexion. Although the test may be performed in the supine or prone position, the senior author prefers the prone position with the knees held tightly together to help eliminate hip rotation. A greater than 15-degree increase in external rotation compared to the contralateral side only with the knee at 30 degrees of flexion suggests an isolated PLC injury. A greater than 15-degree increase at 90 degrees of flexion reflects a concomitant PLC and PCL injury.20 The knee should also be carefully evaluated for anterior and posterior cruciate ligamentous incompetence, in addition to medial-side knee injury. A thorough neurovascular examination is also necessary. The gait status of an individual with suspected PLC insult will also help confirm clinical findings. Because of the role the PLC has in stabilizing varus forces, patients will typically present with a varus thrust or hyperextension at midstance, due to external rotation of the tibia at full extension.5 Some patients may also walk with a flexed knee2,5,21 to avoid pain and instability experienced with hyperextension. DeLeo et al22 reported in a case study a patient with pain in terminal stance and push-off. In this phase of gait, the knee is flexing rapidly from full extension. Stresses to the lateral structures of the knee are increased here, resulting in decreased stance time on the involved limb. Radiographic examination should consist of standard standing bilateral posteroanterior, lateral, and Merchant knee views.

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Figure 55-1 Posterolateral corner injury. Sagittal spin-echo intermediate-weighted magnetic resonance image (2000/20) through the intercondylar notch shows a thickened posterior cruciate ligament (arrows) with intermediate signal intensity throughout, indicative of a torn posterior cruciate ligament. (From Helms CA: The impact of MR imaging in sports medicine. Radiology 2002;224:631–635.)

Plain radiographs may reveal an avulsion fracture of the proximal fibula (arcuate sign), an avulsion of Gerdy’s tubercle, or a Segond fracture (although more common with an anterior cruciate ligament injury). Stress radiographs may show lateral joint space widening. Chronic instability often reveals changes consistent with post-traumatic degenerative joint disease. If malalignment is also suspected, long-cassette hip-to-ankle films should be taken as they may serve beneficial in the planning of a possible osteotomy as an adjunct to ligament repair or recon-

Figure 55-3 Transverse fast spin-echo T2-weighted fat suppressed magnetic resonance image (3000/70) at the level of the joint shows the posterior capsule (left arrow) of the medial side of the joint, which is not evident on the lateral side. This indicates a torn arcuate ligament (which should be seen as a thickening of the lateral capsule at the joint line). In addition, the popliteus tendon (right arrow) has high signal intensity within and a distended tendon sheath. (From Helms CA: The impact of MR imaging in sports medicine. Radiology 2002;224:631–635.)

struction. Magnetic resonance imaging is key in the evaluation of the specific individual components of the PLC of the knee. A high-powered magnet of at least 1.5 T is recommended in order to adequately assess the iliotibial band, long and short heads of the biceps femoris, LCL, popliteus, and the popliteofibular and fabellofibular ligaments (Figs. 55-1 through 55-4). A bone contusion of the anteromedial femoral condyle is also a common finding.

TREATMENT OPTIONS Injuries of the PLC are rarely isolated injuries and are most often the result of significant trauma, with approximately 40% being athletic injuries.14 Although the natural history of posterolateral instability is poorly understood, this injury is associated with the potential for significant morbidity. There is also increased disability when posterolateral instability is part of a combined ligament injury pattern. Unrecognized or inappropriately treated PLC injury has commonly been identified as a leading cause of anterior cruciate ligament reconstruction failure. Nonoperative management is reserved for mild instability without significant functional limitation.23 These patients typically have no varus instability and are free from other associated ligamentous injury. Patients with a negative posterolateral rotation test are also often best suited by nonoperative management. Treatment entails 2 to 4 weeks of immobilization with protected weight bearing for the initial 2 weeks. Figure 55-2 Coronal fast spin-echo T2-weighted fat-suppressed magnetic resonance image (3000/70) reveals a torn lateral collateral ligament (arrow). (From Helms CA: The impact of MR imaging in sports medicine. Radiology 2002;224:631–635.)

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SURGERY If possible, primary surgical repair should be performed within 6 weeks from injury. A concern with isolated repair or recon-

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Figure 55-4 Transverse fast spin-echo T2-weighted magnetic resonance image (3000/70) several centimeters distal to the joint shows high signal intensity surrounding the popliteus muscle (arrow), indicative of injury. At surgery, the popliteus muscle was torn at the musculotendinous junction, and the posterior cruciate, medial collateral, and arcuate ligaments were torn. (From Helms CA: The impact of MR imaging in sports medicine. Radiology 2002;224:631–635.)

struction is varus knee alignment. Varus deformity places increased tensile forces on the repair or reconstruction and may subsequently lead to incompetence and failure of the structures. A high tibial osteotomy may be recommended prior to, or concomitant with, posterolateral repair of reconstruction in this setting. In the case of chronic posterolateral rotary instability (PLRI) in the varus knee, the osteotomy is generally the first stage of a two-stage procedure with ligament reconstruction performed at a later setting.

300 to 350 mm Hg. A no. 10 blade is used to dissect a fullthickness skin flap through a laterally based hockey-stick incision that starts 8 cm proximal to the lateral joint line, immediately posterior to the lateral epicondyle, and courses approximately 7 cm distally between Gerdy’s tubercle and the fibular head (Fig. 55-5). Care is taken to preserve at least a 7-cm skin bridge from other incisions, particularly from an anterior-based incision from open cruciate reconstruction (Fig. 55-6). The interval between the iliotibial band and biceps femoris tendon is developed, which allows exposure of the lateral head of the gastrocnemius and the posterior capsule (Fig. 55-7). The LCL and the popliteus tendon can be evaluated proximally by incising the iliotibial band at the level of the epicondyle. As the peroneal nerve runs posterior to the biceps femoris tendon, it must be carefully protected throughout the procedure (Fig. 55-8). Knee flexion and biceps femoris retraction helps to protect the peroneal nerve. LCL or popliteus avulsion from the femoral origin typically occurs concomitantly and can be repaired with direct sutures to bone, suture anchors, or soft-tissue screws with washers. Popliteus avulsion from the tibia can also be repaired in similar fashion. Disruption of the popliteofibular ligament can be treated by tenodesis of the popliteus to the posterior fibular head, reinforcing it with the fabellofibular ligament if present. Distal LCL avulsion accompanied by a large amount of bone can be repaired with screw or suture fixation. Most primary repairs benefit from tissue augmentation, which helps to allow more expeditious mobilization and rehabilitation.25 When repair is not a feasible option, numerous alternative techniques have been described to address the insufficient PLC. Hughston and Jacobsen26 described advancement of the entire

SURGICAL TECHNIQUE The patient is placed supine on the operating room table, with both the injured and uninjured legs in the extended position. A lateral valgus bar is placed next to the injured thigh. A thorough examination under anesthesia is carried out prior to proceeding with the definitive procedure. A bump of towels is placed under the injured knee. We have found arthroscopic evaluation of the knee with both acute and chronic posterolateral rotatory instability as a valuable adjunct to the open procedure. Noyes et al described the amount of lateral joint line opening under a varus load during arthroscopy. Incompetence of the PLC resulted in at least 12, 10, and 8 of opening at the periphery, mid-portion, and innermost medial edge of the lateral tibiofemoral compartment, respectively.24 In addition, concomitant ligamentous, meniscal, and chondral injuries can be diagnosed and treated during arthroscopy. Open or arthroscopic cruciate reconstruction is at the surgeon’s discretion. Acute PLC repair can be successful in the first 6 weeks following injury, assuming adequate tissue quality without severe injury. Successful surgical repair is aided by early intervention, prior to profound scar formation, in order to allow identification of anatomic structures. At the conclusion of the arthroscopic portion of the procedure, the limb is exsanguinated, and a tourniquet is inflated to

Figure 55-5 Position of preferred lateral incision for posterolateral corner reconstruction. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

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Figure 55-8 Peroneal nerve identification, dissection, and protection are critical in posterolateral corner exposure and reconstruction. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

Figure 55-6 Relationship of the lateral incision to the anterior incision. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

Figure 55-7 Exposure of the posterolateral corner with development of full-thickness skin flaps. Note relationship of the fibular head to Gerdy’s tubercle. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, SpringerVerlag, 2004, pp 143–146.)

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PLC complex. Popliteal bypass procedures have been described using various tissues in order to reconstruct the popliteus muscle tendon unit. Clancy et al27 popularized tenodesis of the biceps femoris to the anterolateral femoral epicondyle. The senior author employs a modified figure-eight fibular-based technique using double-stranded hamstring autograft. Research involving the senior author revealed that both fibular-based and combined tibiofibular-based PLC reconstruction techniques are equally effective in restoring external rotation and varus stability after simulated PLC injury.28 The approach to the PLC of the knee is the same as that for repair. The proximal fibula and biceps femoris tendon are isolated. The femoral fixation site for reconstruction is identified as the point between the footprint of the LCL and the insertion of the popliteus (Fig. 55-9). Next, attention is turned to the fibula. The fibula is drilled with a guide pin in an anterior-toposterior direction, just superior to the fibular neck. Using a 7mm acorn reamer, a tunnel is created over the guidewire (Fig. 55-10). The hamstring graft is then pulled through the fibular head, with the long limb of the graft passed posteriorly and around a 30- to 35-mm cancellous synthes screw with a washer (Fig. 55-11). The anterior limb is also passed around the washer; however, in the opposite direction. This produces a figureeight type arrangement underneath the biceps femoris and iliotibial band. The posterior loop reproduces the popliteofibular complex, while the anterior loop reproduces the LCL (Fig. 5512). The screw is then tightened in place, and the remaining posterior loop is placed through the fibular tunnel again in a posterior-to-anterior direction (Fig. 55-13). The two loops are then tied to one another with 2-0 Vicryl sutures. The posterolateral complex is then tensioned in 30 degrees of knee flexion, with the knee in slight valgus and internal rotation (Figs. 55-14 and 55-15). The posterolateral capsule is then fixed to the posterior aspect of the construct using no. 2 nonabsorbable sutures.

REHABILITATION There is a paucity of literature on the rehabilitation of PLC injuries, treated both nonoperatively and operatively. No con-

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Figure 55-9 Identification of lateral femoral position for posterolateral corner reconstruction between the lateral collateral ligament and the popliteus tendon. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

Figure 55-11 Passage of the double-hamstring autograft through the fibular head. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

trolled studies to date have been done on this region. Isolated low-grade injuries may do well with conservative treatment.5 LaPrade and Wentorf12 suggest that grade I to II PLC injuries can initially be treated nonoperatively in a knee immobilizer in full extension for 3 to 4 weeks non-weight bearing with no motion allowed. Patients may do quadriceps setting and straight

Figure 55-10 Preparation of the fibular head for passage of doublehamstring autograft. A 7-mm reamer is used in an anterior-to-posterior direction over a guidewire. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

Figure 55-12 Reconstruction of the posterolateral corner.

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Figure 55-13 Posterolateral reconstruction. Screw and washer are placed.

Figure 55-14 Fixation of the posterolateral corner “O” autograft. The graft is passed in a figure-of-eight fashion such that the posterior limb (left) serves as the popliteofibular complex and the anterior limb (right) serves as the reconstructed lateral collateral ligament. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, Springer-Verlag, 2004, pp 143–146.)

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Figure 55-15 Fixation of the posterolateral corner graft often allows overlapping of the anterior and posterior limbs with extra tendon. Care is taken to ensure that the tendon is captured by the soft-tissue washer. (From Richards RS, Moorman CT: Open surgical treatment. In Fanelli GC [ed]: The Multiple Ligament Injured Knee. New York, SpringerVerlag, 2004, pp 143–146.)

leg raises. It is currently advised, however, that the leg raises be performed in a brace, with the brace locked at 20 degrees of flexion to minimize the effects of gravity causing either posterior translation or external rotation of the tibia. In this position, a straight leg raise is a misnomer. Bent leg raise is more appropriate terminology. Ultimately, weight-bearing status is at the discretion of the physician. At 4 weeks, LaPrade and Wentorf allow patients to begin range-of-motion exercises and gradual weight bearing. They also propose that closed-chain quadriceps strengthening with no active open-chain hamstring activity is done from weeks 6 to 10. Wilk described, in the case study of DeLeo et al22 a nonoperatively managed PLC injury, that strengthening of the hamstrings, gastrocnemius, popliteus, and hip musculature is indicated to help control varus at the knee. Also, a foot orthosis with a lateral heel wedge may be helpful to unload the lateral structures of the knee during stance phase, as well as a knee brace to offload the medial compartment. A brace may be necessary due to shifting of the axis for tibial rotation to the medial compartment with PLC sectioning.14 The clinician must also be mindful of concomitant cruciate or collateral ligament injury. If present, it will change precautions and indications for therapy. Determining the plan of care for PLC injuries should be managed on a case-by-case basis involving all members of the health care team. In cases of nonoperative management, goals of therapy are to protect the PLC and maintain quadriceps function. Thus, quadriceps setting and bent leg raises with the brace in 20

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degrees of flexion are advocated. Achieving full active extension to 0 degrees is contraindicated for 4 weeks due to the tensile forces that will be placed on the PLC at full extension. Limiting extension ensures that proper healing of the tissues is optimized. As stated previously, weight bearing is at the discretion of the physician, but current standard of practice is for an initial period of protected weight bearing as tolerated with the brace locked at 10 to 20 degrees of flexion. Weight bearing may be indicated because a lack of articular compression deprives articular cartilage of nutrition, which may hasten degeneration of the cartilage matrix.29 Once the patient can bear weight, balance/proprioceptive exercises should be initiated in a closed chain to encourage cocontraction of the hamstrings and quadriceps in stance. Active open-chain knee flexion against gravity is not advised until 6 to 8 weeks after the injury. Pool exercise may also be useful to help with motion and gait status. One study elucidated the results of PLC reconstructions and rehabilitation outcomes. Noyes and Barber-Westin21 reconstructed posterolateral complex injuries using allograft tissues in 20 patients. They reported a 76% success rate by means of stress radiographs and knee stability examinations. The day after surgery, patients did patellar mobilizations, straight (bent) leg raises, electrical muscle stimulation, and isometrics. Patients were non-weight bearing for 4 weeks, and they completed active-assisted range-of-motion exercises six to eight times per day from 10 to 90 degrees. Pool exercises commenced at the third month, and no hamstring activity was done until week 12. Patients were gradually progressed to full weight bearing by the 16th week. Bracing was used for the first 9 months postoperatively to prevent abnormal hyperextension, varus, and external rotation of the tibia. Full hyperextension was avoided until 6 months after surgery. Key considerations in the postoperative care of PLC reconstructions are prevention of (1) varus and external rotation of the tibia, (2) active knee flexion against gravity, and (3) extension/hyperextension of the tibia to protect the grafts. Therefore, no active knee flexion against gravity is done until 12 weeks postoperatively due to the internal rotation of the tibia during the first 10 degrees of flexion and the posterior translation, which places tensile forces on the graft. Passive extension to 0 degrees with gravity eliminated and without overpressure is advocated. Additionally, full hyperextension is not emphasized until up to 3 months postoperatively. Hyperextension should be based on bilateral comparison of the uninvolved limb. Achieving extension of the involved limb should be based on the uninvolved. Contrary to isolated ACL reconstruction in which hyperextension is emphasized immediately, hyperextension after PLC reconstruction can potentially lead to graft failure,30 but 0 degrees of extension is achieved. Not only does it help minimize scar tissue infiltration in the joint, but extension to 0 degrees also helps decrease anterior knee pain. If the knee cannot reach 0 degrees, the quadriceps must contract more forcefully to achieve terminal knee extension needed for heel strike and the midstance portions of gait. Protected motion is also advocated with the brace unlocked, using passive or active-assisted range of motion to tolerance. Complete immobilization is not recommended due to the deleterious effects associated with it, including decreased bone mass, articular cartilage changes, synovial adhesions, muscular inhibition,29 and increased risk of arthrofibrosis due to ligament and capsule stiffness.30 In addition, it leads to loss of lubrication between joint surfaces.29 The paradox is that the knee must be

protected against undue forces, but also must be moved to prevent the negative effects secondary to prolonged immobilization. Following surgical repair, gait is gradually progressed beginning at week 6. It is imperative that assistive devices not be discontinued without normal, nonantalgic gait. Often crutches are discontinued completely, and patients ambulate with a Trendelenburg gait pattern. It is advised that patients progress from bilateral axillary crutches, then to one crutch on the contralateral side, and then a standard cane if necessary. The Trendelenburg gait pattern can cause subtle malfunctions in the kinetic chain that may lead to pain or pathology in other joints, particularly the hip and low back. Careful gait observation should be made by both the physician and rehabilitation professional to ensure that proper gait has been achieved. Because of the non-weight-bearing status, the ipsilateral hip abductors can weaken, complicating gait status once it is allowed at week 6. The gluteus medius stabilizes the ipsilateral pelvis to prevent the contralateral pelvis from dropping inferiorly at midstance. Thus, active hip abduction exercises of the involved limb, standing with a brace, are advocated early to help minimize the presence of the Trendelenburg gait pattern due to gluteus medius weakness. Hip abduction exercises with the hip in neutral and in slight external rotation are effective exercises to be included as part of physical therapy and/or the home exercise program. Resistance should be placed above the knee in order to minimize potential varus forces that would exist if the resistance were placed distal to the knee. Likewise, side-lying exercises are contraindicated initially due to the deleterious effects of varus forces on the reconstructed grafts. Repeating this exercise bilaterally once the patient can fully weight bear will help with control of the involved limb in unilateral stance. Aquatic therapy can be very beneficial for improving range of motion and gait status. Noyes and Barber-Westin21 proposed that this start at 12 weeks. Currently, 6 weeks should be sufficient for the patient to begin careful weight bearing and gait training in the pool. In chest deep water, the patient is approximately 75% unweighted. Buoyancy of water minimizes stress placed on the injured knee.29 Therefore, the water can assist the patient in achieving a normal gait pattern. The patient can be progressed to shallower water, as 50% of body weight is present at waist level. As gait normalizes, this will likely transfer benefit to landbased gait training. A protocol for postoperative rehabilitation is presented in Box 55-2. With proper communication between patient, physician, and rehabilitation professional, safe return to full activity is anticipated following reconstruction of the PLC. In addition, a systematic, graded progression of exercise while being mindful of the healing process will ensure that dynamic stability and strength returns to the involved limb.

COMPLICATIONS Posterolateral corner injuries rarely occur in isolation, and the complex nature of this injury leads to numerous potential complications. Neurologic and vascular injuries may be sustained secondary to the traumatic incident itself. Iatrogenic complications may include neurologic injury and intraoperative fracture during the course of the reconstruction. Failure to appreciate and identify other areas of instability may lead to early failure. In addition, arthrofibrosis, infection, persistent postoperative pain, and painful hardware are also potential complications.

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Box 55-2 Protocol for Postoperative Rehabilitation Phase I: Postoperative weeks 1 to 6 Goals 1. Decrease pain and swelling 2. Maintain patellar mobility 3. Protect against varus, external rotation, and flexion forces 4. Initiate and sustain active quadriceps set 5. Maintain cardiovascular endurance via upper body ergometer Weight-bearing status: Non-weight bearing Brace: Physician preference; but current standard is locked at full extension, unlock for physical therapy at week 4 Exercises 1. Ankle pumps 2. Patellar mobilizations: superior/inferior, medial/lateral 3. Passive extension to 0 degrees without overpressure/with gravity eliminated 4. Quadriceps sets, adductor setting with quadriceps sets, gluteal sets, bent leg raises 5. Begin passive/active-assisted range of motion for flexion at week 4 Phase II: Weeks 6 to 10 Goals 1. Begin weight bearing with unlocked brace 2. Progress to full range of motion in gravity-eliminated position 3. Continue to protect against varus, external rotation, and flexion forces Weight-bearing status: Weight bear as tolerated and progress to full weight bearing Brace: Unlock brace, may discharge when gait is normalized Exercises 1. Active knee flexion in seated position, not against gravity 2. Initiate biking, emphasizing range of motion 3. Initiate pool exercises to help increase range of motion and help with weight bearing 4. Initiate progressive resistance exercise for the quadriceps (i.e., knee extension)

CONCLUSIONS PLC injuries present numerous challenges to the orthopedic surgeon. Expeditious and accurate diagnosis of this condition and all other concomitant injuries is critical in achieving a successful outcome. The decision to pursue nonoperative or operative management should be carefully analyzed and

5. Initiate active knee flexion against gravity at week 10 and progress to progressive resistance as tolerated Phase III: Weeks 12 to 16 Goals 1. Full weight bearing without assistive devices and nonantalgic 2. Begin closed-chain exercises Exercises 1. Bicycle for range of motion and endurance 2. Pool program (strengthening, swimming, walking) 3. Closed-chain exercises: a. Mini-squats b. Front lunges c. Ball/wall squats d. Leg press e. Step ups: forward, side f. Step downs g. Lateral lunges h. Multidirectional lunges 4. Continue isotonic strengthening for the knee extensors, hip abductors/adductors, and hamstrings 5. Stairmaster, elliptical trainer for endurance 6. Proprioceptive/balance exercises a. Progress from stable to unstable surfaces, unidirectional to multidirectional, single plane to multiple plane b. Eyes open, eyes closed c. Cervical movement to help enhance vestibular input Phase IV: 4 to 6 months postoperatively Goals 1. Gradually initiate pool running and agility drills in the pool 2. Continue all strengthening exercises 3. Progress to land-based agility as pool exercises are pain free 4. Gradual return to sports activities at least 6 months postoperatively following isokinetic testing, multidirectional functional and sport-specific testing

based on patient expectation, level of function, and motivation and only after a comprehensive physical examination and review of pertinent radiographic studies. We believe that a fibular-based reconstruction using hamstring autograft in conjunction with a specific, carefully supervised rehabilitation protocol can successfully achieve the goal of a stable and functional knee.

REFERENCES 1. Andrews JR, Baker CL, Curl WW: Surgical repair of acute and chronic lesions of the lateral capsular ligamentous complex of the knee. In Feagin JA (ed): The Cruciate Ligaments: Diagnosis and Treatment. New York, Churchill Livingstone, 1988, pp 425–438. 2. Covey DC: Injuries to the posterolateral corner of the knee. J Bone Joint Surg Am 2001;83:106–118. 3. Maynard MJ, Deng XH, Wickiewicz TL, Warren RF: The popliteofibular ligament: Rediscovery of a key element in posterolateral stability. Am J Sports Med 1996;24:311–315. 4. Recondo JA, Salvador E, Villanua JA, et al: Lateral stabilizing structures of the knee: Functional anatomy and injuries assessed with MR imaging. Radiographics 2000;20:S91–S102.

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5. Davies H, Unwin A, Aichroth P: The posterolateral corner of the knee: Anatomy, biomechanics, and management of injuries. Injury 2004; 35:68–75. 6. Kim YC, Cheng IH, Yoo WK, et al: Anatomy and magnetic resonance imaging of posterolateral structures of the knee. Clin Anat 1997; 10:397–404. 7. Seebacher JR, Inglis AE, Marshall JL, Warren RF: The structure of the posterolateral aspect of the knee. J Bone Joint Surg Am 1982;64:536–541. 8. Kendall FP, McCreary EK, Provance PG: Muscles: Testing and Function, 4th ed. Baltimore, Williams & Wilkins, 1993. 9. LaPrade RF, Ly TV, Wentorf FA, Engebretsen L: The posterolateral attachments of the knee: A qualitative and quantitative morphologic

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10.

11. 12. 13. 14.

15. 16.

17.

18.

19.

analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, lateral gastrocnemius tendon. Am J Sports Med 2003;31:854–860. Sudasna S, Harnsiriwattanagit K: The ligamentous structures of the posterolateral aspect of the knee. Bull Hosp Jt Dis Orthop Inst 1990; 50:35–40. Watanabe Y, Moriya H, Takahashi K, et al: Functional anatomy of the posterolateral structures of the knee. Arthroscopy 1993;9:57–62. LaPrade RF, Wentorf F: Diagnosis and treatment of posterolateral knee injuries. Clin Orthop 2002;402:110–121. DeLee JC, Riley MB, Rockwood CA Jr: Acute posterolateral rotatory instability of the knee. Arthroscopy 2002;18(2 Suppl 1):1–8. Veltri DM, Deng XH, Torzilli PA, et al: The role of the cruciate and posterolateral ligaments in stability of the knee: A biomechanical study. Am J Sports Med 1995;23:436–443. Brunnstrom S: Clinical Kinesiology, 3rd ed. Philadelphia, FA Davis, 1983. LaPrade RF, Resig S, Wentorf F, Lewis JL: The effects of grade III posterolateral complex knee injuries on ACL graft force: A biomechanical analysis. Am J Sports Med 1999;27:469–475. LaPrade RF, Muench C, Wentorf F, Lewis JL: The effect of injury to the posterolateral structures of the knee on force in a PCL graft: A biomechanical study. Am J Sports Med 2002;30:233–238. Hughston JC, Norwood LA Jr: The posterolateral drawer test and external rotation recurvatum test for posterolateral rotatory instability of the knee. Clin Orthop 1980;147:82–87. LaPrade RF, Terry GC: Injuries to the posterolateral aspect of the knee: Association of anatomic injury patterns with clinical instability. Am J Sports Med 1997;25:433–438.

20. Grood ES, Stowers SF, Noyes FR: Limits of movement in the human knee: Effect of sectioning the posterior cruciate ligament and the posterolateral structures. J Bone Joint Surg Am 1988;70:88–97. 21. Noyes FR, Barber-Westin SD: Surgical reconstruction of severe chronic posterolateral complex injuries of the knee using allograft tissues. Am J Sports Med 1995;23:2–12. 22. DeLeo AT, Woodzell WW, Snyder-Mackler L: Resident’s case problem: Diagnosis and treatment of posterolateral instability in a patient with lateral collateral ligament repair. J Orthop Sports Phys Ther 2003; 33:185–194. 23. Chen FS, Rokito AS: Acute and chronic posterolateral rotatory instability of knee. J Am Acad Orthop 2000;8:97–110. 24. Fanelli GC: Treatment of combined anterior cruciate ligament-posterior cruciate ligament-lateral side injuries of the knee. Clin Sports Med 2000;19:493–501. 25. Veltri DM, Warren RF: Anatomy, biomechanics, and physical findings in posterolateral knee instability. Clin Sports Med 1994;13:599– 614. 26. Hughston JC, Jacobsen KE: Chronic posterolateral rotatory instability of the knee. J Bone Joint Surg Am 1985;67:351–359. 27. Clancy WG, Meister K, Craythome CB. Posterolateral corner collateral ligament reconstruction. In Jackson D (ed): Reconstructive Knee Surgery. New York, Raven Press, 1995, pp 143–159. 28. Moorman CT, Clancy WG: American Orthopaedic Society for Sports Medicine. Annual Meeting, July 1, 2002, Lake Buena Vista, FL. 29. Zachazewski JE, Magee DJ, Quillen WS: Athletic Injuries and Rehabilitation. Philadelphia, WB Saunders, 1996. 30. Irrgang JJ, Fitzgerald GK: Rehabilitation of the multiple ligament injured knee. Clin Sports Med 2000;19:545–571.

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56

Multiligament Knee Injuries James R. Gardiner and Darren L. Johnson

In This Chapter Classification Associated injuries Initial evaluation and management Nonoperative management Surgery

INTRODUCTION • A multiligament knee injury is a serious injury that presents the orthopedic surgeon with a complex treatment challenge. • Multiligament knee injuries result from a minimal disruption of two or more of the major stabilizing ligaments of the knee and often result in multidirectional instability patterns. • Knee dislocation may be misleading because the majority of knee dislocations present after having spontaneously reduced. Therefore, the term multiligament knee injury may be more appropriate. • Treatment of this injury may be complicated by associated neurovascular, articular cartilage, meniscal, osseous, and softtissue injuries. • Effective treatment requires the clinician to be aware of the associated injury patterns and to be proficient in the evaluation and treatment of multiligament injuries.

INCIDENCE Acute knee dislocations are a rare event, accounting for less than 0.02% of all orthopedic injuries.1–3 The true incidence is probably unknown because the majority of multiple-ligament-injured knees present after spontaneous reduction. In one series, the incidence of multiligament injuries in an athletically active population was 1.2% of orthopedic trauma.4

RELEVANT ANATOMY A thorough understanding of the complex anatomy surrounding the knee is essential to accurate diagnosis and appropriate decision making during treatment of the multiligament-injured knee. The anatomy of the major stabilizing ligaments of the knee (anterior cruciate ligament [ACL], posterior cruciate ligament [PCL], medial cruciate ligament [MCL], lateral collateral ligament) as well as secondary stabilizers (posterolateral corner, pos-

teromedial capsule, menisci, and musculotendinous units) have been well studied and are thoroughly reviewed in other chapters.5 In addition to knowledge of major stabilizing ligaments, it is important to be familiar with the relevant neurovascular anatomy. The popliteal artery is the continuation of the superficial femoral artery as it passes through the tendinous hiatus of the adductor magnus. The popliteal artery is tethered proximally at the adductor hiatus and distally as it passes under the soleus arch making it susceptible to traction injuries in these areas. The skin surrounding the knee receives a rich blood supply from the superior, middle, and inferior geniculate branches of the popliteal artery. However, this anastomotic ring provides inadequate collateral circulation for lower limb perfusion in the event of disruption of popliteal flow. The sciatic nerve divides proximal to the popliteal space into posterior tibial and common peroneal divisions. The common peroneal nerve courses inferolaterally deep to the biceps femoris and passes around the fibular neck causing it to be more susceptible to injury.

CLASSIFICATION Classification of orthopedic injuries can be useful for both effective communication between physicians and development of appropriate treatment strategies. Multiligament-injured knees can be classified based on the following parameters: (1) joint position, (2) injured structures, (3) energy level, and (4) chronicity. Classification of knee dislocations is summarized in Table 56-1. Historically, knee dislocations like other joint dislocations, have been classified based on the position of the distal bone (tibia) in relation to the proximal bone (femur). Kennedy2 noted five main types of dislocations: anterior (40%), posterior (33%), lateral (18%), medial (4%), and rotational (5%). This classification system is limited because the majority of dislocations present following spontaneous reduction. Although the least common type, the posterolateral dislocation, is well described and is one of the few useful aspects of the positional classification system. The hallmark of this type of dislocation is its frequent irreducibility secondary to “buttonholing” of the medial femoral condyle through the medial capsule and invagination of the MCL into the medial joint space6 (Fig. 56-1). The posterolateral dislocation often produces a dimple sign on the medial aspect of the knee (Fig. 56-2). The anatomic system classifies multiligament-injured knees based on functional evaluation of injured structures,7 which is determined by a thorough clinical examination. The anatomic system clearly defines which structures are injured and can be used to guide surgical planning.

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Table 56-1 Classification of Knee Dislocations Anatomic Classification KDI

Cruciate intact knee dislocation

KDII

Both cruciates torn, collateral intact

KDIII KDIIIM KDIIIL

Both cruciates torn, one collateral torn MCL torn LCL torn

KDIV

All four ligaments torn

KDV

Periarticular fracture-dislocation

Joint Position Anterior

40%

Posterior

33%

Lateral

18%

Rotational

5%

Medial

4%

Energy Level High

Fractures and neurovascular injury common

Low Chronicity Acute

3 mo

Data obtained from references 2, 4, 6, 9, 11.

Figure 56-2 Clinical photograph of a right posterolateral knee dislocation showing dimple sign. Orientation is with the patient’s head toward the top. This photograph corresponds to the magnetic resonance image shown in Figure 56-1.

In addition to the anatomic classification, knee dislocations can be classified based on the energy level or chronicity of the injury. Higher energy level injuries are often associated with additional musculoskeletal or systemic injuries. Low-energy dislocations have a lower incidence of vascular, neurologic, and meniscal injuries.8 In high-energy dislocations, the rate of popliteal artery injury ranges from 14% to 65%. Fifty percent to 60% of patients will have fractures, and 41% will have multiple fractures. Patients with these high-energy injuries often have other significant injuries to their head or chest, which precludes early aggressive treatment of their knee ligaments.9 The chronicity of the injury is also important with regard to associated injuries and surgical planning. Surgical treatment gives improved results in acute versus chronic cases.10 Some structures may be repaired if treated acutely, whereas late treatment may require a reconstruction. A knee dislocation is acute if seen within 3 weeks, subacute if seen between 3 to 12 weeks, and chronic if seen after 3 months.11

MECHANISM OF INJURY Figure 56-1 Coronal magnetic resonance image of a multiligamentinjured knee showing displacement of the medial collateral ligament and medial capsule into joint space.

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The mechanism of injury provides useful information regarding the direction and degree of injury. The mechanisms for the two most common patterns, anterior and posterior dislocations, are well described. Kennedy2 was able to reproduce anterior dislo-

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cation by using a hyperextension force acting on the knee. At 30 degrees of hyperextension, the posterior capsule fails. This is followed at about 50 degrees by the ACL, PCL, and popliteal artery. Posterior dislocations can be caused by a force applied to the anterior proximal tibia in the knee flexed 90 degrees. This has been referred to as the so-called dashboard injury and may be associated with a hip fracture or dislocation. Knee dislocations can also occur from sports-related or lowvelocity mechanisms. Shelbourne and Klootwyk8 reported that the most commonly involved sports were football (35%), wrestling (15%), and running (10%). Industrial accidents and falls are other common mechanisms.2

ASSOCIATED INJURIES All anatomic structures surrounding the knee are at risk of injury following a knee dislocation. By definition, more than one of the four primary ligamentous stabilizers of the knee is disrupted following a multiligament injury. In addition, neurovascular injuries are common. Bony injuries may occur and range from simple avulsions to intra-articular fracture-dislocations. High-energy dislocations may be associated with significant injury to the surrounding soft tissue including skin and myotendinous units. Patients who sustain a high-energy knee dislocation will present with spontaneous reduction up to 50% of the time, leading to delayed or missed diagnosis.9

A

Vascular Injuries Vascular injuries may occur with all types of knee dislocations. The presence of a multiligament-injured knee obligates the clinician to carefully evaluate the circulatory status of the injured extremity. The overall incidence of recognized popliteal vessel injury ranges from 10% to 44%.12–14 The popliteal artery is an end artery for the leg as the genicular arteries provide inadequate collateral circulation to maintain limb perfusion. Obstruction of the popliteal vessels can lead to prolonged ischemia and eventual amputation.

Nerve Injuries The incidence of nerve injuries with knee dislocations is 20% to 30%.15,16 The injury can range from stretching of the nerve (neurapraxia) to transection. The peroneal nerve is most commonly injured, but injuries to the tibial nerve can occur. Injuries to the lateral and posterolateral corner of the knee place the peroneal nerve at increased risk because of its superficial location at the level of the fibular neck. The prognosis of severe peroneal nerve injuries is poor. Complete nerve injuries only recover about 50% of the time.15,17 First-degree injuries (neurapraxia) commonly recover within 1 to 4 months.15

Other Injuries Open dislocations may occur in as many as 30% of high-energy dislocations. The highest incidence is in dislocations that are in the sagittal plane. Cole and Harner11 reported injuries to the patellar tendon or biceps in 20% of these patients (Fig. 56-3). Associated fractures of the distal femur and tibial plateau may occur in up to 30% of high-energy dislocations.11 Patients who sustain high-energy dislocations also often have multiorgan system trauma requiring specialized evaluation and treatment. Recognition and treatment of associated injuries may take precedence and have implications upon definitive treatment of ligamentous injuries.

B Figure 56-3 Sagittal magnetic resonance images of high-energy multiligament knee injury. A, Disruption of anterior and posterior cruciate ligaments. B, Partial quadriceps rupture and open anterior wound.

INITIAL EVALUATION AND MANAGEMENT History and Physical Examination Although some knee dislocations present with obvious deformity, most multiligament knee injuries spontaneously reduce. One must have a high index of suspicion, particularly in the polytrauma setting where these injuries may go overlooked. Important elements from the history include injury mechanism, direction of force, and position of the leg.

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After obtaining a history, a thorough physical examination must be performed. Careful visual inspection should note any deformity, wound, or skin discoloration. Patients with a knee dislocation will often have a large effusion and even swelling of the entire extremity. The presence of a dimple sign or tight compartments must be assessed. A detailed neurovascular examination of both lower extremities must be performed. Evaluation of the sensory and motor functions of peroneal and tibial nerves should be well documented and followed serially. Careful assessment of the circulatory status of the limb should include observation of capillary refill, palpation of the popliteal, posterior tibial and dorsalis pedis pulses, as well as Doppler ankle brachial indices. Keep in mind that a patient with brisk capillary refill and palpable pulses may still have a vascular injury. In the acute setting, swelling and pain often prevent a detailed ligament examination. However, the best possible assessment should be obtained. The four main ligamentous structures include the ACL, PCL, MCL with posteromedial capsule, and the lateral collateral ligament with posterolateral corner. Each of these structures must be systematically evaluated for stability. The most sensitive test for ACL rupture is the Lachman test performed with the knee held in 20 to 30 degrees of flexion.18 The most sensitive test for detecting PCL injury is the posterior drawer test performed with the knee in 90 degrees of flexion.19 The collateral ligaments are assessed by applying varus and valgus stress at both 30 degrees of flexion and full extension. Laxity in full extension denotes disruption of a cruciate ligament and the posteromedial or posterolateral capsule in addition to collateral injury. These patients will exhibit rotatory instability that must be identified initially and addressed at the time of surgery. Techniques for a comprehensive knee examination have been described in a previous chapter.

A

Imaging Upon completion of the initial examination, anteroposterior and lateral radiographs of the affected extremity should be obtained. This should be done prior to any attempts at manipulation. Obtaining radiographs allows for diagnosis of any associated fractures and will assist in planning the appropriate reduction maneuver. Magnetic resonance imaging (MRI) is necessary to evaluate the ligamentous structures and other soft tissues (Fig. 56-4). It may help to diagnose patellar tendon or quadriceps rupture, which would require early repair. MRI may also identify meniscal injuries, articular cartilage lesions, bone bruises, and occult fractures. We recommend performing MRI in all cases in which repair or reconstruction is planned. This imaging study can be obtained in a nonemergent fashion.

B

Reduction An unreduced knee dislocation represents a true orthopedic emergency. A reduction should be performed expeditiously after completion of initial evaluation and radiographs. Following administration of appropriate sedatives, reduction is performed by applying gradual longitudinal traction through the ankle with manipulation of the proximal tibia in the appropriate direction. Following reduction, with the patient still sedated, a repeat examination of the stability of the knee can be performed. Reduction should be confirmed with radiographs. It is imperative to reassess the neurovascular status of the limb following manipulation. Keep in mind that an anteromedial dimple sign indicates a posterolateral dislocation. In this setting, closed reduction is unlikely to be successful and probably should not be attempted.

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C Figure 56-4 Sagittal magnetic resonance images of multiligament knee injury showing anterior cruciate ligament disruption (A), posterior cruciate ligament disruption (B), and fibular collateral ligament disruption (C).

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Because of interposed soft tissue within the medial joint space, open reduction is warranted.20

Stabilization Once reduction has been confirmed radiographically, the knee needs to be temporarily stabilized. Potential modes for temporary stabilization include a hinged knee brace, long-leg splint, and kneespanning external fixation. The choice depends on the patient’s body habitus, presence of concomitant musculoskeletal or systemic injuries, and overall stability of the knee. For most lowenergy injuries, immobilization in full extension with a hinged knee brace or long-leg splint is appropriate. For high-energy injuries, in select polytrauma patients, and patients with significant soft-tissue injuries, external fixation may be more appropriate. Whatever mode of stabilization is selected, it is important to radiographically verify that reduction is maintained immediately after immobilization and at regular intervals thereafter.

Vascular Injuries Popliteal artery injury is often associated with knee dislocation following blunt trauma. The risk of amputation is high if revascularization is not accomplished within a 6- to 8-hour window.1,2,13 Patients who present with signs of vascular compromise, including diminished or absent pulses, pallor, or temperature changes clearly require emergent vascular surgery consultation. However, the most appropriate method of vascular evaluation for a patient with a knee dislocation without signs of ischemia remains controversial.

Historically, authors have advocated routine angiography on all patients with a multiligament-injured knee secondary to the relatively high incidence of popliteal vessel injury.1,2,21,22 Routine angiography is also supported by the fact that as many as 30% of patients with popliteal artery injuries will have palpable distal pulses.9,23 However, more recent literature has supported the role of serial physical examination, including an ankle brachial index with use of selective angiography only if abnormalities are detected on physical examination.13,22 Additional noninvasive techniques include duplex ultrasonography.24 Stannard et al22 performed a prospective cohort study evaluating the role of physical diagnosis in determining the need for angiography. They evaluated 138 consecutive patients with an acute multiligament knee injury. All patients underwent serial physical examination for 48 hours. Arteriography was obtained in patients with a decrease in pedal pulses, temperature or color changes, expanding hematoma, or documented abnormal vascular examination prior to presentation. In their cohort, physical examination had a positive predictive value of 90%, a negative predictive value of 100%, sensitivity of 100%, and specificity of 99%. We have incorporated the use of serial physical examination and selective angiography in our algorithm for initial evaluation and management of multiligament knee injuries. This is based on advocacy of selective arteriography in more recent literature as well as the associated cost and risk of routine arteriography. Table 56-2 provides an algorithm for the initial evaluation and management of multiligament knee injuries.

Table 56-2 Algorithm for Initial Evaluation and Management of Multiligament Knee Injuries Dimple sign 䉲

䉲

No reduction

䉲

䉲

To OR immediately

To OR immediately

䉲

Physical examination

Open reduction

Pulses present

Stable

PE for stability

䉲

䉲

䉲

䉲

Stable

Unstable

䉲

䉲

䉲

Brace IV antibiotics

Immobilize

䉲

䉲

Observe

Radiograph

䉲

Observe

䉲

Unreduced 䉲

To OR 䉲

Reduce

䉲

OR/arteriogram

䉲

䉲

To OR

NL 䉲

䉲

Reduction 䉲

Ex-fix 䉲

Observe

Reduction 䉲

䉲

Reduced

䉲

Vascular consult

䉲

䉲

Pulses absent

䉲

䉲

Unstable

䉲

䉲

Irrigation

Stable 䉲

Immobilize 䉲

Observe

䉲

Unstable 䉲

Ex-fix

䉲

Injury 䉲

Repair Ex-fix 䉲

䉲

Reduction

䉲

䉲

Reduction

Ex-fix

Skin intact

䉲

Open skin

Observe

䉲

Observe

䉲

Ex-fix 䉲

Observe Ex-fix, External fixation; OR, operating room; PE, physical examination. From Wilson TC, Johnson DL: Initial evaluation and management of the acute multiple-ligament-injured knee. Op Tech Sports Med 2003;11:187–192.

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TREATMENT OPTIONS AND RECOMMENDATIONS

ring will obscure tissue planes and repair of individual structures will be difficult.

Definitive management of multiligament knee injuries has not been well studied using prospective, randomized techniques. Interpretation of current literature is made difficult because of the varied combinations of ligamentous, meniscal, and osseous injuries, as well as multiple treatment approaches and outcome measures. The primary goals of treatment include achieving knee stability, maintaining knee motion, and restoring overall knee function to allow for daily activities.

Graft Selection

Nonoperative Management Historically, nonsurgical management of knee dislocations was standard.25–27 Treatment typically consisted of cast immobilization for 4 to 12 weeks. Selecting duration of treatment represented a compromise between stability and motion. Knee stability generally improved while knee motion declined with longer periods of immobilization. Given the results of modern reconstruction techniques, nonoperative management should probably be reserved for those patients who are elderly or very sedentary or have significant medical comorbidities. Nonoperative treatment consists of 6 weeks of immobilization in extension using a cast, brace, or external fixation. The form of immobilization depends on the patient’s habitus, energy level of the injury, and associated soft-tissue, vascular, or systemic injuries. Typically, obese patients, high-energy injuries, and injuries requiring soft-tissue or vascular surgery are best served by treatment in an across-knee external fixator. During the initial period of immobilization, regular radiographs should be obtained to confirm reduction. Initial immobilization is followed by progressive motion and strengthening in a brace.

Surgical Management Principles Most authors currently recommend surgical treatment of acute multiligament knee injuries.3,9–11,27,28 Some disagreement remains concerning surgical timing, surgical technique, graft selection, and rehabilitation protocols. Generally, addressing cruciate ligament injuries as well as all grade III collateral instabilities will allow for the greatest restoration of overall knee function. Careful preoperative planning must include review of MRI, radiographs, initial physical examination, and availability of all equipment and graft sources. Careful examination under anesthesia is performed to confirm the presence of pathologic laxity. Diagnostic arthroscopy should be carried out to confirm ligament injuries and identify any chondral or meniscal injury. Reconstructions should be performed with accurate tunnel placement, strong graft material, and secure fixation. Repairs should be anatomic and secure.

Surgical Timing Absolute surgical indications include irreducibility, vascular injury, open injury, compartment syndrome, and inability to maintain reduction with nonoperative methods. When there are no indications for emergent surgical intervention, reduction, immobilization, and MRI can be performed followed by delayed surgical intervention. Delaying surgery for 7 to 14 days will allow for appropriate vascular monitoring and reduction of swelling. This period will also allow for some capsular healing, which allows the use of arthroscopically assisted techniques with less risk of fluid extravasation. In cases in which collateral ligaments repair is indicated, surgery should not be delayed beyond 3 weeks as scar-

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The physician planning surgical treatment for a multiligamentinjured knee should be adept at using multiple graft sources including autograft and allograft. Most authors currently advocate reconstruction using allograft sources.3,10,28 The advantages of allograft use in surgical management of multiligament injuries include less graft site morbidity, shorter operative time, less surgical dissection in an already traumatized knee, and the potential for less postoperative stiffness. More detailed discussion on the advantages and disadvantages of autograft and allograft tissue are discussed in Chapters 12 and 50.

Combined Cruciate Reconstruction We use a single-stage arthroscopic combined ACL/PCL reconstruction using a bone-patellar tendon-bone allograft for the ACL and an Achilles tendon allograft via a transtibial approach for the PCL. The patient is positioned supine with the operative leg in an arthroscopic leg holder and the well leg widely abducted in the lithotomy position. A tourniquet is applied and used if visualization is impaired. A fluid pump is used judiciously with regular examination for fluid extravasation. Diagnostic arthroscopy is performed and all meniscal and articular pathology is addressed. This is followed by the notchplasty consisting of débridement of the ACL and PCL stump and contouring of the medial and lateral walls and the intercondylar roof. Use of a radiofrequency ablater may help minimize bleeding and improve visualization. Notchplasty should allow for appropriate anatomic tunnel positioning and prevent any graft impingement. Tibial tunnels are created using commercially available ACL and PCL guides. Preparation of the PCL tibial tunnel is always done with the use of an accessory posteromedial portal and a 70-degree arthroscope. The medial meniscal root is used as a landmark for the PCL tibial tunnel position.29 The tip of the guide is placed just posterior to the meniscal root 1 cm off of the tibial plateau. The tunnel should start 4 cm distal to the joint and 2 cm medial to the tibial tubercle. Care must be used in passing the guidewire because of its close proximity to the posterior neurovascular bundles. The ACL tibial guide is placed in the posteromedial footprint of the ACL stump leaving a 2- to 3-cm bridge in the PCL tunnel (Fig. 56-5). Proper guidewire position can be confirmed fluoroscopically, if needed. Femoral tunnels are created next. The ACL femoral tunnel should be positioned at the 10- or 2-o’clock position, leaving a 1- to 2-mm posterior wall. The PCL femoral tunnel is created through the anterolateral arthroscopic portal. It should be positioned in the center of the stump of the anterolateral bundle 2 mm from the articular surface. All soft tissue and sharp edges should be removed from the margins of the tunnels to facilitate graft passage and prevent graft abrasion. PCL graft passage is performed next by passing a long looped wire antegrade through the anterolateral portal into the tibial tunnel. The wire is then used to pass the suture secured to the tendinous portion of the graft retrograde through the tunnel. A blunt trochar placed through the posteromedial portal can assist with graft passage around the corner of the tibial tunnel. A Beath needle is then used through the anterolateral portal to pass the graft into the femoral tunnel, after which it is secured with a bioabsorbable interference screw. The ACL graft is then passed

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ACL PCL

ACL ACL PCL

PCL

A

B

Figure 56-5 Diagram of tunnel placement in combined anterior cruciate ligament (ACL)/posterior cruciate ligament (PCL) reconstruction. (From Rihn JA, Groff YJ, Harner CD, et al: The acutely dislocated knee: Evaluation and management. J Am Acad Orthop Surg 2004;12:334–346.)

in a retrograde fashion and fixed on the femoral side with an interference screw. If repair of collateral structures is required, it should be performed prior to fixation of the grafts on the tibial side. While visualizing the grafts arthroscopically, the knee should be taken through a range of motion to ensure there is no graft impingement (Fig. 56-6) The PCL is tensioned and fixed on the tibial side in 90 degrees of flexion. Prior to fixation, a gentle anteriorly directed force is applied to the proximal tibia to recreate the normal step-off between the tibial plateau and femoral condyle. The PCL is then secured on the tibial side with an interference screw. The ACL is tensioned with the knee in full extension and fixed on the tibial side with an interference screw. Table 56-3 summarizes the order of reconstruction.

Medial-Side Injury Grade I or II MCL injuries alone or in combination with ACL or PCL injuries can be treated successfully nonoperatively with edema control, bracing, early motion, and functional rehabilitation.30,31 Treatment of acute grade III MCL injuries in association with ACL/PCL injuries remains controversial. Treatment recommendations have included nonoperative treatment of the MCL and early reconstruction of the ACL/PCL, nonoperative treatment of the MCL, and delayed cruciate reconstruction, or

Figure 56-6 Arthroscopic view of completed anterior/posterior cruciate ligament reconstruction.

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Table 56-3 Order of Bicruciate Ligament Reconstruction in the Multiligament Injured Knee

ACL, Anterior cruciate ligament; PCL, posterior cruciate ligament. From Cole BJ, Harner CD: The multiligament injured knee. Clin Sports Med 1999;18:241–262.

10,31–33

treatment of all acute grade III injuries. Others have advocated treating grade III MCL tears based on the location of the tear, selecting nonoperative treatment for proximal or midsubtance tears, and treating more distal tears with early repair because of a propensity for poor healing.34,35 It is important to check for involvement of the posteromedial capsule. If patients have laxity to valgus stress in full extension with associated rotatory instability, acute repair of the MCL and posteromedial capsule is warranted. Regardless of the protocol chosen, important principles to follow include accurate diagnosis of both the degree of medial instability and the location of the acute injury. All tools of diagnosis must be used including initial examination, examination under anesthesia, MRI (Fig. 56-7), and arthroscopic findings (Fig. 56-8). Repair of acute medial instability is performed through a straight medial incision extending from the medial epicondyle to 4 cm distal to the joint line. Care must be taken to protect the saphenous nerve. This approach allows access to the superficial MCL, deep MCL, medial meniscus, and posteromedial

Figure 56-7 Coronal magnetic resonance image of medial collateral ligament avulsion off the tibia with proximal retraction.

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Figure 56-8 Arthroscopic picture of medial lift-off.

capsular structures. The superficial MCL should be isolated and the zone of injury identified. The injury will usually be located either proximally or distally, allowing the ligament to be tagged with a locking whipstitch and reflected to allow access to deep structures. Tears in the deep MCL and meniscal capsular attachments are repaired using a minimum of three suture anchors placed just below the articular margin. The posteromedial capsule should be evaluated and repaired mid-substance or reattached with suture anchors if avulsed. The superficial MCL can then be repaired to its anatomic position either proximally or distally and secured with a spiked washer or suture anchors. In cases in which the superficial MCL is injured mid-substance, the repair may be augmented with either a hamstring autograft or an allograft. The medial-side repair should be completed prior to final fixation of the cruciate ligaments.

Lateral-Side Injury Unlike medial-side injury, there is widespread agreement that grade III lateral-side injuries in association with ACL/PCL injury are best treated with acute repair.36,37 Grade III lateral-side injuries most commonly represent avulsions from the tibia/fibula. Direct anatomic repair of all injured structures will provide the greatest chance of favorable outcome.37 The posterolateral corner is approached through a curvilinear incision extending from the lateral epicondyle to Gerdy’s tubercle. A systematic evaluation of all structures should take place including the iliotibial band, biceps femoris, lateral collateral ligament, popliteus, popliteofibular ligament, lateral meniscus, and peroneal nerve. Repair should proceed from deep to superficial with either a direct end-to-end suture repair or suture anchors as needed. Repairs should be performed with the knee in 30 degrees of flexion. In cases of significant mid-substance injury or poor tissue quality, direct repair may be augmented with hamstring autograft, allograft, biceps femoris, or iliotibial band tendon. Numerous techniques have been described.38–40 These same techniques can be applied to cases of chronic laxity requiring reconstructions. We perform reconstructions of the fibular collateral ligament and popliteofibular ligament using a split Achilles tendon allograft fixed on the lateral femoral condyle with an interference screw and passed through tunnels in the proximal tibia and fibula with interference screw fixation.

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Table 56-4 Algorithm for Rehabilitation Following Multiligament Knee Surgery

From Harner CD, Waltrip RL, Bennett CH, et al: Surgical management of knee dislocations. J Bone Joint Surg 2004;86:262–273.

POSTOPERATIVE REHABILITATION Postoperative rehabilitation is an important element in the successful treatment of multiligament knee injuries. A comprehensive postoperative rehabilitation program following multiligament reconstructions has been well described.41,42 A summary is provided in Table 56-4. The knee is placed in a hinged knee brace kept in full extension for the first 4 to 6 weeks. The patient is kept partially weight bearing. For the first 4 weeks, passive extension is emphasized and passive flexion is limited to 90 degrees. After 4 weeks, patients begin closed-chain quadriceps and hamstring exercises. After 6 weeks, the brace can be discontinued with good quadriceps control, and progressive open-chain strengthening and range-of-motion exercises are started. If sufficient motion and strength have been obtained, return to sports and heavy labor can be considered after 9 months.

COMPLICATIONS Given the severity of the injury and the nature of the complex reconstructions, complications with traumatic knee dislocations do occur. Major complications include vascular injury, neurologic injury, compartment syndrome and soft-tissue trauma, and infection associated with open injuries. Other complications include loss of motion, residual laxity, painful hardware, and complex regional pain syndrome.

makes interpreting results difficult. Harner et al10 recently published their results in 33 patients treated with repair or reconstruction of all grade III instabilities at a minimum of 24 months of follow-up. Mean Lysholm score was 87 (range, 50 to 100), average Knee Outcome Survey Activities of Daily Living score was 89 (range, 64 to 99), and final overall International Knee Documentation Committee rating was nearly normal for 11 knees, abnormal for 12, and severely abnormal for eight. These results are similar to ones in other published reports.26–28,43–47 Table 56-5 summarizes subjective assessments of operatively treated multiligament-injured knees.

Table 56-5 Subjective Outcome in Operatively Treated Multiligament Injuries Study

Year

No. of Knees

Lysholm Score

Walker et al

1994

13

84.6 (73–94)

Montgomery et al45

1995

13

80 (60–95)

43

47

Shapiro et al

1995

7

Fanelli et al48

1996

20

91.3 (80–100)

Wascher et al

1994

13

88 (42–100)

Yeh et al46

1999

25

84.1 (79–93)

33

87 (50–100)

44

RESULTS AND OUTCOMES

27

Published results of surgical management of knee dislocations are heterogeneous, small in number, and retrospective. This

Harner et al

2004

74.7 (34–93)

27

Modified from Almekinders and Dedmond.

REFERENCES 1. Green NE, Allen BL: Vascular injuries associated with dislocations of the knee. J Bone Joint Surg Am 1977;59:236–239. 2. Kennedy J: Complete dislocation of the knee joint. J Bone Joint Surg Am 1963;45:889–904.

3. Rihn JA, Groff YJ, Harner CD, et al: The acutely dislocated knee: Evaluation and management. J Am Acad Orthop Surg 2004;12:334– 346. 4. Schenk R: Knee dislocations. Instruct Course Lect 1999;48:515–522.

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5. Goldblatt, JP, Richmond JC: Anatomy and biomechanics of the knee. Oper Tech Sports Med 2003;11:172–185. 6. Quinlan AG: Irreducible posterolateral dislocation of the knee with button-holing of the medial femoral condyle. J Bone Joint Surg Am 1977;59:236–239. 7. Schenk R: Classification of knee dislocations. Oper Tech Sports Med 2003;11:193–198. 8. Shelbourne KD, Klootwyk TE: Low-velocity knee dislocation with sports injury. Treatment principles. Clin Sports Med 2000;19:443–456. 9. Wascher DC: High-velocity knee dislocations with vascular injury. Treatment principles. Clin Sports Med 2000;19:457–477. 10. Harner CD, Waltrip RL, Bennett CH, et al: Surgical management of knee dislocations. J Bone Joint Surg [Am] 2004;86:262–273. 11. Cole BJ, Harner CD: The multiligament injured knee. Clin Sports Med 1999;18:241–262. 12. Miranda FE, Dennis JW, Veldenz HC, et al: Confirmation of the safety and accuracy of physical examination in the evaluation of knee dislocation for injury of the popliteal artery: A prospective study. J Trauma 2002;52:247–251. 13. Armstrong PJ, Franklin DP: Treatment of vascular injuries in the multiple-ligament-injured knee. Oper Tech Sports Med 2003;11:199–207. 14. Mills WJ, Barei DP, McNair P: The value of the ankle-brachial index for diagnosing arterial injury after knee dislocation: A prospective study. J Trauma 2004;56:1261–1265. 15. Monahan TJ: Treatment of nerve injuries in the multipleligament-injured knee. Oper Tech Sports Med 2003;11:208–217. 16. Goitz RJ, Tomaino MM: Management of peroneal nerve injuries associated with knee dislocations. Am J Orthop 2003;32:14–16. 17. Mont MA, Dellon AL, Chen F, et al: The operative treatment of peroneal nerve palsy. J Bone Joint Surg Am 1996;78:863–869. 18. Donaldson WF, Warren RF, Wickiewicz T: A comparison of acute anterior cruciate ligament examinations. Am J Sports Med 1992;10:100–102. 19. Rubinstein RA, Shelbourne KD, McCarroll JR, et al: The accuracy of the clinical examination in the setting of posterior cruciate ligament injuries. Am J Sports Med 1994;22:550–557. 20. Wand JS: A physical sign denoting irreducibility of a dislocated knee. J Bone Joint Surg Br 1989;71:94–102. 21. McCoy GF, Hannon DG, Barr RJ, et al: Vascular injury associated with low-velocity dislocations of the knee. J Bone Joint Surg Br 1987; 69:285–287. 22. Stannard JP, Sheils TM, Lopez-Ben RR, et al: Vascular injuries in knee dislocations: The role of physical examination in determining the need for arteriography. J Bone Joint Surg [Am] 2004;86:910–915. 23. McCutchan JD, Gillham NR: Injury to the popliteal artery associated with dislocation of the knee: Palpable distal pulses do not negate the requirement for arteriography. Injury 1989;20:307–310. 24. Bynoe RP, Miles WS, Bell RM, et al: Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg 1991;14:346–352. 25. Taylor AR, Arden GP, Rainey HA: Traumatic dislocation of the knee: A report of forty-three cases with special reference to conservative treatment. J Bone Joint Surg Br 1972;54:96–102. 26. Richter M, Bosch U, Wipperman B, et al: Comparison of surgical repair or reconstruction of the cruciate ligaments versus nonsurgical treatment in patients with traumatic knee dislocations. Am J Sports Med 2002; 30:718–727. 27. Almekinders LC, Dedmond BT: Outcomes of the operatively treated knee dislocation. Clin Sports Med 2000;19:503–518.

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28. Fanelli GC, Edson CJ: Arthroscopically assisted combined anterior and posterior cruciate ligament reconstruction in the multiple ligament injured knee: 2 to 10 year follow-up. Arthroscopy 2002;18:703– 714. 29. Kantaras AT, Johnson DL: The medial meniscal root as a landmark for tibial tunnel position in posterior cruciate ligament reconstruction. Arthroscopy 2002;18:99–101. 30. Indelicato PA: Isolated medial collateral ligament injures in the knee. J Am Acad Orthop Surg 1995;3:9–14. 31. Hillard-Sembell D, Danile DM, Stone ML, et al: Combined injuries of the anterior cruciate and medial collateral ligaments of the knee. Effect of treatment on stability and function of the knee. J Bone Joint Surg Am 1996;78:169–176. 32. Noyes FR, Barber-Westin SD: The treatment of acute combined ruptures of the anterior cruciate and medial ligaments of the knee. Am J Sports Med 1995;23:380–391. 33. Klimkiewicz JJ, Petrie RS, Harner CD: Surgical treatment of combined injury to anterior cruciate ligament, posterior cruciate ligament, and medial structures. Clin Sports Med 2000;19:479–492. 34. Robins AJ, Newman AP, Burks RT: Postoperative return of motion in anterior cruciate ligament and medial collateral ligament injuries: The effect of medial collateral ligament location. Am J Sports Med 1993;21:20–25. 35. Wilson TC, Satterfield WH, Johnson DL: Medial collateral ligament “tibial” injuries: Indications for acute repair. Orthopedics 2004; 27:89–93. 36. Covey DC: Injuries of the posterolateral corner of the knee. J Bone Joint Surg Am 2001;83:106–118. 37. Veltri DM, Warren RF: Anatomy, biomechanics and physical findings in posterolateral knee instability. Clin Sports Med 1994;13:599–614. 38. Noyes FR, Barber-Westin SD: Treatment of complex injuries involving the posterior cruciate and posterolateral ligaments of the knee. Am J Knee Surg 1996;9:200–214. 39. Veltri DM, Warren RF: Operative treatment of posterolateral instability of the knee. Clin Sports Med 1994;13:615–627. 40. Clancy WG, Sutherland TB: Combined posterior cruciate ligament injuries. Clin Sports Med 1994;13:629–647. 41. Irrgang JJ, Fitzgerald GK: Rehabilitation of the multiple-ligamentinjured knee. Clin Sports Med 2000;19:545–571. 42. Edson C: Postoperative rehabilitation of the multiple-ligament reconstructed knee. Oper Tech Sports Med 2003;11:294–301. 43. Walker DN, Hardison R, Schenck RC: A baker’s dozen of knee dislocations. Am J Knee Surg 1994;7:117–124. 44. Wascher DC, Becker JR, Dexter JG, et al: Reconstruction of the anterior and posterior cruciate ligaments after knee dislocation: Results using fresh-frozen nonirradiated allografts. Am J Knee Surg 1994;27: 189–196. 45. Montgomery IJ, Savoie FH, White JL, et al: Orthopedic management of knee dislocations: Comparison of surgical reconstruction and immobilization. Am J Knee Surg 1995;8:97–103. 46. Yeh WL, Tu YK, Su JY, et al: Knee dislocation: Treatment of high velocity knee dislocations. J Trauma 1999;46:693–701. 47. Shapiro MS, Freedman EL: Allograft reconstruction of the anterior and posterior cruciate ligaments after traumatic knee dislocation. Am J Knee Surg 1995;23:580–587. 48. Fanelli GC, Gianotti BF, Edson CJ: Arthroscopically assisted combined anterior and posterior cruciate ligament reconstruction. Arthroscopy 1996;12:5–14.

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57

Patellofemoral Instability Kevin Charron and Anthony Schepsis

In This Chapter Nonoperative management Surgery Lateral retinacular release Arthroscopic proximal realignment Medial patellofemoral ligament (MPFL) reconstruction Medial tibial tubercle transfer Anteromedialization

INTRODUCTION • Patellofemoral instability encompasses a continuum of abnormal patellofemoral joint mechanics, ranging from subluxation to dislocation, the cause of which can be either traumatic or atraumatic. • Patellofemoral instability is defined as abnormal, clinically symptomatic, lateral, or, in rare cases, medial translation of the patella out of the trochlear groove. In cases of recurrent subluxation, there is lateral translation of the patella early in the flexion range. • Patients may experience a sense of giving way, slipping, or abnormal motion of the patella, unless the patient has permanent lateral tracking of the patella, which is most often secondary to malalignment. • Recurrent subluxation encompasses a spectrum from minor subtle translation of the patella that is not associated with a clinically evident relocation to episodes of major recurrent subluxation when the patella nearly dislocates in the early stages of flexion and then reduces with a clinically apparent snap or shift. • Permanent lateral subluxation is often defined under the category of malalignment and is characterized by a persistent laterally displaced patella through the range of motion (ROM) of the knee, with little or no tendency to recenter in the trochlea. It is often associated with patellar tilt. • The usual mechanism of traumatic patellar dislocation is external rotation of the tibia with concomitant contracture of the quadriceps. • Relevant anatomy, history, physical examination, and imaging modalities that would aid in diagnosis are discussed. • Conservative therapy for the treatment of the various instabilities is briefly discussed.

• Finally, the role of proximal and distal realignment for treatment of patients with patellofemoral malalignment and/or instability is explored. The decision-making process in assessing malalignment/instability of the patellofemoral articulation, the criteria for tibial tubercle transfer in both the medial and anteromedial direction versus proximal realignment, and details of the surgical techniques are addressed.

RELEVANT ANATOMY The anatomy of the entire lower extremity is paramount in the discussion of patellofemoral instability. Starting proximally at the hip, femoral version (anterior or posterior) can affect patellofemoral mechanics. With femoral anteversion, the distal femoral trochlea is internally rotated with a neutral hip alignment. Conversely, with femoral retroversion, the distal femoral trochlea is externally rotated with a neutral hip alignment. Normal femoral anteversion is approximately 14 degrees. Excessive hip anteversion causes the patella to displace laterally. Varying degrees of femoral torsion may also be present, which affects the position of the trochlea. Excessive femoral anteversion with or without internal femoral torsion is usually accompanied by tibial external rotation, which has the effect of further displacing the patella laterally. Dysplasia of the medial or lateral femoral condyle also affects patellofemoral mechanics. If the lateral condyle is hypoplastic, the bony constraint to lateral subluxation is not present in flexion at 20 degrees and beyond. The patella is a sesamoid bone contained within the extensor mechanism. It is made up of a medial and lateral facet separated by a median ridge. Usually the lateral facet is longer and more sloped to match the corresponding condyle. The rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius all send fibers to the extensor mechanism at the proximal aspect of the patella and respective retinaculum. All muscles originate from the proximal femur except for the rectus femoris, which originates on the anterior inferior iliac spine (reflected head) and superior acetabulum (direct head). The orientation of the quadriceps muscle fibers is important in patellofemoral mechanics because they create varying vectors of force on the patella during contraction. The vastus medialis obliquus originates on the medial intermuscular septum and the adductor tubercle and inserts on the medial proximal third of the patella. The vastus medialis obliquus is the most obliquely oriented muscle and therefore provides a medially directed force vector to the patella during extension, which decreases lateral subluxation. All the quadriceps muscles are innervated by the femoral nerve.

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At the distal aspect of the patella is the patellar tendon, which inserts on the tibial tubercle. The tendon is separated from the anterior tibia by the deep infrapatellar bursa. Further posterior to this is the infrapatellar fat pad. Other static restraints to the patella are the medial and lateral patellofemoral ligament and the medial and lateral patellotibial ligament. The MPFL has an almost 90-degree orientation to the patella and therefore is one of the main static restraints to lateral subluxation. The MPFL has been found to be the primary restraint to lateral patellar translation at 20 degrees of flexion, contributing 60% of the total restraining force.1

CLINICAL FEATURES AND EVALUATION History The events surrounding the onset of the knee instability often point to a diagnosis. If the patient’s instability is a result of trauma, most often a ruptured MPFL with or without underlying malalignment may be suspected. In the acute setting, the patient may present with a large hemarthrosis and tenderness over the medial femoral epicondyle and medial border of the patella, in addition to pain or apprehension with lateral translation of the patella. If the patient’s instability is indolent in nature and has occurred over years, most likely the patient has some component of malalignment. In the chronic setting, the patient may give a history of the knee “giving way” with increasing activity. These patients also may complain of an intermittent effusion and pain over the lateral retinaculum and lateral patellar facet. By history, it is important to determine whether the patient has symptomatic instability, either subluxation or dislocation, or purely patellofemoral pain secondary to chondrosis or arthrosis associated with malalignment.

Physical Examination After an appropriate history is taken, the patient is examined standing. Overall varus or valgus alignment of the lower extremity, which can affect patellofemoral mechanics, can be evaluated. A valgus knee tends to increase the quadriceps angle (Q angle) and loading of the lateral facet of the patella. The position of the patella can also be assessed. If the patellae are facing each other when the feet are parallel there may be some degree of femoral anteversion or femoral internal torsion. This is usually accompanied by some degree of tibial external rotation, which can be assessed by palpating the tibial tubercle. The position of the plantigrade foot also can give some insight to overall alignment. With excessive external rotation of the tibia, there is usually a compensatory foot pronation with heel valgus. Leg length discrepancy may also be evaluated at this time by noting any pelvic obliquity. Finally, the patient’s gait may be evaluated for any asymmetry. With proper mechanics, the hip and ankle center should line up so that the overall mechanical axis passes through the center of the knee. Any noticeable pelvic obliquity could be attributed to abductor deficiency. Last, a loaded flexion squat can be performed. Pain and crepitus referable to the patellofemoral articulation is often accentuated by this maneuver. The sitting examination is then performed with the legs flexed 90 degrees over the examination table. Again, the orientation of the patella can be observed. Laterally facing patellae can indicate extensor mechanism malalignment. The tuberosulcus angle can also be measured while the knee is flexed to 90 degrees (Fig. 57-1). It represents the angle between a perpendicular to the transepicondylar axis and a line drawn from the

590

Figure 57-1 The tuberosulcus angle.

midpoint of the patella to the tuberosity. Normally this measures 0 degrees, and greater than 10 degrees is considered abnormal.2 Tibial torsion can also be evaluated by palpating the tibial tubercle. In normal alignment, the tibial tubercle should lie lateral to the midline of the femur, although this is highly variable in the population. Vastus medialis obliquus atrophy can also be appreciated at this point. With flexion and extension of the knee, crepitus can be palpated and patellar tracking observed. The flexion arc in which the patient has pain is sometimes a tipoff as to the location of the patient’s disease. Early range flexion pain and crepitus indicate a more distal lesion, a painful arc and crepitus between 30 and 70 degrees indicate a mid-patellar lesion, and a painful crepitus in greater degrees of flexion indicates a more proximal lesion on the patella. The soft tissues are responsible for stability of the patellofemoral articulation in the first 30 degrees of flexion, whereas the bony anatomy becomes more critical beyond 30 degrees of flexion. At approximately 20 degrees of flexion, the patella should seat fully in the femoral trochlea. A pathologic J sign can be observed as the patella seated in the trochlea subluxates laterally with terminal extension. ROM and muscle strength of the knee and ankle should be documented. From the sitting position, the patient is then placed supine. With the extensor mechanism relaxed, any effusion can be noted and the entire knee should be palpated to include the medial and lateral facets, retinaculum, common extensor tendon, tibial tubercle, and patella tendon. Next the patella should be compressed against the trochlea and moved medially and laterally. Pain during this maneuver implicates the patellofemoral articulation. Lateral glide of more than 50% of the width of the patella is considered abnormal unless there is symmetrical patellar hypermobility associated with generalized ligamentous laxity. A patellar apprehension sign may be encountered when the patient has a sense of dislocation or subluxation with a laterally directed force. Several measurements can now be taken. Leg length can be measured by taking the distance from the anterior superior iliac spine to the tip of the medial malleolus. The Q angle can also be measured (Fig. 57-2). This is measured from the anterior superior iliac spine to the center of the patella to the tibial tubercle. Normal values are up to 15 degrees in the male and up to 18 degrees in the female. The larger Q angles in females are due to the wider pelvis and increase in genu valgum as com-

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Figure 57-2 Measuring the quadriceps (Q) angle. A line is drawn from the anterior superior iliac spine to the center of the patella to the center of the tibial tubercle. The angle between the two is the Q angle.

pared to males. The author believes that the most accurate Qangle measurement is made at 30 degrees of flexion because the patella should be well centered in the trochlear groove by 20 to 25 degrees of flexion. If the Q angle is measured in extension, an inaccurate low value may be obtained since the patella lies laterally in terminal extension from lack of bony constraint. Excessive femoral anteversion, internal femoral torsion, genu valgum, and external tibial torsion all increase the Q angle. A thorough examination would not be complete without a ligamentous examination. Last hamstring tightness should be evaluated by measuring the popliteal angle. The angle can be measured by flexing the hip to 90 degrees, extending the knee to the maximum, and then measuring the angle between the femur and tibia. Values greater than 25 degrees indicate hamstring tightness. From the supine position, the patient should then be placed prone. In this position, hip ROM can be assessed by internally and externally rotating the flexed knees. With the knees flexed in this position, femoral and tibial lengths can be assessed. Finally, quadriceps tightness can be assessed by flexing the knees. With the pelvis level, the heel should come toward the buttocks in a symmetrical level and increased tightness in the anterior thigh, as compared to the contralateral side, could be an indication of quadriceps tightness.

ures the ratio of the length of the patellar tendon to the largest diagonal measurement of the patella on the lateral projection. Normal ratios are 0.8 to 1.2. Ratios less than 0.8 indicate patella baja and ratios greater then 1.2 indicate patella alta. Another similar method is that of Blackburn and Peel,4 who measure the distance from the tibial plateau to the inferior articular surface of the patella as compared to the length of the patella articular surface. A ratio from between 0.54 to 1.06 is normal. Values greater than 1.06 indicate patella alta. This measurement has been found to be more accurate in the evaluation of patella alta and baja. The lateral view can also give an indication to the amount of patellofemoral arthritis by the amount of joint space that is present. The last view obtained is the axial view (Fig. 57-3). Traditional sunrise views are taken with the knee in various degrees of flexion depending on institutional guidelines. Typically they are taken at greater degrees of flexion (i.e., greater than 45 degrees). At these degrees of flexion, almost all patellae are well seated in the trochlea and mild patellofemoral malalignment may be missed. Two standardized views are typically used. The Merchant view5 is taken with the knee flexed to 45 degrees. The x-ray source is placed proximal to the knee with the plate distal to the knee. The congruence angle, described by Merchant, can be measured from this radiograph. On the axial view, the angle between the medial and lateral condyle is bisected. Then a line is drawn from the femoral trochlea to the lowest point on the median ridge of the patella. The angle between these two lines represents the congruence angle. If the line falls medial to the bisector, it is a negative value and if it falls to the lateral side, it is a positive value. Merchant found the average congruence angle in 100 normal subjects was -6 degrees with a standard deviation of 11 degrees. In a normal knee, the median ridge of the patella lies on the medial condyle. The Laurin view6 is another axial view, taken at 20 to 30 degrees of knee flexion. The x-ray tube is placed between the ankles and the x-ray plate is held proximal to the knees. On this view, the lateral patellofemoral angle can be measured. This angle is measured from a line drawn across the most anterior portions of the medial and lateral femoral condyles in the axial view to a line that follows the slope of the lateral patella facet. Normally this angle should increase laterally. In patients with patellar tilt or lateral patellar subluxation, the angle is parallel or increased medially.

Imaging Modalities Evaluation of patellofemoral pain starts with a standard bilateral standing anteroposterior view of the knees. This probably has the least amount of information as it pertains to patellofemoral disease but may give insight into degenerative joint disease and accessory ossification centers of the patella as possible sources of pain. A modification of this radiograph is a flexed knee anteroposterior view called the tunnel view. This gives insight into disease of the femoral condyles and can diagnose an osteochondral defect. With the lateral view of the knee, patella alta (high) or patella baja (low) can be evaluated. The Insall Salvati technique3 meas-

Figure 57-3 Axial view demonstrating marked tilt, subluxation, and arthrosis of the lateral facet.

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Standing mechanical axis view can be taken to assess lower extremity limb alignment. Normally the mechanical axis, a line from the femoral head to the middle of the tibial plafond, should fall just medial to the center of the knee joint. The Q angle, as described before, can also be measured on the radiograph. Varus or valgus angulation at the knees can be measured and an appreciation of femoral anteversion/torsion and tibial torsion can be visualized. A computed tomography (CT) of the knee at various angles of flexion can give insight to the patellofemoral dynamics (Fig. 57-4). Axial images through the midpoint of the patella are taken at 10-degree increments from 0 to 60 degrees of flexion. Congruence angle and lateral patellofemoral angle can be measured from these images at varying degrees of flexion. Another use of CT is the measurement of the anterior tibial tubercle to trochlear groove distance (Fig. 57-5).7 Axial images are taken from the proximal trochlea through the tibial tubercle on the same sequence, with the extremity fixed in extension. It is thought that more than a 2-cm distance is highly abnormal, representing excessive lateralization of the tibial tubercle with a high valgus vector on the knee. Although one study suggests that the normal range is 2 to 9 mm and greater than 10 mm is abnormal,7,8 the exact cutoff between “normal” and “abnormal” would be very difficult to ascertain because of the very wide range of anatomic variations. A final use of CT is in the evaluation of the rotational alignment of the lower extremity. Femoral anteversion/torsion can be evaluated by measuring the angle between the line bisecting the femoral neck and a line drawn across the posterior condyles of the femur on subsequent cuts. In the same way, tibial torsion can be evaluated by measuring the angle between the line across the posterior tibial plateau superimposed on the transmalleolar axis. If excessive femoral anteversion results in patellofemoral malalignment, a femoral derotational osteotomy may be in order. Magnetic resonance imaging can also be helpful in diagnosis. Although CT is better for visualization of bone detail, magnetic

A

B Figure 57-5 The anterior tibial tubercle to trochlear groove distance. A computed tomography measurement of the distance between the center of the trochlear groove and the attachment of the patella tendon to the anterior tibial tubercle. Axial images are taken from the proximal trochlea through the tibial tubercle on the same sequence with the extremity fixed in extension. A, A line is drawn along the posterior femoral condyles on the cut through the deepest portion of the trochlear groove. A perpendicular (x) is drawn from the center of the groove to this line and measured. The distance (a) is measured from this intersection to a fixed point; in this case, the edge of the frame. B, The same parallel line is transposed with a parallel rule to the cut through the midportion of the tendon attachment on the tubercle at the same perpendicular distance (x). The distance (b) is measured to the same fixed point. The anterior tibial tubercle to trochlear groove distance is a - b. In this instance, it was 5 mm, well within normal range.

Figure 57-4 Patellofemoral computed tomography tracking study.

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resonance imaging is more sensitive for osteochondral, ligament, and meniscal injuries that may be caused by a traumatic patellar dislocation. These findings include disruption of the MPFL and osteochondral bone bruises or fractures involving the inferomedial patella and lateral femoral condyle.9–11 Last, in some cases, a bone scan may be useful. With patellar instability, the biomechanical and metabolic processes that maintain homeostasis of the cartilage and soft-tissue structures

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are affected. The loss of this homeostasis is typically undetectable with radiographs or magnetic resonance imaging. The bone scan, on the other hand, can demonstrate a persistently abnormal technetium scintigram of the involved area prior to the development and progression of irreversible degenerative changes that would be evident on radiograph or magnetic resonance imaging.12 In the arena of patellar instability, an area of uptake on the lateral patella facet could mean abnormal articular loading in the face of other normal imaging modalities.

TREATMENT OPTIONS Conservative Treatment Nonsurgical treatment of patellofemoral instability is the cornerstone of treatment. Henry13 reported an approximately 80% success rate in the literature for the conservative treatment of patellofemoral instability. The mainstay of treatment involves the selective strengthening of the vastus medialis obliquus with de-emphasis on strengthening the vastus lateralis. This focus has changed from general quadriceps strengthening that was previously prescribed for patellofemoral pain. McConnell14 has developed a treatment plan for patellofemoral pain that has a reported success rate of 96%. Her method consists of muscle re-education focusing on the vastus medialis obliquus and taping of the patella to modify tilt or subluxation. The use of a patellastabilizing brace is another treatment modality that may have some benefit. Closed-chain exercises, stationary bike, elliptical runner, and other core strengthening exercises help strengthen and stabilize the knee joint without excessive loading of the joint. Prone quadriceps stretching, iliotibial band stretching, and lateral retinacular stretching are paramount. Lower extremity strengthening, patellar stabilization, lower extremity flexibility, and proprioception are important treatment modalities. Correction of excessive foot pronation or supination with orthotics can have a positive effect on alignment in that this limits compensatory external and internal rotation of the tibia, respectively. Nonsteroidal anti-inflammatory drugs may be used as an adjunct to treatment, and a level of activity modification to limit loading of the patellofemoral joint can be beneficial. In the realm of patella dislocations, there are numerous retrospective studies in the literature that detail the success of nonoperative and operative treatment of first-time patella dislocators. Consensus between the studies is problematic due to the varying sample sizes, differing follow-up, varied surgical techniques, and heterogeneity between populations. One prospective, randomized study demonstrated equivalent results between operative and nonoperative treatment for first-time patella dislocation.15 Conservative treatment, which includes immobilization of the knee in extension for 2 to 3 weeks, followed by strength and ROM exercises, has therefore become the author’s treatment of first-time dislocators. The author’s only indications for acute surgical intervention for first-time dislocators include unstable osteochondral fractures and asymmetrical unreduced lateral subluxation of the patella.

Surgical Management When conservative treatment fails to provide satisfactory results, surgery may be indicated. Surgical techniques can be grouped into proximal and distal realignment procedures. Proximal alignment procedures include a lateral release (open or arthroscopic), lateral release and medial plication (open or arthroscopic), and MPFL reconstruction. Distal realignment procedures include the medialization of the tibial tubercle and

anteromedialization of the tibial tubercle. The Maquet technique, anteriorization of the tibial tubercle, has been used mainly to unload the patellofemoral joint in patients with patellofemoral arthritis without malalignment. The Hauser technique is a tibial tubercle osteotomy and moves the tibial tubercle medial, distal, and posterior due to the triangular cross-section of the proximal tibia. This technique has been abandoned because it increases the patellofemoral joint reactive forces, resulting in the subsequent development of patellofemoral arthritis. In this chapter, lateral retinacular release, arthroscopic proximal realignment, MPFL reconstruction, medial tibial tubercle transfer, and anteromedialization of the tibial tubercle are discussed in detail. Lateral Retinacular Release Abnormal patellar tilt increases loading of the lateral patella facet, causes contracture of the lateral retinaculum, and increases the incidence of patellofemoral arthritis on the lateral side. Current indications for lateral release consist of (1) patellofemoral pain with lateral tilt, (2) lateral retinacular pain with lateral tilt or lateral patella position, and (3) tight lateral retinaculum/excessive lateral pressure syndrome.16 This operation is done for pain and is not indicated as a stand-alone procedure for instability. If lateral release is done for instability, the results deteriorate with time. Lateral release is contraindicated with a hypermobile patella. In addition, the authors do not perform lateral release as an isolated procedure for the treatment of recurrent lateral patellar dislocation. Lateral retinacular release can be performed either arthroscopically or open. During knee arthroscopy, the patellar tracking is best observed through a superomedial or superolateral portal. Selective femoral nerve stimulation can be used under general anesthesia to allow active quadriceps contraction and thus evaluate dynamic tracking. If at this point, lateral retinacular release is appropriate, the lateral retinaculum should be divided within 1 cm of the patella starting approximately 2 cm proximal to the proximal pole and extending 2 cm distal to the distal pole. Electrocautery can be used and care must be taken to cauterize the lateral superior geniculate vessels. The tendon fibers of the vastus lateralis should be avoided as this could cause relative weakness of the lateral compartment and a medial patella subluxation. The most common complication of a lateral release is hemarthrosis from laceration of the superolateral geniculate vessels. An open technique can also be employed, which entails an approximately 3-cm longitudinal incision, about 1 cm lateral to the patella. Skin and subcutaneous tissue are divided with a scalpel down to the retinaculum. A Z-plasty is then performed on the transverse fibers of the retinaculum. Once adequate correction is obtained, sutures can be used to prevent further lengthening of the lateral retinaculum. As in the arthroscopic procedure, care is taken to identify and coagulate the superolateral geniculate vessels. Arthroscopic Proximal Realignment Medial reefing is often indicated with a lateral release in proximal realignment. This can be done open, arthroscopically assisted (mini-open), or done all arthroscopically. The author’s ideal indications for proximal realignment include traumatic onset, recurrent episodes associated with an abnormal lateral patellar glide indicating insufficiency of the MPFL and medial soft-tissue restraints, no significant arthrosis of the medial facet, and normal alignment and quadriceps angle. The author uses this arthroscopic technique only in cases of mild instability and uses

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a formal MPFL reconstruction for cases of moderate to severe instability. Using a thigh holder and standard arthroscopy portals, an epidural needle is introduced through the medial retinaculum next to the proximal medial border of the patella. A no. 1 polydiaxone monofilament suture is introduced through the spinal needle into the joint and withdrawn through an accessory portal with a grasper. The spinal needle is then withdrawn from the retinaculum only, into the subcutaneous tissue, and then reinserted into the joint after moving it posterior to the first needle tract. This loop of suture is then withdrawn through the accessory portal and the process is repeated. This procedure can be repeated until the amount of medial imbrication is deemed adequate. An arthroscopic lateral release, if necessary, can then be performed as described previously. The sutures in the medial capsule can then be tied using standard arthroscopic knot-tying techniques. Postoperative Rehabilitation Postoperatively the patient is placed in a hinged knee brace in extension for 1 week followed by ROM exercises with physical therapy. ROM is gradually increased to a maximum of 90 degrees over a 4-week period. Bracing is continued until quadriceps strength returns. The patient is weight bearing as tolerated postoperatively. Results The all-inside technique of proximal realignment has been successful. In Halbrecht’s review17 of 5-year results, 93% of patients who underwent the procedure reported significant improvement. The average Lysholm score improved from 41.5 to 79.3 (P < 0.05). There were no complications or redislocations. Patients in the study reported significant improvement in pain, swelling, stair climbing, crepitus, and ability to return to sports (P < 0.05). Medial Patellofemoral Ligament Reconstruction The author prefers to use formal MPFL in cases of moderate to severe instability. His other indications include traumatic onset, recurrent episodes associated with an abnormal lateral patellar glide (indicating insufficiency of the MPFL and medial softtissue restraints), no significant arthrosis of the medial facet, and normal alignment and quadriceps angle. Technique First, make an incision the length of the patella, located over the junction of the medial and middle thirds of the patella (in line with the medial border of the expansion of the patellar tendon at the distal patellar pole). If a tibial tubercle realignment procedure is indicated, this should be performed first before MPFL reconstruction. The goal of MPFL surgery is to provide a checkrein to lateral displacement of the patella; this surgery is not performed to pull the patella into the trochlea. Perform a subperiosteal dissection, extending medially deep to layers 1 and 2, exposing layer 3 (the capsular layer) at the medial border of the patella. Deeper dissection, between layers 2 and 3, is preferable to dissection superficial to layer 2 because it allows incorporation with advancement of the MPFL (layer 2) superficial to the graft during wound closure. Using a curved clamp to develop the selected tissue interval, bluntly dissect medial retinacular layers between the patella and medial femoral epicondyle. A single-strand semitendinous allograft or autograft approximately 5 to 7 mm in diameter is prepared for the MPFL substitute. If the graft is small in diameter, it may be doubled to achieve the 5- to 7-mm diameter. A running baseball stitch with

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no. 2 FiberWire is placed for approximately 15 mm from one end of the graft to help in seating the graft in the femoral tunnel. If the graft is doubled, it should be run from the two free ends. The origin of the MPFL is now identified on the distal femur. The adductor tubercle and medial epicondyle should be identified. The saddle between these two structures is the femoral origin of the MPFL. A 2.4-mm drill pin is then placed in the center of the saddle. A suture is then wrapped around the drill pin and then attached to the insertion of the MPFL on the patella. The insertion of the MPFL lies on the medial proximal one half of the patella. The knee is placed in 30 degrees of flexion, and the suture is tensioned slightly. The knee is taken through a ROM to evaluate the length change of the suture. Maximum tension should be seen between 0 degrees and 30 degrees, with progressive laxity between 30 degrees and full flexican. The femoral origin point is adjusted to minimize length change of the suture with knee flexion. If lengthening occurs in flexion, replace the pin more distally toward the medial femoral epicondyle. If lengthening occurs in extension, move the pin more proximally toward the adductor tubercle. Slight lengthening will not affect the overall results. Adjustment of the femoral origin of the MPFL is complete when the isometric point is established. Now with the MPFL femoral origin identified, the femoral tunnel can be made with the appropriately sized reamer over the guide pin to a depth of 20 mm. The graft is then fixed in the femoral pilot hole with the appropriately sized Bio-Tenodesis screw. The sutures previously placed in the end of the graft can be brought in through the cannulated Bio-Tenodesis screwdriver to facilitate seating of the graft. The screw should be placed on the medial aspect of the femoral tunnel with the graft exiting laterally. The Bio-Tenodesis screw should be advanced until it is flush with cortical bone. Security of the graft then can be evaluated. Next, a 2.4-mm Beath pin is placed at the insertion of the MPFL on the medial patella, as previously identified. The pin is advanced transversely across the patella until it exits laterally. Isometry should be again tested by provisionally fixating the free end of the graft to the patella. The tendon should be marked at the cortical edge of the patella and cut an additional 15 mm distal to this point. After confirming correct placement of the insertion of the graft, an appropriately sized reamer is placed over the pin and a patella tunnel of 20 mm in depth is made. Usually a 6-mm reamer is used with a 5.5-mm Bio-Tenodesis screw. A no. 2 fiber wire (FiberWire; Artherex, Naples, FL) then is run as a baseball stitch at the distal aspect of the graft for approximately 15 mm. The free ends of the suture are then placed through the eyelet of the Beath pin and pulled into the patellar tunnel to the previously marked depth and fixated with another Bio-Tenodesis screw. The Bio-Tenodesis screw is advanced over the superior portion of the graft until flush with the patellar cortex. A medial imbrication can now be performed if there is redundant medial tissue. The wound is then closed in the standard fashion. Alternatively, a suture anchor technique can be used for patellar fixation. A cancellous bone trough is created in the medial edge of the patella, anterior to the articular surface, from the midwaist superiorly. Two Bio-Suture Taks (Arthrex, Naples, FL) are placed in this trough and the free end of the graft is fixed with suture. Postoperative Rehabilitation Postoperatively the patient is placed in a hinged knee brace in extension for 1 week followed

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Box 57-1 Principal Indications for Medial Tibial Tubercle Transfer 1. Patients with lateral patellar instability and/or patellar malalignment with moderate to severe static malalignment, with radiographic or computed tomography evidence of tilt and/or subluxation 2. Tibial tubercle malalignment with normal or only mild insufficiency of the medial patellofemoral ligament 3. Lateral patellar instability with patella alta 4. A patella with a J-tracking pattern 5. When there is concern about tethering the medial facet by proximal realignment in the presence of advanced medial arthrosis

by ROM exercises with physical therapy. ROM is gradually increased to a maximum of 90 degrees over a 4-week period. Bracing is continued until quadriceps strength returns. The patient is weight bearing as tolerated postoperatively. Return to sports is allowed at 6 months postoperatively if there is full motion, no pain or swelling, and strength at least 80% of the unoperated side. Results Various techniques of anatomic reconstruction of the MPFL have been described and have met with success. At 2year follow-up, Drez et al18 found that 93% of their patients had good to excellent results after MPFL reconstruction. In another study by Gomes et al,19 94% of patients had good to excellent results at over 5 years of follow-up after MPFL reconstruction. Medial Tibial Tubercle Transfer The author’s principal indications for medial tibial tubercle transfer are given in Box 57-1. If significant patella alta is present, tightening the proximal medial restraints will not correct the problem and will create abnormal forces. In these cases, the patellar centers into the groove in higher degrees of flexion. Some of the best results of distal realignment or medial tubercle transfers occur in patients with patella alta and lateral patellar instability. Likewise, J tracking, where the patella “jumps” out laterally in terminal extension, is an indicator of a “valgus vector” from bony malalignment, which starts at the hip from internal femoral torsion. The more practical solution would be to make the correction at the tibial tubercle, although on a theoretical basis, a femoral derotation osteotomy would correct the problem at its source. The advantages of distal realignment are listed in Box 57-2. Numerous studies have looked at the effects of medialization

and anteromedialization on patellofemoral mechanics. The effect of anterior displacement of the tuberosity on patellofemoral contact forces is discussed in a later section. However, there are numerous publications in the literature that show that medial tubercle transfer corrects tilt as well as subluxation and transfers force at the patellofemoral joint from a lateral to a medial direction. In a recent study by Ramappa et al20 it was shown that increasing the Q angle increases patellofemoral contact pressures and transfers forces to the lateral facet of the patella. An increased Q angle also tilts and subluxates the patella laterally. It was further established that medialization corrects the maltracking and partially corrects the increased contact pressures in the patellofemoral articulation. Medial tubercle transfer, however, is contraindicated in patients with a normal Q angle or no clinical or radiographic evidence of tubercle malalignment. In a cadaver study by Kuroda et al,21 medialization in the presence of a normal Q angle increased patellofemoral contact pressures, along with increasing the contact pressures in the medial tibiofemoral compartment. These authors also concluded that overmedialization should be avoided in the varus knee, the knee with medial compartment arthrosis, and the knee with previous total or subtotal medial meniscectomy. Distal realignment is sometimes indicated in combination with proximal realignment when there is both traumatic insufficiency of the MPFL as well as tubercle malalignment. In these cases, both abnormalities need to be corrected. There are a number of disadvantages of distal realignment that should be recognized before performing this procedure. They are listed in Box 57-3. Technique Medial tubercle transfer was first described by Trillat et al22 in 1964. It was then popularized by Cox as the Elmslie-Trillat procedure. Arthroscopy is first performed to address any associated lesions, chondroplasty is performed if necessary, and patellar tracking assessed. At this time, a decision must be made as to whether to perform anteromedialization rather than straight medialization. In general, even in the presence of significant chondral changes at the time of arthroscopy, if the patient is not symptomatic from the chondrosis or arthrosis, straight medialization to correct patellar instability and/or malalignment would be indicated. If the patient has symptomatic arthrosis or chondrosis, the location and severity of the lesion should be noted before deciding which direction to move the tibial tubercle. Furthermore, in some patients with very severe grade IV disease in both the patella and trochlea in diffusely, no further surgery may

Box 57-2 Advantages of Distal Realignment 1. It addresses one of the more common predisposing factors, namely, tubercle malalignment. 2. It allows an aggressive rehabilitation program. 3. These patients are less likely to have range-of-motion problems in comparison with open proximal reconstructions or imbrications. 4. Although pressure transfers go from lateral to medial on the patella when transposing the tubercle medially, one is less likely to tether the medial facet of the patella with an overconstrained proximal realignment. 5. There is less violation of the extensor mechanism. 6. It is well established that medial tuberosity transfer corrects lateral subluxation (congruence angle) as well as lateral patellar tilt (lateral patellofemoral angle).

Box 57-3 Disadvantages of Distal Realignment 1. 2. 3. 4.

It does not address an incompetent medial patellofemoral ligament. It cannot be performed properly before skeletal maturity. There is internal fixation that often requires later removal. There is a potential for posterior neurovascular complications when using anterior to posterior–directed bicortical screws in the proximal tibia. 5. There is the potential for osseous delayed union or nonunion. 6. As mentioned previously, increased loading of the medial tibiofemoral compartment occurs, contraindicating its use in the varus knee or knee with medial compartment arthrosis.

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Figure 57-6 Lateral incision for tibial tubercle medialization (ElmslieTrillat). The tibial tubercle (circle) and Q angle are marked.

Figure 57-7 Exposing the patellar tendon. Both sides of the tendon must be freed up to prevent tethering when the tubercle is shifted.

be indicated at this time and the patient may be a better candidate for other procedures. The decision as to whether to perform a lateral retinacular release, either arthroscopic or open, should be made next. Lateral retinacular release is performed in those cases where there is excessive tightness of the lateral retinaculum secondary to a passive patellar tilt, in patients with symptomatic arthrosis or chondrosis in the lateral compartment of the patellofemoral joint, and radiographic or CT imaging evidence of a decreased lateral patellofemoral angle. Lateral release alone, in these cases, is only indicated for excessive lateral pressure syndrome, with lateral facet pain, a tight lateral retinaculum, minimal or only grade 1 to 2 lateral facet changes, and no subluxation or clinical instability symptoms. The medial tubercle transfer is performed through a small 3to 4-cm longitudinal incision just lateral to the tibial tubercle (Fig. 57-6). A 1 to 1.5 cm thick, 5 to 6 cm long osteoperiosteal shingle with hand osteotomes is created. The patellar tendon is mobilized so that the undersurface of its attachment can be well visualized with retraction (Fig. 57-7). The first cut is performed from lateral to medial with a 1- to 1.5-inch wide hand osteotome 1 cm thick at the level of the tibial tubercle (Fig. 57-8). Care should be made to make this osteotomy directly in the coronal plane. However, if one is to err, err on the side of going from posterior to anterior when going from the lateral to the medial direction so that when the tubercle is transferred, it will move slightly anteriorly and never posteriorly, which would increase patellofemoral contact pressures. A mark is made on the skin distally, 5 to 6 cm distal to the tubercle, and a curved osteotome is used to aim for this point to angle quickly toward the anterior cortex. A small osteotome is used to complete the osteotomy transversely just on the proximal side of the tibial tubercle to prevent propagation into the tibial plateau. Osteoclasis is performed, leaving the distal soft tissues intact, and the tibial tubercle is gently rotated medially (Fig. 57-9). The parameters used by the author are that the patella is fully engaged and congruent by 20 degrees of flexion and that the Q angle is corrected to below 10 degrees as measured intraoperatively. Temporary fixation is achieved with a 3.2-mm drill bit to, but not through, the posterior cortex, at which time a final assessment

of tracking is made (Fig. 57-10). In general, the transfer ranges from a 1- to 1.5-cm shift. If the surgeon is satisfied with the degree of tubercle transfer and the tracking is satisfactory, fixation is performed with a fully threaded 4.5-mm bicortical screw with metal washer (Fig. 57-11). Since this osteotomy is a short, thin osteoperiosteal shingle, the author routinely uses only one bicortical screw, allowing rigid fixation and an aggressive postoperative rehabilitation program. However, if the osteotomy is on the larger side, one can consider fixation with two screws. Care must be taken when drilling through the posterior cortex of the tibia in this area. Drilling should be performed with the knee in at least 90 degrees of flexion and taking care not to plunge through the posterior cortex (Fig. 57-12). In

Figure 57-8 For medialization, a 1 to 1.5 cm thick, 5 to 6 cm long shingle is adequate. It is left attached by periosteum distally at the anterior cortex. The osteotomy is performed with hand osteotomes laterally to medially. The osteotomy must be made directly in the coronal plane for true medialization. Care must be taken not to angle posteriorly or else posteromedialization will occur. This could lead to overloading.

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Figure 57-9 The amount of medialization is measured. A 10- to 15-mm transfer is usually adequate. The Q angle should be corrected to less than 10 degrees.

Figure 57-12 Lateral radiograph of a completed tibial tubercle medialization. The screw should be placed with the knee in flexion to avoid injury to posterior neurovascular structures.

those cases in which MPFL deficiency is a problem and instability and tracking are not fully corrected, it can be addressed, either arthroscopically or open at this time. We use the tourniquet for the open part of this case and then release it prior to closure and achieve hemostasis. A drain is not usually necessary as it is for anteromedialization. The subcutaneous tissues and skin are closed carefully, and the patient is placed in a long-leg brace locked in extension.

Figure 57-10 The osteotomy is temporarily fixed and patellofemoral tracking assessed.

Postoperative Rehabilitation The biomechanics of a flat versus oblique osteotomy have been described by Cosgarea et al.23 In cases of straight medial tubercle transfer with a small thin flat osteotomy, weight bearing can be allowed right away, whereas in a patient with an anteromedialized tubercle, with a larger oblique osteotomy, weight bearing should be prohibited for the first 4 to 6 weeks postoperatively. In general, full ROM is allowed immediately and usually these patients regain full ROM within a couple of weeks after surgical intervention. Protected weight bearing for the first 3 to 4 weeks with the brace locked in extension is encouraged until the patient has good quadriceps control. Since the quadriceps and extensor mechanism are not violated, early quadriceps isometrics are allowed with resisted quadriceps strengthening allowed at 6 to 8 weeks, at which point there is some early bony healing. Results Multiple large series have reported a very high success rate with a low rate of complications.24–26 In summary, the major conclusions of these clinical studies of medial tubercle transfer are the following:

Figure 57-11 The osteotomy is fixed with a 4.5-mm bicortical screw and washer. A second screw and washer can be added if necessary.

1. It is best in young patients without evidence of severe systematic chondrosis or arthrosis. 2. Medial tubercle transfer corrects subluxation (congruence angle) as well as tilt (lateral patellofemoral angle). 3. Adequate postoperative Q-angle correction ( arthrosis Moderate obliquity

Arthrosis > malalignment Maximum obliquity

Figure 57-29 Algorithm for direction of tibial tubercle transfer when distal realignment is indicated.

REFERENCES 1. Desio S, Burks R, Kent B: Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med 1998;26:59–65. 2. Kolowich P, Paulos L, Rosenberg T, Farnsworth S: Lateral release of the patella: Indications and contraindications. Am J Sports Med 1990;18:359–365. 3. Insall J, Goldberg V, Salvati E: Recurrent dislocation and the high-riding patella. Clin Orthop 1972;88:67–69. 4. Blackburn JS, Peel TE: A new method of measuring patellar height. J Bone Joint Surg Br 1977;59:241–242. 5. Merchant AC, Mercer RL, Jacobsen RH, Cool CR: Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am 1974;56:1391–1396. 6. Laurin CA, Levesque HP, Dussault R, et al: The abnormal lateral patellofemoral angle. J Bone Joint Surg Am 1978;60:55–60. 7. Muneta T, Yamamoto H, Ishibashi T, et al: Computerized tomographic analysis of tibial tubercle position in the painful female patellofemoral joint. Am J Sports Med 1994;22:67–71. 8. Beaconsfield T, Hons B, Pintore E, et al: Radiologic measurements in patellofemoral disorders: A review. Clin Orthop 1994;308:18–28. 9. Elias DA, White DM, Fithian DC: Acute lateral patellar dislocation at MR imaging: Injury patterns of medial patellar soft tissue restraints and osteochondral injuries of the inferomedial patella. Radiology 2002;225:736–743. 10. Virolainen H, Visuri T, Kuusela T: Acute dislocation of the patella: MR findings. Radiology 1993;189:243–246. 11. Kirsch M, Fitzgerald S, Friedman H, Rogers LF: Transient lateral patellar dislocation: Diagnosis with MR imaging. AJR Am J Roentgenol 1993;161:109–113. 12. Dye SF, Chew MH: The use of scintigraphy to detect increased osseous metabolic activity about the knee. J Bone Joint Surg Am 1993;75A:1388–1406. 13. Henry JH: Conservative treatment of patellofemoral subluxation. Clin Sports Med 1989;8:261–278. 14. McConnell J: The management of chondromalacia patellae: A long term solution. Aust J Physiother 1986;2:215–223.

15. Nomura E, Inoue M, Kurimura M: Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy 2003; 19:717–721. 16. Fulkerson JP, Kalenak A, Rosenberg TD, Cox JS: Patellofemoral pain. Instruct Course Lect 1992;41:57–71. 17. Halbrecht J: Arthroscopic patella realignment: An all-inside technique. Arthroscopy. J Arthrosc Relat Surg 2001;17:940–945. 18. Drez D, Edwards T, Williams C: Results of medial patellofemoral ligament reconstruction in the treatment of patellar dislocation. Arthroscopy. J Arthrosc Relat Surg 2001;17:3:298–306. 19. Ellera Gomes JL, Stigler Marczyk LR, Cesar de Cesar P, Jungblut CF: Medial patellofemoral ligament reconstruction with semitendinous autograft for chronic patellar instability: A follow-up study. Arthroscopy 2004;20:147–151. 20. Ramappa A, Apreleva M, Harrold F, et al: The effects of medialization and anteromedialization of the tibial tubercle on patellofemoral mechanics and kinematics. AOSSM Instructional Course presented at AOSSM Annual Meeting, July 2003, San Diego, CA. 21. Kuroda R, Kambic H, Valdevit A, Andrish J: Articular contact pressures after tibial tubercle transfer. Am J Sports Med 2001;29:403–409. 22. Trillat A, Dejour H, Couette A: Diagnostic et traitement des subluxation recidivantes de la rotule. Rev Chir Orthop 1964;50: 813–824. 23. Cosgarea A, Schatzke M, Seth A, Litsky A: Biomechanical analysis of flat and oblique tibial tubercle osteotomy for recurrent patellar instability. Am J Sports Med 1999;27:507–512. 24. Cox J: Evaluation of the Roux-Elmslie-Trillat procedure for knee extensor realignment. Am J Sports Med 1982;10:303–310. 25. Shelbourne K, Porter D, Rozzi W: Use of a modified Elmslie-Trillat procedure to improve abnormal patellar congruence angle. Am J Sports Med 1994;22:318–323. 26. Farr J: Distal realignment for recurrent patellar instability. Op Tech Sports Med 2001;9:176–182. 27. Bandi W: Chondromalacia patella und femo-patellare arthrose. Helv Chir Acta 1972;11:1–70.

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28. Maquet P: Un traitement biomecanique: L’arthrose femore-patellaire: L’avancement du tendon rotulien. Rev Rhum Mal Osteoartic 1963;30:779–783. 29. Maquet P: Advancement of the tibial tuberosity. Clin Orthop 1976;115:225–230. 30. Maquet P: Mechanics and osteoarthritis of the patellofemoral joint. Clin Orthop 1979;144:70–73. 31. Maquet P: Biomechanics of the Knee, 2nd ed. Berlin, Springer-Verlag, 1984. 32. Ferguson A, Brown T, Fu F, Rutkowski R: Relief of patellofemoral contact stress by anterior displacement of the tibial tubercle. J Bone Joint Surg Am 1979;61:159–166. 33. Ferguson A: Elevation of the insertion of the patellar ligament for patellofemoral pain. J Bone Joint Surg Am 1982;64:766–771. 34. Ferrandez L, Usabiaga J, Yubero J, et al: An experimental study of the redistribution of patellofemoral pressures by anterior displacement of the anterior tuberosity of the tibia. Clin Orthop 1989;283:183– 189. 35. Fulkerson J, Becker G, Meaney J, et al: Anteromedial tibial tubercle transfer without bone graft. Am J Sports Med 1990;18:490–496. 36. Hungerford D, Barry M: Biomechanics of the patellofemoral joint. Clin Orthop 1979;144:9–15. 37. Nakamura T: Advancement of tibial tuberosity: A biomechanical study. J Bone Joint Surg Br 1985;67:255–260. 38. Pan H, Kish V, Boyd RD, et al: The Maquet procedure: Effect of tibial shingle length on patellofemoral pressures. J Orthop Res 1993;11:199– 204. 39. Radin E: The Maquet procedure: Anterior displacement of the tibial tubercle. Indications, contraindications, and precautions. Clin Orthop 1986;213:241–248. 40. Radin E: Anterior tibial tubercle elevation in the young adult. Orthop Clin North Am 1986;17:297–302. 41. Radin E, Pan H: Long-term follow-up study on the Maquet procedure with special references to the causes of failure. Clin Orthop 1993;290:253–258. 42. Bellemans J, Cauwenberghs F, Witvrouw E, et al: Anteromedial tibial tubercle transfer in patients with chronic anterior knee pain and a subluxation type patella malalignment. Am J Sports Med 1997;25:375–381. 43. Bessette G, Hunter R: The Maquet procedure. A retrospective view. Clin Orthop 1998;232:159–167. 44. Fulkerson J: Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop 1983;177:176–181.

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45. Heatley FW, Allen PR, Patrick JH: Tibial tubercle advancement for anterior knee pain. Clin Orthop 1986;208:215–224. 46. Hirsch D: Experience with Maquet anterior tibial tubercle advancement for patellofemoral arthralgia. Clin Orthop 1980;148:136–139. 47. Koshino T: Changes in patellofemoral compressive force after anterior or anteromedial displacement of tibial tuberosity for chondromalacia patella. Clin Orthop 1991;266:133–138. 48. Leach R, Radin E: Anterior displacement of the tibial tubercle for patellofemoral arthrosis. Orthop Trans 1979;3:291–294. 49. Leach R, Schepsis A: Anterior displacement of the tibial tubercle: The Maquet procedure. Contemp Orthop 1981;3:199–204. 50. Lund F, Nilsson BE: Anterior displacement of tibial tuberosity in chondromalacia patella. Acta Orthop Scand 1980;51:679–688. 51. Pidoriano A, Weinstein R, Buuck D, Fulkerson J: Correlation of patellar articular lesions with results from anteromedial tibial tubercle transfer. Am J Sports Med 1997;25:533–537. 52. Post W, Fulkerson J: Distal realignment of the patellofemoral joint. Orthop Clin North Am 1992;23:631–643. 53. Putnam M, Mears D, Fu F: Combined Maquet and proximal tibial valgus osteotomy. Clin Orthop 1985;197:217–223. 54. Rappaport LH, Browne MG, Wickiewicz TL: The Maquet osteotomy. Orthop Clin North Am 1992;23:645–656. 55. Rozbruch J: Tibial tubercle elevation: A clinical study of 31 cases. Orthop Trans 1979;3:291. 56. Schepsis A, DeSimone A, Leach R: Anterior tibial tubercle transposition for patellofemoral arthrosis: A long-term study. Am J Knee Surg 1994;7:13–20. 57. Schmidt F: The Maquet procedure in the treatment of patellofemoral osteoarthritis. Clin Orthop 1993;294:254–258. 58. Siegel M: The Maquet osteotomy: A review of risks. Orthopedics 1987;10:1073–1078. 59. Sudmann E, Salkowitsch B: Anterior displacement of tibial tuberosity in the treatment of chondromalacia patella. Acta Orthop Scand 1980;51:171–174. 60. Weisbrod, H, Treiman N: Anterior displacement of tibial tuberosity for patellofemoral disorders. Clin Orthop 1980;153:180–182. 61. Cohen Z, Henry J, McCarthy D, et al: Computer simulations of patellofemoral joint surgery: Patient-specific models for tuberosity transfer. Am J Sports Med 2003;31:87–98. 62. Benvenuti J, Rakotomanana L, Leyvraz P, et al: Displacements of the tibial tuberosity: Effects of the surgical parameters. Clin Orthop 1997;1:224–234.

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Tendon Ruptures Jeff C. Brand, Jr.

In This Chapter Quadriceps tendon rupture Surgery—quadriceps tendon repair Patellar tendon rupture Surgery—patellar tendon repair

rior femur just below the level of the lesser trochanter and inserts in the middle layer on the superior medial border of the patella. Its distal fibers contribute to the medial retinaculum. The articularis genu, an anatomic variant, arises deep to the intermedius and inserts on the superior capsule of the knee serving to retract it from the patella.1

Biomechanics

INTRODUCTION • Extensor mechanism disruptions include quadriceps and patellar tendon rupture. • Bilateral atraumatic simultaneous quadriceps tendon ruptures tend to occur in patients with systemic disease. • Diagnosis is made by clinical examination and radiographic findings in most instances. • Surgery is necessary to restore the extensor mechanism anatomy. • Rehabilitation is determined by the type and strength of the repair. • Weakness, atrophy, and functional losses are common postoperative problems.

QUADRICEPS TENDON RUPTURES Relevant Anatomy The quadriceps tendon is the tendinous confluence, approximately 3 cm proximal to the patella, of the vastus lateralis, medialis longus and obliquus, rectus femoris, vastus intermedius, and articularis genu. The tendon is broad based and has a trilaminar depth with fat between the tendon planes. The rectus femoris is the most superficial of the three layers. The rectus direct head arises from the anterior inferior spine and indirect head is from the anterior capsule of the hip. Innervation as for all the quadriceps is from the femoral nerve. It is a two-joint muscle unique among the quadriceps muscles. Distally, fibers form the superficial layer of the quadriceps tendon that traverse over the patella and insert in the infrapatellar tendon. The trilaminar expansion of the quadriceps tendon consists of the superficial layer described, the intermediate layer of the lateralis and medialis, and the deep layer of the intermedius. The lateralis sends fibers to the lateral patellofemoral ligament as well. The vastus lateralis arises from the lateral flare of the greater trochanter along the linea aspera. The vastus intermedius arises from the mid-anterior femur. The vastus medialis originates at the ante-

The patella acts as a moment arm for knee extension through the quadriceps mechanism and patellar tendon attachment on the tibia. Forces in the quadriceps tendon and patellar tendon vary with flexion angle but are consistently reported to be greater at 60 degrees of knee flexion. At 30 and 120 degrees, forces in both structures are roughly one half of these peak values. At 60 degrees of knee flexion, the forces in each tendon are approximately equal. The force in the patellar tendon (FL) is approximately 30% greater than the force in the quadriceps tendon (FQ) at 30 degrees of knee flexion. At 90 degrees of knee flexion, FQ is 30% greater than FL. The patellar contact area moves proximally with increased knee flexion. With the knee in 30 degrees of flexion, the patellar contact area is on the distal portion positioning the patellar tendon at a mechanical disadvantage and increasing forces within the patellar tendon compared to the quadriceps tendon. This suggests that the patella functions as more than a simple pulley that would have equal forces in each the patellar tendon and quadriceps tendon at all knee flexion angles.2 Changing the length of the lever arm by changing the length of either the patellar tendon or the quadriceps tendon can occur with extensor mechanism tendon repair. This will change force loading in each tendon and the contact area of the patella.

Cause of Injury An intact healthy extensor mechanism, particularly the quadriceps tendon, is unlikely to rupture. The tendon most commonly ruptures through a histologically proven degenerative area.3 Patients with bilateral simultaneous quadriceps tendon ruptures frequently have degeneration as a result of a systemic disease. Although the spontaneous atraumatic rupture of bilateral quadriceps tendons simultaneously is a frequent subject of case reports, it is uncommon in case series.

Clinical Features and Evaluation The patient with a quadriceps tendon rupture is commonly a male in the sixth decade of life, may have systemic disease, and suffers an indirect eccentric load to the knee with a misstep. Historically, quadriceps tendon rupture was thought to be rare in the patient younger than 40 years of age.4 Forty-five years ago Scuderi stated, “There should be no difficulty in diagnosing a

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Table 58-1 Clinical Evaluation of Patients with Extensor Tendon Disruption Mechanism of injury Consider systemic medical conditions Hemarthrosis Loss of active knee extension Palpable defect Patella alta (patellar tendon rupture) or baja (quadriceps tendon rupture) on plain radiographs Magnetic resonance imaging if diagnosis is not clinically evident

ruptured quadriceps tendon, but the diagnosis is all too frequently missed.”5 An inability to voluntarily extend the leg, patella baja on exam and a hemarthrosis combined are quite accurate (Table 58-1). Plain radiographs may reveal avulsion fractures and patella baja, which can be assessed with the InsallSalvati method of measurement. Less than 0.8 suggests patella baja (Fig. 58-1). The “tooth” sign seen on the axial patellar radiographs may be an indication of quadriceps tendon degeneration at its insertion on the patella6,7 (Fig. 58-2). Magnetic resonance imaging, as reported in small series, shows a discontinuity in all three layers of the quadriceps tendon.8,9 The patellar tendon, with an intact quadriceps tendon and normal tension in the extensor mechanism, displays a linear or nearly linear appearance. If the quadriceps tendon is ruptured, the patellar tendon has a corrugated or wrinkled appearance due to lack of tension in the extensor mechanism10 (Fig. 58-3). Most authors agree that magnetic resonance imaging is not necessary in patients who have the usual findings of extensor mechanism disruption, but it may be useful when the diagnosis is in doubt.

Surgery Acute Repair A longitudinal incision offers an extensile approach that can be used for secondary procedures such as a total knee arthroplasty.

Figure 58-2 A, Normal patella as seen on a tangential view. B, A superoinferior radiograph of the specimen demonstrates the toothlike structures intimately fused with the anterior cortex of the proximal pole of the patella. (From Greenspan A, Norman A, Kia-Ming Tchang F: “Tooth” sign in Patellar degenerative disease. J Bone Joint Surg Am 1977;59:483–485.)

Figure 58-1 The Insall-Salvati ratio in a normal knee (A) and in one with patella alta (B). LP, length of the patella; LT, length of the patellar tendon. (From Rose PS, Frassica FJ: Atraumatic bilateral patellar tendon rupture. A case report and review of the literature. J Bone Joint Surg Am 2001;83:1382–1386.)

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Figure 58-3 Magnetic resonance imaging of a patient 3 months after quadriceps tendon repair with suture anchors, demonstrating failure of the repair. The end of the quadriceps tendon is attenuated with signal change within the attenuated portion. The patellar tendon is wrinkled, consistent with relaxation of tension within the patellar tendon due to lengthening of the extensor mechanism.

After the incision, the hematoma is evacuated. Intra-articular structures are inspected for further injury to the degree that is possible. The margins of the quadriceps tendon and retinaculum are débrided. As the majority of these lesions occur at the insertion of the tendon onto the superior pole of the patella, the bone of the superior pole of the patella is prepared. Classic descriptions include a trough; however, soft-tissue removal from cortical bone may be adequate as is performed in rotator cuff repair preparation of the greater tuberosity. Three longitudinal drill holes are drilled in the patella. One is drilled in the center of the patella in the coronal plane. A parallel drill hole is positioned on either side of the middle drill hole for a total of three drill holes. An anterior cruciate ligament drill guide may be used to drill the holes in a more controlled fashion.11 Two no. 5 braided Ethibond sutures (Ethicon, Somerville, NJ) or similar suture is passed through the quadriceps tendon in a grasping configuration, such as a Krackow stitch (Fig. 58-4). The sutures are positioned to allow the central limbs of each suture to pass through the central drill hole of the patella. The opposite limb of each suture is passed with a Beath pin or suture passer (Fig. 58-5) through the drill holes along the medial and lateral sides of the patella, respectively. Opposite ends of each suture loop are knotted over the distal pole of the patella (Fig. 58-6). Alternatively, suture anchors drilled and deployed in the position where the bone tunnels would normally be drilled can provide fixation to the patella. The suture from the suture anchors is passed through the tissue in weave or grasping suture.12 Usually there is a defect in the medial and lateral retinaculum that is repaired with no. 2 braided nonabsorbable suture in an interrupted figure-eight fashion. The natural space that is anterior to the repair and deep to the skin should be obliterated in the closure. Meticulous hemostasis and possibly a surgical drain prevent a postoperative hematoma that can become infected. Chronic Repair For patients who have near-normal length of the quadriceps tendon, standard repair techniques perform well. For the patients without normal length and tension in the quadriceps mechanism, the surgeon must decide between measures to add length to the tendon and those meant to substitute for the defect. Often the defect in the quadriceps tendon consists of variable amount of amorphous, nonfunctional scar tissue that should be resected.13 Length may be restored to the quadriceps tendon mechanism through the Codivilla technique described by Scuderi14 (Fig. 58-7). An inverted V is cut through the full thickness of the proximal segment of the quadriceps tendon with the inferior ends of the V ending 1.5 to 2 cm proximal to the rupture. The triangular flap thus fashioned is split into an anterior part of one third of its thickness and the posterior part of two thirds. The tendon ends of the rupture are then apposed with interrupted nonabsorbable sutures. The anterior one third thickness is turned distally and sutured (see Fig. 58-7). The open upper part of the V is closed with interrupted sutures. The stability of the repair is evaluated with passive range of motion (ROM).15

Figure 58-4 Schematic diagram of ligament fixation with the Krackow grasping suture. (From Krackow KA, Thomas SC, Jones LC: A new stitch for ligament-tendon fixation. J Bone Joint Surg Am 1986;68:764–766.)

Postoperative Treatment A hinged rehabilitative brace provides protection, controlled ROM and access to the incision. For the rare patient who may not be compliant with postoperative instruction, a cast may be more secure. Initially the brace is locked into full extension for 1 to 2 weeks to allow wound healing. This period varies depend-

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A

Figure 58-5 A, Hewson suture passer (Smith & Nephew, Memphis, TN). B, The tip of the suture passer.

B

ing on coexistent medical issues, immunosuppressive medications, and repair strength. After wound healing is achieved, progressive ROM starts from 0 to 30 degrees for 1 to 2 weeks, 0 to 60 degrees for the next 1 to 2 weeks, 0 to 90 degrees for the following 1 to 2 weeks. Most braces allow a 15-degree progression of ROM if the surgeon desires a slower progression of ROM. Weight bearing is full from the time of surgery with the hinges of the brace locked in full extension. Until 4 to 6 weeks postoperatively, strengthening is by isometrics, quadriceps-setting exercises, and straight leg raises in the brace with the hinges on the brace locked in full extension. At 4 to 6 weeks, the patient may start closed-chain strengthening. Proprioceptive or neuromuscular activities are an important part of the rehabilitative process as many of these injuries likely result from a misstep. At 10 to 12 weeks, plyometrics and functional activities may be added depending on the patient’s demands and capabilities. This progression of activities can be slowed for chronic repairs or reconstructions of the extensor mechanism. The quality of tissue, quality of the repair, and knee flexion obtained at the time of surgery all are important factors that influence the progression of activities.

Figure 58-6 Technique for quadriceps tendon repair via drill holes in the patella. Sutures (dashed lines) are passed through three parallel drill holes and tied distally. The central two suture strands are passed through the same central hole and tied to the corresponding medial or lateral strand. (From Ilan DI, Tejwani N, Keschner M, Leibman M: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192–200.)

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Results If proven surgical principles and techniques are practiced, patient results are generally good, independent of the quadriceps tendon repair method.4,13,16 Weakness is the most common adverse outcome that may occur as often as 30% or more with isokinetic testing.17 Extensor lag, although less common with more aggressive rehabilitation programs, still affects some patients after repair, and particularly after delayed reconstruction. Return to daily or occupational activities takes approxi-

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Figure 58-7 Codivilla method of quadriceps tendon lengthening and repair. A, Chronic quadriceps tendon tear exposed. Proximal retraction prevents direct opposition of the tear. Dashed lines represent inverted V cut (full thickness) to be made. B, The inverted V cut allows the tear to be approximated and repaired. C, The proximal aspect of the inverted V repaired side to side. A full- or partialthickness flap may be used to augment the repair, as in the Scuderi technique. (From Ilan DI, Tejwani N, Keschner M, Leibman M: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192–200.)

A mately 4 months, but full recovery is longer with some patients. Most patients are able to return to vigorous occupations, but as many as 50% are unable to return to previous recreational activities.18,19 Scuderi stated,5 “It is axiomatic that the earlier a ruptured quadriceps tendon is diagnosed and repaired, the better the end result will be.” A delay in surgical repair results in a greater need for ambulatory aids, a decreased ability to climb stairs, and an increased incidence of an extensor lag. Return to work and recreational activities are similarly affected. Patient satisfaction scores are lower with a delayed surgical repair. Although the best results have been seen in patients who were repaired within 7 days, surgical repair for a chronic rupture is recommended.12,15 Patients with bilateral simultaneous quadriceps tendon rupture do not perform as well as patients with unilateral rupture. The majority of these patients are affected by chronic medical conditions (76%). In one study, results in 57% were considered favorable and 43% had a poor outcome. Older patients did not fare as well as younger patients.20 Complications In a review of multiple series of quadriceps tendon repairs, the most common complication is postoperative stiffness, either extensor lag or loss of flexion. Wound-healing problems and infection are also potential complications. Rerupture of the repair can occur, although it is relatively rare. Other described complications include postoperative hemarthrosis, and deep venous thrombosis or pulmonary embolus.

B

C

the medial and lateral fibers attaching more proximally. The patellar tendon attaches to the anterior aspect of the distal pole of the patella. The nonarticular zone is largely devoid of patellar tendon attachment.21

Cause of Rupture The patellar tendon ruptures through an area of degeneration or impairment3 (Table 58-2). Mechanical impairment may be due to harvest of the middle third of the tendon for ligament reconstruction surgery. Compared to a control group, a test group that experienced harvest of the middle third of the patella in young human cadavers (mean age 24.86 ± 7.13 years) measured a mean area of 48.67 mm2 (49.64% less) and load of 2226.58 N (51% less), and energy level at failure of 32.58 J (45.14% less).22 Cortisone injections into the patellar tendon for inflammatory conditions or anterior knee pain are discussed in several reports as a cause of patellar tendon rupture.6,23 A biochemical investigation demonstrated that dexamethasone significantly decreased cell viability, suppressed cell proliferation, and reduced collagen synthesis in cultured human tenocytes.24

Table 58-2 Patellar Tendon Ruptures Causes

Mechanism

Harvest of the middle third of the patellar tendon for ligament reconstruction22

Mechanical

PATELLAR TENDON RUPTURES Relevant Anatomy

Cortisone injection6,24,33

Decreased cell viability, suppressed cell proliferation, and reduced collagen synthesis

Jumper’s knee6

Degeneration

The patellar tendon is the distal insertion of the extensor mechanism into the proximal tibia through the tibial tubercle. It is obliquely orientated in the coronal plane with the patella lying slightly medial to the tibial tubercle. It is wider and thinner proximally at its attachment on the distal pole of the patella. The patellar tendon fibers merge to attach on the tibial tubercle. Consequently, the tibial insertion is narrower and thicker than the patellar origination. The patellar origination on the distal pole of the patella arcs a crescent in the coronal plane with

1

Rheumatoid arthritis

Fibrosis, synovitis

Obesity1

Fatty degeneration 1

Fluoroquinolones

Osgood-Schlatter disease6,30

Mechanical

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Clinical Evaluation The clinical findings of patellar tendon rupture mirror those of the quadriceps tendon rupture (see Table 58-1). Patients with a patellar tendon rupture are generally younger than those with a quadriceps tendon rupture.

Biomechanics of Repairs In an investigation of elderly cadaveric knees (mean age, 66 years), three methods of patellar tendon repair were loaded in a cyclical fashion for 250 cycles at 0.25 Hz. In the first group, the patellar tendon was sutured with no. 5 Ethibond in a Krackow stitch passed through longitudinal drill holes in the patella (mean gap across the repair site 11.3 ± 0.5 mm). The second group added a no. 5 Ethibond suture augmentation as a cerclage passed through a transverse drill hole at the mid-patella and then passed through a transverse drill hole through the tibial tubercle and tied at 90 degrees of flexion (mean gap, 4.9 ± 0.5 mm). The third group used a 2.0 Dall-Miles cable (Howmedica Inc., Rutherford, NJ) augmentation (mean gap, 3.5 ± 0.8 mm). Although this investigation was a biomechanical evaluation, the authors believed that the Dall-Miles augmentation allowed an accelerated rehabilitation consisting of full weight bearing in extension, knee ROM from 0 to 90 degrees, and isometric quadriceps/hamstring muscle strengthening.25 A similar method of augmentation with the semitendinosus tendon placed through drill holes allowed an accelerated rehabilitation program that obtained ROM through continual passive motion for 2 weeks combined with passive and active-assisted ROM. Low-resistance cycling started at 2 weeks postoperatively. Three of four patients were identical to the contralateral leg with Cybex dynamometer, Lysholm knee scoring scale, onelegged hop test, ROM, and radiographic evaluation.26

Patellar tendon length

Figure 58-8 Preoperative lateral radiograph is taken of the normal knee to obtain the normal patellar tendon length. (From Shelbourne KD, Darmelio MP, Klootwyk TE: Patellar tendon rupture repair using Dall-Miles cable. Am J Knee Surg 2001;14:17–21.)

Acute Repair A longitudinal midline approach to the patellar tendon from the vastus medialis oblique to just beyond the tibial tubercle allows other procedures at the same time or as a delayed procedure.27 Creating thick skin flaps prevents wound-healing complications. A 60-degree lateral radiograph of the contralateral knee preoperatively serves as a guide to patellar tendon length (Fig. 588) that restores normal patellar tracking in all planes. Skin incision and prepatellar bursa excision expose the ruptured patellar tendon. Mid-substance tears and the tendinous portion of the proximal and distal repairs can be sutured with a grasping suture such as the Krackow stitch. For either proximal or distal tears, an anatomic attachment to bone needs to be recreated. The bone should be débrided of soft tissue to allow restoration of the normal tendon to bone insertion. Insertion site anatomy can be restored through either bone anchors or tunnels placed through bone. Transosseous tunnels are favored by history; bone anchors are favored by ease and exposure. A braided no. 5 nonabsorbable suture has been traditionally chosen for these repairs (Fig. 58-9). Newer suture with improved biomechanical properties (Fiberwire; Arthrex, Naples, FL) is currently available. Augmentation with wire,28 Dall-Miles cable,27 or biologic tissue (semitendinosus26) is advocated by some authors. Augmentation can allow a more rapid or accelerated rehabilitation program through improved biomechanical properties of the surgical repair site.25,27 It is most commonly used in circumstances in which tissue quality is considered compromised or when patient compliance with a postoperative program is a concern. Shelbourne et al27 apply the Dall-Miles device after the sutures

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Figure 58-9 Diagram of the repair technique with tendon reattachment through vertical drill holes in the patella using nonabsorbable suture (solid arrow) and reapproximation of the retinaculum using interrupted absorbable sutures (open arrow). (From Kuechle DK, Stuart MJ: Isolated rupture of the patellar tendon in athletes. Am J Sports Med 1994;22:692–695.)

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Figure 58-10 The Dall-Miles cable is placed through the patella and tibia and is clamped at the joint line. The placement of the cable allows knee flexion to approximately 120 degrees without placing undue tension on the patellar tendon repair. (From Shelbourne KD, Darmelio MP, Klootwyk TE: Patellar tendon rupture repair using Dall-Miles cable. Am J Knee Surg 2001;14:17–21.)

are positioned but before they are tied. A drill hole is placed transversely across the patella at the mid-portion. A similar transverse hole is drilled across the tibial tubercle. The DallMiles cable, neutralization wire, or semitendinosus can be tensioned and lateral radiograph obtained with the knee in 60 degrees of flexion that is compared to the preoperative contralateral knee radiograph. The length of Dall-Miles cable or neutralization can be adjusted until the repaired tendon length is equal to the opposite side (Fig. 58-10). Grasping sutures are tied and knee flexion is evaluated for the limits to postoperative rehabilitation. The space anterior to the repair and deep to the skin is closed with meticulous hemostasis and possibly a surgical drain to prevent a postoperative hematoma.

Chronic Repair or Reconstruction If possible, the chronic repair should be performed using the techniques and principles detailed in the acute repair section previously discussed. This approach will not likely be possible beyond 6 weeks from the time of injury. By that time, due to the retraction of the patella alta from the quadriceps muscle, the patellar tendon has healed in an elongated position with biomechanically inferior fibrous tissue. Allograft tissue as a reconstructive option offers ease of use, avoidance of graft site morbidity, availability, and often shorter operating times. Unfortunately, viral or bacterial disease may be transmitted by the allograft tissue. Allograft tissues add to the expense of the operation and are not available in all parts of the world. Anterior cruciate ligament reconstruction results with allograft tissue have been comparable, in some series, to those

results obtained with autogenous tissue. The results of patellar tendon reconstruction are limited to either case reports or small case series. Mills29 published a very complete description of the reconstruction of the patellar tendon with an allograft Achilles tendon, and the reader may wish to refer to this description for further details. Five- to 10-degree flexion contractures are treated with physical therapy, dynamic splinting, and possibly serial casting. Flexion contractures greater than 10 degrees are treated surgically as the first stage of a two-stage reconstruction. The second stage is reconstruction of the patellar tendon. Extensive quadriceps retraction and scarring are treated with a quadricepsplasty. This procedure may reduce flexion after surgery, and the patient should be warned of this possibility. A longitudinal incision from 2 cm proximal to the patella to the distal extent of the tibial tubercle is created. Thick skin flaps are made to protect the vascular supply to the skin edges. The patellar tendon scar is incised in midline providing a sleeve for the allograft. This soft tissue is subperiosteally elevated off the patella and tibial tubercle. Retropatellar and suprapatellar adhesions are resected. The patellar fat pad should be protected and retained if not diseased. A large Weber reduction clamp applies traction to restore the patella to its anatomic position after it is mobilized. If the patella cannot be restored to its anatomic position, a series of quadriceps releases are performed. First, the quadriceps is elevated through the suprapatellar pouch, dissecting between the periosteum of the anterior femur and vastus intermedius with a Cobb elevator. If this fails to restore length to the extensor mechanism, a V-lengthening of the scarred distal vastus intermedius from the undersurface of the quadriceps mass is performed. The next step is to resect the vastus intermedius, maintaining the fibers of the rectus femoris, if inadequate length of quadriceps tendon is not obtained with the measures mentioned previously. The Achilles allograft bone plug is shaped into a rectangular block 30 mm in length, 10 mm in depth, and 10 mm wide. The tendon is divided into a two-tailed graft. The tendinous ends of the graft are tubularized to fit through 6-mm bone tunnels (Fig. 58-11A). A trough is created with a small oscillating saw on the tibial tubercle to match the bone plug on the tendon allograft. The bone plug is extracted from the tibial tubercle with a thin osteotome. A vertical proximal wall of the trough stops graft migration proximally. The bone plug is secured in the trough with two 3.5-mm small fragment cancellous screws (ASIF; Synthes, Paoli, PA). The bone tunnels in the patella are drilled over a Beath pin. The Beath pin can be positioned with the anterior cruciate ligament tibial drill guide. The bone tunnels are parallel and about 8 mm from the midline in the coronal plane. The grafts are passed with the Beath pin. A plain lateral radiograph or fluoroscopy with the knee in 30 to 45 degrees of flexion confirms the correct length of the reconstructed patellar tendon. The allograft tendon tails are sutured with braided nonabsorbable suture material into the quadriceps expansion. The remaining tails are brought over the superficial surface of the patella and sutured to allograft tails (Fig. 58-11B). The soft-tissue envelope is sutured over the graft. Knee flexion is evaluated in order to guide postoperative knee flexion.29

Postoperative Treatment The techniques and principles of rehabilitation discussed in the postoperative treatment section of the quadriceps tendon repair apply to the patellar tendon repair.

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30 mm

C

10 mm

10 mm

A

Figure 58-11 Achilles tendon allograft preparation. Line drawings of the allograft with 30 ¥ 10 ¥ 10-mm bone block, before and after fashioning the two tails of the graft. A, Small-fragment fixation of the calcaneal bone block. Graft passage through the patellar drill holes. B, The limbs of the graft are sutured to the quadriceps tendon and medial and lateral retinaculum and then turned down for suture to the patellar tendon graft as well. (From Mills WJ: Reconstruction of chronic patellar tendon rupture with Achilles tendon allograft. Tech Knee Surg 2004;3:154–162.)

B

The patient who undergoes reconstruction of the patellar tendon with an Achilles tendon allograft follows a similar program but is carefully monitored. Knee motion is not allowed until the wound seals. For 2 weeks, 30 degrees of knee flexion is allowed in a hinged rehabilitative brace. If patellar tendon length is maintained, motion is advanced to 60 degrees of knee flexion for 2 weeks. Again, the position of the patella is con-

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firmed with a plain lateral radiograph. If the position is the same as immediately postoperatively, knee flexion is advanced to 90 degrees. Assuming that patellar tendon length is maintained, unlimited motion is allowed at 6 weeks.29 The quality of tissue, quality of the repair, and knee flexion obtained at the time of surgery determine the progression of activities after repair or reconstruction of the extensor mechanism.

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Results Weakness of the quadriceps muscle may occur in as many as 40% to 50% of patients. Extensor lag is less common in patellar tendon repair compared to those who undergo quadriceps tendon repair. Most patients regain close to full ROM, an argument against the use of augmentation devices and accelerated rehabilitation for repair of the patellar tendon. Unfortunately, patellofemoral incongruence or osteoarthrosis is seen all too frequently on postoperative radiographs, for example, 12 of 29 patients in one series.30 Of the 12 patients, three had unsatisfactory results. All the patients with unsatisfactory results due to pain in the series of Larsen and Lund31 had patellar incongruence. The Insall-Salvati ratio differed more than 10% from the uninvolved knee in 16 of 29 patients in one series of repairs.30 In a series of 10 patients with athletic patellar tendon ruptures treated with immediate suture repair to bone, two of those patients had significant patella alta (InsallSalvati ratios of 0.55 and 0.59) that was increased in each patient from preoperatively. Those two had patellar pain postoperatively that limited their sporting activities.5 Even though patients with patellar tendon repair are generally younger than those with quadriceps tendon rupture, return to preoperative activities is not universal for every patient. Patients with a delayed diagnosis of patellar tendon rupture who undergo reconstruction are less likely to return to full activities. Mills29 reported on five patients with Achilles tendon allograft reconstruction of the patellar tendon. Mean average flexion was 123 degrees. Four of five patients achieved full active terminal extension without an extensor lag. No wound complications or graft ruptures were encountered.

Complications A second operation to remove a cerclage wire is usually necessary as painful hardware or wire breakage is common with this method of augmentation. Other complications closely parallel those described previously for quadriceps tendon repair.

CONCLUSIONS Randomized clinical trials are uncommon involving treatment of extensor mechanism disruption. The body of science on extensor mechanism injuries consists of case series, review articles, and a large number of case reports; as such, clinical decision making relies on data with a low level of clinical evidence. Box 58-1 summarizes the general principles involved in diagnosing and treating extensor mechanism injuries. Due to the strong biomechanical properties of the extensor mechanism, rupture occurs through damaged or degenerative tissue. Particularly in patients with disruption of the quadriceps tendon, systemic disease should be sought and addressed.

Box 58-1 General Principles 1. 2. 3. 4. 5. 6.

Recognize the diagnosis early. Recognize systemic disease. Restore appropriate tension to the extensor mechanism. Repair with grasping suture. Respect the biology of the injury. Rehabilitate appropriate to the patient.

Failure to address these factors may jeopardize postoperative success. A delay in diagnosis and treatment of extensor mechanism disruption is the single most negative impact on outcome from treatment. The clinical findings are straightforward. If the diagnosis is suspected, it is unlikely to be missed. Extensor mechanism length restoration using the contralateral knee as a control is the first priority. Patients with incongruence or malalignment of the patellofemoral articulation after repair or reconstruction are at increased risk of pain.6,30,31 The standard of care is primary repair of the extensor mechanism within 2 weeks of injury with a grasping suture on the tendinous portion of the repair with the suture passed through drill holes. A relatively conservative rehabilitation program focused on restoration of strength, mobility, and functional activities will likely allow the patient to return to daily activities and may allow a return to sporting activities. Augmentation of the primary patellar tendon repair with wire, Dall-Miles cables, suture, and pull-out wire can be advised for patients undergoing an accelerated rehabilitation program. Factors that affect tissue integrity, healing response, or noncompliant patients may be considered for an augmented repair. In general, augmentation is not necessary in the absence of these factors. Repair of the chronically ruptured extensor mechanism presents controversy. Up to 6 weeks after injury a repair may be possible; beyond that time, most authors would recommend the Codivilla V-Y plasty as described by Scuderi for the chronic ruptured quadriceps tendon. Use of allograft tissue, prosthetic devices, and soft-tissue grafts should be confined to individual situations rather than general use. Treatment of the chronic patellar tendon rupture is even more controversial. The first principle is to restore length to the extensor mechanism with the use of the normal side as a control if available. Up to 6 weeks from time of the injury, it may be possible to do a primary suture repair. Proponents of allograft tissue report the use of tendon allograft.29 Autogenous semitendinosis and gracilis may substitute for the patellar tendon after appropriate length is restored.

REFERENCES 1. Ilan D, Tejwani N, Keschner M, et al: Quadriceps tendon rupture. J Am Acad Orthop Surg 2003;11:192–200. 2. Huberti H, Hayes W, Stone J, et al: Force ratios in the quadriceps tendon and ligamentum patellae. J Orthop Res 1984;2:49–54. 3. Kannus P, Jözsa L: Histopathological changes preceding spontaneous rupture of a tendon: A controlled study of 891 patients. J Bone Joint Surg Am 1991;73:1507–1525. 4. Siwek CW, Rao JP: Ruptures of the extensor mechanism of the knee joint. J Bone Joint Surg Am 1981;63:932–937.

5. Scuderi C: Ruptures of the quadriceps tendon. Study of twenty tendon ruptures. Am J Surg 1958;95:626–634. 6. Kelly DW, Carter VS, Jobe FW, et al: Patellar and quadriceps tendon ruptures-jumper’s knee. Am J Sports Med 1984;12:375–380. 7. Greenspan A, Norman A, Tchang FK-M: “Tooth” sign in patellar degenerative disease. J Bone Joint Surg Am 1977;59:483–485. 8. Zeiss J, Saddemi S, Ebraheim N: MR imaging of the quadriceps tendon: Normal layered configuration and its importance in cases of tendon rupture. Am J Roentgenol 1992;159:1031–1034.

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9. Yu J, Petersilge C, Sartoris D, et al: MR imaging of injuries of the extensor mechanism of the knee. Radiographics 1994;14:541–551. 10. Berlin R, Levinsohn E, Chrisman H: The wrinkled patellar tendon: An indication of abnormality in the extensor mechanism of the knee. Skeletal Radiol 1991;20:181–185. 11. Ong BC, Sherman O: Acute patellar tendon rupture: A new surgical technique. Arthroscopy 2000;16:869–870. 12. Richards DP, Barber FA: Repair of quadriceps tendon ruptures using suture anchors. Arthroscopy 2002;18:556–559. 13. Rougraff BT, Reeck CC, Essenmacher J: Complete quadriceps tendon ruptures. Orthopaedics 1996;19:509–514. 14. Scuderi G: Quadriceps and patellar tendon disruption. In Scott W (ed): The Knee. St. Louis, Mosby, 1994, pp 469–478. 15. Yilmaz C, Binnet MS, Narman S: Tendon lengthening repair and early mobilization in treatment of neglected bilateral simultaneous traumatic rupture of the quadriceps tendon. Knee Surg Sports Traumatol Arthrosc 2001;9:163–166. 16. Wenzl M, Kirchner R, Seide K, et al: Quadriceps tendon ruptures—is there a complete functional restitution? Injury 2004;35:922–926. 17. De Baer T, Geulette B, Manche E, et al: Functional results after surgical repair of the quadriceps tendon rupture. Acta Orthop Belg 2002;68:146–149. 18. Konrath G, Chen D, Lock T, et al: Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma 1998;12:273–279. 19. Vidil A, Ouaknine M, Anract P, et al: Trauma-induced tears of the quadriceps tendon: 47 cases. Rev Chir Orthop Reparatrice Appar Mot 2004;90:40–48. 20. Shah K: Outcomes in bilateral and simultaneous quadriceps tendon rupture. Orthopaedics 2003;26:797–798. 21. Basso O, Johnson D, Amis A: The anatomy of the patellar tendon. Knee Surg Sports Traumatol Arthrosc 2001;9:2–5.

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22. Lairungruang W, Kuptniratsaikul S, Itiravivong P: The remained patellar tendon strength after central on third removal: A biomechanical study. J Med Assoc Thailand 2003;86:1101–1105. 23. Kennedy JC, Willis RB: The effects of local steroid injections on tendons: A biomechanical and microscopic correlative study. Am J Sports Med 1976;4:11–21. 24. Wong M, Tang Y, Lee S, et al: Effect of dexamethasone on cultured human tenocytes and its reversibility by platelet-derived growth factor. J Bone Joint Surg Am 2003;85:1914–1920. 25. Ravelin R, Mazzocca A, Grady-Benson J, et al: Biomechanical comparison of patellar tendon repairs in a cadaver model: An evaluation of gap formation at the repair site with cyclic loading. Am J Sports Med 2002;30:469–473. 26. Larson RV, Simonian RT: Semitendinosus augmentation of acute patellar tendon repair with immediate mobilization. Am J Sports Med 1995;23:82–86. 27. Shelbourne K, Darmelio M, Klootwyk T: Patellar tendon rupture using Dall-Miles cable. Am J Knee Surg 2001;14:17–21. 28. Bhargava SP, Hynes MC, Dowell JK: Traumatic patella tendon rupture: Early mobilization following surgical repair. Injury 2004; 35:76–79. 29. Mills WJ: Reconstruction of chronic patellar tendon rupture with Achilles tendon allograft. Tech Knee Surg 2004;3:154–162. 30. Kasten P, Schewe B, Maurer F, et al: Rupture of the patellar tendon: A review of 68 cases and a retrospective study of 29 ruptures comparing two methods of augmentation. Arch Orthop Trauma Surg 2001;121:578–582. 31. Larsen E, Lund PM: Ruptures of the extensor mechanism of the knee joint: Clinical results and patellofemoral articulation. Clin Orthop 1986;213:150–153.

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Arthritis in the Athlete Stephen French and Robert Litchfield

In This Chapter Physical therapy and conditioning Glucosamine/chondroitin sulfate Nonsteroidal anti-inflammatory drugs (NSAIDs) Corticosteroid injection Viscosupplementation Bracing and orthotics Arthroscopy Realignment osteotomy Surgery—high tibial osteotomy Arthroplasty in the athlete

INTRODUCTION • An aging population that desires to remain active has resulted in increased demands on medical providers to treat arthritis in athletic individuals. • Generalized conditioning, reduction in body mass index, and strength and flexibility training have all been shown to be beneficial in improving symptoms. • Glucosamine, chondroitin sulfate, NSAIDs, viscosupplementation, and intra-articular corticosteroids all have a role in the treatment of arthritis. • Unloader bracing is used to improve the distribution of forces through the entire joint. • Realignment osteotomy can provide significant symptomatic relief by redistributing load to more normal articular cartilage while preserving the patient’s own joint.

population. Figures for the United States in the year 2000 indicate that arthritis is a public health burden second only to heart disease in disability expenses, with approximately 38 million people requiring treatment at a cost of $72 billion or 2.5% of the gross national product.1,2 The development and progression of osteoarthritic cartilage changes are influenced by genetic, physiologic, and geometric factors. An error in the DNA sequence for type II collagen that represents an amino acid substitution of one base sequence of cysteine for arginine has been shown to be present in osteoarthritic cartilage.3 There are changes in the load-bearing properties of articular cartilage with age, such as increased cellular death, proteoglycan loss, and a loss of the cartilage matrix. While these changes do occur with age, the symptoms of osteoarthritis are, fortunately, present in only half of the population older than 65 years. The development and progression of symptomatic osteoarthritis are potentiated by a change in the joint architecture. Nonanatomic joint geometry will lead to degeneration of the articular cartilage surface at an increased rate. It is common in the athletic population to have sustained an injury to a joint at an earlier time, such as a small meniscus tear or a low-grade ligament strain, changing the joint architecture slightly, which can later lead to a rapid progression of symptomatic arthritic change. Adults who have previously competed at high-level sports and those who remain active are keenly aware that sporting activities can take a toll on their bodies and lead to the “wear and tear arthritis” that is common in the “master athlete.” They must also be made aware of the tremendous benefits that can be gained from maintaining an active lifestyle, an appropriate body mass index, and good muscle tone and encouraged to continue to participate in activities that are appropriate for their abilities.

TREATMENT OPTIONS One of the goals of modern medicine is to extend the qualityof-life years of the population. Advances in this direction have resulted in a population who is living longer and more active lives. Improvements in workplace productivity, personal income, and better working conditions have also created more time for leisure activities for the population. These factors, combined with the aging “baby boomer” population, who will comprise almost 20% of the United States population aged 60 or older by the year 2020, have created a significant population of “aging athletes” (Population Division of the Department of Economic and Social Affairs of the United Nations Secretariat, 1998). Sports medicine physicians are being challenged to create a treatment strategy for arthritis in the athlete. For the purposes of this volume, we examine the occurrence and treatment of primary osteoarthritis in the adult athletic

Physical Therapy and Conditioning The physician treating symptomatic osteoarthritis has a number of interventions at his or her disposal. Patients with symptomatic osteoarthritis in a weight-bearing joint who have an elevated body mass index can expect an improvement in their symptomatology with a 10% reduction in mass. A dedicated physiotherapy regimen that focuses on improving the strength and flexibility of musculature surrounding an arthritic joint will improve objective pain scores in symptomatic arthritis. The athletic population with arthritis tend to be excellent candidates for a focused physical therapy and conditioning program as they often have participated in these type programs during their competition days. The role of preactivity stretching, maintaining muscle conditioning, and the use of rest, ice, compression, and

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elevation of the affected body part is usually well-known in the adult athlete and should always be encouraged as a first-line therapy and maintenance strategy. The opportunity for group activities such as conditioning classes with goals formed around some manner of competition, weight loss, or strength improvements can be excellent motivational tools.

Nutritional Supplements The use of nutritional supplements is now quite common in the athletic population. Athletes who are experiencing arthritic symptoms are likely to try to treat their pain with the use of nutritional supplements in addition to other modalities. Chondroitin sulfate and glucosamine sulfate are the most commonly used supplements in this role. As substances that are classified as nutritional supplements that have an intended effect of treatment of a medical condition, they have commonly become referred to as “nutriceuticals.” In both osteoarthritis and rheumatoid arthritis, patients have an increased excretion of glucosamine in the urine. As a naturally occurring substance, it stimulates glycosaminoglycan and proteoglycan synthesis, which are involved in the formation and repair of articular cartilage. Chondroitin sulfate is a glycosaminoglycan composed of units of glucosamine with attached sugar molecules. Both chondroitin sulfate and glucosamine are derived from animal sources.4 As dietary supplements, nutriceuticals such as glucosamine and chondroitin sulfate are not subjected to analysis by the U.S. Food and Drug Administration prior to sale. There exists no standardization of testing, and producers regulate the content of their product according to their own guidelines. This has created a concern that substances in this category may not be exactly represented by the labeled amounts of ingredients of the package. A recent consumer monitoring group completed a study that concluded that almost half of the glucosamine/chondroitin supplements tested did not contain the labeled amounts of ingredients.5 To date there has been only one scientific study that has shown an improvement in symptoms with glucosamine compared to placebos. In this study, 212 patients with symptomatic knee arthrosis received either 1500 mg glucosamine daily for 3 years or placebo. A digital knee radiograph study before and after treatment showed progressive joint space narrowing in the placebo group versus no significant narrowing in the glucosamine group. WOMAC (Western Ontario and McMaster University Osteoarthritis Index) knee scores were improved in the glucosamine group and worse in the placebo group.4 With the results of this single study, there is at present no compelling evidence from randomized, double-blind, controlled trials that shows a clear benefit of glucosamine or chondroitin sulfate as a medication for the treatment of painful osteoarthritis. The National Institutes of Health are currently completing what is hoped to be the definitive trial (the Glucosamine/Chondroitin Arthritis Intervention Trial [GAIT]) of these nutritional supplements. The study is designed to determine whether glucosamine, chondroitin sulfate, and/or the combination of glucosamine and chondroitin sulfate are more effective than placebo and whether the combination is more effective than glucosamine or chondroitin sulfate alone in the treatment of knee pain associated with osteoarthritis of the knee.

Nonsteroidal Anti-inflammatory Drugs Athletes may to be used to the concept of minor aches and pains associated with their sporting activity, and “playing with pain”

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is often a common scenario in the athlete with arthritic symptoms. It is also very common for athletes to have taken various analgesic remedies during their competition days and the history of analgesic use should be determined for each patient. As a treating physician of an athlete with arthritic symptoms, it is important to establish the medications that an athlete has used previously for his or her condition and to determine whether the medications have been used on an appropriate dosing schedule. Often medications are taken as an occasional pain reliever on an irregular and inappropriate dosing schedule that may not be of help to the patient and may even be harmful. Our role should be to assess the patient’s symptoms and to create an appropriate treatment plan that can realistically be followed. Pharmaceutical interventions target the painful inflammation from the joint capsule, ligaments, synovium, and subchondral bone, which are responsible for the noxious nerve stimuli and pain of arthritis. Interestingly, articular cartilage does not contain nerve tissue. The transmission of painful stimuli is mediated by prostaglandin synthesis. NSAIDs decrease the production of prostaglandins by inhibiting cyclooxygenase (COX), an enzyme that catalyses the first two steps in the production of prostaglandins from arachidonic acid. Prostaglandins are also involved in the maintenance and protection of gastric mucosa, and it is the disruption of this role that can potentiate NSAIDassociated gastrointestinal bleeding. While NSAIDs remain a mainstay of treatment for management of arthritis related pain, the incidence of NSAIDassociated gastrointestinal bleed complications has created a significant public health burden, where an estimated 33% of the money spent to treat arthritis each year is spent on treatment of NSAID-related gastrointestinal disorders.1 This recognized complication rate has created a tremendous need for the development of NSAIDs that are less harmful to the gastrointestinal tract. COX has more than one form; COX-I has a role in the physiologic maintenance of all tissues, including gastric mucosa, while COX-II is the inducible form of the enzyme involved in the conversion of arachidonic acid to prostaglandins. COXII–specific NSAIDs or COX-II inhibitors were developed to decrease prostaglandin production with less effect on the COXI homeostasis role. COX-II inhibitors have been shown to have a lower rate of gastrointestinal complications at a rate of 0.2% of patients per year of use versus 1.7% of patients per year of use of traditional NSAIDs. COX-II inhibitors as a class of drug include several different proprietary formulae, one of which is sulfonamides or celecoxib (Celebrex). As sulfur-containing compounds, there had been concerns that people with “sulfa allergies” would also have a hypersensitivity reaction to these sulfonamides. However, sulfonamide antimicrobials as a derivative of sulfanilamides are arylamines, while celecoxib is a nonarylamine as is hydrochlorothiazide and DiaBeta (glyburide). A meta-analysis of the North American trials of nonarylamine sulfanilamide COXII inhibitors showed no statistical increase in hypersensitivity reactions in sulfa-allergic patients treated with celecoxib compared to placebo. There may be, however, a cross-reactivity in patients with a confirmed allergy to nonarylamine sulfanilamide compounds such as hydrochlorothiazide and celecoxib, and thus prescribing physicians need to proceed with appropriate caution.1 Recently, concerns regarding the possibility of increased cardiovascular events such as myocardial infarction and stroke in patients taking COX-II inhibitors prompted a voluntary removal of rofecoxib (Vioxx) from the market (Merck and Co. news

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release, “Merck Announces Voluntary Worldwide Withdrawal of Vioxx,” September 30, 2004; available at: www.vioxx.com/), and the U.S. Food and Drug Administration requested a withdrawal of valdecoxib (Bextra) from the market (“FDA Announces Series of Changes to the Class of Marketed Nonsteroidal Anti-inflammatory Drugs [NSAIDs],” April 7, 2005) and a change in the labeling of all NSAIDs (other than aspirin) to reflect the possibility of cardiovascular and gastrointestinal risks. In 1999, researchers had reported that COX-II inhibitors had an inhibitory effect on prostacyclin, which, through its action on the endothelial cells lining blood vessels, maintains thrombosis homeostasis and vascular resistance. With the progression of clinical trials using COX-II inhibitor medications, the possibility of increased occurrence of myocardial and cerebrovascular thrombotic events has been postulated, yet not all COX-II inhibitors appear to have this association, and investigations of the safety of these medications are ongoing. While complete understanding of the clinical safety of all COX-II inhibitor–specific and non-COX-II inhibitor–specific NSAIDs remains to be determined, at present they remain a useful treatment for the inflammation-associated pain of arthritis in the appropriate patient.

Corticosteroid Injections Corticosteroids inhibit the production of the pain mediator prostaglandin from arachidonic acid. Intra-articular steroid injections aim to deliver a higher dose of corticosteroid directly to the site of inflammation and pain in arthritis than would be achievable with oral or intravenous delivery. In addition, highdose local delivery of corticosteroid decreases the vasodilation and permeability of inflammation and may improve the edema and pain of arthritis. Intra-articular steroid delivery has a lengthy clinical history. Recent meta-analyses reported, from the six studies reviewed, an improvement in the various outcome measures at 2 weeks in 74% of patients treated with steroid injection versus 45% of patients treated with placebo. In the three studies that included results at 16 to 24 weeks after injection, the reported improvement decreased to 33% of patients treated with steroid injection versus 16% of patients who received placebo.6,7 Injectable steroid preparations vary in their solubility, and insoluble steroid esters may have a longer duration. More insoluble steroids are appropriate for intra-articular delivery, while soft-tissue injections should use more soluble steroid preparations (such as Celestone [betamethasone]) to limit soft-tissue atrophy.4 While there is no established dose or delivery frequency for the administration of intra-articular steroid in the arthritis literature, the frequency of steroid injections should not exceed one every 3 months.8

Viscosupplementation Arthritis involves changes in the joint surface as well as the synovial fluid within the joint. Osteoarthritic joints have a lower than normal concentration of hyaluronic acid, and viscosupplementation delivers a preparation of hyaluronic acid within the joint with the goal of restoring a more normal joint fluid viscosity and improving the viscoelastic properties for proper joint mechanics. Viscosupplementation has been used in Europe for several years and received U.S. Food and Drug Administration approval in 1997. Hyaluronic acid preparations derived from rooster combs or those manufactured from bacterial cultures are available. Patients with severe hypersensitivity to poultry

products are advised to consider the manufactured preparation. The schedule of injections for viscosupplementation delivery varies by proprietary preparation. While the effect appears to be transient, viscosupplementation has been shown to restore rheologic homeostasis in the osteoarthritic joint with improved WOMAC pain and function scores by 10% to 15% at 12 months following delivery in 62% of patients.9 Many athletes may have previously received intraarticular steroid injections and thus may be quite open to the concept of a trial of viscosupplementation. It is important, however, that patients understand that viscosupplementation will work gradually, does not contain analgesic agents, and requires a full course of injections to determine its effect. The U.S. Food and Drug Administration classifies viscosupplements as a device and not a drug. Medical insurance coverage may reimburse the cost of devices and procedures that are deemed “medically necessary” as treatment for arthritis, according to the labeled uses of the “medical device” as approved by the U.S. Food and Drug Administration. At present, Medicare will provide coverage of hyaluronic acid–based products that are used to treat osteoarthritis of the knee only. Current Medicare policy requires radiographic evidence of the established diagnosis of osteoarthritis and the current approved treatment course will be paid for only if given not more than once every 6 months.

Bracing and Orthotics Symptomatic knee arthrosis is often associated with nonanatomic joint malalignment, which results in uneven load distribution of the weight-bearing axis through the knee. The malalignment may be a result of a previous cartilage injury with cartilage volume loss (such as a meniscal injury that may have been surgically repaired) or a ligament insufficiency leading to attenuation of the remaining structures and nonanatomic joint loading, or it may be due to progressive bone deformation as part of an arthritic process in addition to a primary joint malalignment such as tibia vara. Whatever the cause of nonanatomic joint loading, the concentration of load-bearing forces through one point rather than anatomic distribution of the forces will lead to degenerative joint disease progression at an increased rate. The role of orthotics and bracing in the treatment of osteoarthritis is to attempt to alter the joint architecture to better distribute the effective forces of the weight-bearing axis through the entire joint. Orthotics are intended to realign the foot and ankle to create a solid, stable platform for the rest of the body during the stance phase of weight bearing. Functional knee bracing may be helpful in patients with unicompartmental arthrosis and a malalignment that is correctable with a force that is attainable by the brace.10 Typically this may be a custommolded medial unloader brace for a correctable varus malalignment, with isolated medial compartment symptoms. Custom-molded unloader braces can also be made for valgus malalignment and used with success. Important considerations for the use of unloader bracing and orthotics are whether the implement can achieve the desired correction to relieve the symptoms and whether the patient tolerates the application of this corrective force through the contact points with the implement for the desired period of symptomatic benefit. The well-fitted functional brace will not benefit the patient if use of the brace cannot be tolerated. Discussion of the use of bracing in a protective role for ligaments and menisci is beyond the scope of this chapter, and the

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reader is directed to the position statement of the American Association of Orthopaedic Surgeons on the use of knee braces for a more complete discussion. This resource also contains recommendations for some common clinical scenarios where knee bracing has been considered.

SURGICAL INTERVENTION Arthroscopy and Arthroscopic Débridement Arthroscopic débridement is commonly considered as an intervention for treatment of symptomatic knee arthrosis in the athletic population. There are several theories as to the possible mechanism of benefit of an arthroscopy to relieve arthritic symptoms. With arthroscopy, the irrigation of the joint may remove particulate debris and dilute and remove inflammatory mediators and degenerative enzymes, and it has been postulated that pain impulses may be interrupted by chloride ions from the irrigation solution. Arthroscopic instruments can also be used for mechanical débridement to create a smoother remaining articular surface with stable borders. With intra-articular instrumentation, it is also possible to remove painful impinging osteophytes, débride degenerative meniscal tears, and remove loose bodies. It may also be that the benefit of arthroscopy is in some way a placebo effect.11 The published results of the benefit of arthroscopy have varied, with no standardization of inclusion and exclusion criteria, and no standardization of the outcome measures or the surgical technique of the intervention. This lack of standardization makes prediction of the success rate of arthroscopic débridement for symptomatic knee arthrosis difficult12; however, a nonrigorous meta-analysis indicates that approximately 60% of appropriately selected patients reported improved symptomatology at 3 years postoperatively.4 While many patients report an improvement in their symptoms, arthroscopic débridement does not stop the progression of arthrosis and the benefits predictably decrease with time. Knee arthroscopy primarily involves the use of an arthroscopic shaver to mechanically débride tissue and can be used to attempt to create a smooth cartilage surface. Attempts to use radiofrequency probes to débride irregular osteoarthritic cartilage have been successful in creating débrided surfaces that may be smoother than what is achievable with standard arthroscopic shavers. Radiofrequency energy imparts high temperature on the chondrocytes, which are very temperature sensitive, and may lead to chondrocyte cell death. For treatment of full-thickness lesions, microfracture to promote fibrocartilaginous ingrowth in the area of the lesion has been shown to have good to excellent results for focal lesions.13 Instrumentation such as a microawl is used to penetrate down through the base of the focal lesion, through the subchondral bone, into the vascularized metaphyseal bone. It is postulated that the pluripotent stem cells in the marrow are then released into the area of the focal defect where they form a fibrin clot that can reform into fibrocartilage. Continuous passive range of motion and limited weight bearing for 6 weeks postoperatively may be beneficial to the stability of the fibrocartilage “repair.” As primarily type I cartilage, fibrocartilage expectedly has less rigorous wear characteristics than type II hyaline cartilage, and attempts to encourage more extensive fibrocartilaginous ingrowth for advanced degenerative arthrosis have not been shown to be any more successful than arthroscopic débridement alone.14

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Cartilage Transplantation Focal articular cartilage defects are difficult to treat, and the surgical options for this entity have previously been relatively limited. In addition to the previously discussed microfracture technique that attempts to patch an articular defect with type I fibrocartilage, there are emerging technologies focusing on transplanting viable type II articular cartilage into these defects. “Mosaicplasty” refers to the transfer of full-thickness articular cartilage with its corresponding subchondral bone plug from a non-weight-bearing area of the knee to a corresponding bone plug hole drilled into the base of the full-thickness cartilage lesion. This procedure is technically challenging but its use is increasing. While still considered an advanced surgical principle that is not universally offered, it has shown favorable bone growth and favorable cartilaginous incorporation for focal defects.15

Realignment Osteotomy Knee arthrosis is frequently associated with malalignment. The load across the knee joint is a function of alignment; changes in the axial alignment of the femur or tibia in either the coronal or sagittal plane will influence the distribution of this load resulting in abnormal stresses on articular cartilage. The goal of realignment osteotomy for treatment of knee pain related to arthrosis is to transfer the effective weight-bearing axis from the arthritic cartilage to the more normal cartilage. While the definition of “appropriate” postoperative alignment has been studied extensively, there is no clear consensus on the desired correction angle when performing an osteotomy in the younger patient with a cartilage defect.16 In the patient with varus gonarthrosis, we prefer a weight-bearing line that intersects at a point 62% of the tibial width from the edge of the medial plateau to produce a mechanical axis of 3 to 5 degrees.17 Traditionally, varus gonarthrosis was considered the indication for a valgus-producing osteotomy. The indications for realignment osteotomy have grown to include a correction of valgus malalignment, as an adjunct to ligament reconstruction to help protect the repair and restore joint mechanics, or as an unloading procedure in the event of a significant cartilage defect18 (Table 59-1). The treatment options for an active patient with isolated cartilage lesions are relatively limited, and an osteotomy can be considered as a treatment option to help unload the involved compartment, but there are limitations to the application of this procedure. While a realignment osteotomy through the knee to transfer the load-bearing axis away from the lesion may be a viable treatment, severe degeneration in the opposite tibiofemoral compartment and a gross loss of range of motion will certainly affect the outcome of an osteotomy and may be considered a relative contraindication. A valgus osteotomy should be avoided in those who have previously undergone a

Table 59-1 Indications for Knee Osteotomy Malalignment and arthrosis

Malalignment and instability

Malalignment and arthrosis and/or instability

Malalignment and articular cartilage procedure and/or instability

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Table 59-2 Specific Indications for Individual Osteotomy Techniques

Varus 25 deg

Valgus 15 deg

Increased Tibial Slope

Decreased Tibial Slope

X

X

X X

HTO, High tibial osteotomy.

lateral meniscectomy. However, in the very young athlete with early signs of degenerative joint disease, a lateral meniscectomy should be considered only a relative contraindication, and in the case of severe varus alignment, a high tibial osteotomy to correct to a neutral alignment will preserve favorable joint mechanics (Table 59-2). Higher correction angles may require a change in the traditional fixation implants, but the principles remain the same. Limb alignment is determined by the line extending from the center of the hip to the center of the ankle, that is, the mechanical axis of the limb. This line typically passes immediately medial to the center of the knee, and, by definition, malalignment occurs when this line does not lie close to the center of the knee.19 Sagittal plane alignment should also be considered. This involves evaluation of the posterior tibial slope angle on a lateral radiograph. Tibial slope has been defined as the angle between a line perpendicular to the mid-diaphysis of the tibia and the posterior inclination of the tibial plateau. Measurements based on lateral radiographs have shown the tibial slope of the knee to average 10 ± 3 degrees.

Surgical Technique for High Tibial Osteotomy For the treatment of varus arthrosis, common in athletes, a medial opening, high tibial osteotomy is a very useful tool for correction of alignment in the coronal and sagittal planes. The procedure is carried out through a vertical skin incision, which extends 5 cm distally from the medial joint line and is centered between the anterior tubercle and the posteromedial border of the tibia (Fig. 59-1A). The gracilis and semitendinosus tendons and the superficial medial collateral ligament are preserved and retracted medially to expose the posteromedial border of the proximal tibia (Fig. 59-1B). A guide pin is inserted obliquely along a line proximal to the tibial tubercle starting approximately 4 cm below the medial joint line in the region of the transition between metaphyseal and diaphyseal cortical bone on radiographs and extending to a point 1 cm distal to the lateral joint line. Figure 59-2 illustrates the opening wedge technique, which is monitored throughout with a mobile, low-dose ionizing radiation fluoroscopy unit. The osteotomy is made below the guide pin using a small oscillating saw to breech the medial, anteromedial, and posteromedial cortices. This is followed by narrow, sharp, thin, flexible osteotomes to a point just 1 cm short of the lateral cortex. Frequent imaging helps prevent violation of the

lateral cortex and/or misdirection of the osteotome. The osteotomy is opened gradually to the desired correction angle first with distracting osteotomes to confirm the mobility of the osteotomy and then a calibrated wedge to maintain the appropriate measured distraction. The distracted osteotomy is then fixed with a four-hole Puddu plate secured with two 6.5-mm cancellous screws proximally and two 4.5-mm cortical screws distally. Bone grafting is recommended in all opening wedge osteotomies greater than 7.5 mm. Allograft cancellous bone chips and/or tricortical blocks may be used unless there is an expressed desire by the patient for autograft bone. In our practice, osteotomies less than 7.5 mm are rarely grafted. The pearls and pitfalls of a medial opening wedge osteotomy are presented in Table 59-3. Dissection of the most superior fibers of the patellar tendon insertion on the tibial tubercle improves exposure and protects the patellar tendon when completing the anterior extent of the corticotomy, which must be distal to the patellar tendon insertion. The use of a low-dose ionizing radiation fluoroscope throughout the procedure is critical to ensure all the following: proper guide-pin placement, prevention of lateral cortex violation, avoidance of misdirection of the osteotome, avoidance of intra-articular screw placement, and adequate setting of the bone graft and filling of the defect. The tip of the fibular head is a helpful reference when aiming the guide pin. The correct obliquity of the osteotomy relies on proper placement of the guide pin. For larger corrections, placement should be more horizontal. Greater obliquity increases the risk of fixation failure but, on the other hand, provides increased depth, which may be appropriate for smaller corrections. The osteotomy should always be carried out parallel to the joint line in the sagittal plane and below the guide pin to help prevent intra-articular fracture. The use of thick, traditional-type osteotomes can apply a greater distraction moment when completing the osteotomy and carries an inherent risk of creating an extra- and/or intra-articular fracture. This is considerably minimized with thin, flexible osteotomes (Fig. 59-3). However, these should be advanced with frequent fluoroscopy checks to avoid misdirection. To avoid altering the posterior tibial slope, the distraction of the osteotomy anteriorly (at the tibial tubercle) should be approximately one half its distraction posteromedially. This is facilitated by using trapezoidal distraction block Puddu plates rather than the traditional rectangular version. The plate should be positioned as far posterior as possible along the medial cortex

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Medial joint line

Posteromedial border of tibia

Tibial tubercle

Posteromedial border of tibia Pes anserinus

B

A

Figure 59-1 The surgical approach to medial opening wedge high tibial osteotomy. A, The skin incision is centered between the posteromedial border of the tibia and the tibial tubercle and extends distally from the medial joint line. B, The posteromedial border of the tibia is exposed with a blunt retractor placed deep to the superficial medial collateral ligament. The pes anserinus is left intact.

A

B

D

C

E

Figure 59-2 The use of intraoperative fluoroscopy during medial opening wedge high tibial osteotomy. A, The guide pin is directed toward the tip of the fibular head and from a point 4 cm distal to the medial joint line. Placement should be optimal before proceeding. B, The osteotomy is made below the guide pin. C, The osteotomy is gradually opened to the desired width using a calibrated wedge. D, Fixation is achieved with a four-hole Puddu plate. Care is taken to avoid intra-articular or intraosteotomy screw placement. E, Here the defect has been filled with tricortical bone graft.

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Table 59-3 Pearls and Pitfalls of Corrective Osteotomy Pearls

Pitfalls

All osteotomies

Adequate exposure Use of intraoperative fluoroscopy and guide pins Accurate preoperative planning and radiographic evaluation

Violation of opposite cortex Making asymmetrical bone cuts in sagittal plane Opening the osteotomy before the anterior and posterior cortices are osteotomized

High tibial lateral closing

Make osteotomy 2 cm distal to lateral joint line Complete posterior cortical resection in piecemeal fashion with Kerrison rongeurs

Decreasing tibial slope inadvertently

High tibial medial opening

Use oscillating saw to breach cortex only Make osteotomy below the guidepin Pay particular attention when securing osteotomy plate

Suboptimal guidepin positioning Neglecting the posterior tibial slope when making the osteotomy

to ensure that the distraction is maximized posteromedially and minimized anteriorly. Careful attention to this detail will help decrease the risk of increasing tibial slope on distraction of the osteotomy. Tension of the medial collateral ligament should be assessed during distraction and lengthening by fenestration of the medial collateral ligament may assist in achieving larger corrections. Finally, strict attention to detail is necessary to avoid intraarticular or intraosteotomy screw penetration during fixation of the plate and to ensure that the defect is completely obliterated with bone graft or a substitute; frequent rechecks with fluoroscopy are beneficial.

Figure 59-3 Thin flexible osteotomes used to complete the osteotomy. The osteotomy can then subsequently be opened with distracting osteotomes to the desired correction. This applies less distraction moment on the initial bone cut and thus decreases the chance of intra-articular fracture.

Rehabilitation Following an Osteotomy The rehabilitation schedule is presented in Table 59-4. Early postoperative knee range-of-motion exercises benefit joint healing and articular cartilage nourishment as well as lower limb neuromuscular function. In addition, the return to normal weight bearing is essential for healthy bone turnover and healing. Postoperative physical therapy programs should focus on these components while respecting the desired outcomes of the realignment procedure, which include union and restoring and maintaining alignment. Restoring full range of motion is an important factor in the long-term success of the surgical procedure, and we encourage range-of-motion exercises to begin as soon as possible. Full extension should be achieved by postoperative week 6. If progress is behind schedule, active exercises with slight volitional overpressure are recommended. The weight-bearing progression will depend on the nature of the osteotomy and any other cartilage restoration procedure performed. After an opening wedge osteotomy, patients are restricted to touch weight bearing, equivalent to 25 to 40 pounds, for the first 6 weeks. If any osteocartilaginous procedure has been performed in combination, the opening wedge protocol takes preference. Following closing wedge osteotomy, we allow protected weight bearing for the first 6 weeks. If a cartilage restoration procedure has been performed also, a partial weight-bearing protocol should take preference. From the 6-week mark, the progression of weight bearing is dependent on the appearance of the radiograph at this stage. It would be anticipated that any closing wedge osteotomy could progress to weight bearing as tolerated at this point, with the use of a cane or a single crutch, if consolidation and progression to union are occurring. An opening wedge osteotomy should progress to partial weight bearing for 3 weeks and then to protected weight bearing for 3 weeks if consolidation is evident on the radiograph, and there is no evidence of hardware loosening or change in position. Neuromuscular programs aimed at the maintenance of surrounding joint strength and muscle function, as well as pain management modalities, should be employed during the initial postoperative 6 weeks. During weeks 6 to 12, a more functional program can be instituted, while methods to improve muscular endurance can be instituted after postoperative week 12. Gait retraining and returning to a fully functional state should be additional goals throughout the rehabilitation process. More directed therapy to correct additional functional impairments should also take place after week 12.

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Table 59-4 Postoperative Rehabilitation Guidelines Timeline

Exercise

0–3 wk

Passive range of motion using slider board Pedal rocking on bicycle Isometric quadriceps setting

3–6 wk

Full-circle pedaling on bicycle, very light resistance Active range of motion Side-lying gluteus medius strengthening Hip abduction/adduction, flexion, and extension with resistance fixed above knee, e.g., pulley or resistance tubing Pool exercises, hip abduction/adduction, flexion, and extension; knee flexion and extension Gait pattern training with crutches focusing on proper heel strike/toe off Pool, deep water running or cycling Leg press or squat with weight off-loaded to 24–40 pounds (watch range-of-motion restriction associated with any cartilage/meniscus restoration/repair)

6–9 wk

Pool, shallow water walking as weight-bearing restrictions allow As a general guideline, when 60% of body is submerged, 60% of body weight is off-loaded Standing/seated calf raise Bilateral wobble board balancing as weight-bearing status allows Knee flexion/extension with very light resistance

Upon full weight bearing

Gait training to restore normal gait Step up and step down to work on alignment and eccentric control Elliptical trainer and bicycle for cardiovascular conditioning

Complications of an Osteotomy The list of possible intraoperative, early postoperative, and late postoperative complications following any realignment procedure around the knee is exhaustive. The early complications of upper tibial osteotomy are those of any surgical operation on the lower extremity including compartment syndrome, infection, neurovascular injury, deep vein thrombosis, and pulmonary embolus. These, as well as some that require specific mention, should be included in any list of complications of osteotomy around the knee, namely, delayed or nonunion. The frequency of thromboembolic disease is lower following osteotomy than total knee arthroplasty, and the proper method of prophylaxis is controversial. We currently do not use chemical prophylaxis in patients undergoing knee osteotomy. Mobilization is encouraged on postoperative day 1. Patients with specific risk factors for deep venous thromboembolism or pulmonary embolism are anticoagulated with low molecular weight heparin given subcutaneously for the perioperative period and undergo lower limb venous studies prior to discharge from the hospital. Patients with a history of deep vein thromboembolism or pulmonary embolism are anticoagulated for 6 weeks with Coumadin. The avoidance of intraoperative complications of any osteotomy is especially important with osteotomy around the knee. Intra-articular fracture, intra-articular screw placement, and violation of the opposite cortex with resultant instability of the osteotomy are all avoidable and will all have a significant outcome on the osteotomy. Prevention of these complications by continuous fluoroscopy use is the best form of management; otherwise, early recognition and immediate management are suggested. Intra-articular fracture should be assessed intraoperatively with fluoroscopy and a decision made whether interfragmentary screw stabilization is required. A fracture detected postoperatively may require internal fixation with or without revision of the osteotomy or a simple modification of the postoperative

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rehabilitation protocol with immobilization and non-weight bearing for a period and radiographic monitoring of the fracture. Violation of the opposite cortex in an opening wedge osteotomy of the tibia usually does not require any additional treatment. Under- and overcorrection is a significant concern in tibial realignment osteotomies. Numerous authors have discussed overcorrection into valgus.20,21 Because, cosmetically, producing a valgus deformity is less well tolerated than producing varus alignment, it is best to err on the side of “avoiding excessive valgus.” Critical assessment of the alignment both intraoperatively and in the early postoperative period should take place, and if “overcorrection” or “excessive” varus or valgus correction has occurred, the osteotomy should be revised, as the primary surgical goals have not been attained. Realignment osteotomy about the knee is a very useful tool for the treatment of arthrosis with the benefits of a capacity for correction in multiple planes, the capacity to restore anatomy to a more favorable alignment, and the benefit of maintaining the integrity of the patient’s own joint with the goal of a high level of function (Fig. 59-4).

Arthroplasty in the Athlete Joint arthroplasty has provided a tremendous tool for the relief of arthritis sufferers and is one of the most cost-effective medical interventions available to restore functional lives.22 The goal of arthroplasty is to alleviate pain first and to maintain function. Improvement in function is not the specific intended goal. This is especially true of total knee arthroplasty. With respect to active athletes who are severely affected by arthritis pain, it is most important that this type of patient understand that a unicondylar or a total knee arthroplasty is intended for pain relief, and a modification of activities to avoid high-impact and loading activities would be advised to prolong the life span of the implant. Because the technical challenges of early revision surgery and the morbidity associated with early implant failure are so sig-

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Figure 59-4 A 31-year-old man with isolated medial compartment articular cartilage disease, varus malalignment, and intact anterior and posterior cruciate ligaments. A, The anteroposterior view shows the weight-bearing line (WBL) through the center of the medial compartment and the predicted correction angle. B, Postoperatively, the mechanical axis of the limb is normalized.

WBL

A nificant (autolysis, bone loss, nerve and blood vessel compromise), active and athletic patients who are considering knee arthroplasty are best served by a full understanding of the lim-

B itations of the procedure. In some cases, the procedure must be delayed until the patient reaches the point at which his or her activity level is appropriate for the limitations of the implant.

REFERENCES 1. Laine L: COX-2 selective drugs: Improving safety. Clin Dilemmas 2001;3–6. 2. Reuben S: Orthopaedic applications of COX-2 inhibitors. Orthop Today 2001;5–6. 3. Hochberg M, Brandt K: Guidelines for the medical management of DJD of the hip and knee. J R Coll Physicians Lond 1993;27:391–397. 4. Bert JM, Gasser SI: Approach to the osteoarthritic knee in the aging athlete: Debridement to osteotomy. Instructional course 306. Arthroscopy 2002;18:9107–9110. 5. American Academy of Orthopedic Surgeons: AAOS Research Committee fact sheet: Osteoarthritis, June 2001. 6. Godwin M, Dawes M: Intra-articular steroid injections for painful knees: Systematic review with meta-analysis. Can Fam Physician 2004;50:241–248. 7. Arroll B, Goodyear-Smith F: Corticosteroid injections for osteoarthritis of the knee: Meta-analysis. BMJ 2004;328:869–870. 8. Gaffney K, Ledingham J, Perry JD: Intra-articular triamcinolone hexacetonide in knee osteoarthritis: Factors influencing the clinical response. Ann Rheum Dis 1995;54:379–381. 9. Marshall KW: Intra-articular therapy in knee osteoarthritis: The role of viscosupplementation. Am J Orthop 2001;23–27. 10. Kirkley A, Webster-Bgaert S, Litchfield R, et al: The effects of bracing on varus gonarthrosis. J Bone Joint Surg Am 1999;81:539–548. 11. Moseley JB, O’Malley K, Petersen NJ, et al: A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med 2002;347:81–88. 12. Wai EK, Kreder HJ, Williams JI: Arthroscopic debridement of the knee for osteoarthritis in patients fifty years of age and older. J Bone Joint Surg Am 2002;84:17–22.

13. Miller BS, Steadman JR, Briggs KK, et al: Patient satisfaction and outcome after microfracture of the degenerative knee. J Knee Surg 2004;17:13–17. 14. Bert JM: Role of abrasion arthroplasty and debridement in the management of osteoarthritis of the knee. Rheum Dis Clin North Am 1993;19:725–739. 15. Barber FA, Chow JC: Arthroscopic osteochondral transplantation: Histologic results. Arthroscopy 2001;17:832–835. 16. Coventry MB, Ilstrup DM, Wallrich SL: Proximal tibial osteotomy: A critical long-term study of 87 cases. J Bone Joint Surg Am 1993;75: 196–201. 17. Dugdale TW, Noyes FR, Styer D: Pre-operative planning for high tibial osteotomy. Clin Orthop 1992;274:248–264. 18. Giffin JR, Vogrin TM, Zantop T, et al: Effects of increasing tibial slope on the biomechanics of the knee. Am J Sports Med 2004;32:376–382. 19. Paley D, Herzenberg JE, Tetsworth K, et al: Deformity planning for frontal and sagittal plane corrective osteotomies. Orthop Clin N Am 1994;25:425–465. 20. Insall JN, Joseph DM, Msika C: High tibial osteotomy for varus gonarthrosis. A long-term follow-up study. J Bone Joint Surg Am 1984;66:1040–1048. 21. Yasuda K, Majima T, Tsuchida T, Kaneda K: A ten- to 15-year followup observation of high tibial osteotomy in medial compartment osteoarthrosis. Clin Orthop 1992;186–195. 22. Hawker GA, Wright JG, Coyte PC, et al: Differences between men and women in the rate of use of hip and knee arthroplasty. N Engl J Med 2000;342:1016–1022.

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Overuse Injuries Stephen F. Brockmeier and John J. Klimkiewicz

In This Chapter Patellar tendinosis Quadriceps tendinosis Iliotibial band friction syndrome Popliteus tendonitis Semimembranosus tendonitis Prepatellar bursitis Pes anserine bursitis Infrapatellar fat pad syndrome

INTRODUCTION • Overuse injuries of the knee are a common clinical entity encountered by primary care physicians, general orthopedists, physical medicine and rehabilitation physicians, and sports medicine specialists. • Among the many diagnoses that fit in this category are tendonitis/tendinosis, bursitis, and other chronic and/or degenerative processes that result from repetitive trauma and overuse. • While overuse syndromes occur elsewhere, the knee is the most commonly affected joint. The overall prevalence of these disorders is unknown. In some populations, such as distance runners, the incidence has been estimated to be as high as 30% each year.1 • Management of these disorders can be problematic due to a considerable rate of chronicity and the disability that can be encountered in active patients.

The etiology of overuse injuries can often be attributed to both intrinsic and extrinsic factors. Intrinsic causes can include limb malalignment, leg length discrepancy, muscle/tendon tightness or imbalance, foot abnormalities, and concomitant pathology or injuries about the knee such as meniscal or ligamentous injuries. Extrinsic factors are thought to play a large role in the development of many overuse injuries. The concept of Leadbetter’s “Rule of Toos” in which athletes train too hard, too often, and return to sport too soon and too much after an injury often applies.1 A recent change in the rate, duration, or intensity of activity frequently precedes the development of one of these disorders. Specific activities and training errors are often associated with specific conditions. Overuse injuries are chronic syndromes, initiated by cyclic mechanical trauma. Repetitive trauma to the involved area leads

to an initial injury. The body’s physiologic response to this often subclinical injury includes inflammation about the injured tendon and eventually weakness or dysfunction of the involved muscle(s). A premature return to full activity prior to complete healing can lead to further tissue damage and ultimately chronic degeneration. Many of these syndromes have historically been referred to as tendonitis due to a proposed inflammatory nature of disease. Pathologic and histologic investigation has challenged this terminology. Microscopic evaluation of the diseased tissue has revealed changes consistent with a chronic, degenerative process. Mucoid degeneration or angiofibroblastic hyperplasia is often noted, with a remarkable lack of inflammatory cells.2,3 For this reason, tendonopathy or tendinosis have become the more accurate terminology. The management of these disorders often begins with a period of rest or a decrease in the frequency or intensity of activity. Conservative management, consisting of rest, ice, oral anti-inflammatories, and physical therapy aimed at stretching and strengthening of involved muscle groups, is often successful. Corticosteroid injections may have a role in some of these disorders. Surgical intervention can be indicated in recalcitrant cases after a failed period of nonsurgical management. This chapter addresses some of the more commonly encountered overuse injuries about the knee, including patellar tendinosis, quadriceps tendinosis, iliotibial band friction syndrome, popliteus tendonitis, semimembranosus tendonitis, prepatellar bursitis, pes anserine bursitis, and infrapatellar fat pad syndrome.

PATELLAR TENDINOSIS Also called “jumper’s knee,” patellar tendinosis is a common cause of anterior knee pain in athletes that participate in jumping sports or activities with repetitive knee extension, such as basketball, volleyball, and soccer. The term jumper’s knee was coined by Blazina et al4 in 1973, referring to both patellar and quadriceps tendonopathy. Today, however, the term is usually reserved for only patellar tendinosis. Repetitive eccentric contraction of the extensor that occurs with landing on one leg or kicking is thought to lead to mechanical overload in affected patients.4 This disorder is seen most commonly in adolescents and young adults; symptoms sometimes commence during the adolescent growth spurt as the tendon does not lengthen as fast as the adjacent bone. Multiple predisposing factors have been reported. These include abnormal patellofemoral tracking, patella alta, chondromalacia patella, leg length discrepancy, limb malalignment, and Osgood-Schlatter disease. Patellar tendinosis can occasionally be confused with Sindig-Larsen-Johansson

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disease, which is a traction apophysitis of the distal pole of the patella. This disorder presents in a younger age group. The most frequently affected area is the deep fibers at the tendon’s insertion on the inferior pole of the patella; involvement of the distal tendon at the tibial tubercle is less frequent (one sixth as often).5 Biomechanical evidence suggests that the process likely results from heavy cyclic loading causing a traction injury to the deep fibers of the patellar tendon at its proximal insertion. Others have postulated that repeated impingement of the inferior pole of the patella on the patellar tendon during flexion is causative.6 Pathologically, the process is initiated by microscopic damage to the tendon fibers, leading to an initial inflammatory response and increased vascularity. These physiologic attempts at healing are impeded by repetitive injury. Pathologic changes noted on biopsy include fibroblast proliferation, neovascularization, mucoid degeneration, lipomatosis, and calcification of the tendon, with an absence of inflammatory cells.3,7 Patients typically present with the insidious onset of anterior knee pain and soreness localized to the inferior pole of the patella. Depending on the chronicity of the process, they may report pain after activity, during sports, or a continuous dull ache within the tendon. Ultimately, the pain interferes with the ability to compete and can be present at night, disturbing sleep. Blazina et al4 classified patellar tendonopathy based on the patient’s symptoms. Stage I is characterized by pain experienced after activity. In stage II, pain is present at the beginning of activity, only to disappear and return near the end of activity with muscle fatigue. Stage III is characterized by constant pain both with activity and at rest. Stage IV (added later by Martens et al5) is frank tendon rupture. On examination, the most reproducible finding is point tenderness with palpation of the tendon at the inferior pole of the patella. The tenderness is maximal with the knee in full extension and diminishes with flexion as the tendon is placed under tension. Resisted knee extension and squatting can also be painful. Weakness, tightness, or atrophy of the quadriceps can also be noted. While patellar tendinosis is a clinical diagnosis, imaging can be confirmatory. Plain radiographs are typically normal; however, occasionally one can note abnormalities such as calcification within the proximal tendon. Magnetic resonance imaging (MRI) and ultrasonography are the most useful modalities. MRI evaluation will often reveal an area of increased signal within the deep substance of the tendon, distal to the inferior pole of the patella (Fig. 60-1). The tendon may appear amorphous and often will be increased in thickness.6,8 Ultrasonography can reveal the lesion as a focal area of decreased echogenicity as well as tendon enlargement. Some authors have reported abnormal tendons seen on MRI or ultrasonography in asymptomatic patients.3 Initial management of patellar tendonopathy is conservative. A treatment approach that includes a decrease or cessation of the inciting activity, ice, nonsteroidal anti-inflammatory drugs, and physician-directed physical therapy has been shown to be successful in more than 90% of patients. Most reports are retrospective and review variable populations. However, reported outcomes are consistent, with most patients reporting symptomfree resumption of sports within 6 months. Poorer response is seen in those with concomitant pathology or Blazina stage III disease.9 Rehabilitation should initially focus on quadriceps stretching as well as the correction of any predisposing factors. Isometric exercises to strengthen the quadriceps can be initiated

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Figure 60-1 Magnetic resonance imaging (MRI) of patellar tendinosis. Characteristic MRI findings include increased signal within the deep tendon at the inferior pole of the patella and generalized tendon thickening.

early, but isotonic and isokinetic exercises should be delayed until the patient’s symptoms subside. A gradual advancement to an eccentric quadriceps strengthening program is critical for a successful outcome.1,3,9–11 Accumulating basic science evidence has pointed to a detrimental effect of corticosteroids on tendon tissue. Some authors do advocate corticosteroid injection in more severely affected patients. Complications of injection include resultant tendon rupture and subcutaneous atrophy/skin changes. We do not recommend corticosteroid injection for patellar tendinosis. Operative intervention is generally reserved for recalcitrant patients who have not improved after 3 to 6 months of appropriate conservative management. A number of surgical procedures have been described. The recovery and rehabilitation after operative treatment can be prolonged, frequently lasting 6 to 12 months. While the majority of patients have been reported to have successful results with respect to resolution of pain, the percentage of those who return to their previous level of competition is significantly less after operative treatment.9,12–14 The described surgical techniques involve incision of the proximal tendon with the excision of the degenerative tissue. Often, the inferior pole of the patella is débrided, drilled, or freshened.5,9 The remaining healthy tendon can be imbricated and the paratenon closed. For larger lesions, some authors have advocated a wide excision with reattachment of the tendon using heavy suture. Recently, arthroscopic techniques have been described for this population of patients.12,15 After a diagnostic arthroscopy is performed to examine the intra-articular portion of the patellar tendon and evaluate for concurrent intra-articular pathology, the pathologic tissue and overlying fat pad can be débrided from within the joint using a shaver. A recently published report found arthroscopic tenotomy to be equivalent to open tenotomy with respect to the resolution of symptoms and return to athletics.12

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QUADRICEPS TENDINOSIS Tendonopathy of the quadriceps is much less common than patellar tendonopathy.4 The superior mechanical strength of the quadriceps combined with its improved vascularity provides reasonable protection from significant injury in most patients. However, a similar cascade of microinjury leading to chronic, degenerative tendinosis can occur in some active individuals. The involved portion is commonly at the quadriceps insertion on the superior pole of the patella. Predisposing risk factors can include extensor mechanism malalignment, increased frequency and intensity of activity, and hard playing surfaces.7,10 Most affected patients report less limitation of athletic participation than those with patellar tendonopathy. However, long-standing symptoms can eventually curb performance. In some cases, chronic tendonopathy can lead to partial or frank rupture.7 Patients with quadriceps tendonopathy present with the insidious onset of pain and tenderness at the proximal pole of the patella. A recent increase in running, jumping, kicking, or climbing may be reported. Examination reveals point tenderness over the superior pole of the patella and pain with resisted extension. Attention should be given to the rotational alignment of the limb and to extensor mechanism tracking. As with patellar tendinosis, imaging can be confirmatory with similar findings often seen on MRI or ultrasonography. Nonoperative management of quadriceps tendinosis is almost universally successful. Activity modification, nonsteroidal antiinflammatory drugs, and physical therapy focusing on hamstring flexibility and quadriceps strengthening are generally effective in most patients. Strengthening exercises should build up to eccentric muscle training in order to fortify the tendon to withstand higher stresses. By 3 months, most patients have full resolution and are able to resume activities. Operative intervention is again only indicated after failure of a 3- to 6-month period of conservative treatment. Surgery consists of excision of the diseased tendon and drilling or débridement of the proximal pole of the patella to stimulate healing.10 In the setting of a partial tendon rupture, operative repair is indicated if greater than 50% of the tendon is compromised.

ILIOTIBIAL BAND FRICTION SYNDROME Also called “lateral runner’s knee,” iliotibial band (ITB) friction syndrome is the most common cause of lateral-side knee pain in long-distance runners. Also seen in cyclists, weight lifters, football and soccer players, and cross-country skiers, ITB friction syndrome is an overuse disorder caused by excessive friction between the ITB and the lateral femoral epicondyle.16 Friction is maximal at 30 degrees of knee flexion, which is the position of greatest discomfort. This disorder was described by Renne17 in 1975 in a cohort of marine recruits. He postulated that repeated flexion and extension of the knee during training caused the ITB to rub back and forth over the lateral epicondyle causing direct irritation of the band or periosteum and inflammation of the interposed bursa (Fig. 60-2). The overall incidence has been reported to range from 1.6% to as high as 52% in certain populations.17–19 It is very common in long-distance runners, especially those who run downhill. A number of intrinsic and extrinsic factors have been reported. Prominent lateral femoral epicondyle, genu varum, tightness of the ITB, limb length discrepancy, hindfoot varus, and foot prona-

Figure 60-2 Area of pain and tenderness in iliotibial band friction syndrome. (From Safran MR, Fu FH: Uncommon causes of knee pain in the athlete. Orthop Clin North Am 1995;26:547–559.)

tion have all been implicated. An increase in the distance or frequency of running, a change in training surface, or an increase in downhill training can contribute. When running downhill, the angle of knee flexion at foot strike is decreased. This leads to increased contact between the epicondyle and the ITB. The pathogenesis is often a combination of extrinsic training factors in susceptible individuals. Patients present clinically with lateral-side knee pain that usually begins during a long run. Pain is generally not present at rest but returns with resumption of the offending activity. The pain is often progressive, worsening to the point that the patient has to cease running. Discomfort is often increased with downhill running, and frequently patients can participate in other activities without symptoms. Physical examination findings include point tenderness over the lateral femoral epicondyle, approximately 3 cm proximal to the joint line. Provocative testing using the “creak” test can be helpful. The patient stands with full weight on the affected extremity. A positive test is noted when the patient experiences a stinging pain over the epicondyle at 30 degrees of knee flexion.17 Noble’s test can be confirmatory (Fig. 60-3). It is performed with the patient supine and the affected knee in 90 degrees of flexion. While applying pressure over the lateral femoral epicondyle, the knee is extended and pain is elicited at approximately 30 degrees of flexion.17 Ober’s test is helpful to gauge ITB tightness (Fig. 60-4). The patient is placed in the lateral decubitus position with the affected extremity upward. The uninvolved hip and knee are flexed to correct lumbar lordosis. The affected knee is flexed to 90 degrees and the hip is gently hyperextended and abducted to catch the proximal ITB on the greater trochanter. Tightness in the ITB will prevent the affected limb from adduction below the horizontal created by the patient’s torso.16,18 Imaging is usually not necessary unless other diagnoses are being ruled out. Radiographs are negative in ITB friction syndrome. MRI can be useful to differentiate ITB friction syndrome

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Figure 60-3 Noble’s test for iliotibial band friction syndrome. With the patient supine and the affected knee flexed, the examiner applies pressure over the lateral femoral epicondyle. The knee is extended and pain is elicited at about 30 degrees of flexion. (From Safran MR, Fu FH: Uncommon causes of knee pain in the athlete. Orthop Clin North Am 1995;26: 547–559.)

Figure 60-4 Ober’s test for iliotibial band (ITB) tightness. With the patient in the lateral decubitus position, the uninvolved hip and knee are flexed to correct lumbar lordosis. The affected knee is flexed to 90 degrees, and the hip is gently hyperextended and abducted to catch the proximal ITB on the greater trochanter. Tightness in the ITB will prevent the affected limb from adduction below the horizontal created by the patient’s torso. (From Safran MR, Fu FH: Uncommon causes of knee pain in the athlete. Orthop Clin North Am 1995;26:547–559.)

from other intra-articular pathology. MRI findings in ITB friction syndrome can include focal thickening of the ITB and/or fluid between the ITB and the lateral condyle. Treatment of this disorder is usually conservative. Principles include modification of activity, control of inflammation, and correction of the contributing factors. Training modification includes a period of rest and the cessation of downhill running. Ice, nonsteroidal anti-inflammatory drugs, and phonophoresis can assist with controlling local inflammation. Local corticosteroid injection into the bursa can be helpful to reduce pain and inflammation in the acute phase.20 Shoe modifications or orthotics can help correct foot pronation. Therapy should focus on entire limb kinetics. ITB stretching is essential as well as stretching and strengthening the tensor fascia latae, hip abductors, and hamstrings.16

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Surgical intervention may be warranted in the atypical situation in which a patient fails an appropriate course of conservative treatment. In these recalcitrant patients, surgical release, as described by Noble,19 of the posterior ITB with excision of a 2-cm triangular portion at the level of the lateral epicondyle has been effective. A number of small series have been reported using variations of this technique with satisfactory outcomes.16,18

POPLITEUS TENDONITIS The popliteus travels from its origin on the lateral femoral condyle (tendinous portion) posterolaterally through the popliteal hiatus of the lateral meniscus (intra-articular portion) to form a broad, muscular insertion on the posterior proximal tibia. It functions to derotate the knee joint at the initiation of

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with palpation of the anterior medial tendon of the semimembranosus distal to the joint line and is accentuated with knee flexion and external rotation. The differential diagnosis includes pes anserine bursitis and medial meniscal tear. Treatment is almost always conservative with rest, activity modification, nonsteroidal anti-inflammatory drugs, and physical therapy focusing on hamstring stretching. In the rare refractory patient, surgical exploration, débridement, and drilling of the semimembranosus insertion has been successful.21

PREPATELLAR BURSITIS

Figure 60-5 Evaluation of popliteus tendonitis by palpation in the figurefour position. (From Safran MR, Fu FH: Uncommon causes of knee pain in the athlete. Orthop Clin North Am 1995;26:547–559.)

flexion and aids the posterior cruciate ligament in preventing posterior displacement of the tibia on the femur. Injuries to this structure can occur acutely (with concomitant disruption of the anterior cruciate ligament, posterior cruciate ligament, or the posterolateral corner stabilizers) or chronically with overuse. Overuse injury to the popliteus, called popliteus tendonitis, is not uncommon in active individuals, especially in downhill runners or walkers (backpackers). Hyperpronation of the foot on the affected side due to running on banked terrain has been reported to be associated. Pronation leads to external rotation of the tibia and places chronic stress on the popliteus tendon.16,21 Patients usually complain of the insidious onset of lateral or posterior knee pain. There is usually no history of inciting trauma. Findings on examination include tenderness to palpation over the popliteus tendon at its origin on the lateral femoral condyle. This is best appreciated with the leg in the figure-four position21 (Fig. 60-5). Pain with resisted external rotation can also be noted. The differential diagnosis includes ITB friction syndrome, lateral meniscal tear, and biceps femoris tendonitis. As the ITB and biceps femoris act to resist internal rotation and the popliteus prevents external rotation, pain with external rotation can aid in differentiating these entities. Treatment of popliteus tendonitis includes rest and modification of training techniques in the form of eliminating downhill activities. Ice, ultrasound therapy, iontophoresis, nonsteroidal anti-inflammatory drugs, and physical therapy aimed at stretching can be helpful as well.16 If the patient hyperpronates, orthotics may be beneficial. Symptoms usually resolve over 1 to 2 weeks, and a gradual return to running may be initiated. Uphill running and/or changing sides of the road during runs may help to prevent recurrence.

SEMIMEMBRANOSUS TENDONITIS Semimembranosus tendonitis is an often neglected cause of medial-side knee pain. It occurs in endurance athletes as the result of repetitive loading and unloading and is often associated with other pathologic disorders of overuse. It can result from compensation for other knee problems in the nonathlete.21 Patients present with pain posteromedially just below the joint line that is noted during or after activity. Tenderness is elicited

The prepatellar bursa is a potential space of synovial tissue that functions to decrease the friction between the subcutaneous tissue and the patella. Inflammation of this synovial sac can result from direct trauma, chronic activity or overuse, systemic disease (e.g., gout), or infection. It is most commonly encountered in wrestlers and in those with occupations that require frequent kneeling.22,23 The incidence in wrestlers has been reported to be 9%.22 The proposed mechanism involves repetitive trauma to the bursa leading to aseptic inflammation and chronic anterior knee swelling. Patients present clinically with swelling located superficial to the patella. Knee range of motion is usually painless except at the extremes of flexion (depending on the size of the collection). There is no associated effusion. Thickening and crepitation of the tissue can be seen in more chronic cases. Warmth, erythema, pain, and systemic symptoms signify septic bursitis. This must be confirmed by aspiration, as not all infected bursae are clinically demonstrable. A polymorphonuclear cell count of greater than 75% is the most accurate finding on synovial fluid analysis. Total white blood cell count and glucose levels are less specific.23 Fluid should also be sent for Gram stain, culture, and crystalline analysis. The most common infecting organisms are Staphylococcus aureus and Streptococcus species.23 Following aspiration, treatment of aseptic prepatellar bursitis involves activity modification, compressive wrapping, and antiinflammatory medications. Recurrence is common. Aspiration in combination with immobilization can be helpful in these situations. Surgical excision of the bursa is indicated in multiply recurrent or chronic cases. Septic bursitis is best rectified by surgical excision followed by a period of postoperative antibiotics. Both open and endoscopic techniques for excision have been described.23 Whether treated conservatively or operatively, return to sports or work should be allowed once the inflammation has subsided, and the patient has regained normal strength and range of motion in the involved extremity.

PES ANSERINE BURSITIS The pes anserine bursa is the synovial tissue overlying the attachment of the sartorius, gracilis, and semitendinosus tendons at the pes anserinus (goose foot). It is located approximately 5 to 6 cm below the anteromedial joint line. Inflammation of this bursa (or less commonly the neighboring Voshel’s bursa, which is located just proximal to the pes anserine bursa, deep to the superficial medial collateral ligament) is a potential cause of medial knee pain in runners and athletes who participate in pivoting sports.21 Pes anserine bursitis can be incited by overuse or by direct trauma. Pes tendonitis, while less common, can be superimposed. Patients will present with pain, tenderness, and swelling

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over the pes bursa. In addition, resisted active knee flexion may be painful. This entity must be distinguished from other sources of medial-side pain, including medial meniscal pathology, saphenous nerve entrapment, proximal tibial stress fracture, and degenerative arthritis of the medial compartment. The treatment is conservative with activity modification, ice, moist heat, anti-inflammatory drugs, and physical therapy focusing on hamstring stretching and strengthening modalities. Recalcitrant cases often respond to corticosteroid injections.23 A premature return to activity can lead to recurrence. Surgical excision is rarely indicated.21

INFRAPATELLAR FAT PAD SYNDROME Infrapatellar fat pad syndrome is a disorder associated with anterior knee pain secondary to hypertrophy and inflammation of the infrapatellar fat pad. Also known as Hoffa’s disease, this syndrome is relatively rare. The cause is not fully known, but some have postulated that trauma of the infrapatellar fat

pad occurs in those who participate in activities that entail repetitive maximal extension of the knee. With extension or hyperextension, the fat pad is pinched between the distal femur and the tibial spine leading to injury, hypertrophy, and inflammation.21 Patients present with pain below the inferior pole of the patella, which is exacerbated with activity or knee extension. On examination, tenderness with palpation of the fat pad, deep to the patellar tendon, can be noted. Swelling or an effusion can be present. The bounce test involves passive hyperextension of the knee, which reproduces the patient’s pain.21 Hoffa’s disease is a diagnosis of exclusion. Reduction of symptoms with an injection of Xylocaine into the fat pad can be helpful in confirming the diagnosis.21 In most instances, patients respond to a conservative regimen consisting of rest, ice, and anti-inflammatory drugs. Activity modification with the prevention of hyperextension is effective. In recalcitrant patients, arthroscopic resection of the fat pad may be indicated.21

REFERENCES 1. James SL: Running injuries to the knee. J Am Acad Orthop Surg 1995;3:309–318. 2. Almekinders LC: Tendinitis and other chronic tendinopathies. J Am Acad Orthop Surg 1998;6:157–164. 3. Warden SJ, Brukner P: Patellar tendinopathy. Clin Sports Med 2003; 22:743–759. 4. Blazina ME, Kerlan RK, Jobe FW, et al: Jumper’s knee. Orthop Clin North Am 1973;4:665–678. 5. Martens M, Wouters P, Burssens A, et al: Patellar tendinitis: Pathology and results of treatment. Acta Orthop Scand 1982;53:445–450. 6. Johnson DP, Wakeley CJ, Watt I: Magnetic resonance imaging of patellar tendonitis. J Bone Joint Surg Br 1996;78:452–457. 7. Bottoni CR, Taylor DC, Arciero RA: Knee extensor mechanism injuries in athletes. In DeLee JC, Drez DD, Miller MD (eds): DeLee and Drez’s Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1857–1867. 8. Shalaby M, Almekinders LC: Patellar tendinitis: The significance of magnetic resonance imaging findings. Am J Sports Med 1999;27:345–350. 9. Panni AS, Tartarone M, Maffulli N: Patellar tendinopathy in athletes, outcome of nonoperative and operative management. Am J Sports Med 2000;28:392–397. 10. Panni AS, Biedert RM, Maffuli N, et al: Overuse injuries of the extensor mechanism in athletes. Clin Sports Med 2002;21:483–498. 11. Teitz CC, Garrett, WE, Miniaci A, et al: Tendon problems in athletic individuals. J Bone Joint Surg Am 1997;79:138–152. 12. Coleman BD, Khan KM, Kiss ZS, et al: Open and arthroscopic patellar tenotomy for chronic patellar tendinopathy, a retrospective outcome study. Am J Sports Med 2000;28:183–190.

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13. Ferretti A, Conteduca F, Camerucci E, et al: Patellar tendinosis, a follow-up study of surgical treatment. J Bone Joint Surg Am 2002; 84:2179–2185. 14. Popp JE, Yu JS, Kaeding CC: Recalcitrant patellar tendinitis, magnetic resonance imaging, histologic evaluation, and surgical treatment. Am J Sports Med 1997;25:218–222. 15. Romeo AA, Larson RV: Arthroscopic treatment of infrapatellar tendonitis. Arthroscopy 1999;15:341–345. 16. Nemeth WC, Sanders BL: The lateral recess of the knee: Anatomy and role in chronic iliotibial band friction syndrome. Arthroscopy 1996;12: 574–580. 17. Renne JW: The iliotibial band friction syndrome. J Bone Joint Surg Am 1975;57:1110–1111. 18. Kirk KL, Kuklo T, Klemme W: Iliotibial band friction syndrome. Orthopedics 2000;23:1209–1215. 19. Noble CA: Iliotibial band friction syndrome in runners. Am J Sports Med 1980;8:232–234. 20. Gunter P, Schwellnus MP: Local corticosteroid injection in iliotibial band friction syndrome in runners: A randomised controlled trial. Br J Sports Med 2004;38:269–272. 21. Safran MR, Fu FH: Uncommon causes of knee pain in the athlete. Orthop Clin North Am 1995;26:547–559. 22. Mysnyk MC, Wroble RR, Foster BT, et al: Prepatellar bursitis in wrestlers. Am J Sports Med 1986;14:46–54. 23. Neuschwander DC: Peripatellar pathology. In DeLee JC, Drez DD, Miller MD (eds): DeLee and Drez’s Orthopaedic Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1867–1878.

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61

The Stiff Knee Craig S. Mauro and Christopher D. Harner

In This Chapter Prevention Nonoperative management Surgery Arthroscopic débridement Open débridement

INTRODUCTION • Loss of motion is a common and potentially debilitating problem following knee ligament injury. Depending on the ligament injured and the subsequent repair or reconstruction, loss of motion may involve loss of extension and/or loss of flexion. • Previous studies have identified several risk factors that are associated with loss of motion. The etiology of loss of motion is multifactorial; it may be the result of diffuse joint inflammation and scarring or a mechanical block. • Preventive strategies are the most important means of combating loss of motion. Additionally, early recognition of even a modest loss of motion may lead to an earlier intervention and improved outcome. • Treatment options include nonoperative measures, such as range-of-motion and strengthening exercises, and arthroscopic and open surgical interventions. • Recent studies have demonstrated improved outcomes when steps are taken to prevent, identify early, and aggressively treat loss of knee motion.

CLINICAL FEATURES AND EVALUATION For the purposes of this chapter, the stiff knee is one that has lost some degree of flexion or extension. Throughout the literature, terms such as arthrofibrosis, ankylosis, flexion contracture, and infrapatellar contracture syndrome are used to describe knee motion loss in an attempt to characterize the etiology of the motion loss. To avoid any confusion that may be generated by such descriptions, we use the term loss of motion and, specifically, loss of extension and loss of flexion to describe any decrease from normal knee motion. When a specific diagnosis is discussed, we refer to that entity as it relates to loss of motion. Most people demonstrate some degree of hyperextension in their normal knee range of motion, with men averaging 5 degrees

and women averaging 6 degrees of recurvatum.1 Loss of motion has been defined in various ways in the numerous clinical studies on the subject. Some have defined loss of extension as a loss of greater than 10 degrees relative to the zero-degree position, while others have defined it as a symptomatic lack of motion compared with the other side.2,3 In 2000, the International Knee Documentation Committee (IKDC) revised the IKDC Knee Form, which is a knee-specific measure of symptoms, function, and sports activity.4 One specific modification was a change in the way in which loss of extension is identified. In the original IKDC knee ligament guidelines, loss of extension was defined in terms of the difference from the zero-degree position.5 In the 2000 IKDC Knee Examination Form, extension in the involved knee is compared to that of the normal, noninvolved knee to calculate the motion deficit. The 2000 IKDC Knee Examination Form defines passive motion deficits compared to the noninvolved knee (Table 61-1). These definitions have helped to standardize measurements and communication concerning loss of motion following knee injuries. Loss of motion may be the result of factors specific to a knee injury or, more commonly, the treatment of this injury. Loss of motion may involve loss of flexion and/or loss of extension. Loss of extension usually results in greater functional deficits, as patients may walk with a bent knee gait, which places increased strain on the quadriceps and increases contact forces in the patellofemoral joint.6 Consequently, patients with loss of extension may experience quadriceps weakness, patellofemoral pain, and fatigue.7 Loss of flexion rarely causes functional difficulties unless the knee fails to flex at least 120 degrees. This degree of deficit may interfere with functional activities such as sitting, squatting, stair climbing, and running. The true incidence of loss of motion following knee ligament injury and surgery, as defined by the IKDC classification system, is unknown and, as described previously, very much depends on the injury pattern and surgical intervention. The majority of the research concerning loss of knee motion has been focused on loss of motion following anterior cruciate ligament (ACL) injury and subsequent reconstruction. In 1984, Johnson et al8 reported an incidence of loss of extension of 67.9% and loss of flexion of 76.5% following ACL reconstruction compared to the contralateral side. Since then, authors have reported the incidence of motion loss as between 1% and 25% following ACL reconstruction, with those studies more strictly defining loss of motion demonstrating a higher incidence.2,3,9,10 The incidence of loss of motion is higher in the multiple ligament–injured knee, with some authors reporting an incidence between 18% and 30%.11,12 The risk factors associated with loss of motion have been studied most extensively following injuries to the ACL. As men-

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Table 61-1 Passive Motion Deficit Compared to the Noninvolved Knee Normal

25 degrees flexion 2000 International Knee Documentation Committee/Examination Form.

tioned, an injury pattern involving multiple ligaments, especially the medial collateral ligament, has a higher risk of loss of motion.11,12 Other risk factors for loss of motion that have been identified are related to the surgery itself or postoperative rehabilitation. Several such factors have been described in the ACL reconstruction patient (Table 61-2). Patients with knee dislocations and multiple ligament injuries are at highest risk of loss of motion because of the extensive injury sustained by the tissues during the injury and subsequent reconstruction. Injuries to, and procedures involving, the medial side of the knee may accentuate the fibrotic response of the knee joint, resulting in excessive scar formation and increased loss of motion. Interestingly, patients with multiple ligament injuries who undergo surgery within the first 3 weeks after injury tend to have better subjective functional ratings and better restoration of ligamentous stability.12 This finding may be the result of the easier dissection and repair facilitated by the acute reconstruction prior to the initiation of the fibrous healing response. Further, the timing of surgery in the multiple ligament–injured knee may not affect motion.12 The timing of ACL reconstruction has been a very controversial aspect of reconstructive knee surgery. While several studies have reported that acute ACL reconstruction results in a higher incidence of loss of motion,3,9,13 others have demonstrated no such relationship.14–16 The time frame of an acute ACL reconstruction has traditionally been defined as within 3 weeks of the injury. The association between time from injury to surgery and loss of motion has been attributed to the healing response that begins following any injury. Fibrinogenic cytokines have been shown to promote fibroblast proliferation and extracellular matrix production. Before surgery is performed, it is important to allow the acute sequela of the injury to subside. The quiescence of this episode is manifested by a decrease in swelling, restoration of extension within 5 degrees of the noninvolved side, and the ability of the patient to perform a good quadriceps contraction, such as a straight leg raise without a lag. Even those studies that endorse acute surgery suggest that

Table 61-2 Risk Factors for Loss of Motion After Anterior Cruciate Ligament Reconstruction Acute reconstruction Decreased preoperative motion Graft malposition Poor rehabilitation Excessive immobilization

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restoring the motion deficit preoperatively is an important measure to prevent postoperative loss of motion. Preoperative motion has been demonstrated to be an important risk factor for loss of motion postoperatively in most studies. The preoperative motion may be the most important clinical marker of the inflammatory response that is seen after the initial injury. This response and the consequent risk of motion loss following surgery may be minimized by restoring motion preoperatively. The time from injury to surgery to minimize the risk of loss of extension may vary for each patient, and we believe that the best indicator of when to proceed with ACL reconstruction is restoration of preoperative extension. ACL graft malposition is an important technical factor that may place a patient at risk of loss of motion postoperatively. An anterior tibial tunnel may cause impingement between the graft and the intercondylar notch during terminal extension. This impingement may lead to loss of extension or, ultimately, graft failure. Patients who take part in physical therapy programs that stress early motion and weight bearing tend to have fewer problems with loss of motion.2,9 Excessive immobilization that limits extension following surgery is associated with a higher incidence of loss of extension.3 Achievement of full extension, which may be assisted through bracing and crutches in the early postoperative period, may engage the graft within the intercondylar notch, minimizing hemorrhage and intercondylar notch scarring.

RELEVANT ANATOMY The etiology of loss of motion following ligament surgery is multifactorial but may be attributed to one or more of the following pathoanatomic processes. A mechanical block to flexion or extension may be caused by impingement resulting from an intra-articular block. Alternatively, diffuse inflammation or capsulitis may lead to loss of motion through the development of adhesions and intra-articular scar formation or arthrofibrosis.

Impingement Impingement may be the result of intercondylar notch scarring, a fibrovascular proliferation from the tibial side of the reconstruction, or an anteriorly placed ACL graft. Intercondylar notch scarring may result from bleeding and regrowth of the notch. Also, failure to perform an adequate notchplasty may lead to a physical block to extension.17 An ACL nodule may develop following ACL rupture or reconstruction of the ACL, causing a mechanical block to extension. When the lesion develops following ACL rupture, prior to reconstruction, full extension may be not be achieved within 2 months, even with aggressive rehabilitation. It has been reported that this nodule may develop from the torn fibers of the ligament at the tibial attachment site.18 The ACL nodule that may develop following ACL reconstruction was first described by Jackson and Schaefer19 in 1990, as a “cyclops lesion” because of its arthroscopic appearance. These nodules may arise from the graft and the surrounding tissue overlying the tibia, typically anterolateral to the tibial tunnel (Fig. 61-1). The nodule is composed of fibroelastic connective tissue proliferation, and it is unclear whether the lesion is the result of repetitive trauma to the graft or from hypertrophy of the remains of the native ACL. With knee extension, the cyclops lesion impinges between the graft and the intercondylar notch, preventing full extension.

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A

B

Figure 61-1 A, Cyclops lesion anterior to an anterior cruciate ligament (ACL) graft, viewed arthroscopically. B, Débridement of cyclops lesion with a motorized shaver. C, Probe on the ACL graft after completion of débridement.

C The ideal position of the tibial tunnel is within the ACL footprint. Anterior placement of the graft on the tibial side may lead to impingement of the graft in the intercondylar notch when the knee approaches terminal extension. Impingement from an improperly placed tunnel may lead to graft damage and subsequent fibroproliferation within the notch. Symptoms of impingement include stiffness in the morning that may improve with motion, anterior knee pain, and crepitus at terminal knee extension. Loss of motion with impingement is usually loss of terminal extension, with normal flexion. Usually, the knee is not diffusely inflamed, swelling is minimal, and patellar mobility is not affected.

Capsulitis/Arthrofibrosis Loss of motion following any knee ligament surgery may be due to capsulitis. Capsulitis refers to diffuse periarticular inflammation and swelling. This inflammatory response may lead to varying degrees of arthrofibrosis, a condition of diffuse intraarticular fibrous adhesions. Capsulitis, and the subsequent arthrofibrosis, is the result of cytokine release during the inflammatory response to an injury or surgery. Cytokines stimulate fibroblasts to produce the fibrous adhesions, which leads to the arthrofibrosis.

Shelbourne et al20 developed a classification system of arthrofibrosis based on the motion of the injured knee compared to motion in the uninjured knee. In this classification system, patients with type I arthrofibrosis have an extension loss of 10 degrees or less and normal flexion. Patients with type II arthrofibrosis have greater than 10 degrees of extension loss and normal flexion. Patients with type III arthrofibrosis have greater than 10 degrees of extension loss, greater than 25 degrees of flexion loss, and decreased patellar mobility. Patients with type IV arthrofibrosis have greater than 10 degrees of extension loss, greater than 30 degrees of flexion loss, and patella inferna with markedly decreased patellar mobility. Inflammation in the peripatellar tissues is associated with decreased patellar mobility. Patellar baja may result from the diffuse inflammation because of fibrous hyperplasia of the anterior fat pad. In 1987, Paulos et al21 coined the term infrapatellar contracture syndrome to refer to patients with patellar entrapment associated with loss of extension and flexion despite multiple corrective procedures. The cause of this entrapment is hyperplasia of the anterior fat pad, prolonged immobility, and lack of extension. When the fat pad becomes hyperplastic and adherent to the underlying tibia, the patella has limited excursion, and loss of motion may result.

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Capsulitis results in diffuse constant pain and stiffness. The knee is actively inflamed with diffuse swelling and warmth. Both extension and flexion are limited as a result. Patellar mobility is usually limited and, consequently, contraction of the quadriceps fails to create enough tension to actively extend the knee completely. Arthrofibrosis is the end product of capsulitis, and the knee may demonstrate decreased flexion, extension, and patellar mobility, but the swelling and warmth usually subside.

PREVENTION AND TREATMENT OPTIONS Prevention Preoperative Preoperative steps are the most important interventions to take to prevent loss of motion. Loss of motion following an injury is usually the result of pain, swelling, quadriceps inhibition, and hamstring spasm. A locked knee from a torn meniscus is relatively rare. Treatment in the preoperative period should be focused on decreasing pain and swelling and improving range of motion. Preoperatively, management consists of the use of ice to reduce pain and swelling, range-of-motion exercises, hamstring and calf stretching, and isometric quadriceps exercises. It is also important to counsel the patient about the possible complication of loss of motion and the importance of appropriate physical therapy. Intraoperative Some of the important intraoperative considerations to prevent loss of motion postoperatively were discussed earlier in the clinical features section. Accurate surgical technique and meticulous attention to graft placement are necessary to minimize the risk of loss of motion postoperatively. With ACL reconstruction, improper tibial tunnel placement may lead to motion problems. Most commonly, an anterior tibial tunnel may lead to impingement between the graft and the roof of the intercondylar notch with knee extension.17 Ideally, the tibial tunnel should be drilled within the ACL footprint. For less experienced surgeons, or whenever any surgeon is unsure about tunnel location (especially in revision cases where arthroscopic anatomy is potentially distorted), intraoperative lateral radiographs with the knee in extension are critical. A notchplasty should be performed to allow adequate clearance for the graft within the intercondylar notch. As previously discussed, an inadequate notchplasty or regrowth and scarring of the notch is one of the commonly identified causes of loss of extension following ACL reconstruction. Postoperative An appropriate rehabilitation program that stresses early motion is the most important postoperative measure to take to avoid loss of motion in this period. The goals of the rehabilitation program are to minimize inflammation, restore motion and strength, enhance proprioception and dynamic stability, and return the patient to full function. Our ACL postoperative physical therapy program stresses early motion with passive extension, heel/wall slides, hamstring/calf stretching, and active-assisted range of motion. Straight leg raises, quadriceps sets, half squats/wall slides, standing heel raises, and lateral stepups are important for early postoperative muscle function. It is important to see the patella glide superiorly with the quadriceps sets to prevent infrapatellar contracture syndrome. These exercises may be performed several times daily in the early postop-

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erative period. Modalities such as cold and compression may be helpful to decrease inflammation and swelling. Postoperative rehabilitation following ACL reconstruction must be done in such a manner that minimizes inflammation, pain, and swelling but stresses early motion to minimize adhesive scar formation. During week 1, we lock the knee brace in extension but allow range-of-motion exercises several times during the day. In most cases, we allow the patient to weight bear as tolerated. Beginning week 2, the brace is unlocked for ambulation. We stress the heel-toe gait to emphasize terminal extension. After week 4, the brace and crutches are discontinued if the patient has reached full extension and 100 degrees of flexion, has no knee extensor lag and minimal swelling, and is able to walk without a bent knee gait. Crutches are critical for successful rehabilitation in the first month postoperatively to achieve and maintain terminal extension without development of a bent knee gait. Critical milestones for patients to achieve are full passive extension within 1 week, full active extension within 2 weeks, 90 to 100 degrees of flexion within 2 weeks, and full flexion by 6 weeks. The surgeon should recognize that patients who are not meeting these milestones may require more specific and intense treatment for loss of motion.

Treatment Recognition of loss of motion must occur as early as possible to allow for immediate initiation of treatment. Although the preventative measures described previously are optimal, treatment of loss of motion must be initiated if these measures fail. The treatment process begins with a systematic approach to identify the cause of loss of motion. Successful treatment of loss of motion depends on early recognition of the cause. Early recognition of loss of motion and appropriate intervention should decrease long-term complications for the patient. Some patients experience loss of motion because the affected knee continues to be diffusely swollen, painful, and inflamed in the postoperative period. This type of response may be associated with capsulitis and, if left untreated, arthrofibrosis. When identified in the period of active inflammation, the appropriate treatment for the inflamed knee is anti-inflammatory agents, rest, and ice. Patients may continue with pain-free active rangeof-motion exercises and strengthening but should avoid forceful manipulation of the knee. Stretching techniques should be gentle to avoid aggravation of pain and swelling. Efforts toward regaining motion should be focused on reducing the motion deficit in one direction at a time. We address loss of extension first because it tends to cause more functional deficits and patellofemoral pain if left untreated. Patients should be encouraged to perform quadriceps sets and straight leg raises to minimize any knee extensor lag. A drop-out cast may be used overnight to provide a sustained stretch and prevent further loss of extension. The drop-out cast is constructed by applying a cylindrical long-leg cast with the knee at the end range of extension. Padding is incorporated into the cast anteriorly superior to the patella and posteriorly on the proximal thigh and distal calf to create a three-point pressure system to increase knee extension. After the cast has hardened, a window is cut to expose the anterior aspect of the patella and lower leg. The amount of stretch is then adjusted by incorporating a wedge between the cast and the distal aspect of the calf. The cast is left in place overnight and then removed by splitting it anteriorly over the thigh.

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During the active stage of capsulitis, gentle patellar mobilization is also important. Superior excursion of the patella, which is necessary for proper functioning of the extensor mechanism, may be restored by performing quadriceps sets in terminal extension. This mobilization must not be overly aggressive and must be pain free, as further inflammation of the peripatellar tissues may lead to further delay in restoration of motion. The surgeon, physical therapist, and the patient must have patience in the management of capsulitis. Overly aggressive stretching, manipulation, or surgical intervention during the period of active inflammation may only further inflame the knee and worsen the problem. Once the active inflammation has subsided, which may be 6 months or longer after reconstruction, surgery or manipulation may be considered if the patient has persistent loss of motion. Manipulation under anesthesia is a more invasive means of gently flexing and extending the knee under general or regional anesthesia to loosen scar tissue in patients with arthrofibrosis not responsive to standard physical therapy techniques. Manipulation is most effective for mild arthrofibrosis leading to flexion loss, as knees with greater extension deficits have been shown to achieve significantly less final extension than knees with smaller deficits.22 We believe that manipulation is most effective around 3 months postoperatively, after the acute response has subsided, but before the fibrotic response is complete. Manipulation under anesthesia should be performed gently to prevent chondral damage or stimulation of myositis ossificans or ossification of the medial collateral ligament. When loss of motion appears to be caused by impingement, physical therapy to improve extension should be the focus of the initial management. Gentle stretching techniques that employ a sustained, low-amplitude force should be used. Quadriceps strengthening exercises are stressed to eliminate any quadriceps lag that may be contributing to the loss of extension. A drop-out cast may also be used in this setting to provide a sustained stretch and prevent further loss of extension. If impingement is the suspected cause of loss of motion and extension fails to improve with physical therapy within 2 or 3 weeks, arthroscopic evaluation and débridement of the intercondylar notch (as described in the following section) may be necessary. Aggressive nonoperative manipulation should not be performed in the setting of a physical impingement. Forceful stretching may result in graft failure and will not be successful unless the physical block to motion is removed.

SURGERY Surgical management of loss of knee motion is indicated when nonoperative interventions have failed or if a specific, correctable abnormality exists. Several techniques have been described, including open débridement, arthroscopic débridement, and combined open and arthroscopic débridement.

Arthroscopic Débridement Arthroscopic débridement has been advocated as the first-line surgical treatment for loss of motion. It is often successful and may be performed on an outpatient basis. Loss of extension following ACL reconstruction may be particularly appropriate for arthroscopic intervention, as correction of loss of extension secondary to pathology localized to the notch or scarring may be particularly amenable to this approach.

Prior to undertaking a surgical intervention to address loss of motion, the surgeon should have an idea of the etiology of the loss of motion. Even when the surgeon has a strong suspicion preoperatively of the underlying pathology, it is important to thoroughly visualize all compartments of the knee. We use a diagnostic arthroscopic approach to evaluate the knee in the setting of loss of motion that is similar to the nine-step approach described by Millett et al.23 We create the standard anterolateral and anteromedial portals immediately adjacent to the respective border of the patellar tendon, at previous arthroscopy portal sites if possible. We first evaluate the suprapatellar pouch, the medial gutter, and the lateral gutter, using a motorized shaver to reestablish these spaces if scarring has compromised their visualization (Fig. 61-2). We then turn our attention to the infrapatellar fat pad, which is débrided and mobilized to reestablish the pretibial recess. Any infrapatellar adhesions between the anterior tibia and the fat pad must be débrided to allow patellar mobilization and superior patellar excursion. The medial and lateral retinaculum are then evaluated and released with a motorized shaver if tight or scarred. If the anterior aspects of the menisci are involved in the scarring, this scarring should be released to allow normal anterior-posterior meniscal translation. Evaluation of the intercondylar notch is next. When loss of knee extension following ACL reconstruction is a result of impingement, the offending pathology may be visualized in the intercondylar notch. Proliferation of a cyclops lesion from the tibial side of the reconstruction is usually first visualized with any attempt to visualize the intercondylar notch. This nodule should be débrided, and the intercondylar notch should be evaluated for scarring. Regardless of the presence of a cyclops lesion, intercondylar notch scarring should be débrided to allow the knee to reach as nearly normal extension as possible. Once the excess scarring is excised, the graft should lock into the notch without impinging on it during knee extension. Impingement of the graft in the intercondylar notch may result in failure of the graft to incorporate. The graft insertion should be evaluated for evidence of failure. An inadequate notchplasty may cause impingement and loss of extension following ACL reconstruction. A notchplasty should be performed if there is evidence of continued impingement despite débridement of the notch scarring. In severe cases of intercondylar notch scarring, the ACL and/or posterior cruciate ligament may need to be released. Following intercondylar notch débridement, a drop-out cast may be applied. An anteriorly placed ACL graft may contribute to the loss of motion following ACL reconstruction. In the case of an anteriorly placed ACL graft causing impingement and loss of extension, an adequate notchplasty must be completed to provide the anterior graft the opportunity to reduce into the notch without impingement. If elimination of the impingement is not feasible through notchplasty, the ACL graft may have to be resected. If necessary, revision reconstruction is performed later as a staged procedure. The posterior capsule should be evaluated at its tibial and femoral insertions, as tightness of the posterior capsule may contribute to loss of extension. Some authors advocate release of the posterior capsule if tightness is noted.23 This débridement must be performed carefully, with special consideration given to the neurovascular anatomy of the posterior knee. We do not routinely perform a posterior capsule release and have found a drop-out cast in the postoperative period to be effective for relieving posterior knee tightness.

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A

B

C

D

Figure 61-2 A, Suprapatellar pouch scarring in a patient with severe arthrofibrosis after a tibial plateau fracture (preoperative flexion 60 degrees) 6. Return to function when no joint line tenderness and the patient has successfully completed the Figure 63-2 progression to the required level

LIGAMENT: NONSURGICAL CONCEPTS PARTIAL OR COMPLETE MENISCECTOMY When nonoperative care is unable to provide pain-free function or the knee demonstrates locking, surgical intervention is nearly

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The most commonly used nonsurgical ligamentous approach is that devised for patients following medial collateral injury. This model of what might be termed “functional rehabilitation” for these patients emerged during the 1970s and 1980s. It is now

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widely accepted that the vast majority of isolated medial collateral ligament–injured patients may effectively be treated with a nonoperative approach allowing immediate controlled motion and strengthening.13,14 It is important to note that concomitant injury to other ligaments or structures may alter the opportunity for nonoperative treatment. Typically, a phased rehabilitation approach is implemented starting with maximal protection (protected weight bearing, controlled ROM, quadriceps activation), moderate protection (normalization of gait, strengthening, full ROM), minimal protection (increase strength/power, return to work activities), and return to higher levels as in the later portions of progression as presented in Figure 63-2. Most of these patients proceed through this sequence in approximately 3 to 4 weeks with a partially torn (grade I to II) medial collateral ligament injury but take 6 or more weeks with a complete disruption (grade III). The location of the injury (femoral insertion versus tibial insertion) does affect the early phase, as some surgeons do recommend a period of immobility with grade III tibial disruptions.15 Clinical pearls in the rehabilitation of these patients include the following: 1. When the femoral insertion is the tender site: immediate, controlled ROM and strengthening in the nonpainful portion of the ROM and protected weight bearing is the treatment of choice. 2. If the patient has posterior medial corner tenderness, have the patient wear shoes with a slight heel (1 to 2 inches) during ambulation to minimize knee extension, particularly in the early phases of rehabilitation. 3. If there are concomitant injuries, treatment may not be able to be nonoperative or of the normal progressive nature.

ANTERIOR CRUCIATE LIGAMENT REHABILITATION Reconstructive surgery of the ACL has become one of the most common orthopedic surgical procedures performed in the United States. The surgical technique and graft sources were described in a previous chapter. The surgeon works with the patient to plan the surgery after the patient has regained his or her ROM and normalized muscular function. This may require recommending preoperative physical therapy visits if the patient appears to be having difficulty performing activities independently. The therapist must know the type of graft and fixation used to best design the early phases of the rehabilitation program. In general terms, the normal initial progression/ maximal protection phase is to achieve full extension in the immediate postoperative week, use protected weight bearing until the patient can activate the quadriceps effectively to absorb and transfer loads (1 to 3 weeks), maintain patellar mobility, regain quadriceps control, and prevent development of a chronic effusion. The patient progresses after becoming fully weight bearing to an integrated approach of open- and closed-chain activities. Bilateral closed-chain activities progress to unilateral demands, and core strengthening is often added to be emphasized in the home exercise program. Therapists are urged to be aware of red flags such as difficulty in regaining motion, development of chronic effusion, and inability to adequately control the extremity during normal activities of daily living and functional tasks.

Readers are urged to examine the numerous protocols that are available for these procedures through university and sports medicine center Web sites. It is important to see these materials as guidelines because the unique circumstances of the patient may require adjustments, particularly if the protocol is somewhat time focused in its approach. The special clinical pearls for ACL reconstruction rehabilitation include the following: 1. Prevent problems rather than treat them whenever possible; see problems emerging and treat them early. 2. Imperative: Get extension early and in the first few days, be protective of requested function; do not “beat” a dead extremity. 3. Know which graft is used: If a hamstring graft, avoid isolated open-chain hamstrings for several weeks; if contralateral patellar tendon, implement donor site tendon program; if ipsilateral patellar tendon, get patellar mobility. 4. Quadriceps activation is facilitated by working in flexion and not attempting to activate initially in full extension. 5. Do not discard assistive device until able to activate the quadriceps effectively and demonstrate a normal gait. 6. Integrate your program; do not use just open chain or closed chain; integrate both to gain complete rehabilitation. 7. You may wish to avoid large loads in terminal extension (particularly open chain) during the initial months postoperatively.

POSTERIOR CRUCIATE LIGAMENT REHABILITATION Although ACL injury results in significant disability and joint deterioration, posterior cruciate ligament (PCL) injury is less predictable. Some patients can function well and do not develop symptoms as they “live with” their condition, while others will develop symptoms, often after several years. ACL surgical technique has become well defined, but PCL surgery is more controversial. Nonoperative treatment of PCL disruption is still a common option as the surgical challenges have made for less predictable outcomes. Optimal surgical reconstruction of the PCL remains controversial, with tibial tunnel and inlay techniques described, along with single- and double-bundle reconstructions. Each has potential advantages, with long-term outcomes to be determined.16,17

Nonoperative Treatment The normal instability seen with PCL injury is more of a straight posterior displacement that allows some compensation by the quadriceps. There is greater lateral compartment displacement that manifests as increased external tibial rotation in the PCLdeficient patient. The patients who do not do well typically develop medial compartment arthritis and patellofemoral pain. This is provided via education of the patient as the nonoperative program is instituted. A phased approach to rehabilitation is implemented with the maximal protection including: protected ROM (not greater than 0 to 60 to 70 degrees), protected weight bearing, open-chain quadriceps strengthening, no hamstring strengthening, and control of inflammation. This is followed by moderate protection including full weight bearing, full ROM, emphasis on open-chain quadriceps strengthening, pool activities (which are excellent), and avoiding large closed-chain loaded activities. A functional training program is then used after approximately 10 weeks of the foregoing programs.

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Posterior Cruciate Ligament Reconstruction Rehabilitation The special features of surgical technique make the use of the surgeon’s protocol most important in these patients. The therapist and physician must be able to present the same picture to the patient to maximize outcomes. As a general rule, things are progressed more slowly than in ACL patients as the PCL grafts may have greater inherent risks of stretching or loosening, resulting in instability. The following are general guidelines for PCL reconstruction: 1. 2. 3. 4. 5.

Know the surgeon and the procedure: same ideas Get motion early; do not keep them in strict immobilization Protected weight bearing (bilateral crutches) Protected ROM, 0 to 90 degrees in first 4 to 6 weeks Progression after 6 weeks in the moderate protection phase 6. Long term: avoid large loads in closed-chain exercises (e.g., leg presses, squats); always monitor for the development of arthritic change; thus, be careful with biking activities.

COMPLEX LIGAMENTOUS CONDITIONS The patient with instability related to multiple ligament/capsule injuries is a great challenge for surgeon and therapist as outlined in a previous chapter. Certain combinations, such as ACL or PCL with posterolateral injury require surgical intervention, which make rehabilitation more difficult as the required early postoperative ROM limitations may provide a challenge to normalizing the ROM long term. Ambulatory abnormalities are often seen in these patients as they may have adopted a varus thrust gait preoperatively. A clinical pearl is to keep the knee

flexed during gait by wearing a heel or heel lift under the involved extremity. In the clinic, patients may be instructed in an exaggerated form of this by walking in significant flexion (Groucho walk, as in Groucho Marx). Another activity to avoid is heavy closed-chain loading as the posterolateral corner and PCL both lead to posterior arthritic changes. Open-chain strengthening is often the modality of choice but should be limited in its ROM (typically 90 to 30 degrees) as we do not want to aggressively load the last 30 degrees of extension (thus minimizing loading to the posterolateral corner as well as minimizing possible patellofemoral reaction). Again, it is imperative for the therapist and surgeon to have strong communication and provide a unified standard of expectation. Unfortunately, some of these patients expect too much improvement and are not able to accept that there are limitations as to what level of success will be achieved following surgery and rehabilitation.

CONCLUSIONS Rehabilitation of patients with knee conditions has greatly evolved through the past 25 years. Evidence of clinical and functional improvement is readily available, particularly as it relates to specific conditions. The use of a structured assessment integrated with a functional progression is very appropriate in most nonsurgical patients. A key to success in the more complex situations is the communication between the physician and therapist as they must be certain to provide a consistent message reinforced by each during their interactions with the patient. The functional progression approach is still used with these more challenging patients but with the recognition of special limitations and also expected outcomes following certain interventions.

REFERENCES 1. Malone T, Davies G, Walsh WM: Muscular control of the patella. Clin Sports Med 2002;21:349–362. 2. Lieb FJ, Perry J: Quadriceps function: An anatomic and mechanical study using amputated limbs. J Bone Joint Surg 1968;50:1535–1548. 3. Bolgla L, Malone T: Exercise prescription and patellofemoral pain: Evidence for rehabilitation. J Sport Rehabil 2005;14:72–88. 4. Powers CM, Landel R, Perry J: Timing and intensity of vastus muscle activity during functional activities in subjects with and without patellofemoral pain. Phys Ther 1996;76:946–955. 5. Powers CM, Ward SR, Fredericson M, et al: Patellofemoral kinematics during weight-bearing and non-weight-bearing knee extension in persons with lateral subluxation of the patella; a preliminary study. J Orthop Sports Phys Ther 2003;33:677–685. 6. Wilk KE, Davies GJ, Mangine RE, Malone TR: Patellofemoral disorders: A classification system and clinical guidelines for nonoperative rehabilitation. J Orthop Sports Phys Ther 1998;28:307–322. 7. Alford JW, Cole BJ: Cartilage restoration, part I: Basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med 2005;33:295–306. 8. Alford JW, Cole BJ: Cartilage restoration, part II: Techniques, outcomes, and future directions. Am J Sports Med 2005;33:443–460. 9. Sgaglione NA, Steadman JR, Shaffer B, et al: Current concepts in meniscus surgery: Resection to replacement. Arthroscopy 2003; 19(Suppl 1):161–188.

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10. Mariani P: Accelerated rehabilitation after arthroscopic meniscal repair. Arthroscopy 1997;13:731–736. 11. Barber F: Accelerated rehabilitation for meniscus repairs. Arthroscopy 1997;13:206–210. 12. Tenuta J, Arciero R: Arthroscopic evaluation of meniscal repairs: Factors that effect healing. Am J Sports Med 1994;22:797–802. 13. Vailas AC, Tipton CM, Matthes RD, et al: Physical activity and its influence on the repair process of medial collateral ligaments. Connect Tissue Res 1981;9:25–31. 14. Woo SL-Y, Orlando CA, Gomez MA, et al: Tensile properties of the medial collateral ligament as a function of age. J Orthop Res 1986;4:133–139. 15. Shelbourne KD, Patel DV: Management of combined injuries of the anterior cruciate and medial collateral ligaments. J Bone Joint Surg Am 1995;77:800–806. 16. Noyes FR, Medvecky MJ, Bhargava M: Arthroscopically assisted quadriceps double-bundle tibial inlay posterior cruciate ligament reconstruction. Arthroscopy 2003;19:894–905. 17. Dennis MG, Fox JA, Alford JW, et al: Posterior cruciate ligament reconstruction: Current trends. J Knee Surg 2004;17:133–139.

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64

Thigh and Leg Michael J. Coen

In This Chapter Quadriceps contusion Myositis ossificans Muscle strains Nerve entrapments Exertional compartment syndrome Shin splints Tibial stress fracture Proximal tibial-fibular joint pain

INTRODUCTION • Soft-tissue injuries of the thigh and leg, while not receiving the attention or requiring operative intervention as often as joint injuries, can still be a significant cause of morbidity and lost playing time for the athlete. • The leg is the weight-bearing structure that is the critical column on which balancing and locomotion depend. Any kinematic or kinesiologic compromise may cause significant impact. • We briefly address some of the more commonly seen injuries, mention some of the less prevalent syndromes, and discuss the etiology, evaluation, treatment plans, and prognosis as indicated. With the recent trend of increased sports-mindedness of those of all ages, you will likely see variations of the spectrum of these injuries. • A working cognition of the anatomy, biomechanics, and athletic kinesiology will aid the thought process as you consider how sport-specific injuries are incurred and related.1

THIGH Quadriceps Contusion These injuries are most commonly seen in contact sports. In the United States, quadriceps contusions are typically seen in football where the helmet of a tackler hits a running back in the anterior thigh. The thigh pads are specifically designed to absorb this injury, but sometimes players do not like to wear them (against regulations) because they feel that they slow them down or they may slide off to one side. Quadriceps contusions cause immediate muscular damage,2 intramuscular bleeding, and pain. With severe injuries, the patient may be unable to continue playing. The trainer will typically place an Ace bandage around the thigh, an ice bag, and another Ace bandage over that, trying to apply compression and ice in order to avoid the development

of a large hematoma and decrease the swelling. Depending on the position of the knee at contact and the degree of involvement, flexion (and/or extension) deficits may develop. The degree of difficulty with postinjury range of motion, most specifically regaining flexion, is a significant prognostic indicator.3 The amount of flexion at 48 hours after injury was found by Jackson and Feagin3 to be a predictor of and guide to rehabilitation prognosis and progression. The ice can be removed after about 20 minutes and reapplied every 2 hours. Radiographs are usually not needed immediately. They may be helpful after several weeks to evaluate for myositis ossificans. Immobilization in as much flexion as comfortable for the first 24 hours using an adjustable hinged knee brace may help maintain range of motion. Heat and ultrasound are not used in the initial phase. After the initial injury phase2 and swelling are resolved, the range of motion is gently reestablished without undo stressing of the extensor muscle mass. This may be begun in the inflammatory stage and continued through remodeling.4 Ice massage and soft-tissue techniques are used to try to mobilize the knee and reestablish dynamic functionality of the quadriceps musculature. A progressive resistance exercise program may be undertaken when 90 degrees of flexion is obtained. Prognostic factors include regaining a range of motion of at least 45 degrees of flexion in the first 3 weeks.5 The trainer or therapist needs to be careful with regard to aggressively trying to establish range of motion, as scarring and increased contracture have been noted with aggressive or manipulative attempts to regain knee flexion. Generally, the prognosis is good with return to play at 2 to 3 weeks when the athlete passes isokinetic and functional testing, although in severe cases, it may take several months. The overall outlook for functional return is good, and the risk of myositis ossificans is proportional to the amount of bleeding and degree of the original injury.1 If myositis ossificans becomes a significant factor, range of motion may be more difficult to obtain and the patient may develop a hard mass in that area on a long-term basis. Increased or specialized padding to protect that area for future contact may be appropriate. Excision of myositis ossificans deposits has met with limited success. Compartment syndrome after thigh contusion has been reported, and this entity is discussed later.

Myositis Ossificans Myositis ossificans is the ossification caused by the osteogenic progenitor cells released in the periosteal soft tissue with bleeding and hematoma formation (Fig. 64-1). The mass effect it has on the quadriceps muscle after maturation is usually the only sequelae of formation.3 It is commonly painless, unless reinjured by contusion, but may not decrease in size with time. After ath-

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mentioned medical intervention is undertaken. Medical support is usually adequate for management with resolution of rhabdomyolysis, but, depending on the cause, appropriate compartment release or débridement may also be needed.

Compartment Syndrome of the Thigh Compartment syndrome of the thigh can also be seen on a rare occasion after extensive workouts or contusion to the anterior thigh.6 Symptoms are similar to those in the leg as outlined later in this chapter, which is more commonly seen. A high index of suspicion is needed when pain out of proportion to any injury is reported. Other signs include paresthesias and severe pain with passive motion or stretch of the muscles in the involved compartment. Treatment includes catheter pressure monitoring and fasciotomies as indicated. Compartment pressures7 of more than 30 mm Hg or within 30 of the diastolic blood pressure have both been used as thresholds for considering compartment fascial releases. The thigh has anterior, posterior, and medial compartments. The anterior and posterior compartments can usually be released from a lateral incision. The medial compartment often does not need to be released, and some surgeons will do the lateral incision, release the anterior and posterior compartments, and then check the medial compartment by palpation to see if it is soft.

Muscle Strains Figure 64-1 Myositis ossificans after a quadriceps contusion.

letic thigh contusion, the incidence of myositis ossificans is 9% to 20%.5 Radiographic maturation is usually seen at approximately 4 to 6 months. If a biopsy is performed to rule out osteosarcoma, the biopsy specimen should come from the mature periphery. Serial radiographic follow-up is usually adequate without biopsy. Rarely is the athlete symptomatic or is excision indicated. Increased or specialized padding to protect that area for future contact may be appropriate. If excision is undertaken, it must be done after the bony mass has matured or recurrence may be an issue. Prophylactic treatment with indomethacin postoperatively is recommended.

Rhabdomyolysis Rhabdomyolysis is a disease process whereby damage sustained by the muscle fibers leads to the dissolution of the compromised structural components of the muscle fibers of the involved area. The subsequent elimination of the waste products released can be toxic to the kidneys and can lead to renal failure. Rhabdomyolysis is seen after crushing injuries and contusions but has been reported after extreme overuse episodes such as heavy or maximized weight training. It may be seen as well with compartment syndrome. The patient usually presents with acute pain and swelling in the thigh or involved area. Urine output may decrease with darkening of the urine as the renal involvement becomes more apparent. Laboratory studies will show increased myoglobin in the blood and urine. Fluid support and alkalinization of the patient’s urine is initiated to maintain output, which is monitored with a Foley catheter in a hospital setting. This syndrome usually develops over a period of several hours. The patient’s condition will deteriorate unless the syndrome is recognized and the afore-

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“Pulled” muscles are a common occurrence on the athletic field.8,9 These strains are a physiologic failure of the musculotendinous unit to remain in complete functional continuity. Tissue tension failure can occur at the origin or insertion, muscle belly, and, most commonly, at the musculotendinous junction. Failure may be graded by the degree of involvement of the acting cross-sectional area damaged. The usual mechanism is an overwhelming extension force on an eccentrically contracting muscle.10,11 Warm-up programs may have a preventive effect.12 Treatment is similar to that outlined for a thigh contusion and initially includes rest, ice, compression, and elevation (RICE). Magnetic resonance imaging (MRI) may be helpful to delineate degree of damage. Healing and rehabilitation progress through the three stages of tissue injury, inflammation, and remodeling.3 The different muscles typically involved are discussed. Hamstring Strain Hamstring strains are most commonly seen13 and especially occur in those sports requiring sprinting or jumping. These muscles (long head of the biceps femoris, semimembranosus, semitendinosus) cross two joints so they are susceptible to fast, heavy loads. Strain location can be an avulsion at the origin on the ischial tuberosity. A mid-substance muscular strain is occasionally seen, but failure is most commonly at the musculotendinous junction, at the junction of the middle and distal thigh. The lateral hamstrings are more commonly involved than the medial hamstrings. Poor flexibility and fatigue have been implicated.9 Pain, a pop, or a tearing sensation is usually acutely felt during a jumping or running activity. This most commonly occurs during eccentric contraction of the muscle. There are acute pain and swelling. The degree of strain may be classified as in Table 64-1.14 If the tear is severe with a major portion of the substance involved, a gap or mass may be palpable. This is most easily checked with the athlete lying prone and the knee flexed to about 90 degrees with slight resistance. If the tear is contained within the fascial constraints of the belly, ecchymosis may not be appreciated. However, if the fascial sheath is vio-

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Table 64-1 Hamstring Strain Classification Grade I

Small disruption of structural integrity at musculotendinous junction

Grade II

Partial tear, some musculotendinous fibers remain intact

Grade IIIA

Complete rupture of musculotendinous unit

Grade IIIB

Avulsion fracture at tendon’s origin or insertion site

From DeLee JC, Drez D: DeLee & Drez’s Orthopaedic Sports Medicine: Principles & Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1487–1488.

lated, blood and ecchymosis will usually appear subsequently in the dependent portion of the leg. Immediate care is icing, compression wrapping, and limitation of activities (RICE) with immobilization/crutches as needed. Rehabilitation by the trainer or therapist typically has an acute injury phase, a healing phase with stretching, and a return to activity phase with return to play in a few days to several weeks depending on the degree of strain (Table 64-2).15 Suspected complete tears may be evaluated by MRI, and reattachment of avulsions at the ischial tuberosity has been described. Steroid injections for recalcitrant enthesopathic-type partial tears at the ischial tuberosity may give successful long-term symptomatic relief. If return to activity has been attained, it is important that the athlete continue with a regular stretching program to avoid recurrent injury. Return to play usually is determined by functional evaluation by the team trainer for sprinting and jumping. Quadriceps Strain Quadriceps strains are less common. The rectus femoris is usually involved. This may be because it acts across two joints. Isolation testing of the rectus femoris involves changes in the examination at varying degrees of hip extension. The quadriceps muscle typically works as an antagonist to the hamstrings. Again, injury is usually focused at the musculotendinous junction, but more proximal tears have been described.16 Treatment algo-

Table 64-2 Hamstring Treatment Protocol6 Phase I Rest, ice, compression, elevation (RICE) Phase II Ice, stretch, NSAIDs, electrical stimulation, isometrics ± isotonics, condition Phase III Ice, stretch, NSAIDs ± electrical stimulation, isotonics ± isokinetics,* condition Phase IV Ice, stretch, isokinetics,* running, sport-specific training Phase V Return to sports NSAIDs, Nonsteroidal anti-inflammatory drugs. *Concentric high speeds at first, proceeding to eccentric slow speeds. From DeLee JC, Drez D: DeLee & Drez’s Orthopaedic Sports Medicine: Principles & Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1487–1488.

rithms are similar to those for the hamstrings, but with severe injuries progress may be slower secondary to painful weight acceptance. Conservative care with rehabilitation is successful in the vast majority of patients. Bicycling is often helpful to restore endurance and eliminate fatigue, weakness, and deficits. Most athletes can return to play in 2 to 6 weeks. Neoprene sleeves or shorts may provide symptomatic support. Surgery for proximal tears of the indirect head of the rectus or acute complete tears at the musculotendinous junction16 and chronic attritional microtears with lengthening17 and extension lag has been described. Adductor Strain Adductor strains are a significant cause of lost playing time for athletes in sports that require pushing off from side to side (e.g., skating, baseball, soccer). “Groin pulls” are usually of the adductors (mainly the proximal musculotendinous area of the longus) and pectineus. Preparticipation stretching is the key to prevention. Palpation of the painful structure and increased pain with passive stretching aid in diagnosis. Inguinal hernia should be ruled out by physical examination. “Sports hernias”18 or inflammation/enthesopathy at the insertion on the pubis may be the cause of recalcitrant cases. MRI may be helpful in cases where localization is difficult or treatment is not causing resolution as expected. Treatment is similar to that outlined for hamstring and quadriceps strains, and future preventive stretching is essential to avoid falling into a pattern of recurrent injury. Obturator nerve entrapment may mimic a groin strain but will usually have accompanying symptoms of paresthesias of the inner upper thigh. Surgery for chronic adductor tendonitis has been described.19 Surgery is also considered for acute, complete avulsion injury. However, conservative care allows resolution and return to play in a few weeks in the vast majority of patients.

Femoral Stress Fractures: Shaft Stress fractures of the femoral neck are more commonly seen and are described in Chapter 44. Stress fractures of the femoral shaft20 are occasionally seen and have the typical dull, aching pain seen with other stress fractures that increases with activity and resolves with rest. Usually, a history of changes in training, intensity, or frequency can be elicited from the athlete. Stress fractures are a sign of trabecular bony compromise in the attempt to balance bone remodeling due to unusual loads. Clinical tests as simple as levering the femur over an object (fulcrum test) have been used (Fig. 64-2).21 Bone scan or MRI is used as a diagnostic test. Rest or change of activity level or type will typically allow resolution of symptoms. Pool running can aid in maintaining conditioning with a return to activity in 2 to 4 months.

Saphenous Nerve Entrapment Saphenous nerve entrapment is a rarely seen pain syndrome. The patient will describe paresthesias in a distribution along the saphenous nerve that can fluctuate with activities or exertion. The nerve can be entrapped in Hunter’s canal or the fascial soft tissue on the medial aspect of the thigh. Using Tinel sign to locate the involved area has been helpful as well as a diagnostic (and sometimes therapeutic) injection22 with local anesthetic and a corticosteroid. Release of the nerve from the involved area has been reported with satisfactory results. This is a syndrome that needs to be considered for nonspecific medial distal thigh pain of undetermined cause. Involvement including compression of the superficial femoral artery in the adductor canal (Hunter’s)

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Figure 64-2 The fulcrum test with the examiner’s arm (fulcrum) moved proximally under the thigh. Pain develops when the arm is placed directly under a stress fracture of the femoral shaft and gentle pressure is applied to the dorsum of the knee. (From Johnson AW, Weiss CB, Wheeler DL: Stress fractures of the femoral shaft in athletes-more common than expected. A new clinical test. Am J Sports Med 1994;22:248–256.)

has also been reported.23 Vascular occlusion type of symptoms may be reported, and surgical release has been described.

LEG Compartment Syndrome of the Leg Acute Acute compartment syndrome of the leg is usually caused by injury: bony, muscular, or vascular. This discussion deals mostly with acute compartment syndrome due to muscular contusion and hematoma or bleeding as seen in sports injuries. The pathophysiology is similar to compartment syndrome seen with highenergy bony or vascular injury as seen in a traumatic scenario. This includes increased fluid and pressure contained within the fascial envelope to such a degree that ischemia ensues. A high index of suspicion is necessary. Careful monitoring for pain with passive range of motion and checking compartment pressure measurement is appropriate. Guidelines for compartment pressure indications for fasciotomies vary significantly in the literature, anywhere from 30 mm Hg below diastolic blood pressure to any measurement above a threshold pressure of 30 mm Hg. Treatment for acute compartment syndrome includes fascial release on an emergent basis. This typically involves the anterior and lateral compartments and is done in an open fashion through longitudinal incisions on the lateral24 and, if needed, medial aspects of the leg. There are four anatomic compartments in the leg: anterior, lateral, superficial posterior, and deep posterior (Fig. 64-3).24 The lateral incision is used to identify the intermuscular septum and decompress the anterior and lateral compartments. The fascia is opened anterior and posterior to the

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septum, with care to avoid the superficial peroneal nerve. It is important in doing the release to make certain the entire length of the compartment tightness is released as anatomy can vary and some people have tight areas at the far proximal and distal extremes. Lateral release is usually adequate depending on the area and involvement. If needed, a medial incision is used to release the posterior compartments. This incision is at the posterior aspect of the tibia to release the superficial compartment. By following the posterior aspect of the tibia to the intermuscular septum and dissecting just behind that septum, a careful release of the fascia proximally and distally is performed, thereby releasing the deep posterior compartment. Typically, this provides a visible softening of the compartments, and the wounds are then covered with gauze and later wet-to-dry dressings are applied. Delayed primary closure or skin grafting is done at approximately 5 days after the initial swelling has resolved. Chronic Exertional Compartment Syndrome Chronic exertional compartment syndrome has symptoms similar to those of the acute entity but to a lesser degree and is a more difficult diagnosis to make. Patients typically complain of aching pain or paresthesias (and occasionally vascular complaints) after exercises that stress or challenge the leg muscles.25 Runners complain of insidious pain that begins to limit their activity level. Symptoms originate after beginning activity, and typically resolve after 10 to 30 minutes upon completing the activity. Symptoms most commonly occur in the anterior and lateral compartments. Anterior compartment symptoms include paresthesias in the first web space. Recent studies outlining vascular flow as well as MRI findings in exertional compartment

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Figure 64-3 A, Anterolateral incision for decompression of the anterior and lateral compartments. B, Posteromedial incision for decompression of the superficial and deep posterior compartments. (From Mubarak SJ, Owen CA: Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 1977;59:184–187.)

syndrome have been used to noninvasively evaluate this syndrome. Pre- and postexercise MRI changes in blood flow or fluid in the involved area have been documented, but results of MRI in diagnosing this entity have been equivocal. Invasive catheter measurements for significant increases in pressure postexercise have also been used.26 This is more invasive but currently more reliable and reproducible. After the diagnosis has been made, for symptoms that are significant and recalcitrant to conservative care, release of the involved (typically the anterolateral) compartments has been described. This can be done using a large or small open24 approach as previously described or a percutaneous endoscopic approach.27 This includes three small skin incisions and subcutaneous evaluation of the fascia with use of an endoscope to delineate the intermuscular septum and the fascia anteriorly and posteriorly for release (Fig. 64-4).27 This minimizes the invasiveness with regard to the skin incisions and has been reported to have satisfactory success (approximately 90%). Return to play is typically in a few weeks.

Medial Gastrocnemius Strain (Tennis Leg) Medial gastrocnemius strain, or tennis leg, is a syndrome in which a sudden vigorous load causes pain and often a tearing sensation in the upper calf. Pathophysiology is an eccentric

Figure 64-4 Endoscopic compartment release. The superficial peroneal nerve is seen centrally.

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loading failure at the musculotendinous junction. This muscle spans both the knee and the ankle. It is so named tennis leg because it is commonly encountered in a middle-aged individual during the push-off phase while playing tennis.28 Swelling and sometimes ecchymosis are seen. Seldom is a major defect palpated, but often there may be acute or chronic slight muscle mass loss in that area. Concomitant acute compartment syndrome has been reported.29 As with other muscular strains, the phases of injury, inflammatory healing, and remodeling occur as a rehabilitation course is undertaken. Resolution of symptoms and no significant loss in functional performance are the typical course.

Contusion of the Anterior Tibia Rarely, blows to the tibia may cause a fracture. Much more commonly, these contusions cause a painful soft-tissue injury. This type of injury is seen in youth soccer or sports in which direct blows to the subcutaneous border of the anterior tibia causes hematoma formation. If the hematoma is subperiosteal, it causes severe pain and may result in a significant bony prominence in that area as it consolidates. The use of shin guards for soccer serves to almost eliminate this unless the shin guards are too short, in which case, contusions above the level of the shin guard can occur. While it is impossible to definitively rule out a fracture without a radiograph, percussion of the heel and gentle torsional stressing by rotating the foot may be helpful. Palpation of the noninvolved posteromedial aspect of the tibia may be nontender, thus supporting absence of a fracture. The contusion injury resolves with conservative care, and symptoms are in large part in proportion to the amount of bleeding. Careful padding speeds return to play and any resulting osseous prominence may be permanent.

Shin Splints or Medial Tibial Stress Syndrome Shin splints is a catch phrase for pain in the medial tibial area, usually with overuse activities. Multiple causes30 have been proposed. Soft-tissue sources have been implicated, with tendonitis or periostitis due to overload or unbalanced tendon effects. These can be due to biomechanical sources, such as a foot or ankle malalignment. Poor balancing of the gastrocsoleus posteriorly, the posterior tibialis medially, the anterior tibialis anteriorly, or the peroneals laterally may cause symptoms. The most commonly accepted source of shin splints is a periosteal reaction due to stressing of the insertional fascial areas from the gastrocsoleus or posterior tibialis. Tenderness is elicited by palpation of a length of the involved tibia. Careful evaluation11 of shoes, feet, ankle, tendons, lower extremity alignment, and gait as well as training history should allow changes that will bring symptomatic relief. Orthotics may help with hyperpronation. Rest until symptoms resolve, followed by pool running and bicycling, which may aid conditioning, are recommended until return to play. Surgery has been mentioned for recalcitrant symptoms.31 Radiographs may show a periosteal reaction. A bone scan32 may rule out a transverse osseous involvement (i.e., stress fracture) versus the linear periostitis reaction seen with shin splints.

Tibial Stress Fracture A tibial stress fracture is another source of leg pain in the athlete. Stress fractures in general may be defined as subclinical microfractures that progress to become symptomatic and may even result in a displaced fracture when improperly treated. In the tibia, they are relatively common, representing approxi-

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mately 17% of all stress fractures, and they are the most common stress fracture in the athlete.33 Typically, they occur posteriorly in the proximal or distal third of runners and tend to heal with rest.34 However, they may also occur in other sports and, more significantly, may occur at the anterior mid-diaphysis where healing is less predictable.35 Most patients present with a characteristic history. The leg pain is of insidious onset, associated with repetitive activities, and relieved by rest. Running and jumping sports are most often affected, including track, basketball, volleyball, dance, and football. While the cause is not completely clear, there is an obvious association with overuse. Thus, the athlete may describe an increase in training frequency or intensity, a change of shoes or practice surface, or another variation that could lead to excess biomechanical stresses. At the time of presentation, most often the pain has been present for weeks to months and sometimes even years. The pain may initially occur only after strenuous exercise, later becoming present even with simple walking. It may fluctuate with athletic seasons or gradually worsen with time until the athlete can no longer participate in sports. The examiner should obtain a history regarding amenorrhea in the female, thyroid disease, nutritional deficits, or other factors that may influence bone health. On physical examination, there is typically point tenderness only at the fracture, with relatively normal surrounding soft tissues. In contrast, shin splints are tender over a larger extent of the medial tibia. Symptoms of paresthesias, weakness, or motion restriction are generally absent. Some authors describe the use of tuning forks or distant bony percussion as pain reproductive methods. Imaging studies include radiography, bone scan, computed tomography, and MRI. Radiographs are generally normal for the first few weeks and may take months to show typical abnormalities, which include periosteal reaction, cortical lucency, sclerosis, or even a distinct fracture line. The anterior tibial stress fracture is recognized by its characteristic “dreaded black line”: on a lateral radiograph, this is a thickened area of anterior cortex in the middle third of the tibia with a distinct radiolucent line extending anterior to posterior (Fig. 64-5). While both bone scan and MRI are more sensitive than radiography, a bone scan is thought to be the more sensitive of the two, especially early in the disease course. In fact, it can continue to be positive long after clinical symptoms have resolved and should therefore not be used to monitor healing. The advantages of MRI include its noninvasive nature, ability to visualize soft-tissue pathology, and higher specificity. Treatment of tibial stress fractures depends on location. As stated previously, they most commonly occur on the compressive side of the bone (posterior), typically posteromedially, at the proximal and distal thirds of the bone. Treatment with nonsteroidal anti-inflammatory drugs, ice, physiotherapy, and activity modification generally reduces symptoms within 1 month and allows full sports participation by 3 months. Activity modification includes complete rest until pain free, cross-training, or restriction from running and jumping. Use of a long pneumatic splint has been reported to allow continued sports participation and symptom resolution within a month.36 Treatment of anterior tibial stress fractures is far more controversial. While most authors continue to recommend a trial of conservative treatment, it is well established that, without surgery, the healing rate of these fractures is significantly lower. In addition, the risk of progression to complete fracture is a real, albeit undefined, risk. A review of the literature revealed 15

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symptoms are limited to tenderness or slight swelling in that area. Cysts around the joint may also be symptomatic. Peroneal nerve irritation just posterior to the fibular head may be evaluated using Tinel’s test. Testing the anterior and lateral muscles by resisted dorsiflexion and eversion of the foot will stress the tibial-fibular joint and sometimes elicit symptoms, including pain and popping or shifting in that area. Plain radiographs, fluoroscopy, computed tomography scan, and MRI may be useful, but are frequently normal. A diagnostic/therapeutic injection of local anesthetic and corticosteroid can also be used. Treatment is generally conservative, but surgical stabilization has been described in recalcitrant cases, when instability of the joint is present.

Nerve Entrapment Nerve entrapments in the leg, similar to those previously described for the thigh, can include medially branches of the saphenous nerve, anterolaterally the peroneal39 or superficial peroneal nerve,40,41 and laterally the sural nerve. These are all described in rare cases. Localized areas of possible constriction are best identified by a positive Tinel sign along the course of the involved nerve. A diagnostic and potentially therapeutic injection of local anesthetic and corticosteroid may be helpful, especially if surgical release of constricting fascial soft tissue is considered.41 Figure 64-5 Anterior tibial stress fracture, the “dreaded black line.”

Vascular Entrapment documented stress fractures progressing to complete fracture.37 Both physician and athlete alike should be aware of this possibility and its consequences should the athlete be allowed to continue play prior to documented healing. This same review noted that of 73 attempts at conservative treatment, only 20 (27%) went on to radiographic healing. Surgical treatment has varied widely, including nonunion excision and bone grafting, intramedullary nailing, and plating. Of 57 surgical interventions reported in the literature, 32 (56%) had documented healing within 6 months. Many athletes were able to return to play prior to radiographically proven healing. In general, for patients with a radiographically apparent stress fracture of the anterolateral tibia, early surgery is commonly now employed. The most common surgical treatments are reamed intramedullary nailing and compression plating.

Proximal Tibial-Fibular Joint Pain While not common, inflammation or instability of the proximal tibia-fibula articulation is occasionally seen.38 Symptoms along the interosseous area may be localized to the proximal tibiafibular junction. Often instability is difficult to identify and

Vascular compression entities such as popliteal artery entrapment40 and effort-induced venous thrombosis have been described. Popliteal artery entrapment reportedly causes intermittent claudication, and symptoms may be mimicked by passive dorsiflexion of the foot and checked by Doppler or radiographic studies. Effort-induced venous thrombosis may involve the upper or lower extremity. Diagnosis is confirmed by venous Doppler ultrasonography.

Muscle Herniation In the thigh and more commonly in the leg, aching symptoms may be due to muscle herniation through a defect in the encompassing fascial sheath. These defects can be congenital, spontaneous, or post-traumatic. Herniation sometimes can be grossly seen or palpated. Appreciation may be enhanced with positioning or stressing the muscle belly. MRI or ultrasonography may also be helpful in delineating areas of involvement. The most commonly encountered area of involvement is in the anterolateral distal leg, where the superficial peroneal nerve exits the fascia. If conservative treatment is ineffective, surgery to enlarge the fascial defect (fasciotomy) is performed, eliminating the small confined defect through which the underlying muscle can herniate.

REFERENCES 1. Fu FH, Stone DA: Sports Injuries: Mechanisms, Prevention and Treatment. Baltimore, Williams & Wilkins, 1994. 2. Crisco JJ, Jokl P, Heinen GT, et al: A muscle contusion injury model: Biomechanics, physiology and histology. Am J Sports Med 1994;22:702–710. 3. Jackson DW, Feagin JA: Quadriceps contusions in young athletes: Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am 1973;55:95–105. 4. Noonan TJ, Garrett WE: Muscle strain injury: Diagnosis and treatment. J Am Acad Orthop Surg 1999;7:262–269.

5. Ryan JB, Wheeler JH, Hopkinson WJ, et al: Quadriceps contusions, West Point update. Am J Sports Med 1991;19:299–304. 6. Colosimo AJ, Ireland ML: Thigh compartment syndrome in a football athlete: A case report and review of the literature. Med Sci Sports Exerc 1992;24:958–963. 7. Whitesides TE, Haney TC, Morimoto K, et al: Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:43–51. 8. Garrett WE: Muscle strain injuries. Am J Sports Med 1996;24:S2– S8.

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9. Mair SD, Seaber AV, Glisson RR, et al: The role of fatigue in susceptibility to acute muscle strain injury. Am J Sports Med 1996;24:137– 143. 10. Garrett WE, Nikolaou PK, Ribbeck BM, et al: The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension. Am J Sports Med 1988;16:7–12. 11. Viitasalo JT, Kvist M: Some biomechanical aspects of the foot and ankle in athletes with and without shin splints. Am J Sports Med 1983;11:125–130. 12. Styf J: Entrapment of the superficial peroneal nerve. J Bone Joint Surg Br 1989;71:131–135. 13. Clanton TO, Coupe KJ: Hamstring strains in athletes: Diagnosis and treatment. J Am Acad Orthop Surg 1998;6:237–248. 14. Zarins B, Ciullo JV: Acute muscle and tendon injuries in athletes. Clin Sports Med 1983;2:167–182. 15. DeLee JC, Drez D: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 1487–1488. 16. Hughes C, Hasselman CT, Best TM, et al: Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med 1995;23:500–506. 17. Temple HT, Kuklo TR, Sweet DE, et al: Rectus femoris muscle tear appearing as a pseudotumor. Am J Sports Med 1998;26:544–548. 18. Meyers WC, Foley DP, Garrett W, et al: Management of severe lower abdominal or inguinal pain in high-performance athletes. Am J Sports Med 2000;28:2–8. 19. Akermark C, Johansson C: Tenotomy of the adductor longus tendon in the treatment of chronic groin pain in athletes. Am J Sports Med 1992;20:640–643. 20. Hershman EB, Lombardo J, Bergfeld JA: Femoral shaft stress fracture in athletes. Clin Sports Med 1990;9:111–119. 21. Johnson AW, Weiss CB, Wheeler DL: Stress fractures of the femoral shaft in athletes: More common than expected. Am J Sports Med 1994;22:248–256. 22. Romanoff ME, Cory PC, Kalenak A, et al: Saphenous nerve entrapment at the adductor canal. Am J Sports Med 1989;17:478–481. 23. Balaji MR, DeWeese JA: Adductor canal outlet syndrome. JAMA 1981;245:167–170. 24. Mubarak SJ, Owen CA: Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 1977;59:184–187.

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25. Fronek J, Mubarak SJ, Hargens AR, et al: Management of chronic exertional anterior compartment syndrome of the lower extremity. Clin Orthop 1987;220:217–227. 26. Pedowitz RA, Hargens AR, Mubarak SJ, et al: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990;18:35–40. 27. Ota Y, Senda M, Hashizume H, et al: Chronic compartment syndrome of the lower leg: A new diagnostic method using near-infrared spectroscopy and a new technique of endoscopic fasciotomy. Arthroscopy 1999;15:439–443. 28. Leach RE: Leg and foot injuries in racquet sports. Clin Sports Med 1988;7:359–370. 29. Straehley D, Jones WW: Acute compartment syndrome (anterior, lateral, and superficial posterior) following tear of the medial head of the gastrocnemius muscle. Am J Sports Med 1986;14:96–99. 30. James SL, Bates BT, Osternig LR: Injuries to runners. Am J Sports Med 1978;6:40–50. 31. Detmer DE: Chronic shin splints. Classification and management of medial tibial stress syndrome. Sports Med 1986;3:436–446. 32. Rupani H, Holder L, Espinola D, et al: Three-phase radionuclide bone imaging in sports medicine. Radiology 1985;156:187–196. 33. Morris JM, Blickenstaff LD: Fatigue Fractures: A Clinical Study. Springfield, IL, Charles C Thomas, 1967. 34. Devas MB: Stress fractures of the tibia in athletes or “shin soreness.” J Bone Joint Surg Br 1958;40:227–239. 35. 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 1988;16:250–255. 36. Dickson TB: Functional management of stress fractures in female athletes using a pneumatic leg brace. Am J Sports Med 1987;15:86–89. 37. Hurt JH, Mair SD: Anterior tibial stress fracture: A systematic review of the literature. 2006 (In press). 38. Ogden JA: Subluxation and dislocation of the proximal tibiofibular joint. J Bone Joint Surg Am 1974;56:145–154. 39. Leach RE, Purnell MB, Saito A: Peroneal nerve entrapment in runners. Am J Sports Med 1989;17:287–291. 40. Lysens RJ, Renson LM, Ostyn MS, et al: Intermittent claudication in young athletes: Popliteal artery entrapment syndrome. Am J Sports Med 1983;11:177–179. 41. Safran MR, Garrett WE, Seaber AV, et al: The role of warm-up in muscular injury prevention. Am J Sports Med 1988;16:123–129.

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65

Physical Examination and Evaluation Joel Hurt

In This Chapter Ankle Hindfoot Midfoot Forefoot Special tests

INTRODUCTION • Accurate diagnosis of foot and ankle pathology requires a careful, systematic approach. • Knowledge of the fundamental biomechanics of the foot is essential in making a correct diagnosis. • This chapter describes the foot and ankle examination with regard to the athlete, making mention of relevant biomechanics when necessary.

INSPECTION The foot and ankle physical examination begins with a thorough visual inspection. Begin by noting the athlete’s training shoes if possible. The size, type, and condition of the shoe should be appropriate for the training being done. The force across the foot for each foot strike is approximately 3 times the body weight during running, occurring approximately 3000 times every mile for the average jogger.1 Obviously, a shoe’s ability to absorb force is critical for injury prevention. After 500 miles, remember that a shoe retains less than 60% of its cushion.2 Also, note any abnormal wear patterns. Normally, the heel has a slight tendency to have more wear laterally. Excessive medial sole wear along the heel may indicate overpronation. In a similar fashion, a large degree of distal sole wear over the metatarsals can indicate an equinus contracture or may simply be secondary to the athlete’s normal running style. Comparison with the other shoe is helpful, especially if complaints are unilateral and the shoe wear is not symmetric. Next, make sure that both legs are visible from the knee down. The patient should begin standing, first facing away from and then toward the examiner. As always, throughout the examination, compare any findings with the contralateral side to check for asymmetry. Note the alignment of the hindfoot. As viewed from behind, the heel should be neutral (Fig. 65-1). In addition, provided the knees both face directly forward, the same number of toes should be visible on the lateral side. With

pes planus conditions (e.g., posterior tibialis dysfunction), an increased number of toes will be seen on the lateral side. This “too many toes” sign is usually accompanied by a valgus position of the heel. On double heel rise, the hindfoot should move into a position of relative varus (Fig. 65-2). Failure to do so is most often consistent with a posterior tibialis tendon dysfunction. Likewise, inability to perform a single heel rise (while keeping the knee in extension) may indicate the same pathology of the Achilles tendon-gastrocsoleus complex, or a bony abnormality. If a varus position of the hindfoot is noted on initial examination, a Coleman lateral block test should be performed (see later discussion). Next, the patient should face the examiner. Note overall alignment of the hind-, mid-, and forefoot and the status of the midfoot arch. The talar head may be abnormally protruded medially with a flatfoot deformity. Crossover and hammer toes, hallux valgus, and other distal pathology are best observed in a weight-bearing position. Finally, have the patient walk while carefully watching symmetry, ability to achieve a plantigrade foot, avoidance patterns, and flow of the stance phase (heel strike to toe off). Inspect the feet as the athlete sits on the examination table. Take note of calluses on the side and undersurface of the foot. Note areas of swelling and contusion and reinspect the arch for comparison with the weight-bearing state. An arch that remains flat even while non-weight bearing may indicate a fixed deformity such as a tarsal coalition.

EXAMINATION Hindfoot Palpation should begin at nontender areas to maintain a relaxed, compliant state. Progression to areas of tenderness can help lead to a provisional diagnosis (Figs. 65-3 and 65-4). In the posterior hindfoot, examine the heel cord for continuity, tenderness, and swelling. Achilles tendonitis may present with simply pain or may have associated tendon enlargement. Try to distinguish between tenderness in the tendon itself and pain located more anterior in the retrocalcaneal bursa. In addition, Haglund’s or “pump-bump” deformity will present as a painful bony prominence of the posterior superior calcaneal process (Fig. 65-5). When symptomatic, it usually results in tenderness proximal and lateral to the Achilles tendon insertion. A calcaneal stress fracture may be differentiated from these latter entities by compressing the medial and lateral calcaneal surfaces between the bases of the hands, causing pain when the test is positive. In late childhood and early adolescence, Sever’s disease (calcaneal apophysitis) usually presents with tenderness more distal than the Achilles tendon insertion, at the most posterior and plantar

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Figure 65-1 Neutral hindfoot.

aspect of the calcaneus. On both the lateral and medial hindfoot, tendon sheaths may be identified and then palpated along their course. For instance, instruct the patient to evert the foot in order to tense the peroneal tendons for identification. Pain with resisted eversion as well as localized peroneal tendon tenderness helps to diagnose peroneal tendonitis. This method of examination may be repeated for all tendons in the foot, including the flexor hallucis longus, flexor digitorum longus, and posterior tibialis tendons on the medial hindfoot. Furthermore, in the case of the peroneal tendons, specific signs of tendon subluxation may be sought as indicated. Test by palpating the

Figure 65-3 Lateral side of the foot/ankle. Areas of tenderness correspond to the following diagnoses: 1, retrocalcaneal bursitis; 2, peroneal tendonitis; 3, anterior ankle joint line synovitis; 4, fifth metatarsal base fracture; 5, navicular stress fracture; 6, Morton’s neuroma.

tendons as they pass posterior to the lateral malleolus and have the patient actively move the foot from a position of inversion to eversion. When the test is positive, the examiner will feel the tendons snap over the bone. Occasionally, resisted eversion will be necessary to elicit tendon subluxation.

Ankle Next inspect the ankle joint proper. The medial and lateral malleoli, anterior tibiotalar joint line, and the regions of the deltoid, anterior talofibular (ATFL), and calcaneofibular (CFL) ligaments are all readily available to direct palpation, thus facil-

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Figure 65-2 Single heel rise with hindfoot inversion.

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Figure 65-4 Medial side of the foot/ankle. Areas of tenderness correspond to the following diagnoses: 1, Achilles tendonitis; 2, retrocalcaneal bursitis; 3, calcaneal apophysitis; 4, calcaneal stress fracture; 5, tibialis posterior tendonitis/symptomatic accessory navicular; 6, bunion.

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Forefoot

Figure 65-5 Haglund’s deformity (pump bump).

itating diagnosis. For instance, tenderness to touch over only the ATFL and not the lateral malleolus helps differentiate an ankle sprain from a fracture. Care must also be taken to distinguish tenderness over the ATFL from a painful sinus tarsi, as can occur with sinus tarsi syndrome. When an isolated syndesmotic injury (i.e., high ankle sprain) is suspected, perform the squeeze test by compressing the tibia and fibula at the junction of the middle and distal thirds to reproduce the pain, or, alternatively, dorsiflex and externally rotate the foot while stabilizing the leg at the knee. The resulting torque on the lateral malleolus will cause pain if the syndesmosis is injured. The tibiotalar joint itself should be examined along the anterior joint line where painful spurs can develop, by plantar flexing the ankle and directly palpating the talar dome (to evaluate for osteochondral injury), and by differentiating soft-tissue edema from effusion. Check for an ankle effusion by simultaneously compressing the anteromedial (medial to the tibialis anterior tendon) and anterolateral clear spaces (lateral to the extensor digitorum longus tendon). A distinct fluid wave will be felt when an effusion is present. In addition, the foot is generally held in a slightly plantar-flexed position to relieve intra-articular pressure. Last, painful plantarflexion-dorsiflexion or inversioneversion of the hindfoot will help differentiate tibiotalar versus subtalar joint pathology, respectively.

Midfoot The midfoot joints should be manipulated to check for inflammation. Simply stabilize the hindfoot with one hand and move the forefoot in a circular motion. Follow this up with joint specific palpation including the talonavicular, calcaneocuboid, naviculocuneiform, and tarsometatarsal joints. On the medial side, specifically examine for tenderness over the navicular bone itself (to rule out a stress fracture) as well as at its medial border. This is where both the posterior tibialis tendon inserts and a symptomatic accessory navicular is located. On the lateral midfoot, be sure to check for tenderness over the insertion of the peroneus brevis at the proximal fifth metatarsal. Pain here could be indicative of avulsion fracture, tendonitis, or a symptomatic os peroneum. This should be differentiated from a fifth metatarsal stress fracture (e.g., Jones fracture), which will typically be tender just distal to the metaphysis.

In the forefoot, palpate the metatarsal heads and necks for excessive tenderness to diagnose lesser metatarsal overload (as may occur after bunion surgery) or metatarsal stress fractures, respectively. The pain from an interdigital neuroma (i.e., Morton’s neuroma) is similar in location but localized specifically between metatarsal heads, most often the third interspace. Mediolateral compression of the metatarsal heads may produce a click (Mulder’s click) and generally reproduces the pain of a Morton neuroma, sometimes requiring 20 to 30 seconds of constant pressure. Special attention should be paid to the first metatarsophalangeal (MTP) joint. Hallux rigidus often presents with painful first MTP motion (especially dorsiflexion) and a tender, prominent dorsal spur. Likewise, an obvious hallux valgus deformity (i.e., bunion) will typically be quite tender over the prominent medial first MTP joint line. If there is concern for hallux rigidus, perform the grind test, which entails simultaneous compression and circumduction of the first MTP. Reproduced pain and crepitus is a positive indicator of first MTP osteoarthritis. Lesser MTP synovitis may be diagnosed by direct superior-inferior joint line compression. This condition may also have painful hyperlaxity in the superior-inferior plane. Grasp the proximal phalanx and the corresponding metatarsal head and reciprocally translate up and down; excessive motion combined with pain will often be present. The toes should be separated to visualize painful corns and calluses, and ingrown toenails should be easily distinguished from other sources of discomfort. Common toe deformities include hammer, mallet, and claw toes. A hammer toe entails a neutral or extended MTP joint, a flexed proximal interphalangeal (PIP) joint, and an extended distal interphalangeal (DIP) joint. Often, a painful callous is present on the dorsal skin of the PIP. The second toe is most often affected (due to its longer length), and it is uncommon to find multiple hammer toes on the same foot. A mallet toe presents as a neutral MTP joint, a neutral or extended PIP joint, and a flexed DIP joint. Finally, a claw toe has a flexion deformity at both the PIP and DIP joints. A tender callus generally occurs at the dorsal PIP, similar to a hammer toe. Multiple claw toes are most commonly due to long-term use of shoes that are too constrictive, although other etiologies such as Charcot-Marie-Tooth or MTP inflammatory disease should be considered.

Plantar Surface The plantar surface of the foot should likewise be specifically palpated. In the hindfoot, a painful heel pad should be differentiated from plantar fasciitis. The latter typically has tenderness at the anteromedial border of the calcaneus, whereas the former is more painful in the center of the fat pad. Warts may be distinguished from calluses by their punctuate bleeding when shaved, greater tenderness with side-to-side (versus direct) compression, and the absence of skin wrinkles passing through their substance. On the plantar surface of the first MTP, the sesamoids should be examined for point tenderness as may occur with sesamoiditis or fracture. The plantar surface of the first MTP will similarly be tender after turf toe in which the plantar capsule has been injured or disrupted.

Functional Range of Motion Normal values for joint range of motion can be found in Table 65-1. Start by evaluating the heel cord and gastrocsoleus complex (GSC) for excessive tightness. Passively dorsiflex the foot while the knee is flexed and note the motion. Then pas-

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Table 65-1 Normal Joint Range of Motion5 Ankle

20 degrees of dorsiflexion

50 degrees of plantarflexion

Subtalar

20 degrees of inversion

10 degrees of eversion

First MTP

70 degrees of dorsiflexion

45 degrees of plantarflexion

MTP, metatarsophalangeal.

sively extend the knee while holding the foot dorsiflexed. Because the GSC crosses the knee and ankle joints, when tight, it will force the foot into relative plantarflexion as the knee extends (Figs. 65-6 and 65-7). A supple GSC is essential for prevention of multiple foot injuries including bunions, forefoot overload, and tendonitis. At least 10 degrees of ankle dorsiflexion is required during the support phase of running.3 The tibiotalar joint should then be checked for range of motion while the knee is flexed (to eliminate the GSC contribution). To evaluate the subtalar joint, first place the ankle in a plantigrade position, locking the talus in the ankle mortise. Then passively invert and evert the hindfoot. It is normal to have twice as much inversion. The subtalar joint is critical for accommodating uneven surfaces, and lack of motion here may indicate a tarsal coalition or fibrosed joint as may occur in late stages of posterior tibialis dysfunction. In the midfoot, examination for excessive plantar-dorsal motion (more than approximately 1 cm) of the first tarsometatarsal joint is useful in making treatment decisions for bunions.4 Similarly, the first MTP should be checked to ensure motion, particularly full, painless dorsiflexion that may be limited by hallux rigidus or turf toe.

Neurovascular Examination In most athletes, the neurovascular examination will be relatively normal. However, it is still important to verify, particularly with an established diagnosis of diabetes.

Figure 65-6 Testing for gastrocsoleus complex tightness (knee flexed).

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Figure 65-7 Testing for gastrocsoleus complex tightness (knee extended). Note relative plantarflexion of the foot indicating a tight gastrocsoleus complex.

Neurologic Examination Knowledge of the foot and ankle neuroanatomy is helpful in combining physical examination findings to make a diagnosis. Initial evaluation begins with testing patients for sensation to light touch. If further investigation is indicated, a 5.07 SemmesWeinstein monofilament should be used to test sensation.6 Diabetics and others with distal neuropathies unable to feel this monofilament are thought to be below the threshold for protective sensation and at high risk of neuropathic ulceration. Occasionally, an isolated decrease in sensation may be present in the plantar aspect of toe web spaces with corresponding interdigital neuromas. This finding is highly specific when present.4 To distinguish diffuse distal neuropathy from a superficial peroneal nerve palsy, note that in the latter, the foot dorsum will be numb except for first web space sparing (innervated by branches of the deep peroneal nerve). In patients with previous foot surgery, signs of peripheral nerve injury should be sought. These include point tenderness over a possible neuroma, percussion-induced paresthesias, and anesthesia distal to the suspected injury. All motor units should be checked for strength with standard 0 through 5 grading. Most of the muscle units may be checked with simple manual resistance. For instance, to check the posterior tibialis and accessory foot invertors, have the patient actively invert the foot and then resist that force with the examiner’s hand. Compare with the contralateral side if normal. Not only will this help determine strength and neurologic function, but pain reproduced only with resisted active motion (i.e., not with passive motion) is indicative of pathology in the musculotendinous unit being tested. Two special circumstances should be noted. First, testing of the peroneus longus is not intuitive. To check strength for this tendon, have the patient perform resisted plantar flexion of the first ray (the primary function of the peroneus longus). Second, the GSC is generally too strong to be tested by hand. Even a deficient GSC can typically overcome manual resistance without detection of weakness. Instead, have the patient perform multiple single-limb heel rises and compare with the contralateral side to identify deficits. If any part of the neurologic examination is abnormal, a thorough neurologic assessment should be performed to check for possible etiologies in the proximal leg or the CNS.

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Vascular Examination This generally involves palpation of the dorsalis pedis pulse (just proximal and lateral to the first metatarsal base) and the posterior tibial pulse (approximately 1 cm posterior to the medial malleolus). If pulses are absent or diminished, a full vascular assessment including Doppler pulse pressure measurements is indicated.

SPECIAL TESTS Thompson Test The Thompson test is designed to diagnose an Achilles tendon rupture. Have the patient lie prone on the examining bed with the feet dangling off the end. Start with the normal side by squeezing the calf musculature and noting the normal, brisk plantarflexion of the foot. Next, perform the same maneuver on the leg in question. The test is positive for a rupture if absent (or significantly diminished) plantarflexion is noted. In this case, a palpable defect is usually present in the Achilles tendon (Fig. 65-8).

Figure 65-9 Anterior drawer test.

Coleman Lateral Block Test During examination, if a hindfoot varus deformity is found (as can occur with Charcot-Marie-Tooth disease), it is important to determine whether it is fixed or flexible. The Coleman lateral block test, designed to answer this question, is performed by having the patient stand on a block (approximately 1 inch high) with support under only the heel and lateral metatarsals. Specifically, the first metatarsal is permitted to plantarflex freely. If the deformity is flexible, the hindfoot will correct from a position of varus to neutral. If it is fixed, it will remain in varus, significantly influencing treatment options.

Anterior Drawer Test After an ankle sprain, the anterior drawer test is used to evaluate the integrity of the ATFL and, to a lesser extent, the CFL. It is most useful in cases of suspected chronic ankle instability. Brostrom7 showed that this test’s sensitivity was relatively low in the acute setting secondary to guarding. First, have the patient relax the affected extremity with the knee flexed. Then, stabi-

Figure 65-8 Thompson test. Absent or diminished plantarflexion indicates Achilles tendon rupture.

lize the leg with one hand while grasping the heel with the other hand and applying an anterior force to affect anterior talar translation. Perform in both plantarflexion (tests ATFL) and dorsiflexion (tests CFL). A few millimeters of movement is normal, and variation among different individuals can be significant. Comparison to the contralateral side is thus essential (Fig. 659).

Talar Tilt Test Similar to the anterior drawer test, the talar tilt test is used in cases of suspected chronic ankle instability. However, it differs from the drawer test by examining primarily the CFL instead of the ATFL. Again, with the patient relaxed and the knee flexed, stabilize the leg with one hand and grasp the heel with the other. Then, with the foot first dorsiflexed (for CFL examination) and then plantarflexed (for ATFL examination), invert the hindfoot. Excessive motion may indicate instability of the tibiotalar joint, subtalar joint, or both (Fig. 65-10).

Figure 65-10 Talar tilt test.

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REFERENCES 1. Southmayd W, Hoffman M: Sports Health: The Complete Book of Athletic Injuries. Quick Fox, 1981. 2. Barber FA, Sutker AN: Iliotibial band syndrome. Sports Med 1992;14: 144–148. 3. James SL: Running injuries to the knee. J AAOS 1995;3:309–318. 4. Alexander IJ: The Foot: Examination and Diagnosis. New York, Churchill Livingstone, 1997.

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5. Sammarco GS: Foot and Ankle Manual. Baltimore, Williams & Wilkins, 1998. 6. Brodsky W: Outpatient diagnosis and care of the diabetic foot. Instruct Course Lect 1993;42:121–139. 7. Brostrom L: Sprained ankles: III Clinical observations in recent ligament ruptures. Acta Chir Scand 1965;130:560–569.

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Ankle Ligament Injury and Instability Jeffrey D. Willers and Robert B. Anderson

In This Chapter Acute lateral ankle sprain Chronic ligamentous instability Nonoperative management Surgery—lateral ankle reconstruction Modified Brostrom Modified Brostrom–split Evans Chrisman-Snook

INTRODUCTION • Ankle sprains are among the most common athletic injuries. • The majority of ankle sprains involve the lateral ligament complex. • Chronic instability is a relatively common sequelae. • Associated injuries are common with acute lateral ligament injury and should be considered when symptoms persist. • Rehabilitation generally allows return to sport. • In chronic cases, surgical reconstruction of the lateral ligaments is considered.

Ankle sprains are the most common sports-related and recreational injury, representing an estimated 40% of all athletic injuries.1 Ankle sprains comprise an especially significant percentage of injuries in selective sports: 45% to 53% of all basketball injuries, 21% to 31% of soccer injuries, and 10% to 15% of football injuries that result in time lost.2,3 Jackson et al4 likely reported the truest incidence of ankle injuries in an athletic population in a study of U.S. Military Academy cadets. This study found that approximately one third of all cadets will sustain an ankle injury requiring medical treatment during their 4-year term at the Academy. The vast majority (approximately 75%) of ankle sprains involve injury to the lateral ligament complex. The medial ligaments, however, are infrequently injured with eversion injuries. These medial injuries are rarely isolated injuries but instead usually occur in conjunction with lateral ankle injury or fracture.5 The anterior portion of the deltoid ligament is most frequently injured. An in-depth discussion of medial ligament injury and instability is beyond the scope of this chapter; thus, we focus on lateral ligament injury and instability. Although most ankle sprains do heal with conservative treatment, it has been estimated in multiple studies that long-term

sequelae do occur in a significant percentage of patients (up to 50%).6–9 Chronic instability has been reported to occur in 20% to 42% of patients with acute ankle sprains.10,11

RELEVANT ANATOMY Lateral ankle stability is provided by both static and dynamic restraints. Both the lateral ligaments and the bony configuration of the ankle afford static restraint. The peroneal tendons supply the ankle’s primary dynamic restraint. The bony configuration of the talus contributes approximately 30% of the resistance to rotational forces about the ankle, whereas soft tissues provide the remaining 70%.12 The talus has a flare in its anterior half, which provides significant bony restraint to lateral motion when the talus is engaged in the mortise with the ankle in dorsiflexion. As the talus plantarflexes, the narrower surface of the talus moves into the mortise, resulting in a marked reduction of bony stability and increased susceptibility of the ankle to inversion injury. The lateral ligaments of the ankle are comprised of three main bands (Fig. 66-1): the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL). The ATFL is a thickening of the anterior capsule that courses anteromedially from its origin on the distal anterior tip of the lateral malleolus to insert on the talar body just anterior to the lateral articular surface of the talus. The ATFL is the weakest of the lateral ankle ligaments.13 The CFL is a round (6 to 8 mm in diameter) ligament that originates from the lower anterior border of the lateral malleolus and courses obliquely in a posteromedial direction across both the tibiotalar and subtalar joints to insert on the lateral surface of the calcaneus.14 The CFL imparts stability to both the tibiotalar and subtalar joints. The CFL acts as the floor of the peroneal sheath; thus, injury to the CFL is frequently associated with disruption of the peroneal sheath and infrequently with a tear of the peroneal tendons. Last, the PTFL runs horizontally from its origin on the posterior margin to the lateral malleolus to the posterolateral tubercle of the talus. The lateral ligament complex functions as a unit during ankle motion to provide stability. In the neutral position the ATFL is relaxed, but its strain increases significantly as the ankle moves into plantarflexion. The CFL is relaxed in the neutral position and under significantly increased strain as the ankle is dorsiflexed. The tibiotalar joint is inherently stabilized with stance (loading) due to the configuration of the mortise and the normally valgus positioned hindfoot. Subtalar joint stability is not enhanced by loading but instead relies completely on the ligamentous complex. It is for this reason and the fact that the CFL

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Figure 66-1 Essential anatomy of the lateral ligament complex of the ankle.

imparts stability across both joints that we often consider the presence of combined instability patterns.

ACUTE LATERAL ANKLE INJURY Clinical Features and Evaluation An acute injury to the ankle ligaments is generally apparent from the patient’s history. The patient typically complains of lateral ankle pain and swelling following a forced plantarflexion and inversion injury. Frequently, the history will include a “pop” or “snap” during the traumatic event, but this does not appear to correlate with severity or with long-term sequelae.15 Proper examination should include evaluation of range of motion, swelling, tenderness, and stability. The area of maximal swelling and tenderness is usually indicative of the area of ligament injury; the ATFL is most frequently injured at its fibular origin and the CFL at its calcaneal insertion. Additionally, lateral ligament injuries are commonly categorized by severity into three grades (Table 66-1).16 Many associated injuries can be found in patients with acute lateral ankle injury (Table 66-2).17 These should all be considered when evaluating the patient and thorough examination performed to rule out occult injury.

Diagnostic Studies Although radiographs are frequently obtained in the evaluation of ankle pain, they are often not necessary for the evaluation of ankle sprains. The Ottawa Ankle Rules was developed to establish criteria for performing radiographs.18 According to the Ottawa Ankle Rules, radiographs are necessary only with (1) bony tenderness at the posterior edge or tip of either malleolus,

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(2) inability to bear weight immediately following the injury and for four steps in the emergency department, or (3) bony tenderness at the base of the fifth metatarsal. These criteria reduce the number of unnecessary radiographs without reducing the sensitivity for diagnosing fractures (remains at nearly 100%).18 If indicated, standard radiographs should include three views of the ankle (anteroposterior, lateral, and mortise). The role of stress radiographs of the ankle remains controversial. While numerous articles cite parameters of “significant” instability, the anterior drawer and talar tilt stress radiographs have not been shown to be reliable in diagnosing instability and we have not found them helpful in our decision making process. Magnetic resonance imaging also has a role in the evaluation of select acute ankle injuries. This sensitive test can be benefi-

Table 66-1 Acute Lateral Ankle Injury Grading Grade

Ligament Involvement

Physical Examination

I

Ligament stretch, no tear

Minimal swelling, mild tenderness, no instability, can weight bear

II

Torn ATFL, intact CFL

Moderate swelling and tenderness, difficulty with weight bearing

III

Complete tear of both ATFL and CFL

Marked swelling, diffuse tenderness, inability to bear weight

ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament.

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Table 66-2 Potential Associated Injuries with Acute Lateral Ankle Ligament Injury Ligamentous Injuries Hindfoot sprain Midfoot sprain (Lisfranc) Bony Injuries/Fractures Malleoli (medial, lateral, or posterior) Anterior process of calcaneus Base of fifth metatarsal Lateral posterior talar process Proximal fibula Midtarsal

At approximately 3 weeks following injury, ankle mobilization is initiated through gentle range-of-motion and controlled stretching. When pain-free range of motion and weight bearing have been established, strengthening and proprioception training can begin; timing of this varies depending on severity of the injury. Multiple studies have compared functional treatment/early protected mobilization with both cast immobilization and acute surgical repair (including a large meta-analysis by Kannus and Renstrom20). Functional treatment results in a more rapid recovery of ankle mobility and an earlier return to work or physical activity without sacrificing mechanical stability.21,22 Additionally, if a patient does fail initial nonoperative treatment, delayed reconstruction can be performed even several years following the injury with comparable results to primary repair.

CHRONIC LATERAL ANKLE INSTABILITY

Osteochondral Lesions Talus (usually posterolateral or anteromedial)

Clinical Features and Evaluation

Distal tibia

Patients with isolated chronic lateral ankle instability typically presents with complaints of periodic “giving way” and a history of several previous severe ankle sprains. Although these intermittent episodes are typically associated with a brief period of pain and dysfunction, most patients with isolated instability are essentially pain free between episodes and do not experience mechanical symptoms. If pain is present between episodes of giving way, secondary diagnoses must be considered (Table 664).23

Tendon Injuries Peroneal brevis Peroneal longus Peroneal instability/retinacular tear Os peroneum syndrome Neurapraxic Injuries Superficial peroneal nerve Sural nerve

cial if the clinician suspects associated injuries or, more subacutely, if the recovery is not following the typical course of recovery.

Table 66-4 Lesions to Consider in Patients with Persistent Symptoms and Chronic Lateral Ankle Instability Bone

Treatment Options

Anterior process of calcaneus fracture

Patients with grade I or II ankle injuries respond well to conservative treatment.10,19 A functional treatment protocol is initiated that consists of several phases (Table 66-3). Treatment immediately following the injury consists of RICE (rest, ice, compression, and elevation) with the goal to reduce swelling, hemorrhage, and pain. During the 1- to 3-week period (proliferation phase), protection in the form of taping or bracing should be used. Weight bearing should be initiated as soon as it is tolerated as it is considered beneficial to the healing process.

Lateral/posterior talar process fracture Malleolar fracture Base of fifth metatarsal fracture Anterior ankle bony impingement Tarsal coalition (osseus or fibrous) Ligament Subtalar instability Syndesmosis injury Medial ankle instability Tendon

Table 66-3 Functional Rehabilitation Program Stage

Time After Injury

Treatment

1

Immediate

RICE (rest, ice, compression, elevation)

Acute injury phase

Peroneus longus or brevis tear Peroneal instability/superior peroneal retinacular injury Painful os peroneum syndrome (POPS) Cartilage

2

Proliferation phase

1–3 wk

Protection with tape or brace

Osteochondral lesions of talus or tibia

3

Maturation

3–6 wk

Controlled stretching and range of motion

Neurapraxia of sural or superficial peroneal nerve

4

Remodeling

6–8 wk until 6–12 mo

Continued motion and strengthening with goal of full return to activity

Neural

Soft Tissue Anterolateral ankle soft-tissue impingement Sinus tarsi syndrome

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A complete physical examination of the ankle should include assessing the joint above (knee) and below (subtalar). Lower extremity alignment should also be assessed; hindfoot varus predisposes the ankle to inversion injury. Hindfoot/midfoot mobility should also be evaluated, as it is not uncommon for tarsal coalition to present as recurrent ankle sprain. The peroneal tendons should also always be assessed as they can also be injured. Peroneal examination should involve an assessment of eversion strength, stability of the tendons in the fibular groove, and tenderness and swelling along the course of the tendons. The anterior drawer test evaluates the integrity of the ATFL by assessing the amount of anterior translation of the talus with respect to the tibia. This test is properly performed with the patient sitting, the knee flexed 90 degrees, and the ankle positioned in 10 degrees of plantar flexion. The tibia is stabilized while an attempt is made to draw the talus forward. A positive drawer is defined as greater than 5 mm more than the contralateral side or absolute value of 10 mm of translation.24–26 The quality of the endpoint is also noted. A positive test is only significant if it correlates with the history; Brostrom and Sundelin7 found that only one half of those with a positive anterior drawer had symptomatic instability. The talar tilt test is another common test performed. This test, first described by Faber in 1932, is performed by grasping the calcaneus and talus in one hand while stabilizing the distal tibia in the other. The calcaneus and talus are then inverted. Increased talar tilt, when compared with the contralateral side, indicates rupture of both the CFL and ATFL. Debate remains on what constitutes physiologic tilt; Cox27 reports the normal range of tilt values between 5 and 23 degrees.

Nonoperative Treatment Options As with treatment of acute lateral ankle injuries, functional treatment remains the mainstay of initial treatment for chronic lateral instability. Functional treatment protocols emphasize stretching, muscle strengthening (particularly peroneal), and proprioception.28 Prior to considering surgery, most agree that a trial of a minimum of 6 weeks of aggressive physical therapy should be attempted. Shoe wear modifications or orthotic devices can be used for flexible foot and ankle malalignment and instability. Most patients with lateral ankle instability, particularly those with dynamic supination, will benefit from an external lateral heel wedge. External stabilization of the ankle by taping or braces is also employed. Taping demonstrates excellent initial support, but the amount of support decreases substantially with time, with a 50% reduction at 10 minutes29,30 and no support after 1 hour of exercise.31 A wide variety of commercially available ankle braces exists. These braces consist of rigid or flexible materials in combination with special systems of straps.

Surgical Treatment Options If symptomatic instability persists despite an adequate functional rehabilitation program and bracing, lateral ligament reconstruction is indicated. More than 80 surgical procedures have been described to reconstruct the lateral ankle ligaments. These procedures can be grouped into either anatomic repair or nonanatomic repair. Anatomic repair is preferred as it preserves the natural biomechanics of the ankle. Nonanatomic biotenodesis techniques are used in select cases: obesity, poor soft tissue (revision procedures or connective tissue disorder/generalized

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ligamentous laxity), or high-demand patients at risk of repetitive external varus stresses (e.g., football linemen).23 In patients with osteochondral or impingement lesions, arthroscopy is performed as the primary procedure followed immediately by open lateral ligament reconstruction. In 2000, DiGiovanni et al32 published a retrospective review of associated injuries found during primary lateral ankle ligament reconstruction. They found significant intra-articular pathology: anterolateral impingement lesions (67%), ankle synovitis (49%), loose bodies (26%), and talar osteochondral lesions (23%). Similarly, Komenda and Ferkel33 found a 25% prevalence of chondral injuries in 55 unstable ankles. Others have reported cartilage damage in up to 95% of chronically unstable ankles.34 Due to the high percentage of associated intra-articular pathology in patients with chronic lateral ankle instability, some advocate arthroscopy as the initial diagnostic step during reconstruction of ankle ligaments.

Modified Brostrom Anatomic Lateral Ligament Reconstruction In 1966, Brostrom14 first reported on 60 patients who underwent delayed direct repair of the ATFL and CFL by shortening of the torn ends and midsubstance suturing (Fig. 66-2). Gould et al35 modified this procedure in 1980 by adding an advancement of the extensor retinaculum over the Brostrom repair. The Gould modification reinforces the repair, limits inversion, and helps to correct the subtalar component of instability. Two surgical approaches are commonly used for this procedure: (1) an anterior incision along the distal and anterior border of the fibula (if no extra-articular pathology is suspected) or (2) a curvilinear posterior incision along the posterior border of the fibula (if peroneal tendon or retinacular pathology is suspected). An anterolateral arthrotomy is performed with caution to identify and protect branches of the sural and superficial peroneal nerves. The ATFL and CFL are divided in midsubstance and shortened/imbricated in standard vest-over-pants technique with 2-0 nonabsorbable braided suture. With the ankle in slight plantarflexion and eversion, the CFL sutures are secured first. The posterior heel is suspended and the ATFL sutures are then tied with caution to avoid anterior subluxation of the talus. Last, the repair is reinforced with the Gould modification as the extensor retinaculum is advanced and secured to the distal fibula.

Modified Brostrom–Split Evans Procedure In 1953, Evans36 described a biotenodesis procedure in which the peroneus brevis tendon is released at the musculotendinous junction, rerouted through the fibula, and then reattached to its proximal stump. This procedure was later modified by suturing the tendon back to itself instead of reattaching it to the proximal stump.37 In 1999, Girard et al38 reported on their results of the modified Brostrom-Evans procedure, a procedure that augments the Brostrom reconstruction with the addition of the anterior third of the peroneus brevis (Figs. 66-3 and 66-4). This procedure adds static restraint without a significant sacrifice of dynamic peroneal restraint. The authors believe that the modified Brostrom–split Evans has a role in revision surgery, obese individuals, heavy athletes (e.g., football lineman), laborers, and in patients with generalized ligamentous laxity. It is also our procedure of choice in patients with suspected combined instability patterns. Girard et al38 reported results in 21 patients at an average follow-up of approximately 2.5 years, finding that when compared to the uninjured contralateral side, there was no

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A

B

C

Figure 66-2 Modified Brostrom-Gould anatomic lateral ankle ligament reconstruction. A, Sensory nerve branches shown in relationship to the anterior incision. B, Midsubstance tears of the anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL). C, Modified Brostrom repair with imbrication of the ATFL and CFL. Continued

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Extensor retinaculum

D Figure 66-2—Cont’d D, Gould modification with interior extensor retinaculum–reinforcing repair.

significant difference in ankle plantarflexion or dorsiflexion and no significant loss of peroneal strength. They did report a significant loss of inversion. The surgical technique for the modified Brostrom–split Evans involves a posterior curvilinear incision extending from 4 to 5 cm proximal to the tip of the lateral malleolus along the course of the peroneal tendons to a point approximately 2 cm proximal to the base of the fifth metatarsal. The skin flaps are then elevated to expose the anterolateral ankle capsule, the anterior

distal fibula, and the peroneal tendons with care to avoid damage to branches of the superficial peroneal and sural nerves. The modified Brostrom portion of the procedure is carried out in identical fashion as described in the previous section with the sutures placed in the ATFL and CFL but not immediately tied. The peroneus brevis tendon is then exposed proximally and distally while maintaining the superficial peroneal retinaculum. The anterior one third of the peroneus brevis tendon is isolated distally and, using a no. 2 nylon suture, split from this distal point

Peroneus brevis tendon

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Figure 66-3 Modified Brostrom–split Evans procedure. The end-to-end (shortening with imbrication) Brostrom repair of the anterior talofibular ligament and calcaneofibular ligament is performed with nonabsorbable suture. The anterior one third of the split peroneus brevis is then rerouted through the fibula and secured with either sutures at entrance and exit with suture (shown) or with a biotenodesis screw. (From Girard P, Anderson RB, Davis WH, et al: Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246–252.)

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Figure 66-4 The Gould et al35 modification augments the modified Brostrom-split Evans with the advancement of the extensor retinaculum to the distal fibula. This reinforces the repair, limits inversion, and helps to correct the subtalar component of instability. (Girard P, Anderson RB, Davis WH, et al: Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246–252.)

to its musculotendinous junction. The anterior one third is then transected proximally and brought into the distal aspect of the wound. Next, a drill hole is made in the tip of the lateral malleolus lateral to the articular surface between the insertions of the ATFL and CFL. The drill hole is directed posteriorly and proximally exiting approximately 2.5 cm proximal to the fibular tip. The split portion of the peroneus brevis is passed through the tunnel in a distal-to-proximal direction. Then the sutures of the CFL and ATFL are secured in the manner as described in the modified Brostrom. The peroneal transfer is tensioned with the foot in mild plantarflexion and eversion and secured either with a biotenodesis screw or sutures at its entrance and exit sites in the fibula.

Chrisman-Snook Reconstruction The Elmslie39 procedure is a nonanatomic reconstruction of the lateral ligaments that uses a strip of fascia lata passed through drill holes in the distal fibula and calcaneus. Chrisman and Snook40 modified the Elmslie procedure using a split portion of the peroneus brevis and published their results in 1969. The course of the peroneus brevis graft is designed to recreate the vectors of both ATFL and CFL. The surgical technique for the Chrisman-Snook reconstruction is performed through a posterior curvilinear incision along the course of the peroneal tendons in a manner similar to the modified Brostrom-Evans. The anterior half to the peroneus brevis tendon is identified distally and split from its insertion up to the musculotendinous junction. Next, the anterior half is transected proximally and left attached distally on the base of the fifth metatarsal. In an attempt to replicate the course of the ATFL, the peroneus brevis graft must recreate the insertion of the ATFL on the talus. This can be done by either passing the graft through a small hole at the base of the ATFL’s insertion on the talus or by creation of a bone tunnel. A fibular bone tunnel is then made to recreate the insertion of the ATFL and CFL on the distal

fibula. This is done by fashioning a tunnel that begins anteriorly at the level of the ankle joint and runs anterior to posterior at a 30-degree distal angle, taking great caution to not disrupt the articular surface. The calcaneal insertion of the CFL, a tubercle called the eminenta retrotrochlearis, is identified on the lateral wall of the calcaneus. Two drill holes (1.5 cm apart) are made anterior and posterior to the tubercle. These holes are then joined using curved curets. The next task is passing the peroneus brevis graft. It is first passed from the base of the fifth metatarsal through the bone tunnel or soft tissue on the talus and then through the fibular tunnel in an anterior to posterior direction. With the ankle in neutral position and the hindfoot in gentle eversion, the graft is pulled taut and then sutured to both the periosteum at the anterior distal fibula and to the remaining stump of the ATFL. The graft is passed below the peroneus longus and remaining peroneus brevis tendons and taken in a posterior-to-anterior direction through the calcaneal drill holes. It is sutured back on itself with 2-0 nonabsorbable suture. Additional sutures are then placed at the entry/exit of all bone tunnels. This technique has been simplified (and perhaps improved) with the advent of the biotenodesis screw.

Postoperative Rehabilitation The standard postoperative management consists of 2 weeks of non-weight bearing in a splint followed by 4 weeks weight bearing in a short-leg cast. After cast removal, the ankle is protected in a walker boot or an ankle brace (off-the-shelf), and a home program of range of motion and peroneal strengthening for an additional 4 weeks follows. At the 10-week postoperative mark, the patient’s progress is reassessed and physical therapy initiated for more aggressive motion and strengthening. For the competitive athlete, we recommend that a protective brace be worn for practice and game situations for the first year after surgery.

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REFERENCES 1. Colville MR: Surgical treatment of the unstable ankle. J Am Acad Orthop Surg 1998;6:368–377. 2. Garrick JG: The frequency of injury, mechanism of injury, and epidemiology of ankle sprains. Am J Sports Med 1977;5:241–242. 3. Ekstrand J: Soccer injuries and their mechanisms: A prospective study. Med Sci Sports Exerc 1983;15:267–270. 4. Jackson DW, Ashley RL, Powell JW: Ankle sprains in young athletes. Clin Orthop 1974;101:201–215. 5. Brand RL, Collins MD: Operative management of ligamentous injuries to the ankle. Clin Sports Med 1982;1:119–130. 6. Anderson ME: Reconstruction of lateral ligaments of the ankle using plantaris tendon. J Bone Joint Surg Am 1985;67:930–934. 7. Brostrom L, Sundelin P: Sprained ankles: IV. Histologic changes in recent and “chronic” ligament ruptures. Acta Chir Scand 1966;132:248–253. 8. Freeman MR: Instability of the foot after injuries to the lateral ligaments of the ankle. J Bone Joint Surg Br 1965;47:669–676. 9. Smith RW, Reischl SF: Treatment of ankle sprains in young athletes. Am J Sports Med 1986;14:465–471. 10. Balduini FC, Vegso JJ, Torg JS, et al: Management and rehabilitation of ligamentous injuries to the ankle. Sports Med 1987;4:364–380. 11. Gerber JP, Williams GN, Scoville CR, et al: Persistent disability associated with ankle sprains: A prospective examination of an athletic population. Foot Ankle Int 1998;19:653–660. 12. Stormant DM, Morrey BF, An K, et al: Stability of the loaded ankle. Am J Sports Med 1985;13:295–300. 13. Siegler S, Block J, Schneck CD: The mechanical characteristics of the collateral ligament of the human ankle joint. Foot Ankle 1988;8:234–242. 14. Brostrom L: Sprained ankles. I. Anatomic lesions in recent sprains. Acta Chir Scand 1964;128:483–495. 15. Renstrom P, Theis M: Biomechanics and function of ankle ligaments: Experimental results and clinical application. Sportverletzing Sportschaden 1993;7:29–35. 16. Hamilton WG: Sprained ankles in ballet dancers. Foot Ankle 1982; 3:99–102. 17. DiGiovanni BF, Partal G, Baumhauer JF: Acute ankle injury and chronic lateral instability in the athlete. Clin Sports Med 2004;23:1–19. 18. Stiell I, Greenberg G, McKnight R, et al: A study to develop clinical rules for the use of radiography in acute ankle injuries. Ann Emerg Med 1992;21:384–390. 19. Diamond JE: Rehabilitation of ankle sprains. Clin Sports Med 1989;8:877–891. 20. Kannus P, Renstrom P: Current concepts review: Treatment for acute tears of the lateral ligaments of the ankle. J Bone Joint Surg Am 1991;73:305–312. 21. Konradsen L, Holmer P, Sondergaard L: Early mobilizing treatment for grade III ankle ligament injuries. Foot Ankle 1992;12:69–73.

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22. Eiff M, Smith A, Smith G: Early mobilization versus immobilization in the treatment of lateral ankle sprains. Am J Sports Med 1994;22:83–88. 23. Berlet GC, Anderson RB, Davis WH: Chronic lateral ankle instability. Foot Ankle Clin 1999;4:713–728. 24. Ahouvuo J, Kaartinen E, Slatis P: Diagnostic value of stress radiography in lesions of the lateral ligaments of the ankle. Acta Radiol 1988;29:711–714. 25. Karlsson J, Bergsten T, Lansinger O, et al: Surgical treatment of chronic lateral instability of the ankle joint. Am J Sports Med 1989;17:268– 273. 26. Louwerens JK, Ginai AZ, Van Linge B, et al: Stress radiography of the talocrural joint and subtalar joints. Foot Ankle Int 1995;16:148–155. 27. Cox JS: Surgical and nonsurgical treatment of acute ankle sprains. Clin Orthop 1985;198:118–126. 28. Maki SE, Whitelaw RS: Influence of expectation and arousal on centre of pressure responses to transient postural perturbations. J Vestib Res 1993;3:25–39. 29. Fumich RM, Ellison AE, Guerin GJ: The measured effect of taping on combined ankle motion before and after exercise. Am J Sports Med 1981;9:165–170. 30. Rarick GL, Bigley G, Karst R: The measurable support of the ankle joint by conventional methods of taping. J Bone Joint Surg Am 1962;44:1183–1190. 31. Myburgh KH, Vaughan CL, Isaacs SK: The effects of ankle guards and taping on joint motion before, during and after a squash match. Am J Sports Med 1984;12:441–446. 32. DiGiovanni BF, Fraga CJ, Cohen BE, Shereff MJ: Associated injuries found in chronic lateral instability. Foot Ankle Int 2000;21:809–815. 33. Komenda GA, Ferkel RD: Arthroscopic findings associated with the unstable ankle. Foot Ankle Int 1999;20:708–713. 34. Taga I, Shino K, Inoue M, et al: Articular cartilage lesions in ankles with lateral ankle ligament injury: An arthroscopic study. Am J Sports Med 1993;21:120–127. 35. Gould N, Seligson D, Grassman J: Early and late repair of the lateral ligaments of the ankle. Foot Ankle Int 1980;1:84–89. 36. Evans DL: Recurrent dislocation of the ankle: A method of surgical treatment. Proc R Soc Med 1953;46:343–348. 37. Ottoson L: Lateral instability of the ankle treated by a modified Evans procedure. Acta Orthop Scand 1978;49:302–305. 38. Girard P, Anderson RB, Davis WH, et al: Clinical evaluation of the modified Brostrom-Evans procedure to restore ankle stability. Foot Ankle Int 1999;20:246–252. 39. Elmslie RC: Recurrent subluxations of the ankle joint. Ann Surg 1934;100:364–367. 40. Chrisman OD, Snook GA: Reconstruction of lateral ligament tears of the ankle: An experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am 1969;51:904–912.

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Ankle Intra-articular Injury William I. Sterett and R. Matthew Dumigan

In This Chapter Bony impingement Soft tissue impingement Chondral and osteochondral lesions Surgery—ankle arthroscopy

INTRODUCTION • Intra-articular injuries of the ankle encompass a wide variety of problems, including bony and soft-tissue impingement and osteochondral lesions of the talus. • Bony anterior ankle impingement (footballer’s ankle) is a common cause of chronic ankle pain and loss of dorsiflexion in athletes. Spur formation can occur with or without secondary degenerative changes in the joint. • Persistent pain following an ankle sprain may be a sign of intraarticular soft-tissue impingement. Soft-tissue impingement lesions can occur in the anterolateral and posteromedial aspects of the joint. • Osteochondral lesions of the talus are a well-known cause of chronic ankle pain and should be considered in patients who have persistent ankle pain following a sprain. Treatment of these lesions continues to evolve. • Ankle arthroscopy provides excellent visualization of the joint with decreased operative morbidity and is gaining wider acceptance in the treatment of intra-articular lesions in the ankle.

CLINICAL FEATURES AND EVALUATION Bony Impingement Most patients with anterior bony impingement in the ankle will present with anterior ankle pain and loss of dorsiflexion. Soccer players seem to be particularly prone to this problem due to the repetitive trauma to the anterior capsule. Dancers and runners develop anterior bony impingement because of repetitive dorsiflexion. The pain and loss of motion may worsen slowly over time, but presentation to a physician is often precipitated by an acute injury.1 The diagnosis can be confirmed with anteroposterior and lateral views of the ankle. Dorsiflexion stress radiographs can also be obtained to confirm contact between anterior osteophytes on the tibia and talus.2 The features that should be carefully evaluated on plain radiographs include the

location and size of osteophytes and the presence or absence of joint-space narrowing. Patients with spur formation, loss of dorsiflexion, and persistent pain who fail nonoperative management may be considered for operative treatment.

Soft-Tissue Impingement Soft-tissue impingement lesions in the ankle should be part of the differential diagnosis in patients with persistent symptoms following an ankle sprain. Most patients with a routine ankle sprain demonstrate considerable improvement with 6 weeks of conservative therapy.1 Patients without radiographic changes and symptoms of pain, catching, instability, swelling, stiffness, altered gait, or activity limitation should be carefully evaluated for soft-tissue impingement lesions. Soft-tissue impingement lesions can be classified based on the anatomic location. Most soft-tissue impingement lesions in the ankle occur in the anterolateral aspect of the ankle joint. The Bassett lesion represents impingement of the anterolateral talar body on the distal fascicle of the anteroinferior tibiofibular ligament3,4 (Fig. 67-1). Patients with a Bassett lesion will have a history of an inversion ankle sprain and present with chronic anterolateral ankle pain with normal radiographs. Pain and or popping over the anterolateral ankle with forced dorsiflexion are the most consistent physical examination finding. Another type of anterolateral soft-tissue impingement can result from a tear of the anterior talofibular ligament. The torn soft-tissue becomes a mass of hyalinized connective tissue that impinges in the lateral gutter and has been termed the meniscoid lesion.5 The physical examination for anterolateral impingement is usually nonspecific, but recently a new physical sign was described to aid in the diagnosis.6 The test is performed by placing the foot in a plantarflexed position with direct pressure over the anterolateral ankle. The foot is then brought up to a maximally dorsiflexed position with continued pressure over the anterolateral ankle. Increased pain with this maneuver is caused by pinching of the hypertrophied synovium that is associated with anterolateral impingement lesions between the talus and tibia (Fig. 67-2). A positive test has been shown to be 95% sensitive and 88% specific for synovial impingement. Intra-articular injection of local anesthetic may be used as an adjunct to the physical examination to help differentiate intraarticular from extra-articular pathology. The addition of steroid to the injection may be considered for therapeutic purposes if synovial inflammation is suspected as the cause of the impingement. The diagnosis of anterolateral impingement is usually made based on the history and physical examination findings, but magnetic resonance imaging (MRI) can be considered if the diagnosis is unclear or other pathology is suspected. Recently, a posteromedial impingement lesion was described following severe inversion ankle injury.7 It has been hypothesized

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A Figure 67-1 Diagram of the lateral aspect of the ankle joint. The distal fascicle of the anteroinferior tibiofibular ligament is parallel and distal to the anterior tibiofibular ligament proper and is separated by a fibrofatty septum. Inset: With dorsiflexion, the distal fascicle of the anteroinferior tibiofibular ligament may impinge on the anterolateral aspect of the talus. (From Bassett FH III, Gates HS III, Billys JB, et al: Talar impingement by the anteroinferior tibiofibular ligament. J Bone Joint Surg Am 1990;72:55–59.)

that the deep fibers of the deltoid ligament become crushed between the posterior medial malleolus and the medial talar wall. While most of these lesions seem to resolve spontaneously, some develop chronic inflammation, hypertrophic fibrosis, and metaplasia of the damaged deltoid ligament. Patients will present with deep posteromedial ankle pain that is intensified with direct palpation, plantarflexion, and inversion of the ankle. Plain films and computed tomography are usually negative for this lesion, but bone scans have been useful in confirming the diagnosis.

B

Chondral and Osteochondral Lesions of the Talus Like soft-tissue impingement lesions of the ankle, chondral and osteochondral lesions of the talus will usually present after failed conservative treatment of a presumed ankle sprain. The clinical presentation will be similar to soft-tissue impingement lesions and may include pain, swelling, instability, or catching.8 The physical examination is usually nonspecific, and point tenderness over the lesion may be the only finding. A careful assessment of the lateral ligaments should be made since instability of these ligaments will have implications in the treatment of the talar lesion.1,9 Radiographic examination includes anteroposterior, lateral, and mortise views of the ankle. Stress views can be obtained if lateral ligament laxity is detected on physical examination. Lateral lesions result from inversion and dorsiflexion of the ankle causing impaction between the anterolateral talus and the fibula. The lesions are typically thin, wafer-shaped osteochondral fragments located over the anterolateral talar dome, more likely to be symptomatic, and more closely associated with a history of trauma. Medial lesions result from combined plantarflexion, inversion, and external rotation. The lesions are usually located over the posteromedial talar dome and typically appear as a deep, cup-shaped defect. Unlike lateral lesions, many patients with medial lesions will have no history of trauma.8 Historically, the classification system proposed by

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C Figure 67-2 A, Ankle held in plantarflexion with pressure over anterolateral joint line. B, Ankle ranged from plantarflexed to dorsiflexed position. C, Ankle ranged from plantarflexed to dorsiflexed position with pressure over anterolateral joint line. Worsening pain over pressure alone is a positive test for anterolateral impingement.

Berndt and Harty10 in 1959 has been used to classify osteochondral lesions of the talus: stage I, a small compression fracture; stage II, incomplete avulsion of the fragment; stage III, complete avulsion of the fragment without displacement; and stage IV, complete avulsion of the fragment with displacement. Although computed tomography scans and bone scans have been

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used to further evaluate osteochondral lesions seen on plain films, recent advancements in MRI have made it the preferred diagnostic tool. MRI allows visualization of the articular cartilage and can evaluate the location, size, and stability of a lesion. A recent report has shown that cartilage-sensitive pulse sequence MRI has correlated well with surgical findings and is useful in identifying patients who would benefit from operative versus nonoperative treatment.11

RELEVANT ANATOMY Intra-articular lesions in the ankle can be treated with open or arthroscopic techniques. Knowledge of the local anatomy is important to avoid damage to vital structures. The medial and lateral malleoli, long extensor tendons, and the tibialis anterior are readily visualized and palpated over the anterior ankle and can serve as a guide to identifying neurovascular structures. The superficial peroneal nerve divides into the medial and intermediate dorsal cutaneous nerves approximately 6 to 7 cm above the tip of the fibula. The intermediate dorsal cutaneous nerve courses laterally and passes over the inferior extensor retinaculum near the level of the joint, then crosses the extensor digitorum longus tendons to the fourth and fifth toes distally. The medial dorsal cutaneous nerve is more centrally located and passes superficial to the common extensor digitorum longus tendon at or just distal to the joint line. These two nerves supply the bulk of the sensation to the dorsum of the foot and are at risk with placement of an anterolateral arthroscopic portal or with an anterolateral arthrotomy. The anterior tibial artery and deep peroneal nerve pass deep to the extensor retinaculum over

Figure 67-4 Posterior portals. Posterolateral portal is most commonly used. Posteromedial portal should be used with caution; trans-Achilles portal is not recommended. (From Ferkel TD, Scranton PR: Current concepts review: Arthroscopy of the foot and ankle. J Bone Joint Surg Am 1993;75:1233–1242.)

the central aspect of the anterior ankle. These structures usually run in the interval between the extensor hallucis longus and extensor digitorum longus tendons at the level of the ankle joint and should be palpated and marked prior to making a skin incision. The saphenous nerve and vein can have a variable course but usually cross the ankle just anterior to the medial malleolus. The saphenous nerve is a frequent site of neuroma formation when it is damaged and is at risk with placement of an anteromedial arthroscopic portal or with anteromedial arthrotomy (Fig. 67-3). The posterior surface anatomy is defined by the posterior aspects of the medial and lateral malleoli and the Achilles tendon. The sural nerve and small saphenous vein travel over the posterolateral ankle and are at risk with posterolateral arthroscopic portal placement and posterolateral approaches to the ankle. The sural nerve is also a frequent site of neuroma formation when it is damaged. The tibialis posterior tendon, flexor digitorum longus tendon, posterior neurovascular bundle, and flexor hallucis longus tendon pass in sequential order from anterior to posterior behind the medial malleolus and are at risk with posteromedial arthroscopic portal placement and posteromedial approaches to the ankle. Damage to neurovascular structures in this area is particularly devastating due to significant loss of blood supply as well as the loss of protective sensation over the plantar aspect of the foot (Fig. 67-4).

TREATMENT OPTIONS Figure 67-3 Anterior portals. Use of anterocentral portal is not recommended. (From Ferkel RD, Scranton PE: Current concepts review: Arthroscopy of the foot and ankle. J Bone Joint Surg Am 1993;75:1233–1242.)

Anterior Bony Impingement Anterior bony spurs often become symptomatic when synovial or scar-tissue impingement occurs following acute trauma. In the absence of loose bodies on radiographic evaluation, an initial trial

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of nonoperative treatment should be instituted. This consists of a short course of nonsteroidal anti-inflammatory medications, heel lift, or a short period of immobilization in a weight-bearing cast or walking boot. Injection of local anesthetic with or without steroids can be used for diagnostic and therapeutic purposes.2 Patients who have continued pain and loss of motion with dorsiflexion despite 6 months of nonoperative treatment may be considered for surgical treatment. Important considerations prior to surgery are (1) the duration of symptoms, (2) the size and location of osteophytes, and (3) the degree of joint space narrowing. Long-term follow-up studies have shown superior results in patients with symptoms less than 2 years, those without narrowing of the joint space, those with smaller osteophytes, and those who have removal of anteromedial versus anterolateral osteophytes.12,13 Both open and arthroscopic techniques have been used to successfully treat this problem in selected patients. Arthroscopic treatment offers results similar to open techniques but has decreased operative morbidity, decreased pain, and quicker recovery time.

Soft-Tissue Impingement Lesions Initial management of ankle sprains consists of rest, ice, compression, and elevation. As pain and swelling subside, active range of motion, strengthening, and proprioceptive training are advanced until the ankle regains normal function. Most ankle sprains improve significantly by 6 weeks. Ankle arthroscopy has become the treatment of choice for management of ankle sprains that continue to be symptomatic beyond 6 months.1 Careful assessment of the articular cartilage should be made at the time of arthroscopy since approximately one in four patients will have an associated chondral lesion of the talus. Posteromedial impingement lesions likely represent a small percentage of soft-tissue lesions following inversion ankle injuries but should be considered in the setting of a characteristic physical examination and a positive bone scan. Patients who fail to improve with a trial of conservative management should be considered for surgery. The lesion may be difficult to visualize with the arthroscope, and open excision of the lesion can be performed through a posteromedial approach with an arthrotomy through the base of the tibialis posterior tendon sheath.7

Chondral and Osteochondral Lesions of the Talus Like soft-tissue impingement lesions, chondral lesions of the talus will often have nonspecific physical examination findings and normal radiographs. A high index of clinical suspicion will prompt an MRI confirming the diagnosis. Nonoperative management is similar to that of soft-tissue impingement lesions and should last for approximately 6 months before operative intervention is considered. Patients with continued pain or mechanical symptoms despite appropriate nonoperative treatment may be candidates for surgery. Lateral ligament instability may be present with a chondral lesion and is an important consideration prior to surgery.9 Chondral lesions that are treated without addressing the overlying instability tend to have a worse outcome compared to lesions treated in stable ankles.1 Unless there is evidence of a loose body on plain radiographs or MRI, initial treatment of osteochondral lesions of the talus is nonoperative. Initial treatment can consist of a period of immobilization and limited weight bearing. There are no clear guidelines in the literature that quantify the duration of immobilization or protected weight bearing. The age of the patient and the location, size, and stability of the lesion are

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factors that may contribute to decision making. Historically, lesions that are treated conservatively for up to 12 months still have a good outcome with appropriate surgical treatment.8 Patients with loose bodies at presentation are treated with surgery from the onset, while patients with Berndt and Harty lesions stages I through III with persistent pain, swelling, or mechanical symptoms are considered for surgery after 3 to 6 months of failed nonoperative treatment.14 With the improvements in MRI, the current trend is earlier diagnosis and treatment of osteochondral lesions. Surgical treatment of osteochondral lesions of the talus continues to rapidly evolve, and numerous techniques are available. The advantages and disadvantages of various arthroscopic and open procedures are discussed later in the chapter.

SURGERY Diagnostic Arthroscopy of the Ankle Patient positioning is usually based on surgeon preference. Patients can be placed in a supine position with the leg supported on the table or the leg can be placed in a leg holder and allowed to fall free. Some surgeons use the lateral decubitus position with the patient supported on a beanbag, and some surgeons recommend the prone position when the primary pathology is posterior and posterior portals are planned15 (Fig. 67-5). A standard 4.0-mm 30-degree arthroscope is usually sufficient, but a 2.7-mm 30-degree arthroscope may allow easier maneuverability within the ankle joint. Prior to beginning an ankle arthroscopy, the surface landmarks should be delineated with a marking pen. The dorsalis pedis artery should be palpated and marked, and the saphenous vein and accompanying nerve can be marked just anterior to the medial malleolus. In some patients, the terminal branches of the superficial peroneal nerve can be visualized by grasping the fourth toe and bringing the foot into a plantarflexed and adducted position. Prior to starting the procedure, 10 to 15 mL of saline is injected into the ankle through the anteromedial side of the joint. Invasive or noninvasive distraction devices may be used to improve the visualization in the joint depending on the needs of the procedure. The anteromedial portal is more reproducible and usually established first. A vertical skin incision is made through the skin medial to the tibialis anterior tendon at or just above the joint line. A

Figure 67-5 Patient position for ankle arthroscopy with external traction device.

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Figure 67-6 A, The eight-point anterior examination of the ankle through the arthroscope. B, The seven-point posterior examination of the ankle through the arthroscope. (From Ferkel TD, Scranton PR: Current concepts review: Arthroscopy of the foot and ankle. J Bone Joint Surg Am 1993;75:1233–1242.)

hemostat or blunt obturator is used to dissect through the capsule. The anterolateral portal is then established with the aid of the arthroscope. The skin is transilluminated to look for branches of the superficial peroneal nerve and traversing veins, and a skin incision is made just lateral to the peroneus tertius tendons at or just above the joint line. A central anterior portal has been described, but it engenders unnecessary risk to the anterior tibial artery and deep peroneal nerve and should be avoided.2 Posterior portals include the posterolateral and posteromedial portals. The posterolateral portal is usually considered the “safe” portal and can be established with the use of the arthroscope through one of the anterior portals. The posterolateral portal is made just lateral to the Achilles tendon at the level of the joint line. An 18-gauge needle can be used to localize the correct placement under direct arthroscopic visualization, or alternatively a switching stick can be used through one of the anterior portals. Once this portal is established, it can be used for gravity inflow or as a working portal for posterior pathology.2 The posteromedial portal has not gained wide acceptance due to the risk of damage to the nearby posterior neurovascular bundle. A recent anatomic study has described the safe use of posterolateral and posteromedial arthroscopic portals with the patient in the prone position.15 This allows excellent visualization of the posterior half of the tibiotalar joint, the subtalar joint, and the flexor hallucis longus tendon if posterior ankle joint pathology is to be addressed. Once the portals

are established, a systematic diagnostic arthroscopy following an eight-point examination, as described by Ferkel and Scranton,2 is performed to thoroughly evaluate the ankle (Fig. 67-6).

Arthroscopic Treatment of Anterior Bony Impingement Open removal of anterior osteophytes has been performed in the past with good results. In the past several years, arthroscopy has been increasingly used to treat these lesions with equal effectiveness, but with the benefit of a much easier recovery. The surgery is performed with the patient in the supine position with the leg supported on the operating table, and standard anteromedial and anterolateral portals are established. Nearly all anterior osteophytes will be within the joint capsule and are best visualized without distraction with the ankle in maximal dorsiflexion9,16 (Fig. 67-7). Small joint osteotomes and a 4.0-mm bur are used to take down the osteophytes off the anterior tibia and from the notch on the anterior talar neck. Any hypertrophic synovium or scar tissue in this area is carefully removed with a shaver.

Treatment of Soft-Tissue Impingement Lesions After a thorough diagnostic arthroscopy, anterolateral impingement lesions can be removed with the aid of the arthroscope. Bassett lesions have been found in normal ankles but can become symptomatic in the setting of inversion ankle injuries. This distal

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Figure 67-7 Ankle in maximal dorsiflexion without distraction. (From Van Dijk CN, Tol JL, Verheyen CC: A prospective study of the prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med 1997;24:737–745. Copyright 1997 American Orthopaedic Society for Sports Medicine.)

fascicle will be separate from the anteroinferior tibiofibular ligament by a fibrofatty septum and can be removed without compromising the stability of the syndesmosis. The articular cartilage should be carefully evaluated once the accessory ligament is removed. All abnormal synovium and scar tissue should be removed, and any fraying of the anterior syndesmosis or anterior talofibular ligament should be débrided. Posteromedial impingement lesions may be difficult to visualize and treat with arthroscopic techniques using standard anterior portals. Prone posterior ankle arthroscopy may have a role in treatment of this lesion but has not been described. An open technique has been described in which the tendon sheath of the tibialis posterior tendon is opened, the tendon is retracted anteriorly, and the bed of the tendon sheath is opened to gain access to the posteromedial aspect of the joint. The pathologic tissue tends to “erupt through this incision” and is removed. The incision in the bed of the tendon sheath is left open, and the superficial sheath incision and skin are closed.7

Arthroscopic Treatment of Chondral and Osteochondral Lesions of the Talus Lesions confined to the cartilage alone can be treated arthroscopically with a simple chondroplasty to smooth the articular surface and débride back to normal healthy cartilage (Fig.

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67-8). As stated earlier, strong consideration should be given to stabilizing ankles with lateral ligament instability in the setting of a chondral lesion.1 Treating osteochondral lesions with arthroscopic techniques requires a systematic approach based on the arthroscopic appearance of the lesion. There are numerous techniques available, and the surgeon should be familiar with the advantages and disadvantages of each type of treatment to optimize treatment of a given lesion. Arthroscopy provides excellent visualization of the joint, but some far posteromedial lesions may be difficult to visualize. Therefore, the surgeon should be prepared to convert to an open procedure if necessary. Stage I lesions appear as an area of softened articular cartilage without a definable fragment. If this lesion is symptomatic, then the main treatment decision is whether the articular cartilage should be violated to try to stimulate the lesion to heal. Drilling of an intact lesion can be performed by drilling a 0.062inch Kirschner wire through the intact cartilage and into the base of the lesion. It is believed that the drill holes stimulate revascularization of the avascular fragment. Anterolateral lesions can usually be easily drilled through the anterolateral portal. Posteromedial lesions can be more difficult to access because of their location. With the arthroscope in the anterolateral portal, the ankle is placed in maximal plantarflexion. If the area of softened cartilage can be visualized, then drilling can be performed through the anteromedial portal. If this is unsuccessful, then transmalleolar drilling can be considered. A small joint drill guide is placed over the lesion, and the Kirschner wire is drilled through the medial malleolus and into the lesion (Fig. 67-9).2 These techniques have the advantage of decreased operative morbidity compared to open techniques but injure articular cartilage. An alternative approach allows grafting behind an intact lesion without violating the integrity of the articular cartilage. A small joint drill guide is placed over the lesion, and a guide wire is placed in the sinus tarsi. Retrograde transtalar drilling is then performed under direct arthroscopic visualization (Fig. 67-10).2,8 The tunnel is expanded with a small reamer, and the lesion is grafted with local or distal tibia cancellous bone graft. Stage II lesions have a breach in the articular cartilage, but the fragment is not displaceable. Once the overlying cartilage has been débrided, the underlying bone bed can be addressed. It is important to remove any sclerotic or nonviable bone until bleeding subchondral bone is seen at the base of the lesion.14 Drilling can be performed as described for stage I lesions, or the microfracture technique may be used. The microfracture technique uses specialized awls, and multiple perforations are made in the subchondral plate approximately 3 mm apart.17 Both drilling and microfracture stimulate the release of growth factors and mesenchymal stem cells, which result in filling of the defect with fibrocartilage.16 The advantages of these techniques are decreased operative morbidity compared to open procedures and filling of the defects with fibrocartilage. Two of the potential shortcomings of these techniques are that they are not able to reconstitute significant loss of subchondral bone and long-term durability of fibrocartilage on the talus is not known. Stage III lesions have a breach in the articular cartilage with a displaceable fragment. The size and viability of the fragment as well as the condition of the overlying articular cartilage should be carefully assessed. Some acute traumatic lesions may be candidates for internal fixation (discussed later in chapter). If the lesion is loose and not amenable to internal fixation, then it

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A

B

Figure 67-8 A, Partial-thickness chondral lesion of the talar dome viewed arthroscopically. B, Motorized shaver débriding the lesion. C, Articular surface of the talus after débridement.

C should be removed and the subchondral bed treated as discussed for stage II lesions. Loose lesions will often have a flap of articular cartilage attached to the lesion. In the past, there has been some question about what to do with this cartilage. A recent report has shown that leaving this remaining cartilage in place may obstruct regeneration of healing tissue and that the removal of all degenerative cartilage improves results.9 Stage IV lesions are loose bodies in the ankle joint. Unlike stage I through III lesions, loose bodies are treated surgically as soon as the diagnosis is made. Once again, acute traumatic lesions can be assessed for internal fixation. If the lesion is chronic, nonviable, less than 1 cm in size, or has poor overlying articular cartilage, it is removed.8,14 The site of loose body displacement is débrided, and the subchondral bone bed is treated like stage II and III lesions.

Open Treatment of Osteochondral Lesions Open Débridement Open débridement of osteochondral lesions can be performed through a variety of approaches.18 Most lateral lesions are anterior and can be treated through a standard anterolateral arthrotomy. A skin incision is made just medial to the fibula about 2 cm proximal to the joint and extended 1 to 2 cm distal to the joint. Branches of the superficial peroneal nerve are carefully protected, and the extensor retinaculum is incised. The extensor digitorum longus tendons are retracted medially, and the joint capsule is incised in line with the skin incision. Visualization of the articular surface may be improved with plantarflexion of the ankle. In the rare occurrence of a posterolateral lesion, a fibular osteotomy and incision through the anterior syndesmosis can be performed.

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Figure 67-9 Transmalleolar drilling with a small-joint drill guide inserted through the anteromedial portal. Visualization is through the anterolateral portal. OLT, osteochondral lesion of the talus. (From Ferkel TD, Scranton PR: Current concepts review: Arthroscopy of the foot and ankle. J Bone Joint Surg Am 1993;75:1233–1242.)

Medial lesions may be difficult to visualize both arthroscopically or with a standard medial arthrotomy. In these cases, a medial malleolar osteotomy can be performed. Numerous techniques have been described in an attempt to minimize the complications associated with this procedure. Although this approach provides excellent visualization, there is a risk of malunion, nonunion, hardware complications, and articular cartilage injury.

Internal Fixation Since there are no universally accepted guidelines in the literature, internal fixation of loose or displaced fragments remains somewhat controversial. In general, patients suitable for internal fixation are younger patients with acute traumatic lesions. The ideal type of fragment should be 1 cm or greater and have a large piece of attached subchondral bone, and the overlying articular cartilage should be in good condition.8 The ideal type of fixation is also controversial. Metal implants provide good fixation with excellent biocompatibility but may require a second procedure for removal. This is a particularly difficult problem for posteromedial lesions that required a medial malleolar osteotomy. Bioabsorbable fixation devices are another alternative. These devices have the advantage of not requiring later removal, but bone resorption around the implants remains a concern. Autologous Osteochondral Transplant Autologous osteochondral grafts from the ipsilateral knee are transplanted to the talus using the mosaicplasty technique.19 The procedure can be used as an initial procedure for larger lesions or for revisions that have failed previous arthroscopic procedures. Lesions should be over 1 cm in size, and the cartilage on the remainder of the tibia and talus should be normal. Specialized instruments are used to remove osteochondral plugs from the non-weight-bearing portion of the medial femoral condyle. The talar lesion is then prepared and the plugs are inserted perpendicular to the articular surface. Anterolateral arthrotomies are usually sufficient for lateral lesions, and medial lesions usually require a medial malleolar osteotomy. The procedure replaces the defect with hyaline cartilage and can replace lost subchondral bone stock. Disadvantages include potential donor site morbidity in the knee, and complications associated with open arthrotomies and osteotomies.

Figure 67-10 Use of a drill guide with a tissue-protective cannula in retrograde transtalar drilling of a posteromedial talar dome lesion. (From Stone JW: Osteochondral lesions of the talar dome. J Am Acad Orthop Surg 1996;4:63–73, with permission.)

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Autologous Chondrocyte Transplant One of the newer techniques used to treat osteochondral lesions of the talus is autologous chondrocyte transplantation.20,21 The

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exact indications for this procedure are still evolving but are similar to mosaicplasty. The procedure is performed in two stages. The first stage requires an arthroscopic cartilage biopsy either from the knee or from the non-weight-bearing portion of the anterior talus. The chondrocytes are then grown in culture for approximately 2 to 3 weeks. This is followed by the second procedure that uses an arthrotomy or osteotomy. The lesion is débrided back to normal cartilage with a bleeding subchondral bed. A 10 ¥ 10-mm cortical window is then made in the distal tibia metaphysis, and cancellous bone graft is removed. This graft is packed into the base of the defect to restore subchondral bone stock. A periosteal flap is then harvested from the ipsilateral proximal tibia and is sewn over the defect with a 5-0 polydiaxone monofilament suture. The cultured chondrocytes are then injected under the periosteal flap, and then the flap is sealed with fibrin glue. The theoretical advantage of this procedure is that it replaces lost subchondral bone stock and hyaline cartilage is restored to the articular surface. The two main disadvantages are the high cost of the procedure and the need for two operations. Further research comparing autologous chondrocyte transplantation to other procedures are needed to determine whether the high cost of this procedure is justified in treating osteochondral lesions of the talus.

POSTOPERATIVE REHABILITATION Anterior Bony Impingement Following arthroscopic treatment of anterior bony impingement, patients are placed in a compressive dressing and are partial weight bearing for 3 to 5 days. Active dorsiflexion exercises are started immediately postoperatively and are continued several times daily within the confines of the patient’s comfort. The patient then returns to progressive weight bearing as tolerated.12,13

Soft-Tissue Impingement Lesions Arthroscopic removal of isolated soft-tissue impingement lesions is followed by early range of motion in a compressive dressing. Patients are instructed to weight bear as tolerated as soon as their comfort allows. Once pain and swelling have subsided, strengthening and proprioceptive training are started at 2 to 3 weeks.

Chondral and Osteochondral Lesions The type of procedure and the size of the lesion determine the postoperative rehabilitation. Active and passive range-of-motion exercises are started early in the postoperative course and will precede weight bearing. Restrictions in weight bearing can range from 3 to 6 weeks, with drilling, microfracture, and grafting procedures having longer restrictions than simple débridement.

CRITERIA FOR RETURN TO SPORTS Return to sport after treatment of these lesions is largely based on the patient’s examination. Patients should be carefully assessed for pain, swelling, stiffness, instability, and mechanical symptoms. In the absence of these symptoms, those who undergo isolated removal of soft-tissue lesions or osteophytes can expect an early return to sport once the goals of the postoperative physical therapy regimen have been met. Patients with osteochondral lesions who are treated with drilling, microfracture, or grafting procedures should satisfy both the stated criteria in addition to having radiographic evidence of a stable or

healed lesion. In general, these patients should be kept out of competitive sports for 4 to 6 months.

RESULTS AND OUTCOMES Arthroscopic Treatment of Anterior Bony Impingement At 5- to 8-year follow-up, patients who had removal of anterior osteophytes without preoperative narrowing of the joint space had 77% good to excellent results.12 Radiographic recurrence of the osteophytes occurs in approximately two thirds of the patients, but this does not seem to correlate with recurrence of clinical symptoms.13

Arthroscopic Treatment of Soft-Tissue Impingement Lesions Several small series have shown excellent results after removal of isolated soft-tissue impingement lesions. Good to excellent results can be expected in 80% to 90% of these patients with a high percentage of those being able to return to sport.22

Chondral and Osteochondral Lesions of the Talus Débridement of chondral lesions in stable ankles had good results in 75% of cases, while treatment of similar lesions in unstable ankles showed only 33% good results.1 This confirms the need to restore stability when treating articular cartilage injuries in the talus. Most reports on arthroscopic treatment of osteochondral lesions of the talus using débridement and drilling of the lesion have been favorable with good to excellent results reported in 85% to 90% of cases.14 These results equal or surpass those of traditional open techniques. A recent report on the microfracture technique at 2-year follow-up has shown good to excellent results in 78%.17 Mosaicplasty has also shown encouraging results in treating lesions over 1 cm in size. Good to excellent results have been reported in 94% of patients having this procedure with 2- to 7-year follow-up.19 A few small series of patients treated with autologous chondrocyte transplantation have been reported with good results in most patients.20,21

COMPLICATIONS Most complications that occur as a result of these procedures are related to complications associated with arthroscopy of the ankle. The overall complication rate with ankle arthroscopy is 10%. Most of these complications are neurologic (49%). Of the neurologic complications, 56% involve the branches of the superficial peroneal nerve, 24% involve the sural nerve, and 20% involve the saphenous nerve.2 The use of the central anterior portal has been condemned due to the risk to the anterior tibial artery and deep peroneal nerve, and the posteromedial portal should be used with caution. A good understanding of the local anatomy will minimize complications.

CONCLUSIONS Ankle symptoms that persist following an injury despite nonoperative treatment should be carefully assessed for intra-articular pathology. A high index of clinical suspicion in addition to a thorough history, physical examination, and radiographic studies will often lead to an accurate diagnosis. Arthroscopy is gaining wider acceptance in the treatment of the majority of these lesions, but those who treat these lesions in the ankle should be familiar with the advantages and disadvantages of all available options.

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REFERENCES 1. Ogilvie-Harris DJ, Gilbart MK, Chorney K: Chronic pain following ankle sprains in athletes: The role of arthroscopic surgery. Arthroscopy 1997;13:564–574. 2. Ferkel RD, Scranton PE: Current concepts review: Arthroscopy of the foot and ankle. J Bone Joint Surg Am 1993;75:1233–1242. 3. Bassett FH 3rd, Gates HS 3rd, Billys JB, et al: Talar impingement by the anteroinferior tibiofibular ligament. J Bone Joint Surg Am 1990;72:55–59. 4. Nikolopoulos CE, Tsirikos AI, Sourmelis S, Papachristou G: The accessory anteroinferior tibiofibular ligament as a cause of talar impingement. Am J Sports Med 2004;32:389–395. 5. Lahm A, Erggelet C, Reichelt A: Ankle joint arthroscopy for meniscoid lesions in athletes. Arthroscopy 1998;14:572–575. 6. Molloy S, Solan MC, Bendall SP: Synovial impingement in the ankle. J Bone Joint Surg Br 2003;85:330–333. 7. Paterson RS, Brown JN: The posteromedial impingement lesion of the ankle: A series of six cases. Am J Sports Med 2001;29:550–557. 8. Stone JW: Osteochondral lesions of the talar dome. J Am Acad Orthop Surg 1996;4:63–73. 9. Takao M, Uchio Y, Kakimaru H, et al: Arthroscopic drilling with debridement of remaining cartilage for osteochondral lesions of the talar dome in unstable ankles. Am J Sports Med 2004;32:332– 336. 10. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 1959;41:988–1020. 11. Mintz DN, Tashjian GS, Connell DA, et al: Osteochondral lesions of the talus: A new magnetic resonance grading system with arthroscopic correlation. Arthroscopy 2003;19:353–359.

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12. Tol JL, Verheyen CP, van Dijk CN: Arthroscopic treatment of anterior impingement in the ankle. J Bone Joint Surg Br 2001;83:9–13. 13. Van Dijk CN, Tol JL, Verheyen CC: A prospective study of the prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med 1997;25:737–745. 14. Baker CL, Morales RW: Arthroscopic treatment of transchondral talar dome fractures: A long-term follow-up study. Arthroscopy 1999;15:197–202. 15. Sitler DF, Amendola A, Bailey CS, et al: Posterior ankle arthroscopy: An anatomic study. J Bone Joint Surg Am 2002;84:763–769. 16. Philbin TM, Lee TH, Berlet GC: Arthroscopy for athletic foot and ankle injuries. Clin Sports Med 2004;23:35–53. 17. Thermann H, Becher C: Microfracture technique for treatment of osteochondral and degenerative chondral lesions of the talus: Two year results of a prospective study. Unfallchirurg 2004;107:27–32. 18. Navid DO, Myerson MS: Approach alternatives for treatment of osteochondral lesions in the talus. Foot Ankle Clin 2002;7:635–649. 19. Hangody L: The mosaicplasty technique for osteochondral lesions of the talus. Foot Ankle Clin 2003;8:259–273. 20. Koulalis D, Schultz W, Psychogios B, Papagelopoulos PJ: Articular reconstruction of osteochondral defects of the talus through autologous chondrocyte transplantation. Orthopedics 2004;27:559–562. 21. Koulalis D, Schultz W, Heyden M: Autologous chondrocyte transplantation for osteochondral dissecans of the talus. CORE 2002;395:186–192. 22. DeBerardino TM, Arciero RA, Taylor DC: Arthroscopic treatment of soft tissue impingement of the ankle in athletes. Arthroscopy 1997;13:492–498.

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Ankle Fractures and Syndesmosis Injuries Jeffrey B. Selby

In This Chapter Classification Nonoperative management Surgery Ankle fracture fixation Syndesmosis fixation

INTRODUCTION • Ankle fractures and syndesmosis injuries are a significant source of lost participation in sports. • These injuries are the major differential diagnoses in the much more common ankle sprains and are also frequently missed injuries, when attributed to a simple sprain. • This chapter focuses on the treatment of these more severe injuries that usually cause considerably more impairment and often require surgical fixation.

RELEVANT ANATOMY The ankle is composed of a complex hinge with both bony and ligamentous structures playing a role in stability. This allows for adequate dorsiflexion and plantarflexion during normal gait and provides for stability throughout the hinge motion. The articular surface of the tibia is concave with large anterior and posterior prominences. The medial malleolus is the distal medial portion of tibia and provides for a medial buttress to the talus. The distal fibula or lateral malleolus is the lateral buttress to the talus. It fits into the incisura of the distal lateral tibia, which is concave 75% of the time and is a marker for injury to the syndesmosis. This bony architecture, called the ankle mortise, is not sufficient to keep the talus within the ankle joint despite its conformity with the distal tibia, medial malleolus, and lateral malleolus (Fig. 68-1). The medial malleolus is covered with articular cartilage in contact with the talus except for the region of the deep deltoid ligament. This thick ligament is the primary medial stabilizer to the joint and runs from the posterior colliculus of the medial malleolus to the talus. It restrains external rotation of the talus within the mortise. The superficial deltoid ligament runs from the anterior aspect of the medial malleolus to the talus and is less important as a stabilizer as it is primarily a thickening of the joint capsule (Fig. 68-2). The lateral ligamentous portion of the ankle has three major portions. The major ligamentous restraint to foot inversion and

the most commonly injured ligament in sprains is the anterior talofibular ligament (ATFL). In plantarflexion, the ligament aligns with the fibula and resists inversion of the talus acting as a collateral ligament. In dorsiflexion or neutral position, it resists anterior translation of the tibia as tested in the anterior drawer test of the ankle. The calcaneofibular ligament (CFL) originates in the middle of the distal lateral fibula, traverses deep to the peroneal tendons, and inserts on the calcaneus. This ligament functions as the collateral ligament resisting inversion with the talus in a neutral or dorsiflexed position. There is a posterior talofibular ligament, which runs from the posterior distal fibula to the posterior process of the talus. The syndesmosis has a separate ligamentous structure with three definable ligaments: (1) the anteroinferior tibiofibular ligament, (2) the posteroinferior tibiofibular ligament, and (3) the interosseous ligament. The tibia and fibula are connected throughout their length by the interosseous membrane, and the distal connection of this contributes to the syndesmotic complex. The anteroinferior tibiofibular ligament is the most frequently injured ligament in sprains and in frank diastasis of the syndesmosis.1 It runs from the anterolateral tubercle of the tibia (TillauxChaput tubercle) to the anterodistal fibular shaft and is approximately 20 mm wide and 20 to 30 mm long. The posteroinferior tibiofibular ligament has a deep portion and a superficial portion. The superficial portion originates on the posterolateral portion of the tibia, covers the back of the tibiotalar joint, and runs obliquely down to the posterior aspect of the distal part of the fibula. It is approximately 20 mm wide, 30 mm long, and 5 mm thick and is usually the last structure to tear in syndesmosis injury.2,3 The interosseous ligament runs between the tibia and fibula approximately 1 to 2 cm above the plafond and is considered the primary bond between the tibia and the fibula. It is continuous with the interosseous membrane, which is often torn in syndesmotic injuries, but provides minimal additional strength to the stabilizing syndesmotic ligaments (Fig. 68-3).

BIOMECHANICS The tibiotalar articulation averages about 3 degrees valgus at the plafond. The angle between the plafond and a line drawn from the tip of the medial malleolus to the tip of the lateral malleolus are called the talocrural angle and averages 83 ± 4 degrees.4 The ankle hinge axis runs anterior to posterior from the tip of the medial malleolus to the tip of the lateral malleolus.5 Because of this oblique axis, there is an obligatory internal and external rotation of the foot with plantarflexion and dorsiflexion, respectively. Normal gait requires 10 degrees of plantarflexion, and the normal ankle has mean dorsiflexion of 32 degrees and mean plantarflexion of 45 degrees when a load is applied.6

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obvious if there is gross deformity. Inspection of the skin and soft tissues is performed, dressings applied to open injuries, and deformities are grossly aligned. The neurovascular examination is very important and should be performed both before and after gross realignment of the ankle. A complete sensory examination is performed and motor function is evaluated, although often difficult because of pain limitations. When the injury is not subtle, the extent of the fracture may be obvious, but when subtle, all bony prominences must be palpated. Local tenderness directly over the bone may indicate fracture rather than ligamentous injury. Defects or crepitus can often be palpated at a fracture site. Stability is tested and the ankle is put through a range of motion. It is imperative to palpate the proximal tibia and fibula to ensure that there is not a proximal injury, which is often present in syndesmotic injury.

Imaging

93∞± 2.7∞ Plane of plafond Talocrural angle 83∞± 4∞ Empirical axis

Standard views of the ankle should be obtained in any injury that is suspicious for fracture and include anteroposterior, lateral, and oblique internal rotation (mortise view) views. The mortise view is obtained by placing the leg in 15 degrees of internal rotation with the x-ray beam perpendicular to the flat surface of the table. Stress views are not normally obtained unless syndesmosis injury is suspected. Anteroposterior and lateral views of the entire tibia and fibula are imperative to ensure that there is not a proximal injury. The lateral view helps to rule out injuries to bones other than the mortise such as talus or calcaneus fractures. Computed tomography scans can be obtained as a secondary study if there is significant comminution or suspicion of intra-articular pathology.

Classification Figure 68-1 Bony ankle anatomy. (From Pugh KJ: Fractures and softtissue injuries about the ankle. In Fitzgerald RH, Kaufer H, Malkami AL [eds]: Orthopaedics. St. Louis, Mosby, 2002, p 422.)

The intramalleolar distance increases an average of 1.5 mm when the ankle goes from full plantarflexion to full dorsiflexion. This motion as well as rotation is allowed by the mobile relationship of the tibia and fibula at the syndesmosis. The tibia can rotate 5 to 6 degrees on the talus in walking and almost half of this comes from the inferior tibiofibular joint.7 There is only a 1- to 2-degree increase in external rotation of the fibula with isolated section of the anteroinferior tibiofibular ligament with no effect on frontal plane motion.8 When all the ligaments are cut, there is a 10.2-degree increase in rotation.9

The two main classification schemes used, Lauge-Hansen and Danis-Weber, are helpful in communicating about fractures and in determining the treatment of the fractures. The LaugeHansen classification scheme is most useful in describing the mechanism of injury, so that the forces across the ankle determine the direction and extent of injury. Knowledge of these patterns allows for anatomic reduction and maintenance of reduction with closed means in treating these fractures. The Danis-Weber classification solely describes the injury level of the fibula in relation to the plafond. This is a more simple classification scheme and aids mostly in determining the appropriate operative treatment of the ankle fracture. Both schemes are shown in Figures 68-4 and 68-5.

Goals of Treatment

ANKLE FRACTURES History The mechanism of injury is an important aid in the diagnosis and treatment of ankle fractures. These are usually low-energy injuries in athletic events, and the fractures are usually not open. Medical history is important, and athletes with diabetes or peripheral neuropathies may pose different treatment scenarios. Also, a history of fracture and/or surgery may be helpful in interpreting radiographs and in preoperative planning. The direction of injury is important in treatment and diagnosis of fracture or ligament injury.

Examination Rapidly identifying injuries that may require urgent treatment and those that keep a player from returning to play are usually

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Restoration and maintenance of normal anatomic relationships by the most expedient and least invasive means will lead to fastest rehabilitation and earliest return to sport. Ankle dislocations are grossly realigned on the field, and anatomic reduction is obtained and ensured with radiographs. Many of these injuries have neurovascular and skin compromise, and prompt reduction relieves tension on the skin, nerves, and vessels. Injuries that are stable are usually managed without surgery and unstable injuries are usually managed with anatomic reduction and fixation. Nonoperative Treatment Nonoperative treatment is indicated when the injury did not require a reduction maneuver and the mortise is not widened on standard radiographs. There is usually no medial tenderness to palpation. Subtle medial tenderness to palpation with fracture of the lateral malleolus and without fracture of the medial

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Anterior talofibular Posterior talofibular

Fibulocalcaneal

Figure 68-2 Lateral and medial ankle ligament anatomy. (From Pugh KJ: Fractures and soft-tissue injuries about the ankle. In Fitzgerald RH, Kaufer H, Malkami AL [eds]: Orthopaedics. St. Louis, Mosby, 2002, pp 420–421.)

malleolus may indicate injury to the deltoid ligament and may require stress radiographs to rule out an unstable fracture pattern more adequately treated with surgery. Weber C fractures are rarely stable and are almost always treated surgically. Bimalleolar ankle fractures are difficult to treat with closed means because of their instability. When closed management of bimalleolar ankle fractures is chosen, there must be anatomic alignment ensured with weekly serial radiographs for the first month, then biweekly until healed.

Nonoperative treatment usually consists of closed reduction and casting. With Weber A fractures, a removable boot can be applied, and weight bearing initiated as tolerated. For Weber B fractures treated nonoperatively, a short leg cast is applied and patients are non-weight bearing initially. The mechanism of injury as determined by the history and the Lauge-Hansen classification is reversed, the foot is placed in a plantigrade position, and the cast is molded to resist redisplacement. Maintenance of the normal mortise relationship must be ensured throughout

Interosseous membrane Lateral

Medial

Anteroinferior tibiofibular ligament

Anteroinferior tibiofibular ligament (cut)

Interosseous membrane

Posteroinferior tibiofibular ligament Transverse tibiofibular ligament

Interosseous ligament

Anterior view

A

Lateral

Medial

Posterior view

B

Figure 68-3 A and B, Syndesmosis anatomy. (From Coughlin MJ, Mann RA: Surgery of the Foot and Ankle, 7th ed. St. Louis, Mosby, 1999, p 1134.)

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Danis-Weber Classification

A

B

C

III II III II

IV III

I

IV

I

II

I

II

I IV

I

I

I

Lauge-Hansen Classification Figure 68-4 Classification of ankle fractures. (From Pugh KJ: Fractures and soft-tissue injuries about the ankle. In Fitzgerald RH, Kaufer H, Malkami AL [eds]: Orthopaedics. St. Louis, Mosby, 2002, p 424.)

nonoperative treatment with serial radiographs. Bimalleolar ankle fractures require stabilization above the knee to manage rotatory deforming forces across the ankle (Fig. 68-6). Operative Treatment Surgery is usually indicated in those fractures that are initially unstable or have lost reduction with closed treatment. If the mortise is widened medially more than 4 mm on initial radiographs or there is a Weber C fracture or bimalleolar fracture, closed treatment is much more difficult and can lead to a poor result.10 The detailed description of operative treatment can be found in other texts, and preoperative planning is imperative. The weight-bearing status after surgery is determined by the injury pattern, type of fixation used, and patient compliance. Immobilization is determined by the same factors and varies with different injuries or fixation. Usually patients are placed in a removable orthosis at 2 weeks and are weight bearing by 6 weeks.

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SYNDESMOSIS INJURIES Diagnosis Syndesmosis injuries are a continuum of ankle injuries, but there is a more protracted course than both ankle sprains and ankle fractures. The diagnosis, therefore, is important to rule out in all ankle injuries because it determines the time away from sport and, if missed, can lead to chronic ankle pain and disability. Close attention to these injuries and their early diagnosis may alleviate time and discontent while the athlete wonders why he or she is still not playing after 6 weeks. With fractures, early attention to these injuries decreases the chance of a poor result. Traumatic diastases are usually diagnosed with radiographs, but history and examination are helpful.

History In syndesmosis injury, the patient has well-localized pain located over the anterolateral aspect of the ankle. The patient will

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Figure 68-6 Weber C ankle fracture after open reduction with internal fixation.

Figure 68-5 Weber C ankle fracture.

usually describe an external rotation force as a cause of the injury and occasionally relate pain in areas higher than the plafond. He or she may relate that it feels different from the typical ankle sprain if he or she has had one before. There is often a delayed ecchymosis proximal to the ankle joint. As in ankle fractures, a careful history of injuries such as ankle sprains or fractures is important. In chronic injuries, patients often will describe an ankle sprain that just would not get better.

Examination Swelling and tenderness are usually more precisely located than in a typical sprain. There is very little tenderness and swelling over the anterotalofibular or calcaneofibular ligaments, with tenderness more proximal than a usual ankle sprain. The lateral and medial malleolus must be palpated to rule out fracture, and the entire fibula must be palpated to rule out proximal fracture (Maisonneuve’s fracture). The squeeze test, popularized at West Point, is provocation of pain at the syndesmosis by squeezing the tibia and fibula at midcalf.11 It is poorly studied as a sensitive or specific test but can heighten suspicion of this injury. The anterior drawer test is usually performed and usually negative, although there may be some varus-valgus instability. A more specific test is to hold the leg stabilized with the knee flexed at 90 degrees and apply external rotation stress to the ankle. This reproduces pain at the syndesmosis and should indicate syndesmosis injury unless ruled out by radiographs.

Imaging Standard ankle radiographs may reveal a normal-appearing ankle but may also show subtle signs of injury such as a fleck of bone off the posterior tubercle of the tibia. Radiographs may also reveal chronic injury to the syndesmosis with calcification of the ligaments and interosseous membrane. Diastasis of the syndesmosis is indicated when there is no malleolus fracture and the mortise is widened medially more than 4 mm. This can be variable, and comparison radiographs may be necessary. Another method is to use the amount of overlap of the fibula and tibia of 5 mm on the anteroposterior view or 1 mm on the mortise view. The tibiofibular clear space is the distance between the fibula and the incisura of the tibia 1 cm proximal to the plafond. This normal distance has been found by several studies to be fairly consistent at about 4 mm.12–14 If there are clinical findings of syndesmosis injury and standard radiographs are negative, external rotation stress radiographs are indicated. These can be difficult to interpret and may be limited by patient pain, but if there is obvious widening, it is a useful test. A bone scan may be a way to diagnose injuries that are not diagnosed with stress radiographs limited by patient pain. Magnetic resonance imaging is also very sensitive in detecting ligamentous injury and is becoming more common in helping to determine return to play and prognosis in high-demand athletes. Certainly, if there is any widening of the mortise on any view, the entire fibula must be visualized on radiographs (Fig. 68-7).

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a large clamp with the ankle dorsiflexed. This is viewed on anteroposterior and lateral projection to ensure anatomic reduction. After reduction, the screws are placed percutaneously from the fibula to the tibia at a 20-degree angle posteriorly to anteriorly to ensure placement of the screw into the tibia. The postoperative course is then non-weight bearing for 6 to 8 weeks, followed by weight bearing as tolerated for a few weeks, followed by screw removal at 10 to 12 weeks. Some authors recommend open reduction with direct ligament repair of the syndesmosis. Certainly, if a significant amount of force is required or if the syndesmosis will not reduce, open reduction is indicated, but this is rarely necessary. There is controversy over the size of screws and how many to place. Most recommend either two 3.5-mm cortical screws 1 cm apart, with the inferior screw 1 cm above the plafond, or one 4.5-mm cortical screw. The length of the screw is also debated, with some recommending three cortices and others recommending four. Controversy also exists over whether to remove screws. Screws limit the ability of the fibula to rotate normally. The screws often eventually break, but broken screws rarely cause any sequelae. They are more difficult to remove after they have broken. Regardless of the fixation used, anatomic reduction and maintenance of fixation until the syndesmotic ligaments have healed are the mainstays of treatment. Figure 68-7 Syndesmosis injury.

Treatment of Syndesmosis Injury Treatment of these injuries is based on whether there is diastasis on plain radiographs, diastasis on stress radiographs, or if fracture is present.

Frank Diastasis with Weber B or Weber C Fibula Fracture Surgery of the ankle fracture is usually indicated in this case, and stability of the syndesmosis can be assessed intraoperatively. The cotton test involves a towel clip on the fixed fibula and application of a lateral pull on the fibula. The external rotation

Sprain without Diastasis These injuries are assumed to be stable, and treatment is generally weight bearing as tolerated with or without a high pneumatic brace. For more severe stable injuries, a period of non-weight bearing up to 4 weeks may be employed. Counseling the patient and coach is very important because these injuries have been shown to take an average of 43 days of recovery time.11 This is almost double the recovery time of lateral ankle sprains. Reinjury is common, and return too early can result in a prolonged course. Eighty-six percent of these athletes can be expected to have a good to excellent result, but one third will have mild stiffness and one fourth will have mild activityrelated pain.15 A custom brace to limit rotation can be helpful on return to sports. Sprain with Diastasis on Stress Radiographs These patients do not require surgery as long as the syndesmosis is anatomic. This can be confirmed with computed tomography or magnetic resonance imaging. The patient should be placed in a non-weight-bearing cast or brace for 4 weeks followed by progressive weight bearing for 2 to 4 weeks. Maintenance of reduction should be confirmed during the course of 2 to 3 weeks to ensure proper anatomic healing. Frank Diastasis with or without Proximal Fibula Fracture There is little question that these patients require anatomic reduction of the syndesmosis with operative fixation. There is some discussion over the exact method with which to fix them. The standard teaching is to reduce the syndesmosis closed, using

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Figure 68-8 Syndesmosis reduction and fixation.

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stress test can also be performed with a mortise view of the ankle and external stress applied. Any diastasis at the syndesmosis indicates instability and should be repaired with screws as described previously. The screws can go either through or around the plate so preoperative planning is a must to prepare for possible screw placement. In many bimalleolar ankle fractures, fixation of the medial malleolus restores the medial anatomy and ligamentous structure; thus, syndesmosis screws may not be required. Stress views can help determine whether they are needed (Fig. 68-8 and Table 68-1). Results Most follow-up studies of syndesmosis injuries have few patients. In Fritschy’s report on 10 patients with syndesmotic injury, three were treated surgically and seven with walking casts. They all returned to World Cup skiing, with one having persistent pain.16 Edwards and DeLee reported on six cases of frank diastasis; four patients had good results and two patients

Table 68-1 Treatment of Ankle Fractures Nonoperative

Operative

Weber A Mortise displaced 4 mm Bimalleolar fracture Displaced Weber B

with mild ankle pain and restriction in ankle motion had fair results.17 Syndesmosis injuries appear to add morbidity to ankle fractures and early diagnosis may lead to an improved result both clinically and emotionally because the expectations will be more appropriate.

REFERENCES 1. Bonnin JG: Injuries to the Ankle. Darien, CT, Hafner, 1970. 2. Shereff MJ: Radiographic analysis of the foot and ankle. In Jahss MH (ed): Disorders of the Foot and Ankle, 2nd ed. Philadelphia, WB Saunders, 1991. 3. Sarrafian SK: Anatomy of the Foot and Ankle: Descriptive, Topographic, Functional. Philadelphia, JB Lippincott, 1983. 4. Phillips WA, Schwartz HS, Keller CS, et al: A prospective randomized study of the management of severe ankle fractures. J Bone Joint Surg Am 1985;67:67–78. 5. Inman VT: The Joints of the Ankle. Baltimore, Williams & Wilkins, 1976. 6. Lindsjo U, Danckwardt-Lilliestrom G, Sahlstedt B: Measurement of the range of motion of the loaded ankle. Clin Orthop 1985;199:68–71. 7. Close JR: Some applications of the functional anatomy of the ankle joint. J Bone Joint Surg Am 1956;38:761–781. 8. Rasmussen O: Stability of the ankle joint: Analysis of the function and traumatology of the ankle ligaments. Acta Orthop Scand Suppl 1985;211:1–75. 9. Rasmussen O, Tovberg-Jensen I: Mobility of the ankle joint: Recording ankle movements in the talocrural joints in vitro with and without the lateral collateral ligaments of the ankle. Acta Orthop Scand 1982;53:155–160.

10. Mak KH, Chan KM, Leung PC: Ankle fracture treated with the AO principle—An experience with 116 cases. Injury 1985;16:265–272. 11. Hopkinson WJ, St. Pierre P, Ryan JB, et al: Syndesmosis sprains of the ankle. Foot Ankle 1990;10:325–330. 12. Leeds HC, Ehrlich MG: Instability of the distal tibiofibular syndesmosis after bimalleolar and trimalleolar ankle fractures. J Bone Joint Surg Am 1984;66:490–503. 13. Whiteside LA, Reynolds FC, Ellsasser JC: Tibiofibular synostosis and recurrent ankle sprains in high performance athletes. Am J Sports Med 1978;6:204–305. 14. Gabarino JL, Clancy M, Harcke T, et al: Congenital diastasis of the inferior tibiofibular joint: A review of the literature and report of two cases. J Pediatr Orthop 1985;5:225–228. 15. Taylor DC, Englehardt DL, Bassett FH: Syndesmosis sprains of the ankle and the influence of heterotopic ossification. Am J Sports Med 1992;20:146–150. 16. Fritschy D: An unusual ankle injury in top skiers. Am J Sports Med 1989;17:282–286. 17. Edwards GS Jr, DeLee JC: Ankle diastasis without fracture. Foot Ankle 1984;4:305–312.

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Ankle Tendon Disorders and Ruptures Sharrona Williams and James Nunley

In This Chapter Peroneal tendons Tendonitis Tears and ruptures Dislocation and subluxation Achilles tendon Paratendonitis Retrocalcaneal burstitis Insertional tendonitis Rupture

INTRODUCTION Peroneal Tendons • Peroneal tendon injury must be considered any time a patient presents with lateral ankle pain. • Acute injuries to the peroneal tendons usually present similar to a lateral ankle sprain and often these two injuries occur concomitantly. These injuries are common in the athletic population. • Chronic peroneal conditions are frequently overlooked as a source of chronic lateral ankle pain. • Peroneal tendonitis is usually successfully treated nonoperatively, although recalcitrant cases may respond to surgical débridement. • Attritional tears of the peroneal tendons may do well with conservative treatment. • Peroneal subluxation and dislocation may be managed nonoperatively, but rarely with good results. These injuries usually require surgical intervention. • Surgical outcomes are generally good in cases of subluxation, dislocation, and longitudinal tearing of the peroneal tendons. Achilles Tendon • Achilles tendon overuse injuries are common in the athletic population, especially runners. • Posterior heel pain is usually multifactorial and can include tendonitis, tendonosis, tendonosis with partial rupture, insertional tendonitis, retrocalcaneal bursitis, and subcutaneous tendo-Achilles bursitis. • Most cases of posterior heel pain are successfully treated conservatively. However, if conservative treatment fails, operative treatment has been shown to be effective.1,2

• Achilles tendon ruptures are usually treated operatively in athletes. Operative treatment has shown an advantage over nonoperative treatments in isokinetic strength and return to preinjury activities.3–6 Both percutaneous and open repair techniques are available.

PERONEAL TENDONS Clinical Features and Evaluation Tendonitis Peroneal tenosynovitis commonly presents in athletes and is usually due to repetitive activities, but direct trauma such as ankle fracture, calcaneal fracture, and chronic lateral ankle instability can also be a source. Furthermore, there are anatomic considerations that may cause peroneal tendon inflammation, including crowding of the tendons in the fibro-osseous canal by a low-lying peroneus brevis muscle or the presence of a peroneus quartus muscle/tendon that can also cause overcrowding of the tendon sheath. Tendon irritation can occur at the retromalleolar sulcus, peroneal tubercle, and the os perineum, where the tendons sheaths can become stenosed. Patients may have malalignment at the knee and/or ankle contributing to overload of the peroneals. A cavovarus foot commonly causes more stress on the lateral aspect of the foot and may lead to tenosynovitis, recurrent ankle sprains, or longitudinal peroneal tears. Patients with peroneal tenosynovitis usually complain of pain and swelling at the lateral aspect of the ankle over the peroneals. A palpable thickening over the tendons may be present. The subtalar joint range of motion may be limited secondary to peroneal spasm. The physical examination may reveal pain with passive inversion or resisted eversion and dorsiflexion of the foot. There may be a decrease in peroneal strength as well. If there is doubt about the source of lateral ankle pain, an injection of local anesthesia into the peroneal sheath can be diagnostic for pathology. Anteroposterior and lateral weight-bearing radiographs should be obtained to rule out bony injury.

Tendon Tears and Ruptures Peroneal tendon tears commonly occur in athletes and have the same mechanism as lateral ankle sprains, plantarflexion, and inversion. These injuries often are combined and must be considered especially when, after sufficient time for an ankle sprain to heal, complaints of persistent lateral ankle pain and swelling still exist. Bassett and Speer,7 in a cadaveric study, showed that peroneal tendon tears occur at between 25 and 15 degrees of plantarflexion as the peroneus longus impinges against the tip of the fibula and as the peroneus brevis impinges against the lateral

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wall of the fibula. Acute tendon tears can occur in both the peroneus longus and brevis, as shown in the above study. Attritional or longitudinal tears in the peroneus brevis tendon may occur without any particular inciting event or in patients who have a history of recurrent lateral ankle sprains. These tears typically occur in the retromalleolar region. Sobel et al,8 in an anatomic study of 124 fresh cadavers, found 11.3% with attritional tears of the peroneus brevis tendons centered over the tip of fibula and within the groove; these tears averaged 1.9 cm in length. These authors found no involvement of the peroneus longus tendon. The peroneus longus may act as a wedge and divide the peroneus brevis over the fibrocartilaginous ridge of the posterolateral aspect of the fibula. If the superior retinaculum is incompetent, the tendon is further stressed. Degenerative tears of the peroneus longus are rare, but when they occur, they are usually within the cuboid groove just distal to the os peroneum. The clinical presentation of peroneal tendon tears is similar to peroneal tendonitis, except symptoms are prolonged with more pronounced pain and weakness. Magnetic resonance imaging (MRI) may be diagnostic and can identify tears, tendonitis, tendonopathy, or anomalous muscle, but MRI is less than 100% accurate. Traumatic ruptures of the peroneal tendons, though unusual, do happen secondary to trauma or sports injury. Patients often complain of pre-existing pain or disability. Complete rupture usually occurs at areas where stenosis is present. There are case reports of both peroneal tendons rupturing, but typically only one tendon is involved.9

Dislocation and Subluxation Acute dislocation or subluxation of the peroneal tendons is an uncommon injury that has a traumatic cause. Sport participation is responsible for about 92% of acute peroneal dislocations. Skiing has been reported to cause approximately 66% of the sports injuries.10 Peroneal tendon dislocation may be difficult to distinguish from an acute ankle sprain, but it is rare for both to occur simultaneously. The acute dislocation is caused by a sudden forceful dorsiflexion with simultaneous “violent” reflex contraction of the peroneal muscles. With skiing injuries, the mechanism has been described as forceful peroneal contraction occurring with sudden deceleration and ankle dorsiflexion as the ski tips dig into the snow. Acute injuries frequently exhibit ecchymosis, tenderness, and swelling over the lateral aspect of the ankle and may look similar to a high ankle sprain. Most patients are unable to describe the mechanism of injury, as opposed to lateral ankle sprains, where most are able to describe an inversion injury. There are several findings on physical examination that help make a distinction between lateral ankle sprain and peroneal dislocation; typically, the tenderness is posterior to the fibula with acute dislocation versus anterior over the anterior talofibular ligament or anterior tibiofibular ligament with a sprain. Patients may complain of a painful “snapping” sensation and have apprehension on resisted dorsiflexion and eversion with dislocation. The anterior drawer sign should be negative in peroneal dislocation. Eckert and Davis11 described a classification of acute peroneal tendon dislocation after exploring 73 cases. In grade I injuries, the superior retinaculum and periosteum are stripped off the posterior lateral border of the fibula. The peroneus longus dislocates anteriorly, sitting between the periosteum and the fibula. In grade II injuries, the fibrous rim of the superior peroneal retinaculum is avulsed along with the periosteum of the fibula, mim-

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icking a Bankart lesion in the shoulder. The peroneus longus dislocates anteriorly. In grade III injuries, a bony rim fracture involving the posterior lateral corner of the fibula along with the periosteum and fibrous rim are avulsed by the retinaculum. None of these 73 cases had an actual tear of the superior peroneal retinaculum. In chronic peroneal tendon dislocation, the ankle may appear normal. This injury should be suspected when there is a history of pain with unusual “popping.” A popping or snapping sensation is often reproducible with dorsiflexion and eversion of the foot. Slight swelling and tenderness are usually present posteriorly, and if more significant pain is noted, a tendon tear should be suspected. There may be a complaint of instability, yet the anterior drawer and talar tilt tests remain normal. Standard weight-bearing anteroposterior, lateral, and mortise radiographs should be obtained and inspected for a flake or fibular cortex rim fracture. This finding on radiographs is pathognomonic of grade III tendon dislocation and is found in 10% to 30% of cases. Tenography, computed tomography, and MRI have been used to diagnose peroneal tendon dislocations, with MRI currently the study of choice. MRI has the best ability to define soft-tissue structures including the peroneal tendons, superior retinaculum, and inferior retinaculum.

Relevant Anatomy The peroneus longus and peroneus brevis muscles originate in the lateral compartment of the leg and run distally to course behind the lateral malleolus. The musculotendinous junctions are usually proximal to the superior peroneal retinaculum, but a low-lying brevis muscle can exist, contributing to stenosis within the sheath. The brevis runs deep to the longus and approximately 4 cm proximal to the lateral malleolus, both the brevis and longus pass through the common peroneal sheath. This sheath passes through a fibro-osseous tunnel that is stabilized by the superior peroneal retinaculum, posterior talofibular ligament, calcaneofibular ligament, posterior inferior tibiofibular ligament, and fibula. As the peroneals pass distal to the inferior border of the superior peroneal retinaculum, the synovial sheaths bifurcate into separate sheaths for each tendon. The tendons pass deep to the inferior peroneal retinaculum. The inferior peroneal retinaculum is 2 to 3 cm distal to the fibula and acts as a pulley over both tendons, but it has no significant role in peroneal tendon subluxation. The tendons then pass anterior to the peroneal tubercle of the calcaneus, which can be a source of irritation to the tendons as well. The brevis then crosses anterior to the longus and inserts on the base of the fifth metatarsal. The peroneus brevis is the primary evertor of the foot and has a negligible role in ankle and foot plantarflexion. The peroneal longus enters the deep sole of the foot through a groove in the inferolateral cuboid. This tunnel is another area where stenosis can occur. The os peroneum, an accessory bone located plantar to the cuboid, lateral to the cuboid, or at the calcaneocuboid articulation, is found within the substance of the tendon and ossified in approximately 20% of feet. The os peroneum can also be a cause of stenosing peroneus longus tenosynovitis in the cuboid tunnel. The longus lies directly under the cuneiforms and inserts into the plantar lateral aspect of the base of the first metatarsal. The longus is a weak evertor of the foot but functions primarily to plantarflex the first ray. Both the peroneus longus and brevis are innervated by the superficial peroneal nerve. The peroneus quartus muscle exists in 6.6% of patients according to Zammit and Singh12 and in 22% according to Sobel

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et al.8 It usually arises from the peroneus brevis muscle and inserts into the retrotrochlear eminence of the calcaneus. The presence of this muscle has been associated with longitudinal tears in the brevis, prominent retrotrochlear eminence, and lax superior peroneal retinaculum. The posterior aspect of the distal fibula is also called the retromalleolar sulcus. There is variability in its depth and width. Seventy percent of fibulas have a bony ridge that can add 2 to 4 mm of depth to the sulcus. The width of the sulcus usually ranges from 5 to 10 mm. Edwards13 examined 178 cadaver fibulas but found that 82% had a substantial recess/groove in posterior fibula and 18% were flat or convex, a finding that can contribute to peroneal tendon instability. The superior peroneal retinaculum maintains the peroneal tendons behind the fibula. It averages 10 to 20 mm in width and at least one band runs parallel to the calcaneofibular ligament. Variability exists in the width, thickness, and insertions of the superior peroneal retinaculum. The superior peroneal retinaculum is a condensation of the superficial fascia of the calf and the peroneal tendon sheath. Approximately 2 cm proximal to the tip of the distal fibula, the superior peroneal retinaculum originates from periosteum and is the principal structure injured in acute peroneal tendon dislocation. This structure is also a secondary restraint to ankle inversion. Beck14 elucidated that division of the superior peroneal retinaculum alone is not sufficient to cause peroneal tendon dislocation and that additional fibular pathology is necessary. Laxity in the superior peroneal retinaculum can lead to subluxation and splitting of the tendons.

Treatment Options Tendonitis The conservative treatment modalities available for peroneal tenosynovitis include rest, ice, activity modification, nonsteroidal anti-inflammatory drugs, and orthotic management such as a lateral heel wedge. Occasionally, immobilization in a short-leg walking cast is required for a 4- to 6-week trial. Alternatively, an ankle-foot orthosis for 8 to 12 weeks can be used for immobilization. Steroid injections in the tendon sheath are controversial; if used, the risk of subsequent attrition or rupture must be considered. Tear or Rupture Attritional tendon tears can be managed similar to peroneal tenosynovitis depending on the severity of symptoms. With mild to moderate symptoms, rest, nonsteroidal anti-inflammatory drugs, activity modification, or orthotic management may help. If symptoms are more severe, then immobilization with a cast is necessary. Once again, localized intrasheath steroid injection has been advocated by some authors, but we recommend against this.15 Dislocation or Subluxation Acute Conservative measures for treating acute peroneal dislocation include a below-knee cast in slight plantarflexion and inversion. Non-weight bearing in the cast is generally maintained for 6 weeks; some authors advocate advancing weight bearing in the cast. After discontinuation of the cast, range-of-motion exercises are initiated. A good result after nonoperative treatment of acute peroneal dislocation occurs in 50% to 57% of patients. Eventually, 44% of patients require surgery after nonoperative measures fail. Chronic There is little benefit of conservative treatment for symptomatic chronic peroneal tendon dislocation. Sammarco16

states that conservative treatment does help reduce inflammation or pain, but chronic peroneal tendon dislocation frequently recurs after immobilization is discontinued. Observation is acceptable if subluxating or dislocating peroneal tendons are found incidentally, with an absence of symptoms and no athletic compromise.

Surgery Tendonitis If conservative treatment is unsuccessful for peroneal tendonitis, surgical treatment is considered. A curvilinear incision paralleling the posterior and inferior aspect of the fibula is used to allow for adequate tenosynovectomy. In addition, other pathology found intraoperatively should be addressed. The superior peroneal retinaculum should be maintained. Tear or Rupture When conservative treatment fails for longitudinal peroneal tears, surgical management is indicated. The same curvilinear incision described above following the course of the peroneals is used. The sural nerve is identified and protected. Tendon subluxation or dislocation is assessed. The sheath is opened longitudinally and the tendons are inspected. A tenosynovectomy is performed and the degenerative split débrided. Krause and Brodsky15 proposed a clinical classification of peroneus brevis tears. They recommended that if 50% or more is viable after débridement (grade 1), then repair should be done using a running absorbable suture, tubularizing the tendon (Fig. 69-1). However, if less than 50% of the tendon is viable after débridement (grade 2), then a proximal and distal tenodesis of the brevis to the longus tendon should be performed using an absorbable suture. The tenodesis should be done approximately 3 to 4 cm proximal to the tip of the fibula and 5 to 6 cm below. Any associated pathology including tendon subluxation or chronic ankle instability should be addressed simultaneously. The superior peroneal retinaculum is repaired with suture or drill holes in the fibula. Surgical exploration should be performed for acute peroneal tendon ruptures. A long curvilinear incision over the area of suspected rupture is made. The sural nerve is protected. The anterior talofibular and calcaneofibular ligaments are inspected. The peroneal sheath is incised with preservation of the superior peroneal retinaculum. The proximal and distal ends of the tendon are identified and débrided. The tendon can be repaired with Bunnell, Krackow, or Kessler sutures and an additional running epitenon stitch. The sheath and wound are closed in standard fashion. Dislocation or Subluxation Acute Operative management is considered in the young athletic population. There is a high failure rate of conservative treatment and a better success rate with surgery. Superior peroneal retinacular repair will address acute subluxation or dislocation. The patient can be placed in a prone, lateral, or supine position; we use the lateral position. A 7-cm longitudinal incision, 1 cm posterior to the fibula and following the tendons, is used. The sural nerve is identified and protected. The superior peroneal retinaculum is identified and the defect located. Each tendon should be inspected for concomitant defects. The tendons are retracted and the fibular groove is inspected. If the groove is shallow, flat, or convex, the groove is deepened. The superior peroneal retinaculum is repaired by placing three to four drill holes in the posterolateral margin of the fibula. The sutures

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A

B

D C Figure 69-1 Intraoperative photographs of longitudinal peroneus brevis tear requiring tubularization. A, Planned incision along the course of the peroneal tendons; B, identified tear in the peroneus brevis; C, tubularized tendon; D, débrided portion.

through the superior peroneal retinaculum are advanced through the drill holes. Finally, the retinaculum is imbricated for reinforcement. Chronic There is a multitude of surgical procedures described to address chronic peroneal dislocation: retinaculum reinforcement and repair, tissue transfer, tendon rerouting, bone block, and groove deepening are discussed here. Superior peroneal retinaculum reinforcement entails the same technique as with acute repair. If a fibula avulsion fracture exists, then open reduction and internal fixation are recommended. The advantages of this repair include a small incision, anatomic approach, and avoidance of an osteotomy. The potential disadvantage of this procedure is the failure to correct predisposing anatomy, such as sulcus deformities and insufficient retinaculum. Tissue transfers use tendons and periosteal flaps from other places to recreate or reinforce the superior retinaculum. The most common procedure was described by Jones using a distally attached slip of the Achilles tendon routed through the fibula.

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This stabilizes the peroneals and reinforces the retinaculum. Modifications using the plantaris or peroneus brevis have also been reported. Tendon rerouting relies on the calcaneofibular ligament to constrain the peroneal tendons. Four methods of tendon rerouting have been reported. Platzgummer described dividing the calcaneofibular ligament near the fibular insertion and suturing it over the tendons.10 A modification of this was described by Sarmiento and Wolf who transected the peroneal tendons, passed them below the calcaneofibular ligament, and then repaired them.10 Pozo and Jackson demonstrated another technique, taking the calcaneofibular ligament origin with a predrilled piece of distal fibula.10 The tendons were replaced in the sulcus and the fibula reattached with screw fixation. Poll and Duijfjes reversed this procedure by detaching the insertion of the calcaneofibular ligament with a predrilled piece of the calcaneus.10 Bone Block Bone block procedures attempt to contain the peroneal tendons using the fibula. This procedure was first

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described by Kelly in 1920 by using a partial thickness osteotomy of the distal fibula rotated posteriorly to deepen the fibular groove. DuVries modified this technique by driving a wedge of fibula posteriorly to hold the dislocating peroneal tendons.10

Once the cortex has been weakened, a bone tamp is used to impact the posterior fibular cortex into the medullary canal. This can increase groove depth by 3 to 8 mm. The retinaculum is then closed in a pants-over-vest fashion.

Postoperative Rehabilitation Groove Deepening Groove deepening addresses the shallow or absent retromalleolar groove that often exists in cases of peroneal subluxation or dislocation. The classic groove deepening and newer methods are described. The patient is positioned in the lateral decubitus position. A curvilinear incision starting 5 to 6 cm proximal to the tip of the fibula is made, ending just distal to the fibula. The sural nerve is identified and protected throughout the entire procedure. The entire sheath and retinaculum are visualized prior to incising them just posterior to the border of the fibula. The peroneal tendons are inspected for any associated pathology. Some form of tendon pathology usually exists, primarily longitudinal tearing, and this must be addressed intraoperatively. The retromalleolar sulcus is exposed. Often the groove is shallow, ranging from flat to convex. A saw is used to create a 3-cm long ¥ 1-cm trapdoor within the fibula that is hinged medially (Fig. 69-2). An osteotome is used to elevate the trapdoor. A curet is used to remove 7 to 9 mm of cancellous bone before reinserting the flap into the deepened bed. The retinaculum and periosteum are reattached to the posterolateral border using suture placed through drill holes. The superior peroneal retinaculum is reinforced simultaneously. The more recently described groove-deepening technique is generally easier to perform. Once the retromalleolar sulcus is exposed, an incision just anterior to the origin of the calcaneofibular ligament is made. Care is taken not to incise the calcaneofibular ligament. A periosteal elevator is used to mobilize the soft tissue at the distal fibula. The medullary canal is then reamed using sequential drill bits. The drilling is started at the distal tip of the fibula and advanced proximally into the shaft. The drill bit size is sequentially increased at the most posterior portion of the fibula, being careful not to perforate the cortex.

Tendonitis After peroneal tenosynovectomy, the patient is immobilized until the wound heals. This is followed by range-of-motion exercises and sport-specific strengthening exercises. There is a gradual return to preinjury activities as tolerated. Tear or Rupture If simple débridement and repair or tubularization is performed, the patient is kept non-weight bearing for 2 weeks. This is followed by weight bearing in a short-leg cast for two additional weeks. A removable boot is used at 4 weeks, and range-ofmotion exercises for dorsiflexion/plantarflexion are initiated. At 6 weeks, inversion/eversion and a progressive strengthening program is instituted. Patients are then gradually advanced to full activity. Some authors advocate non-weight bearing for up to 5 weeks and immobilization in a removable boot for up to 10 weeks, especially when a tenodesis is performed.15 After acute repair of the peroneal tendons, the patient is placed in a short-leg walking cast for 6 to 8 weeks. Weight bearing is allowed after 2 weeks. The rehabilitation program consists of range-of-motion, strengthening, and proprioception exercises. Return to competitive sports should be allowed at 5 to 6 months. Dislocation or Subluxation (Acute and Chronic) Patients are maintained non-weight bearing for 2 weeks in a short-leg cast. A walking boot or short-leg cast is used for 4 to 6 weeks. A stirrup brace may be used for several weeks after discontinuation of the boot. At this point, formal physical therapy is introduced to start range of motion and sport-specific strengthening, which is slowly advanced. It may take 4 to 6 months before full range of motion is obtained.

Criteria for Return to Sports Range of motion and full strength must be recovered prior to resuming athletics. After a progressive rehabilitation program, most patients are able to return to athletic activities without limitations by 4 to 6 months.

Results and Outcomes

Figure 69-2 Classic technique for fibular groove deepening in the treatment of peroneal subluxation or dislocation.

Some reported series combine all peroneal injuries when presenting outcomes. Overall, peroneal tendon disorders that require operative intervention have good to excellent outcomes. Alanen et al17 reported a series of 38 patients treated for chronic peroneal tendonitis (five patients), peroneal tears (13 patients) and ruptures (six patients), peroneal subluxation/dislocation (nine patients), and peroneal anomalies (five patients). Eighty percent of the patients were competitive athletes, and 50% of the cases were associated with lateral ankle instability. Ninety percent of the patients had good to excellent outcomes. The outcomes after tenosynovectomy for peroneal tenosynovitis are good to excellent. Peroneal tendon ruptures are uncommon, but of those reported, good to excellent outcomes are obtained. Athletes are able to return to competition without limitations. Bassett and Speer,7 at our institution, reported on acute peroneal tears in athletes that were repaired surgically. The outcomes were generally excellent, with all ankles remain-

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ing asymptomatic while maintaining full athletic activity at follow-up of an average of 7.9 years. Good to excellent clinical results after surgical repair of longitudinal peroneal brevis tears were reported by Krause and Brodsky.15 These authors found that return to maximal function is prolonged but achievable. Surgical reconstruction after acute peroneal dislocation has a success rate of 96%. Patients are able to return to full athletic activities with no limitations. In chronic cases, with retinacular reinforcement and repair, the recurrence rate is about 3%. Of the Jones procedures reported, there have been no redislocations. The main reported complication is loss of motion, occurring in 15% of patients. This is thought to be secondary to the tenodesis effect. There has been no reported recurrence of peroneal dislocation after surgical stabilization with tendon-rerouting procedures. Only minor complications have been reported, including sensory nerve injuries and minor discomfort. Bone block procedures for chronic peroneal tendons dislocation have a redislocation rate of 8%. The overall complication rate after this procedure is up to 30%. Screw-related problems, nonunion, and fracture are reported. With the classic groove-deepening procedure, there are no reported recurrences of subluxation, dislocation, or instability in the 28 reported cases.

Complications In all procedures addressing peroneal pathology, the sural nerve is at risk of injury. The nerve must be identified and protected throughout the procedure. This is one of the most frequent minor complications. Loss of motion after stabilization of the peroneal tendons with rerouting procedures is another potential complication.

Conclusions Peroneal tendonitis usually occurs in the athletic population secondary to overuse but can also occur after a traumatic event. Peroneal tendon disorders must be considered in the evaluation of lateral ankle pain. The mechanism for ankle sprains and peroneal tendon tears are the same, and these injuries often occur concomitantly. Peroneal tendonitis is usually successfully managed conservatively. An adequate trial of all modalities must be given before the option of surgery is considered. Longitudinal peroneal tears are also initially managed conservatively, but when symptoms persist, these tears are successfully managed surgically. Acute peroneal subluxation or dislocation is uncommon and can be frequently difficult to diagnosis. A high index of suspicion must be maintained. There is a 50% success rate for nonoperative treatment in acute injury, and most believe that these injuries have a better outcome when treated surgically. Chronic peroneal dislocation most commonly occurs from misdiagnosed or nontreated acute dislocation. A deficient superior peroneal retinaculum and shallow fibular groove may increase the instability risk. If asymptomatic, conservative measures are employed, but operative intervention is necessary in symptomatic patients. There are multiple procedures with good outcomes available to stabilize the peroneal tendons. At the time of surgery, all pathology must be addressed.

frequency of training must be elicited, as these may be contributory factors. Also, the type of shoes and running surfaces should be noted. During physical examination, mechanical alignment of the entire extremity must be evaluated, checking for a cavus foot, supinated forefoot, hyperpronation, genu varum, or femoral anteversion, all of which have been linked to increased stresses on the Achilles tendon. Paratendonitis Acute paratendonitis occurs most commonly in marathon runners; it is also the result of repetitive stress from cutting, jumping, and pushing off and therefore seen in all types of running athletes. Generally, the area of pain is 4 cm proximal to the calcaneal insertion of the Achilles tendon and the patient exhibits diffuse swelling and discomfort along the tendon. In acute paratendonitis, pain with swelling, warmth, and tenderness are noted and crepitus and pain with ankle motion are consistent findings. The painful arc sign helps distinguish paratendonitis from tendonitis (Fig. 69-3). The spot of tenderness in paratendonitis does not change with range of motion of the ankle, while with tendonitis it does (Fig. 69-4). Palpable tenderness can be noted on both sides of the tendon, but the medial side is more commonly involved. Tender nodules can form within the paratenon. Abnormal biomechanics of the running gait or extrinsic pressure, such as tight shoes, can lead to paratendonitis. Symptoms are typically aggravated by activity and relieved by rest. Retrocalcaneal Bursitis The hallmark of retrocalcaneal bursitis is pain anterior to the Achilles tendon, just superior to its insertion. The bursa becomes hypertrophied, inflamed, and adherent to the tendon. The pain is aggravated with dorsiflexion of the ankle. A positive two-finger squeeze test results in pain with medial and lateral pressure applied anterior and superior to the insertion of the Achilles

ACHILLES TENDON Clinical Features and Evaluation When investigating the causes of posterior heel pain in the athlete, the history of recent change in duration, intensity, and

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Figure 69-3 A positive physical examination sign for paratendonitis is described as the “painful arc sign.” This occurs when the area of pain remains constant with ankle range of motion.

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ciated with retrocalcaneal bursitis or Haglund’s deformity. The cavus foot is less efficient in absorbing shock and places more stress on the lateral side of the Achilles tendon and, thus, has been linked with insertional tendonitis. The physical examination reveals tenderness directly posterior or posterolateral to the insertion of the Achilles tendon. Dorsiflexion of the ankle may be limited secondary to a tight Achilles. Pain is present with active or passive range of motion. Patients with insertional Achilles tendonitis are usually older than patients with paratendonitis or Haglund’s deformity. The lateral heel radiograph may show ossification or spurring off the superior portion of the calcaneus. Ancillary imaging studies such as MRI and ultrasonography are not necessary to make the correct diagnosis. When bilateral, causes of insertional enthesopathy must be considered, including seronegative spondyloarthropathy, gout, fluoroquinolone use, systemic corticosteroids, familial hyperlipidemia, sarcoidosis, and diffuse idiopathic skeletal hyperostosis.

Figure 69-4 The area of pain moves with ankle range of motion if tendonitis exists.

tendon. This must be distinguished from inflammation of the subcutaneous tendo-Achilles bursa, which lies between the posterior aspect of the tendon and the skin and is usually the result of a harsh heel counter or high heels. If retrocalcaneal bursitis is present bilaterally, then the possibility of systemic disease must be considered. Subcutaneous Tendo-Achilles Bursitis This entity is commonly seen with retrocalcaneal bursitis, and frequently there is an element of insertional tendonitis as well. A prominence of the lateral aspect of the posterosuperior calcaneus causes irritation of the retrocalcaneal and subcutaneous bursa as a result of poorly fitting shoes. This has been called Haglund’s deformity or “pump bump.” The bump is usually asymptomatic until irritated by an abrasive heel counter. The prominence is classically present on the lateral side of the tendon at its insertion. This bump is common in women who wear high heels, but also common in hockey players and rock climbers who wear shoes with rigid heel counters. The patient population with this entity tends to be younger than those with isolated retrocalcaneal bursitis. It is not uncommon that these patients with tendo-Achilles bursitis have other features of retrocalcaneal bursitis and insertional tendonitis. Risk factors for Haglund’s deformity include cavus foot, hindfoot varus, hindfoot equinus, and trauma to the apophysis in childhood.18

Achilles Tendon Rupture Achilles tendon ruptures occur most commonly during sports. There is a male predominance occurring in the third to fifth decades. The mechanism is frequently push-off occurring during sprinting and jumping sports resulting in violent ankle dorsiflexion. The patient often describes a sensation of “being kicked in the calf or heel.” The patient’s calf and Achilles tendon should be palpated for continuity. Ecchymosis and swelling should be noted. The Thompson test should be done by placing the patient prone and squeezing the calf muscles. This should indirectly plantarflex the foot if the Achilles tendon is intact. The Thompson test is positive if the foot does not plantarflex. If the Thompson test is equivocal, then the O’Brien’s test can also be done. This is done by placing a needle in the tendon proximal to the suspected area of rupture and passively ranging the ankle. If the needle hub moves in the opposite direction of ankle movement, this confirms an intact tendon distally. Finally, the hyperdorsiflexion sign should be noted. With the patient prone, both knees are flexed to 90 degrees while the examiner maximally dorsiflexes both ankles comparing the injured to the uninjured side. Approximately 20% to 25% of Achilles tendon ruptures are initially misdiagnosed. MRI or ultrasonography are not routinely needed for diagnosis but can be helpful in surgical decision making. Other disease-related factors that place people at greater risk of Achilles rupture include rheumatoid arthritis, lupus erythematosus, hypercholesterolemia, gout, dialysis, renal transplant, steroid therapy, endocrine dysfunction, infection, tumor, autoimmune disorders, diabetes mellitus, and the use of fluoroquinolones.

Relevant Anatomy Insertional Tendonitis True inflammation within the tendon occurs with insertional tendonitis. Patients present with pain over the insertion of the tendon, frequently associated with calcification or spurring seen within the tendon on a lateral radiograph. There is usually pain at the bone-tendon interface that worsens after exercise, and the pain may become constant. Symptoms are usually exacerbated by running up hills and on hard surfaces. A history of poor stretching and increased training are commonly elicited in patients with this problem. Insertional tendonitis has been asso-

The medial and lateral gastrocnemius muscle originates from the posterior aspect of the distal femur while the soleus muscle originates from the posterior aspect of the tibia, fibula, and interosseous membrane. These two tendons from the respective muscles coalesce to form the Achilles tendon, which inserts into the posterior surface of the calcaneus, distal to the calcaneal tuberosity.19 The Achilles tendon internally rotates 90 degrees onto itself, approximately 2 to 6 cm proximal to its insertion, where the posterior portion of the tendon becomes lateral. The area is also hypovascular according to angiographic studies done

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by both Lagergren20 and Carr and Norris,21 and this hypovascular zone correlates with most noninsertional tendonitis, tendinosis, and ruptures. The Achilles tendon is not within a true synovial sheath but is covered by paratenon. The paratenon is penetrated anteriorly by the mesotenal arterioles that feed the tendon through vincula. Other sources of blood supply include the musculotendinous junction and osseous insertion. Deep to the tendon, the retrocalcaneal bursa sits superficial to the bone just proximal to the insertion. Another subcutaneous bursa between the tendon and the skin exists called the retrotendoAchilles bursa or subcutaneous tendo-Achilles. These two areas can also be a source of irritation or inflammation. During normal walking, at heel strike, the subtalar joint everts/pronates and the tibia internally rotates; simultaneously, passive knee extension causes external rotation through the tibia causing the Achilles tendon to absorb the stress. The Achilles is subjected to great stresses that may approach up to 10 times body weight depending on activity level.22 Biomechanical malalignments of the foot including “functional” overpronation and cavus foot have been implicated as causing increased stress on the Achilles tendon, thus inciting tendonitis.23

Treatment Options: Posterior Heel Pain Most cases of Achilles overuse injuries and posterior heel pain are managed conservatively. Kvist23 has reported the most common cause as training errors. Modification of activity or complete rest should be the initial management. Depending on the severity of symptoms, an individualized program should be devised. The key is to allow cross-training, which will keep the athlete in shape; this includes activities such as stationary biking, water therapy, and aqua jogging. As symptoms are diminished, the athlete can advance to the elliptical machine, stair climber, and the NordicTrack as a stepping-stone before resuming running. If symptoms are milder, then training adjustments are made, including a temporary termination of interval training and hill workouts. The training surface must be addressed as well. If the surface is hard or sloped, it must be changed to a softer and flatter surface. Nonsteroidal anti-inflammatory medications are helpful in acute cases of retrocalcaneal bursitis or paratendonitis. In addition, a course of physical therapy, addressing stretching and strengthening, can be advantageous. Stretching should be executed before and after exercises with the knees both flexed and extended. Other modalities that may be helpful include ice, massage, iontophoresis, and phonophoresis. Schepsis et al18 noted that patients with chronic symptoms had limited passive dorsiflexion and benefited from passive static stretching exercises. They also found that in some cases a night splint to hold the foot and ankle dorsiflexed to neutral for 6 to 8 weeks was helpful to maintain passive dorsiflexion. Approximately 10% of patients with retrocalcaneal bursitis will fail conservative treatment. Biomechanical or alignment problems that are causing excessive stress on the Achilles tendon must always be addressed. Orthotic devices may be useful in correcting malalignment problems to keep the foot and ankle in a neutral position. Gross et al24 studied long-distance runners who were given orthotics for their lower extremity complaints. About 20% had a diagnosis of Achilles tendonitis, and of those patients, 75% had great improvement or cure with orthotic shoe inserts. Orthotic devices are most helpful in correcting hyperpronation and leg length discrepancies. Also, a one-fourth– to one-half–inch heel

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pad built into the running shoe may be helpful in reducing stress on the tendon in patients with normal alignment. Finally, after training errors and malalignment problems have been addressed, a program of calf strengthening should be instituted. Eccentric, heavy load calf exercises have been shown to be quite effective in chronic or resistant Achilles overuse syndromes.25 Also, maintenance stretching should be continued. Chronic paratendonitis occurs when symptoms are present for greater than 3 months duration. Nonoperative measures are less successful if there is a delay in treatment. Brisement or distention of the paratenon-tendon interface with lidocaine or other solution can be used in refractory paratendonitis. This is a mechanical lysis of adhesions between tendon and paratenon that occurs by the rapid infusion of 5 to 15 mL of local anesthetic or saline into the peritendinous space. Brisement can be done in the office and can possibly eliminate the need for surgical intervention. There is a 33% success rate with this procedure.

Surgery: Posterior Heel Pain Most patients are successfully treated conservatively, but the ones who fail may benefit from surgical intervention. These patients may have coexisting retrocalcaneal bursitis and insertional Achilles tendonitis or paratendonitis and tendonosis. Schepsis et al18 found that 15% of their surgical cases had a combination of these entities. Obtaining an MRI for preoperative planning may be helpful. Paratendonitis In addressing paratendonitis surgically, some authors advocate a J-shaped incision, starting medial to lateral distal to the Achilles tendon insertion, to turn back the skin for exposure. Others recommend the two-incision (medial and lateral) technique, keeping the skin bridge at least 4 cm wide. We recommend a medial incision. Dissection is carried down to the paratenon, which is freed from the superficial skin and subcutaneous tissue. The paratenon is usually hyperemic, fibrotic, and adherent to the underlying tendon. The affected paratenon is resected, but care is taken not to excise the anterior portion, where the critical blood supply enters the tendon. Complete excision of the paratenon could lead to severe postoperative fibrosis and is not recommended. Insertional Tendonitis Insertional tendonitis is usually seen in older athletes, and surgical exposure has been described with many different approaches. Some authors advocate a longitudinal incision placed either laterally or medially, or a combination of two incisions; however, we advocate the midline longitudinal incision. Full-thickness skin flaps are created until the paratenon is identified. The paratenon layer is then freed from the superficial tissues and split longitudinally, ensuring that a good closure can be obtained. The Achilles tendon is also longitudinally split and distally dissected medially and laterally off the calcaneus, being careful not to entirely detach the tendon. At this point, any degeneration of the tendon is excised along with the retrocalcaneal bursa and the prominence of the posterior os calcis. Two resorbable suture anchors are then used to enhance reattachment of the distal part of the tendon. A 2-0 Vicryl suture is used to reapproximate the Achilles tendon side to side and a 4-0 Vicryl suture is used to close the paratenon.

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Retrocalcaneal Bursitis Open For recalcitrant retrocalcaneal bursitis, the retrocalcaneal bursa should be completely excised. The exposure includes two longitudinal incisions medial and lateral. The bursa is usually hyperemic, thickened, and scarred down to the anterior portion of the tendon. The bursa can hold up to 1 to 2 mL of bursal fluid. There may also be fibrinous loose bodies found within the bursa. After excision of the entire bursa, the prominence of the posterior os calcis should be resected.

compared to nonoperative treatment.4–6,28,29 Proponents of nonoperative treatment maintain that overall complications from surgery including skin necrosis, wound infection, sural neuroma, and adhesions to the skin are high. Problems with wound healing remain the most common and significant problem associated with the operative technique. Achilles tendon ruptures are treated surgically in nearly all athletes, and we discuss both the open and percutaneous methods.

Endoscopic Endoscopic decompression of the retrocalcaneal space can be achieved as well. This is done with the patient either in the prone or supine position. If the patient is supine, the leg holder is applied to the calf, but if prone, the feet are positioned just over the edge of the operating table. The foot is plantarflexed using gravity, while the surgeon can control dorsiflexion of the foot with his or her body. The foot of the table is dropped. A lateral portal is made first at the level of the superior aspect of the calcaneus. A blunt trocar is used to penetrate the retrocalcaneal space. A 30-degree 2.7- or 4-mm arthroscope is inserted, and the medial portal is made under direct visualization at the same level of the calcaneus. The motorized shaver is used to remove the bursa and the periosteal layer off the superior portion of the calcaneus. The foot is then placed in full plantarflexion and the posterior superior rim of the calcaneus removed with an abrader. The insertion of the Achilles tendon should now be visualized and protected. A bur is then inserted to resect the prominence of the os calcis under fluoroscopic guidance. Finally, the shaver is used to smooth the edges and clean debris. The skin is closed with nylon suture.

Surgery: Achilles Tendon Repair

Treatment Options: Achilles Tendon Rupture There is still debate over the best management for Achilles tendon ruptures. The treatment options include nonoperative (cast or brace) and operative treatment. Nonoperative treatment is usually reserved for individuals who are elderly and sedentary and have poor skin quality or other comorbidities that would preclude surgery. Immobilization is provided using a short-leg cast or brace in the equinus position for 4 weeks. The patient is then placed in a neutral walking short-leg cast for 4 more weeks with gradual weight bearing. At 8 weeks, a 2.5-cm heel lift in the shoe is used for another 4 weeks. McComis et al26 developed the concept of functional bracing as an alternative to casting for nonoperative management of Achilles tendon ruptures. Their technique has subsequently been modified and has gained popularity as an acceptable option for selected patients. Wallace et al27 had 140 consecutive patients with acute Achilles ruptures that were treated with combined conservative orthotic management. Initial immobilization includes a non-weight bearing short-leg cast with the ankle in equinus for 4 weeks. At 2 weeks, a rigid polyethylene double-shell patellar tendon–bearing orthosis is fabricated and the cast changed. At 4 weeks after injury, the orthosis is then worn for an additional 4 weeks; during this time, it is removed for ankle and subtalar exercises. The patients are also given gait training and progressed to full weight bearing while wearing the orthotic device. Operative treatment for Achilles tendon rupture is advocated by most surgeons because it allows direct repair, aggressive rehabilitation, and predictable results and has a lower rerupture rate

Percutaneous Technique In 1977, Ma and Griffith introduced percutaneous Achilles tendon repair in 18 patients, reporting no reruptures and only two suture complications.30 Their technique has subsequently been modified and has gained popularity as an acceptable option for selected patients. To successfully perform a percutaneous Achilles tendon repair, the tendon gap must be reducible with the ankle in plantarflexion. The patient is placed in a prone position. A solution composed of a 1:1 mix of 1% lidocaine and 0.5% Marcaine is used to locally anesthetize the skin and subcutaneous tissues. Intravenous medication may be given to sedate the patient. Medial and lateral stab wounds at the level of the tear and 2 cm above and below are made. The subcutaneous tissues are spread using a hemostat. Nylon suture (0 or 1) with Keith needles on both ends is passed transversely through the tendon at the proximal puncture. The needle is then advanced distally from both sides in a crisscross fashion through the tendon at 45-degree angles through the middle puncture hole. The suture is then passed through the tendon into the most distal puncture sites. Finally, the medial suture is passed laterally to meet the other strands where both are tied with the tendon gap closed. A hemostat is used to bury the knot. Nylon suture is used to approximate the skin and an adjustable boot locked in 30 degrees of equinus applied (Fig. 69-5). New devices are available that assist the surgeon in performing the percutaneous method, and early results are encouraging.

Open Technique Open surgical repair of the tendon allows direct visualization and the ability to restore functional length of the musculotendinous unit. The longitudinal skin incision is placed medially to avoid the sural nerve (Fig. 69-6). The tissues are elevated with a full thickness flap until the paratenon is reached. The paratenon is incised and the tendon ends are identified. A minimal to no touch technique for the tendon is used, with a no. 5 nonabsorbable suture with application of simple modified Kessler, Bunnell, or Krackow interlocking stitch. Also an absorbable 2-0 interrupted or running epitendinous suture can be placed. A four-strand repair is advocated to increase strength and allow aggressive rehabilitation. Bulky knots or suture should not be placed directly beneath the incision. The paratenon should be closed over the repair to prevent skin adherence to the tendon. The appropriate tensioning of the repair is crucial, and draping out the contralateral uninjured extremity to allow comparison of ankle dorsiflexion is recommended. The appropriate tension is set with the knee in 90 degrees of flexion. Postoperatively, the patient is placed in a cast or splint with the foot at 30 degrees of equinus to minimize tension on the soft tissues and repair.

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Figure 69-5 A–D, The surgical technique for percutaneous Achilles tendon repair.

Postoperative Rehabilitation: Posterior Heel Pain

Postoperative Rehabilitation: Achilles Tendon Repair

Paratendonitis The patient is placed in a removable boot walker and early motion is started immediately to prevent scarring and fibrosis. Weight bearing is limited until the wound is healed, and progressive weight bearing and strengthening should continue for 2 to 3 weeks. When ambulating without pain, the patient may begin closed-chain activities, such as biking or stair climbing. Running may begin at 6 to 10 weeks after surgery.

Percutaneous Repair The postoperative protocol includes 3 weeks in an adjustable boot locked in 30 degrees of plantarflexion with no weight bearing. During this time, gentle movement of the foot, straight leg raises, and knee range of motion is started. After week 3, the orthosis is adjusted up 5 degrees of dorsiflexion each week until 10 degrees of plantarflexion is achieved. Weight bearing is also increased from toe touch to partial, as tolerated. After 6 weeks, full weight bearing as tolerated is allowed, and at 8 weeks, shoe wear with heel lift is initiated for up to 12 weeks. Throughout this time, light active dorsiflexion of the ankle, muscle strengthening, proprioception exercises, stationary cycling (with heel push only), and soft-tissue treatments commence. Three months postoperatively, closed-chain exercises, cycling, and NordicTrack use should be instituted. Finally, at 6 months, running, jumping, and sports activities are permitted.

Insertional Achilles Tendonitis Wound healing is a major concern after débridement of insertional Achilles tendonitis; therefore, the patient is placed in a short-leg splint for 2 weeks and kept non-weight bearing until the wound is healed. The patient is then placed in a removable boot, and range-of-motion exercises are started. There should be emphasis on active dorsiflexion and a progressive resistance exercise program instituted as tolerated. Sportsspecific training is started at 3 months, and competition begins at 6 months. Retrocalcaneal Bursitis Open The patients are placed in a boot walker for 2 weeks with protected weight bearing. Range-of-motion exercises can be started immediately. A heel lift is used after discontinuation of the boot walker. A progressive exercise program should be instituted. Endoscopic After endoscopic calcaneoplasty, the patient is non-weight bearing and splinted in comfortable equinus for 2 to 3 days. Weight bearing as tolerated is then initiated in a removable boot with a 1-inch heel lift. At this time, range-of-motion exercises are instituted, and the boot is discontinued after 4 weeks. A one-half–inch heel lift in the tennis shoe is then used for an additional 6 weeks. Athletics are not allowed until 3 months after the operation.

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Open Repair Earlier protocols for postoperative rehabilitation after Achilles repair advocated cast immobilization for periods of 6 to 8 weeks with the ankle in equinus. The ankle was placed in progressive dorsiflexion at 2-week intervals. After cast removal, the patient began range-of-motion exercises with a physical therapist. Some authors even advocated a long-leg cast; however, Sekiya et al31 used a cadaveric study to disprove that knee position caused displacement of the Achilles tendon with the ankle plantarflexed. These results suggest that the nonoperative treatment of Achilles tendon ruptures requires immobilization in maximal ankle plantar flexion and that immobilization of the knee may not be necessary to achieve tendon-edge apposition. The detrimental effects of immobilization on tendon and bone healing are well documented. The long-term immobilization of joints while tendons are healing slows the recovery of injured tendons. The remodeling of new collagen fibrils is impeded as well. The flexor tendon work of Gelberman et al32

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A

B

D

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E

Figure 69-6 Open Achilles tendon repair. A, Planned incision medial to the Achilles tendon. B, Tendon rupture identified. C, Tendon edges prepared for repair. D, Nonabsorbable sutures placed. E, Completed repair.

showed that early mobilization leads to increased organization at the repair site and increases strength. Mobilization also decreases muscle atrophy and promotes collagen fiber polymerization. There have now been more reports of favorable results with protocols of early motion after Achilles tendon repairs. Mandelbaum et al33 treated 29 athletes with Achilles tendon rupture using Krackow repair and began range-of-motion exercises 72 hours after surgery, using a posterior splint for 2 weeks. Ambulation was started in a hinged orthosis at 2 weeks. The orthosis

was discontinued at 6 weeks and full weight bearing allowed. Progressive resistance exercises were also initiated. There were no reruptures. Isokinetic strength testing revealed a 2.9% deficit at 6 months and no deficit at 12 months. All patients returned to preinjury activity levels at a mean of 4 months. More recently, authors have proposed early range of motion exercises and early weight bearing with a functional orthosis after surgical Achilles tendon repair. Speck and Klaue34 proposed early mobilization with early full weight bearing after surgical repair of Achilles tendon ruptures. This was instituted to allow

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the tendon to experience tension during healing. Tension improves strength and orientation of collagen fibers as well as vascularity. Twenty patients were treated with a Kessler-type suture repair and plantigrade splint for 24 hours. The postoperative program included 6 weeks of full weight bearing in a removable walker. There were no reruptures. All patients reached their preinjury activity level and showed no statistically significant difference in isokinetic strength. Aoki et al35 reported early active motion and weight bearing after cross-stitch Achilles tendon repair in 22 patients. Twenty of the tendons (91%) healed without rerupture. Patients returned to full sports activity in 13.1 weeks. MRI studies were obtained at 4, 6, 8, 12, 16, and 20 weeks. Excellent healing was seen on the MRI at an average of 12.6 weeks. Akizuki et al36 defined the relative stress on the Achilles tendon during weight bearing with immobilization in varying degrees of plantarflexion. They examined electromyographic activity during ambulation in 10 subjects in normal walking, immobilization with a walker boot in neutral plantarflexion, walker boot with a half-inch heel lift, and a walker boot with a 1-inch heel. They concluded that the stress of the Achilles tendon is determined by the degree of plantarflexion and that a 1-inch heel lift sufficiently minimized plantarflexion activity. Maffulli et al37 did a comparative longitudinal study to determine the effects of early weight bearing and ankle mobilization after repair of Achilles tendon rupture. One group, at 2 weeks, was mobilized with weight bearing as tolerated in the plantigrade position. An anterior below-the-knee slab was secured to the leg with Velcro straps, and patients were instructed by the physical therapist to perform concentric exercises against manual resistance and mobilization within the limits of the anterior slab. The anterior slab was discontinued at 6 weeks. The second group was initially casted in the equinus position and was non-weight bearing for 4 weeks. The patients were casted in the neutral position at 4 weeks and made weight bearing as tolerated. There were no differences found in isometric strength or thickness of the tendon. These results suggest that it is not deleterious to start early weight bearing and ankle mobilization after open repair of Achilles tendon ruptures.

Criteria for Return to Sports: Achilles Tendon Repair Full painless range of motion and strength must be recovered prior to resuming athletics. The average time required before light jogging is 2 to 3 months. Competitive athletic activities are usually allowed by 4 to 6 months; however, decisions to allow the athlete to resume activities are made only if adequate strength gains are present.

Results and Outcomes Paratendonitis Generally, surgical results after resection of chronic paratendonitis are acceptable. The literature varies with reports of 72% to 100% good to excellent results. Schepsis et al18 reported in a series of competitive and serious recreational athletes, 87% satisfactory results after surgical treatment of paratendonitis. The best surgical outcomes of the Achilles tendon disorders occur in paratendonitis. Nelen et al38 reported an 89% satisfactory outcome in 92 cases. Insertional Achilles Tendonitis Maffulli et al39 reported 75% good to excellent results in 21 patients treated surgically for insertional Achilles tendonitis, but

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25% were unable to return to their normal level of sporting activities. Schepsis et al18 achieved an 86% satisfactory result and Nelen et al38 achieved a 73% outcome after surgical intervention for insertional Achilles tendonitis. Retrocalcaneal Bursitis Open Reports in the literature are variable, with success rates ranging from 50% to 90%. Paavola et al1,2 achieved 76% good to excellent results. Schepsis et al18 demonstrated a 71% satisfactory rate in their first series and an increase to 75% in their second series. Endoscopic Leitze et al40 performed a prospective study to compare the endoscopic technique with the standard open technique. They found that postoperative American Orthopaedic Foot and Ankle Society scores were not significantly better, but the endoscopic procedures were associated with fewer complications. The complications included infection (3% versus 12%), altered sensation (10% versus 18%), and scar tenderness (7% versus 18%), in endoscopic and open procedures, respectively. van Dijk et al41 reported 75% excellent results, 20% good results, and 5% fair results, with no surgical complications or postoperative infections in their series. Achilles Tendon Rupture: Nonoperative Treatment In a prospective, randomized comparison between operative and nonoperative management of Achilles tendon ruptures by Moller et al,6 the rerupture rate for the operative group was 1.6% and 20.7% for the nonoperative group. In the quantitative review of Wong et al28 of 645 Achilles tendon ruptures, it was noted that conservative treatment had the highest rerupture rate at 10.7% and skin complications were lowest at 0.5%. In another systematic review of the literature by Kocher et al,5 the probability of rerupture after conservative management was 12.1%, while after operative repair, it was 2.2%. However, the probability of wound complications with conservative treatment was 0.3% compared to 7.5% with operative repair. Wallace et al27 recently reported on 140 patients treated conservatively with combined casting and orthotic treatment. Using the scoring system of Leppilahti, the overall outcomes were 56% excellent, 30% good, 12% fair, and 2% poor. There was a 5.7% rerupture rate including two complete and five partial reruptures. There also was a significant difference in plantarflexion strength, but the authors state that 89% of the patients had no or minimal subjective symptoms of calf weakness. The key point is that only 33% returned to the same level of activity, 54% returned to a lower level of activity, and 9% were unable to return to sports. Josey et al42 reported on 32 patients with Achilles tendon rupture treated conservatively with full weight-bearing cast treatment and found a rerupture rate of 6.25%. These patients also had plantarflexion weakness but overall were satisfied with their treatment. Achilles Tendon Repair Percutaneous Bradley and Tibone43 did a comparative study between percutaneous (1.8-year follow-up) and open surgical repairs (4.6-year follow-up) and found no statistically significant difference in strength, power, or endurance between groups at the 1.8-year follow up. There were two reruptures (13%) in the percutaneous group. FitzGibbons et al44 found a significant difference of a 13% power loss after percutaneous Achilles repair at an average follow-up of 3.8 years. The patients who were

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recreational athletes returned to their preinjury activity level. In the Tomak and Fleming45 study, a 21% power loss after percutaneous repair was found at an average of 34 months of followup. There were no reruptures or sural nerve complications. Despite the loss of plantarflexion power, patients were generally very satisfied with their treatment. There was one recreational athlete who reported weakness. These authors recommend that percutaneous repair be reserved for the recreational athlete only. A cadaveric study comparing the biomechanics of percutaneous repair with that of open repair was done by Hockenbury and Johns,46 who found that percutaneous repairs result in half the strength of open repairs. In the literature, percutaneous repairs have an increased rate of rerupture when compared to open repairs but a lower rerupture rate when compared to nonoperative treatment. The range of repeat rupture after percutaneous repair has been reported from as low as 2.8% to as high as 12%. Haji et al47 recently published a retrospective study of 108 patients comparing percutaneous (38 patients) versus open repair (70 patients) revealing a lower rerupture rate in the percutaneous group (2.6% versus 5.7%, respectively). The percutaneous group had no wound infections and 10.5% transient sural nerve lesions. No significant difference in power was found, but power was defined as normal if the subject was able to stand on his or her tiptoes. There was no mention of return to athletic activities. Open Cetti et al3 conducted a prospective, randomized study to compare operative and nonoperative treatment of Achilles tendon ruptures and also performed a review of the literature. They found that the operative group had a 5.4% rerupture rate compared to a 14.5% rerupture rate in those who received conservative treatment. Another important outcome reported was that 57% of patients returned to their preinjury level of athletics in the operative group. In contrast, in the conservative group, only 29% returned to their preinjury level of athletics. The authors’ literature review revealed a rerupture rate of 13.4% versus 1.4% for nonoperative and operative treatment, respectively. There were fewer minor complications in the nonoperative group than in the operative group. Various methods were used to objectively evaluate functional recovery and mean plantarflexion strength after surgery. After surgical repair, there was an 87% functional recovery compared to 78% with conservative treatment. An increased return to preinjury athletic participation was also noted after surgical treatment. Kellam et al4 reported a retrospective series of 68 patients whose ruptured Achilles tendon were managed operatively. Of the 48 patients who were clinically evaluated, 92% returned to a preinjury level of activity. The rerupture rate in this operative series was 3%, and 13% had incisional complications.

Complications The major complication after Achilles tendon surgery is skin necrosis or superficial infection. Paavola et al2 analyzed complications of 432 consecutive patients after surgical treatment of chronic Achilles tendon overuse injuries. Eleven percent of the patients had complications, including skin edge necrosis in 14 patients, superficial wound infections in 11 patients, partial

rupture in one patient, deep venous thrombosis in one patient, seroma formation in five patients, hematoma in five patients, fibrotic reaction in five patients, and sural nerve irritation in four patients. Most of the complications (54%) involved compromised wound healing. The skin envelope in this region is tenuous and excessive skin mobilization must be avoided. Sural nerve injuries occur most commonly with percutaneous repair of Achilles tendon injuries but can occur with all Achilles tendon operative procedures. The nerve must be either avoided by going medial to the Achilles or visualized and uncompromisingly protected. Reruptures are more common in Achilles tendon ruptures treated nonoperatively, followed by percutaneous repairs. Open repairs have a much smaller occurrence of rerupture. Another complication after treatment of Achilles rupture is lengthening of the tendon. This is more common in closed treatment and percutaneous treatment of Achilles tendon ruptures. Decreased plantarflexion power may result in difficulty with walking, running, or jumping.

Conclusions Most of the Achilles tendon overuse injuries are successfully treated with nonoperative management. This usually consists of a brief period of rest, activity modification, and correction of malalignment with orthotics, and nonsteroidal anti-inflammatory drugs. Other modalities that are helpful include ionophoresis, stretching, eccentric calf strengthening exercises, and a heel lift. Steroid injections are not indicated because this places the Achilles tendon at higher risk of rupture. A gradual, progressive rehabilitation program should be instituted. Nonoperative measures are 90% to 95% successful for acute treatment; however, up to 29% require surgical treatment for chronic problems that fail conservative management.1 Surgical treatment of chronic Achilles tendon overuse injuries obtains approximately 80% satisfactory results. There are options in surgical technique; however, regardless of the approach, meticulous soft-tissue management must be maintained. The major complications of all surgical treatment in this anatomic area include skin edge necrosis, wound infection, sural nerve injury, and fibrotic scar formation. Once the soft-tissue envelope is healed, it is important to start mobilization. Finally, there is still debate regarding the best way to manage Achilles tendon ruptures. Studies have shown that operative repair has the most reliable results, the lowest rate of rerupture, and greater recovery of push-off strength compared to nonoperative treatment. The operative options include open and percutaneous repair. Open repair allows better control of tendon tension and has a lower rerupture rate, but the rate of wound complications is higher. Percutaneous methods present fewer wound complications but sacrifice repair strength and push-off power and risk rerupture or elongation of the tendon. There is also a greater risk of sural nerve injury. We recommend open repair in the athletic population with percutaneous repair as an acceptable alternative in the older, sedentary individual who may be at risk of skin complications. The trend of rehabilitation after Achilles tendon repair has been early mobilization and earlier weight bearing to facilitate healing, decrease atrophy, and shorten rehabilitation. Multiple clinical studies have shown that early weight bearing and mobilization are not deleterious after Achilles tendon repair.

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REFERENCES 1. Paavola M, Kannus P, Paakkala T, et al: Long-term prognosis of patients with Achilles tendinopathy: An observational 8-year follow-up study. Am J Sports Med 2000;28:634–642. 2. Paavola M, Orava S, Leppilahti J, et al: Chronic Achilles tendon overuse injury: Complications after surgical treatment. An analysis of 432 consecutive patients. Am J Sports Med 2000;28:77–82. 3. Cetti R, Christensen SE, Ejsted R, et al: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am J Sports Med 1993;21:791–799. 4. Kellam JF, Hunter GA, McElwain JP: Review of the operative treatment of Achilles tendon rupture. Clin Orthop 1985;201:80–83. 5. Kocher MS, Bishop J, Marshall R, et al: Operative versus nonoperative management of acute Achilles tendon rupture expected-value decision analysis. Am J Sports Med 2002;30:783–790. 6. Moller M, Movin T, Granhed H, et al: Acute rupture of tendo Achillis. A prospective, randomised study of comparison between surgical and non-surgical treatment. J Bone Joint Surg Br 2001;83:843–848. 7. Bassett FH III, Speer KP: Longitudinal rupture of the peroneal tendons. Am J Sports Med 1993;21:354–357. 8. Sobel M, Bohne WH, Levy ME: Longitudinal attrition of the brevis tendon in the fibula groove: An anatomic study. Foot Ankle Int 1990;11:124–128. 9. Pelet S, Saglini M, Garofalo R, et al: Traumatic rupture of both peroneal longus and brevis tendons. Foot Ankle Int 2003;24:721–723. 10. Mann RA, Coughlin MJ: Surgery of the Foot & Ankle, 7th ed. St. Louis, Mosby, 1999. 11. Eckert WR, Davis EA: Acute rupture of the peroneal retinaculum. J Bone Joint Surg Am 1976;58:670–673. 12. Zammit J, Singh D: The peroneus quartus muscle: Anatomy and clinical relevance. J Bone Joint Surg Br 2003;85:1134–1137. 13. Edwards ME: Relations of peroneal tendons to fibula, calcaneus, cuboideum. Am J Anat 1928;42:213–253. 14. Beck E: Operative treatment of recurrent dislocation of peroneal tendons. Arch Orthop Trauma Surg 1981;98:247–250. 15. Krause JO, Brodsky JW: Peroneus brevis tendon tears: Pathophysiology, surgical reconstruction, and clinical results. Foot Ankle Int 1998;19: 271–279. 16. Sammarco GJ: Peroneal tendon injuries. Orthop Clin North Am 1994;25:135–145. 17. Alanen J, Orava S, Heinonen OJ, et al: Peroneal tendon injuries. Report of thirty-eight operated cases. Ann Chir Gynaecol 2001;90:43–46. 18. Schepsis A, Jones H, Haas A: Current concepts: Achilles tendon disorders in athletes. Am J Sports Med 2002;30:287–305. 19. Chao W, Deland JT, Bates JE, et al: Achilles tendon insertion: An in vitro anatomic study. Foot Ankle Int 1997;18:81–84. 20. Lagergren C, Lindholm A: Vascular distribution in the Achilles tendon. An angiographic and microangiograhic study. Acta Chir Scand 1958– 1959;116:491–496. 21. Carr AJ, Norris SH: The blood supply of the calcaneal tendon. J Bone Joint Surg Br 1989;71:100–101. 22. Burdett RG: Forces predicted at ankle during running. Med Sci Sports 182;14:308–310. 23. Kvist M: Achilles tendon injuries in athletes. Sports Med 1994;18:173–201. 24. Gross ML, Dalvin L, Evanski PM: Effectiveness of orthotic shoe inserts in the long distance runner. Am J Sports Med 1991;19:409–412. 25. Alfredson H, Pietila T, Johnson P, et al: Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendonosis. Am J Sports Med 1998;26:360–366. 26. McComis GP, Nawoczenski DA, Dehaven KE: Functional bracing for rupture of the Achilles tendon. Clinical results and analysis of ground-

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27.

28.

29. 30. 31.

32.

33.

34.

35.

36.

37.

38. 39.

40.

41. 42.

43.

44. 45. 46.

47.

reaction forces and temporal data. J Bone Joint Surg (Am) 1997;79:1799–1808. Wallace RG, Traynor IE, Kernohan WG, et al: Combined conservative and orthotic management of acute ruptures of the Achilles tendon. J Bone Joint Surg Am 2004;86:1198–1202. Wong J, Barrass V, Maffulli N: Quantitative review of operative and nonoperative management of Achilles tendon ruptures. Am J Sports Med 2002;30:565–574. Myerson MS: Achilles tendon ruptures. Instr Course Lect 1999;48:219–230. Ma GW, Griffith TG: Percutaneous repair of acute closed ruptured Achilles tendon: A new technique. Clin Orthop 1977;128:247–255. Sekiya JK, Evensen KE, Jebson PJL, et al: The effect of knee and ankle position on displacement of Achilles tendon ruptures in a cadaveric model implications for nonoperative management. Am J Sports Med 1999;27:632–635. Gelberman RH, Woo SL-Y, Lothringer K, et al: Effects of early intermittent passive mobilization on healing canine flexor tendons. J Hand Surg 1982;7:170–175. Mandelbaum BR, Myerson MS, Forster R: Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation. Am J Sports Med 1995;23:392–395. Speck M, Klaue K: Early full weightbearing and functional treatment after surgical repair of acute Achilles tendon rupture. Am J Sports Med 1998;26:789–793. Aoki M, Ogiwara N, Ohta T, et al: Early active motion and weightbearing after cross-stitch Achilles tendon repair. Am J Sports Med 1998;26:794–800. Akizuki KH, Gartman EJ, Nisonson B, et al: The relative stress on the Achilles tendon during ambulation in an ankle immobiliser: Implications for rehabilitation after Achilles tendon repair. Br J Sports Med 2001;35:329–333. Maffulli N, Tallon C, Wong J, et al: Early weightbearing and ankle mobilization after open repair of acute midsubstance tears of the Achilles tendon. Am J Sports Med 2003;31:692–700. Nelen G, Martens M, Burssens A: Surgical treatment of chronic Achilles tendonitis. Am J Sports Med 1989;17:754–759. Maffulli N, Testa V, Capasso G, et al: Calcific insertional Achilles tendinopathy: Reattachment with bone anchors. Am J Sports Med 2004;32:174–182. Leitze Z, Sella EJ, Aversa JM: Endoscopic decompression of the retrocalcaneal space. J Bone Joint Surg Am 2003;85:1488– 1496. van Dijk CN, van Dyk GE, Scholten PE, Kort NP: Endoscopic calcaneoplasty. Am J Sports Med 2001;29:185–189. Josey RA, Marymont JV, Varner KE, et al: Immediate, full weightbearing cast treatment of acute Achilles tendon ruptures: A long-term follow-up study. Foot Ankle Int 2003;24:775–779. Bradley JP, Tibone JE: Percutaneous and open surgical repairs of Achilles tendon ruptures. A comparative study. Am J Sports Med 1990;18:188–195. FitzGibbons RE, Hefferon J, Hill J: Percutaneous Achilles tendon repair. Am J Sports Med 1993;21:724–727. Tomak SL, Fleming LL: Achilles tendon rupture: An alternative treatment. Am J Orthop 2004;33:9–12. Hockenbury RT, Johns JC: A biomechanical in vitro comparison of open versus percutaneous repair of tendon Achilles. Foot Ankle 1990;11:67–72. Haji A, Sahai A, Symes A, et al: Percutaneous versus open tendo Achillis repair. Foot Ankle 2004;25:215–218.

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Midfoot and Hindfoot Steven J. Lawrence

In This Chapter Peritalar dislocations Os trigonum syndrome Lisfranc injuries Navicular stress fracture Plantar fasciitis Tibial nerve entrapment Posterior tibial tendonitis

INTRODUCTION • Sport-related foot injuries generally result from either acute or cumulative injuries. • Most painful foot structures can be examined by direct palpation. • A thorough patient history and physical examination facilitates the formulation of an appropriate differential diagnosis. • The hindfoot and midfoot absorb tremendous torsional and shock-absorbing stresses during athletic endeavors. Hindfoot function and midfoot function are intimately interconnected. • The hindfoot joint complex permits subtle adaptations to uneven terrain. • The midfoot largely functions as a simple block, transmitting forces applied to and from the hindfoot and forefoot. • Midfoot structures are integral components of the longitudinal and transverse arches.

RELEVANT ANATOMY AND BIOMECHANICS Hindfoot and midfoot components are easily delineated. The former is largely composed of its two bony structures, the talus and calcaneus, while the latter is composed of the navicular, the three cuneiforms, and the cuboid. Anatomically, the boundaries of the hindfoot region begin at the subtalar joint and extend to the Chopart (or transverse-tarsal) joint; the midfoot begins at this joint and extends to the Lisfranc (or tarsometatarsal joint) complex. The subtalar articulation links the talus and calcaneus via three articular facets. The Chopart joint comprises the talonavicular and calcaneocuboid joints. The term subtalar joint complex refers to both the subtalar and Chopart joints. In addition to osseous and chondral injuries, soft-tissue structures such

as the capsule, tendon, ligament, nerve, and heel pad may be injured in isolation or combinations during competitive sport. The biomechanics of the subtalar joint complex remain poorly understood; in fact, the joint complex is perhaps the most poorly understood articulation. Efficient locomotion requires alternating flexibility and rigidity of the foot. Flexibility is necessary for shock absorption, while rigidity is required for propulsive activities. The alternating inversion-eversion of the subtalar joint within the gait cycle is necessary for efficient locomotion.1 Subtalar motion is intimately linked to the adduction/abduction and pronation/supination movements of the talonavicular joint. Due to skeletal alignment, natural hindfoot alignment is valgus; therefore, normal hindfoot function is dependent on voluntary control of hindfoot inversion. A competent posterior tibial tendon is, therefore, essential for regulation of subtalar joint control. Midfoot architecture comprises the longitudinal and transverse arches. Bone stability is enhanced by its unique structural design. The second metatarsal base insets into the adjacent cuneiforms in mortise-and-tenon fashion (Fig. 70-1). A dense network of stout, plantar ligaments secure the metatarsal bases to the cuneiforms. The plantar fascia supplies supplemental longitudinal arch support. If midfoot integrity is disrupted, force transmission from the hindfoot to the forefoot (and vice versa) is impaired. If injury is not diagnosed in a timely manner, continued weight bearing may result in midfoot collapse.2 Significant hindfoot or midfoot injury sustained during an athletic injury may result in considerable dysfunction. Overuse injury involving bone and tendon is commonly present in runners and dancers. Periarticular fractures are not infrequent; they are difficult to detect due to intricate three-dimensional foot anatomy. Injury sequelae, especially stiffness and pain, result in impairment in select abilities, such as jumping and ballistic motions, preventing return to elite competition. Therefore, prompt diagnosis, appropriate intervention, and aggressive rehabilitation are essential to optimize outcomes.

SELECT INJURIES Peritalar Dislocations Anatomy Peritalar dislocations are acute hindfoot injuries. They result from an extreme rotational injury. The injury may also be termed a subtalar dislocation. However, since the initial event is a talonavicular dislocation with subsequent subluxation/dislocation of the subtalar joint, the term peritalar dislocation appears to be more anatomically accurate (Fig. 70-2). The condition, therefore, results in complete disruption of the talonavicular joint capsule with a variable interosseous ligament injury.

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Figure 70-1 A schematic representation of the midfoot demonstrating the mortise and tenon-like configuration of the second metatarsal base and the adjacent cuneiforms.

The posterior tibial tendon and a multitude of supporting ligaments including the spring, calcaneofibular, and/or deltoid may also be damaged. Articular injury is not infrequent. The injury subtype is based on the forefoot’s anatomic relationship to the talar head. Although four subtypes are possible, medial and lateral peritalar dislocations comprise the vast majority of injuries. The more common medial peritalar dislocation is thought to result from a forced inversion injury, while its counterpart results from a forced eversion injury.3 Most published series are relatively small with the mechanism of injury associated with high-energy trauma such as motor vehicle accidents, not athletic endeavors. Nonetheless, a peritalar dislocation is not an uncommon athletic injury, especially with basketball players landing on an irregular surface. Clinical Findings A dramatic deformity is typically present; the protruding talar head is palpable on either side of the ankle (Fig. 70-3). Palpation of the uncovered talar head should make the diagnosis evident by clinical means. A thorough neurovascular examina-

Figure 70-2 A lateral radiograph demonstrating a peritalar dislocation. The talonavicular joint is disrupted and the subtalar joint is subluxated.

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Figure 70-3 An anteroposterior radiograph of a lateral peritalar dislocation. The deformity is dramatic with the uncovered talar head noted medially in the subcutaneous tissues.

tion should be performed prior to and following joint reduction. In addition, open injuries occur due to wide displacement and tearing of thin subcutaneous tissues.

Differential Diagnosis Ankle fracture-dislocation

Treatment Options Joint reduction is accomplished in a timely fashion, typically after radiographs have been performed and assessed. Reduction is best performed with the patient under general anesthesia or deep conscious sedation. Suitable anesthesia facilitates relaxation while decreasing the incidence of iatrogenic chondral damage during reduction attempts. Reduction is performed with the knee flexed to 90 degrees to negate the effect of the gastrocnemius. The joint is reduced in steplike fashion. First, one accentuates the deformity. Next, joint distraction is accomplished with application of longitudinal traction. Finally, a reduction maneuver is performed in a direction opposite to that of the injury-producing force.4,5 Irreducible dislocations do occasionally occur, as reduction may be blocked by soft-tissue or bony impediments. Irreducible injuries are most commonly associated with lateral peritalar dislocations. Such instances necessitate an open procedure. This permits excision or reduction of the impediments to reduction. In the instance of a lateral dislocation, the posterior tibial tendon is the most commonly encountered impediment. It may become incarcerated into the joint, blocking reduction. In contrast, with medial peritalar dislocations, the talar head may become buttonholed through the extensor digitorum brevis or the peroneal tendons.5 Typically, once the talonavicular joint has been congruently reduced, the foot is stable. Recurrent dislocations are rare; however, on occasion, insertion of a Kirschner wire is necessary due to a persistent unstable foot.3

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As previously noted, medial peritalar dislocations are decidedly more common than lateral.3,4,6,7 The rate of open injury is variable; Merchan,3 in a series of 39 injuries, documented a 41% rate of open injuries. Compound injuries obviously represent orthopedic emergencies and are managed with urgent irrigation and débridement, reduction, and appropriate antibiotic coverage to prevent deep infection. Peritalar injuries are commonly associated with osteochondral fractures involving the head and/or body of the talus as well as associated foot and ankle fractures, especially metatarsal and malleolar fractures. Multiple authors have highlighted an incidence of associated fractures in the range of 40% or more.3,4,6 These concomitant injuries may adversely affect rehabilitation efforts. A computed tomography study of the hindfoot is recommended to rule out occult injuries not evident by conventional radiography.5,6 Overall, the prognosis following a peritalar dislocation is guarded. In their series of 17 patients, DeLee and Curtis4 found only five patients with range of motion comparable to that of the contralateral, noninjured extremity. Specifically, the average arc of subtalar motion following a medial dislocation was 24 degrees, whereas with lateral dislocations a subtalar arc of 17 degrees was present.4 Similarly, in a report of 18 peritalar dislocations, Garofalo et al7 reported excellent results in only 56% at an average follow-up of 10 years. Subtalar arthrofibrosis and/or post-traumatic arthritis are thought to be primary deterrents to satisfactory outcomes. A subtalar fusion or triple arthrodesis may be considered as a salvage procedure for persistent subtalar dysfunction. Rehabilitation Institution of an aggressive rehabilitation program is vital to optimize outcome following this injury. The program should include foot intrinsic muscle strengthening, ankle and subtalar joint rangeof-motion exercises, and proprioceptive training. Proprioception training enhances the ability of the central nervous system to monitor joint position. Closed-chain exercise and skill-specific training for the athlete’s particular sport demands are essential components of rehabilitation prior to return to competition. Long-term outcome has been associated with multiple factors including direction of the dislocation, concomitant fractures, compound injuries, and length of immobilization.3 Most authors report fewer satisfactory outcomes with lateral peritalar dislocations.3,4,6–8 Range of motion of the subtalar joint appears to directly correlate with the outcome. DeLee and Curtis4 strongly recommend restricting the immobilization period to 3 weeks if possible; otherwise considerable stiffness results. Unfortunately, the presence of a concomitant, unstable fracture may make early mobilization impractical without risking fracture displacement. Aggressive stabilization of associated fractures using internal fixation may permit early rehabilitation, improved outcomes, and a more normal range of joint motion.5 These guarded outcomes must be cautiously viewed, as most series are composed of high-energy injuries rather than lower energy, sport-related injuries. The prognosis for the latter injuries may be more favorable, particularly if associated periarticular injuries are not present and aggressive, timely rehabilitation is instituted.

Os Trigonum Syndrome Anatomic Features The os trigonum is a small oval accessory bone found in less than 10% of the population9 (Fig. 70-4). In 1955, McDougall high-

Figure 70-4 A lateral radiograph of the foot demonstrating a large os trigonum of the posterior aspect of the ankle and subtalar joints.

lighted the painful conditions associated with this accessory bone.10 The ossicle represents an un-united secondary ossification center of the talus. Therefore, its presence alone is not an indication of pathology. However, if an ossicle is present in one foot, it is commonly found in both. The ossicle is located adjacent to the posterolateral talus. Due to its periarticular position, the bone is vulnerable to impingement with ankle plantarflexion. Injury may result from either a single traumatic injury or from repetitive trauma. Furthermore, injury may involve the ossicle or its fibrous connection (synchondrosis) with the talus. The os trigonum syndrome (OTS), therefore, is a painful condition of the posterior triangle of the ankle. The syndrome most commonly involves athletes that perform with the ankle positioned in extreme plantarflexion. Ballet dancers, particularly those who perform en pointe, appear to be the most commonly afflicted athletes. Such athletes may also develop tenosynovitis of the flexor hallucis longus tendon. This latter entity may masquerade as OTS; the two may coexist. Therefore, surgical decompression of the long flexor tendon may be necessary at the time of surgical ablation of the os.11 Clinical Findings Athletes with OTS generally manifest discomfort within the posterior ankle; however, symptoms may be nonspecific. Pain is accentuated with the end range of both passive and active ankle plantarflexion. Resisted isometric ankle plantarflexion, however, should not elicit a painful response. Active or passive ankle dorsiflexion relieves discomfort. Retrocalcaneal bursitis must be distinguished from OTS; the “two-finger squeeze test” is positive with retrocalcaneal bursitis but is negative in OTS (Fig. 70-5). The painful condition may result from either bony or soft-tissue impingement. Radiographic Findings The presence of an os trigonum can be generally confirmed with plain radiographs. Lateral radiographs of the ankle in maximal plantarflexion may demonstrate impingement of the os between the distal tibia and the calcaneus. A bone scan will usually demonstrate intense and localized radionucleotide uptake over the posterior talus if significant injury has occurred (Fig. 70-6).

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Figure 70-5 A photograph demonstrating the two-finger squeeze test. This is a sensitive clinical test for retrocalcaneal bursitis.

Figure 70-6 A bone scan representing localized radionucleotide uptake in the region of the os trigonum. In the proper clinical setting, this study is consistent with os trigonum syndrome.

A computed tomography study may demonstrate an acute fracture or irregular margins of the os trigonum, thereby suggesting the presence of pathology. In the event that diagnosis remains uncertain, OTS may be confirmed by a positive response to a fluoroscopically guided injection of approximately 0.5 mL of a short-acting anesthetic12 (Fig. 70-7).

Differential Diagnosis Achilles tendonitis Retrocalcaneal bursitis Flexor hallucis longus tenosynovitis Subtalar arthritis Calcaneal stress fracture Painful accessory soleus

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Figure 70-7 A fluoroscopic image of the hindfoot confirming appropriate needle location for injection of a symptomatic os trigonum.

Treatment Options Activity restrictions, short-term immobilization, and/or use of nonsteroidal anti-inflammatory medications are cornerstones of conservative management. Commonly, the correct diagnosis is missed or delayed. As previously described, if the diagnosis is uncertain, an injection with a local anesthetic may confirm the diagnosis; an injection with steroid preparation may be therapeutic.12,13 In a series of 19 athletes with OTS, Mouhsine et al13 reported a 84% success rate using one or two fluoroscopically guided steroid injections at 2-year follow-up. The recalcitrant cases were managed with surgical excision with complete relief of symptoms. Abramowitz et al11 reported the outcomes of open surgical resection in 41 symptomatic os trigona. Excellent pain relief and restoration of function was reported at 44-month follow-up; the patients scored an average of 87.6 points on the American Orthopaedic Foot and Ankle Society test (range, 0 to 100). Therefore, resection was recommended if symptoms persisted following 3 months of conservative management. Abramowitz et al observed a trend toward a lower success rate when symptoms had been present for more than 3 years. Finally, iatrogenic sural nerve injury was documented in nearly 20% of their series.11 Marrotta and Micheli14 reported on 16 athletes who underwent open excision of a painful os trigonum. Their series included 12 ballet dancers. Surgical excision was undertaken following failure of conservative management. All patients undergoing excision noted significant improvement of impingement symptoms. All professional dancers returned to full activity; however, two thirds reported occasional discomfort with athletic endeavors. In addition to open resection, an alternative form of ablation, arthroscopic resection, has been performed. In a series of 11 patients, Marumoto and Ferkel15 reported on results following arthroscopic os trigonum excision. At mean follow-up of 35 months, the average American Orthopaedic Foot and Ankle Society score increased from 45 to 86 points. Therefore, this technique may produce superior outcomes due to minimization of scar tissue and shorter recovery times. However, this is a technically demanding procedure; therefore, only surgeons familiar with subtalar arthroscopic techniques should consider this form of minimally invasive excision.

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Chapter 70 Midfoot and Hindfoot

Rehabilitation Conservative management emphasizes means to reduce inflammation. Physical modalities are used. Cross-training techniques are invaluable in maintaining cardiovascular fitness while avoiding irritation of the posterior ankle. Following surgical excision, postoperative rehabilitation programs focus on restoration of ankle and subtalar motion, while increasing strength, power, and endurance to the gastrocsoleus complex. Sural nerve desensitization may be beneficial if hypersensitivity is present. The os trigonum is closely associated with the flexor hallucis longus tendon; therefore, early tendon mobilization should decrease the potential of postoperative tendonsheath scarring.

Lisfranc Injuries Anatomy The foot’s mid-portion functions primarily as a simple block transmitting forces to and from the hindfoot and forefoot. Its composite range of motion is very limited. Midfoot injuries commonly affect the complex osseoligamentocapsular structures of the Lisfranc joint complex. Injury pathomechanics result from either forefoot hyperdorsiflexion or hyperplantarflexion. Such injuries may be either ligamentous, bony, or mixed. Pure ligamentous injuries are commonly underdiagnosed or delayed in diagnosis due to minimal radiographic changes. Furthermore, the midfoot’s inherent bony stability may mask the ligamentous disruption, unless weightbearing radiographs are obtained or stress radiography is performed. Therefore, a high index of suspicion and specialized testing is often necessary to detect occult injuries.2 As previously discussed, the joint complex has unusual bony stability represented by the unique dovetail configuration of the second metatarsal base interlocking into the three cuneiforms. Extensive plantar ligaments connect the metatarsal bases to the cuneiforms and the cuboid. Intermetatarsal ligaments span each of the metatarsal bases except the first and second, where the obliquely oriented Lisfranc ligament is found. This ligament spans the second metatarsal base to the medial cuneiform, providing second metatarsal security. In low-energy athletic injuries, the injury is primarily ligamentous and instability affects only the second metatarsal. However, more extensive injury may occur; the amount and direction of applied energy determine the extent and direction of the Lisfranc disruption. Football-related injuries are not uncommon, especially in linemen. Snowboarding- and windsurfing-related injuries may result as one falls away from the forefoot, which is secured by a foot sling. Clinical Findings Classically, an athlete presents with a painful midfoot and decreased ability to fully weight bear. Swelling and tenderness about the Lisfranc complex are typically present. With isolated stress applied to individual Lisfranc joints, painful clicking may be elicited. Ecchymosis may develop on the plantar aspect of the midfoot.16 The athlete usually cannot stand on tiptoe secondary to pain. However, classic signs and symptoms may not be present due to the wide continuum of pathology. Nunley and Vertullo17 emphasize the uniqueness of athleticsrelated Lisfranc injuries compared to those of high-energy trauma. The radiographic findings are usually subtle. Fractures are rarely present. A sport midfoot injury classification system stratifies these injuries into three subclasses (Table 70-1). Stage I represents a true ligamentous strain; therefore, the ligament is

Table 70-1 Midfoot Sprain Classification Stage I

No diastasis or loss of arch height

Stage II

Diastasis of the I–II metatarsal bases is present with no loss of arch height

Stage III

Diastasis of the I–II metatarsal bases is present with loss of arch height

From Nunley JA, Vertullo CJ: Classification, investigation, and management of midfoot sprain. Lisfranc injuries in the athlete. Am J Sports Med 2002;30:871–878.

intact and competent with no diastasis between the first and second metatarsal bases. In stage II, dorsolateral subluxation of the second metatarsal is radiographically evident; however, despite the diastasis, no loss of arch height is present. Finally, in stage III, both diastasis and loss of longitudinal arch height is apparent on radiographs.17 Typically, midfoot disruption proceeds in steplike fashion. In these injuries, the second metatarsal base commonly subluxates as the initial event18 (Fig. 70-8). The “clear space” between the first and second metatarsal bases should not exceed 2 mm. Radiographs must be carefully scrutinized to ensure anatomic alignment of the metatarsal bases to the cuboid and respective cuneiforms in all projections. A small radiopacity (the fleck sign) in the one-two interspace may represent an avulsion fracture of the Lisfranc ligament, belying a midfoot ligamentous injury. Pathologic forces may propagate proximally between the cuneiforms rather than progressing laterally. Therefore, the softtissue disruption may be longitudinal rather than transverse. Moreover, metatarsophalangeal joint injuries or metatarsal fractures may also accompany midfoot injury.

Differential Diagnosis Metatarsal and tarsal stress fractures

Figure 70-8 An anteroposterior radiograph of the Lisfranc complex demonstrating a widening of the first and second metatarsal bases.

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Ankle and Foot

Treatment Options A continuum of injury occurs and varies from an isolated joint injury (typically the second tarsometatarsal joint) to more extensive joint complex injury. Treatment strategy varies from simple immobilization for simple ligamentous/capsular strains to complex reconstruction with internal fixation for extensive fracture/dislocations. The means to achieve the most suitable outcome remains controversial. Faciszewski et al19 retrospectively studied the long-term outcomes of 15 “subtle” injuries of the Lisfranc joint. “Subtle” injuries were defined as those with a 2- to 5-mm diastasis between the first and second metatarsal bases. Athletes comprised one third of the series. Thirteen of 15 injuries were treated with cast immobilization; the remaining two underwent open reduction and internal fixation. Five of the 13 patients treated with immobilization eventually underwent arthrodesis due to pain and deformity. After review of their series, Faciszewski et al emphasized the value of weight-bearing radiographs. Long-term outcomes were noted to be dependent on an arch height assessment determined by a weight-bearing lateral radiograph. Surgical repair was recommended when significant arch loss was present. Moreover, the measurement of metatarsal diastasis (if