DeLee and Drez's Orthopaedic Sports Medicine, Third Edition: Expert Consult - Online and Print, 2-Volume Set

C o n t r i b u t o r s Karim Abdollahi, MD Clinical Professor of Orthopedic Surgery, Loma Linda University Medical Ce...

Author: Jesse C. DeLee MD | David Drez Jr. MD | Mark D. Miller MD

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C o n t r i b u t o r s

Karim Abdollahi, MD Clinical Professor of Orthopedic Surgery, Loma Linda University Medical Center, Loma Linda; Orthopedic Surgeon, South Coast Medical Center, Laguna Beach, California Thoracic Outlet Syndrome

Shafeeq Ahmed, MD Hospitalist, Cardiovascular Services, Hartford Hospital, Hartford, Connecticut Management of Hypertension in Athletes

Mir Haroon Ali, MD, PhD Resident, Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Heterotopic Bone Around the Elbow

David B. Allen, MD Professor of Pediatrics, University of Wisconsin School of Medicine and Public Health; Director of Endocrinology and Endocrine Fellowship Training, American Family Children’s Hospital, Madison, Wisconsin Diabetes Mellitus

Louis C. Almekinders, MD Attending Surgeon and Cofounder, North Carolina Orthopaedic Clinic, Durham, North Carolina Physiology of Injury to Musculoskeletal Structures

Annunziato Amendola, MD Professor and Director of the University of Iowa Sports Medicine Center, University of Iowa Hospitals and Clinics, Iowa City, Iowa Leg Pain and Exertional Compartment Syndromes; Stress Fractures of the Leg

James R. Andrews, MD Orthopedic Surgeon, Alabama Sports Medicine Center, Birmingham, Alabama Throwing Injuries in the Adult

Robert A. Arciero, MD Professor of Orthopaedic Surgery, University of Connecticut Health Center, Framingham, Connecticut Sports Medicine Terminology

April Armstrong, MD, MSc, FRCSC Assistant Professor, Department of Orthopaedics, Milton S. Hershey Medical Center, Hershey, Pennsylvania The Female Athlete

Robert E. Atkinson, MD Associate Professor and Division Chief, Department of Orthopedic Surgery, University of Hawaii John A. Burns School of Medicine, and Program Director, University of Hawaii Residency Program; Associate, The Queen’s Medical Center, Honolulu, Hawaii Athletic Injuries of the Adult Hand

Geoffrey S. Baer, MD, PhD Assistant Professor of Orthopedic Surgery, Division of Sports Medicine, Department of Orthopedics and Rehabilitation, University of Wisconsin Medical School, Madison, Wisconsin Tendon Injuries of the Foot and Ankle

Roald Bahr, MD, PhD Chair, Oslo Sports Trauma Research Centre, Oslo, Norway Preventing Hamstring Strains

Sue D. Barber-Westin, BS Director, Clinical and Applied Research, Cincinnati Sportsmedicine Research and Education Foundation, Cincinnati, Ohio High Tibial Osteotomy in the Anterior Cruciate Ligament–Deficient Knee with Varus Angulation

Bryce Bederka, MD The Bone and Joint Clinic, Portland, Oregon Leg Pain and Exertional Compartment Syndromes; Stress Fractures of the Leg

J. Michael Bennett, MD Clinical Instructor, Department of Orthopedic Surgery, Sports Medicine, and Arthoscopy, University of Texas at Houston; Orthopedic Surgeon, Fondren Orthopedic Group; Orthopedic Surgeon, Texas Orthopedic Hospital, Houston, Texas Vascular Problems of the Shoulder

Thomas M. Best, MD, PhD Professor and Pomerene Chair in Family Medicine; Chief, Division of Sports Medicine; Director, Primary Care Sports Medicine Fellowship, The OSU Sports Medicine Center, the Ohio State University, Columbus, Ohio Physiology of Injury to Musculoskeletal Structures; Sudden Death in Athletes: Causes, Screening Strategies, Use of Participation Guidelines, and Treatment of Episodes

Bruce D. Beynnon, MS, PhD Professor of Orthopaedics and Rehabilitation, University of Vermont College of Medicine, Burlington, Vermont Relevant Biomechanics of the Knee

vii

viii

Contributors

Mark J. Billante, MD Orthopaedic Surgeon, Greater Austin Orthopaedics, Austin, Texas Knee Replacement in Aging Athletes

Leslie Bonci, MPH, RD Director of Sports Medicine Nutrition, Center for Sports Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Nutrition for Sports

Andrew H. Borom, MD Tallahassee Orthopedic Clinic, Tallahassee, Florida Sports Shoes and Orthoses

James P. Bradley, MD Clinical Professor of Orthopedics, University of Pittsburgh Medical Center; Director, Sports Medicine Department, University of Pittsburgh Medical Center Shadyside Hospital; Director, Sports Medicine Department, University of Pittsburgh Medical Center St. Margaret Hospital, Pittsburgh, Pennsylvania Elbow Injuries in Children and Adolescents; Pediatric Elbow Fractures and Dislocations

Barton R. Branam, MD Physician, Ohio Valley Orthopaedics and Sports Medicine, Cincinnati, Ohio Allograft Tissues

Mark R. Brinker, MD Clinical Professor, Department of Orthopedic Surgery, Baylor College of Medicine; Director, Acute and Reconstructive Trauma Department, Texas Orthopedic Hospital, Fondren Orthopedic Group, Houston, Texas Physiology of Injury to Musculoskeletal Structures

Stephen F. Brockmeier, MD Orthopedic Surgeon, Perry Orthopedics and Sports Medicine, Charlotte, North Carolina Meniscal Injuries

James W. Brodsky, MD Clinical Professor of Orthopaedic Surgery, University of Texas Southwestern Medical School; Fellowship Director, Baylor University Medical Center, Dallas, Texas Stress Fractures of the Foot and Ankle

David E. Brown, MD Clinical Associate Professor of Orthopedic Surgery, University of Nebraska Medical Center; Surgeon, OrthoWest, PC, Omaha, Nebraska Sports Pharmacology: Ergogenic Drugs in Sports

Lauren Brown, BA Research Assistant, Department of Orthopaedics and Rehabilitation, University of Vermont, Burlington, Vermont Relevant Biomechanics of the Knee

Thomas E. Brown, MD Associate Professor, Department of Orthopaedic Surgery, University of Virginia, Charlottesville, Virginia Physical Activity and Sports Participation after Total Hip Arthroplasty

Shawn M. Brubaker, DO Staff, Shasta Orthopaedics and Sports Center, Redding, California Physical Activity and Sports Participation after Total Hip Arthroplasty

Nathan Bruck, MD Instructor, Tel Aviv University Medical School, Tel Aviv; Attending Physician, Sheba Medical Center, Tel-Hashomer, Israel Stress Fractures of the Foot and Ankle

Joseph A. Buckwalter, MD Professor and Head, Department of Orthopaedics and Rehabilitation, University of Iowa, Iowa City, Iowa Physiology of Injury to Musculoskeletal Structures

Wayne Z. Burkhead, MD Orthopedic Surgeon, Private Practice, Dallas, Texas Impingement Lesions in Adult and Adolescent Athletes

Brian Busconi, MD Associate Professor of Orthopaedics and Physical Rehabilitation, University of Massachusetts Medical School, Worcester, Massachusetts Hip and Pelvis

Kenneth P. Butters, MD Orthopedic Surgeon, Slocum Center for Orthopedics and Sports Medicine, Eugene, Oregon Nerve Lesions of the Shoulder

S. Terry Canale, MD Professor and Department Chair, University of Tennessee-Campbell Clinic Department of Orthopaedic Surgery; Staff Physician, Campbell Clinic, Memphis, Tennessee Osteochondroses and Related Problems of the Foot and Ankle

Robert C. Cantu, MD, FACS Medical Director, National Center for Catastrophic Sports Injury Research, University of North Carolina Medical Center, Chapel Hill, North Carolina; Chief of Neurosurgery, Emerson Hospital, Concord, Massachusetts Head Injuries

Robert V. Cantu, MD Assistant Professor of Orthopaedic Surgery, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire Head Injuries

Chang-Hyuk Choi, MD Assistant Professor, Department of Orthopaedic Surgery, Hanyang University Medical School, Hanyang University Hospital, Seoul, Korea Injuries of the Proximal Humerus in Adults

Contributors

Luke Choi, MD Orthopaedic Resident, Department of Orthopaedic Surgery, University of Virginia, Charlottesville, Virginia Overuse Injuries

Thomas O. Clanton, MD Professor and Chairman, Department of Orthopaedics, University of Texas–Houston Medical School, Houston, Texas Sport Shoes and Orthoses; Etiology of Injury to the Foot and Ankle

Jack Clement, MD, PhD Physician, South Texas Radiology Imaging Centers, San Antonio, Texas Basic Imaging Techniques in the Adult; Imaging Considerations in the Skeletally Immature Patient

Brian J. Cole, MD, MBA Professor of Orthopaedic Surgery, Rush University; Director, Cartilage Restoration Center, Rush University Medical Center, Chicago, IIIinois Articular Cartilage Lesion

Fred G. Corley, Jr., MD Professor, Department of Orthopaedics, University of Texas Health Science Center at San Antonio; Professor of Orthopaedic Surgery, Department of Orthopaedic Traumatology, University Health System; Professor of Orthopaedic Surgery, Department of Orthopaedics, University of Texas Medicine Clinic, University of Texas Health Science Center, San Antonio, Texas Arm

Jason A. Craft, MD Assistant Professor, Department of Orthopaedic Surgery, University of Mississippi School of Medicine; Assistant Professor, University Hospital and Clinic, University of Mississipi Medical Center, Jackson, Mississippi Fractures of the Coracoid in Adults and Children; Glenoid and Scapula Fractures in Adults and Children

Ralph J. Curtis, Jr., MD Orthopedic Surgeon, Orthopedic Surgery Association, San Antonio, Texas Anatomy, Biomechanics, and Kinesiology of the Child’s Shoulder; Glenohumeral Instability in the Child

Frances Cuomo, MD Assistant Professor, Department of Orthopaedic Surgery, New York University School of Medicine; Chief, Shoulder and Elbow Service, New York University Hospital for Joint Diseases, New York, New York Injuries of the Proximal Humerus in Adults

ix

Thomas M. DeBerardino, MD Associate Professor, Department of Surgery, F. E. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Director, John A. Feagin, Jr. Sports Medicine Fellowship at West Point; Head Team Physician, United States Military Academy at West Point; Physician, Keller Army Community Hospital, West Point, New York The Team Physician: Preparticipation Examination, On-Field Emergencies, and Ethical and Legal Issues

Richard E. Debski, PhD Associate Professor, Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania Fundamentals of Biomechanics; Functional Anatomy and Biomechanics of the Adult Shoulder

Marc M. DeHart, MD Surgeon, Texas Orthopedics, Sports, and Rehabilitation Associates, Austin, Texas Deep Venous Thrombosis and Pulmonary Embolism

Marlene DeMaio, MD, CAPT, USNR Surgeon, Department of Orthopaedic Surgery, Bone and Joint/Sports Medicine Institute, Naval Medical Center, Portsmouth, Virginia The Female Athlete

Allen Deutsch, MD Clinical Assistant Professor, Department of Orthopaedic Surgery, Baylor College of Medicine; Physician, KelseySeybold Clinic; Physician, St. Luke’s Episcopal Hospital, Houston, Texas Fractures of the Coracoid in Adults and Children; Glenoid and Scapula Fractures in Adults and Children

William W. Dexter, MD Professor, University of Vermont College of Medicine; Director, Sports Medicine Program, Maine Medical Center, Portland, Maine Dermatologic Disorders

David R. Diduch, MD Professor of Orthopaedic Surgery, Head Orthopaedic Team Physician, and Fellowship Director of Sports Medicine, University of Virginia, Charlottesville, Virginia Knee Replacement in Aging Athletes

William Dillin, MD Orthopaedic Surgeon, Kerlan-Jobe Orthopaedic Clinic, Los Angeles and Orange County, California Thoracolumbar Spine Injuries in the Adult

Jeffrey R. Dugas, MD Affiliate Professor, College of Human Services, Troy University, Troy; Fellowship Director, American Sports Medicine Institute, Birmingham, Alabama Throwing Injuries in the Adult

Contributors

Craig J. Edson, MHS, PT Physical Therapist, Geisinger/HealthSouth Rehabilitation Hospital, Danville, Pennsylvania Multiple Ligament Knee Injuries

T. Bradley Edwards, MD Clinical Instructor, Department of Orthopaedic Surgery, University of Texas at Houston; Clinical Assistant Professor, Department of Orthopaedic Surgery, Baylor University; Orthopaedic Surgeon, Fondren Orthopedic Group, Houston, Texas Development of Skills for Shoulder Surgery; Glenohumeral Arthritis in the Athlete

Marsha Eifert-Mangine, EdD, PT, ATC Assistant Professor, Department of Health Sciences, Physical Therapy Program, College of Mount Saint Joseph; Physical Therapist, NovaCare Rehabilitation, Cincinnati, Ohio Use of Modalities in Sports

Frank J. Eismont, MD Leonard M. Miller Professor and Chairman, Department of Orthopaedics; Director, Residency and Fellow Education, University of Miami, Miami; Orthopaedic Surgeon, University of Miami Medical Group, Miami, Florida Thoracolumbar Spine Injuries in the Adult

Hussein Elkousy, MD Volunteer Faculty, Department of Orthopaedic Surgery, University of Texas Health Science Center at Houston; Volunteer Faculty, University of Texas Medical Branch, Galveston; Volunteer Faculty, Baylor College of Medicine, Houston; Staff Surgeon, Texas Orthopedic Hospital, Houston, Texas Development of Skills for Shoulder Surgery; Muscle Ruptures Other Than the Rotator Cuff

Gregory C. Fanelli, MD Chief Emeritus, Sports Medicine and Arthroscopic Surgery, Geisinger Medical Center, Danville, Pennsylvania Multiple Ligament Knee Injuries

Mario Ferretti, MD Researcher, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania Anterior Cruciate Ligament Injuries in the Adult

Gary B. Fetzer, MD Orthopaedic Surgeon,TRIA Orthopaedic Center, Bloomington, Minnesota Lateral and Posterolateral Injuries of the Knee

Larry D. Field, MD Clinical Instructor, Department of Orthopaedic Surgery, University of Mississippi School of Medicine; Director, Upper Extremity Service, Mississippi Sports Medicine and Orthopaedic Center, Jackson, Mississippi Osteochondritis Dissecans of the Elbow; Olecranon Bursitis; Elbow Dislocations in the Adult Athlete and Pediatric Patient

Daniel C. Fitzpatrick, MD, MS Orthopedic Surgeon, Slocum Center for Orthopedics and Sports Medicine, Eugene, Oregon Nerve Lesions of the Shoulder

Kevin R. Ford, MS Research Biomechanist, Cincinnati Children’s Hospital, Cincinnati, Ohio Return-to-Sport Plyometric Training in the Rehabilitation of Athletes following Anterior Cruciate Ligament Reconstruction

Donald E. Fowler Medical Student, University of Virginia, Charlottesville, Virginia Exercise Physiology

W. Anthony Frisella, MD Orthopaedic Surgeon, St. Peters Bone and Joint Surgery, St. Peters, Missouri Injuries of the Proximal Humerus in Adults

Freddie H. Fu, MD, DSc Chairman, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Anterior Cruciate Ligament Injuries in the Adult; Anterior Cruciate Ligament Injuries in the Child

Lorenzo Gamez, MD Assistant Professor of Orthopaedics and Physical Rehabilitation, Department of Orthopaedics, University of Massachusetts Medical School, Worcester, Massachusetts Entrapment Neuropathies of the Foot

Seth C. Gamradt, MD Assistant Professor, Department of Orthopaedic Surgery and Sports Medicine, University of California, Los Angeles, Los Angeles, California Glenohumeral Instability in Adults

William E. Garrett, Jr., MD, PhD Professor, Department of Orthopaedic Surgery, Duke University Medical Center, Durham, North Carolina Physiology of Injury to Musculoskeletal Structures; Sports Medicine Terminology

Gary M. Gartsman, MD Clinical Professor, Department of Orthopaedic Surgery, University of Texas Health Sciences Center at Houston Medical School; Surgeon, Fondren Orthopedic Group, Houston, Texas Adhesive Capsulitis

Contributors

Christian Gerber MD, FRCSEd (Hon) Professor of Orthopaedic Surgery, University of Zürich; Chairman, Department of Orthopaedics, Uniklinik Balgrist, Zürich, Switzerland Suture Materials

Eric Giza, MD Orthopaedic Surgeon, Orthopaedic Sports Medicine Service, University of California, Davis Health System, Sacramento, California Ankle Instability Prevention; Principles of Injury Prevention; Spine-Related Injury Prevention in the Athlete: Trunk Stabilization

S. Raymond Golish, MD, PhD Resident, Department of Orthopaedic Surgery, University of Virginia, Charlottesville, Virginia Design and Statistics in Sports Medicine

Jorge E. Gómez, MD Clinical Professor, Sports Medicine and Pediatrics, University of Texas Health Science Center; Team Physician, University of Texas, San Antonio, Texas Heat Illness; Cold Injury; Altitude

Andreas H. Gomoll, MD Assistant Professor of Orthopaedic Surgery, Harvard Medical School; Orthopaedic Surgeon, Brigham and Women’s Hospital, Boston, Massachusetts Articular Cartilage Lesion

Letha Y. Griffin, MD, PhD Physician, Peachtree Orthopaedic Clinic, Atlanta, Georgia The Female Athlete

Philippe P. Grondin, MD Fellow, Department of Orthopaedics, University of British Columbia, Vancouver, British Columbia, Canada Tendinopathies around the Arm

Andrew J. Grove, MD Adjunct Assistant Professor, Department of Pediatrics, Division of Adolescent Medicine, Medical College of Wisconsin; Primary Care/Sports Medicine Physician, Student Health Service, Marquette University, Milwaukee, Wisconsin Heat Illness; Cold Injury

Dan Guttman, MD Clinical Instructor, Department of Orthopaedic Surgery, University of New Mexico, Albuquerque; Chief of Upper Extremity Surgery and the Hip Arthritis Service, Taos Orthopaedic Institute, Taos, New Mexico Injuries of the Proximal Humerus in Adults

Gregory P. Guyton, MD Attending, Department of Orthopaedics, Union Memorial Hospital, Baltimore, Maryland Entrapment Neuropathies of the Proximal Humerus

xi

Christopher D. Harner, MD Professor, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine; Chief, Division of Sports Medicine; Fellowship Director and Medical Director, Center for Sports Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania

Posterior Cruciate Ligament Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Child

Justin D. Harris, MD Orthopaedic Surgeon, Nebraska Orthopaedic and Sports Medicine, Lincoln, Nebraska Multiple Ligament Knee Injuries

Jennifer A. Hart, MPAS, PA-C Physician Assistant, Department of Orthopaedic Surgery, Division of Sports Medicine, University of Virginia, Charlottesville, Virginia Basic Arthroscopic Principles; Infection: Prevention, Control, and Treatment

Joseph M. Hart, PhD, ATC Assistant Professor of Research, University of Virginia, Charlottesville, Virginia Exercise Physiology

Andrew Haskell, MD Assistant Clinical Professor, University of California, San Francisco, San Francisco; Attending, Palo Alto Foundation Medical Group, Palo Alto, California Biomechanics

Martin J. Herman, MD Associate Professor, Departments of Orthopaedic Surgery and Pediatrics, Drexel University College of Medicine; Attending, St. Christopher’s Hospital for Children and Hahnemann University Hospital, Philadelphia, Pennsylvania Cervical Spine Injuries in the Child

Timothy E. Hewett, PhD, FACSM Associate Professor, University of Cincinnati College of Medicine; Director, Sports Medicine Biodynamics Center, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Return-to-Sport Plyometric Training in the Rehabilitation of Athletes following Anterior Cruciate Ligament Reconstruction

Christopher B. Hirose, MD Orthopaedic Surgeon, Panorama Orthopaedics, Golden, Colorado Etiology of Injury to the Foot and Ankle

xii

Contributors

Nicholas J. Honkamp, MD Staff Physician, Iowa Methodist Medical Center; Private Practice, Des Moines Orthopaedic Surgeons, Des Moines, Iowa

Anterior Cruciate Ligament Injuries in the Adult; Anterior Cruciate Ligament Injuries in the Child; Posterior Cruciate Ligament Injuries in the Child; Posterior Cruciate Ligament in the Adult

Florian G. Huber, MD Orthopaedic Surgeon, Peninsula Orthopaedic Associates; Orthopaedic Trauma Surgeon, Division of Orthopaedic Trauma, Peninsula Regional Medical Center, Salisbury, Maryland Arm

Jack V. Ingari, MD Assistant Professor of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Associate Professor of Surgery, University of Texas Health Sciences Center at San Antonio; Staff, Attending Hand Surgeon, The Hand Center of San Antonio, San Antonio, Texas The Adult Wrist

Darren L. Johnson, MD Professor and Chairman, Department of Orthopaedic Surgery, University of Kentucky School of Medicine; Chief of Orthopaedic Surgery, The Kentucky Clinic, University of Kentucky, Lexington, Kentucky Design and Statistics in Sports Medicine; Allograft Tissues; Medial Collateral Ligament Injuries in Adults; Pediatric Medial Knee Injuries

Rob Johnson, MD Associate Professor, Department of Family Medicine and Community Health, University of Minnesota; Director, Primary Care Sports Medicine, Department of Family Medicine, Hennepin County Medical Center, Minneapolis, Minnesota Infectious Disease and Sports

Robert J. Johnson, MD Professor Emeritus, Department of Orthopaedics, The University of Vermont College of Medicine, University of Vermont, Burlington, Vermont Relevant Biomechanics of the Knee

Ron M. Johnson, PT, MPT, ATC, LAT, ATC, CSCS Facility Director, Excel Sports Therapy, Gulf Coast Rehabilitation, PC, Shiner, Texas Therapeutic Exercise Prescription

James S. Keene, MD Professor of Orthopedic Surgery, University of Wisconsin; Chairman, Division of Sports Medicine, Department of Orthopedic Surgery and Rehabilitation, University of Wisconsin Medical School, Madison, Wisconsin Tendon Injuries of the Foot and Ankle

Sami O. Khan, MD Orthopaedic Surgeon, Resurgens Orthopaedics, Decatur, Georgia Elbow Dislocations in the Adult Athlete and Pediatric Patient

Richard Y. Kim, MD Orthopaedic Surgeon, Hackensack University Medical Center, Hackensack, New Jersey Entrapment Neuropathies around the Elbow

Donald T. Kirkendall, PhD Adjunct Assistant Professor, Department of Exercise and Sport Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Physiology of Injury to Musculoskeletal Structures; Sports Medicine Terminology

Scott H. Kitchel, MD Athletic Medicine Staff, University of Oregon, Eugene, Oregon Thoracolumbar Spine Injuries in the Adult

Sandra E. Klein, MD Assistant Professor, Department of Orthopaedic Surgery, Washington University School of Medicine; Attending, Barnes-Jewish Hospital at Washington University School of Medicine, St. Louis, Missouri Conditions of the Forefoot

William Knopp, MD Assistant Professor, Department of Family and Community Medicine, University of Minnesota School of Medicine; Faculty, Family Medicine and Primary Care Sports Medicine, Methodist Hospital/University of Minnesota Family Medicine Residency Program, Minneapolis, Minnesota Infectious Disease and Sports

Mininder Kocher, MD, MPH Associate Professor of Orthopaedic Surgery, Harvard Medical School; Associate Director, Division of Sports Medicine, Children’s Hospital Boston, Boston, Massachussetts The Young Athlete

Melissa D. Koenig, MD Orthopaedic Surgeon, Kaiser Permanente Medical Group, Houston, Texas Ligament Injuries of the Foot and Ankle in Adult Athletes

Sumant G. Krishnan, MD Assistant Clinical Professor, Department of Orthopaedic Surgery, University of Texas Southwestern Medical Center at Dallas Southwestern Medical School; Staff, Shoulder Service, W.B. Carrell Memorial Clinic, Dallas, Texas Impingement Lesions in Adult and Adolescent Athletes

Contributors

Irving L. Kron, MD Professor and Chairman, Department of Surgery, Division of Thoracic and Cardiovascular Surgery, University of Virginia Health System, Charlottesville, Virginia Vascular Problems—Popliteal Artery Entrapment

John E. Kuhn, MD Associate Professor, Department of Orthopaedics and Rehabilitation, Division of Sports Medicine, Vanderbilt University Medical School; Chief of Shoulder Surgery, Vanderbilt University Medical Center, Nashville, Tennessee Scapulothoracic Disorders in Athletes

Robert F. LaPrade, MD, PhD Professor, Sports Medicine and Shoulder Surgery, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, Minnesota Lateral and Posterolateral Injuries of the Knee

William C. Lauerman, MD Professor of Orthopaedic Surgery, Georgetown University School of Medicine; Chief, Division of Spine Surgery, Georgetown University Hospital, Washington, DC Thoracolumbar Spine Injuries in the Child

Christine Lawless, MD, MBA President, Sports Cardiology Consultants LLC, Columbus, Ohio Sudden Death in Athletes: Causes, Screening Strategies, Use of Participation Guidelines, and Treatment of Episodes

James Lebolt, DO Orthopedic Surgeon, Virginia Sports Medicine and Orthopedic Institute, Christiansburg; Orthopedic Surgeon, Montgomery Regional Hospital, Blacksburg, Virginia Throwing Injuries in the Adult

Igor Cezar da Silva Leitao, MD Assistant Professor, Department of Orthopaedics, Santa Casa de Misericordia de Juiz de Fora, Juiz de Fora/MG, Brazil; Visiting Fellow from Hospital Felicio Rocho, University of Texas Health Science Center at San Antonio, San Antonio, Texas Injuries to the Sternoclavicular Joint in the Adult and Child

Kenneth C. Lin, MD Orthopedic Surgeon, Evergreen Orthopedics, Monroe, Washington Impingement Lesions in Adult and Adolescent Athletes

Thomas N. Lindenfeld, MD Associate Director, Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Complex Regional Pain Syndromes Including Reflex Sympathetic Dystrophy and Causalgia

xiii

Turner C. Lisle, MD Resident, Department of Surgery, University of Virginia, Charlottesville, Virginia Vascular Problems—Popliteal Artery Entrapment

Walter R. Lowe, MD Associate Professor, Department of Orthopedic Surgery, Baylor College of Medicine; Team Physician, Houston Texans, Houston, Texas Superior Labral Injuries

David J. Lunardini, BS Medical Student, University of Virginia, Charlottesville, Virginia Exercise Physiology

Mark W. Maffet, MD Assistant Professor, Department of Orthopedic Surgery, Baylor College of Medicine; Team Physician, Houston Comets; Team Physcian, Houston Baptist University, Houston, Texas Superior Labral Injuries

Jeffrey J. Mair, DO Attending, Riverview Medical Center and Twin Cities Orthopedics, Waconia, Minnesota Lateral and Posterolateral Injuries of the Knee

Robert Mangine, MEd, PT, ATC Adjunct Instructor, College of Mount Saint Joseph; Adjunct Clinical Instructor, Department of Ortho pedics, and Head Football Trainer, University of Cincinnati; Director of Clinical Residency, NovaCare Rehabilitation, Cincinnati, Ohio Use of Modalities in Sports

Roger A. Mann, MD Associate Clinical Professor, Department of Orthopaedic Surgery, University of California, San Francisco, School of Medicine, San Francisco; Director, Foot Fellowship Program, Oakland, California Biomechanics; Entrapment Neuropathies of the Foot

John G. Mastronarde, MD, MSc Associate Professor, Ohio State University; Director, OSU Asthma Center, The Ohio State University Medical Center, Columbus, Ohio Exercise-Induced Bronchospasm

Carl G. Mattacola, PhD Associate Professor and Director, Rehabilitation Sciences Doctoral Program, Division of Athletic Training, University of Kentucky, College of Health Sciences, Lexington, Kentucky Design and Statistics in Sports Medicine

xiv

Contributors

Augustus D. Mazzocca, MD Associate Professor of Orthopaedic Surgery, University of Connecticut, Farmington, Connecticut Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children

Wendy McBride, MD Pediatric Emergency Physician, CarePoint PC, Physician, Sky Ridge Medical Center, Denver, Colorado Heat Illness; Altitude

Kendra McCamey, MD Assistant Clinical Professor, Department of Family Medicine, The Ohio State University Medical Center; Team Physician, Department of Athletics, The Ohio State University, Columbus, Ohio Exercise-Induced Bronchospasm

Michael P. McClincy, BS Medical Student, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Forearm Fractures: Pediatric Elbow Fractures and Dislocations

Edward R. McDevitt, MD Assistant Professor of Surgery, Uniformed Services University of the Health Sciences, Bethesda; Orthopaedic Surgeon, Anne Arundel Medical Center, Annapolis, Maryland Sports Pharmacology: Ergogenic Drugs in Sports; Sports Pharmacology: Recreational Drug Use

Patrick J. McMahon, MD Adjunct Associate Professor, Department of Bio engineering, University of Pittsburgh; Founder, McMahon Orthopedics and Rehabilitation, Pittsburgh, Pennsylvania Functional Anatomy and Biomechanics of the Adult Shoulder

Jennifer J. F. McVean, MD Fellow, University of Wisconsin; Fellow, American Family Children’s Hospital, Madison, Wisconsin Diabetes Mellitus

W. Andrew Middendorf, MPT, ATC Physical Therapist, NovaCare Rehabilitation/University of Cincinnati, Cincinatti, Ohio Use of Modalities in Sports

Chealon D. Miller, MD Resident, Department of Orthopaedic Surgery, University of Virginia, Charlottesville, Virginia Infection: Prevention, Control, and Treatment

Mark D. Miller, MD S. Ward Casscells Professor of Orthopaedic Surgery and Head, Division of Sports Medicine, University of Virginia, Charlottesville; Adjunctive Clinical Professor and Team Physician, James Madison University, Harrisonburg, Virginia Design and Statistics in Sports Medicine; Basic Arthroscopic Principles; Infection: Prevention, Control, and Treatment

Bernard F. Morrey, MD Professor of Orthopedics, College of Medicine, Mayo Clinic; Consultant, Division of Adult Reconstruction, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Biomechanics of the Elbow and Forearm; Tendinopathies around the Elbow

Vasilios Moutzouros, MD Clinical Instructor, Wayne State School of Medicine; Senior Staff, Department of Orthopaedics, Division of Sports Medicine, Henry Ford Center, Detroit, Michigan Osteochondroses

Van C. Mow, PhD Stanley Dicker Professor and Chairman, Department of Biomedical Engineering; Director, Shelley Liu Ping Laboratory for Functional Tissue Engineering Research, Fu Foundation School of Engineering and Applied Science, Columbia University, New York, New York Physiology of Injury to Musculoskeletal Structures

Gregory D. Myer, MS Sports Biomechanist, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio Return-to-Sport Plyometric Training in the Rehabilitation of Athletes following Anterior Cruciate Ligament Reconstruction

Frank R. Noyes, MD Clinical Professor, Department of Orthopaedic Surgery, University of Cincinnati; Chairman, Medical Director, and Chief Operating Officer, Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio High Tibial Osteotomy in the Anterior Cruciate Ligament-Deficient Knee with Varus Angulation

Eugene T. O’Brien Orthopaedic Surgeon, Churchill Evaluation Centers, San Antonio, Texas Wrist Injuries in the Child

Agbecko Ocloo, MD Staff Surgeon, Korle Bu Teaching Hospital, Korle Bu, Accra, Ghana Patellar Fractures

Daniel P. O’Connor, PhD Director, Joe W. King Orthopedic Institute, Houston, Texas Physiology of Injury to Musculoskeletal Structures

Nnamdi Okeke, BS Medical Student, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Anterior Cruciate Ligament Injuries in the Adult

Contributors

Brett D. Owens, MD Assistant Professor, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Assistant Professor, Texas Tech University Health Science Center; Chief, Sports Medicine and Shoulder Service, William Beaumont Army Medical Center, El Paso, Texas The Team Physician: Preparticipation Examination, On-Field Emergencies, and Ethical and Legal Issues

Russ Paine, BS, PT Director of Sports Medicine Research and Rehabilitation, Memorial Hermann Sports Medicine Institute; Team Physical Therapist for Houston Rockets, Houston, Texas Proprioception and Joint Dysfunction; Language of Excercise and Rehabilitation

Selene G. Parekh, MD, MBA Clinical Associate Professor, Duke University; Attending, Division of Orthopaedic Surgery, Duke University Medical Center; Adjunct Faculty, Duke University School of Business, Durham, North Carolina Heel Pain

William D. Parham, PhD, ABPP Dean of Graduate School of Professional Psychology, John F. Kennedy University, Pleasant Hill, California Psychological Adjustment to Athletic Injury

Richard D. Parker, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine; Chairman, Department of Orthopaedic Surgery, Orthopaedic Rheumatologic Institute, Cleveland Clinic Foundation, Cleveland, Ohio Patellar and Quadriceps Tendinopathies and Ruptures; Osteochondroses; Patellofemoral Instability: Recurrent Dislocation of the Patella; Acute Dislocation of the Patella; Chronic Dislocation of the Patella; Patellar Fractures

Johnathan P. Parsons, MD Assistant Professor of Internal Medicine, The Ohio State University; Associate Director, The Ohio State University Asthma Center, Columbus, Ohio Exercise-Induced Bronchospasm

Jayesh K. Patel, MD Chief Resident, Department of Orthopaedic Surgery, University of Kentucky, Lexington, Kentucky Medial Collateral Ligament Injuries in Adults; Pediatric Medial Knee Injuries

Mark V. Paterno, MS, PT, MBA, SCS, ATL Assistant Professor, Department of Pediatrics, Division of Sports Medicine, University of Cincinnati College of Medicine; Coordinator of Orthopaedic and Sports Physical Therapy, Division of Occupational Therapy and Physical Therapy, Cincinnati Children’s Medical Center, Cincinnati, Ohio Return-to-Sport Plyometric Training in the Rehabilitation of Athletes following Anterior Cruciate Ligament Reconstruction

xv

Russell S. Petrie, MD Orthopaedic Surgeon, Newport Orthopaedic Institute, Newport Beach, California Elbow Injuries in Children and Adolescents

Peter D. Pizzutillo, MD Professor, Departments of Orthopedic Surgery and Pediatrics, Drexel University School of Medicine; Director, St. Christopher’s Hospital for Children; Physician, Hahnemann University Hospital, Philadelphia, Pennsylvania Cervical Spine Injuries in the Child

Michael D. Pleacher, MD Assistant Professor of Pediatrics, University of New Mexico, Albuquerque, New Mexico Dermatologic Disorders

Teodor T. Postolache, MD Associate Professor and Director, Mood and Anxiety Program, University of Maryland School of Medicine, Baltimore, Maryland; Director, Institute for Sports Chronobiology, Washington, DC Sleep and Chronobiology in Sports

Matthew T. Provencher, MD Director, Orthopaedic Shoulder, Knee, and Sports Surgery, Department of Orthopaedic Surgery, Naval Medical Center, San Diego, San Diego, California Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children

Anil S. Ranawat, MD Orthopaedic Surgeon, Hospital for Special Surgery, New York, New York Forearm Fractures; Pediatric Elbow Fractures and Dislocations; Posterior Cruciate Ligament Injuries in the Adult; Posterior Cruciate Ligament Injuries in the Child

Michael A. Rauh, MD Clinical Assistant Professor of Orthopaedic Surgery, Department of Orthopaedic Surgery, University Sports Medicine, State University of New York at Buffalo, Buffalo, New York Patellar and Quadriceps Tendinopathies and Ruptures

William D. Regan, MD Assistant Professor of Orthopaedic Surgery, University of British Columbia Faculty of Medicine, Vancouver, British Columbia, Canada Tendinopathies around the Elbow

Scott B. Reynolds, MD Orthopaedic Surgeon, Nebraska Orthopaedic Associates, Omaha, Nebraska Throwing Injuries in the Adult

xvi

Contributors

David R. Richardson, MD Assistant Professor and Director of Residency Program, University of Tennessee-Campbell Clinic Department of Orthopaedic Surgery, University of Tennessee; Staff Physician, Campbell Clinic, Memphis, Tennessee Osteochondroses and Related Problems of the Foot and Ankle

John T. Riehl, MD Resident, Geisinger Pennsylvania

Medical

Center,

Danville,

Multiple Ligament Knee Injuries

David Ring, MD, PhD Associate Professor of Orthopaedic Surgery, Harvard Medical School; Medical Director and Director of Research, Orthopaedic Hand and Upper Extremity Service, Massachusetts General Hospital, Boston, Massachusetts Fractures of the Elbow in the Adult

Kristin N. Rinheimer, MS, PAC Physician’s Assistant, Geisinger Medical Center, Danville, Pennsylvania Multiple Ligament Knee Injuries

Samuel P. Robinson, MD Orthopaedic Surgeon, Jordan-Young Institute, Virginia Beach, Virginia Pediatric Elbow Fractures and Dislocations

Charles A. Rockwood, Jr., MD Professor and Chairman Emeritus, Department of Orthopaedics, University of Texas Health Science Center at San Antonio, San Antonio, Texas Injuries to the Sternoclavicular Joint in the Adult and Child

Scott A. Rodeo, MD Co-Chief, Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York Meniscal Injuries

Anthony A. Romeo, MD Director, Shoulder Service, Department of Orthopaedic Surgery, Rush University, Chicago, Illinois Injuries to the Acromioclavicular Joint in Adults and Children; Sternum and Rib Fractures in Adults and Children

Melvin P. Rosenwasser, MD Robert E. Carroll Professor of Orthopaedic Surgery, Columbia University College of Physicans and Surgeons, New York; Director, Orthopaedic Hand and Trauma Service, New York/Presbyterian Hospital, New York, New York Entrapment Neuropathies around the Elbow

Charles E. Rosipal, MD Physician, GIKK Ortho Specialists, Omaha, Nebraska Injuries to the Sternoclavicular Joint in the Adult and Child

Timothy G. Sanders, MD Visiting Professor, University of Kentucky College of Medicine, Lexington, Kentucky; Director of Education and Research, National Musculoskeletal Imaging, Weston, Florida Imaging of the Glenohumeral Joint

Felix H. Savoie, MD Lee C. Schlesinger Professor and Vice Chairman, Department of Orthopaedic Surgery, Tulane University School of Medicine; Director, Tulane Institute of Sports Medicine, Tulane University Medical Center, New Orleans, Louisiana Osteochondritis Dissecans of the Elbow

David L. Saxton, MD Clinical Faculty, Oklahoma University Medical Center, Oklahoma City, Oklahoma Complex Regional Pain Syndromes Including Reflex Sympathetic Dystrophy and Causalgia

Andrew J. Schorfhaar, DO Assistant Professor and Team Orthopaedic Surgeon, Department of Radiology, Division of Sports Medicine, Michigan State University, East Lansing, Michigan Lateral and Posterolateral Injuries of the Knee

Jon K. Sekiya, MD Associate Professor, Department of Orthopaedic Surgery, University of Michigan, Ann Arbor, Michigan Fundamentals of Biomechanics

Agam Shah, MD Othopaedic Surgeon, Newton-Wellesley Newton, Massachusetts

Hospital,

Hip and Pelvis

Wei Shen MD Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Anterior Cruciate Ligament Injuries in the Adult; Anterior Cruciate Ligament Injuries in the Child

Thomas Shepler, MD Associate Professor of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Staff Physician, Reston HCA Hospital, Reston, Virginia The Pediatric Hand

Holly J. Silvers, MPT ACL Prevention Project Coordinator, Santa Monica Orthopaedic and Sports Medicine Group, Santa Monica, California Anterior Cruciate Ligament Tear Prevention in the Female Athlete; Ankle Instability Prevention

Contributors

Manuj Singhal, MD Physician, Orthopaedic Associates of Lewisville, Lewisville, Texas Medial Collateral Ligament Injuries in Adults; Pediatric Medial Knee Injuries

Timothy Steiner, MD Staff Orthopaedic Surgeon, Orthopaedics of Southern Indiana, Bloomington, Indiana

Patellofemoral Instability: Acute Dislocation of the Patella; Patellofemoral Instability: Recurrent Dislocation of the Patella

Scott P. Steinmann, MD Professor of Orthopedics, Mayo Clinic College of Medicine, Rochester, Minnesota Heterotopic Bone around the Elbow

Ligament Injuries of the Foot and Ankle in the Pediatric Athlete

Dean C. Taylor, MD Professor of Surgery and Director, Duke Sports Medicine Fellowship, Duke University, Durham, North Carolina Sports Medicine Terminology

Samir G. Tejwani, MD Orthopedic Surgeon, Department of Orthopedic Surgery, Division of Sports Medicine, Kaiser Permanente, Fontana, California Elbow Injuries in Children and Adolescents

Richard J. Thomas, MD Attending, Sports Medicine and Orthopaedic Surgery, OrthoGeorgia, Macon, Georgia Olecranon Bursitis

Paul D. Thompson, MD Director of Cardiology and Director of the Athlete’s Heart Program, Hartford Hospital, Hartford Connecticut Management of Hypertension in Athletes

Center,

Danville,

Multiple Ligament Knee Injuries

Steven M. Topper, MD Clinical Assistant Professor, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Attending, The Colorado Hand Center, Colorado Springs, Colorado Wrist Arthroscopy

Joseph S. Torg, MD Professor of Orthopaedic Surgery, Temple University School of Medicine; Attending Staff, Temple University Hospital, Philadelphia, Pennsylvania Cervical Spine Injuries in the Adult

C. Thomas Vangsness, Jr., MD Professor of Orthopaedic Surgery, Department of Orthopaedic Surgery, University of Southern California, Los Angeles, California Osteochondritis Dissecans

Marius von Knoch, MD Associate Professor of Orthopaedic Surgery, University of Duisburg-Essen, Essen, Germany Suture Materials

J. Andy Sullivan, MD Clinical Professor of Pediatric Orthopedics, Department of Orthopedic Surgery, University of Oklahoma, College of Medicine; Attending, Oklahoma University Medical Center, Okalahoma City, Oklahoma

Daniel J. Tomaszewski, MD Attending, Geisinger Medical Pennsylvania

xvii

Keith L. Wapner, MD Clinical Professor of Orthopedic Surgery and Director of Foot and Ankle Orthopedic Fellowship, University of Pennsylvania; Adjunct Professor of Orthopedic Surgery, Drexel College of Medicine, Philadelphia, Pennsylvania Heel Pain

Russell F. Warren, MD Professor, Department of Orthopaedic Surgery, Weill Medical College of Cornell University; Professor of Orthopaedic Surgery and Attending Orthopaedic Surgeon, Hospital for Special Surgery, New York, New York Glenohumeral Instability in Adults

Scott Waterman, MD Sports Medicine Fellow, Keller Army Community Hospital, West Point, New York The Thigh

Robert G. Watkins IV, MD Co-Director, Marina Spine Center, The Marina Hospital, Marina del Rey, California Spine-Related Injury Prevention in the Athlete: Trunk Stabilization

Adam Nelson Whatley, MD Chief Resident, Department of Orthopaedic Surgery, Louisiana State University Health Sciences Center, New Orleans, Louisiana Parsonage-Turner Syndrome

Alexis C. Wickwire, MS Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania Fundamentals of Biomechanics

xviii

Contributors

Kaye E. Wilkins, DVM, MD Professor of Orthopaedics and Pediatrics, University of Texas Health Science Center at San Antonio; Staff Orthopaedic Surgeon, University Hospital, San Antonio; Staff Orthopaedic Surgeon, Christus Children’s Hospital, San Antonio, Texas Injuries of the Proximal Humerus in the Skeletally Immature Athlete

Gerald R. Williams, Jr., MD Professor of Orthopaedic Surgery, Jefferson Medical College; Chief, Shoulder and Elbow Service, The Rothman Institute, Philadelphia, Pennsylvania Glenoid and Scapula Fractures in Adults and Children; Fractures of the Coracoid in Adults and Children

Matthew D. Williams, MD Assistant Professor of Orthopaedic Surgery, Louisiana State University Health Sciences Center, New Orleans; Orthopaedic Surgeon, Acadiana Orthopaedic Group, Lafayette, Louisiana Adhesive Capsulitis; Glenohumeral Arthritis in the Athlete

Michael A. Wirth, MD Professor and Charles A. Rockwood, Jr., MD Chair, Department of Orthopaedics, University of Texas Health Science Center at San Antonio, San Antonio, Texas Injuries to the Sternoclavicular Joint in the Adult and Child

Valerie M. Wolfe, MD Fellow, Department of Orthopaedic Surgery, New York Presbyterian/Columbia Hospital, New York, New York Entrapment Neuropathies around the Elbow

Brett W. Wolters, MD, MS Attending Orthopaedic Surgeon, Memorial Medical Center, Springfield, Illinois Lateral and Posterolateral Injuries of the Knee

Savio L.-Y. Woo, PhD, DSc Whiteford Professor and Director, Musculoskeletal Research Center, Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania Physiology of Injury to Musculoskeletal Structures

Robert M. Wood, MD, FRCS Orthopedic Surgeon, Sports Medicine North, Lynnfield, and North Shore Medical Center, Salem, Massachusetts Etiology of Injury to the Foot and Ankle

Virchel E. Wood, MD Professor, Department of Orthopaedic Surgery, Loma Linda University School of Medicine; Consulting Chief, Hand Surgery Service, Loma Linda University Medical Center, Loma Linda, California Thoracic Outlet Syndrome

Adam Yanke Medical Student, Department of Orthopaedic Surgery, Rush University, Chicago, Illinois Articular Cartilage Lesion

John A. Zavala, MD Chief Resident, Georgetown Washington, DC

University

Hospital,

Thoracolumbar Spine Injuries in the Child

Mary L. Zupanc, MD Professor, Department of Neurology and Pediatrics; Chief, Division of Pediatric Neurology; Heidi Marie Bauman Chair of Epilepsy; Director, Pediatric Comprehensive Epilepsy Program, Medical College of Wisconsin, Milwaukee, Wisconsin Sports and Epilepsy

p r e f a c e

It is an honor and a pleasure to introduce the third edition of the popular textbook DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice. In the preface to the previous edition, we emphasized that the orthopaedic sports specialist must be soundly schooled in a variety of conditions that are not commonly encountered in the dayto-day practice of orthopaedics. We would suggest that with the advent of subspecialty certification in orthopaedic sports medicine, this is even more important today. This textbook, unlike anything else in your library, can help you become properly schooled! So, what’s new in this edition? We have all new chapters, written by experts and leaders in their subspecialty. The contributors have done a fabulous job of reviewing and sharing their experience and the current state of knowledge in their respective fields. For this, we profoundly thank them! We introduce a new 4-color design and format, including full-color intraoperative and clinical images, to this edition. We offer expanded coverage of key topics, including new chapters on arthroscopic principles, allograft tissue, complications in athletes, nutrition, pharmacology, and psychology. We have also asked all contributors to completely update all surgical

procedures from ACL reconstruction to cartilage transplantation to the latest arthroscopic shoulder techniques, including labral and rotator cuff repairs. With this edition we have also created a new website that includes the full content of the text, a self-assessment module, links to PubMed, an image library, content updates, and “bonus” video. We would like to recognize and thank our new web editor, Dr. Scott Montgomery, who is already working hard on developing this website. You can access it at www.expertconsult.com So, this is an exciting new edition. The contributors have done a masterful job. With our new web editor, it will always remain an up-to-date “work in progress.” We are confident that this two-volume treatise will remain the gold standard resource for sports medicine providers. Finally, we offer our sincere appreciation to Kim Murphy, Cathy Carroll, Dan Pepper, Jodi Kaye and all of the staff at Elsevier Science for their unfailing support in producing this third edition of DeLee and Drez! Jesse Delee David Drez Mark Miller

ixx

C H A P T E R

1

Basic Science and Injury of Muscle, Tendon, and Ligament S ecti o n

A

Physiology of Injury to Musculoskeletal Structures 1. Muscle and Tendon Injury Mark R. Brinker, Daniel P. O’Connor, Louis C. Almekinders, Thomas M. Best, Joseph A. Buckwalter, William E. Garrett, Jr., Donald T. Kirkendall, Van C. Mow, and Savio L.-Y. Woo

SKELETAL MUSCLE Structure The primary function of skeletal muscle is to generate force, producing joint and limb locomotion and movement. Muscle also maintains posture, assistsz with joint stability, and generates heat. The muscle moment arm affects the ability to generate joint torques; a larger moment arm requires less muscle force to resist a given externally applied moment. Muscle tissue characteristics include excitability, contractility, elasticity, and extensibility. Muscle originates from bone or dense connective tissue, either directly or from a tendon of origin. The muscle fibers pass distally, usually to a tendon of insertion, and connect with bone. This structural framework supports the musculotendinous unit against injury and organizes the individual units into tissues and organs (Fig. 1A1-1). The muscle-tendon unit crosses one or more joints. Generally, muscles that cross one joint are located close to bone and frequently are involved more in postural or tonic activity (e.g., soleus). Morphologically, one-joint muscles are broad and flat and have slower contraction and increased strength (force output) relative to two-joint muscles. Twojoint or phasic muscles typically lie more superficially (e.g., gastrocnemius, rectus femoris). Compared with onejoint muscles, two-joint muscles are capable of quicker contraction and greater length change but are less effective in producing tension over the full range of motion.

Architecture The muscle fiber is the basic structural unit of skeletal muscle, and the sarcomere is the smallest contractile unit of the fiber. Fibers are grouped into bundles known as fascicles, which are usually oriented obliquely to the longitudinal

axis. Fiber arrangement within the muscle is variable and includes fusiform, parallel, unipennate, bipennate, and multipennate arrangements (Fig. 1A1-2). Fiber architecture plays a major role in muscle function. In general, fusiform muscles permit greater range of motion. Pennate muscles usually produce more force than parallel-fibered muscles of the same weight, but their maximal velocity of shortening is slower, and the work performed can be considerably less.1 A muscle’s force production is proportional to crosssectional area and fiber orientation. Cross-sectional area of muscle is a difficult property to define because there is no location within the muscle belly that is crossed by all fibers. Force production is independent of fiber arrangement when differences in cross-sectional area are considered (Fig. 1A1-3). The fibrous connective tissue network within the muscle is also important. Connective tissue surrounds the whole muscle (epimysium), each bundle of fibers (perimysium), and the individual fibers (endomysium). The connective tissue framework is continuous within the muscle and attaches to the tendon of insertion to produce an efficient means for movement. Tendons provide a wide area for the attachment of muscle fibers.

Myofibrillar Proteins Proteins compose about 12% of the total weight of vertebrate striated muscle. Muscle proteins include myosin, actin, tropomyosin, troponin, and others (Table 1A1-1). Myosin (Fig. 1A1-4) is a hexameric molecule composed of two high-molecular-weight (200,000 Da) heavy chains and four low-molecular-weight light chain subunits (A-1, A-2, and two DTNB units). The myosin molecule can be cleaved by trypsin to yield two fragments, heavy meromyosin and light meromyosin. Papain further cleaves the light

DeLee & Drez’s Orthopaedic Sports Medicine

Fascicle

Fiber Z Band

Z

Myofiber M

Z

H

I Band

I A

M Line

H Zone

A Band

I

I Band Z Band Figure 1A1-1 Schematic drawing of the structure of striated muscle, showing the organizational framework necessary for effective function. (See text for further explanation of structures.)

meromyosin fragment into a globular protein, S-1, and a helical protein, S-2. Myosin’s adenosine triphosphatase (ATPase) activity and actin-combining property are associated with the heavy meromyosin component. Myosin’s solubility properties are associated with the light meromyosin fraction. Functionally, heavy chain meromyosin possesses ATPase activity; light chain meromyosin appears to regulate this action but is not essential for ATPase activity. Actin, tropomyosin, and troponin are incorporated into the thin filaments. Of these, actin is present in the largest amount. Actin molecules are small, spherical structures arranged in the thin filaments as if to form a twisted strand of beads. The polarity of actin and myosin molecules is essential to muscular contraction. Tropomyosin and troponin constitute a protein complex that enables calcium to regulate the contraction-relaxation cycle of actomyosin. Tropomyosin molecules (65,000 Da) are long, thin proteins that attach end to end, forming a

A

B

C

D

Figure 1A1-2 Muscle fiber architecture. A, Parallel; B, unipennate; C, bipennate; D, fusiform.

thin filament. Each actin strand carries its own tropomyosin filament, which lies on the surface near the groove between paired actin strands. Together with the troponin myofibrillar protein, they collectively form native tropomyosin, with two main subunits (α and β polypeptide chains, 34,000 and 35,000 Da, respectively) that differ in cysteine content and electrophoretic mobility. The ratio of these two subunits varies among fiber types.2,3 Native tropomyosin makes actomyosin highly sensitive to calcium concentration. At low calcium concentrations, the tropomyosin threads move out of their actin groove and cover the actin region where the myosin cross-bridges attach. When calcium concentrations approach 10−5 M, tropomyosin binds to its target protein, troponin T, resulting in allosteric conformational changes of the troponin-tropomyosin complex and movement of the tropomyosin further back into the grooves.4 This movement permits actin and myosin to bind, leading to adenosine triphosphate (ATP) hydrolysis and initiation of contraction. Troponin has a globular shape and is located adjacent to the tropomyosin molecule. It is a noncovalent complex of three subunits, troponin T, C, and I, each of which has a distinct physiologic function in muscle. Thin filaments are commonly 1 μm in length, and each troponin-tropomyosin complex is associated with seven actin monomers. C protein is located in the cross-bridge–bearing region of the thick filament. M protein is associated with the enzyme creatine phosphokinase and is localized to the M line in the middle of the thick filament. Titin is an elastic, sarcomeric protein of about 3 million Da that spans the gap between the Z band and the M line in

Basic Science and Injury of Muscle, Tendon, and Ligament

A

C

B Figure 1A1-3 The role of muscle architecture in force development and length change. Length of A is twice that of B; cross-sectional area of A equals that of B, Maximal force of A is one half that of B, whereas maximal length change of A is twice that of B. In C, the force is diminished by only a small factor when fibers are arranged in pennate fashion.

the sarcomere. Titin is thought to account for a significant portion of a muscle’s resistance to stretch when extended under relaxed conditions and may play a central role in protecting the muscle against overstretch.5

Ultrastructure Skeletal muscle has dark and light bands (Fig. 1A1-5). The dark bands are composed of thick filaments with small projections, or cross-bridges, extending from the filament. The primary thick filament protein is myosin. Light bands are composed of thin filaments. The primary thin filament protein is actin. The basic functional unit of skeletal muscle is the sarcomere, which extends from one Z band to the next and is divided into I bands and A bands. The Z band is composed of at least four proteins: α-actinin, desmin, filamin, and zeugmatin. The I band contains actin, tropomyosin, and troponin. The A band consists of myosin and the actintropomyosin-troponin complex. The light bands narrow with contraction and muscle shortening, whereas the dark bands do not change in length. The H zone, which includes the M line, is a region near the center of the A band. At the cellular level, skeletal muscle is postmitotic and multinucleated, with several hundreds to thousands of nuclei per centimeter of fiber length. Each fiber is divided into an array of overlapping domains. Within each domain, the nucleus controls the structural proteins. Any increase in fiber size must be accompanied by an increase in nuclei. Inhibiting the increase of nuclei inhibits the growth of the fiber.6 Nuclei arise from undifferentiated myogenic cells called satellite cells that lie underneath the basal lamina of

Table 1A1-1 Relative Proportions of Myofibrillar Proteins in Rabbit Skeletal Muscle Protein Myosin Actin Tropomyosin Troponin C protein M proteins α-Actinin β-Actinin

Percentage of Total Structural Protein 55 20 7 2 2 50% maximal force) force levels

0

1 2 LENGTH (fraction of optimum) Figure 1A1-8 Tension-length curve of skeletal muscle. L0, rest length.

and thereafter accounts for most of increased force production (Fig. 1A1-9). The common drive principle accounts for the behavior of the firing rates of motor units and provides a simple explanation for the control of motor unit activation.41 Common drive explains that the nervous system does not control the firing rates of motor units individually; rather, it acts on the pool of motoneurons in a uniform fashion.

Contractile Properties The basic feature that differentiates motor units is their contractile properties: time to peak tension in a twitch and the one-half relaxation time. A slow-twitch motor unit possesses a relatively long time to peak tension, whereas a short time to peak tension is characteristic of the fasttwitch motor unit. A prime determinant of a muscle’s time to peak tension is the rate at which myosin splits ATP into adenosine diphosphate (ADP) + inorganic phosphate (Pi). The respective enzyme is referred to as actin-activated myosin ATPase or, more commonly, ATPase.42-45 Under normal physiologic conditions of high concentrations of magnesium, the enzymatic activity of myosin is reduced greatly. High rates of ATP hydrolysis during muscle contraction are due to interactions that remove the inhibitory effects of the divalent cations magnesium and calcium. Differences in the specific ATPase activities of myosin are due to the existence of several isoforms of the protein.14,46,47 Traditionally, myosin isoenzymes have been identified based on their susceptibility to loss of ATPase activity in response to an alteration in pH.46,47 Myosin from slow-twitch muscles is acid stable but alkaline labile, whereas the opposite is true for fast-twitch muscles. The sliding filament theory of skeletal muscle contraction argues that myosin is the most important contractile protein because it hydrolyzes ATP to yield energy for formation of the actomyosin complex. The activity of the ATPase of myosin correlates closely with the intrinsic speed of muscle shortening, thus demonstrating a link between the contractile and biochemical properties of skeletal muscle (Fig. 1A1-10).42 Because the rate-limiting step of muscle contraction appears to be the rate of energy delivery from

30% 0

100

100

0

50

50 33%

0

100 0

100

50

50 39% 0

1 VOLUNTARY FORCES (kg)

100 2

TOTAL PERCENTAGE EXTRA FORCE ACCOUNTED FOR

50

50

0

A

0

100

PERCENTAGE EXTRA FORCE FROM INCREASED RATE

PERCENTAGE EXTRA FORCE FROM RECRUITMENT


20 10 16% 0 20 10 14% 0 20 10 10% 0

B

0

1 2 VOLUNTARY FORCES (kg)

Figure 1A1-9 A, Calculated percentage of increase in force due to recruitment and increased firing rate for three subjects. B, Calculated total percentages of force accounted for by the units studied at various force levels. (From Milner-Brown HS, Stein RB, Yemmon R: Changes in firing rate of human motor units during linearly changing voluntary contractions. J Physiol [Lond] 230:371-390, 1973.)

ATP hydrolysis, one can observe changes in the ATPase of myosin to study alterations in contractile characteristics. Much of skeletal muscle regulation and physiologic adaptation to a given stimulus involves the myosin molecule.48

Adaptability of Mammalian Skeletal Muscle

Actin Activated ATPase - µm P(g × sec)−1

Physiologic overload of skeletal muscle can result in adaptation of all components of the motor unit, including the muscle tissue, the neuromuscular junction, and the

30

Cross-Reinnervation and Electrical Stimulation

25 20 15 10 5 0

corresponding α-motoneuron.26 The plasticity of skeletal muscle has been studied under different conditions to show that the different fiber types within a muscle adapt to various forms of overload in several ways.49-59 Each of these adaptations results in a logical alteration of the morphology and the function of the muscle fiber. Muscle is thought to adapt to the function it performs, which in turn implies that specificity becomes an important factor in any type of functional overload, including exercise training. A variety of stimuli, including cross-reinnervation, electrical stimulation, hypergravity stress, thyrotoxicosis, compensatory hypertrophy, and exercise, have been used to study and elucidate mechanisms for this adaptive response.

0 5 10 15 20 25 30 Contractile Speed - Muscle Lengths/sec

Figure 1A1-10 Relationship between maximal speed of shortening and actin-activated myosin adenosine triphosphatase (ATPase) from a variety of animal species. (From Barany M: ATPase activity of myosin correlated with speed of muscle shortening. J Gen Physiol 50:197-218, 1967, by permission of the Rockefeller University Press.)

The pattern of muscle stimulation plays an important role in determining the functional properties of skeletal muscle.54 Cross-reinnervation experiments have shown that the isometric twitch speed of cat skeletal muscle is determined largely by the motor innervation it receives.50 Motoneurons innervating slow-twitch skeletal muscle generate a sustained, low-frequency pattern of activity; motoneurons innervating fast-twitch muscles generate intermittent bursts of more intense activity.60 Transformation of a fasttwitch muscle into a slow-twitch muscle can be brought about with unaltered innervation by transmitting to the nerve (through implanted electrodes) a frequency pattern that normally is delivered to a slow-twitch muscle.61 Neural influences are also largely responsible for the reciprocal changes that occur in functional59 and biochemical62 properties. Without a change in the frequency pattern of electrical impulses reaching a muscle, crossreinnervation has no significant effect on force-velocity

10


properties of skeletal muscle. These observations discount the theory that a chemotrophic substance affects the physiologic and biochemical differences between fast-twitch and slow-twitch muscle.

Compensatory Hypertrophy Several researchers have induced functional overload in skeletal muscle by ablating synergistic muscles and studying the remaining intact system. This compensatory hypertrophy model has been used to stimulate histochemical and biochemical changes in skeletal muscle fibers. Experiments involving compensatory hypertrophy of the fast-twitch rat plantaris muscle show a decrease in calcium-activated ATPase activity, an increase in the number of histochemically determined alkaline-labile fibers, and alteration of the myosin light chain pattern.49,52,56,57 Changes induced by the compensatory hypertrophy model are not as complete as the changes observed with cross-reinnervation and electrical stimulation. Because compensatory hypertrophy does not directly affect the intact nerve, it more closely represents an ideal physiologic situation. The factors operating in the compensatory hypertrophy model to effect fiber-type transformations are likely the same as those associated with hypergravity stress because neural input is not manipulated in either model. Changes in the soleus and plantaris muscles of rats maintained for 6 months under hypergravity stress reinforce Lomo’s54 conjecture that the pattern of electrical stimulation determines the contractile properties of skeletal muscle. Other models have shown that muscle is capable of responding to a hormonal stimulus.51,53

Exercise Training programs are based on the principles of overload, specificity, and reversibility.63 Overload means that a certain level of stimulus is necessary for adaptation to occur. The specificity concept implies that specific stimuli result in specific responses, that specific training leads to specific adaptations, and that fatigue is specific to the type of exercise performed. Reversibility implies that the effects of training can be reversed with a change in the training stimulus. The adaptive changes of skeletal muscle to endurance exercise are well studied.64,65 Endurance exercise is characterized by activation of large muscle groups that generate high metabolic loads, resulting in adaptation of the respiratory and circulatory transport systems as well as the enzymatic capacity of the muscle. Skeletal muscle has a tremendous potential for adaptation in oxidative potential with endurance training. In certain circumstances, this type of training can double the oxidative capacity of skeletal muscle. For example, a 5-month bicycle ergometer program of 1 hour per day 4 days a week at a load requiring about 75% of maximal oxygen power doubled succinyl dehydrogenase (SDH) and phosphofructokinase (PFK) enzymatic activities.65 By contrast, anaerobic capacity, as measured histochemically by α-glycerophosphate dehydrogenase activity, was increased in the fast-twitch fibers only.65 Mean oxygen uptake increased 13%, and muscle glycogen was 2.5 times higher than before training. The percentages of slow-twitch or fast-twitch fibers, as identified from myosin ATPase activity, were unaffected.

High-force, low-repetition training results in an increase in muscle strength that is proportional to the tissue’s crosssectional area. Some debate exists with regard to whether this increase in cross-sectional area is due to muscle hypertrophy (an increase in the size of the muscle fibers) or to muscle hyperplasia (an increase in the number of muscle fibers). At present, it appears likely that most of the change is due to hypertrophy. Along with an increase in the size of the fibers, an increase in the amount of contractile proteins, particularly myosin, occurs. The contributions of hyperplasia (i.e., fiber splitting, fiber branching, and fiber fusion) to the increase in muscle mass are yet to be determined. There is also a strong neurologic component in strength training. Initial responses to training include an alteration in central nervous system firing of motor neurons to produce a more synchronized, and thus more effective, recruitment of muscle neurons. Prolonged endurance exercise in athletes increases skeletal muscle capillary density.66 This increase in capillary density is highly correlated with the improvement in whole-body maximal oxygen consumption. Another predominant effect of endurance training on skeletal muscle fibers is a marked increase in volume and density of the mitochondria. Prolonged resistance exercise, such as long-term weightlifting and powerlifting, appears to produce fasttwitch fiber hypertrophy, which results in reduced capillary density.67 The percentages of fiber-type composition in human skeletal muscle vary considerably among muscles and among individuals. Certain compositions of fiber types would logically appear advantageous for particular athletic events. Saltin and others9 were the first to show the conversion of type IIb to type IIa fibers; however, the ratio of type I to type II fibers remained constant. Studies reporting increases in the percentage of red compared with white fibers employed oxidative capacity, as measured by SDH or DPNH-diaphorase activity, to classify fibers. In no instance in humans has a change been shown in fiber characteristics as determined histochemically by myosin ATPase. A transition from fast-twitch to slow-twitch fibers can be brought about by increased contractile activity in animal models.68,69 Similar to long-term nerve stimulation, high-intensity endurance running leads to transition of fast-twitch to slow-twitch fibers in the sarcoplasmic reticulum, a decrease in fast-type myosin light chains, and an increase in slow-type myosin light chains. Increased contractile activity may induce changes that are qualitatively similar to changes seen in long-term nerve stimulation. Furthermore, endurance training not only affects the metabolic properties of the muscle fiber but also produces fast to slow transitions in the Ca2+-handling system. As judged by conventional histochemical techniques, type IIb fibers decreased, whereas type IIa and I fibers increased in the plantaris, extensor digitorum longus, and vastus lateralis muscles. Increased contractile activity, brought about in a physiologic manner, is capable of inducing fiber-type transitions in certain instances.68 Similar transformation of type IIb into type IIa fibers and of type IIa into type I fibers have been identified in sedentary human subjects.70 These fiber-type changes were depicted by histochemical staining of myofibrillar ATPase and were accompanied by


an enhancement of the oxidative capacity in all fiber types. Alteration in fiber types with exercise has yet to be shown in highly trained athletes. Skeletal muscle fibers possess the potential for synthesis of all types of myofibrillar proteins. Skeletal muscle fiber transformations appear to occur only when a departure from normal function is severe and sustained. The exact duration, frequency, and magnitude of stimulus required for fibertype transformations are uncertain. The forms of overload discussed here represent nonphysiologic conditions and are not characteristic of physical training. For well-trained athletes, exercise may be unable to meet the necessary requirements to bring about a change in fiber type.

Muscle Injury and Repair Muscle injury results from several mechanisms that are governed by separate pathologic processes. Not enough basic research regarding muscle injury has been done to elucidate the precise changes that occur with injury, and experimental and scientific data regarding prevention and rehabilitation are lacking. A predictable set of events occurs in response to muscle injury, although the molecular mechanisms that regulate and control these events are not well understood. Muscle fiber regeneration begins with the satellite cell, a quiescent cell that is activated with inflammation and repair. These cells are located between the basal lamina and the plasma membrane of individual myofibers. During muscle regeneration, trophic substances released by the injured muscle presumably activate the satellite cells.71 A host of growth factors and cytokines has been shown to cause proliferation of satellite cells and their transformation into myotubes and muscle fibers.72 This process depends in part on the prostaglandin-mediated cyclooxygenase-2 pathway; for instance, cellular muscle repair mechanisms are compromised in cyclooxygenase–2–deficient mice.73 The importance of the cyclooxygenase-2 pathway to muscle repair should be considered when deciding whether to use nonsteroidal anti-inflammatory medications following muscle injury. The postinjury response of the satellite cell appears similar to the process of fetal development, suggesting that the expression of myosin heavy chain isoforms provides a useful marker for regeneration. The time between injury and the initiation of proliferation is affected by several factors, including the type of injury and the metabolic state of the muscle.74 In addition to the regeneration of damaged fibers, successful repair includes the synthesis of collagen. Some connective tissue production is necessary for restoration of the tissue’s tensile strength and architecture; however, animal models have shown that certain conditions, such as immobilization, lead to fibrosis and scarring of the muscle.75 As more is learned about what factors control scar formation, treatment practices may be changed.

Muscle Laceration Laceration of muscle is much more common in trauma than in athletics. After laceration and repair, the two segments of the muscle heal by dense scar formation.76 Muscle does not regenerate across the scar, and functional continuity is

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Transected Isolated Proximal nerve

Figure 1A1-11 Schematic drawing of lacerated muscle. The laceration leaves fibers intact proximally and distally while dividing the central fibers. Scar tissue isolates the distal segment from its nerve supply. (Redrawn from Garrett WE Jr, Seaber AV, Bokswich J, et al: Recovery of skeletal muscle following laceration and repair. J Hand Surg [Am] 9[5]:683-692, 1984.)

not restored. The muscle segment isolated from the motor point loses its innervation. After healing, the segment isolated from the motor point develops the histologic picture of denervated muscle. Electrical mapping studies show that muscle activation does not cross the scar.76 Consequently, the muscle loses a significant proportion of its ability to produce tension. Partial lacerations decrease the ability of the muscle to generate tension, but to a lesser degree than muscles that are transected completely. The isolated segment may be able to transmit force and to shorten, but the active contractile function of the muscle remains only in the portion with an intact nerve supply (Fig. 1A1-11). Treatment should stress the repair or reconstruction of a muscle using its long tendons of origin and insertion as well as the epimysial connective tissue to anchor the repair; muscle tissue alone is inadequate for suture repair.

Muscle Cramps Ordinary muscle cramps are common during and after athletic exercise and are frequent in young healthy people not involved in athletics. Cramps occur most frequently in the gastrocnemius complex and can arise during exercise, at rest, or while asleep. The cause of muscle cramps is uncertain. Their onset frequently follows contraction of shortened muscles. The cramp often originates as fasciculations from a single focus or several distinct foci within the muscle and then spreads throughout the muscle in an irregular pattern. Electromyographic studies reveal fascicular twitching in a single focus, followed by high-frequency discharges within the muscle fibers.77 The entire motor unit is involved, and the initiating source is within the motor nerve fiber rather than within the individual muscle fibers. Specifically, the focus is thought to be located in the terminal arborizations of the motor nerve fibers. Layzer78 supported these findings on peripheral motor nerve involvement and suggested that the disturbance could arise from hyperexcitable motor neurons in the spinal cord. Despite their common occurrence, the cause of muscle cramps during exercise remains poorly understood. Many of the studies to date have been conducted in ultraendurance athletes to investigate the proposed mechanisms, which include dehydration, electrolyte disturbances, and muscle fatigue. Maughan79 followed 90 competitors at the 1982 Aberdeen marathon and found no correlation between hydration status and electrolyte balance and the incidence of muscle cramps.

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Ordinary muscle cramps are also associated with a variety of conditions unrelated to exercise. Excessive sweating or diuresis can cause saline loss and may produce cramps. Patients in renal failure who are on long-term hemodialysis often have muscle cramps. These conditions may be related to an alteration in sodium concentration, and administration of a saline solution sometimes is helpful.80 Low levels of serum calcium or magnesium have been implicated.77 Neither of these ionic disturbances is necessarily present in muscle cramps after exercise, however. The cramp sometimes can be interrupted by forceful stretching of the involved muscle or activation of the antagonistic muscle. After resolution of the knotted and painful contraction, the muscle shows evidence of altered excitability and fasciculations for many minutes after the cramp. The muscle may be painful for several days after the event. Electrolyte and hydration balance is thought to be helpful in preventing cramps, although the value of this treatment has not been proved. Drugs have been more helpful in treating cramps occurring in nonathletic individuals. Quinine sulfate and chloroquine phosphate have been beneficial, particularly for night cramps.81,82 The use of these medications to prevent or control exercise-induced muscle cramps is questionable at this time.

Delayed-Onset Muscle Soreness Muscle pain after unaccustomed vigorous exercise is a common phenomenon in athletes. Muscle soreness is especially marked after the initiation or resumption of training after a period without training. This pain should be distinguished from discomfort occurring during exercise, which is often associated with muscle fatigue. Typically, delayed-onset muscle soreness begins hours after exercise and is prominent on the first and second days after activity. The painful areas are typically located along the tendon or fascial connections within the muscle. Several different pathologic mechanisms have been proposed to explain delayed-onset muscle soreness. Hough83 reported that delayed pain did not necessarily follow more fatiguing work. He found that exercise routines that produced considerable fatigue did not produce as much delayed-onset muscle pain as high-intensity, rhythmic contractions marked by relatively little fatigue or exercises associated with a sudden contraction or jerk. Hough83 proposed that the soreness and reduction in the ability of the muscle to produce tension could be explained by small ruptures within the muscle. Asmussen84 found that negative (eccentric) work produced more delayed-onset muscle soreness than positive (concentric) work, despite the greater fatigue induced by positive work. He concluded that the pain was due primarily to mechanical stress rather than fatigue or metabolic waste products and believed that the location of the injury was the connective tissue within the muscle rather than the muscle fibers.84 Abraham85 investigated the hypothesis that connective tissue breakdown might be associated with delayed-onset muscle soreness by monitoring hydroxyproline, a modified amino acid found almost exclusively in collagen. After a weightlifting program, a significant increase in urinary hydroxyproline occurred in subjects experiencing delayed muscle

s oreness.86 Elevated levels of myoglobin excretion were also noted in subjects who developed pain as well as in subjects who did not develop pain. A correlation thus exists between muscle soreness and collagen breakdown but not between soreness and muscle breakdown. Serum lactic acid concentration is not related to exercise-induced delayed muscle soreness. An alternative theory of muscle soreness implicates muscle spasm and electrical activity as the cause of pain rather than breakdown of connective tissue or muscle fibers.87,88 DeVries87 proposed that exercise produces ischemia that subsequently causes pain, which initiates reflex tonic muscle contraction, which prolongs the ischemia. Using quantitative electromyography, DeVries87 showed that muscular activity can be present when pain is present. Stretching of the muscle diminished the pain and the electromyographic activity. Abraham85 reinvestigated the electromyographic data and was unable to show significant differences in subjects with and without muscle soreness. The weight of the evidence seems to be with the tissue injury theory of muscle damage as a cause of delayed muscle soreness. Electromyographic changes may accompany the tissue injury, so treatment that alters the muscle spasm or electromyographic manifestations may be of benefit for delayed-onset muscle soreness. Studies of delayed-onset muscle soreness have investigated changes that occur on an ultrastructural level (Fig. 1A1-12). Electron microscopy of muscle in subjects with pain in the vastus lateralis after cycling showed significant alterations in the sarcomere and the crossstriations.89 Three days after heavy exercise, 50% of the muscle fibers displayed disorganization of the myofibrillar material. Armstrong90 disputed these findings, showing histologic evidence of injury to less than 5% of muscle fibers active during exercise. It is known that a loss of desmin labeling occurs rapidly after eccentric exercise.91 Z-band streaming, A-band disruption, and myofibril disorganization can be seen within 10 minutes of exercise.92 There appears to be general consensus that the initial injury causing delayed-onset muscle soreness results from mechanical damage or overstretch of the contractile apparatus.93 An inflammatory response quickly follows that is characterized by invasion of neutrophils and the release of cytokines that attract additional inflammatory cells. An unexplored and especially important aspect of inflammation following injury is the role of inflammatory cells in extending injury and possibly directing repair. Neutrophils may promote further damage through the release of oxygen free radicals and lysosomal proteases. Macrophages subsequently invade damaged fibers to phagocytose cellular debris. It is becoming increasingly evident that neutrophils and macrophages play a role in muscle repair, at least in laboratory models.94,95 The clinical significance of these findings awaits further investigation. The pain with delayed-onset muscle soreness generally is described as a dull ache that may be localized to the musculotendinous junction or experienced throughout the muscle. Other clinical findings may include muscle and joint stiffness, swelling, and decreased joint range of motion. A marked reduction in maximal muscle force and power production is typical and may be due to inhibition of voluntary effort secondary to pain as well as to a decline


13

Figure 1A1-12 Transmission electron micrographic (TEM) and light microscopic (LM, inset) views of injured rat soleus muscle fibers immediately after downhill walking. Note the A band disruption and the Z band damage. (TEM from Dr. R. W. Ogilvie. LM from Armstrong RB, Marum P, Tullson P, et al: Acute hypertrophic response of skeletal muscle to the removal of synergists. J Appl Physiol 46:835-842, 1975.)

in the intrinsic force-generating capacity of the muscle as a result of myofiber damage. In some animal models, the decrease in force production follows a biphasic pattern with a secondary loss of muscle contractile force at 48 hours after injury.96 Delayed-onset muscle soreness typically occurs after any unaccustomed physical activity with a strong eccentric component. Prior training with eccentric exercise has been noted to protect against similar injury in humans,97 rats,98 and mice.99 Aging has important effects because muscles from older rats show more injury and recover more slowly than muscles from younger rats.100

exist to determine which pathologic processes are involved. The treatment regimen generally includes rest and ice with an early return to gentle motion.89 Prolonged immobilization has been associated with longer periods of disability than shorter delays in restoration of motion. Active and passive motion should be emphasized, and care is necessary in therapy to avoid reinjury. A study conducted at the U.S. Naval Academy reported that using early immobilization in 120 degrees of knee flexion for the first 24 hours after the injury allowed return to full athletic activity in an average of 3.5 days.104 The general efficacy and effectiveness of such treatment remains to be evaluated.

Muscle Contusions

Myositis Ossificans

Direct trauma to muscle is a common athletic injury, particularly in contact sports. Damage and partial disruption of muscle fibers occur, and intramuscular hematoma frequently results. Direct trauma may affect any muscle, but contusion of the quadriceps and gastrocnemius muscles are most prevalent. The injuries are characterized by tenderness, diffuse swelling or a palpable hematoma, and limitation of motion and strength.

A complication of muscle contusions is the occurrence of myositis ossificans tissue calcification or ossification at the site of injury. Heterotopic bone may form in 20% of patients with a quadriceps hematoma.105 The pathogenesis of heterotopic bone formation is poorly understood. A major risk factor is reinjury during the early stages of recovery.106 Myositis ossificans usually becomes radiologically evident 2 to 4 weeks after injury and often extends to the underlying bone.101 The mass may enlarge or may be symptomatic for several months before stabilizing. History of previous contusion is important because the mass and its radiographic appearance can mimic osteogenic sarcoma (Fig. 1A1-13). The histologic features may be similar if a biopsy is performed early in the course of myositis ossificans. Heterotopic bone often resorbs with time. Normal function is often possible before complete resorption, but the recovery period is longer than that of an uncomplicated contusion. No specific treatment is recommended in

Quadriceps Contusions Adequate acute treatment of muscle injuries is important to limit hematoma formation and inflammation. Jackson and Feagin101 reviewed quadriceps injuries occurring in military cadets and found them to be a significant cause of athletic and occupational disability. The initial injury severity, based on range of motion, correlates well with the severity and the duration of disability.102 The possible pathologic mechanisms were described by Ryan,103 but few scientific data

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of diastolic blood pressure.108 These objective measures are used to increase the reliability of the diagnosis.

Acute Compartment Syndromes

Figure 1A1-13 Radiograph of myositis ossificans of the rectus femoris. This 22-year-old patient suffered a quadriceps contusion that resulted in the condition shown. The resultant heterotopic bone gradually resorbed over time.

addition to the treatment for the contusion. Early surgery may exacerbate heterotopic bone formation and prolong disability. Surgery may be considered later in the disease course to remove the heterotopic bone only if it is causing symptoms and has matured, and no clinical or radiologic improvement can be noted.107

Compartment Syndromes Compartment syndrome is a pathologic condition of skeletal muscle characterized by a rise in intracompartmental pressure above capillary pressure, thus restricting capillary blood flow. Many factors can cause a rise in intracompartmental pressure. The most common cause is muscle edema following transient muscle ischemia. Hemorrhage or direct trauma to muscle can also result in a compartment syndrome. If recognized early, the elevated pressure can be relieved by incising the investing fascia, restoring the circulation and function of the compartmental muscles and neurovascular components. The pathophysiology of compartment syndromes involves increased intracompartmental fluid from hemorrhage or intracellular or extracellular edema. The fluid increases intracompartmental pressure, compromising capillary perfusion and subjecting the muscle within the compartment to ischemic injury. The level of pressure that interferes with capillary circulation is less than that of the major vessels within a compartment. The presence of a pulse distal to the compartment thus does not rule out a compartment syndrome. Clinical evaluation relies on the presence of pain, particularly with passive stretch of the muscles in the involved compartment, increased compartment pressure noted with palpation, and altered nervous function as noted by paresthesias in the sensory distribution of nerves within the compartment. Compartment pressures within the compartment can be measured by needle manometer,108 wick catheter,109 solid-state transducer,110 and noninvasive auscultation. Significant muscle damage can occur with pressures above 30 to 40 mm Hg20 or within 10 to 30 mm Hg

Acute compartment syndromes have been associated with direct trauma to bone or soft tissue. Tibial shaft fractures comprise a large proportion of fractures with compartment syndromes. Direct soft tissue injury and muscle trauma also can result in elevated pressure that compromises tissue perfusion. Indirect injury secondary to exertion is another cause of compartment syndrome. Indirect injuries can be acute or chronic. The acute syndromes are not well understood, but several factors may contribute. Intense muscular activity causes a large rise in interstitial pressure; intermittent pressure levels of greater than 100 mm Hg are common during some forms of exercise.110 Muscle perfusion during such exercise is possible only intermittently between muscular contractions. Increasing exercise also causes a muscle volume increase up to 20% as a result of increased blood content and intracompartmental fluid accumulation. Acute exertional compartment syndromes are uncommon in sports.109 They are typically associated with intense muscular contractions in individuals unaccustomed to such activity, such as military recruits in basic training. Direct measurement of compartment pressures is preferred, although if unavailable, surgical decompression of the muscle and neurovascular components by fascial release probably should be undertaken.

Chronic Compartment Syndromes Chronic exertional compartment syndromes occur more frequently than acute forms. The presenting complaints are usually diffuse pain or a deep ache over the anterior or lateral compartment of the leg, usually after a relatively long exercise period. The pain usually is severe enough to interrupt the activity or reduce the intensity of the exercise. The symptoms are often bilateral, and sensory changes may be present. Occasionally, muscle hernias may be present near the fascial opening through which the distal branch of the superficial peroneal nerve passes (Fig. 1A1-14). Chronic compartment syndrome is difficult to diagnose clinically. Corroboration with objective pressure measurements is the gold standard for diagnosis. Resting pressure values may be slightly higher, but the primary characteristic is pressure elevation above normal during exercise and a slower return to resting value at the end of exercise. A resting pressure of greater than 12 mm Hg and 1-minute recovery pressures of greater than 30 mm Hg or 5-minute postexercise pressure of greater than 20 mm Hg is diagnostic of chronic exertional compartment syndrome.111 For most cases, treatment should begin with relative rest and cross-training to avoid the exacerbating activity. Other treatment options include physical therapy and biomechanical correction. If unsuccessful, elective fasciotomy should be considered.109,111 Subjective improvement and normalization of compartment pressures have been reported. Fascial release adversely affects muscle strength, and these procedures should not be advocated without


Anterior compartment Lateral compartment Superficial peroneal nerve Fascial defect

Medial dorsal cutaneous nerve Intermediate dorsal cutaneous nerve

Figure 1A1-14 Schematic drawing of the relationship of the branches of the superficial peroneal nerve to the fascial defect. (Adapted from Garfin SR, Mubarak SJ, Owen CA: Exertional anterolateral-compartment syndrome. Case report with fascial defect, muscle herniation, and superficial peritoneal-nerve entrapment. J Bone Joint Surg Am 59:404-405, 1977.)

accurate diagnosis and counseling.112 Vigorous exercise should be avoided for 6 to 8 weeks postoperatively.

Medial Tibial Syndrome Medial tibial syndrome, or shin splints, is a syndrome of exercise-related pain localized to the medial aspect of the distal third of the tibia, coursing across the junction of muscle and tendon to bone. This syndrome previously had been ascribed to recurrent deep posterior compartment syndrome.113,114 Objective measurement of pressure within the anterior and posterior compartments, however, has shown no pressure elevation.29 This condition most likely is a stress reaction of the bone or muscle origin in response to repetitive exercise, such as running long distances on hard surfaces. Medial tibial syndrome is more common in athletes with significant hindfoot valgus and midfoot pronation, often called flatfoot.

Muscle Strain Injuries Clinical Studies of Muscle Strain Injury Mechanism of Injury

Muscle strain injuries represent about half of all athletic injuries.115 Epidemiologic studies show that muscle strain injuries occur most often in athletes involved in sports

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requiring bursts of speed or acceleration, such as track and field, football, basketball, rugby, and soccer.116 Strains are injuries caused by stretching or muscle activation during a lengthening (eccentric) contraction.117-119 Muscle may be more prone to injury during eccentric contraction because the passive or connective tissue element of muscle allows significantly higher active muscle force production when muscle is stretched than when it is at static length or allowed to shorten. Certain muscles are more prone to strains than others. The two-joint muscles are at highest risk for injury.120 With these muscles, physiologic joint motion can place the muscles in positions of increased passive tension. For example, the hamstrings increase passive tension as the hip flexes and the knee extends. In addition, twojoint muscles often function in an eccentric manner. With eccentric contractions, the muscle can be considered to be controlling or regulating motion as a function of energy absorption. Much of the muscle action involved with running or sprinting is eccentric.121-124 For instance, during running, the hamstrings act not so much to flex the knee as to decelerate knee extension before foot strike. The muscles most likely to be injured have a relatively high percentage of type II or fast-twitch muscle fibers.125 For unknown reasons, certain muscles within a particular group are more susceptible to strain injury,126 including the adductor longus in the adductors, the biceps femoris in the hamstrings, and the rectus femoris in the quadriceps. The rate of muscle stretch may also affect the site of injury.127 Recent clinical studies have begun to elucidate the relative contribution of the muscle and the tendon to change in overall muscle length during running.128,129 Late swing and early stance have been suggested as potentially injurious phases of the gait cycle for the hamstring muscle group. Studies combining kinematic with electromyogram analysis indicate that the lengthening phase of the hamstring muscles actually starts at about 45% of the gait cycle, with the largest rates of lengthening occurring shortly thereafter.128 Lengthening terminates at about 90% of the gait cycle, that is, in swing phase before foot contact. These observations call into question the hypothesis that hamstring injuries occur after foot strike and raise the possibility that the greatest period of vulnerability is much earlier in the swing phase than previously thought. Structural Changes with Muscle Strain Injury

A muscle strain injury may be partial or complete depending on whether the muscle-tendon unit is grossly disrupted.117 Complete tears produce muscle asymmetry at rest compared with the contralateral contour and a bulge with voluntary contraction on the side of the muscletendon unit that still is attached to bone. Muscle strain injuries can be distinguished clinically from exercise-induced muscle soreness. Both conditions are more prone to occur with eccentric exercise.84,130-132 In both injuries, passive stretching and active contraction of the affected region produce discomfort. A strain injury, however, is an acute and usually painful event that is recognized by the patient at the time of injury, whereas muscle soreness is characterized by focal muscle pain and swelling 24 to 48 hours after exercise.90,133

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Direct muscle injury or contusion causes injury to muscle at the place of contact. Imaging studies have confirmed that the locus of tissue damage in an indirect strain injury occurs at or near the musculotendinous junction.126,134 Reports of surgical exploration of muscle injuries confirm the existence of tears near the muscle-tendon junction in (1) the gastrocnemius medial head (often incorrectly called a plantaris rupture),18,135 (2) the rectus femoris muscle,136 (3) the triceps brachii muscle,137 (4) the adductor longus muscle,138 (5) the pectoralis major muscle,139 and (6) the semimembranosus muscle.3 High-resolution imaging studies have also localized acute hamstring injuries to the muscle-tendon junction (Fig. 1A1-15). Bleeding often occurs after muscle injury, but it often takes a day or more to detect subcutaneous ecchymosis as the blood escapes through the perimysium and fascia to the subcutaneous space.134 Computed tomography has shown an inflammatory or edematous response within the muscle tissue itself.140 In certain instances, a hematoma can form between the muscle tissue and the surrounding fascial compartment, as shown by ultrasonography.141 There has been some interest in using magnetic resonance imaging for prognosis following hamstring strains.142,143 Both T1-weighted and inversion recovery T2-weighted, spin-echo imaging in axial and sagittal planes can be used to determine volume of muscle affected and correlate with length of rehabilitation following a first-time injury.142,143 These studies suggest that magnetic resonance may have some value in predicting return to sport. However, as recently pointed out, there are no consensus guidelines or agreed-on criteria for safe return that completely eliminate the high risk for recurrence.144 Prevention and Treatment

It is difficult to find scientific evidence of the best methods of preventing or treating these often debilitating problems. Most athletes routinely practice stretching largely because it is believed to decrease the risk for muscle injury.145-147 Adequate warm-up also is cited as a way of preventing muscle injury.117,147 Fatigue is thought to predispose muscle to injury,117 as is a prior incomplete injury.116 There have been few clinical or laboratory studies to support any of these hypotheses.148-150 The most commonly applied treatments for muscle injuries (strains, contusions, lacerations) have been rest, ice, compression, elevation, anti-inflammatory drugs, and mobilization. The natural regeneration process can be slow and may produce incomplete healing. The isolation and use of growth factors has opened up a new area for investigation and treatment. The number and diameter of regenerating myofibers and recovery of muscle strength following a contusion injury in mice can be accelerated with the use of basic fibroblast growth factor (b-FGF), insulin-like growth factor (IGF-I), and nerve growth factor (NGF). These growth factors are known to enhance fibroblast proliferation and differentiation into muscle cells in vitro.151 Not all growth factors are beneficial to muscle healing, however. Administration of NS-398, a cyclooxygenase2–specific inhibitor, following muscle laceration in mice resulted in higher expression of transforming growth

Authors’ Preferred Method of Treatment of Muscle Strain Injuries There is no consensus for the treatment of muscle strain injuries.116,117 Various treatment regimens have been adapted empirically from clinical practice. Few studies have been performed to compare the effects of these different treatment strategies. Suggested modalities at various phases of injury include rest, ice, compression, physical therapy to improve joint range of motion and function, bandaging, and medications (topical anesthetics, analgesics, muscle relaxants, and anti-inflammatory agents). Occasionally, surgery has been advocated for persons with complete dissociation of the muscle-tendon unit.154,155 Based on available laboratory and clinical studies, we have devised the following treatment regimen for muscle strain injuries. We avoid immobilization and prefer to begin active stretching and muscle activation as soon as these exercises can be performed without great discomfort. After the initial injury, the tensile strength of the muscle-tendon unit is weaker than normal, and large forces should be avoided. Forces large enough to disrupt the muscle are unlikely to occur in a controlled rehabilitation setting. We stress full recovery of muscle length and joint range of motion. Strengthening exercises are resumed early, and progressive resistance is emphasized. A recent prospective randomized trial demonstrated that a program emphasizing progressive agility and trunk stabilization was superior to a strategy employing static stretching and isolated progressive resistance exercises in individuals with a hamstring strain.156 Although time to return to sport was similar, the risk for reinjury was significantly reduced in the group treated with progressive agility and trunk stabilization exercises. We apply ice during the acute phase of the injury and heat before performing stretching exercises after the acute phase. Therapeutic exercise should be of sufficiently high intensity to impart a strengthening effect. The accommodating resistance of isokinetic devices allows the injured athlete to work at a comfortable level through a full range of motion.

factor-β1 (TGF-β1), which causes fibroblasts to differentiate into fibrotic cells rather than muscle cells, leading to an increase in fibrosis.152 By contrast, inhibition of TGF-β1 with injection of suramin following muscle strain in mice inhibits the production of fibrous scar formation by fibroblasts.153 Further work in this direction may lead to new treatment techniques for muscle strains.

Laboratory Studies of Muscle Strain Injury McMaster157 showed in 1933 that normal tendon did not rupture when the gastrocnemius muscle-tendon unit of rabbits was pulled to failure. Failure occurred at the bonetendon junction, the myotendinous junction, or within the muscle. A series of experiments in a rabbit model showed that activation of normal muscle by nerve stimulation alone


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Energy Absorbed to Failure

Energy Absorbed (Joules)

Group 1

Figure 1A1-15 Acute left biceps femoris muscle strain and chronic right hamstring injury. A prone axial computed tomographic image of the proximal thighs in this patient demonstrates an area of low density in the region of the long head of the left biceps femoris muscle (left arrow), typical of an acute muscle strain. Calcifications are noted in the comparable muscle group on the right side (right arrow), probably due to an old injury in this patient. (From Garret WE Jr, Rich FR, Nikolaou P, Vogler JB: Computed tomography of hamstring muscle strains. Med Sci Sports Exerc 21:506-514, 1989. © The American College of Sports Medicine, 1989.)

produced no disruption of the muscle-tendon unit.158 Gross or microscopic muscle injury required stretch of the muscle. The forces produced at the time of muscle failure were several times the maximal isometric force produced by the activated muscles.158 Passive Stretch

In a rabbit model, muscles stretched from the proximal or distal tendon without preconditioning or muscle activation consistently showed injury near the muscletendon junction (usually distally). A small amount of muscle fiber was left attached to the tendon, usually 0.1 to 1.0 mm in length. The disruption occurred predictably near the muscle-tendon junction within the strain rates tested and for all muscles tested regardless of architectural features or direction of strain. A more recent study showed that at higher rates of stretch, certain muscles tear in the distal muscle belly.127 Injury can be predicted in an animal model to occur at the location of maximal strain.127 Active Stretch

Experiments have been performed to measure the amount of force needed to produce failure, energy absorption before failure, and muscle length before failure in passive and active muscles under conditions simulating powerful eccentric contractions.136 The total amount of strain before failure did not differ among muscles stretched to the point of failure under three conditions of motor nerve activation: (1) tetanically stimulated, (2) submaximally stimulated, and (3) unstimulated. The force generated at failure was only about 15% higher in stimulated muscles. The location of failure, near the myotendinous junction, did not change. The energy absorbed was about 100% higher, however, in muscles stretched to failure while activated (Fig. 1A1-16). These data confirm the importance of considering muscles as energy absorbers. The passive components of stretched muscle have the ability to absorb energy, but the potential

Group 2

Group 3

232 ±47

454 ±67

n=8

258 ±36

516 ±109

0 Hz 64 Hz P < .0003

437 ±111

0 Hz 16 Hz P < .0002

534 ±79

16 Hz 64 Hz P < .01

Figure 1A1-16 Average relative energy absorbed by the muscle-tendon unit before failure in groups 1 through 3. All values are plus or minus the standard deviation. 0 Hz, no stimulation; 16 Hz, wave-summated stimulation; 64 Hz, tetanic stimulation. (From Garrett WE Jr, Safran MR, Seaber AV, et al: Biomechanical comparison of stimulated and nonstimulated skeletal muscle pulled to failure. Am J Sports Med 15:448-454, 1987.)

to absorb energy is increased greatly by concomitant active contraction of the muscle. This concept helps to explain the ability of muscles to prevent injury to themselves as well as the supporting joint structures. Muscles can be injured when they are incapable of withstanding a certain force or strain. The ability of a muscle to withstand force and strain is a measure of energy absorption. In engineering terms, strain energy is the area under the curve relating stress to strain. Muscle can be considered to have passive and active components to absorb energy. The passive component does not depend on muscle activation and is a function of the muscle’s connective tissues, including the muscle fibers themselves and the connective tissue associated with the cell surface and between fibers. The active contractile mechanism of the muscle can double the ability of muscle to absorb energy. Conditions that diminish the muscle’s contractile ability also might diminish the ability of muscle to absorb energy. For example, muscle fatigue and muscle weakness, which suggest that the tissue’s ability to absorb energy is diminished, often are considered as factors predisposing muscle to injury. At low levels of strain, most energy absorption is due to the active rather than the passive elements. Because most physiologic activity in eccentrically contracting muscle occurs at relatively low levels of muscle strain, energy absorption during eccentric contraction is due more to active than to passive force in the muscle. The ability of the muscle to absorb energy not only can protect a muscle but also can protect associated bones and joints.118 Nondisruptive Injury

In nondisruptive stretch-induced injury, muscle fibers do not tear at the junction of the muscle fiber and the tendon but instead tear within those fibers that are a short distance from the tendon.159 In the acute phase, these injuries are marked by fiber disruption and hemorrhage within the muscle (Fig. 1A1-17). By 24 to 48 hours after injury, an inflammatory reaction, including inflammatory

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A

B

Figure 1A1-17 A, Gross appearance of tibialis anterior muscle following controlled passive strain injury. A small hemorrhage (H) is visible at the distal tip of injured muscle at 24 hours. I, injured; C, control. B, Histologic appearance of muscle immediately after passive strain injury. Note the rupture of fibers at the distal muscle-tendon junction, along with hemorrhage. T, tendon; M, intact muscle fibers (Masson stain ×100).� �� (From Nikolaou PK, Macdonald BL, Glisson RR, et al: Biomechanical and histological evaluation of muscle after controlled strain injury. Am J Sports Med 15:9-14, 1987.)

Viscoelastic Behavior of Muscle Among the factors believed to be important in the prevention of injury are innate flexibility, warm-up, and stretching before exercise. Muscle response to stretching classically has been explained on a neurophysiologic basis with reference to stretch reflexes,161,162 although the muscle’s viscoelastic properties probably account for the adaptation to acute stretch. When a ligament or tendon is stretched and held at a constant length, the tension at that length gradually decreases over time,2,163,164 a property known as stress relaxation (Fig. 1A1-19). Additionally, cyclic stretching of ligaments and tendons to the same length results in a decrease in tension with each stretch. Most of the studies pertaining to the viscoelastic behavior of muscle have focused on active force production. Much

less is known about the muscle’s viscoelastic behavior during stretching in a manner relevant to current athletic and rehabilitation regimens. Laboratory studies have confirmed and described mathematically muscle’s viscoelastic behavior127; the relevance of these studies to preventing injury is unknown.

FORCE GENERATION (% Control)

cells and edema, becomes pronounced. By the seventh day, the inflammatory reaction begins to be replaced by fibrous tissue near the site of injury. Although some muscle fibers regenerate, normal histology is not restored, and scar tissue persists.75 Immediately after a nondisruptive injury, muscle can produce about 70% of normal force, but force production decreases within 24 hours to only 50% of normal. Recovery of force production by 7 days is 90% complete (Fig. 1A1-18). The recovery of contractile ability is relatively rapid. The initial loss of function may be a result of the hemorrhage and edema at the site of injury. Another possibility is that oxygen free radicals produced after injury are responsible for the decline in muscle function observed in the first 24 hours after injury.160

100 90 80 70 60 50 40 30 20 10 0

immediate 24 hours

48 hours

7 days

TIME AFTER INJURY Figure 1A1-18 Percentage of control force generation over a range of frequencies versus time after controlled passive injury. Immediately after injury, N = 30; at 24 hours, N = 7; at 48 hours, N = 8; and after 7 days, N = 8. All values are plus or minus the standard error of the mean. (From Nikolaou PK, Macdonald BL, Glisson RR, et al: Biomechanical and histologic evaluation of muscle after controlled strain injury. Am J Sports Med 15:9-14, 1987.)

Basic Science and Injury of Muscle, Tendon, and Ligament 80

Relaxation Sequence

N = 12

Tension (N)

75

5-10 4 3 2 1

70 65 60 0

5

10

15 20 25 30 35 Time (sec) Figure 1A1-19 Relaxation curves for extensor digitorum longus muscle-tendon units subjected to repeated stretch to the same tension. There was a statistically significant (P < .05) difference between the first relaxation curve and the subsequent nine curves. The second relaxation curve also showed a statistically significant difference from the other nine curves (P < .05). There were no differences among curves 3 through 10. (From Taylor DC, Dalton JD, Seaber AV, Garrett WE: Viscoelastic properties of muscle-tendon units. The biomechanical effects of stretching. Am J Sports Med 18:300-309, 1990.)

Effect of Repetitive Stretching on Failure Properties The viscoelastic behavior of muscle-tendon units is separate from reflex effects in the muscle.163 Reflex effects can have great significance in flexibility and performance in sports and exercise, but it is not clear whether these effects have any bearing on the prevention of muscle injury. Stretching often has been advocated to prevent injury. This hypothesis has been tested in a rabbit model.148 Muscles were stretched cyclically using 50% or 70% of the force needed to produce failure in the contralateral leg. Ten cycles at 50% of maximal force resulted in a significant increase in the length of the muscle at failure without affecting force at failure or energy absorption. Many of the muscles that were stretched cyclically to 70% of maximal force, however, showed macroscopic evidence of disruption before completing the 10 cycles; length and force to failure were unaffected in the specimens that showed no disruption. Cyclic stretching induces a protective effect in some cases, but muscles subjected to stretch without preconditioning are actually more subject to injury. Stretch that produces greater than 70% of maximal sustainable force in the muscle can make the muscle more likely to be injured. In summary, a cyclic stretching routine may make muscle less likely to be injured because it increases the length to which a muscle can stretch before failure occurs. Stretching produces significant effects on muscle at physiologic lengths, which produce stress relaxation through viscoelastic effects, and at highly stretched lengths, which affect the mechanical failure properties of muscle.

Effects of Warm-up Warm-up by a short period of muscle activity is emphasized in the prevention of muscle injuries. Viscoelastic materials are sensitive to temperature, which changes within the muscle with activation. Muscle held isometrically and stimulated for one single tetanic contraction lasting 10 to 15 seconds produces a temperature rise of about 1° C within the muscle.136,150 Following this single contraction, more

19

stretch can occur before failure and more force production is possible. These changes may be due in part to the small temperature change within the muscle. These changes, however, also may be due to the effects of stretch on viscoelasticity. Although the total length of the muscle-tendon unit does not change, the region most susceptible to injury probably undergoes some degree of stretch during an isometric contraction as the muscle belly and fibers shorten slightly. The resulting change in failure properties may be related to these stretch effects rather than a temperature change induced by muscle activity.

Summary of Basic Studies on Muscle Injury The cause of most muscle injuries involves powerful eccentric contractions. Disruptive and nondisruptive injuries show pathologic changes near the muscle-tendon junction. Active muscular contraction has an important role in the ability of a muscle to absorb energy. The separate effects of stretch, muscle activation, and temperature are being evaluated with respect to improvement of performance or prevention of injury. Stretch is required to injure normal muscle; strong active contractions involving shortening of the muscle do not appear to create injury. The ability of muscle to withstand stretch may be important in preventing injury. Stretching may increase tissue extensibility because of viscoelastic changes in the muscle. Several stretches that are each held for a specific period seem to be more beneficial than a single stretch. Ballistic stretching should be avoided because high velocities increase stretch forces, and quick shortening does not allow time-dependent or viscous changes to occur in the muscle. Empirically, three to four stretches held for 5 to 10 seconds or more may be optimal. Warm-up increases muscle extensibility. The usual athletic warm-up involves increasing muscle temperature by metabolic activity and stretching the muscles and tendons by active muscle force production. Because extensibility of connective tissue increases with temperature, a warm-up period before a stretching routine may be effective. Longer term adaptations in muscle are important in the prevention of acute injury. Often the physiologic requirement of a muscle in sports is the control or deceleration of a joint or limb. The muscle is required to absorb the kinetic energy of the limb. The ability of the muscle to absorb energy can protect it from injury. Strong muscles can absorb more energy than weak muscles; strong muscles undergo less deformation or stretch than weak muscles. Strengthening may thus help to prevent strain injury. Conditioning has a similar effect. Fatigue is a situation in which the ability of muscle to generate active force is declining. Fatigued muscles can absorb less energy than nonfatigued muscles. Muscle strength and conditioning appear to be valuable components of an injury prevention program, particularly in individuals in whom muscle injury is most likely.

Conclusions More clinical and basic laboratory studies of muscle injuries have become available. Clinical imaging studies provide information about the location and nature of the

20


initial muscle injury and the clinical course. Few studies exist that evaluate or compare means of preventing injury. Such clinical studies would require large numbers of subjects to obtain reliable data. Basic laboratory studies can be helpful in the practical management and prevention of muscle strain injuries. These studies have shown the pathophysiology of muscle stretch injury, and the findings are consistent with clinical observations. As the events of injury and repair are�� better understood, more emphasis is being placed on the treatment and prevention of these injuries and on methods of improving performance.

TENDON Tendons are fibrous connective tissues designed to transmit the force of muscle contraction to bone to effect limb movement. Tendons have a complex architecture: highly aligned matrix containing 90% type I collagen to provide tensile strength; elastin to provide compliance and elasticity; proteoglycans serving as pulse dampeners; and lipids, which may reduce shear stress-induced friction.165-169 On microscopic examination, tendons consist of a network of interlacing fibers with variously shaped cells and ground substance. Eighty-five percent of the dry weight of this structure is collagen, and the mechanical and physiologic behavior of collagen is the most important factor in determining tendon properties.170 Two cell populations are present in the major compartments of tendon. The surface epitenon contains large, polygonal cells (tendon surface cells) in syncytia embedded in a lipid- and proteoglycanrich matrix containing 25% collagen. The internal portion of tendon contains fibroblasts (tendon internal fibroblasts) in syncytial layers amidst linear and branching collagen fascicles and bundles.171-175 The matrix of tendon surface cells contain collagen types I and III, fibronectin, TGF-β, and positive IGF-I and negative modulators of cell division (IGF-I-binding proteins).168,171,172,176 Tendon surface cells are most active in migrating into and populating a wound bed in tendon after injury.165,177-182 Tendon internal fibroblasts migrate and divide less in response to injury.179 Tendon internal fibroblasts and tendon surface cells in mature tendon are present as syncytia situated in layered longitudinal sheets that are intimately connected to each other.183 Within a syncytium, cells are connected by connexin 43 (cx43) and cx32, but between syncytia they are connected only by cx43.183 Cells within the epitenon communicate with cells in the internal compartment by cx43 gap junctions. Tendon internal fibroblasts express IGF-I messenger RNA (mRNA).184 Tendon internal fibroblasts and tendon surface cells cache stores of IGF-I in the tendon epitenon and internal compartment that appear to be used in response to trauma. The epitenon and internal compartment of rat and avian tendon express mRNA for IGFbinding protein (IGF-BP5), particularly in the epitenon tendon surface cells. Rabbit flexor digitorum profundus tendons respond to human recombinant IGF-I by synthesizing DNA and matrix.185 Tendons must be capable of resisting large tensile stresses to perform their primary function, which is to transmit forces from muscle to bone. Tendon also

maintains the length of the moment arm during muscle contraction to optimize force production. In addition to this load-transmitting role, tendons satisfy kinematic requirements (they must be flexible enough to bend at joints) and damping requirements (they must absorb sudden shock to limit damage to muscle).

Structure Tendons and ligaments are both dense, regularly arranged connective tissues, but there are significant differences between them with respect to structure and histologic and biochemical properties.186 The collagen fibers in a tendon are more parallel to the longitudinal axis than is the case in a ligament. The collagen fibers, composed of thinner fibrils, extend the entire length of the tendon. Fibroblasts, which are few in number, are located more centrally in the tendon, between the collagen bundles or fibrils. Present knowledge of tendon morphology is outlined in Figure 1A1-20. The surface of the tendon is enveloped in a white, glistening, synovial-like membrane, called the epitenon. The epitenon is continuous on its inner surface with the endotenon, a thin layer of connective tissue that binds collagen fibers and contains lymphatics, blood vessels, and nerves.187 In some tendons, the epitenon is surrounded by a loose areolar tissue called the paratenon. Typically, the paratenon surrounds tendons that move in a straight line and are capable of great elongation owing to the presence of elastic fibers. This paratenon functions as an elastic sheath permitting free movement of the tendon against the surrounding tissue. Together the epitenon and the paratenon compose the peritendon (Fig. 1A1-21). In some tendons, the paratenon is replaced by a true synovial sheath or bursa consisting of two layers lined by synovial cells. This double-layered sheath, which is lined by synovium, is referred to as a tenosynovium. Within this synovial sheath, the mesotendon carries important blood vessels to the tendon.188 The flexor tendons of the forearm and hand and the Achilles tendon are surrounded by this well-defined sheath lined with synovial cells. In the absence of a synovial lining, the paratenon often is called a tenovagina. The perimysium becomes continuous with the endotenon at the musculotendinous junction. The tendon-bone interface marks the site where collagen fibers enter bone as Sharpey’s fibers, and the endotenon becomes continuous with the periosteum. The insertion of tendon into bone generally is classified into two types. The simpler type, termed direct insertion, occurs when the tendon fibrils pass directly into bone through zones of fibrocartilage with little interdigitation into the surrounding periosteum. As described by Cooper and Misol,189 the tendon inserts into a zone of fibrocartilage, then into a layer of mineralized fibrocartilage, and finally into bone. The periosteum is continuous with the endotendon. Dissipation of force is achieved effectively through this gradual transition from tendon to fibrocartilage to bone. The second type of insertion is more complex and involves the periosteum as well as the underlying bone; the superficial fibrils insert into the periosteum, whereas the deeper fibrils fan out into bone directly. When tendons insert at an angle into the bone, a larger area of fibrocartilage can be found on one


21

Figure 1A1-20 Basic tendon morphology. (Adapted from Kastelic J, Galeski A, Baer E: The multicomposite structure of tendon. Connect Tissue Res 6:11-23, 1978.)

MICROFIBRIL

TENDON

FIBRIL FASCICLE

TROPOCOLLAGEN

Fibroblasts

Waveform or crimp structure

side of the insertion.190 This is thought to be an adaptation to the compressive forces experienced by the tendon on that side. Tendon is well-vascularized tissue, although less so than muscle. The blood supply to tendon has several sources, including the perimysium, periosteal attachments, and surrounding tissues. Blood supplied through the surrounding tissues reaches the tendon through the paratenon, mesotenon, or vincula. A distinction between vascular and the so-called avascular tendons has been made to denote differences in blood supply. Vascular tendons

Fascicular membrane

are surrounded by a paratenon and receive vessels along their borders; these vessels then coalesce within the tendon. The relatively avascular tendons are contained within tendinous sheaths, and the mesotenons within these sheaths function as vascularized conduits called vincula. The muscle-tendon and tendon-bone junctions along with the mesotenon are the three types of vascular supply to the tendon inside the sheath. Other sources of nutrition191,192 include diffusional pathways from the synovial fluid, which provide an important supply of nutrients for the flexor tendons of the hand.

Tendon

Paratenon Peritendon Epitenon Endotenon Fibroblast Primary bundle Fibril Microfibril Collagen fibril Tropocollagen Figure 1A1-21 Structural organization of tendon.

22


The nervous supply to a tendon is sensory in nature. The proprioceptive information supplied to the central nervous system by these nerves usually is picked up through mechanoreceptors located near the musculotendinous junction.

Biochemistry The cellular component of tendon is the tenocyte, which is responsible for the production of collagen and the matrix proteoglycans. Similar to all types of connective tissue, tendons consist of relatively few cells (fibroblasts) and an abundant extracellular matrix. In tendons and ligaments, the main constituent is collagen, along with small amounts of elastin, ground substance, and water. Collagen constitutes about one third of the total protein in the body and is present in large amounts in specialized connective tissues, such as tendon, ligament, skin, joint capsule, and cartilage.

Collagen Twelve different but homologous collagen types are recognized.193 It is convenient to think of two major classes of collagen—those that are fiber forming and those that are not. Collagen types I, II, and III are known as fibril-forming collagens. After being secreted into the extracellular space, these collagens assemble into collagen fibrils. Collagen types I and III are the main forms comprising normal connective tissue. Type I is more common, constituting 90% of the collagen in the body. The remaining collagen types constitute the second major group—the non–fiber-forming group; types IV and V are the basement membrane collagens. The fibroblast is a spindle-shaped, contractile cell that synthesizes connective tissue matrix precursors, including collagen, elastin, and proteoglycans.194,195 Collagen is produced within the fibroblast as a large precursor molecule (procollagen), which is secreted and cleaved extracellularly to form tropocollagen. Soluble tropocollagen molecules form noncovalent cross-links, resulting in insoluble collagen molecules that aggregate to form collagen fibrils. After collagen fibrils have been synthesized in the extracellular space, they are strengthened greatly by the formation of covalent cross-links within and between the constituent collagen molecules. In its normal state, mature collagen can be degraded only by collagenase, whereas ruptured collagen fibrils are susceptible to digestion by trypsin. When isolated collagen fibrils are viewed in an electron microscope (Fig. 1A1-22), they exhibit cross-striations every 64 to 68 nm. This pattern reflects the packing arrangement of the individual collagen molecules in the fibril. Collagen is the strongest fibrous protein in the body. The arrangement of fibers in parallel to their longitudinal axis results in tendon having one of the highest tensile strengths of all soft tissues. All types of collagen have in common a triple helical domain, which is combined differently with globular and nonhelical structural elements (Fig. 1A1-23). The triple helical collagen molecule is stiff compared with a single polypeptide chain. The most common collagen molecule, type I collagen (also found in skin and bone), is composed of three α-peptide chains, each with about 1000 amino acids, resulting in a total

Figure 1A1-22 Electron micrographs of collagen demonstrating the periodicity and the regularity of the molecule. Precipitated from collagen solution by dialysis against 1% sodium chloride. (From Bloom W, Fawcett DW: A Textbook of Histology, 8th ed. Philadelphia, WB Saunders, 1962, p 105. Original investigators: J. Gross, F. O. Schmitt, and J. H. Highberger.)

molecular weight of about 340,000 Da.196,197 The α-chains exist in several different isomeric forms (Table 1A1-3). Type I collagen contains two α1-chains and one α2-chain.198 These three α-chains are wound around each other in a regular helix to generate a rod-like collagen molecule about 300 nm long and 1.5 nm in diameter. Normal human adult flexor tendons are composed largely of type I collagen (>95%); the remaining 5% consists of type III and type IV collagen.199,200 The amino acid sequence of the collagen molecule has been studied extensively to understand the cross-linking mechanism of these structures. They are arranged in a characteristic triple helical pattern that gives the molecule its rod-like form and its rigid properties. Every third amino acid in the α-chain is glycine; other amino acids commonly present are proline (15%) and hydroxyproline (15%).196 Consequently, nearly two thirds of the collagen molecule consists of these three amino acids. Hydroxyproline is derived from proline and is almost unique to collagen, and another amino acid, hydroxylysine, is unique to collagen.

Physical Properties of Collagen The mechanical properties of soft collagenous tissues are highly dependent on their structural integrity, which is determined primarily by the architecture and properties


rupture, abnormal curvature of the spine, and problems with skin breakdown and wound dehiscence.

64 nm Fibril

Elastin

Overlap Zone Microfibrils Hole Zone Packing of molecules

Collagen molecule

23

280 nm

α2 Triple α 1 helix α1

1.5 nm

Elastin is a protein found in connective tissues that permits these structures to undergo changes in length without incurring any permanent change in structure, while expending little energy in the process. Elastin is responsible for the wavy pattern of the tendon when viewed by a light microscope. Tendons of the extremities possess small amounts of this structural protein, whereas elastic ligaments, such as the ligamentum flavum and ligamentum nuchae, have greater proportions of elastin. Elastin in most tendons is found primarily at the fascicle surface201; it usually comprises less than 1% by dry weight. The elastin content of the aorta can be 30% to 60% of dry weight. Elastin, similar to collagen, has lysine-derived cross-links. The amino acids desmosine and isodesmosine are unique to elastin. Their formation depends on the presence of copper. The elastic potential of elastin is due primarily to the cross-linking of lysine residues through desmosine, isodesmosine, and lysinonorleucine.

Ground Substance Collagen α-chain (purity to molecules) Figure 1A1-23 Microstructure of collagen showing the three α-chains of the triple helix. Three separate α-chains are wrapped around each other to form a rope-like, triple-stranded, helical rod. Every third amino acid of the native molecule is glycine.

of the collagen fibers as well as by the amount of elastin present in the tissue. The physical properties of collagen rely on covalent cross-links within and between the molecules. The triple helix conformation of collagen is stabilized mainly by hydrogen bonds. The three chains are held together strongly by hydrogen bonds between glycine residues and between hydroxyl groups of hydroxyproline. This helical conformation is reinforced by hydroxyproline-forming and proline-forming hydrogen bonds to the other two chains. The degree of cross-linking is a key to the tensile strength of collagen and its resistance to enzymatic and chemical breakdown. This conclusion is evident clinically in the condition of lathyrism, in which an absence of cross-linking produces a collagen that is significantly weakened, resulting in an increased incidence of aortic

About 1% of the total dry weight of tendon is composed of ground substance, which consists of proteoglycans, glycosaminoglycans, structural glycoproteins, plasma proteins, and a variety of small molecules. The waterbinding capacity of these structures helps to account for the viscoelastic properties of tendinous materials. Proteoglycans and glycosaminoglycans are thought to be important for stabilizing the collagenous skeleton of connective tissue. Proteoglycans are high-molecularweight macromolecules consisting of a protein core to which glycosaminoglycan side chains are attached. Glycosaminoglycans are macromolecules containing repeated disaccharides composed of a hexosamine residue and a uronic acid residue. Glycosaminoglycans that are abundant in mammalian tissues include hyaluronic acid, chondroitin sulfate, dermatan sulfate, keratan sulfate, and heparin-heparan sulfate. Except for hyaluronic acid, the glycosaminoglycans are negatively charged owing to the presence of sulfate or carboxyl groups, and this confers predictable mechanical and chemical properties on the connective tissue. Regions of tendon that experience primarily tensile forces have a lower proteoglycan content

Table 1A1-3 Principal Collagen Types and Their Properties Type

Molecular Formula

Polymerized Form

Distinctive Features

Tissue Distribution

I

[α-1 (I)]2 α-2(I)

Fibril

Skin, tendon, bone, ligaments, cornea

II

[α-1 (II)]3

Fibril

III

[α-1 (III)]3

Fibril

IV

[α-1 (IV)2 α-2 (IV)]

Basal lamina

Low hydroxylysine Low carbohydrate High hydroxylysine High carbohydrate High hydroxyproline Low hydroxylysine Low carbohydrate Very high hydroxylysine High carbohydrate

Articular cartilage, intervertebral disk, notochord, vitreous body of eye, fetal collagen Skin, blood vessels, internal organs Basal laminae

24


and higher rates of collagen synthesis than areas that experience frictional and compressive forces in addition to tensile forces.202

and development. Gap junction regeneration and function are most likely essential for an organized wound healing response in tendon.

Cellular Interaction

Mechanical Properties of Tendon

Results of light and electron microscopy studies have shown that cells in the epitenon and internal compartment of whole tendon are connected physically to each other.172,183 Epitenon cells and internal fibroblasts in vivo are layered in longitudinal syncytia that appear optimal for rapid, repeated chemical and electrical coupling, similar to osteocytes in bone.203 Cells within tendon and in vitro are coupled and respond to a mechanical perturbation (e.g., a micropipet mechanical stimulation of a target cell plasma membrane) by releasing intracellular calcium stores and propagating a calcium wave to adjacent cells for four to seven cell diameters.204-206 In vivo, tendon fixed with glutaraldehyde under tension contained cells that were indented dramatically, similar to marshmallows squeezed between rods.166 Avian tendon cells express gap junctions and have at least three forms of cx43: a 42-kDa nonphosphorylated form and two intermediate forms of 44 to 47 kDa that are phosphorylated at serine.207-209 Preliminary data indicate that quiescent tendon surface cells have predominantly the nonphosphorylated form of cx43 but have phosphorylated forms during log phase.207 Tendon surface cells and tendon internal fibroblasts express mRNA for cx42, cx43, cx45, and cx45.5 by polymerase chain reaction detection and cloning, but cx43 is the only form detected by Northern analysis.184 The Western blot technique detects cx26, cx32, and cx43, whereas cx32 and cx43 have been visualized by scanning confocal microscopy183 with cx43 appearing to predominate. Quiescent tendon internal fibroblasts have about half each of the 43-kDa nonphosphorylated form and 45-kDa phosphorylated form of cx43 and have all forms during log phase growth. Ingber210 postulated in his tensegrity model that cells are connected and signal through direct mechanical linkage from the matrix through integrins and through the cytoskeletal system to the nucleus.210 Gap junction proteins may not have cytoskeletal connections but are known to pass signaling molecules intercellularly.211-213 A direct response in a cell by perturbing matrix and signaling through an integrin has not been demonstrated, although endothelial cells subjected to shear stress release [Ca2+]ic and cluster integrins at the cell front.214,215 Direct evidence that connexins are involved in signaling and growth control derives from experiments with the c6 glioma cell line, which is poorly electrically coupled.216 If the cells are transfected with cx43 complementary DNA and express the protein, they gain the ability to communicate with neighbors electrically and with a propagated calcium wave in response to a mechanical stimulation.216,217 Loss of cx43 and gap junctions leads to loss of regulation of DNA synthesis and cell division.217 Although cx43 gap junction expression can be up-regulated by mechanical load in tendon cells,165 cx43 is up-regulated by load in osteoblasts and vascular smooth muscle cells as well.218 The connexins may be involved intimately in regulating embryogenesis

The primary function of tendon is to transmit muscle forces to the skeletal system to provide joint and limb locomotion and movement. To do this effectively, tendons must be capable of resisting high tensile forces with limited elongation. Tensile strength of 98 N/mm2 has been reported.219 The densely packed collagen fiber bundles arranged in parallel along the length of the tissue provide efficient resistance to tensile loading; however, tendons have weak resistance to shear and compression forces. Thus, from a functional point of view, tendons are designed to transmit tensile loads with minimal energy loss and deformation. Biomechanical studies of tendon have revealed that the stress-strain relationship is similar to other parallelfibered collagenous tissues, such as ligaments, but not the same as skin, where the collagen fibers are more randomly organized. As with most biologic tissues, tendons show complex time-dependent and history-dependent nonlinear viscoelastic properties.220-223 These properties include stress relaxation (decreased stress with time under constant elongation) and creep (increased elongation with time under constant load) (Fig. 1A1-24). In addition, the shape of the load-elongation curve depends on the previous loading history. Clinically, we recognize these time-dependent and history-dependent characteristics; for example, increased tendinous and ligamentous laxity occurs after exercise. Several models have been developed to describe and predict the mechanical and viscoelastic behavior of tendons and other biologic tissues.222,224,225 Figure 1A1-25 represents a typical load-elongation curve for tendon. Abrahams220 described three distinct regions of such a curve before rupture of the structure. Under tension, the fibers straighten, and the system becomes stiffer. Different components of the structure take up loads at different levels, resulting in a nonlinear, concave, upward load-elongation curve. The initial toe region represents the alignment of fibers in the direction of stress as well as fiber recruitment. In this region, little force is required initially to elongate the tissue, which may protect the tendon from large loads during normal joint motion. The toe region is followed by a steep linear portion of the loadelongation curve, in which most fibers are aligned in parallel to the longitudinal axis of tension and elongation of the helical structure on the fibrillar and macromolecular levels occurs. The slope of the curve in this linear region often is referred to as the elastic stiffness of the tendon. With further loading, small reductions in stiffness sometimes can be observed, which can be attributed to failure of a few fiber bundles. Eventually, major failure of the tendon will occur as the fibers recoil and blossom into a tangled bud at the ruptured end. At strains of 4% to 8%, collagen fibers begin to slide past one another, resulting in disruption of their cross-linked structure. Normal physiologic forces or loads are reported to cause strain of less than 4%,226,227 but certain activities, such as sports, occasionally induce stronger loads. There is a large safety factor because the maximal isometric contractile force of a muscle is usually about


25

X Ultimate failure Load

creep 3

Deformation time

LOAD 2

Deformation 1 Stress

stress relaxation time

Figure 1A1-24 Biomechanical properties of collagen. Under a constant load, the tendon will undergo time-dependent relaxation (creep), whereas under a constant deformation, the structure will undergo stress relaxation (i.e., reduction in load over time).

one third of the maximal load of the tendon, although repetitive loading at submaximal failure loads can result in fatigue and eventual failure of the tendon. The tendon fibroblasts themselves, however, appear to tolerate repetitive tensile loads well. In vitro studies have shown no negative effects on tendon fibroblasts with repetitive stretching up to 25% strain.228 Large variations in mechanical properties of tendons usually are attributable to differences in species, type, and age, as well as testing conditions, such as temperature and humidity. These variables are important to note when comparing the results of different studies. Preconditioning of the specimen through cyclic stretching at low levels of elongation before testing helps to eliminate some of this variation. In addition, one must distinguish between the structural properties of the tendon-bone complex and the mechanical properties of the tendon itself. Structural properties (i.e., linear stiffness, ultimate load, ultimate elongation, and energy absorbed at failure) describe the tensile properties of the tendon-bone complex and are obtained directly from the load-elongation curve. Mechanical properties (i.e., elastic modulus, ultimate tensile strength, ultimate strain, and strain energy density) are represented by the stress-strain relationship and are properties of the tendon itself (Fig. 1A1-26).

Adaptability of Collagen Aging After collagen maturation, the mechanical properties of tendon reach a plateau, followed shortly thereafter by a decrease in tensile strength. This decrease in tensile strength correlates with decreases in both the amount of insoluble collagen and the total collagen present.229 There is a concomitant increase in stiffness,230 which likely is due to a marked increase in collagen cross-linking.231,232 Other

ELONGATION Figure 1A1-25 Typical load-elongation curve to failure showing primary or “toe” region (1), secondary or “linear” region (2), and end of secondary region (3).

extracellular changes include a decrease in the content of mucopolysaccharides and water.

Training Studies of exercise-related changes in tendon properties are inconclusive. Most studies have shown that training results in increased maximal tensile failure load,233-235 which is a structural property of the tendon-bone interface.233,235 The effect of exercise on mechanical properties, cross-sectional area, and collagen content are less clear. These properties in flexor tendons of swine after 1 year of moderate exercise showed no difference from control animals in one study,236 although a similar study observed increases in strength, size, and collagen content in extensor tendons.235 A third study in rabbits234 found that the ultimate load was higher for trained than for nontrained animals, but the weight, water, and collagen contents of the tendons were no different. Flexor and extensor tendons may respond differently to exercise, with flexor tendons having a limited capacity for adaptability and extensor tendons having a greater training potential, although these differences need to be investigated more thoroughly. Ultrastructural investigations have shown that exercise leads to an increased number of collagen fibrils that are thinner in diameter compared with controls.237,238 Studies of exercised rabbits revealed that the collagen fiber crimp angle is increased, whereas crimp length and elastic modulus are lowered.239 Anabolic steroids accentuate these changes and can lead to increased collagen dysplasia.239,240 Further research is needed in this area.

Immobilization Several studies have shown decreased tensile strength241,242 and increased collagen turnover241 in tendon after immobilization. Similar to ligament, tendon shows a decrease in stiffness with immobilization. Many of the differences in these studies may be attributable to differences in age of the animals studied as well as to duration of immobilization.


26

Decrease stress

STRUCTURAL PROPERTIES OF BONE-TENDON COMPLEX (LOAD-DEFORMATION CURVE)

A

Linear slope

Immobilization Energy absorbed Ultimate deformation

Deformation (mm)

Physiologic activities

Exercise

MECHANICAL PROPERTIES MASS

LOAD (N)

Failure load

Increase stress

MECHANICAL PROPERTIES OF TENDON SUBSTANCE (STRESS-STRAIN CURVE)

STRESS (N/m2)

Ultimate stress STRESS AND STRAIN DURATION

Elastic modulus

B

Ultimate strain

Strain (%)

Figure 1A1-26 Representative plots of tensile testing to failure. The structural properties of the tendon-bone complex are obtained from the load-elongation curve (A), and the mechanical properties of the tendon substance are obtained from the stressstrain curve (B).

Based on the available information, Woo and associates243 developed a hypothetical curve that predicts the mechanical response of tendons and ligaments to various periods of exercise and immobilization (Fig. 1A1-27). This diagram suggests that for tendons and ligaments within the normal range of physiologic activity, immobilization results in profound shifts in deformation properties when subjected to increasing forces. Short-term training has little or no observable effect on these properties, and long-term training has a minimal effect. The clinical significance of these animal results suggests that connective tissue is more responsive to a decrease in mechanical stimuli than to progressively increasing loads.

Medication and Tendons Corticosteroid Treatment

Figure 1A1-27 A hypothetical curve showing the nonlinear properties of collagenous tissues and the effects of stress and motion on the equilibrium responses of soft connective tissues. (From Woo SL: Mechanical properties of tendons and ligaments. I. Quasi-static and nonlinear viscoelastic properties. Biorheology 19:385-396, 1982. With permission of Pergamon Press Ltd.)

No area of tendon research has received as much attention in the orthopaedic and sports medicine literature as that of corticosteroid injections into or around tendinous tissue. Glucocorticoids are often used in the treatment of athletic injuries for their marked anti-inflammatory effect. The biosynthesis of collagen is inhibited by glucocorticoids.244 There are case reports of local injections around the Achilles tendon245 and patellar tendon246 resulting in

rupture of the tendinous tissue. The effects of corticosteroids can be systemic as well as local, as shown by reports of bilateral rupture of the Achilles tendon in patients receiving oral glucocorticoid therapy.247,248 Laboratory studies of the effects of corticosteroid injections have produced confusing results. Important variables include the duration of the study, amount of steroid injected, and site of injection. Oxlund249 showed that local administration of hydrocortisone acetate, 20 mg/kg every third day for 24 days, around the peroneal tendons of rats increased the tensile strength and stiffness of muscle tendons with no change in collagen content. In the same study, another group of animals received injections into both knee joint cavities that decreased tensile strength of the posterior cruciate ligament-bone interface. Systemic effects of this local cortisol treatment included decreased thickness and fat content of the skin. A similar study showed that daily intramuscular injections of prednisolone (2 mg/kg/body weight for 14 days) increased the maximal load, maximal stress, and energy absorption for the muscle tendons in rabbits.250 Elastic stiffness, measured after exhaustion of the viscous properties of the tendons, also increased, which was thought to be due to an increased stabilization of the collagen cross-linking pattern. To evaluate the long-term effects of corticosteroid injections, Oxlund251 injected 10 mg/kg of cortisone around the peroneal tendons every third day for 55 days. He found that although the mechanical properties of the tendons were not altered, their dry weight and hydroxyproline content were reduced. The thickness and collagen content of skin remote from the injection site were reduced, although the strength of skin specimens was increased.


As a result of these studies and others, it is currently believed that corticosteroids act on collagenous tissues in two ways.251 Initially, during the first 1 to 2 weeks, corticosteroids induce a relatively fast increase in the mechanical and structural stability of the injected tissues. This increase is believed to be due to a change in the cross-linking pattern of the collagen. With continued treatment, progressive thinning and a reduction in collagen occur as a result of inhibited collagen synthesis, ultimately leading to reduced collagen content. Nonsteroidal Anti-Inflammatory Drugs

Vogel252 was the first investigator to show that indomethacin treatment resulted in increased tensile strength, proportion of insoluble collagen, and total collagen content in rat tail tendons. Carlstedt and coworkers253 examined the influence of indomethacin on the biomechanical and biochemical properties of rabbit tendons and found increased strength in tendon repair after indomethacin treatment. They noted a slight decrease in the amount of soluble collagen, which may have been due to increased cross-linking after indomethacin treatment, and concluded that the increased tendon strength resulted from the increased cross-linkage. The effects of nonsteroidal anti-inflammatory drugs on tendon fibroblasts have been studied in in vitro models. The results suggest that nonsteroidal anti-inflammatory drugs can depress DNA synthesis and stimulate protein synthesis through direct effects on the fibroblasts.254

Tendon Healing Mechanisms of Tendon Injury Injury to tendons can result from acute trauma (e.g., laceration) or repetitive loading (e.g., overuse injury). The former is discussed first with respect to flexor tendon injuries of the hand, and overuse tendinous injuries incurred in sports are covered last. Considerable scientific data are available regarding the acutely traumatized tendon. Much of this work has been done on tendons of the hand owing to their propensity for injury. Injury to tendon can occur in numerous ways; in the hand, avulsion directly from bone and mid-substance transection of the tendon itself are the two major mechanisms. These injuries often occur after crush injuries to the hand, of which 75% involve associated injury to the surrounding soft and hard tissues. The tendons of the hand are also subject to compressive loads when these tendons wrap around articular surfaces and in oblique tendon insertions into bone. During active flexion, the pressure between the pulley and the flexor tendon may be 700 mm Hg.255 These compressive loads are capable of altering the histologic structure of the tendon.256

Primary Tendon Healing As in other areas in the body, tendon healing proceeds in three phases: (1) an inflammatory stage, (2) a reparative or collagen-producing stage, and (3) a remodeling phase. There are two different theories of primary tendon healing, or the healing of two divided tendon ends brought into apposition by sutures.

27

One theory suggests that healing depends on the surrounding tissues and that the tendon itself plays no significant role.198,257-262 This theory holds that the tendon is an inert, almost avascular structure whose cells are incapable of contributing to the healing process. Using a canine model, Potenza259,261 showed that the tendon is invaded by fibrovascular tissue at the location of suture placement. At 28 days, the collagen produced by these fibroblasts is immature, but by 128 days, it is indistinguishable from that of normal tendon. By contrast, several studies191,192,263-268 have suggested that the inflammatory response is not essential to the healing process and that tendons possess an intrinsic capacity for repair. A study of rabbit flexor tendons showed an intrinsic tendon repair response consisting of proliferation of tendon cells and production of mature collagen. Efforts to show the intrinsic capacity of tendon healing previously failed owing to an inability experimentally to isolate the tendon from the inflammatory response. Lindsay and Thomson265 were the first to show (in chickens) that an experimental tendon suture zone can be isolated from the perisheath tissues, and that healing progressed at the same rate as when the perisheath tissues were intact. Later, in isolated segments of profundus tendon in rabbits, these researchers showed that an active metabolic process existed in the experimentally free tendons by the presence of anabolic and catabolic enzymes.266 In addition, sutured free tendon grafts of rabbit flexor tendons healed without adhesions within a vascular synovial environment of the suprapatellar bursa. Consequently, it is now accepted that tendons may possess intrinsic and extrinsic capabilities for healing, and the contribution of each of these two mechanisms probably depends on the location, extent, and mechanism of injury and rehabilitation program used after the injury. Tendon healing begins with the formation of a blood clot and an inflammatory reaction that includes an outpouring of fibrin and inflammatory cells. The degree of inflammation is related to the size of the wound and the amount and type of trauma that has occurred. The presence of nitric oxide also appears to limit the duration and intensity of the inflammatory response following tendon injury.269,270 A clot forms between the two tendon ends and is invaded by cells resembling fibroblasts and migratory capillary buds. This process occurs during the first 3 days after injury. The fibroblasts are believed to arise from the endotenon and epitenon.271 Fibroblasts residing in the endotenon differ from those in the epitendinous tissues.202 The epitendinous fibroblasts resemble synovial cells and are particularly active in response to injury. Mesenchymal cells, which are capable of differentiating into fibroblasts, also appear in the area. A study of patellar tendon injury in a rat model showed that in the first few days of acute injury and inflammation, the mesenchymal cells are primarily from the circulation.272 In the subsequent days and weeks, the number of circulation-derived mesenchymal cells decreases and that of locally derived mesenchymal cells from the tendon tissue itself increases.272 This inflammatory phase is evident until the 8th to 10th day after injury. Collagen synthesis begins within the first week and reaches its maximal level after about 4 weeks. At 3 months, collagen synthesis still proceeds at a rate

28


3 to 4 times normal. Type I collagen is synthesized and extruded into the extracellular space as procollagen, which is converted to type I collagen by the enzyme procollagenase. The expression of procollagen mRNA, and thus the production of procollagen, depends on the presence of TGF-β1273; other growth factors are also expressed throughout the acute inflammatory phase.274 Initially, the collagen fibrils are oriented perpendicular to the long axis of the tendon, but by 2 months these fibrils usually are oriented parallel to the axis of tensile loading. Restoration of the gliding function of the tendon depends on the dissolution and reformation of the collagen fibers during the scar remodeling phase. This phase starts at about the 15th day, and by 28 days, most of the fibroblasts and collagen between the tendon stumps are oriented longitudinally. Collagenase is present in the wound on the second day after injury. Between 4 and 6 weeks, collagen synthesis and collagen degradation reach equilibrium. Collagen maturation and remodeling begin in the third week and can continue for 1 year after injury.275,276 The strength of the tendon repair results from the organization of collagen fibrils at the bone site; these fibrils cross-link with each other and with those of the tendon on each side of the wound.

Biomechanics of Tendon Healing A classic experimental study using the extensor carpi radialis and flexor carpi ulnaris tendons in dogs showed that tensile strength progressed through three phases parallel with the phases of healing: (1) rapid decrease in tensile strength as a result of wound edema, which lasts about 5 days, during which tensile strength depends primarily on the suture; (2) increase in tensile strength, reaching a plateau on about the 16th day; and (3) second increase in tensile strength, beginning between 19 and 21 days and continuing for an undetermined period (length of study was 72 days). The mechanical strength of the healing tendon was related closely to the three histologic phases of the healing process: (1) exudation and fibrous union; (2) fibroplasia; and (3) maturation, organization, and differentiation. Function and motion during the first two phases of healing appeared to increase cellular reaction and separation at the suture lines. Active, unprotected use even after 3 weeks of immobilization may be associated with stretching of the suture line and always leads to an increased cellular response. On the basis of this work, clinicians for the next 40 years immobilized patients with injured tendons until the third phase of the healing process, when range of motion was encouraged to stimulate increased tendon strength and gliding. The strength of an injured tendon that has been sutured properly increases rapidly during the fibroplastic phase, when granulation tissue is produced to repair the defect. Quantitative changes in acid mucopolysaccharides (hydroxyproline and hexosamine) accompany collagen production, and the ratio of wound collagen to mucopolysaccharide content is a direct measure of increasing tensile strength. The strength of the healing tendon increases as the collagen becomes stabilized by cross-links and the fibrils assemble into fibers. A study of rotator cuff repair in sheep showed that the stiffness of the repair construct

uring this stage can be improved by augmenting the d repair with a collagen patch (swine small intestine submucosa), although the patch had no effect on load to failure277 (the long-term effect of xenograft collagen patches on the rate and quality of healing in rotator cuff repair remains uncertain278). During the maturation phase, the mechanical strength of healing tendon increases owing to remodeling and reorganization of the fiber architecture. A gradual shift of collagen production from type III to type I may contribute to increased mechanical strength. Bioscaffolds, in particular porcine small intestinal submucosa (SIS), have also been applied to enhance patellar tendon (PT) healing in rabbits following the harvest of the central third of the PT for anterior cruciate ligament reconstruction.279 A layer of SIS was applied both anterior and posterior to the defect to act as a biologic agent to enhance healing, not as a structural replacement. After 12 weeks of healing, the PT defect filled with more healing neo-PT tissue following SIS treatment than those without treatment, as the cross-sectional area was 68% greater. SIS treatment also resulted in a 57% higher stiffness and a 70% greater ultimate load of the healing central bonepatella tendon-bone (�� BPTB) �� complex compared to without treatment. These results demonstrated the potential of SIS treatment to increase the quantity of healing PT tissue and structural properties of the healing central BPTB complex.

Factors Affecting Healing Active Mobilization Active mobilization in the immediate postoperative period may have a deleterious effect on tendon healing. Early active mobilization ( .91

In order to conduct a study with a power of .80, approximately 10 subjects should be included in each group. (See table at the end of this appendix.) d. Using the effect size and table, find the row that corresponds to n for each group. Then find the power of this study. Power = .83 based on each group containing approximately 10 subjects. Power of t-test of m1 = m2 at a1 = .05 d n

de

.10

.20

.30

.40

.50

.60

.70

.80

1.00

1.20

1.40

8 9 10 11 12 13 14 15 16

.88 .82 .78 .74 .70 .67 .64 .62 .60

07 07 08 08 08 08 08 08 09

10 11 11 12 12 13 13 13 14

13 15 16 17 18 18 19 20 21

19 20 22 23 25 26 27 28 30

25 27 29 31 33 34 36 38 40

31 34 36 39 41 44 46 48 51

38 41 45 48 51 54 57 59 62

46 50 53 57 60 63 66 69 72

61 66 70 74 77 80 83 85 87

74 79 83 86 89 91 93 94 95

85 88 91 94 96 97 98 98 99 Continued


Power of t-test of m1 = m2 at a1 = .05—cont’d d n

de

.10

.20

.30

.40

.50

.60

.70

.80

1.00

1.20

1.40

17 18 19 20 21

.58 .56 .55 .53 .52

09 09 09 09 09

14 15 15 15 16

22 22 23 24 25

31 32 33 34 36

42 43 45 46 48

53 55 57 59 60

64 66 68 70 72

74 76 78 80 82

89 90 92 93 94

96 97 98 98 99

99 99 *

22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 42 44 46 48 50 52 54 56 58 60 64 68 72 76 80 84 88 92 96 100 120 140 160 180 200 250 300 350 400 450 500 600 700 800 900 1000

.51 .50 .48 .47 .46 .46 .45 .44 .43 .42 .42 .41 .40 .40 .39 .39 .38 .38 .37 .36 .35 .35 .34 .33 .33 .32 .31 .31 .30 .29 .28 .28 .27 .26 .26 .25 .24 .24 .23 .21 .20 .18 .17 .16 .15 .13 .12 .12 .11 .10 .10 .09 .08 .08 .07

09 10 10 10 10 10 10 10 10 10 11 11 11 11 11 11 11 11 11 12 12 12 12 12 13 13 13 13 13 14 14 15 15 15 16 16 17 17 17 19 21 23 24 26 30 34 37 41 44 47 53 59 64 68 72

16 16 17 17 18 18 18 19 19 19 20 20 20 21 21 21 22 22 22 23 24 24 25 26 26 27 28 28 29 30 31 33 34 35 36 37 38 40 41 46 51 56 60 64 72 79 84 88 91 93 97 98 99 *

26 26 27 28 28 29 30 30 31 32 33 33 34 34 35 36 36 37 38 39 40 41 43 44 45 46 47 49 50 52 54 56 58 60 61 63 65 66 68 75 80 85 88 91 96 98 99 *

37 38 39 40 41 42 43 44 46 47 48 49 50 50 51 52 53 54 55 57 59 60 62 63 65 66 68 69 70 73 75 77 79 81 82 84 85 87 88 93 95 97 98 99 *

50 51 53 54 55 57 58 59 61 62 63 64 66 67 68 69 70 71 72 74 75 77 79 80 81 83 84 85 86 88 90 91 92 93 94 95 96 96 97 99 99 *

62 64 66 67 69 70 72 73 74 76 77 78 79 80 81 82 83 84 84 86 87 89 90 91 92 93 93 94 95 96 97 97 98 98 99 99 99 99 *

74 76 77 79 80 82 83 84 85 86 87 88 89 89 90 91 91 92 93 94 95 95 96 97 97 98 98 98 98 99 99 99 *

83 85 86 88 89 90 90 91 92 93 93 94 95 95 96 96 96 97 97 98 98 99 99 99 99 99 99 *

95 96 96 97 97 98 98 98 99 99 99 99 99 99 99 *

99 99 99 99 *

*

*

*Power values below this point are greater than .995. From Cohen J: Statistical Power Analysis for the Behavioral Sciences, 2nd ed. Hillsdale, NJ, Lawrence Erlbaum Associates, 1988.

*

117

118


A P P E N D I X

1 C - 2

Comparison of Pearson’s Product-Moment Correlation and Intraclass Correlation Coefficient for Data with Systematic Error

Time

Time

Time

Time

Data

1

2

3

4

1 2 3 4 5 6 7 8 9 10

30 32 34 35 38 40 42 44 46 48

29 31 34 35 39 41 43 45 46 48

30 32 34 35 38 40 42 44 46 48

130 132 134 135 138 140 142 144 146 148

Analysis of Variance Summary Table for Time 1 and Time 2*

Betweensubjects effect Error Time (T1 & T2) Error

SS

DF

MS

F

Sig of F

30420.00

1

30420.0

377.63

.00

725.00 .20

9 1

80.56 ← BMS .20 ← TMS

2.80

9

.31 ← EMS

.64

.443

*The analysis of variance table is used for calculating the Intraclass Correlation Coefficient. DF, degrees of freedom; F, F value; Sig of F, significance of F value; MS, mean square; SS, sums of squares. ICC for Time 1 and Time 2: Between mean square (BMS) = 80.56 Error mean square (EMS) = .31 Trial mean square (TMS) = .20 Mean (X) = 39 Standard deviation (S) = 6.033 k = No. of examiners BMS - EMS ICC (2.1) = BMS + (k - 1) EMS + k[TMS - EMS/N] 80.56 - .31 = 80.56 + (1) .31 + 2[.20 - .31/10] 80.56 .31 = 80.56 + .31 + ( - .022) = .9926 Standard error of measurement (SEM) SEM = s 1 - r = 6.033 1- .9926 = .52

Analysis of Variance Summary Table for Time 3 and Time 4* SS Betweensubjects effect Error Time (T3 & T4) Error

DF

MS

F

Sig of F

158064.0 1

158064.0

2111.276

.000

673.80 9 50000.00 1

74.867 ← BMS 50000.067 ← TMS

.00

.00 ← EMS

9

*The analysis of variance table is used for calculating the Intraclass Correlation Coefficient. Abbreviations defined in summary table for times 1 and 2. ICC for Time 3 and Time 4: Between mean square (BMS) = 74.87 Error mean square (EMS) = .00 Trial mean square (TMS) = 5000 Mean (X) = 88.9 Standard deviation (S) = 50.33 BMS - EMS ICC (2.1) = BMS = (k - 1)EMS + k[TMS - EMS/N] 74.87 - .00 = 74.87 + (1) .00 + 2[50000 - .00/10] 74.87 - .00 = 74.87 + .00 + 1000 = .00743 Standard error of measurement (SEM) SEM = S 1 - r = 50.33 1 - .00743 = 49.95


Pearson’s Product-Moment Correlation for Time 1 and Time 2 Data

T1

T2

X2

Y2

XY

1 2 3 4 5 6 7 8 9 10

30 32 34 35 38 40 42 44 46 48

29 31 34 35 39 41 43 45 46 48

900 1024 1156 1225 1444 1600 1764 1936 2116 2304

841 961 1156 1225 1521 1681 1849 2025 2116 2304

870 992 1156 1225 1482 1640 1806 1980 2116 2304

∑X = 38.9 �� ∑Y = 39.1�� ∑X = 15469�� ∑Y = 15679�� ∑XY = 15571 s = 5.8 s = 6.2 N = No. of pairs df = N - 2 = 8 Critical r at the .05 level = .6319 Note: Data indicate that with an r of .6319 or higher, there is a less than 5 out of 100 chance that the null hypothesis would be rejected incorrectly. NSXY - ( SX) ( SY) r = NSX 2 - ( SX)2 ´ NSY 2 - ( SY)2

Pearson’s Product-Moment Correlation for Time 3 and Time 4: Determination of r When There Was a Systematic Change upon Retest 1 2 3 4 5 6 7 8 9 10

T3

T4

X2

Y2

XY

30 32 34 35 38 40 42 44 46 48

130 132 134 135 138 140 142 144 146 148

900 1024 1156 1225 1444 1600 1764 1936 2116 2304

16900 17424 17956 18225 19044 19600 20164 20736 21316 21904

3900 4224 4556 4725 5244 5600 5964 6336 6716 7104

∑X = 38.9 ��∑Y = 138.9 ��∑X2 = 15469 ��∑Y2 = 193269 ��∑XY = 54369 ��s = 5.8 ��s = 5.8 r= =

NSXY NSX 2 - ( SX )2

- ( SX )( SY ) ´

NSY 2 - ( SY )2

(10 ) 54369 - (38.9)(138.9 ) 10(15469 ) - ( 38.9 )2

´

10(193269 ) - (138.9 )

=

10(15571) - (38.9) (39.1) 10(15469) - (38.9)2 ´ 10(15679) - (39.1)2

543690 - 5403.21 = 154690 - 1513.21 ´ 1932690 - 19293.21

=

155710 - 1520.99 154690 - 1513.21 ´ 156790 - 1528.81

=

=

154189.01 153176.79 ´ 155261.19

=

=

154189.01 (391.3) ´ (394.03)

=

154189.01 154183.939

= 1.00

119

538286.79 153176.79 ´ 1913396.79

538286.79 541267.28 = .994

C H A P T E R�

�2

Surgical Principles S ect i o n

A

Basic Arthroscopic Principles Mark D. Miller and Jennifer Hart

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

OPERATIVE SUITE Arthroscopy is performed most commonly in a standard surgical suite in either a hospital or an ambulatory surgical facility. Office arthroscopy, although advocated by some, may have significant limitations and is used primarily for

diagnosis in selected patients. Newer flexible fiberoptic catheter systems resulted in under-recognition and underestimation of the severity of intra-articular knee disease in one study.2 A relatively large room that can accommodate the bulky arthroscopic equipment is preferred. Storage space for video equipment, shaver blades, instruments, and other equipment should be available in the room or nearby. Dedicated, well-trained operating room personnel are required. Adequate electrical support, lighting, suction, and other logistic concerns should be considered. Equipment sterilization is important. Standard autoclaving is not appropriate for arthroscopes, cables, and many of the instruments used in arthroscopy. Gas sterilization with ethylene oxide is effective, but because of the long turnover times associated with this method, instruments cannot be reused during the same operative day.3 Because of these concerns, most centers have elected to accept high-level disinfection in lieu of sterilization. A newer system that uses peracetic acid (Steris, Menor, Ohio) is convenient and efficacious, and it largely has replaced other methods of sterilization.4

ARTHROSCOPIC EQUIPMENT Arthroscopy requires an arthroscope, a camera, a light source and fiberoptic cable, an irrigation system, cannulas, and various hand and motorized instruments. An arthroscope is a small-diameter fiberoptic instrument that allows direct visualization of joints (Fig. 2A-1).5 It is designed to fit into a sleeve, or cannula. The cannula first is inserted into the joint with a sharp or blunt rod called a trocar, and the trocar is then exchanged for the arthroscope. A fiberoptic cable and camera are attached to the arthroscope, and irrigation fluid is attached to one or more cannulas. A specially adapted video camera usually is attached to the eyepiece of the arthroscope, and images can be recorded directly onto video or onto an accompanying printer (Fig. 2A-2). Arthroscopes are classified according to their diameter and viewing angle. The most commonly used arthroscope is 4 mm with a 25- to 30-degree angle. Smaller arthroscopes 121

122

DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine ��

Figure 2A-1 Top to bottom: Thirty-degree arthroscope with attached cable, 70-degree detached arthroscope, detachable camera cable (left) and sleeve (cannula) (right), trocar for introduction of sleeve, and 30-degree detached arthroscope. (From DiGiovine NM, Bradley JP: Arthroscopic equipment and setup. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 543-556.)

(2.5 and 1.9 mm) can be used for smaller joints (e.g., wrist). Different angles (70 or 90 degrees) sometimes are useful when visualization can be difficult (e.g., posterior knee). Instruments used during arthroscopy include those that are hand operated (e.g., probes, baskets, grabbers) and those that are motorized (e.g., shavers) (Fig. 2A-3). Commercially available shavers of various sizes, shapes, angles, and blades are useful in a variety of situations (Fig. 2A-4). Intra-articular cautery can be useful, and specially adapted tips that can be used with normal irrigating systems are available. Other available systems include special heat probes and lasers. Irrigation is used during arthroscopy for joint distention, improved visualization, and removal of debris. Lactated Ringer’s solution usually is used because it is more physiologic than normal saline.6 A study has suggested, however, that 5% mannitol may prevent excessive loss of proteoglycan from hyaline cartilage.7 Cannulas are used for fluid egress or ingress. Hydrostatic pressure is necessary to maintain joint distention. This pressure can be attained by gravity or through commercially available pumps (Fig. 2A-5).

ARTHROSCOPIC VISUALIZATION One must understand several fundamental concepts to interpret arthroscopic images accurately. First, the typical arthroscope does not look straight ahead but instead is directed at a 25- to 30-degree angle off the axis.8 This angle allows greater visual control and improves the field. The arthroscopist can keep the arthroscope stationary and rotate the viewing angle, allowing a 60-degree view from a 30-degree scope (Fig. 2A-6). Another consideration is that an object’s size as seen on the monitor is magnified. The degree of magnification varies with the distance of the object from the lens of the arthroscope. Judging distances and size requires practice. Knowing the dimensions of an instrument, such as an arthroscopic probe, helps in determining the relative size

Figure 2A-2 Top to bottom: Arthroscopic cart showing camera, light source with cable, video equipment, and printer. A monitor (not shown) can be placed on top of the cart. (From DiGiovine NM, Bradley JP: Arthroscopic equipment and setup. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 543-556.)

of the object being visualized. It is helpful to know about normal versus abnormal findings in each joint.

ARTHROSCOPIC TECHNIQUE Extreme care should be taken in positioning the extremity for arthroscopy to avoid any compression that can result in neurapraxia. The nonoperative side is padded and protected, and excessive traction or unnecessary motion of the operative extremity is avoided. Numerous positioning and traction devices are commercially available and are often helpful. Tourniquets, when used, should be as wide as possible, and tourniquet time should be minimized. Surgical preparation and draping should be performed carefully to seal the operative field and to create a sterile environment. A joint-specific systematic diagnostic examination should be done before any therapeutic procedures are performed. A complete arthroscopic examination usually can be performed in a few minutes, and then a complete operative plan can be confirmed or modified according to these findings.

ARTHROSCOPIC COMPLICATIONS Any operation carries a risk for complications, and arthroscopy is no exception.9 Perhaps the most common complication is inadvertent damage to the intra-articular

Surgical Principles

Figure 2A-3 Probes (top two instruments) and baskets (bottom three instruments) come in a variety of sizes and angles. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

123

Figure 2A-5 Commercially available arthroscopy pump allows precise control of flow rate and hydrostatic pressure. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

structures.10 This risk is inversely proportional to the surgeon’s experience and the care with which the surgeon performs the procedure. Proper portal placement, gentle technique, and attention to detail are crucial. The exact prevalence and long-term sequelae of this lesion are unknown, but studies involving second-look arthroscopy and animal models have shown that this is a true risk and that the lesions do not tend to fill with time.11,12 Certain joints such as the hip are at increased risk for iatrogenic cartilage injury, and techniques of portal placement and traction have been described to help decrease the risk in this joint.13 Instruments can break, especially when older, unserviced instruments are used.14 Nerve or vessel injury can result from improper portal placement. A thorough knowledge of local anatomy is needed before performing arthroscopy. In joints at particular risk (e.g., the elbow), the nick and spread method is preferred. The skin only is cut with a blade, and a small hemostat is used to clear the way before inserting instruments with this method. Tourniquet

paresis can be reduced with a wide cuff and by limiting tourniquet time to less than 90 minutes whenever possible.15 Positioning devices (e.g., leg holders) can have a tourniquet effect, even when the tourniquet is not inflated. Fluid extravasation has been reported,16 although the incidence of this complication can be reduced with careful placement of inflow cannulas and proper use of inflow pumps. Synovial fistula formation is a rare complication of arthroscopy and is usually remedied by 7 to 10 days of immobilization and, occasionally, delayed closure. Infection is an extremely rare complication of arthroscopy, usually the result of a break in sterile technique.17 High-dose antibiotics and arthroscopic irrigation and débridement may be indicated in severe cases.18 An unusual, but potentially life-threatening, complication of knee arthroscopy is the development of a postoperative deep vein thrombosis (DVT) or pulmonary embolism (PE). Although the risk for these events is low, careful screening of risk factors must be done to identify patients who require routine prophylaxis. These risk factors include things such as increased body mass index (BMI), personal or family history of clotting disorder, advancing age, and

Figure 2A-4 Arthroscopic shavers come in a variety of sizes, angles, and blades. (From Ciccotti MG, Shields CL, El Attrache N: Meniscectomy. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 591-613.)

Figure 2A-6 Rotation of a 30-degree arthroscope allows a 60-degree view. (From Crane L, Sullivan DJ: Instrumentation. In McGinty JB [ed]: Operative Arthroscopy. New York, Raven Press, 1991, p 6.)

124


Box 2A-1 Relative Risk Factors for Postoperative Deep Venous Thrombosis or Pulmonary Embolism in Knee Arthroscopy One-Point Factors Age 40-59 yr Surgery shorter than 45 min Body mass index > 25 kg/m2 Pregnant or 1 mo postpartum Chronic obstructive pulmonary disease Varicose veins Inflammatory bowel disease Preoperative bed rest Two-Point Factors Age 60-70 yr History of malignancy in past Surgery longer than 45 min Postoperative immobilization > 72 hr Three-Point Factors Age 70-75 yr Personal or family history of clot Factor V Leiden deficiency Thrombophilia Five-Point Factors Hip, pelvis, or leg fracture Multiple trauma History of stroke Limb paralysis

history of malignancy. We use the system described in Box 2A-1 to identify patients who need prophylactic treatment for thromboembolic events. Any patient with more than three points as defined by these guidelines is considered to be at increased risk and should be treated.19,20

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

Knee Arthroscopy Indications Arthroscopy has diverse application in various forms of knee disease. Diagnostic arthroscopy helps to confirm suspected knee injuries. Arthroscopic synovectomy can be useful for synovial biopsies to aid the diagnosis of rheumatologic

Figure 2A-7 Arthroscopic positioning with a commercially available leg holder for the operative leg and a well-padded gynecologic leg holder for the nonoperative extremity. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 50.)

isorders, to remove diseased synovium, and to resect d synovial folds or plicae. A six-portal technique is favored for complete synovectomy. Treatment of meniscal disease is perhaps the most common application of arthroscopy. Meniscal tears account for about half of knee injuries that require surgery.21 Osteochondral lesions commonly are addressed arthroscopically. Injuries to the cruciate ligaments can be diagnosed easily with arthroscopy; endoscopic reconstruction of these ligaments is one of the most common orthopaedic procedures. Other procedures that sometimes are aided with arthroscopy include tibial plateau fracture reduction, reduction and fixation of tibial eminence fractures, loose body removal, anterior fat pad débridement, lateral release for patellar malalignment, and irrigation and débridement of septic arthritis.

Positioning and Portal Placement Two different forms of positioning are commonly used for knee arthroscopy. The patient can be placed supine on the operating table, and a lateral post can be used for countertraction. Alternatively, the operative leg can be positioned in a commercially available leg holder (Fig. 2A-7). The operative leg is allowed to hang freely over the end of the operating table, and the opposite leg is positioned in a well-padded leg holder, with care taken not to compress the peroneal nerve. Standard arthroscopic portals for knee arthroscopy have traditionally included a superomedial or superolateral

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Patella

PSM SL

Trochlea

SM

PM PL FM FL

PCL ACL

IM

MP IL Figure 2A-9 Normal arthroscopic anatomy of the knee. (Inset shows posteromedial aspect of the knee as seen through the notch.) ACL, anterior cruciate ligament; PCL, posterior cruciate ligament. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 51.) Figure 2A-8 Arthroscopic portals for knee arthroscopy. FL, far lateral; FM, far medial; IL, inferolateral; IM, inferomedial; MP, midpatellar; PL, posterolateral; PM, posteromedial; PSM, proximal superomedial; SL, superolateral; SM, superomedial. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 50.)

ortal for fluid inflow and outflow and inferomedial and p inferolateral portals positioned just above the joint line on both sides of the patellar tendon for arthroscopy and instrumentation (Fig. 2A-8). Newer arthroscopic fluid control systems have now made the use of superior portals optional. The use of a far proximal superior portal can still be helpful for visualization of patellar tracking. The inferolateral portal usually is used during diagnostic arthroscopy. Accessory portals for the knee include the posteromedial, posterolateral, far medial and lateral, and proximal superomedial portals. The posteromedial portal is often helpful for visualizing the posterior cruciate ligament22 and the posterior horn of the medial meniscus.23 The posterolateral portal, located between the iliotibial band and the biceps tendon, sometimes is helpful, but extreme care should be taken to ensure that the portal is anterior to the biceps tendon to avoid injury to the peroneal nerve. Other portals include the midpatellar portal; far medial and lateral portals (sometimes helpful for instrument placement in hard to reach areas); and the proximal superomedial portal, located 4 cm proximal to and in line with the medial edge of the patella (for assessment of patellar tracking).

Arthroscopic Anatomy As with any joint, systematic examination of the knee is appropriate. Before positioning the patient, a complete examination under anesthesia is conducted to assess

instability in all planes. An arthroscopic cannula is placed in the superomedial or superolateral portal for inflow and outflow (although the use of these superior portals is now optional with many of the new pump systems), and the arthroscope is introduced into the inferolateral portal. Although many examination sequences are possible, it is important to visualize the suprapatellar pouch, patellofemoral joint, medial and lateral gutters, medial and lateral compartments (meniscus and articular cartilage), and intercondylar notch (cruciate ligaments) in all patients. Accessory viewing portals are established as necessary if other areas need to be evaluated. A posteromedial portal can be helpful whenever medial meniscus pathology is suspected but is unable to be identified from the anterior portals. This portal is established by introducing the arthroscopic cannula into the back of the knee by directing it from anterior to posterior on the notch side of the medial femoral condyle. Care must be taken to avoid the saphenous nerve and vein while using the spinal needle to establish the portal. Once the arthroscope is in the posterior aspect of the knee, the posterior horn of the medial meniscus can be visualized. A 70-degree scope may be helpful. After a complete evaluation of the joint (Fig. 2A-9), all surgical pathology is addressed.

Hip Arthroscopy Indications The indications for hip arthroscopy are more limited than for other joints. Because of its anatomy, the hip joint is difficult to access through arthroscopy, and maneuverability is difficult. Arthroscopy may be indicated for cases of loose bodies, torn labral tissue, articular cartilage lesions, synovial or ligamentum teres impingement, and refractory pain of undetermined cause. Arthroscopy can be used in

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young arthritic patients to delay the need for total joint arthroplasty.24 A more recent indication for hip arthroscopy includes the treatment of internal and external snapping hip. Results have proved perhaps even superior to the more traditional open techniques of lengthening Z-plasty and iliopsoas tendon release.25,26 Benefits again include shorter operation times and recovery periods with fewer surgical complications, with the added benefit of allowing the arthroscopist to evaluate for the presence of intra-articular pathology at the same time.

Positioning and Portal Placement Two positions are popular for hip arthroscopy: the supine and the lateral decubitus positions. The latter, developed by Glick and colleagues27 after their initial dissatisfaction with the supine position, is performed with the patient on his or her side, with the involved hip on top. The patient is placed in the lateral decubitus position on a fracture table with a peroneal post, and traction is applied through the footplate, skeletal traction, or a commercially available external traction device. The leg is abducted 45 degrees and forward-flexed 10 degrees.27 About 50 pounds of traction is necessary to distract the hip 8 to 10 mm for arthroscopic visualization.24 The supine position was reintroduced by Byrd,28 who also used a fracture table. A padded peroneal post is lateralized to the operative side, the hip is positioned in extension and 25 degrees of abduction, and traction is applied. Fluoroscopy is recommended for either position to confirm entry into the joint. Portals are similar for both positions and include the anterior, anterolateral (anterior trochanteric), and posterolateral (posterior trochanteric) portals (Fig. 2A-10). The anterior portal is established at the intersection of a sagittal line drawn distally from the anterosuperior iliac

spine and a transverse line across the superior margin of the greater trochanter. The arthroscope can be inserted into this portal in a direction 45 degrees cephalad and 30 degrees toward the midline. Although this portal places the lateral femoral cutaneous nerve at risk, studies show that the nerve, which arborizes before this point, lies lateral to this portal.29 The other two portals are established at the anterior and posterior margins of the superior edge of the greater trochanter. These portals lie about 4 cm below the superior gluteal nerve, and the posterolateral portal is about 3 cm superior to the sciatic nerve.29 The surgical approach to the iliotibial band for the treatment of snapping hip is made with laterally based portals to access the superficial aspect of the band. The iliopsoas tendon can be released either from the lesser trochanter or accessed from the peripheral compartment.30 Special extra-long cannulas and sheaths (5.25 inches) have been developed for hip arthroscopy. Surgical instruments and the arthroscope can be exchanged easily with these cannulas. Cannulated trocars are commercially available to allow insertion over a guidewire that can be introduced through a large-diameter spinal needle, which facilitates portal placement.

Arthroscopic Anatomy Most of the hip joint can be visualized with the arthroscope (Fig. 2A-11).31 Eighty percent or more of the femoral head can be seen, and the insertion of the ligamentum teres into the anteromedial portion of the femoral head is a readily identifiable landmark. The acetabulum is well visualized with the horseshoe-shaped, lunate surface of the acetabulum that extends to the peripheral labrum and central acetabular fossa. The acetabular fossa extends inferiorly and is filled with vascular adipose tissue extending to the transverse ligament. Viewing the joint through different portals helps evaluate all forms of hip disease.

AL

AW

L

FH

LT

FH

PW PL

Figure 2A-10 Portals for hip arthroscopy include the anterior portal and two portals adjacent to the superior edge of the greater trochanter. (From Miller MD, Cooper DE, Warner JJP: Review of Sports Medicine and Arthroscopy. Philadelphia, WB Saunders, 1995.)

Figure 2A-11 Arthroscopic anatomy of the hip. AL, anterior labrum; AW, wall of acetabulum; FH, femoral head; L, labrum; LT, ligamentum teres; PL, posterior labrum; PW, posterior wall. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRIArthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 101.)

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risk, the anterocentral (dorsalis pedis artery and deep peroneal nerve) and posteromedial (posterior tibial artery and tibial nerve) portals usually are not recommended.

Ankle Arthroscopy Indications The most accepted indication for ankle arthroscopy is removal of loose bodies. This situation is uncommon but may be a result of osteochondritis dissecans or traumatic osteochondral injuries. These lesions can be débrided or repaired with arthroscopic techniques. Synovial or osteophytic impingement is perhaps the most common indication for ankle arthroscopy.32-34 Another procedure that is gaining acceptance is arthroscopically assisted tibiotalar arthrodesis.35 Other relative indications for ankle arthroscopy include adjunctive treatment of fractures, stabilization procedures, and synovectomy for rheumatologic conditions.

Arthroscopic Anatomy

Positioning and Portal Placement

Indications for shoulder arthroscopy are evolving, but there are proponents and opponents for each proposed application, and the controversy continues. Shoulder arthroscopy has been applied to the diagnosis and treatment of shoulder instability, impingement syndrome, distal clavicle problems, rotator cuff disease, inflammatory and degenerative diseases of the shoulder, adhesive capsulitis, sepsis, and other diagnoses. Arthroscopy has been advocated for débridement of loose tissue and washout of degenerative arthritis,38 treatment of adhesive capsulitis,39,40 irrigation and débridement of septic joints,41 removal of foreign bodies, and a variety of other procedures.

Most surgeons perform ankle arthroscopy with the patient supine. Several commercially available ankle distracters are available and provide enough distraction for adequate visualization. Alternatively, the patient’s knee and leg can be positioned over the end of the operating table, and a gauze bandage loop can be fashioned as the surgeon’s foot provides a distraction force.36 The standard 4.0-mm arthroscope can be used for most procedures, although small arthroscopes (2.7 mm) may be helpful for areas that are more difficult to visualize (e.g., the posterior ankle). A 3.5-mm-diameter shaver is often helpful for ankle arthroscopy. The most commonly used portals are the anteromedial and anterolateral portals.37 The anteromedial portal is placed just medial to the tibialis anterior tendon at the level of the ankle joint. A spinal needle helps to localize this site and instill saline into the joint. The anterolateral portal is established just lateral to the peroneus tertius tendon at the joint line level (Fig. 2A-12). The nick and spread technique helps to establish these portals to ensure that superficial nerves and veins are avoided. A posterolateral portal, placed just lateral to the Achilles tendon, can be used for outflow or occasionally to visualize the posterior ankle. A 70-degree arthroscope placed through an anterior portal usually provides adequate visualization of the posterior ankle, however. Because of the significant neurovascular

Anterolateral

Anteromedial

The anterolateral portal is used most commonly for visualization. The joint should be evaluated systematically (Fig. 2A-13). The lateral sulcus and tip of the fibula usually can be visualized. The medial sulcus and tip of the medial malleolus is best seen with the arthroscope placed in the anteromedial portal. Pathology is addressed as necessary.

Shoulder Arthroscopy Indications

Positioning and Portal Placement Two methods of positioning are popular: the lateral decubitus position and the beach-chair position (Fig. 2A-14). The lateral decubitus position involves placement of the patient with the affected arm up; traction is used to suspend the arm. Transient neurapraxia can be a common problem with this positioning.42 Other disadvantages of this position are that regional anesthesia is poorly tolerated, conversion to an open procedure is difficult, the capsular anatomy is distorted, and arm positioning can be more

Posterolateral

Figure 2A-12 Portals for ankle arthroscopy are anteromedial, anterolateral, and posterolateral. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 134.)

Figure 2A-13 Arthroscopic anatomy of the ankle. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 134.)

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Figure 2A-14 Lateral decubitus and beach-chair positioning for shoulder arthroscopy. (From Miller MD, Chhabra A, Hurwitz S, et al: Orthopaedic Surgical Approaches. Philadelphia, Saunders, 2008.)

ifficult.43 Because of these problems, the beach-chair posid tion was developed by Warner.44 This positioning allows easy access for arthroscopy without the disadvantages of other positions. The most commonly used arthroscopic shoulder portals are the posterior, anterosuperior, anteroinferior, and lateral portals. The superior, or Neviaser, portal and the posterolateral portal (of Wilmington) are used by some surgeons as accessory portals (Fig. 2A-15). The posterior portal, placed 2 cm medial and 2 to 3 cm inferior to the

Arthroscopic Anatomy

5 2 1

posterolateral corner of the acromion, is used primarily for arthroscopic visualization. The anterosuperior portal, located lateral to the coracoid and just distal to the anterior edge of the acromion, is used most commonly for instrumentation. The anteroinferior portal, located about 2 cm below the anterosuperior portal just above the subscapularis tendon (visualized arthroscopically), is used primarily for arthroscopic Bankart repair. The lateral portal is used for instrumentation during bursoscopy. The superior (or supraspinatus or Neviaser) portal is located at the corner of the supraspinatus fossa and is oriented slightly anteriorly and laterally. This portal is used for visualization of the anterior glenoid and may be helpful in addressing superior labral and biceps injuries. The posterolateral portal (port of Wilmington) is used most commonly for superior labral repairs.

4

3

Clavicle 5

1

Acromion

2

3

Coracoid 4 Figure 2A-15 Arthroscopic portals for shoulder arthroscopy. 1, Posterior; 2, anterosuperior; 3, anteroinferior; 4, lateral; 5, superior or Neviaser portal. (From Miller MD, Cooper DE, Warner JJP: Review of Sports Medicine and Arthroscopy. Philadelphia, WB Saunders, 1995.)

Although many sequences are recommended for arthro scopic evaluation of the shoulder, it is important to visualize and palpate the biceps tendon, labrum, glenohumeral articular surfaces, glenohumeral ligaments, and rotator cuff at a minimum (Fig. 2A-16). During bursoscopy, the superior surface of the rotator cuff, the inferior acromion, and the acromioclavicular joint should be evaluated. The interface of the biceps tendon and superior labrum most commonly is visualized first to allow the surgeon to become oriented; the surgeon can then address the possibility of a superior labral anterior-to-posterior lesion (SLAP). The labrum is inspected and probed to detect any labral injury (Bankart tear), especially in a patient with anterior instability. Separation of the superior labrum from the glenoid may be normal.45 The articular surfaces of the glenoid and humerus are examined for any articular injuries or degenerative joint disease. By rotating the arm, one can visualize most of the proximal humerus. With the arthroscope positioned posterior and inferior to the superior surface of the glenoid,

Surgical Principles

129

Direct posterior Proximal medial Posterolateral Anteromedial

Proximal lateral Anterolateral

Figure 2A-16 Arthroscopic anatomy of the shoulder. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 160.)

internal rotation of the humerus allows visualization of a Hill-Sachs defect, or impression fracture, associated with anterior instability. The glenohumeral ligaments, which represent thickenings of the joint capsule, can then be evaluated. The superior glenohumeral ligament arises just anterior to the long head of the biceps tendon in the rotator interval (between the biceps and subscapularis). The middle glenohumeral ligament drapes over the subscapularis tendon. The inferior glenohumeral ligament complex is composed of two bands, anterior and posterior, and attaches to the inferior labrum. Arthroscopy of the inferior axillary pouch, the rotator cuff insertion (superiorly), and the subacromial bursa completes the examination.

Elbow Arthroscopy Indications Although the indications for elbow arthroscopy are evolving, it is a well-accepted technique for removal of loose bodies, irrigation of an infected joint, synovectomy, and osteophyte excision. Loose or foreign bodies can be removed easily from the joint using the contralateral portal.46-48 A septic joint can be irrigated with only two portals (proximal-medial and posterolateral).49 Osteophytes can be removed using arthroscopic burs and generous irrigation.50 Synovectomy can be accomplished through anterior and posterior portals and can provide considerable pain relief in patients with chronic synovitis.51 Other proposed procedures include arthroscopic capsular52 and radial head excision.49

Positioning and Portal Placement Elbow arthroscopy can be done with the patient supine53 or prone.54 The prone position, which is more popular, allows improved arthroscopic manipulation and better visualization without the use of an overhead suspension device.49

Figure 2A-17 Arthroscopic portals for elbow arthroscopy. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRIArthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 197.)

The soft spot, or anconeus triangle (defined by the lateral epicondyle, tip of the olecranon, and radial head) should be palpated, and 30 to 50 mL of fluid should be injected to distend the capsule before establishing arthroscopic portals. Three portals commonly are used for elbow arthroscopy: the proximal-medial, posterolateral, and anterolateral portals. A fourth portal, the direct posterior portal, can be established when posterior instrumentation is necessary. A final portal, the proximal-lateral portal, has been advocated for improved safety (Fig. 2A-17).55-57 The nick and spread method should be used when establishing all arthroscopic portals around the elbow because of the attendant neurovascular risk. The proximal-medial portal is the primary diagnostic arthroscopic portal with the patient in the prone position.49 This portal is located 2 cm proximal to the medial epicondyle, just anterior to the intermuscular septum. The arthroscopic sheath should contact the anterior surface of the humerus and is directed toward the radial head. The posterolateral portal is made in the anconeus triangle and can be used for inflow and outflow. The arthroscope can be introduced into this portal to allow visualization of the posterior joint. Some authors favor establishing this portal proximal and posterior to this location, 2 cm proximal to the tip of the olecranon and adjacent to the lateral edge of the triceps tendon. The anterolateral portal is established 3 cm distal and 2 cm anterior to the lateral epicondyle with the elbow flexed 90 degrees. The portal can be established with an inside-out technique using a blunt rod. The radial nerve is at risk with this portal and is immediately adjacent to the portal in 50% of cases.57 The direct posterior portal is

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made 2 cm proximal to the tip of the olecranon, through the triceps tendon, and is used primarily for instrumentation in the posterior joint. The proximal-lateral portal was developed to reduce the risk associated with other portals.56 It is located 1 to 2 cm proximal to the lateral epicondyle, directly on the anterior surface of the humerus. As with the proximalmedial portal, the trocar is kept in direct contact with the anterior humerus during insertion. The proximal-lateral portal has been advocated in lieu of the more hazardous anterolateral portal.58 The radial head and capitellum can be well visualized through this portal. The anteromedial portal, located 2 cm distal and 2 cm anterior to the medial epicondyle, can jeopardize the anterior branch of the medial antebrachial cutaneous nerve and the median nerve and usually is not recommended. The standard anterior portals used in elbow arthroscopy should be proximalmedial and proximal-lateral portals. The anteromedial and anterolateral portals, if necessary, should be established proximal to the radial head.

Arthroscopic Anatomy With the arthroscope placed in the proximal medial portal, the humeroulnar and radiocapitellar joints, the coronoid fossa, and the medial and lateral gutters can be well visualized (Fig. 2A-18). The posterior joint (olecranon and olecranon fossa) can be well visualized through the posterolateral portal.

Wrist Arthroscopy Indications Wrist arthroscopy is becoming increasingly useful in the diagnosis and treatment of wrist disorders. Treatment of injuries to the triangular fibrocartilage complex

(TFCC), treatment of ligament injuries, fracture management, and treatment of wrist disease are enhanced with arthroscopy. Type 1C volar rim tears of the TFCC that involve the origins of the ulnotriquetral and ulnolunate ligaments are managed with an open procedure after arthroscopic identification. The treatment of these injuries is controversial, but two good choices currently exist. Bednar and Osterman59 advocated direct repair augmented with a strip of the flexor carpi ulnaris tendon. The other option is to advance the origin of the ulnotriquetral and ulnolunate ligaments into the triquetrum with a bone anchor. Type 1D tears of the radial attachment of the TFCC by definition involve the dorsal radioulnar ligament or the volar radioulnar ligament, or both. Tears close to the radial attachment of the TFCC, which spare the dorsal radioulnar ligament and volar radioulnar ligament, are best considered type 1A tears and are treated with débridement. Arthroscopic reduction and fixation of intra-articular distal radius fracture is being employed more frequently. In the search for the most appropriate and beneficial treatment for this difficult injury, the arthroscope has some important potential advantages.52,58

Positioning and Portal Placement Wrist arthroscopy is performed with the patient supine. Wrist distraction (10 to 12 pounds) usually is achieved with a commercially available traction device. A small 1.9- to 2.7-mm arthroscope and small joint instruments with a maximal diameter of 3.0 mm are used. Arthroscopic portals around the wrist are designated based on their location in reference to the dorsal extensor compartments (Fig. 2A-19). The standard portals for any diagnostic wrist arthroscopy are the 3-4, the 4-5, and

STT MCR 1-2

MCU 6U 6R 4-5

1 6

Figure 2A-18 Arthroscopic anatomy of the elbow. (Inset, posterior view.) (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 198.)

5

4

3

3-4

2

Figure 2A-19 Arthroscopic wrist portals. Numbers indicate wrist extensor compartments and associated portals. MCR, midcarpal radial; MCU, midcarpal ulnar; R, radial; STT, scaphotrapeziotrapezoid; U, ulnar. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 220.)

Surgical Principles

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

Arthroscopic Anatomy A thorough and complete wrist arthroscopy details the anatomy of the articular surfaces, intrinsic carpal ligaments, extrinsic carpal ligaments, and TFCC (Fig. 2A-20). Proceeding from radial to ulnar in the radiocarpal joint, the following structures are observed: radial styloid, radioscaphocapitate ligament, long radioulnate ligament, scaphoid proximal pole, radius scaphoid facet, scapholunate interosseous ligament, radioscapholunate ligament (ligament of Testut), lunate proximal pole, radius lunate facet, short radiolunate ligament, TFCC (including the dorsal and volar radioulnar ligaments), ulnolunate ligament, ulnotriquetral ligament, lunatotriquetral interosseous ligament, and triquetrum proximal pole. Proceeding from radial to ulnar in the midcarpal joint, examination of the following structures is accomplished: STT, capitate proximal pole, scaphoid distal pole, scapholunate interval stability, lunate distal pole, lunatotriquetral interval stability, triquetrum distal pole, capitohamate interval, hamate proximal pole. The ligaments that cross the midcarpal joint often are difficult to visualize because of overlying synovium. If a midcarpal instability is suspected, visualization can be accomplished by débriding the synovium carefully. The ligaments in question include the radioscaphocapitate, ulnocapitate, triquetrocapitate, and triquetrohamate.

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

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Figure 2A-20 Arthroscopic wrist anatomy. (From Miller MD, Osborne JR, Warner JJP, Fu FH [eds]: MRI-Arthroscopy Correlative Atlas. Philadelphia, WB Saunders, 1997, p 221.)

C

r i t i c a l

P

o i n t s

• Appropriate diagnosis with physical examination and imaging studies remains of particular importance. • Arthroscopy has the advantage of less invasive surgical approach, shorter operative time, and potentially faster recovery. • Arthroscopic surgery is not without risk, and extreme caution should be used in patient selection, portal placement, and careful technique. • Indications for arthroscopic surgery are variable, depending on the joint, and are constantly evolving. • Arthroscopic techniques should never replace the surgeon’s ability to perform standard open approach surgical procedures.

S U G G E S T E D

R E A D I N G S

Coward DB: General principles and instrumentation of arthroscopic surgery. In Chapman MW (ed): Operative Orthopaedics. Philadelphia, JB Lippincott, 1988, pp 1549-1559. DiGiovine NM, Bradley JP: Arthroscopy equipment and setup. In Fu FH, Harner CD, Vince KG (eds): Knee Surgery. Baltimore, Williams & Wilkins, 1994. Jackson RW: Quovenis quovadis: Evolution of arthroscopy. Arthroscopy 15: 680-685, 1999. Johnson LL: Arthroscopic Surgery: Principles and Practice, 3rd ed. St. Louis, CV Mosby, 1986. Olsen EJ, King NA: Arthroscopic anatomy. In Fu FH, Harner CD, Vince KG (eds): Knee Surgery. Baltimore, Williams & Wilkins, 1994, pp 77-99.

R eferences Please see www.expertconsult.com

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S ect i o n

B

Suture Materials Marius von Knoch and Christian Gerber

Essentially, no orthopaedic procedure is carried out without the use of sutures. The selection of the type and size of the suture material is, however, often related to what a surgeon has learned empirically during training rather than to logical conclusions based on material properties and imposed demands. The role of the type and size of suture material and the surgical suturing technique in the development of fixation failure are not uniformly established. The technique of tying knots in combination with arthroscopic techniques has been given particular attention recently.1 It is established that the success of orthopaedic operations (e.g., tendon or ligament repairs) depends on the type of suture material used and the technique.2-9 Thus, a more precise analysis of the role of sutures and suturing techniques is needed to allow a more scientifically based selection of material and of suturing and knotting technique. Among the several forms in which surgical sutures are available today are braided, unbraided, absorbable, nonabsorbable, hybrid, polyblend, and sutures of different materials.10 This chapter aims to describe different types of sutures and discuss advantages of and indications for different forms.

IMPOSED DEMANDS ON SUTURE MATERIALS Different demands are imposed on surgical suture materials. Their importance or priority may change with the specific application of the suture material considered. A variety of mechanical, biomechanical, and biologic properties should be considered when a specific suture material is selected. Such properties include the following: 1. Biologic characteristics a. Biocompatibility b. Antimicrobial characteristics 2. Mechanical characteristics a. Ultimate tensile strength b. Elasticity and deformation under load (gap formation under tensile load) c. Abrasion resistance d. Adequate maintenance of mechanical properties during healing (absorbable sutures) e. Knotting properties (ease of knotting, loss of strength after tying knots, knot slippage, number of knots necessary for stability, knot prominence) 3. Handling characteristics a. Ease in practical use

BIOLOGIC CHARACTERISTICS AND BIOCOMPATIBILITY A number of studies have assessed the compatibility of different suture materials, either by means of semiquantitative analysis of the histologic foreign body reaction to the implanted material or by means of experimental or clinical testing of the healing properties of the sutured tissues.7,11-22 Biocompatibility depends on the type of suture material, its structure (braided versus monofilament), the amount of material implanted, and the site of implantation.23 Three principal phases of healing of soft tissues to bone have been identified in animal experiments: inflammation, repair, and remodeling.10 Each phase can be influenced by specific characteristics of the sutures used, and a rational choice leads to clinical success. The initial inflammatory reaction is characterized by the presence of polymorphonuclear cells, lymphocytes, and monocytes. This acute inflammatory foreign body reaction peaks between days 2 and 7. By day 4, mononuclear cells start to predominate, and fibroblasts appear. By day 7, mature fibroblasts are present; the foreign material becomes encapsulated in a fibrous mantle by day 10.23 At that point, no further tissue reaction is expected if the implanted material is nonabsorbable. Most currently used nonabsorbable materials are inert and are therefore extremely well tolerated. Absorbable materials elicit a “second” boost of inflammatory reaction at the time of their resorption. The intensity of this reaction depends on the specific chemical process that leads to resorption and on the amount of material to be resorbed. Previous reports of lytic response after implantation of PGA (polyglycolic acid) sutures have led to the use of less reactive polymers. A higher rate of material degradation has been associated with an increased cellular response.24 Among currently used degradable materials are PGA, PLLA (poly-l-lactic acid), PDS (polydioxanone), poly-D, PDLLA (l-lactic acid), and their copolymers.24 In general, a higher percentage of PLA is associated with slower resorption than with PGA.10 Suture materials such as polyglactin (Vicryl), polyglycolic acid (Dexon Plus), polyglyconate (Maxon), poliglecaprone 25 (Monocryl), polydioxanone (PDS), and poly(l-lactide/glycolide) (Panacryl) are absorbed by simple hydrolysis, whereas catgut requires enzymatic degradation, which tends to provoke a much more intense soft tissue reaction. Of the commonly used materials, monofilament stainless steel provokes the least amount of foreign body reaction in skin and other musculoskeletal tissues. Almost no foreign body reaction is seen after implantation of nylon,

Surgical Principles

polypropylene (Prolene), polyester (Ethibond, Tevdek, Ti-Cron), polybutester (Novofil), or absorbable materials (Maxon and PDS). Polyglycolic acid (Dexon Plus) and polyglactin (Vicryl), which are dissolved by simple hydrolysis, also elicit a minimal foreign body response but are probably tolerated somewhat less well than polydioxanone (PDS) and polyglyconate (Maxon).16,17,19,25 The tissue response may be more pronounced if these materials are used in the skin. Catgut and, at the time of its resorption, chromic catgut cause a moderate to intense inflammatory response.14,26 Silk, which used to be the standard material for skin closure, is probably the least well tolerated of all materials still in use, and its application experimentally has been proved to compromise the results of intra-articular ligament repairs.7,19 Optimal selection of materials for skin closure has also been shown clinically to reduce the incidence of wound infection (polydioxanone plus polypropylene versus chromic catgut plus silk).22 A monofilament structure has a variety of biologic advantages. There is less surface area exposed to the body so that the foreign body reaction is less intense than that seen with multifilament sutures.23 Because less suture material is exposed to hydrolysis, monofilament sutures retain their mechanical properties longer.12 There is increasing concern that braided capillary materials may favor the propagation of infection, whereas noncapillary materials or monofilament sutures do not.11,23 It appears that bacteria can colonize these materials, not so much on the surface of the suture as within it, where immunocompetent cells have insufficient access. This accounts for the lack of support for the use of multifilament sutures in situations of potential contamination.13 Sutures with antimicrobial coatings are under development.27 A silver-doped bioactive glass powder was used to coat resorbable Vicryl (polyglactin 910) and non-resorbable Mersilk surgical sutures, thereby imparting bioactive, antimicrobial, and bactericidal properties to the sutures. Laboratory testing showed that the bioactive glass coating did not affect dynamic mechanical and thermal properties of the sutures. Resorbable sutures with bioactive coatings may open new opportunities for the use of antimicrobial sutures in surgery. Because the implantation of braided suture material very close to the skin incites a much more intense and lasting reaction than burying the suture material in wellvascularized tissue, and because contamination very close to the epidermis is always possible, we suggest that the use of braided suture materials immediately beneath the epidermis should be avoided. Clearly, the presence of large amounts of suture material incites more intense foreign body reactions. Therefore, sutures with optimal strength and knotting characteristics are needed so that small sutures requiring few throws for a stable knot can be used.

MECHANICAL CHARACTERISTICS Suture Strength From an engineering standpoint, ultimate tensile strength should be measured in relation to the cross section of the material tested. Material properties become system

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roperties when the suture material is knotted. For pracp tical purposes, however, the orthopaedic surgeon selects the suture size exclusively according to the United States Pharmacopeia (USP) size, which is designed in numbers ranging from 12-0 to 6. When comparing data from different suture materials of different sizes, it should be understood that the cross section (or the diameter) of one material with a specific USP number may be different from the cross section of another material with the same USP number.26 In addition, we never use unknotted sutures in daily practice. This system appears reasonable because the surgeon is not interested in verifying the diameter of a certain suture and because essentially all sutures invariably fail at the site of the knot.28,29 Until recently, only thin suture materials had been widely tested, and the mechanical properties of heavier materials (e.g., sizes 0 to 6) were only sparsely documented.12,15,16,25,29-32 Repairs of large musculotendinous units are performed with the use of thick sutures, which have so far not been proved adequate, let alone optimal, for their respective applications. We recently tested the mechanical in vitro properties of the heavier sutures (gauges 0 to 3).28 Not all suture materials were available in all sizes. Maximal tensile in vitro strength of comparably sized sutures was historically found for monofilament stainless steel sutures and for absorbable monofilament materials (polyglyconate [Maxon] and polydioxanone [PDS]). Braided absorbable polyglactin (Vicryl) and polyglycolic acid (Dexon Plus), as well as braided polyester (Mersilene, Ethibond, Tevdek), showed excellent ultimate tensile strength, whereas nylon (Dermalon, Prolene) was somewhat weaker. Our own previous data were in rough agreement with those found in the literature. In contrast to the study of Bourne and colleagues, we did not find a decrease in the ultimate tensile strength of wet sutures compared with dry material.12 Recently, high-strength polyethylene polyblend sutures have been introduced that are less prone to breakage during knotting. The first of these sutures was introduced under the trade name FiberWire and has rapidly been accepted and used by the orthopaedic community. These sutures are characterized by a core of fine strands of UHMWPE (ultra–high-molecular-weight polyethylene), which is surrounded by braided polyester. Other brand names are Magnum Wire, Ultrabraid, Force Fiber, MaxBraid PE, and Hi-Fi. All these latter sutures are composed exclusively of UHMWPE.24 A partially resorbable suture of this new kind is Orthocord, which consists of a UHMWPE sleeve covering a resorbable PDS core. While the PDS core dissolves over time, the nonresorbable UHMWPE sleeve retains some of the initial stability.24 Suture abrasion is mainly observed during knot tying.33 Different modes of abrasion have been described, among which are abrasion against bone, abrasion during sliding through a knot pusher or through an anchor eyelet, or inherent abrasion at the knot site.34 A biomechanical study showed that polyblend sutures may be advantageous over conventional Ethibond with respect to abrasion resistance.33 As a result, failure of tendon to bone repair with new polyblend sutures can occur at the suture-tendon margin, as slippage of the anchor, or as eyelet failure of an

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absorbable anchor.35 The cutting characteristics of different sutures through tendon have not been well established to date. In a mechanical study performed at our institution, four types of polyblend sutures were tested: FiberWire, Herculine, Orthocord, and Ultrabraid.36 Fretting resistance was tested on eyelets of metallic and absorbable suture anchors. The ultimate strength of a polyblend suture material was 2- to 2.5-fold compared with Ethibond and PDS sutures. The resistance to fretting was up to 500fold better than that of Ethibond or PDS sutures. This makes polyblend sutures particularly useful with metallic edges of anchors or prostheses or with absorbable anchor eyelets.

DEFORMATION UNDER TENSILE LOAD Although monofilament sutures tend to be more compliant, they are favored for certain arthroscopic techniques because they can be passed more easily through arthroscopic instruments.37 Both suture elongation under load and thread or knot failure, however, may lead to gap formation and may impair successful healing and functional recovery.6,33 The very strong, absorbable monofilament polyglyconate (Maxon) and polydioxanone (PDS II) sutures are very compliant under tensile loads, as opposed to the also very strong and absorbable, but braided, polyglycolic acid (Dexon) and polyglactin 910 (Vicryl) sutures, which are very stiff. Among the commonly used nonabsorbable sutures, only monofilament stainless steel sutures are stiff; the other monofilament sutures (polypropylene and nylon) are very compliant. The most commonly used nonabsorbable braided suture material has been polyester and has been partially replaced by polyblend sutures. Clinically, it may be advantageous to use a very compliant suture, especially a running type, because it may yield rather than break.38 For tendons, suture repair techniques that prevent gapping are considered optimal because scar and adhesion formation is reduced and early functional treatment, which promotes remodeling, can be undertaken.4,36 An optimal tendon-to-bone repair should not allow gap formation under tensile load, but moderate extensibility may be beneficial for healing. If a rotator cuff tendon is sutured to a trough in the greater tuberosity, transosseous suture loops of roughly 7 cm are tied over the proximal humeral cortex or a miniplate. If such repairs are brought under a tension of, for example, 200 N, which is possible when the arm is lowered, the elasticity of the suture material alone may allow gapping of the repair. Under a load of 200 N, the suture material properties alone would allow the following gaps: 2.2 mm for Ethibond No. 3, 3.2 mm for Ethibond No. 1, 6.7 mm for Surgilon No. 1, and 9.1 mm for PDS II No. 1.28 Therefore, suture material alone may prevent stable anchoring of a tendon in bone if the repair is subjected to load; the selection of appropriate suture material is critical. Also, it is extremely important to know the loads to which a repair will be subjected to determine the optimal suture material.

MAINTENANCE OF MECHANICAL PROPERTIES IN VIVO It is widely believed that nonabsorbable suture materials maintain their strength during healing. This is true for braided polyester (Ethibond), which remains stable after implantation.39 It is surprising, however, that Ethilon and Prolene, which both are nonabsorbable, lose 56% and 74%, respectively, of their initial ultimate tensile strength 6 weeks after subcutaneous implantation.39 Even greater changes in the mechanical properties of absorbable suture materials are demonstrated after implantation.39 Catgut loses its strength essentially within 1 week. Polyglactin 910 (Vicryl) loses about 50% of its initial ultimate tensile strength after 2 weeks, and then loses 75% by 3 weeks and 100% by 4 weeks.12 The material is absorbed after 56 to 90 days.14,40 Polyglycolic acid (Dexon Plus) has similar mechanical properties in vivo; 20% of its initial strength is lost within the first week, 50% is lost by 2 weeks, and essentially 100% is lost by 4 weeks.21 Dexon Plus remains in the wound longer than Vicryl and is resorbed only after about 120 days.40 Poly glyconate (Maxon) loses its strength distinctly less rapidly; its very high initial strength is reduced by roughly 50% after 3 weeks and is almost completely lost by 6 weeks.12,39 Polydioxanone (PDS) is initially somewhat less strong. Because it seems to be hydrolyzed more slowly than Maxon, it is already distinctly stronger at 3 weeks after implantation and maintains about 14% to 50% of its initial breaking strength for 6 weeks.12,39 Its resorption requires roughly half a year.14 Of particular interest is another absorbable suture material, poly(l-lactide/glycolide) (Panacryl). According to the manufacturer, Panacryl maintains 80% of its ultimate tensile strength for 3 months after in vivo implantation and maintains 60% of its strength for half a year. Full absorption occurs after 1.5 o 2.5 years. For absorbable sutures, Panacryl preserves its mechanical properties longer than any other suture material; it almost behaves as a nonabsorbable suture. The in vivo behavior of new polyblend sutures is not well established to date. The selection of the appropriate suture material depends on the expected type and rate of wound healing. For simple adaptation of subcutaneous tissue that is not under tension, the rapid resorption of polyglycolic acid or of polyglactin 910 may be desirable. Because the fibroblastic response dictates that a healing wound will rapidly regain strength between days 5 and 14, and because collagen content increases until day 42 with subsequent remodeling of the wound, a suture material such as polyglyconate (Maxon) may have optimal resorption characteristics for a wound that is under slight tension.23 If a tendon or fascia is repaired under moderate tension and a longer period of protection is desired, a material such as polydioxanone (PDS) may be optimal. If, however, prolonged holding power is required and gapping is to be prevented, braided polyester (Ethibond, Tevdek, Mersilene) or a polyblend polyethylene suture may be the best choice. Any recommendation in favor of polyblend polyethylene sutures is based on current knowledge, whereas clinical proof of its superiority remains to be established.

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KNOTTING PROPERTIES Tera and Åberg have introduced an internationally accepted terminology for knotting techniques.29 They distinguished between parallel and crossed knots and established that in general, parallel knots are more stable than crossed knots. Knotting properties appear to be similar for different sizes of the same material.25,41 Knots are indeed of great importance because suture material almost invariably fails at the site of the knot.15,28,29 Stainless steel loses little strength when knotted, whereas catgut and silk lose a large part of their strength when knotted.29,41 Indeed, the failure strength of suture material may be reduced by 10% to 70% by tying a knot.15 Slipping of the knot depends on the number of throws and on the material. In general, any knot with six throws should not slip.12 We were, however, able to show that the 2 = 1 = 1 configuration leads to stable knots for all tested sutures, and this is our preferred technique, although some sutures may require even fewer throws.28 Zechner and colleagues have shown that the reduction in tensile strength can be partly prevented if knots are tied in the horizontal branch of the suture rather than in the region where linear stress is applied.42 Although one may believe that knots of monofilament sutures slide easily, therefore necessitating multiple knots, this is not true; polyglyconate has excellent knotting properties, as have other monofilament sutures.12,17,21,28 The braided absorbable sutures tend to slip less when wet.1 Knotting is more delicate in coated materials such as Ti-Cron (braided

A

Figure 2B-2 Roeder’s knot security depends on the number of initial turns around the standing part.

polyester) because coating reduces friction and therefore favors slipping of the knot. Coated and particularly stiff sutures are better knotted with double throws.15,21 Several new arthroscopic sliding knots have been introduced. Ten commonly used knots were tested in a mechanical study: Dines knot, Duncan loop (Fig. 2B-1A), Tennessee slider (see Fig. 2B-1B), field knot, giant knot, Roeder’s knot (Fig. 2B-2), Nicky’s knot (Fig. 2B-3), SMC knot, Snyder knot, and Weston knot.43 Knots were tested for forward and backward sliding characteristics, loop security before securing with half-hitches, resistance to sliding, knot security after securing with three alternating half-hitches on alternating posts, resistance to sliding, and distance to failure. The Dines knot performed best, exhibiting superior biomechanical characteristics in six of seven measured categories. The only category in which the Dines knot did not perform superiorly was forward sliding, indicating that the Dines knot can be rated as intermediate in ease of placement.43 Another study investigated the optimal knot configuration for maximal knot and loop security.44 A static surgeon’s knot provided the best balance of loop security and knot security within the knot configurations tested in that study. A sliding knot without the addition of three reversing half-hitches on alternating posts had both poor loop

B

Figure 2B-1 A, The Duncan loop is a typical sliding knot. B, Tennessee slider. The loop strand is thrown around the post and loop strand one time and then around the post strand only. It is then brought up between the parallel limbs between the first and second loops.

Figure 2B-3 Nicky’s knot is a one-way sliding knot with high initial holding capacity. It maintains tension on soft tissue while additional hitches are being tied.

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security and knot security and was not recommended. The addition of three reversing half-hitches on alternating posts improved knot security of all sliding knots tested and improved loop security of most of the sliding knots tested. The addition of three reversing half-hitches on alternating posts improved the knot security of all sliding knots to adequately resist predicted in vivo loads. The Roeder knot with three reversing half-hitches on alternating posts provided the best balance of loop security and knot security within the sliding knot configurations tested in that study regardless of suture type. Tying a surgeon’s knot or a sliding knot with three reversing half-hitches on alternating posts using No. 2 FiberWire increased knot security over the same knot tied with No. 2 Ethibond. In another mechanical study, performance characteristics of three different knots were compared between standard Ethibond suture and a braided, high-strength polyethylene suture and were in accordance with the aforementioned results.45 In contrast to this, it has been observed by other investigators under different testing conditions that FiberWire knots may be more prone to knot slippage and failure than Ethibond knots.46 At least two throws more than with conventional sutures have to be used for knot tying according to our experience.36 Accordingly, it has been described that up to seven knots are required to secure a polyblend suture.47 It was concluded that polyblend sutures may be most suitable in regions with subcutaneous fat in order to prevent frictional problems in tight spaces, such as the pulley space of the long head of the biceps tendon. In our hands, the sliding knot is the most convenient surgically; it corresponds to a parallel square knot and has the same properties.48 It should be noted, however, that a double throw for the first knot increases tensile strength in a statistically significant manner.28 If such a double throw is pinched with a ribbed needle holder, the tensile strength of sutures sized 0 to 3 is not significantly impaired. Pinching a smaller-sized thread reduces the tensile strength by up to 30%, however.12,28 As an arthroscopic knot, we prefer to use Nicky’s sliding knot.

HANDLING PROPERTIES Modern suture materials are available with atraumatic precision needles, which are adapted to the intended use of the suture and thus essentially solve needle problems. Among suture materials, stainless steel has little popularity despite its soft tissue tolerance because of its stiffness and its potential for breaking if the suture is kinked.2 Braided, high-strength polyethylene sutures have become very popular among orthopaedic surgeons. In vitro testing of these sutures has been very promising. Clinical data will show whether the increased costs for using these sutures are warranted. Handling of the sutures remains a matter of personal preference, and there are no clear-cut advantages of one suture over another in regard to handling properties. In our practice, we have seen no distinct handling disadvantages of these sutures.

A u t h o r s ’ P r e f e rr e d M e t h o d Personal Approach to the Selection of Sutures

To fix large tendons to bone, we prefer polyblend polyethylene sutures. As a sliding knot, we prefer to apply Nicky`s knot. For tendon sutures, we use fine polypropylene (Prolene) or polydioxanone (PDS). They are somewhat elastic but have extremely high tensile strength, and polydioxanone maintains its mechanical properties sufficiently long to allow tendon healing.24 If strength needs to be maintained, as in closures of aponeuroses (fascia lata), we prefer to use heavier elastic running sutures with polydioxanone. In subcuticular tissue, the breaking strength of the suture can be lost rapidly, so 4-0 polyglyconate (Maxon) appears optimal. For sutures placed very close to the skin, as well as in situations with questionable contamination, we try to avoid the use of braided suture materials. For closure of the skin, we prefer polypropylene (Prolene), 4-0 or 3-0. We do not use very rapidly absorbed polyglactin (Vicryl Rapid) or polyglycolic acid (Dexon), which have been recommended for skin closure, but they can be used for approximation of subcuticular tissues.49-51 Within the skin, these materials tend to cause irritation and may serve as a wick, promoting contamination. We have no use for any form of catgut.52 The selection of suture remains personal in every field of surgery but should be done on a rational basis.53

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r i t i c a l

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l High-strength polyethylene polyblend sutures are less prone to breakage during knotting. l These sutures are characterized by a core of fine strands of UHMWPE (ultra—high-molecular-weight polyethylene), which is surrounded by braided polyester. l Polyblend sutures may be advantageous over conventional Ethibond with respect to abrasion resistance. The ultimate strength of a polyblend suture material is 2- to 2.5-fold compared with Ethibond and PDS sutures. The resistance to fretting is up to 500-fold better than that of Ethibond or PDS sutures. l Failure of tendon to bone repair with new polyblend sutures can occur at the suture-tendon margin, as slippage of the anchor, or as eyelet failure of an absorbable anchor.

S U G G E S T E D

R E A D I N G S

Abbi G, Espinoza L, Odell T, et al: Evaluation of 5 knots and 2 suture materials for arthroscopic rotator cuff repair: Very strong sutures can still slip. Arthroscopy 22:38-43, 2006. Elkousy HA, Sekiya JK, Stabile KJ, McMahon PJ: A biomechanical comparison of arthroscopic sliding and sliding-locking knots. Arthroscopy 21:204-210, 2005. Mahar AT, Moezzi DM, Serra-Hsu F, Pedowitz RA: Comparison and perfomance characteristics of 3 different knots when tied with 2 suture materials used for shoulder arthroscopy. Arthroscopy 22:614. e1-e2, 2006. Wüst M, Meyer DC, Favre P, Gerber C: Mechanical and handling properties of braided polyblend polyethylene sutures in comparison to braided polyester and monofilament polydioxanone sutures. Arthroscopy 22:1146-1153, 2006.

R efer�� ences Plea�� se see www.�� expertconsult.com

Surgical Principles

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Allograft Tissues Barton R. Branam and Darren L. Johnson

The use of allograft tissues in orthopaedic surgery is increasing yearly. The most commonly used musculoskeletal allografts are bone grafts and those used for ligament reconstruction. Osteochondral and meniscal allografts are also available to the surgeon for more complex joint reconstructions. The main driving force behind the keen interest in allograft tissue use is that it eliminates the need to harvest autogenous graft tissue. The reduction of donor site morbidity and rapid rehabilita tion are enticing, especially to the sports medicine surgeon. Meniscal transplantation or reconstruction relies totally on allograft tissue sources. Many find the idea of an ample supply of “spare parts’’ very appealing. Before implantation, we must understand the science behind the procurement, the steriliza tion, the storage, and the clinical use of allograft tissue before we can confidently offer them as an option to patients. The purpose of this chapter is to describe the current concepts re garding the science and use of allograft tissues for knee recon structive surgery.

Besides the elimination of donor site morbidity, the ben efits of using allografts instead of autografts include smaller incisions as well as the ability to choose among various graft types and sizes. This allows the surgeon to “customize” the specific graft to the exact patient’s needs. The ability to prepare graft tissues for implantation before the surgical procedure starts is also a benefit in saving tourniquet time, total operating room time, and overall surgical morbidity. This is a great asset for the surgeon working without an experienced assistant. Furthermore, the reduction in oper ating room time, the elimination of autogenous graft har vesting, and the decreased need for postoperative analgesia arguably offset the cost of the allograft tissue used. There are risks that go along with the use of allograft tissue, which must be explained accurately to the patient during preoperative counseling. Although remote, there is an estimated risk for disease transmission with musculo skeletal allografts of about 1 in 1.5 million.1-8 This risk has been reduced and more clearly defined as allograft tissue processing has become more controlled with the establish ment of the standards of the American Association of Tissue Banks9 (AATB) and the U.S. Food and Drug Adminis tration (FDA). The other risks with the use of allograft tissue are a slower remodeling incorporation process, with the potential for an adverse immune response.10-13 The immune response is often described as subclinical, although further research is needed in this area.

HISTORY Allograft tissue has been used in orthopaedic surgery since the late 19th century. MacEwen reported using allograft bone in 1880.14 Lexer first reported osteoarticular allograft

use in 1908.15 In 1925, Lexer reported his results on 23 whole-joint and 11 hemijoint transplantations around the knee, with a declared 50% successful outcome.15 Both Shino and coworkers and Noyes and associates began using allograft tissues for ligament reconstruction in 1981 and have subsequently provided long-term data from these cases.16-20 Finally, meniscal allograft transplantation was first reported in 1984 by Milachowski and colleagues.21 The operative techniques and the postoperative reha bilitation protocols in knee reconstructive surgery have evolved significantly. For example, ligament fixation meth ods and rehabilitation protocols after knee ligament recon struction continue to evolve and improve outcomes. With this in mind, it is difficult to compare clinical outcome data from earlier studies on allografts to those done more recently. It is especially important to give critical attention to the methods of procurement, sterilization, and storage of the allografts when reviewing the literature. Allografts are not all processed in the same way. Differ ences in sterilization and storage have a tremendous bear ing on clinical outcome. For example, the use of ethylene oxide to sterilize allograft tissue was popular in the 1980s because of its effectiveness in killing bacteria, viruses, and fungi. It was later found, however, to cause a synovial reac tion as well as bone changes after implantation. Ethylene oxide residue levels on graft tissues are now strictly regu lated.22,23 Similarly, the use of gamma irradiation to sterilize allograft tissues has been regulated owing to a dose-related weakening of the collagen. This effect was not appreci ated fully until the late 1980s and the early 1990s, when a number of studies proved and quantified the effects of different radiation levels on the biomechanical properties of allograft tissues.12,16,18,24-29 With these examples alone, it is easy to understand the need to regulate the processing of allograft tissues. Today, the two major regulatory bod ies that monitor the processing of allograft tissues are the FDA and the AATB. The first bone bank reported on was established in 1942.30 Bone banks later increased in number as regional tissue banks became popular in the 1950s. The AATB was founded in 1976 and has been the major influence on the standardization of allograft tissue processing.9 Accredita tion by the AATB requires a periodic examination and review of the tissue bank, its methods, and its employees. The AATB provides accreditation for the recovery, process ing, and distribution of allograft tissue. Accreditation cer tification lasts 3 years. Standards are reviewed and updated annually. On-site inspections by the AATB were started in 1986. Consequently, a number of tissue banks have failed to meet certain requirements on occasion. Membership in the AATB is voluntary, but without its accreditation,

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a tissue bank lacks credibility in the medical community. It is highly recommended that orthopaedic surgeons use only tissue banks accredited by the AATB. It is estimated that there are more than 150 tissue banks; less than 100 of them are currently accredited by the AATB. Lack of accredita tion should be a red flag to the surgeon concerning the safety and quality of allograft tissue. Conversely, compliance with FDA standards is a strict requirement. In 1993, the FDA issued regulations for allograft donor screening.12 In 1994, FDA personnel con ducted on-site evaluations that ultimately led to some tissue bank closures. All the tissue banks in the United States today have been evaluated by the FDA and must remain in com pliance with FDA regulations to stay open. This process has been a tremendous step forward in bringing more unifor mity to allograft studies in the orthopaedic literature. Allograft safety is being addressed by other groups besides the FDA and AATB. In 1987, the Musculoskeletal Transplant Foundation (MTF) was founded by academic orthopaedic surgeons determined to provide allograft tis sue of the highest quality and safety. In the founding year, the MTF distributed about 1500 units of tissue from about 100 donors. In 2002, almost 300,000 units of tissue were distributed from 4431 donors. In more than 15 years and more than 2 million units of tissue transplanted, the MTF has had no confirmed cases of allograft-associated infec tion.31 The Tissue Banking Project Team (TBPT) was formed by the American Association of Orthopaedic Sur geons in February 2002. The goal of the TBPT is to work together with the FDA and Centers for Disease Control and Prevention (CDC) to formulate guidelines for the safe use of musculoskeletal allografts by evaluating cur rent tissue banking procedures in relation to orthopaedic practice.32 Effective July 1, 2005, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) released new hospital standards and requirements perti nent to the tissue banking industry.33 This is applicable to hospitals and specimens found in clinical laboratories, surgical centers, and outpatient centers. This requires overseeing of the individual tissue program within the institution. This essentially includes evaluation, monitor ing, and documentation of all steps of the process within the institution, including the reporting and prompt inves tigation of any adverse event.34 Allograft use in orthopaedics is becoming increas ingly popular. In 2006, about 1.5 million bone and tissue allografts were implanted. Donors have increased from about 6000 in 1994 to more than 22,000 in 2005.34 Despite the recent marked increase in musculoskeletal allograft implantation, there is currently no consensus among or thopaedic surgeons regarding the exact indications for use of allograft tissue, particularly in the sports medicine com munity. The greatest tool in determining the efficacy of treatment efforts is the blinded randomized prospective study of similar patient populations, in significant num bers, treated by different methods with long-term followup. There is a paucity of this type of literature to help us come to a consensus regarding the use of allografts simply because these types of studies involving allograft tissues are extremely hard to do. Surely, as more organizations take an interest and active role in ensuring the safe use of allografts, the number of adverse events will diminish.

Double-blinded, randomized, prospective studies com paring allograft to autograft tissue for knee ligament reconstructive surgery are virtually impossible. Because the patient is required to give informed consent regarding graft choice before the surgery, the choice is not blinded to the patient. The patient’s decision on which graft type to use also eliminates randomization. Furthermore, it is impractical to blind the surgeon to graft choice during the operation. Independent examiners and patients would see any differences in surgical incisions as an obvious indica tion of the type of graft used. Therefore, it is important to understand the potential for bias in any clinical outcome data on allografts because the studies are not blinded and are without true randomization.

PROCUREMENT The AATB printed its first edition of Standards for Tissue Banking in 1984. In keeping up with the rapid changes in allograft science, the publication has gone through mul tiple revisions. The 11th edition of Standards9 was pub lished in 2006 and can be ordered online at the AATB’s website, http://www.AATB.org. This information should be understood thoroughly by the clinician to assist in edu cating patients about musculoskeletal allografts. The screening of donors is the first line of defense in preventing the transmission of disease with allograft tissue. A questionnaire filled out by the donor, the next of kin, the significant life partner, or other relevant individuals is used to detail the medical, social, and sexual history of the donor. A check for drug use, neurologic diseases, autoim mune disorders, metabolic diseases, collagen disorders, and exposure to communicable diseases or unprotected sex is included. If any one of these risk factors is positive, it disqualifies the potential donor. A physical examination and, if available, an autopsy report from the donor are used to detect signs of infectious disease, such as hepatosplenomegaly, lymphadenopathy, oral thrush, or cutaneous lesions (e.g., Kaposi’s sarcoma). The donor is also checked for evidence of sexually trans mitted disease, and the genitals and anus are examined for cutaneous lesions or condyloma. Any suggestion of sexually transmitted disease or anal sex disqualifies the potential donor. As outlined in the most recent Standards, several medical conditions, including rheumatoid arthritis, systemic lupus erythematosus, polyarteritis nodosa, sar coidosis, and clinically significant metabolic bone disease, preclude musculoskeletal tissue donation in addition to the general exclusion criteria.9 The donor’s blood and serum are tested with aerobic and anaerobic cultures. The AATB requires several infectious disease tests: anti–HIV-1, anti– HIV-2, nucleic acid test (NAT) for HIV-1, hepatitis B surface antigen, total antibody to hepatitis B core antigen, antibodies to the hepatitis C virus (HCV), NAT for HCV, antibodies to human T-lymphotropic virus type I and type II, and syphilis. The harvested tissue is also cultured for aerobic and anaerobic organisms. If a donor is exposed to certain pathogens close to the time of death, a window of vulnerability exists in which an infection can go undetected with serum antibody tests. Initially, nucleic acid testing was not a requirement of tis sue banks. As of March 9, 2005, the AATB requires NAT

Surgical Principles

screening for HIV and HCV.35 Rather than looking for antibodies, NAT uses a highly sensitive polymerase chain reaction (PCR) test to look for the actual genetic material of the viruses.34 PCR testing decreases the window period from about 4 to 6 weeks to 10 days for viral RNA.36 The AATB outlines very specific guidelines in regard to the timing and technique of tissue harvesting. Tissue excision for musculoskeletal and osteoarticular allografts should begin within 24 hours of asystole provided that the body was cooled or refrigerated within 12 hours of asystole. However, harvesting should commence within 15 hours of death if the body was not cooled. The harvesting of tis sues should be performed under the same standard sterile technique used in the operating room for all surgical cases. Some institutions allow the procurement of tissues to be carried out in a “clean’’ or substerile fashion. These insti tutions rely on tissue sterilization at a later date. There is no provision for a substerile technique in the AATB Standards, however.9 After harvesting, the grafts are aseptically wrapped and appropriately labeled. The tissues are usually cooled and taken to the tissue bank. The maximal allowed time for the tissues to remain at wet ice temperatures before final processing or freezing is no longer than 72 hours. Osteo articular allografts may remain at wet ice temperatures for 5 days before processing. Osteoarticular and musculoskeletal allograft tissue are kept in a bacteriologically and climatecontrolled environment while processed.9

STERILIZATION Tissue processing and sterilization is a delicate balance between preserving the biologic function of the tissue and removing potentially infectious agents. The ideal method of allograft sterilization would eliminate all poten tial pathogens from the graft without compromising the viability of the graft or its biomechanical properties and would not cause any morbidity to the eventual recipient. Currently, there is no ideal method. Gamma irradiation and antibiotic soaks are acceptable methods of second ary sterilization after graft procurement. Less common methods include heat and ultraviolet radiation. All these methods are less than ideal and therefore make it neces sary to adhere to strict sterile technique during procure ment and initial storage phases. Processing methods must be validated to reduce the risk for tissue contamination and cross-contamination. Bacteriostasis can cause false-negative culture results of allograft tissues, which can be problematic with spore-forming bacteria.31 However, unless a sporicidal method is used to process the tissue, the tissue should not be considered sterile, and there is risk for possible bacterial infection.37 Sterile is considered to be the absence of all living or potentially living microorganisms at the steril ity assurance level (SAL) of 10-6. This means that there is a 99.99% probability that the tissue is sterile, which is the same percentage for the total hip or knee implant that might be needed later. Ethylene oxide is an effective agent against bacterial, fungal, and viral agents on nonporous surfaces and is com monly used to sterilize surgical instruments. Ethylene oxide was previously a popular and accepted method for sterilizing musculoskeletal allografts. However, Jackson

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and associates found a 6.4% incidence of persistent intraarticular reaction in patients who received an allograft for anterior cruciate ligament (ACL) reconstruction that was sterilized with ethylene oxide.22 The AATB requires elimination of residual ethylene oxide or its breakdown products to less than specified levels.9 Increased graft fail ure and chronic synovitis associated with ethylene oxide sterilization have caused most tissue banks to discontinue its use.32,34,36 Gamma irradiation historically has been the most widely used method of secondary sterilization of musculoskeletal allograft. Bacillus pumilis spore control strips are used to confirm that the radiation load is effective in sterilizing the tissue against bacteria. This typically requires a radiation load of at least 1.5 megarad. The elimination of HIV with gamma irradiation requires higher doses of radiation, esti mated to be greater than 3.5 megarad.5 Gamma irradiation levels of 3.0 megarad have been proved to significantly alter the mechanical properties of a goat infrapatellar ten don.26 In this model, a 27% reduction of maximal failure force and a 40% reduction in the energy-to–maximal force ratio were observed in infrapatellar tendons treated with 3 megarad of radiation when compared with untreated control models.24 Furthermore, human infrapatellar tendons treated with 4 megarad have a significant reduction in lin ear stiffness and maximal force compared with untreated control models.27 Therefore, HIV cannot be eliminated from allograft tissues using gamma irradiation without compromising the mechanical properties of the graft. Currently, 2.5 megarad is the recommended maximal dose to avoid altering the biomechanical structure of the graft while providing maximal bacterial eradication.36 Antibi otic soaks are typically used synergistically with low-dose gamma radiation. Antibiotic solutions kill bacteria and viruses; however, the effect is limited by incomplete tissue penetration.32 There is no one best way to sterilize allograft tissue. All sterilization processes have the potential to affect bio mechanical and biologic properties. Techniques simply vary with each tissue bank. The graft is swabbed and is checked for bacterial contamination at the conclusion of the sterilization process in most cases. Several major pro cessing companies use specific and unique techniques to disinfect allograft tissue. Allowash formula (LifeNet, Vir ginia Beach, Va) combines irradiation, ultrasonics, cen trifugation, and negative pressure with reagents, including biologic detergents, antibiotics, alcohols, and hydrogen peroxide to increase solubilization and the removal of lip ids, bone marrow, and blood elements.34 The BioCleanse technique (Regeneration Technologies, Gainesville, Fla) uses a low-temperature chemical sterilization process with liquid sterilants that perfuse the inner matrix of the tissue. This is followed by irradiation.34 More than 300,000 grafts have been implanted without a known infection. The pro cess has been validated by the FDA to kill implanted spores and viruses.38 The Clearant Process (Clearant, Los Ange les, Calif) freezes the tissue, extracts the water, and adds dimethlysulfoxide as a radioprotectant. The tissue is then treated with 50 kGy of radiation, which is 2 to 4 times the dose recommended to avoid damaging cells.34 The search for a perfect mechanism of sterilization is ongoing, with further refinement techniques expected in the future.

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STORAGE The ideal method of allograft preservation would main tain the viability of the cells, would not alter the collagen matrix, and would enable indefinite storage in a conve nient, cost-effective manner. Reducing the antigenicity of the graft tissue and secondary sterilization would be desir able as well. An ideal method does not exist, similar to our current situation with sterilization. Deep freezing, freeze drying, cryopreservation, and fresh (osteochondral) are the current methods employed to preserve musculoskeletal allograft tissue. Deep freezing is the most commonly used method of preservation for allografts used in ligament reconstruc tion.39 Grafts preserved by deep freezing, referred to as fresh frozen grafts, undergo the freezing process twice: once during quarantine and then finally for storage on the shelf before use. Marrow elements and blood must be removed from the graft before the initial freeze. After the tissue is removed from quarantine, is is thawed to room temperature and soaked in antibiotic solution. Secondary sterilization with gamma irradiation may or may not be used, depending on the preferences of the individual tissue bank. Finally, the tissue is packaged without any solution and frozen rapidly to −80° C. The graft can be stored at this temperature for 3 to 5 years.40 One benefit of deep freezing is the reduced antigenic ity of the graft, which is accomplished by the destruction of cellular antigens. This process reduces the potential for the host to mount an immune response once the graft is implanted. Unfortunately, however, the viability of the cells in the graft is not maintained with deep freezing. Ice crystal formation kills the cells and is also believed to be detrimental to the collagen matrix. This problem calls into question the use of deep freezing as a potential method of preserving articular or meniscal cartilage allograft tissue. In these tissues, cell viability may be critical to long-term success. It is believed that multiple freezings are increas ingly detrimental to the graft tissue collagen matrix41; as more ice crystals are formed in the graft collagen matrix, more damage is done. Cryopreservation methods use chemicals to remove cel lular water and controlled-rate freezing to prevent crys tal formation. After procurement, tissues designated for cryopreservation are cooled to wet ice temperatures for up to 48 hours. During this short period of quarantine, the graft is cleared for final processing. The tissues are then soaked in antibiotic solution at ambient temperatures for 24 hours. The tissue is placed into a storage container filled with a cryoprotectant solution of dimethyl sulfoxide or glycerol. The cryoprotectant displaces cellular water. The controlled-rate freezing then ensues. The controlled-rate freezing is completed at a tempera ture of about −135° C. The final storage uses liquid nitro gen at a temperature of about −196° C. The grafts can be stored at this temperature for up to 10 years. The higher temperatures used in deep-freezing storage (−80° C) allow ice crystals to continue to grow and re-form. The liquid nitrogen storage temperature (−196° C) used for cryo preservation does not allow this type of crystal turnover. Cryopreservation is one method of storage for meniscal allografts because cellular viability is largely maintained.

Many surgeons prefer ligament reconstruction allografts preserved by this method as well. Jackson and associates, however, have shown that preserved cells in allografts used for ligament reconstruction do not survive long after implantation.42 Using DNA-probe analysis, they found that the donor cell DNA is no longer present in allograft ligament reconstructions after 4 weeks in a goat model. This absence of the donor tissue DNA occurred without any detectable sign of immune rejection. Their study sug gests that neither fresh nor cryopreserved allograft liga ments maintain cellular viability after implantation and rely totally on host cell repopulation for graft incorpo ration and remodeling. The most significant benefit of cryopreservation clearly is the elimination of ice crystal formation, which can damage and weaken the collagen in the graft. Freeze drying is also used to preserve allograft tissue used for ligament reconstruction and is distinctly different from cryopreservation or deep freezing. Freeze drying has the advantage of allowing ambient storage temperatures after processing is completed. The graft can be rehydrated for use up to 5 years later. Freeze drying is the most costefficient means of storage. Procured tissues designated for freeze drying are cleaned to remove marrow elements and blood and are frozen during a period of quarantine. After the tissues are cleared and removed from quarantine, they are thawed and soaked in antibiotic solution for 1 hour at ambient tem peratures. Secondary sterilization with ethylene oxide or gamma irradiation may be done at the discretion of the tis sue bank. Freeze drying, or lyophilization, is then carried out. In this process, alcohol replaces water within the tissue to a residual moisture level of 5% or less. A vacuum pro cess then removes the alcohol from the tissue. This process ultimately kills all the nucleated cells in the graft. The tissue is very dry and stiff after lyophilization. It is important not to manipulate the graft because of its vul nerability to fracture. The tissue is prepared for surgery by soaking it in a physiologic solution for at least 30 minutes before any type of handling. It may take up to 24 hours for ligament-sized tissue to rehydrate totally. A number of studies have evaluated the biomechanical and clinical properties of freeze-dried grafts used for liga ment reconstruction.22,23,25,43-46 Most studies show that the freeze-drying process alone has minimal effect on the bio mechanical properties of allograft bone, tendon, or liga ment as long as the specimens are not repeatedly frozen and thawed. More pronounced differences in freeze-dried grafts compared with other grafts have been demonstrated in clinical studies after implantation. For example, Indeli cato and associates showed a significantly higher incidence of both subjective instability and a pivot shift in ACL reconstructions done with freeze-dried grafts compared with fresh frozen grafts.43 One benefit of freeze drying may be that it potentially helps neutralize HIV. In 1985, three different recipients converted to HIV positive after receiving a fresh frozen allograft from the same infected donor.1,4,7 Recipients of freeze-dried grafts from the same donor did not become infected with HIV. Although anecdotal, there is a sugges tion that freeze drying assists in neutralizing HIV. This potential benefit cannot be totally relied on, however,

Surgical Principles

because HIV has been cultured successfully from freezedried bone. Crawford and associates recently performed a study on tendon and cortical bone from cats infected with retrovirus. The retrovirus was not inactivated by the lyophilization process, and the authors concluded that freeze drying should not be relied on to inactivate retrovi rus in musculoskeletal allografts.47 In the case of osteochondral allografts—grafts that involve articular cartilage and its subchondral bone—the viability of the chondrocytes may be critical. Cellular viability is best maintained when transplanted in a fresh fashion without long-term storage.13,18,29,48-52 Freezing of osteochondral allografts has been shown to decrease the viability of articular cartilage chondrocytes severely. Some tissue banks establish a 45-day shelf life for osteochondral allografts. There is a decrease in the percentage of viable chondrocytes after 24 hours. Fresh grafts have a higher risk for disease transmission because of the lack of steril ization that occurs with secondary sterilization and storage processing.

RISK FOR INFECTION The predominant concern regarding the ultimate safety of allograft use is the risk for infection. To date, there is only one reported case of HIV transmission using a musculo skeletal allograft,1,4,7 and it occurred in 1985. The donor tissue, a patellar tendon graft, came from an AATB-certified tissue bank. Donor screening was carried out by family interview, medical history review, and enzyme-linked immunosorbent assay for HIV. All the screening test results were negative, and the tissue was accepted. The graft was not processed with removal of blood or bone marrow. The graft that caused the transmission of HIV was not second arily sterilized and was fresh frozen. Other tissues from the same donor (fascia lata, Achilles tendon, and patellar ten don) were processed and freeze dried and did not cause HIV infection after implantation into three other recipi ents. NAT testing for HIV is now an AATB require ment. HIV is an RNA virus; however, it infects the DNA of the white blood cell. Because white blood cell DNA is stable in cadaver blood for up to 48 hours, PCR testing for HIV is effective in detecting the infected white blood cell DNA and consequently highly effective in allograft screening.38 In 1995, Conrad and associates reported two separate cases of hepatitis C transmission through musculoskeletal allografts.6 Both patients were recipients of a fresh frozen allograft patellar tendon graft. Neither graft was processed with blood and marrow element removal, nor were the grafts secondarily sterilized. Twelve other musculoskel etal allografts from the same donor that were processed and irradiated did not transmit hepatitis C to the eventual recipients. Recently, 38 patients received allograft tissue from one infected donor, and at least 6 patients tested posi tive for HCV. One of the patients had received a patellar tendon allograft. The infection in the donor was unde tected by the tissue bank. Ultimately, the donor was found to be anti–HCV antibody negative, HCV RNA positive.53 A patient underwent anterior and posterior spinal fusion in March 1998 with cancellous allograft bone. Six weeks after surgery, he developed acute hepatitis, and in May 1998,

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tests for hepatitis C antibodies were negative. In August 1998, he tested positive for hepatitis C RNA, and in November 1998, he tested positive for hepatitis C antibod ies. He had no known risk factors and it was believed that he acquired the virus through the bone graft.54 This illus trates that there is a clear window for negative serologies despite the presence of disease. The AATB now mandates NAT testing for HCV. It is an RNA virus but, in contrast to HIV, does not attach to white blood cell DNA. It is continuously cleared from the serum by immune system enzymes, and the half-life of HCV in cadaver blood can be a few hours unless the blood sample is obtained early after death and cooled. PCR testing for HCV is less effective in tissue banking than in blood banks and can produce a 15% to 25% false-negative rate in tissue banks.38 Further more, hepatitis C has been found in about 1.1% of donors, in comparison to HIV, which is present in only 0.03% of donors.38 Risk for allograft-associated bacterial infection is clearly a concern as well. As of March 2002, the CDC identified 26 cases of musculoskeletal allograft infection. Investiga tion ensued after the postoperative death of a 23-year-old man who received an osteochondral femoral graft. He developed pain at the surgical site on postoperative day 3, which rapidly progressed to shock; the patient died on postoperative day 4. Premortem blood cultures grew Clostridium sordellii. Another patient received a fresh femoral condyle graft and a frozen meniscal allograft from the same donor. He also developed septic arthritis; however, cul tures for anaerobic bacteria were not obtained. The body of the donor was refrigerated 19 hours after death, and the tissue was procured 23.5 hours after death. The CDC sub sequently cultured C. sordellii from nonimplanted donor tissue. The tissue bank had cultured the aseptically har vested tissue only after soaks in an antibiotic and antifungal solution. Thirteen of the 26 patients with a musculoskel etal allograft–associated bacterial infection were infected with Clostridium. Eleven of these patients, including the 2 previously described patients, received tissues processed by the same tissue bank. Eight of the allografts were used for ACL reconstruction. Eleven were frozen, and 2 were fresh. All were processed aseptically, but none was termi nally sterilized. Of the 13 other patients, 11 patients were infected with gram-negative bacilli; 5 were polymicrobial and 2 were negative by culture. Eight of the 13 patients had evidence implicating the allograft. Eight patients received grafts that were not terminally sterilized, and 3 patients received grafts that had reportedly undergone gamma irradiation.37 It is clear after this investigation that sporeforming bacteria are potential pathogens. The CDC made several recommendations based on this investigation and ultimately stated that “Unless a sporicidal method is used, aseptically processed tissue should not be considered ster ile. Health-care providers should be informed of the pos sible risk for bacterial infection.”37 The general risk for postoperative wound infection with musculoskeletal allografts is negligible with small grafts. Large musculoskeletal allografts have an infection rate sim ilar to that of other sterilized prosthetic implants. Tomford reported no wound infections in 287 patients who received a small bone or soft tissue allograft.8 A large intercalary bone graft used for joint revision or tumor reconstruction

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was involved in all 13 wound infections found in this series. All the grafts in this series had negative culture results before implantation, and the cause of infection was not thought to be a result of graft contamination. The infec tion rate in the large revisions and reconstructions with allograft was found to be comparable to similar cases using metallic prosthetic implants. None of the pathogens could be traced to the donor or the tissue bank. Clearly, musculoskeletal allograft–associated viral and bacterial infection is still a concern. This underscores the importance of choosing a tissue bank that is accredited by the AATB. Surgeons should be familiar with the processes of the tissue bank that they choose in order to ensure the safe use of allografts. The surgeon has the ultimate choice between autograft and allograft tissue. This fortunately is not life or death surgery. Therefore, all risks must be con sidered before allograft use.

ALLOGRAFTS FOR LIGAMENT RECONSTRUCTION There is no absolute indication for the use of allograft tissue in knee ligament reconstruction other than a lack of autogenous tissue. In multiple-ligament knee recon structions, allograft is often the tissue of choice because of the need for more than one ligament graft.55-60 This choice reduces donor morbidity and operative time sig nificantly. Otherwise, the choice to use allograft tissue instead of autograft is at the discretion of the surgeon and the patient. Most of the controversy regarding the use of allografts concerns the use of allograft tissue for primary reconstruc tion of the ACL. This debate largely arises because of the frequency of this procedure as well as the familiarity that most orthopaedic surgeons have with it. Autograft ACL reconstruction is a procedure with an enormous amount of outcome data with good and excellent results. Surgeons who prefer autogenous tissue also cite the risk for infection, the potential for an immune response, and a potentially higher failure rate as other reasons not to use allograft for primary ACL reconstruction. Surgeons who prefer allograft tissue for ACL reconstruction cite no donor morbidity, less post operative pain, smaller incisions, less operative time, and comparable results in terms of knee stability as reasons for their graft choice.61 The difficulty in reaching a consensus is largely due to a lack of long-term data on the outcome of primary ACL reconstruction with allograft compared with auto graft using similar surgical and rehabilitation techniques in a uniform patient population. Surgeons, therefore, rely on animal studies and the available clinical outcome data, which are difficult to interpret because of differences in patient populations. Allograft studies cannot be “lumped’’ together because of differences in surgical and rehabilita tion techniques, tissue processing, patient populations, and outcome measurement tools. Also, multiple, different types of allograft tissues are used for ligament reconstruc tion, including patellar tendon, Achilles tendon, and all soft tissue allografts. It is not recommended that different tissue types be lumped together as allografts in terms of outcome after ligament reconstruction. One must be very

critical when analyzing the literature on allograft outcome studies because not all “allografts” are the same. Animal studies have been done to evaluate allograft and autograft ligament histologic incorporation and bio mechanical properties at various stages of healing.10,28,44,45 The process of graft revascularization and incorporation for allograft tissue has been found to be similar to that for autograft tissue. This was demonstrated in the classic study by Cordrey and associates using a rabbit model.10 They found that the revascularization and the collagen turnover in the allograft ligaments were the same as in autografts, except that the allografts took longer to go through the process. Infrapatellar tendon allograft ACL reconstruc tions in dogs have been shown to be grossly and histologi cally similar to the native ACL 1 year after implantation in two separate studies.62,63 Biomechanical differences between allograft and auto graft ACL reconstructions have been demonstrated using a goat model.42 In this study, Jackson and coworkers found that the allograft ACL reconstructions had a maximal loadto-failure ratio that was 27% of normal, compared with 62% of normal for autograft reconstructions. This find ing is in contrast to the study by Nikolaou, who demon strated 90% of normal strength in cryopreserved allograft ACL reconstructions after sacrifice at 36 weeks in a dog model.64 It is likely that allograft ligament reconstructions are weaker than autografts during graft incorporation, but this has yet to be proved clinically significant in terms of increased graft failures.12 Despite a slower rate of graft incorporation, the clini cal results of allograft ACL reconstruction have been promising. Shelton and associates compared bone–patellar tendon–bone allograft and bone–patellar tendon–bone autograft ACL reconstructions and found no difference in pain, effusion, stability, range of motion, patellofemo ral crepitus, or thigh circumference after 24 months.65 Harner and colleagues found no statistical difference in the 3- to 5-year outcome for ACL reconstructions using fresh frozen nonirradiated allograft tissue compared with autograft ACL reconstruction, with the exception that the autograft patients had a higher incidence of terminal extension loss.61 Interestingly, the allograft group in Harn er’s study had better knee scores than the autograft group in two different ratings systems, but this was not statisti cally significant. In a later publication, Harner stated that his indications for allograft ACL reconstruction include increased age, low activity level, and patient preference.32 Also, Noyes and coworkers reported 89% good to excellent results in ACL reconstructions done with bone–patellar tendon–bone and fascia lata allografts after 2 years and noted that bone–patellar tendon–bone allografts had bet ter arthrometric results.66 Revision ACL reconstruction is a situation in which allograft tissue may be particularly useful. Often, in a failed ACL reconstruction, previous autogenous tissue has been used, limiting options for graft selection during revi sion surgery. Revision ACL reconstruction often requires increased tunnel size (because of tunnel lysis) and the need for larger bone plugs or tissue.32 Allograft tissue may pro vide for larger soft tissue grafts (increased tensile strength),32 which could be optimal in the setting of a salvage operation with gross instability or combined instability in multiple

Surgical Principles

directions. Tissue choices for revision ACL reconstruction include patellar tendon, Achilles tendon, and all soft tis sue grafts, including anteroposterior tibialis tendons and iliotibial band. Fewer published outcome studies address the use of allograft tissue for posterior cruciate or collateral ligament reconstruction. Allograft tissue is often the graft of choice for these complex cases. Noyes and Barber-Weston, as well as Bullis and Paulos, have provided studies on the use of allografts for these types of reconstructions, with good results.58,59,67,68 In addition, the data available on allograft for ACL reconstruction appear to support its use for poste rior cruciate ligament or collateral ligament reconstruction or augmentation after primary repair. Consideration should be strongly given to allograft use in reconstruction of the multiligamentous knee. Not only are multiple ligaments injured with knee dislocations but the injury also often includes damage to menisci, articu lar cartilage, and neurovascular structures. Advantages of allografts include a sufficient amount of tissue to recon struct all injured ligaments, decreased surgical time, imme diate motion, and decreased donor site morbidity in an already traumatized knee. Minimizing incisions, intraop erative tourniquet time, postoperative pain, and postopera tive knee stiffness are additional benefits.32

MENISCAL ALLOGRAFTS The role of the meniscus in the preservation of articular cartilage has been increasingly appreciated since Fairbank’s 1948 article on postmeniscectomy degenerative changes to the knee.69 Lee and colleagues70 evaluated changes in tib iofemoral contact areas and stresses after serial meniscec tomies of the posterior horn of the medial meniscus. They concluded that the peripheral portions of the medial menis cus provide greater contribution to increasing contact areas and decreasing mean contact stresses than does the central portion and that the increase in peak contact stresses are proportional to the amount of the removed meniscus. Fur thermore, they showed that in terms of load bearing, loss of hoop tension (i.e., segmental meniscectomy) is equal to total menisectomy.70 Most surgeons make a concerted effort to minimize the removal of meniscal tissue during partial meniscectomy and to repair the meniscus whenever possible, particularly in the knee with an ACL injury. An injury to the meniscus resulting in near-total meniscec tomy was without a good solution until meniscal allograft reconstruction was pioneered. Milachowski was the first to attempt meniscal allograft reconstruction in 1984.21,71 A few years later, Arnoczky used a dog model to demonstrate peripheral healing, cellular repopulation, and the lack of immune response after meniscal allograft reconstruction and therefore proved the feasibility of the procedure.72 Since then, knee sur geons have been defining the indications and refining the procedure.48,73-75 Selecting the appropriate patient is critical for a success ful outcome after allograft meniscal transplantation. The ideal candidate is physiologically young, has had a previous meniscectomy, has developed pain over the involved tib iofemoral compartment, and has minimal articular carti lage changes without significant bipolar disease.32,36 Limb

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alignment and ligament stability are critical and must be addressed before meniscal transplantation or at the index procedure. Meniscal transplantation can also be combined with osteochondral allograft when necessary.32,76 Patient compliance and realistic expectations are important in obtaining a good outcome. Contraindications include obe sity, rheumatoid arthritis, metabolic diseases, gout, and infection.36 The success of meniscal allograft reconstruction has been most predictable in patients with ligamentous sta bility, physiologically normal alignment, and minimal articular cartilage damage. It is not uncommon to find significant irreparable damage to a meniscus with little to no arthritic change after an acute ACL tear. Meniscal allograft transplantation may be planned in conjunction with ACL reconstruction. Implantation of the meniscal allograft is technically much easier to perform before the ACL reconstruction is completed and should precede the ACL reconstruction when combining the procedures. Reconstructing the meniscus and the ACL may have a synergistic effect on the stability of the knee and the survival of both grafts. Sekiya and associates77 recently performed a retrospective review of 28 patients who underwent combined ACL reconstruction and menis cal allograft transplantation. Nearly 90% had normal Lachman and pivot shift scores at an average 2.8 years after surgery. Joint space narrowing was not significantly different from that of the contralateral knee. They con cluded that restoration of meniscal function could pro tect the cartilage and improve joint stability.77 Yoldas and coworkers78 evaluated meniscal allograft transplanta tion with and without combined ACL reconstruction in 31 patients. No difference was found between which meniscus was transplanted, concurrent ACL reconstruc tion, or degree of arthrosis found at surgery. Twentytwo patients were greatly improved, 8 were somewhat improved, and 1 was unchanged.78 Sizing of the meniscal allograft is critical to outcome. Plain radiographs of the patient’s knee are sent to the tissue bank to compare to donor radiographs. Any magnification in the radiographs must be accounted for. Without proper sizing, the meniscus cannot share and distribute the load across the articular cartilage. Central hypocellularity and shrinkage of meniscal allografts have been a problem in 15% to 30% of the cases reported.12,18,29,75,79 It is believed that this occurs because the more central chondrocytes in the meniscus do not receive enough nutrition. The more peripheral cells in the meniscal allograft are more likely to survive. Graft selection is important for meniscal allograft suc cess. Most meniscal allografts are fresh frozen or cryo preserved. In 1993, Jackson and colleagues80 used a goat model to show that host cell repopulation of the graft takes place within several weeks after transplantation. Given that host cells repopulate the graft, fresh frozen grafts are appropriate.32,36,80 Fresh frozen grafts are cheaper than cryopreserved grafts, and freezing the graft kills the cells and diminishes the potential for an immune response. The advantages of cryopreserved tissue are maintenance of cellular viability and the possibility of prolonged storage. This allows ample time for serologic testing of the graft and appropriate sizing.32,36

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The technique of transplantation has been refined sig nificantly. Early meniscal allograft transplantation was done through a moderate-sized arthrotomy that included releasing the collateral ligament. The modern techniques are done arthroscopically, assisted by small arthrotomies without disruption of the collateral ligaments. The menis cus is attached to bone plugs (medial) or to a bone bridge (lateral) fashioned to key into drill holes (medial) or a slot (lateral). The periphery of the meniscus is fixed with cur rent meniscal repair suture techniques. Multiple studies have been published regarding the clin ical results of meniscal allograft transplantation.16,18,81-89 There is significant variability in mean length of follow-up, assessment techniques, and results. Cook90 concisely sum marized conclusions from meniscal allograft transplanta tion. In general, patient satisfaction exceeds 75%, and about 90% of patients would have the procedure again. Fresh frozen and cryopreserved allografts perform equally well. Functional outcomes are better for lateral meniscal allografts than for medial meniscal allografts. All treatable pathologies of the knee should be treated before or simul taneous with the meniscal allograft transplantation. Finally, rehabilitation is important for a successful outcome.90 Meniscal allograft surgery continues to evolve. The untoward effects of a meniscal-deficient knee are well doc umented. Advances in tissue processing increase the safety of allograft surgery. There is currently no simple solution for symptomatic patients with a previous meniscectomy. At this time, meniscal allograft transplantation is the most viable option for young patients with localized symptoms who have had a prior meniscectomy.

OSTEOCHONDRAL ALLOGRAFTS Treatment of articular cartilage injury and defects remains a challenging problem for the orthopaedist, especially in physiologically younger and active patients. Osteochon dral injury can be disabling with pain, mechanical symp toms, and swelling. These lesions can generate irregular surfaces and predispose the joint to further articular carti lage damage and meniscal pathology.32,36 If symptomatic, some surgical treatment options include microfracture, abrasion arthroplasty, and drilling. These procedures result in healing of the defect with fibrocartilage. More aggressive surgical techniques include autologous chon drocyte implantation, osteochondral autograft transplan tation, or osteochondral allograft. Factors determining the appropriate procedure include the size, depth, location of the defect, activity level, physiologic age of the patient, and associated knee pathology.36 Osteochondral allografts are indicated for patients with full-thickness articular cartilage defects larger than 2 cm.32 This deficit is usually the result of trauma, osteochondri tis dissecans, or avascular necrosis.32 Contraindications include rheumatoid arthritis, generalized arthritis, and corticosteroid-induced osteonecrosis.36 As with meniscal transplantation, associated meniscal pathology, ligamen tous instability, or limb malalignment must be addressed.32 Advantages of osteoarticular allograft over autograft include the ability to harvest a much larger graft and the ability to obtain tissue from a younger donor with healthier cartilage.32,36 The graft can be sized with radiographs with

a disparity in size of less than 10%.32 The goal of trans plantation is to achieve an anatomic articular surface with minimal step-off at the host-donor cartilage interface.32 Osteochondral allografts are typically implanted fresh or cryopreserved because the viability of the chondrocytes is critical to success. Fresh typically means that the graft was harvested within 24 hours of the donor’s death and implanted within 7 days.91 Fresh grafts preserve chondro cyte viability at the expense of increased risk for disease transmission, increased immunogenicity, and more diffi culty in sizing.36 Recent studies have been performed to evaluate chondrocyte viability after storage of the grafts. Williams and associates92 looked at hypothermically (4° C) stored sheep knee condyles at various time inter vals between 1 and 60 days. Mean chondrocyte viability decreased over the storage interval, with a preponderance of nonviable chondrocytes in the superficial layer. Decreases in matrix proteoglycan and matrix dynamic modulus were seen as well. Allen and colleagues93 evaluated chondrocyte viability and extracellular matrix quality in unused cartilage from 16 consecutive allografts after tissue bank processing and storage. They found that after a mean storage time of 20 days, there was a decrease in cell viability, especially in the superficial zone, as well as a decrease in cell density and metabolic activity. Matrix and biomechanical properties were preserved. Pearsall and coworkers91 assessed 16 refrig erated (2° to 8° C) osteochondral allografts that had been refrigerated for an average of 30 days from donor expira tion to implantation. The grafts were evaluated at the time of implantation. No significant correlation was noted with chondrocyte viability. The authors concluded that refrig erated osteochondral allografts can be maintained for up to 44 days, with an average chondrocyte viability of 67%. This last study is encouraging because the goal is to implant a graft with maximal chondrocyte viability while placing the patient at the least possible risk.36 Alternatively, cryopre served grafts maintain up to 80% viability of cells, have greater storage time, and are less immunogenic.36 How ever, cryopreserved grafts reveal early articular degenera tion and decreased chondrocyte viability compared with fresh grafts32,94 and yield inferior results.36 Zukor and coworkers have reported on more than 100 cases and showed that the best results were in patients with focal traumatic unipolar lesions.95 Osteochondritis disse cans and bipolar lesions that were treated had less favor able results. Of the 92 knees treated in this series, a 75% success rate was found at 5 years, and the rate declined to 63% at 14 years. An 85% success rate in the treatment of small (2 to 4 cm2) lesions of osteochondritis dissecans was reported by Garret.96 Success was determined by the appearance of normal articular cartilage on second-look arthroscopy. The subchondral bone did not incorporate, and the articu lar cartilage fragmented in those that failed. This finding is further proof that the incorporation of the subchondral bone is critical to the outcome of these grafts. Several studies have recently evaluated osteochondral allografts. Gross and colleagues97 performed a prospec tive, nonrandomized study of fresh allografts for unipolar femoral condyle defects (60 patients with average 10-year follow-up) and fresh allografts for reconstruction of the tib ial plateau (65 patients with average 11.8-year follow-up).

Surgical Principles

Kaplan-Meier survivorship showed 95% femoral graft survival at 5 years and 85% at 10 years. Twenty-one of 65 patients with a tibial plateau allograft were converted to total knee arthroplasty at an average of 9.7 years. KaplanMeier survivorship revealed 95% survival at 5 years, 80% at 10 years, and 65% at 15 years. Spak and Teitge98 looked at 14 fresh osteochondral allografts of the patella or patel lofemoral joint for patellofemoral arthritis in 11 patients younger than 55 years with a mean follow-up of 10 years. Knee scores and functional scores improved. At last follow-up, 8 of 14 grafts were in place, and 3 nonsurviv ing grafts had lasted more than 10 years. Emmerson and associates99 looked at 66 knees in 64 patients who under went osteochondral allograft transplantation for osteo chondritis dissecans of the femoral condyle. The average patient age was 28.6 years (15 to 54 years), and the average follow-up was 7.7 years (range, 2 to 22 years). Seventy-two percent of patients had good or excellent results, and only 1 patient had a fair result. Ten patients underwent reop eration. Finally, McCulloch and coworkers100 performed a prospective evaluation of prolonged fresh osteochon dral allografts of the femoral condyle in 25 patients with a mean follow-up of 35 months. The grafts were stored at 4° C and implanted at a mean of 24 days after procure ment. Statistically significant improvements were seen for the Lysolm and International Knee Documentation Com mittee scores. Patients reported 84% satisfaction and felt their knee functioned at 79% of their contralateral knee. This study validates the basic science study performed by Pearsall and colleagues.91 It is important to consider these promising results in light of the fact that there is no per fect solution to articular cartilage defects in young active patients and that these are very difficult problems to treat.

SUMMARY There is a great deal of science in the processing of muscu loskeletal allograft tissues and in their use in patients. More groups are becoming interested and involved in the moni toring and assurance of the safe use of allografts. Allograft safety has improved significantly during the past 15 years. It is critical that the orthopaedic surgeon use grafts only from AATB-accredited tissue banks. The surgeon must be familiar with the processes of the bank supplying their allograft. Not all tissue banks use the same donor screen ing, tissue harvesting, tissue processing, safety purification methods, and secondary sterilization techniques. Implan tation of allograft tissue can cause infection with significant morbidity and mortality. It is critically important for the surgeon to weigh the risk and benefits of allograft tissue compared with autograft tissue and discuss this with the patient. Ultimately, it is you as the surgeon who is the “tissue banker,” at least in the patient’s view. Encouraging results from recent studies indicate that musculoskeletal allografts will be used more in the future. There is currently a clear role for the safe use of musculoskeletal allografts in ligament reconstruction, meniscal transplantation, and chondral defects.

C

r i t i c a l

P

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o i n t s

l

rthopaedic surgeons should only use allograft tissues O obtained from an AATB-accredited tissue bank. The use of allograft tissue is only as safe as your tissue source or tissue bank. l It is important to be familiar with the processes of the tis sue bank from which one obtains the tissue grafts. Not all tissue banks are the same. l It is important to obtain grafts that were appropriately stored to preserve the critical properties necessary for successful transplantation, that is, fresh or cryopreserved storage for osteochondral allografts. l Disease transmission can be a problem with musculoskel etal allografts, and unless a sporicidal method of second ary sterilization is used, a graft should not be considered sterile. Secondary sterilization does not guarantee sterility or safety. l Allografts may be used for any ligament reconstruction, but revision ACL surgery and multiligamentous knee injuries are situations in which allograft tissue may be particularly indicated. l Patient selection is critical to the outcomes of menis cal allograft transplantation and osteochondral allograft transplantation. Associated knee pathology should be treated before these procedures or at the index surgery. l Outcomes of osteochondral allograft surgery are encour aging given this difficult problem in a relatively young patient population.

S U G G E S T E D

R E A D I N G S

American Association of Tissue Banks: Standards for Tissue Banking. MacLean, Va, American Association of Tissue Banks, 2006. Caldwell PE 3rd, Shelton WR: Indications for allografts [review]. Orthop Clin North Am 36(4):459-467, 2005. Centers for Disease Control and Prevention: Update: Allograft-associated bacterial infections—United States, 2002. MMWR Morb Mortal Wkly Rep 51:207-210, 2002. Cook JL: The current status of treatment for large meniscal defects [review]. Clin Orthop 435:88-95, 2005. Gross AE, Shasha N, Aubin P: Long-term follow-up of the use of fresh osteochon dral allografts for posttraumatic knee defects. Clin Orthop 435:79-87, 2005. Lee SJ, Aadalen KJ, Malaviya P, et al: Tibiofemoral contact mechanics after se rial medial meniscectomies in the human cadaveric knee. Am J Sports Med 34(8):1334-1344, 2006. Rihn JA, Harner CD: The use of musculoskeletal allograft tissue in knee surgery. Arthroscopy 19(Suppl 1):51-66, 2003. Shelton WR: Arthroscopic allograft surgery of the knee and shoulder: Indications, techniques, and risks. Arthroscopy 19(10 Suppl 1):67-69, 2003. Spak RT, Teitge RA: Fresh osteochondral allografts for patellofemoral arthritis: Long-term followup. Clin Orthop 444:193-200, 2006. Vangsness CT, Wagner PP, Moore TM, Roberts MR: Overview of safety issues concerning the preparation and processing of soft-tissue allografts. Arthroscopy 22(12):1351-1358, 2006.


C H A P T E R

3

Nonorthopaedic Conditions S ect i o n

A

Infectious Disease and Sports Rob Johnson and William Knopp

Infectious disease in athletes poses unique circumstances and challenges. The circumstances of an ill-timed infection can prevent training or competition with little advanced warning. The challenges are to promptly recognize the problem, initiate appropriate treatment, return the athlete to practice and play safely, and prevent spread amongst teammates, coaches, and contacts (family, friends, and spectators). The average adult experiences one to six upper respiratory tract infections (URTIs) per year.1 This translates into about 100 million URTIs and 250 million days of activity restriction.2 And this only represents the risk for the common rhinovirus! Added to common infections, the infectious exposures posed by the athletes’ training regimen, travel, and daily communal training and competition environments virtually guarantee that infectious disease will affect the athlete.3 Pathogens can single out the recreational athlete, the regular exerciser, the citizen competitor, or the team-sport athlete at every level of competition. Consequently, the sports and team physician must be knowledgeable of the more common threats and possess the skills to diagnose and treat them.

EFFECTS OF TRAINING AND COMPETITION ON THE IMMUNE SYSTEM The effects of exercise and training are addressed in two different ways: the effects of a single bout of exercise and the long-term effects and observations. A brief review of the components of the immune system provides a context for interpreting the data regarding the acute and chronic effects of exercise on the immune system and illness. The innate immune system is the body’s broad, nonspecific, first line of defense consisting of the skin, mucous membranes, upper and lower respiratory systems, specific cell types such as phagocytes and natural killer (NK) cells, humoral factors such as cytokines, and various complement factors.4 Within the mucous membrane is secretory

immunoglobulin A (IgA) that identifies and alters viral particles to enhance control and removal of the virus. The release of cytokines and complement is the initial response of the immune system to an infectious stimulus. This response activates and controls the T cells and B cells that represent a specific response of the acquired immune system to the infectious agent. T- and B-cell activity is specific to the infectious agent, viral or bacterial. Both T cells and B cells have memory for the specific infectious agent maintaining antibodies against the agent. The duration of memory and antibody activity is highly variable. An initial response of the immune system to an acute, intense bout of exercise is an increase in leukocytes, predominantly composed of neutrophils, with a mild increase in lymphocytes and monocytes.5,6 This acute response is triggered by catecholamines and cortisol. NK cells increase 150% to 300% immediately after an exercise bout of less than 1 hour, but then fall to less than baseline within 30 minutes after exercise.7 An exercise session lasting more than 1 hour fails to incite a similar NK-cell response. Macrophages also increase with an acute exercise bout. This response is blunted in athletes who train regularly, but levels are still higher than those in untrained individuals.7 Secretory IgA concentrations are impaired by long, intense exercise sessions.8,9 Based on this information, there is no correlation of these depressed levels with a higher rate of respiratory infection. Another study of secretory IgA levels over the course of a football season, however, demonstrated both significantly diminished levels of IgA and a diminished secretory rate of IgA.10 The outcome measured was the incidence of URTIs. The lower IgA levels and secretion were associated with more URTIs. The level of IgA was a predictive factor in the risk for developing URTI. Cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and IL-6, another factor within the innate immune system, increase with a single bout of intense exercise.11 Some factors show dramatic increases. A summary of the effects of a single bout of exercise is shown in Table 3A-1. 147

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TABLE 3A-1 Immune System Function Changes

High

with Exercise

Increased after Acute Exercise Bout

Increased after Training Period

Neutrophil concentration Monocytes (chemotaxis, adhesion) Dendritic cell concentration (T-cell inducer) Th2 dominance (bacterial protection)

NK-cell function Monocyte function Vaccination response

Decreased after Acute Exercise Bout

Th1 dominance (viral protection) Decreased after Training Period

NK-cell function Delayed-type hypersensitivity Lymphocyte function Mucous immunoglobulin A production Monocytes (major histocompatibility complex enzymes) (Adapted from Malm C: Exercise immunology: The current state of man and mouse. Sports Med 34[9]:555-566, 2004.)

The response of the immune system to a single bout of exercise demonstrates acute increases during or immediately after exercise, followed by levels decreasing to or below baseline, giving support to the open-window theory.7 This hypothesis suggests that the athlete is at increased risk for infection if exposed to pathogens during the “window” of decreased immune surveillance. The concern for the athlete is to observe precautions in exposure and hygienic practices to reduce risk during this vulnerable period. Animal studies have looked at this very issue. Inoculation of rats after an exhaustive bout of exercise showed that the rats were protected against infection compared with another group that was already infected and performed a similar bout of exercise. The infected group had progression to more severe symptoms.12,13 Another study comparing trained mice with untrained mice showed less damage to the myocardium after infection with either bacterial or viral pathogens in the trained mice.14 The trained mice, however, also showed more severe symptoms and outcomes when exercising after they were infected. The effects of long-term training on the immune system are largely reflected in the epidemiologic studies of training and infection. Generally, individuals who train aerobically on a regular basis perceive themselves as having fewer infections than untrained people.15 Several randomized studies by Nieman support this perception.7 These studies demonstrated that near-daily physical activity reduces the number of days of reported illness. Other research shows a 23% decrease in URTIs in people who train on a regular basis, and another found that URTI development is inversely related to the level of moderate physical activity.16,17 Marathoners training in excess of 97 km (60 miles) per week self-reported twice the rate of URTI than those training at distances of less than 97 km.18 Marathoners also self-reported URTI at a rate of 33% within 2 weeks of completing a marathon, compared with controls who reported a rate of 15%.19 Using total training time or volume to explain infection risk is probably oversimplification because other factors, including stress, malnutrition, and weight loss, are likely contributors to infection risk.20

Average

Low Sedentary

Moderate

Very high

Exercise workload Figure 3A-1 Infection risk (J-curve). (Adapted from Nieman DC: Current perspective on exercise immunology. Curr Sports Med Rep 2:239-242, 2003.)

The effects of regular exercise on the immune system are summarized in Table 3A-1. As a result of randomized and epidemiologic studies of regular exercisers, Nieman proposed a J-curve theory for infection risk.7 He hypothesized that the untrained and elite athletes at opposite ends of the training spectrum are at greater risk for infectious illness than those who train moderately (Fig. 3A-1). The data to support this, however, are either conflicting or insufficient for those at the upper end of the training spectrum. Interestingly, athletes diagnosed with overtraining syndrome, presumably at the high end of the training spectrum, demonstrated normal cell counts and fewer infections than well-trained athletes.21,22 Similar immune function benefits can be observed in the older population. Training in the elderly population results in improved immune function compared with those who do not train.23 Vaccination response in elderly people is also improved in those who exercise regularly.24 In summary, those who exercise regularly have fewer infections than those who are sedentary and those who train at high levels and for long durations. If exposed to infection after an intense bout of exercise, the athlete is relatively protected. If already symptomatic with an infection, intense exercise may increase the severity of the illness. For those training on a regular basis or competing at a high level, preventing illness is a priority. Nieman offers common-sense recommendations to reduce infection risk7: 1. Minimize other stressors. 2. Ensure adequate nutritional intake, especially carbohydrates. 3. Avoid fatigue from “excessive” training. 4. Ensure adequate rest during training cycles. 5. Avoid rapid weight loss. 6. Avoid infectious exposure and inoculation. 7. Minimize or avoid potential infectious exposures before important competitions. 8. Obtain appropriate vaccines.

Nonorthopaedic Conditions

EPIDEMIOLOGY OF OUTBREAKS The most typical scenario for infectious disease is a single athlete contracting an infection by droplet, aerosolized, fecal-oral, or more rarely, blood-borne transmission. The athlete is diagnosed and treated with minimal disruption of the training cycle and competition. A more troublesome development is the occurrence of an outbreak of infectious illness. In a review of infectious disease outbreaks in athletes (1966-2005), Turbeville and colleagues found three modes of transmission: direct (skin-to-skin), indirect (respiratory, fecal-oral, body fluids), and common source (e.g., equipment, water bottles, soap, towels, whirlpools).3 Football, accounting for 34% of the reported infectious outbreaks, wrestling (32%), and rugby (17%) were the most common sports reporting outbreaks. A variety of other sports reported infrequent outbreaks. The responsible pathogens varied much more than the affected sports. Herpes simplex virus (22%) and Staphylococcus aureus infection (22%) accounted for most of the football, wrestling, and rugby outbreaks. Enteroviruses (19%) and tinea (14%) ranked next in frequency. The only aerosolized pathogen implicated in sports-related outbreaks was measles, responsible for 5% of the outbreaks. The sports and organisms most often involved support the finding of skin as the most commonly affected site of infectious outbreaks.

RESPIRATORY INFECTIONS Upper Respiratory Infection The “common cold” is just that—common. The average adult experiences one to six URTIs per year, caused 40% of the time by rhinoviruses.1 Athletes experience the same potential exposure and consequently will be infected at some time, likely during their competitive seasons. Cold exposure, especially in outdoor sports during the fall and winter seasons and indoor ice arenas, may increase the risk by drying the mucosal surfaces of the respiratory tract, adversely affecting the cilia and inhibiting the ability to serve as an effective barrier to viral illness.25 Parainfluenza and influenza illnesses also place athletes and physically active people at risk. These agents occur as more seasonal phenomena. The URTI, a self-limited illness, usually presents with onset of nasal congestion, rhinorrhea, lethargy, sore throat, cough, and low-grade fever. The symptoms may intensify over 3 to 5 days, then slowly resolve. Analgesics and antipyretics (acetaminophen, ibuprofen) and decongestants or decongestant-antihistamine combinations may be used for symptomatic treatment. Decongestant nasal sprays, such as oxymetazoline, may also be used. Be careful to limit their use to 4 to 5 days to minimize the likelihood of rhinitis medicamentosa (mucosal dependence on topical decongestants). Sinusitis and otitis media are potential, but infrequent, complications of URTIs. The effects of both individual exercise and training sessions and long-term training on infectious disease have previously been discussed. The important consideration, then, becomes whether to train or compete during the

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illness or to rest and resume training and competition when symptoms permit. Based on animal studies, exercising after acquiring a bacterial infection may intensify the symptoms.12,13 Does this same risk apply to the common cold? Certainly, we have all witnessed media reports or actual contests where “sick” athletes performed at high levels with no apparent adverse effects. Are these performances exceptions or are they the rule? Sedentary subjects who performed exercise after naturally acquiring a URTI did not experience an effect on the symptoms or duration of the illness compared with nonexercising controls.26 A 3-year study of elite swimmers with mild illness and the effect on competitive performance demonstrated that female swimmers had a 32% chance of a beneficial effect, 31% chance of a trivial effect, and 37% chance of harmful effect on performance.27 Compare this to male swimmers, who had a 17% chance of beneficial effect, 31% chance of trivial effect, and 52% chance of harmful effect on performance. These results imply confounding factors of forced rest or modifying training because of the illness or, perhaps, that the individual’s perception of illness and effects or lack of effects can be overcome by effort. Viral and bacterial pharyngitides are other common URTIs. Certainly, identifying group A, β-hemolytic streptococcal infections is important for the potential sequelae of glomerulonephritis or rheumatic fever with associated valvular involvement. Viral pharyngitides, in association with rhinoviruses and influenza viruses, are far more common than streptococcal infections in adults (about 10% of adult sore throats) and more common in childhood and adolescence (about 50%). Participation with these illnesses can be treated as other viral illnesses, a topic that is discussed later. Sinusitis is a potential complication of, or comorbidity with, URTIs. The initial symptoms may resemble those of URTI. Consider the diagnosis of acute bacterial sinusitis in those who have URTI symptoms, usually lasting longer than 7 days and less than 4 weeks, accompanied by two of the following findings: purulent nasal discharge; maxillary, tooth, or facial pain or tenderness; unilateral maxillary sinus tenderness; or worsening of URTI symptoms after an initial course of improvement.28 Infectious mononucleosis poses additional return-to-play considerations and is discussed in a separate section. Available data suggest that participating with a URTI is athlete dependent. The risk appears to be only performance related without significant disease sequelae.

Lower Respiratory Infection Lower respiratory infections are less common than URTIs. Acute bronchitis and pneumonia constitute the common spectrum of lower respiratory infectious illness. Acute bronchitis, the most common lower respiratory illness in adults, is inflammation of the respiratory tree (trachea, bronchi, bronchioles).29 The responsible pathogens are most commonly of viral origin, including influenza A and B, parainfluenza viruses, coronaviruses, rhinoviruses, and adenoviruses. Bacterial sources are also implicated in bronchitis but are less common. The typical presenting symptoms are dry cough (lasting less than 3 weeks) and mild lassitude. Physical examination findings may be scant.

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Auscultation of the chest can occasionally yield course breath sounds or wheezes. The diagnosis is made based on history and examination. A chest radiograph is rarely necessary. Treatment is symptomatic. The cough, which may be exacerbated with exertion or lying down, can be treated with β2-agonist inhalers because bronchoconstriction is often the cause. Antibiotics are rarely indicated in treating acute bronchitis. If the cough persists for more than 3 weeks, further diagnostic investigation is warranted.29 Pneumonia is the other common cause of lower respiratory infection. Although the symptoms may be similar to those of bronchitis, the cough is productive of purulent sputum and is accompanied by fever, myalgias, and fatigue. Chest auscultation reveals crackles. Chest radiograph confirms the clinical suspicion. If influenza A or B is suspected, amantadine, rimantadine, or oseltamivir is an appropriate treatment choice. If bacterial causes are likely, a macrolide or doxycycline is an appropriate choice.29 Return-to-play decisions have been made based on tradition, individual experience, and expert opinion. Solid evidence is lacking as we guide athletes back to play after respiratory infections. An elevated temperature (commonly cited as 100.6° F, 38° C) can impair muscle strength, pulmonary perfusion, cognitive function, increase metabolic parameters, and increase insensitive fluid losses, all factors that can impair athletic performance.4,30 Fortunately, this is an objective measure, whereas many of the other recommendations involve subjective interpretations. The elevated body temperature is a relative guide for the clinician to place in the context of the history, symptoms, and physical examination. A common guideline developed by Eichner is a reasonable, practical approach to safely returning athletes to participation.31 He labels this process, the “neck check.” If the symptoms are all occurring above the neck (sore throat, congestion, rhinorrhea), participation is probably okay. If the symptoms include myalgias, elevated body temperature, or significant cough, participation is probably unwise. Included as a part of the neck check, probably the most practical of the recommendations, is a brief warm-up. If after a brief warm-up there is no worsening of symptoms, participation may be considered. If symptoms worsen, participation should be terminated. Animal studies raise the possibility of worsening symptoms of an illness when performing high-intensity exercise after symptoms of illness have occurred.13

INFECTIOUS MONONUCLEOSIS Infectious mononucleosis carries clinical implications (splenomegaly, fragile spleen) for athletes that other infectious illnesses lack. For that reason, careful consideration is necessary in the diagnosis and decision making regarding return to play. Infectious mononucleosis is a viral illness caused by the Epstein-Barr virus (EBV) and is spread by salivary contact. The incubation period is long, ranging from 30 to 50 days after exposure.32 The typical clinical presentation consists of a 3- to 5-day prodrome of lethargy, headache, and loss of appetite. For the next 5 to 15 days, the athlete experiences the more typical symptoms of sore throat, fever, swollen glands (particularly the posterior submandibular nodes), and

fatigue.33 The peak incidence of infectious mononucleosis occurs in the 15- to 21-year-old group, the most common years of competitive athletic participation. In fact, in the college age group, 1% to 3% are infected annually.34 Commonly, younger children may have infectious mononucleosis with minimal or no symptoms. As a result, many adults, without a specific recollection or clinical history of infectious mononucleosis, are seropositive (by heterophil antibody test, or Mono-Spot test) when tested.35,36 When presented with an athlete with a sore throat and fatigue, a history consistent with mononucleosis, and physical findings suspicious for mononucleosis, further evaluation is necessary to confirm the diagnosis. Laboratory results consistent with mononucleosis include a leukocytosis (white cell count, 15,000 to 25,000) with an absolute lymphocytosis (10% to 20% atypical) and a positive heterophil antibody test (typically the Mono-Spot).37,38 The heterophil antibody test usually becomes positive 5 to 7 days after the onset of the prodromal symptoms. The sensitivity of the heterophil antibody test is 63% to 85%, and the specificity is 84% to 100%.39 The low sensitivity is thought to be related to performing the test too early in the course of the illness before the test is expected to yield positive results. When the heterophil antibody test is positive, but the clinical course and physical examination are inconsistent with the diagnosis of infectious mononucleosis, the next step is to obtain the EBV IgG virally encoded antigen (VCA) and EBV IgM VCA serologies to determine whether the illness is, indeed, an acute case of infectious mononucleosis. EBV IgG VCA levels begin to rise within the first few days of the illness and decline from a maximum after 2 to 3 months to a steady-state level that may remain present for life. EBV IgM VCA represents an acute response appearing during the early symptoms and declining to undetectable levels after 1 to 3 months. Because the heterophil antibody screening tests for infectious mononucleosis are IgG based, a person’s heterophil antibody test may remain positive for a lifetime.40 If the implications for return to play were insignificant, confirming the diagnosis in atypical cases would be unimportant. Because splenomegaly associated with infectious mononucleosis has the potential for a substantial delay in returning to play interfering with a considerable portion of an athlete’s season, testing for the EBV serologies to confirm the diagnosis is recommended. If EBV IgG is present, but IgM is not, the illness is not infectious mononucleosis, and the athlete can return to play when symptoms permit. Liver function tests may increase 2 to 3 times above normal, usually peaking by the second or third week and returning to normal by the fifth week.33 These tests are probably not clinically relevant unless the athlete appears icteric. They seldom affect the clinical course and returnto-play decisions. Obtaining a “rapid strep” test to evaluate for concomitant group A, β-hemolytic streptococcal infection is advised. Studies of infectious mononucleosis have shown a coexisting group A, β-hemolytic streptococcal infection in 30% of cases.33 Treatment of infectious mononucleosis is supportive. Analgesics can be used to treat pain and fever. Rest or relative rest and no sport or training participation for at


least 3 weeks from illness onset is recommended because spontaneous splenic rupture is thought to be a risk during this time frame. In practice, if the tonsils are swollen enough to cause the individual to have difficulty handling oral secretions, a short course of prednisone can be used to reduce tonsillar hypertrophy. Use of corticosteroids does not otherwise alter the course of infectious mononucleosis. The controversial issues with infectious mononucleosis, then, involve splenomegaly and return-to-play decisions. During the course of mononucleosis, the spleen undergoes lymphocytic infiltration with enlargement within the first few weeks. The lymphocytic infiltration distorts the normal anatomy and support structures of the spleen, causing both enlargement and increased fragility.41 These changes result in an increased risk for splenic rupture but otherwise have no effect on the course of the illness. Splenomegaly in infectious mononucleosis is estimated to occur in 50% to 100% of cases.38,42 Splenic rupture associated with infectious mononucleosis occurs in 0.1% to 0.2% of cases.33 Case reports have documented both spontaneous rupture and rupture as a result of athletic activity. These same case reports showed that the timing of rupture occurs between day 4 and day 21 from the onset of symptoms. Clinical determination of splenomegaly is unreliable.43 As a result, various imaging techniques have been assessed for accuracy in determining spleen size. Computed tomography, magnetic resonance imaging, and ultrasound of the spleen are accurate in assessment, but defining the normal spleen size proves more difficult. A recent study of college athletes performed during their preparticipation examinations showed that 7% of asymptomatic athletes had spleens that exceeded the accepted normal size range.44 In general, male athletes had larger spleens than female athletes, and white males had larger spleens than African American males. Because of the variability of normal spleen size, the most effective means of using ultrasound is to obtain a baseline splenic ultrasound at admission to either high school or college for comparison in the event of mononucleosis occurring at a later time. However, this is both logistically and economically impractical given the low incidence of mononucleosis in these populations. Thus, we are left with clinical decision making based on experience, or the best evidence available. The usual standard of care in regard to return to play applies. The athlete should be free of symptoms, have a normal energy level, be well hydrated, and have no palpable splenomegaly; the athlete participating in a noncollision sport should be at least 21 days beyond the onset of symptoms. Rarely does splenomegaly continue beyond the fourth week. Although the timing of return to play for collision sports remains controversial, safe return is possible by the third to fourth week after the onset of symptoms. Many team physicians continue to use some form of imaging to assist in these decisions, but the wide variability of normal spleen size makes interpretation of the imaging unreliable. If a preseason, baseline splenic size has been determined, following the infectious mononucleosis spleen with serial ultrasounds to peak spleen size and resolution provides the clinician with objective return-to-play information.32 Again, however, this is expensive and impractical.

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After confirming the diagnosis of infectious mononucleosis by a combination of clinical and laboratory information, the athlete should refrain from physical activity until at least 3 weeks from the onset of symptoms. Return to play is permitted if the athlete is completely symptom free and has no palpable spleen. Return to collision sports may be entertained at this time, but more safely, based on available information and practice tradition, at 4 weeks.

CARDIAC INFECTIONS Myocarditis Myocarditis is an uncommon phenomenon, in general, and is even less common in athletes. The consequences, however, have serious potential. Myocarditis, in most studies of exertional sudden death, is cited as a cause of death 10% to 42% of the time.45-47 As a result, physicians working with athletes with illness must be vigilant for symptoms suggestive of cardiac involvement. Myocarditis is defined as an inflammation of the myocardium with myocellular necrosis.48 The clinical diagnosis may be difficult because of variable symptoms at presentation. Some patients may be completely asymptomatic but then rapidly develop symptoms of congestive heart failure, syncope, and even sudden death as a result of a rhythm disturbance.48 Although this course is atypical, one must be suspicious of any symptoms of chest pain, rapid heart rate, and tachypnea following a recent, seemingly innocuous, viral illness. The incidence of myocarditis is low, ranging in frequency from 0.001% to 0.2 %.47 Men are diagnosed more frequently than women (62% versus 38%), and the affected individuals are usually younger than 40 years.47 The infectious cause is most often Coxsackie B virus, followed by human immunodeficiency virus (HIV), adenovirus, and cytomegalovirus (CMV). Medications such as doxorubicin may also be responsible as a chemical cause of myocarditis. Ampicillin, sulfa, lithium, hydrochlorothiazide, and indomethacin may cause myocarditis mediated by a hypersensitivity reaction.48 When myocarditis occurs, the acute phase may last up to 3 days. The subacute phase (days 4 to 14) is mediated by the immune response to the infectious process. It is this response that causes the myocardial damage.48 If, during the chronic phase (variably from days 15 to 90), the immune response continues, causing further myocardial damage, cardiomyopathy may result. If the immune response is moderate, complete recovery is likely. In fact, there are estimates suggesting that 5% of asymptomatic people have myocarditis with viral illnesses but recover completely.49 Diagnosing myocarditis is largely based on history and physical examination findings of tachypnea, tachycardia, S3, apical murmur, rales on chest auscultation, and distended neck veins. Information supporting the diagnosis includes elevations of several blood tests, including creatine kinase, troponin, erythrocyte sedimentation rate (ESR), and C-re active protein. The electrocardiogram is usually abnormal, but the changes are nonspecific. The chest radiograph may demonstrate increased left ventricular size. If the athlete

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has findings consistent with a diagnosis of myocarditis, consult a cardiologist for possible biopsy and further treatment recommendations. For most, the treatment is supportive with symptom management and diuretics and angiotensinconverting enzyme inhibitors when necessary.48 Although complete recovery is the usual result, 10% to 30% of patients may have a dilated cardiomyopathy. As many as 10% may be at risk for death due to congestive heart failure or arrhythmias.50 According to the guidelines published by the 36th Bethesda Conference, there should be 6 months of recovery before considering return to play.51

Pericarditis Pericarditis is defined as an inflammation of the pericardial sac. As with myocarditis, pericarditis has return-to-play implications. Thus, the sports physician must be familiar with the problem and its athletic implications. Pericarditis is typically infectious in origin, with viral pathogens most often responsible. URTIs often precede pericarditis.52 Of all causes of chest pain presenting to emergency departments, 5% are diagnosed as pericarditis.53 Of those diagnosed, most are in young adults.54 When pericarditis occurs, the inflammatory process, infectious disease, or other cause (e.g., hypersensitivity reaction, autoimmune disease) results in vascular permeability, causing fluid to accumulate within the pericardial sac. Given enough fluid within the pericardial sac, the fluid serves as a constraint to left ventricular filling and causes subsequent cardiac dysfunction. Clinical signs and symptoms suggestive of pericarditis include flu-like symptoms with chest pain and friction rub at the left middle and lower sternal border with ST elevation in all leads of the ECG. Sinus tachycardia may also be seen.55 Other confirmatory tests include echocardiography and elevated ESR. Cardiac enzymes are typically normal. Because most episodes of pericarditis are self-limited, the primary treatment is supportive. Nonsteroidal antiinflammatory drugs can be given in uncomplicated cases. For more severe situations, corticosteroids can be used, but these are rarely necessary. Most symptoms resolve within 2 weeks.55 Pericardiocentesis is rarely indicated. The 36th Bethesda Conference recommendations for athletes and physically active individuals urge no activity during the acute phase (usually 2 weeks). After the acute phase, athletes may return to activity when there is no evidence of active disease.51 If there is evidence of myocardial involvement, return-to-play decisions should be the same as those recommended for myocarditis, that is, 6 months of recovery. Recurrence of pericarditis is rare in the situation of infectious pericarditis. However, when no cause can be identified (idiopathic pericarditis), the recurrence rate may be as high as 15% to 30%.56

INFECTIOUS DIARRHEA Athletes and physically active adults develop infectious diarrhea with a frequency similar to a sedentary population. Rare outbreaks may develop as a result of specific sports competition.

Common causes of community-acquired diarrhea are Salmonella, Shigella, and Campylobacter species, Escherichia coli O157:H7, and Clostridium difficile infection.57 Most are self-limited illnesses and need only supportive treatment such as rehydration, dietary modification, and, possibly, antidiarrheal agents. If the diarrhea is associated with a significant fever or blood in the stool, stool cultures are obtained to identify the causative agent. When the responsible pathogen is identified, treatment is begun with the appropriate antibiotic, including a quinolone for suspected Shigella species infection or a macrolide for suspected Campylobacter species infection.57 For a diarrheal illness without fever or bloody stool that persists for more than 7 days, consider other pathogens such as parasites (especially with travel outside the athlete’s usual locale), such as Giardia, Cryptosporidium, or Cyclospora species infection. In this situation, obtain a stool sample for ova and parasites. If symptoms warrant, consider evaluation for inflammatory bowel disease. Treatment is based on the organism identified by the examination for stool pathogens.57 Specific gastrointestinal outbreaks associated with water-sport activities have been reported. Leptospirosis (spirochete of various Leptospira species) has been identified in tri-athletes exposed to contaminated fresh water during the swimming portion of the event.58 Paddle-sport athletes are also at risk if exposed to contaminated water. Symptoms of fever, nausea, vomiting, and diarrhea occur following an incubation period of 2 to 20 days. A late phase of the illness may cause aseptic meningitis, rash, or uveitis. Those with severe symptoms may have to be hospitalized for parenteral therapy. Those with mild to moderate symptoms may be treated with doxycycline, 100 mg twice daily for 7 days, or amoxicillin, 500 mg 4 times a day for 7 days.58 Giardia species outbreaks have also been associated with fresh-water paddle and swimming sports.58 Persistent, intermittent diarrhea is the prominent physical complaint with this illness. Stool samples for ova and parasites yield the diagnosis 70% of the time. Direct stool antigen assay has a sensitivity of 98%.58 The recommended treatment is metronidazole, 250 mg 3 times a day for 5 to 7 days.

URINARY TRACT INFECTIONS Diagnosis of urinary tract infection (UTI) is one of the most common diagnoses of infectious disease, and athletes are also be afflicted with this annoying problem.59 Half of all women in the United States and Canada report at least one UTI over the course of a lifetime.60 Based on these data, women athletes are more likely than male athletes to report symptoms consistent with UTI during the course of training and competition. Typical presenting symptoms are urgency, dysuria, and urinary frequency. Dipstick urinalysis positive for leukocyte esterase (specificity, 94% to 98%; sensitivity, 75% to 96%) or nitrites accompanying the classic symptoms is usually adequate for the diagnosis.61 A urine culture with sensitivities is confirmatory but not necessary in the uncomplicated UTI. For someone with a history of recurrent UTIs, the culture and sensitivities become increasingly valuable to identify specific pathogens.


Treatment of an uncomplicated UTI is with t rimethoprim-sulfamethoxazole, 160/800 mg twice a day for 3 days. For a treatment failure or history of resistant organisms, ciprofloxacin, 250 mg twice daily for 3 days, or nitrofurantoin, 100 mg twice daily for 7 days, is an acceptable choice. For postmenopausal female athletes, the treatment choices are identical, except the duration of therapy is extended to 7 days.62 Men have a low incidence of UTIs, especially in the most active age group, 15 to 50 years of age. As a result, research and recommendations for treatment are limited. Diagnosis and treatment are similar to that in women. Treatment, however, should be for at least 7 days because the likelihood of complications is higher in men. Nitrofurantoin has poor tissue penetration and is not recommended in men.62,63

BLOOD-BORNE INFECTIONS Human Immunodeficiency Virus About 1 million Americans are infected with HIV. The acute infection of HIV is similar to that of mononucleosis or CMV and includes fever, malaise, and lymphadenopathy, but not all individuals develop symptoms during the acute infection. There is a long asymptomatic state lasting for many years during which the person is healthy and unaware that he or she is infected and allowing spread of the disease.64 As the infected person’s CD4 counts decline, he or she will develop opportunistic infections and neoplasms and, ultimately, overt acquired immunodeficiency syndrome (AIDS). Because of its extremely long asymptomatic period, the potential for transmission is high. HIV is present in body fluids, but only blood poses a significant risk for transmitting the virus. Direct contact of body fluids with open wounds or mucous membranes is required for infection. There is no evidence that an individual can acquire HIV through intact skin. There is only one suspected case of possible transmission of HIV in a professional soccer player in Italy in 1990, but there is insufficient evidence to confirm transmission.64 Given the prevalence of the disease and no confirmed transmission of HIV in the athletic setting, the risk for transmission from one athlete to another is exceedingly low. One study calculated the risk to an NFL football player to be 1 per 85 million games.64 The risk for an athlete acquiring HIV is greatest off the field of play through unsafe sexual practices; shared needles with the use of ergogenic aids such as anabolic steroids, growth hormone, and erythropoietin; and illicit parenteral drug use. Because an effective vaccine for HIV is not available and treatment at this point is not curative, prevention is paramount. Universal precautions should be used without exception by all coaches and medical personnel when caring for athletes. Athletes with open wounds that can bleed in competition should be protected in such a way that they can withstand the demands of competition. If an athlete has anything more than a superficial scratch or abrasion, he or she should be removed from competition until the wound is appropriately covered and blood

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soaked clothing removed and replaced. A detailed list of preventive measures has been documented by the American Academy of Pediatrics65 and the American Medical Society for Sports Medicine (AMSSM) and American Orthopedic Society for Sports Medicine (AOSSM).64 The detailed measures recommended by the AMSSM and AOSSM follow: 1. Pre-event participation includes proper care for existing wounds. Abrasions, cuts, or oozing wounds that may serve as a source of bleeding or as a portal of entry for blood-borne pathogens should be covered with an occlusive dressing that will withstand the demands of competition. Likewise, care providers with healing wounds or dermatitis should have these areas adequately covered to prevent transmission to or from a patient. 2. Necessary equipment or supplies important for compliance with universal precautions should be available to caregivers. These supplies include latex or vinyl gloves, disinfectant, bleach (freshly prepared in a 1:10 dilution with tap water), antiseptic, designated receptacles for soiled equipment or uniforms (with separate waterproof bags or receptacles appropriately marked for uniforms and equipment contaminated with blood), bandages or dressings, and a container for appropriate disposal of needles, syringes, or scalpels. 3. During the sports event, early recognition of uncontrolled bleeding is the responsibility of officials, athletes, and medical personnel. Participants with active bleeding should be removed from the event as soon as this is practical. Bleeding must be controlled and the wound cleansed with soap and water or an antiseptic. The wound must be covered with an occlusive dressing that will withstand the demands of the activity. When bleeding is controlled and any wound properly covered, the player may return to competition. Any participant whose uniform is saturated with blood, regardless of source, must have that uniform changed before returning to competition. 4. The athletes should be advised that it is their responsibility to report all wounds and injuries in a timely manner, including those recognized before the sporting activity. It is also the athletes’ responsibility to wear appropriate protective equipment at all times, including mouth protectors, in contact sports. 5. The care provider managing an acute blood exposure must follow the guidelines of universal precautions. Appropriate gloves should be worn when direct contact with blood, body fluids, and other fluids containing blood can be anticipated. Gloves should be changed after treating each participant, and as soon as practical after glove removal, hands should be washed with soap and water or antiseptic. 6. Minor cuts and abrasions commonly occur during sports. These types of wounds do not require interruption of play or removal of the participant from competition. Minor cuts and abrasions that are not bleeding should be cleansed and covered during scheduled breaks in play. Likewise, small amounts of bloodstain on a uniform do not require removal of the participant or a uniform change.

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7. Lack of protective equipment should not delay emergency care for life-threatening injuries. Although HIV is not transmitted by saliva, medical personnel may prefer using airway devices. These devices should be made available whenever possible. 8. Any equipment or area (e.g., wrestling mat) soiled with blood should be wiped immediately with paper towels or disposable cloths. The contaminated areas should be disinfected with a solution prepared with 1 part household bleach to 10 parts water and should be prepared fresh daily. The cleaned area should be dry before reuse. Persons cleaning equipment or collecting soiled linen should wear gloves. 9. Postevent considerations should include re-evaluation of any wounds sustained during the sporting event. Further cleansing and dressing of the wound may be necessary. Also, blood-soiled uniforms or towels should be collected for eventual washing in hot water and detergent. 10. Procedures performed in the training room are also governed by adherence to universal precautions. Care providers should wear gloves. Any blood, body fluids, or other fluids containing blood should be cleaned in a manner as described previously. Equipment handlers, laundry personnel, and janitorial staff should be advised to wear gloves whenever contact with bloody equipment, clothing, or other items is anticipated. Appropriate containers for the disposal of needles, syringes, or scalpels should be available. 11. Members of the athletic health care team are considered to be covered by Occupational Safety and Health Administration guidelines. Assessment of the application of these guidelines must be made on an individual basis. This application may include consideration for hepatitis B virus (HBV) immunization for some personnel who are involved with the athletic health care team. No recommendation has been specifically made for the immunizations against HBV for athletes in particular. However, several groups now recommend universal immunization against HBV of the newborn and college-age groups.64 The decision to allow the participation of an athlete who is HIV positive should be individualized and should involve the athlete, his or her parents (if appropriate), the athlete’s personal physician, and the team physician. Factors affecting the decision to participate should include the athlete’s current state of health, the status of the HIV infection, the nature and intensity of training, the potential contribution of stress from athletic competition, and the potential risk for transmission. Although the data are limited, the following exercise guidelines have been suggested66: 1. Exercise is a safe and beneficial activity for the HIVinfected person. 2. HIV-infected individuals should begin exercising while healthy and adopt strategies to help them maintain an exercise program throughout the course of their illness. 3. HIV-infected persons, through the use of exercise, can play an important role in the management of their illness, while improving quality of life.

4. Exercise has the potential of other subtle and effective behavioral therapeutics benefits regardless of ethnicity, exposure category, or gender and is particularly promising in areas in which pharmacologic treatments are not readily available (e.g., underdeveloped countries). Mandatory testing is not recommended by any organization because of the extremely low risk for athletic transmission and because mandatory testing would not result in preventing transmission in sport. The ethical, moral, legal, medical, financial, and logistical considerations in mandatory testing for HIV or other blood-borne illnesses are challenging and beyond the scope of this discussion. Testing for HIV should be performed if there is a known exposure or the athlete has had multiple sexual partners, uses intravenous (IV) drugs or ergogenic aids, has sexual contact with at-risk persons, has had other sexually transmitted diseases including HBV, or had a blood transfusion before 1985.64 If an athlete is HIV positive, this information can be used to protect and treat the infected athlete, his or her sexual partner, and other athletes. Because of patient-doctor confidentiality matters, the athlete’s physician should not reveal an athlete’s HIV status to the coach, the school, or anyone involved with the athlete. This is to protect the athlete’s ability to participate in athletics safely and without discrimination. The present laws protect the physician from any legal responsibility for not revealing an athlete’s HIV status.65

Hepatitis A, B, C, D, and E Five viruses cause the majority of infectious hepatitis in the United States: hepatitis A, B, C, D, and E. The prevalence of infectious hepatitis among competitive athletes in not known.67 The risk for acquiring hepatitis as a result of active participation in sports is extremely low, and the athlete is much more likely to acquire these infections from off-field activities. Although there are no official recommendations requiring immunization, it is recommended that all athletes be immunized against HBV, and athletes who will compete in areas at high risk for hepatitis A virus (HAV) should also receive HAV vaccination. As of 2007, it is recommended that all children born in the United States be immunized against HAV and HBV. The symptoms and signs of all forms of hepatitis are similar and may include asymptomatic infection, anorexia, malaise, fatigue, myalgia, arthralgia, diarrhea (more common in children), jaundice, headache, right upper quadrant pain and fever (more common in HAV), serum sickness syndrome, pharyngitis, hepatomegaly, splenomegaly, and in rare cases, fulminant hepatitis. Lymphadenopathy is not a common symptom of infectious hepatitis but is commonly seen in infectious mononucleosis, CMV infection, and HIV infection. HAV is endemic in developing countries, and about 40% of adults in the United States show serologic evidence of prior infection. It is an RNA picornavirus that is transmitted by fecal-oral, direct person-to-person contact, or through contaminated drinking water. Incubation is 15 to 60 days, and individuals are most contagious in late incubation. Fifteen percent of infected individuals have prolonged or relapsing hepatitis. Fulminant hepatitis and death rarely occur. Because of genetic stability throughout


the world, chronic infection with HAV rarely occurs. An effective vaccine is available. Hepatitis E virus (HEV) is a single-stranded RNA virus that, like HAV, is enterically acquired by fecal-oral transmission through consumption of contaminated drinking water or food, but not by person-to-person transmission. HEV is most common in Asia, Mediterranean countries, and Central America. The prevalence of HEV is low in the United States, where virtually all cases of HEV are among travelers returning from endemic areas.67 Incubation is 15 to 60 days. The symptoms, signs, and course of illness are similar to those of HAV. There is no immunization for HEV. HBV, a DNA hepadnavirus, is transmitted parenterally, by sexual contact, perinatally, and potentially during athletic activities in which an athlete comes in direct contact with another athlete’s blood or body secretions. The incubation period is 45 to 160 days. Most individuals recover completely, but 6% to 10% progress to chronic infection each year. The peak age of infection is 20 to 39 years. The most common mode of transmission is heterosexual contact, but about one third of infected individuals have no known risk factors.67 Hepatitis C virus (HCV), an RNA flavivirus, occurs when there is contact with blood or blood products, primarily through transfusion (now less than 1% who receive a blood or blood product transfusion), injecting drugs (including anabolic steroids with shared needle use), and needle-stick exposure. Sexual transmission is less common. Incubation is 14 to 180 days. Seroprevalence of HCV in the United States is 1.8%.68 The concern about acquiring hepatitis C is that up to 70% of individuals develop chronic infection, and about one fourth of these develop cirrhosis. In fact, HCV is the most common reason for liver transplantation in the United States. Unlike HAV, HCV mutates rapidly and escapes immune surveillance by the host. There is no effective vaccine for HCV. Hepatitis D virus (HDV), a defective single-stranded RNA virus, requires coinfection with HBV for viral replication. An individual who has detectable hepatitis B surface antigen is at risk for coinfection with HDV. Incubation is 42 to 180 days. HDV is prevalent worldwide but is more commonly seen in Africa, Central Asia, Italy, and the Middle East. The overall prevalence in the United States is low except in IV or intramuscular drug users. Transmission is primarily parenteral and less frequently through sexual contact. Coinfection with HBV and HDV results in a more severe acute hepatitis and essentially guarantees progression to chronic hepatitis. As with hepatitis C, there is no effective vaccine for HDV. The AMSSM and AOSSM have each published position statements that state that acute viral hepatitis should be viewed like other viral infections and that specific activity and athletic participation recommendations should be based on the individual’s clinical condition.64 In athletes who have chronic hepatitis, multiple studies have examined the effect of endurance exercise on liver function, and no studies have found significant changes in liver function.67 Chronic persistent viral hepatitis should be viewed much like HIV. Although no firm recommendations have been made for chronic persistent hepatitis, the recommendations used for exercise and competition should be similar to those for athletes with HIV.67 Using hygienic practices such as not sharing food and water and thorough hand washing before meals can prevent

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transmission of HAV and HEV. Outbreaks of HAV have occurred in multiple sports because of poor hygienic practices.67 Only one case of athletic transmission of HBV has been documented: multiple high school sumo wrestlers in Japan were infected after being exposed to a wrestler with known HBV who had multiple scars that often bled during competition. The only other documented case of bloodborne pathogen transmission occurred in Swedish crosscountry athletes who acquired HBV after cleaning their superficial skin wounds with water from a common, contaminated source.65 To date, there is no known transmission of HBV or HCV in the United States during practice or competition.67 Therefore, because the risk for transmission is extremely low, when appropriate precautions are taken, an athlete with chronic persistent hepatitis should be allowed to practice and compete in all sports.

Lyme Disease Lyme disease is a tick-borne systemic illness caused by the spirochete Borrelia burgdorferi. This spirochete is carried by the Ixodes scapularis tick (black-legged or deer tick) in the eastern United States and the Ixodes pacificus (western black-legged tick) in the western United States. Lyme disease is most prevalent in the Northeast and Upper Midwest but has a widespread distribution throughout the United States. Heavily infested tick habitats, such as wooded areas containing trees, brush, leaf litter, woodpiles, and long grass, pose a risk to the outdoor athlete.69 Lyme disease has three stages. Stage 1 (early localized) presents with influenza-like symptoms, regional lymphadenopathy, myalgia, headache, and in most cases, the classic erythema migrans rash. Stage 2 (early disseminated) presents weeks to months later, and any of the following can occur: atrioventricular block, myopericarditis, pancreatitis, malaise, fatigue, regional or generalized lymphadenopathy, migratory pain in joints, bone, muscle, brief arthritis, meningitis, Bell’s palsy, cranial neuritis, radiculoneuritis, and secondary annular lesions. Stage 3 (late chronic) can present months to years later as fatigue, prolonged arthritis, encephalopathy, polyneuropathy, leukoencephalitis, lymphocytoma, and acrodermatitis chronica atrophicans.69 The symptoms of arthralgia and myalgia may mimic musculoskeletal injury. Consequently, Lyme arthritis must be included in the differential diagnosis of joint and muscle problems that present atypically. Laboratory testing must be used appropriately to avoid excessive false-positive and false-negative test results. The two-step approach of the Centers for Disease Control and Prevention (CDC) combines the pretest probability, the time since onset of the disease, and the Western blot test IgM (symptom onset less than 4 weeks) and IgG (all tests) titers. If the CDC criteria are used, the specificity of the two-step approach is 99% to 100%.70 Treatment of stage 1 Lyme disease includes oral doxycycline, 100 mg twice a day; amoxicillin, 500 mg 3 times a day; cefuroxime, 500 mg twice a day; or erythromycin, 250 mg 4 times a day—all for 14 to 21 days. Treatment of stage 2 or 3 or resistant stage 1 includes ceftriaxone, 2 g IV daily; cefotaxime, 2 g IV every 4 hours; or penicillin G, 24 million units IV every 24 hours—all for 14 to 21 days. There are other oral and IV regimens that can be used based on local resistance patterns.70

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The Lyme disease vaccine (LYMErix) has been removed from the market, and at present no vaccine for Lyme disease exists. To avoid Lyme disease, insect repellants containing N,N-diethyl-3-methylbenzamide (DEET), permethrin applied to clothing, or permethrin-impregnated clothing can prevent tick bites; also useful are protective clothing, such as boots and socks. Because the tick usually must be attached for at least 48 hours before transmitting the infection, frequent tick checks are essential to prevent the disease. C

r i t i c a l

P

o i n t s

l Moderate

exercise enhances the immune system. an acute, intense bout of exercise, the athlete may be transiently at increased risk for infection. This is the open-window hypothesis. l The neck check is a simple clinical tool to assist the team physician in determining return to play in an athlete with illness. If symptoms occur above the neck, participation is possible if the athlete feels okay after warm-up. If symptoms occur below the neck, participation is discouraged. l Concerns regarding splenomegaly and fragile spleen accompanying infectious mononucleosis suggest no activity for 3 weeks after onset of symptom, with return to collision sports 3 to 4 weeks after onset of symptoms. l HIV transmission during sports activity has not been reported. l Athletes, athletic trainers, and physicians should observe universal precautions in the training room and on the s ideline. l Transmission of HBV during sports activity is rare. No cases of transmission among athletes have been reported in the United States. l Following

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American Medical Society for Sports Medicine (AMSSM) and the American Orthopedic Society for Sports Medicine (AOSSM): Human immunodeficiency virus (HIV) and other blood-borne pathogens in sports. Joint position statement, 1995. Beck CK: Infectious disease in sports. Med Sci Sports Exerc 32(7 Suppl):S431-S438, 2000. Brenner I, Shek P, Shephard B: Infection in athletes. Sports Med 17:86-107, 1994. Lorenc TM, Kernan MT: Lower respiratory infections and potential complications in athletes. Curr Sports Med Rep 5:80-86, 2006. Malm C: Exercise immunology: The current state of man and mouse. Sports Med 34(9):555-566, 2004. Metz JP: Upper respiratory tract infections: Who plays, who sits?. Curr Sports Med Rep 2:84-90, 2003. Nieman DC: Nutrition, exercise and immune system function. Clin Sports Med 18:537-548, 1999. Nieman DC: Current perspective on exercise immunology. Curr Sports Med Rep 2:239-242, 2003. Turbeville SD, Cowan LD, Greenfield RA: Infectious disease outbreaks in competitive sports: A review of the literature. Am J Sports Med 34(11):1860-1865, 2006. Waninger KN, Harcke HT: Infectious mononucleosis and return to play. Clin J Sport Med 15(6):410-416, 2005.


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Management of Hypertension in Athletes Shafeeq Ahmed and Paul D. Thompson Hypertension is the most common cardiovascular roblem in athletes, although the prevalence of hypertenp sion among athletes is about 50% lower than that in the general population.1 The risk for developing hypertension in both athletes and the general population is increased among blacks and with age, a family history of hypertension, diabetes, obesity, and renal disease. Although awareness, treatment, and control of blood pressure have improved, blood pressure control remains inadequate in many patients.2 According to the World Health Organization, inadequate blood pressure control is responsible for 49% of cases ischemic heart disease and 62% of cerebrovascular disease events, with little variation by sex. In addition, inadequate blood pressure control is the number one attributable risk factor for death throughout the world.3 This chapter describes the diagnosis and treatment of hypertension in athletes based on the Seventh

report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) and the 36th Bethesda Conference Task Force 5 recommendations.

CLASSIFICATION OF BLOOD PRESSURE JNC 7 classifies hypertension into prehypertension and stage 1 and stage 2 hypertension (Table 3B-1). Most athletes with hypertension have either prehypertension or stage 1 hypertension. Hypertension can be classified into primary, or idiopathic, and secondary hypertension. Primary hypertension refers to that with no detectable underlying cause, whereas secondary hypertension refers to hypertension secondary to some other disease process.


Table 3B-1 Classification of Blood Pressure in Adults Type

SBP (mm Hg)

Normal Prehypertension Stage 1 hypertension Stage 2 hypertension

1 min, PTA > 24 hr, PCCS > 7 days Any LOC

LOC, loss of consciousness; PTA, post-traumatic amnesia (anterograde/retrograde); PCCS, postconcussion signs/symptoms other than amnesia. Data from Cantu RC: Posttraumatic retrograde and anterograde amnesia: Pathophysiology and implications in grading and safe return to play. J Athl Train 36:244-248, 2001.

resuscitation. The athlete should be suspected to have sustained a cervical spine fracture and should be transported on a fracture board, with the head and neck immobilized, to a hospital with neurosurgery service. All athletes with severe concussion should be evaluated for possible intracranial bleeding.

Postconcussion Syndrome The postconcussion syndrome consists of headache (especially with exertion), labyrinthine disturbance, fatigue, irritability, and impaired memory and concentration. The true incidence of this syndrome is not known. Persistence of symptoms reflects altered neurotransmitter function and usually correlates well with the duration of post-traumatic amnesia, and it suggests that the athlete should be evaluated by computed tomography (CT) and neuropsychiatric testing. Before an athlete is allowed to return to play after a head injury, the criteria in Table 15-2 should be met. Otherwise, the athlete risks cumulative brain injury as well as the second-impact syndrome. TABLE 15-2 Criteria for Return to Play after Concussion Grade 1

Grade 2

Grade 3

Athlete may return to play in 2 wk if asymptomatic at rest and with exertion for 7 days

Athlete may return to play in 1 mo if asymptomatic at rest and exertion for 7 days

Minimum of 1 mo; may return to play then if asymptomatic for 1 wk; consider terminating season

Terminate season; may return to play next season if asymptomatic

First Concussion

Athlete may return to play that day in select situations if clinical examination results are normal at rest and with exertion; otherwise return to play in 1 week Second Concussion

Return to play in 2 wk if asymptomatic for 1 wk

Third Concussion



Second-Impact Syndrome Second-impact syndrome is defined as a rapid brain swelling and herniation after a second head injury in a still symptomatic athlete.7,8 Between 1980 and 1998, the National Center for Catastrophic Sports Injury Research in Chapel Hill, North Carolina, identified 35 probable cases of second-impact syndrome in football players alone. Autopsy or surgery and MRI findings confirmed 17 of these cases. An additional 18 cases, although not conclusively documented with autopsy findings, most likely resulted from secondimpact syndrome. The syndrome, first described by Schneider in 1973, occurs when the athlete has had a head injury—often a concussion or worse, such as a cerebral contusion—and sustains a second injury before the symptoms associated with the first have cleared.9 The initial symptoms are typically postconcussive and may include visual, motor, or sensory changes as well as difficulty with thought and memory processes. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head.

Physical Examination and Testing Although concussion is the most common athletic head injury, the leading cause of death from athletic head injury is intracranial hemorrhage. There are four types of hemorrhage, of which every trainer and team physician must be aware: epidural, subdural, intracerebral, and subarachnoid. Because all four types of intracranial hemorrhage may be fatal, rapid and accurate initial assessment and appropriate follow-up are mandatory after an athletic head injury.

On-Field Evaluation Initial evaluation of a “down” athlete should include assessment of level of consciousness. If the athlete is unconscious, evaluation and treatment should follow the ABCs of ATLS resuscitation. If the patient is face down or lying on the side, he or she should be carefully logrolled into the supine position. Evaluation of the airway and assessment of respirations is the first concern. Whenever possible, the helmet should be left on and the facemask removed for airway access, with the neck manually immobilized. The helmet should be removed only in the rare instance that facemask removal

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does not provide adequate airway access. The helmet, when left on, can be taped onto a fracture board to help stabilize the upper spine. Pupils should be assessed for size and symmetry. Response to verbal and noxious stimulus should be evaluated. The patient with prolonged loss of consciousness should be transported to a medical facility with neurosurgical services. CT scanning should be performed to evaluate possible intracranial hemorrhage. Contusion or injury of the brain, as seen with any intracerebral hematoma, usually causes headache and, often, an associated neurologic deficit, depending on the area of the brain involved. The injury may also precipitate a seizure. If a seizure occurs, it is important to logroll the patient onto the side. By this maneuver, any blood or saliva rolls out of the mouth and nose, and the tongue cannot fall back to obstruct the airway. A padded tongue depressor or oral airway can be inserted between the teeth. Fingers should not be inserted into the mouth of an athlete having a seizure because amputation can easily result. Traumatic seizures typically last 1 to 2 minutes. The athlete will then relax, and transportation to the nearest medical facility can occur. The awake athlete should be evaluated on the sidelines for continued signs and symptoms of head injury. The athlete’s level of consciousness, memory, speech, coordination, reflexes, vision, concentration, hearing, and gait should be evaluated. Symptoms such as headache, nausea and vomiting, confusion, dizziness, sensitivity to light, irritability, and amnesia should be evaluated. Symptoms should be assessed both at rest and with exertion. The athlete with persistent symptoms should not return to competition. The athlete with worsening headache, nausea and vomiting, or decreased level of consciousness should be transported to a medical facility for further evaluation.

Imaging If intracranial hemorrhage is suspected, CT scan is the modality of choice. CT scan will rapidly diagnose the location, type, and extent of bleeding and assist with operative decision making (Fig. 15-2). If there is a concern for carotid dissection or stroke, MRI with magnetic resonance angiogram can be obtained. Positron-emission tomography has been used to evaluate patients with persistent symptoms.

Treatment Options Nonoperative Initial treatment of a mild concussion requires the player to be removed from the game and observed on the bench. After a sufficient time (as short as 15 to 30 minutes), if the athlete has no headache, dizziness, or impaired concentration (including orientation to person, place, and time and full recall of events that occurred just before the injury), return to game may be considered. Before returning to the game, the player should be asymptomatic at rest and demonstrate movement with the usual dexterity and speed during exertion. If an athlete has any symptoms during rest or exertion, continued neurologic observation is essential. Various neuropsychological tests and tests of balance and coordination have been developed to help determine whether the athlete may safely return to competition.

These tests may play a role at the professional and perhaps collegiate level, but their complexity and expense may preclude routine use (see Table 15-2).

Operative Surgical intervention may be required following an athletic head injury that results in intracranial bleeding. A full discussion of operative indications is beyond the scope of this chapter, but it is important to know the types of injuries for which surgery may be necessary. The four general types of intracranial hematomas include epidural, subdural, intracerebral, and subarachnoid. Epidural Hematoma

An epidural hematoma is usually the most rapidly progressing intracranial hematoma. It is frequently associated with a fracture of the temporal bone and results from a tear of the middle meningeal artery supplying the cover (dura) of the brain. This hematoma accumulates between the skull and the covering of the brain and may reach a fatal size in 30 to 60 minutes. The athlete typically has a loss of consciousness followed by a lucid interval, but this does not always occur. Thus, the athlete may initially remain conscious or regain consciousness after the head trauma and then experience an increasing headache and a progressive decline in level of consciousness. This occurs as the clot accumulates and the intracranial pressure increases. If an epidural hematoma is present, it will almost always declare itself within 1 or 2 hours from the time of the injury. The brain substance is usually free from direct injury; thus, if the clot is promptly evacuated, full recovery is to be expected. Because this lesion may be rapidly fatal if missed, all athletes receiving a major head injury must be observed closely and frequently, preferably during the ensuing 24 hours. This observation should be done at a facility where full neurosurgical services are immediately available. Subdural Hematoma

With a subdural hematoma, the athlete usually does not regain consciousness, and the need for immediate neurosurgical evaluation is obvious. A subdural hematoma occurs between the brain surface and the dura, and so it is located directly on the brain. It is the most common fatal athletic head injury. A subdural hematoma usually results from a torn vein running from the surface of the brain to the dura or from diffuse injury to the surface of the brain. It may also result from a torn venous sinus or even a small artery on the surface of the brain. Unlike an epidural hematoma, a subdural hematoma is often associated with injury to the brain tissue. If the symptoms of a subdural hematoma are severe enough to necessitate emergent surgery, the mortality rate is high, not because of the clot itself, but because of the associated brain injury. Intracerebral Hematoma

Intracerebral hematoma is a third type of intracranial hemorrhage seen after head trauma. In this instance, the bleeding is into the brain substance itself, usually from a torn artery. Bleeding may also result from rupture of a congenital vascular lesion, such as an aneurysm or arteriovenous malformation. Intracerebral hematomas are not

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Figure 15-2 Computed tomographic scans of intracranial hemorrhage. A, Epidural hematoma, B, subdural hematoma, C, subarachnoid hematoma, D, intracerebral hematoma.

A

B

C

D

usually associated with a lucid interval and may be rapidly progressive. Death occasionally occurs before the injured athlete can be transported to a hospital. Because of the intense reaction such a tragic event precipitates among fellow athletes, family, students, and community, it is imperative to obtain a complete autopsy to clarify the causative factors. The autopsy often reveals a congenital lesion that may indicate the cause of death was other than presumed and potentially unavoidable. Subarachnoid Hemorrhage

The final type of intracranial hemorrhage is subarachnoid, confined to the cerebrospinal fluid space along the surface of the brain. After head trauma, such bleeding is usually

the result of disruption of the tiny surface brain vessels and is analogous to a bruise, but it can also result from a ruptured cerebral aneurysm or arteriovenous malformation. As with the intracerebral hematoma, there is often brain swelling. Because bleeding is superficial, surgery is not usually required unless a congenital vascular anomaly is present. After intracranial hemorrhage, prophylactic anticonvulsant therapy is usually given for 1 week, and a long course may be indicated if the patient actually experienced a seizure. Because the chance of post-traumatic epilepsy is less than 10% with a concussion or contusion, anticonvulsant therapy is given only if late epilepsy actually occurs.

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WEIGHING THE EVIDENCE Sports-related head injuries receive substantial public attention and are responsible for 70% of traumatic athletic deaths and 20% of permanent disability related to sports.10 Mild to moderate concussion has been recognized as an epidemic in sports, and it can have an impact on the scholastic performance of the athlete. Even a single, mild sports-related concussion can temporarily affect neuropsychological test responses.11 According to the National Center for Catastrophic Sports Injury Research, sports with the highest risk for head injury per 100,000 participants are football, gymnastics, and ice hockey. The absolute numbers of severe head injuries are highest from football because more than 10 times as many people play football as each of the other two sports. Box 15-2 lists some of the most hazardous sports for head and spine injury. Concussion is a common injury at the professional level. In the National Football League, it is estimated that 100 to 120 concussions occur per year, or about one every two to three games.12 In professional soccer, 52% of players have reported at least one concussion in their career.13 The National Hockey League has seen an increase in the number of concussions, with the rate from 1997 to 2002 more than triple that of the preceding decade.14 Multiple theories have been proposed for the increase, such as bigger, faster players, new equipment, and harder boards and glass. Fortunately the rate has reached a plateau since 1997, which was the year the National Hockey League instituted its concussion program. There is some evidence to suggest that younger athletes may be at higher risk for concussion. For example, the concussion rate for collegiate soccer players is estimated at 1 per 3000 athletic exposures, whereas the rate for high school players has been reported at 1 per 2000 exposures. Among Canadian amateur hockey players aged 15 to 20 years, 60% have reported sustaining a concussion during either a practice or a game. Authors have expressed

BOX 15-2 Sports with the Highest Risk for Head Injury Auto racing Boxing Cycling Equestrian sports Football Gymnastics Hang-gliding Ice hockey Lacrosse Martial arts Motorcycling Parachuting Rugby Skiing Soccer (goalie) Track (pole vaulting)

A u t h o r ’ s P r e f e r r e d M e t h o d Athletes who have sustained a prolonged loss of consciousness or exhibit neurologic deficits should be triaged to a medical center for further evaluation. Abbreviated neurologic examinations such as the Glasgow Coma Scale are useful in predicting outcome after a severe head injury (Table 15-3).16 On arrival at a medical center, a full neurologic examination should be performed, including assessment of mental status, speech, memory, motor and sensory function, cranial nerve function, and reflexes (normal and abnormal). CT scan is helpful in evaluation of potential intracranial hemorrhage and skull fracture. MRI study will identify more diffuse injury such as diffuse axonal shear.17 TABLE 15-3 Glasgow Coma Scale Sign

Evaluation

Score

Eye opening (E)

Spontaneous To speech To pain None Obeys Localizes Withdraws Decorticate Decerebrate None Oriented Confused conversation Inappropriate words Incomprehensible sounds None

4 3 2 1 6 5 4 3 2 1 5 4 3 2

Best motor response (M)

Verbal response (V)

Total EMV score by adding best response in each category. Range from 3-15.

1

concern that injury during adolescence may impair the plasticity of the developing brain.15

POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Postoperative care following a traumatic athletic head injury is the same as for any trauma patient. Whether an athlete should be allowed to return to competition after intracranial surgery is an area of controversy and beyond the scope of this chapter. The ultimate goal when discussing athletic head injuries is prevention. The increased attention on head injuries in sports has made athletes, trainers, physicians, and fans more aware of the potential dangers of brain injury in sports. Football was one of the first sports to focus on prevention of head and neck injury, as evidenced by the rule change in 1976 prohibiting initial contact with the head (spear tackling). The number of fatalities due to head injuries in football has declined from a high of 162 during the 10-year span of 1965 to 1974 to a low of 32 during the 10 years of 1985 to 1994.18

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BOX 15-3 Return to Play in Head Injury Because the subject does not lend itself to prospective, randomized studies, the guidelines for return to play after a traumatic brain injury are based largely on retrospective analysis and judgment. A primary goal is to avoid secondary injury such as a more severe concussion or worse yet a second-impact syndrome. It is for this reason that athletes who remain symptomatic after even a grade 1 concussion should not return to play. Another goal is to prevent the long-term effects of multiple minor traumatic brain injuries that can lead to permanent changes such as the classic description of dementia pugilistica seen in boxers. It is with these aims in mind that the guidelines in Table 15-2 were developed. Factors other than the concussion severity must be weighed in the return-to-play decision. The athlete’s concussion history, including total number, time between injuries, and severity of the blow causing the concussion are important factors. When making the return-to-play decision, one should consider all pieces of the concussion puzzle and when in doubt, err on the side of caution: “If in doubt, sit them out.”

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Cantu RC: Guidelines for return to contact sports after a cerebral concussion. Phys Sportsmed 14:76-79, 1986. Cantu RC, Mueller FO: Brain injury-related fatalities in American football, 19451999. Neurosurgery 52(4):846-853, 2003. Ghiselli G, Schaadt G, McAllister DR: On-the-field evaluation of an athlete with a head or neck injury. Clin Sports Med 22(3):445-465, 2003. Grindel SH: Epidemiology and pathophysiology of minor traumatic brain injury. Curr Sports Med Rep 2:18-23, 2003.

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l Sporting activities account for about 20% of head injuries per year in the United States. l About 70% of traumatic athletic deaths result from head injury. l A concussion can occur without a loss of consciousness (grade 1). l Repetitive minor brain injury (concussion) can lead to permanent neurologic changes. l An athlete who returns to competition still symptomatic from a prior concussion may risk suffering a secondimpact syndrome. l The four types of intracranial hemorrhage include epidural, subdural, intracerebral, and subarachnoid. l Athletes with an epidural hematoma may have a brief lucid interval following initial loss of consciousness. l For the unconscious athlete, the ABCs of trauma care should be followed. l Rule changes have had a positive impact on the incidence of head and neck injuries in football.

Okonkwo DO, Stone JR: Basic science of closed head injuries and spinal cord injuries. Clin Sports Med 22(3):467-481, 2003. Schneider RC: Head and neck injuries in football: Mechanisms, treatment, and prevention. Baltimore, Williams & Wilkins, 1973.


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Cervical Spine Injuries 1. Cervical Spine Injuries in the Adult Joseph S. Torg

This chapter presents guidelines for classification, evaluation, management, and return to play criteria for injuries that occur to the cervical spine and related neural structures as a result of participation in competitive and recreational activities. Although all athletic injuries require careful attention, the evaluation and management of cervical spine injuries should proceed with particular caution. The actual or potential involvement of the nervous system creates a high-risk situation in which the margin for error is low. An accurate diagnosis is imperative, but the clinical picture is not always representative of the seriousness of the injury at hand. An intracranial hemorrhage may present initially with minimal symptoms yet follow a precipitous downhill course, whereas a less severe injury, such as neurapraxia of the cervical spinal cord associated with alarming paresthesias and paralysis, will resolve swiftly and allow a return to activity. Although the more severe injuries are rather infrequent, this low incidence coincidentally results in little, if any, management experience for the on-site medical staff.

EMERGENCY MANAGEMENT There are several principles that should be considered by individuals responsible for athletes who may sustain injuries to the cervical spine.1,2 1. The team physician or the trainer should be designated as the person responsible for supervising on-the-field management of the potentially serious injury. This person is the “captain” of the medical team. 2. Previous planning must ensure the availability of all necessary emergency equipment at the site of potential injury. At a minimum, this should include a spine board, a stretcher, and equipment necessary for helmet removal and the initiation and maintenance of cardiopulmonary resuscitation. 3. Previous planning must ensure the availability of a properly equipped ambulance as well as a hospital equipped and staffed to handle emergency neurologic problems.

4. Previous planning must ensure the immediate availability of a telephone for communicating with the hospital emergency room, ambulance, and other responsible individuals in case of an emergency. Managing the unconscious or spine-injured athlete is a process that should not be done hastily or haphazardly. Being prepared to handle this situation is the best way to prevent actions that could convert a repairable injury into a catastrophe. Be sure that all the necessary equipment is readily accessible and in good operating condition and that all assisting personnel have been trained to use it properly. Onthe-job training in an emergency situation is inefficient at best. Everyone should know what must be done beforehand so that on a signal, the game plan can be put into effect. A means of transporting the athlete must be immediately available in a high-risk sport such as football and “on call” in other sports. The medical facility must be alerted to the athlete’s condition and estimated time of arrival so that adequate preparation can be made. The availability of the proper equipment is essential! A spine board is necessary and is the best means of supporting the body in a rigid position. It is essentially a fullbody splint. By splinting the body, the risk for aggravating a spinal cord injury, which must always be suspected in the unconscious athlete, is reduced. In football, appropriate instruments are also essential if it becomes necessary to remove the facemask. A telephone must be available to call for assistance and to notify the medical facility. Oxygen should be available and is usually carried by ambulance and rescue squads, although it is rarely required in an athletic setting. Rigid cervical collars and other external immobilization devices can be helpful if properly used. Manual stabilization of the head and neck is recommended if other means are not available. Properly trained personnel must know, first of all, who is in charge. Everyone should know how to perform cardiopulmonary resuscitation and how to move and transport the athlete. They should know where emergency equipment 665

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is located, how to use it, and the procedure for activating the emergency support system. Individuals should be assigned specific tasks beforehand, if possible, to prevent duplication of effort. Being well prepared helps alleviate indecisiveness and second-guessing. Prevention of further injury is the single most important objective. Do not take any action that could possibly cause further injury. The first step should be to immobilize the head and neck by supporting them in a stable position (Fig. 16A1-1). Then, in the following order, check for breathing, pulse, and level of consciousness. If the victim is breathing, simply remove the mouth guard, if present, and maintain the airway. It is necessary to remove the facemask only if the respiratory situation is threatened or unstable or if the athlete remains unconscious for a prolonged period. Leave the chin strap on. After it is established that the athlete is breathing and has a pulse, evaluate the neurologic status. The level of consciousness, the response to pain, the pupillary response, and any unusual posturing, flaccidity, rigidity, or weakness should be noted. At this point, simply maintain the situation until transportation is available or until the athlete regains consciousness. If the athlete is face down when the ambulance arrives, change his or her position to face up by logrolling the athlete onto a spine board. Gentle longitudinal traction should be exerted to support the head without attempting to correct alignment. Make no attempt to move the injured person except to transport him or her or to perform cardiopulmonary resuscitation if it becomes necessary. If the athlete is not breathing or stops breathing, the airway must be established. If face down, he or she must be turned to a face-up position. The safest and easiest way to

accomplish this is to logroll the athlete. In an ideal situation, the medical support team is made up of five members: the leader, who controls the head and gives the commands; three members to roll; and another to help lift and carry when it becomes necessary. If time permits and the spine board is on the scene, the athlete should be rolled directly onto it. Breathing and circulation are much more important at this point, however. With all medical support team members in position, the athlete is rolled toward the assistants—one at the shoulders, one at the hips, and one at the knees. They must maintain the body in line with the head and spine during the roll. The leader maintains immobilization of the head by applying slight traction and by using the crossed-arm technique. This technique allows the arms to unwind during the roll (Fig. 16A1-2).

A

B

A

C B Figure 16A1-1 A, Athletes with suspected cervical spine injury may or may not be unconscious. All who are unconscious, however, should be managed as though they had a significant neck injury. B, Immediate manual immobilization of the head and neck unit. First check for breathing. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

Figure 16A1-2 A, Logroll to a spine board. This maneuver requires four individuals: the leader to immobilize the head and neck and command the medical-support team, and the remaining three individuals positioned at the shoulders, hips, and lower legs. B, Logroll. The leader uses the crossed-arm technique to immobilize the head. This technique allows the leader’s arms to unwind as the three assistants roll the athlete onto the spine board. C, Logroll. The three assistants maintain body alignment during the roll. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

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Figure 16A1-3 Head and helmet must be securely immobilized. A, Remove cage-type masks by cutting the plastic loops with Dura shears, EMT scissors, or Trainer’s Angel. Make the cut on the side of the loop away from the face. B, Remove the entire mask from the helmet so that it does not interfere with further resuscitation efforts. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

The following guidelines are outlined by Kleiner and colleagues3: Heavy persons, including many athletes, can be handled more efficiently with a six-plus-person lift; this is also preferred for suspected spine injuries. The Inter-Association Task Force recommends that the six-plus-person lift be used along with a scoop stretcher whenever possible. In the athletic arena, there are usually a sufficient number of certified athletic trainers, physicians, and EMS personnel on hand to effectively administer the six-plus-person lift. For the six-plus-person lift, rescuer 1 immobilizes the neck. The rescuer’s hands are placed on the athlete’s shoulders (under the shoulder pads) with the thumbs pointed away from the athlete’s face. The athlete’s head will then be resting between the rescuer’s forearms. The other six rescuers position themselves along the athlete’s sides: one on each side of the chest, pelvis, and legs. The hands are slid under the athlete and equipment, if any, to provide a firm, coordinated lift. To lift, rescuer 1 gives the command “prepare to lift; lift. ” The assistants lift the athlete 4 to 6 inches off the ground. It is imperative to maintain a coordinated lift and to prevent any movement of the spine. One of the rescuers at the thigh level must control the legs with his or her arms toward the feet so the splint can be slid into place from the foot end. After the splint is in place, while positions are maintained, rescuer 1 gives the command “prepare to lower; lower, ” and the athlete is lowered onto the splint. In the case of larger athletes, as many as 10 individuals should participate in the lift, with one on each side of the chest and pelvis, two at the legs, one at the head, and one with the splint. The Inter-Association Task Force does not recommend the use of fewer than fourplus-persons to lift athletes suspected of having a spinal injury, even smaller athletes and children, in part due to the weight of the athlete while wearing protective equipment.3

The facemask should be removed from the helmet as quickly as possible any time a player is suspected of having a spinal injury, even if still conscious and regardless of respiratory status. The type of mask that is attached to the helmet determines the method of removal. Bolt cutters are used with the older single- and double-bar masks. The newer masks that are attached with plastic loops should be removed by cutting the loops with an instrument capable of cutting through the newer loop straps made of harder plastic, such as Dura shears, EMT scissors, or the Trainer’s Angel. Remove the entire mask so that it does not interfere with further rescue efforts (Fig. 16A1-3). Once the mask has been removed, initiate rescue breathing following the current standards of the American Heart Association. After the athlete has been moved to a face-up position, quickly evaluate breathing and pulse. If there is still no breathing or if breathing has stopped, the airway must be established. The jaw thrust technique is the safest first approach to opening the airway of a victim who has a suspected neck injury because in most cases it can be accomplished by the rescuer grasping the angles of the victim’s lower jaw and lifting with both hands, one on each side, displacing the mandible forward while tilting the head backward. The rescuer’s elbows should rest on the surface on which the victim is lying (Fig. 16A1-4). If the jaw thrust is not adequate, the head tilt–jaw lift should be substituted. Care must be exercised not to overextend the neck. The fingers of one hand are placed under the lower jaw on the bony part near the chin and are lifted to bring the chin forward, supporting the jaw and helping tilt the head back. The fingers must not compress the soft tissue under the chin, which might obstruct the airway. The other hand presses on the victim’s forehead to tilt the head back (Fig. 16A1-5). The transportation team should be familiar with handling a victim with a cervical spine injury, and they should be receptive to taking orders from the team physician or

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Figure 16A1-4 Jaw thrust maneuver for opening the airway of a victim with a suspected cervical spine injury.

the trainer. It is extremely important not to lose control of the care of the athlete; therefore, be familiar with the transportation crew that is used. In an athletic situation, arrangements with an ambulance service should be made ahead of time. An appreciation of the controversy that currently exists between emergency medicine physicians and technicians on one hand and team physicians and athletic trainers on the other regarding helmet removal is in order. Existing emergency medical services guidelines mandate removal of protective headgear before transport of an individual suspected of having a cervical spine injury to a fixed medical installation. These guidelines were implemented with motorcycle helmets in mind to facilitate both airway accessibility and application of cervical spine immobilizing devices. Clearly, such a procedure contradicts the longstanding principle adhered to by team physicians and athletic trainers of leaving the helmet in place on the football player suspected of having a cervical spine injury until he or she is transported to a definitive medical facility. It must be emphasized that this particular problem is of more than academic interest. Specifically, there have been occasions in which emergency medical technicians under the direction of emergency room physicians unfamiliar with the nuances of the relationship between helmet, shoulder pads, and the injured cervical spine have precipitated turf battles by refusing to move the injured player before helmet removal. Again, such episodes represent more than an honest difference of opinion. Such episodes are clearly detrimental to the health and wellbeing of the injured player. It is my view that removal of the football helmet and shoulder pads on site exposes the potentially injured spine to both unnecessary and awkward manipulation and disruption of the immobilizing capacity of the helmet and shoulder pads. Also, removal of the helmet alone subjects a potentially unstable spine to hyperlordotic deformity. I agree with the National Collegiate Athletic Association Guidelines for helmet removal.4 Unless there are

Figure 16A1-5 Head tilt—jaw lift maneuver for opening the airway. This is used if jaw thrust is inadequate or if a helmet is being worn.

special circumstances, such as respiratory distress coupled with an inability to access the airway, the helmet should never be removed during the prehospital care of the athlete with a potential head and neck injury unless the following conditions are present: 1. The helmet does not hold the head securely, such that immobilization of the helmet does not immobilize the head. 2. The design of the sport helmet is such that even after removal of the facemask, the airway cannot be controlled and ventilation cannot be provided. 3. After a reasonable time, the facemask cannot be removed. 4. The helmet prevents immobilization for transportation in an appropriate position. When helmet removal is necessary in any setting, it should be performed only by personnel trained in this procedure. If removal of the helmet is needed to initiate treatment or to obtain special radiographic studies, a specific protocol needs to be followed. With the head, the neck, and the helmet manually stabilized, the chin strap can be cut. While stability is being maintained, the cheek pads can be removed by slipping the flat blade of a screwdriver or bandage scissors under the pad snaps and above the inner surface of the shell. One individual provides manual stability of the chin and the neck, and the other workers stabilize the head by placing their thumbs or index fingers into the ear holes on both sides. By pulling both laterally and longitudinally, the helmet shell can be spread and eased off. If a rocking motion is necessary to loosen the helmet, the head and neck unit must not be allowed to move. Those individuals participating in this important maneuver must proceed with caution and must coordinate every move.

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Figure 16A1-6 A, Four members of the medical support team lift the athlete on the command of the leader. B, The leader maintains manual immobilization of the head. The spine board is not recommended as a stretcher. An additional stretcher should be used for transporting the patient over long distances. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

Supporting the concept of leaving the helmet on is the work of Swenson and associates5 and Gastel and colleagues.6 Swenson and associates studied sagittal cervical alignment in live subjects with various combinations of helmets, shoulder pads, and no equipment. They concluded that football players with a potential cervical spine injury should be immobilized for transport with both helmet and shoulder pads left in place, thereby maintaining the neck in a position most closely approximating normal. Gastel and colleagues performed a similar study using stable and surgically destabilized cadaver spines. They concluded that to maintain a neutral position and minimize secondary injury to the cervical neural elements, both the helmet and the shoulder pads should be either left on or removed in the emergency setting. Lifting and carrying the athlete requires five individuals: four to lift, and a leader to maintain immobilization of the head. The leader initiates all actions with clear, loud verbal commands (Fig. 16A1-6). The same guidelines apply to the choice of a medical facility as to the choice of an ambulance: Be sure it is equipped and staffed to handle an emergency head or neck injury. There should be a neurosurgeon and an orthopaedic surgeon to meet the athlete on arrival. Radiographic facilities should be standing by. Once the athlete is in a medical facility and permanent immobilization measures have been instituted, the helmet can be removed. The chin strap may now be unfastened and discarded. The following protocol is recommended3,4: The helmet should be removed in a controlled environment after radiographs have been obtained and only by qualified medical personnel with training in equipment removal. Helmet removal should never be attempted without thorough communication among all involved parties. One person should stabilize the head, neck, and helmet while another person cuts the chin strap. Accessible internal helmet padding, such as cheek pads, should be removed, and air padding should be deflated before removal of the helmet, while a second assistant manually stabilizes the chin and back of the neck, in a cephalad direction, making sure to maintain the athlete’s position. The pads are removed

through the insertion of a tongue depressor or a similar stiff, flat-bladed object between the snaps and helmet shell to pry the cheek pads away from their snap attachment. If an air cell–padding system is present, deflate the air inflation system by releasing the air at the external port with an inflation needle or large-gauge hypodermic needle. The helmet should slide off the occiput with slight forward rotation of the helmet. In the event the helmet does not move, slight traction can be applied to the helmet, which can then be gently maneuvered anteriorly and posteriorly, although the head-neck unit must not be allowed to move. The helmet should not be spread apart by the ear holes3,4 because this maneuver only serves to tighten the helmet on the forehead and occiput region (Fig. 16A1-7). Despite the advent of such high-technology imaging modalities as computed tomography (CT) and magnetic resonance imaging (MRI), the initial radiographic examination of a patient with suspected or actual cervical spine trauma remains a routine radiographic examination. The preliminary study, performed while immobilization of the head, the neck, and the trunk is maintained, includes an anteroposterior and lateral examination of vertebrae C1 to C7. If major fracture, subluxation, dislocation, or evidence of instability is not evident, the remainder of the routine examination, including open mouth and oblique views, should be obtained. Depending on the neurologic and comfort status of the patient, lateral flexion and extension views should be obtained at some point. CT and MRI may provide more detailed information; however, horizontally oriented fractures and subtle subluxations are best identified on the routine radiographs. The choice of imaging technique depends on the results of the routine examination, the neurologic status of the patient, the preference of the responsible physician, and the availability of the imaging modalities.

THE AMBULATORY PATIENT Fortunately, it is the rare athlete with a cervical spine injury who presents with neurologic impairment. Important physical findings indicative of injury in an individual

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A

B

Figure 16A1-7 A, The helmet should be removed only when permanent immobilization can be instituted. The helmet may be removed by detaching the chin strap, removing cheek pads, deflating air padding, and gently pulling the helmet off in a straight line with the cervical spine. B, The head must be supported under the occiput during and after removal of the helmet. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

ithout neurologic findings are (1) presence of a wry neck w or torticollis posture; (2) limitation of cervical motion; and (3) presence of paravertebral muscle atrophy in subacute and chronic cases. An individual presenting with a history of trauma and one or more of these findings requires a careful neurologic examination and appropriate imaging studies.

CERVICAL SPINE INJURIES Athletic injuries to the cervical spine may involve the bony vertebrae, the intervertebral disks, the ligamentous supporting structures, the spinal cord, the roots, the peripheral nerves, or any combination of these structures. The panorama of injuries observed runs the spectrum from the “cervical sprain syndrome ” to fracture-dislocations with permanent quadriplegia. Fortunately, severe injuries with neural involvement occur infrequently. Those responsible for the emergency and subsequent care of the athlete with a cervical spine injury should possess a basic understanding of the variety of problems that can occur. The various athletic injuries to the cervical spine and related structures are the following: 1. Nerve root–brachial plexus injury 2. Stable cervical sprain 3. Muscular strain 4. Nerve root–brachial plexus axonotmesis 5. Intervertebral disk injury (narrowing-herniation) without neurologic deficit 6. Stable cervical fractures without neurologic deficit 7. Subluxations without neurologic deficit 8. Unstable fractures without neurologic deficit 9. Dislocations without neurologic deficit 10. Intervertebral disk herniation with neurologic deficit 11. Unstable fracture with neurologic deficit 12. Dislocation with neurologic deficit 13. Quadriplegia 14. Death

Criteria for return to contact activities after congenital and traumatic problems of the cervical spine are included at the end of this chapter.

Nerve Root–Brachial Plexus Injury The most common and poorly understood cervical injury is pinch-stretch neurapraxia of the nerve roots and the brachial plexus (Fig. 16A1-8).7 Typically, after an impact involving the head, neck, or shoulder, a sharp burning pain is experienced in the neck on the involved side that may radiate into the shoulder and down the arm to the hand. There may be associated weakness and paresthesia in the involved extremity lasting several seconds to several minutes. Characteristically, there is weakness of shoulder abduction (deltoid), elbow flexion (biceps), and external humeral rotation (spinatus). The key to the nature of this lesion is its short duration and the presence of a full, pain-free range of neck motion. Although most of these injuries are short lived, they are worrisome because of the occasional plexus axonotmesis that occurs. The youngster whose paresthesia completely abates and who demonstrates full muscle strength in the intrinsic muscles of the shoulder and upper extremities, and who, most important, has a full, pain-free range of cervical motion may return to his or her activity.8,9 The “burner syndrome ” has been attributed to different mechanisms. Bateman10 believed that root lesions were rarely involved in injuries to athletes, whereas peripheral nerve lesions were common. He recognized that direct blows as well as other mechanisms could result in varying peripheral nerve injuries about the shoulder. Chrisman11 described lateral neck flexion away from the involved side resulting in cervical sprain and traction injury to the cervical nerve roots. Rockett12 reported operative findings in patients with persistent burners. He noted scarring of the C5 and C6 nerve roots at their point of emergence from the vertebra between the anterior and middle scalene. He suggested that repetitive tightening of the scalenes causes trauma to the nerve roots with resultant scarring.

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C4 C5 Dorsal scapular n. (Rhomboid minor and major)

C5 To longus and scalene m.

NK

C5-C6 Suprascapular n. (Supraspinatus infraspinatus)

ER

P UP

C5-C6 Upper subscapular n. (Subscapularis)

C7

to n. vius la c K b su RUN T

LE

DD

MI

ER

LA TE

RA L

W LO R

C

D

R

O

Phrenic n. (diaphragm) C8

K

N

CO

RD

C5-C6 Lower subscapular n. (Subscapularis teres major)

C5-C6 Musculocutaneous n. (Coracobrachialis biceps brachialis)

C6

U TR

U TR

T1

Long thoracic n. (Serratus anterior)

IO

ER

ST

C5-C6 Axillary n. (Deltoid teres minor)

Lateral pectoral n. (Pectoralis major)

D

PO

L

IA

ED

R CO

M

Medial pectoral n. (Pectoralis major and minor) Thoracodorsal n. (Latissimus dorsi) (C6-C8)

Median n. C6-T1 (C7-T1)

Medial brachial cutaneous Medial antebrachial cutaneous

no motors

Ulnar n. Radial n. (C6-T1) Figure 16A1-8 Diagram of the brachial plexus demonstrating the location of Erb’s point (arrow). Presumably, brachial plexus stretch injuries result from traction of the plexus at this point. (From Torg JS: Athletic Injuries to the Head, Neck and Face, 2nd ed. St. Louis, Mosby-Year Book, 1991.)

Clancy13,14 has suggested a more distal injury. He believes that burners are brachial plexus injuries. Electrodiagnostic evidence indicated that plexus axonotmesis involved only the upper trunk. He noted different mechanisms of injury and suggested that the point of plexus injury may vary depending on neck, arm, and shoulder position. Neck hyperextension, shoulder depression, neck hypertension with lateral bend to the side of injury, and contralateral neck flexion with ipsilateral shoulder depression were some mechanisms reported. Clancy13,14 also recommended classifying these injuries based on the staging system of Seddon.15 Neurapraxia, the mildest form of injury, represents a reversible aberration in axonal function. Focal demyelinization can occur, producing an electrophysiologic conduction block or conduction slowing. Complete recovery usually occurs immediately or within a maximum of 2 weeks. Axonotmesis is an injury in which the axon and the myelin sheath are disrupted, but the epineurium remains intact. Wallerian degeneration occurs distal to the point of injury; functional recovery may occur, but it can be incomplete and unpredictable. The most severe injury, neurotmesis, is rarely seen in athletes

and results in complete disruption of the nerve. Prognosis is poor, and generally recovery does not occur. Clancy13,14 has defined cervical nerve pinch syndrome as those injuries that recover within 2 weeks; most likely, these represent neurapraxia. The term brachial plexus injury is reserved for injuries with weakness or sensory changes lasting longer than 2 weeks. In our opinion, the term brachial plexus injury should be reserved for anatomic localization. Many of these injuries are mixed lesions, and classification by Seddon’s system15 serves mainly to aid in describing a potential recovery course and prognosis. Robertson16 indicated that brachial plexus injury at Erb’s point is most likely to be a stretch injury. He reported that all patients became symptomatic after contact, causing ipsilateral shoulder depression and lateral neck flexion to the opposite side. Kelly and coworkers17,18 investigated the relationship between burners and cervical stenosis in younger patients aged 15 to 18 years. A review of 69 cervical spine radiographs demonstrated a significant decrease in the Torg ratio (the ratio of the anteroposterior diameter of the spinal cord to the anteroposterior diameter of the vertebral body)

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as compared with the control group. They hypothesized that developmental cervical stenosis predisposes an athlete to experience burners as a result of concomitant foraminal narrowing with nerve root compression. Meyer19 studied 40 patients with “stingers” at the University of Iowa from 1987 to 1991. The mechanism was reported as extension-compression in 34 subjects and brachial plexus stretch in 6 subjects. Cervical spine radiographs were analyzed and compared with a control group of asymptomatic football players. Players with stingers demonstrated a statistically significant incidence of spinal stenosis of at least one cervical segment as defined by a Torg ratio of less than 0.8. For the stinger group, 47.5% had a ratio less than 0.8 for at least one level, compared with 25.1% in the asymptomatic group. No patient in the group with brachial plexus stretch injuries had a Torg ratio of less than 0.8. Meyer concluded that there is a relationship between cervical stenosis and the occurrence of nonparalyzing extension-compression injuries. It is clear that the typical burner can be caused by various injury mechanisms. History, physical examination, and appropriate diagnostic studies help differentiate between brachial plexus and cervical nerve root lesions. Brachial plexus injuries are more likely to occur in younger patients with less well-developed neck musculature. Usually, these are traction injuries resulting from lateral neck flexion away from the involved area and shoulder depression to the side of involvement. Neck pain can be present but is usually not a prominent feature. When pain is present, cervical spine radiographs are necessary. Typically, pain and paresthesias involving the arm and the shoulder are transient. On examination, Spurling’s test result is negative (Fig. 16A1-9). Weakness typically involves the deltoid, the spinati, and the biceps and might not be evident initially on clinical examination, making a follow-up visit necessary.

Figure 16A1-9 Spurling’s maneuver. The examiner applies pressure to the head, forcing the cervical spine into extension and lateral flexion toward the symptomatic side. This reproduces the pathomechanics of those injuries resulting from compression of the cervical nerve roots or the dorsal root ganglion in the involved intervertebral foramen.

Root lesions result from compression of the nerve root or dorsal root ganglion in the intervertebral foramen and are generally associated with radiologic evidence of cervical disk disease and developmental stenosis. In football players, these injuries usually occur when the player reaches the college or professional level. Hyperextension with lateral neck flexion is the common mechanism of injury. Neck pain and a decreased cervical range of motion may be present. Spurling’s test result is positive. Plain radiographic findings may be normal or may demonstrate loss of normal cervical lordosis and the changes of degenerative disk disease. MRI is indicated in patients with a persistent neurologic deficit and prolonged or recurrent symptoms and will demonstrate either acute disk herniation or degenerative disk disease with asymmetric disk bulging. In our experience, patients often have developmental spinal stenosis, degenerative disk disease, and asymmetric disk bulging that results in root irritation with cervical hyperextension. Persistence of paresthesia, weakness, or limitation of cervical motion requires that the individual be protected from further exposure and that he or she undergo neurologic, electromyographic, and roentgenographic evaluation. Persistent or recurrent episodes require a complete neurologic and radiographic or other imaging work-up. If routine roentgenographic films of the cervical spine are negative and a preganglionic root lesion is suspected, MRI, plain myelography, or CT myelography should be considered. Disk herniation, foraminal narrowing, and extradural intraspinal masses should be considered in the differential diagnosis. A complete electromyographic examination, including both nerve conduction studies and a needle electrode examination, may be helpful. These studies should be delayed for 3 to 4 weeks from the time of the initial injury. Nerve conduction studies should include both routine conduction and sensory nerve action potential evaluations. Electrode evaluation of the cervical spine musculature will differentiate between preganglionic root injuries and plexus disorders. Initial management must be directed at evaluation of the cervical spine, the shoulder girdle, the affected upper extremity, and the peripheral nervous system. The first obligation of the physician is to rule out a serious cervical spine injury. A patient history of bilateral symptoms or symptoms including the lower extremities should alert the physician to the possibility of cord neurapraxia, cervical spine fracture, or ligamentous injury. In this instance, the spine should be immobilized until injury is ruled out. If a player complains of neck pain, a complete cervical spine evaluation is mandatory, including radiographic examination. Characteristically, the signs and symptoms are transient and resolve within minutes. In athletes whose pain and paresthesias abate, a normal neurologic examination is required, and most important, a full pain-free range of cervical motion must be seen before return to activity is allowed. Also, players must demonstrate normal strength on clinical examination before they return to participation. Those patients who have recurrent symptoms without weakness require careful follow-up; continued symptoms associated with weakness preclude further athletic participation.

Spinal Injuries

Figure 16A1-10 Crucial in the effective management of the athlete with recurrent burners is the implementation of an aggressive, year-round neck and shoulder muscle strengthening program. Effective are variable-resistance isotonic “neck machines.”

In brachial plexus injuries, prevention is based on an aggressive neck and shoulder strengthening program (Fig. 16A1-10). Neck rolls, or devices such as the cowboy collar, and high-profile shoulder pads also help prevent injuries by limiting the extent of lateral flexion and extension (Fig. 16A1-11).

A

673

Electrodiagnostic studies may be helpful but are not mandatory in the management of burners secondary to brachial plexus injury. Speer20 demonstrated that although there was no correlation between initial physical findings and the results of electrodiagnostic testing, evidence of muscular weakness 72 hours after the injury did correlate with positive electromyographic results. Bergfeld21 reported that electromyographic changes continue to appear long after weakness has apparently been resolved according to clinical examinations; therefore, abnormal electromyographic findings should not be used as a criterion for exclusion from athletic participation. In summary, the burner pain syndrome or stinger results from either of two distinct injury patterns: traction to the brachial plexus or compression of the cervical nerve roots. Brachial plexus injuries are typically traction neurapraxias occurring in younger athletes as a result of shoulder depression and lateral neck flexion away from the side of injury. Cervical root injuries typically occur in older players. They are hyperextension injuries and are associated with degenerative disk changes, often in combination with developmental cervical stenosis.22 Criteria for return to athletic participation include absence of symptoms, normal strength, and painless, full range of motion of the cervical spine. Players who experience one or more burners should wear appropriate neck rolls or a cowboy collar to prevent extreme hyperextension and lateral bending of the cervical spine (Fig. 16A1-12). A year-round neck and shoulder muscle strengthening program will aid in the prevention of the burner syndrome.12

Acute Cervical Sprain Syndrome An acute cervical sprain is a collision injury frequently seen in contact sports. The patient complains of having “jammed” his or her neck, with subsequent pain localized to the cervical area. Characteristically, the patient pre sents with limitation of cervical spine motion but without radiation of pain or paresthesia. Neurologic examination is negative, and roentgenograms are normal.

B

Figure 16A1-11 Frontal (A) and lateral (B) views of the cowboy collar. This device, which is worn under the shoulder pads, effectively limits the extremes of extension and lateral bending of the cervical spine.

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Figure 16A1-12 The combined action of the football helmet, the cowboy collar, and the shoulder pads effectively limits the extremes of lateral bend of the neck.

Stable cervical sprains and strains eventually resolve with or without treatment. Initially, the presence of a serious injury should be ruled out by performing a thorough neurologic examination and determining the range of cervical motion. Range of motion is evaluated by having athletes perform the following actions: actively nod their head, touch their chin to their chest, extend their neck maximally, touch their chin to their left shoulder, touch their chin to their right shoulder, touch their left ear to their left shoulder, and touch their right ear to their right shoulder. If the patient is unwilling or unable to perform these maneuvers actively while standing erect, proceed no further. The athlete with less than a full, pain-free range of cervical motion, persistent paresthesia, or weakness should be protected and excluded from activity. Subsequent evaluation should include appropriate roentgenographic studies, including flexion and extension views to demonstrate fractures or instability. In general, treatment of athletes with “cervical sprains” should be tailored to the severity of the injury. Immobilizing the neck in a soft collar and using analgesics and antiinflammatory agents until there is a full, spasm-free range of neck motion is appropriate. Individuals with a history of collision injury, pain, and limited cervical motion should have routine cervical spine roentgenograms. Also, lateral flexion and extension roentgenograms are indicated after the acute symptoms have subsided. Marked limitation of cervical motion, persistent pain, or radicular symptoms or findings may require MRI to rule out intervertebral disk injury.

Intervertebral Disk Injuries Acute herniation of a cervical intervertebral disk associated with neurologic findings and occurring as an isolated entity is rare in the athlete. Acute onset of transient quadriplegia in an athlete who has sustained head impact but has negative cervical spine roentgenographic findings

should prompt consideration of an acute rupture of a cervical intervertebral disk. The syndrome of acute anterior spinal cord injury, as described by Schneider,23,24 may be observed in individuals with instability associated with acute disk herniation: “The acute anterior cervical spinal cord injury syndrome may be characterized as an immediate acute paralysis of all four extremities with a loss of pain and temperature to the level of the lesion, but with preservation of posterior column sensation of motion, position, vibration and part of touch.”23,24 The pressure of the disk is exerted on the anterior and lateral columns, whereas the posterior columns are protected by the denticulate ligaments. MRI or a CT myelogram should be performed to substantiate the diagnosis. Anterior diskectomy and interbody fusion for a patient with neurologic involvement or persistent disability because of pain should be considered. Albright and colleagues25 studied 75 University of Iowa freshmen football recruits who had had roentgenograms of their cervical spines after playing football in high school but before playing in college. Of this group, 32% had one or more of the following: “occult” fracture, vertebral body compression fracture, intervertebral disk-space narrowing, or other degenerative changes. Of this group, only 13% admitted having a positive history of neck symptoms. The development of early degenerative changes or intervertebral disk-space narrowing in this group was attributed to the effect of repetitive loading on the cervical spine as a result of head impact from blocking and tackling. Acute and chronic cervical intervertebral disk injury without frank herniation or neurologic findings occurs with considerable frequency in the athlete. Associated with a history of injury are neck pain and limited cervical spine motion. Roentgenograms may demonstrate disk-space narrowing and marginal osteophytes. Magnetic resonance imaging frequently demonstrates disk bulge without herniation. In general, management is conservative; permission to engage in activity is withheld until the youngster is asymptomatic and has a full range of cervical spine motion.

Cervical Vertebral Subluxation without Fracture Axial compression-flexion injuries incurred by striking an object with the top of the helmet can result in disruption of the posterior soft tissue supporting elements with angulation and anterior translation of the superior cervical vertebrae. Fractures of the bony elements are not demonstrated on roentgenograms, and the patient has no neurologic deficit. Flexion-extension roentgenograms demonstrate instability of the cervical spine at the involved level, manifested by motion, anterior intervertebral disk-space narrowing, anterior angulation and displacement of the vertebral body, and fanning of the spinous processes. Demonstrable instability on lateral flexion-extension roentgenograms in young, vigorous individuals requires aggressive treatment. When soft tissue disruption occurs without an associated fracture, it is likely that instability will result despite conservative treatment. When anterior subluxation greater than 20% of the vertebral body is due to disruption of the posterior supporting structures, posterior cervical fusion is recommended.

Spinal Injuries

Cervical Fractures or Dislocations: General Principles Fractures or dislocations of the cervical spine may be stable or unstable and may or may not be associated with neurologic deficit. When fracture or disruption of the soft tissue supporting structure immediately violates or threatens to violate the integrity of the spinal cord, implementation of certain management and treatment principles is imperative. These include the following: 1. Protection of the cord from further injury 2. Expeditious reduction 3. Attainment of rapid and secure stability 4. Implementation of an early rehabilitation program The first goal is to protect the spinal cord and the nerve roots from injury through mismanagement. It has been estimated that many neurologic deficits occur after the initial injury. That is, if a patient with an unstable lesion is carelessly manipulated during transportation to a medical facility or subsequently managed inappropriately, further encroachment on the spinal cord can occur. Second, once appropriate roentgenograms have been obtained and qualified orthopaedic and neurosurgical personnel are available, the malalignment of the cervical spine should be reduced as quickly and gently as possible. This will effectively decompress the spinal cord. When dislocation or anterior angulation and translation are demonstrated roentgenographically, immediate reduction is attempted with skull traction using Gardner-Wells tongs. These tongs can be easily and rapidly applied under local anesthesia without shaving the head in the emergency room or in the patient’s bed. Because these tongs are spring-loaded, it is not necessary to drill the outer table of the skull for their application. The tongs are attached to a cervical traction pulley, and weight is added at a rate of 5 pounds per disk space, or 25 to 40 pounds for a lower cervical injury. Reduction is attempted by adding 5 pounds every 15 to 20 minutes and is monitored by lateral roentgenograms. Unilateral facet dislocations, particularly at the C3-C4 level, are not always reducible by using skeletal traction. In such instances, closed skeletal or manipulative reduction under nasotracheal anesthesia may be necessary. The expediency of early reduction of cervical dislocations must be emphasized.26 It has been proposed that the presence of a bulbocavernous reflex indicates that spinal shock has worn off and that except for recovery of an occasional root at the site of the injury, neither motor nor sensory paralysis will be resolved regardless of treatment. The bulbocavernous reflex is produced by pulling on the urethral catheter. This stimulates the trigone of the bladder, producing a reflex contraction of the anal sphincter around the examiner’s gloved finger. Although the presence of a bulbocavernous reflex is generally a sign that there will be no further neurologic recovery below the level of injury, this is not always true. The presence of this reflex does not give the clinician license to handle the situation in an elective fashion. Malalignments and dislocations of the cervical spine associated with quadriparesis should be reduced as quickly as possible, by

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whatever means necessary, if maximal recovery is to be expected. In most instances in which a vertebral body burst fracture is associated with anterior compression of the cord, decompression is logically effected through an anterior approach with interbody fusion. Likewise, intervertebral disk herniation with cord involvement is best managed through anterior diskectomy and interbody fusion. In patients with cervical fractures and dislocations, posterior cervical laminectomy is indicated only rarely when excision of foreign bodies or bony alignment of the spine is the most effective method of decompression of the cervical cord. Indications for surgical decompression of the spinal cord have been delineated. A documented increase in neurologic signs is the clearest mandate for surgical decompression. Further observation, expectant waiting, and procrastination in this situation are contraindicated. Persistent partial cord or root signs, with objective evidence of mechanical compression, are also an indication for surgical intervention. The use of parenteral corticosteroids to decrease the inflammatory reactions of the injured cord and the surrounding soft tissue structures is indicated in the management of acute cervical spinal cord injuries. The efficacy of methylprednisolone in improving neurologic recovery when given in the first 8 hours has been recently demonstrated. The recommended regimen is a bolus of 30 mg/kg of body weight of methylprednisolone administered intravenously followed by an infusion of 5.4 mg/kg/hour for 23 hours. It is essential that the regimen be started within 8 hours of the injury. Although the results of the National Acute Spinal Cord Studies have been critical of this regimen, it remains in keeping with the standard of care.27,28 The third goal in managing fractures and dislocations of the cervical spine is to effect rapid and secure stability to prevent residual deformity and instability with associated pain as well as to prevent the possibility of further trauma to the neural elements. White and coworkers recognized that the literature is neither always clear nor consistent in describing what constitutes an unstable cervical spine.29,30 Using fresh cadaver specimens, they performed load displacement studies on sectioned and unsectioned two-level cervical spine segments to determine the horizontal translation and rotation that occurred in the sagittal plane after each ligament was transected. The experiments constituted a quantitative biomechanical analysis of the effects of destroying ligaments and facets on the stability of the cervical spine below C2 in an attempt to determine cervical stability. The express purpose of the study was to establish indications for surgical treatment to stabilize the spine. Although the intent of the study was to define clinical instability to formulate treatment standards and was not intended to establish criteria for a return to contact athletics, it appears that their findings are relevant to the latter issue. White and colleagues described clinical stability as the ability of the spine to limit its patterns of displacement of physiologic loads to prevent damage or irritation of the spinal cord or the nerve roots.29,30 They delineated four important findings. First, in sectioning the ligaments, small increments of change in stability occur, followed without warning by sudden, complete disruption of the spine under stress. Second, removal of the facets alters the motion

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s egment such that in flexion there is less angular displacement and more horizontal displacement. Third, the anterior ligaments contribute more to stability in extension than the posterior ligaments, and in flexion, the posterior ligaments contribute more than the anterior ligaments. The most relevant finding from the standpoint of criteria for return to contact sports is the fourth one. The adult cervical spine is unstable, or on the brink of instability, when one or more of the following conditions is present: (1) all the anterior or all the posterior elements are destroyed or are unable to function; (2) more than 3.5 mm of horizontal displacement of one vertebra exists in relation to an adjacent vertebra, measured on lateral roentgenograms (resting or flexionextension); or (3) there is more than 11 degrees of rotation difference compared with that of either adjacent vertebra measured on a resting lateral or flexion-extension roentgenogram (Figs. 16A1-13 and 16A1-14). The method of immobilization depends on the postreduction status of the injury. The literature has delineated the indications for using nonsurgical and surgical methods to achieve stability.31,32 These concepts for managing cervical spine fractures and dislocations may be summarized as follows: 1. Patients with stable compression fractures of the vertebral body, undisplaced fractures of the lamina or lateral masses, or soft tissue injuries without detectable

eurologic deficit can be adequately treated with tracn tion and subsequent protection with a cervical brace until healing occurs. 2. Stable, reduced facet dislocation without neurologic deficit can also be treated conservatively with a halo jacket brace until healing has been demonstrated by negative lateral flexion-extension roentgenograms. 3. Unstable cervical spine fractures or fracture-dislocations without neurologic deficit may require either surgical or nonsurgical methods to ensure stability. 4. Absolute indications for surgical stabilization of an unstable injury without neurologic deficits are late instability after closed treatment and flexion-rotation injuries with unreduced locked facets. 5. Relative indications for surgical stabilization in patients with unstable injuries without neurologic deficit are anterior subluxation greater than 20%, certain atlantoaxial fractures or dislocations, and unreduced vertical compression injuries with neck flexion. 6. Cervical spine fractures with complete cord lesions require reduction followed by stabilization by closed or open means, as indicated. 7. Cervical spine fractures with incomplete cord lesions require reduction followed by careful evaluation for surgical intervention.

4

5 –2° 6

+20° >3.5 mm –4°

7

ABNORMAL ANGLE

= 20 – (–2) = 22 = 20 – (–4) = 24

>11°

Figure 16A1-13 Abnormal angulation between two vertebrae at any one interspace is determined by comparing the angle formed by the projection of the inferior vertebral body borders with that of either the vertebral body above or the vertebral body below. If the angle at the interspace in question is 11 degrees or greater than that of either adjacent interspace, it is considered by White and associates to be clinical instability. (From White AA, Johnson RM, Punjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 109:85, 1975.)

Figure 16A1-14 The method for determining translatory displacement, as described by White and colleagues. Using the posteroinferior angle of the superior vertebral body as one point of reference and the posterosuperior angle of the vertebral body below, the distance between the two in the sagittal plane is measured. A distance of 3.5 mm or greater is suggestive of clinical instability. (From White AA, Johnson RM, Punjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 109:85, 1975.)

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Alar ligaments

Odontoid

TAL A

B

Figure 16A1-15 A, The atlantoaxial complex as seen from above. B, The disruption of the transverse ligament (TAL) with intact alar ligaments results in C1-C2 instability without cord compression. (Redrawn from Hensinger RN: Congenital anomalies of the atlantoaxial joint. In The Cervical Spine Research Society Editorial Committee: The Cervical Spine, 2nd ed. Philadelphia, JB Lippincott, 1989, p 242.)

The fourth and final goal of treatment is rapid and effective rehabilitation started early in the treatment process. A more specific categorization of athletic injuries to the cervical spine can be made. Specifically, these injuries can be divided into upper cervical spine, midcervical spine, and lower cervical spine injuries.

Upper Cervical Spine Fractures and Dislocations Upper cervical spine lesions involve C1 through C3. Although they rarely occur in sports, several specific injuries that can occur to the upper cervical vertebrae deserve mention. The transverse and alar ligaments are responsible for atlantoaxial stability (Fig. 16A1-15). If these structures are ruptured from a flexion injury with translation of C1 anteriorly, the spinal cord can be impinged between the posterior aspect of the odontoid process and the posterior rim of C1. The patient gives a history of head trauma and complains of neck pain, particularly with nodding, and may or may not present with cord signs. Roentgenographically, lateral views of the C1-C2 articulation demonstrate increase of the atlantodens interval. This interval is normally 3 mm in the adult. With transverse ligament rupture, it may increase up to 10 to 12 mm depending on the status of the alar and accessory ligaments. Note that increase in the atlantodens interval may be seen only when the neck is flexed. Fielding states that atlantoaxial fusion may be the “conservative” treatment for this lesion.33 He recommends posterior C1-C2 fusion using wire fixation and an iliac bone graft. Fractures of the atlas were described by Jefferson in 1920.34 These may be of two types: posterior arch fractures or burst fractures. Posterior arch fractures are more common, and with a brace support, they go on to achieve satisfactory fibrous or bony union. Burst fractures result from an axial load transmitted to the occipital condyles, which then disrupt the integrity of both the anterior and posterior arches of the atlas (Fig. 16A1-16). Roentgenograms

demonstrate bilateral symmetrical overhang of the lateral masses of the atlas in relation to the axis, with an increase in the paraodontoid space on the open mouth view. Clinically, the patient characteristically has pain and imitates the nodding motion. These fractures are considered stable when the combined lateral overhang of the atlas measures less than 7 mm. When the transverse diameter of the atlas is 7 mm greater than that of the axis, a transverse ligament rupture should be suspected (Fig. 16A1-17). Treatment, as recommended by Fielding, includes head-halter traction until muscle spasm resolves, followed by a brace support.33 If flexion-extension roentgenograms subsequently demonstrate significant instability, fusion may be indicated. Fractures of the odontoid have been classified into three types by Anderson and D’Alonzo.35 Type I is an avulsion of the tip of the odontoid at the site of the attachment of the alar ligament and is a rare and stable lesion. Type II is a fracture through the base at or just below the level of the superior articular processes. Type III involves a fracture of

Figure 16A1-16 Schematic representation of the four-part comminuted burst fracture of the atlas as seen from above. (Redrawn from Jefferson G: Fracture of the atlas vertebra. Br J Surg 7:407–422, 1919. By permission of the Publishers ButterworthHeinemann Ltd.)

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Figure 16A1-17 Illustration of a comminuted Jefferson fracture with both the transverse ligament intact (stable configuration) and a transverse ligament rupture (unstable configuration). (Redrawn from White AA, Punjabi MM: Clinical Biomechanics of the Spine. Philadelphia, JB Lippincott, 1978, p 204.) Y

X

Stable

the body of the axis (Fig. 16A1-18). When the odontoid is not displaced, planograms may be required to identify the lesion. The mechanism of odontoid fractures has not been clearly delineated; however, they appear to be due to head impact. All routine cervical spine roentgenographic studies should include the open mouth view to identify lesions involving the odontoid as well as the atlas. If these are negative, and if a lesion in this area is suspected,

Type I

Type II

Type III

Figure 16A1-18 Illustration of the three types of odontoid fractures in both the anteroposterior and lateral planes. Type I is an oblique avulsion fracture from the upper portion of the odontoid. Type II is a fracture of the odontoid process at its base. Type III is an odontoid fracture through the body of C2. (Redrawn from Anderson LD, D’Alonzo RT: Fractures of the odontoid process of the axis. J Bone Joint Surg Am 56:1663–1674, 1974.)

X + Y ≥7 mm Unstable

planograms or bending films may further delineate pathologic changes in this area. Managing type II fractures is a problem. It has been reported that 36% to 50% of these lesions treated initially with plaster casts or reinforced cervical braces fail to unite. Cloward has reported that 85% of his patients heal within 3 months when treated with the halo brace.36 Current management involves more aggressive surgical management with early posterior stabilization by means of wiring and fusion. It is necessary to stabilize fibrous unions or nonunited fractures of the odontoid surgically if they are demonstrated to be unstable on flexion and extension views. Stabilization may be effected through either posterior C1-C2 wire fixation and fusion or anterior odontoid screw fixation. Fractures through the arch of the axis are also known as traumatic spondylolistheses of C2, or hangman’s fractures. These are relatively rare lesions. The mechanism of injury is generally recognized to be hyperextension. This injury is inherently unstable, but it has been shown to heal with predictable regularity without surgical intervention.

Midcervical Spine Fractures and Dislocations Acute traumatic lesions of the cervical spine at the C3-C4 level are rare and are generally not associated with fractures. These lesions are classified as follows: (1) acute rupture of the C3-C4 intervertebral disk; (2) anterior subluxation of C3 on C4; (3) unilateral dislocation of the joint between the articular processes; and (4) bilateral dislocation of the joint between the articular processes.26,37,38 An episode of transient quadriplegia in an athlete who has sustained head impact but has a cervical spine roentgenogram with negative findings suggests acute rupture of the C3-C4 intervertebral disk. The syndrome of acute anterior spinal cord injury, as described by Schneider and associates,23,24 may be observed. A cervical myelogram or an MRI will substantiate the diagnosis. Anterior diskectomy and interbody fusion may be the most effective treatment of this lesion. Anterior subluxation of C3 on C4 is a result of a shearing force through the intervertebral disk space that disrupts the interspinous ligament as well as the posterior supporting structure. Roentgenograms demonstrate narrowing of the intervertebral disk space, anterior angulation and translation of C3 on C4, an increase in the distance between

Spinal Injuries

Figure 16A1-19 Roentgenogram demonstrates C3-C4 subluxation as manifested by anterior intervertebral disk space narrowing, anterior angulation, displacement of the superior vertebral body, and fanning of the spinous processes. (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17–25, 1991.)

Figure 16A1-20 Unilateral C3-C4 facet dislocation resulting in complete motor and sensory deficit distal to the lesion. There is fanning of the spinous processes of C3 and C4 and more than 20% anterior displacement of the body of C3 on C4 (arrow). (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17–25, 1991.)

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the spinous processes of the two vertebrae, and instability without fracture of the bony elements (Fig. 16A1-19). Spinal fusion may be necessary for adequate stabilization in such cases, in contrast to cervical spine instability caused by fracture, in which adequate reduction and subsequent bony healing result in stability. When the patient has posterior instability, posterior fusion is preferable to an anterior interbody fusion. Unilateral facet dislocation at C3-C4 may result in immediate quadriparesis. This injury involves the intervertebral disk space, the interspinous ligament, the posterior ligamentous supporting structures, and the one facet with resulting rotatory dislocation of C3 on C4 without fracture (Fig. 16A1-20). At this level, strong skeletal traction does not usually yield a successful reduction, and closed manipulation under general anesthesia is necessary to disengage the locked joint between the articular processes. Bilateral facet dislocation at the C3-C4 level is a grave lesion (Fig. 16A1-21). Skeletal traction may not reduce the lesion, and the prognosis for this injury is poor.

Lower Cervical Spine Fractures and Dislocations Lower cervical spine fractures or dislocations are those involving C4 through C7. In injuries resulting from various athletic endeavors, most fractures or dislocations of the

Figure 16A1-21 Bilateral facet dislocation at the C3-C4 level demonstrates anterior angulation as well as translation greater than 50% of the width of the vertebral body associated with spinous fanning. The lesion resulted in quadriplegia. (From Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine: Analysis and classification. Am J Sports Med 19:17–25, 1991.)

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cervical spine, with or without neurologic involvement, involve this segment. Although unilateral and bilateral facet dislocations occur, they are relatively rare. Most severe, athletically incurred cervical spine injuries are fractures of the vertebral body with varying degrees of compression or comminution.39

Unilateral Facet Dislocations Unilateral facet dislocations are the result of axial loading, flexion-rotation types of mechanisms. The lesion may be truly ligamentous without an associated vertebral fracture. In such instances, the facet dislocation is stable and is usually associated with neurologic involvement. Roentgenograms demonstrate less than 50% anterior shift of the superior vertebra on the inferior vertebra. Attempts should be made to reduce the facet dislocation by means of skeletal traction. As with similar lesions described at the C3-C4 level, it may not be possible to effect a closed reduction. In this instance, open reduction under direct vision through a posterior approach with supplemental posterior element bone grafting should be performed.

Bilateral Facet Dislocations Bilateral facet dislocations are unstable and are almost always associated with neurologic involvement. These injuries are associated with a high incidence of quadriplegia. Lateral roentgenograms demonstrate greater than 50% anterior displacement of the superior vertebral body on the inferior vertebral body. Immediate treatment, as described previously, consists of closed reduction with skeletal traction. Such lesions are generally reducible by means of skeletal traction and are then treated by halo-brace stabilization

A

and posterior fusion. It should be noted that instability is directly related to the ease with which the lesion is reduced because the easier it is to reduce, the easier it is to re-dislocate. If skeletal traction is unsuccessful, either manipulative reduction under sedation or general anesthesia or open reduction under direct vision is recommended. When the dislocation is reduced closed and the reduction is maintained, immobilization should be effected by use of the halo brace for 8 to 12 weeks. Corrective bracing should continue for an additional 4 weeks.

Vertebral Body Compression Fractures Compression fractures of the vertebral body are a result of axial loading. Vertebral body fractures of the cervical spine can be classified into five types.40

Type I Simple wedge or vertebral end-plate compression fractures of the cervical vertebrae are common injuries that respond to conservative management and rarely are associated with neurologic involvement (Fig. 16A1-22). It is important to differentiate these lesions from compression fractures that are associated with disruption of the posterior element soft tissue supporting structures. The latter lesions are unstable and are frequently associated with neurologic involvement, including quadriplegia.

Type II An isolated anteroinferior vertebral body or “teardrop” fracture is without displacement, has intact posterior elements, and is not associated with neurologic involvement

B

Figure 16A1-22 A and B, Type I vertebral body end plate compression fracture involving the superior aspect of C6 (arrows). Extension and flexion views demonstrate absence of evidence of instability. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

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Figure 16A1-23 Type II anteroinferior vertebral body fracture demonstrates the characteristic isolated teardrop fracture. Lateral roentgenograms of the lesion demonstrate maintenance of adjacent disk space height as well as a lack of subluxation or spinous process fanning. If there is no disruption of the posterior elements, this is a relatively stable lesion. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

Figure 16A1-24 Type III comminuted burst fracture of C4 with displacement of fragments into the vertebral canal (arrow). (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

(Fig. 16A1-23). This is a relatively stable fracture and may be treated conservatively.28,41

Cervical Spinal Stenosis with Cord Neurapraxia and Transient Quadriplegia

Type III

Characteristically, the clinical picture of cervical cord neurapraxia (CCN) with transient quadriplegia involves an athlete who sustains an acute transient neurologic episode of cervical cord origin with sensory changes that may be associated with motor paresis involving both arms, both legs, or all four extremities after forced hyperextension, hyperflexion, or axial loading of the cervical spine.47,48 Sensory changes include burning pain, numbness, tingling, or loss of sensation; motor changes consist of weakness or complete paralysis. The episodes are transient, and complete recovery usually occurs in 10 to 15 minutes, although in some cases gradual resolution does not occur for 36 to 48 hours. Except for burning paresthesia, neck pain is not present at the time of injury. There is complete return of motor function and full, pain-free cervical motion. Routine roentgenograms of the cervical spine show no evidence of fracture or dislocation, but a demonstrable degree of cervical spinal stenosis is present.

Comminuted burst vertebral body fractures have intact posterior elements, but displacement of bony fragments into the vertebral canal may place the cord in jeopardy. Late settling of the fracture with deformity can occur. Surgical stabilization is recommended (Fig. 16A1-24).

Type IV The axial load three-part–two-plane vertebral body fracture consists of three fracture parts: (1) an anteroinferior teardrop; (2) a sagittal vertebral body fracture; and (3) disruption of the posterior neural arch.42-46 This lesion is unstable and is almost always associated with quadriplegia. Careful evaluation of the routine anteroposterior roentgenogram or CT scan is necessary to appreciate the sagittal vertebral body fracture, a finding that portends a grave prognosis (Fig. 16A1-25).

Type V This is a vertebral body three-part–two-plane compression fracture associated with disruption of posterior elements of an adjacent vertebra. This is an extremely unstable fracture (Fig. 16A1-26).

Determination of Spinal Stenosis: Method of Measurement To identify cervical stenosis, a method of measurement is needed. The standard method, the one most commonly employed for determining the sagittal diameter of

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A

C

B

D

Figure 16A1-25 A, A three-part–two-plane fracture of C6. Lateral view demonstrates prevertebral soft tissue swelling and an anteroinferior fracture fragment of C6 involving the entire vertebral body height and one third of the vertebral body width. There is about 1 mm of posterior displacement of the inferior aspect of the posterior vertebral body. The C6-C7 intervertebral disk space is minimally narrowed posteriorly with associated capsular disruption and “fanning.” B, Frontal view demonstrates a faint, linear radiolucency through the C6 vertebral body indicating a sagittal vertebral body fracture (arrow). There is mild lateral mass displacement. C, Computed tomographic examination demonstrates the sagittal fracture extending completely through the vertebral body with disruption of the lamina on the right. D, Diagrammatic representation of the three-part–two-plane vertebral body compression fracture demonstrates the anteroinferior teardrop as well as the sagittal vertebral body fractures and associated fracture through the lamina. (A, From Torg JS, Pavlov H, O’Neill MJ, et al: The axial load teardrop fracture. Am J Sports Med 19:355–364, 1991.)

the spinal canal, involves measuring the distance between the middle of the posterior surface of the vertebral body and the nearest point on the spinolaminar line. Using this technique, Boden and colleagues49 reported that the average sagittal diameter of the spinal canal from the fourth to

the sixth cervical vertebra in 200 healthy individuals was 18.5 mm (range, 14.2 to 23 mm). The target distance he used was 1.4 m. Others have noted that values of less than 14 mm are uncommon and fall below the standard deviation for any cervical segment. Other measurements

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A

683

B

Figure 16A1-26 A, Type V compression fracture of the vertebral body associated with fractures of the neural arch of an adjacent vertebra. Settling and posterior displacement of the superior vertebral segment occur. B, Distraction of the superior vertebral segment with skeletal traction permits visualization of fractures through the pedicles (arrow) of C6 in addition to the three-part–two-plane fracture of the body of C5. (From Torg JS [ed]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982.)

reported in the literature vary greatly. The variations in the landmarks and the methods used to determine the sagittal distance, as well as the use of different target distances for roentgenography, have resulted in inconsistencies in the so-called normal values. Therefore, the standard method of measurement for spinal stenosis is a questionable one.

On the basis of these observations, it may be concluded that the factor that explains the described neurologic picture of CCN is diminution of the anteroposterior diameter of the spinal canal, either as an isolated observation or in association with intervertebral disk herniation, degenerative changes, post-traumatic instability, or

The Ratio Method An alternative way to determine the sagittal diameter of the spinal canal was devised by Pavlov and colleagues and is called the ratio method.50 It compares the standard method of measurement of the canal with the anteroposterior width of the vertebral body at the midpoint of the corresponding vertebral body (Fig. 16A1-27). The actual measurement of the sagittal diameter in millimeters, as determined by the conventional method, is misleading both as reported in the literature and in actual practice because of variations in the target distances used for roentgenography and in the landmarks used for obtaining the measurement. The ratio method compensates for variations in roentgenographic technique because the sagittal diameter of both the canal and the vertebral body is affected similarly by magnification factors. The ratio method is independent of variations in technique, and the results are statistically significant. Using the ratio method of determining the dimension of the canal, a ratio of the spinal canal to the vertebral body of less than 0.80 is indicative of cervical stenosis. I believe that the ratio of the anteroposterior diameter of the spinal canal to that of the vertebral body (SC/VB ratio) is a consistent and reliable way to determine cervical stenosis (Fig. 16A1-28) in those individuals who have experienced episodes of CCN. The ratio has a very low predictive value, however, and should not be used as a screening tool.

a b

ratio =

a b

Figure 16A1-27 The ratio of the spinal canal to the vertebral body is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line (a) divided by the anteroposterior width of the vertebral body (b). (From Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354–1370, 1986.)

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A

B

Figure 16A1-28 A and B, A comparison between the ratio of the spinal canal to the vertebral body of a stenotic patient and the same ratio in a control subject is demonstrated on lateral roentgenograms of the cervical spine. The ratio is about 1:2 (0.50) in the stenotic patient compared with 1:1 (1.00) in the control subject. (From Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:1354–1370, 1986.)

c ongenital anomalies. In instances of developmental cervical stenosis, forced hyperflexion, or hyperextension of the cervical spine, the caliber of an already narrow canal is further decreased, as explained by the pincer mechanism of Penning (Fig. 16A1-29).51 In patients in whom stenosis is associated with osteophytes or a herniated disk, direct pressure can occur, again when the spine is forced in the extremes of flexion and extension. It is further postulated that with an abrupt but brief decrease in the anteroposterior diameter of the spinal canal, the cervical cord is mechanically compressed, causing transient interruption of either motor or sensory function, or both, distal to the lesion. The neurologic aberration that results is transient and completely reversible. A review of the literature has revealed few reported cases of transient quadriplegia occurring in athletes. Attempts to establish the incidence indicate that the problem is more prevalent than may be expected. Specifically, in a population of 39,377 exposed participants, the reported incidence of transient paresthesia in all four extremities was 6 per 10,000, whereas the reported incidence of paresthesia associated with transient quadriplegia was 1.3 per 10,000 in the one football season surveyed. From these data, it may be concluded that the prevalence of this problem is relatively

Figure 16A1-29 The pincers mechanism, as described by Penning, occurs when the distance between the posteroinferior margin of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the subjacent vertebra decreases with hyperextension, resulting in compression of the cord. With hyperflexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior margin of the inferior vertebra would be the “pincers.” (Redrawn from Torg JS, Pavlov H, Gennario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:13541–370, 1986.)

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4 5 1 2

1 4 2 5

5 4 1 2

2 4 1 5

17

1 College 2 Professional 3 Transient 4 Quadriplegic 5 Control

16

Canal

18

19

football. None of the 77 quadriplegic individuals (cohort 4) had an episode of neurapraxia of the spinal cord before the catastrophic injury. Also, none of the 45 high school, college, and professional players who had an episode of transient neurapraxia (cohort 3) became quadriplegic. These data, in combination with the absence of developmental narrowing of the cervical canal in the quadriplegic group (cohort 4), provide evidence that transient neurapraxia of the cervical cord and an injury associated with permanent catastrophic neurologic sequelae are unrelated (Fig. 16A1-30). Therefore, developmental narrowing of the cervical canal in a spine that has no evidence of instability is neither a harbinger of nor a predisposing factor for permanent neurologic injury. The data did not reveal an association between developmental narrowing of the cervical canal and quadriplegia. The major factor in the occurrence of cervical quadriplegia in football players is a tackling technique in which the head is used as the primary point of contact, with resulting transmission of axial energy to, and subsequent failure of, the cervical spine. The findings of this study demonstrated the high sensitivity, low specificity, and low predictive value of the ratio of the diameter of the cervical spinal canal to that of the vertebral body, precluding its use as a screening mechanism for determining the suitability of an individual for participation in contact sports. Developmental narrowing of the cervical canal without associated instability does not predispose an individual to permanent catastrophic neurologic injury and therefore should not preclude an athlete from participation in contact sports. More recently, a group of 110 patients with CCN has been studied. In this report, a classification system of CCN was developed, and MRI data were analyzed using a new computerized measurement technique.53 CCN was classified according to the type of neurologic deficit: plegia for episodes with complete paralysis; paresis for episodes

3 3

15

high and that an awareness of the causes, manifestations, and appropriate principles of management is warranted.47 Characteristically, after an episode of CCN with or without transient quadriplegia, the first question raised concerns the advisability of restricting activity. In an attempt to address this problem, 117 young athletes have been interviewed who sustained cervical spine injuries associated with complete permanent quadriplegia while playing football between the years 1971 and 1984. None of these patients recalled a prodromal experience of transient motor paresis. Conversely, none of the patients in this series who had experienced transient neurologic episodes subsequently sustained an injury that resulted in permanent neurologic injury. On the basis of these data, it was concluded that a young patient who has had an episode of CCN with or without an episode of transient quadriplegia is not predisposed to permanent neurologic injury because of it.47 Subsequent to the description of neurapraxia of the cervical cord with transient quadriplegia, a number of issues concerning the disorder have arisen. An epidemiologic study evaluating 45 athletes who had an episode of transient neurapraxia of the cervical spinal cord revealed the consistent finding of developmental narrowing of the cervical spinal canal. The purpose of the study was to determine the relationship, if any, between a developmentally narrowed cervical canal and reversible and irreversible injury of the cervical cord with use of various cohorts of football players and a large control group. Cohort 1 was composed of 227 college football players who were asymptomatic and had no known history of transient neurapraxia of the cervical cord. Cohort 2 consisted of 97 professional football players who also were asymptomatic and had no known history of transient neurapraxia of the cervical cord. Cohort 3 was a group of 45 high school, college, and professional football players who had at least one episode of transient neurapraxia of the cervical cord. Cohort 4 was composed of 77 individuals who were permanently quadriplegic as a result of an injury while playing high school or college football. Cohort 5 consisted of a control group of 105 male subjects who were not athletes and had no history of a major injury of the cervical spine, an episode of transient neurapraxia, or neurologic symptoms.52 The mean and standard deviation of the diameter of the spinal canal, the diameter of the vertebral body, and the ratio of the diameter of the spinal canal to that of the vertebral body were determined for the third through sixth cervical levels on the radiographs of each cohort. In addition, sensitivity, specificity, and positive predictive value of the ratio of the diameter of the spinal canal to that of the vertebral body of 0.90 or less were evaluated. The findings of this study demonstrated that a ratio of 0.80 or less had a high sensitivity (93%) for transient neurapraxia. These findings also support the concept that the symptoms result from a transient reversible deformation of the spinal cord in a developmentally narrowed osseous canal. The low predictive value of the ratio (0.2%), however, precludes its use as a screening mechanism for determining the suitability of an athlete for participation in contact activities. Axial load, degree of instability, and the period of time from injury to reduction have been implicated as factors in permanent neurologic injury in athletes who play tackle

685

3 3

C3

C4

C5

C6

Cervical Spine Level Figure 16A1-30 Profile plot of the mean diameter of the spinal canal, demonstrating a significantly smaller value in cohort 3 compared with that in all other cohorts (P < .05). With the numbers available, no significant difference was found among cohorts 1, 2, 4, and 5. (From Torg JS, Naranja RJ Jr, Pavlov 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 78:1308-1314, 1996.)

DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� .9

.9

.8

.8

.7

.7 Probability of Recurrence

Probability of Recurrence

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.6 .5 .4 .3

.5 .4 .3

.2

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.1 0

0 6

A

.6

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8 9 10 11 12 13 MRI Disk Level Canal Diameter (mm)

.3

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B

.4 .5 .6 .7 .8 .9 1 1.1 1.2 1.3 X-ray Spinal Canal/Vertebral Body Ratio

Figure 16A1-31 Graphs developed using regression analysis in which the risk for recurrence can be plotted as a function of the disk-level diameter measured on magnetic resonance imaging (A) and the spinal canal–to–vertebral body ratio calculated on the basis of x-ray films (B). The construction of these plots is based on the result that increased risk for recurrence is inversely correlated with canal diameter. Future patients with cervical cord neurapraxia can be counseled regarding their individual risk for recurrence based on the particular size of their spinal canal.

with motor weakness; and paresthesia for episodes that involve only sensory changes without motor involvement. The CCN grade was defined by the length of time that the neurologic symptoms persisted: grade I, less than 15 minutes; grade II, greater than 15 minutes but less than 24 hours; and grade III, greater than 24 hours. The CCN pattern was defined by the anatomic distribution of all the neurologic symptoms: quad, episodes that involve all four extremities; upper, episodes involving both arms; lower, episodes involving both legs; and hemi, episodes involving an ipsilateral arm and leg. Using this classification system, the incidence of CCN type was plegia in 44 cases (40%), paresis in 28 (25%), and paresthesia in 38 cases (35%). CCN was grade I in 81 cases (74%), grade II in 17 cases (15%), and grade III in 12 cases (11%). The pattern was quad in 88 cases (80%), upper in 17 cases (15%), lower in 2 cases (2%), and hemi in 3 cases (3%). To study the relationship of the spinal cord to the spinal canal, a computerized system was developed to analyze magnetic resonance images. This system consisted of a personal computer and a color scanner with a transparency adapter. Images were digitized on the scanner and then uploaded using an imaging software package. The midsagittal T1and T2-weighted images were digitized. Using a graphics digitizer pad with a resolution of 0.01 mm, the following measurements were made at levels C3-C7: To quantify spondylitic narrowing, the disk level canal diameter was measured as the shortest distance between the intervertebral disk and the body posterior elements; the cord diameter was determined by measuring the transverse diameter of the spinal cord at the appropriate level; and the space available for the cord was calculated by subtracting the spinal cord diameter from the disk-level canal diameter. Follow-up evaluation was obtained by questionnaire, telephone interview, or office evaluation and was available for 105 of the 110 cases. Sixty-three patients (57%) returned to contact activities after their first episode of CCN. Of this group, 35 patients (56%) experienced a second episode of CCN. Once again, there were no permanent or catastrophic neurologic injuries related to the occurrence of CCN. Patients returning to football had a

higher recurrence rate than those returning to other sports. Thirty-two of 52 football players (62%) who returned to the sport experienced a recurrence, compared with 3 of 11 players (27%) who returned to other sports. All radiologic measurements except spinal cord diameter were predictive or recurrent. The patients’ age, level of sports participation, radiographic findings, MRI findings, clinical CCN classification, and radiologic classification did not have predictive value in determining which patients were at risk for recurrence. The presence of disk herniation, cord compression, degenerative disk disease, or any other finding was not an indicator of whether patients would suffer future episodes of CCN. Based on the finding that narrowing of the canal is a causative factor of CCN, the recurrence and diameter data were analyzed and correlated. Graphic plots were constructed using logistic regression analysis of the percentage risk for recurrence versus the disk-level canal diameter and the SC/VB ratio. The plots demonstrated a strong inverse correlation between the risk for recurrence and the disklevel canal diameter and SC/VB ratio (Fig. 16A1-31). Of note, there is one reported case of a professional football player who had congential stenosis and sustained a partial cervical spinal cord injury manifested by mild upper extremity dysesthesias and mild weakness of the wrist extensors and biceps.96

PREVENTION Athletic injuries to the cervical spine that result in injury to the spinal cord are infrequent but catastrophic events. Accurate descriptions of the mechanism or mechanisms responsible for a particular injury transcend simple academic interest. Before preventive measures can be developed and implemented, identification of the mechanisms involved in the production of the particular injury is necessary. Because the nervous system is unable to recover significant function after severe trauma, prevention assumes a most important role when considering these injuries. Injuries resulting in spinal cord damage have been associated with football,49,54-58 water sports,59-63 wrestling,64 rugby,65-69 trampolining,70-72 and ice hockey.73,74 The use

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of epidemiologic data, biomechanical evidence, and cinematographic analysis has (1) defined and supported the involvement of axial load forces in cervical spine injuries occurring in football; (2) demonstrated the success of appropriate rule changes in the prevention of these injuries; and (3) emphasized the need for employment of epidemiologic methods to prevent cervical spine and similar severe injuries in other high-risk athletic activities. Identification of the cause of football-related cervical quadriplegia and its prevention center on four areas: (1) the role of the helmet-facemask protective system; (2) the concept of the axial loading mechanism of injury; (3) the effect of the 1976 rule changes banning spearing and the use of the top of the helmet as the initial point of contact in tackling; and (4) the necessity for continued research, education, and enforcement of rules.

A

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The protective capabilities provided by the modern football helmet have resulted in the advent of playing techniques that have placed the cervical spine at risk for injury, with associated catastrophic neurologic sequelae. Available cinematographic and epidemiologic data clearly indicate that cervical spine injuries associated with quadriplegia occurring as a result of football are not hyperflexion accidents. Instead, they are due to purposeful axial loading of the cervical spine as a result of spearing and head-first playing techniques (Fig. 16A1-32). As a causative factor, the modern helmet-facemask system is secondary, contributing to these injuries because of its protective capabilities that have permitted the head to be used as a battering ram, thus exposing the cervical spine to injury. Classically, hyperflexion has been emphasized as playing a role in cervical spine trauma, whether the injury was

B

D

Figure 16A1-32 A, With the advent of the polycarbonate helmet-facemask protective device, use of the top or crown of the helmet as the initial point of contact in blocking and tackling became prevalent. Contact is made, the head abruptly stops, the momentum of the body continues, and the cervical spine is literally crushed between the two. In this instance, the fracture-dislocation transected the spinal cord. B, The injured player collapses, having been rendered quadriplegic. C, Further collapse is noted. D, The player is evacuated on a spine board and stretcher. (Photos courtesy of Randy Green, Vanderbilt Student Communications.)

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due to a diving accident, trampolining, rugby, or American football. Epidemiologic and cinematographic analyses have established that most cases of cervical spine quadriplegia that occur in football have resulted from axial loading. Far from being an accident or an untoward event, techniques are deliberately used that place the cervical spine at risk for catastrophic injury (Fig. 16A1-33). Recent laboratory observations also indicate that athletically induced cervical spine trauma results from axial loading.56-58,75 Mertz and colleagues,76 Hodgson and Thomas,77 and Sances and colleagues78 measured stresses and strains within the cervical spine when axial impulses were applied to helmeted cadaver head-spine-trunk specimens. They were able to produce fractures of the lower cervical spine when the impulse was applied to the crown of the helmet. Hodgson and Thomas determined that direct vertex impact imparted a larger force to the cervical vertebrae than forces applied further forward on the skull. Gosch and associates79 investigated three different injury modes (hyperflexion, hyperextension, and axial compression) in anesthetized monkeys and concluded that axial compression produced cervical spine fractures and dislocations. Maiman and coworkers,80

Roaf,81-83 and White and associates29 demonstrated vertebral body fractures in the lower cervical spine caused by the axial loading of isolated spinal units. Roaf subjected spinal units to forces differing in direction and magnitude and concluded that hyperflexion of the cervical spine was an anatomic impossibility. In contrast, he was able to produce almost every variety of spinal injury with a combination of compression and rotation. Bauze and Ardran84 postulated that axial loads were responsible for cervical spine dislocations as well as fractures. They demonstrated that failure of the facet joints and posterior ligaments occurred when axial loads were applied to cadaveric spines. When the lower portion of the spine was flexed and fixed, and the upper part extended and free to move forward, vertical compression produced bilateral dislocation to the facet joints without fracture. If lateral tilt or axial rotation occurred as well, a unilateral dislocation was produced. The forces observed were all less than those required for bony failure and allowed facet dislocation without associated bony injury. Nightingale and associates85 analyzed the relationships among head motion, local deformations of the cervical

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Figure 16A1-33 A, Subject (No. 37, foreground) lines up in front of ball carrier in preparation for tackling. B, Preimpact position shows tackler about to ram ball carrier with the crown of his helmet. C, At impact, contact is made with the top of the helmet. Although the neck is slightly flexed, it is clearly not hyperflexed. The major force vector is transmitted along the axial alignment of the cervical spine. D, The tackler recoils following impact.

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Figure 16A1-34 A, When the neck is in a normal upright anatomic position, the cervical spine is slightly extended because of the natural cervical lordosis. B, When the neck is flexed slightly, to about 30 degrees, the cervical spine is straightened and converted into a segmented column.

spine, and injury mechanisms using a cadaver head and neck model that had experienced impact in an anatomically neutral position. They observed that classic concepts of flexion and extension of the cervical spine do not apply as a mechanism of injury to a vertically impacted head. They further concluded that straightening of the cervical spine before injury may be a necessary element of the compressive flexion mechanism. In the course of a collision activity, such as tackle football, most energy inputs to the cervical spine are effectively dissipated by the energy-absorbing capabilities of the cervical musculature through controlled lateral bending, flexion, or extension motion. The bones, the disks, and the ligamentous structures can be injured when contact occurs on the top of the helmet when head, neck, and trunk are

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positioned in such a way that forces are transmitted along the longitudinal axis of the cervical spine. When the neck is in the anatomic position, the cervical spine is extended as a result of normal cervical lordosis. When the neck is flexed to 30 degrees, the cervical spine straightens (Fig. 16A1-34). In axial loading injuries, the neck is slightly flexed, and normal cervical lordosis is eliminated, thereby converting the spine into a straight segmented column. Assuming head, neck, and trunk components to be in motion, rapid deceleration of the head occurs when it strikes another object, such as another player, trampoline bed, or lake bottom. This results in the cervical spine being compressed between the rapidly decelerated head and the force of the oncoming trunk. When the maximal amount of vertical compression is reached, the straightened cervical spine fails in a flexion mode, and fracture, subluxation, or unilateral or bilateral facet dislocation can occur (Fig. 16A1-35).86 Refutation of the “freak accident” concept with the more logical principle of cause and effect has been most rewarding in dealing with problems of football-induced cervical quadriplegia. Definition of the axial loading mechanism—in which football players, usually defensive backs, make a tackle by striking an opponent with the top of their helmet—has been a key element in this process. Implementation of rule changes and coaching techniques eliminating the use of the head as a battering ram has resulted in a dramatic reduction in the incidence of quadriplegia since 1976. Data on cervical spine injuries resulting from participation in football have been compiled by a national registry since 1971.56,58 Analysis of the epidemiologic data and cinematographic documentation clearly demonstrates that most cervical fractures and dislocations were due to axial loading. On the basis of these observations, rule changes banning both deliberate “spearing” and the use of the top of the helmet as the initial point of

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Figure 16A1-35 Biomechanically, a straight cervical spine responds to an axial load force like a segmented column. Axial loading of the cervical spine first results in compressive deformation of the intervertebral disks (A and B). As the energy input continues and maximal compressive deformation is reached, angular deformation and buckling occur. The spine fails in a flexion mode (C), with resulting fracture, subluxation, or dislocation (D and E). Compressive deformation to failure with a resultant fracture, dislocation, or subluxation occurs in as little as 8.4 msec. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sport Med 1:12–27, 1991.)


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30 32 25 20 15 10 5 0

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1995 1994 1993 1992 1991 1990 1989 1988 1987 1986 1985 1984 1983 1982 1981 1980 1979 1978 1977 1976 1975 Year Figure 16A1-36 The yearly incidence of permanent cervical quadriplegia for all levels of participation (1975 to 1995) decreased dramatically in 1977 following initiation of the rule changes prohibiting the use of head-first tackling and blocking techniques.

contact in making a tackle were implemented at the high school and college levels. Subsequently, a marked decrease in cervical spine injury rates has occurred. The incidence of permanent cervical quadriplegia decreased from 34 cases in 1976 to 5 in the 1984 season (Fig. 16A1-36). I believe that most athletic injuries to the cervical spine associated with quadriplegia also occur as a result of axial loading. Tator and colleagues studied 38 acute spinal cord injuries caused by diving accidents. They observed, “In most cases the cervical spine was fractured and the spinal cord crushed. The top of the head struck the bottom of the lake or pool.”87 Scher, reporting on vertex impact and cervical dislocation in rugby players, observed, “When the neck is slightly flexed, the spine is straight. If significant force is applied to the vertex when the spine is straight, the force is transmitted down the long axis of the spine. When the force exceeds the energy-absorbing capacity of the structures involved, cervical spine flexion and dislocation will result.”67 Tator and Edmonds73 reported the results of a national questionnaire by the Canadian Committee on the Prevention of Spinal Injuries due to Hockey, which recorded 28 injuries involving the spinal cord, 17 of which resulted in complete paralysis. They noted that in this series, the most common mechanism involved was a check, in which injured players struck the boards “with the top of their heads, while their necks were slightly flexed.” Reports in the recent literature on the mechanism of injury involved in cervical spine injuries resulting from water sports (diving), rugby, and ice hockey support our thesis.

PATHOPHYSIOLOGY OF CERVICAL CORD INJURY AS IT RELATES TO THE PRINCIPLES OF CORD RESUSCITATION Cervical cord injuries have resulted in reversible, incompletely reversible, and irreversible neurologic deficits. An explanation for this variable response to injury has been obtained from the study of the histochemical responses of a squid axon injury model to mechanical deformation.88 The spinal cord is considered an element with a low modulus of

rigidity in which compressive macroscopic loads applied to the cord result in localized tension within the tissue. Various macroscopic deformations result in local elongation. With axial elongation of the cord, all elements experience stretch. With extension or flexion, the tension in the cord will vary across the diameter. Highly localized loading, such as shearing from subluxation of the vertebral elements, or focal compressions, such as a weight-drop experiment, result in elongation of the elements in the direction of the long axis of the cord. The effects of mechanical deformation of the axon membrane lead to an alteration in membrane permeability as a result of the development of nonspecific defects in the membrane. This allows calcium to flow into the cell and results in depolarization of the membrane. The giant axon of the squid was used as the tissue model to determine the effects of high strain and uniaxial tension to various degrees of stretch in concert with the neurophysiologic changes of the single axon. These experiments showed that the degree of mechanical injury to the axon influences the magnitude of the calcium insult and the time course of the recovery phase. A low rate of deformation produces only a small reversible depolarization. The axon responds to the increased intracellular calcium by pumping it extracellularly with no residual deficit. As the rate of loading is increased, the magnitude of the depolarization and the recovery time to the original resting potential increase in a nonlinear fashion. The axon may or may not fully recover depending on the ability of the cell to pump calcium. With a large influx of calcium, intracellular calcium pumps may be overwhelmed, resulting in irreversible injury. The excess intracellular calcium results in activation of calcium-activated neutral proteases, which lead to cytoskeletal depolymerization and the accumulation of proteins intracellularly. The resulting increased osmotic pressure causes the cell to swell and eventually rupture (Fig. 16A1-37). In addition to the immediate and direct effect of mechanical deformation on the cytosolic calcium concentration within the axon, it has been shown that high strain rate elongation of isolated venous specimens elicits a spontaneous constriction. This mechanically induced vasospasm has the effect of altering blood flow in various regions as a function of the level of vessel stretch. Ultimately, the outcome for the neural tissue will depend synergistically on the level of calcium introduced into the cytosol and the degree to which the metabolic machinery of the cell may be compromised by regional reduction in blood flow.88

Clinical Correlation The clinical evidence of varying degrees of recovery to cervical spine injury correlates with the squid axon model. Cord neurapraxia and transient quadriplegia, a completely reversible lesion, are associated with developmental narrowing of the cervical spine. Cord deformation occurs rapidly and is attributable to a hyperflexion or hyperextension mechanism. Disruption of cell membrane permeability leads to a small increase in intracellular calcium, but spinal stability and cell anatomy are not disturbed, and the deleterious effects of local anoxia secondary to venous spasm do not impede recovery of axonal function.

Spinal Injuries 1o Resting axon 1o+∆1 Stimulus controlled strain and strain rate Ca++

Ca++ 1o

Elevated intracellular calcium

Excess calcium produces CANP and cytoskeletal depolymerization Accumulation of vesicles and elevated protein solution Increased osmotic pressure with cell swelling

Elevated intracellular hydrostatic pressure and axolemma rupture Figure 16A1-37 Schematic representation of the effects of elevated intracellular calcium concentration on cell viability. Specifically, elevated cytosolic-free calcium in excess of 50 m will result in calcium-activated neutral protease (CANP), which can damage protein structures of the cell.

Cervical cord lesions with incomplete reversibility are often associated with instability, such as is seen with subluxation or unilateral facet dislocation, whereby the cord undergoes maximal elastic deformation. It is proposed that lack of full recovery is attributable to prolonged duration of deformity with local anoxia inhibiting cell membrane function and a reduction of intracellular calcium concentrations. Irreversible cord injury with permanent quadriplegia results from an axial load mechanism, which causes a fracture or dislocation that renders the spine markedly unstable. The cord undergoes functional plastic deformation with anatomic disruption of axonal integrity.

Management Implications: Principles of Cervical Cord Resuscitation These observations support the concept that acute spinal cord injury with concomitant subluxation and dislocation should be reduced promptly. This approach contradicts previous approaches that recommended gradual reductions of cervical dislocations over a prolonged period of time.

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Recent studies have documented the efficacy of methylprednisolone in the management of acute spinal cord injuries. These observations suggest the possible efficacy of other pharmacologic agents that would increase vasodilation and local blood flow and counteract the effects of local cord anoxia or enhance the removal of intracellular calcium. Correlation of both reversible and irreversible spinal cord injury with the effect of neuronal and small vessel deformation has clearly indicated the potential for neurologic recovery by reversing the effects of increased intracellular calcium ion concentration and tissue anoxia. Presumably, these observations suggest that it is secondary cord injury caused by hypoxia and aberration in cell membrane potential that are largely responsible for irreversible neurologic deficits. Thus, the concept of spinal cord resuscitation is proposed as an attempt to reverse secondary changes that occur to obtain maximal neurologic recovery. Such measures would include prompt relief of cord deformation, administration of intravenous corticosteroid, measures to facilitate spinal cord perfusion, and pharmacologic agents to facilitate the return of the calcium pump mechanism.89

CRITERIA USED TO GAUGE RETURN TO CONTACT ACTIVITIES AFTER CERVICAL SPINE INJURY Injury to the cervical spine and associated structures as a result of participation in competitive athletic and recreational activities is not uncommon. It appears that the frequency of these various injuries is inversely proportional to their severity. Whereas Albright and colleagues25 have reported that 32% of college football recruits sustained “moderate” injuries while in high school, catastrophic injuries with associated quadriplegia occur in fewer than 1 in 100,000 participants per season at the high school level. As indicated, the variety of possible lesions is considerable and the severity variable. The literature dealing with diagnosis and treatment of these problems is considerable. However, conspicuously absent is a comprehensive set of standards or guidelines for establishing criteria for permitting or prohibiting return to contact sports (boxing, football, ice hockey, lacrosse, rugby, wrestling) following injury to the cervical spinal structures. The explanation for this void appears to be twofold. First, the combination of a litigious society and the potential for great harm should things go wrong makes “no” the easiest and perhaps most reasonable advice. Second and perhaps most important, with the exception of the matter of transient quadriplegia, there is a lack of credible data pertaining to postinjury risk factors. Despite a lack of credible data, this chapter will attempt to establish guidelines to assist the clinician as well as the patient and his or her parents in the decision-making process.90 Cervical spine conditions requiring a decision as to whether or not participation in contact activities is advisable and safe can be divided into two categories: (1) congenital or developmental conditions, and (2) post-traumatic conditions. Each condition has been determined to pre sent either no contraindication, relative contraindications, or an absolute contraindication on the basis of a variety of parameters. Information compiled from more than

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1200 cervical spine injuries documented by the National Football Head and Neck Injury Registry has provided insight into whether various conditions may or may not predispose to more serious injury.56-58 A review of the literature in several instances provides significant data for a limited number of specific conditions. Analysis of many conditions predicated on an understanding of recognized injury mechanisms has permitted categorization on the basis of “educated” conjecture. And last, much reliance has been placed on personal experience that must be regarded as anecdotal. The structure and mechanics of the cervical spine enable it to perform three important functions. First, it supports the head as well as the variety of soft tissue structures of the neck. Second, by virtue of segmentation and configuration, it permits multiplanar motion of the head. Third, and most important, it serves as a protective conduit for the spinal cord and cervical nerve roots. A condition that impedes or prevents the performance of any of the three functions in a pain-free manner either immediately or in the future is unacceptable and constitutes a contraindication to participation in contact sports. The following proposed criteria for return to contact activities in the presence of cervical spine abnormalities or following injury are intended as guidelines only. It is fully acknowledged that for the most part they are at best

A

redicated on anecdotal experience, and no responsibility p can be assumed for their implementation. Critical to the application of these guidelines is the implementation of coaching and playing techniques that preclude the use of the head as the initial point of contact in a collision situation. Exposure of the cervical spine to axial loading is an invitation to disaster and makes all safety standards meaningless.

Congenital Conditions Odontoid Anomalies Hensinger91 has stated that “patients with congenital anomalies of the odontoid are leading a precarious existence. The concern is that a trivial insult superimposed on already weakened or compromised structure may be catastrophic.” This concern became a reality during the 1989 football season when an 18-year-old high school player was rendered a respiratory-dependent quadriplegic while making a head tackle that was vividly demonstrated on the game video. Postinjury roentgenograms revealed an os odontoideum with marked C1-C2 instability (Fig. 16A1-38). Thus, odontoid agenesis, odontoid hypoplasia, and os odontoideum are all absolute contraindications to participation in contact activities.

B

Figure 16A1-38 Inherent instability at C1 in a patient with an os odontoideum. This condition resulted in respiratory-dependent quadriplegia following a spear tackle by this 18-year-old high school football player. The reduction in the space available for the cord is vividly demonstrated by the lateral extension (A) and flexion (B) postinjury views. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sport Med 1:12–27, 1991.)

Spinal Injuries

Spina Bifida Occulta This is a rare, incidental roentgenographic finding that presents no contraindication.

Atlanto-occipital Fusion This rare condition is characterized by partial or complete congenital fusion of the bony ring of the atlas to the base of the occiput. Signs and symptoms are referable to the posterior columns as a result of cord compression by the posterior lip of the foramen magnum and usually occur in the third or fourth decade. They usually begin insidiously and progress slowly, but sudden onset or instant death has been reported. Atlanto-occipital fusion as an isolated entity or coexisting with other abnormalities constitutes an absolute contraindication to participation in contact activities.

Klippel-Feil Anomaly This eponym is applied to congenital fusion of two or more cervical vertebrae. For purposes of this discussion, the variety of abnormalities can be divided into two groups: type I—mass fusion of the cervical and upper thoracic vertebrae (Fig. 16A1-39); and type II—fusion of only one or two interspaces (Fig. 16A1-40). To be noted, a variety of congenital problems have been associated with congenital fusion of the cervical vertebrae and include pulmonary, cardiovascular, and urogenital problems. Pizzutillo92 has pointed out that “children with congenital fusion of the

Figure 16A1-39 Type I Klippel-Feil deformity with multiple-level fusions and deformities as demonstrated on the lateral roentgenogram. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injuries. Clin J Sport Med 1:12–27, 1991.)

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c ervical spine rarely develop neurologic problems or signs of instability. However, he further states that “the literature reveals more than 90 cases of neurologic problems … that developed as a consequence of occipital cervical anomalies, late instability, disk disease, or degenerative joint disease.” These reports included cervical radiculopathy, spasticity, pain, quadriplegia, and sudden death. Also, “more than two thirds of the neurologically involved patients had single level fusion of the upper area, whereas many cervical patients with extension fusions of five to seven levels had no associated neurologic loss.” Despite this, a type I lesion, a mass fusion, constitutes an absolute contraindication to participation in contact sports. A type II lesion with fusion of one or two interspaces with associated limited motion or associated occipitocervical anomalies, involvement of C2, instability, disk disease, or degenerative changes also constitutes an absolute contraindication to participation. On the other hand, a type II lesion involving fusion of one or two interspaces at C3 and below in an individual with a full cervical range of motion and an absence of occipitocervical anomalies, instability, disk disease, or degenerative changes should present no contraindication.

Developmental Conditions Developmental Narrowing (Stenosis) of the Cervical Spinal Canal This condition and its association with CCN and transient quadriplegia has been well defined.47,52,88 The definition of narrowing or stenosis as a cervical segment with one

Figure 16A1-40 Type II Klippel-Feil deformity with a one-level congenital fusion at C3-C4 involving both the vertebral bodies and the lateral masses. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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or more vertebrae that have a SC/VB ratio of 0.8 or less is predicated on the fact that 100% of all reported clinical cases have fallen below this value at one or more levels. To be noted, 12% of asymptomatic controls also fell below the 0.8 level, as did 32% of asymptomatic professional and 34% of asymptomatic college players. In the group of reported symptomatic players, there was in every instance complete return of neurologic function, and in those who continued with contact activities, recurrence was not predictable. Clearly, the presence of developmental narrowing of the cervical spinal canal does not predispose to permanent neurologic injury. Eismont and colleagues have indicated, on the basis of experience of cervical fractures or dislocations resulting from automobile crashes, that the degree

of neurologic impairment was inversely related to the anteroposterior diameter of the canal.93 As a result of the all-or-nothing pattern of axial load football spine injuries, this phenomenon has not been observed in sports-related injuries. The presence of a SC/VB ratio of 0.8 or less is not a contraindication to participation in contact activities in asymptomatic individuals. I further recommend against preparticipation screening roentgenograms in asympto matic players. Such studies will not contribute to safety, are not cost effective, and will only contribute to the hysteria surrounding this issue. In individuals with a ratio of 0.8 or less who experience either motor or sensory manifestations of CCN, there is a relative contraindication to return to contact activities. In these instances, each case must be determined on an individual basis depending on the understanding of the player and his or her parents and their willingness to accept any presumed theoretical risk (Fig. 16A1-41). An absolute contraindication to continued participation applies to those individuals who experience a documented episode of CCN associated with ligamentous instability, MRI evidence of cord defects or swelling, symptoms or positive neurologic findings lasting more than 36 hours, or more than one recurrence.

Spear Tackler’s Spine

Figure 16A1-41 The ratio of the spinal canal to the vertebral body is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line divided by the anteroposterior width of the vertebral body. A ratio of less than 0.8 indicates the presence of developmental narrowing (stenosis). Lateral roentgenogram of a 20-year-old intercollegiate football player who had one episode of transient quadriplegia that lasted 10 minutes following a hyperflexion injury. The canal “to” vertebral body ratios are narrow from C3 through C7. Specifically, the ratio at C4 measures 0.6. This player returned to active playing for two seasons without a recurrence. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

Analysis of material more recently received by the National Football Head and Neck Injury Registry has identified a subset of football players with “spear tackler’s spine.”94 The entity consists of (1) developmental narrowing (stenosis) of the cervical canal; (2) persistent straightening or reversal of the normal cervical lordotic curve on an erect lateral roentgenogram obtained in the neutral position; (3) concomitant preexisting post-traumatic roentgenographic abnormalities of the cervical spine; and (4) documentation of the individual employing spear tackling technique (Fig. 16A1-42). In two instances in which preinjury roentgenograms and video documentation of axial loading of the spine due to spear tackling were available, a C3-C4 bilateral facet dislocation resulted in one and C4-C5 fracture-dislocation in the other, both players being rendered quadriplegic. It is postulated that the straightened “segmented column” alignment of the cervical spine, combined with head-first tackling techniques, predisposed these individuals to an axial loading injury of the cervical segment. Thus, this combination of factors constitutes an absolute contraindication to further participation in collision sports.

Traumatic Conditions of the Upper Cervical Spine (C1-C2) The anatomy and mechanics of the C1-C2 segments of the cervical spine differ markedly from those of the middle or lower segments.95 Lesions with any degree of occipital or atlantoaxial instability portend a potentially grave prognosis (Fig. 16A1-43). Thus, almost all injuries involving the upper cervical segment that involve a fracture or ligamentous laxity are an absolute contraindication to further participation in contact activities (Fig. 16A1-44). Healed,

Spinal Injuries

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Figure 16A1-42 Roentgenograms of a 19-year-old intercollegiate linebacker with spear tackler’s spine. A, On the anteroposterior view, the cervical spine is noted to be tilted toward his left. This represents a wry neck attitude frequently seen in those with either acute or chronic cervical injury. B, The lateral view demonstrates several manifestations of spear tackler’s spine: (1) a cervical kyphosis, (2) developmental narrowing of the cervical canal, and (3) an old compression injury of C5. The kyphotic deformity was fixed in both flexion and extension. He subsequently sustained a bilateral C3-C4 facet dislocation and was rendered quadriplegic as a result of spear tackling.

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Figure 16A1-43 The atlas-dens interval (ADI) is the distance on the lateral roentgenogram between the anterior aspect of the dens and the posterior aspect of the anterior ring of the atlas. In children, the ADI should not exceed 4.0 mm, whereas the upper limit in the normal adult is less than 3.0 mm. C1-C2 instability is vividly demonstrated in the extension (A) and flexion (B) views. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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Figure 16A1-44 A, Lateral roentgenogram of the cervical spine in the erect neutral position of a 21-year-old college football player demonstrates anterior translation of C6 on C7 of greater than 3.5 mm (arrows). B, A computed tomographic scan of C6 in the axial plane demonstrates a fracture through the lateral mass (arrow). Persistent displacement despite healing of the fracture constitutes an absolute contraindication to further participation in contact sports. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

nondisplaced Jefferson fractures, healed type I and type II odontoid fractures, and healed lateral mass fractures of C2 constitute relative contraindications provided the patient is pain free, has a full range of cervical motion, and has no neurologic findings.35 Because of the uncertainty of the results of cervical fusion, the gracile configuration of C1, and the importance of the alar and transverse odontoid ligaments, fusion for instability of the upper segment constitutes an absolute contraindication regardless of how successful the fusion appears roentgenographically.

Traumatic Conditions of the Middle and Lower Cervical Spine Ligamentous Injuries The criteria of White, Punjabi, and colleagues for defining clinical instability were intended to help establish indications for surgical stabilization (see Figs. 16A1-13 and 16A1-14).29,30 However, although the limits of displacement and angulation correlated with disruption of known structures, no one determinant was considered absolute. In view of the observations of Albright and colleagues that 10% (7 of 75) of the college freshmen in their study demonstrated abnormal motion, “as well as on the basis of our own experience, it appears that in many instances some degree of minor instability” exists in populations of both high school and college football players without apparently leading to adverse effects. The question, of course, is, what are the upper limits of “minor” instability? Unfortunately, there are no data available relating this question to

Figure 16A1-45 Lateral roentgenogram of the cervical spine taken in the erect neutral position demonstrates an anterosuperior compression defect in the vertebral body of C5 (arrow). This limbus deformity resulted from a previous compression injury to the ring epiphysis. There is no evidence of angulation, displacement, or instability of the spine. Such a radiographic finding would not constitute a contraindication to further participation. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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the clinical situation that allow reliable standards. Clearly, however, lateral roentgenograms that demonstrate more than 3.5 mm of horizontal displacement of either vertebra in relation to another or more than 11 degrees of rotation than either adjacent vertebra represent an absolute contraindication to further participation in contact activities. With regard to lesser degrees of displacement or rotation, further participation in sports enters the realm of “trial by battle,” and such situations can be considered a relative contraindication depending on such factors as level of performance, physical habits, position played (i.e., interior lineman or defensive back), and so on.

2. A healed stable end-plate fracture without a sagittal component on anteroposterior roentgenograms or involvement of the posterior or bony ligamentous structures (see Fig. 16A1-22) 3. Healed spinous process “clay shoveler” fractures Relative contraindications apply to the following healed stable fractures in individuals who are asymptomatic and neurologically normal and have a full pain-free range of cervical motion: 1. Stable undisplaced vertebral body compression fractures without a sagittal component on anteroposterior roentgenograms: The propensity for these fractures to settle, causing increased deformity, must be considered and carefully followed (Fig. 16A1-46). 2. Healed stable fractures involving the elements of the posterior neural ring in individuals who are asympto matic, neurologically normal, and have a full pain-free range of cervical motion (Fig. 16A1-47): In evaluating radiographic and imaging studies to find the location and subsequent healing of a posterior neural ring fracture, one must understand that a rigid ring cannot break in one location.73 Thus, healing of paired fractures of the ring must be demonstrated.

Fractures The following healed stable fractures in an asymptomatic patient who is neurologically normal and has a full range of cervical motion can be considered to present no contraindication to participation in contact activities: 1. Stable compression fractures of the vertebral body without a sagittal component on anteroposterior roentgenograms and without involvement of either the ligamentous or the posterior bony structures (Fig. 16A1-45)

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Figure 16A1-46 A, Lateral roentgenogram of the cervical spine taken while the patient was in a cervical brace demonstrates undisplaced compression fracture of the vertebral body of C5. Notable is the fact that there is no associated angulation, displacement, intervertebral disk space narrowing, facet incongruity, or fanning of the spinous processes. B, Lateral flexion view demonstrates pathologic angulation as defined by White and associates. There is no translation, disk space narrowing, facet incongruity, or fanning of the spinous processes, suggesting a stable lesion. The increased angulation is attributed to the deformity of the vertebral body. Assuming that no progression of the deformity or evidence of instability occurred and that the patient had a pain-free neck with a normal range of motion, this situation would constitute a relative contraindication to participation in contact activities depending on the player’s level, position, and willingness to accept risk for reinjury. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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Figure 16A1-47 A, Computed tomographic scan of a vertebral neural arch in the transverse plane demonstrating a hairline fracture through the lateral mass (open arrow) as well as a more evident nondisplaced fracture through the ipsilateral lamina (closed arrow). B, The patient was treated in a halo brace with satisfactory evidence of healing as demonstrated on computed tomographic scan. Following immobilization and the return of normal pain-free motion, he was permitted to return to contact activity after rehabilitation was fully effected and pain-free cervical range of motion and paravertebral muscle strength returned. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

Absolute contraindications to further participation in contact activities exist in the presence of the following fractures: 1. An acute fracture of either the body or posterior elements with or without associated ligamentous laxity 2. Vertebral body fracture with a sagittal component (see Fig. 16A1-25) 3. Fracture of the vertebral body with or without displacement with associated posterior arch fractures or ligamentous laxity (Fig. 16A1-48) 4. Comminuted fractures of the vertebral body with displacement into the spinal canal 5. Any healed fracture of either the vertebral body or the posterior components with associated pain, neurologic findings, and limitation of normal cervical motion 6. Healed displaced fractures involving the lateral masses with resulting facet incongruity

Intervertebral Disk Injury There is no contraindication to participation in contact activities in individuals with a healed anterior or lateral disk herniation treated conservatively (Fig. 16A1-49) or in those requiring an intervertebral diskectomy and interbody fusion for a lateral or central herniation who have a solid fusion, are asymptomatic and neurologically negative, and have a full pain-free range of motion. A relative contraindication exists in individuals with either conservatively or surgically treated disk disease with residual facet instability. An absolute contraindication exists in those with an acute or chronic “hard disk”

Figure 16A1-48 Lateral roentgenograms of the cervical spine in the erect neutral position demonstrate an anterosuperior compression defect in the vertebral body of C6. In addition, there is fanning of the C5-C6 spinous process, indicating posterior instability due to disruption of the intraspinous and posterior longitudinal ligaments (arrows). This situation constitutes an absolute contraindication to contact sports. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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erniation with associated neurologic findings, pain, or h significant limitation of cervical motion (Fig. 16A1-50).

Status after Cervical Spine Fusion A stable one-level anterior or posterior fusion in a patient who is asymptomatic, neurologically negative, and pain free and has a normal range of cervical motion presents no contraindication to continued participation in contact activities (Fig. 16A1-51). Individuals with a stable two- or three-level fusion who are asymptomatic and neurologically negative and have a pain-free full range of cervical motion have a relative contraindication. Because of the presumed increased stresses at the articulations of the adjacent uninvolved vertebrae and the propensity for development of degenerative changes at these levels, it appears that this patient is the rare exception who should be permitted to continue contact activities (Fig. 16A1-52). In individuals with more than a three-level anterior or posterior fusion, an absolute contraindication exists as far as continued participation in contact activities (Fig. 16A1-53).

Figure 16A1-49 Magnetic resonance sagittal image of the cervical spine in a 17-year-old high school football player with a history of neck injury. An anterior intervertebral disk herniation with disk space changes �� is seen �� at the C5-C6 level. At the time of follow-up examination, the youngster was asymptomatic and neurologically normal and had a pain-free range of cervical motion. He was permitted to return to contact activities. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

Figure 16A1-50 A sagittal magnetic resonance image of the cervical spine of a 17-year-old high school football player who complained of posterior neck pain while butt blocking as well as a right unilateral transient radiculopathy or “burner.” Visualized are intervertebral disk herniations at C4-C5 and C5-C6 that are indenting the spinal cord at both levels (arrows). Although the neurologic examination was normal, the presence of a wry neck attitude, limited neck extension, congenital canal narrowing (stenosis), and reversal of the normal cervical lordosis on roentgenogram precluded the individual from participation in contact sports. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

Figure 16A1-51 Lateral roentgenogram of a 28-year-old professional ice hockey player who underwent a successful onelevel interbody fusion at C5-C6 for instability. He subsequently played 2 years without a problem. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

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C l Managing

Figure 16A1-52 Lateral roentgenogram of the cervical spine of a 28-year-old former professional football player who had undergone a C4-C5-C6 posterior fusion for a posttraumatic instability. He subsequently returned to play 2 years of professional football; however, he developed stiffness, neck discomfort, and limited motion. The individual who elects to return to contact activities following more than a two-level fusion must understand that the probability of symptoms resulting from degenerative changes at the articulations above and below the fusion is increased. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

Figure 16A1-53 Lateral roentgenogram of an 18-yearold who had injured his neck playing football when he was 13 years old. At that time, a three-level posterior fusion and wiring was performed; however, it appears that periosteal stripping of adjacent vertebrae above and below resulted in a five-level fusion. Such a situation is an absolute contraindication to participation in contact activities. (From Torg JS, Glasgow SG: Criteria for return to contact activities following cervical spine injury. Clin J Sport Med 1:12–27, 1991.)

r i t i c a l

P

o i n t s

the unconscious or spine-injured athlete requires planning and preparation. All necessary equipment should be readily accessible and in good operating condition and all personnel trained in its proper use. Onthe-job training in an emergency situation is inefficient at best and a potential catastrophe at worst. l The “burner” pain syndrome or “stinger” results from two distinct injury patterns. Brachial plexus traction injuries, commonly seen in younger athletes, result from ipsilateral shoulder depression and contralateral neck flexion. Cervical root injuries, typically occurring in older players, are due to cervical hyperextension associated with degenerative disk changes, often in combination with developmental cervical stenosis. Criteria for return to athletic participation include absence of symptoms, normal strength, and painless full range of cervical spine motion. l Intervertebral disk injury without frank herniation and neurologic findings associated with a history of injury, neck pain, and limited cervical motion are frequently seen in collision activities. MRI frequently demonstrates disk bulge without herniation. Management is conservative, with return to activity after the individual is asymptomatic and has a full range of pain-free cervical motion. l The principles of spinal cord resuscitation include (1) protection from further injury; (2) administration of methyl prednisolone; (3) expeditious reduction; (4) rapid and secure spinal stabilization; and (5) implementation of an early rehabilitation program. l Anatomic variation and response to injury best define the cervical spine into upper (C1-C2), middle (C3-C4), and lower (C4-C7) segments. l Clues indicative of a serious cervical spine injury in the ambulatory patient are presence of a wry neck or torticollis posture, limitation of volitional cervical motion, and presence of paravertebral muscle atrophy. An individual presenting with a history of trauma and one or more of these findings requires a careful neurologic examination and appropriate imaging studies. l Cervical spinal stenosis with cervical cord neurapraxia is an acute transient neurologic episode of cervical cord origin with sensory changes that may be associated with motor paresis involving both arms, both legs, or all four extremities after forced hyperextension, hyperflexion, or axial loading of the cervical spine. Such episodes are transient, usually lasting 10 to 15 minutes, and except for paresthesia, neck pain is not present. There is complete return of motor function and full pain-free cervical motion. Routine radiographs characteristically demonstrate cervical spinal stenosis. l Available data indicate that individuals who have an episode of CCN with or without an episode of transient quadriplegia are not predisposed to permanent neurologic injury. The problem, however, is the propensity for reoccurrence, which is predictable. l The primary mechanism for athletic injuries of the cervical spine is axial loading, which occurs in American football when an individual strikes an opponent with the top or crown of the helmet. The implementation of rules changes and coaching techniques eliminating the use of

Spinal Injuries

the head as a battering ram has resulted in a dramatic reduction in the incidence of quadriplegia. l Criteria for return to athletic activity have been categorized as no contraindication, relative contraindication, and absolute contraindication depending on availability or lack of available risk data. As a general rule, return to activity requires that the individual have a stable cervical spine, be pain free and neurologically negative, and have a full range of cervical motion.

S U G G E S T E D

R E A D I N G S

Boden BP, Tacchetti RL, Cantu RC, et al: Catastrophic cervical spine injuries in high school and college football players. Am J Sports Med 34�� -8:1223-1232, 2006. Koffler KM, Kelly JD: Neurovascular trauma in athletes. Orthop Clin N Am 33:523-534, 2002. Kwon BK, Vaccaro AR, Grauer JN, et al: Subaxial cervical spine trauma. J Am Acad Orthop Surg 14:78-79, 2006.

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Spivak JM, Connolly PJ (eds): Orthopedic Knowledge Update, 3rd ed. Rosemont, Ill, American Academy of Orthopedic Surgeons, 2006. Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neurapraxia: Classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 87:743850, 1997. Torg JS, Guille JT, Jaffe S: Current concept review: Injuries to the cervical spine in American football players. J Bone Joint Surg Am 84:112-122, 2002. Torg JS, Thibault L, Sennett B, et al: The pathomechanics and pathophysiology of reversible, incompletely reversible and irreversible cervical spinal cord injury. Clin Orthop 321:259-269, 1995. Torg JS, Vegso JJ O’Neill J, Sennett B: The epidemiologic, pathologic, biomechanical and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 18:50-57, 1990.


S ecti o n

A

Cervical Spine Injuries 2. Cervical Spine Injuries in the Child Peter D. Pizzutillo and Martin J. Herman

The pursuit of excellence in athletic endeavors has resulted in the development of highly effective training programs for adolescent athletes that have made them bigger, stronger, and faster than young athletes of a generation ago. The emphasis on winning is generated by pressures within the athlete and is enhanced by peers, parents, coaches, and society in general. Society likes “a winner.” Tremendous pressures are placed on young athletes to perform well not only for the satisfaction enjoyed in sports but also as a passport to a lifetime of success. This milieu has led to significant medical problems in athletes with the popularization of steroids, psychological turmoil due to unrealistic expectations, and the “burnout” phenomenon. Competitive behavior has become more aggressive and physical. Even a highly skilled finesse sport such as basketball is now played as a contact sport. Football and ice hockey have evolved from contact sports to the level of collision sports. The result is an increased incidence of injury in young athletes. Forty-four percent of injuries sustained in students 14 years of age and older are due to sports activity.1 In a high school survey conducted by Paulson,1 80 of 100 participants in football sustained an injury

during the playing season. This compares with 75 of 100 participants in wrestling, 44 of 100 participants in softball, 40 of 100 female participants in gymnastics, 28 of 100 male participants in gymnastics, 35 females and 29 males of 100 participants in track and cross-country, 31 of 100 male participants in basketball, 30 of 100 participants in soccer, and 18 of 100 male participants in baseball. This survey reflects all levels of severity; however, it is significant that 7% of high school teenagers were hospitalized as the result of sports injuries. Football injuries accounted for 20% of these cases, and basketball injuries accounted for 17.4%. Spinal injuries occur during sports activities but are less common than other musculoskeletal injuries. Although catastrophic injuries do occur, most injuries are minor soft tissue contusions, sprains, and paraspinal muscle strains. In a review of all spinal injuries in 406 children admitted to a level-one pediatric trauma center, sports was the most common mechanism of injury for children aged 10 to 14 years2; 68% of children had paravertebral soft tissue injuries. In a review of consecutive children treated at another pediatric level-one trauma center,3 27% of cervical spine injuries were sports-related; most of these injuries

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occurred in adolescent boys and were isolated injuries. Analysis of the National Pediatric Trauma Registry from 1994 to 1999 for all cervical fractures, dislocations, and spinal cord injuries without radiographic abnormalities (SCIWORA) revealed that 66 of 408 children sustained these injuries during sports.4 Catastrophic spinal cord injury from cervical spine trauma is rare in children and adolescents. Although motor vehicle crashes are the most common mechanism, spinal cord injuries occur during sports activities,3,4 particularly collision sports and diving. A review of patients with spinal cord injury at several regional rehabilitation centers revealed that 10% to 20% of spinal cord injuries were due to sports-related accidents.5,6 From 1950 to 1989, 90% of fatal football injuries involved head or neck injuries.7 The modern helmet and facemask were developed in the 1950s and 1960s, and these devices led to increased use of the head in blocking and tackling techniques, resulting in an increase in deaths from head injury.8 In the 1970s, helmets were improved to protect the brain. A subsequent decrease in fatalities due to head injury followed, but the level of cervical spine injuries was sustained, primarily due to “spearing” techniques in tackling.9 In January 1976, the National Collegiate Athletic Association (NCAA) and the National Federation of State High School Associations (NFSHSA) formally adopted high school, college, and coaching rules that prohibited tackling or blocking with a helmeted head because of the vulnerability of the cervical spine to injury in this position. This single step has resulted in a significant decrease in serious cervical spine injury.10 Since 1977, there has been one fatality for every 10 million athlete exposures in football at the high school, college, and professional levels. The incidence of nonfatal but catastrophic injuries is difficult to report reliably because of incomplete recording of injuries.11,12 The National Football Head and Neck Injury Registry has been functional since 1955 and has provided much of the information that is used today for analysis. The decreasing rate of cervical spine injury in football is attributed to improvements in equipment, changes in game rules that better protect the athlete, more effective conditioning of the athlete, and better coaching of basic playing techniques, especially blocking and tackling. Similar developments are necessary to reverse the increasing incidence of cervical spine injury in other sports. Severe head and spinal injuries occur in other collision sports as well as in noncontact sports activities. Ice hockey is another collision sport in which severe head and spinal injuries occur.13,14 Between 1943 and 1999, 271 major spinal injuries were reported in Canadian ice hockey players, with 49% of these occurring in players 16 to 20 years of age.15 The most common mechanisms were impact with the boards and checking or pushing from behind. Education of coaches and players and rules changes by organized hockey have reduced the incidence of these injuries in recent years. From 1978 to 1982, the National Registry of Gymnastic Catastrophic Injuries documented 20 incidents of injury, including 17 patients with permanent quadriplegia and 3 deaths.16 These injuries occurred in skilled performers during practice settings. Analysis of this group revealed that permanent spinal cord injury was closely associated with use of the trampoline,17 especially when attempting

to perform a somersault. In many states, the trampoline has now been banned from physical education classes and is used only with spotters and physical restraints in teaching new skills in gymnastics. Catastrophic neurotrauma involving the cervical spinal cord has also occurred in rugby,16,18,19 wrestling20 and diving.21-23 Diving injuries account for 4% to 14% of spinal cord injuries in young patients24; most of these occur outside of organized programs.21 Downhill skiing had a mortality rate of 1.7% in 430 patients reported from Lake Tahoe in a 14-year study.25 Thirteen patients in this group had permanent radiculopathy, and 4 had permanent myelopathy. Cervical spine injury in skiers is frequently associated with concurrent head injury. The martial arts have contributed to cervical spine fractures and dislocations, usually as the result of a forceful foot strike to the head or a fall onto the head and neck area. At least 17 deaths have been reported in judo and karate as a result of this mechanism.26 Interestingly, soccer26 and boxing27 have not been associated with a high incidence of cervical spine injury.

ANATOMY OF THE CERVICAL SPINE Cervical spine injury in children younger than 8 years of age is uncommon and differs from injury in older adolescents and adults by virtue of site and mechanism of injury.28,29 The problem of evaluation of the cervical spine in childhood is complicated by the fact that much of the cervical spine is unossified and is undergoing progressive radiographic changes as ossification and growth proceed. By 8 years of age, the cervical spine has developed the adult configuration. Before the age of 1 year, the anterior ring of C1 is unossified, and it may be difficult to determine whether the upper cervical spine is unstable (Fig. 16A2-1). Between 3 and 6 years of age, the basilar synchondrosis becomes visible and may be mistaken for fracture at the base of the odontoid. By 6 years of age, the inner diameter of the spinal canal of the entire cervical spine has reached the adult level. In the child younger than 8 years, extension of the spine causes a spurious impression of subluxation of the anterior arch of the atlas over the superior aspect of the dens, which is not yet ossified. From infancy to 8 years of age, lateral neutral radiographs of the cervical spine reveal an increase in the angulation of the facet joint from 30 degrees to 60 degrees. In the younger child with a facet joint angle of 30 degrees, a greater degree of freedom in flexion and extension exists that may contribute to the appearance of pseudosubluxation commonly seen at the C2-C3 and C3-C4 levels. In the first decade of life, flexion-extension lateral radiographs of the cervical spine may reveal an atlantodens interval up to 5 mm, whereas the adult interval should not exceed 3.5 mm. Incomplete ossification of the cervical spine creates the appearance both of a truncated odontoid, until its tip ossifies at 10 to 12 years of age, and of apparent wedging of the vertebral bodies on lateral radiographs until ossification is more complete at 10 years of age. Whereas most fractures in adults occur in the lower cervical spine, the upper cervical spine is involved in up to 70% of cervical spine fractures in children. The relatively

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Figure 16A2-1 Lateral radiograph of the immature cervical spine reveals absence of the anterior arch of C1, presence of the basilar synchondrosis, and apparent wedging due to unossified vertebral bodies.

large size of the child’s skull may be a significant factor in injury of the upper cervical spine in this age group. A marked differential in elasticity between the spinal column and the spinal cord has been identified in the young child. The clinical expression of this differential in elasticity has been popularized by Pang and Wilberger30 in their report of SCIWORA in children. Pang and Wilberger’s study documented the presence of serious neurologic damage of the upper cervical cord in the absence of cervical spine osseous damage on initial radiographic evaluation in children younger than 8 years.

RECOGNITION AND PRIMARY TREATMENT The lifelong consequences of catastrophic spinal cord injury are of such magnitude that it is imperative that personnel dealing with athletes on a regular basis be well educated about the possibility of injury during practice and game conditions. Education alone can increase awareness of this problem and may indeed spare the injured athlete from further neural damage caused by mismanagement on the field. There is considerable difficulty in maintaining a high index of suspicion for spinal injury because severe neck injury does not frequently occur. The very mention of spinal cord injury creates an immediate emotional response among athletes, coaching staff, and the athletes’ families. In competitive conditions, whether in practice or in actual game situations, it can be quite difficult to evaluate the injured athlete adequately

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and manage problems on the field. Preparation and education of everyone involved in the athlete’s care in the event of nonfatal catastrophic spinal cord injury is of the utmost importance. A properly equipped ambulance with attendants trained in safe transport of individuals with neurologic damage and identification of hospital facilities that have the capability of dealing with catastrophic neurologic injury must exist well in advance of injury in order to provide the optimal environment for the injured athlete’s treatment. The development of regional spinal cord injury centers has provided a network of experienced staff throughout the country who can provide the very best of care for the spinal cord–injured athlete. Education of emergency medical technicians has significantly decreased the incidence of secondary neural injury that was formerly caused by improper immobilization during transport. Ongoing educational efforts are needed to maintain current proficiency and to improve our existing level of care. The management of the athlete with a severe spinal injury requires rapid assessment with protection of vital structures.31 If the athlete is unconscious, quadriparetic, or quadriplegic, or has significant paresthesias or dysesthesias involving the upper and lower extremities, the cervical spine must be considered unstable and must be protected.32 The head and neck should immediately be immobilized in a neutral position. If the patient is in the prone position, an organized logroll maneuver may be performed in which the head and neck are turned as one unit with the patient’s trunk. This can be managed by having one member of the emergency team control the head and neck while grasping the shoulder area in order to prevent changes in flexion or extension. In addition to level of consciousness, it is important to determine the patient’s respiratory and circulatory status. If the athlete uses a mouthpiece during sports activity, the mouthpiece should be removed. Football players should have their facemasks removed, but the helmet and chin strap should be left in place until the athlete is evaluated neurologically. If the patient is not breathing, it is important to position the jaw in an appropriate forward attitude to open the airway without overextending the neck. If the jaw thrust maneuver is not successful in restoring breathing, rescue breathing must be initiated. The athlete must be transported in an expedient manner but under safe conditions to an appropriately identified medical facility capable of dealing with these problems. In athletes younger than 8 years of age, care must be taken to avoid the forced flexion of the cervical spine that occurs on a flat spine board because of the relative increased size of the head in relation to the size of the chest.33 A standard flat board can be used with a towel roll beneath the shoulders to create a more neutral position of the cervical spine. The minimal components provided by the evaluating facility should include a neurosurgeon, an orthopaedic surgeon, and adequate radiographic capability.

ACUTE SOFT TISSUE INJURY Acute soft tissue injury of the cervical spine may involve the disk, ligaments, muscle, and fascia. Typically, these injuries are the result of a collision or fall onto the head and neck

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complex. The athlete usually complains of neck pain or neck and shoulder pain without distal radiation of pain or paresthesias. Physical examination reveals a limited range of motion of the cervical spine, usually in the presence of mild to moderate paraspinal muscle spasms, with no evidence of motor, sensory, or reflex changes in the upper or lower extremities. Radiographs of the cervical spine are normal and show no evidence of subluxation or dislocation but may reveal straightening of the cervical lordosis. Acute injury involving the fascia, muscle, or ligaments of the neck without disruption and instability should be treated symptomatically. A rehabilitation program comprising range of motion exercises and restitution of strength of the neck and shoulder girdle is important before gradual resumption of sports activity. The painful phase of soft tissue injury usually does not last more than 5 to 10 days and will allow the athlete to resume sports activity. If rehabilitation is not included as an integral part of the return-to-play program, the athlete will demonstrate a chronic decrease in range of motion of the cervical spine and diminished strength of the neck, especially in the flexor muscle group. Limitation of motion and weakness of the neck may lead to secondary injury with low-grade fascial, muscular, or ligamentous injury that perpetuates a vicious cycle of disability. Effective treatment of chronic cervical sprains and strains, therefore, includes a rehabilitation program designed to stretch out contracture of the cervical soft tissues and reconstitute the strength of the surrounding cervical and shoulder musculature. It is extremely important that children and adolescents who have sustained apparent innocuous injury to the cervical spine be re-evaluated on a serial basis. Herkowitz and Rothman34 reported development of instability of the cervical spine in individuals who initially demonstrated no radiographic evidence of bony or soft tissue abnormality. Subacute instability of the cervical spine is due to elastic and plastic deformation of the ligamentous and disk structures and may result in neurologic deficits in individuals who were initially neurologically normal. Children in the first decade of life who sustain neck injuries but appear to be normal by radiographic and neurologic testing need careful follow-up. Pang and Wilberger’s report30 primarily involved victims of vehicular injury and included only four sports injuries, but it demonstrated that 52% of patients with SCIWORA experienced the onset of serious neurologic problems an average of 4 days after their initial injury. Pollack and colleagues35 reviewed 42 children with spinal cord injury and found that within 10 weeks of the first injury, 8 children had a second spinal cord injury with more serious neurologic consequences; central or partial cord injury occurred in all 8, and 3 patients had severe quadriparesis or paraparesis. Pollack and colleagues proposed an arbitrary protocol that includes immobilization of the cervical spine in a brace for 3 months with no sports activity, close clinical follow-up, and repeat somatosensory evoked potentials (SSEPs) at 6 weeks. If dynamic radiographic studies and physical examination of the cervical spine are normal at the 3-month follow-up examination, the individual is ready to begin the return to sports. Full range of motion of the neck with demonstrated stability of the cervical spine on flexion-extension lateral radiographs and the absence of sensory or motor loss are required

before the athlete is allowed to return to competitive sports activity. Acute herniation of the cervical nucleus pulposus has been reported in adult sports activity36 but is rare in the child or adolescent athlete. Its presence can result in catastrophic neurologic injury with compromise of the anterior spinal cord.37 These patients experience a sudden onset of neck pain with radiation to both shoulders, arms, and hands, and they tend to hold the head tilted to the side of the disk lesion. Interscapular pain is commonly reported. When the head is tilted to the side of the lesion and then extended, there is an increase in pain. Herniation of the cervical disk most commonly occurs at the C5-C6 and C6-C7 levels. The immediate concern is to differentiate the acute herniated disk from the “burner lesion” that results in searing pain in a radicular distribution. A detailed neurologic assessment and an appropriate radiographic evaluation including computed tomography (CT) and magnetic resonance imaging (MRI) are usually required. Treatment of acute disk herniation in adolescent athletes requires decompression of the spinal canal. Repetitive axial compression of the cervical spine may result in chronic changes involving the disk. Albright and colleagues38,39 reported radiographic evidence of neck injury in 32% of freshman college football players in their preseason evaluations. Half of this study group had a past medical history of neck pain and showed abnormal radiographic findings involving the cervical spine. Linebackers and defensive backs were most commonly involved; running backs and wide receivers were at greater risk than linemen. Among athletes in whom the preseason physical examination or past medical history suggested a cervical spine problem, half demonstrated radiographic abnormalities of the cervical spine involving disk degeneration. Most of the athletes were unaware of any significant neck problems and had not sought prior medical evaluation. Axial loading appears to be the most important injury of the cervical spine. Torg and colleagues40 demonstrated that axial forces transmitted to the cervical spine in slight extension are dissipated primarily by the cervical muscles. When the neck is flexed 30 degrees, it becomes a straight segmented column. Axial forces applied under these conditions are transmitted directly to the vertebrae, ligaments, and disk rather than being dissipated by muscle. These observations have led to improvements in tackling and blocking techniques to reduce the frequency of cervical spine injury.

FRACTURES AND DISLOCATIONS Atlanto-occipital Instability Atlanto-occipital instability is usually the result of violent forces and is frequently fatal.41-43 Although atlanto-occipital instability has not been reported in sports injuries, it is conceivable that its incidence may be higher than suspected because appropriate diagnostic tests for spinal stability are not always conducted in acute fatalities, and there has not been much attention directed at the atlanto-occipital junction in the past.

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Athletes with Down syndrome are of special concern. The recent observation that individuals with Down syndrome may have atlanto-occipital hypermobility that excludes them from contact sports and from axial loading sports is important. In addition to the more commonly reported atlantoaxial instability, atlanto-occipital instability must be ruled out before athletes with Down syndrome can be medically cleared for sports activities (Fig. 16A2-2).

Jefferson Fracture When a high axial load is delivered from the apex of the skull to the cervical spine, tremendous forces are generated at the junction of the occipital condyle and the ring of the atlas.44 Low-level forces result in fractures of the posterior atlantal arch that are stable and can be successfully treated with immobilization by orthotics. When severe force is applied, a burst fracture of the atlas involving disruption of both anterior and posterior arches allows progressive displacement of the lateral masses of the atlas, producing consequent vascular and neurologic compromise. Most patients who have sustained injuries to the ring of the atlas are neurologically intact and must be evaluated in an expedient manner to avoid delay in diagnosis and secondary neurologic compromise. Patients with an injury of the ring of the atlas complain of neck pain and have severely restricted motion of the cervical spine in flexion, extension, lateral side bending, and lateral rotation. In the presence of a normal neurologic examination, a high index of suspicion of fracture of

Figure 16A2-2 Lateral radiograph of the upper cervical spine reveals significant anterior translation (arrows) of the occiput on the cervical axis.

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the atlas is required when evaluating patients with a skull fracture or severe laceration of the scalp that suggests axial loading. Routine radiographs of the upper cervical spine are difficult to interpret, especially when the head is tilted in response to paravertebral muscle spasm. Detailed inspection of the ring of the atlas on both lateral and open mouth anteroposterior radiographs is required to determine the relationship between the lateral masses of the atlas and the axis. When the open mouth anteroposterior radiograph reveals combined overhang of the lateral masses of the atlas on the axis of more than 7 mm, instability and disruption of the transverse ligament must be assumed. computed tomographic imaging is a routine part of care of athletes with a suspected cervical spine fracture, especially when there is difficulty in obtaining adequate information from routine radiographs. Computed tomographic scans provide excellent detail in evaluation of an injury of the atlas (Fig. 16A2-3). Fractures of the anterior and posterior arches of the atlas, as well as the relationship of the odontoid to the anterior arch of the atlas, can be precisely evaluated on computed tomographic scans. Although most fractures of the atlas heal by nonoperative immobilization techniques, such as a halo brace, there is an occasional need for surgical fusion.45

Acute Atlantoaxial Instability Acute atlantoaxial instability is usually the result of severe flexion forces imposed on the cervical spine. If the atlantodens interval is greater than 5 mm in children, the transverse ligament is compromised and instability is present (Fig. 16A2-4). Posterior fusion of the atlas and axis is required to avoid spinal cord compression. Special concern exists about individuals with Down syndrome who are athletically active. The standard radiographic parameters of stability of the cervical spine in individuals without Down syndrome are not appropriate for judging stability in individuals with Down syndrome. Natural history studies indicate that one third of adults with Down syndrome demonstrate a radiographic appearance of instability at all levels of the cervical spine, but only 3% of these individuals experience neurologic problems. Caution must be exercised in evaluating individuals with Down syndrome to avoid undertreatment or overtreatment. Many children and adolescents with Down syndrome are actively involved in sports activities such as basketball, swimming, and horseback riding. Like other athletes, these individuals and their families derive a great deal of satisfaction, pride, and joy in their athletic accomplishments. A blanket prescription against sports involvement needlessly deprives these athletes of the sense of accomplishment that accompanies athletic endeavor and diminishes their selfesteem. On the other hand, children and adolescents with Down syndrome who demonstrate radiographic evidence of cervical instability should be advised against participation in sports activities that potentially endanger neural function, such as diving and gymnastics (Box 16A2-1). In the presence of neurologic dysfunction and radiographic cervical instability, surgical stabilization of the cervical spine is necessary to preserve existing neural function and to prevent progressive loss.

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B

A

C Figure 16A2-3 A, Lateral radiograph reveals a break in the cortex (arrowhead) of the posterior arch of C1. B, Open mouth view reveals bilateral symmetrical overhang of the lateral masses of C1 on C2 (arrowheads) C, Computed tomography reveals a disruption in the ring of C1 in both the anterior and posterior arches.

Rotary Atlantoaxial Subluxation Children may demonstrate the insidious onset of wry neck deformity in association with posterior pharyngeal inflammation. Clinical examination of the involved child reveals a “cock-robin” attitude of the head with tilt of the head toward one shoulder and rotation of the chin toward the opposite shoulder. The patient demonstrates mild to moderate limitation of flexion and extension and nearly full lateral rotation to the side opposite the head tilt. In contrast, there is minimal lateral rotation toward the side of the head tilt. Cervical muscle spasm or localized soft tissue tenderness is usually absent. In addition, there is no prominence of the sternocleidomastoid muscle on the side of the head tilt, as is seen in congenital muscular torticollis. Most involved children are neurologically intact. Routine radiographs of the cervical spine should be supplemented by open mouth and lateral flexion-extension views of the upper cervical spine. Adequate lateral evaluation may be difficult to obtain if the radiology technician aligns the patient in the standard fashion for a lateral view

of the cervical spine because of the rotation and tilt of the skull and atlas. To avoid the confusing features caused by rotation and lateral tilt, the technician should be instructed to obtain a lateral radiograph of the skull to include the upper cervical spine. A lateral view of the skull using this technique will reveal a true lateral view of the atlas and permit more reliable interpretation of the relationship between the atlas and the axis. In the presence of malrotation, the lateral radiograph may spuriously suggest instability at the atlanto-occipital junction as well as at the atlantoaxial junction. In addition, the lateral mass of the atlas may appear anteriorly as a triangular wedge, the so-called sail sign (Fig. 16A2-5A). Lateral flexion-extension radiographs in neutral rotation are needed to reliably evaluate the degree of stability of the upper cervical spine as well as the existence of fixed rotary displacement between the atlas and axis. Computed tomographic scans have been extremely helpful in documenting the degree of displacement of the lateral mass of the atlas in relationship to the axis, the spatial relationship of the odontoid to the anterior arch of the atlas,

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Box 16A2-1 Recommendations for Activity Restrictions for the Athlete with Down Syndrome Based on Atlanto-Dens Interval*

1. ADI < 5 mm: no restrictions 2. ADI = 5 mm to 10 mm: spinal fusion: no collision sports

*Measured on high-quality “true” lateral cervical spine radiograph or physician-directed fluoroscopic examination.

s tability is proved, the patient may be weaned to a soft cervical collar and begun on gentle range of motion exercises as well as isometric strengthening exercises. Repeat lateral flexion-extension radiographs of the cervical spine should be performed 6 weeks later to rule out recurrent instability. If instability persists following immobilization or if recurrent instability develops, posterior atlantoaxial surgical fusion is indicated.

Fracture of the Odontoid Figure 16A2-4 Lateral flexion radiograph of the cervical spine reveals significant anterior displacement of the ring of C1 from the odontoid in a patient with Down syndrome with hypoplastic odontoid.

and the space available for the cord dorsal to the odontoid (see Fig. 16A2-5B). Parke and colleagues46 demonstrated a rich network of sinusoidal vessels draining directly from the posterior pharynx to the soft tissues about the atlas and axis. During inflammatory states, such as those occurring with upper respiratory tract infection, hyperemia results in dissolution of the attachment of the transverse ligament to the anterior arch of the atlas. With progressive dissolution, gross instability occurs with loss of orientation of the lateral masses of the atlas and axis. Treatment initiated before 4 weeks of clinical expression is successful in resolving rotary subluxation of the atlas and axis by nonsurgical methods. After 4 weeks, surgical stabilization is frequently required to maintain stability even when anatomic alignment can be regained by traction techniques (see Fig. 16A2-5C).47 Children and adolescents who present with a mild degree of rotary subluxation of the atlas and axis should be placed in a cervical collar and prohibited from recreational and sports activity. With more severe degrees of subluxation or fixed rotary subluxation, the patient should be protected and treated as an inpatient. Patients are initially treated by halter cervical spine traction or by halo traction in mild hyperextension and longitudinal traction. Once anatomic reduction has been obtained, the patient is immobilized either in a halo vest or a Minerva cast. After a 6- to 8-week period of immobilization, lateral flexion-extension radiographs of the cervical spine out of the cast or brace are needed to document stability. If

Fractures of the odontoid in children may be difficult to assess, especially in the presence of an unossified basilar synchondrosis. Acute separation of the odontoid through the basilar synchondrosis can occur in children younger than 7 years of age. Spontaneous reduction may occur, but marked widening of the retropharyngeal space is usually observed on radiographic evaluation of these patients.41 MRI evaluation may also reveal occult injury. With ossification of the ossiculum terminale, avulsion of the tip of the odontoid may be inadvertently suspected on radiographs. Lateral flexion-extension radiographs document the presence or absence of stability. In children older than 7 years, a type II odontoid fracture is more common and may be associated with nonunion as it is in adults. Most type II odontoid fractures heal through the use of nonsurgical techniques of immobilization such as halo vest stabilization but may require surgical fusion.48

Hangman’s Fracture The term hangman’s fracture refers to fractures involving the pedicle of the second cervical vertebra. These fractures are frequently the result of motor vehicle crashes or falls and do occur in children and adolescents.49 The most common mechanism of injury is that of extension and distraction, although other mechanisms have been suggested, including axial loading in extension and flexion. With bilateral disruption of the axial pedicles, the atlas and the anterior elements of the axis move as a single unit in flexion and extension. Schneider described anterior displacement of the “cervicocranium” with enlargement of the upper cervical spinal canal in flexion that spares the spinal cord from injury.8 The patient with a hangman’s fracture may present with neck pain and cradling of the head in the absence

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A

C

B Figure 16A2-5 A, Lateral radiograph of the cervical spine in a patient with rotary subluxation of C1-C2 presents a triangular wedged appearance of the anterior arch of C1. B, Computed tomography of C1-C2 reveals malalignment of the axis of the vertebrae with anterior translation of the lateral mass of C1 on C2. C, Lateral flexion radiograph reveals solid fusion between C1 and C2 without evidence of displacement.

of objective neurologic abnormalities. With persistent anterior displacement of the cervicocranium, neurologic deficits eventually develop. Early identification is of paramount importance. In addition to routine radiographs, computed tomographic scans of the cervical spine have allowed precise delineation of fracture patterns. Most patients with hangman’s fracture may be treated with gentle traction followed by halo vest or cast for 3 months. Lateral flexion-extension radiographs are necessary to demonstrate osseous healing and intersegmental stability. In the presence of nonunion or disruption of the C2-C3 disk, surgical fusion is indicated either by anterior fusion of C2 to C3 or posterior cervical fusion involving C1, C2, and C3.

Fracture of the Subaxial Cervical Spine Injury to the lower cervical spine from C3 to C7 may involve injury to the anterior elements of the spinal column, to the posterior elements, to the lateral elements, or

to a combination of sites. Clinical problems include facet dislocation with or without fracture, lamina fractures, and avulsion fractures of the spinous processes. Lateral mass fractures and pedicle fractures are uncommon in the subaxial spine compared with the incidence of injury in the upper cervical spine. The anterior elements of the spinal column are usually injured in flexion, with resultant compression fractures of the vertebral body and injury to the disk. Although disruption of the posterior longitudinal ligament is not common in athletic injuries, disruption may occur, especially with a flexion-distraction mechanism associated with significant intersegmental instability and the potential for neurologic catastrophe. As with injury at other levels, immediate immobilization of the spine is of extreme importance to prevent additional loss of neurologic function. Fracture at the C3-C4 vertebral level is rare.43 Athletic injuries most commonly result in injury at vertebral levels ranging from C4 to C7.14,22,35,50-55 Facet dislocation may be unilateral or bilateral and may occur with or without

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associated fracture. Unilateral facet dislocation is usually the result of axial loading in combination with flexion and rotation and does not usually result in neurologic damage. In the absence of facet fracture, the injury is primarily ligamentous and capsular, and the spine maintains its stability. Lateral radiographs of the cervical spine with unilateral facet dislocation reveal anterior translation of one vertebra on another of about 25%. Reduction of facet dislocation is obtained by closed traction techniques; occasionally, inability to reduce facet dislocation by closed methods necessitates open reduction with posterior fusion of the involved levels. Bilateral facet dislocation is a much more serious injury and occurs primarily through a mechanism of flexion. The spine is unstable in this situation and is associated with severe neurologic deficit including quadriplegia. Lateral radiographs of the cervical spine with bilateral facet dislocation reveal translation of more than 50% of one vertebra on another. These dislocations can usually be reduced by traction, immobilized in a halo cast, and stabilized by posterior fusion of the involved cervical vertebrae. Lamina fractures are difficult to diagnose on routine radiographs owing to the obliquity of the lamina in relation to the axis of the x-ray. CT is more reliable in identifi cation of lamina fractures. Fractures of the lamina do not usually participate in compression of neural tissue and heal with immobilization. Avulsion fractures of the spinous process are the result of vigorous exertion and are termed the clay shoveler’s fracture. The spinous process of the seventh cervical vertebra is most frequently involved. Treatment of the clay shoveler’s fracture is symptomatic because no subsequent instability results from this avulsion fracture. Injury of the anterior elements of the spinal column primarily involves axial loading resulting in compression fracture of the vertebral body. The extent of injury varies from a wedge fracture, which is stable, to the severely comminuted burst fracture, which is unstable and involves intrusion of bony elements into the spinal canal. The wedge fracture is common and is not associated with neurologic compromise. The posterior elements, including the ligamentous structures, are intact, and the spinal column remains stable. If disruption of the posterior elements is associated with anterior compression fracture of the vertebral body, stability is most likely compromised, and surgical stabilization is necessary. When progressive escalation of forces is experienced by the neck with axial loading, more severe injury of the vertebral body occurs, ranging from nondisplaced fracture fragments to wide displacement of bone and compromise of the spinal canal. Disruption of the posterior elements is more frequent with severe flexion and distraction forces and creates an extremely unstable clinical situation with severe neurologic compromise, including quadriplegia. Anterior decompression of the spinal canal with fusion is required, followed by posterior spinal fusion. Patients with facet dislocation or moderate to severe degrees of compression fracture require evaluation of the spinal canal to eliminate the possibility of concomitant extruded disk material (Fig. 16A2-6). Neurologically intact individuals with facet dislocation have been rendered quadriplegic following closed reduction owing to compromise of the anterior spinal cord by extruded disk material. If a disk is extruded, anterior surgical decompression of the

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Figure 16A2-6 Patients with a severe compression fracture and disruption of the posterior soft tissues require further evaluation to rule out disk extrusion into the spinal canal.

disk should be performed, followed by reduction of facets with anterior and posterior spinal stabilization. Subacute or late instability of the cervical spine should be suspected in the presence of facet dislocation. Herkowitz and Rothman34 reported on six neurologically intact patients with no bone or soft tissue abnormalities on initial radiographs. Four patients had unilateral facet dislocations; one had a perched facet at C5-C6; and one had subluxation at C4-C5. Each patient subsequently developed radiographic changes indicating intersegmental instability with attendant neurologic compromise. It is important to perform repeat physical examinations and radiographic studies within 3 weeks of injury to rule out the existence of subacute instability. Once instability has been identified, surgical stabilization is required.

SPINAL CORD INJURY Spinal cord injury results from violent forces imposed on the spinal column. Injury may be direct, as in complete transection or bony compression of the spinal cord, or indirect as a result of hemorrhage, swelling, or secondary ischemia. With the clinical presentation of complete motor and sensory loss, transection of the spinal cord is likely and is irreversible. Incomplete lesions of the spinal cord usually present as mixtures of described syndromes. When severe forces are imposed by axial load on the cervical spine, a burst fracture of the vertebral body may result, producing bony impingement on the anterior spinal artery

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with motor loss below the injury level and loss of sensations of pain and temperature. These deficits are usually permanent, and the degree of loss is equal in both upper and lower extremities. Severe flexion-extension moments applied to the cervical spine in the presence of spinal stenosis or secondary degenerative changes, which may occur in high school athletes, result in central cord hemorrhage and ischemia with primary involvement of the corticospinal tracts. Nonspecific sensory loss may be observed in the presence of incomplete motor loss involving all extremities. The upper extremities are usually significantly weaker than the lower extremities. Central cord involvement has a relatively favorable prognosis with varying degrees of recovery. Hemisection of the spinal cord results in loss of ipsilateral motor function and contralateral pain and temperature and is designated Brown-Séquard syndrome. Posterior spinal cord syndrome is a rare lesion in sports, with ischemia of the posterior spinal artery resulting in loss of dorsal column function and preservation of anterior cord function. These clinical syndromes do not usually appear in pure form but rather as parts of more complex lesions, most commonly involving a combination of central cord injury and BrownSéquard syndrome. The “burning hands syndrome” was first described by Maroon in 1977 as severe burning dysesthesias and paresthesias of both hands due to injury to the central fibers of the spinal tract.56 The injury is usually the result of ischemia. Wilburger and colleagues57 used MRI and SSEP to demonstrate that the burning hands syndrome was a reversible insult to the sensory pathways of the spinal cord. Vascular insults may result in thrombosis or embolization. In 1970, Schneider and associates58 reported seven cases of cervicomedullary injury in football players that resulted from “spearing.” Five of the athletes had no radiographic evidence of fracture or dislocation, although two showed evidence of atlantoaxial instability. Schneider and coworkers postulated that vertebrobasilar insufficiency with hypoperfusion of either the vertebral or basilar arteries could result in intramedullary cavitation and hemorrhage. A second possible mechanism of injury suggested by these authors involved acute arterial or venous obstruction from the brain due to uncal herniation through the tentorial notch. The final mechanism postulated by Schneider and colleagues involved high-velocity impact to the top of the head such that the brain interacts with the cervicomedullary junction, which is tethered by the dentate ligaments, resulting in secondary hemorrhages of the cervicomedullary junction. Fortunately, vascular injury of this sort in athletic events is uncommon. Of great concern is the problem of transient quadriplegia. Torg and colleagues55,59 described this problem as acute but transient episodes of sensory changes that may be associated with motor paresis in either both arms, both legs, or all four limbs following a forced hyperextension, hyperflexion, or axial load to the cervical spine. Complete recovery usually occurs in less than 15 minutes. Of interest is Torg’s report of 32 athletes with transient quadriparesis and associated developmental cervical spine stenosis.59 The degree of canal stenosis may be enhanced in flexion and extension by the “pincer mechanism” described by Penning60 or by infolding of the lamina ligaments, which

are capable of narrowing the spinal canal by 30% in hyperextension. Torg noted that 17 of the reported 32 athletes demonstrated developmental spinal stenosis. Only 4 of the 17 were able to return to play without permanent problems. Of the remaining 15 athletes without stenosis, 5 had congenital cervical fusions, and only 1 of these returned to play; 4 athletes had evidence of cervical instability, and 1 of these returned to competition; and of 6 athletes with degenerative disk changes, none returned to sports without problems. Therefore, of the group of 32 patients reported by Torg and associates, only 6 were able to return to play without problems. Although Torg and associates implied that athletes who have sustained transient quadriplegia with coincident developmental spinal stenosis should be discouraged from returning to competition, they conclude that athletes with transient quadriplegia and no demonstrated stenosis should be able to return to sports activity without a predisposition to permanent neurologic injury. The subset sample size is small in this study and does not allow formulation of a firm conclusion about the safety of return to competition. Transient quadriplegia in young athletes demands a detailed orthopaedic, neurologic, and imaging evaluation to rule out factors that may prohibit continued sports participation.61,62 In one review of 13 children between the ages of 7 to 15 years who had an episode of transient quadriplegia, all from sports activities, none had evidence of congenital stenosis based on measurements of the spinal canal diameter or the Torg ratio.63 The authors concluded that hypermobility of the cervical spine and not stenosis was the reason for the episode of transient quadriplegia. Evaluation of larger study groups of involved athletes is required before strong recommendations can be formulated about return to competition. The skeletally immature athlete who sustains this injury, even when clinical recovery is full and imaging of the cervical spine is normal, in the authors’ opinion is most safely treated by restriction from contact sports and other activities with risks for recurrent injury. “Burners” are described as episodes of searing pain in the upper extremities that follow the radicular distribution.7,40,64-67 Burners tend to occur after acute extension of the neck or a lateral stretch of the neck to the side opposite the painful arm with depression of the shoulder, as in a tackling maneuver. The symptoms usually last a few seconds in the initial episodes. The involved athlete allows his arm to hang limply at the side and then shakes or rubs the hand or arm vigorously to diminish the unpleasant searing pain. Numbness tends to last longer than the weakness; however, with repeated episodes, progressive residual weakness is observed. College football players have reported that burners last longer with increased frequency of the episodes, and occasionally persistent weakness, sensory loss, and pain are experienced whenever the arm is used. Rockett’s66 observations during surgical exploration of patients with burners document scarring at the C5-C6 nerve roots as they emerge between the anterior and posterior lamellae of the transverse processes. He subsequently recommended decompression of the nerve roots with lysis of nerve adhesions. Poindexter and Johnson65 performed electromyographic (EMG) evaluation of burners and suggested that they are the result of C6 radiculopathy rather than stretch of the brachial plexus.

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The initial complaints of athletes with burners suggest the diagnosis of acute herniated nucleus pulposus; however, with burners, the range of motion of the cervical spine remains normal, and symptoms are short lived. Burners, or “stingers” as they are also known, have been reported at least once in the careers of more than 50% of football players.64 During on-field evaluation, the affected player holds his head in a forward, stiff position to avoid extension and rotation of the neck. The presence of motor or sensory loss or arm or neck pain precludes return to play during that game until further evaluation is performed. In players who have sustained repeated injuries, full range of motion of the cervical spine and normal strength of the neck and shoulder girdle should be present before the athlete is permitted to return to competition.68 If weakness persists despite rest and rehabilitation, radiographic evaluation, EMG analysis, and MRI are needed to rule out less common lesions such as a herniated nucleus pulposus. EMG changes may persist in the absence of objective neurologic deficits for several years and cannot be used as a parameter for determining return to competition. Preventive measures that have been recommended to decrease the frequency of burners include neck and shoulder strengthening exercises, increasing the thickness of shoulder pads, and using neck rolls.

CONGENITAL ANOMALIES Congenital anomalies of the cervical spine primarily involve failure of formation or failure of segmentation of the vertebrae. Guidelines for participation in sports activities for young athletes with congenital anomalies have been based mostly on expert opinions, case reports, and biomechanical analyses because of the small number of children with known abnormalities who participate in these activities.69 Occipitalization of the atlas has been associated in neurosurgical literature with neurologic compromise; however, occipitalization is not usually associated with stenosis at the foramen magnum or with instability. The exception is the patient with occipitalization of the atlas and congenital fusion of C2-C3 in whom secondary hypermobility and instability frequently develop at the atlantoaxial junction. Instability has also been reported in individuals with hypoplasia of the odontoid in the presence of occipitalization of the atlas. Instability at this level requires posterior fusion of the occiput to the axis. Congenital absence of the posterior arch of the atlas is a rare congenital anomaly that is not usually associated with instability (Fig. 16A2-7). Lateral flexion-extension radiographs of the cervical spine as well as MRI evaluation are helpful to rule out cervical spine instability and chronic spinal cord impingement. In the absence of the posterior arch of the atlas, it is the author’s recommendation that athletes refrain from high-impact loading activities such as contact or collision sports and diving. Os odontoideum may be the result of nonunion or fracture through the body of the odontoid or congenital deformity. Lateral flexion-extension radiographs are required to document stability. Athletes with a stable os odontoideum should avoid impact-loading sports, including contact and collision sports. Individuals with an unstable os odontoideum require posterior surgical stabilization of the atlas

Figure 16A2-7 Lateral radiograph of the cervical spine reveals a complete absence of the posterior arch of C1 with no instability at C1-C2.

and axis. The normal spine that has undergone single-level spinal fusion should not be considered normal, and such an individual should not be allowed to return to full sports activity. There are no scientific data on the response of the surgically fused spine to forces imposed by sudden motion and the forces experienced in athletic activity. High-impact loading in the form of contact and collision sports and high diving should be avoided by this patient population. Congenital absence of the pedicles is a rare congenital anomaly that is usually alarming when viewed radiographically. If lateral flexion-extension radiographs demonstrate stability, however, there is no known reason to restrict the athlete’s activity. Congenital scoliosis of the cervical spine is not associated with instability. Mixed bony lesions may be noted with widening of the interpedicular distances suggestive of intraspinal lesions such as diastematomyelia. If appropriate radiographic studies and MRI eliminate the existence of intraspinal lesions and instability, involved athletes should be permitted to participate in all sports activities. Congenital fusion of the cervical spine, referred to as the Klippel-Feil syndrome, presents with a host of patterns that span the spectrum from single-level fusion to multiple levels of fusion to complete fusion from C2 to C7 (Fig. 16A2-8). It is extremely important to document the integrity of the occipitocervical junction in patients with Klippel-Feil syndrome to rule out instability. In the subaxial cervical spine, lateral flexion-extension radiographs may demonstrate anteroposterior translation of vertebrae as well as anterior gaping of open disk spaces.

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Figure 16A2-8 Lateral radiograph of the cervical spine reveals congenital fusion of C1 and C2 and also of C3, C4, C5, and C6.

In the absence of progressive radiographic changes in stability and of neurologic deficits, individuals with KlippelFeil syndrome should be observed; however, progressive translation or angular deformation at an open disk space should lead to exclusion of these patients from contact and collision sports and possibly to surgical stabilization of the unstable segment. The high association of renal anomalies in those with congenital scoliosis or congenital fusion of the cervical spine demands evaluation of the renal system by ultrasound to rule out clinically important anomalies. Unilateral absence of a renal system is the most common anomaly and is a significant factor in restricting involved individuals from contact sports (Fig. 16A2-9).The authors’ recommendations for play restrictions of collision sports for children with congenital cervical anomalies are listed in Box 16A2-2.

CONCLUSION Neglect of injury to the cervical spine can result in catastrophic neurologic damage as well as death. During the past decade, the study of mechanisms of sports injuries involving the neck has resulted in a significant decrease in the incidence of catastrophic and fatal injuries involving the cervical spine by means of alterations in competitive rules and the education of athletes and coaches in safe techniques of play. Comprehensive conditioning programs

Figure 16A2-9 Intravenous pyelogram demonstrates complete absence of one renal system with hydronephrosis of the remaining system.

Box 16A2-2 Contraindications to Collision Sports for Pediatric Athletes with Congenital Cervical Spine Anomalies (Authors, Recommendations) Absolute Contraindications •�� Occipitalization of C1 combined with C2-C3 fusion or odontoid hypoplasia •�� Os odontoideum •�� Subaxial fusions with instability* of the segments cephalad or caudad to the fusion mass •�� One episode of cervical cord neurapraxia (transient quadriplegia) •�� Congenital cervical spondylolisthesis •�� Atraumatic occiput–C1 instability Relative Contraindications •�� Occipitalization of C1 without segmental instability •�� Congenital absence of the posterior arch of C1 without segmental instability •�� Subaxial fusions without instability of the segments cephalad or caudad to the fusion mass *Stability determined on lateral flexion-extension cervical radiographs by anteroposterior translation of vertebrae as well as anterior gaping of open disk spaces.

Spinal Injuries

t ailored to the neck and shoulder girdle improve the athlete’s ability to resist damaging forces. Equipment deficits have been responsibly addressed by manufacturers with design improvement in such items as football pads, cervical rolls, and helmets. The “unexpected” contributes to the excitement experienced in sports. Unfortunately, it is a limiting factor that precludes the reduction of serious or fatal injury to zero. Most serious cervical spine injuries can be eliminated by strict adherence of coaches and officials to the rules of competition, use of effective equipment, instruction of athletes in safe techniques, and identification of high-risk athletes, combined with subsequent conditioning before competition.31 Team orthopaedic surgeons should educate the coaching staff about the serious nature of injury to the cervical spine. Injury to the soft or hard tissues of the neck requires attention to treatment guidelines and a comprehensive rehabilitation program that fosters full range of motion of the neck as well as normal strength. There have been no rigorous studies designed to prove that proper conditioning and preparation for competition decreases the incidence of injury of the cervical spine; however, the uncertainty of sports demands that the competitive athlete be in optimal physical condition during competition. Safe and effective competition requires appropriate mental and psychological preparation as well as physical conditioning to complement the state-of-the-art equipment available. It is only by adherence to a disciplined program that the incidence of serious and catastrophic cervical spine injuries can be lowered.

C

r i t i c a l

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l Due to a low incidence of spinal injury in the young athlete, a high index of suspicion is needed to expedite early diagnosis and treatment. l Radiographs of the cervical spine of individuals in the first decade of life are difficult to evaluate due to incomplete ossification of vertebral elements and increased mobility compared with the adult spine.

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l The team physician and coaches should identify local medical facilities experienced in the care of spinal injury prior to initiation of practice or game schedule. l Recurrent “burners” result in limited motion of the neck, with weakness of the neck, upper back, and shoulder girdle; these issues must be resolved prior to return to play. l While most individuals with Down syndrome may participate in sports without restrictions, those with ADI greater than 5mm are restricted from collision sports. l Latent instability of the cervical spine must be suspected in the presence of facet dislocation. l Athletes with transient quadriplegia associated with spinal stenosis are permanently restricted from collision sports.

S U G G E S T E D

R E A D I N G S

Frankel HL, Montero FA, Penny PT: Spinal cord injuries due to diving. Paraplegia 18:118–122, 1980. Schneider RC, Livingston KE, Cave AJE, et al: Hangman’s fracture of the cervical spine. J Neurosurg 22:141, 1965. Steinbruck D, Paeslack V: Analysis of 139 spinal cord injuries due to accidents in water sports. Paraplegia 18:86–93, 1980. Williams P, McKibbin B: Unstable cervical spine injuries in rugby: A 20-year review. Injury 18:329–332, 1987. Wroble RR, Albright JP: Neck and low back injuries in wrestling. Clin Sports Med 5(2):295–325, 1986. Wu WQ, Lewis RC: Injuries of the cervical spine in high school wrestling. Surg Neurol 23:143–147, 1985.


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Thoracolumbar Injuries 1. Thoracolumbar Spine Injuries in the Adult William Dillin, Frank J. Eismont, and Scott Kitchel

Consider who we, as physicians, might see in the bend of time. Will she be 14 years old, suspended in the rings above the floor mat, each bodily gyration, each release and catch the animation of physical grace? Will he pose before the last hole, straddling his tee shot, knowing full well his best hole is the 19th, and strike with all the twisting force that his middle-aged trunk can consider, the longest distance of the weekend? At 90, will she walk at dawn, chasing the last wisp of darkness, arms pumping, feet striking asphalt, her spine battling load and gravity? Will he crash into the last defender with will and force, tumbling the last few feet into the end zone? Will her head be down, her upper back cringing, her arms exhausted as she rolls her chair towards the finish line? Will he clutch the undersurface of his board, spinning away from the upper edge of the half pipe, with earth and ice waiting his return? Will she glide past them, as they reach for her, ascending in a single mellifluous leap towards the rim? Will he hear nature’s footsteps in the rising sea, leap freely from his prone position, and tightrope top and bottom turns before the impact zone? Will she see yet another batter in the endless weekend of games, winding once again and curling spin and speed with bodily deception? Will he soar like a swan in flight from water, his kite 100 feet above, his body engaged in twist and twirls before inevitable return to the ocean’s side? Will she plant her pole in the steep slope in the outback and wipe the sweat from her eyes of her weekend tour? Will his racquet reach the apex of his toss, slicing the soft round ball in chosen direction? Will she look upon the course of trees and feel the blur of nature with each heartbeat as she runs? Will the world seem tame to his address, the bat that once was on his shoulder, the ball lost beyond the fence? Will she pirouette and point and unfurl her arms to sounds she cannot hear? At dusk, will he gather himself for a final water start onto his board, his sail arced forward to catch the wind, slipping silently across the water at nature’s speed—a single fin? Will he or she be one of us? (Fig. 16B1-1). And why might we be there? Is it the test of opposition? Is it the struggle to the end? Is it contest? Is it measurement? Is it fulfillment? Is it the dream? Is it our nature? “Exercise ferments the Humours, casts them into their proper Channels, throws off Redundancies, and helps Nature in those secret Distributions, without which the Body cannot subsist in its Vigour, nor the Soul act with Cheerfulness.1 So who are we? Can we distinguish between an exerciser and athlete? Is the competitive long-distance runner the athlete and the daily jogger, who burns a routine distance

and time, not for a race but for health, an exerciser? Will the same injury have separate and unequal meanings to the two of them? “The Greeks understood that mind and body must develop in harmonious proportions to produce a creative intelligence. And so did the most brilliant intelligence of our earliest days—Thomas Jefferson—when he said, not less than two hours a day should be devoted to exercise. If the man who wrote the Declaration of Independence, was Secretary of State, and twice President, could give it two hours, our children can give it ten or fifteen minutes.”2 As we integrate mind and body and twin them to exertion, what can we do with injury? Who will our future injured be? As the scientific evidence compounds promoting quality of life, and longevity of life is linked to weekly duration of exercise, health maintenance may be derived from consistency. And consistency may come from the successful management of injury that avoids deconditioning. “Those who think they have not time for bodily exercise will sooner or later have to find time for illness.”3 For every professional athlete, for every college athlete, for every high school athlete engaged in performance sports, we will encounter many from the group of “everyman and everywoman” slugging though their exercise routine. What are we to consider in the spectrum of injury? Is there a difference between achieving a zone of activity and the continuous striving for performance enhancement? Can injury be separated from the individual goal of exercise or the insistent demand of an individual in a dedicated sport? Who will we see in the factory of biology? We will see the young and the old and everyone in between—their biologic potentials for injury having some common elements and age-related discrepancies. We will see the male and female, the able and disabled, the reluctant, the resigned, and the conditioned zealot. We will see failure of biologic material exposed to continuous, repetitive load over time, or failure with exposure to sudden force in an instant. We will see the unprepared reach for goals way beyond their training and capacity and wonder why an injury occurs. We will see the fully trained to peak and perform, hurt, and wonder why this injury at this time. We will see the rates and types of injury vary among the chosen sports. We will see the common injuries of daily life sustained during exercise or derived from daily life and amplified and delimited in the presence of exercise. We will encounter the various motivations that surround a particular injury, and to cure the biology, we will also treat the psychology. We will see the full fluctuation of what biology reveals in

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715

lliocostalis thoracis

Spinalis thoracis Figure 16B1-1 Professional and amateur windsurfers share the north shore Maui waters at Kanaha.

failure, and we may be the guiding hosts for its recovery. We may be called on to provide advice for prevention and search a meager science for verifiable answers. No injury exists without context, and for us, knowing the context is vital to treating the injury. To our forefathers we turn for advice. “Medicine is not only a science; it is also an art. It does not consist of compounding pills and plasters; it deals with the very processes of life, which must be understood before they may be guided.”4 To the fundamental process of life we now turn as we examine injury to the thoracic and lumbar spine during exercise.

ANATOMY The anatomies of the thoracic and lumbar spines are sufficiently different that they are considered separately. Anatomy is discussed to correlate its practical application with common injury patterns.

Thoracic Spine The thoracic vertebral column is responsible for the support of the thorax and protection of the thoracic spinal cord and provides the origin for the ribs. There are 12 thoracic vertebrae that articulate with one another through the diarthrodial facet joints as well as the intervertebral disks. The typical thoracic vertebra is roughly heart shaped and midsize between the cervical and lumbar vertebrae. The size of these vertebrae increases gradually from the 1st to the 12th in a caudad direction. The pedicles are placed toward the upper end of the bodies, with the laminae arising from these in a more superoinferior direction, allowing them to overlap one another. The spinous processes are typically long and slender with a slight caudad direction so that they overlap the succeeding vertebrae. The thoracic vertebral arch is a small, round spinal canal that protects the thoracic spinal cord. A distinguishing factor of the thoracic vertebrae is that they articulate with the ribs and bear facets for these articulations. The thoracic vertebrae articulate with the head and the tubercle of the rib arising from them as well as the head of the rib below their own segmental level.

Longissimus thoracis

Figure 16B1-2 Musculature of the thoracic spine.

These articulations between the thoracic vertebrae represent a three-joint complex including the intervertebral disk as well as the facet joints. The stability of these articulations is strengthened further by the rib cage; this has two consequences for the thoracic spine. First, it is an extremely stable region because of these articulations and the supporting rib cage. Second, because of the frontal plane orientation of the joints and the rib cage, the thoracic spine is the least mobile of the spine regions. Ligamentous support is provided to the articulations of the thoracic spine from many locations. Ventrally, there is a strong anterior longitudinal ligament that runs continuously along the entire length of the thoracic spine. The posterior longitudinal ligament similarly runs in continuity over the length of the thoracic spine along the dorsal aspect of the vertebral bodies, forming the anterior wall of the vertebral canal. The facet joints in the thoracic spine have capsular ligaments, which provide stability and limit the excursion of these joints. Dorsally, the ligamentum flavum is less developed in the thoracic spine than its cervical or lumbar counterparts. The supraspinous and intraspinous ligaments are membranous sets of fibers that run between spinous processes. In the thoracic spine, the interspinous ligament provides only minimal stability. The individual fibers of the supraspinous ligament are arranged so that the more superficial fibers extend over several spinal segments, whereas the deeper, shorter fibers bridge only half spines. The musculature of the thoracic spine and thorax contributes a portion of its stability (Fig. 16B1-2). The muscles of the thoracic spine generally run in a longitudinal fashion. They have multiple origins and insertions arising from

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DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Dura Dorsal root

Spinal nerve Dorsal ramus

Ventral root Figure 16B1-3 Segmental spinal nerve innervations of spinal muscles.

many consecutive vertebrae or ribs and inserting into many consecutive vertebrae or ribs more caudad. These muscles seem particularly complex because of the great amount of fusion that takes place between adjacent segmental muscles to form longer ones and the tangential splitting that results in a number of superimposed layers. For the purposes of this chapter, it is not important to know the specific muscle names but merely that they can be grouped broadly according to the general direction of the muscle bundles and their approximate lengths. The longer muscles of the back can be categorized into the splenius, the erector spinae, and the transversospinalis groups. The splenius muscles arise from the midline and run laterally as well as cephalad. They are responsible for spine rotation as well as extension. The erector spinae group is the largest muscular mass of the back. These muscles arise along the midline and run nearly directly longitudinally in the thoracic spine. They are the predominant extensors of the thoracic spine. The transversospinalis muscles lie deep to the erector spinae and are much shorter. These muscles arise from the transverse processes and run cephalad to the spinous processes. They are predominantly rotators of the spine but also participate in extension.

A

Deep to these major muscle groups are a series of small segmental muscles that run between spinous processes or between transverse processes. These muscles include the interspinalis and intertransversarial. Both of these muscle groups are functionally less important in the thoracic spine. The muscles of the back are covered posteriorly by a dense fascia that separates them from the overlying structures. The fascia is continuous, with connections from the cervical spine through the sacrum. In the thoracic spine, this fascia is thin and transparent except where it blends into the muscle origin. The innervation of these back muscles is by the dorsal rami of the segmental spinal nerves (Fig. 16B1-3). The dorsal rami typically slant inferiorly as they proceed through the muscles, supplying muscle caudad to the level of the origin of each nerve. A few of the more lateral deep muscles may be innervated by ventral rami of the spinal nerves. The blood supply of the thoracic spine is from the segmental arteries (Fig. 16B1-4). Each thoracic vertebra is related to a pair of segmental intercostal arteries from the aorta. Each segmental vessel gives off twigs to the anterolateral aspect of the vertebral body, and larger vessels enter the vertebra from the vertebral canal. The dorsal branches of the segmental arteries are distributed mostly to the musculature of the back but give off spinal branches as they pass through the intervertebral foramen. These spinal branches enter the epidural space as well as anastomosing above and below corresponding vessels to form the major supply of the dura, nerve roots, and spinal cord. The vessels to each vertebral body come from the segmental arteries entering above and below the body so that each body typically receives nourishment from four arteries. These arteries pass between the posterior longitudinal ligament and the vertebral body, usually penetrating the bone by a common opening. The venous drainage of the vertebral column parallels the arterial supply and enters the internal vertebral plexus that surrounds the spinal cord. There is significant

B

Figure 16B1-4 Blood supply of thoracic spine. A, Lateral view. B, Posterior view.

Spinal Injuries

anterolateral drainage from the vertebra directly into the segmental veins, which ultimately drain into the vena cava.

Lumbar Spine The lumbar vertebrae are the last five vertebrae of the vertebral column. They are particularly large and heavy when compared with the vertebrae of the cervical or thoracic spine. Their bodies are wider transversely than anteroposteriorly. The pedicles of the lumbar spine are short and heavy, arising from the upper part of the body. Compared with the thoracic spine, the transverse processes project more laterally and ventrally. From the posterior surfaces of the superior articular processes, there are marked enlargements, called the mammillary process. The laminae are shorter vertically than the bodies; this causes a gap between the lamina at each level, which is bridged only by ligaments. The spinous processes are broader and stronger than those in the thoracic spine; they project in a dorsal direction with little caudad angulation. The articulations in the lumbar spine are the same three-joint complex. The joints are oriented in a more sagittal plane. This orientation allows the lumbar spine to have relatively more flexion and extension than its thoracic counterpart but significantly less rotation. This joint alignment also allows for lateral flexion in the lumbar spine. The same basic ligamentous structures are present in the lumbar spine as in the thoracic spine. The anterior longitudinal ligament is relatively thicker in the lumbar spine. The ligamentum flavum is much stronger than its thoracic counterpart. This increased strength is in part due to the fact that it serves as a bridge between adjacent laminae where there is no bony overlapping. The facet joint capsules of the lumbar spine are thicker and stronger in the lumbar spine, as are the supraspinous and infraspinous ligaments. The stability of the lumbar spine is related much more directly to the ligamentous structures than the thoracic spine because of the loss of stability added by the rib articulations and rib cage. The musculature of the lumbar spine is organized in the same pattern as that of the thoracic spine. As one moves more caudally into the lumbar area, the muscles of the superficial groups tend to become larger and stronger. These muscles provide some stability to the lumbar

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spine as well as being the primary extensors of this region. The enveloping fascia in the lumbar spine is thicker and stronger than its thoracic counterpart. This fascia has been divided into three distinct layers, which provide stability as well as compartmentalization in the lumbar spine. The nerve and blood supply of the lumbar spine is functionally identical to that of the thoracic spine. The segmental vessels and the nerves run courses similar to the thoracic spine and provide similar function.

Intervertebral Disk The intervertebral disk is the fibrocartilaginous structure that forms the articulation between adjacent vertebrae. It provides a strong union, while allowing the degree of intervertebral motion necessary for function. Disks of the various portions of the spinal region differ considerably in size but are basically identical in their organization. They all consist of two components: the outer, laminar fibrous container (or anulus), and the inner, semifluid mass (the nucleus pulposus) (Fig. 16B1-5). The anulus fibrosus is a concentric series of fibrous lamellae. Its major function is to withstand tension from the torsional stresses of the vertebral column as well as the horizontal extensions of the compressed nucleus that it contains. The anulus is attached to the vertebral body through a blending of the fibers with the vertebral periosteum as well as the longitudinal ligaments. The nucleus pulposus occupies a concentric position within the confines of the anulus. Its major function is that of a shock absorber. The nucleus pulposus exhibits viscoelastic properties under applied pressure, responding with elastic rebound. There is no definite structural interface between the nucleus and the anulus. The two tissues blend imperceptibly. The disks make up about one fourth of the height of the entire spinal column. Moving from cephalad to caudad, the disks become larger in their cross-sectional area as well as thicker when measured from one vertebral end plate to the next. The thoracic disks are heart shaped compared with the more oval form seen in the lumbar spine. The blood supply and nutrition of the intervertebral disk is achieved primarily by diffusion from the adjacent vertebral end plates. The anulus is penetrated by capillaries for only a few millimeters. The disk is not inert; the normal disk tissue has a high rate of metabolic turnover. The disk itself has no direct innervation. Sensory fibers are abundant, however, in the adjacent longitudinal ligaments. The pain attributable to disk disease most likely is carried through those fibers.

Spinal Cord and Cauda Equina

Figure 16B1-5 Anatomy of the thoracic disk.

In the thoracolumbar spine, it is important to differentiate between spinal cord and cauda equina. The spinal cord typically ends at the thoracolumbar junction, and caudad to that level is the cauda equina. The cauda equina is merely a collection of nerve roots that are traversing the spinal canal until they exit at their appropriate foramen. This differentiation is important because of the differences in structural anatomy and the responses to injury of the spinal cord and cauda equina.

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The thoracic spinal cord is generally wider laterally than it is deep in the anteroposterior direction. The cord is smaller in the thoracic region than its cervical counterpart. The average anteroposterior depth found by Elliott5 was about 9 mm. An average anteroposterior vertebral canal diameter is 17 mm. The cord occupies about half of the space available within the vertebral column. The major function of the thoracic spinal cord is the transmission of nerve impulses, from the periphery to the brain and from the brain to the peripheral muscles. The tapered lower end of the spinal cord is the conus medullaris. From this point caudad, only individual nerve roots exist and are grouped together as the cauda equina. These nerve roots pass caudad until they reach the appropriate level, where they pass out through the vertebral foramen. The response of the spinal cord to injury is different from the response of the cauda equina. The nerve roots in the cauda equina recover from injury in the same fashion as a peripheral nerve. Injury to the spinal cord is generally irreversible, however, and has permanent consequences. This fact is important when considering injuries of the thoracolumbar spine with associated neurologic deficits.

BIOMECHANICS The thoracolumbar spine is a complex, three-dimensional structure with coupled motion characteristics.6 The thoracolumbar spine is capable of flexion, extension, lateral flexion, and rotation. The total range of motion is the result of a summation of the limited movements permitted between the individual vertebrae. The musculature and ligaments have key roles in the initiation and control of movements as well as in supporting the bone structures. The individual motions vary considerably in the different vertebral regions. Although all thoracolumbar vertebrae are united in the three-joint system of the intervertebral disk and the two zygapophyseal articulations, the size and shape of the intervertebral disk as well as the shape and orientation of the articular joints determine the types and range of motion available at an individual intervertebral articulation. The most common movement of the vertebral column is flexion. Flexion requires an anterior compression of the intervertebral disk, along with a gliding separation of the articular facets at the zygapophyseal joint. This movement is limited by the posterior ligamentous complex and the dorsal musculature. Extension is a more limited motion, producing posterior compression of the disk along with gliding motion of the zygapophyseal joint. Extension is limited by the anterior longitudinal ligament as well as the ventral musculature. The laminae and spinous processes limit extension by direct apposition. Lateral flexion necessarily is accompanied by some degree of rotation. It involves lateral compression of the intervertebral disk, along with a sliding separation of the zygapophyseal joint on the convex side, whereas an overriding of this joint occurs on the concave side. Lateral flexion is limited by the intertransverse ligament as well as the extension of the ribs. Rotation is related most directly to the thickness of the intervertebral disk. It involves compression of the anulus

fibrosus fibers. Rotation also is limited directly by the geometry of the zygapophyseal joints. The disk limits rotation by resistance to compression in the anulus. Normal range of motion for the thoracolumbar spine cannot be considered without also considering the synchronous motions of the cervical spine. The entire vertebral column moves as a whole in all planes of motion. The column can rotate about 90 degrees to either side of the sagittal plane. Most of this rotation is accomplished in the cervical and thoracic sections. Flexion of 90 degrees is possible, using cervical, thoracic, and lumbar regions. About 90 degrees of extension is also possible, but this occurs primarily in a combination of the cervical and lumbar regions. Lateral flexion, which must be accompanied by some rotation, is allowed to nearly 60 degrees. This is primarily a cervical and lumbar function. The mobility of the thoracolumbar region is not uniform throughout any of its segments. The upper thoracic spine is impaired greatly in its motion by the rib cage. The articular facets in this region are oriented in the frontal plane. The lower thoracic region allows more flexion and extension because the disk and vertebral bodies progressively increase in size. Also, in the lower thoracic spine, the articular facet joints begin to turn more toward the sagittal plane, permitting greater flexion and extension but limiting rotation. The lumbar region is oriented to allow significant amounts of flexion, extension, and lateral flexion. The zygapophyseal joints are oriented in the sagittal plane, however, locking them against rotation (Fig. 16B1-6). This orientation allows a gliding action of the joints that permits the neural arches to separate and approximate during flexion and extension. The lumbosacral joints change their orientation so that they are midrange between frontal and sagittal planes. This alignment allows some rotation; however, this is limited by the iliolumbar ligaments. The essential function of the lumbosacral joints is to buttress the fifth lumbar vertebra in relation to the sacrum. Each region of the spine has its own characteristic curvature. These curves allow upright posture while maintaining the center of gravity over the major weight-supporting structures of the pelvis and lower limbs. The normal thoracic kyphosis places the thoracic vertebrae posterior to the center of gravity. This kyphosis compensates for the normal cervical lordosis, which allows the head to be held in its erect position. The lumbar lordosis brings the middle of the lumbar spine anterior to the center of gravity, allowing erect posture. The transitional vertebrae between each major spinal segment intersect the center of gravity and appear to be the most unstable regions of the spine. This fact is emphasized by the high incidence of fractures and dislocations in the transitional regions. The biomechanics of the intervertebral disk emphasize its functional competency. The anulus fibrosis receives most forces transmitted from one vertebral body to the other. It is constructed best to resist tension and shear. This resistance is accomplished by the radial alignment of the progressive lamellae of the anulus. Experimental analysis has shown that different portions of the anulus respond differently to the same degree of tension. It appears that the peripheral anulus has the greatest recovery, whereas the medial sections are more distensible.

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Spinous process of T5 Supraspinous ligament

Articular process of T8

Interspinous ligament

Interspinous ligament Articular process of L3 Articular process of L2

Capsule Articular process of T9

A

Ligamentum flavum

Ligamentum flavum Intervertebral disk

B

Figure 16B1-6 Zygapophyseal joints of thoracic (A) and lumbar (B) spine.

The nucleus pulposus is designed best to resist compression forces. It receives primarily vertical forces from the vertebral bodies and redistributes them in a radial fashion to a horizontal plane. The internal pressure of the nucleus distorts the anulus, which, with its resiliency, allows recovery from the pressure. The tension of the intervertebral ligaments and anulus preloads the disk. This preloading increases stability in the spine. Through this function, the disk must dissipate and transfer the axial thrust necessary to permit erect posture and motion.7 The spine must act as a flexible boom. The spine is the fulcrum of a first-class lever system.

CLINICAL EVALUATION Evaluation of the thoracolumbar spine in athletes must follow the same sound principles as any clinical evaluation. The essentials include an accurate, problem-oriented history; spine and lower extremity evaluation; physical examination; and appropriate and specialized diagnostic studies based on the history and physical examination. It is essential that the clinician develop a reproducible standardized method of obtaining the evaluation so that there are no omissions or missing clinical information that would prevent an accurate diagnosis. The injured athlete is highly motivated to return to preinjury activity. The evaluation must lead to a working diagnosis so that treatment may begin and return the athlete to participation as soon as possible.

History One of the keys to an accurate diagnosis of any thoracolumbar spine problem is a carefully taken history. The athlete generally understates his or her complaints and generally omits any past spine problems or injuries. The history should include the patient’s chief complaint, a discussion of the present illness, a past history of any spinal or general orthopaedic problems, and a brief discussion of any family history of back problems. A commonsense approach is essential in this process. A good clinician allows the athlete to render the story in his

or her own words but elicits the important information. History taking varies widely in extent and length of time as the clinical situation dictates. Often, after an acute injury, only a brief history is obtained, but the clinician should return at a later time to obtain a more complete history of any previous problem or injury predisposition. Spending a little extra time obtaining a complete history provides great dividends in understanding the athlete’s problem and working toward a correct diagnosis. The chief complaint must be provided by the athlete. This should key the clinician into a certain line of history taking related to that specific body part. The history of the present illness enlarges on this chief complaint. This history can be obtained from the injured athlete and from other participants who may have witnessed the injury or who were present at the time. The most common initial complaint in spine problems is pain. It is important to attempt to localize and characterize the pain. The onset of the pain, as related to the time of injury, may provide important information regarding the diagnosis. Diffuse aching pain in the lumbar spine that began the day after an extended workout would lead the clinician into checking for a musculoligamentous type of overuse injury. The most important part of the history is the present illness. This part of the history should work toward a chronologic development of the spine pain, its character, and any improvement between its onset and the examination of the patient. The temporal onset of the pain gives the clinician a clue to the correct diagnosis. Mechanical causes of back pain have a sudden, acute onset. Often the athlete reports that the onset of pain is associated with a specific activity. The pain generally starts immediately or within a few hours. A more insidious onset of pain should alert the clinician to consider medical causes of low back pain. A history of the duration and frequency of the pain is essential. The clinician should ascertain whether the pain is episodic or more persistent. Most mechanical pain of the thoracolumbar spine is intermittent. The frequency of the episodes varies depending on the exposure of the athlete.

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The duration of the pain can lead the clinician to an accurate diagnosis. Most muscular strains are relieved within a week. Disk problems generally require longer to resolve. A history of the quality of the pain itself must be obtained. The quality of the pain and its intensity can be helpful in identifying its source. The patient should be allowed to describe the pain in his or her own words, without being led by the examiner. The intensity of the pain must be ascertained. It is often difficult for the athlete to describe pain intensity; this may be facilitated by asking the athlete to rank the pain on a scale of 0 to 10, with 0 being absence of pain and 10 being the worst pain ever felt. Localizing the pain to a specific area in the thoracolumbar spine is helpful. The pain may be localized to a specific midline structure or may radiate out from there into the adjacent soft tissues. A key to the evaluation of thoracolumbar spine discomfort is any radiation of the pain. It is especially important to differentiate strictly back pain from pain that may radiate into the leg or foot. Pain that radiates into the lower leg is suggestive of nerve root impingement, such as occurs with disk herniation. The athlete should be questioned carefully about any aggravating or alleviating factors. Generally, mechanical lesions of the thoracolumbar spine improve with supine positioning and worsen with increased activity. Not all thoracolumbar spine movements necessarily exacerbate muscle strain pain. A careful history defines which movements appear to help or aggravate the pain. Questioning the athlete regarding specific variances in pain related to time of day helps to sort out mechanical disorders from underlying inflammatory problems. In the typical muscle strain injury, the athlete notes that the pain is worse at the end of the day, after he or she has been active. Medical disorders, such as inflammatory arthropathies, cause stiffness in the morning when attempting to get out of bed. During the day, the stiffness lessens. Underlying tumors of the spine or spinal cord generally cause increased pain at night because the pain is increased with recumbency and is more noticeable with the loss of other sensory input while in bed. A past history of spinal problems is a key to accurate diagnosis. The patient should be asked at several different times in several different ways if he or she has had any previous spine problems. Questions about childhood and adolescence should be included. A preexisting condition of the spine may lead the clinician to an accurate diagnosis because a previous problem may recur or may predispose to a new injury. In this portion of the history, a brief time should be spent discussing any family history of spine problems with the athlete. Familial predisposition to back problems is characteristic of many medical illnesses, including disk degenerative conditions, ankylosing spondylitis, Reiter’s syndrome, and other spondyloarthropathies. As more older athletes become involved with highdemand workout schedules, it is important to remember that these athletes have other social and occupational activities that may contribute to their spine problem. In such an athlete, it is essential to obtain an occupational history to determine what tasks the athlete may be performing at work that may contribute to spine problems. Individuals required to do heavy lifting at their jobs are at risk for developing mechanical low back pain. Review of

leisure-time activities is important to look for predisposing causes of the spine problem. The patient history is the essential foundation on which the remainder of the diagnostic process is constructed. By taking a little extra time and listening carefully to the athlete’s description of the chief complaint, the clinician should be able to generate a list of potential diagnoses to direct the remainder of the history taking and physical examination.

Physical Examination After carefully obtaining the history, a problem-oriented physical examination is the next step in the diagnostic process. Physical examination takes a variety of forms, depending on when the examination is performed. The clinician should never feel limited by time in evaluating acute injuries of the thoracolumbar spine. In the acute setting of an injury to the spine, enough time must be taken to rule out injuries that could produce instability or threaten the neurologic structures before moving the patient. On the field, management of acute spine injuries must be approached with caution because of the potential neurologic sequelae of inadequate immobilization or transportation of the unstable spine. If there is any question of a spinal column injury with neurologic symptoms, it is important to immobilize the athlete in the position in which he or she was found and not attempt to move the athlete. No attempt should be made to remove equipment, such as a football helmet or part of the uniform. The athlete may be immobilized on a spine board or immobilized without change in body position by a scoop, such as is used by emergency medical personnel. This process takes time and should not be rushed so that there is a minimal risk for increased neurologic injury or manipulation of the spine. The athlete and the provider are better served by overimmobilizing the injured athlete than by attempting to move him or her in a hurry to allow completion of the athletic event. A spine board always should be available for transporting the spine-injured athlete. This board often is available because emergency medical personnel are at the scene of the athletic contest. When no medical emergency personnel are on hand, the institution should have a spine board available for transporting these athletes. All athletes with evidence of injury to the spine and neurologic signs or symptoms should be transported immobilized on a spine board. Athletes who have significant pain in the spine secondary to a high-velocity injury should be transported immobilized on a spine board because of the potential for spinal instability, which could lead to neurologic sequelae. Any athlete who is in too much pain to allow mobilization simply on the basis of muscle spasm should be transported on a spine board. It cannot be overemphasized that adequate immobilization and careful transportation prevent possible catastrophic neurologic injury in athletes with spinal column injuries. The clinician should not hesitate to take all the time needed and should have adequate equipment available before any attempt is made to transport the injured athlete. The essentials of the physical examination of the thoracolumbar spine are no different from those for examination

Spinal Injuries

of any other region of the body. The objective of the examination is to show the physical abnormalities that sort out the possible pathologic conditions elicited during the history taking. Essentials include inspection, palpation, rangeof-motion testing, and neurologic examination. Inspection of the patient as a whole and of the thoracolumbar spine in particular should be carried out initially with the patient in the standing position and disrobed sufficiently to allow the spine to be seen. The patient should be viewed from behind as well as laterally and anteriorly. From behind, the level of the shoulder should be noted as well as any lateral curvature or cervical scoliosis. The patient should stand with the head centered over the pelvis and feet. Any deviation at one location in the spine must be compensated for by an opposite deviation elsewhere if the patient is standing erect. A list occurs if the thoracic vertebrae are not centered over the sacrum. The list may be measured by dropping a perpendicular line from the first thoracic vertebra and measuring how far this falls to the right or left of the gluteal cleft. When viewing the patient in the lateral plane, any exaggeration or decrease of the normal spine curvature should be noted. Particularly, any increase in thoracic kyphosis or decrease in lumbar lordosis is significant. The lower extremities should be viewed in the lateral plane. Particular attention should be paid to any flexion or extension deformities of the hips and knees. Inspection from the front of the patient should include the position of the head and level of the shoulders. It is generally easy to view the iliac wings, and these should be of equal height. There should be no tilt to the pelvis. The skin about the thoracolumbar spine should be inspected, noting the superficial structures. Particular attention should be paid to any skin lesion, such as café-au-lait spots or a tuft of hair over the spine. After adequate inspection of the thoracolumbar spine, the next step in a complete examination is palpation of the area of tenderness. The primary area of tenderness should be palpated, but because this will cause the patient maximal discomfort, it is wise to palpate certain other anatomic landmarks first. Tenderness should be assessed over the spinous process at each level. The paraspinal muscles should be palpated looking for tenderness as well as muscle spasm. The sacroiliac joints and the sciatic notches should be palpated for tenderness, and deep palpation of the posterior thighs should be performed. When an area of maximal tenderness is identified, palpation should be carried out in an attempt to identify the primary structure that is tender at that level. The tenderness may be superficial, such as that seen with the spinous processes or dorsal musculature, or it may be more deep and diffuse, such as that related to a fracture or disk injury. There may be no area of point tenderness in many musculoligamentous-type injuries of the thoracolumbar spine. Assessing the range of motion of the thoracolumbar spine is important to identify the problem adequately. The absolute range of motion is not of major significance because there is a great deal of individual variance. Range of motion of the lumbar spine should be assessed for flexion-extension and lateral flexion. The reported average range of forward flexion is 40 to 60 degrees. Forward flexion is a complex motion of the lumbar spine, sacroiliac

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joints, and hip joints. It may be significantly influenced by tightness of the hamstrings if the gauge is the athlete’s ability to touch the toes. Extension is considered average at 20 to 35 degrees. There should be about 20 degrees of side bending, right and left. Rotation of the lumbar spine is limited and difficult to assess because it occurs in symmetry with the thoracic spine. The major thoracic motion to be evaluated is rotation. With the feet in place, the patient is rotated at the shoulder level. Rotation to nearly 90 degrees can be achieved in the average athlete. While assessing the range of motion, the patient should be asked to squat in place. This tests not only the general muscle strength of the lower extremities but also joint function. If the patient is unable to squat, it should be assessed whether this is secondary to pain or some specific decreased function in the lower extremities. When an athlete with an injury to one of the functional units of the spine attempts to bend or rotate, this motion is inhibited by protective muscle spasm. The lumbar spine may be observed not to have a normal curve in the erect position and not to reverse its lordosis with attempts at flexion. This observation is highly suggestive of protective muscle spasm. If the protective spasm is unilateral and predominantly affects the tissue on one side of the spine, a scoliosis may develop. Scoliosis also may develop from nerve root irritation on one side of the spine, such as occurs with disk herniation. After the patient has flexed forward fully, it is helpful to observe how he or she regains the erect posture. This gives clues to tissue injury as well as muscle integrity. Normally, the return to the erect position is accomplished by a derotation of the pelvis without changes of spine curvature until the patient has come up to 45 degrees. During the terminal 45 degrees, the low back resumes its lordosis. Pain caused by any motion should be noted. Pain precipitated by flexion is a nonspecific finding and may be related to many pathologic conditions. Pain with extension generally is related to an increase of the lordosis forces across the facet joints or stresses in the pars interarticularis; this in turn narrows the foramen where the nerve roots exit the spine and compresses the posterior disk. Pain with hyperextension generally can be related to a pathologic condition involving the facet joints, pars interarticularis, posterior disk structures, or neuroforamen. The pain may be back pain, leg pain, or both. No special significance should be placed on pain with lateral bending. Lateral bending causes ligamentous or muscular stretching and may be restricted in many conditions. In some cases, pain that increases with flexion to the ipsilateral side may be related to articular facet disease or lateral disk protrusion. This should be considered if radicular pain is elicited with lateral bending. Similarly, limitations of rotation are nonspecific. These limitations may be secondary to muscle spasm within the thoracic spine or simple increases in pain with this motion. A more helpful way of checking rotation is to seat the patient, stabilizing the pelvis and hips. This not only limits the rotation of the spine but also gives a more specific view of spine rotation, eliminating that from the hips and pelvis. A neurologic examination of the thoracic and lumbar spine must include sensory and motor evaluation of the thorax and the lower extremities. In the thoracic spine, this

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TABLE 16B1-1 Muscle Testing of the Lower Extremities Nerve Root

Muscle Group

L1 L2 L3 L4 L5 S1

Hip flexion Hip flexion Knee extension Foot dorsiflexion-knee extension Big toe extension-foot eversion Foot plantar flexors-knee flexion

L4 L5

Reflex L1 Knee jerk Posterior tibial Ankle jerk

S2

L2

S2

L3 L4

L3

evaluation is limited by sensory overlapping and the multiple levels of innervation. Sensation can be assessed most sensitively by light-touch examination of the thorax. Motor examination of the thoracic and paraspinal musculature is difficult in the athlete with thoracolumbar spine problems because of pain and attendant muscle spasm. Neurologic examination of the lower extremities in the patient with thoracolumbar spine pain is particularly important. Neurologic examination is essential in a patient who complains of any leg pain, numbness, or weakness. This evaluation must include motor strength testing, lighttouch sensation, reflex testing, sciatic and femoral nerve tension signs, and assessment of sacral motor and sensory function. Initial assessment of lower extremity strength can be made in rough terms by asking the patient to squat, then return to an erect position. This rough motor examination can be supplemented by asking the patient to walk first on the heels, then on the toes. Any weakness seen in toe walking is suggestive of weakness in the triceps sura musculature. Difficulty with heel walking is consistent with ankle dorsiflexion weakness. When this evaluation has been completed, the patient is seated on the table with the legs dangling off the side. Muscle testing in the lower extremities is performed, including the hip flexors, adductors, quadriceps, hamstrings, tibialis anterior, foot everters, extensor hallucis longus, and foot plantar flexors (Table 16B1-1). This information is recorded according to the standard nomenclature on a 0-to-5 scale. Any specific deficits are noted. A sensory examination of the lower extremities is carried out by light-touch testing (Fig. 16B1-7). This test is performed most easily by simple light stroking of the thighs and legs in all different dermatomes. Any specific deficit is noted and retested. We do not routinely advocate sharp-dull discrimination or position-sense testing unless other deficits have been found. Reflex examination of the lower extremities is carried out in the sitting position. This examination should include an evaluation of knee jerks and ankle jerks. The knee jerk reflex is mediated primarily through the L4 nerve root. The ankle jerk is mediated by the S1 nerve root. These reflexes are recorded in the standard 0-to-4 nomenclature. The patient is asked to lie supine on the examining table for evaluation of nerve root tension signs. The classic test of sciatic nerve irritation is the straight leg raising test.8 The intent of this test is to stretch the dura and nerve roots, reproducing leg pain. The patient experiences pain along the anatomic course of the sciatic nerve into the lower leg, ankle, and foot. Symptoms should not be produced until the leg is raised to at least 30 to 35 degrees. When the leg

S1

S5 S4 S3

L5 L4

S1

S1 S2

L4 L5

L5 S1

S1 L5

Figure 16B1-7 Dermatomal innervation of the lower extremities.

has been elevated beyond 70 degrees, no further stretching of the nerve roots and dura occurs. To be considered positive, the test must reproduce the patient’s radicular symptoms. Production of back pain does not indicate a positive result (Fig. 16B1-8). Many other sciatic nerve root tension tests have been described. In Lasègue’s test,9 the patient lies supine with the hip flexed to 90 degrees. The knee is extended slowly until the radicular pain is reproduced. This test is likely less specific than the straight leg raising test because hip and knee joints are moved. The bowstring sign10 is performed with the knee flexed to 90 degrees and the body bent forward to lengthen the course of the sciatic nerve. The examiner’s finger is pressed into the popliteal space to increase further the tension on the sciatic nerve. A positive test occurs if the patient’s pain increases down the leg. Milgram’s test11 is another sciatic nerve tension sign. The patient lies in the supine position, then raises both extended legs several inches above the examining table. This movement increases intra-abdominal pressure and intrathecal pressure. The patient is asked to hold the position for 30 seconds. The test is positive if the maneuver re-creates the radicular leg pain. Nerve tension signs of the femoral nerve have been described. The most popular names for these tests are reverse straight leg raising and femoral nerve tension sign. This testing is performed with the patient in the prone position. The knee is flexed to 90 degrees. The hip is extended with the pelvis fixed to the table. Recreation of anterior thigh radicular pain is considered a positive test. Sacral sensory and motor function is not checked routinely in the athlete unless it is indicated by the history or other portions of the physical examination. To assess this function adequately, evaluation of perianal sensation,

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A

B

C

Figure 16B1-8 A, Straight leg raising test. B, Femoral stretch test. C, Milgram’s test.

sphincter tone, contractility of the anal sphincter, and the superficial anal reflex is required. This reflex is mediated by the S2, S3, and S4 nerve roots. Touching the perianal skin should cause contraction of the anal sphincter and external anal muscles. The history and physical examination can be modified depending on the circumstances and the individual. The complete history and physical examination cannot be carried out on the field of competition while the competition is delayed. The clinician should never feel rushed when evaluating a patient with a thoracolumbar spine injury, however, and should not consent to move the patient until he or she is convinced there is no evidence of serious injury. Only a small portion of this evaluation may be carried out acutely, and the remainder of it should be done as soon as possible. The importance of a careful history and physical examination cannot be overemphasized. When this portion of the

evaluation is completed, a working diagnosis or differential diagnosis should be established. This diagnosis guides the clinician through the remainder of the evaluation process, including the use of diagnostic testing.

Diagnostic Testing Evaluation of thoracolumbar spine pain in the athlete frequently includes many radiographic techniques used to visualize the structures of the thoracolumbar spine. These tests can be extremely helpful in establishing the diagnosis and treatment plan. It is essential to obtain the radiographic images in a timely fashion and to interpret them properly to allow determination of the true diagnosis. The underlying problem that complicates the relationship between thoracolumbar spine pain and radiographs is the progressive anatomic changes that occur naturally in the thoracolumbar spine over time. This is generally not a problem in

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young athletes, but as more older athletes pursue competition, it becomes more of an issue. By the age of 50 years, 95% of adults who come to autopsy show evidence of disk space narrowing, calcification, or marginal sclerosis.12 In a similar series of living patients, degenerative changes are present in 87%.13 Conversely, only 5% of people younger than age 20 years have evidence of abnormal radiographic findings without symptoms. A radiograph of the thoracolumbar spine is the initial film made in the radiographic diagnosis of spine problems.14 The advantages are availability, low exposure of tissue to radiation, speed, and relatively low cost. Tangential radiographs offer good resolution of bone structures but do not show the soft tissue structures. It is not possible to image the entire thoracic and lumbar spine in one series of radiographs. It is appropriate to center the x-ray beam over the area of identified pathology. In general, only anteroposterior and lateral views are indicated initially. Oblique views provide limited information in specialized settings but should not be included routinely. The normal radiographic anatomy of the thoracic spine is shown in Figure 16B1-9. In this anteroposterior projection, the spinous processes, transverse processes, pedicles, facet joints, and laminae can be visualized. Each of these structures should be visualized at every level, with particular attention paid to the levels of the patient’s pain or discomfort. The normal lateral radiographic anatomy of the thoracic spine is shown in Figure 16B1-10. The bodies of the vertebrae, pedicles, spinous processes, and intervertebral

disk spaces are seen best in the lateral projection. The normal thoracic kyphosis can be seen to form a smooth curve. The thoracic intervertebral foramina can be visualized in the lateral view. The normal radiographic anatomy of the lumbar spine in the anteroposterior projection is shown in Figure 16B1-11. As in the thoracic spine, this projection best visualizes the transverse processes, spinous processes, pedicles, facet joints, and laminae. Particular attention should be paid to the alignment of the spinous processes and any lateral movement of the lumbar spine or rotation appearing as a deviation in the alignment. Particular attention should be paid to the transverse processes, which are clearly visible on this view. Often, direct blows to the lumbar spine result in fractures of the transverse processes. The facet joints in the lumbar spine run in a vertical orientation and are adjacent to the pedicles. Changes within the facet joint may be suggestive of degenerative disease. The soft tissue shadow of the psoas muscle can be seen in the anteroposterior projection. Any asymmetry of the psoas shadow should be taken only in its clinical context because this may be affected by positioning, spine rotation, or muscle contraction. The lateral radiographic anatomy of the lumbar spine is shown in Figure 16B1-12. In this projection, the bodies of the vertebrae, intervertebral disk spaces, pedicles, and spinous processes are well seen. One should be able to observe the normal lumbar lordosis with the posterior aspects of the bodies lining up to form a smooth curve. Movement of a single vertebral body in the horizontal plane, forward or backward, causes a disruption of this curve. The disk

Figure 16B1-9 Normal anteroposterior anatomy of the thoracic spine.

Figure 16B1-10 Normal lateral anatomy of the thoracic spine.

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Figure 16B1-11 Normal anteroposterior anatomy of the lumbar spine.

Figure 16B1-12 Normal lateral anatomy of the lumbar spine.

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Figure 16B1-13 Oblique projection of the lumbar spine.

spaces generally should increase in size from L1 to L4. The lumbar intervertebral foramina are seen best on this view. Oblique projections of the lumbar spine are particularly useful in showing pathology within the facet joints or pars interarticularis.15 These projections should be obtained when pathology within one of these two regions is suspected. They are not of value in every series of spine radiographs. An oblique view of the lumbar spine is shown in Figure 16B1-13. In this projection, the facet joint is seen in profile and can be examined for asymmetry or degenerative change. The pars interarticularis also is well visualized. In visualizing these familiar Scottie dogs, the neck of the dog is represented by the pars interarticularis; the nose, the transverse process; the eye, the pedicle; the ear, the superior articular process; and the front legs, the inferior articular process. A collar, or disruption of the neck, is suggestive of spondylolysis (Fig. 16B1-14). Other specialized views of the thoracic or lumbar spine may be indicated in specific pathologic conditions. Lateral flexion-extension views may supplement the evaluation of either the thoracic or the lumbar spine when instability is suspected.8 There is great margin for error in lateral flexion-extension views based on the ability to reproduce the position and the interpretation of the examiner. It is important to remember the limitations of plain radiographs.16 Radiographs do not visualize the contents of the spinal canal, such as the spinal cord, dural structures, or spinal ligaments. They do not visualize the disk itself but merely the space that it is occupying. Significant destruction of bone may exist that does not show up on plain films. Rauschning15 showed that 50% of the medullary bone of a

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Figure 16B1-14 Spondylolysis of the lumbar spine. Figure 16B1-16 Bone scan of stress fracture of pars interarticularis.

Figure 16B1-15 Normal bone scan.

vertebral body must be destroyed before it can be seen on plain radiographs. Radionuclide imaging, or bone scanning, is a sensitive technique for the detection of bone abnormalities. A small dose of radioisotope, generally technetium, is injected intravenously and allowed to circulate through the entire body through the bloodstream. Any process that disturbs

the normal balance of bone production and resorption produces abnormalities on bone scans. Increased osteoblastic activity is associated with increased concentration of the radionuclide tracer. Interruption of metabolic activities of bone results in a decreased amount of visible tracer. Radionuclide imaging depends on blood flow to bone. It also depends on the rate of bone turnover. In young athletes, the epiphyseal and metaphyseal bone plates are areas of increased bone activity and show up as areas of increased radionuclide concentration. Bone scan images are obtained with a scintillation camera that detects the emission of gamma radiation. A large-field camera may be used to cover the entire skeleton, or spot views may be taken in the area of maximal interest. Projections may be obtained in anteroposterior and lateral planes to allow localization of the increased radionuclide tracer. Images can be taken at different times after injection of the radionuclides; this allows differentiation between blood flow abnormalities and bone metabolism abnormalities. A normal bone scan mirrors the response of normal bones to mechanical pressures (Fig. 16B1-15). Radionuclide imaging is useful in circumstances in which radiographic changes lag behind increased bone activity17; this is particularly true in the detection of stress reactions of the pars interarticularis (Fig. 16B1-16). The major limitation of radionuclide bone scanning is its low specificity. Although it is extremely sensitive in picking up any abnormality of the bone blood flow or metabolic activity, it is extremely nonspecific. In the evaluation of thoracolumbar spine pain in the athlete, bone scanning should

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not be considered until after a routine series of radiographs has been obtained. If an area of point tenderness persists that does not have correlating radiographic abnormalities, a bone scan should be considered. Bone scans are indicated early in the evaluation of stress fractures or stress reactions of the pars interarticularis, such as occur in young gymnasts. Bone scans should never be used as a first-line test and should be reserved for specific indications. Computed tomography (CT) is useful for evaluating abnormalities of the thoracolumbar spine because of its complex three-dimensional, spatial anatomy.18 CT images not only re-create anteroposterior and lateral radiographs but also allow cross-sectional imaging in all three planes. CT images best assess bony configuration and structure and show graded shadings of soft tissue, such as ligaments, disks, nerve roots, and fat. CT allows excellent visualization of the paraspinal soft tissues. CT scanning should be used to confirm clinical findings derived from the history and physical examination. CT is not a tool for primary diagnosis, but rather one for confirmation of this diagnosis when a primary bony abnormality is considered. Many studies19,20 have shown that routine CT scanning for thoracolumbar pain is not useful or costeffective. CT scanning should be directed to the area of pathology and should not be used as a shotgun technique to evaluate the whole spine. A CT section of the lumbar spine contains different anatomic structures depending on the level of the cross section. Each CT cut is able to assess only one slice of the skeleton. Abnormalities that are not contained in that plane are not viewed by the CT scanner. Figure 16B1-17 shows a typical CT scan cross section through the intervertebral disk. CT scanning of the thoracolumbar spine in the athlete is particularly useful for the diagnosis of bony abnormalities.21 This examination generally is most useful in the evaluation of significant trauma involving fractures of the thoracolumbar spine in which the question of spinal canal impingement needs to be answered. CT scanning is helpful in the evaluation of tumors of the thoracolumbar spine for localizing the lesion and determining its extent.

The usefulness of CT scanning alone to identify significant disk herniations continues to be questioned. Many clinicians still believe that myelography must be used with CT scans to obtain adequate information about disk pathology. Magnetic resonance imaging (MRI) appears to have advantages that supersede those of myelography and CT scanning in the diagnosis of disk pathology. MRI allows excellent visualization of the soft tissues. As the imaging technology has advanced, MRI has become progressively more useful in the diagnosis of problems of the thoracolumbar spine. MRI is now the imaging modality of choice for all soft tissue injuries of the thoracolumbar spine. MRI also has a role in evaluation of bone injuries when they are causing significant impingement of soft tissue structures, such as the nerve roots. The principle behind MRI involves the generation of a magnetic field by protons of hydrogen atoms. Hydrogen atoms are the major constituent of water, which is found in varying amounts in all structures of the body. MRI allows visualization of all body structures and is not limited by direct changes in the density of tissues, as are other radiographic techniques. A normal MRI image of the lumbar spine is shown in Figure 16B1-18. MRI allows visualization of the vertebral column, intervertebral disk, and spinal canal. The axial views show the paravertebral soft tissues, the spinal canal, and the disk or vertebral body. At this time, MRI is an excellent technique for viewing the spinal canal and soft tissues about the spine, including the nerve roots and intervertebral disks.22-24 In injuries commonly seen in the athletic spine, MRI is a superb technique for visualizing disk pathology, nerve root compression, and ligamentous injury associated with hemorrhage. MRI is an excellent technique for characterizing primary changes occurring within the spinal cord or nerve roots, intramedullary tumors, and syringomyelia.

Figure 16B1-17 Computed tomographic cross section through intervertebral disk.

Figure 16B1-18 Normal magnetic resonance imaging scan of the lumbar spine.

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Two other radiographic techniques bear discussion in the evaluation of thoracolumbar spine injuries in the athlete—tomography and diskography. In a limited number of patients, tomography presents a useful alternative to CT or MRI, particularly if CT or MRI is not available. Tomographic slices through the vertebral bodies and posterior elements may define bony abnormalities. Diskography is performed by inserting a spinal needle into a disk space, then injecting radiopaque dye.25,26 Information is obtained by the radiographic appearance of the dye, the injection pressure used, and the reproduction of the patient’s pain during the test. There continues to be controversy at present concerning the validity of diskography. Radiographically, it is a sensitive technique to image the internal architecture of the disk when it is combined with CT scanning. The clinical significance of diskography must be assessed in conjunction with the patient’s pain response when the disk is injected. Diskograms rarely are indicated in the management of thoracolumbar spine pain in athletes. Instrumented kinetic muscle testing of the thoracolumbar spine is used infrequently in athletes. At this time, there are no studies documenting the ability of this technique to evaluate the thoracolumbar spine in athletes. With time and further studies, it is hoped that instrumented kinetic muscle testing may prove to be successful in the rehabilitation of the athletic spine as well as in predicting certain deficiencies that may predispose the athlete to injury.

REHABILIATION CYCLE The acutely injured athlete often doesn’t follow a linear route from injury to return to play (Fig. 16B1-19); ironically, re-expression of clinical symptoms or true recurrence may complicate rehabilitation. In addition, evolution of a biologic process, such as the transition from a lumbar anular tear to a lumbar disk herniation, may cause different clinical symptoms. Often the rehabilitation restores physical capabilities but may not change the underlying biologic process. Rehabilitation should be an ongoing restoration process with the ability to be adaptable in the face of acute change in function. The reduction or resolution of clinical spinal symptoms may occur by either conservative or surgical methodologies. In some instances, reduction of activity may entail immobilization. Activation is the beginning of movement and load as it applies to the spine. The activation process may be more sequential and gradual if it follows a period

Injury

Rehabilitation

Recovery

Figure 16B1-19 Linear route from injury to return to play that the acutely injured athlete often does not follow.

Reduction/ Resolution of symptoms

Return to play

Sportsspecific functionaltiy

Activation

Functional restoration

Figure 16B1-20 Diagram showing the cycle of rehabilitation

of immobilization. If possible, the activation process may occur simultaneously with reduction or resolution of symptoms. Functional restoration follows the activation process. Functional restoration is the restoration of strength, flexibility, balance, coordination, and aerobic and anaerobic conditioning. After functional restoration is achieved, and the athlete has symptomatic improvement, sport-specific functionality can be restored, which may include not only sport-specific drills but also other unique conditioning factors relevant to that sport. This process is often superimposed on, and continues with, general and spinal functional restoration. Once an athlete demonstrates sport-specific functional capacity and symptom control, he or she may be ready to return to play. The return-to-play decision is made in the context of multiple factors: the nature of the injury, the nature of the treatment, the individual athlete, and the exact requirements of the sport applied to the athlete. A cyclic rehabilitation program (Fig. 16B1-20) has been proposed that is both conceptual and specific and allows for transitioning up and down a ladder of activity and restriction based on creating certain rehabilitation goals.27 Unfortunately there is currently no universal, evidencebased standard of rehabilitation that applies to either specific spinal pathologies, specific sports, framework of injury, recovery, or return to play.

LUMBAR SPINE STABILIZATION (CORE STRENGTHENING) A recent analysis of literature related to core strengthening found multiple synonyms that included lumbar stabilization, dynamic stabilization, neuromuscular retraining, neutral spine control, muscular fusion, and trunk stabilization.28,29 Core strengthening has an historical past. Joseph Pilates, for example, focused on girdle strength by recruiting the

Spinal Injuries

deep trunk muscles.28 Core stability has been defined as an active support mechanism generated from intra-abdominal pressure and tensioning of the thoracolumbar fascia and deep lumbar stabilizers.30 It therefore requires the core strength of musculature. Core strength includes the entire trunk region, including pelvis, lumbar spine, and scapulothoracic region, with those regions providing a solid base of support for extremity movement.28 From the sports perspective, core strength is translated to core stability, which facilitates precise maintenance of lumbar and pelvic posture. Conversely, inadequate core strength can lead to poor core stability and may decrease biomechanical efficiency and increased risk for injury.28 Although theoretically sound, the diversity of what constitutes core strengthening programs and its lack of adequate objective measurement have hampered obtaining evidence-based data. It is important to investigate and understand the mechanisms and actions by which strength contributes to stability and how stability is achieved and maintained during static and dynamic tasks.28 Lumbar stabilization is the ability of the spine to be subjected to active and passive loads without failure. Stability is a dynamic process that includes both static positions and controlled movement.31 Panjabi has described a concept of stability focused on three components: bone and ligaments, muscle function, and neural control.32 Segmental stability is achieved by the interplay and interdependence of these three factors. Accordingly, instability can result from tissue damage, which makes the segment more difficult to stabilize, from insufficient muscle strength or endurance, or from poor muscular control. He believes that instability is usually a combination of all three factors.31 There is an essential relationship between stiffness and movement of the motion segment in order to dissipate forces and minimize energy expenditure.31 The neuromuscular system is responsible for modulating stiffness and movement to match the demands of internal and external forces.31 Spinal musculature may be considered both segmental and global. The lumbar spine consists of motion segments that are interrelated and coordinated with coupled functionality that contributes to normal physiologic curves (lordosis) and permits global movement of the entire unit. There are both segmental and global groups of muscles. The deep muscles in the lumbar spine control the intersegmental motion and the superficial muscles control more global motion. The deep muscles originate or insert on the lumbar vertebrae and are largely responsible for the control of stiffness and relationship between the vertebrae. The large superficial muscles of the trunk generate torque for spinal motion, are responsible for global motion, and handle external loads applied to the spine.31,33 There are theories about the role of activation of spinal musculature and the potential role of global muscles substituting for impaired deep muscle when the deep muscles are dysfunctional.31 Proper sequencing of muscle activation and appropriate response to movement and load may be functionally important and is a focus of further research. Interestingly, complex lumbar spine function may also include more generalized functions such as lumbopelvic stability, which requires control of whole-body equilibrium.31 Some

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authors feel there is a close link between lumbar stabilization, posture, balance, and proprioception.31 One thorough review of lumbar stabilization raised five clinical concerns31: (1) whether or not exercise could reverse the changes seen in muscle mass, fiber type, strength, and endurance; (2) whether or not exercise could change neural firing patterns so that patients with low back pain could recruit their muscles in the same way as patients without back problems; (3) whether or not exercise could improve the proprioceptive and balance problems in patients with back pain; (4) whether or not patients with back pain or other spinal damage could participate in a stabilization program; and (5) whether or not lumbar stabilization could improve clinical outcome of patients with back pain.31 From a sports medicine perspective, the task is not just activities of daily living but the mechanical demands of a particular sport. Clearly, the functions of stability (load) and movement must be addressed to allow the spine to meet these demands as it passes along its age-related degenerative cascade and to function adequately. One recent study evaluated patients with various abnormalities on lumbar MRI scans.34 Back pain and disability were assessed both before and up to 12 months after therapy, and any improvements were compared to the baseline MRI findings. Eighty-nine percent of patients had one or more of the following findings: disk bulging, high intensity zones within the disk, or end-plate or bone marrow changes in at least one lumbar segment. Only 11% patients had none of these changes at any level.34 The two most salient points of the study were, not surprisingly, that MRI abnormalities showed minimal association with baseline symptoms and had no significant negative influence on the outcome after therapy.34 As in other studies, there is often little or no correlation between function and morphology. The relationship between specific pathologies, core strengthening, and eventual outcome has been investigated. In two separate studies with homogenous pathologies, patients benefited from a core strengthening program. Specific stabilizing exercises were applied to symptomatic patients with low back pain and radiographic evidence of spondylolisthesis and spondylolysis. Low back pain improved with exercises targeted to the deep abdominal and lumbar multifidi muscles.35 Postoperatively, patients who had dynamic lumbar stabilization had a better outcome than those who had no exercise or had a nonspecific exercise program.36 One study tried to predict treatment response to a stabilization exercise program for patients with low back pain based on clinical parameters.37 This study concluded that the clinical examination (history and physical) could elicit the factors that predicted success or failure with a trunk stabilization program. Another study compared outcomes of patients with low back pain who received treatments that were either matched or unmatched to subgroups that were based on the patient’s initial clinical presentation.38 The subgroups were based on the type of treatment believed most likely to benefit the patient (i.e., manipulation, stabilization exercise, or specific exercise). The patients were also randomly assigned to one of the three treatment protocols. This study concluded that nonspecific low back pain was not a homogenous condition. Outcomes could be improved

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when patient grouping was used to help guide treatment decision making.38 The clinical implication of that study was that subgroups of patients with low back patients exist and that there is a difference in their response to conservative, exercise-based treatment. Clinical, mechanical, and observational features of both acute and chronic low back pain may yield a better classification system for active therapeutic management than does imaging alone. One study evaluated stratification of load during exercise and attempted to quantify spine stability and loading by comparing eight stabilization exercises.39 The purpose of the study was to determine the relationship between strengthening and load, thereby allowing a continuum of lumbar spine rehabilitation decision making. That study attempted to provide clinicians with a better sense of the loads imposed on different spinal tissues and the resulting lumbar spine stability that occurred while performing commonly prescribed stabilization exercises.39 The graphical representation of exercise compared stability with compression and abdominal training with extension (Fig. 16B1-21). Matching clinical subgroups with directed and specific exercise programs depends partially on the mechanical demands on the spine that are anticipated. The level of endurance of the different trunk muscles and the production of certain motor patterns are linked with lumbar spine health.38-42 In some patients, the predominant goal for therapy is the need to minimize compressive load penalties and avoid certain deviated spine postures.39 Further research is required to permit the clinician to choose the appropriate matched variables involving stability and compression load with the appropriate subgroup of patients. One recent study demonstrated that patients with an acute first episode of low back pain treated with a lumbar stabilization program had a reduced risk for pain recurrence than a control group.43 The exercise group had a recurrence rate of 30% at 1 year and 35% in the 2- to 3-year follow-up period.43 The control group, on the other hand, had a recurrence rate of 84% at 1 year and 75% at 2 to 3 years.43

There are some challenges to the concept of core strengthening in treating recurrent back pain. A randomized, controlled trial comparing spinal stabilization exercises with conventional physiotherapy for recurrent low back pain concluded that patients with low back pain had similar improvement with both treatments. There appeared to be no additional benefit to specific spinal stabilization exercises over a conventional physiotherapy package for patients with recurrent low back pain.44 Other critics have stated that conventional physical therapy is as effective as core stabilization in treating low back pain. A systematic review of randomized controlled trials evaluating a segmental stabilizing program for low back pain concluded that segmental stabilizing exercises were no more effective than other physiotherapy interventions.45 For the management of low back pain in sports-related circumstances, exercise programs are an important adjunct in back rehabilitation. It makes sense that the components of a core strengthening or lumbar spine stabilization program would be important for return to sports, where significant loads are imposed on the lumbar spine. Lumbar stabilization exercises directed at the following four areas are thought to be important by some authors31,46: (1) deep musculature (such as the multifidi) that provide intersegmental lumbar vertebral control; (2) muscles (such as the transverse abdominis, diaphragm and pelvic floor) that increase intra-abdominal pressure to increase lumbar stability; (3) global muscles (such as the latissimus dorsi, quadratus lumborum, and superficial spine flexors and extensors) that control trunk movement and co-contraction during activities such as walking and lifting; and (4) precise neural control of these muscles.31,46 In conclusion, it is tempting to speculate that future work may bring a refinement to the evidence regarding core strengthening and low back pain. By creating accurate subgroups of patients with low back pain and matching objective load and stability data to the various subgroups, the clinician may have the tools to direct individual patients toward appropriate exercise pathways.

Higher Compression–Higher Stability Fpn_arm/leg Emphasis on Abdominals Abdcurl SideBridge Higher Compression-Moderate Stability Abdcurl SideBridge Bridge_leg

Lower Compression–Moderate Stability Fpn_leg Bridge

Emphasis on Extensers Fpn_leg Fpn_arm/leg Sitting on a chair Bridge Sitting on a ball Bridge_leg Lower Compression–Lower Stability Figure 16B1-21 Exercises recommended for specific goals. (Redrawn from Kavcic N, Grenier S, McGill SM: Quantifying tissue loads and spine stability while performing commonly prescribed low back stabilization exercises. Spine 29:2319-2329, 2004.)

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COLD THERAPY AND HEAT THERAPY There is little evidence suggesting that either heat or cold therapy is better for many spinal conditions. A Cochrane review addressed the issue of heat or cold for low back pain.47 This review concluded that there was limited evidence to support superficial heat and cold therapy for low back pain and that there was a need for better randomized controlled trials. In a small number of trials, there was moderate evidence that heat wrap therapy provided a slight short-term reduction in pain and disability in patients with a mix of acute and subacute low back pain. The addition of exercise was found to further reduce pain and improve function, but there was insufficient evidence to evaluate the effects of cold for low back pain, and there was conflicting evidence for any differences between heat and cold for low back pain.47

MEDICATIONS A review of 50 randomized controlled clinical trials assessing medications and low back pain found that there was evidence to support the effectiveness of nonselective nonsteroidal anti-inflammatory drugs in acute and chronic low back pain. Similarly, there was evidence to support muscle relaxants in acute low back pain and antidepressants in chronic low back pain.48 A Cochrane review of nonsteroidal anti-inflammatory medications also supported their use in acute low back pain but did not state whether one was more effective than others.49 Corticosteroids have been advocated in radiculopathy but have a less clear indication in the treatment of low back pain.50 It is generally recommended to use a proton pump inhibitor �� concomitantly �� for patients taking nonsteroidal anti-inflammatory medications to reduce gastrointestinal complications.51-60

INJECTION: DIAGNOSTIC AND THERAPEUTIC IN THE THORACIC AND LUMBAR SPINE The injured athlete may resolve an acute clinical syndrome involving the thoracic or lumbar spine regions by the natural history of the clinical problem, medication management, alteration of activity followed by active rehabilitation, and ultimately return to sports participation. Clinical subsets may include athletes who experience acute recurrent selflimited episodes, acute recurrent episodes with chronic smoldering clinical symptoms, or chronic persistent symptoms that may interfere with performance. Under these circumstances, questions naturally arise regarding a different level of diagnostic and therapeutic intervention. The logical trail for potential anatomic pain generators is the level of evidence assumed to establish the source. The diagnostic assessment and therapeutic modulation of these potential sources of pain has been summarized by Boswell and colleagues.61 The contained information reveals the changing nature of evidence criteria and its anticipated change with time. The definition of a structure capable of generating axial or referred pain in the thoracic or lumbar spine has some

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TABLE 16B1-2 Ability to Identify the Source of Back Pain Percentage of Patients Pain Source

Pang et al (1998)77

Facet joint Facet joint and nerve root Facet joint and sacroiliac joint Lumbar nerve root irritation Internal disk disorder Sacroiliac joint Sympathetic dystrophy No cause identified Total

24 24 4 20 7 6 2 13 100

Manchikanti et al (2001)78

40 13 26 2 19 100

From Boswell MV, Trescot AM, Datta S: Interventional techniques: Evidence-based practice guidelines in the management of chronic spinal pain. Pain Physician 10:7-111, 2007.

precepts. The structure should have a nerve supply, be capable of causing pain similar to that seen clinically, be susceptible to diseases or injuries known to be painful, and be shown to be a source of pain in patients, using reliable and valid diagnostic techniques.61,62 The source of pain identification is coupled to the strategy of managing that painful source. In some instances, it may not really matter whether the pain source is identified because the therapeutic option is either unpalatable or unconfirmed or disproportionate to the level of symptoms. Even the accuracy of identification of specific anatomic sites and the interpretation of testing are challenged by some authors.63-76 Two studies using diagnostic blocks as the strategy for determining pain source in the absence of other noninvasive evidence produced the results shown in Table 16B1-2.77,78 The anatomic arguments and literature sources supporting the facet (zygapophyseal) joints, the intervertebral disk, dorsal root ganglion, sacroiliac joint, postlaminectomy syndrome, and spinal stenosis as potential the pain-generators are well documented by Boswell and colleagues.61 Interventional techniques use chemical means such as local anesthetics and steroids. For example, local anesthetics interrupt the pain-spasm cycle and nociceptor transmission, whereas corticosteroids reduce inflammation.61 Diagnostic interventional techniques may either suppress pain from an anatomic structure or stimulate pain from a suspected anatomic structure. Alleviation of pain from an anatomic source by diagnostic blockade makes inherent sense, but there is variability in accuracy of injection and in sensitivity and specificity for each structure and invasive test. Pain stimulation from an anatomic structure may demand an even greater degree of difficulty in interpretation because the patient is asked to separate a potentially painful experience inherent in the test itself from the usual experience of their pain, known as concordant pain. The balance between the degree of intervention, level of disability, and often a season-based time constraint for return to sports participation requires experience and judgment. Familiarity with the spinal pathologies in the nonsports environment is helpful in assessing the context of routine activities of daily living versus performance-oriented

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sports. Added to the texture of decision making are potential career choices in the professional setting and physical achievement with a variety of goals in the amateur environment. Interventional techniques may be used for their short-term value in relieving pain, serving as a symptom suppression vehicle to facilitate transition into functional rehabilitation or other therapeutic considerations. The evidence reviewed by Boswell and associates summarizes and characterizes the long-term relief from interventional procedures as being moderate to limited.61 Further discussion of the various injection techniques and level of evidence is beyond the scope of this chapter. Interested readers are referred to the work by Boswell and colleagues.61

TRIGGER POINT INJECTION A recent review summarized the role of trigger point injections in the nonoperative management of acute and chronic low back pain.79 This study recommended against using trigger point injections in nonspecific categories of acute or chronic low back pain.79 It concluded that injections could be considered for patients with back pain secondary to suspected myofascial syndrome, thought to be to the result of hyperirritable foci of taut muscle bands.79,80 Trigger point injections are often used in the context of a more comprehensive program of physical therapy and medication and the number of injections should be limited.79 Other studies have also concluded that myofascial trigger point injections should only be used within the framework of other treatment modalities.81 The choice of chemical agents for trigger point injections varies widely among clinicians. For example, one recent study compared botulinum toxin A to bupivacaine trigger point injections for the treatment of myofascial pain syndrome and concluded there was no outcome difference between the two and thus recommended the more economical bupivacaine.82 Critics of trigger point injections point out the lack of scientific evidence supporting its use. One study found no benefit to botulinum toxin A trigger point injections for cervicothoracic myofascial pain.83 Another study recommended against the use of trigger point injections generally because of lack of sufficient evidence to support their usage.84

THORACOLUMBAR SPRAINS AND STRAINS The sports medicine physician will be confronted by patients with soft tissue injury in the thoracic and lumbar spine sustained during participation in sports activities or precipitated in the nonsports environment but with symptoms interfering with performance and activity. Since 80% to 90% of the adult population will experience nonspecific low back pain during their lifetime, at least transient interference in sports is common. In general, recovering from soft tissue injuries of the thoracic and lumbar spine should have a favorable course. The biggest issue is the timing of injury and lost playing time, especially in competitive athletics. Bono cited three different studies showing the influence of low back pain and playing time: 30% of college football players lost time,

38% of professional tennis players, and 90% of professional golfers.85-88 A sprain may be defined as an injury to a ligament that may affect individual fibers but does not disrupt the continuity of the structure.85 The muscle fibers may be disrupted at the junction of muscle and tendon or within the muscle itself.85

Thoracic The key points in the evaluation of soft tissue injuries in the thoracic spine are an accurate history and physical examination. It is important to determine whether or not there was a direct blow or twisting mechanism that caused soft tissue injury. Pain location and onset are often helpful in evaluation of soft tissue strains and injuries, but specific recall may not always be possible but may be represented by a change in activity or alteration of training. The most common injury of the thoracic spine in athletes involves the soft tissues. Soft tissue injuries are either musculoligamentous strains or sprains or contusions related to a direct blow. In the differential diagnosis of thoracic region pain and athletes, Karlson linked anatomic location with injury probability. Pain located in the superior thorax was correlated with first rib stress fractures; pain located in the mid-thorax anteriorly is most likely costochondritis; pain located in the mid-thorax anterolaterally to posteriorly was most likely a rib stress fracture; pain located in the mid-thorax posteriorly was considered most likely rib subluxation; pain located in the inferior thorax was most likely a slipping rib.89 Other muscular injuries include the intercostal muscles, the serratus anterior muscle, and miscellaneous muscle avulsions.89 Physical examination findings of importance include the location and the size of the area of tenderness. Consideration of the differential diagnosis of thoracic area symptoms may lead to further diagnostic testing, or confidence in history and physical examination may allow the clinician to confirm a soft tissue diagnosis. Most strains and sprains of the thoracic region are treated like other areas of the body. Controlling the inflammatory process by local measures (e.g., cold therapy) and nonsteroidal anti-inflammatory medicine may facilitate reduction of clinical symptoms. A program of rehabilitation, reconditioning, and sport-specific training will allow a gradual return to full participation. The time required for this process to occur is often a function of the extent of injury and the nature of the aggravating factor related to a specific sport that induced the injury. Stretching to allow return to normal range of motion and muscle strengthening theoretically reduce the risk for repeat injury. Contusions of the thoracic spine are usually related to a direct blow to the bony elements or the paraspinal musculature. Muscle spasm, loss of range of motion, and considerable pain accompany this type of injury. Reduction in inflammation is important as the initial phase of treatment, which may include local modalities as well as medication. Once pain has subsided, the next goal is achieving normal range of motion and normal function. Normal range of motion includes rotation, lateral flexion, and extension of the thoracic region. Muscle conditioning and stretching should be targeted to these functions. Initially, isometric

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muscle contraction is begun while there is still significant pain and loss of motion. When pain and muscle spasm subside, stretching of the thoracic spine is instituted, again primarily involving lateral flexion and rotation motions. Ballistic stretching is absolutely contraindicated. Since individual flexibility among athletes varies, no specific guideline can be given as to the amount of lateral flexion and rotation that can be achieved. The return to sports requires sufficient range of motion and pain control so that the athlete is not risking further injury by splinting of the thoracic spine.

Lumbar One recent study found that muscle strains were the most frequent injury and that acute back injuries were significantly more common than either overuse injuries or injuries associated with preexisting conditions.90 It is important to describe the event leading to pain from a lumbar strain as well as the provocative and palliative factors. It is also important to determine whether there is an underlying chronic condition contributing to the problem. Clinical observation of muscle spasm, restricted range of motion, and localized tenderness should be sought. X-rays are usually not helpful but may be valuable in determining whether underlying structural abnormalities are present. After an acute injury, a short period of cold therapy to limit localized tissue inflammation and edema should be instituted for about 48 hours. In general, the most debilitating portion of the musculoligamentous injury is the associated muscle spasm. This spasm can be controlled with the use of antispasmodic medications. A short trial of a lightweight lumbosacral corset may also help to control muscle spasm and may make the athlete feel more comfortable. When the initial period of spasm and pain has been controlled, treatment is directed toward rehabilitation, which includes strengthening and regaining normal range of motion. There have been attempts to classify low back pain in athletes that has no radicular component.91 Exercise within a pain-free zone of motion and restriction of painful postures are fundamental principles.91

Anterior column

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Return to sports participation after lumbar ligamentous strains and sprains requires an individualized program for the athlete based on the particular demands of the sport.

THORACIC AND LUMBAR FRACTURES The potential injuries derived from the wide variety of sports activities means that almost every thoracic and lumbar fracture pattern may be encountered. Clearly some sports are inherently riskier than others in this regard. Hang gliding, mountaineering, racecar driving, skiing, and snowboarding would presume a different risk profile than sports such as golf, tennis, and long-distance running. Some authors have classified the incidence of thoraciclumbar spine injuries by anatomic zones: T11-L1 (52%), L1-L5 (32%), T1-T10 (16%).92 Important considerations in the evaluation of thoracolumbar trauma include neurologic status, spinal stability, and associated internal organ injury. In the more mature athlete, consideration for preexisting bone quality may be a factor in susceptibility to fracture. The history of the mechanism and force of injury may also be important to lead the astute clinician to search for more occult spinal injury. The neurologic status of the patient is paramount and is a critical consideration in terms of potential nonoperative versus operative treatment and ultimate return to play. The anatomic level and severity of neurologic involvement may produce a variety of neurologic patterns. Decision making for surgical treatment of thoracolumbar fractures depends on three factors: injury mechanism and pathology, neurologic status, and posterior ligament integrity.93 Although there are multiple classifications systems to assess mechanism of injury and inherent spinal stability, the three-column classification of spine injury is commonly used (Fig. 16B1-22).94-98 The spine is divided into three distinct columns, and injuries to these columns become the basis of classification.98 The anterior column is represented by the anterior longitudinal ligament and the anterior portion of the vertebral body.98 The middle column comprises

Middle column

Posterior column

Figure 16B1-22 The commonly used three-column classification system to assess mechanism of injury and inherent spinal stability.

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the remaining part of the vertebral body and the posterior longitudinal ligaments.98 The posterior boundary of the middle column is the origin of the pedicles.98 The posterior column is composed of the remaining posterior elements, including pedicle, lamina, facet joint, spinous process, and posterior soft tissues.98 Use of this classification system forms the basis for evaluating whether a fracture is stable or unstable and influences treatment decisions. If there is a suspected fracture at the time of injury, immobilization on a spine board should be performed if there is any question regarding spinal stability or the risk for additional neurologic impairment. The injured athlete is immobilized and then can then be safely transferred to where further assessment of stability and neurologic status can be performed. The mechanism and other important historical features of the injury should be recorded. This includes not only the description of the event but the immediate and subsequent symptoms experienced by the athlete. Exact location and description of axial pain, presence of numbness, weakness, or pain in the lower extremities, even if only transient, should be sought. Prior history of spine-related problems should be obtained. Physical examination may be limited because of pain, but inspection and palpation and a thorough neurologic examination should be performed. Imaging should include anterior-posterior and lateral radiographs. Since the three-column classification system is used to assess spinal stability, particular attention should be paid to the lateral x-ray. Dynamic x-rays in flexion and extension are often not useful initially because of limited motion from pain. Visualization of the x-ray pattern may suggest compromise to the spinal canal or potential instability secondary to ligamentous injury. Ligamentous injury in the posterior column may be suspected when there is abnormal spacing between two adjacent spinous processes compared with other levels. The spinal canal can be assessed by CT scanning, which can provide axial, sagittal, coronal, and three-dimensional imaging. In the absence of neurologic injury, a CT scan is generally more valuable than an MRI in providing information about bony anatomy and fracture classification. MRI provides superior information regarding soft tissues, ligament, disk, and neural structures.92 In the injured athlete, treatment determinations in traumatic spinal injuries are focused on fracture configuration, spine stability, and neurologic status.

r etroperitoneal or intra-abdominal process. The presence of hematuria should raise a red flag for possible renal injury and should warrant further evaluation. Some authors have suggested CT scanning if plain radiographs reveal lumbar transverse process fractures to make sure there are no other concomitant spinal fractures.101 In a review of professional football players with transverse process fractures “associated visceral injuries were rare and the time lost from sports is only an average of 3.5 weeks.”102 Treatment is directed at pain reduction and allowing adequate time for biologic healing of the fracture to occur, although healing of the transverse process often does not occur because of distraction of the fracture fragment from muscle pull. Healing is often judged by x-ray evaluation and by direct palpation of the site of injury. Once painless range of motion is achieved and mobilization and strengthening of the trunk accomplished, return to active sports is permitted. In noncontact sports, equipment changes may not be necessary to protect the area, but in contact sports, padded equipment modification may be helpful in reducing the risk for reinjury.

Thoracic Compression Fractures The most common fracture in the thoracic spine region is the compression fracture (Fig. 16B1-23). Compression fractures result from failure of the anterior bone column in compression as a flexion moment occurs. There is usually a significant history of trauma in the younger athlete to generate the force required to produce a thoracic compression fracture. Diminishing bone mass from osteoporosis may predispose to fracture in the older athlete. Although the middle column is intact with a compression fracture, and canal compromise

Lumbar Transverse Process Fractures Direct trauma to the lumbar area may cause fractures of the transverse processes or other posterior elements. These fractures are stable and are rarely associated with neurologic injury. Intra-abdominal injuries can occur in association with fractures of the transverse process or with blunt trauma to the area of the costovertebral angle. A high index of suspicion for retroperitoneal and intra-abdominal processes is warranted in athletes who have a fracture of the transverse process.99,100 Examination of the abdomen may reveal guarding or tenderness, and tenderness in the costovertebral angle should raise concern about possible abdominal injury, particularly to the kidney. Further consultation or directed assessment may be necessary to diagnose a

Figure 16B1-23 Thoracic compression fracture not visualized on lateral radiograph in mature recreational walker but identified on bone scan.

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is therefore unlikely, it is important to be sure that the neurologic examination is normal and that there is no associated transient neurologic abnormality. Physical examination may reveal point tenderness and guarded range of motion. Usually the diagnosis of compression fractures of the thoracic spine is made by anteroposterior and lateral x-rays. The lateral x-ray is usually diagnostic of compression fracture. The amount of compression can be determined by comparing the height of the anterior and posterior aspects of the vertebral body. Careful evaluation of other vertebral bodies may reveal more than one compression fracture. Most compression fractures in athletes will show less than 25% compression of the anterior vertebral body compared with the posterior vertebral body. If anterior vertebral body compression is more than 50% of the posterior vertebral body height or adjacent intervertebral bodies, CT should be considered to assess the spinal canal. Compression fractures with less than 25% compression deformity are treated symptomatically with analgesia and possibly immobilization in a thoracic orthosis and exclusion from sports. The purpose of bracing is to provide immobilization for pain relief and to prevent further flexion of the thoracic spine, which could increase the deformity. The duration of bracing depends on pain relief and the underlying bone quality. The two most common forms of braces are the Jewett extension orthosis and a molded polypropylene thoracolumbar spine orthosis (TLSO). Cement augmentation techniques (e.g., kyphoplasty and vertebroplasty) involve the injection of cement into the compression fracture and have become more popular techniques for the treatment of the osteoporotic compression fracture.103-105 Vertebroplasty involves the percutaneous instillation of liquid cement into the fractured vertebra, whereas kyphoplasty expands the vertebral body through inflation of a balloon, which creates a void for the placement of viscous cement (RF12-F14). Their role in the treatment of vertebral compression fractures in younger individuals, including young athletes, is unknown.

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Thoracolumbar Burst Fractures Burst fractures of the lumbar spine are caused by direct axial loading of the spine or by a combination of flexion and axial loading. This injury involves not only the anterior column but also the middle column in compression and is frequently associated with bony retropulsion into the spinal canal and neurologic involvement. Thoracolumbar burst fractures without neurologic involvement and with mild to moderate canal narrowing can be managed conservatively (Fig. 16B1-24).106,107 Burst fractures involving more than 50% of the vertebral body, producing more than 50% bony impingement of the spinal canal, or having more than 20 degrees of kyphosis at the level of fracture have traditionally been considered indications for surgery.108 Surgical goals include restoring anatomic height of the vertebral body, providing spinal stability, and achieving spinal canal decompression by either direct or indirect decompression. The surgical approach may be anterior, posterior, or combined. Anterior spinal surgery involves a retroperitoneal approach to the affected segment, corpectomy with removal of bony fragments from the spinal canal, and vertebral body reconstruction of the corpectomy defect and stabilization. Spinal canal restoration can also be accomplished with posterolateral decompression of the bony fragments in the canal and vertebral height restoration with indirect decompression by distraction-lordosis and instrumentation. Combined anterior and posterior approaches can also be used with the anterior approach ensuring adequate spinal canal decompression and middle column reconstruction with biomaterials, followed by posterior instrumentation fusion to ensure adequate stability for early mobilization of the patient. Whether an anterior, posterior, or combined approach is used, the patient is typically mobilized in a TLSO for 3 months.

Thoracolumbar Fractures Summary Other injury patterns not described in this chapter include distraction-flexion injuries, fracture-dislocations, and distraction-extension injuries. Characteristics and Figure 16B1-24 A 38-year-old dentist involved in a dune buggy “hard landing” sustained a burst fracture of L1 without neurologic deficit and was treated with a thoracolumbar spine orthosis. She is asymptomatic and has returned to normal sports activities but not dune buggy riding.

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Figure 16B1-25 Sacral stress fracture in a female collegiate basketball player with complaints of back and leg pain. She successfully returned to collegiate basketball after conservative treatment.

t reatment of these injuries is beyond the scope of this chapter but have been described elsewhere.92,109 In the context of acute thoracolumbar injury evaluation, appropriate immobilization and transportation without precipitation or aggravation of existing neurologic injury forms the initial principle of management. History, physical examination, and diagnostic imaging (plain x-ray, MRI, CT) form the cornerstone of assessment and in deciding on surgical or nonsurgical treatment of these injuries. Decision making for the surgical treatment of thoracolumbar fractures concentrates on three factors: injury morphology, neurologic status, and posterior ligament integrity.93

SACRAL STRESS FRACTURE In 1989, Volpin and associates reported on stress fractures of the sacrum following strenuous activity.110,111 In their series of three cases, sacral stress fractures were identified in a military population.111 The concept of fracture in the sacrum without direct trauma is either due to insufficiency in bone mass (osteoporosis) and subsequent failure or repetitive microtrauma from overuse leading to fatigue fracture. Sacral stress fractures result from concentration of the body forces that are dissipated from the spine to the sacrum and ala.110,112 The usual causes of athletic stress fractures, generally, is an increase in the intensity and duration of a sports activity or a change in the way the athletic activity is performed, resulting in concentrated load on the affected anatomic structure. Sacral stress fractures should be considered in the differential diagnosis of low back and leg pain in the athlete (Fig. 16B1-25).

An underlying metabolic bone disease may lead to insufficiency fracture in the athlete. Older athletes may have osteoporosis as a contributing factor to insufficiency fracture. The typical sacral stress fracture in the athlete may begin with either an acute history or the development of insidious unilateral buttock, upper thigh, or low back pain. There are no pathognomonic physical examination findings diagnostic of sacral stress fractures. Various physical maneuvers designed to load the area have been described, such as the hopping test.110,113 MRI scan of the pelvis and single-photon emission computed tomography (SPECT) and bone scan typically reveal the stress fracture. A three-phase protocol to diagnose and manage pelvic stress injuries in the athlete has been described.114 Phase I involves stopping the painful activity, including substituting non–weight-bearing activities such as swimming or cycling for weight-bearing activities in order to maintain aerobic capacity. Phase II is initiated after a 3- to 5-day pain-free interval. This phase employs light-weighted exercises to facilitate strength and correct strength imbalances. Sport-specific rehabilitation is initiated at this time. Phase III focuses on return-to-sport specific activity with gradual progression every other day to normal activity.114 This process of recovery can take from 3 to 18 weeks.115

Kyphosis and Scoliosis Spinal deformity may be encountered in adolescents and young adults as an intrinsic structure rather than a derivative of sports participation. Scoliosis may be defined as a coronal plane pathology and kyphosis as abnormal curvature in the sagittal plane.

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The classification of scoliosis can be related to its underlying generation: congenital (present at birth), neuromuscular (deformity associated with impaired neuromuscular states), and idiopathic (undefined). The typical athlete with scoliosis most likely will have congenital or idiopathic scoliosis.116-118 The classification of kyphosis is also related to presumptive underlying cause: congenital (present at birth), neuromuscular (sagittal plane deformity associated with impaired neuromuscular states), postural (related to posture), Scheuermann’s disease (vertebral body wedging and associated end plate changes).119 In the sports medicine context, spinal deformity is usually an incidental finding, rather than a result of specific injury. Inspection and palpation may reveal the underlying deformity: asymmetry of shoulder and pelvic height, abnormalities in spinal contour expressed as prominent asymmetric thoracic chest wall or paralumbar musculature, round back posture, or leg-length inequality associated with the spinal deformity. Exclusion of neurologic abnormalities is important in assigning spinal deformity. Radiographic evaluation of suspected spinal deformity includes standing posteroanterior and lateral x-ray views. These views allow the quantitative measurement of the projected curves, which is a critical factor in deciding treatment. There are four general patterns of curvature: thoracic, lumbar, thoracolumbar, and double major curves. The rationale for full spine standing anteroposterior and lateral x-rays is the ability to assess all the potential curves that might be associated with deformity. These curve patterns have been classified by King and colleagues and more recently by Lenke and associates.120,121 Plain x-ray coronal plane measurements include the determination of the central sacral vertical line, the end vertebrae, the apical vertebra, and the stable vertebra. Kyphosis is a normal physiologic curve in the thoracic spine and has a normal range of 20 to 40 degrees. Scheuermann’s kyphosis is defined by the following characteristics: anterior wedging greater than 5 degrees involving three or more consecutive vertebral bodies, kyphosis greater than 45 degrees on the standing lateral x-ray, irregularity of the vertebral end plates, and Schmorl’s nodes, which are depressions in the vertebral bodies from ballooning of the disk into the vertebral end plate.122 Other abnormalities may be seen in patients with Scheuermann’s kyphosis, including mild scoliosis and spondylolisthesis.122 Curves less than 25 degrees can be observed for progression.122 Bracing should be considered in the skeletally immature patient for curves measuring 30 to 45 degrees, or for curves greater than 25 degrees with documented progression of more than 5 degrees.122 Conservative management of Scheuermann’s kyphosis consists of bracing at 50 degrees in addition to an exercise program.122 Round back deformity (not possessing the radiographic criteria of Scheuermann’s) is treated with thoracic extension exercises. In general, indications for surgical intervention for scoliosis include curve progression despite bracing, curves greater than 40 degrees in the skeletally immature, and curves greater than 50 degrees with a mature skeleton.122 Indications for surgery in Scheuermann’s kyphosis include curves greater than 70 degrees, intractable pain,

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curve progression, neurologic compression, cardiopulmonary compromise, and significant trunk deformity.122,123

Adult Scoliosis Scoliosis may be encountered in the adult years as a derivative of preexisting adolescent scoliosis or as a new-onset deformity. The patterns of deformity, the amount of concomitant degenerative changes in the spine, the natural history of deformity progression, and the clinical presentation are different in the adult as compared with the adolescent with scoliosis.124 Indeed, it is often the symptoms from the associated degenerative change that results in clinical presentation in the adult with scoliosis. These changes include spinal stenosis, spondylolisthesis, rotational subluxation, lumbar hyperlordosis, and rigidity of the curve.124 The Scoliosis Research Society has recently defined a classification system for adult spinal deformity that is different from the adolescent. This classification system is a radiographic classification as opposed to clinical classification, in which there are six major coronal deformities and a single sagittal plane deformity without associated thoracic or lumbar coronal deformities that would meet the requirements of the primary coronal deformity.124 The goal of this classification system is the recognition that there are unique challenges related to adult scoliosis that are inherently different from adolescent growth period issues. The specifics of this classification are beyond the scope of this chapter and are described elsewhere.124-131

Degenerative Lumbar Scoliosis Degenerative lumbar scoliosis presents a difficult combination of multiplanar deformity. A radiographic study of degenerative lumbar scoliosis tried to define x-ray parameters and canal measurements.132 Associated degenerative changes such as hypertrophy of the ligamentum flavum, posterior disk bulging, and bony overgrowth are thought to be more likely to contribute to stenosis regardless of the scoliosis.132 Degenerative scoliosis may exist without neurologic symptoms, or it may occur in association with spinal stenosis with symptomatic back and leg symptoms. A quantitative radiographic and clinical analysis demonstrated that lateral listhesis, L3 and L4 obliquity, lumbar lordosis, and thoracolumbar kyphosis were significantly correlated with pain.133 Degenerative lumbar scoliosis in association with lumbar spinal stenosis usually involves the L3 and L4 nerve roots, which are foraminally compressed in the concave side of the curve, and the L5 and S1 nerve roots, which are compressed in the lateral recess on the convex side of the curve.134 Sports medicine considerations for management of the active older athlete with adult scoliosis typically involve traditional nonoperative measures.135 There will be active individuals with some measure of deformity who wish to maintain their levels of performance. In addition, many individuals with superimposed osteoporosis and adult scoliosis will need to strike a balance between desired level of performance and symptom overload. The complexity of surgical decision making, as it applies to adult scoliosis, is beyond the scope of this discussion.

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THORACIC DISK HERNIATION Thoracic disk herniation can occur spontaneously without a significant history of trauma or specific athletic causation. The most commonly involved levels are T9-10, T10-11 and T11-12.136 A retrospective review of thoracic disk herniations found that 27% of the patients had surgery and 73% were treated conservatively.137 This study concluded that thoracic disk herniations only occasionally lead to surgery and that many patients return to active lifestyles without the need for surgery.137 Another study reviewed the natural history of asymptomatic thoracic disk herniations and concluded that the patients rarely developed symptoms during the period of review.138 In a study of serial thoracic MRI scans assessing degenerative changes, thoracic disk herniation was present in 10% of subjects on the initial scans, and 27% of patients improved radiographically.139 An additional 1.5% of subjects were found to have another thoracic disk herniation at the time of follow-up MRI.139 In another review of thoracic disk herniations, initial symptoms included pain in 57% of patients, sensory disturbance in 24%, motor involvement in 17%, and bowel and bladder dysfunction in 2% of patients.140,141 The presenting signs and symptoms on the initial evaluation involved motor or sensory symptoms in 61% of patients and bowel and bladder dysfunction in 30%.140,141 Chest wall or upper abdominal pain may result from intercostal nerve root involvement from posterolateral thoracic disk herniations.142-145 Central disk herniations may be painless but can present with lower extremity neurologic dysfunction. Lower extremity paresis or paralysis may be a presenting finding.142,146 Symptoms mimicking a C8 radiculopathy can occur with T1-T2 herniated disk involving T1 nerve root.147 Physical examination may reveal dermatomal numbness in the distribution of an involved intercostal nerve from a posterolateral herniation. Spinal cord compression from a central disk herniation may present with spastic paraparesis and long tract findings, such as hyperreflexia, clonus, and upgoing plantar response (Babinski sign).148,149 Abdominal and cremasteric reflexes should be sought as part of the examination.150 Diagnostic studies include MRI and myelography followed by CT (CT-myelography). MRI directly visualizes the thoracic spine, including the disk and the neural elements, and reveals any spinal cord compression. Thoracic CT-myelography may also be helpful in delineating anatomic defects and location of a thoracic disk herniation when MRI is inconclusive. The treatment of thoracic disk herniation depends on the clinical syndrome and location of the disk herniation. A posterolateral herniation that does not compress the spinal cord and only involves an isolated nerve root producing intercostal nerve root pain may be treated conservatively. If the pain is severe and does not resolve, surgical intervention can be considered. With more central thoracic disk herniations leading to neurologic signs and symptoms, surgery may be required. Surgical options include anterior excision through a transthoracic approach for disk spaces T4 through T12140-151 or minimally invasive video-assisted

thoracoscopic surgery for central herniations.152-154 Posterior costotransversectomy may be used for paracentral and lateral disk herniations with the approach from the side of the disk herniation.140,155,156 The costotransversectomy involves removal of pedicle, hemilamina, facet joint, and medial rib to allow access to the canal.140 Posterior transpedicular strategies involve unilateral removal of pedicle and facet to gain access to the thoracic spinal floor while avoiding the spinal cord.157-159 Alternatively, a transfacet approach can be used that provides limited exposure for access to the central canal but can provide good exposure for lateral disk herniations.140,160,161 Return to full sports activity is dependent on the clinical circumstance and the nature of the treatment. For conservatively treated patients without neurologic deficits, return to full sports activity without restriction can be anticipated after an adequate rehabilitation program is completed. For thoracic disk herniations surgically decompressed without fusion and having complete recovery, the decision for return to sport participation should be individualized. Following thoracotomy with disk excision and fusion, many surgeons would not allow contact sports, although some would consider this on an individualized basis (Fig. 16B1-26). A solid bony fusion should be achieved, and neurologic recovery must be complete for the patient to return to sports after successful rehabilitation.

THORACIC SPINAL STENOSIS Thoracic spinal stenosis is less common than either cervical or lumbar spinal stenosis because of the relative lack of motion of the thoracic spine. Thoracic spinal stenosis can occur from calcified disk protrusions, posterior vertebral body osteophytes, ossification of the posterior longitudinal ligament, facet joint or lamina hypertrophy, or ossification of the ligamentum flavum.162-166 Congenital narrowing of the spinal canal may also exist and can be a contributor to stenosis. If a critical diminution of space available for the spinal cord results, then neurologic findings may ensue. The most common presentation for symptomatic spinal stenosis involves a gait disorder characterized by spastic gait. Lower extremity numbness with a defined sensory level at or below the level of spinal cord compression may also be present. Lower extremity weakness and bowel and bladder symptoms may also occur. The full spectrum of upper motor neuron findings may be elicited, including lower extremity hyperreflexia, clonus, and abnormal plantar response (Babinski sign). From an athletic perspective, thoracic spinal stenosis is most likely to present in older patients with acquired (degenerative) narrowing of the spinal canal. Younger patients may become symptomatic from a combination of a preexisting congenital narrow canal with superimposed degenerative changes. Asymptomatic thoracic spinal stenosis does not require surgical intervention. Return to full participation in sports in the asymptomatic individual with thoracic spinal canal stenosis depends on the nature of the sport, the degree of narrowing, and the clinician’s opinion as to the potential for injury. There are no unequivocal guidelines for these decisions.

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Figure 16B1-26 A 35-year-old recreational athlete with the delayed onset of long tract lower extremity symptoms with thoracic disk herniation treated with transthoracic decompression and interspace fusion with rib graft. Neurologic symptoms resolved, and he is in active rehabilitation in preparation for return to recreational sports.

If clinical findings of spinal cord compression are present, surgical treatment is indicated. The choice of surgical approach is often dictated by the location of spinal cord compression (Fig. 16B1-27).167 For predominantly anterior compression, an anterior approach would be preferred. For predominant posterior pathology or posterolateral compression of the spinal cord, a posterior decompressive laminectomy may be performed.167

Recent studies have shown satisfactory results for thoracic laminectomy for thoracic spinal stenosis.168-170 However, one study noted a 14.5% neurologic complication rate with posterior decompression for thoracic spinal stenosis.171 After resolution of neurologic symptoms following posterior thoracic decompressive laminectomy, return to sports participation can be considered, although collision sports should probably be avoided.

Figure 16B1-27 Middle-aged recreational walker with subtle onset of gait disorder rapidly progressing to extreme difficulty walking. Posterior thoracic decompression resolved the clinical symptoms in this patient with a combination of congenital narrowing and facet joint encroachment into the spinal canal.

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LUMBAR DEGENERATIVE DISK DISEASE Lumbar degenerative disk disease is a universal age-related condition consisting of morphologic changes in the lumbar motion segment. These changes may be symptomatic or asymptomatic. Disk pathology, including focal disk protrusions and anular tears, are common in the asymptomatic population.172 Degenerative changes in the lumbar spine are present in virtually everyone by middle age.173 These changes consist of disk degeneration and marginal osteophyte formation of the vertebral bodies with remodeling changes in the facet joints. Disk degeneration is generally thought to be the primary pathologic process, with facet joint changes occurring secondarily. Because about 80% of the population has been estimated to experience transient back pain at some point in time, there is clearly an interface where degenerative changes may contribute to an active symptomatic state and periods of time where the architectural changes are asymptomatic. It should be remembered that back pain is a symptom and not a diagnosis, and both spinal and nonspinal causes of low back pain must be considered. Spinal causes of back pain are numerous and can include the disk, facet joints, bones, ligaments, muscles, and nerves. Extraspinal causes of low back pain include both intra-abdominal and intrapelvic conditions, such as ulcer disease, abdominal aortic aneurysm, renal conditions, endometriosis, and many other conditions. The natural history of low back pain is relatively benign, with up to 90% of patients having resolution within 6 weeks and only 1% having low back pain for longer than 1 year.174 Because symptoms may resolve quickly, imaging is usually not indicated for acute low back pain if noninvasive conservative treatment is planned. Recurrence of low back pain is common, with subsequent episodes occurring in 20% to 67% of patients.175,176 It can be difficult to identify the cause of low back pain. The degenerative changes commonly seen on imaging studies may not be the source of pain.177,178 MRI has not been found to be a reliable predictor of future low back pain in asymptomatic patients.179 In addition, MRI is typically static imaging, which may not predict what actually occurs during dynamic activity and under loading. It has been found that structural abnormalities on MRI do not preclude successful lumbar spine rehabilitation.180 If it is important to identify the source of pain, invasive diagnostic testing is indicated. Usually this involves either the stimulation of pain or the suppression of pain from a particular anatomic site. Although theoretically logical, invasive testing has variable accuracy in its ability to localize the pain generator.181 In addition, invasive testing cannot reliably localize all potential pain generators, such as the disk, ligament, muscle, tendon, or facet joint. In general, there is little value in attempting to identify the source of low back pain unless such identification has therapeutic implications. If identifying a specific anatomic pain generator can lead to specific treatment, for example, surgery, then such testing is potentially valuable. If the patient is going to continue with conservative treatment, such as physical therapy or oral medications, then the information obtained from invasive testing is unlikely to be valuable.

Figure 16B1-28 Spine pain: loaded with sensors.

The degenerative disk cascade was developed by Kirkaldy-Willis.182-184 This model presumes the interplay of the three-joint complex: the intervertebral disk and the paired posterior facet joints.184 This tripod forms the basic building block of the spine: the motion segment. The lumbar spine is thus composed of stacked motion segments that are interconnected to form a physiologic posture (lordosis in the lumbar spine and kyphosis in the thoracic spine). The degenerative disk disease cascade is characterized by periods of mechanical dysfunction, instability, and restabilization.182 An athlete may be seen in any phase of the degenerative cascade. The question often arises about whether the injury occurred because of some predisposition to injury from the degenerative cascade process or whether the injury caused the morphologic architectural degenerative changes. This is usually a question that cannot be answered definitively (Fig. 16B1-28).

Anular Tear Within the degenerative cascade, radial tears of the disk occur. The anulus fibrosus can be a source of pain because of its sensory innervation in its outer layers.185-188 The intervertebral disk is a syndesmosis, which is essentially a fibrous union. Anatomic changes in the anulus consisting of fissuring or frank tears occur and may be a potential source of pain.186-188 Controversy exists about whether MRI can identify a disk with a radial tear producing an area of bright signal on T2-weighted imaging (a high-intensity zone) as being symptomatic or asymptomatic.189-191 The hallmark invasive diagnostic test to determine whether the disk is the source of a patient’s back pain is lumbar diskography. Diskography involves injection of a dye into the disk and recording the patient’s pain response as either painless, concordant (reproducing the patient’s typical pain), or discordant (producing atypical pain). A less important feature of diskography is the radiographic image that it produces, either normal or abnormal. Diskography

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makes theoretical sense but is often challenged on an evidence-based basis.192-203 Some authors think that pressure-controlled manometric diskography can distinguish between asymptomatic and symptomatic anular tears, although this is controversial.204

Facet Joint The paired posterior facet joints are capable of producing pain based on their neural innervation.205-207 The facet joint is a diarthrodial joint with synovium and cartilaginous surfaces. The diagnosis of the facet joint as a source of pain is based on injection of the joints under x-ray control and producing pain relief.206,207 However, there are many challenges to the accuracy of facet injection as a diagnostic tool, and its utility is not universally accepted.206

Degenerative Disk Disease in the Athlete There is controversy surrounding the question of whether athletes have a higher incidence of low back pain and more degenerative lumbar changes than the general population. One study of Olympic athletes suggested a higher prevalence of and more lumbar disk degeneration than the normal population when using historical controls.208 Back pain and plain x-ray changes in the thoracolumbar spine were reviewed in elite wrestlers, gymnasts, and soccer and tennis players 14 to 25 years of age.209 Symptomatic back pain was reported in 50% to 85% of athletes, and x-ray abnormalities were found in 36% to 55% of athletes.209 The authors concluded that such high-demand athletes were subjected to increased symptoms.209 In a landmark study comparing elite athletes to control subjects, back pain was found to be less common in athletes than in controls, and there were no significant differences in hospitalizations or pensions.210 Not surprisingly, weightlifters and soccer players had more degenerative changes than runners and shooters.210 In a follow-up study, athletes did not report a higher frequency of back pain than nonathletes despite having significantly more radiologic abnormalities.211 Some anatomic changes, such as progressive loss of disk height or new-onset disk space narrowing, correlated with back pain.211 Another review of the epidemiology of low back pain in athletes suggested that, although common, episodes of low back pain were often short-lived.212 Because different sports produce different stresses on the spine, back strengthening programs might theoretically reduce the incidence of low back pain in athletes.212 The effect of mechanical load on low back pain in athletes is unclear. In a study of intercollegiate rowers, 32% experienced low back pain during college, and those who were symptomatic had a greater incidence of low back pain later in life compared with those who remained asymptomatic.213 The lifetime prevalence of back pain in the rowers did not differ from that of the general population, although the asymptomatic intercollegiate rowers had a lower incidence of low back pain than the general population as the study progressed. In another study, elite athletes competing in cross-country skiing, rowing, and orienteering were matched to nonathletic controls.214 The elite athletes had more low back pain during periods of training

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and competition.214 The implication of these studies is that elite athletes in these endurance sports may have increased mechanical demand on the lumbar spine and more symptoms. For the nonelite athlete or casual exerciser, it is desirable to find a mechanical corridor that allows endurance and load training but keeps symptoms to a minimum.215 One recent study showed that two primary risk factors for long-term spinal problems were sports-related injuries and overuse in triathletes.216 An unanswered question is whether or not future scientific evidence will result in a change in training methods to reduce the mechanical load on the thoracolumbar spine, thereby reducing the incidence of low back pain.

Surgery for Degenerative Disk Disease Lumbar surgery in the athlete typically involves surgery for disk herniation, spinal stenosis, spondylolisthesis, or instability. The goals of surgery for instability in the athlete involve either motion segment elimination (fusion) or motion segment preservation (artificial disk replacement or dynamic stabilization techniques). A recent review comparing fusion to nonoperative care for chronic low back pain concluded that lumbar fusion may be more efficacious than unstructured, heterogeneous nonoperative care but that fusion may not be better than a structured rehabilitation program that includes cognitive-behavior therapy (Figs. 16B1-29 and 16B1-30).217 A 1-year follow-up study comparing fusion surgery with a conservative physical therapy �� regimen for �� degenerative disk disease showed no advantage for surgery.218,219 A randomized trial comparing fusion to conservative treatment for chronic low back pain showed superior outcome in the fusion group.220-224 No particular fusion technique was found to be superior to the other techniques.222,224 Dynamic neutralization stabilization has been advocated as an alternative to fusion, but the clinical success of such techniques and their applicability to the athlete remain to be proved.225-228 Motion preservation with artificial disk replacement is a newer technology whose long-term outcome and complications are unknown.229-240 One study demonstrated the superiority of a particular type of lumbar artificial disk replacement compared with circumferential fusion for one-level degenerative disk disease.240 Although motion preservation is an appealing concept for the athlete, the issues of durability and long-term clinical outcome remain unanswered. Furthermore, the theoretical advantage of reducing adjacent segment degeneration bordering interbody surgery remains unproved.

LUMBAR DISK HERNIATION Lumbar disk herniation is produced by protrusion of the nucleus pulposus through the outer covering of the disk, known as the anulus fibrosus. This protrusion of nuclear material may take multiple anatomic forms, commonly described as a protrusion, an extrusion, or a sequestration.241 This deformation may be sufficient in size and location to produce mechanical compression of the surrounding neurologic structures. An extruded disk disrupts the anulus fibrosus but maintains some continuity with the

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Figure 16B1-29 Middle-aged female runner treated with nonsteroidal antiinflammatory medications for low back pain. She currently runs 18 miles per week.

parent disk. A sequestered fragment, commonly known as a free fragment, is displaced from the disk space and isolated from it. From a practical point of view, the net effect is mechanical compression of the spinal nerve root or roots by the disk material. The clinical onset of a symptomatic lumbar disk herniation may vary widely. Crescendo back or buttock pain may be the precursor to radicular leg pain. This may occur suddenly or gradually, may occur without preceding back or buttock symptoms, and may present with sudden dramatic

Figure 16B1-30 Lumbar degenerative disk disease in a female professional basketball player who returned to professional basketball after conservative treatment.

radicular pain.242 It is common for a patient to be able to describe the day and time of the acute onset of radicular pain but not necessarily be able to relate it to a specific activity. A lumbar disk herniation is not always associated with a specific event, even in the sports population. The level and the anatomic location of the herniation (central, posterolateral, foraminal, or extraforaminal) determine which spinal nerve may be affected.243 In addition, a herniated disk may produce a wide variety of clinical signs and symptoms such as numbness, weakness, and pain.

Spinal Injuries

Lumbar disk herniations most commonly produce calf pain because the most common location of a herniation is at the L4-5 and L5-S1 levels, producing mechanical compression of either the L5 or S1 nerve roots, respectively. Proximal anterior thigh pain may result from involvement of the L2, L3, or L4 spinal nerve roots. There are three clinical patterns related to lumbar disk herniation that can influence treatment implications: cauda equina syndrome, progressive neurologic deficit, and radicular pain. Cauda equina syndrome can result from a large lumbar disk herniation that affects the sacral nerve roots (S2, S3, and S4). The cauda equina syndrome is characterized by a loss of control of bowel and bladder function. The treatment of this condition is urgent surgical decompression to maximize the chance of bowel and bladder recovery.241 It is ideal for surgery to take place in the first 24 to 72 hours of this clinical syndrome.244-248 However, some authors have not shown a temporal relationship between onset of cauda equina symptoms and functional bowel and bladder recovery.249 The second clinical condition, which may also accompany cauda equina syndrome, is progressive lower extremity neurologic deficit. A progressive neurologic deficit constitutes an absolute indication for urgent or emergent surgical intervention.241 Controversy exists regarding established, nonprogressive lower extremity neurologic deficits secondary to lumbar disk herniation. Some clinicians advocate conservative care based on the fact that most studies have not shown a difference in outcome and ultimate return of strength between surgical and nonsurgical treatment for nonprogressive lower extremity motor weakness.250-252 Recent studies have shown a correlation among functional motor recovery, the degree of preoperative lower extremity weakness, and the timing of surgery.253,254 Clearly, in the athletic population in which performance is a major concern, surgical intervention is a consideration in the presence of even nonprogressive lower extremity motor weakness. Radicular pain derived from a lumbar herniated disk may be sufficiently intense to warrant surgical intervention during the early phase of clinical presentation. This is, however, an exception to the general principle of trying conservative treatment for a period of time for at least 4 to 6 weeks because about 80% of patients with radicular pain secondary to lumbar disk herniation significantly improve without surgical intervention.255-257

Clinical History and Physical Examination The key clinical questions to be asked of the patient are about the onset, duration, and location of pain; the presence or absence of normal bowel and bladder function; and the presence and distribution of any numbness or weakness in the lower extremities. Inspection of the lumbar spine may demonstrate a truncal list either toward or away from the anatomic location of the herniation; the side of the list appears to be independent of the location of the disk herniation.258 Range of motion of the lumbar spine may be restricted because of back pain, and leg pain may be produced by either back extension or flexion, suggesting a dynamic component to neurologic compression. Neurologic examination

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involves reflex, sensory, and motor examination of the lower extremities and a rectal examination, if there is any suspicion of cauda equina syndrome. A careful clinical examination may suggest which nerve root is affected by a lumbar disk herniation and allow correlation with imaging studies.258-264 Tension signs are an important indicator of nerve root inflammation. These signs include the straight leg raising test, contralateral straight leg raising test, femoral stretch test, and Lasègue’s sign. The straight leg raising test is considered positive if the patient’s typical leg pain is reproduced in the arc between 0 to 70 degrees of leg elevation. A contralateral straight leg raising test is positive when the asymptomatic leg is elevated and produces opposite (symptomatic) leg pain. Foot dorsiflexion of the symptomatic leg during performance of the straight leg raising test may produce radicular pain (Lasègue’s sign). Of note, the straight leg raising test reflects compression and inflammation primarily involving the L5 and S1 nerve roots. Mechanical pressure and inflammation involving the L2, L3, and L4 nerve roots is elicited during the femoral nerve stretch test, which is either performed with the patient prone while the involved hip is extended or is performed with the patient in the lateral decubitus position while the upper (symptomatic) hip is extended. The test is positive if the patient’s pain is reproduced in the femoral nerve distribution (anterior thigh).

Diagnostic Imaging The gold standard for imaging of a lumbar disk herniation is MRI. In most patients, MRI defines the relevant spinal anatomy, including a lumbar disk herniation and neural compression. If the MRI is of suboptimal quality, if the patient cannot tolerate the procedure, if there are contraindications to its use (e.g., the presence of a cardiac pacemaker), or if the suspected pathology is not clearly visualized, other diagnostic tests should be performed. In most instances, this would be a traditional lumbar myelogram with a postcontrast CT scan. In rare circumstances, CT diskography may be helpful in further identifying questionable pathologies such as a foraminal or extraforaminal lumbar disk herniation.

Conservative Treatment In the absence of a cauda equina syndrome or a progressive neurologic deficit, conservative (nonoperative) management of lumbar disk herniation is the initial standard of treatment because most lumbar disk herniations do not require surgery. Conservative measures include activity restriction, physical therapy, medication management, and spinal injections (epidural steroid injections or selective nerve root blocks). In a retrospective study of lumbar disk herniations, Hakelius demonstrated that 38% of patients with a lumbar disk herniation were improved by 1 month, 52% by 2 months, and 73% by 3 months.257 Two subsequent studies suggested that the optimal timing of surgical intervention was within 3 months.255-256 Clearly there is a point at which the optimal timing of surgery needs to be balanced with giving the patient an adequate trial of conservative management.265-273

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Box 16B1-1 Anatomic Zones for Stenosis Central canal stenosis Lateral recess stenosis Foraminal stenosis Extraforaminal stenosis

Figure 16B1-31 Lumbar disk herniation in a 38-year-old professional basketball player with preoperative weakness in the left anterior tibial muscle and left leg pain treated with lumbar microdiskectomy and eventual return to professional basketball (same season).

Surgery The goal of surgery is the removal of mechanical compression from the involved lumbar spinal nerves. The goal of surgery is resolution or lessening of leg pain, not back pain. Surgery is less predictable in resolving motor or sensory deficits than in improving radicular leg pain.255,259,260,261,274,275 The gold standard surgical procedure is subtotal lumbar diskectomy.276-280 The anatomic location of a disk herniation and other associated pathology may mandate additional bone, ligament, or facet joint resection to adequately decompress the nerve. There is no proven advantage of microsurgical decompression to standard diskectomy.281,282 A recent Cochrane update suggested that diskectomy provides quicker relief from acute sciatica from lumbar disk herniation than does nonoperative treatment. Furthermore, microdiskectomy gave comparable results to those of traditional diskectomy, with little evidence regarding outcome from other newer and less invasive techniques.282

Return to Sports Return to sports participation after symptomatic lumbar disk herniation, whether treated operatively or nonoperatively, depends on the amount of back or leg pain, neurologic status of the patient, and demands of the particular sport. A study of professional and Olympic athletes operated on for lumbar herniated disk with a microscopic diskectomy technique showed an average return to sports at 5.2 months, with 88% achieving successful return to play at their previous level (Fig. 16B1-31).283 In another study of elite athletes and return to play, 90% returned to prior intercollegiate sports following a single-level microdiskectomy, but none of the three athletes undergoing two-level diskectomies, nor the single athlete undergoing percutaneous diskectomy, returned to his or her sport.284

LUMBAR SPINAL STENOSIS Lumbar spinal stenosis, or neurogenic claudication, is broadly defined as narrowing of the central or foraminal canal through which the neurologic elements pass. The

Spinal Alignment Normal Spondylolisthesis Scoliosis Kyphosis Multidirectional malalignment

spinal nerve roots emerge from the spinal cord as the cauda equina and then course though the central spinal canal, exiting through the neural foramen bilaterally at each level of the lumbar spine. At each level of the spine, the nerve root passes below the pedicle of that same level; for example, the L5 nerve root passes below the L5 pedicle. The L1 nerve roots exit most proximally and the sacral nerve roots most distally. The spinal nerve roots may be crowded together centrally within the dural sac from extrinsic compression as the spinal canal concentrically narrows, or a single nerve root may be compressed individually as it exits the spinal canal. Central spinal stenosis is a global compression of the dural sac. One study comparing stenotic canals with normal canals found that the mean transverse area of the dural sac in the stenotic canals was 89.6 mm2 ± 35.1 mm2, compared with the normal canals, where the mean transverse area was 178 mm2 ± 50 mm2.285 This study concluded that constriction of the transverse area of the cauda equina to less than 75 mm2 will cause increased pressure within the nerve roots.285 A good correlation was found between reduced cross-sectional area and narrowed anteroposterior diameter of the dural sac.285 Structures contributing to neural compression included hypertrophic ligamentum flavum, disk protrusion, hypertrophic facet joints and laminae, and olisthesis. In acquired stenosis, the minimum cross-sectional area often occurs at the interfacet level.285 These age-related degenerative changes contribute to typical central lumbar spinal stenosis. At some point, the neural elements may become crowded together by the progressive degenerative process and may reach a critical level such that symptoms develop (Box 16B1-1).285 Lateral lumbar spinal canal stenosis may occur from neural compression at various anatomic zones.286,287 The lateral recess of the spinal canal has been divided into three zones based on the trajectory of the spinal nerve root: the entrance, the midzone, and the exit zone.286,287 Entrance zone lateral recess stenosis is located medial to the superior articular process of the facet joint where the nerve could be compressed between the anterior disk and the posterior facet joint.286,287 Midzone lateral recess stenosis occurs at the pars interarticularis and inferior to the pedicle. Exit zone lateral recess stenosis involves the intervertebral foramen. Although various studies have reported on the minimal cross-sectional area of the cauda equina required to produce

Spinal Injuries

symptoms of spinal stenosis, they are of little practical and clinical value and are not commonly used.288 Other studies have reported that no statistically significant correlation was found between the severity of symptoms of spinal stenosis and dural cross-sectional area.289 In general, imaging cannot differentiate symptomatic from asymptomatic individuals.290 It is therefore clear that imaging alone cannot predict symptomatic lumbar spinal stenosis. The underlying premorbid structure of the spine clearly plays a role in the potential for future development of symptoms. The presence of asymptomatic underlying congenital stenosis or structural abnormalities such as spondylolisthesis, scoliosis, kyphosis, or multidirectional malalignment can predispose to symptoms if normal agerelated changes, such as facet arthrosis, minor disk bulging, or herniation, occur. What role does spinal stenosis play in the athletic population? With people living longer and wanting to remain athletically active, clinical spinal stenosis will likely be encountered by many sports medicine physicians. In a review of a 5-year hospital admission cohort with a diagnosis of lumbar spinal stenosis, it was found that 9.8% were younger than 51 years old.291 The clinical onset of spinal stenosis is usually gradual but relentless as the critical space available for the neural elements is reduced. Sudden and dramatic nerve root symptoms may result from a long-standing severely obstructed spinal canal or from a sudden worsening of an underlying stenotic canal from a concomitant disk herniation. Most patients, however, describe a gradual and progressive increase in clinical symptoms, which can lead to a significant reduction in their activities in order to control their symptoms. A common complaint of golfers with symptomatic spinal stenosis, for example, is leg symptoms with walking, even if they use a riding cart. One study compared 100 patients with lumbar herniated disks, 100 patients with lateral recess stenosis, and 100 patients with central canal stenosis to determine symptoms and physical examination features of these disorders.292 The duration of symptoms before surgery and analgesic use was found to be significantly shorter in patients with disk herniations than in patients with stenosis. Tension signs (positive straight leg raising or femoral nerve stretch test) were more common with disk herniation than lateral stenosis and were uncommon with central stenosis.292 Because central spinal canal stenosis may occur at any intervertebral level, multiple nerve roots may be affected, and diffuse leg symptoms may be present unilaterally or bilaterally. Central spinal canal stenosis may produce only severe back pain and bilateral buttock pain without radicular leg symptoms, whereas foraminal stenosis typically produces radicular leg symptoms. Although spinal stenosis may produce the cauda equina syndrome, or progressive measurable neurologic deficits, it most commonly presents with few objective neurologic findings. Neurogenic claudication is characterized by buttocks pain or by leg pain, weakness, or numbness originating from spinal nerve compression elicited during standing or walking.293-295 The distribution of symptoms in the lower extremities may conform to sciatic or femoral nerve patterns or may simultaneously involve spinal nerve roots with both a sciatic and femoral nerve distribution. The

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TABLE 16B1-3 Vascular versus Neurogenic Claudication Evaluation

Vascular

Neurogenic

Walking distance Palliative factors Provocative factors Walking uphill Bicycle test Pulses Skin Weakness Back pain Back motion Pain character

Fixed Standing Walking Painful Positive (painful) Absent Loss of hair, shiny Rarely Occasionally Normal Cramping, distal to proximal Uncommon

Variable Sitting, bending Walking, standing Painless Negative (painless) Present Normal Occasionally Commonly Limited Numbness, aching, proximal to distal Occasionally

Atrophy

common presenting history is one of buttocks pain or leg pain, numbness, or weakness exacerbated by walking and standing and relieved by sitting or bending forward.293-295 The reason for this is that the spinal canal is narrower when standing and walking than when sitting. Patients with stenosis therefore characteristically assume a flexed or sitting posture to produce canal enlargement and relieve their leg or buttocks symptoms. Neurogenic claudication must be distinguished from vascular claudication, which has a different etiology and slightly different clinical features (Table 16B1-3).296 One distinguishing feature of vascular claudication is the production of leg symptoms while in a position of lumbar spine flexion, as in riding a bicycle.297 This position of flexion while riding a bicycle typically does not produce symptoms in a patient with spinal stenosis because sitting increases the size of the spinal canal and reduces spinal nerve compression.297 Some authors have used the combination of a treadmill test and a bicycle test to help distinguish vascular from neurogenic claudication.298 From a diagnostic perspective, normal arterial Doppler studies essentially rule out vascular claudication. There are few studies on the natural history of lumbar spinal stenosis. One study of 32 patients observed over a 4-year period found that 70% of the patients remained unchanged, 15% improved, and only 15% worsened.299 This study supports the concept that the surgical decisions are related to quality-of-life factors and not simply to the anatomic configuration of the spinal canal.299 In general, surgical treatment of spinal stenosis involves decompression of the stenotic segments (Fig. 16B1-32). Whether only symptomatic areas should be decompressed or all stenotic segments, both asymptomatic and symptomatic, should be decompressed is an area of controversy and beyond the scope of this discussion. Similarly, the decision of whether to perform a concomitant fusion with the surgical decompression is often controversial and not pertinent to this discussion. Early surgical intervention is mandated for stenotic patients with cauda equina syndrome or with progressive neurologic deficit. For most patients with spinal stenosis, however, the decision about surgery rests on the degree to which symptoms interfere with the patient’s quality of life.

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Figure 16B1-32 Middle-aged recreational walker with an iatrogenic spinal stenosis and associated spondylolisthesis treated with anterior-posterior fusion and decompression. Postoperatively, the patient walks 40 minutes 5 times per week.

Physical Examination Inspection of the lumbar spine may be normal or may demonstrate postural abnormalities such as loss of lumbar lordosis, forward posturing, scoliosis, or kyphosis. Range of motion of the lumbar spine may be restricted, and back or leg symptoms may be exacerbated by back extension. Tension signs, such as the straight leg raising test and the femoral nerve stretch test, are often negative. It is important to examine both hip joints for painful or restricted range of motion because of the potential of having concomitant hip disease with spinal stenosis. Neurologic examination of the lower extremities is usually normal or nonfocal. A rectal examination should be performed if there is any suspicion of cauda equina syndrome. Because lumbar spinal stenosis often coexists with cervical stenosis (tandem stenosis), an upper extremity neurologic examination should also be performed to look for evidence of long tract signs that might indicate the presence of cervical myelopathy.300,301

of activity, physical therapy, medication management, and spinal injections (epidural steroid injections or selective nerve root blocks).302,303

Surgery

The lumbar MRI is the standard initial diagnostic imaging test for suspected lumbar spinal stenosis. However, lumbar myelography with a postcontrast CT are also valuable for surgical planning and for identification of pathologic levels in patients with spinal stenosis. CT is commonly used for patients who cannot tolerate MRI, in patients with contraindications to MRI (e.g., presence of a cardiac pacemaker), in patients with spinal deformity, or in patients who have had prior spinal instrumentation in whom metal artifact might obscure visualization with MRI.

The goal of surgery is spinal nerve decompression and restoration of functional activity by reduction or resolution of the leg symptoms provoked by walking or standing. The surgical strategy for lumbar spinal stenosis involves neural decompression and possible correction of any associated deformity or instability by fusion (Fig. 16B1-33). Current surgical techniques include traditional decompression or less invasive surgery. The role of such minimally invasive surgery remains to be proved.304-306 Both traditional and minimally invasive decompression should be able to address the full spectrum of compressive pathology and preserve stability.307-328 Interspinous distraction devices have recently been approved for surgical treatment of spinal stenosis.329-332 The theory behind such devices is that they produce a focal kyphosis at the stenotic segment, thereby opening the spinal canal and producing relief of symptoms arising from that level. Although conceptually attractive, their intermediate and long-term outcome is unknown. It is unlikely, however, that they would play a significant role in the older athletic population. Finally, it is important to realize that stenosis is generally a condition of older age and is therefore often associated with other age-related comorbidities. Surgical outcome is heavily influenced by multiple factors, including the number and types of such comorbidities.333-345

Conservative Treatment

Congenital Spinal Stenosis

Assuming that there is no evidence of a cauda equina syndrome or a progressive neurologic deficit, most patients with symptomatic spinal stenosis undergo a course of conservative management. Because lumbar stenosis is generally slowly progressive, this nonoperative phase may continue for some time. Conservative treatments include restriction

Congenital lumbar spinal stenosis is a type of stenosis in which there is a congenital narrowing of the spinal canal.346 Under such circumstances, minimal additional age-related structural changes can produce significant incremental compression of neurologic structures within the spinal canal. Although typical acquired lumbar spinal

Diagnostic Imaging

Spinal Injuries

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Figure 16B1-33 Recreational golfer treated with laminectomy, facet fusion, and facet-pedicle vertebral fixation with 4.5 36-mm shaft screws for symptomatic lumbar spinal stenosis and associated degenerative lumbar spondylolisthesis.

stenosis is associated with an older population, congenital spinal stenosis is likely to be symptomatic much earlier in life and often manifests in the prime of athletic careers (Figs. 16B1-34 and 16B1-35). Congenitally short pedicles are a common recognizable radiographic feature of congenital spinal stenosis. One radiographic analysis of lumbar congenital spinal stenosis noted a significantly smaller cross-sectional area of the canal at all measured lumbar levels. Pedicles were markedly shorter in the congenital stenosis group at each lumbar level. In addition, anteroposterior canal diameter was significantly smaller than in control patients.347 The congenital spinal stenosis patient was found to be symptomatic at a younger age, with fewer degenerative changes and with multiple levels of involvement compared with degenerative spinal stenosis.347 Congential narrowing of the canal is a risk factor for additional pathology, such as a herniated disk, to become symptomatic.348 Congenital lumbar spinal stenosis is likely to be encountered in the younger athletic population.

Degenerative Lumbar Spondylolisthesis Degenerative spondylolisthesis, also known as spondylolisthesis with an intact neural arch, differs from isthmic spondylolisthesis in which there is a defect in the pars interarticularis (Table 16B1-4). Because of the intact neural arch, degenerative spondylolisthesis results in central canal narrowing as a result of the anterolisthesis of the affected vertebra. Isthmic spondylolisthesis does not result in central canal narrowing because the posterior elements remain in their normal position as the vertebral body slips forward. Vertebral translation in degenerative spondylolisthesis occurs as a result of both disk degeneration and facet arthrosis.349 Intersegmental instability results from inability of the lumbar facet joints to withstand shear forces, resulting in the slippage.350 The amount of forward slipping is typically 30% or less of the superior vertebra on the inferior vertebra.351 The most common location of degenerative spondylolisthesis is at L4-5, in contrast to isthmic spondylolisthesis, in which the L5-S1 level is most commonly involved.351

Figure 16B1-34 A 17-year-old football player with the sudden onset of progressive motor weakness in both lower extremities treated with lumbar decompression and diskectomy for symptomatic congenital lumbar spinal stenosis with a central disk herniation. He experienced a full neurologic recovery but decided not to return to football.

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Figure 16B1-35 A 26-year-old professional basketball player with congenital spinal stenosis and symptomatic lumbar disk herniation treated with a lumbar microdiskectomy. He returned to professional basketball during the same season as his surgery.

Degenerative spondylolisthesis is a condition of older age, rarely occurring before 40 years of age, in contrast to isthmic spondylolisthesis, which occurs in youth, generally around the age of 10 years. Its clinical presentation is usually that of typical lumbar spinal stenosis. Anatomically, both the central and lateral recess zones become stenotic, and the traversing nerve root is usually more commonly affected than the exiting nerve root. For example, a degenerative spondylolisthesis at the L4-L5 level would more commonly affect the traversing L5 nerve root than the exiting L4 nerve root. Therefore, lateral calf pain (L5 dermatomal distribution) is more commonly the presenting symptom than anterior thigh pain (L4 dermatomal distribution). The diagnosis of degenerative lumbar spondylolisthesis should be made from a standing lateral x-ray because supine views may not reveal a slippage.352 Some authors have noted that spinal motion may affect the sagittal alignment of spondylolisthesis, with flexion typically exacerbating the slip and extension often reducing it.353 Dynamic axial loading during MRI has been described and advocated to demonstrate whether the slip is dynamic and changes with positioning.354,355 The initial treatment of degenerative spondylolisthesis is conservative and is the same as with typical lumbar spinal stenosis without spondylolisthesis. A recent study showed

TABLE 16B1-4 Degenerative versus Isthmic Spondylolisthesis

Age of onset Level Pars interarticularis Central canal Foraminal canal Degree of slip

Degenerative Spondylolisthesis

Isthmic Spondylolisthesis

Older than 40 yr Any level; most commonly at L4-5 Intact Narrowed Narrowed Less than 30% of inferior vertebral body

About 10 yr Any level; most commonly L5-S1 Lysis Patent Narrowed No limit

surgery was superior to conservative care in both pain and function in symptomatic degenerative spondylolisthesis and spinal stenosis.356 The most commonly performed surgical procedure for lumbar degenerative spondylolisthesis is fusion with or without instrumentation, although there may be some select instances in which decompression without fusion is performed.349,357-361 A recent analysis of hospital data showed that decompression with fusion was less likely to require additional surgery compared with decompression alone.361 In addition, the presence of a solid fusion was associated with a better long-term outcome than if a pseudarthrosis was present.360

Isthmic Spondylolisthesis Isthmic spondylolisthesis and spondylolysis result from a stress fracture of the pars interarticularis. There are some anatomic variants, which include an acute fracture involving the pars and fractures of either the pedicle, facet, or lamina.362 Fracture of the pars without an associated slip (anterolisthesis) is termed spondylolysis. Spondylolisthesis refers to the presence of an associated anterior subluxation of the involved vertebra on the subjacent vertebra.363 It is classified (graded) by the degree of anterior displacement of the upper vertebra on the lower vertebra (Fig. 16B1-36). Other radiographic parameters have been described but are of limited clinical value.364-367 Stress fractures of the pars commonly occur during the childhood and adolescent growth period when the spine is exposed to repetitive stresses. Spondylolysis is thought to represent a fatigue fracture, usually as a result of repetitive mechanical stresses, or occasionally as a result of a single load of sufficient force to cause failure.362 Single-photon emission computed tomography (SPECT) or MRI may detect the stress reaction in bone consistent with a potentially evolving stress fracture (Fig. 16B1-37). The morphology of the pars fracture can be seen best by computed tomography (CT). Pars defects may be either unilateral or bilateral, and at a single vertebral level or at multiple levels, although most commonly at L5-S1. In

Spinal Injuries

Figure 16B1-36 Classification of spondylolisthesis: grade I, 0% to 25% slip; grade II, 25% to 50% slip; grade III, 50% to 75% slip; grade IV, 75% to 100% slip; grade V, spondyloptosis (complete displacement of upper vertebra in front of lower vertebra). (From Wiltse LL, Winter RB: Terminology and measurement of spondylolisthesis. Clin Orthop 117:23-29, 1976.)

some patients with a unilateral stress fracture, the contralateral pars or pedicle may show a stress reaction which can be detected on either SPECT or MRI. Most low-grade (grade I or II) isthmic spondylolistheses do not progress after the age of 18 years.368 Progressive

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slipping may occur in adults as a result of associated degenerative changes in the disk at the slip level.369 The degree of forward slipping does not necessarily correlate with the amount of pain. For example, a highgrade slip may be asymptomatic, whereas a low-grade slip may be symptomatic. Isthmic spondylolisthesis may vary in presentation and clinical effect. Clinical symptoms include back pain, leg pain, leg numbness, or leg weakness. In the teenage years, back pain and hamstring spasm may dominate the clinical picture, with the back pain exacerbated with activity. In middle age, with the onset of degenerative disk space narrowing, the clinical symptoms may suggest stenosis, with leg pain predominating and worsened by walking and standing. This is due to compression of the exiting nerve root by a combination of foraminal narrowing produced by collapse of the disk and involvement of the nerve from the overlying fibrocartilaginous pars defect. Most adolescents with acute spondylolysis can be successfully managed by conservative measures, such as activity restriction, bracing, and lumbar trunk strengthening. Most are capable of eventually returning to their particular sport. Patients with chronic spondylotic defects and low-grade spondylolisthesis can usually be managed with a conservative care regimen also. Injection of the pars under fluoroscopic guidance can indicate whether the pars is the source of the patient’s back pain. Some authors have advocated pars defect repair in patients with minimal or no slip and a normal disk by MRI, but the mainstay of surgical treatment is fusion of the affected segment. As individuals age, degeneration within the affected disk can lead to low back pain and leg pain.370 Under these circumstances, surgical intervention may be warranted and may include a variety of decompressive and fusion options. The symptoms of acute spondylolysis may resolve, and patients may return to their sport when they are symptom free and can handle increasing spinal loads and the demands of their particular sport. Treatment usually entails a progressive program that begins with achieving

Figure 16B1-37 Single-photon emission computed tomography (SPECT) imaging with increased tracer uptake and matching magnetic resonance imaging with edema in pars area.

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Figure 16B1-38 Middle-aged marathon runner who returned to sport after an anterior-posterior fusion for adult isthmic spondylolisthesis.

pain-free motion. This is followed by attaining the ability to perform their usual daily activities, followed by the ability to run and to strengthen supporting musculature, ultimately progressing to sport-specific drills. Return to play with isthmic spondylolisthesis is often correlated with the grade and progression of the slip. Patients with nonprogressive low-grade spondylolisthesis may return to play after progressive and pain-free reintroduction of loads of daily activities, trunk strengthening, and specific sports drills. Patients with high-grade slips are more problematic and require more individualized decision making. The outcome following conservative and surgical treatment of adult isthmic spondylolisthesis has been examined. Some studies have demonstrated improved function and more pain relief with surgery than with exercise.371 A randomized, controlled, 9-year follow-up study comparing a conservatively treated group of patients undergoing physical therapy with a surgical group undergoing posterolateral fusion, either with or without instrumentation, showed that patients who underwent fusion reported better outcome than conservatively treated patients.372 The authors thought that the long-term outcome of conservatively treated patients likely reflected the natural course of the condition and that no significant long-term improvement should be expected in adult patients with symptomatic isthmic spondylolisthesis. It was thought that most patients would continue to have substantial pain, functional disability, and a reduced quality of life over many years.372 In another study, the preoperative and postoperative SF-36 (Short Form-36) scores of adult patients with isthmic spondylolisthesis were compared.373 Significant improvement in six of eight scores was noted, and 55% of scores were within the normal range.373 The best operation among different surgical strategies for adult isthmic spondylolisthesis remains unclear. In adult patients with unstable low-grade isthmic spondylolisthesis,

posterior instrumented fusion was compared with combined anterior-posterior fusion.374 The 2-year outcomes following combined anterior-posterior surgery were statistically superior to posterior fusion for unstable spondylolisthesis, although the differences between the two groups lessened after 6 months. The benefits of combined fusion must be balanced against the morbidity and costs associated with the additional surgery.374 Other authors also believe that combined anteriorposterior fusion procedures might be preferred for adult isthmic spondylolisthesis (Fig. 16B1-38), although the literature does not provide a definitive answer.375 A review of the literature on fusion for low-grade adult isthmic spondylolisthesis was unable to determine the best surgical technique for fusion (posterior lumbar fusion, posterior lumbar interbody fusion, anterior lumbar interbody fusion, use of instrumentation or not). The outcomes of fusion are generally good, but reports vary widely.376 Instrumentation is thought to play a beneficial role in achieving reduction and fusion for low-grade isthmic spondylolisthesis, although this perception has yet to be conclusively proved. For the sports medicine physician, an asymptomatic adolescent with isthmic spondylolisthesis may develop symptoms in middle age with age-related degeneration of the spondylolisthetic segment. Conservative treatment remains the first line of treatment, but surgery often achieves an excellent outcome with return to active sports participation.

RETURN-TO-PLAY DECISIONS One area of controversy for the sports medicine specialist and spine subspecialist is the decision about return to play after thoracolumbar spine injury. Often, philosophy more than science dictates the decision about return to play because there are no prospective, randomized, double-blind studies on which to base many of the

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Figure 16B1-39 A 38-year-old professional radio host and high-level recreational hockey player with successful index lumbar microdiskectomy and two repeat additional microdiskectomies for recurrent lumbar disk herniation. After surgery, the patient is pain free, and neurologically intact. Whether the patient returned to contact sports is unknown.

decisions. Therefore, the nature of the injury, the clinical signs and symptoms, and the type of treatment are key ingredients in the decision-making process.377 It might be assumed that decisions regarding return to play after cervical spine injuries would generate consensus of opinion. A 2001 survey of spine surgeons, however, demonstrated lack of consensus in the ability and level of return to play based on clinical scenarios of 10 cervical spine–injured patients.378 There was wide variability in the recommendations made for return to play. Spine subspecialists tended to recommend return to play at a higher impact level of play than sports medicine subspecialists. Clinicians who had been in practice longer selected a return to play at a lower impact level than clinicians who were more recently in practice. Categorization may help conceptualize sports in terms of potential risk categories, but there is no prospective study using these categories for determining return to play. Risk categorization is therefore a balance between the potential for recurrence of symptoms and the potential for catastrophic injury. Therefore, even in the analysis of risk categories of the cervical spine, there is more assumption than science, and no concrete data exist to help the clinician with many decisions. Most opinions regarding return to play are based on certain common features: being asymptomatic or having minimal symptoms, having normal or near-normal active range of motion, and achieving functional restoration of strength and endurance.377-381 If these are achieved, the athlete may progress to sport-specific drills and conditioning and ultimately to full competitive play. There will always, however, be assumptions about the potential for

recurrent injury based on the nature of the sport and the position the athlete plays. Repeat surgery at the same level of the spinal region may influence the decision to return an athlete to full performance.379 Some authors believe that repeat or additional surgery in the same spinal region is a contraindication for return to contact sports (Fig. 16B1-39).379 Reasons for this include potential instability produced by multiple procedures at the same level. Regional anatomic considerations play a role in making return-to-play decisions. Despite little surplus space surrounding the spinal canal in the thoracic spine, the relative immobility of the thoracic spine provides stability. The bony elements of the rib cage, together with the paraspinal musculature and sternum, increase thoracic stability by 20% to 40%.379,382 Three zones of the thoracic spine have been described: a midzone, proximal, and distal junctional zone.379 The bony structures change when transitioning from the cervical spine to the thoracic spine. In addition, the facet orientation changes from coronal in the upper thoracic spine to sagittal in the lower thoracic spine. Furthermore, the size of the thoracic vertebral bodies increases from proximal to distal in the thoracic spine.379 The cervicothoracic and thoracolumbar junctions are areas of potential instability and risk for injury because of the transition from a fixed segmental structure in the mid-thoracic spine to the more mobile cervical and lumbar spine. There is debate about whether spinal instrumentation should stop at the cervicothoracic junction or should continue to the more stable thoracic spine. One recommendation is that athletes be restricted from contact play if they undergo an instrumented fusion that crosses the cervicothoracic or

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thoracolumbar junction, or if a fusion terminates at either junctional transition area.379 This restriction did not apply to athletes fully recovered from thoracic decompression and fusion that did not involve the transitional zones, assuming that they fulfilled all other criteria for return to play.379 There are two common lumbar conditions that frequently affect athletes: lumbar disk herniation and lumbar spondylolisthesis. Successful conservative or surgical treatment of lumbar disk herniation is not a contraindication to return to full contact sports as long as all other criteria for return to play are met. Return to play following surgery for the athlete with spondylolysis or spondylolisthesis is less clear. Return to play following posterolateral fusion, with or without instrumentation or direct repair of the pars interarticularis, is permitted provided that the athlete is pain free and neurologically intact and that the spine is structurally sound.379 Because the spinal cord typically terminates at the L1-2 level, only spinal nerves pass through the lumbar canal, and nerve root compression is much better tolerated than spinal cord compression. Because of the capacious nature of the lumbar canal relative to the size of the neural elements, the lumbar spine has a degree of tolerance to stenosis not present in any other region of the spine. In the lumbar spine, therefore, more anatomic narrowing and compression are needed to produce neurologic deficits than in other regions.379 Recommendations for return to contact sports after spinal surgery have been summarized by Burnett and Sonntag (Table 16B1-5).379 A survey of surgeons found significant variations in surgeon opinion regarding the timing and level of return to sports in children and adolescents after spine surgery.381 Patients treated surgically for scoliosis and low-grade spondylolisthesis (Meyerding grade I and II) were generally allowed to resume low-impact noncontact sports and return to gym class by about 6 months after surgery. For higher-grade spondylolisthesis (grades III and IV), many surgeons withheld noncontact sports for slightly longer, and most surgeons recommended restricting contact sports for a full year. Most surgeons recommended that patients undergoing fusion for scoliosis and high-grade spondylolisthesis never return to collision sports. Return to play after nonoperative and operative treatment for thoracic and lumbar spine injuries revealed a wide range of expert opinion.

CONCLUSION Reconsider then who we, as physicians, do see in the bend of time. Will she be 14 years old, suspended in the rings above the floor mat, each bodily gyration, each release and catch the animation of physical grace—acute spondylolysis? Will he pose before the last hole, straddling his tee shot, knowing full well his best hole is the 19th, and strike with all the twisting force that his middle-aged trunk can consider, the longest distance of the weekend—lumbar anular tear? At 90, will she walk at dawn, chasing the last wisp of darkness, arms pumping, feet striking asphalt, her spine battling load and gravity—thoracic compression fracture? Will he crash into the last defender with will and force, tumbling the last few feet into the end zone—lumbar transverse process fracture? Will her head be down, her upper back cringing,

Table 16B1-5 Recommendations for Return to Contact Sports after Spinal Surgery*

Op Location/Procedure Cervical Occiput–C2 region Subaxial region Posterior foraminotomy single-level multilevel laminectomy (with or without fusion)/laminoplasty single level 2 level >2 level Anterior diskectomy fusion/arthroplasty single level 2 level >2 level foraminotomy single level multilevel corpectomy single level multilevel Thoracic Cervicothoracic junction zone Midthoracic with deformity without deformity �� Thoracolumbar junction zone Lumbar diskectomy/laminectomy/laminoplasty single level multilevel anterior or posterior fusion/arthoplasty single level multilevel

Return to Contact Sports No

Yes Yes Yes Yes No

Yes Yes Yes No No Yes Yes No Yes Yes Yes Yes

*To be considered eligible for a full return to activity, patients must be pain free, neurologically intact, and have completed an uneventful rehabilitative course. From Burnett MG, Sonntag VKH: Return to contact sports after spinal surgery. Neurosurg Focus 21 (4): E5, 2006.

her arms exhausted as she rolls her chair toward the finish line—thoracic muscle strain? Will he clutch the undersurface of his board, spinning away from the upper edge of the half pipe, with earth and ice waiting his return—lumbar burst fracture—on impact? Will she glide past them, as they reach for her, ascending in a single mellifluous leap towards the rim—asymptomatic thoracic scoliosis? Will he hear nature’s footsteps in the rising sea, leap freely from his prone position, and tightrope top and bottom turns before the impact zone—congenital lumbar stenosis with sudden back pain? Will she see yet another batter in the endless weekend of games, winding once again and curling spin and speed with bodily deception—lumbar muscle sprain? Will he soar like a swan in flight from water, his kite 100 feet above, his body engaged in twist and twirls before inevitable return to the ocean’s side—lumbar strain with radiographic evidence of Scheuermann’s disease? Will she plant her pole in the steep slope in the outback and wipe the sweat from her eyes of her weekend tour—structural but asymptomatic lumbar spinal stenosis? Will his racquet reach the apex of his toss, slicing

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the soft round ball in chosen direction—acute lumbar herniated disk? Will she look on the course of trees and feel the blur of nature with each heartbeat as she runs—sacral stress fracture? Will the world seem tame to his address, the bat that once was on his shoulder, the ball lost beyond the fence—adult isthmic spondylolisthesis? Will she pirouette and point and unfurl her arms to sounds she cannot hear— grade II asymptomatic isthmic spondylolisthesis? At dusk, will he gather himself for a final water start onto his board, his sail arced forward to catch the wind, slipping silently across the water at nature’s speed—lumbar degenerative disk disease? He or she will be one of us.

C l Thoracic

r i t i c a l

P

o i n t s

and lumbar fractures should be evaluated for spinal stability, neurologic status, and associated injury. Spinal stability and neurologic status govern nonoperative and operative treatment choices. The three-column theory of spinal stability by Denis is often used to assess stability. Minor fractures involve the spinous process, transverse process, pars interarticularis, and facet joints. Major fractures involve compression fractures, burst fractures, fracture-dislocations, and flexion-distraction injuries. Immobilization before movement of the injured athlete should be performed if there is any question regarding spinal stability or neurologic involvement. Sacral stress fracture may be due to overuse with repetitive microtrauma, a fatigue fracture, inadequate bone mass, or an insufficiency fracture. Imaging is likely to make the diagnosis: pelvis MRI, SPECT scan, or bone scan. l Scoliosis is a coronal plane deformity, and kyphosis is a sagittal plane deformity. Most athletes with scoliosis have congenital or idiopathic types. Most athletes with kyphosis have congenital, postural, or Scheuermann’s types. Spinal deformity can be measured on full spine, standing anteroposterior, and lateral x-rays. Most athletes with spinal deformity are diagnosed because of other clinical events and not sports injuries. Most athletes with spinal deformity treated conservatively can participate in sports within the context of the conservative treatment. Most athletes with spinal deformity that is surgically treated will not be precluded from noncontact sports. l Thoracic disk herniations may present with unilateral chest wall or abdominal pain. Central thoracic disk herniations may compress the spinal cord, causing long tract symptoms and clinical findings: weakness and numbness in the legs and bowel and bladder dysfunction. Surgery is indicated for neurologic findings. Anterior transthoracic surgery provides access to the spinal canal for spinal cord decompression and thoracic diskectomy and interspace fusion. Alternative posterior approaches are the costotransversectomy and transpedicular approaches to canal decompression and diskectomy, but these have certain anatomic and technical limitations. l Thoracic spinal stenosis may occur as the result of degenerative changes narrowing the spinal canal. Congenital narrowing with superimposed degenerative changes may

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lead to earlier presentation of symptoms. Thoracic-level spinal cord compression may be expressed clinically as a range from a subtle myelopathic gait disorder on one extreme to paralysis on the other. Surgical intervention should be directed by an approach that addresses the most compressed aspect of the spinal cord. l Imaging evidence of degenerative disk disease is common in athletes but is not necessarily related to symptoms. The natural history of degenerative disk disease and the symptom of low back pain have a relatively benign course. Invasive diagnostic testing in the lumbar spine would ideally be reserved for anticipated probable change in treatment based on the clinical condition of the patient and the likelihood of finding the pain generator. Low back pain in athletes associated with degenerative disk disease is usually treated conservatively. Eighty percent of lumbar herniated disks resolve within 3 months. Imaging must correlate with clinical findings (look at the patient and then the MRI scan). Loss of bowel or bladder function or progressive motor deficit is a surgical condition. Static neurological deficit and leg pain are not mandatory surgical conditions (requires judgment and evaluation of clinical effect and clinical course). The final common denominator of surgical value is spinal nerve decompression and not the title of the operation. l Spinal stenosis is a structural definition. The clinical expression of spinal stenosis involves back pain, leg pain, leg numbness, or leg weakness associated with walking or standing. Neurogenic claudication is the term used for dynamic leg symptoms associated with structural lumbar spinal stenosis. Stenotic patients usually experience worsening symptoms when their lumbar spine is extended and improvement when their lumbar spine is in flexion. l Isthmic spondylolisthesis is defined as a forward slippage of the cephalad vertebra on the caudad vertebra due to defects in the pars interarticularis. Isthmic spondylolisthesis can be graded based on the degree of slipping of the cephalad vertebra on the caudad vertebra. Most people with spondylolysis and low-grade spondylolisthesis respond to conservative treatment and successfully return to their particular sport. Occasional adolescent and young adult patients with isthmic spondylolisthesis will evolve into candidates for pars repair or segmental lumbar fusion. Older adults with isthmic spondylolisthesis may become symptomatic with superimposed degenerative changes in the affected motion segment. Some symptomatic adults with isthmic spondylolisthesis respond to surgical intervention involving decompression and fusion.

R E F E R E N C E S Please see www.expertconsult.com

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Thoracolumbar Injuries 2. Thoracolumbar Spine Injuries in the Child William C. Lauerman and John A. Zavala

Injuries to the thoracolumbar spine and associated back pain represent a relatively small proportion of sports injuries. About 10% of all sports injuries involve the spine, with certain sports (e.g., gymnastics, football, rowing) representing greater risks, particularly to the low back.1 In our experience, it is not uncommon to see skeletally immature athletes presenting with back pain; indeed, among the children and adolescents in our practice, thoracolumbar spine injuries likely represent 20% to 25% of sports injuries with pain persisting for greater than 1 month. When considering the pediatric athlete with back pain, it is helpful to be familiar with the prevalence of back pain in a general population of children and adolescents. Although the prevalence of low back pain in children younger than the age of 10 years has been reported to be as low as 1% to 3%, it increases in teenagers, varying among different researchers but reported to be as high as 20% to 25%.2 Relatively few children or adolescents present for treatment. When involved in organized sports requiring daily training and regular competition, however, the athlete with a complaint of persistent back pain will often visit the trainer or the physician. These complaints may stem from either isolated or repetitive trauma; in many cases, they may not be related to sports participation at all. It is essential, however, to address the athletic component of the pain complaint simultaneously, including timely return to participation, while bearing in mind the prevalence, the differential diagnosis, and the expected response to treatment of pediatric back pain in general. Appropriate management of the skeletally immature athlete with a back injury or persistent back pain often requires persistence, diplomacy, and luck. Increasingly, young children are participating in organized sports with schedules for training and competition and training techniques that may not match the physiology of the growing skeleton. In addition, attention to appropriate training and stretching regimens, including stretching of the neck and the low back, may be lacking; this is particularly true in elementary school children. Other factors to be considered when evaluating the underage athlete with persistent back pain are the desires and the motivation of the athlete. Although most athletes at all levels enjoy their chosen sport, we occasionally see grade school and, in particular, high school athletes with persistent complaints of back pain who subconsciously or consciously seem to be signaling a desire to gracefully avoid that sport and move on to a different activity. Sometimes

a limited desire of the child or adolescent to participate in sports does not match the enthusiasm of the parents to have the child play. Back pain can provide an acceptable exit strategy for the child to deal with what may represent unrealistic expectations on the part of the parent. Pain can be a mechanism for the child to cope with parental stresses. Factoring this into the management of the pediatric athlete with back pain is important but requires finesse, and suspected lack of enthusiasm should never represent a reason not to evaluate a complaint of pain.3 Finally, the reaction of the parents to what is all too often a protracted course of low back pain with attendant activity restrictions may add to the clinician’s challenge. Many parents find it unfathomable that a child can have back pain, let alone pain that eludes diagnosis and treatment. Reassuring the family of the relatively common nature of the problem being addressed is frequently quite helpful.

RELEVANT ANATOMY AND BIOMECHANICS The thoracolumbar spine comprises most of the vertebral column and contrasts the relatively rigid thoracic spine with the increased mobility of the lumbar spine. The thoracic spine receives its inherent stability from the thoracic rib cage. The erector spinae muscles function bilaterally to produce back extension and unilaterally to produce lateral bending. Deep to the erector spinae is the transversospinal musculature, which contributes to extension, lateral bending, and rotation of the vertebral column. Muscular strains involving the erector spinae and transversospinalis muscles are common in the athletic population. Important ligamentous structures include the anterior and posterior longitudinal ligaments, interspinous ligaments, and the supraspinous ligaments. The lumbosacral articulation has been demonstrated to be exposed to the highest forces in the thoracolumbar spine. The oblique inclination of the sacrum subjects the neural arch to both anterior compressive and shear forces. The erector spinae also place increased stress on the neural arch in the erect stance. There are a number of factors predisposing to back injuries and back pain in the growing child and adolescent, including the presence of a skeletally immature spine composed of the disk–vertebral body complex, the ligaments, and the musculotendinous unit. The adolescent growth

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spurt places the soft tissue structures of the spine at particular risk, because of a difference in maturation between the osseous components of the spine and the soft tissue structures. Full maturation of the bony pars interarticularis does not occur until early in the third decade. Tight lumbodorsal fascia and hamstring muscles may impose increased stress on the spine, thereby predisposing to back pain. The disk–vertebral body complex is also unique in the growing child. Before skeletal maturity, the cartilaginous and bony end plates are densely adherent to one another, but the ring apophysis, which extends peripherally along the margins of the vertebral body and is intimately adherent to the anulus, is at risk for injury.4 Such injuries to the ring apophysis can present clinically and radiographically as pediatric disk herniations.

CLASSIFICATION Thoracolumbar spine injuries in pediatric athletes can be broken down into two broad categories: those related to acute trauma and those involving chronic pain, possibly owing to chronic repetitive trauma (Table 16B2-1). Athletes with a history of acute trauma often describe a fairly significant and acute history of back pain. This may include either a significant traumatic event, or a relatively minor event that unmasks an underlying minor pain and brings these symptoms to clinical attention. In attempting to sort out the potential diagnoses, it is helpful to determine whether the athlete was truly asymptomatic before the significant symptoms began and whether a significant trauma occurred at the time of the onset of symptoms. Several manifestations of acute trauma may be seen. Fracture or dislocation of the anterior column of the thoracolumbar spine is unusual. When it occurs, the usual mechanism is an axial load, typically with the patient describing a fall on the buttocks either from a height or at a relatively rapid speed (Fig. 16B2-1). More commonly the injury is a relatively benign compression fracture, often occurring in the lower thoracic spine or at the thoracolumbar junction. Some compression fractures at the thoracolumbar junction are not easily seen on plain radiographs. When significant pain or tenderness is present at this location, plain radiographs of the thoracolumbar junction must

Table 16B2-1 Injury Classification of Thoracolumbar Injuries Acute Fracture-dislocation

Chronic

Isthmic spondylolysis and spondylolisthesis (type IIA and IIB) Acute pars fracture (type IIC) Lumbar disc injury, diskogenic pain Disk herniation Apophyseal injury Disk degeneration Acute traumatic disk herniation Overuse syndrome Infection Spinal deformity Spinal tumor Infection

Figure 16B2-1 A 14-year-old boy was thrown from his bike during a competition, landed on his head and neck, and experienced the sudden onset of mid-thoracic pain. He was neurologically normal. Plain lateral radiography demonstrated mild wedging at T6 and T8 and a more significant wedge compression fracture of T7 (arrowheads). The absence of endplate irregularity or Schmorl’s node formation differentiates this from Scheuermann’s kyphosis, which would also involve multilevel wedging.

be carefully scrutinized. If radiographss are inconclusive or if a neurologic deficit is present, even if transiently, computed tomography (CT) or magnetic resonance imaging (MRI) should be performed. Acute traumatic fractures of the pars interarticularis have been reported but are exceedingly rare.5 The acuity of the pars fracture itself can be difficult to determine based merely on the presence of sudden onset of back pain. It can also be difficult to radiographically distinguish an acute fracture of the pars from a subacute or chronic fracture. Initial evaluation consists of plain lateral radiographs and, when in doubt, should include oblique radiographs and single-photon emission computed tomography (SPECT). CT is also useful in defining the defect at the pars interarticularis,6 although it can still be difficult to be certain that the radiographic abnormality is truly acute. MRI is the best study to diagnose an acute pars fracture by marrow changes at the pars. Most patients who have back pain and are found to have a pars fracture have had a preexisting spondylolysis rather than an acute fracture. Appropriate counseling regarding the goals of treatment is essential in this setting. Disk injuries may also occur as a result of acute trauma, although at least 50% of symptomatic disk herniations in both adults and adolescents present with the insidious onset of back pain or leg pain, or both.7-9 In contrast to adult patients with a symptomatic disk herniation, disk

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herniation in the pediatric athlete may or may not involve radiculopathy. Back pain is the most common complaint in the child or adolescent with disk herniation, with less than half of all patients initially describing radicular symptoms. It is relatively rare to see a functionally significant, or worsening, neurologic deficit, but the presence of subtle neurologic abnormalities should be determined. The possibility of cauda equina syndrome, including urinary retention, should also be borne in mind. A positive tension sign (straight leg raising test or bowstring sign) is present in almost all pediatric patients with a clinically significant disk herniation. Chronic back pain in a pediatric athlete should, for the most part, be approached as one would approach back pain in the pediatric population at large. The differential diagnosis is varied, but in the athlete, the symptoms are much more likely to be due to repetitive trauma or an overuse syndrome. Although the diagnosis of an overuse syndrome may be considered initially, other diagnoses should be considered in those patients who fail to respond to treatment. Spondylolysis and associated spondylolisthesis are common causes of low back pain, particularly in children younger than 10 years and in adolescents.10 Occult spondylolysis is the most common provisional diagnosis in adolescents referred to us with recalcitrant back pain. It is noteworthy that this diagnosis is frequently found to be erroneous in the adolescent population. It is also worth noting that spondylolysis is present in 5% to 6% of the normal population at skeletal maturity and is frequently asymptomatic. Fredrickson and colleagues noted spondylolisthesis in 75% of a group of school-aged children with spondylolysis.11 Spondylolysis is more common in males and in certain ethnic groups, such as Aleutian Eskimos.12 Ninety percent or more of the defects are found at L5, and although they are virtually never present in newborns, 75% of pars defects occur—and can be radiographically documented—by age 6 years.11 The remaining 25%, occurring in later childhood and adolescence, likely account for the well-known association between spondylolisthesis and certain high-risk sports such as gymnastics, football (especially in interior linemen), and weightlifting.13,14 It has been demonstrated that football players with spondylolysis have a higher incidence of back pain than those with disk abnormalities and spinal instability.15 The acute onset of back pain, therefore, even in the presence of a defect in the pars interarticularis, cannot always be assumed to be caused by this defect (Fig. 16B2-2). Spondylolisthesis has been classified based upon the cause of the slippage (Box 16B2-1).16,17 The most common form of spondylolisthesis in all age groups is type II (isthmic), and this is the most prevalent by far in the pediatric population. Isthmic spondylolisthesis involves a defect in the pars interarticularis. The possible types of disorder of the pars include fatigue fracture of the pars (type IIA), elongation of the pars (type IIB), and acute fracture of the pars (type IIC). The concept of fatigue fracture of the pars interarticularis as the underlying disorder in spondylolysis was first popularized by Wiltse.17,18 It is believed that in certain individuals, the pars is susceptible to repetitive hyperextension stresses and that there is therefore a hereditary predisposition to this susceptibility. Elongation of the pars interarticularis (type IIB) may be seen without frank

Figure 16B2-2 A 16-year-old football player was struck in the back during a game and suffered acute onset of low back pain. Plain lateral radiography demonstrates isthmic spondylolisthesis at L5-S1. By the time of his orthopaedic evaluation, he was asymptomatic, and he has been symptom free for more than 2 years.

fracture and may permit the development of anterolisthesis. Acute traumatic fracture of the pars (type IV), although rare, may also be seen.5 Diskogenic back pain can be seen infrequently in the pediatric athlete. The patient typically presents with a chronic history of nonspecific back pain, which occasionally radiates into the buttocks and the thighs. The potential causes of such pain include disk herniation, apophyseal injury, and disk degeneration. The latter includes socalled juvenile diskogenic disease, which appears on MRI as decreased water content on T2-weighted imaging, Schmorl’s nodes, and end-plate irregularities. This can be

Box 16B2-1 Classification of Spondylolysis Wiltse-Newman I. Dysplastic II. Isthmic A. Lytic-fatigue fracture of pars B. Elongated pars C. Acute pars fracture III. Degenerative IV. Traumatic V. Pathologic From Wiltse LL, Newman PH, Macnab I: Classification of spondylolysis and spondylolisthesis. Clin Orthop 117:23-29, 1976.

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seen in either the thoracolumbar or lumbar spine with vertebral body flattening or wedging. In the lumbar spine, this condition has been referred to as lumbar Scheuermann’s disease.19 This condition is commonly seen in association with back pain in young adults and is occasionally seen in the pediatric athlete. Chronic overuse syndrome is common in the adolescent athlete with persistent low back pain. This should, however, be a diagnosis of exclusion, and a thorough radiographic work-up should be performed before making this diagnosis. Axial low back pain is the typical complaint, with minimal radiation into the buttocks, the thighs, or the legs. Relief with rest or activity restrictions is typical. Most pediatric athletes have back injuries or back pain that falls into one of the above categories. The remaining few can have back pain from less common conditions in the pediatric population, such as spinal deformities. Adolescent idiopathic scoliosis, although not typically painful, can be associated with mild to moderate pain (Fig. 16B2-3). This condition should only rarely require activity limitation, and the athlete who voluntarily restricts sports participation should be thoroughly evaluated for other causes of pain. Causes of painful scoliosis include tumors such as osteoid osteoma or osteoblastoma as well as intraspinal lesions. Hyperkyphosis is another cause of back pain in the adolescent, and pain is a relatively common presenting complaint of juvenile patients with Scheuermann’s kyphosis.

Figure 16B2-3 A 14-year-old swimmer had a 6-month history of mild low back pain that did not interfere with her participation in sports. Physical examination suggested scoliosis, which was confirmed on this plain anteroposterior radiograph. Her pain improved with a stretching and strengthening regimen, and the scoliosis, which progressed, was treated with nighttime bracing.

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A number of tumors of the spine, although all quite rare, may present with back pain in the child or the adolescent. These include lesions of the posterior elements, such as osteoid osteoma or osteoblastoma; lesions of the anterior column, including eosinophilic granuloma, lymphoma, or primary malignancy such as Ewing’s sarcoma; and lesions of the spinal cord or cauda equina, such as ependymoma, astrocytoma, or neuroblastoma (Fig. 16B2-4). The presence of severe pain, pain at rest, and neurologic findings should trigger a more aggressive diagnostic work-up. Infectious conditions of the spine, such as disk space infection and vertebral body osteomyelitis, can occur in the pediatric population, particularly in younger children, in whom the mean age at presentation is 6 to 7 years. A history of constitutional symptoms such as fever, chills, or weight loss is common, and a history of a recent infection, such as an upper respiratory or skin infection, is frequent. The presence of pain at rest is also relatively common. Finally, metabolic abnormalities, generalized systemic malignancies such as leukemia or lymphoma, and visceral disorders should be considered.

EVALUATION Clinical Presentation and History Taking a thorough history is the key to the diagnosis and management of the pediatric athlete with back pain. The diagnostic and therapeutic goal, which should be clearly expressed to the patient and the parents, is return to full activity with minimal or no symptoms. Often, a concise diagnosis cannot be made, and overemphasis on obtaining a concrete diagnosis can lead to frustration, unnecessary imaging studies, and needless limitation of activity. History taking begins with inquiry about possible trauma. Although it is helpful to try to identify a traumatic episode, in our experience, this is uncommon. The patient should be asked about the onset of pain, whether it is acute or insidious, and whether there was any preexisting pain before the event or the day in which it was noticed. Frequently, a relatively long history of gradually worsening pain, culminating in a single day or event when the pain was noticed, can be elicited. When a traumatic episode can be identified, it is important to inquire about the presence of any transient neurologic signs or symptoms at the time of onset (e.g., inability to move an extremity, extremity or whole-body numbness, or loss of bowel or bladder function). Although these are extremely rare with sports injuries to the thoracolumbar spine, their occurrence, if present, should be elicited. Many pain complaints are chronic and of insidious onset. A helpful mnemonic to aid in the history is CLEAR: C represents the character of the pain complaint (e.g., burning, stabbing). L represents the location of the pain. Clinical terms such as back, buttocks, hips, or spine frequently mean different things to different people, and it is essential to have the patient accurately define where he or she experiences the pain. This can be difficult, particularly with younger children, but is essential in the evaluation of any persistent complaint. E represents exacerbation: What makes the pain worse? This is usually activity, but certain

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B

A Figure 16B2-4 A 14-year-old girl who presented after injuring her back playing soccer complained of diffuse back pain and tingling in her feet. A, On plain anteroposterior radiography, there is collapse of T10, irregularity of both pedicles, and a prominent soft tissue mass. B, Sagittal magnetic resonance images demonstrate a pathologic fracture, proved on biopsy to be caused by lymphoma.

activities and positions may be particularly painful and should be determined. A stands for amelioration: What can the patient do to lessen the pain? In general, rest reduces or relieves most musculoskeletal back pain. The child or the adolescent who clearly describes pain that occurs at night and awakens him or her needs to be evaluated much more aggressively than the typical teenager with activityinduced back pain. Finally, R stands for radiation: Where does the pain go? True radicular pain (typically pain that radiates below the knee) is seen in only 1% to 2% of children or adolescents with back complaints but, when present, should be identified.9 It is important to determine what the appropriate evaluation is, based on the severity of the patient’s complaints. Pain is truly subjective and therefore impossible to quantify, but certain factors provide insight into the magnitude of the problem. This is particularly true in children and adolescents who, when given a choice, will nearly always pursue their preferred activities and rarely have secondary gain issues. It is important to inquire about any interference with daily activities. Is the child missing school? Is he or she participating in sports? Are any medications

being used to help with the pain? Anything other than occasional interference with preferred activities represents a potentially more serious problem that mandates further evaluation. The presence or absence of neurologic symptoms should be determined. The presence of leg pain or paresthesias may signify nerve root compression or irritation. The presence of L’hermitte’s sign, a radiating electric sensation down the back and into the legs with forward flexion of the neck, is rare but may represent an underlying intraspinal abnormality masquerading as a sports injury. Bowel or bladder dysfunction is unusual, but it is important to inquire about its presence to avoid missing a cauda equina syndrome. The presence of new-onset enuresis should also be determined. Although the treatment of back pain in this population is fairly standardized, it is important to inquire about any previous treatment and the patient’s response to it. Since activity restriction is often the initial treatment, its prescription, and the response to it, should be identified. It is also important to determine whether the patient was compliant with any prescribed restrictions. The clinician

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should inquire as to whether or not physical therapy was done and what it entailed. The patient should be asked about whether physical modalities or an active back exercise program was prescribed. It is important to define which exercises were pursued and the completeness or incompleteness of compliance. Any history of medication usage and the response to it should also be sought. Finally, the previous use of bracing or casting should be explored. Identifying the type of brace, the regimen prescribed, patient compliance, and whether any sports participation was attempted while in the brace provides a foundation for further treatment options. With children, it is generally important to obtain a thorough general medical history. This includes getting a birth history, determining the presence of any developmental milestone delays, and taking both a general family history and a history of any spinal disorders such as scoliosis or spondylolisthesis. A review of systems should be obtained, and the presence of any constitutional symptoms such as fever, chills, or weight loss should be noted. Finally, the presence of any psychosocial factors such as depression should be identified.

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Box 16B2-2 Typical History and Physical Examination Findings Spondylolysis and Spondylolisthesis •�� Back pain with back extension maneuvers •�� Usually acute exacerbation of chronic low grade pain •�� Limited forward flexion due to hamstring tightness •�� Palpable step-off of lumbar spinous processes (for highgrade slip) •�� Tenderness with pressure on and movement of affected spinous process Lumbar Disk Herniation

•�� Pain with sitting or any maneuver that increases intraabdominal pressure (e.g., cough or sneeze)

•�� Often of sudden onset •�� Significant back pain and stiffness with postural abnor-

mality (sciatic list) abnormalities often absent, but may have weakness or reflex change •�� High incidence of positive tension sign (straight leg raising sign, bowstring sign, or femoral nerve stretch test)

•�� Neurologic

Physical Examination and Testing Examination of the patient with a low back complaint begins with inspection, which cannot be performed adequately unless the patient is in an examining gown that opens in back, is disrobed down to underpants and bra, and has shoes and socks off. Inspection of the skin is performed, and the presence of any skin lesions, such as caféau lait spots or hairy patches, is noted. Asymmetry of the shoulders, the pelvis, the scapulae, and the skin creases is noted. Adam’s forward bend test—having the child bend forward to touch his or her toes and noting asymmetry of the ribs or the flank—is suggestive of scoliosis and should be performed. The child’s gait is then observed, including having the child walk on the heels and toes. A broad-based gait may suggest an underlying disorder such as myelopathy. This may be further evaluated by having the patient perform tandem gait (having the patient heel-toe walk as in a sobriety test). Palpation of the back is then performed. Palpation helps define exactly where the painful area is, or was, located. The exact site of tenderness is noted, whether in the midline, in the paraspinal region, in the buttocks, or over the trochanteric bursae. Palpation may also identify a stepoff in the lower lumbar spine, suggesting a high-grade spondylolisthesis. Range of motion of the spine should be tested. Limitation of forward flexion may represent disk disease, although hamstring tightness or spasm, commonly seen with spondylolysis and spondylolisthesis, may also limit forward flexion. Pain on extension of the lumbar spine, particularly with a painful catch, is commonly seen with spondylolysis or spondylolisthesis. A positive single-legged hyperextension test has been thought to signify the presence of an active spondylolysis, but a recent report suggests that this test is a poor predictor of active spondylolysis in adolescent athletes with low back pain.20 Although neurologic abnormalities are exceedingly rare in pediatric patients with back pain, a neurologic

e xamination should be performed. The presence of leg atrophy or asymmetry should be noted. Light-touch sensory testing, motor strength assessment, and testing of the reflexes should be performed. Deep tendon reflexes may be normally brisk in this age group. The presence of upper motor neuron findings such as spasticity, hyperreflexia, clonus, extensor plantar response (Babinski’s sign), or asymmetry of the superficial abdominal reflexes should also be noted. Tension signs, such as the straight leg raising sign, the bowstring sign, and the femoral nerve stretch test, should also be assessed because they are highly sensitive for disk herniation in this population.3,9 The history and physical examination features of, and distinction between, spondylolysis or spondylolisthesis and disk herniation are listed in Box 16B2-2. Examination of associated nonspinal areas is also important, including the abdominal contents, the hips, and when indicated, the sacroiliac area (by testing for Faber’s or Gaenslen’s sign). Because back pain may be due to nonspinal causes, the clinician should examine the abdomen and hips, when indicated.

Imaging Radiographic imaging studies are costly, time-consuming, and sometimes inaccurate in identifying the source of back pain in all age groups, including children and adolescents. Furthermore, it is relatively uncommon for a radiographic abnormality to alter treatment in the early phase of back pain. It is essential to bear in mind that a radiographic diagnosis does not need to be made in most cases at the time of initial assessment. This includes conditions such as spondylolisthesis and disk herniation. The decision for imaging in the pediatric athlete with back pain is determined, therefore, by several factors, including the severity and duration of symptoms and the response to previous treatment. Although uncommon, a history of

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Figure 16B2-5 Lateral radiograph from an 11-year-old swimmer with a 2-month history of back pain. Six weeks earlier, he had stopped participating in swimming, and he had been housebound for 1 week before this image was taken. This radiograph demonstrates end-plate erosion and vertebral body involvement at T9-T10 (arrowhead) consistent with diskitis and vertebral osteomyelitis.

acute trauma, particularly associated with neurologic signs or symptoms, constitutes an indication for imaging. There is no universally accepted algorithm for imaging in the pediatric patient with back pain, whether an athlete or not. In the acute setting, we frequently find it helpful to institute treatment before obtaining radiographss and to assess and monitor the child’s response to the treatment. If the patient does not improve, plain radiographs are obtained, and treatment may be altered. If no further improvement is seen, more sophisticated imaging, such as MRI, may be obtained and treatment adjusted accordingly. Plain radiographs are the usual initial imaging test. They are indicated in a pediatric athlete with a history of acute trauma in whom fracture is suspected. We typically obtain plain radiographs in adolescents with significant symptoms lasting more than 3 to 4 weeks or in children or adolescents with severe pain or those who are unable to attend school (Fig. 16B2-5). The standard lumbar radiographic series includes standing anteroposterior (AP) and lateral views of the lumbar spine as well as a spot lateral (coned down) view of L5-S1. Plain lateral radiographs can identify 80% of pars defects (Fig. 16B2-6) and essentially all cases of spondylolisthesis.21 These views also identify virtually all significant fractures, such as compression fracture of the vertebral body. If a pars defect is suspected but not identified on the plain AP and lateral views, oblique views of the lumbar spine are ordered (Fig. 16B2-7), but these are not routine in our practice because of the significant increase in radiation they produce. Standing posteroanterior (PA) and lateral scoliosis radiographs are ordered if truncal asymmetry or hyperkyphosis is present on physical examination (see Fig. 16B2-3). It is important to recognize that hyperkyphosis, with or without mild secondary scoliosis, is frequently misinterpreted by primary care practitioners as scoliosis; therefore, all initial scoliosis evaluations should include a lateral radiograph.

Figure 16B2-6 A plain lateral radiograph of the lumbar spine from a 15-year-old soccer player with low back pain for 8 months demonstrates lysis of the pars interarticularis at L5 (arrowhead) without spondylolisthesis.

Figure 16B2-7 A defect in the pars interarticularis of L5 (arrowhead) is seen on this oblique radiograph. The normal bony continuity of the pars (the “neck of the Scotty dog”) of L3 and L4 can also be appreciated.

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Figure 16B2-8 Coronal (A) and sagittal (B) single-photon emission computed tomographic images from a 15-year-old boy with uptake in the region of the L5 pars interarticularis, consistent with spondylolysis.

A higher frequency of radiographic thoracolumbar abnormalities is present in the adolescent athlete compared with controls. Repetitive hyperflexion of the immature spine is thought to result in anterior disk herniation (marginal Schmorl’s nodes), whereas tension shear is thought to result in abnormalities of the vertebral ring apophysis.22 A higher frequency of anterior end-plate lesions have been demonstrated in competitive adolescent skiers, wrestlers, and gymnasts.23 Nuclear imaging with technetium-99m bone scanning can be helpful in identifying occult lesions of the spine not seen on plain radiographs. The sensitivity of technetium is enhanced with SPECT, which provides tomographic images of the radiotracer in the lumbar spine (Fig. 16B2-8). SPECT scanning is the preferred imaging modality for identifying occult pars interarticularis lesions.24 It is also sensitive, although nonspecific, for identifying other bony lesions such as tumors of the posterior elements, apophyseal fractures, and diskitis. Some of these lesions may be missed on MRI. Although technetium scanning is sensitive in identifying occult cases of spondylolysis, it is less useful in determining the acuity of an injury because a bone scan may be abnormal for up to 18 months after fracture. CT is also helpful in certain conditions, particularly in the evaluation of spondylolysis.6 Although not as sensitive as SPECT scanning, CT using 3-mm parallel cuts is a very sensitive modality for identifying pars defects. It is also very specific for differentiating pars defects from sclerosis of the pars or the pedicle, from tumors such as osteoid osteoma or osteoblastoma, or from apophyseal injuries. In addition, CT is useful for monitoring healing of a pars defect. CT

provides the best definition of the bony anatomy of the posterior elements of the lumbar spine. MRI is commonly employed, although it may not provide significant therapeutically useful information in the pediatric or adolescent athlete with acute pain. MRI in a pediatric athlete with acute pain is of limited usefulness and should be restricted until after a trial of conservative treatment has been tried. Despite its limitations, we do employ MRI initially for patients with clear-cut neurologic signs or symptoms and for patients who are clinically deteriorating. Similarly, a history of constitutional symptoms merits early evaluation with MRI. We also typically use MRI in the pediatric athlete with functionally disabling pain for longer than 3 months. Although 3 months may still be relatively early in the disease process, patient and parent expectations generally mandate its use. The obvious advantages of MRI are that it is noninvasive, does not deliver any ionizing radiation, and provides orthogonal imaging of the entire lumbar spine. It is the test of choice for herniated nucleus pulposus.25 The clinician should be aware that disk abnormalities are common in asymptomatic individuals, even adolescents. Besides identifying disk herniations, MRI also is ideal for defining other changes in the disk, such as disk degeneration or infection. MRI is thought by some clinicians to be less sensitive and less specific than either SPECT or CT in identifying pars defects. The usefulness of MRI in spondylolisthesis, however, is in its ability to identify the presence or absence of foraminal stenosis on the parasagittal images. Such foraminal stenosis is a common cause of radicular leg pain in the patient with spondylolisthesis, particularly high-grade slips.

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In cases in which surgery is elected in the pediatric patient with spondylolysis or spondylolisthesis, we routinely perform MRI to exclude other sources of pain. MRI is also helpful in identifying and defining rare, but ominous, causes of back pain in children and adolescents. These include intraspinal diseases such as tumors, intraspinal lipoma, and tethered cord, which usually present with neurologic findings. Tumors of the anterior column, although rare, and infections of the spine are also optimally imaged with MRI. On the other hand, MRI is inferior to CT for defining bony lesions of the posterior elements.

TREATMENT OPTIONS Initial Nonoperative Treatment Most pediatric athletes presenting with new-onset back pain respond quickly to a series of general measures (Box 16B2-3). Therefore, it is rarely essential to make a specific diagnosis early in the course of the patient’s complaints. Furthermore, it is rarely cost-effective to order sophisticated imaging of children or adults with recent-onset back pain except in unusual circumstances. Most pediatric athletes present with a more chronic pain of insidious onset. These patients should be evaluated for so-called red flags, which are potential indicators of a more serious underlying condition such has fracture, infection, or tumor. These red flags include night pain, fever, weight loss, neurologic symptoms or signs and constitutional symptoms. The presence of incapacitating pain causing the patient to stay home from school or to be bedridden should lead to a more aggressive evaluation. Similarly, a history of constitutional symptoms such as unexplained weight loss, fever, or chills or the presence of significant neurologic signs or symptoms suggests the need for prompt imaging.3 Unless one or more red flags are present, most patients are placed on activity restrictions and are started on generic treatments such as moist heat, stretching, and over-the-counter medications such as acetaminophen or ibuprofen. The goal of this approach is to rule out more serious underlying disease and to return the patient to full activity with minimal or no pain. This may require relatively frequent re-evaluation. We typically bring the pediatric athlete with back pain back for re-evaluation on a weekly basis for the first 2 or 3 weeks and then every 2 or 3 weeks thereafter until acceptable resolution of the pain has occurred. In most cases, improvement will occur. Depending on the duration of the patient’s symptoms, their severity, and the rapidity of improvement, the athlete is allowed to gradually return to his or her daily activities and is then started on a program of back stretching and strengthening exercises under the guidance of a physical therapist. Once the exercise program has been mastered without recurrence of pain, gradual resumption of athletic activities is allowed. Because pain is a strictly subjective complaint, it is difficult to define objective guidelines for when the patient can resume specific activities. We find that the most useful guideline is the presence of minimal or no pain, full range of motion, and a normal neurological examination.

Another aspect of the management of the pediatric athlete with ongoing back pain is counseling. The athlete and, in particular, the parents often do not understand that back pain, even in a child, is a relatively common occurrence. It is imperative that the physician reinforce the fact that this condition may occasionally involve a prolonged recovery. It also needs to be emphasized that, although it is exceedingly frustrating for the family, the exact cause of the pain may not be determined. The appropriate role of imaging studies is to guide treatment; they should therefore be obtained only when they can reasonably be expected to have a significant impact on therapeutic decision making. In general, imaging is rarely helpful, and therefore not indicated, in the first 2 to 4 weeks of symptoms. We typically wait 2 to 4 weeks before obtaining plain radiographs for those individuals whose back pain fails to significantly improve. If plain radiographic findings are negative and the pain persists, we consider an MRI after 6 to 12 weeks of symptoms. When there is particular concern about the presence of a spondylolysis, we often proceed to SPECT before getting an MRI. If the MRI is normal and symptoms persist for 6 months or longer, we often recommend technetium bone scanning.

Diagnosis and Nonoperative Treatment of Spondylolysis and Spondylolisthesis Spondylolysis with or without spondylolisthesis (slippage) is a chronic fatigue fracture of the pars interarticularis. It results from both hereditary and environmental factors (nature and nurture). The child or adolescent with spondylolysis or spondylolisthesis typically presents with a history of chronic low-grade back pain, sometimes with an acute exacerbation. The degree of slippage is based on Meyerding’s classification, whereby the superior aspect of the sacrum is divided into quarters and the slip is described as the relationship of the L5 vertebral body to the sacrum (S1).26 Grade I represents a slippage of 0% to 25% of L5 on S1; grade II is 25% to 50% slip; grade III is 50% to 75% slip, and grade IV is more than 75% anterolisthesis. Spondyloptosis refers to the situation in which the body of L5 sits anterior to the sacrum—a slip of more than 100%. Most children with spondylolysis have either no slippage or a low-grade (grade I or II) spondylolisthesis, and therefore many of the more dramatic associated physical findings seen with high-grade slips (e.g., flattening of the buttocks, a transverse abdominal crease, or gait alterations) are absent. In the thin patient, a palpable step-off of the lower lumbar spinous processes may be appreciated, and there is frequently painful limitation of extension associated with a painful catch on back extension. Hamstring spasm is frequently present, and forward flexion may be limited because of the tight hamstrings. Diagnostic studies start with plain radiography. A standing spot lateral view identifies 80% of pars defects but may be supplemented with oblique views if needed. SPECT is the most sensitive study for identifying occult pars defects that are not seen on plain radiographs. CT is helpful to more clearly define the pars fracture (Fig. 16B2-9). CT can help differentiate an acute fracture of the pars from a chronic fracture.

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Box 16B2-3 Treatment Options Acute Lumbar Strain •�� Limited period of activity restriction •�� Moist heat and tissue massage •�� Nonsteroidal anti-inflammatory drugs (NSAIDs) •�� Stretching and strengthening program •�� Gradual return to play Spondylolysis and Spondylolisthesis

•�� Activity restriction with or without bracing •�� NSAIDs •�� Physical therapy with core strengthening (stabilization program) and stretching stabilization if pain > 1 year or high-grade (grade III or IV) spondylolisthesis

•�� Surgical

Lumbar Disk Herniation

•�� Initial period of restricted activity •�� NSAIDs and moist heat •�� McKenzie’s back program (generally an extension program)

•�� Surgical treatment if unacceptable pain for 6-12 weeks (physical and radiographic findings must correlate) or progressive weakness or cauda equina syndrome

Overuse Syndrome •�� Plain radiography, magnetic resonance imaging, and bone scan correlate (must rule out other conditions) •�� Activity restriction, NSAIDs, moist heat, and physical therapy program •�� Alternative treatments may be considered (chiropractic, acupuncture) •�� Gradual resumption of activities •�� If recurrence: change to less competitive level of athletic participation or change sport

The primary goal of treatment is relief of back pain and the resumption of full activities, including sports. The goal is not to heal a pars fracture or to reduce a slippage because most individuals with spondylolysis or spondylolisthesis are asymptomatic, or minimally symptomatic, even with these abnormalities. The goal of treatment is to render the patient asymptomatic or minimally symptomatic. It is important to stress this from the outset to the athlete and the parents. Most patients with symptomatic spondylolysis or spondylolisthesis are started on an initial trial of nonsteroidal anti-inflammatory drugs (NSAIDs), moist heat, and activity limitation. Depending on the severity and the duration of the patient’s symptoms, athletic participation may be either restricted or eliminated. As the symptoms resolve, athletic participation is gradually resumed, and the patient is weaned off medication and is usually started on a lumbar stabilization program. The athlete is encouraged to continue these exercises, even if he or she is asymptomatic, for at least one season and frequently longer. Unfortunately, some patients either fail to respond or suffer a recurrence of pain. In these circumstances, we typically repeat the course of treatment and try to ensure that compliance has been adequate. Another option in this

Figure 16B2-9 Axial computed tomographic image of a 17year-old football player demonstrating unilateral spondylolysis with sclerosis of the contralateral pars.

setting is the use of bracing; a number of patients respond to a Boston antilordotic brace worn on a full-time basis initially, with gradual weaning over a 6- to 12-week period.27 In general, the goal of bracing is to render the patient asymptomatic rather than to promote healing of a pars fracture. Fracture healing is very unlikely, and when it does occur, it is most likely to do so in a young child with a recent fracture and with no slippage. Physical therapy modalities such as ultrasound, electrical stimulation, and massage are only rarely used but may be helpful to provide temporary relief of symptoms.27 Electrical stimulation has also been tried for spondylolysis when an initial trial of conservative treatment has failed. A few small retrospective case series have demonstrated some success with electrical stimulation. However, these results may not be generalizable to the entire population, and additional clinical research is required.28 Acute fracture of the pars interarticularis (type IV) is unusual, but when it is identified early, fracture healing can sometimes be achieved. The most reliable method of immobilizing the lumbosacral junction is a pantaloon spica cast, although some authors report an acceptable healing rate with other types of bracing.27 Serial CT can be useful in following the progression of the defect to healing.

Operative Treatment of Spondylolisthesis Although most patients with spondylolysis or spondylolisthesis are either asymptomatic or respond to nonsurgical treatment, surgery is occasionally required. Intractable pain after 1 year of appropriate treatment is the most common indication for surgery. A therapeutic dilemma arises in the patient who achieves acceptable symptomatic relief by activity restriction but is unable to resume athletic activity without symptoms. Surgery may be considered under such circumstances, but return to high-level sports competition following surgery is unpredictable. Other less common indications for surgery include a significant or worsening neurologic deficit or the presence of cauda

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A

B

Figure 16B2-10 A and B, Serial lateral radiographs over a 15-month period demonstrating dramatic progression of isthmic spondylolisthesis in an adolescent athlete. Progression of this type is somewhat uncommon and is usually associated with pain, as it was in this boy, whose symptoms quickly resolved after L5-S1 fusion and cast immobilization.

equina syndrome. These are unlikely except in a highgrade slip or spondyloptosis. In addition, a progressive slip (Fig. 16B2-10) or a slip of greater than 50% in a skeletally immature child generally mandates prophylactic stabilization, regardless of symptoms. The traditional gold standard surgical treatment is a posterior spinal fusion. For an L5 spondylolysis or lowgrade L5-S1 slip, fusion from L5 to the sacrum is typically performed. In situ noninstrumented posterolateral fusion with autogenous iliac crest bone graft and cast immobilization has a very high success rate with minimal morbidity.21 Laminectomy or nerve root decompression is rarely necessary in the pediatric population, even in the presence of leg pain. The role of instrumentation as an adjunct to posterolateral fusion for the child with spondylolisthesis is a controversial issue. In the smaller, skeletally immature patient (typically 90 kg). Slawski and Cahill155 reported a 79% bilateral involvement with weightlifters once they present to the physician with symptoms.

Radiographically, a Zanca view (cephalic tilt of 10 to 15 degrees), when taking AP radiographs of the AC joint, provides the best image of the distal clavicle. The changes are represented by a loss of subchondral bone detail at the distal clavicle, cystic appearance in the subchondral area and osteoporosis to the distal third of the clavicle. Late manifestations include a distinct widening of the AC joint with cysts and lucencies at the clavicular end of the acromion. A bone scan is useful in assessing the biologic activity at the distal clavicle and can be used to support the diagnosis of distal clavicle osteolysis. Pitchford and Cahill’s154 conservative treatment of atraumatic osteolysis of the distal clavicle is directed toward eliminating the provocative maneuvers causing it. Unfortunately, many power athletes require the weight training to maintain and increase strength as well as their overall body mass if they want to remain competitive. Pitchford and Cahill154 suggested the following surgical indications for the treatment of distal clavicle osteolysis: (1) a confirmed diagnosis of atraumatic osteolysis, and (2) an unwillingness on the part of the athlete to accept a lower level of performance. The surgical procedure is a distal clavicle resection that can be performed with open or arthroscopic techniques. In summary, atraumatic osteolysis of the distal clavicle is a cumulative stress on the distal clavicle caused by muscular forces across the AC joint with press-type maneuvers. This entity predominantly occurs in weightlifters but may be seen in athletes who use weightlifting for strength and conditioning. The clinical history and examination, combined with appropriate radiographs, allows for the correct diagnosis. The diagnosis is supported by a positive bone scan. The treatment of choice is avoidance of the activities associated with increased symptoms. When this fails, distal clavicle resection may be indicated.

Intra-articular Acromioclavicular Joint Fractures Minimally displaced distal clavicle fractures or acromial fractures are relatively stable owing to the ligamentous stability provided by the AC, coracoclavicular, and coracoacromial

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Figure 17C-40 A, Radiograph of the AC joint demonstrating widening of the AC joint and loss of subchondral cortical detail of the distal clavicle (arrow). B, Radiograph of the AC joint demonstrating osteoporosis of the distal clavicle and cortical thinning. C, Radiograph of the AC joint demonstrating cystic changes (arrowheads) and loss of subchondral integrity. D, Radiograph of AC joint demonstrating cystic changes of the clavicular portion of the acromion (arrowheads) and widening of the AC joint. (From Pitchford MR, Cahill BR: Osteolysis of the distal clavicle in the overhead athlete. Operative Tech Sports Med 5:74, 1997.)

ligaments. These are generally treated nonoperatively with success unless there are extenuating effects (open injury, neurovascular compromise). A sling for comfort, then early range of motion and shoulder strengthening exercises when pain permits, is recommended. Some of these fractures may predispose the joint to early post-traumatic arthrosis. When indicated by the persistence of pain unrelieved with nonoperative treatment, a distal clavicle resection is performed.

Acromioclavicular Injuries in the Child The developmental anatomy of the shoulder provides insight regarding the type of injuries that occur in a skeletally immature athlete. At 1 year of age, there is an ossification center seen at the tip of the coracoid. At age 10 years, the base of the coracoid and upper fourth of the glenoid have ossified, and these fuse to the scapula by the age 15 years. Near puberty, the acromion forms between two and five ossification centers that fuse by the age of 22 years. Failure of the acromion ossifications to fuse can occur without any loss of shoulder function. In children, the classification of AC injuries is based on the position of the clavicle with respect to the periosteal sleeve and intact ligaments. This classification system has been reported by Curtis and colleagues and is organized in a similar progression as the adult or skeletally mature patient classification scale (Fig. 17C-41).156

Figure 17C-41 Acromioclavicular ligament injuries. Displacement of the distal clavicle occurs through a tear in the periosteal tube. This occurs in children who sustain a severe force to the shoulder. The AC and costoclavicular ligaments remain intact through the periosteal tube. (From Beim GM, Warner JP: Clinical and radiographic evaluation of the acromioclavicular joint. Oper Tech Sports Med 5:68, 1997.)

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Type I injury: sprain of AC ligaments with the periosteal sleeve intact Type II injury: partial disruption of the periosteal sleeve with slight winding of the AC joint Type III injury: periosteal tube disrupted with instability of the distal clavicle, superior displacement 25% to 100% of the distal clavicle on the AP radiograph Type IV injury: periosteal tube disrupted, distal clavicle displaced posteriorly through or into trapezius muscle seen on axial lateral radiograph Type V injury: periosteal tube disrupted, deltoid and trapezial detachment, clavicle displaced subcutaneously greater than 100% of the normal Type VI injury: inferior displacement of the clavicle behind the coracoid process Fracture of the coracoid through the common growth plate with the upper glenoid fossa may mimic an AC injury, but the coracoclavicular interspace remains intact.118 The axillary view best demonstrates a fracture to the coracoid. This should be suspected in AC injuries within the first three decades of life. A computed tomographic scan is indicated if there is any concern of a displaced fracture involving the glenohumeral joint.

l Capsule

and capsular ligaments are primary restraints to AP translation. The main contribution of the coracoclavicular ligaments is vertical stability—they mediate synchronous scapulohumeral motion and strengthen AC articulation. l Distal clavicle resection of even less than 1 cm may have residual posterior instability. l AC injuries present clinically as acute (direct or indirect injury; see Box 17C-2) or chronic (arthrosis, degenerative AC joint); diagnostic tests and injections help to differentiate the causes of shoulder pain. l AC injuries are suspected in weightlifters, overhead repetitive lifters, and some throwers, in whom the subcutaneous joint with fascial covering is easily injured. l Physical examination and radiographs determine the neurovascular status of the upper extremity and evaluate the neck and sternoclavicular joint for associated injuries; attempt to localize pain to AC joint (AC compression, cross-body adduction, and other tests); and assess skin condition for tenting (type IV if posterior tenting). l Types I and II AC injuries are treated nonoperatively. Treatment of type III injuries remains controversial. Types IV, V, and VI injuries are usually treated operatively.

Treatment in Children The treatment of AC joint injuries in skeletally immature athletes is typically nonoperative because the most common injuries are type I, II, and III. Nonoperative treatment consists of a sling for pain control over the first 3 to 7 days, ice, nonsteroidal anti-inflammatory medications, and mild analgesics as needed. Most athletes in this age group do not require physiotherapy, but if limitations in range of motion are present after 2 to 4 weeks, a short course of physiotherapy is beneficial. Eidman and colleagues62 reported that conservative treatment of these injuries have gone on to heal without clinically relevant sequelae. Nuber and Bowman25 report in their chapter that surgical treatment of type IV, V, and VI injuries is successful. Replacement of the clavicle into its periosteal sleeve with suturing the sleeve closed and then fixation of the coracoclavicular lag screw or transacromial fixation is recommended. The fixation is then removed after 4 to 6 weeks before physical therapy is started in the child.

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Chronopoulos E, Kim TK, Park HB, et al: Diagnostic value of physical tests for isolated chronic acromioclavicular lesions. Am J Sports Med 32:655-661, 2004. Debski RE, Parsons IM, Woo SL, Fu FH: Effect of capsular injury on acromioclavicular joint mechanics. J Bone Joint Surg Am 83:1344-1351, 2001. Fakuda K, Craig E, AN K, et al: Biomechanical study of the ligament systems of the acromioclavicular joint. J Bone Joint Surg Am 68:434-439, 1986. Mazzocca AD, Santangelo SA, Johnson ST, et al: A biomechanical evaluation of an anatomical coracoclavicular ligament reconstruction. Am J Sports Med 34:236246, 2006. Rockwood CJ, Williams G, Young DC: Disorders of the acromioclavicular joint. In Rockwood CJ, Matsen F (eds): The Shoulder, 3rd edition. Philadelphia, Saunders, 2004, pp 521-595. Schlegel TF, Burks RT, Marcus RL, Dunn HK: A prospective evaluation of untreated acute grade III acromioclavicular separations. Am J Sports Med 29:699703, 2001. Tienen TG, Oyen JF, Eggen PJ: A modified technique of reconstruction for complete acromioclavicular dislocation: A prospective study. Am J Sports Med 31:655-659, 2003. Walton J, Mahajan S, Paxinos A, et al: Diagnostic values of tests for acromioclavicular joint pain. J Bone Joint Surg Am 86:807-812, 2004. Weaver J, Dunn H: Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg Am 54:1187-1194, 1972.

o i n t s

he AC joint is diarthrodial, providing 6 degrees of freeT dom. The collagenous disk between joints predictably degenerates with age. l The shoulder is stabilized by static (AC, CC, and CA ligament, and capsule) and dynamic (deltoid, trapezius) structures.


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Injuries to the Glenoid, Scapula, and Coracoid 1. Glenoid and Scapula Fractures in Adults and Children Allen Deutsch, Jason A. Craft, and Gerald R. Williams, Jr.

The scapula is intimately linked to shoulder function and mobility. It links the appendicular and axial skeletons through the clavicle and the acromioclavicular, sternoclavicular, and glenohumeral joints and presents a stable platform for the upper extremity. Injury to the scapula may disrupt normal shoulder function. The incidence of scapular fracture has been reported to be 3% to 5% of shoulder girdle injuries1,2 and 0.4% to 1% of all fractures.3,4 The low incidence of scapular fracture is due to its protected position along the rib cage, the enveloping musculature, and its relative mobility, which permits dissipation of forces. Scapular fractures most commonly involve the scapular body (49% to 89%), the glenoid neck (10% to 60%), and the glenoid cavity (10%).5-10 Scapular fractures are usually sustained as the result of severe trauma. Most series report motor vehicle or motorcycle crashes as the cause of injury in more than half of cases.5,6,8-10 Associated injuries are common, including rib fracture, pneumothorax, and head injury. Rowe11 reported that 71% of the patients in his series of scapular fractures had other associated injuries: 45% had fracture of other bones, including the ribs, sternum, and spine; 3% sustained a pneumothorax; 4% sustained brachial plexus injuries; and 19% sustained other shoulder girdle dislocations. A recent multicenter trauma review of scapular fractures found that they were associated with 1.1% of all blunt trauma admissions. Despite being relatively rare, 99% had associated injuries, with rib fractures (43%) and lower and upper extremity fractures (36% and 33%) being the most common. However, 28% and 27% had associated intrathoracic trauma and head trauma, respectively.12 These numbers highlight the large amount of force required to obtain these fractures and reinforce the need to fully evaluate that patient for associated injuries. Several classification systems for scapular fractures have been reported in the literature. Zdravkovic and Damholt13 divided scapular fractures into three types: type I fractures, or fractures of the body; type II fractures, or fractures of the apophyses (including the coracoid and acromion); and type III fractures, or fractures of the superior lateral angle (i.e., scapular neck and glenoid). Zdravkovic and Damholt13 considered the type III fracture to be the most difficult to treat; these represented only 6% of their series. Thompson and coworkers14 presented a classification system that divided these fractures according to the likelihood that associated injuries would be present. Their cases resulted from blunt trauma. Class I fractures included fractures of the coracoid and acromion process and small

fractures of the body. Class II fractures included glenoid and scapular neck fractures. Class III fractures included major scapular body fractures. Thompson and colleagues14 reported that class II and class III fractures were much more likely to have associated injuries. Wilber and Evans10 described 40 patients with 52 scapular fractures. The patients were divided into two groups on the basis of fracture location: group I, which included patients with fractures of the scapular body, neck, and spine; and group II, which included patients with fractures of the acromion process, coracoid process, or glenoid. They reported unsatisfactory results of treatment of patients in group II because of residual pain and loss of glenohumeral motion. Ideberg15,16 devised a classification system of five types of scapular fracture with an associated intra-articular glenoid component. This system was modified by Goss17,18 with inclusion of six types. Type I fractures involve the glenoid rim and are subdivided into Ia, anterior rim; and Ib, posterior rim. Type II to V fractures extend from the glenoid fossa to various exit points along the scapula. Type II fractures exit the lateral border of the scapula, below the infraglenoid tubercle. Type III fractures exit the superior border and typically extend medial to the base of the coracoid. Type IV fractures extend directly across the scapula to the medial border and usually exit superior to the scapular spine. Type V fractures are combinations of types II to IV. Type VI fractures encompass glenoid fractures with extensive intra-articular comminution (Fig. 17D1-1).17 Goss19 described the superior shoulder suspensory complex, consisting of the glenoid, coracoid, acromion, distal clavicle, coracoclavicular ligaments, and acromioclavicular ligaments. This bone–soft tissue ring maintains the normal, stable relationship between the upper extremity and the axial skeleton. Single disruptions of the superior shoulder suspensory complex, such as an isolated scapular neck fracture, are usually anatomically stable because the integrity of the complex is preserved, and nonoperative management yields good functional results. When the complex is disrupted in two places (double disruption), such as a scapular neck fracture with an acromioclavicular joint disruption, a potentially unstable anatomic situation is created. Because the superior shoulder suspensory complex includes the glenoid, acromion, and coracoid, many double disruption injuries involve the scapula. Open reduction is indicated for double disruptions that are accompanied by significant displacement, which may lead to delayed union, malunion, or nonunion as well as long-term functional deficits.

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Figure 17D1-1 Classification of fractures of the glenoid cavity. Type Ia, anterior rim fracture; type Ib, posterior rim fracture; type II, fracture line through the glenoid fossa exiting at the lateral scapular border; type III, fracture line through the glenoid fossa exiting at the superior scapular border; type IV, fracture line through the glenoid fossa exiting at the medial scapular border; type Va, combination of types II and IV; type Vb, combination of types III and IV; type Vc, combination of types II, III, and IV; type VI, comminuted fracture. (Modified from Goss TP: Scapular fractures and dislocations: Diagnosis and treatment. J Acad Am Orthop Surg 3:22-33, 1995.)

Ia

II

Ib

III

Va

Vb

IV

Vc

VI

ANATOMY The scapula is enveloped by multiple layers of muscles. The anterior surface provides attachment for the subscapularis, the serratus anterior, the omohyoid, the pectoralis minor, the conjoined tendon of the coracobrachialis and short head of the biceps, the long head of the biceps, and the long head of the triceps (Fig. 17D1-2). The posterior surface of the scapula provides muscle attachment sites for the levator scapulae, the rhomboid major, the rhomboid minor, the latissimus dorsi, the teres major, the teres minor, a portion of the long head of the triceps, the deltoid, the trapezius, the supraspinatus, the infraspinatus, and a portion of the omohyoid (Fig. 17D1-3). The intramuscular position of the scapula provides it with great mobility and a protective cushion that are no doubt responsible for the low incidence of scapular injury. The proximity of neurovascular structures to the scapula places them at risk for injury. The pectoralis minor tendon inserts at the base of the coracoid process and the lateral border of the suprascapular notch. The brachial plexus and axillary artery travel posterior to the pectoralis minor tendon. The suprascapular nerve passes under the transverse scapular ligament as it passes through the suprascapular notch to innervate the supraspinatus muscle, whereas the suprascapular artery passes over the ligament. The suprascapular nerve continues through the spinoglenoid notch, or the junction between the base of the acromion and the

Coracobrachialis and short head of biceps Pectoralis minor Omohyoid

Biceps, long head

Triceps

Serratus anterior

Subscapularis

Figure 17D1-2 The muscle attachments to the anterior surface of the scapula. (Modified from Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Shoulder Omohyoid m. Supraspinatus m.

Trapezius m.

Biceps m.

Levator scapulae m. Deltoid m.

Rhomboideus minor m.

Triceps m. Infraspinatus m.

Rhomboideus major m.

Teres minor m.

Teres major m. Latissimus dorsi m.

Figure 17D1-3 The muscle attachments to the posterior surface of the scapula. (Modified from Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

neck of the scapula, to innervate the infraspinatus muscle. At the medial border of the scapula, the dorsal scapular and spinal accessory nerves course along with the branches of the transverse cervical artery. The osseous components of the scapula, which consist of the body and spine, the coracoid process, the acromion process, the glenoid, and the inferior angle, arise from several ossification centers.20-22 At birth, the body and spine form one ossified mass. The coracoid process, the acromion process, the glenoid, and the inferior angle are cartilaginous, however. The coracoid process is a coalescence of four or five centers of ossification. The center of ossification for the midportion of the coracoid appears at the age of 3 to 18 months and may be bipolar. The ossification center for the base of the coracoid, which includes the upper third of the glenoid, appears at 7 to 10 years. Two ossification centers appear at the age of 14 to 16 years: a center for the tip and a shell-like center at the medial apex of the coracoid process. The ossification centers for the

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base and the midportion of the coracoid coalesce during adolescence at 14 to 16 years of age. The other ossification centers fuse at 18 to 25 years of age (Figs. 17D1-4 and 17D1-5). The acromion is a coalescence of two or three centers of ossification that appear between the ages of 14 and 16 years, coalesce at the age of 19 years, and fuse to the spine at the age of 20 to 25 years. Failure of the anterior acromion ossification center to fuse to the spine gives rise to the os acromiale. This unfused apophysis is present in 2.7% of random patients and is bilateral in 60% of cases.23 The size of the os acromiale depends on which of the four ossification centers of the acromion have failed to fuse (Fig. 17D1-6). The most common site of nonunion is between the meso-acromion and the meta-acromion, which corresponds to the mid-acromioclavicular joint level. An axillary lateral radiograph clearly demonstrates the lesion (Fig. 17D1-7). Norris24 has reported that the os acromiale has been mistaken for fracture and that there is an association between the os acromiale and a rotator cuff tear. The inferior angle of the scapula arises from an ossification center that appears at the age of 15 years and fuses with the remainder of the scapula at the age of 20 years. The vertebral border arises from an ossification center that appears at 16 to 18 years of age and fuses by the 25th year. The glenoid fossa ossifies from four sources: (1) the coracoid base (including the upper third of the glenoid), (2) the deep portion of the coracoid process, (3) the body, and (4) the lower pole, which joins with the remainder of the body of the scapula at 20 to 25 years of age. Because many athletes are adolescents and because many of the apophyses do not fuse until the age of 25 years, caution must be exercised in interpreting radiographs of the scapula. The os acromiale is the most frequently quoted unfused apophysis and can be confused with fracture.23,24 In addition, the physes at the base of the coracoid and the tip of the coracoid process can be difficult to distinguish from fracture. In the appropriate setting, a radiograph of the contralateral scapula is useful in determining whether a radiographic “line” is truly a fracture or an unfused apophysis.

Figure 17D1-4 A normal ossification pattern at the base of the coracoid. A crescent-shaped center is seen at the apex of the coracoid. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

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Figure 17D1-7 Os acromiale. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

CLINICAL EVALUATION Figure 17D1-5 An epiphyseal line is seen across the upper third of the glenoid because this portion of the glenoid ossifies in common with the base of the coracoid. This may be confused with a fracture and is the precise location of most type III glenoid fractures. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

PA MTA PA = Pre-acromion

History Scapular fractures in athletes can result from either direct or indirect mechanisms of injury. Although most athletes are not subjected to the high-energy trauma associated with motor vehicle crashes, direct blows to the scapula can occur with enough force to cause fracture in contact sports such as hockey and football. Direct blows to the acromion can cause either acromion fracture or acromioclavicular separation. In addition, direct blows to the scapula or to the lateral aspect of the shoulder can cause scapular body fractures or glenoid fractures. Alternatively, glenoid fractures can be the result of indirect trauma incurred during a violent glenohumeral dislocation or a fall on an outstretched arm.

MSA = Meso-acromion

MSA BA

MTA = Meta-acromion

Physical Examination

BA = Basi-acromion

The athlete with a scapular fracture typically presents with the arm adducted and protected from all movements. Abduction is especially painful. Although ecchymosis is less than expected from the degree of bone injury present, severe local tenderness is a reliable finding.25 Athletes with scapular body fractures or coracoid process fractures often complain of increasing pain with deep inspiration secondary to the pull of the pectoralis minor or serratus anterior muscles. Frequently, rotator cuff function is extremely painful and weak secondary to inhibition from intramuscular hemorrhage. This has been described as a pseudorupture of the rotator cuff26 and usually resolves within a few weeks. Scapular fracture is often associated with other injuries that need more urgent treatment. Significant associated injuries have been reported to occur in 35% to 98% of all patients with scapular fractures.25 The highest incidence of serious associated injuries occurs in fractures sustained during high-speed motor vehicle crashes.6,8-10,14,27 McLennen and Ungersma28 reported 16 pneumothoraces in 30 patients who presented with fractured scapulae.

A

B Figure 17D1-6 A, The diagram represents the ossification centers of the acromion. B, The most common site of failure of ossification lies between the meso-acromion and the metaacromion. (Modified from Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

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Of the 16 pneumothoraces, 10 were delayed in onset from 1 to 3 days. The authors recommended a follow-up chest radiograph, physical examination, and blood gas determination for all patients with scapular fractures. Other series have reported an overall incidence of pneumothorax associated with scapular fracture of between 11% and 38%.6,14,27 Ipsilateral rib fractures,14 pulmonary contusion,14,27 arterial injury,27 and brachial plexus injury6,8,9,14,27 have also been reported in association with scapular fractures. Physical examination should be directed toward detecting any of these possible associated injuries.

RADIOGRAPHIC EVALUATION Most scapular fractures can be adequately visualized on routine radiographic views. A true anteroposterior view of the scapula, combined with an axillary or true scapular lateral view, demonstrates most scapular body or spine fractures, glenoid neck fractures, and acromion fractures (Figs. 17D1-8 through 17D1-10). “Special” views may be required in selected circumstances. The Stryker notch view, as described later in this chapter section, is useful for coracoid fractures25 (Fig. 17D1-11). The apical oblique view described by Garth and colleagues29 and the West Point lateral view30,31 are useful for evaluating anterior glenoid rim fractures. Computed tomography (CT) is a useful adjunct in evaluating intra-articular glenoid fractures. The contralateral normal shoulder, as well as the involved shoulder, may be scanned to provide a means for comparison of the pathologic findings noted in the involved shoulder, especially in adolescents.25 CT allows confirmation of the size, location, and degree of displacement of fracture fragments and detects the presence of instability. Three-dimensional images can be generated as well (Fig. 17D1-12). These three-dimensional computed tomographic reconstructions are useful in surgical planning. With appropriate software, the humeral head can be subtracted from the image so that an unobstructed view of the scapula and glenoid can be obtained if needed. Glenoid rim fractures associated with glenohumeral instability pose perhaps the most difficult decisions for treatment of fractures of the scapula among athletes. The

Figure 17D1-8 An anteroposterior view of the glenoid showing an anterior-inferior glenoid fracture.

Figure 17D1-9 A tangential scapular lateral view (trauma series lateral view) showing a displaced scapular body fracture with a bayonet position.

athlete does not always relay a history of glenohumeral dislocation in association with the initial injury. Because the decision regarding operative or nonoperative treatment of these glenoid rim fractures depends on whether they are associated with instability,25 the physician should make every attempt to verify the presence or absence of instability. In this regard, stress views with or without fluoroscopic control or an examination under anesthesia may be helpful.

Figure 17D1-10 The fractured base of the acromion with a posterosuperior humeral head dislocation is well seen on a tangential scapular lateral view.

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Fracture of the neck of the scapula is the second most common scapular fracture.25 The glenoid articular surface is intact, and the fracture line most often extends from the

suprascapular notch area across the neck of the scapula to its lateral border inferior to the glenoid. The glenoid and coracoid may be separated or may remain as an intact unit. Although glenoid neck fractures are often affected, their displacement is limited by an intact clavicle and by the acromioclavicular and coracoclavicular ligaments.1 Displacement, however, does occasionally occur in these fractures. It is often measured in terms of displacement percentage, amount of medialization of the glenoid, and the glenopolar angle compared with the normal side. The glenopolar angle,39 a measure of glenoid rotational displacement, is defined as the angle between the plane of the glenoid and a line running from the superior glenoid to the inferior pole of the scapula as seen on an anteroposterior radiograph. Optimal treatment of these fractures is debatable; most series report good functional results in patients with glenoid neck fractures regardless of the method of treatment7,23,40,41 (Fig. 17D1-13). Hitzrot and Bolling42 in 1916 stated that manipulation and traction had no effect on displaced glenoid neck fractures and that the results were so satisfactory without reduction that attempts to achieve reduction were unnecessary. Armstrong and Vanderspuy6 reported that six of seven of their patients with glenoid neck fractures had some residual stiffness, but no patient had a functional disability. Zdravkovic and Damholt13 came to the same conclusion in their report, in which patients had an average of 9 years of follow-up. A large meta-analysis by Zlowodzki and associates43 that reviewed 520 fractures in 22 case series found that 88% of fractures (7 of 8) that involved only the neck and were treated surgically had a good or excellent outcome. However, 77% (80 of 104) of those treated conservatively had a good or excellent outcome as well. Most authors recommend closed treatment of glenoid neck fractures.32-34,36 For displaced fractures, DePalma33 recommended closed reduction and olecranon pin traction for 3 weeks, and Bateman32 favors closed reduction

Figure 17D1-12 Three-dimensional computed tomographic scan showing the amount of medialization and caudal displacement of the glenoid component of the glenoid neck fracture.

Figure 17D1-13 A healed glenoid neck fracture with marked medial displacement and full range of motion. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 17D1-11 A fracture of the base of the coracoid, seen best on a Stryker notch view. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

TREATMENT OPTIONS IN ADULTS The recommended treatment of specific types of scapular fracture varies according to whether the fracture is intraarticular or extra-articular. Most extra-articular fractures (i.e., glenoid neck, scapular body or spine, acromion, and coracoid fractures) are managed nonoperatively.32-36 Intraarticular fractures, particularly those associated with glenohumeral instability, are managed operatively.11,15,33,37,38

Extra-articular Fractures Glenoid Neck Fracture

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and a shoulder spica cast for 6 to 8 weeks in cases in which “shortening of the neck is sufficient to favor subluxation or interfere with abduction.” However, McLaughlin35 casts doubt on the usefulness of closed reduction in these fractures because most of them are affected and difficult to move. Lindholm and Leven34 found that all fractures healed in the position displayed at the time of the original injury (i.e., without additional displacement). Recently, van Noort and van Kampen44 reported on their results of nonoperative treatment of glenoid neck fractures. Of 13 patients, four had greater than 1 cm displacement, but no correlation could be made between displacement and outcomes. In fact, SF-36 scores were similar to agematched controls. Other authors1,45 have recommended open reduction of glenoid neck fractures (Fig. 17D1-14). Gagey and colleagues45 reported only one good result among 12 displaced glenoid neck fractures with closed treatment. They recommended open reduction and internal fixation (ORIF) because the displaced glenoid would “disorganize the coracoacromial arch.” These poor results were recently corroborated in a study by Pace and coworkers.46 They followed nine patients with scapular neck fractures for at least 2 years. None of the fractures was displaced more than 8 mm medially, 40 degrees angulated, or 100% translated. Despite these minimal displacements, all patients had some pain in the shoulder at rest or with work, and 33% had functional, measurable weakness. They attributed this pain and weakness to magnetic resonance imaging (MRI)– documented rotator cuff tendinopathy and subacromial bursitis caused by the glenoid malunion changing the cuff forces from compression to shear. Surgery and nerve exploration should also be considered for those fractures associated with a suprascapular nerve palsy confirmed by electromyography.7,47 Ada and Miller5 described 24 patients with displaced scapular neck fractures. Of the 16 treated conservatively, 50% complained of night pain, 40% had weakness of abduction, and 20% had decreased range of motion. ORIF was used to treat eight patients with scapular neck fractures having greater than 40 degrees of angulation or more than 1 cm of medial displacement of the glenoid surface. None of these patients complained of night pain, and all regained at least 85% of abduction. Romero and colleagues48 found that a glenopolar angle of less than 20 degrees (normal, 30 to 45 degrees) correlated to more severe pain, loss of function, and motion. Goss19 introduced the concept of the superior shoulder suspensory complex composed of a clavicle– acromioclavicular joint strut, the coracoclavicular ligament linkage, and the superolateral scapula (Fig. 17D1-15). He thought that injuries at two of these sites rendered an unstable “floating shoulder” and required operative stabilization. However, many authors noted that fractures of the glenoid neck and clavicle were frequently minimally displaced. The concept of an unstable floating shoulder was clarified in a biomechanical study by Williams and associates.49 They proved that in order to get significant displacement with ipsilateral scapular neck and clavicle fractures, there must also be injures to the coracoclavicular or acromioclavicular ligaments. These injuries have been managed both conservatively

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and operatively, with good functional results reported for both treatment methods. Ramos and associates50 reported 92% good or excellent results in 16 patients treated conservatively with aggressive rehabilitation. Williams and associates51 correlated functional outcome with medial glenoid displacement in nine patients treated nonoperatively. Six patients with 2.2 cm or less of medial displacement had good or excellent results. They recommended that nonoperative management be considered in fractures with less than 3 cm of medial displacement of the glenoid. Edwards and coworkers52 obtained excellent clinical results with nonoperative treatment of 20 patients with less than 5 mm of scapular displacement. Van Wellen and colleagues53 described successful treatment of ipsilateral displaced glenoid neck and clavicle fracture with balanced traction. Hardegger and coworkers1 recommended open reduction and scapular fixation for displaced glenoid neck fractures associated with a fracture of the clavicle or disruption of the coracoclavicular ligaments (Fig. 17D1-16). They postulated that a severe displacement in these injuries would result in “functional imbalance” of the shoulder mechanism. Leung and Lam54 managed these injuries with open reduction of both the clavicle and scapula fractures because of “loss of the normal lever arm of the cuff.” They reported good or excellent functional results in all but 1 of the 15 patients they treated. Herscovici and associates55 believed that this injury disrupts the suspensory structures, leading to anteromedial displacement of the glenoid and ptosis of the shoulder due to muscle forces and the weight of the arm. They used open reduction of the clavicle in seven patients with excellent functional results. However, a study by Labler and colleagues,56 in which they reviewed their treatment of 17 ipsilateral clavicle and scapular neck fractures, underscores the fact that not all these injuries need ORIF and that the decision should be individualized depending on displacement. In their series, nine patients underwent ORIF of both fractures if possible, but at least of the clavicle, and eight were treated conservatively. The patients undergoing ORIF had more displaced fractures than the nonoperatively treated patients. Nevertheless, an equal number in each group obtained good and excellent results. The investigators thought that much of the outcome in their series was related to associated injuries. They recommended ORIF if displacement of the neck was more than 25 mm or the glenopolar angle was reduced 30 degrees compared with the opposite side. This algorithm is supported by van Noort and colleagues,57 who organized a multicenter study of floating shoulder injuries. Of the patients treated conservatively, those with a minimally displaced glenoid had average Constant scores of 85, but those patients with caudal dislocation of the glenoid had average Constant scores of 42 (Box 17D1-1).

Scapular Body Fracture Fracture of the body of the scapula is the most common type of scapular fracture and is correlated with the highest incidence of associated injury.25 When injury is the result of high-energy trauma, these fractures may be comminuted and displaced. Cain and Hamilton40 reported five scapular fractures in professional football players that were

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A

C

E

B

D

Figure 17D1-14 A, Anteroposterior radiograph of the scapula shows the difficulty determining fracture orientation on some radiographs. B, Three-dimensional CT better illustrates the fracture configuration. C-E, Postoperative radiographs show fixation of the scapular neck and body fractures, restoring the normal lever arm of the shoulder joint.

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Box 17d1-1 Glenoid Neck Fractures 1. Isolated glenoid neck fracture a. Nonoperative treatment i. 20 degrees glenopolar angle difference iii. Suprascapular nerve palsy—with exploration iv�� . �� Intact lateral border fragment that impinges on humeral head in external rotation 2.�� Glenoid neck fracture with clavicle fracture a.�� Nonoperative treatment i. 1 cm glenoid medialization 4�� . �� >20 degrees glenopolar angle difference

Figure 17D1-15 Diagram showing the linkage that is important in the superior shoulder suspensory complex.

Figure 17D1-16 Postoperative anteroposterior radiograph showing techniques of fixation of a “floating shoulder” injury.

the result of direct blows to the shoulder. The musculature surrounding the scapula makes nonunion a rare occurrence. Scapular malunion is rarely associated with clinical symptoms.2,11,33,36 Consequently, most authors favor a sling, ice, and supportive measures until the initial pain subsides2,11,35,36 Neer58 and Bateman32 reported immobilization using cross-strapping with adhesive moleskin in a nonambulatory patient with a scapular body fracture. This type of immobilization, however, has occasionally been associated with residual shoulder stiffness.35 On occasion, scapular malunion results in painful crepitus interfering with range of motion that may require removal of a bone prominence.59 Nordqvist and Petersson60 found poor long-term results in some patients with more than 10 mm of displacement. Cole61 includes 100% translation of the lateral border of the scapula in his indications for fixation of extra-articular scapula fractures. Usually these fractures are associated with spine or acromion fractures or with glenoid fractures. In these instances, the treatment of the body fracture is dictated by the associated fractures. Unusual causes of scapular body fractures include indirect injury, low-energy injury, and stress fracture. These injuries are treated nonoperatively with early mobilization. Wyrsch and coworkers62 reported a scapular body fracture in a professional boxer who sustained the injury during an attempted punch that completely missed the opponent. This injury was caused by a voluntary muscle contraction and was treated successfully with progressive active range

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Figure 17D1-18 Axial magnetic resonance imaging in a patient with superiorly displaced acromion fracture, showing complete disruption of posterior rotator cuff with defect in posterior deltoid. Also, the subscapularis is ruptured, and the biceps tendon has displaced from the groove. Figure 17D1-17 Scapular Y radiograph showing superiorly displaced acromion fracture with posterosuperior humeral head dislocation.

of motion and physical therapy. Deltoff and Bressler63 described the case of a scapular fracture sustained while a man was performing push-ups. McAtee64 reported an isolated scapular body fracture in a 41-year-old man playing touch football. Scapular body stress fracture has been reported in an elderly woman who had used a cane for ambulation.65 All these fractures were treated with a short period of protection and progressive range of motion.

Acromion Fracture Acromion fractures make up only 8% to 10% of all scapula fractures,1,9,10,66 and although fractures of the acromion are rare, when they do occur, it is usually the result of one of two mechanisms. First, an acromion fracture can result from a downward blow directly applied to the superior aspect of the acromion. Second, acromion fracture can result from superior displacement or dislocation of the humeral head (Fig. 17D1-17). When the injury is a result of a downward blow to the acromion, acromioclavicular dislocation is much more common than acromion fracture. Caution should be used in distinguishing this minimally displaced fracture from an os acromiale. Os acromiale usually has a more sclerotic border than an acute fracture, and in questionable cases, a radiograph of the contralateral side may be helpful because the os acromiale is bilateral in 60% of cases.23 The supraspinatus outlet view may be useful in estimating the amount of displacement if any is present.67 Significant displacement of an acromion fracture resulting from a downward blow to the acromion should alert the clinician to possible associated brachial plexus avulsions.25,68 Significant superior displacement of the acromion associated with superior displacement or dislocation of the humeral head should alert the clinician to possible injury

to the rotator cuff (Fig. 17D1-18).68 Fortunately, when a fracture does occur, it is usually minimally displaced. Less common mechanisms of acromion fractures include avulsions of the acromion from muscular over-pull and stress fractures from overuse. Most acromion fractures, because they are minimally displaced, should be treated closed.2,10,11,36,68 McLaughlin35 stated that “bony union is the rule, despite the presence or absence of immobilization, provided the fragments are in apposition.” Neer68 recommended symptomatic treatment only. Wilber and Evans,10 on the other hand, reported residual stiffness in patients with acromion fractures. They recommended cast immobilization in 60 degrees of abduction, 25 degrees of flexion, and 25 degrees of external rotation for 6 weeks. Most authors recommend ORIF for markedly displaced acromion fractures to reduce the acromioclavicular joint and prevent nonunion, malunion, and secondary impingement (Figs. 17D1-19 and 17D1-20).11,58,68 In a large meta-analysis study, Zlowodzki and associates43 examined data from many scapular fracture studies. Those that treated acromion fractures were combined and showed 70% good results with operative treatment and 82% good results with nonoperative treatment. There was no way to examine the indications for fixation across the different studies, and some of the studies included fractures not isolated to the acromion. Gorczyca and associates69 highlight the importance of looking for these injuries when the mechanism is suggestive. Their patient, with an unrecognized, nondisplaced acromion fracture, was allowed to bear weight with a platform walker. The acromion fracture then displaced and required operative treatment. Their surgical indications included displacement enough to effect deltoid function and lead to impingement in a manual laborer. Kuhn and associates70 recommended a classification system to help determine the need for operative intervention. Type I fractures with minimal displacement and type II displaced fractures without a decrease in the subacromial

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shots and contraction of the posterior deltoid as the club struck the golf ball. Stress fractures have also been reported after subacromial decompression secondary to thinning of the acromion.74-76 However, if after nonoperative trials the stress fractures have not healed and are symptomatic, good results can be obtained with ORIF (Box 17D1-2).77

Glenoid (Intra-articular) Fractures

Figure 17D1-19 Postoperative anteroposterior radiograph showing open reduction with internal fixation of acromion and suture anchor repair of rotator cuff.

space warrant nonoperative treatment. In type II displaced fractures in which the subacromial space is diminished by the inferior pull of the deltoid on the acromial fragment; ORIF is required to prevent secondary impingement. All the fractures were treated conservatively in this study, and 5 of 19 (26%) went on to nonunion. Stress fractures of the acromion may occur in athletes. These injuries should be managed nonoperatively. Ward and colleagues71 reported a stress fracture at the base of the acromion in a professional football player resulting from repeated microstresses secondary to weightlifting and blocking assignments. Veluvolu and associates72 reported a case of an acromial stress fracture in a jogger using arm weights while running. Hall and Calvert73 described a woman golfer who sustained a stress fracture at the base of the acromion as a result of repetitive stress by repeated

Historically, intra-articular glenoid fractures—in the absence of associated glenohumeral instability—have been managed nonoperatively.10,25 Intact glenohumeral ligaments prevent gross displacement of the fracture and maintain a stable shoulder that many authors have had success treating nonoperatively11,15,36,37 (Figs. 17D1-21 and 17D1-22). Surgical intervention was initiated only for glenoid fractures associated with glenohumeral instability.78,79 These reports were limited because standardized outcome measures were lacking and the incidence of late glenohumeral arthritis was unknown. Surgical treatment of glenoid fractures has received greater attention recently.17,18,41,54,66,80-87 Indications for ORIF of intra-articular glenoid fractures depend on fragment size, fracture displacement, and stability of the glenohumeral joint.11,15,17,18,33,37,38,41,54,66,80-87 Glenoid rim fractures (type I) are usually sustained during traumatic glenohumeral subluxation or dislocation. In the setting of recurrent anterior instability, Rowe and coworkers11,38 recommended excision of an anterior rim fragment of up to 25% of the articular surface with repair of the capsule back to the remainder of the glenoid. DePalma33 believed that glenohumeral instability will result if the fragment is greater than 25% of the anterior rim, greater than 33% of the posterior rim, or displaced more than 10 mm. He recommended immediate open reduction for these situations.33 Rockwood37 recommended open reduction of the fragment with screw fixation if the fracture involves at least 25% of the glenoid

Box 17D1-2 A cromion Fractures Mechanisms 1. Downward blow on acromion (rule out brachial plexus injures) 2. Superior blow by humeral head (rule out rotator cuff injures) 3. Avulsions 4. Stress fractures (numbers 3 and 4 are managed conservatively unless symptomatic nonunion or displacement occurs)

Figure 17D1-20 Axillary lateral radiograph showing open reduction with internal fixation of acromion and reduction of the glenohumeral joint.

Kuhn Classification 1. I—Minimally displaced (nonoperative; early range of motion, minimal deltoid use until healed) 2. IIa—Displaced without subacromial space decrease (nonoperative) 3. IIb—Displaced with subacromial space decrease (open reduction and internal fixation) From Kuhn JE, Blasier RB, Carpenter JE: Fractures of the acromion process: A proposed classification system. J Orthop Trauma 8:6-13, 1994.

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Figure 17D1-21 Combined glenoid articular fracture with satisfactory position. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

Figure 17D1-22 This fracture healed well without problems and with good preservation of the joint surface. (From Rockwood CA, Matsen FA [eds]: The Shoulder. Philadelphia, WB Saunders, 1990.)

A

C

B

D

Figure 17D1-23 Anteroposterior radiograph (A) and computed tomographic scan (B) of an anterior glenoid rim fracture (type Ia) involving about 33% of the articular surface, resulting in anterior instability of the shoulder. The fracture was repaired with five suture anchors through an anterior deltopectoral approach. Postoperative radiographs show anatomic reduction (C) and a reduced glenohumeral joint (D).

Shoulder

B

A

C

869

D

E

F

Figure 17D1-24 Anteroposterior (A) and axillary (B) radiographs show a large displaced anteroinferior glenoid rim fracture, type Ia. Its position and displacement are better evaluated with sagittal (C) and axial (D) images. E and F, Postoperative radiographs showing excellent reduction of the fragment and glenohumeral joint using a headless compression screw system.

and is associated with instability. A biomechanical study by Gerber and Nyffeler88 showed that an anterior rim defect that was 50% of the maximal anteroposterior diameter of the glenoid would lead to 30% loss of anterior stability. Although debate exists among surgeons about the amount of displacement and the size of the fragment that are acceptable, it is well accepted that rim fractures associated with persistent or recurrent instability should undergo ORIF.1,15,25,33,37,78,86,87 The size of the glenoid rim fragment and the quality of the bone determine the method of fixation to stabilize the fragment. Anterior glenoid rim fragments that are too small to accommodate a screw can be reduced and stabilized with suture anchors in the glenoid and sutures passed through the fragment and

tied (Fig. 17D1-23). Screw fixation can be used for large enough fragments with good bone quality (Figs. 17D1-24 and 17D1-25). Good results have been obtained with arthroscopically assisted reduction and percutaneous fixation of a displaced intra-articular glenoid fractures using cannulated screws,81 K-wires,41 or transglenoid sutures.89 Careful monitoring of fluid extravasation and assessment for compartment syndrome are recommended, as is having a low threshold to convert to open reduction if adequate reduction cannot be obtained arthroscopically. If the rim fracture is comminuted, the fragment can be excised, and a tricortical graft harvested from the iliac crest can be internally fixed to the glenoid rim.17 The results of operative fixation of glenoid rim fractures have been successful;

870


A

B

C Figure 17D1-25 Anteroposterior radiograph (A) and magnetic resonance image (B) demonstrate a posterior glenoid fracture involving about 40% of the articular surface, leading to posterior subluxation of the humeral head. Note the comminution extending down into the articular surface and lateral scapular body. This fracture was repaired by limited internal fixation to restore the posterior glenoid rim and glenohumeral stability (C).

Shoulder

B

A

C

E

871

D

Figure 17D1-26 A, Anteroposterior radiograph shows an intra-articular glenoid fracture involving the superior half of the glenoid (type III). B, Computed tomography demonstrates involvement of the coracoid process. C and D, The fracture was reduced and fixed with a superior-toinferior lag screw and an anterior plate. E, The patient regained full forward elevation and had an excellent result.

872


most authors reported restoration of glenohumeral stability and good functional results.25,41,78,80,81,86,87,89,90 For glenoid fossa fractures of types II to V, the amount of articular displacement and the degree of comminution determine the need for ORIF (Fig. 17D1-26). Goss17,18 recommended ORIF for an articular step-off of 5 mm, fracture separation of enough distance to preclude reliable healing, and subluxation of the humeral head out of the center of the glenoid. Kavanagh and associates82 described successful surgical treatment of displaced (4 to 8 mm) intra-articular fractures of the glenoid fossa. They emphasized that uncertainty still remained with regard to the amount of glenoid articular incongruity that could be accepted without risking long-term pain, stiffness, and post-traumatic degenerative arthritis. Poppen and Walker91 demonstrated that transarticular forces of 0.9 times body weight can be generated at the glenohumeral joint by lifting a 5-kg mass to shoulder height with the elbow extended. This suggests that disruption of articular congruence probably leads to unacceptable joint contact stress. Soslowsky and coworkers92 demonstrated that the maximal thickness of glenoid articular cartilage is 5 mm. On the basis of this information, several surgeons have adopted displacement of 5 mm or more as the indication for reduction and stabilization.66,78,79,82,93 The results of operative fixation of glenoid fossa fractures have been less predictable. Bauer and colleagues66 reported greater than 70% good or very good functional results for patients treated surgically for grossly displaced fractures of the glenoid rim, neck, fossa, and acromion. Leung and associates79 reported nine excellent and five good results in 14 patients treated surgically for displaced intra-articular glenoid fractures. Mayo and associates84 reviewed 27 displaced glenoid fossa fractures treated with ORIF at 43 months of follow-up and found that 82% of patients had good or excellent results. Three patients had articular incongruities measuring 2 mm or less. Ruedi and Chapman93 maintain that glenoid fractures that result in incongruity and instability benefit from ORIF to prevent arthritic changes. Recently, Schandelmaier and associates94 found Constant scores averaging 94% of the uninjured side in a series of operatively treated glenoid fossa fractures evaluated from 5 to 23 years postoperatively. Worse results were related to brachial plexus injures and infection. Overall, the large meta-analysis by Zlowodzki and associates43 found that 82% (45 of 55) of operatively treated glenoid fractures obtained good and excellent results, whereas only 67% (6 of 9) of those treated nonoperatively obtained equal outcomes. For type V and VI fractures, the degree of glenoid comminution determines treatment. ORIF is employed if the degree of comminution is minor and will allow stable fixation. If comminution is too severe to permit fixation of all fragments, limited reduction and stabilization of the articular segment are performed. Caution should be used in approaching these comminuted fractures because failed attempts at fixation disrupt the limited remaining soft tissue envelope. In selected cases with humeral head subluxation, partial fixation of larger fragments may be used to allow reduction of the humeral head, but any fixation used should

Box 17D1-3 Intra-Articular glenoid fractures 1. Type I (Ia—anterior, Ib—posterior) a. No shoulder instability i. Early range of motion ii. Strengthening b. Instability i. Ia—Anterior approach; Ib—posterior approach 1. Fragment fixation 2. Large fragment a. Screws 3. Small, comminuted fragment a. Suture anchors 2. Types II to IV a. Nonoperative i. 5 mm displacement ii.�� Humeral head subluxation 3.�� Types V and VI (comminuted) a.�� Nonoperative—sling, early range of motion i.�� Severe comminution ii.�� Centered humeral head b.�� Operative i.�� Large fragments to accept fixation partial open reduction with internal fixation, with humeral head subluxation

allow early passive range of motion exercises. If fracture comminution prevents even limited fixation, nonoperative management is employed. Techniques of nonoperative management include sling and swathe immobilization and early range of motion, immobilization in an abduction splint and range of motion above the splint if possible, or traction and range of motion as allowed by the traction17 (Box 17D1-3).

TREATMENT OPTIONS IN CHILDREN The criteria for operative treatment of scapular and glenoid fractures in children and adolescents are not known. These types of injuries are extremely uncommon in children and adolescents. In addition, the capacity for remodeling in children makes the amount of tolerable displacement less certain. The amount of glenoid or scapular remodeling possible as a function of age is not known. Therefore, treatment recommendations must be made intuitively, based on the age and projected growth remaining. Nonoperative treatment is recommended for most scapular fractures in children. The only potential exceptions to this rule are displaced glenoid fossa fractures, floating shoulders with greater than 3 cm of displacement of the glenoid fragment, and glenoid rim fractures that are associated with recurrent or persistent glenohumeral instability.

Shoulder

Authors’ Preferred Method

o f T r e a t m e n t i n

Glenoid Neck Fracture

Most glenoid neck fractures are impacted and stable and do not require any reduction to obtain a good clinical result. Symptomatic local care, followed by passive exercises, will result in a rapid return of motion. Strengthening exercises may be instituted at 4 to 6 weeks. In the case of a double disruption of the superior shoulder suspensory complex, including the glenoid neck and another portion of the superior shoulder suspensory complex, surgical management becomes necessary if displacement at one or both sites in unacceptable. Reducing and stabilizing one of the disruptions will usually indirectly reduce and stabilize the other, if the reduction is performed acutely (within 1 week of injury). Ipsilateral glenoid neck and clavicle fractures are managed operatively if medial displacement of the glenoid neck fracture is more than 3 cm or if the intact lateral border fragment is positioned in such a way that it would impinge on the humeral head in external rotation. In most acute cases, reduction and stabilization of the clavicle will reduce and stabilize the glenoid neck. If clavicular fixation fails to reduce the medial displacement of the glenoid neck, reduction and fixation of the glenoid neck are carried out. Criteria for Return to Athletics. Healing is normally complete after about 6 weeks. Return to sports should be delayed, however, until range of motion has returned to normal and the strength of the shoulder is 90% of that of the uninvolved extremity. This normally takes 3 to 4 months. Body and Spine Fractures

Assuming that serious associated injuries have been ruled out, symptomatic treatment is indicated for virtually all patients with this type of fracture. Ice and sling immobilization are used initially. Within 1 to 2 weeks, passive range of motion and stretching exercises can be instituted. As pain and swelling subside, active range of motion and progressiveresistance exercises can be instituted. Criteria for Return to Athletics. The athlete should be withheld from competition until the fracture has healed and there is a full range of motion (typically 6 to 12 weeks). Foam padding over the posterior aspect of the scapula helps cushion blows that may be encountered when the athlete returns to contact competition. Acromion Fractures

Most acromion fractures are stable and are minimally displaced. Therefore, a sling is required for only 3 to 5 days. When pain diminishes enough to permit exercise, active and passive range of motion exercises are begun. Resisted deltoid exercises are avoided for 6 weeks to allow fracture union. In the instance of a displaced acromion fracture, ORIF are performed with tension band or compression screw fixation for distal fractures or a 3.5-mm malleable reconstruction plate for more proximal injuries. Caution should be exercised to rule out the presence of os acromiale, rotator cuff tear, or brachial plexus injury. Criteria for Return to Athletics. The athlete with an acromion fracture, regardless of whether it was displaced

873

Adults

and required fixation, should be withheld from competition until fracture union is complete and range of motion is pain free. This normally requires between 6 and 12 weeks. If the fracture was accompanied by a complication, such as a rotator cuff tear or brachial plexus injury, appropriate treatment should be instituted and return to sport delayed accordingly. Glenoid Fracture: Stable Glenohumeral Joint

Glenoid fossa fractures with less than 5 mm of displacement that are not associated with instability are treated symptomatically, with a sling for immobilization, until pain permits range of motion exercises (7 to 10 days). Glenoid rim or fossa fractures involving 20% or more of the articular surface that are displaced more than 5 mm are treated surgically. Types II to V glenoid fossa fractures with displacement of 5 mm or more are treated surgically. The approach depends on whether extensile exposure of the lateral angle of the scapula is required. Extensile exposure of the anterior aspect of the lateral scapular border is limited because of the axillary nerve. The posterior approach is the most utilitarian and is used for most type II, IV, and V fractures. An extensile exposure may be obtained by reflecting the posterior deltoid origin from its attachment on the scapular spine (Fig. 17D1-27). Displaced type III glenoid fossa fractures usually do not require exposure of the lateral scapular border and can frequently be stabilized through an anterior deltopectoral approach. If the posterior cortex is comminuted, a posterior deltoid-splitting approach may be used in place of an anterior approach. Rehabilitation is similar for operatively and nonoperatively treated glenoid fossa fractures without glenohumeral instability because both are stable. Passive mobilization is instituted within the first week of injury or surgery. Activeassisted range of motion is added at 4 weeks. Strengthening exercises are added as range of motion is restored and absence of pain permits (typically 6 to 8 weeks). When nonoperative management is undertaken (i.e., less than 5 mm of displacement), close follow-up with radiographs and physical examination is necessary to document maintenance of glenohumeral stability. Criteria for Return to Athletics. Return to sport is possible after fracture union has occurred, range of motion has reached its maximal level, and strength has returned to within 90% of that of the opposite extremity (typically 3 to 4 months, depending on the type of fracture). The athlete should be warned about the possibility of the development of glenohumeral arthritis, particularly if he or she is involved in a sport that places a large demand on the shoulder. Glenoid Fracture: Unstable Glenohumeral Joint

Anterior glenoid fractures (type Ia) associated with glenohumeral instability are best treated with surgical repair. If the fragment is of good quality and large enough to accept a small fragment screw, ORIF through an anterior deltopectoral Continued

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Adults—cont’d

Figure 17D1-27 Posterior extensile exposure of the glenoid. The skin incision begins at the base of the scapular spine and extends laterally, parallel to the scapular spine. At the posterolateral corner of the acromion, the incision turns distally and medially and parallels the lateral border of the scapula (A). The posterior deltoid is reflected from its origin on the scapular spine from its most medial attachment to the posterolateral corner of the acromion. The interval between the infraspinatus and teres minor is indicated by the curved arrow (B). The infraspinatus insertion is sharply divided and retracted medially, thereby protecting the supraspinatus nerve at the supraspinatus notch (C). The teres minor and the axillary nerve are retracted laterally, providing excellent exposure to the posterior scapula (D). A plate is applied to the posterior aspect of the glenoid (E).

approach is performed. The fragment is reduced and held provisionally with a temporary wire, and definitive fixation is performed with a standard 3.5-mm cortical screw, a partially threaded cancellous screw, or a variable pitch headless compression screw. Smaller fractures may be fixed with suture

anchors placed in the glenoid and sutures passed through the fragment. If the fragment is too small to accommodate a screw or suture, it is excised, and the anteroinferior capsule is repaired to the raw surface of the remaining glenoid. Pendulum exercises are begun immediately postoperatively.

Shoulder



Two to 3 weeks after surgery, the patient is encouraged to use the arm for everyday living activities, and gentle passive flexion and external rotation exercises are begun. At 6 to 8 weeks, stretching and strengthening exercises are instituted. Posterior glenoid fractures (type Ib) with significant displacement or posterior glenohumeral instability require operative intervention through a posterior approach. A deltoid-splitting approach is usually adequate. If the fragment is not too large, this may be combined with a muscle-splitting, internervous approach between the infraspinatus and teres minor or an infraspinatus-splitting approach. The more distal interval (i.e., between infraspinatus and teres minor) is preferred if the fragment involves the inferior third of the glenoid or if the fragment is large. This exposure can be made extensile by reflecting the infraspinatus and elevating the dorsal portion of the teres minor origin. If exposure of the midportion of the posterior glenoid is required, an infraspinatus-splitting approach may be more appropriate. If the fragment represents 25% or more of the articular surface,


of

Adults—cont’d

it is reduced and stabilized with a screw. Smaller fragments are excised, and the capsule is reattached to the remaining glenoid. Criteria for Return to Athletics. Regardless of whether the fragment has been excised or fixed, the presence of glenohumeral instability dictates postponement of a return to competition. Rehabilitative efforts should concentrate on passive range of motion until fracture union has occurred. Further therapy should emphasize restoration of glenohumeral stability through rotator cuff and scapular stabilizer muscle exercises. Return to sport is possible after glenohumeral stability has been achieved, range of motion is restored, and strength has returned to within 90% of that of the opposite extremity (typically 4 to 6 months for anterior instability and 6 to 9 months for posterior instability). The athlete should be warned about the possibility of the development of glenohumeral arthritis, particularly if he or she is involved in a sport that places a large demand on the shoulder.

Treatment

All extra-articular scapular fractures in children who are 12 years and younger are treated nonoperatively initially. This recommendation is based on the belief that most of these fractures will heal and that the potential for remodeling is significant. The only exception to this rule is a displaced (>3 cm) glenoid neck fracture in combination with a displaced, ipsilateral clavicle shaft fracture (i.e., a floating shoulder). Under these circumstances, the clavicle is reduced anatomically and fixed rigidly with a plate and screws. Glenoid rim fractures in children who are 12 years and younger are not treated operatively unless they are associated with recurrent or persistent glenohumeral instability or are displaced 1 cm or greater. The indications in children older than the age of 12 years for operative treatment are the same as for adults. The surgical techniques for stabilization

in

Children

of glenoid rim fractures in children are the same as those described for adults. In children who are 12 years and younger, the technique of placing suture anchors within the remaining, uninvolved glenoid and passing sutures through the osseocartilaginous glenoid rim is preferred. Anchors with long-term absorbable (i.e., 3 months) sutures are preferred. Glenoid fossa fractures in patients older than 12 years are treated similarly to glenoid fossa fractures in adults. The potential for remodeling is greater in children who are 12 years and younger. The amount of residual displacement that is capable of being remodeled is not known. ORIF is currently performed in glenoid fossa fractures with 1 cm or greater of articular displacement. The surgical techniques, postoperative rehabilitation, and timing for return to athletics are the same as for adults.

S U G G E S T E D C

r i t i c a l

P

o i n t s

l Scapular fractures are relatively rare.

l The muscular envelope provides protection and dissipation of forces. l Usually, large direct forces are required for fracture, so the orthopaedist needs to evaluate for associated injuries. l Multiple ossification centers fuse at various times in the adolescent scapula, making comparison radiographs of the opposite scapula important when evaluating injuries in these patients.

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R E A D I N G S

Cole P: Scapula fractures. Orthop Clin North Am 33(1):1-18, 2002. Goss TP: Double disruptions of the superior shoulder complex. J Orthop Trauma 7:99-106, 1993. Goss TP: Scapular fractures and dislocations: Diagnosis and treatment. J Acad Am Surg 3:22-33, 1995. Niggebrugge AH, van Hesden HA, Bode PJ, van Vugt AB: Dislocated intraarticular fractures of the anterior rim of the glenoid treated by open reduction and internal fixation. Injury 24:130-131, 1993. Ramos L, Mencia R, Alonso A, Ferrandez L: Conservative treatment of ipsilateral fractures of the scapula and clavicle. J Trauma 42:239-242, 1997.


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S ect i o n

D

Injuries to the Glenoid, Scapula, and Coracoid 2. Fractures of the Coracoid in Adults and Children Allen Deutsch, Jason A. Craft, and Gerald R. Williams, Jr.

Fractures of the coracoid process of the scapula are uncommon and have received especially little attention in the sports medicine literature. Injury may occur as an apparently isolated phenomenon or in association with other injuries around the shoulder girdle. The coracoid process of the scapula serves as an anchoring point for the attachment of multiple ligaments and muscles. Ligaments include the coracohumeral and coracoacromial ligaments and the conoid and trapezoid components of the coracoclavicular ligaments. These last two ligaments perform an essentially suspensory function, exerting a static upward force on the scapula through the coracoid process.1 On the contrary, the muscular attachments exert a dynamic, active, and largely inferior force on the coracoid. The muscular origins comprise the pectoralis minor from the body and tip of the coracoid and the conjoined tendon from the tip. The conjoined tendon consists of the coracobrachialis and the short head of the biceps brachii. Consideration of these ligamentous and muscular attachments to the coracoid will give some insight into the proposed mechanisms of coracoid fracture. The location of the coracoid fracture (i.e., tip, body, or base in relation to the musculoligamentous structures) also determines the stability of the fracture and hence the propensity for displacement.

MECHANISM OF INJURY Mariani2 has suggested that direct and indirect mechanisms cause acute coracoid fracture. The direct type of injury appears to be a relatively rare phenomenon, probably because of the coracoid’s deep-seated, sheltered anatomic location. Therefore, a direct external blow to the coracoid severe enough to result in fracture usually involves massive trauma more common to motor vehicle crashes than to sporting endeavors. Direct trauma to the coracoid from the interior may arise in two circumstances, however. Anterior translation of the humeral head in subcoracoid glenohumeral dislocations may result in a direct coracoid impact that is sufficient to cause fracture.3-6 This too must be considered an uncommon injury, but it has been proposed that the combination of glenohumeral dislocation with coracoid fracture may be underdiagnosed. As discussed later, this shortcoming may be related to the difficulty of obtaining a good axillary lateral radiograph in an acutely painful shoulder or to the widespread practice of relying on the more difficult to interpret and less readily reproducible scapular lateral radiograph.

McLaughlin7 considered glenohumeral dislocation the most common cause of coracoid fracture. It has also been suggested that an undetected coracoid fracture might account for occasional cases of prolonged convalescence after glenohumeral dislocation3 and may conceivably be confused with recurrent anterior instability or rotator cuff disease. Wong-Chung and Quinlan described fracture of the coracoid tip that prevented closed reduction of an anterior glenohumeral dislocation.8 The other direct mechanism of coracoid fracture would in theory involve a blow to the lateral clavicle causing inferior displacement and impact with the coracoid.2 This would result in acromioclavicular ligamentous disruption but would preserve the coracoclavicular ligaments. Although this scenario appears not to have received specific attention in the literature, it is possible that some apparently isolated, undisplaced coracoid fractures might arise in this manner. The stress radiograph, discussed later, would be of particular relevance in this situation. So-called indirect mechanisms probably account for most fractures of the coracoid process. An indirect mechanism is probably most often responsible for isolated coracoid fractures.2,9 Smith10 described this mechanism in terms of a sudden, violent, and resisted contraction of the conjoined tendon and pectoralis minor. Wyrsch and associates described a case of an extra-articular scapula fracture with extension into the coracoid process in a professional boxer resulting from a violent muscle contraction.11 Mariani2 concluded that the coracoid is especially vulnerable to the stress of muscular action when the arm is in the position of abduction and extension. Benton and Nelson12 also drew attention to the stress placed on the coracoid when the arm is in this position. Another indirect mechanism of coracoid fracture involves a direct blow or fall onto the point of the shoulder,13 causing superior subluxation or dislocation of the lateral clavicle. Rather than the more common rupture of the coracoclavicular ligaments, the coracoid (proximal to the coracoclavicular ligaments) may fail.10,14-18 The pain accompanying the coracoid fracture may overshadow the acromioclavicular disruption so that, again, this injury may be misinterpreted as an isolated coracoid fracture if stress radiographs are not obtained.2,10 More commonly, however, the acromioclavicular dislocation is recognized, and the coracoid process fracture is unappreciated. Avulsion fractures of the coracoid resulting from strong traction forces have also been reported.19

Shoulder

Box 17D2-1 Coracoid Fracture Basics A. Rare injury B. Mechanisms 1. Direct a. External source (e.g., motor vehicle collision) b. Anterior humeral head dislocation c. Inferiorly displaced distal clavicle with acromioclavicular (AC) separation 2. Indirect a. Inferior: conjoined tendon and pectoralis minor avulsion b. Superior: superior AC separation with failure through coracoid instead of coracoclavicular ligaments c. Rare i. Suture tied under coracoid for AC reconstruction ii. Stress fractures

In addition to these direct and indirect mechanisms involving significant trauma, repetitive forces of a lesser degree have been reported by a number of authors to be a source of coracoid stress fracture. Boyer9 and Sandrock20 in separate reports described a fracture of the coracoid base in a young female trap shooter. The position of the gun butt directly over the coracoid tip was confirmed radiologically. Symptoms resolved, and the fracture healed when shooting was stopped. This appears to be an example of repetitive direct trauma resulting in stress fracture. A case of indirect trauma resulting from repetitive muscular action and leading to coracoid stress fracture in its distal half was reported by Benton and Nelson.12 They described a 19-year-old tennis player with a 4-year history of shoulder pain. It had been of insidious onset and was aggravated during serving. This patient eventually required excision of the distal fragment and reattachment of the conjoined tendon. Nontraumatic causes of coracoid fractures have also been described secondary to nonresorbable coracoclavicular cerclage fixation during acromioclavicular reconstruction, as well as in association with massive rotator cuff tears (Box 17D2-1).21

877

reviously mentioned case report by Benton and Nelson12 p of a distal stress fracture in a young tennis player. These problems of union and displacement and hence the possibility of persistent symptoms appear to be related to the location of the fracture in relation to the coracoclavicular ligaments.1 A fracture within the broad area of the attachment of these ligaments is likely to be splinted and minimally displaced. As the fracture line moves toward the tip and hence beyond the attachments of the conoid and trapezoid ligaments, however, the coracoid tip becomes increasingly subject to the displacing action of the pectoralis minor and the conjoined tendon.4,12 Coracoid fracture has been described in association with acromioclavicular separation and glenohumeral dislocation. Montgomery and Loyd16 described two adolescents with coracoid apophyseal avulsion at the site of attachment of the coracoclavicular ligament. Combalia and colleagues described a case of a 12-year-old boy who sustained an acromioclavicular dislocation with epiphyseal separation of the coracoid process as a result of a fall during a soccer match.25 Certain other associations have also been recognized. Zilberman and Rejovitzky24 encountered coracoid fractures in conjunction with clavicular shaft and acromion fractures. Wolf and colleagues5 described a combination of coracoid base fracture and avulsion of a thin spicule from the superior border of the scapula medial to the coracoid. This pattern of injury may be due to the fact that the fragments are connected by the suprascapular ligament. Acromioclavicular separation with coracoclavicular ligament disruption and coracoid fracture has also been described.26,27 Neurologic injuries may also be seen with coracoid fractures.13 The brachial plexus deep to the coracoid and pectoralis minor may be contused, resulting in either specific or subtle patchy neurologic deficits. Basal coracoid fractures may especially result in suprascapular nerve entrapment and may be confused with rotator cuff tears (Fig. 17D2-1).13

CLINICAL FEATURES OF CORACOID FRACTURES History

PATTERN OF CORACOID FRACTURE The pattern of coracoid fracture is variable. Most such fractures occur through the base of the process,2,3,9,22,23 and this is almost invariably the case with associated acromioclavicular injuries. Basal coracoid fractures may very rarely involve a significant portion of the superior portion of the glenoid articular surface. Fractures of the body or tip of the coracoid process of the scapula without acromioclavicular injury appear to be related more to violent muscular action1,4,12,24 but have been associated with anterior glenohumeral dislocation.6 These more distal fractures also appear to be more troublesome in terms of delayed union or nonunion and the related problem of displacement.4 Both these problems are well demonstrated in the

The history of coracoid fractures caused by shoulder injury is not particularly specific. About one third of reports of coracoid fractures attribute the injury to a motor vehicle crash.14 The next most common history obtained is that of a fall onto the point of the shoulder or a direct blow to the shoulder. It is of interest that football injuries involving both these mechanisms appear regularly in the literature. Typical football injuries have included a fall onto the shoulder, a direct blow from running into a goalpost, and apparently impact sustained during a rugby scrum.2 A fall backward onto the extended abducted and externally rotated arm also appears to be a well-established mechanism1,4 and may be brought out in the history. As previously discussed, coracoid stress fracture appears to be a real entity in sportsmen.4,9,20 A history of acute injury is conspicuously absent, and recalcitrant symptoms

878


A

B

Figure 17D2-1 A, The coracoid process serves as the insertion of the pectoralis minor and the origin of the conjoined tendon of the coracobrachialis and the short head of the biceps. Reflection of the pectoralis reveals the proximity of the underlying brachial plexus. B, The suprascapular nerve is at risk with fractures of the coracoid base that extend into the superior scapular notch.

of insidious onset may pose a diagnostic dilemma. Pain is an invariable complaint with acute fracture of the coracoid but may be poorly localized at the front of the shoulder. Pain may be aggravated by arm movements that exert muscular forces onto the coracoid. The patient may recognize these particular movements, which include elbow flexion,28 shoulder flexion with the elbow extended,2,12 and combined shoulder abduction, extension, and external rotation.28 Similarly, the patient may volunteer the fact that the pain is aggravated by deep inspiration owing to pectoralis minor activation.2,12 As with all shoulder girdle injuries, neurologic symptoms13 may be prominent, especially in the form of transient paresthesias. This is not surprising in view of the intimate relationship of the major neurovascular structures to the coracoid and pectoralis minor.

Physical Examination Unless there has been an associated injury to the acromioclavicular joint or a glenohumeral dislocation, there will usually be no striking external abnormality. Falls onto or direct blows to the shoulder may, of course, result in localized areas of contusion or abrasion. Despite the deep-seated location of the coracoid process, swelling or loss of definition in the deltopectoral interval may be detected.28 Marked localized tenderness on palpation is a key finding. Specific stress tests2,12,28 such as resisted elbow flexion, resisted straight-arm raising, and coughing may also sharply localize discomfort to the coracoid region. Whenever suspicion of a coracoid injury is raised, attention should be specifically directed to the acromioclavicular joint and vice versa. Local acromioclavicular tenderness, swelling, subluxation, or obvious superior dislocation of the lateral clavicle may be apparent. As always, comparison with the normal shoulder may be of considerable assistance. Neurologic examination is mandatory in cases of coracoid fracture. Because deficits may be patchy and subtle, a thorough brachial plexus assessment is essential. Special emphasis should be placed on suprascapular nerve evaluation because of the risk for entrapment.13

Diagnostic Studies The anteroposterior view should be part of the routine shoulder series and is of particular relevance in detecting associated acromioclavicular injuries or fractures (Fig. 17D2-2).5,24 Although it is possible to diagnose some coracoid fractures with a plain anteroposterior radiograph,28 it is likely that most will be overlooked without additional views (Fig. 17D2-3).12 This is because the coracoid process is foreshortened and projected over the acromion and the spine of the scapula in this view.29 Many authors have stressed the value of the axillary lateral view in diagnosing coracoid fractures,3,6,9,12-14 but even this view may fail to demonstrate a basal coracoid fracture (Fig. 17D2-4).29 Froimson28 has also pointed out that the abduction required for a good axillary lateral view may be difficult to obtain because of the pain it provokes in patients with acute coracoid fractures. A much better profile of the coracoid, including the base, can be obtained by tilting the x-ray beam in a cephalic direction. This obviates the need to move the patient’s arm. Most authors recommend a supine position

Figure 17D2-2 Combined coracoid process fracture and acromioclavicular dislocation as demonstrated on routine anteroposterior radiograph.

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Figure 17D2-3 A, A coracoid process fracture that is well visualized on a routine anteroposterior radiograph. B, Fractures of the base of the coracoid process can be difficult to visualize on routine anteroposterior views.

with a 30- to 35-degree cephalic tilt.2,6,17,24,29 Froimson found that a cephalic tilt of as much as 45 to 60 degrees was quite useful. Although the Stryker notch view was originally intended to identify the Hill-Sachs lesion characteristic of anterior glenohumeral dislocations, the authors have found this technique especially useful in studying coracoid fractures (Fig. 17D2-5).30 Kopecky and colleagues22 reported on the value of computed tomographic scanning when doubt exists. The authors have also found that this modality is helpful in clarifying coracoid fracture morphology (Fig. 17D2-6). Specific attention should be paid to the acromioclavicular joint in the presence of coracoid fracture. Despite acromioclavicular dislocation, the coracoclavicular distance will be maintained (Fig. 17D2-7).2,10,14 Erect anteroposterior films of both shoulders are necessary to compare the coracoclavicular distance on the injured side with the uninjured side. Although stress views may be helpful in some cases, most often they are not required.

A

Normal coracoid epiphyses or apophyses should not be confused with fractures.12,30 The coracoid process forms from two ossification centers. The basal ossification center also forms the upper third of the glenoid, whereas the other forms the main body of the coracoid. The basal epiphyseal plate fuses at puberty. Smaller accessory ossification centers that are shell-like and rounded may be seen medial to the coracoid base or at its very tip (Fig. 17D2-8). Cottalorda and colleagues described a case of a 15-year-old boy who suffered a displaced epiphyseal separation as a result of a direct fall onto the shoulder while participating in judo.31 The only other diagnostic study apart from radiography that may be necessary is electromyography, which is indicated if suprascapular nerve entrapment is suspected.13 This most often occurs subacutely when the pain associated with the acute fracture has subsided and strength of the supraspinatus and infraspinatus can be accurately assessed.

B

Figure 17D2-4 A, Fractures of the tip of the coracoid process are frequently well visualized on an axillary lateral radiograph. B, Basal fractures of the coracoid process can be difficult to demonstrate, even on an axillary lateral radiograph.

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Figure 17D2-7 An anteroposterior stress radiograph in patient with a combined coracoid process fracture and an acromioclavicular dislocation reveals that the coracoclavicular interspace has been maintained.

Figure 17D2-5 The Stryker notch view is helpful in demonstrating basal coracoid process fractures that are difficult to visualize on other routine views.

Treatment Options Acute isolated fracture of the coracoid base is almost invariably nondisplaced and is treated conservatively with the expectation of a good result.1 If the acromioclavicular joint is sound, the basal fracture is splinted by the coracoclavicular ligaments, and displacement is minimal. Fracture surfaces are relatively large and predominantly cancellous. Prompt union is generally anticipated. Nonunion is infrequent, may be related to premature return to vigorous activities, and may require bone grafting and screw fixation (Fig. 17D2-9). Essentially, the basic treatment ought to be symptomatic—resting the affected arm in a sling,

Figure 17D2-6 Computed tomographic scanning is occasionally useful for clarifying the morphology of certain coracoid fractures.

a dministering analgesia for the initially severe pain, and gradually mobilizing the shoulder as symptoms regress and radiographic healing occurs. Basal coracoid fracture with suprascapular nerve palsy is a rare indication for early operative exploration, especially if there is any displacement of the fracture with narrowing of the suprascapular notch (Fig. 17D2-10). The prognosis for recovery from suprascapular entrapment appears to be poor once cancellous bone has formed in the region of the suprascapular notch.13 As the location of an isolated coracoid fracture approaches the tip of the coracoid process, opinions about treatment diverge. The closer the fracture gets to the tip of the coracoid process, the smaller is the stabilizing effect of the coracoclavicular ligaments and the greater is the propensity for displacement or nonunion exerted by the muscular attachments at the tip. Rowe32 recommends simple approximation of fragments with nonresorbable sutures in this situation, whereas McLaughlin7 considers that fibrous union is not uncommon and is rarely accompanied by any residual symptoms (Fig. 17D2-11). Benton and Nelson described late surgical treatment of a displaced coracoid fracture that irritated the surrounding soft tissue structures.12 Marked displacement and delayed union of these more distal fractures may significantly delay recovery.1,4,12 Moreover, surgical management of significantly displaced fractures frequently yields satisfactory results. When surgical management is selected, the choice is between fixation of the fragment (Fig. 17D2-12) and, if it is especially distal, excision of the fragment and reattachment of the pectoralis minor and conjoined tendon to the residual coracoid stump. Similarly, for a combined coracoid fracture and acromioclavicular dislocation, there appears to be no single best line of management. Martin-Herrero and coworkers33 reviewed seven patients with coracoid fractures. Four had associated acromioclavicular joint injuries, but all had “good or very good” results at final follow-up with conservative treatment. Bernard and associates,14 in a comprehensive review of this dual injury, found that surgical and nonsurgical methods of treatment appear to offer equally favorable results. It is also of interest that coracoid nonunion appeared to be no more common with this injury. Should nonunion arise, its combination with complete acromioclavicular dislocation appears to be compatible with a functional pain-free result.15

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Figure 17D2-8 A, The normal basal coracoid physis as demonstrated on the Stryker notch view. B, The normal ossification center at the tip of the coracoid process.

A

B

Figure 17D2-9 A, Stryker notch view demonstrating nonunion of the base of the coracoid process in an 18-year-old football player. B, The nonunion was fixed through an anterior deltopectoral approach with an interfragmentary screw and bone graft.

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Figure 17D2-10 The scapula viewed from posterior, with the spine of the scapula and acromion removed. The basilar coracoid fracture is displaced and impinging on the suprascapular nerve through the suprascapular notch.

Acromion

Displaced Superior transverse scapular ligament

Humeral head

Entrapped suprascapular nerve

Cut end of scapular spine

Scapula

Posterior view acromion removal

Eyres and coworkers recently described a classification system for coracoid fractures that is based on the size of the coracoid fragment and whether a clavicle fracture or an acromioclavicular separation is present.34 They recommend surgical treatment of displaced fractures that extend into the glenoid or scapular body, fractures associated with clavicle fracture or acromioclavicular separation, and fractures with interposed coracoid fragments preventing reduction of glenohumeral joint dislocation. Ogawa and colleagues described their experience with treatment of 67 coracoid fractures.35 Most patients had associated injuries, including acromioclavicular separations, clavicle fractures, and scapula fractures, that disturbed the link between the scapula and the clavicle. They recommended open reduction and internal fixation of

coracoid fractures that were posterior to the attachment of coracoclavicular ligaments to restore the scapuloclavicular connection to permit early therapy. When one is dealing with athletes with combined acromioclavicular dislocation and a displaced coracoid base fracture, the unusual physical demands of their sport may influence treatment more toward anatomic restoration. If this course is taken, the fracture location itself may preclude coracoclavicular fixation techniques, and trans articular pins may become necessary (Fig. 17D2-13).10 Screw fixation of the coracoid back to the body of the scapula is technically difficult but may be indicated if the fracture is not fixed acutely. Under these circumstances, direct fracture exposure is necessary to accomplish reduction.

Figure 17D2-11 A, Axillary lateral view demonstrating an acute fracture of the coracoid in a 42-year-old woman who sustained a glenohumeral dislocation. This patient also suffered concomitant suprascapular nerve palsy and was managed nonoperatively. Continued

A

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Figure 17D2-11, cont’d B and C, At 2 years’ follow-up, the suprascapular nerve palsy had resolved, the patient had returned to all previous activities, and physical examination revealed small deficits in forward elevation and internal rotation.

B

C

Figure 17D2-12 Anteroposterior (A) and axillary lateral (B) images show excellent reduction and fixation of an unstable distal coracoid fracture.

A

B

Figure 17D2-13 Combined coracoid process fracture and acromioclavicular dislocation treated with reduction and acromioclavicular wires.

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of

Treatment

Without Acromioclavicular Dislocation

Fractures of the Distal Coracoid Process

Because the coracoclavicular and acromioclavicular ligaments remain intact in this injury, the fracture is stable. Therefore, treatment with a sling for comfort is sufficient. Pendulum exercises should be encouraged to prevent loss of motion in the shoulder; however, overhead elevation is restricted for 4 to 6 weeks to allow healing to occur at the base of the coracoid process. The athlete may return to competition after complete healing of the fracture and return of a full, painless range of motion. This usually requires 6 to 10 weeks.

Treatment of these fractures is symptomatic. Most patients become asymptomatic in 8 to 10 weeks regardless of the presence or absence of nonunion. Should a symptomatic nonunion result, excision of the fragment and reattachment of the pectoralis minor or conjoined tendons to the residual coracoid stump are curative. The athlete can return to competition when pain allows a full range of motion. This normally occurs about 4 to 6 weeks after injury (Box 17D2-2).

With Acromioclavicular Dislocation

When a coracoid process fracture is accompanied by a severely displaced acromioclavicular dislocation, open reduction with internal fixation is usually indicated. The displacement criteria for fractures of the coracoid base that involve the articular surface of the glenoid are more stringent than the criteria for fractures without articular involvement. Articular displacement of 5 mm or greater is treated with open reduction and internal fixation. Fixation options are limited because of the fracture of the coracoid process. Reduction and fixation of the acromioclavicular joint must be accompanied by reduction of the coracoid base and intraarticular glenoid component. Therefore, despite the small risk for acromioclavicular arthritis, fixation with transarticular smooth pins is indicated. The pins are removed after 6 to 8 weeks when radiographs reveal healing of the fracture. Before the pins are removed, the patient is not permitted to raise his or her arm overhead. If the fracture is not reduced within 1 week, reduction of the acromioclavicular dislocation will most likely not result in simultaneous reduction of the coracoid fracture. Under these circumstances, direct exposure of the coracoid base fracture is required. Interfragmentary screw fixation is performed. After pin removal, fracture healing, and restoration of a full, pain-free range of motion, the athlete may return to competition. It is not necessary to wait for screw removal in those treated with interfragmentary screw fixation. Return to competition is encouraged after restoration of a full, painfree range of motion. This normally requires 8 to 12 weeks.

POSTOPERATIVE MANAGEMENT AND REHABILITATION The postoperative rehabilitation of coracoid process fractures is the same as the nonoperative management of fractures that do not require surgery. This is because fractures selected for nonoperative management are either minimally displaced and stable or displaced without the need for anatomic reduction. Likewise, operatively treated fractures have been rendered stable. Pendulum exercises are instituted within 7 to 10 days of injury or surgery. Supine passive flexion to 90 degrees or less and passive external rotation are added 3 to 4 weeks after injury or surgery.

Box 17D2-2 C oracoid Fracture Treatment Outline A. Basal fractures 1. Nonoperative treatment a. Nondisplaced basal fractures i. Splinted by intact coracoclavicular ligaments

ii. Cancellous surface allows reliable healing b. Sling for comfort c. Progressive range of motion as healing allows 2. Operative treatment a. Associated suprascapular nerve palsy b. Extension into glenoid articular surface c. Associated operative acromioclavicular joint separation B. Nonbasal fractures 1. More distal fractures lose splinting of coracoclavicular ligaments 2. Conjoined tendon and pectoralis minor place distracting forces at fracture 3. Operative treatment a. More than 1 cm displacement b. Symptomatic nonunion c. Displacement precluding glenohumeral reduction after anterior shoulder dislocation

External rotation is particularly important in coracoid base fractures because scarring at the coracohumeral ligament attachment site may result in loss of passive external rotation. Passive and active-assisted overhead elevation is permitted 6 weeks after injury or surgery. An overhead pulley is useful in allowing the athlete to improve overhead elevation progressively. Rotator cuff and deltoid strengthening exercises are added 6 to 8 weeks after surgery. As these exercises are progressed, the important scapular rotators are also strengthened. Return to athletic competition is determined individually based on attainment of a pain-free range of motion and strength that approaches 90% of the uninjured side.

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r i t i c a l

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o i n t s

l Suspicion is the key to diagnosis, especially with direct blow to the shoulder or with an AC joint separation. l Pain is experienced with use of muscles attached to coracoid (pectoralis minor—deep inspiration; elbow flexion—short head biceps tendon; shoulder flexion with elbow extended—coracobrachialis). l A thorough brachial plexus examination is necessary because of proximity (especially axillary, musculocutaneous nerves).

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R E A D I N G S

Garcia-Elias M, Salo JM: Nonunion of a fractured coracoid process after dislocation of the shoulder. J Bone Joint Surg [Br] 67:722, 1985. Gil JF, Haydar A: Isolated injury of the coracoid process: Case report. J Trauma 31:1696, 1991. Martin-Herrero T, Rodriquez-Merchan C, Munera-Martinez L: Fracture of the coracoid process: presentation of seven cases and reveiw of the literature. J Trauma 30:1597-1599, 1990. Ogawa K, Yoshida A, Takahashi M, Ui M: Fractures of the coracoid process. J Bone Joint Surg [Br] 79:17-19, 1997. Wong-Chung J, Quinlan W: Coracoid process preventing closed reduction of anterior dislocation of the shoulder. Injury 20(5):296-297, 1989.


S E C T I O N

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Scapulothoracic Disorders in Athletes John E. Kuhn

Scapulothoracic disorders include crepitus and bursitis, two related conditions that are not infrequently seen in the athletic population; scapular winging; and scapulothoracic dyskinesis. These conditions are often related to alterations in normal scapulothoracic kinematics. Before describing these conditions, it is important to understand the anatomy of the scapulothoracic articulation.

ANATOMY AND BIOMECHANICS OF THE SCAPULOTHORACIC ARTICULATION Seventeen muscles have their origin or insertion on the scapula (Box 17E-1, Fig. 17E-1), making it the cornerstone for coordinated upper extremity activity. These muscles include the rhomboideus major and minor, the levator scapulae, the serratus anterior, the trapezius, the omohyoid, and the pectoralis minor. Scapular winging or scapulothoracic dyskinesis may occur as a result of dysfunction of these muscles. The rotator cuff muscles (supraspinatus, infraspinatus, subscapularis, and teres minor) contribute 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 scapulohumeral muscles provide power to the humerus and include the deltoid, the long head of the biceps, the short head of the biceps, the coracobrachialis, the long head of the triceps, and the teres major. Almost every functional upper extremity movement has components of scapulothoracic and glenohumeral motion.

Box 17E-1 Muscles with Origins or Insertions on the Scapula Scapulohumeral Muscles Long head of biceps Short head of biceps Deltoid Coracobrachialis Teres major Long head of triceps Scapulothoracic Muscles Levator scapulae Omohyoid Rhomboid major Rhomboid minor Serratus anterior Trapezius Pectoralis minor Rotator Cuff Muscles Supraspinatus Infraspinatus Subscapularis Teres minor From Kuhn JE: The scapulothoracic articulation: Anatomy, biomechanics, pathology and management. In Iannotti JP, Williams GR Jr (eds): Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams &Wilkins, 1999, pp 817-845.

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DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Conjoined tendon of coracobrachialis and biceps

Trapezius muscle

Pectoralis minor muscle Scapular notch Omohyoid muscle

Omohyoid Coracoid muscle Superior angle Levator scapular muscle Supraspinatus muscle Rhomboid minor muscle Infraspinatus muscle Medial border

Acromion Deltold muscle Glenoid fossa Scapula neck Triceps(long head)

Teres minor muscle

Serratus anterior muscle Subscapularis muscle

Lateral border

Rhomboid major muscle Teres major muscle Inferior angle Latissimus dorsi muscle Figure 17E-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. (Redrawn from Kuhn JE: The scapulothoracic articulation: Anatomy, biomechanics, pathology and management. In Iannotti JP, Williams GR Jr [eds]: Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams &Wilkins, 1999, pp 817-845.)

While at rest, the scapula is anteriorly rotated relative to the trunk about 30 degrees.1,2 The medial border of the scapula is also rotated, with the inferior pole diverging away from the spine about 3 degrees. The scapula is also tilted forward about 20 degrees in the sagittal plane when viewed from the side.1 It is thought by some that deviations in this normal alignment may contribute to glenohumeral instability, and likely contribute to scapulothoracic crepitus and bursitis.

Bursae around the Scapula The normal smooth gliding motion of the scapula on the chest wall occurs as a result of multiple scapulothoracic bursae. Two major, or anatomic, bursae and four minor, or adventitial, bursae have been described for the scapulothoracic articulation (Box 17E-2, Fig. 17E-2). The major bursae are easily and reproducibly found,3,4 whereas the adventitial bursae are not. The first major bursa is found in the space between the serratus anterior muscle and the chest wall. The second major bursa is located between the subscapularis and the serratus anterior muscles.3,5,6 The superomedial angle and the inferior angle of the scapula appear to be the two anatomic regions involved in patients with scapulothoracic bursitis. When symptomatic, these areas tend to develop inflamed bursae; however, these bursae may be adventitious because they are not found reliably.3,7,8 When scapulothoracic bursitis affects the inferior angle of the scapula, most authors agree that the inflamed bursa lies between the serratus anterior muscle and the chest wall.6,9,10 This bursa has been called the infraserratus bursa6 and the bursa mucosa serrata.10,11 The second and more common site of scapulothoracic bursitis

occurs at the superomedial angle of the scapula. Codman believed that the inflamed superomedial angle bursa was also an infraserratus bursa, lying between the upper and anterior portion of the scapula and the back of the first three ribs.6 O’Donoghue also believed that the bursa between the serratus anterior and the chest wall was the involved bursa in athletes with pain and crepitus.12 Von Gruber, on the other hand, identified a bursa in this region between the subscapularis and the serratus anticus muscles, which he called the bursa mucosa angulae superioris scapulae.13 Williams and colleagues identified a third major bursa, the scapulotrapezial bursa, which lies between the superomedial scapula and the trapezius muscle.4 This bursa contains the spinal accessory nerve but is not thought to be a source of scapulothoracic crepitus or bursitis. A third minor or adventitial bursa, which Codman believed was the site of painful crepitus in scapulothoracic crepitus, was called the trapezoid bursa, and is found over the triangular surface at the medial base of the spine of the scapula under the trapezius muscle.6 Some believe that these minor bursae are adventitial and develop in response to abnormal pathomechanics of the scapulothoracic articulation.3,7,8 It would not be surprising, then, to find these bursae inconsistently or in different soft tissue planes.

SCAPULOTHORACIC CREPITUS Pathophysiology Symptomatic scapulothoracic crepitus has been described by a number of different authors and has been called the snapping scapula,9 the washboard syndrome,14 the scapulothoracic

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Box 17E-2 Bursae Around the Scapula

Box 17E-3 Causes of Scapulothoracic Crepitus

Major/Anatomic Bursae Infraserratus bursae: between serratus anterior and chest wall Supraserratus bursae: between subscapularis and serratus anterior muscles Scapulotrapezial bursae: between superomedial scapula and the trapezius

Interposed Tissue

Minor/Adventitial Bursae Superomedial Angle of the Scapula Infraserratus bursae: between serratus anterior and chest wall Supraserratus bursae: between subscapularis and serratus anterior Inferior Angle of the Scapula Infraserratus bursae: between serratus anterior and chest wall Spine of Scapula Trapezoid bursae: between 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.

syndrome,15 the rolling scapula,7 the grating scapula,16 and the scapulocostal syndrome.17 Boinet18 was the first to describe this disorder in 1867. Thirty-seven years later, Mauclaire19 classified scapulothoracic crepitus into three groups: “froissement” was described as a gentle friction sound and was thought to be physiologic, “frottement” was a louder sound with grating and was usually pathologic, and “craquement” was a loud snapping sound and was always pathologic. These scapular noises are thought to occur from two sources, either from anatomic changes in the tissue interposed between the scapula and the chest wall or by incongruence in the scapulothoracic articulation (Box 17E-3). Extrapolating from Milch,9 frottement may

Infraserratus bursa Supraserratus bursa

Infraserratus bursa Supraserratus bursa Trapezoid bursa Infraserratus bursa

Figure 17E-2 Bursae of the scapula. The locations of both anatomic and adventitial bursae are shown. (Redrawn 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.)

Muscle Atrophy Fibrosis Anatomic variation Bone Rib osteochondroma Scapular osteochondroma Rib fracture Scapular fracture Hooked superomedial angle of scapula Luschka’s tubercle Reactive bone spurs from muscle avulsion Other Soft Tissue Bursitis Tuberculosis Syphilitic lues Abnormalities in Scapulothoracic Congruence Scoliosis Thoracic Kyphosis From Kuhn JE, Hawkins RJ: Evaluation and treatment of scapular disorders. In Warner JJP, Iannotti JP, Gerber C (eds): Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 357-375.

s uggest soft tissue pathology or bursitis, whereas craquement may suggest bony pathology as the source of symptomatic scapulothoracic crepitus. It is interesting to note that Codman was able to make his own scapula “sound about the room without the slightest pain”6 and was likely demonstrating froissement. In every instance, the air-filled thoracic cavity acts as a resonance chamber, much like a string instrument,20 and amplifies these noises. Pathologic conditions affecting muscle in the scapulothoracic articulation include atrophied muscle,9 fibrotic muscle,9,13,21 and anomalous muscle insertions.22 The most common bony pathology in the scapulothoracic space that may give rise to scapulothoracic crepitus is the osteochondroma, arising either from the ribs23 or the scapula (Fig. 17E-3).21,24,25 Malunited fractures of the ribs or scapula are also capable of creating painful crepitus.9,26,27 Abnormalities of the superomedial angle of the scapula, including a hooked superomedial angle24,28 or Luschka’s tubercle (which originally was described as an osteochondroma, but has subsequently come to mean any prominence of bone at the superomedial angle),9,27,29 have also been implicated as sources for scapulothoracic crepitus. Others11,20,30 implicate reactive spurs of bone that are created by the microtrauma of chronic, repeated small periscapular muscle avulsions. Certainly, any bony pathology that causes scapulothoracic crepitus is capable of forming a reactive bursa around the area of pathology.31,32 In fact, at the time of resection of bony pathology, a bursa is frequently seen. Bursae can become inflamed and painful in the absence of bony

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who participate in sports that require repetitive overhead activity are commonly affected.12 There may be a familial tendency toward developing symptoms.7 Patients may relate a history of mild trauma that precipitates symptoms,41 and scapulothoracic crepitus may be bilateral in some patients.5 A space-occupying lesion, such as an osteochondroma, should be suspected if fullness or winging is identified on inspection of the scapula. Palpation or auscultation while the shoulder goes through a range of motion may help to identify the source and location of the periscapular crepitus.5,42 Supplemental radiographs, which include tangential views of the lateral scapula, computed tomography, or magnetic resonance imaging may be helpful in identifying anatomic pathology. Figure 17E-3 Osteochondroma of the scapula causing scapulothoracic crepitus. Note the increased signal in the bursa surrounding this osteochondroma of the scapula.

pathology and may, by themselves, become a source of crepitus.33 Other soft tissue pathologies that have been implicated in scapulothoracic crepitus include tuberculosis lesions in the scapulothoracic region and syphilitic lues,9 which are exceedingly rare in athletes. A common source of scapulothoracic crepitus in athletes involves abnormalities in congruence of the scapulothoracic articulation. Both scoliosis34,35 and thoracic kyphosis7 have been implicated as sources of scapulothoracic crepitus. In many athletes, thoracic kyphosis is common36,37 and may be the most likely source of scapulothoracic crepitus. Scapulothoracic dyskinesis38,39 may position the scapula in such a way as to promote contact between the superomedial angle and the ribs. This disorder is described later. Winging of the scapula has also been associated with scapulothoracic crepitus. Winging may be described as primary, secondary, or voluntary.40 Primary scapular winging results from identifiable anatomic disorders that directly affect the scapulothoracic articulation. Secondary scapular winging usually accompanies some form of glenohumeral joint pathology. This type of winging resolves once the glenohumeral pathology has been addressed. Voluntary winging, although rare, often has psychological overtones. Any form of winging may be associated with scapulothoracic crepitus. The more common causes of scapular winging in athletes are neurologic and include damage to the fifth cervical nerve root causing palsy of the rhomboid muscles; damage to the spinal accessory nerve causing trapezius palsy; and, as has been described in a number of athletic events, damage to the long thoracic nerve, causing serratus anterior palsy. Long thoracic nerve injury causing scapular winging is typically a neurapraxic or stretch injury to the nerve that occurs during play and typically resolves spontaneously within 1 year.40

Evaluation The patient with symptomatic scapulothoracic crepitus may be able to identify the location of the crepitus, pointing to the superomedial angle or the inferior angle. Athletes

Treatment As exemplified by Codman,6 it is important to recognize that scapulothoracic crepitus is not necessarily a pathologic condition. Scapular crepitus has been found in 35% of normal asymptomatic people.43 As a result of this, patients with hidden agendas or psychiatric conditions may not respond to treatment as well as other patients. However, if the athlete presents with pain, winging, or other disorders of the scapulothoracic articulation, the scapulothoracic crepitus is considered pathologic. Most athletes do not require surgical treatment of scapu lothoracic crepitus, particularly if the crepitus is related to soft tissue abnormalities, altered posture, or scapulothoracic dyskinesis.5,44 Treatment in these athletes should include postural exercises designed to prevent sloping of the shoulders.5,44,45 A figure-of-eight harness may be a useful tool to remind patients to maintain upright posture. Exercises to strengthen periscapular muscles are also thought to be important.5,12,44,45 Systemic nonsteroidal anti-inflammatory drugs, as well as local modalities such as heat, massage, phonophoresis, and ultrasound, and the application of ethyl chloride to trigger points may also prove useful.5,12,44 Injections of local anesthetics and corticosteroids into the painful area have also been recommended.7,12,41,44-46 Caution must be used because there is a risk for creating a pneumothorax.41 Using these means, most athletes are expected to improve significantly12,46; however, for those who fail, a number of operations have been described. In addition, athletes with clearly defined bony pathology such as an osteochondroma are unlikely to improve with conservative treatment.47 Resection of the bony pathology is usually necessary to alleviate symptoms with a high likelihood of success.12,21,26 Historically, some authors have used muscle plasty operations to treat scapulothoracic crepitus, which include those described by Mauclaire, who reflected a flap of the rhomboids or trapezius and sutured it to the undersurface of the scapula.19 This is thought to be inadequate, however, because the muscle flap may atrophy with time, and symptoms could return.47 Rockwood has excised a rhomboid muscle avulsion flap with the elimination of snapping and pain.41 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 scapula48 and, more commonly, on the superomedial angle.7,25,27,28,42,47,49

Shoulder

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Suprascapular artery and nerve

Trapezius m. Spine of scapula

Area of scapula to be resected Rhomboideus minor m. Supraspinatus m. Infraspinatus m.

A

C

The surgical technique for the resection of the superomedial angle of the scapula begins with the patient in the prone position (Fig. 17E-4). An incision following Langer’s lines is made just lateral to the medial border of the scapula, from the superior angle to the scapular spine. The soft tissue is dissected down to the spine of the scapula. The periosteum over the spine is incised, and a plane is developed between the superficial trapezius and the underlying scapula. Next, a plane is developed between the supraspinatus and the rhomboids, and the levator scapulae muscles along the medial border of the scapula starting at the spine of the scapula. The supraspinatus is elevated in a subperiosteal plane from the supraspinatus fossa. The medial scapulothoracic muscles are dissected from the medial border of the scapula, and the dissection in this subperiosteal plane is carried around the medial border 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. Caution is warranted, because the resection is carried laterally, to avoid injury to the dorsal scapular artery and the suprascapular nerve in the suprascapular notch. After resecting the bone, the reflected muscles fall back into place, and the medial border of the supraspinatus is repaired to the rhomboidlevator flap. 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

B

Figure 17E-4 Surgical approach for excision of the superomedial angle of the scapula. A, The 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. (Redrawn 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.)

begun after 6 weeks, and resistance exercises follow after 8 to 12 weeks. Complications associated with partial scapulectomy include pneumothorax and postoperative hematoma; in younger patients, bone may try to re-form, but this rarely produces symptoms. The reported results for this procedure are generally good.7,25,28,47,49,50 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.32,47

SCAPULOTHORACIC BURSITIS Symptomatic scapulothoracic crepitus is typically accom panied by an inflamed scapulothoracic bursa. It is important to realize that although these two conditions are frequently found together, an athlete may have crepitus without pain, and another may have scapulothoracic bursitis without crepitus. As described earlier, symptomatic scapulothoracic bursitis appears to affect two areas of the scapula, the superomedial angle and the inferior angle. These bursae, when inflamed, are thought to be adventitious.3,7,12

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Evaluation Scapulothoracic bursitis may accompany painful scapular crepitus or may exist as a separate entity. Patients generally complain of pain with activity and may have audible and palpable crepitus of the scapulothoracic articulation. Usually the scapular crepitus associated with bursitis is of a much lesser quality and nature than that described with bony pathology. Periscapular fullness is frequently appreciated in thinner athletes. This may become significant enough to produce noticeable scapular winging. Scapular winging has been identified in 50% of patients with a snapping scapula and no bony abnormalities.12 Patients may describe minor trauma as a predisposing event.19,42 More commonly, repetitive overhead activities in work or athletics have been implicated.17,44,46 The repetitive motion may irritate soft tissues until a chronic bursitis and inflammation develops. The bursa then undergoes scarring and fibrosis, with crepitus and pain to follow. Like scapulothoracic crepitus, this scapulothoracic bursitis in athletes is related to postural abnormalities and scapulothoracic dyskinesis. O’Donoghue recommended injecting local anesthetic into the bursa as a diagnostic aid.12

Treatment The initial treatment of scapulothoracic bursitis regardless of its location is conservative, beginning with rest, analgesics, and nonsteroidal anti-inflammatory drugs. Physical therapy to improve posture, heat, and local steroid injections have also been recommended.10,17,44 Efforts to strengthen periscapular muscles and stretching are frequently added.10,18,44 For patients who continue to have symptoms despite conservative treatment, surgery may be beneficial. Sisto and Jobe10 described an open procedure for resecting a bursa at the inferior angle of the scapula in four major league baseball pitchers. All pitchers had pain during the early and late cocking phases, as well as during acceleration, and could no longer pitch (Fig. 17E-5). Only one of the four patients presented with scapulothoracic crepitus, but all had a palpable bursal sac ranging in size from 1 to 2 cm, best seen with the arm abducted to 60 degrees and elevated forward 30 degrees. All four pitchers failed conservative therapy and underwent a bursal excision through an oblique incision just distal to the inferior angle of the scapula. The trapezius muscle and then the latissimus dorsi muscle were split in line with their fibers, 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 after 6 weeks. This progressed as symptoms permitted to full-speed throwing. After this procedure, all four pitchers were able to return to their former level of pitching. Similarly, McCluskey and Bigliani47 performed an open excision of a symptomatic superomedial scapulothoracic bursa in nine patients and noted a thickened, abnormal bursa between the serratus anterior and the chest wall at the time of surgery. Their surgical technique involved

Infraserratus bursa

Figure 17E-5 Bursa at the inferior angle of the scapula in throwers. This is an infraserratus bursa and has been described in baseball pitchers, in whom an excision of the bursa has allowed a return to throwing. (Redrawn 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.)

making a vertical incision medial to the vertebral border of the scapula. The trapezius is dissected free, and a subperiosteal dissection is used to free the levator scapulae and rhomboids from the medial border of the scapula. A plane is developed between the serratus anterior and the chest wall. The thickened bursa is resected and any bony projections removed. The medial periscapular muscles and trapezius are reapproximated to the scapula. The skin is closed in a routine fashion. The patient uses a sling for comfort and begins passive motion and pendulum exercises immediately. After 3 weeks, active motion is allowed, with strengthening begun at 12 weeks. With this technique, 88% of patients with symptomatic scapulothoracic bursitis had good or excellent results. One patient with a fair result also required muscle transfers for trapezius winging.47 Similar results for bursectomy have been reported by others.51 Resection of the symptomatic scapulothoracic bursa has been performed endoscopically as well.3,5,46,52-56 Ciullo and Jones5 have one of the largest and earliest endoscopic series 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 were 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.5 Matthews and colleagues46,57 have described the technique for scapulothoracic endoscopy. Patients can be placed in the prone or lateral position; however, the lateral position is preferred because it allows for arthroscopic evaluation of the glenohumeral joint and the subacromial space. In addition, if the arm is extended and maximally internally rotated, the scapula will fall away from the thorax improving access to the bursae.

Shoulder

Figure 17E-6 Portals used for scapulothoracic bursoscopy. Portals are placed 3 cm medial to the medial scapular border with the most superior portal being placed below the level of the scapular spine.

Three portals are used that are placed at least 2 cm from the medial border of the scapula in the region between the scapular spine and the inferior angle (Fig. 17E-6). For the middle portal, a spinal needle is inserted into the bursa between the serratus anterior and the chest wall. This needle should be inserted midway between the scapular spine and the inferior angle, at least 3 fingerbreadths medial to the medial border of the scapula to avoid injury to the dorsal scapular artery and nerve. The bursa under the serratus anterior can be distended with fluid before a stab wound is made in the skin and the blunt obturator and endoscope are inserted. Deep penetration may traverse the serratus entering the axillary space and should be avoided. After this initial middle portal has been established, a superior portal placed 3 fingerbreadths medial to the vertebral border of the scapula just below the spine penetrates the interval between the rhomboideus major and rhomboideus minor. This portal allows 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 (Fig. 17E-7). The

A

891

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. As presented at numerous meetings, the arthroscopic techniques for performing a scapulothoracic bursectomy appear to have early promising results, and to date no cases of injury to the long thoracic nerve, dorsal scapular artery, suprascapular nerve, axillary contents, or thoracic cavity have been reported. Despite this, few series of patients treated arthroscopically for scapulothoracic bursitis have been published in the peer-reviewed literature, and this technique remains investigational at this time.

SCAPULOTHORACIC DYSKINESIS As one might expect, abnormalities in scapulothoracic motion that change the position of the scapula relative to the chest wall are related to the development of scapulothoracic crepitus and bursitis. Burkhart and colleagues have described a condition known as the SICK scapula.58 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. This is a static finding at rest but is similar to scapular dyskinesis described by Kibler and McMullen, in which the scapula moves abnormally during arm elevation.59 Myers and colleagues studied scapulothoracic motion in a population of throwing athletes and compared this to a control population.60 They found 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. Interestingly, all these positions may be related to the pectoralis minor muscle. Su and colleagues have demonstrated that scapular kinematics may be altered in symptomatic swimmers, an effect that is magnified with fatigue associated with a practice.61 Many

B

Figure 17E-7 Arthroscopic photographs of the scapulothoracic bursa. Landmarks are conspicuously absent. A, View through the superior portal. The shaver and cautery device are used to débride the bursa. The subscapularis fascia is seen superiorly. B, A similar view looking at the inferior aspect of the scapulothoracic space.

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authors62-66 have evaluated muscle firing patterns in a number of athletes with shoulder pain and have noted that dysfunction of the serratus anterior is an early finding in many of these athletes. It is conceivable that weakness of the serratus anterior may predispose the overhead athlete to compensatory pectoralis muscle firing, which alters the dynamic position of the scapula during sport activities. This may lead to other problems as the normal function of the glenohumeral joint is altered. The altered position of the scapula would lead to increased strain on the posterior capsule structures during the deceleration of throwing, which could lead to tightness in the capsule and muscle leading to the glenohumeral internal rotation deficit. Static scapular position abnormalities then develop. With the altered position of the scapula, the acromion is in a position to produce impingement of the rotator cuff. In addition, the tight posterior capsule would lead to superior humeral head migration during elevation and external rotation of the arm, further jeopardizing the rotator cuff. Our understanding of this constellation of findings in the shoulder of overhead athletes is in its infancy, yet an interplay between a weak serratus and overfunctioning pectoralis minor appears to be important.

Evaluation Patients with scapulothoracic dyskinesis may not direct the physician toward the scapula and complain of pain in the glenohumeral joint. Standing behind the athlete and inspecting the scapulae from the back demonstrates asymmetry at rest, with the affected shoulder frequently depressed and the scapula protracted and tilted forward. Mild scapular winging may be present, with the inferior angle and the medial border of the scapula prominent. Patients frequently have pain to palpation just medial to the coracoid at the insertion of the pectoralis minor. Asking the patient to elevate the arm in the frontal plane and in the scapula plane reveals asymmetry in scapulothoracic motion, called scapulothoracic dyskinesis. In the presence of rotator cuff pathology, this may be related to decreased firing of the middle and lower trapezius.67 It appears to be also related to a shortened pectoralis minor tendon.68,69 Patients with this scapular dyskinesis often present with rotator cuff pain. These patients have positive impingement signs and pain when testing supraspinatus strength in a position of scaption. This pain will be reduced and measured strength will improve if the scapula is reduced to the chest wall, a test known as the scapular retraction test.70,71 It has been noted that core stability is typically poor in these patients.59 Checking the athlete for a Trendelenburg sign and observing the single-leg knee bend can be helpful to look for weakness and problems with balance. In baseball pitchers, asymmetry is often seen such that the stride leg has more weakness than the lead leg.

Treatment Treatment of scapulothoracic dyskinesis is through exercise and modalities of physical therapy. Kinetic chain– based rehabilitation programs have been recommended39,60 because many of the patients with scapulothoracic kinematic abnormalities have weakness in the core stabilizers of

the trunk. Stretching tight structures is important. A major contributor to scapular dyskinesis is a tight pectoralis minor tendon. Borstad and Ludewig demonstrated the door jamb stretch to be the best method to stretch a tight pectoralis minor.72 The posterior capsule, which is commonly found to be tight, can effectively be stretched.73,74 Although a variety of methods exist to stretch the posterior capsule, stretching across the body appears particularly effective.75 Strengthening of key muscle groups—the serratus anterior, low trapezius, rhomboids, and rotator cuff—is usually included in the rehabilitation.59 Many of these methods of rehabilitation have not been evaluated prospectively or with randomized trials, and as such, the work is currently in its infancy. Clearly much more work is needed to define pathologic scapulothoracic kinematics and their effect on other shoulder pathologies.

SUMMARY A variety of scapulothoracic conditions can affect the athlete’s shoulder. These include winging in a variety of forms, crepitus and bursitis, and dyskinesis of the scapulothoracic articulation. Scapular winging in athletes most commonly results from a long thoracic nerve neuropraxic injury, and these athletes 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 shoulders5,45 and periscapular muscle strengthening.5,12,45,46,59 A figure-of-eight harness may be a useful tool to remind patients to maintain upright posture. Local modalities, nonsteroidal anti-inflammatory drugs, and local injections have also been recommended. In athletes with refractory symptoms, surgical correction may be considered; however, there are only a few reports in the literature for this select population, so it is difficult to predict outcomes with regard to returning to sport. Scapular dyskinesis is only now under study as a source of shoulder pathology, and early results suggest the effects of scapular dyskinesis may be of critical importance. General considerations for treating scapular dyskinesis include exercises to improve core stability, stretch the pectoralis minor, stretch the posterior capsule, and strengthen the serratus and low trapezius.59 More work is needed to gain a complete understanding of scapulothoracic problems in the athlete.

C l Scapular

r i t i c a l

P

o i n t s

bursitis may exist with or without scapulothoracic crepitus, and scapulothoracic crepitus may exist with or without bursitis. l Scapular winging is most commonly neurologic and in athletes is the result of a neurapraxic injury to the long thoracic nerve. These injuries usually recover spontaneously but may take a year or longer. l Scapulothoracic bursitis is often seen in athletes. Initial treatment is nonoperative. When nonoperative measures fail, open or arthroscopic bursectomy may help.

Shoulder l Scapulothoracic

dyskinesis is common in athletes with shoulder pain and is characterized by an altered position of the scapula at rest (sick scapula) or during motion (scapula dyskinesis). l The esssence of treatment for scapulothoracic dyskinesis involves improving core stability, stretching pectoralis minor and posterior glenohumeral joint capsules, and strengthening the serratus and low trapezius.

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Kuhn JE, Plancher KP, Hawkins RJ: Scapular winging. J Am Acad Orthop Surg 6:319-325, 1995. Kuhn JE, Plancher KP, Hawkins RJ: Symptomatic scapulothoracic crepitus and scapulothoracic bursitis. J Am Acad Orthop Surg 6(5):267-273, 1998. Manske RC, Reiman MP, Stovak ML: Nonoperative and operative management of snapping scapula. Am J Sports Med 32(6):1554-1565, 2004. Williams GR Jr, Shakil M, Klimkiewicz J, Ianotti JP: The anatomy of the scapulothoracic articulation. Clin Orthop 357:237-246, 1999.


S U G G E S T E D

R E A D I N G S

Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part III. The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19(6):641-661, 2003. Kibler WB: Role of the scapula in the overhead throwing motion. Contemp Orthop 22:525-532, 1991. Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 11(2):142-151, 2003.

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F

Sternum and Rib Fractures in Adults and Children Matthew T. Provencher, Augustus D. Mazzocca, and Anthony A. Romeo

Rib and sternum injuries are relatively rare in athletes and more commonly result from motor vehicle crashes.1,2 In children, this type of fracture can be a marker of either severe trauma or abuse.3-6 This section defines the classification of rib and sternal fractures, the mechanism of injury, the physical assessment, and the treatment for both pediatric and adult athletes.

RIB FRACTURES Rib fractures can be divided into two main categories: stress fractures (indirect) and traumatic fractures (direct). Traumatic fractures are caused by either a blow from a blunt object, which fractures the ribs in direct contact, or compression of the entire thorax, which results in fractures of multiple ribs.7 Stress fractures can occur in ribs that are subjected to repetitive mechanical loading during a particular activity. The complete history generally provides insight into which of these categories applies (Table 17F-1).

Traumatic Rib Fractures The mechanism of traumatic rib fracture or injury is a direct blow from a blunt object. In athletics, this blow generally comes from an anterior direction, causing a more lateral

rib fracture or an injury to the costochondral junction.8,9 Athletes will recall the injury and will sometimes report that the “wind” was knocked out of them. It is important to identify which and how many ribs are injured because fractures of the first four or last two ribs, multiple fractures, and flail segments may result in injury to surrounding structures.8 The definition of flail chest has historically been involvement of three or more ribs that are fractured in two or more places. Clinically, this term has changed to include any chest segment that exhibits paradoxical motion during respiration. Injuries to the kidney, the spleen, or the liver may not be readily clinically apparent. Splenic trauma has been reported in up to 20% of left lower rib fractures, and liver trauma has been reported in 10% of right lower rib fractures.9 Pneumothorax and hemothorax must be ruled out by auscultating the chest and palpating for subcutaneous air. Progressive shortness of breath is also an ominous indicator in this situation. Rib fractures that presented to a level I trauma center9 (7147 total fractures over 5 years) demonstrated a high incidence of associated injuries (94%), hemothorax or pneumothorax (32%), or lung contusion (26%), with as many as one third developing pulmonary complications. Although not as prevalent in pure athletic trauma, one should be vigilant to evaluate for concomitant injuries, especially in the case of multiple rib fractures.

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Table 17F-1 Typical Findings in Rib and Sternum Fractures

Acute Rib Fractures

Rib Stress Fractures

Sternum Fractures

Recall injury— More chronic onset “wind” knocked out

Direct motor vehicle trauma (automobile racing) Assess for shortness Suspect in most upper Direct injury: of breath, cardiac segment (1st rib) in relatively flexible symptoms weightlifting and inferior sternum is throwing flexed posteriorly and fractured, or sternomanubrial dislocation can occur Exclude Middle rib cage (ribs Indirect injury: pneumothorax 5-9) in rowers flexion-compression (auscultate) and of cervical spine— hemothorax posteriorly displaces (palpation and manubrium and inspection) anterior displacement of the sternum Pain during deep Evaluate personal Rib and spine inspiration dietary and fractures may be hormonal history associated Assess costochondral Lateral radiograph junction for step-off of sternum (sternal view) Chest radiograph— Ultrasound may aid assess for in diagnosis and pneumothorax identify retrosternal fluid Rib series—oblique Evaluate for views of involved mediastinal segment widening, which usually indicates more severe visceral or substernal pathology Ultrasound may Pediatric population: improve accuracy, sequential fusion of especially at sternum, which is costochondral not complete until junction about age 21 yr

In the case of infant, toddler, or child traumatic rib fracture, one should maintain a high level of suspicion for nonaccidental trauma (NAT).3-5 These rib fractures may be difficult to identify in NAT with a routine skeletal survey. The combination of conventional and high-detail skeletal radiography and possibly ultrasound may improve the diagnosis. The risk for complications and mortality increased with the number of ribs fractures and was usually a harbinger of additional pathology.3 Regardless, it has been argued that in children younger than 3 years, the positive predictive value of a rib fracture to identify NAT is greater than 90%.3

Examination Physical examination usually elicits pain during palpation as well as during deep inspiration. A hematoma is an indicator of a displaced rib fracture produced by injury to the intercostal vessel. In palpating the costochondral junction, one may also palpate a step-off, which aids in the diagnosis of costochondral fracture-dislocation. Two radiographic examinations (chest series and rib series) are important in diagnosing rib fractures. A chest

Table 17F-2 Treatment Options in Rib and Sternum Fractures

Acute Rib Fractures


Sternum Fractures

Symptomatic treatment Rest, ice, oral analgesics Intercostal rib block (injection) if especially painful on inspiration Rib binder may improve comfort

Symptomatic treatment Rest, ice, oral analgesics Investigate causes— sport mechanics (rowing, lifting, throwing) Physical therapy— critical to strengthen serratus anterior, and sports mechanics evaluation

Symptomatic treatment Rest, ice, oral analgesics Avoid contact sports until completely pain free

Bone mineral density may be indicated— dietary and hormonal evaluation

Sternomanubrial dislocation may warrant reduction and is usually stable once reduced. Treatment is similar to above.

series (posterior-anterior and lateral) is needed to rule out pneumothorax. A rib series includes oblique views of the clinically involved segment. Injuries to the costochondral junction are not well seen on radiographs. Magnetic resonance imaging (MRI) or computed tomography (CT) may be needed to confirm the suspected diagnosis of a costochondral injury. Ultrasound has also been advocated to diagnose acute rib fractures, with the potential for improved diagnostic accuracy over conventional radiography.10

Treatment Treatment of traumatic rib injuries is primarily symptomatic (Table 17F-2). Most of these fractures are stable. Stable rib fractures are nondisplaced or minimally displaced and do not involve more than two consecutive segments. The first mode of treatment is oral analgesic medication to relieve pain, which mainly occurs during inspiration. If this does not relieve the pain, an intercostal “rib block” may offer some temporary relief of spasm. A long-acting medication such as bupivacaine is used. It is infiltrated along the intercostal nerve of the fractured rib and the ribs above and below it. Some success has also been reported with the use of “rib binders,” which may splint the fracture, keeping it more stable so that activities of daily living are more comfortable.11

Return to Athletics The criteria for return to play with rib fractures are stability of the injury with no soft tissue complications (e.g., pneumothorax, hemothorax, or liver, spleen, or kidney contusion) and an improvement in pain (Table 17F-3). This is usually seen about 2 to 3 weeks after injury. The athlete can return to play at this time using a rib belt; he or she is further protected for about 6 to 8 weeks by a flak jacket (Fig. 17F-1) so that the rib can heal completely. It has been reported that nonunion is not a complication of

Shoulder

Table 17F-3 Return to Play in Rib and Sternum Fractures

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these injuries if there is persistent pain lasting longer than 6 to 8 weeks.

Acute Rib Fractures


Sternum Fractures

Stress Fractures

Stability of the rib segments (usually 2-3 wk) Any soft tissue or visceral injuries healed (usually 2-3 wk)

Pain free for 2-4 wk

Pain free (usually 6-8 wk), pain >12 wk is rare If sternomanubrial reduction, may take 6-12 wk for return to play

Stress fractures or indirect injury to the ribs usually involves muscle contractions that result in subthreshold bending, causing microfracture. This microfracture is additive and eventually causes pain. A stress fracture is caused by the inability of the bone to withstand subfracture threshold force in a repetitive fashion. There is an imbalance between bone formation and bone resorption. It is also important to realize that a stress fracture is a normal response to an abnormal stress, whereas an insufficiency fracture is an abnormal response to a normal stress. Stress fractures have been reported to occur in the first rib in baseball players12-15 (Fig. 17F-2) and also as a more acute phenomenon in basketball players. Fractures of the lower ribs have been reported in golfers and rowers.16-20 Karlson19 reviewed rib stress fractures in rowers and found that those occurring in the anterolateral to posterolateral aspects of ribs five through nine are most often associated with long-distance training and heavy load per stroke. It was also noted that the similarity between these stress fractures and fractures caused by chronic coughing suggests a similar mechanism of injury. The actions of both the serratus anterior and the external oblique abdominal musculature on the rib may cause these stress fractures because of the repeated bending forces of both rowing and coughing. Mintz21 used an MRI analysis technique, and McKenzie22 analyzed rowing mechanics to implicate the serratus anterior in the causation of stress fractures. Avulsion fractures of the floating ribs may also result from the opposing pulls of the latissimus dorsi, the internal obliques, and the serratus posterior inferior muscles (Fig. 17F-3).15 It has also been suggested17,23 that exercise-induced rib stress

May return if no visceral pathology and ribs stable at 2-3 wk. Wear rib belt and flak jacket for up to 8 wk May return earlier (1-2 wk) if few (4 weeks) and secondary (≥4 weeks) hemiarthroplasty in elderly patients.94 The results of late reconstruction have been found to be inferior to those after reconstruction of acute fracture and to be more technically demanding with increased complications. Beredjiklian and colleagues95 and Norris96 evaluated 39 cases of malunion of the proximal aspect of the humerus. Sixty-seven percent of patients were deemed to have satisfactory results at an average of 44 months’ follow-up. The authors suggest that a delay in the operative treatment of the malunion of the proximal aspect of the humerus has a negative impact on outcome as a result of many factors, including disuse atrophy and more mature soft tissue scarring associated with prolonged malunion.

Open Reduction and Internal Fixation versus Humeral Head Replacement for Four-Part Fractures Some authors have questioned the effectiveness of prosthetic replacement, especially in terms of functional outcome. In 1993, Hawkins and Switlyk evaluated humeral

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A

C

B

Figure 17J1-14 A, Anteroposterior view of a three-part proximal humerus fracture treated with intramedullary rodding. B, Axillary lateral view before treatment. C, Anteroposterior view after treatment.

head replacement in 20 three- and four-part fractures in patients with an average age of 64 years.97 The results were variable. Eighteen patients (90%) had mild or no pain; however, active forward elevation averaged only 72 degrees. Movin and coworkers reported poor functional results after shoulder replacement in 29 proximal humerus fracture patients followed for 2 to 12 years.98 They concluded that treatment of severe proximal humerus fractures with a prosthesis did not give complete pain relief and resulted in impaired shoulder function. Zyto and colleagues also reviewed the outcome of 27 patients after hemiarthroplasty for three- and four-part fractures of the proximal humerus.99 Results were disappointing, and they recommended open reduction and fixation. Bigliani and colleagues evaluated 29 cases of failed primary prosthetic replacement for displaced proximal humerus fractures.100 Most of the failure factors were technical errors of surgery. Detachment of either the greater tuberosity or both tuberosities occurred in 15 shoulders (52%). Malposition of the prosthesis occurred in 7 cases (24%). Loosening of the humeral component occurred in 12 shoulders (41%), and all but 1 of these were uncemented. Inadequate rehabilitation postoperatively or patient noncompliance with restrictions contributed to failure in 9 patients (31%). In 1991, Jakob reported a much lower rate of avascular necrosis in four-part valgus-impacted fractures than with true four-part fractures. In this series of 14 fractures, treated either with closed reduction and percutaneous K-wires or with minimal internal fixation, the authors obtained 74% excellent or satisfactory results at an average 4-year follow-up.101 Subsequently, Darder and associates presented 64% good to excellent results with tension band wiring and K-wires in the treatment of four-part fractures,

although the mean age of their patients was 59 years.75 They suggested that two groups, those with significant comminution plus fracture-dislocation, and patients older than 75 years, should be treated with hemiarthroplasty. Esser also treated 16 three-part and 10 four-part fractures employing the use of a modified cloverleaf plate in a young population.102 At an average follow-up of 6 years, results were excellent or good in 92%. In 1997, Resch and associates published the results of a 4-year study of 9 three-part fractures and 18 four-part fractures treated with percutaneous reduction and screw fixation.103 The average age was 54 years, with follow-up of 2 years. Average ConstantMurley scores of 91 for three-part fractures and 87 for four-part fractures were obtained. Thirteen of 18 fourpart fractures were of the valgus-impacted type. Hoellen and coworkers compared minimal osteosynthesis with primary prosthetic replacement in 30 four-part fractures of the proximal humerus.104 After 1 year, the results were similar in both groups, although there were two revision surgeries and four cases of implant removal in the minimal osteosynthesis group. In older patients, the authors recommended prosthetic replacement. Robinson and associates recommended using the vascularity of the head as a guide to prosthetic replacement in complex fracturedislocations, and advocated primary prosthetic replacement in the absence of arterial backbleeding in the older (>60 years) patient.105

Summary On the basis of recently published reports, some controversy remains regarding optimal treatment for fourpart fractures. It should be kept in mind that precise identification of fracture configuration and bone quality

1048 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine ��

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Figure 17J1-15 A, Anteroposterior view of a four-part proximal humerus fracture. B, Intraoperative radiographs of a trial prosthesis can be used to assess humeral height and the relationship of the humeral head to the greater tuberosity and the glenoid. C, Anteroposterior view after treatment with a humeral head replacement.

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are most important when choosing treatment methods. When ORIF is planned in the valgus-impacted fourpart fracture without osteoporosis, a soft tissue–sparing approach with minimal but stable fixation is recommended. However, it is suggested that older patients and true four-part fractures are best treated with primary replacement. In lesser fractures, such as three-part fractures, in which the tendinous attachments or bone is too frail to accept rigid fixation, arthroplasty remains the better alternative.

Complications Avascular Necrosis The most important factors in the development of avascular necrosis are fracture type, degree of displacement, and the treatment method selected. In four-part fractures, the reported incidence varies between 13% and 34%, whereas the incidence in three-part fractures is reported to range from 3% to 14%.75 Brooks and colleagues studied the effect of simulated four-part fractures on the vascularity of the humeral head.106 In most cases, perfusion was prevented, but if the head fracture extended distally below the articular surface medially, some perfusion of the head persisted by the posteromedial vessels. This finding suggested the importance of identifying the size of the fracture fragments and configuration of the fracture. Lower rates of avascular necrosis with valgus-impacted four-part fractures have been noted. It is postulated to be the result of the intact medial soft tissue hinge. This has been confirmed by Hertel and coworkers, who demonstrated that the most important factors predictive of loss of blood supply were loss of the medial calcar bony hinge and a fracture pattern with a short metaphyseal extension.107 When the medial hinge is intact, preservation of its integrity is of utmost importance in an attempt to prevent interruption of blood supply.100,103 Gerber and colleagues reported on 25 patients with a partial or complete collapse of the humeral head caused by post-traumatic avascular necrosis.97,108,109 Initial treatment consisted of ORIF in 19 cases, including 9 cases of minimal internal fixation. Five cases were treated with closed reduction and percutaneous pinning. The comparative outcome results were gained from two groups of patients based on radiographic analysis. Group 1 consisted of 13 patients with avascular necrosis and collapse in the absence of malunion, and group 2 included 12 patients with additional malunion. The clinical outcome was significantly related to the anatomic alignment of the fragments of the humerus at the time of healing. The exact pathogenesis of the poor outcome in patients with coexisting avascular necrosis and malunion is not well known, but it is believed that in addition to bony impingement caused by tuberosity malunion, malposition of the head segment prevents optimal function of the cuff muscles. The authors therefore recommended that a proximal humeral fracture that is at risk for avascular necrosis should be reduced anatomically if jointpreserving treatment is selected. If anatomic reduction cannot be obtained, other treatment options such as arthroplasty should be considered.

Neurovascular Injury Axillary nerve injury remains the most common peripheral nerve injury affecting the shoulder after glenohumeral joint dislocation and displaced proximal humeral fractures. During the acute phase of injury, the shoulder should be rested, and when clinically indicated, an extensive rehabilitation program should be initiated, emphasizing range of motion and strengthening of the shoulder girdle muscles. If no recovery is observed by 3 to 6 months after injury, surgical exploration may be indicated.110 Visser and associates compared electromyographic findings in shoulder dislocations and fractures of the proximal humerus with clinical neurologic examination in 215 patients.111 Electromyographic disorders were noted in 133 patients (62%), with testing of sensibility and clinical reflexes proving to be unreliable indicators for electromyographic abnormalities. The findings of this study implied that by clinical examination alone, a large number of axonal lesions remain undetected.

Nonunion Nonunions are most frequently encountered at the surgical neck. Nonunions are more frequent after ORIF.96 Surprisingly, up to 23% of patients undergoing these procedures may develop nonunion. Patients may have virtually no functional use of their shoulder and experience pain. Successful treatment is reliable in relief of pain and potentially can restore function. Usually, the diagnosis can be made with simple plain radiographs; however, CT may be helpful in the identification of tuberosity union and position. Surgical reconstruction for nonunion of the surgical neck often results in significant improvement in pain but much more modest improvement in active motion and function.112,113 Jupiter and Mullaji reported on the treatment of nonunion of proximal humerus fractures in the elderly patient with weak bone, resorption at the fracture site, contracture of the glenohumeral joint, and associated medical conditions.114 A blade plate, designed specifically for the treatment of these nonunions, was used in nine patients (mean age, 66 years) who had painful nonunion with a mean duration of 22.5 months. Autologous bone grafting was used in all cases. Eight nonunions followed displaced two-part proximal humeral fractures: five had been initially treated nonoperatively and four with medullary nails. After a mean of 6.5 months (range, 4 to 28 months), union had been achieved in all but one patient. Functional evaluation revealed good results in five patients, fair results in three, and one poor result. Use of the blade plate offered a successful method of stable internal fixation in these complex cases, although locking plates are gaining favor for this indication.

Malunion Tuberosity malunion can lead to significant shoulder dysfunction if it is associated with arthritic changes or fixed contracture. Conditions that contribute to the malunion or nonunion include osteoporotic bone, premature or aggressive rehabilitation, high-energy multitrauma, long


head of biceps tendon interposition, and inadequate stability of operative stabilization. A relatively painless malunion may not require surgical management. However, symptomatic malunion may be treated with excision of the bony prominence with soft tissue release, osteotomy, and realignment, or prosthetic replacement if the articular surfaces are involved. Plain radiographs can be inadequate and even misleading in determining tuberosity displacement. The addition of CT in the evaluation of tuberosity malunions can improve assessment of displacement and assist in determining treatment options.37,115

and 4 three-part fractures.117 The results revealed that age and poor general condition of the patient, as well as the difficulty of the surgical technique, more than the rehabilitation, were related to the poor results observed after shoulder replacement. The discrepancy between active and passive elevation suggests that limited motion is not caused by shoulder stiffness and glenohumeral scarring but instead by weakness of the deltoid or external rotators, especially in the presence of greater tuberosity migration.

Loss of Motion

Myositis ossificans and heterotopic ossification can occur after fracture of the proximal humerus but most often pre sent little if any clinical significance. Because the degree of myositis can usually be correlated with the severity of the soft tissue injury, fracture-dislocations have the highest incidence.2 The heterotopic ossification rarely forms a block to motion, although many patients have decreased motion secondary to soft tissue contracture.

Early passive range of motion is the goal of both ORIF and replacement surgery. It is imperative to continue exercises because patients usually do not attain their maximal result until 12 to 18 months after surgery.116 Boileau and associates reported prognostic factors during rehabilitation after shoulder replacement for 42 four-part fractures


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Myositis Ossificans

Treatment

Two-Part Greater Tuberosity Fractures

Lesser Tuberosity Fractures

Once the deltoid-splitting approach has been performed and adhesions lysed, debris and hematoma are removed to clean the fracture bed and allow for anatomic reduction of the tuberosity. The tuberosity fragment is identified and mobilized with heavy nonabsorbable sutures such as No. 5 Tevdek or Ethibond, placed at the bone-tendon interface to incorporate the strong rotator cuff tendon (Fig. 17J1-16). This area is often stronger and holds suture more securely than when the sutures are placed through osteoporotic tuberosity bone, where they may easily cut out. To completely reduce the tuberosity, it is important to place sutures at the level of the superior, middle, and inferior facets to overcome the displacement forces of the supraspinatus and teres minor. Based on these rotator cuff insertions, the fragments may be pulled superiorly, posteriorly, or in both directions at the time of injury, depending on the fracture location within the tuberosity. Sutures therefore must be placed in a manner that not only brings the superior facet downward but also brings the inferior facet forward. With this configuration of suture placement, the fracture can then be reduced. If the fragment is large, it may require removal of a small amount of cancellous bone to allow reduction. At this point, drill holes are placed around the periphery of the bed in the shaft and humeral head. By definition, there is an associated rotator cuff tear either in the rotator interval between the supraspinatus and subscapularis or more posteriorly between the supraspinatus and infraspinatus. It is helpful to repair this tear after reducing but before securing the fragment to the head and shaft to take tension off of the tuberosity fixation. It is essential to repair the tear in the cuff to restore optimal function. The tuberosity is now securely fixed to the shaft through the drill holes, using the heavy nonabsorbable sutures at the bonetendon interface in a figure-of-eight fashion (Fig. 17J1-17). The deltoid is meticulously closed, also with nonabsorbable suture.

The displaced isolated lesser tuberosity fracture is a rare lesion with a minimum of clinical experience reported. Although it is difficult to be dogmatic about treatment, most authors would agree that if a portion of the articular surface is involved with the tuberosity fracture or a significant block to internal rotation exists, then ORIF is warranted. Fixation of these fractures is performed in a manner similar to that described for greater tuberosity fractures, although exposure for the anteromedial displacement seen is better afforded by a deltopectoral or anterior axillary approach. The anterior axillary approach differs from the standard deltopectoral only in that the skin incision is vertical and made in the anterior axillary crease for better cosmesis. The skin is undermined superiorly and medially to gain the necessary exposure. The remainder of this approach is as described for the deltopectoral approach. The subscapularis and lesser tuberosity fragment are then identified with external rotation and forward elevation of the arm. The subscapularis and lesser tuberosity are then mobilized with heavy nonabsorbable suture and reduced into the freshened bed. Drill holes are placed in the head and shaft around the bed’s periphery, and the fragment is secured as previously described for the greater tuberosity. Some authors have used a cannulated screw in place of suture fixation, although this is not our preference (Fig. 17J1-18). Excision of the fragment by shelling it out of the subscapularis and anterior capsule and with subsequent reattachment of the subscapularis has also been described with some success. Inasmuch as the deltoid origin has been left intact, the interval between the deltoid and pectoralis is easily closed. Two-Part Surgical Neck Fractures

ORIF of displaced surgical neck fractures is most easily performed through the deltopectoral approach. Once the fracture is adequately exposed, the shaft and head are

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Treatment—cont’d

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Figure 17J1-16 A, Superior skin incision (dotted line) is begun just lateral to the coracoid and extends 7 to 8 cm in Langer’s lines over the lateral margin of the anterolateral corner of the acromion. B, Mobilization of the greater tuberosity fragment with heavy nonabsorbable suture placed at the bone-tendon interface at the superior, middle, and inferior facets to correct both superior and posterior displacement. (A, From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 143.)

obilized, and the fracture site is curetted. The humeral m shaft is mobilized gently, and control of the humeral head is gained either by placing heavy suture at the tuberosity bonetendon interfaces or with skin hooks to reduce the head on top of the shaft. Reduction is obtained by forward elevation of the shaft while gently pulling on the sutures controlling the head. The fracture is then impacted and the arm lowered while keeping tension on the sutures through the cuff to prevent loss of reduction. Once adequate reduction is achieved, fixation is accomplished with a locking proximal humerus plate. It should be emphasized that sutures placed into the rotator cuff will allow better mobilization of the head fragment and will also be incorporated into the plate, increasing the stability of the construct. Heavy nonabsorbable suture incorporating the tuberosities and cuff to the shaft in addition to the locked plate construct will provide excellent, rigid fixation and allow for very early and aggressive rehabilitation, important in a patient considering a return to sport. This augmented fixation is of even greater importance when there is associated comminution of the fracture site with less inherent reduction stability. While reduction is maintained, the locked plate is placed over the lateral aspect of the humeral shaft. A key

c onsideration is the height of the plate. A plate placed too high along the greater tuberosity will cause impingement in the subacromial space and reduce the ability to forward-flex and abduct the arm. A plate placed too low will compromise fixation in the humeral head (Fig. 17J1-19). Once the correct height of the plate is determined, we fix the plate to the shaft with a nonlocking cortical screw. The proximal portion of the plate is then fixed provisionally into the head with K-wires. At this point, a fluoroscopic image is taken to check the position of the plate. If it is malpositioned, the provisional K-wires are removed and the position adjusted until it is correct: parallel to the shaft of the humerus and more than 5 mm distal to the tip of the greater tuberosity. Once the position of the plate is confirmed and appropriate, locking screws are placed through the appropriate guide into the humeral head. It is important to ensure that no screw has penetrated into the joint space, which can be accomplished only by a careful fluoroscopic survey encompassing an arc of at least 90 degrees. Unrecognized screw penetration causing chondrolysis is a disastrous complication that can only be avoided by fastidious checking of screw lengths. If a screw has been found to penetrate the joint, it can be exchanged for a screw that is 10 mm shorter without significantly compromising fixation. Nonlocking (to secure Continued



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Figure 17J1-17 A, Displaced greater tuberosity fracture seen on an anteroposterior radiograph. B, On an axillary radiograph, the posterior displacement can be appreciated. C, Tuberosity fragment is secured to its bed with No. 5 Tevdek sutures in figure-of-eight fashion, incorporating the strong cuff tendon after closure of the rotator cuff tear. (A, From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 146.)

the plate to the shaft) followed by locking screws are then placed into the humeral shaft. At this point, an assessment of stability and range of motion is undertaken. Finally, previously placed sutures may be incorporated from the rotator cuff tendons into the plate. This allows fixation into the tendinous cuff to be combined with plate fixation into the strong cortical bone of the humeral shaft. Three-Part Fractures

ORIF of these fractures merely combines the techniques described for two-part tuberosity and surgical neck fractures. However, it is here that the anatomy becomes difficult. Strict attention to detail and anatomic landmarks can ease the task at hand. Again, the deltopectoral approach is employed. The

biceps tendon now becomes the lighthouse for identifying the somewhat complicated anatomy. It may be found underneath the pectoralis major insertion and should be protected if the pectoralis is released. Following the biceps superiorly will lead to the rotator interval, which is incised to the glenoid to gain further exposure and facilitate mobilization of fracture fragments. The displaced medial lesser or lateral greater tuberosity is then mobilized, as previously described, with heavy nonabsorbable suture. Once identified, the head and its attached tuberosity may be mobilized in a similar manner, gaining control of the possibly dislocated head by gentle traction on sutures placed at the tuberosity bonetendon interface, assisted with a blunt Darrach retractor for leverage back into the joint.

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Figure 17J1-18 Treatment of a lesser tuberosity fracture with open reduction and minimal internal fixation with a cannulated screw. (From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 146.)

Once control of the fragments is obtained, the displaced tuberosity is first reduced and fixed to the head and intact tuberosity with heavy suture through drill holes (Fig. 17J1-20). The fracture is now converted to a two-part surgical neck fracture. The head-tuberosity fragment can be fixed to the shaft using a locking plate as for a two-part fracture. Alternatively, the head-tuberosity fracture can be repaired using a tension band construct augmented with intramedullary Ender rods. We prefer this technique for three-part fractures, described later. Once adequate reduction of the tuberosity to the head is achieved with heavy nonabsorbable suture, the head fragment is reduced onto the shaft. Again, heavy suture or wire incorporating the tuberosities and cuff are placed, which will be supplemented with intramedullary nails in a tension band configuration. Eighteen-gauge wire may be substituted for suture, inasmuch as it will provide greater immediate stability, but the risk for breakage, migration, and irritation in the subacromial space must be weighed. Therefore, we prefer suture whenever possible. Ender nails (3.5 mm) are superior to straight rods or pins such as Rush rods, in that they afford three-point fixation and therefore enhance rotational stability. The addition of the tension band configuration with intramedullary nails has been found to add even greater longitudinal and rotational stability over that of either tension banding or intramedullary nailing alone (Fig 17J1-21). This augmented fixation is of even greater importance when there is associated comminution of the fracture site with less inherent reduction stability. While reduction is maintained, small longitudinal incisions are made in the direction of the rotator cuff fibers over

the lesser tuberosity and just outside the articular surface for nail insertion. Ender nails are preferred here, not only for stability, as previously discussed, but also for the ability to place figure-of-eight suture or wire through the eyelet. The slot of the Ender nail is long, however, and an appreciable amount of metal may still protrude proximally. Therefore, the nail can be modified with an additional hole above this slot for suture or wire incorporation. This allows for deeper insertion of the nail into the humeral head, placing the tip well below the cuff tendons (Fig. 17J1-22). The site for nail insertion is dependent on the lack of associated fractures within the tuberosity chosen to achieve maximal rigidity. When no other fractures are identified, the greater tuberosity is the better choice, inasmuch as two nails may be used here as opposed to only one in the lesser tuberosity. Therefore, anterior and posterior longitudinal incisions are made in the supraspinatus tendon over the greater tuberosity, and an awl is used to penetrate the bone. The posterior nail is best placed initially because levering on this partially inserted nail will aid in holding the reduction and preventing the humeral head from falling posteriorly. The second nail is then inserted more anteriorly, about 1.0 to 1.5 cm from the first. It is advantageous to use nails of different lengths to prevent the possibility of a stress riser distally. Nails between 22 and 27 cm in length are generally adequate. Before the nails are completely buried, two drill holes are made in the shaft lateral to the biceps tendon for tension band suturing or wiring. Figure-of-eight suture or wire (No. 5 Tevdek or 18-gauge wire) is passed through the eyelets of the nails, passing it deep to the rotator cuff tendon between the nails to prevent proximal migration, and then through the predrilled holes in the shaft. Before the suture is tied or both limbs of wire are twisted, the nails are impacted well below the cuff, and fracture reduction is evaluated. Once the figure-of-eight is secured, range of motion and fixation stability are assessed carefully to guide the postoperative rehabilitation without stressing the repair. The rotator cuff incisions and deltopectoral interval are closed, usually over suction drainage. Four-Part Fractures, Head-Splitting Injuries

In four-part fractures and head-splitting injuries, humeral head replacement is the treatment of choice, especially in elderly patients. It should be emphasized that four-part fractures are exceedingly rare in young patients. Valgus-impacted fractures have been reported to have lower rates of osteonecrosis (9% to 11%), and ORIF is therefore possible. ORIF is performed by elevating the impacted head and relocating the tuberosities. It is also imperative to fill the void with cancellous bone chips.103 Minimal osteosynthesis can be performed with 1.8-mm K-wires to secure the head to the shaft, and numerous sutures are used to anchor the tuberosities to each other and the shaft. A locking plate may be added and the tuberosities secured to the plate, with additional fixation into the head. This is a procedure best performed in young, healthy bone. The technique of humeral head replacement uses a deltopectoral approach and leaves the origins and insertions intact. It is important to identify and then mobilize the fracture Continued



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B

Figure 17J1-19 A, Placement of the locking plate at least 5 mm below the lesser tuberosity will reduce the chance of subacromial impingement when the arm is abducted. B, This plate is placed too proximal along the shaft, increasing the risk for plate impingement.

Figure 17J1-20 This three-part fracture is reduced to two parts by securing the involved tuberosity to the head and the lesser tuberosity with multiple sutures. The exact construct depends on the anatomy of the fracture. (From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 151.)

fragments. Skin hooks can aid in retrieving retracted fragments. No. 5 Tevdek/Ethibond suture is placed carefully at the tuberosity bone-tendon interface. By avoiding placing sutures through bone, fragmentation of comminuted or osteoporotic bone is prevented. Humeral positioning is critical in determining the correct height, version, and sizing of the component and head. Secure prosthesis fixation always requires cement. Drill holes are placed in the shaft medial and lateral to the bicipital groove for tuberosity fixation, and then No. 5 nonabsorbable sutures are passed through these drill holes before cementing. The goal in tuberosity reconstruction is to obtain healing of the tuberosities to the shaft and to each other. Tuberosity stay sutures, which were previously placed at superior, middle, and inferior tendinous insertions, are now used to secure the tuberosities to the prosthetic fin, to each other, and to the shaft, respectively. It is important to secure the tuberosities below the head. The inferior sutures are first secured to the shaft, then to the fin, and finally to the other tuberosity. Wire fixation should be avoided because of the potential for breakage. Tuberosities are held together with a towel clip before tying the final sutures. The rotator interval is then repaired with nonabsorbable No. 1 Tevdek/Ethibond suture. Range of motion is then tested, and the tuberosity repair is inspected.

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A B

D

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Figure 17J1-21 A and B, Fixed tuberosity and head unit are reduced and secured to the shaft with a nail inserted into the intact lesser tuberosity. C, Figure-of-eight sutures or wires are used to secure the greater tuberosity and the humeral head segments to the shaft through four predrilled holes. D, Clinical example of similar injury 1 year after open reduction and internal fixation of three-part anterior fracture-dislocation. (A, From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 152.) Continued



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Figure 17J1-22 Modified 3.5-mm Ender nail with additional hole above the eyelet to allow deeper insertion below the rotator cuff. (From Cuomo F, Zuckerman JD: Proximal humerus fracture. In Browner BD [ed]: Techniques in Orthopaedics, vol 9. New York, Raven Press, 1994, p 152.)

REHABILITATION Intensive rehabilitation after proximal humeral fractures is essential to maximize the functional result after treatment. In the athletic patient, it is especially important to avoid the common complications of stiffness and decreased function. The limits of postoperative rehabilitation are based on the limits of the repair. Physician-supervised postoperative rehabilitation plays a vital and integral part in the management of displaced proximal humerus fractures and is paramount for optimal results. The primary goal of surgical reconstruction is to obtain fixation secure enough to allow early passive motion and active-assisted exercises. Early motion is necessary to prevent intra-articular and extra-articular adhesions, which may be extremely difficult to eliminate nonoperatively. In most cases, passive range of motion is begun on the first postoperative day in the form of pendulums and passive forward elevation in the plane of the scapula. Dependent on the fixation rigidity noted at surgery, external rotation with a stick and elevation are also added in the immediate postoperative setting, usually within 1 to 2 days. These passive exercises are performed 4 times daily until healing has occurred, at which point more advanced stretching is begun. Internal rotation behind the back is held for 6 weeks when the greater tuberosity has been fixed to avoid stressing the repair. In the case of lesser tuberosity fractures, external rotation is limited to a point, determined at surgery, that will not place tension on the tuberosity fixation. Active range of motion is not initiated until adequate bone and tendon healing has occurred, usually at 6 weeks, with resistive and strengthening exercises added at about 3 months in the form of Thera-Band or surgical tubing. Progressive improvement in range of motion and strength

will continue over a full year’s duration; therefore, a physician-supervised rehabilitation program is essential throughout this time to maximize results. A four-phase program is used for rehabilitation. In the initial phase, passive and assisted range of motion exercises are performed within the limits of the repair or fracture stability until the fracture is deemed to be healed. In the second phase, active range of motion and advanced stretching exercises are instituted. Early resistance exercises, both isometric and isotonic, are begun. The third phase moves toward advanced stretching exercises as well as isotonic and isokinetic strengthening. The final fourth phase is activityspecific exercise, which attempts to return the athlete to his or her sport. In the initial phase of rehabilitation, exercises are performed more frequently for a shorter duration. A common protocol consists of exercises performed 4 to 5 times daily for 10 to 15 minutes. The use of moist heat before exercise helps to relieve discomfort and make the soft tissues more supple. Analgesics are used for pain control as necessary. The first phase consists of pendulum exercises along with supine assisted elevation exercises. These can be accomplished with the use of either an overhead pulley mounted to a frame, a 3-foot stick, or the opposite hand. Hand and elbow range of motion exercises are begun in this initial phase (Fig. 17J1-23A and B). A stick is used to perform supine external rotation stretching. In the second phase, active range of motion is initiated with cane-assisted active forward elevation, activities of daily living, isometrics, and further stretching, that is, internal rotation behind the back (see Fig. 17J1-23C). When the fracture is deemed to be clinically and radiographically healed, the third phase is begun. The third phase of exercises includes more advanced stretching

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exercises such as wall stretch for both elevation and external rotation. Isotonic exercises needed to strengthen the components of the rotator cuff and three components of the deltoid are performed using a pulley and weight system. The trapezius and rhomboids are strengthened using a hand-held weight for shoulder shrugs and scapular retraction exercises. As healing progresses and strengthening advances, isokinetic strengthening can be used in both internal and external rotation as well as flexion-extension planes. Attention should be given to the fact that a weak rotator cuff can allow superior shear of the humeral head and therefore can propagate impingement. Care is taken to keep the strengthening exercises out of the impingement planes until adequate cuff strength has been regained (Fig. 17J1-24). The final phase of rehabilitation is sport specific. Ballistic overhead activities in the throwing plane can be performed using surgical tubing or isokinetic equipment (Fig. 17J1-25). Subcomponents of the sport-specific activity can be performed until the athlete completes the entire sport-specific motion in a pain-free fashion. Return to play is variable, depending on the severity of the fracture (Box 17J1-5).16

Muscle Ruptures Involving the Proximal Humerus Region Excluding the Rotator Cuff Injuries to the musculotendinous unit are quite common in sport-related activities. Most cases result only in partial injury and rarely cause long-term disability for the athlete. Partial injuries or muscle strains may cause pain, loss of strength, and decrease in function leading to significant interference with athletic performance. Muscle strains and tendinitis probably represent the most frequent causes of missed playing time in competitive athletes.16 Complete avulsion injuries to major tendons can lead to substantial functional disability. With complete disruption of a musculotendinous unit or the muscle belly, significant alteration of joint biomechanics results. Because most complete tendinous avulsion injuries result in retraction of the tendon by muscle contraction and shortening, permanent dysfunction may occur unless appropriate anatomic repair is carried out.

A

C

B

Figure 17J1-23 Rehabilitation phase I and II. A, Pendulum exercise. B, Forward elevation using overhead pulley. C, Internal rotation stretching using opposite hand (a phase II exercise).


A

B

C

Figure 17J1-24 Rehabilitation phase III (strengthening). A, External rotation with Thera-Band. B, Internal rotation. C, Scapular retraction.

A

B

Figure 17J1-25 Rehabilitation phase IV (sport-specific exercise). Ballistics using Thera-Band in throwing position.

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Box 17J1-5 R eturn to Play in Proximal Humerus Fracture After painless range of motion and bridging callus on radiography are apparent, a conservative estimate should require 12 weeks of additional rehabilitation. Early range of motion will minimize stiffness and allow earlier return to play. Strengthening exercises are held until radiographic evidence of healing is apparent.

Most significant muscle ruptures occur when an actively contracting muscle group is overloaded by the application of a load or extrinsic force that exceeds tissue tolerance.118 In the athlete, this overload can occur acutely with the application of a single macrotraumatic force, or it can occur chronically with the application of multiple submaximal forces at a rate that exceeds the body’s ability to respond. Muscles and tendons clearly do respond to stress and applied demand by varying their strength and dimensions.119 Tendons become thicker with repeated stresses, and their collagen fibers become more appropriately oriented for function. Repetitive stress can eventually damage tendon tissue if the rate of application of the stress is more rapid than the body’s ability to respond. Healing of microscopic fiber failure occurs by the formation of scar and granulation tissue, which leads to an area within the tendon of altered mechanical properties. It is in this area that macrofailure will eventually occur.16 In the normal state, it has been shown that tendon appears to be stronger than the muscle belly and the tendon-bone interface.118 However, in the case of repetitive microtrauma to tendons, as often occurs in sports, this “normal” situation is modified and may lead more commonly to tendinous rupture. Both the rate of force application and the mechanism of injury affect the site of rupture.119 An additional factor that can affect the normal state of muscle-tendon unit physiology and biomechanics is the use of anabolic steroids. In response to reports in recent years of frequent abuse of steroids by certain groups of athletes, much research has begun to understand better the changes that develop in the human system.120,121 Abuse of anabolic steroids may increase the risk for injury to the muscle-tendon unit both by direct effects on structure and physiology and indirectly through changes in biomechanics.120

Rupture of the Pectoralis Major Rupture of the pectoralis major is an uncommon injury that most commonly occurs in skeletally mature men. A recent review of the literature reports a meta-analysis of 112 cases with enough data to evaluate cause, rupture site, injury mechanism, and treatment outcomes.122 All patients were men. This injury occurred most commonly in sports during weight training, weightlifting, or wrestling when the arm was externally rotated and abducted. Most reported ruptures are complete and are located at the insertion to the humerus. Work-related injuries occur more often at the musculotendinous junction. The prognosis was related neither to the age of the patient

nor to the location of the rupture. Surgical treatment, preferably within the first 8 weeks after the injury, had a significantly better outcome than nonoperative treatment or delayed repair.122 McEntire and colleagues completed a review, revealing that only 45 cases had been reported before the 11 cases noted in their series.123 Pectoralis major rupture, therefore, is a relatively rare injury, with about 150 reported cases in the literature. Significantly, most of the patients sustained rupture of the pectoralis major while involved in sports. Weightlifting was by far the most common activity, followed by rugby, wrestling, other contact sports, and even windsurfing.124 This injury has been reported in all age groups, but patients in the third and fourth decades are affected predominantly. There has never been a case reported in a female.125-132 This most likely reflects the fact that men in the early middle-age groups are historically more commonly involved in contact sports and have traditionally had greater involvement in weightlifting.

Anatomy The pectoralis major muscle arises as a broad sheet of muscle from the mid-clavicle, sternum, ribs, and external oblique fascia (Fig. 17J1-26). The muscle is often described as having two parts or “heads,” an upper clavicular head, and a lower sternocostal head. Muscle fibers, composed of a flat tendon about 5 cm broad, converge toward their insertion distal to the crest of the greater tuberosity of the humerus. The tendon consists of two laminae placed one in front of the other that commonly blend together inferiorly. The fibers from the clavicular head run in line to form the anterior lamina of the tendon. The more distal and deep fibers of the sternocostal head run upward and laterally to form the posterior lamina, those with the lowest origin having the highest insertion, giving a twisted appearance to the muscle.10 Dissections performed by Kretzler and Richardson showed the tendon to be about 1 cm long on the anterior surface and perhaps 2.5 cm long on the deeper or posterior surface.128 The tendon is quite thin and appears to be a coalescence of the anterior and posterior vesting fasciae rather than a true tendon or musculotendinous junction.

Laminated tendon

Pectoralis major m.

Figure 17J1-26 The two “heads” of the pectoralis major muscle, which arise from a broad area on the chest and converge into a flat laminated tendon that attaches to the proximal humerus.


Grossly, the pectoralis major forms the smooth, rounded appearance of the anterior axillary fold. The muscle is innervated by the medial and lateral pectoral nerves, which branch directly from the medial and lateral cords. The primary function of the pectoralis major muscle is adduction and medial rotation of the humerus. The muscle can also function to flex the humerus if it is extended behind the plane of the body. With the arm at the side, the upper or clavicular portion of the muscle is most effective, but as the shoulder is abducted, the lower portion of the muscle provides the bulk of the power.10

Classification Pectoralis major ruptures can be classified by the degree and location of the rupture. The degree of rupture can be classified as either complete or incomplete. Most cases are undoubtedly partial or incomplete and represent strains of the muscle belly or musculotendinous junction. Most cases in the literature that have come to surgery involved complete ruptures. Avulsion-type injuries involving the tendon at or near the humeral insertion tend to predominate.122,123 Incomplete and complete ruptures at the musculotendinous junction or in the substance of the muscle belly have also been reported in association with a direct blow.125,126,132,134,135

Clinical Evaluation History and Mechanism of Injury Patients with an acute rupture of the pectoralis major usually present with a definite history of injury. The typical injury occurs when the patient is lifting weights or receives a direct blow. The patient experiences an immediate, severe pain and a tearing sensation with burning at the site of injury. Some patients describe an audible pop or snap associated with a complete rupture of the tendon. The most common mechanism of injury is indirect and is related to excessive tension on a maximally contracted muscle. Weightlifting, specifically the bench press, is an example of this mechanism.123,128,132 Ruptures have also been reported to occur while windsurfing, being dragged behind a moving vehicle, and attempting to break a fall. These injuries can be associated with a fracture or dislocation of the proximal humerus. Direct trauma to the muscle as in wrestling, rugby, football, or other contact sports has also been reported.123,124,135-138 The most common activity associated with complete rupture was the bench press weight lift. This indirect mechanism is associated with the development of excessive muscle tension and usually results in an avulsion type of injury at or near the tendinous insertion into the humerus. An attempt to break a fall on an outstretched hand can also apply a severe indirect force to the muscle-tendon unit that can result in rupture. Wolfe and colleagues reported on nine weightlifters with pectoralis ruptures and designed an anatomic cadaver study to determine the mechanism of injury.139 They concluded that the short, inferior fibers have a mechanical disadvantage in the final portion of the eccentric phase of the lift. Continued application of high loads to these maximally

stretched fibers of the sternal head produces rupture of the pectoralis major. Direct blows are also associated with injury to the pectoralis major and may occur within the substance of the muscle belly. In wrestling, there seems to be a propensity to disrupt the muscle at the sternoclavicular head by direct contact. McEntire and colleagues, in their review of the literature, proposed that some of the previously reported cases of pectoralis major rupture may actually represent congenital absence of the muscle.123 Complete avulsion of both the sternal and clavicular heads may also occur in older individuals.125

Physical Examination The patient with acute rupture of the pectoralis major pre sents with the affected extremity splinted across the chest and often supported by the opposite hand. Early swelling and ecchymosis occur across the chest, axilla, and upper arm region. Pain with shoulder motion is present. Distal rupture is associated with asymmetry of the anterior axillary fold as the muscle retracts medially and superiorly. There is commonly a prominent bulge involving the retracted muscle belly. A palpable defect is present at the site of injury but may be obscured initially by swelling. Weakness is present with attempted adduction and internal rotation of the arm. Clinical diagnosis immediately after injury can be difficult because ecchymosis, swelling, and severe pain can obscure the exact location and extent of injury. Consequently, it may be very difficult in the acute setting to distinguish between complete and partial ruptures. Some authors advocate repeated physical examinations over a 4week period (Fig. 17J1-27).132 In chronic cases, the retracted muscle belly may be very prominent, and asymmetry from side to side is noticeable. A defect in the anterior axillary fold gives a webbed appearance to the anterior axilla. The most reliable clinical examination finding is weakness in adduction and internal rotation. In chronic cases, the patient often complains of a dull, aching pain with activities that require heavy muscle power.

Imaging Plain radiographs of the shoulder, chest, and scapula are usually normal unless a bony avulsion has occurred.140 A loss of the normal pectoralis major shadow has been described but is very subtle.128,141 Liu and colleagues reported on Cybex isokinetic muscle testing, CT, and ultrasonography to help in making the diagnosis.142 Magnetic resonance imaging (MRI) is the optimal imaging technique to study the normal and abnormal conditions of the pectoralis major muscle and tendon unit. The normal pectoralis major myotendinous unit has low signal intensity on both T1- and T2-weighted images. Lee and associates described anatomic landmarks for recognition of injuries to the muscle and myotendinous unit.143 These include the quadrilateral space, or the origin of the lateral head of the triceps, as the superior boundary and the deltoid tuberosity as the inferior boundary of the intact tendon of insertion. Failure to visualize a normal insertion within these boundaries should prompt a search for

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A

B

Figure 17J1-27 A, Clinical presentation of an acute rupture of the pectoralis major tendon at rest. Note the mildly webbed appearance of the axilla. B, Webbing and deformity on the right are accentuated by stressing the pectoralis with resisted contraction.

r upture and retraction of the tendon medially. MRI can be valuable in making or confirming an early diagnosis, which can avoid surgical delay. Early diagnosis has the advantage of avoiding adhesions, muscle retraction, and atrophy and thus preventing the delayed return of the athlete to competition (Fig. 17J1-28).129

Treatment Many authors agree that partial ruptures of the pectoralis major tendon and incomplete lesions of the muscle belly itself respond to conservative treatment.123,141,144-146 These partial injuries are characterized by less swelling, ecchymosis, and pain than complete injuries. When adduction is

A

resisted, no defect in the tendon is palpable. Initial treatment begins with ice, rest, and control of the hematoma followed by a program of progressive range of motion and strengthening exercises. Slow return to strength is the rule. These injuries usually heal without major deformity or significant strength deficit. They often require a 6- to 8-week course of recovery before return to stressful lifting activities. Both surgical and nonsurgical treatment methods for complete rupture of the pectoralis major have been described.127,128,132,145 Three major parameters can be assessed when describing results of treatment after this injury: pain, strength, and cosmetic deformity. Nonoperative treatment is similar to that described for incomplete injuries.

B

Figure 17J1-28 A, T1-weighted magnetic resonance image of an acute rupture of the pectoralis major tendon. B, T2-weighted image. Note the detachment of the tendon from its insertion on the humerus as well as medial retraction.


perative management for complete tears within the tenO don can be carried out by reattaching the tendon through drill holes or suture anchors in the humeral cortex at its anatomic insertion site.122,129,138,139,147,148 If the tear is at or near the musculotendinous junction, repair can be accomplished by an end-to-end technique. In a review of 29 cases by Park and Espinella, only 58% of patients with rupture of the pectoralis major treated by nonoperative means showed good results.149 In the same series, the authors report 90% good to excellent results in those patients treated surgically. Zeman and colleagues reported four of four cases treated surgically had excellent results.132 In five patients treated conservatively, significant strength deficits existed that limited return to athletic competition. Late repair has been shown to be effective in improving pain, strength, and function in a high percentage of cases.128,132,150 Delayed repair for up to 4 to 6 weeks does not appear to affect the result. Several reports of late repairs from 3 months to 5 years discuss successful results. Anbari and associates recently reported a delayed repair successfully performed 13 years after the initial injury, although the authors caution this was possible only because the ruptured sternal portion of the muscle was scarred to the intact clavicular portion and had not retracted.151 The authors described all


of

late repairs with some residual deficiency of strength but good overall results.128,147,150,151 Because many of these injuries occur in athletes, most authors have recently advocated surgical repair to obtain complete recovery and restoration of the full strength of the muscle.128,129,132,133,135 Pavlik and colleagues surgically repaired an acute rupture in one wrestler who 3 months later went on to win an Olympic gold medal.138 Wolfe and associates found that surgically treated patients showed comparable torque and work measurements, whereas conservatively treated patients demonstrated a marked deficit in both peak torque and work/repetition.139 Schepsis and colleagues retrospectively studied 17 cases of distal pectoralis major muscle rupture to compare the results of repair in acute and chronic injuries and to compare operative and nonoperative treatment.148 Isokinetic testing revealed that acute injuries treated surgically demonstrated the highest adduction strength (102% of the opposite side) compared with chronic injuries (94%) or nonoperative treatment (71%). There were no statistically significant subjective or objective differences in outcome between the patients treated operatively for acute or chronic injuries, but these patients fared significantly better than patients treated nonoperatively.148

Treatment

For partial ruptures involving predominantly the muscle belly, we prefer nonoperative treatment. Initially, the patient’s arm should be immobilized in a sling, and ice should be applied. Pendulum exercises are begun on the second or third day, followed by slow, progressive shoulder range of motion exercises. Strengthening exercises are begun at about the fourth week, and slow progression to isotonic and isokinetic exercises is allowed. Typically, recovery takes 6 to 8 weeks. Early diagnosis of complete rupture is helpful in advising the patient about treatment options. Diagnosis can usually be based on clinical data, but if there is a question,

MRI is a helpful adjunct to obtain additional information. Complete ruptures within the substance of the tendon or avulsion from the humerus should be repaired to bone (Fig. 17J1-29). An anterior axillary incision is used, and the tendon is isolated. The tendon is usually thin and small and is sometimes difficult to identify owing to rotation into the muscle belly and large hematoma. Heavy No. 5 nonabsorbable sutures are woven in a Bunnell-type fashion from the musculotendinous junction out through the end of the tendon. Even if some lateral tendon remnant is found at the humerus, we believe the musculotendinous unit should be

Pectoralis major m.

Distal portion of deltopectoral incision

A

Distal stump

Figure 17J1-29 Surgical repair of a ruptured pectoralis major tendon. A, The distal portion of a deltopectoral incision is used.

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of

Treatment —

cont’d

Bony trough

B

Repaired

Figure 17J1-29, cont’d B, The tendon is repaired with multiple No. 5 nonabsorbable sutures.

anchored back to bone. A bony trough is developed in the cortex of the humerus, and multiple drill holes are made in the adjacent cortex. The tendon is advanced into the trough and anchored by passing the sutures through the adjacent

Postoperative Management and Rehabilitation A sling is worn postoperatively for the first month. Gentle shoulder range of motion exercises are begun early in the first week. Further stretching and range of motion exercises are initiated to obtain a full range of motion by the sixth or eighth week. Light isotonic exercises are begun at about 6 weeks, and slow progression to advanced strengthening and functional activities is made during the first 3 months. Return to full unrestricted weightlifting is often delayed until 6 months after the repair.

Criteria for Return to Sports Participation The patient with a partial or complete injury who is treated conservatively should regain full shoulder motion and protective strength before return to competition is allowed. The patient treated by surgical repair often requires 6 months to return to full strength. Before return to heavy athletic competition, full range of motion should be achieved.16

drill holes. If there is residual tendon remaining on the humerus, this can be oversewn for double reinforcement of the repair.

three major portions of the deltoid that converge on a common insertion point midway down the humerus at the deltoid tuberosity. The axillary nerve is the primary innervation for the deltoid muscle. It passes beneath the glenohumeral joint to exit posteriorly at the quadrangular space, then branches into anterior and posterior divisions that course on the deep surface of the deltoid about 6 to 8 cm distal to its origin. The axillary nerve innervates both the deltoid and the teres minor and provides sensation for the upper lateral arm. Functionally, the deltoid provides power for flexion, extension, and abduction of the glenohumeral joint. It also forms the bulk that covers and protects the underlying rotator cuff and the shoulder joint itself.10

Supraspinatus m. Posterior third of deltoid m.

Rupture of the Deltoid Complete rupture of the deltoid muscle is a rare clinical entity, although contusions and strains are not uncommon in both throwing and contact sports. Little has been written about injury to this muscle, yet even minor injuries can seriously affect athletic performance.141,152-154

Anatomy and Biomechanics The deltoid is the primary motor for the shoulder girdle. It arises from the anterior clavicle, the acromion, and the spine of the scapula (Fig. 17J1-30). There are

Middle third of deltoid m. Clavicular head of pectoralis major m.

Subscapularis m.

Figure 17J1-30 The three major portions of the deltoid, originating on the clavicle, the acromion, and the spine of the scapula. Insertion is midway down the humerus at the deltoid tuberosity.


Clinical Evaluation History and Mechanism of Injury Minor injuries to the deltoid such as strains and contusions are common in athletic activities. Usually a direct blow to the upper arm while it is in abduction or forward elevation is the cause. Deltoid muscle strains have also been described in throwing sports. The anterior deltoid can be injured during acceleration, whereas the posterior deltoid is subject to injury during deceleration. Injury to the origin of the deltoid can occur with grade V acromioclavicular dislocations when the distal clavicle ruptures through the deltotrapezius fascia. Complete disruption of the deltoid is quite rare and appears to be associated with crushing injuries or severe direct blows received during major trauma from the outside. A few rare examples have been reported in the literature, usually associated with cases of severe trauma such as those described by Gilcreest and Albi in 1939155 and McEntire and colleagues in 1972.123 Recently, Blazar and Morisawa both reported on the spontaneous detachment of the deltoid origin in patients with chronic, massive rotator cuff tears. These detachments were associated with an acute and sudden onset of shoulder weakness and minimal pain.152,153 One series described more than 1000 musculotendinous injuries that contained no cases of deltoid rupture.156 It is important to note that rupture of the deltoid is perhaps most commonly associated with surgical intervention.141,154,157 The deltoid muscle is commonly detached from its origin on the clavicle and acromion in a number of shoulder procedures. Inadequate reattachment of the deltoid origin followed by early institution of resistance exercises can result in retraction of the deltoid distally. This is an extremely difficult problem to reconstruct later, and therefore early diagnosis following detachment and retraction of the deltoid is important. Permanent loss of deltoid function owing to detachment can result in a severe functional deficit that may preclude return to athletic competition.

Treatment In most strains and contusions involving the deltoid muscle, local conservative treatment is all that is necessary. Ice is applied in the acute phase, with immobilization in a sling as symptoms warrant. After several days, heat, gentle mobilization, stretching, and slowly progressive strengthening exercises are usually all that is required to return to full function. Management of postoperative dehiscence requires early diagnosis followed by surgical reattachment. Deltoid disruption after shoulder surgery is associated with poor function. Sher reported on 24 patients who underwent direct repair or rotational deltoidplasty reconstruction for detached muscle origin after shoulder surgery.154 Two patients required a shoulder fusion for intractable pain. Overall, 1 (4%) excellent, 7 (29%) good, and 16 (67%) unsatisfactory results were observed. A poor outcome was associated with a prior lateral acromionectomy, involvement of the middle deltoid, a massive rotator cuff tear with weakness in external rotation, and a residual postoperative defect larger than 2 cm. Only in select cases was repair or deltoidplasty thought to improve function and pain.

Authors’ Preferred Method of Treatment Partial injuries and contusions should be treated with ice and rest in the acute phase, followed by progressive range of motion exercises, heat, and strengthening. Complete healing and return to sport can be expected. Complete disruption and dehiscence following previous shoulder surgery should be treated surgically. Every attempt should be made to anchor these injuries back to bone. Protection in an abduction splint is almost always necessary to decrease any tension on the repair. Passive motion should be instituted early, but active exercise is delayed for at least 6 weeks. Prognosis after this injury is guarded.


Rupture of the Subscapularis

In the acute deltoid strain without rupture, local tenderness and mild swelling may be the only clinical signs. Ecchymosis may be present in the case of a contusion caused by a direct blow. Shoulder motion is often limited, and weakness secondary to pain may be present. Examination after acute complete rupture will demonstrate massive injury with swelling, deformity, and ecchymosis. With complete avulsion, there is loss of the normal shoulder contour, direct tenderness, and often a palpable defect. Weakness and limited abduction are present. Because this injury usually occurs after massive multiple trauma, masking by the additional injuries may make immediate recognition difficult. In postsurgical dehiscence of the deltoid, the defect is usually palpable in the region of the previous attachment. This late detachment can also be difficult to diagnose because of local swelling.

As an isolated tear, this is an extremely rare injury.155,158,159 Recently, Gerber and Krushell presented a series of 16 cases of this injury that required surgical treatment.160 Partial ruptures have been documented by many authors in association with anterior dislocation of the glenohumeral joint.58,128 In the traumatic situation, subscapularis tendon avulsions are often associated with avulsion fractures of the lesser tuberosity.161,162

Anatomy The subscapularis muscle arises from the subscapular fossa on the deep surface of the scapula and inserts by a broad tendinous attachment into the lesser tuberosity of the humerus. It is the anterior part of the musculotendinous rotator cuff. The subscapularis forms the upper border of the quadrangular and triangular spaces with the axillary

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nerve, posterior humeral circumflex vessels, and scapular circumflex vessels passing beneath it. It has an important function in internal rotation of the humerus and acts as a dynamic humeral head stabilizer.10

Clinical Presentation History and Mechanism of Injury Although poorly described in the literature, the mechanism of injury is similar to that for an anterior dislocation. A fall on the outstretched arm in abduction as the patient attempts to bring the arm into an adducted position is often the mechanism of injury. The cause of injury as forceful hyperextension or traumatic external rotation of the adducted arm has also been described.160 The patient presents with pain, anterior swelling, and decreased mobility around the joint. If the injury is associated with anterior instability, the apprehension test is positive. With an isolated injury, weakness of internal rotation is present along with increased passive external rotation. Gerber and Krushell described a clinical test for evaluation of the integrity of the subscapularis that they termed the lift-off test.160 The patient places the arm in internal rotation with the dorsum of the hand on the back. If the patient is unable to lift the hand off the back, incompetence of the subscapularis can be suspected. Additionally, one can hold the patient’s hand in internal rotation away from the back and then release. Inability of the patient to hold the hand away from the back is consistent with subscapularis incompetence.

Recommended Treatment In cases associated with anterior dislocation, the subscapularis rupture is repaired during anterior reconstruction. Surgical repair or reconstruction of isolated ruptures has been reported with good results.159,160 In cases associated with lesser tuberosity avulsion, treatment by direct reattachment with either sutures or screw fixation has been described.161,162

Anatomy This large muscle arises in the back from the lower six thoracic spinous processes, the thoracolumbar fascia, the posterior part of the iliac crest, the lower three or four ribs, and the inferior angle of the scapula. It attaches to the upper medial humerus, forming the posterior axillary fold. It is a powerful adductor of the humerus and acts as an extensor of the humerus when the shoulder is flexed. The thoracodorsal nerve arising from the posterior cord supplies the latissimus.10

Clinical Evaluation History and Mechanism of Injury In most cases of muscle strain and contusion of the latissimus dorsi, swelling, ecchymosis, and deformity are notably absent. Tenderness to direct palpation of the muscle belly and pain when adduction of the shoulder is resisted are the major clinical signs. The latissimus is stressed during the throwing motion when the arm is rapidly decelerated during follow-through. Kawashima and colleagues164 and Spinner and associates166 have described the only cases of complete rupture of the latissimus dorsi tendon. In one case, this was associated with a complete rupture of the pectoralis major in a patient who suffered a severe industrial crush injury. Pain, ecchymosis, and swelling of the posterior axillary fold and tenderness to palpation were present. The other case was associated with an avulsion of the conjoined tendons of the latissimus and teres major muscles.164,166 There is also one report of an isolated teres major tendon injury in a baseball pitcher diagnosed by MRI.167 Lazio and coworkers reported on two cases of ruptures of the latissimus dorsi as a result of the surgical approach in transthoracic and thoracoabdominal approaches to the spine.165 In each case, the patient presented 3 to 6 months postoperatively with a large painful mass along the posterior axillary line adjacent to the surgical incision.

Recommended Treatment Authors’ Preferred Method of Treatment We recommend primary repair of injuries to the subscapularis tendon with or without avulsion fracture. If the bone fragment is large, it may be repaired with screw fixation. If it is a tendinous avulsion or a small portion of bone, repair with heavy sutures through drill holes is preferred.

Latissimus Dorsi Injuries Injuries to the latissimus dorsi are extremely rare. Complete rupture has been described only in conjunction with rupture of the pectoralis major and the teres major in severe trauma and after anterior spine surgery.163-166 Pain in the region of the latissimus dorsi can occur in throwing athletes as a result of muscular strain and in contact sports as a result of contusion.

Surgical repair of complete rupture by direct suture has been reported with complete return of function.164 Partial injuries should be treated like other acute strains of the musculotendinous unit. In the acute phase, rest, ice, and stretching are the mainstays, followed by a program of progressive motion, heat, ultrasound, and strengthening exercises.

C l The

r i t i c a l

P

o i n t s

surgeon undertaking fixation using a locking plate must use meticulous care to avoid penetration of screws into the joint. This involves a careful examination of the screw position in a minimum of 90 degrees of shoulder rotation, using either manipulation of the patient’s arm or arcing of the fluoroscope. Two isolated views are not adequate.

1066 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� l Fixation of three-part fractures using tension band and Ender nails requires that the tuberosity fragment first be reduced to the head fragment, converting the fracture to a two-part fracture. l We describe and prefer a technique of suture fixation through the cuff combined with intramedullary Ender nails to fix the head/tuberosity fragment to the shaft; however, a locking plate is also a good option (as for two-part fracture). l Proximal humerus fractures in younger sporting patients are usually high-energy injuries. l Fractures often occur in association with a dislocation, especially in a younger patient. l A neurovascular examination is essential to document function, especially of the axillary nerve. l An adequate axillary radiograph is an absolute requirement for classification. l Treatment is determined by fracture classification and patient function. l Anatomic, rigid stabilization is the goal of operative treatment, regardless of technique. l There are multiple methods of fracture fixation, none of which has been definitively proved superior to others.

S U G G E S T E D

R E A D I N G S

Egol KA, Kubiak EN, Fulkerson E, et al: Biomechanics of locked plates and screws. J Orthop Trauma 18:488-493, 2004. Fankhauser F, Boldin C, Schippinger G, et al: A new locking plate for unstable fractures of the proximal humerus. Clin Orthop 430:176-181, 2005. Gerber C, Schneeberger AG, Vinh TS: The arterial vascularization of the humeral head: An anatomical study. J Bone Joint Surg Am 72:1486-1494, 1990. Hertel R, Hempfing A, Stiehler M, et al: Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg 13:427433, 2004. Keener JD Parsons BO, Flatow EL, et al: Outcomes after percutaneous reduction and fixation of proximal humeral fractures. J Shoulder Elbow Surg 16:330-338, 2007. Neer CS II: Displaced proximal humerus fractures: Parts I and II. J. Bone Joint Surg Am 52:1077-1103, 1970. Nho SJ, Brophy RH, Barker JU, et al: Innovations in the management of displaced proximal humerus fractures. J Am Acad Orthop Surg 15:12-26, 2007. Park MC, Murthi AM, Roth NS, et al: Two-part and three-part fractures of the proximal humerus treated with suture fixation. J Orthop Trauma 17:319-325, 2003. Rose PS, Adams CR, Torchia ME, et al: Locking plate fixation for proximal humeral fractures: Initial results with a new implant. J Shoulder Elbow Surg 16: 202-207, 2007. Sperling JW, Cuomo F, Hill JD, et al: The difficult proximal humerus fracture: Tips and techniques to avoid complications and improve results. Instr Course Lect 56:45-57, 2007.


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Injuries of the Proximal Humerus 2. Injuries of the Proximal Humerus in the Skeletally Immature Athlete Kaye E. Wilkins

PHILOSOPHY OF TREATING FRACTURES OF THE PROXIMAL HUMERUS IN CHILDREN The High-Performance Athlete It will become obvious that there are many methods of treating the various fractures that occur in the proximal humerus in the immature athlete. In many instances reference will be made for singling out a specific treatment for the so-called high-performance athlete. This usually entails achieving an anatomic reduction by surgical intervention. This is in contradistinction to waiting for some misalignment to naturally remodel over the ensuing months or

even years. Depending on remodeling alone to resolve the misalignment may result in the individual having less than total motion and possibly total function of the involved shoulder. For almost all individuals this may not result in any problem of performing the usual ordinary tasks of life. For an athlete who, for example, is a very talented baseball pitcher, any minor reduction in motion or shoulder function can inhibit the ability to achieve the ultimate pitching potential. The athlete may have to change to playing in the outfield rather than continuing pitching. Certainly for those individuals who are presently participating at the high-performance level, there is no argument but to provide the treatment that will have the best chance of restoring both the anatomic alignment and function of the shoulder.

Shoulder 1067

The Non–High-Performance Athlete What about those athletes who are not participating at high-performance levels? This can present a dilemma to the treating physician and parents. The real question is what the future holds for this injured athlete. At the point of the injury, this may not have yet been determined. Although this athlete may not become engaged in a life of high-performance sporting participation, he or she may be involved in an occupation that would involve the need to perform heavy overhead work such as would be required of a painter or carpenter. Should not this lower level athlete be offered the same level of treatment? That is a question that can be answered only by a full explanation to the parents (and possibly to the patient as well) of the advantages and risks of all the modalities of treatment available for the injury sustained.

Offer Only the Best In summary, all pediatric athletes, regardless of their level of performance, should be offered all the modalities of treatment for their specific proximal humeral injury. The advantages, risks, and rehabilitation needs for each treatment available for that injury pattern should be outlined in detail so that the athlete and family can make the appropriate decision. In addition, should the initial treating surgeon not be able to perform all of the modalities available, it may appropriate to refer the athlete to an individual who can. It is also important that the treating surgeon be objective and not allow his or her prejudices to color the description of the modalities available.

EPIDEMIOLOGY Incidence of Shoulder Injuries Uncommon Shoulder injuries are relatively uncommon in the overall picture of injuries to the pediatric musculoskeletal system. Although fractures to the upper extremities per se are the most common injuries seen in the pediatric age group, most are distal rather than proximal. In his study of 8682 fractures in children, Landin1 found that 22.7% involved the distal forearm, 8.1% involved the clavicle, and only 2.2% involved the proximal end of the humerus. Most clavicular fractures after the age of 10 years occurred in boys and occurred during falls or contact sports. In a more recent review of 6493 children’s fractures by Cheng and coworkers,2 fractures about the shoulder accounted for less than 5% of all fracture types.

Almost No Sequelae In looking at the long-term sequelae of pediatric sportsrelated injuries, Marchi and coworkers3 found that none of those injuries occurring in the shoulder region had any long-term sequelae in young athletes. The highest

incidence of injuries with long-term sequelae was seen in the ankle and elbow regions.

Organized Sporting Events Increasing Incidence In Landin’s overall global review of all pediatric fractures, only 21% occurred in organized sporting events.1 In fractures associated with sporting events, there have been increases not only in participation but also in the number of injuries. Landin1 found that in the three decades from 1950 to 1980, there was a fivefold increase in the incidence of injuries to children from sporting activities.

Male Predominance in Sports In another study that looked only at fractures of the proximal humerus, Kohler and Trillaud4 found that 22% of 136 fractures occurred during sporting events. In their series, 60% of the patients were male. The peak age incidence was 10 to 14 years of age. Two thirds of the fractures involved the proximal metaphysis, and the other third involved the physeal plate.

Nonorganized Sports Higher Risks In the pediatric age group, most sporting activity occurs outside the organized educational setting. This has been a growing trend over the past 20 years. In the pediatric setting, many studies1,5,6 have found that far more injuries occur in nonorganized play activities. It was estimated in 1980 that nearly 30 million young people aged 6 to 21 years were involved in nonscholastic athletic programs.7 In contrast, in organized interscholastic sports in 1981,8 only 5.35 million young people were active participants. In the same study, the most popular sport reported for boys was football. For girls, basketball was the leader.

Female Preponderance In Landin’s study1 fractures of the proximal humerus accounted for only 2.2% of all fractures in children. More of these fractures occurred in girls. In his series of children in Sweden between the ages of 9 and 10 years, fully 50% of the fractures resulted from falls that occurred with horseback riding. Almost all of these patients were girls. Even when horseback riding injuries were removed from the overall group, there was still a preponderance of girls. In this same study, Landin found that the incidence of females sustaining fractures of the proximal humerus had increased dramatically since 1970. This large preponderance of girls sustaining fractures of the proximal humerus was also found in another study from Sweden.9

Horseback Riding In Landin’s series, the sporting event that produced the highest percentage of shoulder injuries was horseback riding (Fig. 17J2-1).1 Twenty-eight percent of the injuries


Summary In summary, the overall risk for injury to the pediatric athlete is related to the nature of the sporting event, the age of the participant, and the method by which the players are grouped. There appears to be a greater risk for injury in the skeletally immature individual among participants in nonorganized recreational or play activities than in players who are under some type of adult supervision.

Sport-Specific Trauma Sports injuries can be divided into two categories: macrotrauma and microtrauma. Macrotrauma usually results in an acute failure of the osseous structures. Microtrauma, conversely, is usually the result of repetitive stresses so that the failure occurs over a prolonged period.

Macrotrauma

Figure 17J2-1 A proximal humeral metaphyseal greenstick fracture in an 11-year-old girl who fell from a horse. Note that the fracture is incomplete with minimal displacement.

sustained from horseback riding involved the proximal humerus, and another 9% involved the clavicle.

Age Fear of Crippling Injuries Age is a factor in the overall incidence of athletic injuries in the pediatric age group. In 1956, the American Medical Association (AMA) published a statement warning against the participation of skeletally immature individuals in organized contact athletic events.10 The AMA stated categorically that such participation was unsafe because of the large number of physeal or growth injuries that could occur. Subsequent follow-up studies11 showed that this fear of so-called crippling injuries was unfounded. In fact, injuries to the physes accounted for less than 5% of all sports injuries.

Age-Related Injuries Injuries are age related.12 Among grade school athletes, the injury rate is very low. The injury rates increase steadily with age so that the maximal rates are seen in the high school age group.13

In 1978, Garrick and Requa14 surveyed the overall incidence of injuries over a 2-year period in high school sports. They mainly looked at macrotrauma injuries. Macrotrauma injuries occur as a sudden failure of bone. Predictably, football and wrestling produced the greatest number of injuries, whereas swimming and tennis had the lowest injury rates (Fig. 17J2-2). In reviewing the incidence of macrotrauma shoulder injuries in football,15-20 bicycling,20-23 skiing,24 snowboarding,25 and wrestling,8,26 the overall incidence of true acute failure of the osseous structures is very low. In these sporting events the failure usually occurs in the soft tissues securing the glenohumeral and acromioclavicular joints. There are three major sporting events in which there can be a high incidence of acute failure of the osseous structure of the proximal humerus while engaged in the sport: baseball, football, and horseback riding. Baseball

Fractures of the humeral shaft in pediatric baseball players are relatively rare but do occur.27,28 Usually, they are related to some inherent defect in the bony structures (Fig. 17J2-3). Ireland and Andrews27 described a case in a young pitcher with an acute avulsion of the coracoid epiphysis. Football

Most injuries to the shoulder in football result in macrotrauma (i.e., fracture of the clavicle or glenohumeral dislocation). The overall injury rate increases with age. In the little league age group, the rate of football injuries overall was only 7.8%, compared with 17% in high school players.17 When specific body areas are examined, the percentage of football injuries involving the shoulder is fairly consistent, ranging from 8% to 12%.16,17,26,29 The shoulder ranks second after the knee in overall injuries sustained in football. There appears to be an increased incidence of shoulder injuries in more recent years. Culpepper and Niemann16 theorized that this was due to the outlawing of spearing, which brought a return of shoulder-body contact to tackling. In one study of recurrent anterior shoulder dislocations requiring surgical correction, 49% of the patients sustained their initial injury in football.23 In another study

Shoulder 1069 Figure 17J2-2 Injury rates for macrotrauma for various athletic events in high school sports. (From Garrick JG, Requa RK: Injuries in high school sports. Pediatrics 61:465, 1978.)

90 FOOT BALL

80

WRESTLING 70 2-yr rate Male Female

Injuries / 100 participants

60

1st yr 2nd yr 50 SOFTBALL 40

CROSS COUNTRY

20

BASKET BALL

SOCCER

GYM

30

CROSS COUNTRY VOLLEYBALL

10 BADMINTON

TRACK & FIELD

GYM

TRACK & FIELD BASKET BALL

BASEBALL

SWIMMING

SWIMMING

TENNIS TENNIS

0

of acromioclavicular injuries, 41% of patients sustained their initial injury in football.20 Horseback Riding

Trauma sustained by young horseback riders most frequently involves head and neck injuries. Next to head injuries, however, is skeletal trauma, with two thirds of fractures occurring in the upper extremity.30 In Sweden, the major cause of fracture of the proximal humerus in girls (see Fig. 17J-1) is falling off a horse.1

Microtrauma Injuries due to microtrauma are especially prevalent in the shoulder region. The discussion of microtrauma injuries involving the physis will be presented in detail in the final section of this chapter dealing with stress injuries of the proximal humeral physis.

STRUCTURE OF THE PROXIMAL HUMERUS The proximal humerus is composed of the epiphysis, the physeal plate, and the metaphysis, all of which have unique biomechanical properties. These properties contribute to the specific injury patterns seen in this area. A review of the unique structural anatomy of this area will give the reader a better understanding of both the mechanism and the treatment of injuries that occur in the proximal humerus.

It also must be remembered that the soft tissues, such as the muscles, tendons, capsule, and periosteum, also play a prominent role in the susceptibilities of the osseous tissues of the proximal humerus to failure.

Epiphyseal Development Two Ossification Centers The proximal humeral epiphysis is a hemispherical structure containing a cone-shaped physeal plate. The physis is more proximally directed posteriorly, which provides some intrinsic stability (Fig. 17J-4). The hemispherical epiphysis contains the articular surface and the greater and lesser tuberosities. The epiphyseal mass is formed by two separate ossification centers, which fuse to form a single center by about 7 years of age and are completely fused to the proximal humerus by 17 or 18 years of age.31

Ossification Process This serial development of the proximal humeral epiphysis has been studied in great detail by Ogden and his coworkers.32 The initial contour of the physis is transversely oriented. At birth, there is usually no radiographically discernible ossification center. The first center develops as the capital or articular center at about 2 months of age (Fig. 17J2-5). At 7 months of age, a second center develops in the area of the greater tuberosity. By 3 years, these centers have enlarged and matured, with the physis assuming


its conical shape. When the individual reaches 7 years of age, there is a complete fusion of these two centers. The physis becomes more conical in shape. From 10 to 13 years of age, the greater tuberosity ossification center expands until it completely fills the cartilaginous space on the lateral portion of the epiphysis.

Physeal Closure By 14 years of age, the physis begins to close, starting in the center and extending peripherally.

Metaphysis Development When the epiphyseal centers fuse, the lateral metaphyseal cortex becomes thicker. It is composed almost entirely of cortical bone up to the physis, whereas the cortex on the medial metaphysis remains thin with a trabecular structure. This is thought to be one of the reasons that the Thurston-Holland metaphyseal fragment in the Salter-Harris II fracture occurs medially. As the physis closes, the medial metaphyseal cortex increases in density. Even though the cortex on the medial side is thicker, it has developed some trabecular pattern next to the physis. This produces an inherent weakness on the medial side of the proximal humerus.

Muscle Attachments Figure 17J2-3 This 12-year-old sustained an acute fracture while simply throwing a baseball during practice. This fracture occurred through a cystic osseous defect in the proximal humeral diaphysis (arrows).

Anterior view

The proximal humeral epiphysis has four muscles attached to it. In the greater tuberosity posterolaterally are the teres minor, infraspinatus, and supraspinatus. The subscapularis

Posterior view

B

A Figure 17J2-4 A, Line drawings of the proximal epiphysis and physis demonstrating the conical configuration. B, This SalterHarris type I physeal injury demonstrates the conical configuration as well. (A, From Grant JCB: An Atlas of Anatomy, 5th ed. Baltimore, Williams & Wilkins, 1962.)

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2 Mo.

3 Mo.

7 Yr.

9 Yr.

7 Mo.

10 Yr.

2 Yr.

13 Yr.

3 Yr.

14 Yr.

Figure 17J2-5 The schematic development of the proximal humeral epiphysis and metaphysis from age 2 months to 14 years. (From Ogden JA, Conlogue GJ, Jensen P: Radiology of postnatal skeletal development: The proximal humerus. Skeletal Radiol 2:153-160, 1978.)

inserts into the lesser tuberosity anteriorly. The pectoralis major attaches distally to the anterior metaphysis. In addition, the deltoid muscle inserts more distally at the diaphyseal-metaphyseal junction. When these two parts are separated by a fracture, there can be considerable displacement of the fragments. The dynamic effects of these muscles’ insertions on the epiphysis and metaphysis of the proximal humerus are demonstrated in Figure 17J2-6.

Capsular Attachments The glenohumeral joint capsule on the medial side attaches distally past the edge of the articular surface to the metaphysis. This means that a portion of the proximal physis lies intra-articularly within the shoulder joint (Fig. 17J2-7).

osterior circumflex humeral arteries, which arise from the p third part of the axillary artery.

Anterior Source Most of the blood supply to the osseous humeral head comes from the anterior ascending branch of the anterior circumflex artery.33 This artery ascends proximally along the upper end of the bicipital groove and then enters the head by branches that pierce the greater and lesser tuberosities. Once inside the humeral head, this artery assumes

Attachment of capsule

Blood Supply With the exception of the suprascapular artery, the blood supply to the shoulder arises from the second and third parts of the axillary artery (Fig. 17J2-8). The major supply to the proximal humerus comes from the anterior and

Physeal plate

Supraspinatus Infraspinatus Teres minor

Subscapularis

Pectoralis major

Figure 17J2-6 Effect of muscle forces on the proximal humeral epiphysis and metaphysis. (From Dameron TB: Fractures and dislocations of the shoulder. In Rockwood CA Jr, Wilkins KE, King RE [eds]: Fractures in Children, vol 3. Philadelphia, JB Lippincott, 1984.)

Figure 17J2-7 The relationship of the physeal plate and the glenohumeral capsular attachment to the proximal humerus is shown. The medial end of the physeal plate extends across an area covered by articular cartilage in the area noted by the dashed line. This area of metaphysis is intra-articular. (From Dameron TB: Fractures and dislocations of the shoulder. In Rockwood CA Jr, Wilkins KE, King RE [eds]: Fractures in Children, vol 3. Philadelphia, JB Lippincott, 1984.)


Suprascapular a. Anterior circumflex humeral a.

Transverse cervical a. Inferior thyroid a. Thyrocervical trunk Subclavian a. Highest thoracic a. Thoracoacromial a.

Posterior circumflex humeral a.

Box 17J2-1 O sseous Failure Patterns of the Proximal Humerus

I. Fractures of the proximal humeral physis II. Pure metaphyseal fractures III. Avulsion of the lesser tuberosity IV. Stress fracture of the proximal physis

Lateral thoracic a.

Profunda brachii a.

Subscapular a. Superior ulnar collateral a. Brachial a.

Figure 17J2-8 The arteries of the shoulder region. (From O’Rahilly R: Gardner-Gray-O’Rahilly: Anatomy, 5th ed. Philadelphia, WB Saunders, 1986.)

a form like that of the lateral epiphyseal artery of the femoral head. That is, it forms an arcuate system from which branches radiate at right angles to the periphery of the epiphysis.

Posterior Source A small amount of blood supply originates from the posterior humeral circumflex artery. This artery enters the epiphysis through a small portion on the posteromedial surface of the humeral head, which is similar to the medial epiphyseal arteries of the femoral head.

Muscular Sources A part of the blood supply also arises anterolaterally through the rotator cuff into the greater tuberosity. Because much of the blood supply enters through the muscular attachments to the proximal humeral epiphysis, avascular necrosis of the humeral head is extremely rare after a fracture through the proximal humeral physis (see “Avascular Necrosis.”).

INCIDENCE OF FRACTURES OF THE PROXIMAL HUMERUS It is difficult to determine the true incidence of pure physeal versus metaphyseal fractures of the proximal humerus because many of the reported series combine both into the generic category of fractures of the proximal humerus.3,34-37 The specific incidence of each of the various fracture subtypes is discussed in each of the sections dealing with the specific fracture types.

SPECIFIC FRACTURE PATTERNS Failure of the bony structure of the proximal humerus can occur in one of four patterns. These are listed in Box 17J2-1. The first three occur as a result of acute macrotrauma. The

last pattern is the result of repetitive microtrauma. Each of the failure patterns is discussed in detail in the following section. When there is failure of the proximal osseous structures, the position of the fracture fragments is determined by the muscles that remain attached to the separate fragments and the periosteal coverings. Thus, the nature of the fracture pattern is determined by whether the fracture occurs through the physis or metaphysis Because the proximal humerus is the area where most of the growth and remodeling of the humerus occurs, the incidence and patterns of fractures in this area are much different from those in the shaft. There is more leeway in accepting less than an anatomic alignment of the fracture fragments because of the increased remodeling potential in this area.

FRACTURES OF THE PROXIMAL HUMERAL PHYSIS Structural Aspects Variable Strength The presence of the physeal plates about the shoulder provides bony matrices of lesser strength than those provided by the adjacent capsules, ligaments, or even in some cases periosteum. The physes have an age-related variability in strength. The physis and its perichondrial ring weaken just before maturity.38 This fact is borne out in a clinical setting in the classic study by Peterson and Peterson.39 They found that the greatest incidence of physeal injuries occurred between the ages of 11 and 12 years in girls and 13 and 14 years in boys.

Role of the Periosteum The periosteum serves to provide some stability between the physis and the metaphysis. It can also help to direct the remodeling process. The thickness is not uniform around the proximal humerus. The varying degrees of thickness can be a factor in the failure pattern.

Thinnest Anteriorly In laboratory studies on humeri obtained from stillborn infants, Dameron and Reibel36 found that posterior displacement of the metaphysis was extremely difficult to accomplish. They attributed this to the fact that the periosteum of the metaphysis was considerably thicker posteromedially. Anterior displacement of the metaphysis was relatively

Shoulder 1073

easy to achieve because of the thinner periosteum on the anterolateral surface.

Provides Stability If it remains intact, the periosteal sleeve can also stabilize an undisplaced fracture. Once the metaphyseal fragment has torn the periosteum, all of its intrinsic stability is lost.

Guides Callus Formation The intact periosteal sleeve serves as a guide to the callous formation when the fracture fragments have become markedly displaced. This is an important factor in the remodeling process (see Fig. 17J2-12C).

Incidence Pure Physeal Injuries The most recent large review of physeal injuries has been that by Peterson and coworkers in 1994.40 Their series looked at 951 physeal injuries in Olmsted County, Minnesota, from 1979 to 1988. In this group, only 1.9% involved the proximal humerus, which was less than the range of 2% to 6.7% in four other previous series totaling 3326 cases.39,41-43

Salter-Harris I or II Almost all physeal fractures in this area are either SalterHarris type I or II.4,36,44 Type I fractures are less common and occur usually in younger children (i.e., younger than 10 years). Almost all the physeal fractures among individuals older than 10 years are Salter-Harris type II lesions.4,36 Because of the flexibility of the shoulder, forces acting directly against the articular surface or perpendicular to the physis are rarely applied to the proximal humerus.

Figure 17J2-9 Radiograph showing muscle force displacement. The epiphyseal fragment is rotated into flexion, abduction, and external rotation (white arrow). The metaphyseal fragment is forced cephalad by the pectoralis and deltoid muscles (black arrow).

Fragment Displacement Loss of Adduction Force When the failure occurs through the proximal physis, the adducting force of the pectoralis major muscle has been completely lost. Thus, the epiphyseal segment has become totally under the control of the muscles that rotate the proximal humerus to produce a distinct fracture pattern.

Epiphyseal Rotation When the proximal epiphysis becomes disrupted from the metaphysis, the unopposed action of the muscles on the epiphysis tends to pull this fragment into flexion, abduction, and external rotation (Fig. 17J2-9).48

Other Salter-Harris Injuries

Signs and Symptoms

As a result, Salter-Harris type III and IV fracture patterns are extremely rare.44-47 Lee and coworkers46 recently described a case of a Salter-Harris type III fracture pattern in which the humeral head epiphysis was dislocated and displaced posterior to the glenoid labrum. They pointed out that this was unusual because if there is complete separation of the epiphyseal fragment, it usually lies anterior to the glenoid. The type V lesions, which often result in the development of a varus deformity of the humerus, are usually the result of nontraumatic injuries that occur during early infancy or childhood and thus are usually not seen with athletic events.

Displacement Dictates Swelling

Anatomic Characteristics Intracapsular Fracture The capsule attaches to both the epiphyseal and metaphyseal cortices. Thus, a physeal fracture passes through the medial physeal plate, creating a line that is intra-articular in location (see Fig. 17J2-7).48

The differentiation between fractures of the proximal physis and metaphysis of the proximal humerus may be difficult clinically. In undisplaced metaphyseal fractures, especially those in which cortical integrity is maintained, there may be only minimal swelling. The tenderness is usually localized over the proximal humerus. In physeal fractures and metaphyseal fractures with displacement, there is usually considerable bleeding into the soft tissues of the deltoid area, which produces marked swelling. The athlete with these types of fractures is usually uncomfortable and holds the extremity adducted to the chest. The weight of the extremity is often supported at the elbow and forearm with the opposite hand.

Clinical Signs Not Specific The only major differential clinical finding occurs with complete fractures of the proximal physis. The maximal point of tenderness is usually more proximal. With the


physeal injuries, the distal metaphyseal fragment usually is laterally displaced. In this case it may be possible to define the prominence of the proximal metaphyseal fragment by palpating it under the anterolateral deltoid. However, with the severe swelling and pain that occur with these displaced physeal injuries, the ability to palpate these structures is severely limited. The final differentiation is usually dependent on the radiographic findings.

Evaluate for Ipsilateral Injuries It is important to assess all the nerves of the upper extremity to rule out a concomitant injury to any of the peripheral nerves of the brachial plexus. The vascular status of the upper extremity needs to be evaluated. Because the force was transmitted from the hand longitudinally, the entire extremity must be checked for the occurrence of less obvious ipsilateral fractures, especially in the distal radial metaphysis.

Mechanism of Injury Older Age Group The exact mechanism of proximal humeral physeal injuries is not completely clear. Physeal fractures are more common among athletes nearing skeletal maturity.

Multiple Mechanisms One of the first to truly analyze the mechanisms of proximal humeral physeal injuries was Williams in 1981.49 He did this by examining different displacement patterns of these fractures in his patients. It was determined that four forces could be applied to the proximal physis either singly or in combination. Only six variations of this, however, are likely to occur in the clinical situation: (1) pure extension; (2) pure flexion; (3) forced extension with lateral rotation; (4) forced extension with medial rotation; (5) forced flexion with lateral rotation; and (6) forced flexion with medial rotation. It is hoped that a better reduction can be obtained when the mechanism is determined according to the fracture patterns and the position of the patient’s upper extremity.

Displacement Dictated by Local Architecture The periosteum is weaker on the anterolateral aspect of the proximal humerus. In fractures involving the humeral physis, the proximal metaphyseal fragment is usually forced anteriorly and laterally through this weakened area. Neer and Horowitz42 reasoned that this force resulted from a direct blow to the shoulder by a posterolateral shearing force that adducted the humeral shaft and forced it anteriorly. Dameron,27 in contrast, believed that the force was directed longitudinally up the upper extremity as it was used to break a fall in a backward direction. The force originating as the hand hits the ground is transmitted proximally through the humeral shaft with the shoulder extended and adducted. This forces the metaphysis anteriorly, laterally, and cephalad. The horizontal alignment of the physis in the anterolateral portion of the proximal

humerus facilitates this displacement in an anterolateral direction. The combination of a stronger posteromedial periosteum and compressive posteromedial forces results in the triangular metaphyseal fracture fragment occurring in this area.

Metaphysis Slips Anterolateral When the periosteum disrupts, the proximal portion of the metaphysis tends to displace anterolaterally to the intertubercular groove under the long head of the biceps (Fig. 17J2-10).47

Classification Two Types Proximal humeral physeal fractures can be either acute or chronic. In the acute injuries, there is immediate partial or complete displacement of the physis from the adjacent metaphysis. The chronic type represents a stress injury, which is discussed at the end of this chapter.

Acute Injuries Fractures of the proximal humeral physis can be classified by location, degree of displacement, and stability. The degree of stability usually depends on the degree of initial displacement and the magnitude of the injury. The most commonly accepted classification of displacement is that proposed by Neer and Horowitz,42 who separated the displacement into four grades (Box 17J2-2). It should be noted that Neer and Horowitz in their original article42 used the term width of shaft instead of width of physis to denote the degree of routine displacement. In their illustrative cases, however, they demonstrated displacement of the physis. Thus, I have taken the license to correct this anatomic inaccuracy because the actual displacement is measured by the amount of physeal displacement, not by the amount of displacement of the proximal shaft, which is actually the metaphysis.

Radiographic Studies Routine Imaging Usually, routine roentgenograms are enough to demonstrate the presence of the fracture. The proximal and lateral displacement of the metaphyseal portion is usually obvious on routine anteroposterior views of the shoulder. It may be necessary to use transthoracic lateral or oblique scapular views to determine the degree of apex anterior angular displacement between the separate fracture fragments (see Fig. 17J2-10B).

Computed Tomography In some cases in which there may be a complex fragment pattern, a computed tomographic scan with horizontal cuts or three-dimensional reconstruction may be helpful in determining the fracture patterns and degree of displacement.

Shoulder 1075

A

C

Radiographic Comparison There is a distinct difference in the displacement of the fracture fragments between the proximal physeal and proximal metaphyseal fractures (Fig. 17J2-11). With the completely displaced fractures of the proximal physis, the distal fragment lies lateral to the epiphyseal fragment. Because the proximal fragment is rotated, the long axes lie at an angle to each other. With the metaphyseal fractures, the Box 17J2-2 Grades of Displacement Grade I—less than 5 mm Grade II—up to one third the width of the physis Grade III—up to two thirds the width of the physis Grade IV—greater than two thirds the width of the physis, including total displacement From Neer CS, Horowitz BS: Fractures of the proximal humeral epiphyseal plate. Clin Orthop 41:24-31, 1965.

B

Figure 17J2-10 A Salter-Harris type II fracture of the proximal humerus physis. Posteroanterior (A) and transthoracic (B) views show that the metaphyseal fragment (solid line) is anterolateral to the epiphyseal fragment (dashed line). C, Axillary lateral view confirms that the proximal metaphyseal fragment is anterior to the head.

pectoralis tendon insertion on the distal fragment forces it to lie medial to the proximal metaphyseal segment. Because there is some attachment of the pectoralis tendon on the proximal fragment, this proximal fragment lies with its long axis relatively parallel to the distal fragment.

Treatment In choosing the appropriate treatment plan, two major factors must be evaluated. The first is the degree of rotation and displacement of the proximal fragment. The second is the remodeling capacity of the patient.

Proximal Fragment Rotated In displaced fractures of the proximal humeral physis, rotation of the proximal fragment often occurs because there is an absence of adductor forces on this fragment. The adductor forces act entirely on the distal metaphyseal fragment


Figure 17J2-11 Left, With the completely displaced fractures of the proximal physis, the distal fragment lies lateral to the epiphyseal fragment. Because the proximal fragment is rotated, the long axes (lines) are at an angle to each other. Right, With the metaphyseal fractures, the pectoral tendon displaces the distal fragment to lie medial to the proximal metaphyseal segment. Because there is some attachment of the pectoral tendon on the proximal fragment, this proximal fragment is not rotated and thus lies with its long axis relatively parallel to that of the distal fragment (lines).

(see Fig. 17J2-9). In addition, the distal insertion of the deltoid muscle on the distal fragment provides a force that tends to retract the metaphyseal fragment proximally.

At no other physis in the body is there a larger proportion of contribution to longitudinal growth than at the proximal humeral physis. About 80% of the longitudinal growth occurs in this area.3,44,50 As a result, the remodeling potential in this area is tremendous. The younger the athlete, the greater is the potential for remodeling. Because of the wide range of motion of the glenohumeral joint, the residual varus that may remain usually does not result in any functional limitation.44 Shortening of these fractures is also well tolerated because of the independent function and non–weight-bearing status of the upper extremity. It must be emphasized, however, that there needs to be at least 12 to 18 months of growth remaining in the proximal humeral physis for adequate remodeling to be achieved.

f ragments into a more anatomic position. In some cases, a primary closed reduction is performed, either with sedation or under general anesthesia, and then the reduction is maintained by external support. The reduction is usually achieved by bringing the distal shaft fragment into flexion and some abduction and external rotation to align it with the flexed, abducted, and externally rotated proximal fragment.48 The real question concerns whether an anatomic reduction is necessary. Many series34,37,42,44,45,52-54 have shown that for most individuals, even those who have considerable initial displacement, simple immobilization often produces satisfactory results for most athletic activities not requiring high-performance upper extremity skills (Fig. 17J2-12). Baxter and Wiley44 found in their retrospective review that the manipulative process improved the arm’s position in only one third of the patients in whom it was attempted. When there was an improvement in position, the final result was no better than that seen in patients in whom an equal displacement had been accepted. These authors questioned whether active manipulation had had any effect on the final outcome.

Specific Treatment Methods

Maintaining the Reduction

As with most fractures, there are both closed and surgically invasive techniques that can be used in the management of fractures of the proximal humeral physis.

Once obtained, the reduction must be maintained nonoperatively by either a cast or some type of traction.

Remodeling Capacity

Closed Methods Obtaining a Reduction The argument for reduction of the fragments is that it decreases the degree of shortening that develops if the malalignment is allowed to remain.48,51 Various closed methods have been advocated to realign the fracture

Cast Methods

If the fracture is stable after the reduction, it can be immobilized alongside the chest. If it is not stable, this position of flexed abduction and external rotation must be maintained with either a shoulder spica cast in the salute position or a commercial splint. Neither immobilization technique is well tolerated by the athlete or the parents. The “Statue of Liberty” position with a spica cast should be avoided because of its potential to cause injury to the brachial

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Figure 17J2-12 No initial reduction. A, Anteroposterior image of this 12-year-old soccer player who sustained a Neer type III displaced fracture of the proximal humeral physis. B, Lateral image taken along the axis of the scapula. The metaphysis is anterior (black dotted line), and the epiphyseal segment is angulated posterior (white dotted line). C, Images obtained 6 weeks after the fracture demonstrate new bone (black arrows) forming along the intact inferior periosteal sleeve. The prominence of the fracture surface of the metaphyseal fragment is being resorbed. D, By 7 months after injury, there is considerable remodeling of the proximal humerus. Clinically, this patient still lacks full abduction (E) and external rotation (F).

plexus or to lead to development of vascular compromise to the upper extremity.22,47 Although this method of treatment was recommended in the past,55 it has now been universally abandoned. With the minimally invasive surgical techniques now available, combined with the unreliability of a cast to adequately maintain the reduction achieved, there is almost no indication for the use of casts in the treatment of these fractures. Traction Methods

Some37 have used the traction produced by the hanging arm cast to achieve a reduction or to improve the final fracture position. This method may not be effective if the cast is applied late after the fracture clot has congealed. The hanging arm cast usually requires that the patient sleep in the upright position. Having to sleep in this position can produce considerable discomfort in the early phases of the fracture healing process. Overhead skeletal olecranon traction can be used for patients in whom the usual external immobilization techniques cannot be used. It is a good method of achieving and maintaining a reduction, but it requires extensive hospitalization and has all the problems associated with the management and care of the skeletal pin or screw. The major indication for this method in an athlete would be a severely comminuted fracture or concomitant injuries that require a period of recumbent positioning.

Maintenance Difficult Nonoperatively Often after the reduction is obtained, it can be lost unless something is added surgically to the treatment process to stabilize the fragments (Fig. 17J2-13).

Operative Intervention The High-Performance Athlete It must be remembered, however, that these aforementioned series using nonoperative methods were treating individuals who were engaged mainly in normal activity. What about the high-performance athlete? Is there a greater need to achieve a more anatomic reduction in athletes? This question must be answered when such an athlete sustains this type of fracture.

Percutaneous Stabilization The major indication for operative stabilization is to maintain as near anatomic reduction as possible in an athlete who needs to regain a full range of shoulder motion. A semiclosed method of operative management involves reducing the fracture by closed methods first, and then stabilizing it with pins placed across the fracture site percutaneously under image intensifier guidance. There are two methods of stabilizing the fragment using a percutaneous technique.


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One involves inserting the pins obliquely across the fracture site. The second involves passing the pins proximally up the intramedullary canal. Direct Insertion

Figure 17J2-13 Loss of reduction. A, Injury image of a 12-year-old soccer player who sustained this Neer stage III displaced fracture of his left proximal humerus. B, An anatomic reduction was obtained by inserting a threaded pin into the proximal shaft to facilitate the manipulation. However, nothing was done to stabilize the reduction. C, After reduction, the upper extremity was simply placed aside the chest. As a result, the prereduction position of the fracture fragments recurred. By 2 weeks, some early callus developed along the inferior periosteal sleeve (arrows). D, Fortunately, after 6 months, there had been considerable remodeling of the fracture site.

The stabilizing pins or nails can be inserted directly in an oblique manner across the fracture site. It is best to direct the pins cephalad from the metaphysis into the epiphysis rather than antegrade from the epiphysis in to the metaphysis (Fig. 17J2-14A and B). These percutaneous techniques have the advantage of maintaining fracture alignment, with the arm in the normal position supported only with a splint or collar and cuff. Because of rapid healing, the pins can be removed within 2 to 3 weeks. There are many disadvantages of this technique. The first is that the pins may be difficult to insert because the shoulder must be abducted to maintain the reduction. Because of the oblique angle insertion that must be used, it is often difficult to gain entrance into the lateral cortex of the proximal humeral metaphyseal segment. The tips of the pins often keep slipping off the cortex. The other disadvantage is that the penetration of the pins through the substance of the deltoid muscle often inhibits the initiation of early motion. The antegrade insertion of the pins from the epiphysis to the metaphysis should be avoided because it will eliminate any chance of starting early motion as the pins bind up the rotator cuff (see Fig. 17J2-14C). In inserting the pins in this manner, there can be production of scar tissue in the cuff, which can result in a permanent loss of shoulder motion. The decision about whether to leave the ends of the pins outside the skin is usually left to the treating surgeon. More recently, cannulated screws have become a popular method of stabilizing the fragments (Fig. 17J-15).The use

of these cross screws to stabilize the fragments eliminates some of the disadvantages of using the oblique pins. However, these screws are not appropriate in those immature athletes who have more than 2 years of growth remaining because the threads in the screws apply compressive forces across the fracture site, which can produce a growth arrest. Intramedullary Nails

Retrograde intramedullary flexible nails also can be used in those fractures that require an anatomic reduction be maintained (Fig. 17J-16).56 The nails are inserted distally from the metaphysis in the supracondylar area. The entrance points can be either both through the lateral supracondylar column or one each through the medial and lateral supracondylar columns. Passage of the nails proximally using the medial and lateral approaches is easier but requires care to avoid injuring the ulnar nerve when inserting the nail in the medial column. The advantage of the intramedullary technique is that the deltoid muscle is not violated and bound by the pins when they are passed percutaneously. Thus, circumduction motion can be initiated earlier when the nails are passed intramedullary. The disadvantage of the intramedullary technique is that the prominence of the nail ends at their entrance sites may inhibit motion at the elbow if they are left protruding too much.

Open Reduction On rare occasions, a satisfactory reduction may not be able to be obtained by a simple manipulation. In these situations, the surgeon will need to resort to performing an open reduction.

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C Figure 17J2-14 Percutaneous pins. A, An image of a Neer type IV displaced proximal humeral physeal fracture in the dominant extremity of a 13-year-old high-performance quarterback. B, Anatomic reduction was achieved by closed reduction and was secured by percutaneous pin fixation placed in a retrograde direction.

Rarely Indicated

Primary open operative reduction just to improve the position has almost no role in treatment of this fracture. The major absolute indications are the rare open fractures and fractures with vascular injuries. Other relative indications include comminuted intra-articular Salter-Harris type III and IV injuries and cases in which large amounts of periosteum or the biceps tendon have become interposed in the fracture site (Fig. 17J2-17). In the high-performance athlete, the risks of an open surgical intervention must be weighed against the need to obtain a nearly anatomic reduction. Poor Results

series of 39 patients who were treated nonoperatively. In the 9 patients who were treated operatively, there was a high rate of complications. The deficiency in this review is that they did not evaluate specifically the patients who used their upper extremities for high-performance activities. Also, it can be said that those undergoing surgical intervention had more severe injuries.

Subjective and Objective Findings Unfortunately, closed reduction alone is undependable in ensuring that the reduction obtained will be maintained. There are many other series35,36,44,45,55,57 that reported

In general, the open reduction of these fractures has produced poor results, which often are worse than the results of comparable fractures managed closed.54 Nilsson and Svartholm37 believed that the poor outcomes seen after an open reduction were the result of the surgical intervention and not the fracture. This conclusion was echoed 20 years later by Baxter and Wiley,44 who stated that open reduction improved the displacement in only three of seven patients, inflicting a cosmetically unattractive scar for no obvious advantage.

Weighing the Evidence No Controlled Studies Unfortunately, there are no double-blind controlled or comparative studies to compare the results of operative (which includes closed reduction and percutaneous fixation) with pure nonoperative management. The most recent work to confirm the good results of nonoperative management is the article by Beringer and coworkers.34 They demonstrated excellent results in their

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Figure 17J2-15 Percutaneous screw fixation. A, Injury image of a 15-year-old male basketball player who sustained the Neer stage II fracture of his dominant shoulder. B, Following the reduction, the fracture was stabilized with a cannulated screw placed percutaneously. (Courtesy of Dr. John Edeen, San Antonio, Texas.)


3-4 cm

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Figure 17J2-16 A, Skin incision and entrance sites. The skin is incised for 3 to 4 cm over the lateral aspect of the distal humerus starting about 1 cm proximal to the prominence of the lateral condyle. The two entrance sites (dotted circles) are placed 1 to 2 cm apart on the anterior lateral surface of the lateral supracondylar column. If medial-lateral entrance sites are used, a separate anteromedial incision (bold circle) is also placed over the medial supracondylar column to make the medical entrance site. B, First entrance site. The first site is usually the most proximal site. The awl is started first at 90° until it engages the cortex. It is then angled cranially gradually 45° as it drills through the cortex. C,The first nail is inserted through its entrance site and advanced proximally. The second entrance site is then made distal and anterior with the awl. The handle of the awl is leaned against the first nail to guide it until it has penetrated the cortex. (Note: This is a lateral projection.) D,The second nail is inserted and both nails are advanced proximally to the fracture site. E, Reduction and fixation. The fracture fragments are reduced by abducting and slightly externally rotating the distal fragment. Each nail is then separately advanced into the proximal fragment. F, Final position. Once both nail tips have been secured in the head, the pins are cut distally. Notice the tips have the desired divergence. (From Dietz HG, Schmittenbecher PP, Slongo T, Wilkins KE: AO Manual of Fracture Management, Elastic Stable Intramedullary Nailing (ESIN) in Children. Davos Platz, Switzerland, AO Publishing, 2006, pp 25-30.)

good results with nonoperative management alone. In some of these series, there were reports of both subjective complaints and objective findings of minor decreases in shoulder motion in the older patients. The major question is how these minor deficiencies affect the function of the upper extremity in the high-performance athlete. Are the athletes who are near skeletal maturity (the commonly accepted age for males is 15 years58) able to return to their preinjury level of performance?

Results after Operative Intervention Dobbs and coworkers58 recently studied a group of patients 15 years and older in whom a Neer stage I or II reduction was obtained by open or closed method followed by pin or screw stabilization. In all the patients who were examined 4 years after surgery, there was near-normal glenohumeral motion and excellent strength. The important finding in this series was that all of these patients were able

to regain preinjury functional use of the involved upper extremity.

Specific Poor Nonoperative Results The first citation in the literature that relates to poor results in the high-performance athlete has been described by Dameron and Rockwood.48 This involved a 14-year-old track star who sustained a displaced Salter-Harris II fracture of the proximal humerus while pole vaulting. At the time of healing, there was a small proximal lateral spur on the anterolateral aspect of the metaphysis due to proximal migration of the distal fragment. When the patient had fully recovered, he was able to play football but was unable to participate in throwing sports because of a restriction of about 20 degrees in flexion and abduction. Sherk and Probst55 also reported loss of shoulder motion along with high-performance function in the older athletes who had less than an anatomic reduction.

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Figure 17J2-17 Open reduction. A, Image taken after an attempted closed reduction of an almost skeletally mature male demonstrated a persistent gap between the proximal metaphyseal and epiphyseal fragments. (The anteroposterior and lateral radiographs are seen in Fig. 17J2-10A and B.) The decision was made that the sporting activities of this athlete required as close to an anatomic reduction as possible. B, At open surgery, the periosteum and biceps tendon were found to be interposed between the fragments. Once this tissue was removed, the fragments were reduced anatomically and secured with cannulated screws.

The Author’s Experience

of shoulder motion 18 months after fracture to require an osteotomy to regain her motion to a functional level (Fig. 17J2-19). Thus, there is both direct and indirect evidence to support the concept that with the high-performance throwing athlete nearing maturity, an aggressive surgical approach may be necessary to obtain and maintain an anatomic reduction.

I had experience with a high-performance pitcher who was treated nonoperatively and had a minor residual deformity (Fig. 17J2-18). After the fracture, he had enough residual restriction of motion that he could no longer pitch effectively and had to change to playing the outfield. Another young pubertal girl whose fracture was initially inadequately reduced had sufficient restriction

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Figure 17J2-18 High-performance athlete. Anteroposterior (A) and lateral (B) injury radiographs of a high-performance 14-yearold baseball pitcher who sustained a displaced proximal humeral physeal fracture.


D C Figure 17J2-18, Cont’d Anteroposterior �(C) and lateral (D) radiographs taken 6 months after the fracture show some incongruity of the proximal humerus. Although mild, this injury was severe enough to interfere with his ability to pitch at a high level.

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Figure 17J2-19 Malunion. A, Injury film of an adolescent female basketball player who sustained a significantly displaced proximal humeral physeal injury. The proximal spike of the metaphyseal fragment (dotted line) was very prominent (arrow). B, Eighteen months later, she still could not abduct past 120 degrees, which interfered with her basketball skills. The prominence of the metaphyseal spike remained (arrow). C, A valgus osteotomy was performed, which corrected the varus of the head and allowed her to assume full abduction. (Photo courtesy of Dr. Earl A. Stanley, Jr, University of Texas Health Science Center at San Antonio.)

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Author’s Preferred Method

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Treatment

Minimally Displaced

The Neer I or II fractures can usually be treated with a simple sling and allowing the initiation of early active motion when the pain and swelling have subsided. Because this involves the physis, the healing process is very rapid, and there is the laying down of callus very early. This early callus stabilizes the fracture fragments to allow the initiation of early motion. It must be emphasized that this must be active motion at all times. Passive motion should never be used in the early recovery process. Significantly Displaced

In markedly displaced physeal fractures, sufficient reduction must exist to ensure uninhibited motion of the glenohumeral

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joint. In the athlete close to maturity, this may be as little as a Neer I displacement pattern. This is especially true for those athletes who need full glenohumeral motion for throwing, gymnastics, or swimming activities. In such cases, an anatomic reduction is achieved first by manipulation. In the past, I had used percutaneous pins or screws to stabilize these fractures. In inserting these devices, the deltoid muscle is violated, which can delay the resumption of shoulder motion. Recently, I have found intramedullary flexible nails to be more satisfactory for fixation (Fig. 17J2-20). They allow the patient to start motion almost immediately and do not have risk for infection associated with pins protruding from the skin. In inserting the pins in the distal humerus, I prefer to use the separate medial and lateral entrance sites rather than the two lateral entrance sites. See Figure 17J2-16.

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G Figure 17J2-20 Author’s retrograde nailing. A, The injury image of a mature 14-year-old female swimmer who sustained this Neer grade IV fracture of her left proximal humeral physis. B, The fracture was able to be reduced to a nearly anatomic position by abducting the extremity. C, When the extremity was allowed to return to the side of the body, the original fracture malalignment recurred. Because it was determined that a nearly anatomic alignment of the proximal humerus would need to be achieved for her to regain her ability to perform her swimming activities on a high level, the decision was made to secure the fragments in a nearly anatomic position with retrograde nails. �� The AO technique �� (as demonstrated in Figure 17J2-16) was used; both nails are passed retrograde up to the fracture site. D, With this athlete, the nails were advanced retrograde from separate medial lateral entrance sites. E, Once the nails had been advanced retrograde to the fracture site, the fracture was reduced by abducting the extremity. F and G, After the reduction, the nails were then advanced into the proximal fragment a sufficient distance to provide adequate stabilization. Stabilization is enhanced by providing separation of the tips. Continued



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I have found that external immobilization methods are cumbersome and uncomfortable and are not well accepted by the patient, in addition to being unreliable in maintaining the position of the fragments. Open Reduction

In my experience, I have found few indications for an open reduction. In the very rare open fractures or fractures with vascular compromise, I would not hesitate to perform an open reduction. In an athlete in whom there is interposed tendon or other tissue, one would have to weigh the risks of surgical damage to the shoulder muscles against the ben-

efits of achieving an anatomic reduction. In my limited experience, the most common tissue interposed has been the local periosteum. The diagnosis of interposed tissue is made by having a persistent gap between the fragments when attempting a closed reduction. This interposed tissue can limit shoulder motion by either the persistent incongruity of the proximal humerus or tethering the long head of the biceps. Once the decision has been made to achieve as anatomic a reduction as possible, an open reduction with internal fixation using a deltopectoral approach (see Fig.17J-17A) usually achieves an adequate reduction.

Postfracture Management

Criteria for Return to Athletic Activity

Nonoperative Cases

Patients can return to their athletic activities in a noncompetitive setting as soon as they have regained nearly full range of motion of the shoulder. They should not be allowed to return to their athletic activities in a competitive setting until the upper extremity has regained full strength. A good parameter for determining the return of upper extremity strength is when the athlete can perform 10 to 20 push-ups.

Initial Rest In those cases managed totally nonoperatively, the patient is supported in a sling and allowed to wait until the pain and swelling have subsided enough to start early shoulder motion. Initially the motion is in the form of circumduction exercises. This type of motion can usually be initiated after the first week. Once early callus begins to appear, the athlete can begin to actively abduct the shoulder. This usually consists of the patient starting to walk the fingers up a wall. It must be emphasized that all this activity is in the form of active motion. In these early stages, passive motion should never be employed.

Physical Therapy Once the athlete is able to actively abduct the shoulder to at least 90 degrees, formal physical therapy can be initiated. The emphasis needs to be on strengthening the muscles of the shoulder girdle as well as the other muscles of the upper extremity that have become weakened because of disuse.

Operative Cases In those cases in which there has been operative intervention, postoperative management is essentially the same. The initial rest period may be slightly prolonged in patients who have undergone an open reduction to allow the incision to heal before starting active motion. Usually, there is sufficient healing after a week to allow the amount of motion that the patient will use in the early stages. In patients in whom the fragments were stabilized with pins obliquely passed through the skin and deltoid muscle, the pins may inhibit the initiation of early motion. Usually, there is sufficient callus and internal stability by 3 weeks to remove the pins so that uninhibited motion can begin. This inability to initiate early shoulder motion is one of the major disadvantages of using the pins, which are directly inserted through the skin and muscle.

Complications The complications associated with proximal humeral fractures can be divided into nonskeletal and skeletal complications.

Nonskeletal Nonskeletal complications are rare with injuries in this area. Baxter and Wiley44 described one patient with complete disruption of the brachial artery at the lateral border of the axilla. In some patients, they also found severe tenting of the skin, which required operative intervention to prevent skin necrosis. Dameron and Reibel36 reported one case of brachial plexus paresis in a patient treated in a Statue of Liberty cast. Transient axillary nerve paralysis has also been described.47 Usually, however, these problems resolve by the time the athlete is ready to start the recovery or rehabilitation phase.

Skeletal The major skeletal complications include growth arrest, avascular necrosis, late malunion, and dislocation of the humeral head.

Growth Arrest This complication has been described in only one case in the recent English literature.46 Although there was a varus deformity of the humeral head and neck, the function of the upper extremity was the same as the uninjured extremity.

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Avascular Necrosis Although avascular necrosis of the humeral head is not uncommon in comminuted fractures of the proximal humerus in adults, it is extremely rare in the skeletally immature athlete. An article by Martin and Parsons59 described a case of a 14-year-old who had a Neer II physeal injury. The patient was not symptomatic until 7 months after the fracture. One year later, the lesion had healed with no significant deformity. In the two other cases described in the recent literature, the patients were asymptomatic, and there was no effect on the function of the shoulder.46,60 Lipscomb61 in 1975 described a case of localized avascular necrosis producing a condition similar to osteochondritis dissecans of the knee that developed in an athlete from a chronic stress injury involving the proximal humeral epiphysis. This resulted in a loose body that needed to be removed surgically.

Late Malunion Residual varus angulation and shortening, although they do occur, are rarely a problem among athletic individuals.44 In some adolescents in whom a fracture is not reduced anatomically just before the onset of skeletal maturity, there may be sufficient deformity to produce a disabling loss of motion. In these patients, the surgeon must weigh the benefits of surgical intervention against the risks of the procedure (see Fig. 17J2-19).

Figure 17J2-21 Many proximal humeral metaphyseal fractures present as a simple, nondisplaced incomplete fracture (arrow) with minimal greenstick angulation.

fractures involving the physis and the metaphysis. These differences are discussed in detail in the following section.

Anatomic Characteristics

Dislocation

Area of Remodeling

Almost all the physeal fracture patterns described in the major series of fractures of the proximal humeral physis are Salter-Harris I or II fracture patterns.4,34,36,44,53,55,58 In the recent literature, six cases involving fractures of the proximal humeral physis were associated with a dislocation of the shoulder.46,60,62-65 These cases all had Salter-Harris III or IV fracture patterns. Salter-Harris III and IV fractures are rarely seen in the proximal humerus. The reason given is that the shoulder has such a free range of motion. The Salter-Harris III and IV patterns are more commonly seen in those joints in which the motion is limited to only one plane.46 Often it is difficult to determine the exact position of the epiphyseal fragment on the routine radiographic images. Usually either CT or magnetic resonance imaging (MRI) is needed to determine the exact location of the proximal and distal fragments. With the exception of one case,46 the epiphyseal fragment was situated anterior in the joint. Of the six cases reported, four required an open reduction

When bone is laid down at the physis, it is produced as cancellous or quantity bone. This is why the cross-sectional area of this region is greater. With time, this quantity bone is remodeled into the stronger cortical bone of the diaphysis. Thus, we have in the diaphysis quality bone. Because the bone in the metaphyseal area is undergoing remodeling, its cortex is inherently thinner and also weaker. Thus, it is less resistant to compressive and tension forces. As a result, we see in the pediatric age group failure patterns such as minimally displaced greenstick-type fractures (Fig. 17J2-21).

METAPHYSEAL FRACTURES OF THE PROXIMAL HUMERUS In most of the articles and textbooks dealing with fractures of the proximal humerus, there is little differentiation between those fractures involving the physis and the proximal metaphysis. Unfortunately, the structure, incidence, and treatment principles differ considerably between those

Pathologic Fractures The metaphysis is also the most common location for a unicameral bone cyst. As a result, the incidence of pathologic fracture is frequent in this area (Fig. 17J2-22). In Kohler and Trillaud’s review covering 20 years of proximal humeral fractures,4 one fourth of the metaphyseal fractures occurred through unicameral bone cysts

Muscle Forces Because the location of the fracture line is more distal in the metaphysis, it is at the insertion of the pectoralis major tendon on the proximal humerus. Thus, this tendon is situated on both fragments. There is usually enough of the insertion on the proximal fragment to counteract the rotation of the proximal epiphysis such as is seen with the pure physeal fractures. The major portion of the tendon


is situated on the proximal portion of the distal fragment. If the facture is complete, the force of this tendon on this distal fragment tends to force it anterior and medial. On the anteroposterior projection, the two fracture fragments usually are in a somewhat parallel alignment to lie in bayonet apposition (Fig. 17J2-23).

Extra-articular Fracture The distal location in the metaphysis places the fracture line well outside the joint capsule. As a result, any malunion of the fracture fragments will not impinge on the motion of the joint. Limited abduction of the shoulder is rarely seen following these fractures. This makes the metaphyseal fractures less likely to result in any loss of shoulder function in the high-performance athlete. This fact also has a bearing on the indications for surgical intervention to achieve an anatomic reduction.

Incidence Younger Age Group Proximal metaphyseal fractures are characteristically predominant in children younger than 10 years of age. The mechanism of the fracture probably is the same as that causing proximal humeral physeal fractures. The combination of a weaker metaphysis and a stronger perichondrial physeal ring probably accounts for the occurrence of the fracture in the metaphysis rather than the physis in this younger age group.

Figure 17J2-22 This fracture through a large unicameral bone cyst occurred after minimal trauma. The developmental defect greatly weakens the bone, making it susceptible to pathologic fracture. Coracobrachialis m. Supraspinatus m.

Subscapularis m.

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Deltoid m.

M Pectoralis major m.

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Figure 17J2-23 Metaphyseal muscle forces. A, The pectoralis major is the main deforming force on the distal metaphyseal fragment. The deltoid muscle tends to decrease the rotation on the proximal fragment. B, Image of a complete fracture of the proximal humeral metaphysis in which the proximal and distal fragments are aligned in parallel bayonet apposition.

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Less Concern in the Athlete Because metaphyseal fractures are usually seen in the first decade, they are only rarely a factor of concern in the older high-performance athlete.

Signs and Symptoms As stated previously, the degree of swelling is dictated by the amount of displacement of the fracture fragments. The simple undisplaced metaphyseal fractures may have minimal swelling with no deformity. In those fractures that are completely displaced, there will be considerable swelling and discomfort. Because of the swelling, it may be difficult to palpate the ends of the fracture fragments. In those that are completely displaced and the fragments are in bayonet apposition, it is theoretically possible to palpate the fracture surfaces as being more distal than with the pure physeal fractures. From a practical standpoint, the young athlete is so uncomfortable that he or she will not allow much in the way of palpation at the fracture site. Thus, the differentiation between the two types of fracture patterns is dependent on the radiographic image (see Fig. 17J2-11).

Classification of Metaphyseal Fractures Ogden47 classifies metaphyseal fractures into two types. In the first type, the cortex remains intact. These are usually torus or greenstick fractures (see Fig. 17J2-21). In the second type, there is loss of cortical integrity with either angular or translocation displacement (see Fig. 17J2-23).

Radiographic Studies These fractures are usually straightforward and obvious on routine radiographic projections. The standard lateral projection, which is usually obtained by abducting the shoulder, may be difficult to obtain in the acute situation because of pain and swelling. In this situation, the transthoracic view may be used. The transthoracic projections are sometimes difficult to evaluate. There is almost never an occasion to obtain special studies such as CT for these fractures.

Treatment of Proximal Humeral Metaphyseal Fractures With few exceptions, metaphyseal fractures of the proximal humerus can be managed conservatively. There are very few operative indications.

Nonoperative Management Undisplaced Fractures Simple metaphyseal fractures that are undisplaced or only minimally angulated usually can be treated quite adequately with a collar and cuff. In the acute stage, added comfort may be achieved by binding the arm to the chest with a circular elastic bandage. Most of these fractures are intrinsically stable; thus, shoulder motion can be initiated early. In the pediatric athlete, it is extremely important to regain

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Figure 17J2-24 Bayonet remodeling. A, Injury film of an 8year-old baseball player who sustained a proximal metaphyseal fracture. The bayonet apposition and shortening were accepted. Initially, the boy was treated with a simple collar and cuff, supplemented with an Ace bandage. B, Radiograph obtained 4 months after injury shows remarkable remodeling. The range of motion and strength of the shoulder have since returned to the preinjury level.

shoulder motion as soon as possible to achieve maximal rehabilitation.

Displaced Fractures In the completely displaced metaphyseal fracture, little abduction of the proximal fragment is usually present because some adduction force is maintained by both the pectoralis major and the latissimus dorsi on the proximal metaphysis (see Fig. 17J2-23). As a result, these fractures often develop bayonet apposition. Although shortening occurs because of the longitudinal pull of the triceps, biceps, and deltoid muscles, it is usually not sufficient to cause any functional or cosmetic residua. These fractures usually can be treated quite well using a collar and cuff plus a thoracic elastic bandage. Healing with the bayonet apposition (although it may initially concern the parents) usually results in an acceptable cosmetic and functional result, even in the adolescent patient (Fig. 17J2-24).

Operative Indications Olecranon Traction About the only time treatment with overhead olecranon traction would be warranted would be with the multipleinjury trauma patient who is confined to a recumbent position. This situation would be extremely unlikely to occur with the immature athlete. The only other possible indication would be severe comminution of the metaphyseal fragments. The traction maintains the reduction until there is sufficient callus and intrinsic stability at the fracture site


to allow the traction to be discontinued. Once the traction is removed, the upper extremity can be supported by no more than a collar and cuff.

Percutaneous Stabilization Because the nonoperative methods produce such satisfactory results, about the only indication for pins would be in the athlete who is at or near maturity. As with the physeal fractures, the reduction is usually first obtained by closed methods and then stabilized with pins. These can be placed directly across the fracture fragments or retrograde with intramedullary pins.66 One special indication for surgical stabilization would be a fracture in either the ipsilateral or contralateral upper extremity, in which surgical stabilization would facilitate early mobilization (Fig. 17J2-25).

Open Reduction

A

Other than the rare open fracture, there is probably no indication to perform an open reduction of a proximal humeral metaphyseal fracture. The only possible exception is treatment of an athlete who is approaching skeletal maturity in whom an anatomic reduction is deemed necessary for the athlete to achieve full functional recovery.

B

Weighing the Evidence

Figure 17J2-25 Metaphyseal intramedullary pins. A, Radiograph of an 8-year-old girl who sustained a contralateral displaced lateral condyle in addition to this displaced proximal humeral metaphyseal fracture. B, In an effort to facilitate early recovery of both injuries, the proximal humeral metaphyseal fracture was initially stabilized with retrograde intramedullary pins.


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The absence of articles devoted exclusively to the treatment of metaphyseal fractures of the proximal humerus makes the evaluation of any method of treatment based on the principles of evidence-based medicine impossible. Fortunately, in the citations dealing with the overall fractures of the proximal humerus, metaphyseal fractures heal well with any method of treatment.

Treatment

For undisplaced or minimally displaced fractures of the proximal humeral metaphysis, I use a collar and cuff supplemented with an elastic bandage, and I strap the extremity to the chest wall. Within a few days, the elastic bandage strap is discontinued, and the cuff is gradually lowered until the elbow is at 90 degrees. At this time, circumduction exercises of the shoulder are begun. The remainder of the postoperative course is carried out the same as for the physeal fractures. In those complete metaphyseal fractures that are in bayonet apposition, I usually accept this position and treat them similarly to the minimally or undisplaced fractures. Patients with these fractures may be slower to recover their range of motion. It usually requires a major degree of explaining to convince the parents that these will completely remodel. I usually keep pictures or radiographs of previous cases handy to convince them (Fig. 17J2-26). In patients who are very near skeletal maturity, I usually do a closed reduction and then secure the fragments with percutaneous intramedullary pins (Fig. 17J2-27). I have only one instance in which I treated a proximal humeral metaphyseal fracture with an open reduction. This patient had an associated closed head injury which made the

A

B

Figure 17J2-26 Full bayonet remodeling. A, Image of a young child who had sustained a complete fracture of the proximal humeral metaphysis 6 weeks previously. The bayonet apposition was accepted. B, Two years later, the proximal humerus had completely remodeled. This is a good example of the remodeling capacity of the proximal humerus.

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A

D

of


C

B

Figure 17J2-27 Author’s intramedullary metaphyseal nailing technique. Anteroposterior (A) and lateral (B) injury images taken of a high-performance tennis player who was involved in an automobile accident. Fortunately, this was his only major musculoskeletal injury. Because of his need to have an anatomic reduction to ensure his continued high-performance upper extremity function, it was elected to attain as anatomic a reduction as possible and stabilize it with retrograde intramedullary flexible nails. Anteroposterior (C) and lateral (D) images demonstrating the position of the ends of the nails separated in the humeral head.

usual closed treatment impossible. It was a difficult procedure. Had there not been an associated head injury, I would have treated this patient by the usual closed methods. It was difficult to determine whether the reduction obtained by an open procedure produced any better functional results in the long term over accepting the inevitable malreduction that was developing in this patient. The rehabilitation protocol and criteria for returning to competitive athletic activities are essentially the same as outlined following physeal fractures of the proximal humerus.

The complications associated with fractures of the proximal humeral metaphysis are much less than those associated with the fractures of the proximal humeral physis. There is much less loss of shoulder motion. The problems associated with growth disturbance are essentially nonexistent. The shortening that is seen with the fractures that heal in bayonet apposition is usually not of any functional or cosmetic significance. (Table 17J2-1)

TABLE 17J2-1 Typical Findings: Differences between Proximal Humeral Physeal and Metaphyseal Fractures Age Fracture location Radiographic findings Treatment options

Proximal Humeral Physis

Proximal Humeral Metaphysis

More common after 10 years of age Intra-articular, thus more malunion may alter motion Fragments angulated to each other Metaphyseal fragment usually lies lateral to the epiphyseal fragment May require surgical reduction and stabilization in those patients near skeletal maturity

Usually seen before the age of 10 Extra-articular, thus malunion less likely to affect shoulder motion Fragments lie parallel in bayonet apposition Metaphyseal fragment usually lies medial to the epiphyseal fragment Extremely rare to require any surgical intervention


AVULSION OF THE LESSER TUBERCLE Avulsion of the lesser tubercle by the subscapularis tendon is uncommon in the skeletally immature patient.67-70 Levine and coworkers provide the most extensive analysis of this type of fracture in their case report and review.57

Mechanism The most commonly reported mechanism is one of a forced external rotation against a resisting force. This can occur in wrestling.57

BOX 17J2-3 Typical Findings: Avulsion of the Lesser Tubercle

• This injury is rare in the skeletally immature. • Often the diagnosis in unappreciated on the

initial evaluation. • Radiographic findings may be subtle. • Most require the establishment of an anatomic reduction. • If left unreduced, it may result in significant loss of shoulder motion. • Because there is the need to achieve soft tissue healing, the recovery period may be slower and prolonged.

Diagnosis Late Diagnosis These fractures may be difficult to diagnose acutely. Levine and coworkers,57 in their review of the published reports of this injury, found that 50% of the cases reported in the skeletally immature and adolescents were diagnosed late. These were patients who presented with chronic shoulder pain following an injury.

Clinical Appearance There may be point tenderness over the anterior aspect of the shoulder. The patient’s apprehension is accentuated by abducting the shoulder to 90 degrees and attempting to externally rotate the shoulder. This apprehension can be lessened with shoulder stabilization using downward pressure on the upper arm in the supine position.57

Imaging Studies The findings may be subtle on the routine radiographs. The axillary view provides the best image of the fragment.71 MRI or CT usually is necessary to adequately assess the displacement of the tubercular fragment.57

Treatment Nonoperative Management If the fragment is essentially nondisplaced, it can be obtained with nonoperative management. This requires close follow-up to be sure that the fragment does not displace late.72

Operative Management Because of the fear of subsequent nonunion, malunion, or anterior impingement, it has been recommend by some that these fragments be replaced surgically.57 If untreated, these avulsions by the subscapularis and shoulder capsule can result in loss of shoulder motion. This can be disabling in a high-performance athlete who uses that upper extremity for throwing. Once the exostosis has developed, it may require surgical removal to permit full recovery of the shoulder motion. For this reason, some authors57,67,70 have

recommended primary reattachment of the tubercle in all young athletes if recognized acutely. The tuberosity is reattached using a variety of drill holes, suture anchor fixation, or small fragment screw fixation. Care must be taken in the skeletally immature athlete to avoid procedures that can create a premature growth arrest. In general, the results with acute fixation of the fragment have enabled a full return to athletic function in 3 to 6 months.57,71,73,74

Weighing the Evidence Because of the rarity of this injury, there have been no double-blind comparison studies. In the long-term review of their few cases, Ogawa and Takashi72 reported superior results in those treated operatively.

Postoperative Management The reports in the literature are simple case reports, so there are few guidelines to the postoperative management. Because this involves a soft tissue and bone repair, there is a longer healing time than with just fracture healing. Levine and coworkers57 placed the patient initially in a sling. Active shoulder internal and external rotation was restricted to 45 degrees for the first 6 weeks. The patient’s range of motion and strength were then gradually increased with aggressive physical therapy. By 4 months, when the motion and strength had returned to normal, the athlete was allowed to return to full competitive activity (Box 17J2-3).

STRESS FRACTURES OF THE PROXIMAL HUMERAL PHYSIS One area of skeletal weakness that is susceptible to failure with repeated microtrauma is the proximal humeral physeal plate. The failure usually occurs as a stress fracture of the proximal humeral physis.

Incidence Because rotational forces applied to the shoulder are especially prevalent in the pitching activity associated with baseball, the proximal humeral stress fractures involving

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the physis are most commonly seen in the immature baseball player. This injury has also been seen in gymnasts,75 badminton players,76 and cricketers.77

In baseball, however, elbow problems predominate in immature players. Shoulder pain and chronic problems do not develop until adolescents are in their late teens.78-81 Some authors have speculated that the late incidence of shoulder problems is related to abnormal pitching patterns because of other chronic elbow conditions that have developed during the immature athlete’s earlier years.78,81

behind. Next, the forearm and hand are whipped forward, owing in large part to forces generated by the pectoralis major and latissimus dorsi. The third, or follow-through, phase involves coordination of the forearm muscles to release the ball at the proper time and with the proper spin. The deceleration forces generated in this phase are unique to baseball and tennis. This phase puts stretch on the posterior capsule and external rotators that can be a source of the posterior shoulder pain syndrome. Richardson29 found that during this phase there might also be stress on the rhomboids and levator scapulae insertions, which produces pain along the medial scapular border.

Little Leaguer’s Shoulder

Both Rotational and Compressive Forces

One area of skeletal weakness that is susceptible to failure with repeated microtrauma is the proximal humeral physeal plate. The failure usually occurs as a stress fracture of the proximal humeral physis. Dotter50 first described this entity as little leaguer’s shoulder in 1953. Since then, numerous cases have been described in the literature.60,61,66,82-85 All these cases occurred in high-performance male pitchers who were 11 to 13 years old. In the cases presented, all except one responded to rest for the remainder of the season plus a vigorous preseason conditioning program the following year.86 In only one case was operative intervention necessary. This was an individual described by Lipscomb61 in whom a localized avascular necrosis of the epiphysis developed, producing a loose body that had to be removed surgically.

Tullos and King88 found that the pitching patterns among adolescents and adults were remarkably similar. The forces generated during pitching are very large, especially when rotation is considered. Gainor and coworkers89 pointed out that pitching involves both rotational forces from the internal and external rotators of the shoulder and compressive forces from the flexors and extensors of the elbow. They calculated that internal rotational torque is 14,000 inchpounds just before release of the ball. The kinetic energy produced is 27,000 inch-pounds during the throw. These forces are four times greater than those generated in the lower extremity when an athlete is kicking a ball. In addition, they are greater than the forces required to fracture an isolated cadaver humerus. These are usually repeated rotational forces applied to the physis.

Shoulder Problems among Adolescents

Causative Factors Repetitive Rotational Forces This is usually the result of the repeated rotational forces that develop at the proximal humerus in the immature athlete. The opposing proximal muscular attachments (rotator cuff) and deltoid, pectoralis major, and triceps attachments distally render the extracapsular proximal humeral physis particularly vulnerable to repetitive rotational microtrauma.87

Forces around the Baseball Pitcher’s Shoulder Pitching Phases Tullos and King88 divided pitching activity into three phases (Fig. 17J2-28): cocking, acceleration, and follow-through. First is the cocking phase, in which the shoulder is markedly externally rotated. This tightens the triceps and biceps as well as both the internal and external rotators across the shoulder. This part of the throwing act in the adolescent pitcher results in increased external and decreased internal rotation arcs in the shoulder. Richardson29 pointed out that during this phase, the internal rotators and adductors are at maximal stretch. If the body or shoulder moves forward too soon, the arm has to catch up by putting an excessive load on these structures, thereby creating an inflammatory tendonitis that is the most common cause of anterior shoulder pain among adolescent pitchers. The second, or acceleration, phase consists of two parts. First, the shoulder is brought forward with the forearm

Pitching Techniques In addition to chronic repetitive rotational and compressive forces across the shoulder, there appear to be other factors that may create microtrauma in young, skeletally immature pitchers. Albright and associates78 observed in their extensive study of little league pitchers that the incidence of symptoms reflected the form of pitching rather than the age of the pitcher. Those who had poor pitching skills were more likely to become symptomatic. For this reason, Slager81 advised that the first emphasis of immature pitchers should be on the development of skills and control; as they mature, emphasis can then be placed on increasing the speed of pitching.

Social Factors Social pressures can also be a factor. Torg and associates85 found that in comparable age groups, those who performed in a less competitive environment were less likely to develop symptoms in the throwing arm than those who were subjected to high competitive pressures.

Signs and Symptoms Clinical Presentation and History Patients complain of gradually increasing lateral shoulder pain with aggravation by throwing and later at rest. There is usually no history of trauma or neurologic involvement.


A

C

Cocking phase

B

Acceleration phase 1st stage

D

Follow-through phase

Acceleration phase 2nd stage

Figure 17J2-28 Phases of pitching. A, Cocking phase. B and C, Acceleration phase. D, Follow-through phase. (From Woods GW, Tullos HS, King JW: The throwing arm: Elbow joint injuries. J Sports Med 1[Suppl 4]:45, 1973.)

Physical Examination and Testing Physical examination shows localized lateral tenderness to palpation over the proximal humerus with painful external rotation. Loss of range of motion and swelling are uncommon findings.

Imaging The common radiographic finding is a widening of the proximal humeral physeal plate (Fig. 17J2-29). Associated findings in about half of patients may include demineralization, sclerosis, cystic changes, and lateral fragmentation of the proximal humeral metaphysis.90 MRI and bone scan studies do not add information but may be more sensitive in the early stage of physeal injury when plain radiographs remain normal. Oblique coronal T1-weighted images reveal widening of the proximal lateral humeral physis and

increased signal intensity indicative of periosteal and bone marrow edema on T2-weighted images. Follow-up MRI or bone scan studies in an uncomplicated course are not indicated.

Treatment These fractures usually respond well to rest for the remainder of the season. There must also be a vigorous muscle conditioning program. The pitching technique may need to be critically evaluated and any errors corrected.

Complications If the player continues to participate by ignoring the pain, a slippage of the proximal physis can occur75 (Box 17J2-4).

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A

B

Figure 17J2-29 Baseball shoulder. A, This 13-year-old high-performance little league pitcher experienced pain while throwing toward the end of the season. This radiograph demonstrates widening of the physis (arrows), which is indicative of a stress fracture through the physis, or baseball shoulder. B, Radiograph of normal left side for comparison.

BOX 17J2-4 Typical Findings: Stress Fractures of the Proximal Humeral Physis

• Commonly referred to as “baseball shoulder” • Due to repetitive rotational forces applied

to the roximal humeral physis p • Manifest by local tenderness with pain accented by rotation of the shoulder • Radiographically demonstrated as widening and fragmentation of the physis • Treated by prolonged rest and correction of pitching techniques • If not treated early, the proximal humeral physis can slip, producing joint incongruity.

C l Most

r i t i c a l

P

o i n t s

injuries from sporting events in the pediatric age group occur in males in nonorganized sporting events. l The weakest periosteum of the proximal humerus is over the anterolateral aspect of the metaphysis. This is where the initial failure occurs with fractures involving the proximal humeral physis. l Most fractures of the proximal humeral physis are SalterHarris I or II failure patterns. l Fractures of the proximal humeral physis occur more commonly in the first decade of life. Fractures involving the proximal humeral metaphysis occur more commonly in the second decade of life. l Fractures involving the proximal humeral physis can usually be managed conservatively up until about 3 years before skeletal maturity. Once the athlete approaches skeletal maturity, efforts should be directed toward obtaining and maintaining as near anatomic reduction as possible. Failure to accomplish this in the high-performance athlete can result in loss of function of the upper extremity. l Because fractures of the proximal humeral metaphysis are extra-articular and occur in the younger age group, they rarely require operative intervention.

l The proximal humeral metaphysis often contains pathologic bone such as unicameral bone cysts. This predisposes this area to fractures occurring with minimal trauma. l Avulsions of the lesser tubercle of the proximal humerus often present late as the initial radiographic findings may be subtle and overlooked. l Most avulsion fractures of the lesser tubercle require an open reduction to obtain an anatomic alignment. l The management of stress fractures (little leaguer’s shoulder) of the proximal humeral physis requires a prolonged period of rest as well as an examination of the pitching techniques of the pediatric athlete.

S U G G E S T E D

R E A D I N G S

Adams JE: Little league shoulder: Osteochondrosis of the proximal humeral epiphysis in boy baseball pitchers. Calif Med 105:22-25, 1966. Beringer DC, Weiner DS, Noble JS, Bell RH: Severely displaced proximal humeral epiphyseal fractures: A follow-up study. J Pediatr Orthop 18:31-37, 1998. Dobbs MB, Luhmann SL, Gordon J, et al: Severely displaced proximal humeral epiphyseal fractures. J Pediatr Orthop 29:208-215, 2003. Levine B, Pereira D, Rosen J: Avulsion fractures of the lesser tuberosity of the humerus in adolescents: Review of the literature and case report. J Orthop Trauma 19:349-352, 2005. Neer CS, Horowitz BS: Fractures of the proximal humeral epiphyseal plate. Clin Orthop 41:24-31, 1965. Sanders JO, Cermack MB: Fractures of the proximal humerus. In Rockwood CA, Matsen FA, Wirth MA, Lippitt SB (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 2004, pp 1307-1325. Sarwark JF, King EC, Luhmann SJ: Fractures of the proximal humerus. In Beaty JH, Kasser JR (eds): Rockwood and Wilkins’ Fractures in Children, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 104-715. Webb LX, Mooney JF: Proximal humeral fractures. In Green NE, Swintowski MF (eds): Skeletal Trauma in Children, 3rd ed. Philadelphia, WB Saunders, 2003, pp 334-337.


�rthopaedic �� S �ports �� Medicine �� 1094 DeLee & Drez’s� O

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Adhesive Capsulitis Gary M. Gartsman and Matthew D. Williams

The stiff shoulder presents a persistent diagnostic and therapeutic challenge. “Peri-arthritis scapulo-humerale” was the first description of the stiff shoulder by Dulay1 in 1872, and manipulation under anesthesia was reported as the treatment of choice. Frozen shoulder, a term coined by Codman,2 provided a clear description of the presentation and examination of patients with stiff shoulder regardless of etiology. In a natural history study, Reeves reported on three phases of the frozen shoulder that persists over a course of 1 to 3 years: freezing, frozen, and thawing.3 Thickened capsular tissues led Nevaiser to describe adhesive capsulitis as a term indicative of pathologic alterations in the capsule of stiff shoulders.4 There are four basic conditions that produce shoulder stiffness: idiopathic adhesive capsulitis,3,5 endocrine disorders,6,7 post-traumatic stiffness,8 and postoperative stiffness (Box 17K-1).9 Idiopathic adhesive capsulitis is a painful and disabling condition believed to be self-limited that resolves after 1 to 2 years.5 The primary cause of this condition is unknown and remains controversial. Restriction on active and passive motion is due to capsular thickening and contracture.4 Although patients do improve over time, comparison to the uninvolved contralateral shoulder demonstrates residual limitation of movement and function.10 In addition, many patients suffering from pain and disabling loss of motion are not willing to undergo a protracted conservative course and request early operative intervention. Although patients with diabetes are at increased risk for development of shoulder stiffness, the pathophysiology of the contracture and its relation to diabetes is not understood.11 The stiffness in diabetic patients is reported to be more painful and more recalcitrant to conservative therapy than idiopathic capsulitis in the nondiabetic population.6,7 Effective treatment resulting in improvements in motion

Box 17k-1 conditions causing a stiff shoulder Idiopathic adhesive capsulitis Diabetes Thyroid disorder Degenerative arthritis Post-traumatic stiffness Rotator cuff tear Labral tear Fracture malunion Postoperative stiffness

and pain is attainable in diabetic adhesive capsulitis with arthroscopic release.6,12 The degree of pain and impairment in post-traumatic stiffness is related to the severity of the trauma. Postoperative stiffness may result from scarring in the area of surgical treatment (subacromial adhesions after rotator cuff repair, anterior glenohumeral capsular contracture after a Bankart procedure),9 and profound glenohumeral joint contractures can occur after surgical treatment that does not violate the capsule.12,13

RELEVANT ANATOMY AND BIOMECHANICS Glenohumeral joint stability is preserved through concavity-compression by balanced muscular forces of the rotator cuff.14 Passive restraints such as capsular tissues and the glenohumeral ligaments serve as checkreins that become taught at extremes of motion to resist abnormal glenohumeral rotation and translation and maintain a congruent joint.14,15 The stiff shoulder may be characterized by the direction of motion loss. For instance, global loss of mobility in idiopathic adhesive capsulitis is characterized by circumferentially rigid capsular tissues and glenohumeral ligaments. Throwing athletes with restricted internal rotation have contractures isolated to the posterior capsule. Loss of external rotation with the arm adducted points to rotator interval stiffening.16,17 Decreased external rotation in abduction exposes the anteroinferior structures as the cause for restricted movement.18 Understanding the function of soft tissue restraints of the glenohumeral joint under normal conditions aids in understanding patterns of motion restriction in stiff shoulders with capsular contracture. Releasing a tight capsule eliminates the impediment to shoulder motion and allows the primary stabilizing mechanisms, the rotator cuff, to keep the joint congruent. Capsular release results in increased translation of the humeral head in all planes of motion, but not an increased incidence of dislocation.19 The captured shoulder is characterized by extraarticular adhesions secondary to prior surgery.20 Severe subacromial bursal and subdeltoid adhesions clinically simulate the global loss of shoulder mobility found in the contracted capsule of idiopathic capsulitis patients. However, arthroscopic examination proves the intra-articular capsule benign and compliant. Circumferential inspection of the bursal surface is possible arthroscopically and allows thorough adhesion release.

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EVALUATION History and Clinical Presentation The classic presentation of patients with adhesive capsulitis, regardless of the underlying cause, is that of painful and restricted shoulder motion.13,21 Pain is constant and often unremitting, interfering with sleep and activities of daily living. Overhead activities and reaching behind the back is painful or impossible secondary to contracture. Rapid shoulder movement causes severe pain. Patients report decreased motion, both active and passive, that is often less than half the mobility of the opposite side (Box 17K-2 ).

Physical Examination Measurements of shoulder mobility using reproducible tests should be recorded for both active and passive motion. Active and passive motion recordings that are discordant point toward a diagnosis other than adhesive capsulitis. Evaluation of motion should always be compared with assessments made of the uninvolved extremity. Motion planes recorded are elevation, abduction, and external rotation with the arm in adduction and 90 degrees or maximal abduction. The highest vertebral level the patient can reach behind their back with the thumb extended measures internal rotation. The examiner must remember that scapulothoracic motion may increase the effective range of motion and should be held in check. Stabilizing the scapula with a hand on the inferior border will protect against scapulothoracic motion and provide more accurate measurement of glenohumeral motion. In addition to motion, a complete neurovascular examination, including muscle strength about the shoulder, should be included in the physical examination (see Box 17K-2).

Imaging Radiographs including anteroposterior, axillary, and supraspinatus outlet views should be obtained and are often normal. Plain films document any glenohumeral abnormality, including arthritis; post-traumatic, postsurgical changes; or disuse

Box 17k-2 history and presentation History No memorable inciting event Minimal traumatic event Recent surgery Concomitant medical issues Diabetes Thyroid dysfunction Presentation Pain and limited motion Night pain Pain with activities of daily living (particularly overhead or reaching behind the back) Severe pain with rapid shoulder movement

osteopenia.21 Arthrography is described as an adjunctive test for adhesive capsulitis (a contracted glenohumeral joint has a limited joint volume),22,23 but has no relationship to loss of motion.22 Magnetic resonance imaging allows the evaluation of associated pathology, including rotator cuff and labral tears. Additionally, reports in radiology literature correlate the thickness of rotator interval and inferior capsular tissues (3 to 4 mm) with the diagnosis of adhesive capsulitis.24,25

TREATMENT OPTIONS The treatment options for adhesive capsulitis range from nonoperative physical therapy to operative intervention, including manipulation under anesthesia and either arthroscopic or open capsular release. The efficacy of nonoperative treatment depends on the cause of the stiffness; post-traumatic and postsurgical stiffness seem to respond poorly to physical therapy.8,21 Regardless of the cause, a trial of conservative therapy is warranted for a period (we use 6 months as a baseline) before operative intervention (Box 17K-3).

Nonoperative Modalities In a prospective functional outcome study of conservative treatment of idiopathic adhesive capsulitis, Griggs and colleagues5 reported on 71 patients over a mean follow-up of 22 months. Passive exercises, including pendulums, forward elevation, external rotation, horizontal adduction, and internal rotation, were completed 5 times per day (91% participated in organized physical therapy). Pain scores at rest and with activity were significantly improved, as were the increases in range of motion attained. Ninety percent were satisfied with their outcome despite residual differences in motion between the affected and unaffected shoulders. Five patients were unhappy with the nonoperative results and underwent operative intervention. Other reports support the conclusion that nonoperative therapy is effective at reducing pain and increasing motion in patients with idiopathic adhesive capsulitis.10

Closed Manipulation Closed manipulation under anesthesia is generally regarded as the second-line treatment of the stiff shoulder after failure of nonoperative therapy. Nevaiser and Nevaiser22 and Harryman8 have described methods of closed manipulation. Manipulation is reported as effective in recovering motion in patients with adhesive capsulitis.26,27 The procedure is not without risk, with possible complications including humeral

Box 17k-3 treatment options Nonoperative Physical therapy Nonsteroidal anti-inflammatory drugs Corticosteroid injection (intra-articular) Operative Manipulation under anesthesia Arthroscopic capsular release Open capsular release


fracture, dislocation, and soft tissue injury such as rotator cuff and labral tears and possible neurovascular injury. Manipulation alone without direct arthroscopic visualization does not allow for documentation of concomitant lesions or visualization of the effectiveness of the manipulation.

Arthroscopic Release Arthroscopic treatment of adhesive capsulitis is advantageous in that it enables visualization and release of both intra-articular and extra-articular adhesions without the need for open surgery that requires dividing the subscapularis tendon. Active range of motion can be initiated immediately after surgery, reducing the incidence of new scar tissue formation.28 Arthroscopic capsular release safely and reliably improves shoulder mobility in adhesive capsulitis.6,12,13,27,29-33 Postoperative time to full motion and activity is 3 to 6 months,30 and in contrast to those treated with nonoperative modalities, most patients regain motion similar to the contralateral extremity.6,8,13 In a direct comparison of manipulation and arthroscopic release, OgilvieHarris and colleagues27 reported similar gains in range of motion between the two groups but significantly improved pain relief and ultimate restoration of function in the arthroscopically treated group.

Open Release Advances in arthroscopic techniques have decreased the indications for open capsular release. Familiarity with intraarticular and extra-articular arthroscopic shoulder anatomy allows the surgeon the freedom to address all the components of the stiff shoulder without open surgery. However, knowledge of open capsular release techniques should also be familiar. Open capsular release is indicated when anatomy is distorted precluding safe arthroscopic release, when arthroscopic treatment fails, or in patients with postoperative or post-traumatic stiffness associated with malunited fractures or hardware requiring removal. The surgeon should be prepared to abort an arthroscopic release and proceed with open surgery in the event of a complication, inability to adequately discern tissue planes, or difficulty identifying landmarks for release. Several reports in the literature discuss the success of open release for capsular contractures.34-36 Key points in

open release for stiff shoulders include lysis of deltoid adhesions, rotator interval release,17,37 adequate subscapularis release or lengthening of the subscapularis if necessary, and inferior capsular release.

Weighing the Evidence Literature discussing the treatment of adhesive capsulitis supports the efficacy of all modalities: nonoperative, manipulation under anesthesia, and arthroscopic and open capsular releases. Treatment recommendations have evolved over time with improvements in surgical techniques and outcomes. Conservative therapy for adhesive capsulitis is effective owing to the self-limited nature of the condition; stiff shoulders will regain motion over time.5,10 However, the prolonged course of adhesive capsulitis pushes the patient and physician toward more aggressive treatment. Manipulation under anesthesia effectively loosens the stiff shoulder and helps regain motion without surgery.26,27 However, manipulation does not allow visualization of the joint, resulting in the possibility of incomplete release. Surgical intervention with open capsular release provides improved mobility after surgery, but at the expense of subscapularis transection and its associated risks.34-36 Arthroscopic capsular resection and adhesion release provide visualization of intra-articular and extra-articular pathology and allow the surgeon to address both. Patients proceed with active motion immediately after arthroscopic release and may regain nearly complete return of function.6,12,13,27,29,30-33 There are few direct comparison studies of treatment options in the literature, making it impossible to define the most efficacious modality. Therefore, nonoperative methods should be exhausted before operative intervention, and the surgeon should choose the most appropriate operative procedure, either open or arthroscopic, consistent with his or her comfort and skill level.

POSTOPERATIVE PRESCRIPTION Steroids Regardless of the cause of the stiffness, all patients are started on a methylprednisolone dose pack the day of surgery. Cortisone is not injected into the joint after capsular

Author’s Preferred Method Indications and Contraindications

Surgical intervention is discussed with the patient if after 6 months of appropriate nonoperative treatment there remains persistent pain and restricted motion. Severe stiffness is defined as 0 degrees of external rotation and less than 30 degrees of abduction, whereas moderate stiffness is a decrease of 30 degrees in either plane as compared with the opposite shoulder. Restriction of internal rotation is not considered an indication for arthroscopic release despite the fact that it may be significant to the patient. The throwing athlete poses an exception to this rule in that posterior capsular contracture and restricted internal rotation may be

an isolated problem readily addressed arthroscopically. If after 6 months of therapy, the patient reports decreased pain but continued stiffness, nonoperative treatment is prolonged for at least 2 more months. Our rationale is that the decrease in pain may herald the “thawing” phase and spontaneous resolution without surgery. Operative release is indicated if the contracture has not improved by 2 additional months. We proceed more aggressively with surgery if motion has not improved or worsens by 4 to 6 months after the initiation of therapy. In our practice, there are few contraindications to arthroscopic release: intervention during the inflammatory

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A u t h o r ’ s P r e f e r r e d M e t h o d — c ont ’ d or freezing phase of adhesive capsulitis, and significant fracture malunion requiring osteotomy or hardware requiring removal. Any surgery during the inflammatory phase could increase capsular irritation and accelerate or worsen contractures and should be avoided during this time. Treatment of traumatic stiffness from mildly malunited greater tuberosity fractures or proximal humerus fractures may be attempted arthroscopically. Previous open procedures or trauma often cause scar formation extra-articularly, anterior to the subscapularis. Although we routinely address these contractures with the arthroscope, release in these situations is difficult and requires in-depth knowledge of arthroscopic anatomy and skill (Box 17K-4).

in abduction and adduction are applied to the shoulder only if it responds to elevation and abduction. If external rotation improves, proceed with internal rotation in maximal abduction, followed by cross-body adduction, then behindthe-back internal rotation. Ensuring that the contractures respond to abduction and elevation before proceeding with rotational torque will decrease the incidence of humeral fracture. Regardless of the amount of mobility achieved with manipulation, we proceed with arthroscopy. If full motion was obtained, the capsular release can be documented for completeness or surgically released if found to be insufficient. Manipulation techniques are effective for extracapsular contractures but often leave capsular contractures intact that must be addressed for optimal results.28,38

Technique for Arthroscopic Release

Examination proceeds under anesthesia. Range of motion of both shoulders is examined and recorded in elevation, abduction, and external rotation with the arm adducted at the side. Internal and external rotation are also recorded with the arm in maximal abduction. Before soft tissue release, hydrocortisone is administered intravenously. A trial of gentle closed manipulation is performed on all patients before proceeding with arthroscopic release. Gentle is a relative term but in this case applies to a small amount of force used to move the shoulder in abduction and elevation. Contracted shoulders amenable to closed manipulation will move with minimally applied force. External rotation forces

Box 17k-4 indications and contraindications Surgical Indications Failure of nonoperative treatment Persistent pain and stiffness after 6 months of care No improvement or worsening of external rotation after 4 to 6 months Quantitative Evaluation of Stiffness Severe stiffness 0 degrees of external rotation ≤30 degrees of abduction Moderate stiffness Loss of motion of 30 degrees in external rotation or abduction versus contralateral side Arthroscopic Contraindications Hardware requiring removal Significant fracture malunion requiring osteotomy Factors increasing difficulty of arthroscopic release Prior instability procedure requiring subscapularis takedown* Post-traumatic stiffness* Fracture malunion coupled with stiffness* Surgical Contraindications Release during the freezing phase of idiopathic adhesive capsulitis *These conditions may require open release.

Arthroscopic Technique—Joint Entry

Entering the stiff shoulder is difficult secondary to the reduced joint volume and thick capsule. Articular cartilage damage may be caused by forcefully pushing a trocar into the glenohumeral joint. Generally, a standard metal cannula and blunt trocar are effective owing to their stiffness and the surgeon’s ability to palpate the posterior bony structures. The entry point for the trocar is located superiorly because the glenohumeral joint is widest at this point and the potential for articular damage is reduced (Fig. 17K-1). The skin incision should be located at the posterior joint line to allow adequate maneuverability inside the joint. The trocar is inserted until bone is palpated. Internal and external rotation of the arm allows the surgeon to feel whether the trocar is positioned over the humeral head (will feel the rotation) or the posterior glenoid. The objective is to palpate the superior glenoid rim and advance the trocar at that point (Fig. 17K-2).

Superior

Superior entry

Inferior entry

Inferior

Figure 17K-1 Location of joint entry. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 146.) Continued


A u t h o r ’ s P r e f e r r e d M e t h o d — c ont ’ d

A

Figure 17K-3 Contracted rotator interval. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 146.)

B Figure 17K-2 Palpate bone to determine the entry point. A, Glenoid palpation—trocar is too medial. B, Palpate the humeral head—trocar is too lateral; aim medially and enter the joint. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 146.)

will often be found contracted (Fig. 17K-3). The soft tissues within these borders are excised using a motorized soft tissue resector. We use the Dyonics Electroblade (Smith & Nephew Endoscopy, Andover, Mass) that is a combination motorized soft tissue resector and electrocautery. The anterior cannula pierces the rotator interval. The resector is passed into the joint through the cannula, which is then pulled back out of the joint leaving the tissues accessible to the shaver. After tissue excision, the cannula is advanced back into the joint to maintain joint access, and the resector is removed. The arthroscope is removed from the posterior cannula at this point, leaving it within the joint. Gentle closed manipulation is completed as previously described. Should full motion be attained, we inspect the capsule with the arthroscope to ensure complete capsular release and humeral head location. We proceed to the next step and release the anterior capsule if full range of motion is not obtained with manipulation.28,38 Anterior Capsular Release

Inside the joint, attention is directed to viewing the rotator interval. A spinal needle is used to localize anterior portal placement superior to the subscapularis tendon. A 5-mm cannula and trocar are inserted after skin incision. After successful placement of the arthroscope and anterior cannula, we begin our capsular releases, proceeding from the rotator interval to the anterior capsule and finally to the inferior and posterior capsular tissues. The subacromial space is inspected for extra-articular adhesions following intra-articular releases. Rotator Interval Release

The boundaries of the rotator interval are the biceps tendon medially, the superior border of the subscapularis tendon inferiorly, and the humeral head laterally. The rotator interval

The key landmark for beginning the anterior release is the point at which the middle glenohumeral ligament crosses the subscapularis tendon (Fig. 17K-4). The plane between these two structures should be exploited using a resector or a blunt dissector. Initially the shaver is used to transect the middle glenohumeral ligament until the rolled edge of the subscapularis is clearly visualized. At this point, the blunt dissector is used to complete the tissue separation. Using a Harryman soft tissue punch (Smith & Nephew Endoscopy, Andover, Mass), a 5- to 10-mm strip of anterior capsule is removed. The resection includes the middle glenohumeral ligament and superior portion of the anteroinferior glenohumeral ligament (Figs. 17K-5 to 17K-11). The humeral head may be translated laterally after this release to improve visualization and access to the inferior capsule.

Shoulder 1099


Figure 17K-4 Contracture of the anterior capsule. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 147.)

Inferior Capsular Release

A lateral translation force to the proximal humerus is applied by an assistant who allows the arthroscope to enter anteriorly and inferiorly and improves visualization of the anteroinferior glenohumeral ligament and inferior capsule. Using the soft tissue punch, the bottom blunt jaw is used to transect the anteroinferior glenohumeral ligament and inferior capsule from anterior to posterior (Figs. 17K-12 and 17K-13). The transection should be competed as far from the glenoid rim as possible. Severe contracture of the axillary pouch will limit ability to reach the inferior capsule. Attention must be turned to the release of the posterior and posteroinferior capsule first to gain adequate access to the inferior axillary pouch.

Figure 17K-5 Identify the superior margin of the middle glenohumeral ligament. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 147.)

Figure 17K-6 Divide the superior portion of the middle glenohumeral ligament. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 147.)

Under arthroscopic visualization, the anterior cannula is removed, and a metal cannula and trocar are inserted in its place. The arthroscope is then moved from the posterior cannula to the anterior cannula. The posterior metal cannula is exchanged for a small plastic cannula under visualization. Using the motorized tissue resector, 5 to 10 mm of posterior capsule is excised (Fig. 17K-14). The small cannula is removed, and a cannula large enough to accommodate the soft tissue punch is then placed through the posterior incision (Figs. 17K-15 and 17K-16). The posteroinferior capsule is resected using the punch for a distance of about 10 mm. Similar to the anterior release, we keep the punch 5 to 10 mm lateral to the glenoid rim to avoid injury to the labrum. A third trial of manipulation

Figure 17K-7 Cauterize or resect the middle glenohumeral ligament covering the subscapularis tendon. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 147.) Continued



Figure 17K-8 Cautery to the middle glenohumeral ligament covering the subscapularis. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 148.)

Figure 17K-10 Blunt dissection anterior to the subscapularis tendon. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 148.)

is often successful in releasing the remaining capsule in the axillary pouch. The inferior capsule is inspected from the posterior portal; if it is still intact after manipulation, it is transected with the punch through the anterior portal (Figs. 17K-17 to 17K-19). The blunt tissue dissector may be used to release adhesions anterior to the subscapularis tendon.

lateral subacromial portal, providing visualization anteromedially and anteroinferiorly. An anterior subacromial portal can be made, or a small cannula is directed into the subacromial space through the anterior incision. The shaver can be directed anteromedially and anteroinferiorly from here to release adhesions anterior to the subscapularis tendon. Far medial or inferior adhesions can be reached more easily with the shaver through an accessory portal located just distal to the anterolateral corner of the acromion. Acromioplasty should not be performed as an adjunctive procedure after capsular release because of increased risk for forming recurrent subacromial adhesions.

Subacromial Inspection and Bursectomy

The subacromial space is inspected, and the motorized tissue resector is used to excise the bursal tissue and any extra-articular adhesions (Figs. 17K-20 and 17K-21). Extra-articular adhesions between the subscapularis and the conjoined tendon are evaluated with the arthroscope in the

Figure 17K-9 Cautery to middle glenohumeral ligament covering the subscapularis. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 148.)

Figure 17K-11 Blunt dissection posterior to subscapularis tendon. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 148.)


Figure 17K-12 Contracture of the inferior capsule. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 148.)

Figure 17K-15 Insert a large cannula posteriorly. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 149.)

Figure 17K-13 Soft tissue punch release of anteroinferior capsule. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 149.)

Figure 17K-16 View of completed posterior capsular resection. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 149.)

Figure 17K-14 Shaver resection of the posterior capsule. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 149.)

Figure 17K-17 Return arthroscope to the posterior portal and complete inferior capsular resection. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 150.) Continued



Figure 17K-20 Resection of subacromial adhesions. Figure 17K-18 Punch resection of inferior capsule. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 150.)

Figure 17K-21 Complete subacromial adhesion release. Figure 17K-19 Complete inferior capsular resection. (From Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003, p 150.)

release because it will extravasate through the incompetent capsule and lose effectiveness. A subacromial injection of 1 mg of hydrocortisone is used after release of posttraumatic and postsurgical stiffness. Diabetes is a contraindication to steroid treatment (Box 17K-5).

Physical Therapy after Arthroscopic Release Following arthroscopic release, a pillow is used to keep the arm in slight abduction and to avoid internal rotation. During the initial postoperative examination in the hospital, the patient’s arm should be taken through a range of motion (not painful secondary to the interscalene block). The rationale for this important step is to demonstrate to

the patient that motion has been improved and to impress upon the patient that success will depend on compliance with postoperative therapy protocols. Continuous passive motion (CPM) is started the day of surgery and continued for 2 weeks at home. The CPM chair is used for 1-hour sessions 4 times each day. At 2 weeks’ follow-up in the clinic, the CPM is discontinued if shoulder range of motion is improving. Specific range of motion exercises prescribed are passive elevation and external rotation in a supine position using a dowel or pulley. Full range of motion and use of the shoulder is encouraged. Additional follow-up visits are at 6 weeks, 3 months, and 6 months. Patients are allowed immediate full use of the shoulder for all activities as pain allows (see Box 17K-5).

Shoulder 1103

Box 17k-5 Postoperative prescription Medications Hydrocortisone given intravenously during surgery Methylprednisolone dose pack, after surgery No steroids in diabetic patients Continuous Passive Motion Chair Begin the day of surgery Continue for 2 weeks: 1-hour session, four sessions per day Two-week follow-up: stop if motion is satisfactory Directed Home Exercises Supine passive elevation and external rotation Full active use of the extremity as tolerated

s tatistically significant improvements in pain, external rotation, abduction, and function in a group of diabetic patients with adhesive capsulitis released arthroscopically. Diabetic patients generally achieve slightly less improvement than those without diabetes and have a higher incidence of recurrence. A review of the complications of arthroscopic and open release is given in Box 17K-6. Open release of the stiff shoulder is also a successful operation for patients recalcitrant to conservative management.34-36,39 Lusardi and associates34 and MacDonald and colleagues36 reported increases in motion and decreased pain in patients treated with open capsular release secondary to postoperative capsular contracture. Ozaki and colleagues17 and Omari and Bunker39 documented nearly complete return of normal motion and improved pain scores following open release of adhesive capsulitis.

Repeat Contracture Release Repeat contracture release is scheduled if full range of motion is not obtained by 3 months after the initial procedure. Manipulation under anesthesia is generally effective for achieving full range of motion in these repeat situations.

RESULTS The results of arthroscopic release for adhesive capsulitis is well documented. Harryman and colleagues30 reported on 30 patients whose affected shoulder motion improved from 41% of the unaffected shoulder to 93%. They also reported pain relief and significant functional improvements. Warner and colleagues13 documented average Constant score improvement of 48 points and motion improvements of 49 degrees flexion, 45 degrees external rotation, and eight spinous processes of internal rotation. Final motion regained was within a mean of 7 degrees of the unaffected shoulder. Ogilvie-Harris and Myerhall6 reported

Box 17K-6 Complications Manipulation Humerus fracture Glenohumeral dislocation Neurovascular injury Arthroscopic Release Axillary nerve injury Subscapularis tendon transection Labral injury Inadequate release Recurrence Open Release Neurovascular injury Subscapularis dehiscence Inadequate release Infection Recurrence

C

r i t i c a l

P

o i n t s

l Complete

a thorough history and physical examination with reproducible measurements of active and passive motion. l Take plain radiographs to document bony pathology. l Proceed with conservative therapy for 6 months. l Do not operate during the freezing stage of disease. l Follow a routine procedure for releases: rotator interval, anterior capsule, anteroinferior capsule, posterior capsule, and then inferior release. l Treat with preoperative methylprednisolone and postoperative oral methylprednisolone (Medrol) dose pack (except in diabetic patients). l Examine the subacromial bursa and release all extracapsular adhesions. l Encourage active and active-assisted range of motion immediately after surgery.

S U G G E S T E D

R E A D I N G S

Farrell CM, Sperling JW, Cofield RH: Manipulation for frozen shoulder: Longterm results. J Shoulder Elbow Surg 14:480-484, 2005. Griggs SM, Ahn A, Green A: Idiopathic adhesive capsulitis: A prospective functional outcome study of nonoperative treatment. J Bone Joint Surg Am 82:1398-1407, 2000. Harryman DT II: Shoulders: frozen and stiff. Instr Course Lect 42:247-257, 1993. Harryman DT, Matsen FA, Sidles JA: Arthroscopic management of refractory shoulder stiffness. Arthroscopy 13:133-147, 1997. Neviaser RJ, Neviaser TJ: The frozen shoulder: Diagnosis and management. Clin Orthop 223:59-64, 1987. Ogilvie-Harris DJ, Myerhall S: The diabetic frozen shoulder: Arthroscopic release. Arthroscopy 13:1-8, 1997. Shaffer B, Tibone JE, Kerlan RK: Frozen shoulder: A long-term follow-up. J Bone Joint Surg Am 74:738-746, 1992. Warner JJP: Frozen shoulder: Diagnosis and management. J Am Acad Orthop Surg 5:130-140, 1997. Warner JJP, Answorth A, Marks PH, et al: Arthroscopic release for chronic refractory adhesive capsulitis of the shoulder. J Bone Joint Surg Am 78:1808-1816, 1996.



S e c t i o n

L

Glenohumeral Arthritis in the Athlete Matthew D. Williams and T. Bradley Edwards

Glenohumeral joint degeneration is a disabling condition. Pain and loss of shoulder mobility reduce a patient’s functional capacity, even to the point of affecting basic activities of daily living. These disabilities are especially difficult hurdles for patients desiring active lifestyles. Primary arthritis of the shoulder is atypical, but especially rare in young people. Usually, glenohumeral degeneration in these patients is due to an underlying diagnosis or secondary cause. Treatment is challenging because it not only must reduce pain and improve function in the short term but also must be durable for the life of the patient. Modalities range from conservative care aimed at pain modulation to surgical intervention with joint-sparing orreplacing techniques. Proper treatment selection and outcomes depend on understanding the etiology of the joint degeneration, the age of the patient and the patient’s functional demands, and the efficacy and durability of treatment options. The ultimate goal in treating glenohumeral arthritis in the active population is pain relief and restoration of optimal function.

CLASSIFICATION Glenohumeral arthritis has multiple etiologies (Box 17L-1). Primary osteoarthritis may affect the shoulder joint but is uncommon in patients younger than their sixth decade. The secondary causes of arthritis are subdivided into atraumatic and traumatic conditions. Atraumatic conditions include inflammatory arthritis such as rheumatoid disease. Box 17l-1 Classification of Glenohumeral Arthritis Primary osteoarthritis Secondary osteoarthritis Atraumatic conditions Inflammatory arthropathy (rheumatoid arthritis) Osteonecrosis—avascular necrosis Post-traumatic conditions Postfracture Dislocation arthropathy Post-traumatic osteonecrosis Postsurgical conditions Capsulorrhaphy arthropathy Chondrolysis Implant complications Rotator cuff tear arthropathy

Osteonecrosis and its subsequent articular collapse is also an atraumatic cause of glenohumeral arthritis. Traumatic causes of shoulder arthritis include arthritis following fracture and instability (dislocation arthropathy). Capsulorrhaphy arthropathy (arthritis following anterior or posterior stabilization procedures) and chondrolysis are postsurgical complications. Massive rotator cuff tears do occur in the active and athletic population and left untreated may theoretically cause secondary rotator cuff arthropathy; however, the average age at presentation of these patients is 77 years, and most rotator cuff tears resulting in arthropathy are degenerative.1

Primary Osteoarthritis Primary osteoarthritis of the glenohumeral joint is rare, and most patients who present with primary glenohumeral arthritis are older than 60 years of age.2-4 The etiology of primary joint degeneration is unknown. Stiffness of the glenohumeral joint, joint space narrowing, humeral head osteophytes, and an intact rotator cuff characterize primary osteoarthritis of the shoulder as classically described by Neer.5 An inferior osteophyte present on the glenoid and humeral head is a classic finding (Fig. 17L-1),6,7 and chronic posterior subluxation, posterior glenoid erosion, and tight anterior structures limiting external rotation are also features.7,8 Recently, Walch and associates9 described a group of patients with static posterior subluxation of the humeral head preceding the development of osteoarthritis. Posterior subluxation may be the first radiographic indication of emerging arthritis (Table 17L-1).

Dislocation Arthropathy Traumatic dislocation of the shoulder produces articular cartilage injury secondary to shear and impaction, with an incidence of chondral and osteochondral lesions of 47% and 46% respectively.10,11 Neer described glenohumeral arthritis after anterior shoulder instability in 1982.7 The term dislocation arthropathy was coined and classified by Samilson and Prieto in their 1983 report on 74 patients with glenohumeral instability and arthritis.12 The development of arthritis was associated with increased age at the initial event; the direction of dislocation, with posterior dislocations inducing more degenerative change than anterior dislocations; and associated glenoid fractures. The number of dislocation events and previous stabilization procedures were not associated with the development of arthritis.12 Several reports have agreed that arthritis after instability

Shoulder 1105

is associated with older age of the patient at the time of injury and the length of time since the injury occurred.13-15 The impact of previous stabilization surgery and of numerous dislocation episodes has been a point of debate.15-18 Recently, in a multicenter study of patients undergoing arthroplasty for arthritis secondary to instability, Matsoukis and colleagues19 reported no differences between patients treated operatively and those treated nonoperatively for their instability in regard to arthritis severity. The incidence rate of arthritis after dislocation treated nonoperatively averages between 10% and 20% (see Table 17L-1).13-15

Capsulorrhaphy Arthropathy

Figure 17L-1 Anteroposterior radiograph of primary osteoarthritis. Inferior osteophyte is visible at the inferior glenoid and humeral head.

Glenohumeral arthritis in patients with prior instability procedures is well documented and discussed in the literature. The term capsulorrhaphy arthropathy, coined by Matsen and colleagues,20 describes overtightening of the capsule either anteriorly or posteriorly resulting in abnormal translation of the humeral head opposite the capsulorrhaphy. Nonanatomic glenohumeral translation results in atypical biomechanics, asymmetric cartilage wear, and ultimately arthritis (Fig. 17L-2). Biomechanical models have demonstrated that selective capsular plication causes alterations in humeral head translation.21-24 Capsulorrhaphy arthropathy affects predominantly young male patients with a mean age of 45 years.25 Factors implicated in the development of arthritis include length of followup, external rotation contracture of the operative shoulder, and age at the time of initial trauma, with older patients

TABLE 17L-1 Typical Findings Diagnosis

Presentation and History


Imaging

Primary osteoarthritis

Pain and decreased motion No identifiable cause

Restricted range of motion External rotation contracture Palpable crepitus

Rheumatoid arthritis

Pain and decreased motion Joint swelling Diagnosis of rheumatoid arthritis

Restricted range of motion Shoulder effusion Painful crepitance

Avascular necrosis

Shoulder pain Suggestive history with positive risk factors

Near-normal motion Crepitus—often palpable Pain at midrange positions

Post-traumatic arthritis

Pain and decreased motion Subjective complaints of instability Antecedent fracture or dislocation

Restricted range of motion Positive or negative instability examination

Capsulorrhaphy arthropathy

Pain and decreased motion History of glenohumeral stabilization procedure

Restricted range of motion Painful at midrange positions

Chondrolysis

Pain with activity Difficulty achieving motion goals in therapy Recent shoulder surgery (arthroscopic)

Pain out of proportion to expected examination Restricted range of motion Palpable crepitus

Joint space narrowing Osteophytes Sclerosis Subchondral cysts Posterior humeral subluxation Regional osteopenia Joint space narrowing Periarticular erosions Medial glenoid erosion Superior humeral head migration if rotator cuff involved Sclerosis commonly Subchondral crescent sign Subchondral collapse Images dependent on stage of disease Joint space narrowing Radiographic signs of fracture Osteophytes Sclerosis Hill-Sachs lesions Anterior or posterior glenoid bone loss Joint space narrowing Sclerosis Osteophytes Signs of previous operative intervention Glenohumeral space narrowing


cuff repair protocol.44 The remaining five cases occurred after shoulder arthroscopy in young patients, all younger than 20 years.42,43 Radiofrequency ablation (RFA) was used in four of the cases and thought to be a contributor to the onset of chondrolysis because RFA has been shown to cause cartilage destruction and chondrocyte death.45,46 However, the direct causal relationship of thermal devices and cartilage death was questioned in a review of more than 14,000 arthroscopic shoulder procedures using thermal devices with no incidence of chondrolysis.47 The final case involved use of a bupivacaine pump intra-articularly for pain control. Gomoll and colleagues recently reported on the chondrotoxic properties of bupivacaine, questioning the routine postoperative use of intra-articular bupivacaine infusion pumps.48 The pathophysiology of cartilage death and degeneration in the glenohumeral joint following arthroscopy is not understood. There is no described treatment protocol for glenohumeral chondrolysis in the literature (see Table 17L-1).

Rheumatoid Arthritis

Figure 17L-2 Anteroposterior radiograph of capsulorrhaphy arthropathy that developed in a patient after an anterior stabilization procedure.

being more susceptible.15 Dislocation arthropathy is associated with many of the same predisposing factors as capsulorrhaphy arthropathy with the exception of previous surgery. Reports have found no difference in patients treated operatively for instability and patients treated nonoperatively, calling into question whether dislocation arthropathy and capsulorrhaphy arthropathy are actually different entities (see Table 17L-1).19,26,27 Surgical procedures for anterior glenohumeral instability have evolved over time and may be divided into anatomic and nonanatomic repairs. Anatomy-preserving procedures are the Bankart28 and capsular shift.29 Nonanatomic procedures include the Putti-Platt,30 MagnusonStack,31 Bristow,32 and Latarjet.33 Arthropathy following anterior reconstructive procedures for instability occurs after both anatomic and nonanatomic repairs, and severity correlates to the length of time since surgery. Degenerative changes have been reported in 30% to 61% of shoulders treated with the Putti-Platt procedure at 9- to 26-year follow-up.17,34,35 The Latarjet-type coracoid transfer is associated with a 49% incidence of arthritis at an average 14 year’s follow-up.15,36,37 Anatomic Bankart repairs and later joint degeneration are also time dependent. The increasing incidence of arthritis is reported from 0% to 63% over a 6- to 19-year follow-up.18,32,38-41

Chondrolysis Chondrolysis of the glenohumeral joint is a rare and devastating condition described in only a handful of cases, all of whom were young patients.42-44 Two reported cases were caused by a chondrotoxic stain used during a rotator

Rheumatoid arthritis is an inflammatory condition of the synovium that results in synovial hyperplasia and a disabling secondary erosive arthritis. Overall prevalence is 1% with a female predominance and shoulder involvement in more than 90% of patients with chronic rheumatoid disease.49 Early complaints are pain, swelling, and decreasing shoulder motion. As the disease progresses, extra-articular structures become involved and painful: the subacromial bursa, acromioclavicular joint, and even rotator cuff.50 Rheumatoid shoulders undergo medial migration of the humeral head into the glenoid. The encroachment is typically into the central glenoid with joint space narrowing. The bone quality is generally osteopenic with periarticular erosions (Fig. 17L-3).51 Periarticular bony invasion of rheumatoid disease tends to affect the humeral head superior and medial to the greater tuberosity. Bony lesions (cysts) at the insertion of the rotator cuff tendons, coupled with the tendon degeneration associated with rheumatoid disease, may lead to cuff compromise. Rotator cuff–deficient shoulders will have superior humeral head migration and uneven joint erosion. The late result of rheumatoid disease affecting the shoulder is painful joint destruction, loss of bone stock, rotator cuff compromise, and poor function.50,52 Evaluating patients with rheumatoid arthritis is difficult secondary to the concomitant pain generators that may be present. Rheumatoid patients often suffer with cervical involvement and radiculopathy or myelopathy that can confound the shoulder examination with secondary pain and weakness. A thorough history and physical examination in association with appropriate imaging—magnetic resonance imaging (MRI) and computed tomography (CT)53,54—and diagnostic injections may be necessary to delineate the causes of pain in order to properly direct treatment (see Table 17L-1).

Osteonecrosis Vascular compromise and death of bone are the end result of osteonecrosis, otherwise known as avascular necrosis (AVN) or aseptic necrosis.55 The pathogenesis

Shoulder 1107

Figure 17L-3 Rheumatoid arthritis—concentric medial migration of the humeral head.

of osteonecrosis of the humeral head parallels that of the femoral head. Loss of microcirculation in the epiphyseal bone leads to marrow necrosis. Resorption of necrotic bone proceeds more rapidly than trabecular bone replacement and subsequent subchondral weakness results. Collapse of the articular surface secondary to fractures in weak subchondral bone results in articular incongruency and degeneration. The vascular network supplying the humeral head stems from the anterolateral branch of the anterior humeral circumflex artery.56 Injury to this principle vessel threatens the blood supply to the entire humeral head. Osteonecrosis of the proximal humerus results from numerous traumatic and atraumatic causes, most frequently systemic corticosteroids and trauma (see Table 17L-1).57-64 Pain is the most common complaint of patients with osteonecrosis and includes night pain with difficulty sleeping and pain interfering with simple activities of daily living.64,65 These patients are generally younger than those presenting with primary osteoarthritis.66,67 Although near-normal range of motion may be present, mechanical symptoms are not uncommon secondary to articular cartilage lesions or joint incongruity. Pain is reliably reproduced with the shoulder flexed or abducted near 90 degrees owing to the involvement of the superior central portion of the humeral head that contacts the glenoid in this position.65 Osteonecrosis of the proximal humeral head is classified according to the system reported by Cruess.68 The six-stage system is based on the classification of femoral head osteonecrosis described by Ficat and Arlet.69,70 Similar to osteonecrosis in the femoral head,

Figure 17L-4 Collapse of the subchondral bone—Arlet and Ficat stage 4 osteonecrosis.

c ollapse of the subchondral bone in the humerus is heralded by the crescent sign, and final stage of disease is illustrated by radiographic degeneration on both sides of the joint (Fig. 17L-4).

PATIENT EVALUATION Presentation and History Although there is not a classic or pathognomonic history for glenohumeral arthritis, most patients complain of increasing pain coupled with a progressive loss of shoulder mobility. Common complaints also include “noise” and crepitus, feelings of “catching,” and instability complaints. Instability complaints are subjective in nature, generally without history of frank dislocation, and are usually related to the mechanical catching of incongruent articular surfaces. Morning stiffness usually improves through the day, and sleep is affected by night pain. Primary glenohumeral arthritis is uncommon in the young population and an exhaustive history and physical examination should be completed to identify underlying primary diagnoses. The history should contain episodes of trauma, therapy or surgical procedures, medications including steroid use, family history, and recreational and social factors. Questions directed to participation in sports, organized or recreational, including questions about training, conditioning, and position should be answered.


The physical examination should begin with the cervical spine to rule out pathology that could confound examination and treatment outcomes in the shoulder. Should the cervical spine examination demonstrate positive findings, it is incumbent on the evaluating physician to treat or refer this patient for proper care of their associated conditions. The shoulder examination begins with visual examination with the patient exposed to evaluate muscular atrophy. Palpation for tenderness around the shoulder, including the sternoclavicular and acromioclavicular joints, is important. Disregarding a painful acromioclavicular joint can result in misdiagnosis and poor outcomes after treatment of other pathology. Mobility is paramount to successful outcomes in shoulder surgery and active and passive motion should be documented. Motion is evaluated by elevation in the plane of the scapula, abduction, external rotation with the arm at the side and abducted 90 degrees, and internal rotation by vertebral level reached with the thumb outstretched behind the back. Accurate delineation of painful motion is important in accurate diagnosis and treatment of shoulder arthritis. Typically, end range of motion pain is secondary to impingement, osteophytes, and capsular contracture. Midrange motion pain is indicative of articular surface damage or inflammation or synovial inflammation and is of prognostic value in directing surgical treatment.71 Glenohumeral crepitus should be noted, as should discrepancy between active and passive motionpain. Impingement signs should be documented as well as pain along the long head of the biceps. Strength testing of the rotator cuff is improved by isolating each tendon. Jobe’s test is used for the supraspinatus.72 The infraspinatus is tested using the external rotation lag sign and external rotation strength with the arm adducted at the side.73 The horn blower’s sign (external rotation with the shoulder abducted 90 degrees) tests teres minor

A

B

integrity.74 Subscapularis strength is tested using the belly press test and the lift-off test.75

Imaging Combining a thorough history and physical examination with proper imaging gives the best chance of proper diagnosis and successful treatment. Radiographic evaluation of glenohumeral arthritis provides an illustration of the extent of disease, and standard views should be taken of each patient. Standard radiographs for evaluation of the shoulder in our practice include an anteroposterior view in neutral rotation, a scapular outlet view, and an axillary view (Fig. 17L-5). Additional radiographic studies are obtained if necessary, for example, a glenoid profile or Bernageau view to assess instability.51,76,77 These views document the position of the humeral head in relation to the glenoid, the presence of osteophytes, bone quality, relative glenohumeral joint space, and visualization of glenoid bone loss. CT arthrograms are obtained to evaluate glenoid bone stock, morphology and version, and rotator cuff muscle and tendon quality if surgery is a consideration. The morphology, bone quality, and bone loss are important to document. Glenoid version is assessed using the technique described by Friedman and colleagues (Fig. 17L-6).78 The classification system of Walch and associates is used to assess glenoid wear in the anteroposterior plane for biconcavity (Fig. 17L-7).79,80 Rotator cuff muscle quality is documented because fatty infiltration has been shown to affect the results of unconstrained shoulder arthroplasty in patients with primary osteoarthritis.81 The classification system of Goutallier is used to determine prognosis.82 Routine MRI of patients with radiographically documented glenohumeral arthritis is not part of our diagnostic protocol.

C

Figure 17L-5 Standard radiographic views used in our clinical practice: anteroposterior (A), scapular outlet (B), and axillary (C) views.

Shoulder 1109 Figure 17L-6 Assessment of glenoid version as described by Friedman and colleagues. (From Friedman RJ, Hawthorne KB, Genez BM: The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am 74:1032-1037, 1992.)

α

α = Amount of Retrovision

A

Axis of Scapula

B

TREATMENT

Nonoperative

The aims of treating glenohumeral arthritis are pain reduction and restoration of mobility and function. In older patients, as in the knee and hip, a total shoulder arthroplasty effectively replaces the painful joint surfaces and allows return of function. In young patients, however, the durability of a treatment option must be weighed against the age of the patient and the patient’s functional goals. Nonoperative treatment should be aggressively pursued and exhausted before surgical intervention. Surgical options include joint-sparing techniques such as arthroscopic débridement and glenoidplasty that are temporizing treatments to delay replacement. Some diagnoses are not adequately treated with conservative or minimally invasive surgery and require arthroplasty at a young age to regain function. The mainstay of a successful outcome, whether nonsurgical or surgical, is patient education: explanation of the natural history of the disease process and functional prognosis, management of acute and chronic pain, and clear delineation of a treatment plan.

Nonoperative treatment modalities include physical therapy, nonsteroidal anti-inflammatory drugs (NSAIDs), injectable corticosteroids, and viscosupplementation. Physical therapy is the primary defense against stiffness and muscle atrophy caused by disuse secondary to pain.83,84 Therapists are excellent patient educators, helping patients modify tasks and activities of daily living to make them easier and less painful. Range of motion is maintained using both active and active-assisted exercises. Advancement of motion and resistance training should be tailored to the individual patient based on pain. Painful activities serve to decrease compliance and exacerbate the disease process. Medical interventions include NSAIDs and corticosteroid injections among others. NSAIDs are effective for the treatment of arthritis pain.85 Intra-articular corticosteroid injections also provide symptomatic relief, yet there remains much discussion and no definitive recommendations for their use despite being a fundamental part of arthritis care. Viscosupplementation using hyaluronic acid has been used for arthritis therapy in the knee with

A1

B1

A2 B2

C

Figure 17L-7 The classification system of Walch and associates is used to assess biconcavity and glenoid wear in the anterior-posterior plane. (From Walch G, Badet R, Boulahia A, Hhoury A: Morphologic study of the glenoid in primary osteoarthritis. J Arthroplasty 14:756-760, 1999.)


c ontroversial results.86 Viscosupplementation agents are not yet approved for treatment of glenohumeral arthritis. The efficacy of oral glucosamine and chondroitin sulfate in the treatment of arthritis is also controversial, but this supplement remains popular with the patient population.87,88

Joint-Sparing Techniques Arthroscopic Débridement Diagnosis of glenohumeral arthritis and cartilage lesions in young patients is often made incidentally unless radiographic changes or a predisposing underlying condition is present (Fig. 17L-8).89-91 Arthroscopy provides a minimally invasive approach to directly address chondral lesions in the shoulder and allows early rehabilitation and return to activities for patients unresponsive to conservative modalities.92 Although arthroscopic débridement and associated procedures are temporizing treatments that do not change the course of the underlying process, they can provide pain relief and functional improvement.93-96 Weinstein and colleagues94 reported on 25 patients who underwent arthroscopic débridement for isolated chondral lesions. Results correlated positively with the extent of cartilage damage. Seventy-six percent of the patients had sustained pain relief at an average 34-month follow-up. In another report, grade IV osteochondral lesions were treated with arthroscopic débridement. Pain relief was at a maximum within 5 weeks of surgery, and 88% of patients had sustained pain relief at 2 years. Lesions larger than 2 cm2 were associated with earlier return of pain.93 In addition to débridement, full-thickness chondral defects have been managed with microfracture, similar to that performed in the knee for full-thickness cartilage defects.97,98 Shoulder pain in patients with glenohumeral arthritis may be due to concomitant pain generators as well as the cartilage lesions. Subacromial bursitis and impingement,99 acromioclavicular joint pain,100 partial rotator cuff

tears,101,102 labral tears, long head of the biceps tendon lesions,103 and capsular contractures104 should be addressed at the time of arthroscopic surgery. Failure to address these associated lesions will worsen postoperative results.

Glenoidplasty Glenoidplasty and osteocapsular arthroplasty are arthros copic alternatives to arthroplasty in the young patient with glenohumeral arthritis. Posterior subluxation of the proximal humerus causes nonconcentric glenoid wear and glenoidplasty is the restoration of glenoid morphology from a biconcavity to a single concavity. Recreating the concavity of the glenoid reduces posterior humeral subluxation, increases the effective joint surface, which decreases point loading, and increases joint stability. Using an arthroscopic bur, the anterior glenoid is removed until flush with the posterior glenoid. In addition to stabilizing the joint, glenoidplasty serves to reduce tension in anterior soft tissue restraints, thereby improving external rotation that is often restricted in these patients.105 The primary recommendation for glenoidplasty and other arthroscopic joint-sparing procedures is pain relief. Results suggest predictable relief of rest pain and mechanical glenohumeral impingement at extremes, but pain relief in mid-arc range of motion pain is not predictable. Postoperative functional recovery is related directly to pain relief. Motion gained intraoperatively is often lost in the postoperative period, resulting in unpredictable functional outcomes. Clinically, factors associated with good results include pain at extremes of motion, rest pain, and painless crepitus. Radiographically, large humeral osteophytes, glenoid biconcavity secondary to posterior humeral subluxation, and loose bodies are also positive prognosticators. Important negative prognostic signs for success are pain in the mid-arc of motion, painful crepitus, small osteophytes, and no glenoid biconcavity. Severe pain in the mid-arc of motion is a contraindication to glenoidplasty because of its association with severe arthritis as well as glenoids without biconcavity.105 Osteocapsular arthroplasty involves removing humeral osteophytes and releasing soft tissue capsular contractures. Capsular releases should be performed from the rotator interval to the posterior-inferior axillary recess to gain maximal mobility. Osteophytes can be a source of pain and may limit mobility—both of which are improved by this procedure. Accessory portals or enlarged portals may be required to remove large osteophytes or loose bodies. Kelly and colleagues106 reported on a group of patients with an average age of 50 years with glenohumeral arthritis and restricted range of motion treated using glenoidplasty and osteocapsular arthroplasty. More than 85% of the patients reported improvement in both pain and range of motion at average 3-year follow-up.

Arthroscopic Treatment of Rheumatoid Arthritis and Osteonecrosis Figure 17L-8 Isolated humeral head osteochondral lesion in a young patient found at arthroscopy for a suspected superior labral lesion.

Arthroscopic procedures are also used in the early treatment of rheumatoid disease. Hypertrophic synovial tissue incites the bony and articular destruction; therefore, synovectomy helps to slow disease progression. Synovectomy

Shoulder 1111

may be effected medically, surgically, or with a combination of modalities.107-109 Arthroscopic synovectomy results in increased motion and decreased pain in 80% of patients; however, it is only indicated early in the disease process. When radiographic signs associated with joint destruction are visible, synovectomy is no longer a viable option.110 Associated arthroscopic procedures may be performed, including subacromial bursectomy and rotator cuff repair or débridement if irreparable. Regeneration of the hypertrophic synovium may occur, requiring repeat synovectomy. Early treatment of proximal humeral osteonecrosis includes arthroscopy and core decompression. Results have been shown to be related to the severity of humeral head involvement.111 Mont and colleagues112 first described core decompression for humeral osteonecrosis in 1993. Ficat and Arlet stages I and II osteonecrosis have successful treatment rates of 94% and 88%, respectively, after decompression.113 Results decreased to 70% for stage III and only 14% success for stage IV. Core decompression may increase the time until arthroplasty in stage III disease, but its indications are controversial. Core decompression is not indicated with stage IV or V disease.

Joint-Resurfacing Techniques Osteochondral Allograft Patients with full-thickness cartilage defects of the humeral head that fail treatment with arthroscopic débridement and microfracture techniques are candidates for open treatment. Humeral lesions are replaced with matched osteochondral allograft implantation (Fig. 17L-9). Championed in the knee and used in the shoulder for large defects secondary to instability,114-117 osteochondral allografts are a viable and effective means to fill localized and diffuse chondral defects in the humeral head. Two years after osteoarticular allografting in 18 patients for instability defects, Miniaci and colleagues117 reported no repeat instability and no allograft complications. Gerber and associates115 treated

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four patients with humeral osteoarticular allografts. At 60 months, three patients had little or no pain and minimal functional disability; one failure occurred secondary to necrosis of the humeral head at 6-year follow-up. The non–weight-bearing glenohumeral joint provides a forgiving environment for allograft incorporation and sympto matic relief of grafted full-thickness defects.

Humeral Head Resurfacing In addition to traditional hemiarthroplasty and total shoulder arthroplasty, humeral head resurfacing implants are available as treatment options for the younger patient. A benefit of these implants is that implantation requires minimal bone resection, and no stem is inserted into the canal, alleviating the complication of periprosthetic humeral shaft fracture.118-121 Humeral head resurfacing implants provide for complete surface replacement or partial surface replacement. An indication for resurfacing humeral arthroplasty is AVN of the humeral head with an area of necrosis less than 25% of the humeral head. Larger defects compromise the fixation of a resurfacing design, and a stemmed implant is necessary. Another indication is a very young patient requiring arthroplasty, usually secondary to chondrolysis. In our practice, complete resurfacing implants are not used along with prosthetic glenoid reconstruction or in a humeral head without adequate proximal bone, that is, in proximal humeral fracture patients or large AVN defects. Without resection of the humeral head, as done for traditional humeral implant placement, glenoid exposure is difficult and may result in improper glenoid component positioning, leading to poor results. Partial humeral resurfacing implants (Hemicap, Arthrosurface Inc., Franklin, Mass) are used for focal chondral lesions that fail arthroscopic management (Fig. 17L-10). Contraindications for partial humeral head arthroplasty are lesions larger than 35 mm (represents the largest implant available), nonlocalized disease, and insufficient bone to support the implant. Although these implant designs are smaller and require less bony

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Figure 17L-9 A, Large osteochondral lesion in a young patient. B, Intraoperative view of matched osteochondral allograft being impacted into position. C, Resurfaced lesion with matched osteochondral allograft.


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Figure 17L-10 A, Focal full-thickness osteochondral lesion. B, Complete coverage of the lesion using a metallic resurfacing implant.

resection, they are no less invasive to implant than a conventional prosthesis.

Biologic Resurfacing Biologic resurfacing of focal glenoid chondral lesions or glenoid arthritis is a viable alternative to total shoulder arthroplasty in the young patient. Focal glenoid lesions that fail arthroscopic techniques (i.e., débridement and microfracture) can be “covered” with a soft tissue graft. Tissues used to resurface the glenoid are autologous fascia lata, anterior shoulder capsule, Achilles allograft, meniscal allograft, and porcine tissue.122-125 Morphologic abnormalities of the glenoid should be realized and addressed concomitantly with biologic resurfacing. Preparation of the glenoid for the graft includes reaming to correct any anterior or posterior wear and removing any remaining cartilage to bleeding bone. Hemiarthroplasty of the proximal humerus or a humeral resurfacing implant coupled with a biologically resurfaced glenoid alleviates many of the complications associated with glenoid component wear and loosening in younger patients in short-term follow-up (Fig. 17L-11). Nowinski and associates evaluated 26 shoulders treated with glenoid resurfacing using a variety of techniques over a 5- to 13-year follow-up.123 All were treated with cementless hemiarthroplasty for the humeral disease. An overall 81% good to excellent result was reported for the treatment group and improved results were documented with fascia lata or Achilles grafts. Twenty-one of the patients returned to predisease activities, including heavy manual labor and sports; however, biologic resurfacing did not protect the glenoid from erosion.123 Yamaguchi and colleagues126 reported on results of seven patients

Figure 17L-11 Biologic glenoid resurfacing using a fascia lata autograft. Graft being positioned for final suturing intraoperatively.

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treated using meniscal allograft over a 5-year follow-up. All reported improvements in pain and had restoration of the joint space on radiographs.

Arthroplasty Neer introduced shoulder arthroplasty in the 1950s.127 Advances in prosthesis design and surgical techniques have improved function in patients undergoing shoulder arthroplasty. Shoulder arthroplasty is an effective treatment option for degenerative conditions of the glenohumeral joint, including primary osteoarthritis, post-traumatic arthritis, inflammatory arthritis, osteonecrosis, and capsulorrhaphy arthropathy. The results of shoulder arthroplasty are dependent on the condition of bone and soft tissue structures and the underlying etiology of disease. Pain recalcitrant to other treatment modalities is the most common indication for replacement; however, patients also improve statistically in regard to motion, strength, and function after arthroplasty. Primary osteoarthritis of the glenohumeral joint that is unresponsive to nonoperative therapy or that fails joint-preserving surgical treatments such as arthroscopic débridement is an indication for shoulder arthroplasty (Fig. 17L-12). Results of primary osteoarthritis treated

Figure 17L-12 Anteroposterior radiograph of a total shoulder arthroplasty for primary osteoarthritis using an anatomic humeral component and an all-polyethylene glenoid component.

with shoulder arthroplasty are found in focused studies2,128-132 and in series of nonhomogenous diagnoses including primary osteoarthritis.7,133,134 In a series of more than 200 patients, Godenèche and colleagues128 reported 77% good or excellent objective results based on the Constant score.135,136 Mean forward elevation of their cohort improved 50 degrees from 94 degrees preoperatively to 145 degrees postoperatively, and ageadjusted Constant scores improved from an average of 38 preoperatively to 97 postoperatively. Subjective results were equally impressive; 94% of patients were satisfied or very satisfied.128 Edwards and associates2 showed statistically significant improvement in postoperative values over preoperative scores for all variables, including Constant scores, pain, mobility, activity, and strength, in patients with osteoarthritis treated with arthroplasty. These results compare favorably with the results of the other series on arthroplasty for primary osteoarthritis. Preoperative factors affecting results of shoulder arthroplasty in osteoarthritis include rotator cuff tears, muscle degeneration, and glenoid morphology (in total shoulder arthroplasty). Small supraspinatus tears have little effect on outcomes after arthroplasty,81 but larger tears have a negative impact on active forward elevation and strength.128,133 Rotator cuff tears have little effect on postoperative pain relief.128 Fatty degeneration of the rotator cuff muscles affected postoperative results, and decreased forward elevation and strength were noted in patients with Goutallier82 grade 2 or higher fatty infiltration in the infraspinatus and grade 3 or higher in the subscapularis.128 Historically, glenoid resurfacing has been a point of debate because the indications for glenoid resurfacing were poorly defined and the decision to resurface was largely based on the skills and comfort level of the operating surgeon. Glenoid radiolucencies are a concern with total shoulder arthroplasty and have an incidence of 29% to 90%.7,128,134,137-139 Advancement in components, glenoid preparation, and implantation and cementing techniques in response to glenoid radiolucencies have lowered their overall incidence (Fig. 17L-13).140-144 Indications for glenoid resurfacing and arthritis include an intact rotator cuff, small reparable rotator cuff tear, glenoid incongruity, and loss of glenoid cartilage.145,146 Arthritis in conjunction with massive rotator cuff tear or inadequate glenoid bone stock is an indication for hemiarthroplasty or reverse shoulder arthroplasty.145,146 The reverse shoulder prosthesis should be reserved for elderly patients and as an implant of last resort, not routinely considered in young and active patients with glenohumeral arthritis. The literature has indicated that total shoulder arthroplasty provides improved results over hemiarthroplasty,134,147-149 but early series were too small to prove statistical significance. However, a meta-analysis by Kirkley and coworkers150 showed superiority of total shoulder arthroplasty compared with hemiarthroplasty. Additionally, Edwards and associates2 compared hemiarthroplasty to total shoulder replacement in a large multicenter study of 600 patients, which was powerful enough to show statistical significance. Total shoulder arthroplasty outperformed hemiarthroplasty, with statistical significance in nearly all measured parameters, including Constant scores, pain, motion, strength, activity scores, and active anterior


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Figure 17L-13 A and B, Intraoperative views of a resurfaced glenoid using an all-polyethylene glenoid component.

elevation and external rotation. Of important note, there was no difference in complication rate or reoperation rate. Both hemiarthroplasty and total shoulder arthroplasty provide pain relief, but total shoulder replacement is statistically superior to hemiarthroplasty. Humeral head replacement alone is reported to have poorer results and an increased incidence of revision when compared with total shoulder arthroplasty.149

Arthroplasty for Inflammatory Arthritis Shoulder arthroplasty and its results for patients with rheumatoid disease and inflammatory arthritis have been reported.147,151-156 Although preoperative symptoms are improved or relieved with both hemiarthroplasty and total shoulder arthroplasty for this condition, choice of implant is a source of controversy. Basmania and colleagues156 reported improvement in pain and motion over preoperative values for 45 patients with rheumatoid arthritis treated with arthroplasty. Hemiarthroplasty achieved improved range of motion in this group as well as improved subjective satisfaction over total shoulder patients. Other studies recommend total shoulder arthroplasty in the face of inflammatory arthritis.147,155,157 In contrast, other studies show no significant differences in outcome between the two modalities in rheumatoid disease.153,158 Rheumatoid arthritis associated with a large rotator cuff tear is an indication for reverse shoulder arthroplasty, but only in older patients without another reasonable surgical alternative.159,160

Arthroplasty for Instability Arthropathy Neer and associates7 first reported on the results of shoulder arthroplasty for osteoarthritis following instability surgery, with 16 of 17 patients reporting satisfactory to excellent results. Total shoulder arthroplasty and hemiarthroplasty for arthritis after instability surgery resulted in 77% excellent or satisfactory outcomes and 23% unsatisfactory results at 3-year follow-up in a study by Bigliani and colleagues.161 No distinction in postoperative outcome was made between hemiarthroplasty and total shoulder arthroplasty patients. Multiple procedures before the arthroplasty were cited as the reason for inferior outcomes compared with arthroplasty for primary arthritis. Other patient series report marked improvements in pain and mobility, including external rotation and abduction, after total shoulder arthroplasty for arthritis after instability repair.162,163 Revision rates are higher in these patients than in primary osteoarthritis.163 Matsoukis and colleagues19 reported on 55 patients with glenohumeral arthritis and a history of anterior dislocation treated with arthroplasty, 27 of whom had a previous stabilization procedure. Glenoid resurfacing was done on 39 patients. Younger patients scored higher on outcome studies than older patients but not significantly. Total shoulder arthroplasties demonstrated improved postoperative function compared with hemiarthroplasties. In contrast to other studies, patients with history of instability surgery and those treated nonoperatively before the arthroplasty demonstrated no differences in postoperative outcomes.19

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Author’s preferred method Patients who present and are diagnosed with glenohumeral articular cartilage degeneration in our practice are treated according to the severity of their disease and according to their functional goals. The major component in determining a treatment protocol is severity of disease. All patients are given a trial of conservative management consisting of NSAIDs, selective rest, and activity modification for 6 to 12 weeks regardless of their condition. After this initial trial, we either continue on a conservative course using corticosteroid injections as necessary—not more than one injection every 6 months—or discuss operative intervention. For focal articular humeral head defects less than 35 mm in diameter, arthroscopic débridement of the lesion, microfracture, and contracture release as indicated is the initial surgical option. A period of 6 months is allowed for improvement after débridement. If patients remain symptomatic after 6 months, we fill the defect with a matched osteoarticular allograft if the patient is younger than 30 years, or with a metallic device (Hemicap, Arthrosurface Inc., Franklin, Mass) if they are older (Fig. 17L-14). Focal chondral lesions of the glenoid are managed similarly to those found on the humeral head. Arthroscopic

techniques are used initially. Should symptoms not improve or worsen, biologic glenoid resurfacing using fascia lata autograft is completed. Isolated biologic glenoid resurfacing is used only in the presence of a normal humeral head articular surface. Nonfocal articular lesions or larger osteochondral defects caused by osteonecrosis or chondrolysis are treated using a variety of methods. In the absence of glenoid involvement and defects less than 25% of the humeral head, complete resurfacing implants are used without glenoid resurfacing. Large osteonecrotic lesions with bone loss contraindicating the use of a resurfacing implant are treated with a stemmed anatomic hemiarthroplasty.164 Involvement of the glenoid in patients younger than 40 years is addressed with biologic glenoid resurfacing using a fascia lata autograft. In older patients, we proceed to stemmed humeral components and glenoid resurfacing using all-polyethylene glenoid implants (total shoulder arthroplasty) (Fig. 17L-15). Glenohumeral arthritic conditions secondary to primary osteoarthritis, rheumatoid arthritis, extensive traumatic arthropathy, or capsulorrhaphy arthropathy are managed surgically after failure of conservative measures. Diffuse

Focal full-thickness chondral lesions of the humeral head Initial treatment: Arthroscopic débridement and microfracture

Treatment failure?

Isolated humeral head lesion

Isolated glenoid lesion

30 years old: Metallic resurfacing humeral implant

Fascia lata autograft resurfacing

Humeral head lesion with glenoid involvement

Diffuse involvement (humeral head + glenoid)

40 years old: Total shoulder arthroplasty Figure 17L-14 Treatment algorithm for decision making in the treatment of focal osteochondral lesions. Continued


A u t h o r ’ s p r e f e r r e d m e t h o d — c ont ’ d involvement of both sides of the glenohumeral joint in these conditions precludes a lasting functional outcome from arthroscopic débridement in our opinion. For these patients, we proceed with total shoulder arthroplasty. Total

shoulder arthroplasty is used over hemiarthroplasty even in younger patients (>40 years), secondary to the improved functional results and durability of modern total shoulder prostheses.

Nonfocal chondral lesions

Primary osteoarthritis Dislocation arthropathy Capsulorrhaphy arthropathy Rheumatoid arthritis Chondrolysis

If 40 years old: Total shoulder arthroplasty using stemmed humeral component

Osteonecrosis

Normal glenoid

Complete metallic humeral resurfacing implant or stemmed hemiarthroplasty— no glenoid resurfacing

Glenoid involvement

If 40 years old: Total shoulder arthroplasty using stemmed humeral component Figure 17L-15 Treatment algorithm for decision making in the treatment of nonfocal osteochondral lesions.

REHABILITATION

Arthroplasty Rehabilitation Protocol

Rehabilitation after arthroscopic treatment of arthritic lesions is focused on regaining and maintaining functional range of motion. Range of motion activities, including active and active-assisted range of motion, are begun within 1 week of surgery. Strengthening is started after acceptable motion is achieved in a pain-free arc. Hydrotherapy, discussed later in our protocol following arthroplasty, is also used after arthroscopic treatments for glenohumeral joint lesions (Table 17L-2).165

The surgical procedure, arthroscopic or open, the type of prosthesis used, and associated procedures performed determine the type of postoperative orthosis and the duration it is required. Table 17L-3 presents postoperative orthosis protocols. All patients begin hand, wrist, and elbow mobility exercises on postoperative day 1; patients undergoing unconstrained shoulder arthroplasty or resurfacing procedures without performance of an associated posterior TABLE 17L-3 Type of Postoperative Orthosis Used

TABLE 17L-2 Time for Initiation of Hydrotherapy Procedure Arthroscopic procedures Unconstrained arthroplasty Resurfacing arthroplasty Osteochondral grafting Unconstrained arthroplasty and posterior capsulorrhaphy Reverse shoulder arthroplasty

Hydrotherapy Initiated (Postoperative Week) 1 1 1 1 1 3 to 4

and Duration of Usage Procedure Performed

Type

Duration (wk)

Arthroscopic procedures Unconstrained hemi or total shoulder arthroplasty Resurfacing arthroplasty Osteochondral grafting Unconstrained arthroplasty and posterior capsulorrhaphy Reverse shoulder arthroplasty

Simple sling Simple sling

1-2 as needed 2-4

Simple sling Simple sling Neutral rotation sling Neutral rotation sling

2-4 2-4 4 4

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TABLE 17L-4 Limitation of Motion in Physical Therapy to Protect Repairs Procedure Performed

Motion Limited

Unconstrained total shoulder arthroplasty* Posterior capsulorrhaphy* (associated procedure)

External rotation past neutral Internal rotation, horizontal adduction

Duration of Limitation (wk) 4 4

*With the exception of these procedures, no limitations on range of motion are imposed.

c apsulorrhaphy are also instructed in pendulum exercises. The exercises are performed 3 to 5 times per day for about 15 minutes and are continued throughout the rehabilitative program. Hydrotherapy is used for all arthroplasty patients unless contraindicated because of deep venous thrombosis, fear of water, or chlorine allergy. Hydrotherapy is performed using a warm (35° C) rehabilitation pool to improve comfort without increasing body temperature and risk for inflammatory response. Supports accommodate straps and harnesses used in the rehabilitation process. The surgical wound is covered with a waterproof, air-permeable, hypoallergenic adhesive dressing, and patients are equipped with a mask and snorkel. The

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inability to swim is not a contraindication to hydrotherapy rehabilitation, but anxiety and fearfulness of aquatic rehabilitation are contraindications. In this instance, we use a land-based program incorporating the same exercises used in the rehabilitation pool. Land-based therapy is effective in obtaining similar results to hydrotherapy; however, it generally takes longer to reach mobility goals, and patients tend to complain of more pain. Daily (5 to 7 days per week depending on availability) sessions in the pool last 30 to 45 minutes. Exercises designed to gain elevation, extension, horizontal adduction, internal rotation, and external rotation are performed in sets of 10 repetitions. The unaffected extremity is used for passive and active-assisted movement. An active gentle breaststroke motion with the palms horizontal to decrease water resistance is allowed with the patient supported by a harness and the shoulders submerged. Table 17L-4 provides motion limitations in physical therapy to protect soft tissue repairs. Short land-based verification sessions follow pool sessions to affirm improvements in mobility achieved in the pool. Modalities, such as cryotherapy, are used as required at the discretion of the therapist. Analgesic medication is provided for 6 weeks following surgery for postoperative discomfort.165 Shoulder motion exercises with total-body immersion are proposed to all patients but are not compulsory. Patients are fitted with weighted belts and instructed to

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Figure 17L-16 Capsular stretching exercises completed underwater in hydrotherapy or as part of a land-based therapy protocol. A, The siesta position with fingers interlocked behind the head. B, Anterior capsular stretching by external rotation. C, Posterior capsular stretching with internal shoulder rotation.�


hold their breath as they kneel or recline supine on the bottom of the pool. Mobility gains are accelerated when exercising in the insulated underwater environment.165 Once 140 degrees of elevation is obtained, the “siesta” position is reached with the hands clasped behind the head. Internal rotation of the shoulder in this position stretches the posterior capsule, and external rotation stretches the anterior (Fig. 17L-16). From the siesta position, the arms may be raised, and the triple-locking position is obtained, which stretches the inferior capsule (Fig. 17L-17). The siesta and triple-locking positions form a patient-directed program implemented after discharge from formal therapy sessions.165 Patients are re-evaluated after 5 weeks of hydrotherapy. Water therapy is discontinued and a land-based self-rehabilitation regimen begins once acceptable motion is achieved. The siesta and triple-locking stretches are performed several times per day indefinitely. Additional sessions of hydrotherapy are ordered at 6-week intervals as needed. Most patients graduate to the self-directed program by 3 months after surgery. Patients without access to a physical therapist with a rehabilitation pool may learn the program from an experienced therapist and complete the program independently in any public or private pool. Additionally, patients adept at performing the exercises in the hydrotherapy program are allowed to work independently with only periodic monitoring by a trained therapist.

Return to Play After arthroscopic joint-sparing procedures, open procedures, and arthroplasty, activities of daily living generally resume by 6 weeks after surgery. Patients are asked to gradually resume their normal activities; this serves to increase strength and stamina with minimal risks.

TABLE 17L-5 Timetable to Resume Golf and Tennis Six Weeks Three Months after Surgery after Surgery Golf

Putting

Tennis

Four or Five Months after Surgery

Six months after Surgery

Half-swing Full swing with Unrestricted with 7-iron all clubs from play from a tee a tee Gentle ground Slowly increase Unrestricted strokes intensity (no play overheads)

All patients are encouraged to pursue their preoperative activities and sporting events; however, we limit patients to noncontact sports. Most of our patients desire to continue or begin playing golf and tennis after arthroplasty. Restriction on immediate return to play protects the subscapularis. A timetable for return to golf and tennis is given in Table 17L-5. We do not specifically recommend strengthening exercises as part of the rehabilitation program; however, some of our younger patients participate in weightlifting as part of their fitness regimen. Upper extremity weightlifting is allowed 6 months after surgery. Weightlifting for maintenance of muscle tone is encouraged, but powerlifting exercises are restricted. Our patients remain active after shoulder reconstruction, participating in trap shooting, water-skiing, snow-skiing, and mountain climbing 6 months after undergoing shoulder arthroplasty.

COMPLICATIONS Complications associated with arthroscopic procedures for treatment of the degenerative glenohumeral joint are extremely rare. Open shoulder reconstruction procedures are more prone to complications, with an incidence of nearly 20%. Tables 17L-6 and 17L-7 contain a list of common complications encountered during and after shoulder reconstruction and their treatment. The complications are discussed in relation to specific anatomic structures: humerus, glenoid, and soft tissues. TABLE 17L-6 Intraoperative Complications and Treatment Location

Complication

Treatment

Humerus

Iatrogenic diaphyseal fracture

Humerus

Iatrogenic tuberosity fracture Iatrogenic glenoid fracture

Reduction and fixation— long stem prosthesis, allograft struts and cables as necessary Suture fixation (adjust postoperative rehabilitation) Rim fractures—no treatment required Glenoid body fractures— bone grafting and staged reconstruction Avoid with proper exposure—large defect may require reverse prosthesis Avoid overzealous retraction—follow with observation Avoid medial dissection; emergent intraoperative vascular surgery consult

Glenoid

Rotator cuff

Figure 17L-17 The inferior capsule is stretched using the triple-locking position by raising the arms from the siesta position.

Tendon disruption

Neurovascular Axillary and injury musculocutaneous nerve injury Neurovascular Large vessel injury injury

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TABLE 17L-7 Postoperative Complications and Treatment Location/Diagnosis

Complication

Treatment

Wound

Hematoma

Humerus

Dehiscence Component loosening

Symptomatic; nonoperative protocol Irrigation and débridement if drainage persists > 7 days Symptomatic; local wound care Rule out infection Revision to a larger or cemented stem Nonoperative fracture care Operative indications: complete displacement, >30 degrees angulation, loosening, nonunion Revision surgery Revision to total shoulder arthroplasty Revision surgery Revision surgery with posterior capsulorrhaphy. or revision to reverse prosthesis Revision to reverse prosthesis Attempt at repair if acute. or revision to reverse prosthesis Revision to smaller component Arthroscopic release if failed 6 mo of nonoperative therapy Irrigation and débridement with component retention Six weeks of intravenous antibiotics Removal of components and intravenous antibiotics Revision surgery or resection arthroplasty, case specific

Periprosthetic fracture Glenoid

Component loosening Glenoid erosion (following hemiarthroplasty) Poor prosthetic alignment Capsule related (posterior instability most common) Rotator cuff related Failed subscapularis repair Prosthesis related Capsule related Early (within 6 wk)

Instability

Stiffness Infection

Late (after 6 wk)

C l Primary

r i t i c a l

P

o i n t s

glenohumeral arthritis in athletes is rare; therefore, an underlying diagnosis or secondary cause should be excluded. l Treatment should not be focused on short-term gains only, but directed toward durable results for the life of the patient. l Successful outcomes hinge on appropriate diagnosis and assessment of the functional demands of the patient and understanding the efficacy of treatment options. l A primary aim of the physical examination is to rule out confounding issues before focusing on the glenohumeral joint. l Pain is the most common indication for arthroplasty, yet motion, strength, and function also improve statistically after glenohumeral replacement. l Radiographs and CT should be used to define bony morphology and soft tissue quality; these influence treatment selection and results. l Treatment algorithms should be followed from conservative measures through surgical intervention in a stepwise manner in the treatment of glenohumeral arthritis. l A defined rehabilitation plan and structured goals should accompany treatment planning and patient education perioperatively.

S U G G E S T E D

R E A D I N G S

Edwards TB, Boulahia A, Kempf JF, et al: The influence of the rotator cuff on the results of shoulder arthroplasty for primary osteoarthritis: Results of a multicenter study. J Bone Joint Surg Am 84:2240-2248, 2002. Edwards TB, Kadakia NR, Boulahia A, et al: A comparison of hemiarthroplasty and total shoulder arthroplasty in the treatment of primary osteoarthritis: Results of a multicenter study. J Shoulder Elbow Surg 12:207-213, 2003. Friedman RJ, Hawthorne KB, Genez BM: The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am 74:1032-1037, 1992. Gartsman GM, Roddey TS, Hamerman SM: Shoulder arthroplasty with or without resurfacing the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am 82:26-34, 2000. Liotard JP, Edwards TB, Padey A, et al: Hydrotherapy rehabilitation after shoulder surgery. Tech Shoulder Elbow Surg 4:44-49, 2003. Neer CS II: Replacement arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am 56:1-13, 1974. Neer CS, Watson KC, Stanton FJ: Recent experience in total shoulder replacement. J Bone Joint Surg Am 64:319-337, 1982. Samilson RL, Prieto V: Dislocation arthropathy of the shoulder. J Bone Joint Surg Am 65:456-460, 1983. Walch G, Boileau P: Prosthetic adaptability: A new concept for shoulder arthroplasty. J Shoulder Elbow Surg 8:443-451, 1999.



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Nerve Lesions of the Shoulder Daniel C. Fitzpatrick and Kenneth P. Butters

SUPRASCAPULAR NERVE PALSY Suprascapular neuropathy has been reported in many types of athletes.1-3 Injury to the suprascapular nerve secondary to compression or traction most commonly occurs at either the suprascapular notch or the spinoglenoid notch. A direct blow or forceful scapular protraction may cause traction on the nerve at Erb’s point or kinking at either the suprascapular or spinoglenoid notch.4 When the injury occurs at the suprascapular notch, pain and motor weakness of both the supraspinatus and infraspinatus muscles may result. Compression of the suprascapular nerve by a ganglion at the spinoglenoid notch is a well-known clinical entity,5-9 resulting in isolated infraspinatus palsy, which often presents as painless posterior shoulder atrophy and weakness.

Anatomy and Biomechanics The suprascapular nerve arises from C5-C6 at the upper trunk of the brachial plexus, where it passes deep to the trapezius and the omohyoid. It enters the supraspinatus fossa through the suprascapular notch beneath the transverse scapular ligament (Fig. 17M-1). Together, the suprascapular notch and the overlying ligament form the suprascapular fossa. The suprascapular notch may assume various shapes, most commonly U-shaped (48% to 84%) and varies from flat to enclosed with bone.10,11 The width of the transverse scapular ligament parallels the size of the notch—that is, a larger bony notch results in a larger foramen.11 The nerve continues deep to the supraspinatus, innervating it with two motor branches, and sends sensory branches to the glenohumeral and acromioclavicular joints. There is no cutaneous sensory distribution from the suprascapular nerve. The nerve then reaches the lateral edge of the spine of the scapula and descends through the spinoglenoid notch, entering the infraspinatus fossa and innervating the infraspinatus. The spinoglenoid ligament passes from the spine of the scapula to the glenoid neck and posterior shoulder capsule. Its attachment into the posterior capsule results in tightening of the spinoglenoid ligament with cross-body adduction and internal rotation. The ligament is described in 14%12 to 100%13 of patients. Demirhan and associates14 found the spinoglenoid ligament present more commonly in men (64% to 36%), whereas Plancher and colleagues found the ligament to be present in equal proportions in men and women.13 Cummins and colleagues15 classified two types of spinoglenoid ligament: type I, a thin fibrous band (60%); and type II, a distinct ligament (20%), with an absent ligament in 20%. Bigliani and coworkers16 found the average

distance from the supraglenoid tubercle to the nerve at the suprascapular notch was 3 cm. The distance from glenoid rim to spinoglenoid notch is 1.8 to 2.1 cm.16,17 The suprascapular nerve is relatively fixed at its origin in the brachial plexus and at its terminal branches into the infraspinatus, resulting in several possible sites of injury.3 The two most commonly described locations of injury are the suprascapular fossa and the spinoglenoid notch. Although there is no translation of the nerve at the suprascapular fossa, the nerve forms an angle as it passes through the fossa. Nerve contact with the suprascapular ligament is accentuated with depression, retraction, or hyperabduction of the shoulder. This resulting “sling effect” may result in traction injury to the nerve.11 Cadaver studies18 also show that extremes of scapular motion can render the suprascapular nerve taut and clinically may result in suprascapular nerve injury.19,20 Ferretti and colleagues21 suggested an alternate mechanism of nerve compromise by hyperabduction of the shoulder with eccentric contraction of the infraspinatus resulting in compression of the suprascapular nerve at the spinoglenoid notch. Nerve compression against the

Suprascapular n.

Transverse scapular ligament

Spinoglenoid ligament

Infraspinatus m.

Figure 17M-1 Anatomy of the suprascapular nerve. (Redrawn from Black KP, Lombardo JA: Suprascapular nerve injuries with isolated paralysis of the infraspinatus. J Sports Med 18[3]: 225-228, 1990.)

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A

B

Figure 17M-2 Magnetic resonance image of the right shoulder shows a ganglion at the superior and posterior glenoid compressing the infraspinatus branch of the suprascapular nerve at the spinoglenoid notch.

lateral margin of the spine of the scapula by supraspinatus and infraspinatus tendons at their point of juncture is also thought to result in nerve injury.21 Ganglion cysts are a common cause of compressive injury to the suprascapular nerve. They result from superior labral tears, with the cyst expanding into the posterior scapular region, which is devoid of overlying muscle or tendon. Compression of the infraspinatus branch typically occurs as the nerve passes through the spinoglenoid notch (Fig. 17M-2).22 Suprascapular nerve palsy has also been reported following distal clavicle fractures and after resection of the distal clavicle.23,24 The nerve is located only 1.4 cm behind the clavicle and within 2 to 3 cm of the acromioclavicular joint (Fig. 17M-3).

Clinical Evaluation The athlete may have a history of trauma, but more often the complaint is vague posterior shoulder discomfort and weakness of insidious onset. Because there is no cutaneous distribution from the suprascapular nerve, pain is thought to arise from the articular branches to the acromioclavicular and glenohumeral joints. If the lesion is at the spinoglenoid notch, distal to the acromioclavicular and glenohumeral branches, the presentation may be one of painless atrophy of the infraspinatus and external rotation weakness. Diagnosis of suprascapular nerve compression by physical examination is difficult. It requires careful shoulder examination, including visual inspection of the posterior shoulder and testing of external rotation and supraspinatus strength. A complete neurologic evaluation of the neck and proximal extremity is also required. Pain is an inconsistent finding, but when present, it is usually located in the posterior shoulder and radiates to the arm; it may be worse with adduction of the shoulder.25 Posterior shoulder atrophy,

especially in the infraspinatus fossa, is an important finding (Fig. 17M-4). Because it is covered by the trapezius, supraspinatus atrophy may be difficult to observe. Weakness is a classic finding; however, weakness of the supraspinatus is not as easily exposed as that of the infraspinatus. Post and Mayer found suprascapular notch tenderness in seven of nine patients.25 Posterior ganglion cysts compressing the suprascapular nerve are thought to be associated with superior labral injuries. Compression typically occurs at the spinoglenoid notch, although cysts at the suprascapular notch have been described.26 Patients with clinical signs suggestive of a labral tear and wasting of the infraspinatus muscle warrant further diagnostic work-up, including magnetic resonance imaging (MRI) and electromyography (EMG) and nerve conduction velocity studies. Fractures of the scapula are also associated with associated nerve palsy. Edeland and Zachrisson described 18 scapular fractures, 7 with clinical involvement of the suprascapular nerve and only 1 with positive electromyographic findings.27 Treatment of suprascapular neuropathy after scapular fracture should probably include early exploration of the nerve with neurolysis and notch resection.

Diagnostic Studies A work-up for a patient with suprascapular nerve palsy should include shoulder views and, if necessary, a cervical spine series. A 30-degree cephalic tilt radiograph to visualize the suprascapular notch is helpful, especially in patients with fractures (Fig. 17M-5). MRI is useful in the evaluation of patients with suprascapular nerve palsy.28 Acute entrapment may be differentiated from chronic injury on T2-weighted images based on increased signal in the affected supraspinatus or

1122 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Figure 17M-3 Superior view of the suprascapular nerve showing its proximity to the acromioclavicular joint and posterolateral clavicle.

Medial border of scapula

Infraspinatus

Spine of scapula

Superior angle

Acromion

Supraspinatus Suprascapular n.

Infraspinatus

Suprascapular notch and ligament

Greater tuberosity

1.4 cm 2-3 cm

Supraspinatus Bicipital groove

Coracoid process

Lessor tuberosity

Clavicle

Acromioclavicular joint

infraspinatus muscles. Chronic compression appears as typical denervation changes, including decreased bulk and fatty infiltration of the muscles.29 Ganglion cysts in the supraspinatus fossa causing compression of the suprascapular nerve can be readily identified on MRI, as can associated pathology such as SLAP (superior labrum, anterior to posterior) tears and rotator cuff tears. Less common causes of suprascapular nerve palsy such as schwannoma30 and interneural ganglion31 have also been identified on MRI. Ultrasound is also reported as an effective diagnostic tool for the identification of paralabral cysts and associated rotator cuff tears.32 Ultrasound has the added benefit of

allowing aspiration of paralabral cysts, with symptomatic improvement in 86% of patients in one series.33 The authors’ experience was not nearly as successful. A local anesthetic block in the suprascapular notch area is a useful part of a series of diagnostic injections. Electrical evaluation should include both EMG of the entire shoulder girdle, including the paraspinus muscles, and nerve conduction studies from Erb’s point to the supraspinatus. Normal latency values in nerve conduction studies are 1.7 to 3.7 msec to the supraspinatus and 2.4 to 4.2 msec to the infraspinatus. Nerve conduction studies should be abnormal to confirm the diagnosis of suprascapular nerve

Figure 17M-4 Rotator cuff atrophy.

Figure 17M-5 Radiograph of suprascapular notch fracture with 30-degree cephalic tilt.

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compression. Electromyographic abnormalities can also occur with brachial neuritis, cervical root compression, and incomplete brachial plexus stretch. Additionally, some think that electromyographic studies may be normal with an obvious clinical suprascapular nerve deficit,34,35 confirming the need for the nerve latency examination. Compression with ganglia may involve only one of the three or four suprascapular nerve branches to the infraspinatus, so electromyographic recordings should be done at more than one location within the muscle.

Treatment Treatment of a patient with closed, acute suprascapular nerve injury is initially conservative, with follow-up of the problem at frequent intervals, including electrical studies. A patient with a chronic condition (6 to 12 months) and well-established atrophy requires surgery, as does a patient with suprascapular nerve palsy associated with acute scapular fracture in the area of the suprascapular notch. The symptomatic patient with a ganglion cyst compressing the suprascapular nerve also benefits from surgical decompression.5-9,26

Spinoglenoid Notch Compression When a spinoglenoid ganglion is discovered as the cause of suprascapular nerve palsy, arthroscopy should be done to repair or débride associated labral lesions and decompress the labral cyst.36 Piatt and coworkers reported 97% patient satisfaction in a group treated with labral repair and open or arthroscopic decompression of the cyst versus 57% satisfaction in a nonoperative treatment group.8 Several authors have reported cyst resolution and return of nerve function following arthroscopic decompression of the cyst.5-9,26 Arthroscopic decompression of the cyst may be performed through a preexisting labral tear; however, if no labral tear is present, a capsulotomy is required. The preoperative MRI is useful for planning the exact location of the capsulotomy, which may be performed with an electrocautery device or a shaver. The cyst is visualized with the arthroscope in the posterior portal. A blunt probe is placed in the labral tear or capsulotomy until the characteristic amber-colored cyst fluid is visualized. Decompression is achieved by placing a shaver within the cyst and evacuating the fluid. The cyst wall may be removed using the shaver, but care must be taken to avoid iatrogenic injury to the suprascapular nerve. The shaver is pointed at the glenoid neck during removal, and dissection should not extend greater than 1 cm medial to the posterior labral attachment to the glenoid.9 Associated labral pathology is then addressed. Youm reported cyst resolution and return of nerve function following repair or débridement of an associated SLAP lesion without attempts at cyst débridement in 10 patients.37 If open decompression of the nerve at the spinoglenoid notch is necessary with excision of ganglia, a surgical approach to the posterior glenoid is performed. This approach is begun with a deltoid split over the glenohumeral joint with limited deltoid detachment laterally from the acromion. The superior edge of the infraspinatus is

identified, and at most, the upper one half of that tendon is detached, leaving a humeral side stump for repair.38 The size of the exposure needed is based on the MRI position of the ganglion and the size of the patient. Aspiration and steroid injection of posterior-superior ganglia is also good initial treatment, with one report of only one in five cases developing recurrent cyst. In painless infraspinatus muscle palsy without a cyst, function is usually good with nonoperative care. Asymptomatic ganglia without nerve findings may not require treatment.21,36,39,40

Suprascapular Notch Compression Compression of the suprascapular nerve at the suprascapular notch that fails nonoperative treatment may benefit from decompression. Most reports show good return of function in selected patients following open surgical decompression.41-43 Arthroscopic decompression has also been reported.44 Open surgical decompression of the suprascapular nerve at the suprascapular notch is performed with the patient in the lateral decubitus position. A skin incision is made parallel to the spine of the scapula, and subperiosteal removal of the trapezius attachment to the spine exposes the superior border of the supraspinatus. The upper border of the supraspinatus is carefully retracted inferiorly and posteriorly to expose the superior surface of the scapula and the suprascapular notch and ligament. The suprascapular artery crosses above the ligament and the nerve below. Ligament excision and appropriate bony resection should be performed with a laminectomy rongeur. Rask reported two cases in which repeat decompression of the nerve with bony resection gave good results; he recommends wide notch resection as primary treatment.45 Certainly, if there is any question about the nerve being free, notch resection is indicated. In thin individuals, a less extensile trapezius-splitting approach can be used through a strap incision across the spine of the scapula 2 cm medial to the acromioclavicular joint. The trapezius is split 5 cm in length centered over the skin incision.

Sports Suprascapular nerve injury may present after specific trauma, with chronic onset of pain or weakness, or with insidious painless muscle atrophy. Bateman stated that “athletic stress,” especially throwing, produces a backward and forward rotation of the scapula and suprascapular nerve compression at the notch.46 Jobe and colleagues have stated that in the athlete, the nerve is often injured as it passes around the lateral spine of the scapula, sparing the supraspinatus.47 In patients with spinoglenoid notch lesions, a program of therapy may allow the elite pitcher to return to high-level competition, assuming the infraspinatus is not completely denervated. Jobe and colleagues’ electromyographic studies showed that only 30% to 40% of the maximal strength of the infraspinatus is used during throwing. Therefore, in the case of a partial nerve injury, a return to pitching is possible.47 Ferretti and associates2 studied asymptomatic volleyball players and found that 12 of 96 had isolated partial infraspinatus paralysis mostly in


the dominant shoulder; some had electrical abnormalities, others had muscle atrophy, and there was a 15% to 30% loss of external rotation power.2 They suggested that the cause was nerve tension at the spinoglenoid notch when the arm is cocked in maximal stretch and during follow-through. In a long-term study, Ferretti had 35 such patients with isolated infraspinatus atrophy and re-examined 16 patients at 5.5 years of average follow-up.21 All were still able to play volleyball at a high level with atrophy unchanged. He also found the incidence of subacromial impingement in this series to be no higher than in the general population of volleyball players. Suprascapular neuropathy has been reported with acute shoulder dislocation in a cyclist48 and with sudden onset after a hard throw from center field in a professional baseball player.49 The literature is confusing in that it refers to problems with the suprascapular nerve as both compression syndrome and nerve traction injury. The overall good response to conservative management suggests that traction injury rather than compression may be the cause. In the absence of a compressing lesion, rest from sports or other inciting causes may be helpful. Return to activity is permitted according to the judgment of the physician, based on factors in the course of follow-up, including the extent of the initial paralysis, electrical studies, symptoms, and improvements in the muscle examination with therapy. Surgical exploration of a well-localized lesion should be performed if conservative management of 3 to 6 months has failed.

LONG THORACIC NERVE PALSY Anatomy Long thoracic nerve palsy causing paralysis of the serratus anterior with winging of the scapula is a rather disabling lesion. This pure motor nerve is formed from roots of C5, C6, and C7, which branch shortly after they exit from the intervertebral foramina. Branches of C5 and C6 form the upper trunk of the nerve, which passes anteriorly through the middle scalene muscle. It then joins the lower trunk from C7 to form the long thoracic nerve. The nerve courses behind the brachial plexus to perforate the fascia of the proximal serratus anterior. It then passes medial to the coracoid on the frontal view and has an overall length of 30 cm (Fig. 17M-6).50 The nerve supplies a single muscle, the serratus anterior, which covers much of the lateral thorax and acts with the trapezius to position the scapula for elevation. It arises from the upper nine ribs and attaches at the deep surface of the scapula along the vertebral border. The muscles may be separated into upper, intermediate, and lower portions. The upper and intermediate portions are supplied by the upper division of the long thoracic nerve and produce shoulder protraction. The lower portion is primarily responsible for scapular stabilization.51 These portions typically work together to draw the scapula forward and rotate its inferior angle upward. The serratus anterior also acts as an accessory inspiratory muscle, as is seen in runners who fix their scapulae by holding their thighs to catch their breath after a race.

Long thoracic n.

Serratus anterior m.

Figure 17M-6 The brachial plexus. (Modified from Haymaker W, Woodhall B: Peripheral Nerve Injuries. Philadelphia, WB Saunders, 1956.)

Etiology of Disorders Isolated serratus anterior palsy may result from acute injury, chronic irritation, or brachial neuritis. Hester and colleagues described a tight fascial band between the inferior aspect of the brachial plexus and the region of the middle scalene insertion on the first rib.52 They noted the long thoracic nerve to “bow-string” over this band with shoulder abduction and external rotation. Medial and upward rotation of the scapula further compressed the nerve. Other authors have described internal traction on the nerve secondary to asynchronous motion between the arm and scapula as a cause of acute traction injury to the nerve.53 Long thoracic nerve palsy may also occur with prolonged recumbency or intraoperative stretch during thoracic surgery. Serratus anterior weakness following transaxillary first rib resection is not uncommon and has a good prognosis, although complete paralysis has a poor outlook.47 Other causes of nerve palsy include backpacking and shoveling. Proposed traumatic mechanisms include crushing of the nerve between the clavicle and the second rib, tetanic scalenus medius muscle contraction, and nerve stretch with head flexion or rotation and lateral tilt with ipsilateral arm elevation or backward arm extension.50 The outcome of acute traction injuries is good.11 Because the nerve is deeply located, a direct blow seems unlikely to cause isolated palsy. Serratus anterior rupture has been reported in patients with rheumatoid arthritis.4 The long thoracic nerve is often affected by the poorly understood syndrome of brachial neuritis. Brachial neuritis is a clinical syndrome of unknown cause and is the most common cause of serratus anterior palsy in our experience. Significant pain lasting a variable time—days to weeks— precedes loss of function in one or more shoulder girdle proximal extremity muscles. Sensory loss does not exclude

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Figure 17M-7 Scapular winging is often discovered during weight training as the scapula protrudes with resisted elevation or contacts the flat surface during bench press. If weightlifting is thought to be the cause, resumption of participation should await return of nerve function. Return to sports by patients with long thoracic nerve palsy depends on the demands placed on the upper extremity by the sport.

the syndrome. In the literature, there is a good prognosis for recovery, with 36% of patients recovered by the end of the first year and 75% by the end of the second year.54 Some improvement may occur after 2 years.48 Recurrent long thoracic nerve palsy is rare.50 Parsonage and Turner55 coined the term neuralgic amyotrophy (brachial neuritis) in 136 military personnel, 30 of whom had isolated serratus anterior paralysis. They also noted a right-sided predominance.

Clinical Evaluation Paralysis of the serratus anterior causes winging and a lack of scapular stabilization, limiting active shoulder elevation to 110 degrees in patients with complete lesions.50 Winging of the scapula is usually brought out with resisted active arm elevation or by doing a push-up while leaning against a wall (Fig. 17M-7). Scapular winging secondary to a long thoracic nerve palsy is characterized by elevation and retraction of the scapula such that the scapula moves toward the midline and slightly superior.53 Bertelli described the shoulder protraction test to identify upper trunk long thoracic nerve injuries.51 In this test, the patient is placed in the supine position and asked to elevate (protract) the shoulder. Ability to protract the shoulder indicates an intact upper trunk of the nerve. A patient with an early palsy may present with subtle changes in the ability to perform his or her sport, along with decreased active range of motion of the shoulder and altered scapulohumeral rhythm. The onset of long thoracic nerve palsy may be painful, as in brachial neuritis, or it may be more

subtle, involving problems with weightlifting or the feeling of pressure from a chair against the winging scapula while one is sitting. After an acute injury, several weeks may pass before marked scapular winging is evident. Gregg and colleagues believe that time is needed for the trapezius to stretch out and for scapular winging to become evident.50 Electromyographic studies confirm the diagnosis of long thoracic nerve palsy. Conduction studies should be performed from Erb’s point to the serratus anterior muscle on the anterolateral chest wall. Causes of winging other than serratus anterior palsy include trapezius palsy, painful shoulder conditions resulting in splinting of the glenohumeral joint, winging associated with multidirectional instability, and voluntary winging. The appearance of winging with arm elevation due to serratus anterior palsy differs from that of winging due to trapezius palsy. When the serratus anterior muscle does not function, the inferior tip of the scapula is pulled medially and posteriorly. With trapezius paralysis, the scapular body is held in position, and the medial border merely becomes more prominent, a more subtle deformity. In neither type of winging is the scapula rotated laterally to facilitate arm elevation.

Treatment Cessation of the suspected inciting activity is important. Shoulder braces cannot begin to normalize the force couple on the scapula between the serratus anterior and the trapezius. However, in the case of severe serratus winging, braces may prevent stretching out of the trapezius muscle. Surgically, pectoralis minor transfer56,57 to the lateral inferior scapula for dynamic support has been reported. Transfer of the pectoralis major (sternal head) with fascia lata extension to the inferior border of the scapula is the currently favored reconstruction.58 Fortunately, surgical treatment is seldom needed.

Sports Sports have been implicated as a cause of isolated serratus anterior palsy,48,50,59 with traction injury—single or repetitive—to the long thoracic nerve being the proposed mechanism. In one series, the repetitive trauma of tennis and archery was thought to be the cause of the lesion in 5 of 20 patients. Other sports implicated in this type of injury are basketball, football, golf, gymnastics, and wrestling.60

ACCESSORY NERVE PALSY Anatomy The spinal accessory nerve is a pure motor nerve innervating the trapezius and sternocleidomastoid muscles. The nerve leaves the jugular foramen at the base of the skull, goes through the upper third of the sternocleidomastoid muscle, and crosses the posterior triangle of the neck. It is here that it is superficial and vulnerable to injury. The nerve enters the trapezius and is the predominant motor nerve to that muscle. Root fibers from C3 and C4 also innervate the trapezius and may blend with the accessory


A

B

Figure 17M-8 A, Drooping of the right shoulder when the patient is relaxed. B, There is no voluntary elevation of the shoulder on the right compared with the left.

nerve; some feel that this C3-C4 contribution is only proprioceptive.61 The accessory nerve is small—only 1 to 3 mm in diameter.62 Scapular stabilization and elevation result from the balance of the forces between the trapezius and serratus anterior. The upper trapezius elevates and tilts the scapula, raising the point of the shoulder and assisting in arm elevation, respectively. The lower trapezius works with the rhomboids to retract the scapula and balance the pull of the serratus anterior. The nerve may be damaged, as it is most commonly, during a posterior triangle node biopsy. Sports injuries are typically by a direct blow—for example, with a hockey stick or in a traction injury with a cross-face maneuver in wrestling.63 Stretch injury resulting from distal upper extremity distraction and contralateral head rotation has been reported.64

Clinical Evaluation The patient complains of a sagging shoulder and incomplete arm elevation with loss of strength (Fig. 17M-8). The symptoms may be quite severe owing to muscle spasm and brachial plexus traction neuritis. Examination shows a drooping of the shoulder and a deepening of the supraclavicular fossa after trapezius atrophy has occurred. Winging of the scapula occurs with resisted arm elevation and with active external rotation against resistance.65 Winging secondary to trapezius palsy differs from that seen with a serratus anterior palsy in that the scapula lowers and translates to the midline while the inferior angle is drawn up by the levator scapulae. The levator scapulae is palpable and is seen as a band of muscle in the neck; rhomboid contraction is also palpable on attempted scapular adduction. EMG is used to provide the definitive diagnosis, but its role in determining prognosis for recovery has been questioned.66

Treatment Most athletic injuries to the spinal accessory nerve are closed and initially treated with observation.53 Good functional results are generally expected with closed injuries.66 Teboul and colleagues thought that exploration was indicated if no clinical or electrical signs of improvement existed at 3 months.67 However, they also showed good results with neurolysis up to 20 months after injury if the trapezius responded to interoperative electrical stimulation of the nerve. If the nerve injury has lasted longer than 20 months, reconstruction is advised. Clinical indications for exploration or reconstruction include a symptomatic patient with upper extremity drooping, aching, numbness, and incomplete active arm elevation. Adjacent scapular muscles cannot substitute for a paralyzed trapezius with muscle strengthening alone. The current operation of choice was described by Bigliani and associates.68 The levator scapulae and rhomboids are moved to a more lateral insertion on the scapula to substitute for the upper, middle, and lower trapezius. Other operations described include a scapular suspension with fascial grafts from the vertebral spine to the medial scapula or from the ribs to the scapula, and scapulothoracic fusion.69

Sports Spinal accessory injuries in sports are rare. Cases have been reported of a wrestler and a hockey player63 with closed accessory nerve palsy, and the authors have seen a rugby player with palsy resulting from a direct blow; all recovered nerve function with observation. Winging is less obvious and often is less disabling with trapezius palsy than with serratus anterior palsy. However, shoulder function in an athlete with accessory nerve palsy is often inadequate for competition.

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Bencardino JT, Rosenberg ZS: Entrapment neuropathies of the shoulder and elbow in the athlete. Clin Sports Med 25:465-487, 2006. Bertelli JA, Ghizoni MF: Long thoracic nerve: Anatomy and functional assessment. J Bone Joint Surg Am 87:993-998, 2005. Duralde XA: Neurologic injuries in the athlete’s shoulder. J Athl Train 35:316-328, 2000. Friedenberg SM, Zimprich T, Harper CM: The natural history of long thoracic and spinal accessory neuropathies. Muscle Nerve 25:535-539, 2002. Piatt BE, Hawkins RJ, Fritz RC, et al: Clinical evaluation and treatment of spinoglenoid notch ganglion cysts. J Shoulder Elbow Surg 11:600-604, 2002. Plancher KD, Peterson RK, Johnston JC, Luke TA: The spinoglenoid ligament: Anatomy, morphology, and histological findings. J Bone Joint Surg Am 87:361365, 2005. Teboul F, Bizot P, Kakkar R, Sedel L: Surgical management of trapezius palsy. J Bone Joint Surg Am 86:1884-1890, 2004. Westerheide KJ, Dopirak RM, Karzel RP, Snyder SJ: Suprascapular nerve palsy secondary to spinoglenoid cysts: Results of arthroscopic treatment. Arthroscopy 22:721-727, 2006. Youm T, Matthews PV, El Attrache NS: Treatment of patients with spinoglenoid cysts associated with superior labral tears without cyst aspiration, debridement, or excision. Arthroscopy 22:548-552, 2006.

l Suprascapular neuropathy occurring at the suprascapular notch presents with pain and motor weakness of both the supraspinatus and the infraspinatus. l Suprascapular neuropathy occurring at the spinoglenoid notch presents with isolated infraspinatus palsy occurring as painless atrophy. l Spinoglenoid notch cysts occurring as a result of superior labral tears are a common cause of suprascapular neuropathy. l MRI and EMG/NCV studies of the entire shoulder girdle are valuatble in the work-up of suprascapular nerve compression. l Scapular winging secondary to a long thoracic nerve palsy affecting the serratus anterior muscle is characterized by medial, posterior, and slight superior displacement. l Scapular winging secondary to a spinal accessory nerve palsy affecting the trapezius is characterized by prominence of the medial boarder of the scapula.


S e c t i o n

N

Thoracic Outlet Syndrome Karim Abdollahi and Virchel E. Wood

HISTORY Thoracic outlet syndrome (TOS) was described by Paget as an effort thrombosis of the subclavian vein in 1875 and was discussed similarly by von Schroetter in 1884.1 In 1740, Hunauld2 first described compression of the thoracic outlet secondary to a cervical rib. In 1919, Stopford and Telford showed that the neurovascular structures could be compressed by the first thoracic rib and that surgical removal of this rib would alleviate symptoms of the compression.3 The first cervical rib removal was performed by Coote4 in St. Bartholomew’s Hospital in 1861. Twenty-nine years later, the second case of a cervical rib was removed. Murphy5 was the first to remove a normal first thoracic rib for TOS in 1910. TOS has been called by various names (Box 17N-1).

ANATOMY The thoracic outlet involves the area of the shoulder girdle and thorax in which the subclavian artery and vein exit the chest cavity and combine with the brachial plexus, passing

through the scalene triangle over the first rib and under the clavicle to enter the axillary region of the shoulder (Fig. 17N-1). The anatomic boundary of the thoracic outlet consists of the superior surface of the first rib and the anterior scalene muscle and the middle scalene muscle, both of which insert into the first rib. The clavicle overrides the neurovascular structures and applies pressure on the thoracic outlet if it is displaced or positioned posteriorly. Neurovascular compression within the thoracic outlet involves the subclavian artery, the subclavian vein, or the brachial plexus within this area. Compression may involve a cervical rib abnormality or the anterior or middle scalene muscle, or it may occur at the costoclavicular or subclavian tendon junction, at the level of the first rib, or as far laterally as the pectoralis minor insertion into the coracoid process.6 Anatomic factors include an inadequate intrascalene triangle (which may be due to anterior or middle scalene hypertrophy or spasm), a high first thoracic rib, or descent of the shoulder girdle with age, allowing a sagging effect and compression of the neurovascular structures. Congenital


Box 17n-1 synonyms for thoracic outlet syndrome Shoulder-hand syndrome Paget-Schroetter syndrome Cervical rib syndrome First thoracic rib syndrome Scalenus anterior syndrome Brachiocephalic syndrome Scalenus minimus syndrome Scalenus medius band syndrome Costoclavicular syndrome Humeral head syndrome Hyperabduction syndrome Nocturnal paresthetic brachialgia Fractured clavicle syndrome Pneumatic hammer syndrome Cervicobrachial neurovascular compression syndrome Effort vein thrombosis Rucksack paralysis Pectoralis minor syndrome Cervicothoracic outlet syndrome Subcoracoid syndrome Syndrome of the scalenus medius band Naffziger’s syndrome Acroparesthesia

C1 C2 C3

Middle scalene m.

C4 Anterior scalene m.

C5

Upper branchial plexus A

Lower branchial plexus Coracoid process

B

C6 C7 T1

C Axillary

factors, such as a cervical rib, a rudimentary or anomalous first thoracic rib, variant scalene muscles, an elongated transverse process, or adventitial fibrotic bands, may be present.7 Wood and Marchinski8 described anomalous muscles such as the axillopectoral muscle (4% to 8%), chondroepitrochlear muscle, and subscapularis-teres-latissimus muscle (5.2%). Further considerations include traumatic factors, such as fracture of the clavicle, injuries to the cervical vertebrae, dislocation of the head of the humerus, and atherosclerosis of the major arteries at the isthmus of the neck of the humerus.9 Kofoed10 emphasized the necessity of ruling out cervical disk herniation in the evaluation of TOS. Differential diagnoses in TOS include any pathology creating pain in the neck, arms, or shoulders (Box 17N-2). Roos11 observed that 98% of his patients with TOS had anomalous fibrous muscular bands that probably irritated or compressed the brachial plexus. Nine different bands were described. The most frequent is type 3, which is a fibromuscular structure originating on the neck of the first rib and passing horizontally across the thoracic outlet to lie between the T1 root of the plexus and the subclavian artery (Fig. 17N-2). Type 7 is a fibrous cord attaching to the anterior surface of the anterior scalene passing under the subclavian vein to attach to the posterior surface of the sternum (Fig. 17N-3). The other seven types have been described in detail.11 TOS usually involves the lower plexus, but when the upper plexus is involved, other abnormalities may be present. Roos11 described five types of anomalies that primarily involve the relationship between scalene muscles and the upper brachial plexus. The patient presents clinically with symptoms of median nerve compression. The most frequent upper plexus anomaly is type 3, in which the anterior scalene muscle passes between the roots and trunks of the plexus (Fig. 17N-4). TOS may be caused by compression in the subcoracoid space, which is immediately posterior to the origin of pectoralis minor from the coracoid process.12 When performing Wright’s hyperabduction maneuver, the neu-

a. v.

Pectoralis minor m.

Figure 17N-1 Compression of neurovascular structures may occur at three points. The brachial plexus may be compressed between the anterior and the middle scalene muscles, causing upper thoracic outlet syndrome (A). Most commonly, compression occurs between the clavicle and the first rib (B). The pressure effect between the pectoralis minor and the rib cage is specifically assessed when performing Wright’s hyperabduction maneuver (C). a, Artery; m, muscle; v, vein.

Box 17n-2 Differential Diagnosis of Thoracic Outlet Syndrome Cervical radiculopathy (caused by disk protrusion, osteophytes) Cervical arthritis causing radiating pain to shoulder Shoulder bursitis (impingement syndrome, rotator cuff tendinitis) Glenohumeral joint instability (subluxation of humeral head irritating the brachial plexus) Brachial plexus neuritis (Parsonage-Turner syndrome) Peripheral nerve compression (cubital and carpal tunnel syndromes) Neoplasm of the spinal canal Rheumatologic conditions (fibromyalgia, myositis, fibrositis, Raynaud’s phenomenon) Thromboangiitis Neoplasm of the peripheral nerve Apical pulmonary neoplasm Mass effect (axillary tumor)

Shoulder 1129

Type 3 Type 7

Figure 17N-2 Type 3 is the most frequent type of anomalous band encountered in thoracic outlet syndrome. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome: The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

Figure 17N-3 A type 7 band found in thoracic outlet syndrome may cause venous thrombosis. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome: The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

rovascular bundle gets stretched by the coracoid process and compressed by the pectoralis minor in the subcoracoid space and may lead to loss of radial pulse or to paresthesias, or both. Effort thrombosis of axillary or subclavian vein appears to be related to overstretching of the venous wall or occluding pressure against the vein by the first rib.

which the neck or upper torso was injured.13 In our cases, the problem with the ulnar nerve alone was the most common symptom,14 followed by problems of the artery and the median nerve alone in 12%. There were many combinations of symptoms. Two of our patients were admitted to the hospital for a heart attack, and two other patients had Raynaud’s phenomenon. Three women had unilateral breast swelling and severe breast pain. Shoulder pain in athletes usually is due to musculos keletal problems, such as impingement syndrome and glenohumeral instability. Less commonly, the shoulder pain may be caused by TOS. Repetitive throwing activities in the extended, abducted, externally rotated position of the arm aggravate the symptoms (Fig. 17N-5). Pressure on the brachial plexus and artery, especially during overhead exertions, may result in fatigue, aching, and inability to perform competitive activities such as swimming.15 The swimmer may present with complaints of inability to keep fingers together during the pull-through phase of the swimming strokes. The water polo athlete may have trouble grabbing, holding, and throwing the ball. These symptoms are due to weakness in the intrinsic muscles of the hand, which suggests compromise of C8 and T1 nerve roots. Effort thrombosis of the subclavian vein (PagetSchroetter syndrome) has been reported in a competitive swimmer.16 TOS of vascular origin occurs in only 2% of

SYMPTOMS Although pain, weakness, and neurovascular deficits are associated with TOS, often the symptoms are quite bizarre and may be intermittent. Awareness of the occurrence of TOS and the presence of clinical objective findings are necessary to diagnose this syndrome. Neurologic symptoms consist of weakness, fatigability, numbness, and tingling, particularly in the distribution of posterior and medial cords of the brachial plexus. A pain diagram with a questionnaire can be helpful. Vascular symptoms consist of ischemia, claudication, cold intolerance, swelling with venous congestion, and occasional thromboembolic phenomena with distal arterial occlusion. Symptoms are especially pronounced with arm elevation above the level of the shoulder, particularly during throwing, combing the hair, or sleeping with the arm above the head. Half of our patients indicated that a single traumatic event precipitated TOS, such as a motor vehicle crash in


Anterion scalene m.

Figure 17N-4 In a type 3 anomaly, the anterior scalene muscle passes between the roots and the trunks of the plexus. (From Wood VE, Ellison DW: Results of upper plexus thoracic outlet syndrome operation. Ann Thorac Surg 58:458-461, 1994.)

patients; 97% present with neurologic symptoms. Athletes may present with generalized aching, fullness, and swelling of the arm. If acute, swelling may be significant; superficial veins may not drain with arm elevation. The incidence is higher in young, physically active males 15 to 40 years old.15 Ten of our patients presented with a venous thrombosis, Figure 17N-5 Axillary artery compression by the pectoralis minor muscle at the coracoid process insertion in the throwing athlete.

which represented 3% of our patients with TOS. PagetSchroetter syndrome has been reported in several overhead athletes, including weightlifters (Fig. 17N-6). Because aquatic athletes are primarily overhead athletes, one may expect a higher incidence of TOS in this population. Swimmers require controlled, repetitive power strokes at the extremes of abduction and external rotation of the shoulder.12 If the athlete complains of tightness and pain about the shoulder at the point the hand enters the water, the physician should be alerted to the possibility of TOS. Water polo also subjects the shoulder to repetitive abduction and external rotation in throwing and in blocking a shot. In upper TOS, athletes may complain of pain in the lower face and ear; headaches; and radiation of the pain to shoulder, thumb, and index and middle fingers.12 This presentation should be distinguished from swimmer’s ear (otitis externa). Patients also may complain of weakness or fatigue in the upper extremity muscles. Priest and Nagel17 described tennis shoulder as a depression or drooping of the exercised shoulder that they attributed to stretching of the muscles that elevate the shoulder and hypertrophy of the extremity. Shoulder droop may induce TOS by increasing the pressure at the thoracic outlet. Symptoms may be reduced by strengthening the shoulder-elevating muscles (levator scapulae, rhomboids, and upper trapezius). Rayan18 reported on two young athletes with TOS resulting from a cervical rib. Their symptoms increased with sporting activities. They responded well to resection of the cervical rib. Four cases of TOS in athletes were reported by Strukel and Garrick.3 Their patients responded well to conservative treatment. TOS is seen not only in the throwing athlete3 but also in heavy, muscular athletes, such as weightlifters, football players, and athletes who may sustain traction injuries to

Shoulder 1131

A

B

Figure 17N-6 A, This weightlifter developed effort vein thrombosis with swelling and pain in the left arm. B, The venogram shows multiple clots. This was called Paget-Schroetter syndrome in the older literature. (From Wood VE, Twito RS, Verska JM: Thoracic outlet syndrome: The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988.)

the upper arm and chest. Direct trauma that results in rib fractures, transverse process fractures, clavicular fractures, and shoulder dislocations may precipitate thoracic outlet symptoms.19

PHYSICAL EXAMINATION The physical examination is the most important aspect of diagnosing TOS. Adequate time must be allowed to perform the initial evaluation. The female athlete should be in a gown with her hair up. The shoulders should be observed for slouching. The physician should note if the breasts are large. The physician should look for any shoulder asymmetry, especially unilateral drooping or hypertrophy, as may be seen in professional tennis players, shot putters, javelin throwers, and other overhead athletes. The physician should note any venous engorgement or arm swelling (vein thrombosis). The physician should palpate the clavicle for deformity and the supraclavicular area for a cervical rib. Muscles and bones around the shoulder should be palpated, and the physician should document areas of tenderness, especially areas where the patient complains of pain. Sensation may be tested by static and moving two-point discrimination. We prefer the 10 test, in which the same area in both upper extremities is touched and the patient is asked to rate the symptomatic side 0 to 10 with 10 being normal sensation (as felt on the asymptomatic side) and 0 being no sensation at all. By sensory testing, one can attempt to distinguish between lower TOS (ulnar nerve distribution) and upper TOS (median nerve distribution). If pathology at the nerve root level is suspected, the physician should test sensation by dermatomes and note any reflex asymmetry. Motor weakness, such as with intrinsic muscles of the hand, may be subtle. Comparison to the opposite side is essential.

The physician should test for distal sites of nerve compression, such as carpal or cubital tunnel syndromes, before doing provocative maneuvers for TOS.20 This practice helps minimize false-positive findings of peripheral nerve compression that are seen when the brachial plexus is irritated by provocative maneuvers first.

PROVOCATIVE SIGNS For a test to be positive, either the symptoms must be reproduced or the radial pulse must shut off. If the pulse shuts off, the opposite side also should be tested. Less value is placed on a positive test result if the pulse shuts off on the asymptomatic arm also. The physician should ask the patient if the baseline paresthesia gets worse with the maneuver and returns to baseline after the maneuver. Between tests, the physician should give the patient a few seconds to shake his or her hand and recover from paresthesias caused by the maneuver.

Adson’s Test The physician palpates the radial pulse and abducts the arm slightly (Fig. 17N-7). The physician asks the patient to hyperextend the neck and turn it to the affected side and inhale deeply. Diminution or obliteration of the pulse probably is due to compression of the axillary artery by the anterior scalene muscle. The patient should turn the head to the opposite side (reverse Adson’s test) to test compressive effect of the middle scalene.

Halstead’s Maneuver The physician has the patient retract the shoulders downward and backward to draw the clavicle closer to the first rib (Fig. 17N-8). The physician palpates the pulse and asks about worsening paresthesias.


Roos’ Test Both shoulders are abducted 90 degrees and externally rotated 90 degrees (Fig. 17N-10). The patient opens and closes both hands rapidly for 3 minutes. The physician asks the patient if the two hands feel different from each other and if there are any paresthesias or numbness in the involved hand. A cold sensation or rapid fatigue is suggestive of arterial compromise. A patient with TOS is unable to keep the arms and hands elevated because of an ischemic, vascular type of pain.

Retroclavicular Spurling’s Test

Figure 17N-7 Adson’s test: Hold patient’s arm in slight abduction while palpating the radial pulse. Ask the patient to extend the neck and rotate toward the affected side. Adson’s test is positive if the patient reports paresthesias or if the pulse fades away.

The physician places the thumb flat and deep into the retroclavicular space and attempts to compress the brachial plexus and vascular structures (Fig. 17N-11).21 The physician should ask the patient if he or she has increasing numbness or tingling in the hand. If the answer is yes, the test is performed on the opposite side as a control. Wright,22 in his series of 150 asymptomatic normal subjects, found that 92.6% had obliteration of the radial pulse in at least one upper extremity tested in the elevated position. In our experience, the best objective test to diagnose TOS is Roos’ test.7 The retroclavicular Spurling’s test is

Wright’s Hyperabduction Test The physician passively abducts the patient’s shoulder to 180 degrees and extends it to compress brachial plexus and vessels between the pectoralis minor and the rib cage (Fig. 17N-9). This maneuver also stretches the structures under the coracoid process. The physician should palpate the pulse and ask about worsening paresthesias.

Figure 17N-8 Halstead’s maneuver: Ask patient to pull shoulders backward and downward to depress the clavicle against the first rib. Halstead’s maneuver is positive if the patient reports paresthesias or if the pulse is diminished.

Figure 17N-9 Wright’s hyperabduction maneuver: Passively abduct the affected side to 180 degrees while palpating the radial pulse. Paresthesias or diminution of the pulse suggests a positive test.

Shoulder 1133

Figure 17N-10 Roos’ test: Ask the patient to abduct and externally rotate the shoulders and open and close both hands simultaneously for up to 3 minutes. Worsening paresthesias on the affected side indicate a positive Roos’ test.

our second most reliable objective test. We believe that at least three or four of the aforementioned five signs should be clearly positive to make the diagnosis of TOS.

DIAGNOSTIC STUDIES Diagnostic tests consist of routine chest, cervical spine, and shoulder radiographs. Radiographic evaluation for cervical ribs (Fig. 17N-12), anomalous first and second ribs, pathologic clavicular fractures, and space-occupying lesions such as tumor or aneurysm must be ruled out. Arteriography documents arterial compression and possible aneurysm formation about the first rib. Venography documents venous compression or occlusion (see Fig. 17N-6). Peripheral vascular studies, including pulses,

Figure 17N-11 Retroclavicular Spurling’s test: Press the thumb down into the space behind clavicle. Paresthesia into the ipsilateral hand indicates a positive test.

Figure 17N-12 Prominent cervical rib seen on the right can compress the neurovascular structures in the thoracic outlet.

blood pressure measurements, and Doppler studies, aid in the diagnosis of thoracic outlet compression and occlusion of the arterial supply to the arm. Electromyography and nerve conduction velocity are negative in most cases of TOS. This test still is recommended, however, because it can help diagnose cervical radiculopathy, carpal tunnel, and cubital tunnel syndromes, which can be seen commonly as part of a double-crush phenomenon.23 These other sites of compression can be treated to decrease symptoms. MRI has been used to evaluate TOS.24-26 Using special techniques in an open MRI scanner, patients were imaged at 0 and 90 degrees and compared with normal subjects. A significantly smaller distance between the rib and the clavicle was seen in the patients with TOS. On coronal views, the compression of the brachial plexus often could be visualized in abduction. Gadolinium-enhanced magnetic resonance angiography, in the neutral and the abducted position, is a good screening test for patients suspected of having TOS. More recently, lidocaine injection into the scalene muscles has been promoted to help confirm the diagnosis of TOS.27,28 Under fluoroscopic and electromyographic guidance the anterior and middle scalene muscles are anesthetized using lidocaine, which temporarily paralyzes the muscles. With relaxation of these two muscles, there will be less compression on the upper brachial plexus. Shortly after the injection the provocative tests for TOS are repeated and accurately documented. The athlete is also asked to estimate (in percentage) how much relief they obtained from the injection. If physical signs show improvement and the patient reports significant reduction of symptoms shortly after these injections, he or she would be a candidate for injection of botulinum toxin into the same scalene muscles or surgical decompression. Unfortunately, there is no single test that is diagnostic for TOS. The diagnosis is based on the history, physical findings, and supportive diagnostic testing.


NONSURGICAL TREATMENT In most cases, nonoperative treatment is the initial form of management when the diagnosis of TOS is suspected.29 The treatment program includes patient education, behavior modification, and joint mobilization exercises.30 If successful, this program is followed continually and should not be terminated. Continued evaluation and monitoring of the patient are necessary. Behavior modification consists of altering sleep patterns, working patterns, and driving patterns and taking general precautions for activities that could compromise the thoracic outlet. Faulty posture must be corrected. Shoulder exercises with emphasis on gradual scapular retraction and shoulder range of motion increase joint motion and allow the cervical spine to achieve axial body and extremity extension and open the thoracic outlet space. Diaphragmatic breathing exercises often are indicated to aid in respiration when there is hypertrophy of the accessory muscles of the chest and neck. In particular, elevation of the rib cage by the pectoralis minor and scalene muscles should be eliminated because this tendency decreases the thoracic outlet space. Weak musculature about the neck and shoulder should be strengthened, and shoulder posture should be improved. The upper trunk muscles, such as the serratus anterior, middle and lower trapezius, latissimus dorsi, and rhomboids, must be strengthened. Joint mobilization techniques for the sternoclavicular, acromioclavicular, and scapulothoracic joints improve and increase the costoclavicular space. Likewise, mobilization of the occiput on the atlas facilitates axial extension body movements and improves the symptoms of TOS. Specific joint mobilization and therapy programs have been outlined by Smith.31 Conservative management should produce improvement in symptoms 1 to 3 months after the onset of symptoms. Physical therapy should not continue indefinitely and should be discontinued if it substantially exacerbates the symptoms.

SURGICAL TREATMENT When symptoms persist or become worse with conservative management, surgical intervention may be necessary.32 Patients with severe, intractable pain; disability; arterial or venous compromise, or neurologic compromise fall into this category.33 Surgery ranges from resection of the scalenus anterior, described by Adson in 1927,34 to removal of the first thoracic rib, described by Murphy5 in Australia and Brickner35 in the United States. Anterior and supraclavicular approaches have been used by these authors for first rib resection. Another approach used by Clagett36 was a limited posterior thoracotomy incision, and a transaxillary


of

approach was used by Roos.37 First rib resections now are done most commonly according to the techniques of Roos through a transaxillary approach. In addition to first rib resection, this approach allows the possibility of performing a thoracic sympathectomy at the same time for pain relief. Scalenectomy by itself does not provide predictable relief of TOS symptoms. Strict attention must be paid to the pathology, and when other causes appear to be operative, they must be corrected. Such correction may include cervical rib resection or excision of callus after a fractured clavicle. Vascular changes, particularly aneurysmal dilation or thromboembolism of the intima of the vessel, must be addressed and corrected surgically at the time of thoracic outlet decompression. In certain instances, a combination of supraclavicular and transaxillary approaches has been used for decompression of the thoracic outlet, first rib resection, and vascular reconstruction, including brachial plexus exploration as indicated. Edwards and colleagues38 performed 52 transaxillary first rib resections in 46 patients, and 42 patients (91%) had immediate improvement in symptoms after surgery, but symptoms recurred in 3 patients 6 to 8 months postoperatively. Donaghy and colleagues’39 surgical treatment of suspected neurogenic TOS relieved pain and sensory disturbance in 90% of patients but was less effective for relieving muscle weakness (50%). Thrombosis of the subclavian or axillary vein may require fibrinolytic therapy with intravenous streptokinase.16 When recannulation of the vein is confirmed by venogram, after an appropriate period of warfarin treatment (about 4 months), a first rib resection is recommended. The postoperative care is simple. The patient is allowed limited range of motion of the arm for 3 to 4 weeks for activities of daily living. Gentle active range of motion is encouraged. At 4 weeks, if the range of motion of the shoulder is restricted, we send the patient to physical therapy for range of motion, scar tissue management, and strengthening exercises. By 2 months, the patient should have full use of the operated extremity.

CRITERIA FOR RETURN TO SPORTS PARTICIPATION Resumption of sports depends on return of range of motion, strength, and endurance in the shoulder girdle and upper extremity. A recovery period of 6 months to 1 year usually is required to maximize functional return in competitive athletes. In the case of effort thrombosis of axillary or subclavian vein, retirement from competitive swimming is likely because of the long-lasting effects.15

Treatment


Conservative treatment of TOS is aimed at reducing inflammation around the brachial plexus; improving the posture of neck, shoulders, and upper back; and treating muscle spasms.12,40 Nonsteroidal anti-inflammatory medications and oral steroids should help decrease nerve irritation.

Therapists experienced in dealing with TOS can work on improving flexibility of the shoulder to allow more space between the clavicle and the first rib. Correcting posture and improving muscle balance should decrease compression of the neurovascular structures (Fig. 17N-13).

Shoulder 1135


of

T r e a t m e n t — cont ’ d

ALGORITHM FOR TOS History & physical examination consistent with TOS

Equivocal

Work-up for other compression neuropathy (e.g., cervical radiculopathy, carpal tunnel syndrome)

Yes C-spine radiograph to R/O cervical rib

Physical therapy 4-8 wk

If better

If positive

Home exercise program

If not better Work-up for other compression neuropathy with EMG/NCS and/or neck MRI

If positive

Treat the diagnosed condition

If negative Lidocaine injection of scalene muscles

Consider Botox injection of scalenes or surgery

Good response

No good response Re-evaluate for other conditions: rheumatologic disorder fibromyalgia Figure 17N-13 Algorithm for the treatment of thoracic outlet syndrome.

Most upper extremity sports, such as tennis, baseball, and all water sports, involve repetitive overhead motions. A period of rest from the offending activity should help. The athlete should be advised to avoid sleeping with the arms overhead either prone or supine. Muscle spasm is thought to play a role in causing TOS. Stretching of scalenes, pectoralis major and minor, trapezius, and levator scapulae may help relieve symptoms or prevent symptoms in the future. Success of conservative treatment of TOS is reported to be 50% to 90%.12 Our experience has shown, however, that many patients cannot tolerate physical therapy and become much worse. A negative response to therapy may be helpful in the decision process as to when surgery should be done. Another nonoperative approach would be injection of the anterior and middle scalene muscles with botulinum toxin.27,28 This would be done under fluoroscopic and electromyographic guidance in athletes who responded to the lidocaine injection in the same muscles discussed previously under Diagnostic Studies. Chemodenervation of the scalene muscles in this manner can reduce symptoms for about

3 months on the average. These injections could be repeated every 3 to 6 months, but the subsequent injections can be less effective in some patients. Surgical Technique

Roos37,41,42 described the operative technique for the transaxillary approach in several articles and gave many valuable pointers for success. We briefly describe our current technique, which is modified from that of Roos. The patient is placed on a table (usually covered with an air cushion) with the hips in a straight lateral position and the thorax tilted 60 degrees, with sandbags supporting the back for easy manipulation of the arm. The buttocks are taped in a crisscross fashion for stability, a pillow is placed between the legs, and the legs are strapped to the table. The incision is made transversely in the axilla at the point where the hairline first breaks from the rib cage up to the axilla when the arm and shoulder are elevated properly toward the ceiling. If one gets too high in the axilla, the fat Continued



of

T r e a t m e n t — cont’d

and lymph nodes from axillary fat make dissection impossible. If one gets below the third rib, the hole becomes extremely deep, making dissection difficult. The transverse incision is curved slightly in the shape of a parabola so that it lies in the axillary skin lines, becoming almost imperceptible after 6 months. One of the first structures encountered is the intercostal brachial nerve in the midfield coming from the second intercostal space. Although this may be thought to be a blood vessel, it should not be ligated. The intercostal brachial nerve is protected best by dissecting it free along with a sleeve of adipose tissue. The arm position is extremely important. One assistant will be in charge of distracting the upper arm while the patient’s shoulder is held in 90 degrees of abduction. The patient’s elbow is flexed to 90 degrees and interlocks with the assistant’s elbow while the assistant’s other arm holds onto the patient’s wrist to get effective distraction and exposure in the axilla. The procedure is well described by Roos.37 The surgeon dissects immediately to the chest wall, at which point all of the structures fall away until the first rib becomes visible. Often the superior thoracic artery lies in the field near the first rib. The artery is ligated easily using vascular clamps. We use a Cobb elevator to remove the soft tissues from the anteroinferior surface of the first rib. When the soft tissues are dissected free, the Cobb elevator is directed posteriorly under the first rib to open up the surrounding field. Theoretically, removing the rib subperiosteally invites recurrence. We and others have not found this to be a problem, but resecting it extraperiosteally invites almost certain damage to the pleura. We next take a right-angle clamp and carefully tease all of the structures from the superior surface of the rib, including the scalenus anterior, subclavius, and a portion of the ligament between the first rib and the anterior clavicle (although this is cut more easily with a knife). All of the abnormal muscle structures inserting on the first rib are teased free, with the muscle fibers spread carefully and the pleura protected at all times. The scalenus medius muscle is teased from the first rib. The surgeon now can remove the first rib safely; a special rib cutter and a nerve root retractor (designed by Roos) are indispensable at this point. We have modified the rib cutter

C l The

r i t i c a l

P

o i n t s

main source of compression is between the first rib and the clavicle. l A physical therapist experienced in TOS is important to get good results. l During provocative maneuvers, shutting off of the radial pulse is more important than paresthesias alone. We do not recommend rib resection unless the pulse shuts off. l Rule out other sources of compression neuropathy before considering surgery for TOS. l Resection of the first rib is associated with more complications and longer recovery time than carpal tunnel release or ulnar nerve decompression at the elbow.

to one that is smaller and cuts at a 60-degree angle. The rib cutter is placed as far posterior as possible so that the T1 nerve root is visualized away from the tips of the rib cutter. The posterior part of the rib is cut, and using two Kocher clamps, the rib is pulled gently from the rib cage. Particularly in women, the rib can be avulsed by a gentle pull from the sternocostal junction. If it is impossible to remove the rib from the sternocostal junction, it can be cut anteriorly with the rib cutter. With these maneuvers, one can obtain, in most cases, the entire first rib except for the posterior stump. The stump should be cut and left short so that it lies posterior to the T1 nerve root; the remaining first rib should be less than 2 cm in length. A box rongeur is used to trim the first rib back to the level of the transverse process of the seventh cervical vertebra. If a cervical rib is 2 cm or less, resection usually is not necessary, but the muscles coming from its tip should be removed. At this point, the pleura is checked carefully for holes by putting saline into the wound and overinflating the lungs. If a pneumothorax is found, a chest tube is placed into the hole. The skin is reapproximated with a subcutaneous and subcuticular stitch, and the wound is left undrained because there have been few problems with infection. The chest tube usually is removed the following day. Roos11 suggested that a clinical presentation of upper or lower plexus symptoms is an appropriate criterion to use in selecting the surgical approach for relieving thoracic outlet compression. Because the upper plexus lies beneath the anterior scalene muscles, we recommend an anterior scalenotomy through the superior clavicular approach for upper plexus symptoms as well as a transaxillary resection of the first rib. A first rib resection is recommended for the relief of lower plexus symptoms; scalenectomy and first rib resection are performed easily through the transaxillary approach. If there is any indication that the thoracic outlet is not decompressed thoroughly, one should not hesitate to do a combined approach. Removal of the first rib is a surgical procedure that must be thought out carefully and executed meticulously because it is a procedure often associated with malpractice suits. The TOS operation is not a procedure that lends itself well to teaching, and it is not a procedure easily mastered.43 The procedure requires at least two assistants.

S U G G E S T E D

R E A D I N G S

Adson AW: Cervical ribs: Symptoms, differential diagnosis for section of the insertion of the scalenus anticus muscle. J Int Coll Surg 16:546, 1951. Brickner WM: Brachial plexus pressure by the normal first rib. Ann Surg 85:858872, 1927. Edwards DP, Mulkern E, Barker P: Trans-axillary first rib excision for thoracic outlet syndrome. J R Coll Surg Edinb 44:362-365, 1999. Hagspiel KD, Spinosa DJ, Angle JF, et al: Diagnosis of vascular compression at the thoracic outlet using gadolinium-enhanced high-resolution ultrafast MR angiography in abduction and adduction. Cardiovasc Intervent Radiol 23:152154, 2000. Nichols HM: Anatomic structures of the thoracic outlet. Clin Orthop 207:13-20, 1986. Roeder DK, Mills M, McHale JJ, et al: First rib resection in the treatment of thoracic outlet syndrome: Transaxillary and posterior thoracoplasty approaches. Ann Surg 178:49-52, 1973. Roos DB: Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 163:354-358, 1966.

Shoulder 1137 Roos DB: Experience with first rib resection for thoracic outlet syndrome. Ann Surg 173:429-442, 1971. Roos DB: Congenital anomalies associated with thoracic outlet syndrome: Anatomy, symptoms, diagnosis and treatment. Am J Surg 132:771, 1976. Wood VE, Biondi J: Double-crush nerve compression in thoracic outlet syndrome. J Bone Joint Surg Am 72:85-87, 1990. Wood VE, Marchinski LJ: Neurovascular abnormalities associated with congenital anomalies. In Rockwood CA (ed): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 142-163.


S e c t i o n

O

Vascular Problems of the Shoulder J. Michael Bennett

Vascular injuries of the shoulder are relatively uncommon and are often associated with direct trauma. Most acute sports-related vascular injuries occur with contact sports; however, repetitive motion and congenital malformation can lead to many chronic syndromes that can become painful and debilitating. Symptoms can be misinterpreted and attributed to one of the more common shoulder musculoskeletal abnormalities. Early recognition of vascular compromise is essential to avoid potentially catastrophic outcomes from misdiagnosis.

and pectoral branches. The third section is distal to the lateral border of the pectoralis minor and contributes the largest branch of the axillary artery, the subscapular artery. The subscapular artery further divides into the scapular circumflex and the thoracodorsal artery. The anterior and posterior humeral circumflex arteries are the last two remaining branches from the axillary artery before it becomes the brachial artery. The posterior humeral circumflex descends posteriorly into the quadrilateral space

ANATOMY A thorough understanding of the vascular anatomy of the shoulder is necessary to fully understand the complete spectrum of vascular injury (Fig. 17O-1). Blood flow to the upper extremity begins with the heart. On the right, the subclavian artery branches from the innominate artery. On the left, the subclavian artery arises directly from the arch of the aorta. The subclavian artery then enters the thoracic outlet and extends to the lateral border of the first rib. The thoracic outlet is composed of the upper border of the first rib, inferior border of the clavicle, and anterior and middle scalene muscles. From the lateral border of the first rib to the inferior border of the latissimus dorsi, the subclavian becomes the axillary artery. The artery travels beneath the pectoralis minor and is divided into three sections, with the number of branches from each section corresponding with the number of the section. The first section is above the superior border of the pectoralis minor and gives off the superior thoracic artery inferiorly, which supplies vessels to the first, second, and third intercostal spaces. The second section travels deep to the pectoralis minor consisting of the lateral thoracic and the thoracoacromial arteries, which further arborize into clavicular, acromial, deltoid,

Anterior scalene muscle

Posterior humoral Suprascapular circumflex artery artery Axillary Anterior artery humoral circumflex artery

Subclavian artery

Pectoralis minor muscle

Subscapular artery

Figure 17O-1 Arterial anatomy of the shoulder demonstrates arterial relationships to surrounding musculoskeletal structures and potential sites of compression.


with the axillary nerve. The anterior humeral circumflex artery is smaller than the posterior branch and travels laterally around the front of the surgical neck of the humerus, supplying most of the blood supply to the humeral head. The humeral head is perfused by the arcuate artery, which is an anterolateral ascending branch of the anterior circumflex artery that enters the bone in the area of the intertubercular groove and supplies branches to the lesser and greater tuberosities. The subclavian vein begins as a branch from the brachiocephalic vein medially and becomes the axillary vein at the lateral border of the first rib. At the inferior border of the latissimus dorsi, the axillary vein becomes the basilic vein, and it continues distally. The cephalic vein is a superficial vein that pierces the clavipectoral fascia and empties into the axillary vein. The axillary and cephalic veins are responsible for most of the venous drainage in the shoulder. The lymphatics end in the thoracic and right lymphatic ducts.

CLINICAL PRESENTATION The differential diagnosis of shoulder pain and swelling should include vascular injury. Vascular lesions have been described in baseball, volleyball, tennis, cycling, marksmanship, and kayaking athletes.1 Initial symptoms are vague and nonspecific; however, complaints of easy fatigability, venous congestion, pallor, coolness of the hand, paresthesias, diminished pulses, and cold intolerance should increase suspicion of a vascular lesion. The throwing athlete is at particular risk for developing a vascular injury. The increased stresses across the shoulder can place vascular structures at risk. Other potential causes to consider include penetrating and blunt trauma, thrombosis, and compression by muscle, tendon, fascia, callus, or bone.

Figure 17O-2 Adson’s test indicates subclavian arterial compression between the scalene muscles when there is a diminished radial pulse with arm extension, external rotation, and the patient facing the involved extremity.

PHYSICAL EXAMINATION A thorough history emphasizing timing of symptoms, activities, and precipitating causes is necessary. Physical examination of both upper extremities should include inspection of the hands and fingers, looking for ulcerations, cold intolerance, capillary refill, color differences, and nailbed abnormalities.2 Standard range of motion, strength testing, blood pressure, shoulder swelling, auscultation of the axilla and brachial artery, Allen’s test, and pulse palpation from the wrist to the shoulder should be evaluated. The position of the arm is important and should be tested at the side and in abduction and external rotation to identify any clinically significant differences that would need further neurovascular evaluation. In addition to the extremities, the cervical spine and clavicle must be thoroughly examined. Vascular compression in the cervical region can be evaluated using Adson’s test, the costoclavicular maneuver, and the hyperabduction maneuver. Adson’s test (Fig. 17O-2) indicates subclavian arterial compression between the scalene muscles when there is a diminished radial pulse with arm extension, external rotation, and the patient facing toward the involved extremity. The costoclavicular maneuver (Fig. 17O-3) indicates compression among the structures between the clavicle and the first rib when there is a diminished pulse after thrusting the shoulders back in an erect posture. For the hyperabduction maneuver (Fig. 17O-4), the arm is extended, abducted, and externally rotated with the patient facing away from

Figure 17O-3 The costoclavicular maneuver indicates compression among the structures between the clavicle and the first rib when there is a diminished pulse after thrusting the shoulders back in an erect posture.

Shoulder 1139

Figure 17O-5 Arteriogram demonstrating an axillary artery aneurysm after a gunshot injury to the right shoulder. (Courtesy of Drs. Raphael Espada and James B. Bennett.) Figure 17O-4 For the hyperabduction maneuver, the arm is extended, abducted, and externally rotated with the patient facing away from the affected extremity, which compresses the axillary artery as it passes underneath the insertion of pectoralis minor and the coracoid process.

the affected extremity, which theoretically compresses the axillary artery as it passes underneath the insertion of the pectoralis minor and coracoid process.3

IMAGING Once a history and physical examination have been obtained, a systematic diagnostic work-up is indicated. Standard radiographs of the cervical spine and shoulder should be obtained to rule out bony abnormalities associated with vascular compromise such as a cervical rib, a mass occupying bone lesion, fracture, or dislocation. If a vascular lesion is suspected, a Doppler ultrasound of the extremities is the best initial screening test1,4; however, its use should be limited as a dynamic test. Arteriography remains the gold standard for the diagnosis of arterial injuries. Magnetic resonance angiography (MRA) has gained recent popularity for its detailed images of blood vessels and blood flow without having to insert a catheter into the area of interest, minimizing the risk for arterial damage. In all cases, a vascular consultation is recommended to aid in the initial evaluation and work-up.

VASCULAR TRAUMA Vascular injury to the shoulder can occur secondary to blunt or penetrating trauma. Most traumatic vascular injuries to the shoulder occur from penetrating trauma such as bone fragments or a foreign object (Fig. 17O-5). Axillary artery injury has been associated with scapular neck fractures, humeral neck fractures, and clavicle fractures. Vascular status and fracture pattern must be quickly assessed with plain films and a thorough physical examination followed by arteriography or MRA (if indicated). If surgery is indicated, the injury must be addressed within 6 hours to reduce risk for limb ischemia. Although blunt

trauma-induced injury is in the minority, the consequences from delay in diagnosis can be just as devastating. Shoulder mobility can create injury from traction and avulsion of underlying neurovascular structures without creating a bony injury. Low-energy shoulder dislocations or highenergy traction injuries such as scapulothoracic dissociation can lead to similarly poor outcomes if a misdiagnosis or delay in diagnosis is made.

Scapulothoracic Dissociation Scapulothoracic dissociation (SCD) describes a complete disruption of the scapulothoracic joint and its underlying neurovascular structures, which can be associated with acromioclavicular separation, displaced clavicle fracture, or sternoclavicular disruption. Vascular lesions have been reported in 88% of patients, and severe neurologic injuries occur in 94% of patients. One study reported a 10% mortality rate and nearly 100% of deaths were associated with vascular lesions.5 Overall, clinical outcome after SCD is uniformly poor. Outcomes such as flail extremity, early amputation, and death have been reported.6 The scapula, clavicle, acromioclavicular joint, and the surrounding ligamentous, tendinous, and capsular structures create a superior shoulder suspensory complex. Injuries to single components of the complex may be treated nonoperatively because the complex maintains a stable construct. However, if two or more components are compromised, the complex is unstable and requires at least partial repair to restore stability.6

Shoulder Dislocation Anterior shoulder dislocation is a common injury with potential complications associated with the initial dislocation as well as the reduction. Fortunately, vascular injury associated with anterior dislocation is rare. Because of anatomic location and primary restraints, the axillary artery remains at risk with this type of injury. There are a number of mechanisms that have been proposed to describe arterial injury. Some authors have proposed that the artery is fixed by the circumflex scapular artery, which reduces the


artery’s mobility on impact and can lead to arterial disruption.7,8 Others have suggested9 that the pectoralis minor acts as a fulcrum against which the artery is angulated, contused, and ruptures as the humeral head displaces the artery anteriorly (Fig. 17O-6). Vascular injuries secondary to shoulder dislocation occur primarily in older patients with stiffer, calcified, more delicate vessels. Other injuries to the axillary artery include axillary artery occlusion, which has been documented with luxatio erecta, and pseudoaneurysm (Figs. 17O-7) and can occur after recurrent anterior dislocations.9 In addition to arterial injuries, venous injuries such as venous thrombosis (Fig. 17O-8) can have a delayed presentation with unilateral extremity swelling and pain. Noninvasive Doppler imaging or venography can be used for diagnosis.

Sternoclavicular Dislocation Posterior sternoclavicular joint dislocation is a rare entity, with only 120 cases documented in the medical literature since it was first described by Sir Astley Cooper in 1824.10 The sternoclavicular joint is the articulation between the medial clavicle and the manubrium of the sternum. The joint is considered to be gliding with an intra-articular

disk, allowing up to 60 degrees of angulation in extremes of shoulder girdle movement.10 Younger patients have a higher rate of dislocation due to increased joint laxity. Stability of the joint is maintained with anterior ligaments and a thicker, stronger posterior ligament. The proximity of the brachiocephalic vein and innominate artery on the right and the common carotid artery and subclavian vein on the left can make posterior dislocation of the sternoclavicular joint a potentially life-threatening injury. Compressive or violent force is usually required to cause a dislocation, although a few cases of atraumatic dislocation have been reported.11 Contact sports and motorcycle injuries are the most common causes worldwide.12,13 Symptoms include pain, inability to move the affected shoulder, and a palpable depression on the affected side. Rarely, patients may present with dyspnea or respiratory compromise and immediate reduction is indicated. Other life-threatening complications, which can occur in up to 25% of cases, include tracheal damage, hemopneumothorax, and damage to the larynx with vocal cord palsy.13 Standard radiographic views can be difficult to interpret; therefore, computed tomography (CT) evaluation in stable patients is the ideal method for confirming the suspected diagnosis. CT angiography can delineate related injuries, and intravenous contrast can be used to enhance computed tomographic interpretation of vascular injuries. Treatment of posterior dislocation is immediate reduction. Attempt at closed reduction is made and if unsuccessful or the joint is found to be unstable, open reduction is indicated. If open reduction is indicated, a cardiothoracic surgeon should be present or on standby. Arteriography can be used before and after reduction; however, because of its invasive nature, it is reserved for selected cases.10

VASCULAR INJURY IN THE ATHLETE Subclavian and Axillary Artery Occlusion

Figure 17O-6 During anterior dislocation, the pectoralis minor can act as a fulcrum against which the artery is angulated and contused, and it ruptures as the humeral head displaces the artery anteriorly.

The axillary artery is a continuation of the subclavian artery and is responsible for perfusing the entire upper extremity. There are a number of anatomic compression sites along this pathway that may lead to arterial occlusion. Compression can occur at the subclavian artery as it angulates over a cervical transverse process, cervical rib, or first rib or is compressed by the anterior scalene muscle. Symptoms may include intermittent blanching of the hand and fingers associated with cooler temperatures, fatigue, and exertional pain. Physical examination may reveal a diminished or absent radial pulse, supraclavicular bruits, and a positive Adson’s test. The diagnosis is confirmed with arteriography. Treatment involves a first rib resection. An acute arterial occlusion is an emergency, and immediate surgery is indicated with first rib resection, removal of the thrombus, and embolectomy.14 In 1945, Wright first demonstrated occlusion of the axillary artery from direct compression of the pectoralis minor as the arm is brought into a position of hyperabduction.3,15 Tullos and colleagues further expanded on this description to include a position of abduction, extension, and external rotation, which is consistent with the cocking phase of the throwing cycle. They concluded

Shoulder 1141 Figure 17O-7 Diagnosis and treatment of a large pseudoaneurysm in a patient after recurrent shoulder dislocations. (Courtesy of Drs. Raphael Espada, Baylor College of Medicine, Houston, TX, and James B. Bennett, the Fondren Orthopedic group, Houston, TX.)

that repetitive throwing can lead to repeated local trauma to the artery creating intimal damage and the development of subsequent thrombosis.3,16 Symptoms included claudication pain, rapid fatigue, poor control of the pitch, diminished or absent distal pulses, cyanosis, and decreased skin temperatures particularly in the position of hyperabduction and external rotation. Noninvasive Doppler studies can be diagnostic; however, definitive diagnosis is made with arteriography (Fig. 17O-9). Treatment of this condition is usually surgical, and options include thrombectomy,

sympathectomy, segmental excisions, bypass with vascular graft, anastomosis, and angioplasty.16-19

Thrombosis of the axillary venous system was first described by Sir James Paget in 1875 and by Von Schroetter in 1884. This condition has been termed effort-induced thrombosis because of its frequent association with repetitive vigorous activity or blunt trauma with direct or indirect injury to the

Figure 17O-8 Venogram demonstrating venous thrombosis, which can be a complication after dislocation. (Courtesy of Drs. Raphael Espada and James B. Bennett.)

Figure 17O-9 Arteriogram demonstrating axillary artery thrombosis. (Courtesy of Dr. Raphael Espada.)

Effort Thrombosis


axillary vein. The basilic vein becomes the axillary vein at the lower border of the teres major muscle, which becomes the subclavian vein at the lateral margin of the first rib. There are several points along its anatomic course where venous compromise may occur. Compression occurs with hyperextension of the neck or hyperabduction of the arms and can occur between the first rib and the clavicle, the subclavian muscles, or the costocoracoid ligament.20,21 Risk factors for the development of a thrombus include a hypercoagulable state, dehydration, oral contraceptives, and vascular injury. The repetitive throwing motion involved with overhead athletes stretches the subclavian vein and can predispose to the development of tears within the intima of the vein. Symptoms occur within 24 hours of the inciting trauma or activity and consist of activity-related fatigue, dull and aching extremity pain, numbness, and swelling. Often, patients describe a “heaviness” of the upper arm and shoulder following activities. Physical examination may reveal superficial venous dilation, extremity cyanosis, swelling, and a painful axilla or deltopectoral groove. Pulses and neurologic examination can be normal. The physical findings may become more prominent with exercising testing. Diagnosis is made with history and physical examination and can be confirmed using venography. The venogram will show complete occlusion of the axillary or subclavian vein with extensive collateral venous return. Once the diagnosis is made, the first line of treatment for effort-induced thrombosis is conservative, emphasizing rest, heat, and elevation of the involved extremity. Pain and swelling will resolve within 3 to 4 days; however, many of these patients continue to suffer symptoms.17,22 In the acute phase, heparin, followed by warfarin, is often used to inhibit progression of the thrombus. Recently, thrombolytic agents such as streptokinase have been found to be effective in the lysis of acute clots less than 2 weeks old; however, these agents are ineffective with chronic clots. Early thrombectomy with simultaneous decompression of the thoracic outlet or first rib resection following fibrinolytic therapy has been associated with good long-term results.17,23

of the extremity for longer than 1 minute. Dampening of the radial pulse may also occur with the arm in this cocked position. In chronic cases, there may be atrophy of the deltoid. Neurologic examination and electromyographic studies are usually normal. Diagnosis may be confirmed using bilateral dynamic subclavian arteriograms. Cahill and Palmer2,24 found that with abduction and external rotation, the PHCA remained patent in the asymptomatic shoulder and became obstructed in the symptomatic shoulder. Mochizuki and associates25 found that asymptomatic volunteers demonstrated angiographic occlusion of the PHCA while in the cocked position. Angiography is nonspecific and should serve only as a supplement to a clinical diagnosis. The standard treatment is nonoperative for patients with quadrilateral space syndrome. Rest, modification of activities, and the initiation of a formal therapy program is the first line of treatment. Therapy should emphasize stretching the posterior capsule and teres minor. If conservative measures fail, surgical decompression of the quadrilateral space through a posterior approach is indicated. The surrounding muscles, tendons, and fibrous bands that constrain the space are released, removing all pressure on the neurovascular bundle when the shoulder is brought into abduction and external rotation. Cahill and Palmer reported 16 of 18 patients with good or excellent results and 2 of 18 with no change in symptoms after decompression.24 Further interpretation of the results associated with decompression is difficult owing to the small number of cases and the short follow-up.

Thoracic Outlet Syndrome Thoracic outlet syndrome involves compression of the neurovascular structures supplying the upper limb as they course from the neck to the axilla. The boundaries of compression include the clavicle, the scapula, and the first thoracic rib or cervical rib. Etiology, symptoms, and treatment are further discussed in Chapter 17N.

Quadrilateral Space Syndrome The quadrilateral space is defined as the area enclosed by the teres minor superiorly, the humeral shaft laterally, the teres major inferiorly, and the long head of the triceps medially. Within this space traverses the axillary nerve and posterior humeral circumflex artery (PHCA). In 1983, Cahill and Palmer first described the “quadrilateral space syndrome,” which involves compression of the PHCA or the axillary nerve within the quadrilateral space.1,24 Compression can occur from fibrous bands within this space, creating tension across the neurovascular bundle with abduction and external rotation of the affected extremity. Typical patients are between 25 and 50 years of age. Symptoms are unilateral and often involve the dominant extremity. The symptoms described are nonspecific and include pain and paresthesias not associated with a traumatic event. These symptoms progressively worsen with abduction and external rotation. Clinical findings include tenderness to palpation over the quadrilateral space in addition to reproduction of symptoms with abduction and external rotation

c

r i t i c a l

P

o i n t s

l Early recognition of vascular compromise is essential to avoid potentially catastrophic outcomes from misdiagnosis. l Initial symptoms are vague and nonspecific; however, complaints of easy fatigability, venous congestion, pallor, coolness of the hand, paresthesias, diminished pulses, and cold intolerance should increase suspicion of a vascular lesion. l The position of the arm is important and should be tested at the side and in abduction and external rotation to identify any clinically significant differences that would need further neurovasuclar evalution. l Standard radiographs of the cervical spine and shoulder should be obtained to rule out bony abnormalities associated with vascular compromise such as a cervical rib, a mass occupying bone lesion, fracture, or dislocation.

Shoulder 1143

l Arteriography remains the gold standard for the diagnosis of arterial injuries. l Vascular injuries secondary to shoulder dislocation occur primarily in older patients with stiffer, calcified, more delicate vessesls. Other injuries to the axillary artery include axillary artery occlusion, which has been documented with luxatio erecta, and pseudoaneurysm and can occur after recurrent anterior dislocations. l The proximity of the braciocephalic vein and innominate artery on the right and the common carotid artery and subclavian vein on the left can make posterior dislocation a potentially life-threatening injury. l Risk factors for the development of a thrombus include a hypercoagulable state, dehydration, oral contraceptives, and vascular injury. l The repetitive throwing motion involved with overhead athletes stretches the subclavian vein and can predispose to the development of tears within the intima of the vein.

S U G G E S T E D

R E A D I N G S

Baker CL, Liu SH: Neurovascular injuries to the shoulder. J Orthop Sports Phys Ther 18(1):360-364, 1993. Baker CL, Liu SH, Blackburn TA: Neurovascular compression syndromes of the shoulder. In Andrews JR (ed): The Athlete’s Shoulder. New York, Churchill Livingstone, 1994, pp 261-273. Baker CL, Thornberry R: Nerovascular syndromes. Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, pp 176-188. Beeson MS: Complications of shoulder dislocation. Am J Emerg Med 17(3):288299, 1999. Durgas JR, Weiland AJ: Vascular pathology in the throwing athlete. Update on Management of sports Injuries 16(3):477-485, 2000. Marone PJ: vascular lesions about the shoulder girdle: Shoulder injuries in sports. Wellesley Hills, MA, Aspen Publishers, 1992, pp 129-132. Mirza AH, Alam K, Ali A: Posterior sternocalvicular dislocation in a rugby player as a cause of silent vascular compromise: A case report. Br J Sports Med 39(5):e28, 2005. Nuber GW, McCarthy WJ, Yao JS, et al: Arterial abnormalities of the shoulder in athletes. Am J Sports Med 18(5):514-519, 1990. Ryu RK, Dunbar WH, Kuhn JE, et al: Comprehensive evaluation and treatment of the shoulder in throwing athlete. Arthroscopy 18(9):70-89, 2002. Schulte KR, Warner JP: Uncommon causes of shoulder pain in the athlete. Orthop Clin N Am 26(3):505-528, 1995. Tullos HS, Erwin WD, Woods GW, et al: Unusual lesions of the pitching arm. Clin Orthop 88:169-182, 1972.


S e c t i o n

P

Parsonage-Turner Syndrome Adam Nelson Whatley

Parsonage-Turner syndrome, also known as brachial neuritis or neuralgic amyotrophy, is a condition of unknown etiology. It affects the brachial plexus and causes pain followed by weakness of the shoulder and upper extremity. It has been described numerous times in the literature since it was first reported by Parsonage and Turner in 1948.1 The classic presentation begins with an acute onset of sharp pain in the shoulder region. As the pain subsides, weakness arises in the shoulder musculature. Diagnosis of this condition is primarily clinical in nature and is exceedingly difficult in the acute stage. There is a 3:2 male-to-female ratio in the idiopathic form of the disease, although a hereditary form of the disease has been reported widely in the literature.2 Age of onset is usually in the second or third decade, but cases have been reported ranging in age from neonates to patients in their eighth decade. The exact cause is unknown, but the current hypothesis is one of an immune-mediated response to a patient’s own peripheral nerves.2 This theory is supported by the fact that about half of attacks are preceded

by some event that can trigger the immune system, including infection, surgery, pregnancy and puerperium, mental and strenuous physical stress, immunizations, and immunomodulating treatment regimens (interleukin-2 or interferon-α2).2

RELEVANT ANATOMY AND BIOMECHANICS The brachial plexus comprises the ventral rami of spinal nerve roots from C5 to T1. These rami, or roots, form subsequent trunks, divisions, cords, and terminal branches that innervate the shoulder and upper extremity. The brachial plexus resides in the upper shoulder region between the anterior and middle scalene muscles. It encircles the subclavian artery and enters the upper arm through the axilla. The brachial plexus is the site of many traumatic and atraumatic conditions, which must be considered in the differential diagnosis of Parsonage-Turner syndrome.


CLASSIFICATION There is no classification system for Parsonage-Turner syndrome at the time of the writing of this chapter.

EVALUATION Clinical Presentation and History Patients who present with Parsonage-Turner syndrome most commonly (96%) complain of severe pain in or around the shoulder girdle and upper arm.2 There are few if any disorders in the shoulder and arm region that are so extremely and persistently painful at onset. The pain usually (61%) wakes the patient from sleep in the middle of the night or early in the morning.2 Ninety-four percent of patients report an inability to return to sleep.2 The pain is most often described as burning, aching, or throbbing and quantified as severe in nature. Often the pain radiates down the arm and occasionally extends below the elbow. This distal radiation is characteristic of patients with diffuse lesions or lesions that involve the lower brachial plexus.3 Most patients present with right-sided symptoms, and two thirds of patients demonstrate scapular winging.2 These painful symptoms usually maintain their intensity for a period ranging from a few hours to 2 to 3 weeks.1 Pain is exacerbated in the acute stage by any movement around the shoulder. In contrast, Valsalva or neck motion does not affect the symptoms.1 Waxman described the flexionadduction sign as patients keeping the shoulder adducted and the elbow flexed to decrease discomfort.4 These painful symptoms precede generalized weakness, although in some cases pain and weakness coincide. Eightyfive percent of patients report some degree of subjective weakness during the first month of symptoms, and 70% report weakness during the first 2 weeks.5 This weakness involves lower motor neurons in the brachial plexus and is represented by flaccidity followed by generalized wasting of the affected musculature. The pattern of involvement most often follows an upper brachial plexus distribution (71%). Half of these upper brachial plexus cases demonstrate long thoracic involvement, and 21% do not.2 Females present with middle or lower plexus distribution in 23% of cases compared with 11% of males.2 Fifteen percent of cases demonstrate signs of distal autonomic nervous system dysfunction, such as hand edema and vasomotor instability.2 Seventeen percent of these idiopathic cases involve nerves outside of the brachial plexus, including the lumbosacral plexus, phrenic nerve, or recurrent laryngeal nerve. Very infrequently, the facial nerve or abdominal nerves are involved. These atypical cases are seen more frequently (56%) in the hereditary form.2 Often patients present demonstrating the “coat pocket sign,” which entails suspending the affected extremity by lodging the hand in the ipsilateral coat pocket to reduce painful symptoms. The differential diagnosis of Parsonage-Turner syndrome should include the following: rotator cuff pathology, subacromial impingement, adhesive capsulitis, calcific tendinosis, diskogenic cervical spine disorders, poliomyelitis, amyotrophic lateral sclerosis, herpes zoster, tumors of the

spinal cord and brachial plexus, traumatic compressive nerve injuries, and ganglion cysts.6 Accurate diagnosis is difficult to achieve if the disease is in the acute phase during presentation; however, it can prevent unwarranted testing or surgery that may be indicated by a misdiagnosis and can guide earlier appropriate therapies.7 It can mimic other conditions, but there is a characteristic rapid and spontaneous resolution of pain in Parsonage-Turner syndrome. It remains a diagnosis of exclusion in some patients.

PHYSICAL EXAMINATION AND TESTING Examination The characteristic weakness in Parsonage-Turner syndrome may present in one of several patterns: muscles innervated by one peripheral nerve, muscles innervated by multiple peripheral nerves, muscles innervated by one or more nerve trunks, or muscles innervated by a combination of peripheral nerves and trunks.8 The most commonly affected peripheral nerve is the axillary nerve, followed by the suprascapular, long thoracic, and the musculocutaneous nerve.9 However, cases involving the anterior interosseous, radial, and median nerves have been reported in the literature.5,10-12 Classically, the deltoid demonstrates some degree of weakness, but the supraspinatus, infraspinatus, serratus anterior, biceps brachii, triceps, and extensors of the wrist and fingers have also been known to be affected. Diaphragmatic paralysis can be caused by phrenic nerve involvement and presents with shortness of breath and tachypnea. Atrophic changes of the affected muscles usually occur to some degree during the course of the disease. Interestingly, one third of cases demonstrate other areas of subclinical involvement.2 It is imperative to pay close attention to other upper extremity musculature and cutaneous sensation that the patient does not directly complain about in order to avoid diagnostic errors.

Testing There is only a limited role in laboratory testing in the diagnosis of Parsonage-Turner syndrome because most standard laboratory values (complete blood count, erythrocyte sedimentation rate, electrolytes, liver function tests, and urinalysis) are within normal limits.12 Cerebrospinal fluid, although reported in few affected patients to be abnormally elevated in protein, is not an efficient marker because of the potential comorbidity of lumbar puncture.5,8 Immunoassays are largely noncontributory because immunoglobulin M and immunoglobulin G have been reported to be elevated in only one patient.13 Electromyography (EMG) has been used effectively in the diagnosis of Parsonage-Turner syndrome. Its uses range from aiding in accurate initial diagnosis to the prediction of eventual recovery. EMG is helpful in localizing the area affected by the disease process and confirming the presumptive diagnosis. It is also useful in differentiating between Parsonage-Turner syndrome and traumatic etiology. Although the reading is at times variable, an acute denervation indicating axonal neuropathy is often demonstrated.14 Nerve conduction

Shoulder 1145

velocity is often within normal limits but is sometimes delayed. Testing 3 to 4 weeks after onset often demonstrates fibrillation potentials, positive waves, delayed distal latencies, and decreased amplitude of action potentials.3,6,9,15-17 Interestingly, EMG in the face of Parsonage-Turner syndrome spares the paraspinal musculature. EMG is also useful in detection of subclinical pathology in the contralateral (otherwise silent) upper extremity.5 EMG demonstrates reinnervation and recovery of muscular function, which is important in helping to predict functional outcome.

Imaging Plain radiographic imaging of the cervical spine and shoulder usually is normal and noncontributory. One exception is the initial presentation of inferior glenohumeral subluxation occurring up to 2.5 weeks after onset in cases with deltoid and rotator cuff involvement.18 This finding usually resolves on overall symptomatic relief. Plain radiographs of the chest demonstrate hemidiaphragmatic elevation in cases involving one or both phrenic nerves.5,19 Standard magnetic resonance imaging (MRI) usually demonstrates only the secondary changes in affected muscles, including early high intensity in T2-weighted images in the subacute stage (1 to 3 months) and diffuse muscular atrophy and fatty replacement (mean of 5 weeks after onset) with T1-weighted images in the months following onset of symptoms.20 Only infrequently have pathologic changes been demonstrated in neural elements in the face of Parsonage-Turner syndrome with standard MRI (3 of 50 cases).21 Magnetic resonance neurography is more sensitive than standard MRI in peripheral neural element pathology22,23 and has been shown in studies to be sensitive in the acute stage (within 1 month of onset) in the diagnosis of Parsonage-Turner syndrome.20 It has been shown to confirm the diagnosis in the case of one 27-year-old man demonstrating thickened, hyperintense upper trunk changes consistent with plexitis.24 This methodology holds some promise in the advancement of a radiologic basis of diagnosis in patients with Parsonage-Turner syndrome.

TREATMENT OPTIONS Nonoperative The overall nature of Parsonage-Turner syndrome is one of a benign and self-limited disease. Treatment is largely supportive, and no one treatment regimen has been shown to alter the course of the disease process.12 Corticosteroids have been shown to reduce pain in a few patients during the very early stages.5 Analgesics are somewhat effective in the treatment of debilitating pain. Rest of the affected extremity is often advocated because movement often exacerbates pain,25 and immobilization has been used effectively to limit pain from stretching affected muscles. One method of immobilization is to employ a standard shoulder sling to ensure maintenance of full normal range of motion with dedicated active and passive range of motion exercises to the shoulder and elbow a few times per day. Physical therapy is widely recommended but has not been shown

to have any effect in reducing time to recovery compared with no formal therapy.5 Massage and electrical stimulation have been cited as beneficial, but there are no subjective data to support this claim.12 The neurology literature has reported good response in decreasing pain with a multimodal pharmaceutical approach. One such regimen includes the combination of a long-acting nonsteroidal anti-inflammatory drug and an opiate (sustained-release diclofenac, 100 mg, with sustained-release morphine, 10 to 30 mg twice daily).21 Co-analgesics such as gabapentin, carbamazepine, and amitriptyline are also recommended for control of second-phase pain, which is characterized by spontaneous or movement-induced shooting pains and tingling sensations due to aberrant impulse firing in damaged, hypersensitive portions of the brachial plexus.2 These medications are used in delayed-onset cases and are not indicated for the treatment of acute pain.

Operative Operative treatment of Parsonage-Turner syndrome is indicated only in cases in which there is no long-term improvement. Such cases involve muscle transfers or fusions to compensate for permanent muscular deficit. Reported procedures include scapulothoracic stabilization for a case with persistent serratus anterior and rhomboid deficit, and tendon transfers to thumb, fingers, and wrist for a case involving persistent radial nerve deficit.26

POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Overall recovery is usually good, with complete restoration of strength and function. A longer duration of active painful symptoms and longer time to full recovery are typical in cases with multiple nerve involvement or bilateral involvement.1,5,8,9 Isolated upper trunk pathology, which is the most common distribution, usually resolves more quickly and without complications.5 In all cases of Parsonage-Turner syndrome, improvement in both strength and sensation occur as early as 1 month after onset but can take up to 3 years if recovery is reached at all. Tsairis and colleagues reported complete recovery in 36% by 1 year, 75% within 2 years, and 89% within 3 years.5 Sensory and motor recovery parallel each other. Recurrence of symptoms is seen occasionally (1) and higher Blackburne-Peel measurement (>0.805) (Fig. 22A-14). With disruption of the quadriceps tendon, there is a distal migration of the patella and a resulting lower InsallSalvati ratio (5 degrees Retropatellar crepitation Positive apprehension test Redislocation frequency Late problems Kujala score

Posterior Splint (n = 17)

Bandage/Brace (n = 23)

15%

6%

13%

27%

6%

17%

67%

53%

52%

53%

53%

48%

38%

47%

57%

47% 80

21% 82

32% 74

Adapted from Maenpaa H, Lehto MU: Patellar dislocation: The long-term results of nonoperative management in 100 patients. Am J Sports Med 25(2): 213-217, 1997.

a lateral buttress, and patients began supervised physical therapy immediately following evaluation of their injury. Therapies consisted of initial straight-leg raises followed by stationary bicycle for passive and active motion, and isotonic and isometric quadriceps strengthening. Return to full activities was allowed when tenderness subsided and isotonic quadriceps strength was symmetric, taking between 3 and 8 weeks. Two thirds of the knees had good to excellent results following a first-time acute dislocation, compared with only 50% of those with a recurrent dislocation. Overall, 73% were satisfied with their knees, but 16% were not and eventually elected to have surgical stabilization. Whether immobilized or not, those with acute patellar dislocation can expect a lengthy rehabilitation period before return to sport. Atkin and associates prospectively studied the recovery during the first 6 months following injury in 74 patients.1 Only 16% returned to sport by 6 weeks. At 6 months, 69% had returned to sport, despite more than half having continued difficulty with kneeling and squatting.

OPERATIVE TREATMENT If deemed necessary, operative treatment of acute patellar dislocation should be used to reestablish patellofemoral stability and treat any osteochondral injury that may

be present. In restoring stability, the approach should be to “repair, reconstruct, release, or realign.” After careful and complete evaluation of the injured knee, any combination of these principles may be needed to tailor a treatment plan to the individual. Repair and reconstruction should be directed at identifiable soft tissue injuries on the medial side of the knee. Release or lengthening of the lateral retinaculum should be aimed at restoring soft tissue balance of the patellofemoral joint, taking care not to destabilize the patella.59 Realignment procedures should be used to address clear underlying anatomic malalignment. Unfortunately, no one procedure or combination of these procedures has produced reproducible and uniformly excellent results. In a systematic review of the literature on primary patellar dislocations, Stefancin and Parker identified only five studies comparing nonoperative and operative treatment head to head, only two of which are randomized, prospective studies (Table 22C1-7).25 In a nonrandomized study, Hawkins evaluated 27 patients with either nonoperative treatment with a cylinder cast for an average of 3 weeks or operative treatment with arthrotomy, excision of osteochondral fragments, repair of the medial retinaculum, advancement of the vastus medialis, and lateral release followed by a cylinder cast for 5 to 6 weeks.60 Fifteen percent of patients treated nonoperatively sustained a redislocation in the follow-up period, whereas there were none in the operative group. More important, the study showed that 40% to 70% of patients can anticipate residual symptoms of anterior knee pain, and 20% to 30% will experience feelings of instability despite treatment method. Cash and Hughston similarly showed no dislocations in their operative treatment group, which underwent acute medial ligament repair without lateral release or realignment, compared with 36% of those treated nonoperatively.54 Recently, Buchner and colleagues retrospectively evaluated primary patellar dislocations in 126 patients after an average of 8 years.61 The four treatment groups consisted of nonoperative; arthroscopy only; open surgery with reconstruction of the medial retinaculum, realignment, and lateral release; and open surgery with fixation of a loose osteochondral fragment. The overall recurrence rate was 26%, with no significant difference between treatment groups. In addition, there was no statistical difference between treatment groups in activity level, function, pain, or subjective evaluation. Nikku and associates have published the only two prospective, randomized trials comparing nonoperative to

TABLE 22C1-7 Results of Randomized Clinical Trials Comparing Operative and Nonoperative Treatment of Acute Patellar Dislocation

Knees Study (2005)61

Buchner et al Cash & Hughston (1988)54 Hawkins et al (1986)60 Nikku et al (2005)62 Nikku et al (1997)63

Good to Excellent Results

Redislocation Rate

Follow-up (yr)

Nonoperative

Operative

Nonoperative

Operative

Nonoperative

Operative

8.1 8.0 2.8 2.1 7.0

63 74 20 55 57

63 29 7 70 70

67% 58% 71% 81%

76% 82% 70% 67%

27% 36% 14% 27% 39%

25% 10% 0% 31% 17%

Adapted from Stefancin JJ, Parker RD: First-time traumatic patellar dislocation: A systematic review. Clin Orthop 455:93-101, 2007.

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operative treatment of primary patellar dislocation.62,63 Their operative group was treated with repair, duplication, or augmentation of the medial retinaculum with or without lateral release, and a subset of patients with subluxation only on examination under anesthesia were treated with isolated lateral release. Postoperative care was identical in both treatment groups. In their initial report of 125 patients with an average follow-up of 2 years, there was no significant difference in the patients’ subjective opinion, recurrent episodes of instability or subluxation, and redislocation between treatment groups. The only statistical difference was a slightly higher Hughston Visual Analog Scale (VAS) score in the nonoperative group.63 In 2005, Nikku re-evaluated 127 patients from the same study group at a mean follow-up of 7 years.62 No statistical significance was shown between treatment groups with respect to subjective Kujala, Hughston, and Tegner scores, or incidence of instability or redislocation. Risk factors for poor subjective outcome and recurrent instability were identified: lower Kujala scores were associated with female gender, loose bodies, and an initial history of instability in the contralateral knee, and a high recurrence rate was associated with young age and initial contralateral instability. Late operation was performed in nearly half of the study participants, signifying the frequency of long-term problems associated with acute patellar dislocation, despite the initial treatment. In general, operative indications for treatment of the acute dislocation of the patella in the adult are controversial. The most commonly cited indications for initial operative treatment are osteochondral loose bodies, palpable defects in the vastus medialis insertion, obvious tear in the medial retinaculum, and persistent asymmetric subluxation. With better imaging and more awareness of its importance, tear or avulsion of the MPFL should be added on this list.

Arthroscopy Arthroscopy of the knee following acute patellar dislocation has become more widely accepted. Arthroscopy is a minimally invasive procedure that allows direct visualization of the articular surfaces and can be done alone or in combination with open procedures. However, as MRI techniques have improved, the use of arthroscopy is becoming more therapeutic than diagnostic. Chondral and osteochondral injuries can be documented, excised, or fixed with the use of arthroscopic equipment. Recently, minimally invasive medial retinacular repair by suture anchor to the patella has been suggested by Fukushima, but the technique involved is technically difficult and does not address lesions at the adductor tubercle.64

Lateral Release Release of the lateral retinaculum has been used alone or in combination with other procedures in the treatment of acute patellar dislocation. Open lateral release was popularized by Merchant and Mercer in 1974.65 Arthroscopic lateral release was first described by Chen and Ramanathan in 1984 and has become a commonly performed, but controversial, adjunct to arthroscopy of the knee in acute

patellar dislocation.66 The concept of creating a “balanced laxity” in the patellofemoral joint is based on equalizing the soft tissue tension on both sides of the patella, that is, cutting the lateral side and allowing it to scar in a lengthened position balances out the stretched or torn medial retinaculum and patellofemoral ligament. Although this has been shown to decrease patellar tilt, it has not been shown to decrease lateral subluxation. Although it is often cited as treatment for recurrent lateral dislocations, there is little published on the use of lateral release in acute dislocations. At two-year follow-up, Dainer and colleagues showed no recurrent dislocations and 93% good to excellent results with arthroscopy alone, but a 27% recurrence rate and only 73% good to excellent results with concomitant lateral release.67 Jensen and Roosen concluded in a nonrandomized trial that lateral capsulotomy offered no advantage in preventing chondromalacia following acute patellar dislocation.68 More recently, Panni and coworkers showed that lateral release was less favorable in treating instability than pain. Threeyear results showed 72% satisfactory outcomes, dropping to 50% at 8-year follow-up with only 60% return to sports.69 There is considerable controversy in the concept of balancing the patella with a lateral release because it may contribute to lateral patellar dislocation instead of helping prevent it. Desio and associates showed in a biomechanical cadaveric model that the intact lateral retinaculum actually prevents lateral patellar displacement, contributing 10% of the restraining force. In a recent biomechanical study, Christoforakis and colleagues found that the force required to displace the patella 10 mm following lateral release was reduced by 16% to 19% from 0 to 20 degrees of knee flexion.70 Clinically, several studies have confirmed these findings, reporting recurrent lateral dislocations almost exclusively in groups treated with lateral release.15,67,68 In addition to recurrent lateral problems, iatrogenic medial subluxation and dislocation following lateral release have been observed by several authors.59,71 Hughston and Deese reported on 54 patients with worsening symptoms following arthroscopic lateral release and found that 50% demonstrated medial subluxation or dislocation that was not present preoperatively.59 Partially based on this issue, a survey of the International Patellofemoral Study Group was conducted to determine the current views regarding lateral release. Results were published in 2004, showing that only 7% of respondents would consider a lateral release in a first-time lateral patellar dislocation with a tight lateral retinaculum, and 37% would consider a history of lateral patellar dislocation as a contraindication to lateral release.72 In light of these findings, one should be aware of the potential complications and use lateral release with caution in cases of acute lateral patellar dislocation.

Medial Retinacular Repair Disruption or stretching of the medial retinaculum and MPFL always accompanies lateral patellar dislocation. Therefore, the mainstay of early surgical treatment in the acute first-time patellar dislocation is repair or reefing of the medial soft tissue structures, often accompanied by lateral release. In 1978, Boring reported on immediate


s urgical repair of the acute patellar dislocation in 17 patients, of which 8 had repair or reefing of the medial retinaculum. In all of the surgical groups, there was no recurrent dislocation, but 12 knees were described as painful at follow-up. Fourteen patients were satisfied with their outcome, and there was no difference in outcome between medial retinacular reefing and medial transfer of the patellar tendon.73 Cash and Hughston also reported on a group treated with acute medial repair. Although the details of their repair are not described, they reported no recurrent dislocations and no subsequent operative reconstruction in this treatment group. Good to excellent subjective results were reported in 91% of those with contralateral congenital extensor mechanism abnormality and in 80% of those with a normal contralateral knee.54 Vainionpaa and colleagues prospectively reviewed 55 acute dislocations treated with medial retinacular repair, augmented with lateral release in 37 for tight lateral retinaculum with lateralization of the patella. Dislocation recurred in only 9%. Despite 80% good to excellent results, the incidence of discomfort, snapping, and giving way noticeably increased over the 2-year follow-up period. One patient had loss of motion requiring manipulation at 12 weeks.15 In 1993, Harilainen and Sandelin prospectively studied 53 patients treated with medial retinacular suturing or reefing and lateral capsular release. At an average of 6.5 years of follow-up, the redislocation rate was 17%, with all occurring in women.74 Maenpaa and Lehto performed medial reefing in 270 patellar dislocations, with concomitant release of the lateral retinaculum in 235. The overall subjective result was good to excellent in 70% with a recurrence rate of 17%. In accordance with other authors’ findings, the subjective results and recurrence rates were less favorable with a prior history of instability and a nontraumatic mechanism.75 In 2005, Buchner retrospectively studied operative treatment with medial retinacular repair combined with a lateral release, with an average 8 years of follow-up. The redislocation rate was 27% and statistically similar to nonoperative and arthroscopy groups. At follow-up, the Tegner activity score was 4.5, the Lysholm score was 85, and subjective success was realized in 80%. All were statistically similar to nonoperative and arthroscopy groups.61 Also in 2005, Nikku reported on an operative group of 63 patients treated with repair of medial retinaculum or augmentation of the MPFL, with a 7-year follow-up. Fifty-four had a concomitant lateral release. Although 67% had episodes of postoperative instability, recurrent dislocation occurred in only 31%, demonstrating no statistical difference from the nonoperative group. Good to excellent results were found in 67%.62

Medial Patellofemoral Ligament Repair and Augmentation Repair or reefing of the medial retinaculum often does not completely address the medial-sided pathology after acute patellar dislocation. The importance of the MPFL for stability of the patella has been proved in cadaveric models, and several studies have shown a high incidence of avulsion of the MPFL from the adductor tubercle. Repair of retinacular injury does not restore continuity of the medial

restraints in cases of MPFL avulsion from the adductor tubercle. Continuity can be restored by direct repair, augmented repair, or reconstruction with graft at the site of injury. Reconstruction is usually reserved for cases of recurrent dislocation and will be discussed in depth in the following section. In 1996, Sallay and associates were the first to report on direct repair of the MPFL. Twelve patients were evaluated at 2-year follow-up; there were no redislocations, although four had episodes of sharp pain that may have represented subluxation. Good to excellent results were found in only 58% with an average Lysholm score of 81. After 4 weeks of immobilization, two patients suffered loss of motion requiring manipulation under anesthesia.16 Ahmad and coworkers also reported on direct repair of the MPFL. A limited series of eight acute patella dislocations were treated with direct repair of the MPFL to the adductor tubercle along with lateral release and repair of the vastus medialis obliquus (VMO) to the adductor magnus tendon. At 3 years’ follow-up, the average Kujala score was 92, and patient satisfaction was 96%. Despite these impressive results, athletes were able to return to only 86% of their preinjury level.76 Although several augmentation procedures were previously described, Gallie and Lemesurier were the first to report a “reconstruction” of the medial structures with graft in 1924. They described a procedure “anchoring” the patella in place with a strip of fascia to an isometric point on the medial femoral condyle. The procedure was performed on seven patients with no recurrence and “perfect functional results.”3 Since then, several authors have reported on augmentation procedures with less than perfect results. In 1993, Avikainen and associates performed augmentation of the MPFL with the distal 8 cm of adductor magnus tendon in 14 patients, 10 with acute dislocation. There was one recurrence at 2.5 years. There were 86% good results, but no excellent results.77 Recently, Nomura published the 5-year results of an augmented repair of the MPFL with a slip of the medial retinaculum. Despite recurrent subluxation in four of five knees, excellent results were reported in three of five, with an average Kujala score of 97.78 Although there have been favorable results with both MPFL repair and augmentation of the MPFL, there are no randomized, prospective studies comparing them to each other or to nonoperative treatment. Further investigation is needed before these procedures can be recommended in the case of acute patellar dislocation.

REHABILITATION A structured rehabilitation program is essential following acute patellar dislocation, despite treatment method. The program should be supervised by a certified physical therapist or athletic trainer familiar with these injuries. Initial goals should be to advance weight-bearing and regain both active and passive range of motion. Subsequently, closed kinetic chain strength training and proprioceptive exercises should begin, followed by functional and sportspecific training. The ultimate goal should be a stable, functional, and asymptomatic knee with strength equal to the uninjured side.

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Return to play should be allowed only when the following criteria have been met: Subjectively, there should be no pain, swelling, or sensation of instability. Objectively, there should be no effusion, no tenderness or apprehension, and a full range of motion without pain. Quadriceps strength should be at least 80% of the contralateral side, as determined by functional testing. Once running and cutting can be performed without symptoms, the athlete is allowed unrestricted return to competition. The benefit of patellar bracing after dislocation is unclear. Effective bracing should augment the static and dynamic stabilizers of the patella.79 Dynamic MRI studies have shown improvement in the position of the laterally subluxated patella with bracing; whether this clinically extrapolates to a rapidly moving athlete is unclear.80,81 Unfortunately, no randomized, prospective studies evaluating patellar bracing for instability exist.

Authors’ Preferred Method Treatment of acute patellar instability requires a thorough history, physical examination, radiographic and MRI examination, and differentiation between instability and disability. Usually a large osteochondral fracture and instability are the predominant issues, and care must be taken to educate the patient regarding expectations and outcomes. An individualized treatment plan should be developed for each patient. In other words, care must be taken not to treat each patient the same. Rehabilitation is the usual treatment for the acute patellar dislocation. Immobilization in extension is usually the initial treatment for the first 10 to 14 days. Rehabilitation as outlined previously is then initiated. Rehabilitation is chosen both to strengthen and increase endurance in the operative candidate unless a large osteochondral fracture is present, in which case operative treatment is initiated. The operative patient undergoes an examination under anesthesia and diagnostic arthroscopy as part of the surgical procedure. It is imperative to rule out other forms of instability, such as anterior cruciate instability. In addition, chondral or osteochondral loose bodies or changes on the patella or trochlear groove are important considerations in the treatment algorithm. If an associated meniscal injury is encountered, it should be recognized and treated as well. Patellofemoral tracking can be assessed as well. Based on the previous discussion, decisions are made regarding proximal and distal realignment.

C

r i t i c a l

P

o i n t s

l

wo distinct groups of patella dislocations exist: those T with normal anatomy and a traumatic event, and those with predisposing anatomy and a history of subluxation without a traumatic event. l The medial patellofemoral ligament is the main restraint to lateral patellar subluxation. The medial retinaculum, medial patellotibial ligament, and lateral retinaculum are secondary restraints. l The medial patellofemoral ligament is nearly universally disrupted in lateral patellar dislocation. l The mechanism of dislocation can be a direct blow or an indirect rotation of the body on a valgus, flexed knee relative to a fixed foot. The indirect mechanism is more common. l Clinical examination should include palpation for defect in the medial retinaculum and evaluation of apprehension of the patella to a lateral force. l Imaging should include plain radiographs and MRI to evaluate for evidence of chondral and medial retinacular injury. l Head-to-head studies show no difference in outcome when comparing conservative with early surgical treatment in acute lateral patellar dislocations. l Surgical treatments include arthroscopic débridement, medial retinacular repair, medial patellofemoral ligament repair, and augmentation. Care should be taken to evaluate the location of the medial lesion because retinacular repair will not address avulsion of the medial patellofemoral ligament from the adductor tubercle. Lateral release should be done only in select cases. l Structured rehabilitation is essential for optimal recovery despite treatment method.

S U G G E S T E D

R E A D I N G S

Amis AA, Firer P, Mountney J, et al: Anatomy and biomechanics of the medial patellofemoral ligament. Knee 10(3):215-220, 2003. Fithian DC, Paxton EW, Post WR, Panni AS: Lateral retinacular release: A survey of the International Patellofemoral Study Group. Arthroscopy 20(5):463-468, 2004. Fithian DC, Paxton EW, Stone ML, et al: Epidemiology and natural history of acute patellar dislocation. Am J Sports Med 32(5):1114-1121, 2004. Insall J, Salvati E: Patella position in the normal knee joint. Radiology 101(1):101104, 1971. Stanitski CL: Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med 23(2):146-150, 1995. Stefancin JJ, Parker RD: First-time traumatic patellar dislocation: A systematic review. Clin Orthop 455:93-101, 2007.



S e c t i o n

C

Subluxation and Dislocation 2. Patellofemoral Instability: Recurrent Dislocation of the Patella Timothy Steiner and Richard D. Parker

Patellofemoral instability is a complex topic. Significant advances have occurred in our knowledge about the anatomy and function of the patellofemoral joint, which has resulted in a better understanding of the evaluation and treatment of patellar instability.

ANATOMY Stability of the patella depends on the complex balance of forces imposed by static restraints and dynamic stabilizers around the knee. The static restraints are twofold: the bony architecture of the patellofemoral joint and the surrounding soft tissue structures, primarily those of the medial retinaculum and medial patellofemoral ligament (Fig. 22C2-1). The dynamic restraints consist of muscular forces that act on the patella, especially the quadriceps (Fig. 22C2-2). The importance of each structure has been well studied, but only recently has the relative contribution of each been defined. Senavongse and Amis reported the biomechanical contributions of the articular, retinacular, and muscular stabilizers of the patella.1 When compared with an intact knee,

Figure 22C2-1 Static restraints of the knee. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

flattening of the lateral facet of the femoral trochlea had the greatest effect on patellar stability, reducing the force necessary for displacement by 70% at 20 degrees of knee flexion. Sectioning of the medial retinacular structures, including the medial patellofemoral ligament, reduced the displacement force by 49% in full extension, with lessening effects during knee flexion. Relaxing the vastus medialis had a smaller but more consistent effect on stability, reducing the force by 30% throughout the midrange of

Figure 22C2-2 Dynamic restraints of the knee. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Patella 1549

A

B

C

Figure 22C2-3 Anteversion of the femur. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

knee motion. The patella was found to be most unstable at 20 degrees of flexion, both in the intact knee and in all test groups. These quantitative findings help define the relative contributions of each factor, which warrant individual discussion. Although one may tend to focus on the knee and its surrounding structures, the entire lower extremity, from hip to foot, should be considered in the patient with recurrent patellar dislocation. For ease of discussion, lower extremity anatomy in this chapter is separated into its bony and soft tissue elements.

Bony Anatomy The bony anatomy of the femur, tibia, and patella contribute to the stability of the patella. Abnormalities of the femur include increased anteversion of the femoral neck, torsion of the femoral shaft, hypoplasia of the lateral femoral condyle, and dysplasia of the femoral trochlea. Tibial abnormalities include increased external tibial torsion and variable location of the tibial tuberosity. Morphology of the patella also plays an important role in its stability. Before discussing the individual bones, the overall alignment of the leg should be addressed. Abnormalities in alignment, genu valgum and genu varum, are dictated by the combined morphology of the femur and tibia. These abnormalities cause the quadriceps pull to be out of alignment with the trochlear groove, leading to a sidedirected vector on the patella. In genu valgum, this vector is directed laterally, which can lead to lateral dislocation if medial restraining forces are overcome.2 The anatomy of the entire femur is important in patellofemoral mechanics. At the proximal end, the version of the femur is a measure of the anterior or posterior projection of the femoral neck and head. In the transverse plane, this is defined as the angle between a line through the long axis of the femoral neck and a line through the center of the femoral condyles (Fig. 22C2-3). Normal femoral anteversion varies, with anatomic, biplane radiographic and computed tomography (CT) data ranging from 6 to 48 degrees, with most between 7 and 20 degrees.3 An increase in femoral anteversion causes the distal femur and

Figure 22C2-4 Torsion of femur and/or tibia. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

atellofemoral articulation to face medial when the femop ral head lies neutral in the acetabulum. A decrease in version, or retroversion, causes the opposite effect. Torsional deformity can also be present anywhere along the length of the femur, leading to a similar effect on the alignment of the patellofemoral joint or an amplification of abnormalities caused by increased anteversion of the femoral neck. Abnormalities in femoral rotation are often seen in combination with external tibial torsion, causing the patellas to point medially toward each other when the feet are facing forward (Fig. 22C2-4). These torsional abnormalities, alone or in combination, tend to displace the patella laterally by a side-directed force similar to that seen in genu valgum. Although distinctly different, this may appear as an increased quadriceps angle when viewed in the coronal plane only. The bony anatomy of the distal femur has a very different but equally significant role in stability of the patella (Fig. 22C2-5). Recognized by Albee nearly a century ago, the medial and lateral portions of the femoral trochlea act as a buttresses to displacement of the patella.4 Any reduction in the size of this buttress confers lessening resistance


Figure 22C2-6 Articular surface of patella. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Figure 22C2-5 Trochlear depth and patellar shape contribute to stability. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

toward subluxation or dislocation of the patella. Seen alone or in combination, this reduction in size may present in different ways. Trochlear dysplasia presents proximally as a shallow trochlear floor relative to the medial and lateral condyles, whereas a hypoplastic lateral condyle presents as an isolated deficiency in the size of the lateral condyle, as depicted by the height of the lateral side seen on an axial radiograph. At 45 degrees of flexion, the height of the lateral condyle should be 1 cm more anterior than the medial condyle. One must be careful not to be fooled by “illusory dysplasia,” or the appearance of a lateral condylar deficiency secondary to excessive rotational deformity of the femur.5 Multiple studies have demonstrated that the bony stability of the femoral trochlea is the most important stabilizer of the patella,1,6,7 and sufficient trochlear restraint may compensate for other anatomic deficiencies. The patella is a sesamoid bone of irregular shape that lies within the extensor mechanism of the knee. Its anatomy is well described, with a convex anterior surface and a complex, cartilage-covered posterior articular surface. The inferior pole is nonarticular, and the remaining superior pole is divided into medial and lateral facets divided by a central ridge. An additional odd facet at the most medial edge of the patella may be found. The lateral facet is longer and more sloped, and the subchondral bone density is highest at its proximal facet.8 These anatomic differences are likely adaptations derived to match the larger forces imparted by the larger, wider, and more prominent lateral femoral condyle. Wiberg devised a classification system in the axial plane, and Grelsamer devised one in the sagittal plane.9,10 A correlation exists between Wiberg type and lateral patellofemoral ligament width, suggesting a

evelopmental manifestation of muscular forces around d the patella.11 The contact area of the patella changes throughout the range of knee flexion (Fig. 22C2-6). As knee flexion increases, the contact area moves from the distal to the proximal pole of the patella, and the odd facet contacts only in deep flexion, where the lateral and odd facets separately contact the femoral condyles.12 Unfortunately, the complex shape of the patella and matching contours of the femoral trochlea are not seen on plain radiographs because the varying thickness of articular cartilage is radiolucent. The bony anatomy of the tibia is also important in the stability of the patella. As previously discussed, external tibial torsion often accompanies abnormalities in femoral anteversion. The tibial tuberosity is the distal attachment of the extensor mechanism, and its location on the tibia affects the alignment of the patellar tendon. The combination of external tibial torsion and lateral placement of the tibial tuberosity can cause a deleterious change in the quadriceps angle. One must not forget to include the bony anatomy of the foot. Although distant from the knee, deformities in the foot cause changes in the alignment of the lower extremity. Pronation of the foot is easily seen on physical examination as valgus in the heel. Excessive valgus at the subtalar joint causes obligatory internal rotation of the tibia, whereas varus causes external rotation.

Soft Tissue Anatomy The soft tissue elements that contribute to patellar stability include muscles, tendons, and ligaments that act as static restraints and dynamic stabilizers of the patella. The quadriceps muscle is intimately involved because of its direct attachment to the patella by way of the quadriceps tendon. The ligamentous structures are particularly important because of their role as checkreins in the static stability of the patella, on both the medial and lateral sides. These ligamentous structures arise within the retinacular tissue and include patellofemoral and patellotibial ligaments. The quadriceps muscle is the most important dynamic stabilizer of the patella. It is named for its four portions: rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis (Fig. 22C2-7). Only the rectus femoris crosses both the hip and knee joints, with its origin at the anterior inferior iliac spine of the pelvis. The other muscles originate

Patella 1551

on the proximal shaft of the femur. All four muscles insert in a layered arrangement into the proximal half of the patella through the quadriceps tendon, with the rectus femoris inserting most anterior and the vastus intermedius most posterior. All but the vastus intermedius continue as a tendinous expansion over the top of the patella to become part of the patellar tendon.13,14 The vastus medialis and lateralis also provide connection to the tibia through the attachment of their investing fascia to the medial and lateral patellar retinacula, respectively. Each portion of the quadriceps muscle imparts a different force vector based on the angle of its tendinous insertion. In 1968, Lieb and Perry measured the obliquity of the quadriceps muscles with respect to the long axis of the femur in the frontal plane13: the vastus lateralis was 12 to 15 degrees lateral, and the rectus femoris was 7 to 10 degrees lateral. They described the vastus medialis as consisting of two distinct parts, which they called the vastus medialis longus and vastus medialis oblique (VMO), with a marked difference in the angle of their fibers. The angle of fibers in the oblique portion measured 50 to 55 degrees medially, but only 15 to 18 degrees medially in the longus portion. They also reported distinctly different anatomy, with oblique fibers originating off the intermuscular septum and adductor tubercle and inserting on the proximal third of the medial patellar border. Farahmand and colleagues reported similar angles of 15 and 47 degrees for the long and oblique portions, respectively,7 and Andrikoula and associates recently reported 45 degrees from the rectus for the vastus medialis as a whole.15 Despite these numbers, some estimate the oblique portion to have an angle as high as 55 to 65 degrees.16 Special attention has been paid to the oblique portion of the vastus medialis and also of the vastus lateralis. Hallisey

Figure 22C2-7 Quadriceps musculature. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

and coworkers described the vastus lateralis oblique with distinct anatomy from the long portion. The oblique originates off the lateral intermuscular septum with three distinct patterns of insertion. The mean angle of insertion was statistically different by sex at 48 degrees in men and 38 degrees in women.17 Andrikoula recently reported 26 degrees with respect to the rectus femoris, whose own vector lies lateral to the femur.15 These angles are significantly higher than the 12 to 15 degrees for the entire vastus lateralis previously reported by Lieb and Perry.13 The high angle of insertion of the medial and lateral oblique muscle bellies results in a large portion of the muscular force directed perpendicular to the long axis of the thigh. Although not proved, these perpendicular forces may serve as dynamic stabilizers of the patella in addition to their role as knee extensors. Recent work by Panagiotopoulos and colleagues has shown that the distal attachment of the VMO may also dynamically tension the medial patellofemoral ligament, providing additional medial support to the patella, confirming previous work by Sallay and associates.18,19 Although the quadriceps muscles provide extension to the knee and dynamic balance to the patella, the remaining soft tissue structures provide static restraint. Both the medial and lateral retinacula contain intrinsic fibers and thickenings that have been described as distinct ligamentous structures named the patellofemoral, patellotibial, and patellomeniscal ligaments (Fig. 22C2-8). Additionally, a thickening on the lateral side runs transversely from the iliotibial band to the patella and is named the iliopatellar band (Fig. 22C2-9). Kaplan first described the epicondylopatellar ligaments, which are now called patellofemoral ligaments.20 Warren and

Figure 22C2-8 Medial patellofemoral ligaments. MPFL, medial patellofemoral ligament; MPML, medial patellomeniscal ligament; MPTL, medial patellotibial ligament. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

1552 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Figure 22C2-9 Lateral thickening of iliotibial (IT) band to the patella called the iliopatellar band. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Marshall subsequently described the anatomy of the medial side of the knee in a three-layered pattern; the medial patellofemoral ligament (MPFL) resides in the second layer, deep to the vastus medialis.21 Although Reider and colleagues found a distinct ligament in only 35% of knees, most authors report a nearly universal existence of the structure.11 The MPFL originates near the adductor tubercle, with additional fibers arising from the superficial portion of the medial collateral ligament, and it inserts on the proximal two thirds of the medial border of the patella, with additional fibers inserting on the quadriceps tendon. The MPFL is 5 cm in length and averages 1.9 cm in width, becoming wider at its insertion than its origin.15,22 The tensile strength of the ligament has been found to be 208 Newtons.23 The anatomy of the patellotibial and patellomeniscal ligaments is less well studied. On the medial side, they reside deep to the patellofemoral ligaments in the third layer.21 The medial patellotibial ligament (MPTL) originates at the inferomedial border of the patella and inserts on the anteromedial tibia. Its insertion is 1.5 cm below the joint line and 1.5 cm medial to the patellar tendon, lying 20 to 25 degrees oblique to the patellar tendon.18 The medial patellomeniscal ligament (MPML) originates near its patellotibial counterpart on the inferomedial border of the patella. It inserts broadly on the anterior horn of the medial meniscus, with fibers fanning out posteriorly.15 Both the MPML and MPTL are relatively thin and only 3 to 6 cm. No studies have quantified their tensile strength.18 The lateral retinaculum is composed of only two layers. The superficial oblique retinaculum spans the iliotibial band to the patella, blends with the quadriceps expansion, and becomes thinner in its distal portion. The deep transverse retinaculum is thicker but ends at the inferior border of the patella. It consists of the lateral patellofemoral, patellotibial, and iliopatellar ligaments. In distinction from the medial side, no patellomeniscal ligament exists; rather, fibers of the patellotibial ligament insert on both the proximal tibia near Gerdy’s tubercle and on the anterior horn of the lateral meniscus.14,24 The size and existence of the lateral patellofemoral ligament (LPFL) is variable. Reider and associates identified the ligament in only 13 of 48 specimens but noted a correlation between ligament width and Wiberg shape of the patella.11 Like the MPFL, recent studies have shown nearly universal existence of the LPFL.25 Although no lateral sectioning studies exist, several authors have recognized

medial patellar instability following a lateral release, which severs the LPFL.26-28 Two studies have examined the tension of the LPFL during knee motion. Luo showed a significant increase in LPFL tension at 30 degrees of flexion during passive knee motion in vitro, whereas Ishibashi showed maximal tension at 120 degrees of flexion in vivo in patients with lateral patellar instability.29,30 Most patellar dislocations are lateral, and biomechanical studies have concentrated on the importance of the medial ligaments in patellar stability (Fig. 22C2-10). Conlan published the first biomechanical study that focused on the medial supporting structures of the knee. Using sequential sectioning and a laterally directed load with the knee in full extension, he demonstrated that the MPFL contributed 53% of the restraining force to lateral displacement; the

Figure 22C2-10 Most dislocations of the patella are lateral because of the sum of the vectors directing the patella laterally. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Patella 1553

TABLE 22C2-1 Results of the Sectioning Studies Percentage of Patellar Stability Contribution Determined by Study Structure Contributing to Static Patellar Stability

Conlan et al (1993)187

Desio et al (1998)159

Hautmaa et al (1998)9188

Panagiotopoulos et al (2006)18

Medial patellofemoral ligament Medial patellotibial ligament Medial patellomeniscal ligament Medial retinaculum Lateral retinaculum

53

60

50

50

5

3

25

13

22

13

25

24

11 —

3 10

5 —

13 —

MPML was a secondary restraint, contributing 22%. In a similar work, Desio later confirmed these findings at 20 degrees of knee flexion, with the MPFL and the MPML contributing 60% and 13%, respectively. Interestingly, the lateral retinaculum was also found to contribute 10% of the restraining force to lateral displacement. Conversely, Hautmaa measured displacement of the patella under constant load as the medial structures were sectioned in two different sequences. Sectioning of the MPFL caused a 50% increase in displacement in both cases, whereas sectioning the patellotibial and patellomeniscal ligaments together increased displacement by 25%. Recent studies have confirmed the results of these early works. Panagiotopoulos measured displacement under a constant load in a sequential sectioning study to determine the relative contribution of each structure to static patellar stability. The MPFL contributed 50%, the MPML contributed 24%, and the MPTL and medial retinaculum each contributed 13%.18 The results from all the sectioning studies mentioned are summarized and referenced in Table 22C2-1.

CLINICAL PRESENTATION The patient with recurrent patellar dislocation may or may not have had a classic episode of acute patellar dislocation. Often, the patient complains that the knee “gives way” and commonly reports weakness of the leg. Occasionally, the

TABLE 22C2-2 Most Common Symptoms of Patellofemoral Subluxation Symptom

Patients Reporting (%)

Pain going down stairs Pain on flexion Weakness Giving way Swelling Pain going up stairs Locking

76 75 73 61 60 54 50

From Henry JH: Conservative treatment of patellofemoral subluxation. Clin Sports Med 8(2):261-278, 1989.

patient reports feeling the kneecap “slide out of place” or “pop” into or out of place. The femur is often in a position of internal rotation on a fixed tibia, regardless of whether episodes occur during daily activities or sporting events. Many patients with recurrent instability complain of pain. In a study of 465 patients with the diagnosis of patellofemoral subluxation, pain represented the top two most commonly reported symptoms (Table 22C2-2). A careful history is essential to separate pain related to instability from other patellofemoral problems.

PHYSICAL EXAMINATION A careful and complete physical examination is necessary for accurate diagnosis and proper clinical decision making. Examination should not be limited to the affected knee but should include examination of the entire lower extremity of both sides. Information should be gathered by examining the patient in the upright, sitting, and supine positions while barefoot and dressed in shorts. The physical examination should begin with observation. Obesity, posture, and body habitus should be noted. Skin should be examined on the extremities; prior surgical and traumatic scars should be noted, as should any evidence of vasomotor abnormality. Any muscular asymmetry of the thigh or calf should be confirmed with circumferential measurements at a standard distance above and below the knee. The size and location of the vastus medialis muscle belly should be noted because a lower insertion is considered more efficient in resisting lateral subluxation.31

Quadriceps Angle Because the quadriceps angle, or Q angle, can be measured in the standing, sitting, or supine positions, it is discussed first. The Q angle is a commonly used measurement in the evaluation and treatment of patellofemoral disorders (Fig. 22C2-11). Because it is easily measured, it is often used in clinical practice. However, it is important to stress that the Q angle should not be used as the sole factor in surgical decision making in recurrent patellar subluxation.32 The Q angle was first described in 1847 by Cruveilhier as the angle between the vector of the quadriceps tendon and the vector of the patellar tendon.33 Clinically, these


the Q angle at varying degrees of knee flexion and found decreasing values as flexion increased,37 a finding similar to that of Sojbjerg and coworkers.38 In general, the Q angle decreases from supine to standing to sitting examination. It is widely accepted that females have higher Q angles than males, an observation that has been attributed to the wider pelvis, shorter femur, and increased genu valgum seen in females.39,40 However, Horton demonstrated that males actually have a longer distance between greater trochanters and that there is no relationship between hip width and Q angle. Further analysis showed that although the ratio of femur length to hip width was greater in females, it did not correlate to Q angle. When measuring the Q angle with the leg extended, the value may be erroneously low if the patella lies superior and lateral to the trochlear groove. This should be considered during the examination, especially in those with patella alta, a J sign, or obvious lateral displacement of the patella. On the contrary, the Q angle may be falsely elevated by excessive femoral anteversion, femoral torsion, external tibial torsion, and genu valgum.

Standing Examination

Figure 22C2-11 Standing Q angle. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

vectors are simplified as lines from the anterior superior iliac spine to the midpatella and from the midpatella to the tibial tubercle. The logic behind the Q angle is best summarized with a two-dimensional free body diagram of the patella. The vertically oriented resultant vectors balance each other out, whereas the horizontally oriented resultant vectors add up to a large laterally directed vector (see Fig. 22C2-10). The theoretical problem then becomes clear: a larger Q angle results in a larger laterally directed force that must be resisted by the bony and soft tissue restraints previously discussed. When the restraints are overcome, dislocation or instability may result. Although a larger Q angle theoretically causes more lateral force, the clinical significance is unclear. Aglietti and associates demonstrated no significant difference in the Q angle of patients with patellar subluxation compared with healthy controls,34 and Fairbank and coworkers showed no difference between adolescents with and without knee pain.35 Because the Q angle can be measured in the standing, supine, or sitting position, a complete assessment should include all three. Insall’s original description of 50 normal knees with an average Q angle of 14 degrees did not specify the position of measurement. A review of the literature demonstrates a range from 8 to 16 degrees for males in the supine position and from 15 to 19 degrees in females. Woodland showed that the standing Q angle was statistically higher than supine for both male and female subjects, although only by roughly 1 degree.36 Q angles in the standing position range from 11 to 20 degrees in males and 15 to 23 degrees in females. Johnson and colleagues examined

Standing alignment should be viewed from the front, back, and side. In the sagittal plane, recurvatum may indicate systemic hypermobility, and lack of full extension may indicate fat pad impingement or flexion contracture. Coronal plane observations may include leg-length discrepancy, patella alta or baja, and genu varum or valgum. A sharp varus angulation in the proximal tibia may be present and is termed the bayonet sign. Excessive femoral anteversion and internal tibial torsion may give the appearance of “squinting,” or inward pointing, of the patella. The patella should be observed with the feet in a comfortable position and with the feet facing forward; those with excessive external tibial torsion may show squinting only in the latter position. If suspected, abnormalities in femoral anteversion should be measured by observing maximal prone internal and external hip rotation as well as rotation of the leg at the position of maximal prominence of the greater trochanter.41 Similarly, transmalleolar axis and thigh-foot angle should be used to confirm excessive tibial torsion, although the latter does not set apart abnormalities of the foot. These rotational abnormalities may be part of a larger constellation of findings called miserable malalignment, in which squinting of the patella from excessive femoral anteversion and outward tibial rotation are accompanied by tibia vara, patella alta, and an increased quadriceps angle.42 Finally, the feet should be examined in the weightbearing position. From behind, hindfoot alignment can be observed; valgus may indicate foot pronation, a compensatory position that allows a plantigrade foot in subjects with genu varum or tibia vara. Foot pronation causes obligate internal tibial rotation, with little change noted at the knee joint.43,44 Although controversial in the pathogenesis of patellofemoral pain, this combination of findings may alter patellofemoral mechanics.45,46 The conclusion of the standing examination should include an observation of the patient’s gait. Observation of the whole body should note antalgia or limping. A quadriceps avoidance gait with reduced knee flexion in stance

Patella 1555

A

B

Figure 22C2-12 A, Normal patella position on physical examination. B, Patella alta; note the patella tilting upward. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

may be present.47 A Trendelenburg gait with a drop in the contralateral pelvis during stance phase indicates gluteus medius weakness; this change in pelvic obliquity tightens the ipsilateral iliotibial band, a common source of knee pain. Then, attention should focus on the patella during gait. Catching, jumping, or any other abnormal movements should be noted as the patella enters and leaves the trochlea near full extension.

Sitting Examination The patient should next be examined in the sitting position, with the knees flexed 90 degrees over the table. The position of the patella and the tibial tubercle should be observed. Patella alta or baja is easily observed from the side (Fig. 22C2-12). Normally, the patella should sit at the distal end of the femur with the proximal pole in line with the anterior portion of the femur. In patella alta, the patella will lie more proximal with its anterior surface tipped up. If there is also patellar tilt, the knees will have the so-called grasshopper-eyes appearance. The position of the tibial tubercle should be observed in relation to the center of the patella. In flexion, the patella is centered in the trochlea, and the tibia derotates (Fig. 22C2-13). Any deviation of the tubercle laterally from the center of the patella is called the tubercle sulcus angle (Fig. 22C2-14). In normal subjects, this angle averages 4 degrees,37 and an abnormal angle has been postulated to be greater than 10 degrees.48 Because the patella is centered in the trochlea at 90 degrees of knee flexion, the tubercle sulcus angle may correlate with the radiographic measurement of tibial tubercle–to-trochlear groove (TT-TG) distance.

Figure 22C2-13 The patellar tendon and tibial tuberosity should line up with the knee flexed 90 degrees. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)


Next, the musculature surrounding the knee should be examined. The VMO belly is important in dynamic stabilization of the patella. Lieb and Perry concluded that the only function of this muscle was for alignment of the patella.13 Electromyographic studies subsequently showed that the VMO was most active in the last 30 degrees of extension, a time in which the patella is unconstrained by the trochlea.49,50 The size and location of insertion of the VMO are of importance. A well-developed and symmetrical VMO is ideal, with muscle bulk arising near the adductor tubercle and inserting on the proximal third of the patella. A more distal insertion on the patella provides even more resistance to lateral movement of the patella.31 Finally, tracking of the patella should be observed in the sitting position. The term J sign refers to an abnormal tracking pattern in which the patella sits lateral to the femoral sulcus in full extension; the movement of the patella appears in the shape of an upside-down J as the knee goes from flexion into full extension. Conversely, the patella starts laterally and makes an abrupt shift medially as it enters the femoral trochlea at the initiation of flexion. Although tracking can be seen during a weightbearing squat, tracking during both active and passive motion can be observed in the sitting position. An exact cause of this pathologic motion has not been defined, but Post has postulated that VMO deficiency may be to blame if the J sign is observed during active motion, and underlying bone morphology and soft tissue imbalance may be the cause during passive motion.51 The presence of a J sign during active or passive motion is clearly abnormal, and the J sign did not appear in a study of 210 asymptomatic men and women.37

Figure 22C2-14 Tubercle sulcus angle. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Supine Examination The patient should be asked to lie comfortably on the examination table. The knee is first observed for evidence of effusion. A large effusion is often visible as a swelling in the suprapatellar pouch and an obliteration of the normal dimples adjacent to the patellar tendon at the joint line. Unless the patella has recently dislocated, a large effusion is usually absent. It should be noted that a large effusion may accompany an acute patellar dislocation, but it should not be tense because of the necessary disruption of the retinaculum. A ballotable patella without obvious visual clues may indicate a moderate effusion. If not readily observed, the joint should be milked for evidence of a small effusion. If present, even a moderate effusion can cause reflex inhibition of the quadriceps muscle. Inhibited by only 20 mL of intra-articular saline, the vastus medialis has been shown to be even more sensitive to effusion than the rectus femoris or the vastus lateralis.52 Care should be taken to differentiate an intra-articular effusion from extra-articular swelling, which presents as immobile, thickened soft tissue. Any abnormalities in skin temperature and color around the knee should also be assessed as possible indicators of diffuse synovitis or infection. Structures around the knee should be systematically palpated (Fig. 22C2-15). First, the peripatellar structures should be evaluated. Tenderness at the proximal and distal poles of the patella may indicate insertional tendinitis, and tenderness within the quadriceps or patellar tendon may indicate more diffuse tendinitis. Pain at the medial border of the patella may represent injury to the MPFL, which should be palpated along its length to its origin at the adductor tubercle. The insertion of the nearby VMO should also be palpated for pain or defect. In patients with prior operative scars, the operative area should be examined for neuroma. These areas are highly innervated,53,54 and a diagnostic injection of local anesthetic can be used to confirm a suspected diagnosis. The medial articular facet can be palpated by displacing the patella medially with the knee in 30 degrees of flexion; the patella tilts laterally,

Figure 22C2-15 Palpation of the peripatellar structures is important. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Patella 1557

Figure 22C2-16 Lateral pull test; with contraction, the patella should move a bit laterally. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

uncovering the medial facet.55 Pain on the lateral border of the patella is commonly found in excessive lateral pressure syndrome and should be differentiated from pain on the lateral femoral condyle as a result of osteochondral fracture after dislocation. Finally, the medial and lateral joint lines should be evaluated for tenderness that may represent meniscal tear, arthrosis, or tear of the patellomeniscal ligament along its course to insertion on the anterior horn of the medial meniscus.55 Active and passive range of motion should be evaluated next. Any deficit or asymmetry should be measured for future reference. During motion, the patella should be observed for abnormal tracking and palpated for patellofemoral crepitation. A resisted straight-leg raise should be performed to rule out disruption or injury to the extensor mechanism. Evaluation of patellar mobility is an essential part of the examination and should include passive testing for patellar tilt, glide, apprehension, and compression with comparison to the contralateral leg. The position of the knee is important in evaluating these criteria because the patella becomes captured in the femoral trochlea by 30 degrees of flexion. If this difference in stability is not found, the possibility of underlying trochlear dysplasia or patella alta should be considered. Before passive stability testing, the movement of the patella under isometric quadriceps contraction should be observed in full extension. During this lateral pull test, the position of the patella should be observed before, during, and after contraction; normally, the patella should move straight superiorly or superiorly and laterally in equal proportions, and any excessive lateral movement indicates an abnormal pull of the quadriceps tendon48 (Figs. 22C2-16 and 22C2-17).

Figure 22C2-17 The resultant lateral vector. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Patellar tilt is used to determine whether the medial or lateral soft tissue restraints are excessively tight and should be performed with the knee extended and the quadriceps relaxed (Fig. 22C2-18). The examiner pushes down on the medial patella while lifting the lateral patella, taking care not to dislocate the patella. Normally, the patella should correct to neutral with the anterior surface of the patella parallel to the examination table. Decreased tilt, or

Figure 22C2-18 Passive patellar tilt. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)


inability to reach the neutral position, is indicative of tight lateral structures. Patellar glide demonstrates the integrity of the medial and lateral patellar restraints by passively translating the patella to each side with the quadriceps relaxed (Fig. 22C2-19). Lateral glide is a test of the medial structures, and medial glide is a test of the lateral structures. Although Kolowich and colleagues described this test with the knee in 20 to 30 degrees of flexion, examination in full extension isolates the soft tissue restraints by removing the bony contact of the patella in the trochlea.48 The degree of glide is graded in four levels, determined by the amount of translation relative to the width of the patella divided into quadrants. A deficient medial or lateral restraint is defined as glide of three or four quadrants in the respective direction.48,51 Grading of both patellar tilt and glide is highly variable among observers,56 which has led to the use of instrumented measurement of patellar displacement.57-59 Skalley and associates attempted to quantify normal medial and lateral motion with a handheld force gauge and concluded that medial and lateral displacement was limited by ligamentous restraints only with manually produced displacement more reproducible.60 Fithian and associates used a similar device to quantify patellar balance as the difference between instrumented medial and lateral displacement with good interobserver and intraobserver reliability.57 Despite the benefits of objective translational data, these instruments are not widely used in clinical practice. Translation of the patella that causes a feeling of impending dislocation is called apprehension.61,62 The apprehension test is the classic examination in acute patellar dislocations and is often positive in patients with recurrent dislocations. The patella is translated laterally with the knee flexed 20 to 30 degrees and the quadriceps relaxed. In a positive test, the patient feels the patella about to dislocate and contracts the quadriceps involuntarily. The patient may look apprehensive about a recurrent dislocation.61 Although pain usually accompanies the apprehension, the latter is considered the major element of a positive test.

The apprehension test may also be used for medial instability, which is most commonly an iatrogenic injury following a lateral release.26-28 Several other tests for medial subluxation should be used to evaluate patients with failed patellofemoral surgery. Fulkerson has described a test that attempts to reproduce the reduction of a medially subluxated patella.63 The patella is manually displaced medially as the knee is flexed; the test is positive if sudden relocation of the patella into the trochlear groove reproduces the symptoms. The gravity subluxation test is also used for evaluation of iatrogenic medial dislocation from previous lateral release.64 The patella is displaced medially while the patient is in the lateral decubitus position; an inability to actively reduce the patella against gravity by muscular contraction demonstrates incompetence of the lateral supporting structures. Compression of the patella against the trochlea may cause pain in patients with articular lesions, which may be the result of a previous patellar dislocation. Compression should be done with the knee in fixed positions of flexion, taking care to compress only the patella and not the surrounding soft tissue structures. The degree of knee flexion may predict the location of articular damage on the patella because the contact area moves proximally on the patella as flexion increases. Suspicion of an articular cartilage lesion should be confirmed with imaging studies for operative planning. The supine examination should be concluded with evaluation of lower extremity flexibility. Tightness is most commonly encountered in the hamstrings, where excessive tightness requires more quadriceps force for extension of the knee during gait; the result is increased pressure across the patellofemoral joint. Hamstring flexibility is best assessed by measuring the popliteal angle. In the supine position, the hip is flexed 90 degrees, with the contralateral leg extended. The maximal extension of the knee in this position is a measure of hamstring tightness. Gastrocnemius and soleus tightness should also be assessed with the patient in the supine position. The flexibility of both muscles can be judged by ankle dorsiflexion with the knee extended. With the knee flexed, the gastrocnemius is relaxed, and the soleus is isolated. In both positions, the ankle should dorsiflex 15 to 20 degrees past neutral. Limitation causes a compensatory increase in subtalar pronation, increasing internal tibial rotation during gait. Iliotibial band tightness has been correlated with lateral knee pain and should be assessed with Ober’s test.65 In the lateral decubitus position with the affected knee up, the leg abducted, brought into full extension, and then adducted toward the table. Tightness or pain may be elicited. Comparison should be made with the opposite side.

IMAGING Radiographs

Figure 22C2-19 Patellar glide. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)

Imaging of the patellofemoral joint should begin with a complete series of plain radiographs in all cases of recurrent patellofemoral dislocation. Radiographs should include standing anteroposterior, 45-degree standing posteroanterior, 30-degree flexion lateral, and axial views. If any

Patella 1559

malalignment is detected on clinical examination, a standing, full-length alignment film should also be obtained.

The Anteroposterior Radiograph In recurrent patellar dislocation, the standing anteroposterior and 45-degree posteroanterior views offer little useful information. Patella fractures and bipartite patella are most easily seen on these views. Additionally, joint space narrowing, subchondral sclerosis, and osteophytes associated with tibiofemoral arthritis are easily seen. With the knee in neutral rotation, medial and lateral position of the patella can be quantified, but subluxation is best quantified on the axial view. Although patella alta and baja can be seen, they are best quantified on the 30-degree lateral view.

The Lateral Radiograph The 30-degree flexion lateral view provides a wealth of information about the patellofemoral joint, including morphology of the femur as well as size, shape, and position of the patella. To provide the most useful and accurate information, the radiograph must be a true lateral, showing overlap of the distal and posterior cortices of the medial and lateral femoral condyles.

A

B

D

E

The height of the patella is most easily seen on the lateral radiograph. Because patella alta is a known risk factor in recurrent patellar dislocation, height of the patella should always be determined. A number of techniques have been described using the lateral radiograph (Fig. 22C2-20). The method of Blumensaat determines the height of the patella based on the projection of the roof of the intercondylar fossa on a 30-degree flexion lateral (see Fig. 22C2-20F).66 The anterior projection of this line should intersect the inferior pole of the patella; if the line passes below, patella alta is present. This method is hindered by anatomic and positional variation. The knee must be in exactly 30 degrees of flexion for accurate determination of patellar height. In addition, Brattström pointed out a second potential problem with this method after demonstrating a wide variation in the angle of Blumensaat’s line. On the lateral radiographs of 100 patients, he found that the angle between Blumensaat’s line and the longitudinal axis of the femur ranged from 27 and 60 degrees, showing that a 10-degree variation in the angle would equal a 10-mm difference in patellar height.67 Even when modified to normalize the angle of the line, Blumensaat’s method shows poor correlation with other patellar indices.68 The method of Labelle and Laurin requires the knee be flexed 90 degrees for the lateral radiograph, a position that

C

F

Figure 22C2-20 A, Insall-Salvati ratio. B, Grelsamer’s modification of the Insall-Salvati ratio. C, Blackburne-Peel measurement. D, Caton-Deschamps measurement. E, Labelle-Laurin measurement of patellar position. F, Blumenstaat’s measurement of patellar position. (Reprinted with the permission of The Cleveland Clinic Center for Medical Art & Photography © 2008.)


is used clinically to determine patella alta (see Fig. 22C220E). Using this method, patella alta is determined by the projection of the anterior cortex of the femur in relation to the proximal pole of the patella. In their original study, this line passed above the patella in 97% of knees. Based on these findings, patella alta is diagnosed by intersection of this anterior femoral line with any portion of the patella.69 Patellar height ratios are popular among clinicians because they are independent of knee flexion angle, easily recalled, and simple to use. The Insall-Salvati ratio was described in 1971 and has remained the most identifiable index for patellar height. It is based on the ratio of the length of the patellar tendon divided by the greatest length of the patella (see Fig. 22C2-20A). The normal ratio defined by the authors was 1.0, plus or minus 20%. Therefore, patella alta is defined as an Insall-Salvati ratio greater than 1.2.70 Unfortunately, difficulty in determining the exact insertion of the patellar tendon and abnormal morphology of the nonarticular portion of the patella may falsely alter this ratio. In addition, patellar tendon length varies between sexes in the normal population.71 For these reasons, a modified Insall-Salvati ratio was proposed by Grelsamer and Meadows in 1992.72 This modified ratio is defined as the distance from the inferior articular surface of the patella to the patellar tendon insertion divided by the length of the articular surface (see Fig. 22C2-20B). Using this method, patella alta is defined as a ratio greater than 2.0, a point at which only 3% of controls would be falsely identified as patella alta.72 In a recent study, the traditional Insall-Salvati ratio was found to be more reproducible; there was agreement in classification in 67% of radiographs using the traditional method, compared with 47% agreement using the modified method proposed by Grelsamer.73 Blackburne and Peel described a ratio that is independent of the length of the patellar tendon, once again citing the difficulty in measuring the true length of the patellar tendon (see Fig. 22C2-20C). Their ratio is based on the anterior projection of the tibial plateau and is defined as the ratio of the length of the perpendicular line from the lower end of the patellar articular surface to the tibial plateau line divided by the length of the articular surface. In their study of 171 normal knees and 58 with recurrent subluxation of the patella, they defined a ratio of 0.8 to be normal and a ratio greater than 1.0 to describe patella alta.74 Caton and Deschamps also devised a ratio to address the difficulty in measuring the length of the patellar tendon.75 Their ratio is defined as the ratio of the distance from the inferior articular surface of the patella to the anterosuperior border of the tibia divided by the length of the articular surface of the patella (see Fig. 22C2-20D). Patella alta is defined as a ratio greater than 1.2. A summary of the indices of patellar height is provided in Table 22C2-3. Several recent studies have compared the different techniques of measuring patellar height. In 1996, Berg looked at the Insall-Salvati, the modified Insall-Salvati, the Blackburne-Peel, and Caton-Deschamps indices using three blinded observers and radiographs of 15 asympto matic knees. The Blackburne-Peel ratio was found to be the most reproducible, having the lowest standard error and least intraobserver error. Interestingly, the authors

TABLE 22C2-3 Indices of Patellar Height Measurement

Normal

Alta

Baja

Insall-Salvati70

1.0 — 0.8 1.2 >2.0 >1.0 >1.2 Visual

30 degrees

No 60 degrees of flexion to full extension ++ Active or passive Quantitative 30 min Radiation exposure

No 45 degrees of flexion to full extension + Active or passive Quantitative or qualitative 20 min None

+++ Passive Quantitative 15 min Radiation exposure

Adapted from Muhle C, Brossmann J, Heller M: Kinematic CT and MR imaging of the patellofemoral joint. Eur Radiol 9(3):508-518, 1999.

In 1991, Shellock and associates introduced a new pulse sequence that allowed imaging of the patellofemoral joint during active motion, a way to quantify the effect of both static and dynamic patellar stabilizers.133 Brossmann and colleagues subsequently studied 13 patients with patellar maltracking and 15 controls with motion-triggered cinematic MR imaging.134 During active motion scans, there were significant differences in all measurement parameters between groups; these differences were not universally present during passive motion scans. Subsequent studies have confirmed these findings.135 Kinematic MRI provides useful information but is currently limited by availability. A summary of imaging modalities is presented in Table 22C2-7.

NONOPERATIVE TREATMENT Nonoperative treatment of chronic patellar dislocations with immobilization followed by rehabilitation has produced dismal results, with nearly half of patients having recurrent dislocations or continued symptoms. Immobilization following recurrent episodes of patellar dislocation is of little benefit, although it may be used in the short-term for patient comfort. An attempt at rehabilitation should be reserved for the patient who experiences only occasional dislocation and displays no obvious anatomic or radiographic abnormalities that may predispose to recurrent episodes. Those with dislocation in activities of daily living or gross anatomic deficiencies will likely need operative treatment. In some patient populations, a trial of rehabilitation is warranted to show commitment to getting well because surgical treatment often requires an extended period of postoperative rehabilitation for success. Although numerous prospective studies exist on the nonoperative treatment of acute patellar dislocation with rehabilitation, no studies exist on its use in recurrent patellar dislocation. If chosen, rehabilitation may be augmented by the use of a patellar orthosis if tolerated by the patient. Palumbo first proposed a brace with a pad to prevent lateral patellar translation, which proved subjectively beneficial in 39 patients with subluxation. Since that time, several kinematic MRI studies have examined the position of the patella with and without the use of a brace. Shellock and colleagues demonstrated qualitative improvement in patellar position in 76% of subjects and cited bony dysplasia and

patella alta as reasons for failure.136 In a subsequent study also using qualitative measures, they showed a similar rate of improvement but cited obesity and patella alta as reasons for failure.137 Only one study has used quantitative measures to evaluate patellar position on kinematic MRI; Muhle and associates138 showed no significant difference in patellar tilt, bisect offset, and lateral patellar displacement with and without a patellar brace during active motion. Given these results, bracing should be applied only to patients who meet criteria for rehabilitation: occasional dislocators without gross anatomic abnormalities.

OPERATIVE TREATMENT Operative treatment for recurrent dislocation of the patella should be directed at the underlying pathology that can be determined from careful evaluation of history, physical examination, and imaging studies. There is a tendency for less experienced patellofemoral surgeons to perform the same operation, anterior medialization of the tibial tuberosity with lateral release, for all cases of patellar instability. However, surgical treatment should be customized to the causative pathology found in each patient. According to Andrish, the first principle in the operative treatment of patellar instability is to individualize, customize, and normalize to correct the offending pathoanatomy and not to create a secondary pathoanatomy to compensate for the primary pathoanatomy.139 This philosophy is clearly reflected in the recent literature as increasing reports of MPFL reconstruction and trochlear osteotomy have been devised to address loss of medial retinacular integrity and trochlear dysplasia, respectively.

Distal Realignment Procedures Most surgeons immediately think of extensor mechanism reconstruction procedures when dealing with recurrent patellar instability. Distal realignment techniques can be divided into those that transfer the bony insertion of the patellar tendon and those that involve soft tissue transfer, with the former reserved for patients who have reached skeletal maturity. Modern bony techniques are based on the description by Roux in 1888, which included transposition of the patellar tendon insertion, tightening of the medial structures, and lateral retinacular release.140 Shortly thereafter, Goldthwait described a soft tissue realignment

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that involved transposition of the lateral half of the patellar tendon under the remaining medial half with attachment to the soft tissue of the pes anserine.141 In 1938, Hauser reported a procedure that became synonymous with extensor mechanism realignment142; this procedure involves a distal and medial transfer of the tibial tuberosity onto the medial surface of the tibia with concomitant release of the lateral retinaculum and imbrication of the medial retinaculum. By today’s standards, the degree of transposition is considered extreme and fraught with complications. The placement of the tibial tuberosity on the sloping medial border of the tibia not only medializes the patella but also places it in a position posterior to its original location, increasing patellofemoral contact forces. Short-term results were favorable in cases of recurrent patellar dislocation, with up to 70% good to excellent results.143 However, suspicion of increased contact pressures was confirmed with long-term results that showed progression to arthritis in the same number of patients at 7 to 18 years.144-146 More recently, Barbari and coworkers showed that only 29% of 54 patients were stable and free from pain at 8 years of follow-up, with a high incidence of both patellofemoral and tibiofemoral arthritis.147 The Elmslie-Trillat procedure allows medialization without posterior transfer of the tibial tuberosity in combination with lateral release and medial capsular reefing. At a short-term follow-up of 3 years, Cox reported a 7% rate of recurrent dislocation but 73% good to excellent results.148 At 26-years’ follow-up in a subset of the same patients, only 7% had sustained a recurrent dislocation, and good to excellent results remained in 54%. Incidence of arthritis was not quantified by radiograph, but visual analog scale pain scores averaged 48.149 Modifications of this procedure and its subsequent outcomes are too numerous to mention. Anteromedial tibial tuberosity transfer was first described in 1983 by Fulkerson.150 In this procedure, an osteotomy of variable obliquity allows the degree of anterior and medial transfer to be independently adjusted to address the patient’s individual pathology. Biomechanical studies have demonstrated beneficial effects of the procedure. Molina showed that the most predictable way of increasing contact area and decreasing patellofemoral stress is transfer of the tuberosity 1 cm anterior and 0.5 to 1 cm medial.151 Recent studies have looked at contact pressures following anteromedialization procedures. On the trochlear side, Beck and coworkers showed that contact pressures are decreased and shift medially with anteromedial transfer.152 On the patellar side, Ramappa and colleagues showed that the shift in force to the lateral facet was better corrected by medialization than anteromedialization, although both corrected maltracking and reduced the overall contact force.153 In addition to these findings, Fulkerson has pointed out that anteromedial transfer also unloads the distal pole of the patella, a common source of pain.154 Although the intent of the anteromedialization procedure is to reduce an abnormal Q angle and correct lateral tracking of the patella, some authors believe there are untoward effects. Arendt and associates have shown that medialization externally rotates the tibia and alters patellar rotation, rather than stabilizing the patella.155 Huberti

and Hayes showed that decreasing the Q angle not only resulted in decreased lateral facet load but also was always associated with increased loads elsewhere in the joint.156 Alteration of these loads following tuberosity transfer may lead to early medial facet arthrosis. Studies on the clinical implications of these biomechanical results in the specific patient population with recurrent patellar dislocation are few and of short-term follow-up only. Bellemans and colleagues evaluated 29 patients with chronic knee pain associated with patellar subluxation.157 Kujala scores significantly improved from 43 to 89, and Lysholm scores increased from 62 to 92 at a mean of 32 months following anteromedialization. In 2005, Dantas and coworkers reviewed a more specific group of 24 knees with recurrent patellar dislocation treated by anteromedialization with lateral retinacular release.158 At a mean 52 months’ follow-up, the average Lysholm score improved from 63 to 98, with no recurrent dislocations.158 Longer term studies are needed to evaluate the true value of the procedure.

Lateral Retinacular Release or Lengthening The lateral retinaculum is an important structure that contributes to both lateral and medial stability of the patella.130,132 Although often performed in combination with other procedures, isolated release of the lateral retinaculum has been described in the treatment of lateral instability.160-163 Multiple studies have demonstrated that isolated lateral release is effective in reducing patellar tilt; however, the clinical implications in instability are unclear.164,165 There are no randomized, prospective studies comparing isolated lateral release to other methods of treatment. In 2007, Ricchetti reviewed the lower level evidence comparing isolated lateral release and that performed in combination with medial soft tissue realignment.166 Groups treated with isolated lateral release showed significantly greater odds of recurrent instability and dislocation. The controversy surrounding lateral retinacular release is reflected in Fithian’s survey of the International Patellofemoral Study Group on the role of the lateral release.167 In this survey completed by a group of surgeons with unparalleled interest and experience in the treatment of the patellofemoral joint, 37% of respondents said that lateral patellar dislocation is actually a contraindication to lateral release. Only 11% of respondents considered recurrent lateral patellar dislocation as a clinical scenario for which they would consider lateral release. If chosen, lateral release should be done with caution; multiple authors have shown iatrogenic medial subluxation of the patella as a complication of this procedure, suggesting that lateral release may worsen cases of lateral patellar dislocation.26,28,168,169 If a tight lateral retinaculum is indeed the offending pathology, a lengthening should be performed as described by Larsen and colleagues.170 In this technique, the oblique fibers of the superficial lateral retinaculum are incised just lateral to the patella to the depth of the deep transverse layer. A plane is developed between the two layers to the lateral epicondyle, where the deep layer is released. The two layers can then be sutured together in a length appropriate for soft tissue balance.


Lateral retinacular release should be performed as an adjunct to other procedures chosen to address the primary offending pathology. In this situation, most authors recommend that it be performed to address residual patellar tilt or limited medial translation.171 The release should be performed as the final procedure, preferably suturing it together in a lengthened position that allows the most normal intraoperative patellar tracking.

Proximal Realignment Procedures The goal of proximal realignment surgery is to reestablish a dynamic balance of forces around the patella. In 1979, Insall and associates described the “tube” realignment for the treatment of chondromalacia patella.172 The procedure consists of release of the medial and lateral retinacular tissue, which are sewn together over the quadriceps proximal to the patella. Modifications of this procedure involving a lateral release with a lateral and 1-cm distal advancement of the vastus medialis were later described in the treatment of patellar dislocation. Scuderi and colleagues reported on 60 knees treated with this procedure for recurrent dislocation of the patella refractory to conservative management.173 At 3.5 years’ follow-up, there were good to excellent results, with significantly better results achieved in males and those younger than 20 years of age. There was only one recurrent dislocation, but 11 patients required further operation or manipulation. Zeichen and associates also reported midterm results of the procedure with 6 years’ follow-up on 36 patients.174 Only one patient sustained a recurrent dislocation, and good to excellent results were achieved in 63% of patients. Andrish pointed out that distal advancement of the vastus medialis may reduce the obliquity of the muscle vector and reduce its mechanical effectiveness.139 To increase the obliquity, the posteromedial portion of the tendon should be advanced, as described by Ahmad and coworkers.175

Trochleoplasty and Trochlear Osteotomy The importance of trochlear dysplasia in recurrent patellar dislocation is well accepted. Classic studies by Brattström and Dejour and associates demonstrated a 10-degree increase in femoral sulcus angle in patients with patellar instability and a “crossing sign” in 96% of patients with objective patellar instability, respectively.5,78 Procedures to treat the dysplastic trochlea were described long before these radiographic parameters popularized the concept of trochlear dysplasia; investigators proposed gouging of the femoral trochlea in the late 19th century, and Albee first proposed the lateral femoral osteotomy in 1915.4,176 Bony procedures that address the dysplastic trochlea can be divided into two main categories: those that deepen the trochlea (trochleoplasty) and those that elevate the anterior portion of the femoral condyles (trochlear osteotomy). Numerous variations in these techniques and retrospective case series of their results have been published. However, there are no prospective, randomized studies in the literature that support the use of these techniques. Albee’s lateral femoral osteotomy addresses dysplasia by elevating the lateral condyle to provide a buttress to lateral motion of the patella.4 Weiker and Black reported

the results of this procedure in six knees that had undergone an average of 3.8 procedures before presentation.177 At 8 years’ follow-up, functional status was improved in four knees, despite a high perioperative complication rate. Inability to regain motion in three of six knees resulted in one closed manipulation under anesthesia and two open lyses of adhesions.177 In contrast, Koëter and colleagues reported no loss of motion at a mean 4 years’ follow-up in a recent study of 19 knees undergoing the same procedure for objective patellar instability with isolated trochlear dysplasia.178 The authors cited meticulous surgical technique in combination with postoperative CPM for maintaining range of motion. Functional improvement was reported in 16 of 19 knees, and pain relief during activities was reported in 12 knees. Progressive osteoarthritis was noted in 2 knees, a possible complication recognized by both Koëter and Weiker. The risk for patellofemoral pain and arthrosis from increased contact pressure in the lateral aspect of the patellofemoral joint has been recognized as a limitation of the Albee procedure. Kuroda published a biomechanical study of cadaveric knees that evaluated the patellofemoral contact pressures following elevation of the lateral condyle by 3, 6, and 10 mm.179 No significant change was noted at 3 mm, but significant increases in pressure were noted at 45 degrees of flexion with 6 mm of elevation and at 15 and 45 degrees with 10 mm of elevation. Unfortunately, the clinical significance of this is unknown. Masse first devised a procedure to address dysplasia by deepening the trochlea rather than elevating the femoral condyles.180 The initial procedure involved simple impaction of the prominent cartilage but was subsequently modified to remove subchondral bone before impaction. In Dejour and colleagues’ modification of this technique, the subchondral bone of the trochlea is removed with a bur and the overlying cartilage is first incised, then impacted and fixed. Verdonk evaluated 13 knees treated with Dejour’s procedure at a mean follow-up of 18 months. Using the Larsen-Lauridsen score, 59% had fair or poor results, but an equal number had good or very good results on subjective scoring. Five patients suffered postoperative arthrofibrosis. The study is limited by a short follow-up period and a population that included both patients with instability and pain. Donell recently published results of the same procedure at a mean follow-up of 3 years. Radiographically, the trochlear boss was reduced from 8 to 0 mm, and the Kujala score improved from 48 to 75. One patient required reoperation for arthrofibrosis and six had bothersome patellofemoral crepitus. In an effort to improve on the Dejour technique, Bereiter and Gautier described a technique in which an osteochondral wedge is removed from the femoral trochlea, allowing for deepening of the underlying cancellous bone and replacement of the cartilage in a deepened position.182 Schöttle and colleagues evaluated 19 knees at a mean 3 years’ follow-up using this procedure for the treatment of recurrent patellar instability with trochlear dysplasia.183 No dislocations recurred, and good to excellent results were achieved in 16 of 19 knees, despite persistent apprehension in 2 knees. Two knees had poor results that were attributed to degenerative changes of the trochlea noted during surgery. Radiographic parameters were also

Patella 1569

e valuated before and after surgery, showing an increase in the mean depth of the trochlea from 1 to 7 mm, a decrease in the TT-TG distance from 20 to 10 mm, and an improvement in the patellar inclination angle from 22 to 8 degrees. In a similar study with 8 years’ follow-up, von Knoch and coworkers showed less promising results.184 Although pain improved in half the patients, it worsened in one third. There were no redislocations and one continued subluxation, and all patients but one were able to return to a higher level of sporting activity. Radiographic findings showed that the trochlear depth increased from 0 to 5 and that the trochlear bump decreased from 4 to 0. Radiographic findings of grade 2 or worse osteoarthritis in the patellofemoral joint were absent preoperatively but found in 30% postoperatively. The results of these studies evaluating both trochlear deepening and condylar elevating procedures show that dysplasia can clearly be reduced on radiographic follow-up and that stability can likely be restored. However, the risks for short-term postoperative stiffness and long-term patellofemoral arthrosis from an incongruent patellofemoral articulation and increased contact forces remain legitimate concerns.

Medial Patellofemoral Ligament Reconstruction In the past several decades, restoring soft tissue restraints has become an important surgical principle in the treatment of unstable joints.185 Examples of this include anterior cruciate ligament reconstruction of the knee, anterior talofibular ligament reconstruction of the ankle, Bankart repair of the shoulder, and ulnar collateral ligament repair of the elbow. The principle of reconstruction of the MPFL of the knee is no different. In addition to the patellofemoral articulation, the MPFL is an important passive stabilizer of the patella that serves as a “check rein” to lateral patellar motion.186 Historically, emphasis has been placed on realignment surgery, but Davis and Fithian state that there exists no evidence that any amount of malalignment will cause dislocation unless passive stabilizers are damaged.185 Studies have shown that the MPFL is universally disrupted in patellar dislocation and that its integrity is of primary importance in lateral stability of the patella.19,129,159,187-190 In cases of recurrent instability of the patella, the MPFL may be torn, stretched, or healed in an elongated position, allowing excessive translation and subsequent episodes of subluxation or dislocation. Instrumented physical examination and stress radiographs have demonstrated this increased lateral laxity compared with that in controls and in contralateral knees in patients with patellar instability.57,105 Although first used in the operative treatment of acute patellar dislocation, primary repair of the medial retinaculum for recurrent patellar dislocation was suggested by Sargent and Teipner in 1971.191 The technique involved shortening of the retinaculum with suture repair to the roughened bone of the proximal patella in eight patients with recurrent patellar dislocation; there were no recurrent dislocations in the 16-month follow-up period. Although Fithian and Meier described a detailed modification of Sargent’s technique, no other literature exists on

the results of isolated primary repair in recurrent patellar dislocation.192 Since the identification of the MPFL as the primary restraint, several investigators have looked at primary repair of the ligament at its origin on the adductor tubercle19,175,193 and at its insertion on the patella in acute dislocation.191 It is important to point out that if primary repair is the chosen method of treatment, the entire MPFL must be imaged and explored because injury away from the proposed site of repair will liken the possibility of failure. In the early 1900s, a number of techniques were published for reconstruction of the “proximal transverse retinaculum,” including fascial transplantation, transposition of the hamstring tendons, and transposition of the medial half of the patellar tendon.194 In 1924, Gallie published the premise for modern techniques of MPFL reconstruction. The technique used bone tunnels and involved “tethering the patella itself, by strand of tendon or fascia, to the internal condyle of the femur at the point which forms the centre of the circle through the arc of which the patella moves on flexion and extension of the knee.”195 Nearly a century ago, this technique fulfilled all of the modern principles of ligament reconstruction as suggested by Teitge and Torga-Spak: selection of a sufficiently strong and stiff graft, isometric graft placement, correct tension, adequate fixation, and no condylar impingement.196 Since confirmation of the MPFL as the primary restraint in lateral patellar translation in the early 1990s, much attention has been focused on reconstruction of this structure in an attempt to restore stability, as evidenced by more than 50 recent publications in the English literature of various reconstructive techniques. Before modern reconstruction techniques using free grafts, tenodesis procedures as described by Galeazzi were sometimes performed for recurrent patellar dislocation.197 These procedures were often used in children to avoid growth disturbance of the proximal tibia from distal realignment procedures.198-200 Avikainen and coworkers proposed augmentation of medial retinacular plication with tenodesis of the distal adductor magnus tendon to the medial border of the patella in adults; they reported 12 good, but no excellent, results and 1 recurrent dislocation in 14 patients.194 Augmentation is still used by some in cases in which direct repair can be done after acute dislocation.201 Despite favorable results, attention has turned toward more anatomic procedures of MPFL reconstruction for recurrent cases of instability. Soon after the biomechanical reports proving the importance of the MPFL were published, techniques of reconstruction for recurrent dislocation began to surface. In 1992, Ellera Gomes proposed a surgical technique using a polyester graft placed in an isometric position. Eightythree percent of the 30 patients showed significant improvement in their symptoms at 39 months’ follow-up.202 Results were significantly worse results in patients with concomitant chondral pathology, but good to excellent results were found in 96% of those without. Nomura and associates also published a technique using a polyester Leeds-Keio artificial ligament covered by a medial retinacular slip.203 At 6 years’ follow-up, 96% of 27 patients had good to excellent results. Mild stiffness and recurrent apprehension were reported as occasional complications in both studies.


Implantation of artificial material is controversial, but the histologic changes in these polyester grafts have been well studied; 6 years after implantation, small but regularly aligned collagen fibers were found encasing the polyester, with a near-normal bimodal pattern of collagen size seen at 8 years’ follow-up.204,205 Despite the apparent success of artificial graft materials, soft tissue autograft remains the gold standard for all ligament reconstruction procedures. A number of donor sites have been reported, including patellar tendon,206 quadriceps tendon,96,196,207 adductor magnus tendon,96,196 medial retinaculum,208 and most commonly, hamstring tendon.209-217 Although the tensile strength of all these graft choices far exceed the 208-Newton tensile strength of the native MPFL,218 the graft must not be expected to hold the patella in place once engaged in a normal trochlea. Rather, it should guide the patella into the trochlea in the first 10 to 30 degrees of flexion, allowing bony constraint to stabilize the patella thereafter.139 A number of technical notes have been published on reconstruction of the MPFL, all of which describe slight variations in the method of restoring the tether between the origin and insertion of the native ligament.196,207,209,213,216,219 Methods of fixation include sutures, spiked washers, staples, bone tunnels, bone anchors, and interference screws. In a recent study, Mountney and colleagues showed that compared with suture anchors, blind tunnels, and sutures alone, a through-tunnel technique of graft fixation was the only fixation method statistically equivalent to the strength of the native MPFL.218 The MPFL has a broad, thin structure, and the exact origin and insertion are difficult to define. Nevertheless, some authors believe that isometric placement of the graft in reconstruction is essential for proper function and longevity of the graft as evidenced by some of the early reconstruction techniques.196,202,216 In a recent study of 11 cadaveric knees, Steensen and colleagues showed that the most isometric points in the native MPFL are the inferior portion of its patellar attachment and the superior portion of its femoral attachment.220 In cases in which the native origin and insertion are no longer identifiable after rupture, these points can be estimated at positions 23 mm from the superior pole of the patella and at the most superior aspect of the anterior portion of the medial epicondyle. Variation in the location and length of the graft can greatly alter the compressive forces at the medial aspect of the patellofemoral joint. Elias and Cosgarea showed that a combination of a graft that is 3 mm short and positioned 5 mm proximal on the femur results in significantly higher compressive forces on the medial patellar cartilage from 30 to 90 degrees of flexion.221 The clinical significance of these findings is unknown. In an in vitro, head-to-head study, Ostermeier and colleagues examined MPFL loading and stabilization of the patella after medial tibial tuberosity transfer versus ligament reconstruction in a MPFL-deficient knee under physiologic loading.222 Maximal loading of the MPFL occurred in full extension, when bony constraint is absent. Despite its traditional use in the treatment of patellar dislocations, tibial tuberosity transfer showed no significant relief of MPFL loading and did not stabilize the patella during lateral loading. MPFL reconstruction alone did restore stability to the

patella under load; ligament load was reduced, likely owing to difference in cross-sectional area between the native MPFL and the semitendinosis graft. Although no randomized, prospective trials exist on the outcome of isolated MPFL reconstruction in vivo, a number of retrospective studies have shown very promising results at midterm follow-up. A summary of these results is presented in Table 22C-8. Good to excellent results in these reports of isolated MPFL reconstruction range from 80% to 96%, with almost nonexistent cases of recurrent dislocation. Reports of MPFL reconstruction in combination with realignment procedures have also been published. Mikashima and colleagues retrospectively reviewed 40 patients treated with an Elmslie-Trillat procedure with or without concomitant MPFL reconstruction. There was no residual apprehension in cases with ligament reconstruction, compared with 30% in those without at 2-year followup without a significant difference in Kujala scores.223 MPFL reconstruction has also been used to treat offending causes of recurrent dislocations. Steiner and colleagues retrospectively reviewed 34 cases of MPFL reconstruction in patients with isolated trochlear dysplasia and recurrent patellar instability; those with other risk factors, including patella alta, large Q angle, and rotational deformities, were excluded.96 Good to excellent results were found in 91% of patients at 5 years’ follow-up, and knee scores were comparable to results of other studies of MPFL reconstruction in patients without dysplasia (see Table 22C2-8). Schöttle published a case report of MPFL reconstruction in a patient with rotational deformities of the femur and tibia and showed a correction in the position of the patella and no recurrent dislocations in a 10-month followup.224 Although results of these studies are promising, care should be taken to correct the offending pathology first and foremost.

Arthroscopic Treatment In the current era of minimally invasive surgery, some authors have attempted fully arthroscopic stabilization for recurrent dislocation of the patella. Procedures that have been advertised as minimally invasive include those using mini open medial capsular reefing in combination with arthroscopic lateral release225,226 and arthroscopically assisted procedures.227 However, only a few studies have reported fully arthroscopic stabilization of the patella. In 1986, Yamamoto first described a completely arthroscopic technique for repair of the medial retinaculum in acute patellar dislocations,228 but Henry and Pflum were the first to report an arthroscopic patellar realignment and stabilization for recurrent dislocations and subluxations.229 Their technique involved plication of the medial retinaculum using spinal needles to pass sutures, which were tied percutaneously. They experienced no recurrent dislocation over a 6-year period in an unspecified number of patients. Halbrecht described a similar technique with intra-articular, rather than percutaneous, knot tying with 2-year follow-up in 29 subjects; 93% subjectively felt significantly better, and the mean Lysholm score improved from 42 to 79.230 Objective radiographic measures showed significant improvement in congruence angle, lateral patellofemoral angle, and lateral translation. Hašpl and

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TABLE 22C2-8 Results of Medial Patellofemoral Ligament Reconstruction Knees

Graft Type

Lateral Retinacular Release

Follow-up (yr)

Results

6

Hamstring

−

7.4

Deie et al (2005)233

46

Hamstring

NR*

5.0/10.0

Drez et al (2001)211

15

Hamstring

+

2.6

Ellera Gomes (1992)202

30

Polyester

+

3.3

Ellera Gomes et al (2004)212

16

Hamstring

+

5.0

Fernandez et al (2005)214

30

Hamstring

±

3.2

Mikishima et al (2006)215

24

Hamstring

NR*

2.0

Nomura et al (2000)203

27

Polyester

±

5.9

Nomura et al (2005)201

5

Retinaculum

±

5.9

Nomura & Inoue (2006)234

12

Hamstring

±

4.2

Schottle et al (2005)217

15

Hamstring

NR*

4.0

Steiner et al (2006)96

34

Adductor, quadriceps

−

5.5

Redislocations: 0/6 Subluxation: 0/6 Apprehension: 2/6 Kujala mean: 96.3 Redislocation: 0/46 Subluxation: 4/46 Apprehension: 4/46 Kujala mean: >90 Redislocation: 0/15 Subluxation: 1/15 Apprehension: 0/15 Kujala mean: 88.6 Fulkerson mean: 93.0 Tegner mean: 6.7 Good to excellent: 13/15 Redislocation: 0/30 Subluxation: 1/30 Apprehension: 0/30 Redislocation: 0/16 Subluxation: 0/16 Apprehension: 1/16 Good to excellent: 15/16 Redislocation: 0/30 Subluxation: 0/30 Apprehension: 0/30 Good to excellent: 29/30 Redislocation: 0/24 Subluxation: 0/24 Apprehension: 1/24 Kujala mean: 95.2 Redislocation: 1/27 Subluxation: 1/27 Apprehension: 2/27 Good to excellent: 26/27 Redislocation: 0/5 Subluxation: 4/5 Apprehension: 1/5 Kujala mean: 97.6 Good to excellent: 4/5 Redislocation: 0/12 Subluxation: 0/12 Apprehension: 0/12 Good to excellent: 10/12 Kujala mean: 96.0 Redislocation: NR Subluxation: NR Apprehension: 3/15 Kujala mean: 85.7 Good to excellent: 13/15 Redislocation: 0/34 Subluxation: 0/34 Apprehension: NR Kujala mean: 90.7 Lysholm mean: 92.1 Tegner mean: 5.1 Good to excellent: 31/34

Study Deie et al

(2003)210

*Not registered.

colleagues subsequently described a technique in which the medial retinaculum was reefed from a working cannula that remained extra-articular on the medial side of the knee.231 At 13 months’ follow-up, 17 patients with a history of patellar instability had experienced no recurrence.

Ali recently reported a 4-year follow-up of 38 knees treated by all arthroscopic lateral release with medial plication. All the aforementioned arthroscopic techniques included a concomitant lateral retinacular release, the risks of which have been previously discussed.


Authors’ Preferred Treatment Treatment of chronic patellar instability requires a thorough history, physical examination, radiographic and MRI examination, and differentiation between instability and disability. Regardless of whether disability or instability is the predominant issue, care must be undertaken to educate the patient regarding expectations and outcomes. An individualized treatment plan should be developed for each patient. In other words, care must be taken not to treat each patient the same. Rehabilitation is chosen both to strengthen and increase endurance in the operative candidate or for treatment in the patient who has never had rehabilitation or who cannot comply with operative treatment. Operative treatment is the mainstay of treatment for the symptomatic recurrent patellar instability patient. Each patient undergoes an examination under anesthesia and diagnostic arthroscopy as part of the surgical procedure. It is imperative to rule out other forms of instability, such as anterior cruciate instability. In addition, chondral or osteochondral loose bodies or changes on the patella or trochlear groove are important consideration in the algorithm of treatment. If an associated meniscal injury is encountered, it should be recognized and treated as well. Patellofemoral tracking can be assessed as well. Based on the discussion in the previous sections, decisions are made regarding proximal and distal realignment, reconstruction of the MPFL, and lateral retinaculum lengthening or release.

C

r i t i c a l

P

o i n t s

bony congruity of the patellofemoral joint is the most significant contributor to patellar stability. l The medial patellofemoral ligament is the primary soft tissue restraint to lateral patellar dislocation, followed by the patellotibial ligament.

l Patella alta, trochlear dysplasia, increased patellar tilt, and increased tibial tuberosity–to–trochlear groove distance are radiographic findings that are associated with objective patellar instability. l Instrumented stress radiographs are simple to perform and provide objective radiographic evaluation of patellar mobility. l A course of nonoperative treatment with physical therapy should be attempted before surgical treatment. l Surgical treatment should be directed at the offending pathology determined through history, physical examination, and imaging studies. l Pain, recurrence, and patellofemoral arthrosis are possible complications of any procedure following multiple patellar dislocations.

S U G G E S T E D

R E A D I N G S

Amis AA, Firer P, Mountney J, et al: Anatomy and biomechanics of the medial patellofemoral ligament. Knee 10(3):215-220, 2003. Dejour H, Walch G, Nove-Josserand L, Guier C: Factors of patellar instability: An anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc 2(1):19-26, 1994. Fulkerson JP, Gossling HR: Anatomy of the knee joint lateral retinaculum. Clin Orthop 153:183-188, 1980. Hughston JC, Deese M: Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med 16(4):383-388, 1988. Kolowich PA, Paulos LE, Rosenberg TD, Farnsworth S: Lateral release of the patella: Indications and contraindications. Am J Sports Med 18(4):359-365, 1990. Kuroda R, Kambic H, Valdevit A, Andrish J: Distribution of patellofemoral joint pressures after femoral trochlear osteotomy. Knee Surg Sports Traumatol Arthrosc 10(1):33-37, 2002. Steiner TM, Torga-Spak R, Teitge RA: Medial patellofemoral ligament reconstruction in patients with lateral patellar instability and trochlear dysplasia. Am J Sports Med 34(8):1254-1261, 2006.

l The


S e c t i o n

D

Patellar Fractures Agbecko Ocloo and Richard D. Parker

Patella fractures are relatively uncommon injuries constituting about 1% of all skeletal injuries.1 They are usually the result of significant trauma and less commonly through participating in sporting events. The mechanism of injury is either a direct blow to the patella or an indirect force applied to the patella through the extensor mechanism. The various fracture patterns are usually representative

of the injury mechanism. These fractures can be broadly divided into displaced and nondisplaced fractures. Both nonoperative and operative management may be employed with good outcomes depending on the age and activity level of the patient, the fracture pattern, and the amount of displacement. Multiple techniques have been described for the surgical treatment of displaced fractures.

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The salient points of surgical treatment include anatomic reduction and rigid internal fixation that will allow early knee motion and rehabilitation.

SG

ANATOMY AND BIOMECHANICS The patella is the largest sesamoid bone in the body. It ossifies from a single center which usually makes its appearance in the second or third year, but may be delayed until the sixth year. More rarely, the bone is developed by two centers, placed side by side. Ossification is completed about the age of puberty. Incomplete ossification results in a bipartite patella. The patella is a flat triangular bone with a base or superior border which is thick and gives attachment to the quadriceps muscle. The medial and lateral borders are thinner and converge below. They give attachments to the vastus lateralis and medialis. The apex is pointed and gives attachment to the patella ligament. The posterior articular surface of the patella is divided by a vertical ridge and then again into thirds by two horizontal ridges. The lateral facet is larger than the medial. The lower facets articulate first with the trochlear groove in early flexion followed by the middle and then the upper facets. In full flexion, the most medial aspect of the patellar articular surface, designated the crescentic or odd facet, is the main contact point. The patella articulates with the trochlear groove of the distal femur and undergoes approximately 7 cm of excursion from extension to full flexion. The patellofemoral contact is initiated at about 20 degrees of flexion. The forces generated across the patellofemoral joint are tremendous, ranging from half of body weight for normal walking to nearly eight times body weight for jumping from a small height.2 Because of these forces, the articular surface of the patella is the thickest in the body. The average thickness is more than 1 cm. The blood supply to the patella is from a vascular anastomotic ring lying in the thin layer of loose connective tissue covering the rectus expansion (Fig. 22D-1). The main vessels contributing to this anastomotic ring are the supreme genicular, the medial superior genicular, medial inferior genicular, lateral superior genicular arteries and the anterior tibial recurrent artery. Nutrient vessels pass obliquely into the anterior surface of the patella from this complex network. Disruption of this supply by injury and subsequent surgical dissection can result in avascular necrosis. Rates of 3.5% to 24% have been reported after patellar fracture.3

CLASSIFICATION Fracture patterns of the patella are classified by their configuration and are usually consistent with the mechanism of injury. Indirect forces usually produce a nondisplaced or minimally displaced transverse fracture of the central or distal third or more uncommonly, a vertical fracture. Blunt injury to the patella either from a direct blow or from a fall onto the flexed knee, produces a comminuted stellate patella fracture. However, vertical or transverse patterns can also be produced. Do not forget that stress fractures can occur, too. Fractures are further designated displaced or nondisplaced,

LSG

MSG

LIG

MIG

ATR

Figure 22D-1 Schematic arterial blood supply to the patella. LSG, lateral superior geniculate; SG, superior geniculate; MSG, middle superior geniculate; MIG, middle inferior geniculate; ATR, anterior tibial recurrent; LIG, lateral inferior geniculate.

which is defined as more than 1 to 2 mm of articular separation or 3 to 4 mm of fracture separation.

EVALUATION Clinical Presentation and History Patellar fractures result either from an indirect force applied through the strong contraction of the quadriceps mechanism against a flexed knee or from a direct force, such as a fall onto a flexed knee or blunt trauma to the anterior patella. The subcutaneous location of the patella places it at risk for injury from direct impact. Traumatic separation of a bipartite patella can occur.4 This group of patients has a dull ache or pain in the knee prior to the traumatic episode. Reports of patella fractures after anterior cruciate ligament (ACL) reconstruction using the central third bonepatella tendon-bone autograft is being reported in the literature.5 Patients with patella fractures usually present with a painful, swollen knee after either direct trauma to the knee or a fall when an attempt was made to stop suddenly or “catch oneself.” Weight bearing is painful and depending on the competence of the medial and lateral retinacula, the patient may be able to extend the knee.


TREATMENT OPTIONS Nonoperative Initial treatment of patellar fractures should include splinting in extension and application of ice. The indications for nonoperative treatment are:

Figure 22D-2 Significantly displaced patellar fracture with disruption of the extensor retinaculum.

Physical Examination and Testing Localized tenderness and a hemarthrosis are typically present. It is important to examine the skin around the knee for abrasions and lacerations. In their presence intra-articular communications with the skin wound need to be ruled out. Open fractures will require immediate surgical débridement. With a displaced fracture, a gap between the two fracture fragments can be palpated. The integrity of the extensor mechanism needs to be evaluated. On occasion, a patient may be limited by pain instead of extensor mechanism disruption. For further evaluation of this, an aspiration of the hemarthrosis under sterile conditions followed by injection of intra-articular lidocaine can be performed.

Imaging Most patellar fractures can easily be diagnosed with standard radiographs (Fig. 22D-2). Radiographic evaluation includes anteroposterior, lateral and Merchant views. The anteroposterior view is used to assess for fragmentation, but visualization can be difficult owing to overlap of the distal femur. The lateral view best reveals the degree of fragmenting of the fracture or separation of fragments. Some vertical and osteochondral fractures are best seen on tangential or Merchant views. Osteochondral, marginal, and especially chondral injuries can more accurately be evaluated with magnetic resonance imaging. Other diagnostic studies, including computed tomography, bone scans, and conventional tomography, have been described but provide little additional clinical value. Bone scans have been reported to be helpful in evaluating patella stress fractures in athletes.6 A bipartite patella can be confused with an acute fracture and must be considered when radiographs reveal a small fragment separated from the main portion of the patella. In most cases these secondary ossification centers are located in the superolateral pole. The separation is minimal and the borders are usually smooth. Contralateral radiographs are of assistance if the variant is also present.

1. Undisplaced fractures with intact articular surface. There should be minimal displacement of fragments (10 mm opening with valgus stress at 30 degrees of flexion

The patient’s gait should be observed as the patient walks into the room or at some point during the examination. Gait may be misleading because patients with a complete MCL tear may walk with a barely perceptible limp. Hughston and colleagues found that 50% of athletes with grade III injuries could walk into the office unassisted and reported that a complete disruption of the medial compartment can occur “without subsequent significant pain, effusion, or disability for walking.”12 However, patients with an MCL tear may exhibit a vaulting-type gait in which the quadriceps is activated to allow for medial stabilization. This differs from the patient with an ACL or meniscus tear who may walk with a bent knee gait because of an effusion. Similar to any orthopaedic injury, the neurovascular status of the limb should be assessed. Pedal pulses should be palpated along with assessing sensation over the dorsum, plantar, and first web space of the foot. Compartments should be felt to rule out compartment syndrome, and the ability to dorsiflex and plantarflex the ankle and great toe should be assessed. On the skin, the physician should look for edema, effusion, and ecchymosis to help localize the site of injury. It is important to differentiate between localized edema and an intra-articular effusion. Isolated MCL injuries usually have localized swelling, and intra-articular pathology, such as an ACL or peripheral meniscal tear, may indicate a hemarthrosis. Severe medial complex injuries with an ACL tear frequently have no evidence of effusion because the capsular rent is large enough to allow extravasation of fluid. In addition, on examination, if there is hemarthrosis, the examiner should exclude other causes such as a torn cruciate, patellar dislocation, osteochondral fracture, and peripheral meniscal tear. Along with assessment of swelling, palpation of the anatomic sites of attachment can provide clues to the diagnosis. The entire course of the MCL should be palpated from proximal to distal. Pain at the medial femoral epicondyle signifies injury at the femoral insertion of the MCL. With tibial-sided injuries, patients have pain along the proximal tibia below the pes anserinus adjacent to the tibial tubercle. Mid-substance tears exhibit pain at the joint line, which also occurs with meniscal tears, posing a diagnostic dilemma. Hughston and colleagues showed that point tenderness can accurately identify the location of injury in 78% of cases, and localized edema can identify a tear in the medial side 64% of the time.12 A valgus injury that disrupts the MCL can also result in lateral meniscus tears or osteochondral fracture to the lateral condyle or lateral tibial plateau, so palpation of the lateral joint line should also be performed. Valgus stress testing at 30 degrees of knee flexion is still the gold standard for assessing damage to the MCL. This

test should be performed with the foot in external rotation because increased instability will be noted if the knee moves from internal to external rotation. For larger patients, 30 degrees of flexion can be achieved by dropping the foot a few inches over the table. The examiner then grasps the ankle and applies a valgus stress with the other hand resting on the fibular head to assess the amount of opening and the quality of the end point compared with the uninjured side. The laxity of the MCL can be recorded based on a grading system or the amount of opening. Based on the Noyes classification, 5 to 8 mm of medial opening signifies a significant collateral ligament injury with “impairment of the ligament’s restraining effect.”6 The grading system has three grades: (1) stress examination produces little to no opening with pain along the line of the collateral ligament; (2) some opening to stress occurs but with a firm end point; (3) there is significant opening of the joint with no end point. After assessing the degree of opening, a repeat valgus stress should be performed with the examiner palpating the medial meniscus to assess if it subluxates in and out of the joint, indicative of injury to the meniscotibial ligament.13 In addition to valgus testing in flexion, opening of the medial joint should be assessed with the knee in full extension. The cruciates, POL, posteromedial capsule, and MCL all contribute to stability in full extension. Asymmetric joint opening compared with the contralateral side should alert the physician to the possibility of a combined MCL injury with a cruciate tear or posteromedial complex injury. The ACL should be assessed with Lachman’s test because the pivot shift is difficult to perform owing to guarding and the loss of the pivot axis with abduction instability. In addition, the posterior cruciate ligament and lateral ligament should be examined. Along with cruciate injury, patellar instability and tearing of the vastus medialis obliquus are associated with laxity in full extension. Hunter and colleagues14 found 18 of 40 laterally displaceable patellas on stress radiographs in patients with medial-sided injuries and a 9% to 21% incidence of damage to the extensor mechanism with medial ligament injury. In addition to valgus testing at 30 and 0 degrees, Slocum’s modified anterior drawer test and anterior drawer in external rotation should be tested to assess for medial-sided injuries (Table 23C1-2).

Imaging Radiography, arthrography, magnetic resonance imaging (MRI), and arthroscopy can provide information in knee injuries. All knees should receive radiography with anteroposterior, lateral, and sunrise views. These radiographs should be evaluated for occult fractures, lateral capsular sign (Segond’s fracture), ligamentous avulsions, old PellegriniStieda lesions (old MCL injury) (Fig. 23C1-8), and loose bodies. In adolescent and pediatric patients, stress radiographs help differentiate between physeal injuries versus ligamentous injuries. MRI without contrast is the imaging study of choice for evaluating MCL tears because it is less invasive and provides detail for lesions of the medial meniscus, the superficial MCL, POL, posteromedial complex, and semimembranosus tendon (Fig. 23C1-9). In addition, MRI is beneficial in assessing injuries to anterior and posterior

1630 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 23C1-2 Methods for Examining the Medial Collateral Ligament Examination

Technique

Valgus stress at 0 and 30 degrees

Illustration

Grading

Significance

Valgus force applied to tibia while stabilizing the femur. This should be done at 0 and 30 degrees of flexion and should be compared with the opposite leg.

Grade I: 0- to 5-mm opening, firm end point Grade II: 5- to 10-mm opening, firm end point Grade III: 10- to 15-mm opening, soft end point

Slocum’s modified anterior drawer test

Valgus force in 15 degrees of external rotation and 80 degrees of flexion

This test is positive if there is a noticeably increased prominence of the medial condyle compared with the other side.

Anterior drawer test in external rotation

Anterior drawer test at 90 degrees of knee flexion with an external rotation applied to proximal tibia

This test is positive if there is a noticeably increased anterior translation of the medial condyle.

Opening at 30 degrees occurs from isolated medial collateral ligament (MCL) injuries. Valgus stress at 0 degrees is associated with other ligament tears (anterior cruciate ligament, posterior collateral ligament, or posterior oblique ligament). The disruption of the deep MCL allows the meniscus to move freely and allows the medial tibial plateau to rotate anteriorly, leading to an increased prominence of the medial tibial condyle. A disruption of the MCL alone should not lead to an increased anteromedial translation. An increased anteromedial translation indicates an anteromedial rotatory instability that involves an injury of the posteromedial structures.

cruciate ligaments, meniscus, and osteochondral structures. Loredo and associates showed that intra-articular contrast may help highlight and better define the structures of the posteromedial complex but still concluded the assessment of the posteromedial complex was difficult.15 They found that the posteromedial complex was best visualized on the coronal and axial images. Indelicato and Linton stated that MRI can provide advantages in four circumstance: (1) when the status of the ACL remains uncertain despite physical examination, (2) when the status of the meniscus is in

uestion, (3) when surgical repair of the MCL is indicated q and localization of the tear will help limit the exposure, and (4) when an unexplainable effusion occurs during rehabilitation.16 However, MRI does not always provide concrete diagnosis, and the clinical examination becomes the deciding factor. Examination under anesthesia is another tool the physician can use to assess the injury pattern in patients who present late, or in patients in whom the office examination and MRI do not provide a diagnosis. Norwood and coworkers found on examination under anesthesia that

Figure 23C1-8 A and B, PellegriniStieda lesion. (Reproduced with permission from Pavlov H: Radiology for the orthopedic surgeon. Contemp Orthop 6:85, 1993.)

A

B

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Figure 23C1-9 Magnetic resonance image showing medial collateral ligament tear.

18% of patients had anterolateral rotatory instability that was not suspected preoperatively.17 In addition to MRI, arthrograms can be used to evaluate meniscal disease and capsular tearing with extravasation of contrast material. Kimori and colleagues found arthrography to be more useful than arthroscopy in diagnosing tears of the meniscotibial and meniscofemoral ligaments.18 With the increased use of MRI, arthroscopy is used infrequently as a diagnostic tool. ACL and meniscal tears may be identified on MRI. Also, it is rare to find an intrasubstance medial meniscal tear in an isolated MCL rupture because meniscocapsular separation occurs, and the fulcrum to load the medial compartment and tear the medial meniscus is lost.

TREATMENT OPTIONS Treatment of the MCL and medial-sided knee injuries can be divided into operative and nonoperative approaches. Numerous factors, including the timing, severity, location, and associated injuries such as an ACL tear, need to be taken into account when formulating a treatment plan. The MCL has the greatest capacity to heal of any of the four major knee ligaments because of its anatomic and biologic properties.19,20 As a result of multiple biomechanical, clinical, and functional studies, the trend has been toward a conservative, nonsurgical method for most MCL injuries. Recently, posteromedial corner injuries have been recognized as a separate entity from MCL injuries and may need to be addressed more aggressively because of rotational laxity and instability.5 Isolated tears of the MCL, grade I and II, do well with nonoperative management. Routinely, partial tears are treated with temporary immobilization and protected weight-bearing with crutches. Once the swelling subsides, range of motion, resistive exercises, and progressive weightbearing are initiated. Nonsteroidal anti-inflammatory drugs can be used to help with pain and swelling. Studies have shown no deleterious effect of nonsteroidal drugs on ligament healing.21 Numerous authors have shown excellent results with nonoperative treatment of grade I and II MCL tears.22-25 Ellsasser and associates looked at 74 knees

in professional football players and achieved a 98% success rate with a nonoperative protocol.22 They had strict inclusion criteria to ensure isolated MCL injury: (1) up to grade II laxity with a firm end point in flexion, (2) no instability to valgus stress in extension, (3) no significant rotatory or anteroposterior subluxation, (4) no significant effusion, and (5) normal stress radiographs. In this series, patients were treated with crutches, no brace, and progressive weightbearing. Ellsasser thought, based on his experience, that by 1 week patients should progress to full extension, no effusion, and decreased tenderness. The players returned to football in 3 to 8 weeks. The only failure occurred in a patient with an osteochondral fracture that was found later. Derscheid and Garrick performed a prospective study looking at 51 grade I and grade II MCL injuries in college football players.23 They used a nonoperative rehabilitation protocol with a knee immobilizer initially. Players with a grade I injury returned to full participation at an average of 10.6 days, and players with grade II injury returned at an average of 19.5 days. At long-term follow-up, these patients showed slight increases in medial instability. Injured knees had a higher incidence of reinjury than control knees, but this was not statistically significant. Bassett and associates24 and Hastings25 studied the use of cast brace in treating isolated MCL ruptures. Both studies found early return to athletics with the use of the cast brace. Nonoperative treatment varies from casting to functional bracing to no bracing, and good outcomes occur with all three forms of treatment. Management of grade III injuries remains much more controversial. Grade III injuries not only involve complete disruption of its fibers but also are frequently associated with additional ligamentous injuries. Fetto and Marshall found an 80% incidence of concomitant ligamentous injuries with a grade III MCL tear, with 95% of the associated injuries being an ACL tear.26 Early authors recommended primary repair for grade III injuries. O’Donoghue stressed the importance of immediate repair of complete tears of the MCL.27 Hughston and Barrett supported primary repair of all medial structures, including the superficial MCL and POL.28 They believed that repair and advancement of the posterior oblique ligament was key to restoring medial stability. Their results were good to excellent in 77% to 94% of patients. Muller reported 65% good and 31% excellent results in repair of isolated grade III MCL injuries.2 He repaired the superficial MCL avulsion with screw and washers and intrasubstance tears with a combination of approximation and tension-relieving sutures. In addition to Hughston, O’Donoghue, and Muller, Collins29 and Kannus30 have written that surgical intervention is necessary for complete ruptures of the MCL. Even though early authors demonstrated good results with surgical repair of the MCL, recent literature has focused on the nonoperative management of grade III MCL injuries. Fetto and Marshall were among the first to assess outcomes after nonoperative treatment of grade III MCL injuries.26 They studied 265 MCL injuries and found that patients with grade II injuries did much better than grade III injuries (97% compared with 73%). Initially, in their study, all grade III injuries received operative intervention. However, there were some patients with grade III injuries that were not operated owing to skin lesions and infection.


At follow-up, patients with operative treatment of isolated MCL ruptures had no improved outcome compared with the nonsurgical group. This incidental finding led the way for more prospective studies to investigate the role of nonoperative treatment in isolated grade III MCL injuries. Indelicato prospectively compared operative to nonoperative treatment of isolated third-degree ruptures.31 All patients underwent examination under anesthesia and arthroscopy to rule out any other pathology, such as ACL and meniscal tears. He found objectively stable knees in 15 of 16 patients treated operatively and in 17 of 20 patients treated nonoperatively. Both groups followed a rigid rehabilitation protocol including casting at 30 degrees of flexion for 2 weeks and then 4 weeks longer in a cast brace with hinges that allowed motion from 30 to 90 degrees. Subjective scores were higher in the nonsurgical group, with good to excellent results of 90% in the nonsurgical group and 88% in the surgically repaired group, suggesting there was no benefit to surgical intervention. Indelicato also showed that patients treated with early motion returned to football 3 weeks earlier than immobilized patients. In a subsequent study by Indelicato and associates, they showed that conservative approach in complete MCL ruptures was successful in collegiate football players.32 All players were managed with a functional rehabilitation program, and 71% had good to excellent results. Similar to Indelicato, both Reider and colleagues33 and Jones and associates34 found excellent outcomes in athletes with isolated grade III medial ligament injuries treated conservatively and agreed that nonoperative treatment of these lesions is justified. Reider and colleagues looked at 35 athletes who were treated with early functional rehabilitation for isolated grade III tears.33 Of these, 19 patients returned to full, unlimited activity in fewer than 8 weeks. At an average follow-up of 5.3 years, outcomes based on subjective and objective measurements were comparable to earlier investigations employing a surgical repair. In 1985, Jones reported his results on 24 high school football players who returned to competition at an average of 34 days.34 Management consisted of 1 week of immobilization followed by gradual range of motion and strengthening. The knee was tested weekly with valgus stress, and instability was reduced to grade 0 or 1 by 29 days. No increased incidence of reinjury was found the following spring. Even though Indelicato, Fetto and Marshall, Jones, and Reider found excellent results with nonoperative treatment, Kannus studied 27 patients with grade III lesions at an average 9 years of follow-up.30 Patients were found to have poor outcomes (Lysholm score of 66) and degenerative changes on radiographs. Kannus concluded that early surgical repair would prevent deterioration. A careful review of the patients showed that 16 of 27 had greater than 2+ Lachman score, and 10 of 27 had anterolateral instability. This study did not show that nonoperative treatment has poor outcomes, but associated injuries need to be addressed, such as ACL, to prevent poor long-term outcome. Combined injury to the MCL and ACL represents a completely different entity than isolated MCL injury. The ACL is a primary restraint to anterior displacement and acts as a secondary stabilizer to valgus stress, especially in full extension. Conversely, the MCL is the primary restraint to valgus stress at 30 degrees of flexion. Therefore, injury

to the MCL and ACL results in both anterior and valgus instability and can significantly compromise knee function. Even though the apparent consensus that solitary MCL rupture can be treated nonoperatively, the optimal treatment for a concurrent ACL and MCL injury remains controversial. Two controversial studies regarding the management of combined ACL and MCL injury have been addressed in the literature. The first issue pertains to the various surgical options available for managing these injuries. Three principal surgical options exist: (1) surgical repair of both ligaments, (2) ACL reconstruction and nonoperative MCL management, and recently (3) operative management of MCL with nonoperative ACL treatment. ACL reconstruction with nonoperative management of the MCL remains the most popular option. The second controversial issue regarding combined injuries is whether early or late ACL reconstruction provides better functional and long-term results. Early authors recommended surgical intervention for both ligamentous structures in concomitant ACL and MCL ruptures.26,36,37 Fetto and Marshall had 79% unsatisfactory outcomes in patients treated operatively for ACL and MCL tears.26 Even though studies have shown operative repair of all ligaments results in stable, functional knees, there was a high incidence of knee motion postoperative complications.38-40 Other authors have stated that isolated operative MCL repair and nonoperative ACL reconstruction leads to good results. Hughston and colleagues reported that 94% of their patients with combined ACL and MCL injury and treated with only MCL reconstruction returned to their preinjury levels of athletic performance.41 They stated that the key to obtaining excellent results was reconstruction of the POL and posteromedial structures. Noyes and Barber-Westin criticized Hughston and Barrett’s method of reporting results and stated that the results may have been overly optimistic. However, Hughston continued to report good results at 22 years of follow-up.35 In addition to Hughston, Shirakura and associates reported excellent results in 14 patients with combined lesions but reconstruction of the MCL only; however, they did not report anteroposterior instability.42 Conversely, Frohlke and coworkers reported poor results with solitary MCL repair.43 They performed arthroscopically guided repair of the MCL, which led to functional stability in 68% of knees, but clinical testing of all 22 knees showed abnormal or severe abnormal examination. Most authors, however, suggest that nonoperative treatment of the MCL with reconstruction of the ACL provides good to excellent results. Shelbourne and Porter demonstrated good to excellent results in 68 patients with ACL reconstruction and nonsurgical management of an MCL tear.44 They also showed that these patients achieved a greater range of motion and more rapid strength gains than patients with surgical repair of both ligaments. Similarly, Noyes and Barber-Westin demonstrated a higher incidence of motion problems when MCL and ACL were treated operatively, and they recommend arthroscopic reconstruction of the ACL with nonoperative management of the MCL after recovery of range of motion and muscle function.45 In a prospective randomized study, Halinen and associates treated 47 consecutive patients with combined ACL and grade III MCL injuries.46 All patients

Knee 1633

underwent early ACL reconstruction within 3 weeks of injury. The MCL was treated operatively in 23 patients and nonoperatively in 24 patients. All patients were available for follow-up at a mean of 27 months. The nonoperative treatment of the MCL led to results similar to those obtained with operative treatment, with respect to subjective function, postoperative stability, range of motion, muscle power, return to activities, and Lysholm score. Halinen and colleagues concluded that MCL ruptures did not need to be treated operatively when the ACL was reconstructed early. In a retrospective study, Millett and colleagues reported on 19 patients with a complete ACL injury and a minimal grade II MCL tear who underwent early ACL reconstruction and nonoperative treatment of the MCL.47 At 2-year follow-up, subjective evaluation showed a Lysholm score of 94.5 and Tegner activity score of 8.4. Clinical examination revealed good range of motion and strength. No patient experienced graft failure or required subsequent surgery. The second controversial issue regarding combined ACL and MCL injury is whether early or late ACL reconstruction provides optimal return of function and long-term results. Based on animal studies, MCL healing is adversely affected

by ACL insufficiency.48 Therefore, it has been proposed that early ACL reconstruction will improve healing of the MCL. Both Halinen and colleagues46 and Millett and associates47 showed good subjective scores and minimal loss of motion complications with early ACL reconstruction (within 3 weeks). Conversely, Petersen and Laprell demonstrated poorer results with early ACL reconstruction compared with late ACL reconstruction in combined injuries.49 All patients underwent nonoperative treatment of MCL injury, and early ACL reconstruction was performed within 3 weeks and late ACL reconstruction after a minimum of 10 weeks. The late reconstruction group had a lower rate of loss of motion and higher Lysholm scores compared with the early reconstruction group. The literature supports nonoperative treatment of the MCL tear with surgical reconstruction of the ACL. This is the trend that most surgeons are currently using. However, early versus late reconstruction continues to be a subject of debate, with studies supporting both sides. Other factors such as preoperative and postoperative rehabilitation protocol along with bracing may need to be further analyzed to help better assess whether early or late reconstruction is more beneficial.

Authors’ Preferred Method Before proceeding with a treatment plan, it is essential to know the extent of injury. Initially we perform a thorough history and physical examination. With MCL injuries, we assess the grade of injury of the MCL and also any associated ligamentous, meniscal, posteromedial corner, or patellar injuries. We obtain radiographs as a routine diagnostic tool to rule out fracture or any signs of chronic

edial insufficiency (Pellegrini-Stieda lesion) and chronic m ACL deficiency (deep femoral notch sign, peaked tibial spines, cupula lesion). The use of MRI is dependent on the grade of the MCL lesion and associated injury. Isolated grade I or II injuries can be diagnosed on clinical examination and do not require MRI. However, in a grade I or II injury with an indeterminate cruciate examination and Figure 23C1-10 Algorithm for treatment of mcl injuries. ACL, anterior cruciate ligament; MCL, medial collateral ligament; PT, physical therapy.

Suspected MCL Injury? Examine

Isolated Grade I or II MCL

Isolated Grade III or MCL with associated injuries

MRI

Rehab

Isolated Grade III MCL

ACL/MCL

Femoral Avulsion Isolated Grade III

Rehab, PT, regain motion

Full ROM

Tibial Avulsion

MCL Repair/Reconstr

MCL unstable ACL Reconstruction

Continued


Authors’ Preferred Method—cont’d

Figure 23C1-11 Coronal magnetic resonance image shows complete avulsion of the superficial and deep medial collateral ligament with an unattached medial meniscus.

effusion, we order an MRI. In contrast, we perform MRI on all grade III injuries because the site of involvement, tibia or femur, is important in our decision making. In addition, most grade III lesions are associated with concomitant ligamentous injuries. Figure 23C1-10 presents our treatment algorithm. We treat isolated grade I and II MCL injuries conservatively. In the first 48 hours, we encourage rest, ice, compression, and elevation to help reduce swelling. In addition, we place all patients in a hinged knee brace and provide crutches for protected weight-bearing. If patients have significant pain and valgus laxity, initially we lock the brace in extension. Once the swelling subsides and pain is improved, we encourage aggressive range of motion exercises and straight leg raises with quadriceps-setting exercises. Once the patient

Figure 23C1-12 Arthroscopy confirms gross laxity of the medial compartment with complete disruption of medial support structures and a free-floating meniscus.

has regained full range of motion and ambulation without a limp, crutches and the brace can be discontinued. Stationary bicycle and progressive resistive exercises are instituted as tolerated. Once full range of motion and 80% strength of the opposite side have been achieved, closed-chain kinetic exercises and jogging are allowed. In athletes, once they have achieved 75% of the maximal running speed, sport-specific training is allowed. Return to sports is permitted after the patient has strength, agility, and proprioception equal to the other side. We recommend a functional brace for contact or high-risk sports. In grade I sprains, patients usually return to sports in 10 to 14 days; because immobilization is temporary, patients regain strength and motion quickly. However, return to play after grade II sprains is much more variable. With grade II sprains, the period of immobilization can be up to 3 weeks to allow the pain to dissipate. Therefore, patients can lose more strength and motion with increased time of immobilization compared with grade I sprains. Patients are allowed to return when they have equal strength, and there is no pain with valgus stress. The treatment of grade III MCL sprains has significantly evolved over the past 20 years. The general consensus has been to treat isolated grade III injuries conservatively. We believe that the treatment of grade III injury is dependent on not only the specific location of the MCL rupture but also the degree of laxity on physical examination as well as the quantity of the arthroscopic drive-through sign. A case example is that of a 16-year-old high school football player who sustained a contact MCL and ACL injury treated operatively in a staged fashion. Figures 23C1-11 to 23C1-14 highlight the treatment plan. This allowed full return to contact sports 1 year from injury. Although most femoralsided tears can be treated successfully conservatively, complete tibial-sided avulsions of the deep and superficial MCL, although rare, often heal with residual laxity. In athletes who

Figure 23C1-13 Open surgery confirms complete avulsion of the medial collateral ligament from the tibia with a free-floating, unattached medial meniscus between the articular cartilage of the medial femoral condyle and tibial plateau.

Knee 1635

Authors’

preferred method—cont’d

Figure 23C1-14 Magnetic resonance image showing tibial-sided avulsions.

articipate in level I sports, frequently we favor operative p repair of these tibial-sided complete avulsions that display retraction of the deep or superficial MCL on MRI (Fig. 23C1-15).50 Figures 23C1-16 and 23C1-17 highlight a case example of a Division I football player with a tibial-sided complete MCL avulsion with gross laxity and an impressive arthroscopic drive-through sign treated surgically. Our rehabilitation protocol for grade III lesions is placement in a long-leg hinged knee brace locked in extension with weight-bearing as tolerated on crutches for 2 weeks. In the first 4 weeks, our goal is to have the patient attain nearly full range of motion and normal gait pattern with full

Figure 23C1-15 Arthroscopy 3 months after fixation at the time of primary anterior cruciate ligament reconstruction shows complete healing of meniscus and elimination of the drive-through sign.

Figure 23C1-16 Coronal magnetic resonance image shows tibial-sided avulsion of the medial collateral ligament with retraction and a contrecoup bipolar bone bruise lesion laterally, which suggest a high-energy injury pattern.

weight-bearing in a hinged knee brace, and begin quadriceps and hamstring strengthening. In contrast, patients who undergo a repair of the MCL follow a different protocol. Postoperatively, a hinged knee brace is locked from 30 to 90 degrees for 3 weeks, followed by unlimited motion. Weight-bearing is limited for 3 weeks with crutches and then progressed to full weight by 4 to 6 weeks. Bracing is discontinued at 6 weeks, and nonimpact conditioning is allowed, with running started by 3 months.

Figure 23C1-17 Arthroscopy confirms a drive-through sign with liftoff of the medial meniscus from the tibia requiring open repair of medial structures.


POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS The treatment of MCL injuries has evolved into nonoperative management. Therefore, rehabilitation is pivotal and is the primary modality for treatment. There is no one perfect rehabilitation protocol that will work with every athlete. When reviewing the literature, there is no apparent consensus on the most efficacious rehabilitation protocol, and protocols are usually based on surgeon preference and experience. Steadman,51 Bergfeld,52 O’Connor,53 Cox,54 and Wilk and colleagues55 have had excellent success with their individual protocols for treatment of MCL injuries. To effectively treat MCL injuries, the grade of the injury must be determined because the parameters of rehabilitation are based on the degree of injury. Look at Table 23C1-3 for general principles to follow in rehabilitation of MCL. Isolated grade I sprains are treated with rest, ice, compression, and elevation for the first couple of days to help reduce swelling. Patients are allowed weight-bearing as tolerated with use of an assistive device if there is pain with walking. The only exception is patients with significant valgus deformity because they will place more stress on the MCL, affecting healing. In these patients, it may be safer to allow them partial weight-bearing for a couple of weeks. With grade I MCL tears, immobilization in a brace is rarely required, and if patient compliance is of concern, a short leg hinged brace is used to control valgus and rotational stresses. Range of motion is begun immediately to prevent arthrofibrosis and stiffness. In addition, quadriceps strengthening and closed chain exercises are started. Once the patient regains full range of motion, resistive exercises are begun along with sport-specific drills. Isolated grade II injuries are treated similarly to grade I injuries with rest, ice, elevation, and compression. Because grade II injuries involve a greater degree of damage to the ligament with increased valgus instability, a long-leg hinged brace is usually needed. Patients are allowed to progressively bear weight as tolerated in the brace; however, if the patient is having significant pain, the brace can be locked in extension until the pain subsides, usually in 1 week. Assistive devices are used until the patient has a

TABLE 23C1-3 Principles for Rehabilitation of the Medial Collateral Ligament Phase

Goals

Criteria for Progression

Maximal protection phase

Early protected range of motion (ROM) Decrease effusion and pain Prevent quadriceps atrophy Full painless ROM Restore strength Ambulation without crutches Increase strength and power

No increase in instability No increase in swelling Minimal tenderness Passive ROM at least 10-100 degrees No instability No swelling or tenderness Full painless ROM

Moderate protection phase Minimal protection phase

nonantalgic gait. Active range of motion exercises are started immediately. During the early period, quadriceps strengthening is done in a non–weight-bearing fashion with straight leg raises, quadriceps-setting exercises, and electrical stimulation. Once the patient has achieved full range of motion and functional strength, proprioceptive and agility drills can be initiated. Isolated grade III injuries usually involve disruption of both the superficial and deep fibers. Therefore, the rehabilitation process is slower, and a longer period of immobilization is required. The treatment of grade III injuries can be divided into stages. In the first phase (about 4 weeks), the patient should wear a brace locked in extension and progressively increase weight-bearing to attain a normal gait pattern. Also, the patient needs to perform range of motion exercises with strengthening of quadriceps and hamstrings. In phase II, 4 to 6 weeks, the patient continues to attain full range of motion, unlock the brace, and achieve quadriceps and hamstring strengthening. After 6 weeks, the brace can be discontinued if the patient has a nonantalgic gait and has regained quadriceps strength for daily ambulation. Phase III starts after 6 weeks and includes squatting, light jogging with agility drills, and continued strengthening to return to sports. After surgical repair of an isolated MCL, the patient is locked in 30 degrees and allowed toe-touch weight-bearing for 3 weeks. The patient is encouraged to continue range of motion from 30 to 90 degrees. The patient also continues strengthening of the quadriceps and hamstring in brace. After 3 weeks, the patient is allowed to progress to full weight-bearing with full-time brace wear to continue to protect the repair. The brace can be worn unlocked to allow free range of motion as well as valgus and rotational stability. From 3 to 6 weeks, the goal is to restore full range of motion along with continued strengthening with closed kinetic chain exercises. After 6 weeks, the patient continues to progressively increase activities with resistive and sportspecific exercises. Combined injuries of the MCL and ACL require additional steps to be taken compared with the rehabilitation of isolated MCL tears. Reviewing the literature as stated previously on ACL and MCL injuries, conservative treatment of MCL followed by surgical reconstruction of ACL is the favored management. Initially the protocol focuses on the severity of the MCL injury. For example, a grade I MCL injury with an ACL injury will proceed with the protocol presented earlier for grade I injuries. The patient will quickly regain range of motion and functional strength, and then the surgeon can proceed with reconstruction of the ACL. Conversely, the patient with a grade III injury with an ACL injury will take much longer owing to the slower protocol for type III injuries. Regaining range of motion and functional strength training may take 8 to 10 weeks. Therefore, ACL reconstruction with a type III injury will take longer to proceed. Once the ACL is reconstructed with conservative treatment of the MCL, the rehabilitation protocol follows one for an ACL. After a combined ACL reconstruction and medial-sided repair, the knee is braced in full extension, and a standard ACL protocol is followed. In combined ACL and MCL injury, it is important to remember that ACL rehabilitation takes precedence over medial-sided repair.

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Outcomes were thoroughly discussed in the treatment section. However, nonoperative treatment for grade I and II sprains is well accepted in the literature. Ellsasser and colleagues showed in 74 professional football players with isolated grade I and II MCL sprains return to play in 3 to 8 weeks and excellent results in 98%.22 Similarly, Derscheid and Garrick demonstrated in 51 college football players with grade I and II sprains return to play at 10.6 days and 19.5 days, respectively.23 Indelicato, Reider, and Jones and their associates found excellent results with conservative management of grade III sprains with return to sports by 8 weeks.32-34 Complications of MCL ruptures are rare in the literature. Failure to diagnose associated ligament injuries, such as ACL, can lead to long-term instability and degenerative problems. In addition, missed associated meniscal tears and articular cartilage defects can lead to continued pain. Atrophy and arthrofibrosis are rare complications given the aggressive rehabilitation protocols with early motion and strengthening. Infection is a rare complication with surgical reconstruction. Residual pain can occur after grade I sprains, usually near the femoral origin, possibly because of a small neurovascular bundle.2 Treatment consists of an injection or anti-inflammatory medication. In addition to pain, patients with femoral-sided lesions are more prone to have loss of motion and associated stiffness.

CRITERIA FOR RETURN TO PLAY See Box 23C1-1.

Box 23C1-1 Return to Play

• Full range of motion • No instability • Muscle strength 85% of contralateral side • Proprioception ability satisfactory • No tenderness over medial collateral ligament • No effusion • Quadriceps strength; torque/body weight • Lateral knee brace (if necessary)

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l The superficial MCL is the primary static stabilizer against valgus and external rotation stress. l Posteromedial corner structures include the posterior horn of the medial meniscus, POL, semimembranosus expansions, meniscotibial ligaments, and oblique popliteal ligament.

l The posteromedial corner provides static and dynamic restraint to anteromedial rotatory instability. Concomitant injuries, such as ACL, PCL, meniscus tear, and patellar injuries, with MCL injury should be ruled out. l Valgus laxity at 30 degrees occurs with isolated MCL injury. l Valgus laxity at 0 degrees occurs with combined MCL and ACL or posteromedial complex injury. l Grade I or II MCL injury is treated conservatively with rehabilitation. l Isolated grade III injury is treated conservatively. Combined grade III ACL and MCL injury is treated with rehabilitation of the MCL and then reconstruction of the ACL if the MCL heals. Watch for nonhealing of tibialsided MCL lesions. If nonhealing, repair the tibial-sided MCL and reconstruct the ACL.

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Fanelli GC, Harris JD: Surgical treatment of acute medial collateral ligament and posteromedial corner injuries of the knee. Sports Med Arthrosc Rev 14:78-83, 2006. Halinen J, Lindahl J, Hirvensalo E: Operative and nonoperative treatments of medial collateral ligament rupture with early anterior cruciate ligament reconstruction. Am J Sports Med 34:1134-1140, 2006. Hughston JC, Eilers AF: The role of the posterior oblique ligament in repairs of acute medial (collateral) ligament tears of the knee. J Bone Joint Surg Am 55: 923-940, 1973. Indelicato PA, Hermansdorfer J, Huegel M: Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate players. Clin Orthop 256:174-177, 1990. Jacobson KE, Chi FS: Evaluation and treatment of medial collateral ligament and medial-sided injuries of the knee. Sports Med Arthrosc Rev 14:58-66, 2006. Noyes FR, Barber-Westin SD: The treatment of acute combined ruptures of the anterior cruciate and medial collateral ligament of the knee. Am J Sports Med 23:380-389, 1995. Petersen W, Laprell H: Combined injuries of the medial collateral ligament and the anterior cruciate ligament: Early ACL reconstruction versus late ACL reconstruction. Arch Orthop Trauma Surg 119:258-262, 1999. Sims WF, Jacobson KE: The posteromedial corner of the knee: Medial-sided injury patterns revisited. Am J Sports Med 32:337-345, 2004. Warren LF, Marshall JL: The supporting structures and layers on the medial side of the knee. J Bone Joint Surg Am 61:56-62, 1979. Wilk KE, Andrews JR, Clancy WG: Nonoperative and postoperative rehabilitation of the collateral ligaments of the knee. Oper Tech Sports Med 4:192-201, 1996.



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Medial Ligament Injuries 2. Pediatric Medial Knee Injuries Jayesh K. Patel, Manuj Singhal, and Darren Johnson

Knee injuries in children are rather complex given the broad spectrum of patients in regard to age and maturity. In this section, we describe the basic anatomy of the pediatric knee, focusing on, in particular, the medial aspect of the knee and the medial collateral ligament (MCL). Much has been written regarding adult MCL injuries, but few studies focus on pediatric knee injuries. As the world of organized sports incorporates younger and younger children, knee injuries are become more prevalent and complex. We focus on studies and literature pertaining to only the pediatric population.

ANATOMY The growth plates of the distal femur and the proximal tibia, as well as the ligamentous structures, are all vulnerable to injury. The ligaments and cartilaginous structure of the knee start to develop at about the eighth week of embryonic development.1 The distal femoral epiphysis is the largest and most rapidly growing growth plate in the body. It grows an average of 10 to 11 mm per year. It is the first secondary ossification center to appear in the body and is present at birth in fullterm newborns.1,2 The distal femur contributes roughly 40% of the length of the entire leg. It fuses at about 14 years of age in girls and at 16 years of age in boys. The distal femoral epiphysis is the last epiphysis to fuse in adults.2 The rapid growth of the distal femoral epiphysis increases its vulnerability to injury. The proximal tibial epiphysis is seen at about 2 months of age. There is an additional secondary epiphysis that develops in the tibial tubercle between the ages of 9 and 14 years.1 The proximal tibia grows at rate of about 6 to 7 mm per year.3 By the age of 16 years in girls and 18 years in boys, the proximal tibia is fused. It contributes about BOX 23C2-1 Layers of the Medial Side of the Knee 1. Layer I—sartorius fascia 2. Layer II—superficial medial collateral ligament, posteromedial capsule 3. Layer III—deep medial collateral ligament, capsule of knee joint

27% of the entire length of the leg.2 The distal femur is twice as likely to be injured compared with the proximal tibia. The medial structures of the knee are divided into three distinct layers. Layer I includes the deep sartorius fascia. Layer II includes the superficial MCL and the ligaments of the posteromedial capsule. Layer III is the deep MCL and the knee capsule (Box 23C2-1; see also Chapter 23C1).1,2,4 The superficial MCL, layer II, originates over a large region of the medial femoral epiphysis that extends to the physis. It finally inserts on the metaphyseal region of the proximal tibia. The deep MCL also originates at the distal femoral epiphysis and extends to the epiphyseal perichondrium of the proximal tibia.1,2 Both the distal femoral physis and the proximal tibia physis are extracapsular and extrasynovial.1

HISTORY AND PHYSICAL EXAMINATION The most important tool in diagnosing any injury is the history and physical examination. This holds true especially in the pediatric population, even though sometimes it is tough to obtain. The history should include multiple questions, including but not restricted to precipitating and exacerbating events and whether the mechanism of injury was low or high energy (e.g., motor vehicle crash versus twisting the knee playing soccer). A key question is the presence or absence of an effusion. The presence of effusion can narrow the differential diagnosis (Box 23C2-2). The five main causes of an effusion in the knee are fracture, BOX 23C2-2 differential Diagnosis of Medial-Sided Knee Injuries

• Fracture—proximal tibia, distal femur • Medial collateral ligament injury • Medial meniscal tear • Discoid meniscus • Legg-Calvé-Perthes disease • Slipped capital femoral epiphysis • Functional knee • Tumor

Knee 1639

meniscal pathology, patella dislocation, ligamentous injury (anterior cruciate ligament [ACL] tear), and cartilage damage. It is important to note whether the effusion happened within 24 hours or was delayed in its presentation. The presence of locking, popping, or catching prompts diagnostic questions leading to intra-articular pathology. The parents are asked about limping and swelling of the limb. The patient’s age and the absence or beginning of menses are important regarding physeal injuries. The accuracy of a history is difficult in young patients because they frequently forget the mechanism of injury, have difficulty describing their symptoms, and may exhibit a lack of cooperation or inconsistencies with verbal questioning.5 Harvell and associates found that the accuracy of preoperative clinical diagnosis in preadolescent children was only 55%, and that it increased to 70% in adolescent patients.6 Functional knee pain should also be in the differential diagnosis. This entity develops to allow children to deal with environmental stressors and emotional outburst.5 The next important step is the physical examination. This should always begin with analysis of the patient’s gait. The differentiation between an antalgic and a Trendelenburg gait can help narrow the differential. The examination of the hip is important in children. All patients between 5 and 15 years of age presenting with knee pain should have their hip evaluated.5 Many pathologic conditions of the hip can present as medial-sided knee pain, including slipped capital femoral epiphysis or Legg-Calvé-Perthes disease. It is important to observe for the presence of a lateral thrust or asymmetry between foot progression angles. In children, examination of the normal knee is helpful. First, it places the patient at ease before causing pain, and second, it gives the physician the ability to compare findings, especially if the patient has increased physiologic laxity. With children, establishing a good rapport and understanding helps facilitate the physical examination. Once a full examination of the normal knee has been performed and full range of motion and ligamentous and neurovascular examination recorded, the physician can focus on the injured knee. This begins with visual inspection, making note of lacerations, abrasions, ecchymosis, and swelling that may help to point toward the injury. The presence of an effusion is important in determining intra-articular pathology. As stated earlier, an effusion can narrow the differential diagnosis to include meniscal injury, ligamentous injury, fracture, patella dislocation, or cartilage damage. The presence of quadriceps atrophy occurs with long-term immobilization or altered gait. Palpation of the entire knee in a systematic way is crucial. Joint line tenderness has been shown to correlate with meniscal pathology.20 Reproduction of pain or popping with flexion and extension maneuvers with rotation, such as McMurray’s test and Apley’s grind test, is suggestive of meniscal injuries. Numerous studies have shown that in young patients, these tests are not particularly accurate.1,7,19,21 Ligamentous examination should follow basic range of motion evaluation. The most commonly described is Lachman’s test, looking for ACL injury. Lachman’s test is the most sensitive test for the presence of anterior laxity.22 The posterior drawer test is used to determine the competency of the posterior cruciate ligament (PCL). Valgus

stress to the knee at 30 degrees of flexion tests the competency of the MCL. If there is laxity to valgus stress at full extension, one should be alert to the fact there might be a multiligamentous injury. Varus stress at 30 degrees of flexion tests the strength of the lateral collateral ligament; laxity with varus stress at full extension should warn to a possible posterior collateral ligament or ACL injury. After a basic physical examination and history are performed, imaging techniques can be used to further evaluate the knee. These examinations include radiography, magnetic resonance imaging (MRI), and computed tomography (CT), if needed.

INJURIES TO THE MEDIAL COLLATERAL LIGAMENT Injuries to the knee in children result in fractures or physeal injuries more commonly than ligament disruptions because of the weakness of the growth plate relative to the strength of the ligaments in a skeletally immature patient. Injuries to the MCL are divided into three grades according to the American Medical Association Standard Nomenclature of Athletic Injuries. Grade I shows no knee instability with no medial opening on stress radiographs. Grade II includes partial anatomic discontinuity and mild functional instability. The injury presents with mild (0 to 5 mm) or moderate (6 to 10 mm) displacement with valgus stress to the injured knee. Radiographs present with some medial opening. Grade III demonstrates gross instability with displacement of greater than 10 mm and no end point with valgus stress.9,10 Isolated MCL injuries are rare, and therefore the literature is scarce. Most ligamentous injuries are associated with a physeal fracture.11,12 Injuries to the MCL are usually found in patients with high-energy trauma. Clanton reviewed 932 patients with knee injuries. Only 9 of these patients had ligamentous injuries with open physes, all younger than 14 years. Five children were hit by automobiles; one was in a motorcycle crash; one in a go-cart crash; one fell out of a moving vehicle; and one fell from a merry-go-round. Five patients had injuries to the MCL: two were torn from the meniscofemoral portion, and three were torn from meniscotibial portion of the MCL.12 Kannus reviewed 33 patients who sustained knee ligament injuries in skeletally immature patients. They found 13 patients with grade II MCL strains, 1 patient with grade III MCL strains, 4 with combined ACL and grade II MCL, and 1 with combined ACL and grade III MCL injuries.10 The extent of injury can be correlated to a careful history and examination. The examination should include a full knee examination and should be directed to the amount of valgus instability. The test is performed at 30 degrees of flexion, and a valgus strain is applied. This test is also performed at full extension to rule out other ligamentous instabilities that can occur with MCL tears. A medial opening between 5 and 10 mm suggests an incomplete injury, grade II. A medial opening greater than 1 cm with no end point points to a grade III injury or complete disruption of the MCL. One must also assess the competency of the ACL and PCL by performing Lachman’s test and the posterior drawer test (Box 23C2-3; see Chapter 23C1).


BOX 23C2-3 Signs and Symptoms of Medial Collateral Ligament Tear enderness to palpation along insertion or origin of • T medial collateral ligament • Pain with valgus stress • Opening to valgus stress at 30 degrees of flexion

Diagnostic Testing The two most important modalities are plain and stress radiographs. If more imaging is need, MRI may be warranted to evaluate ligamentous and meniscal pathology. The first step would be to obtain radiographs to assess for fractures—anteroposterior and lateral views of the knee. If a child presents with chronic knee pain, anteroposterior and frog-leg lateral views of the ipsilateral hip may be warranted to rule out hip pathology. The next modality of choice is MRI. This can be employed if intra-articular or ligamentous injury is suspected. In children, however, clinical examination is more sensitive in determining the extent of the knee injury.13 Kocher and colleagues found a lower sensitivity (61.7% versus 78.3%) and specificity (90.2% versus 95.5%) with the diagnostic performance of MRI studies in children younger than 12 years than in adolescents 12 to 16 years of age, respectively.14 This correlates to prior studies that have shown lower values of sensitivity and specificity for the diagnosis of meniscal injuries (sensitivity, 50% versus 100%; specificity, 46% versus 95%) and ACL injuries (sensitivity, 64% versus 78%; specificity, 94% versus 100%) in children compared with adults. The data clearly show that clinical examination and history are the keys to diagnosing injuries of the knee in children.

Treatment Most MCL injuries in children can be treated nonoperatively. Deciding which ones to operate on is difficult. Treatment principles of MCL injuries are the same as in adults (see Chapter 23C1). Grade I MCL strains are all treated nonoperatively. Grade II MCL strains are also treated nonoperatively, but they tend to have a longer recovery period. The controversy revolves around grade III MCL tears. Numerous studies have shown nonoperative treatment to be effective. Jones and associates retrospectively evaluated 24 high school football athletes with isolated grade III MCL injuries.15 They found 22 cases in which knee stability was achieved at an average of 29 days. The athletes returned to play competitive football at a mean of 34 days. Kannus and Jarvinen reviewed 32 patients with grade II or III injuries to the ligaments of the knee and concluded that grade II injuries in adolescents can be treated nonoperatively but that grade III injuries show long-term functional instability and some early posttraumatic osteoarthritis.10 The study had many deficiencies, including combining multiligamentous injuries with the isolated MCL results. This could explain the long-term instability found in the knees with grade III injuries. Most authors agree that nonoperative treatment is the standard of care for grade III injuries.

Authors’ Preferred Method We start treating grade I and II MCL using a hinged knee sleeve for 2 to 3 weeks, with activity modification and physical therapy focusing on quadriceps and hamstring strengthening. Grade III MCL injuries are also treated nonoperatively. They are placed in a hinged knee brace locked at 30 degrees of flexion with non–weight-bearing for 2 weeks. Patients are allowed to bear weight 2 to 4 weeks after injury and progress as tolerated. They begin passive range of motion and physical therapy at this time. Patients are allowed to return to athletic competition when they have no pain or instability. They are also assessed based on their physical examination. If laxity with valgus stress remains, the athlete is held from activities until examination mirrors the opposite knee (Box 23C2-4; see Chapter 23C1).

BOX 23C2-4 Treatment of Medial Collateral Ligament Injury Grade I—hinged knee sleeve, physical therapy Grade II—hinged knee sleeve, protected immobilization for 2 to 4 weeks, physical therapy Grade III—hinged knee brace locked at 2 to 4 weeks, non-weight-bearing for 2 to 4 weeks, passive range of motion, physical therapy

FRACTURES OF THE MEDIAL KNEE Fractures to the physeal aspects of the knee are more common than ligamentous injuries in children. Physeal fractures are relatively uncommon, accounting for only 1% of all pediatric fractures.11 They can be divided into two groups: (1) distal femoral epiphyseal fractures, which account for about 5% to 15% of all physeal fractures16,24 and (2) proximal tibial epiphyseal fractures, which account for less than 2% of all physeal fractures (Box 23C2-5).16 The rate and magnitude of the injuring force are the determining factors for whether there will be a ligamentous injury or a physeal fracture. High-magnitude forces at low velocity result in physeal injuries, and low-magnitude forces at high velocity result in ligament injuries.17 Physeal fractures are divided according to the Salter-Harris classification, types I thru IV (Fig. 23C2-1). Salter-Harris I injuries are complete separation of the epiphysis from the

BOX 23C2-5 Anatomic Location of Fractures around the Knee

• Distal femoral epiphysis or physis fracture • Proximal tibial epiphysis or physis fracture • Patella sleeve fracture • Tibial tubercle fractures • Tibial spine fractures • Osteochondral fractures

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Type I

Type II

Type III

Type IV

Type V

Figure 23C2-1 Classification of epiphyseal fractures according to the Salter-Harris system. In type I fractures, the fracture line traverses the physis, staying entirely within it. In type II injuries, the fracture line traverses the growth plate for a variable length and then exits obliquely through the metaphysis. Type III fractures also begin in the physis but exit through the epiphysis toward the joint. Type IV fractures involve a vertical split of the epiphysis, physis, and metaphysis. Type V fractures are crush injuries to the physeal plate. (Redrawn from Edwards P, Grana W: Physeal fractures about the knee. J Am Acad Orthop Surg 3:63-69, 1995.)

metaphysis without bone fracture. Type II injuries have a line of separation that extends from the epiphyseal plate out through a portion of the metaphysis; this produces the Thurston-Holland fragment. Most of these injuries occur in children older than 10 years. These are the most common type of injury seen in physeal fractures. Type III injuries are intra-articular; the fracture line begins from the joint surface into the physis than exits perpendicular to the physis. Type IV injuries are also intra-articular. The injury begins at the joint surface through the physis and exits through the metaphysis, resulting in a complete split. Type V injuries are rare but involve a crushing injury to the epiphysis and physis.8

Distal Femoral Epiphyseal Fractures History and Physical Examination Patients with distal femoral epiphysis fractures usually present with limited range of motion, inability to bear weight, large effusion of the knee, and tenderness along the physis (Box 23C2-6). Obvious deformity of the knee can be detected on visual inspection. With anterior displacement, the patella can be prominent, and anterior skin dimpling can be seen. With posterior displacement, the distal metaphysis becomes prominent at or above the patella. Crepitus with range of motion can also be felt.

BOX 23C2-6 Signs and Symptoms of Fractures around the Knee

• Inability to bear weight • Tenderness to palpation over growth plate or epiphysis • Knee effusion, hemarthrosis • Pain with range of motion • Crepitation • Visual deformity of knee

Imaging The first step in evaluating for a physeal injury after the history and physical examination is obtaining plain radiographs. Standard anteroposterior and lateral radiographs are required to establish a diagnosis (Fig. 23C2-2). If there remains a concern for fracture, oblique radiographs and radiographs of the contralateral side can be helpful. When there is apparent laxity to the knee and plain radiographs are normal, stress radiographs can be obtained to rule out physeal separation compared with ligamentous injury. MRI or CT can also be obtained to rule out nondisplaced injuries (Fig. 23C2-3). MRI can also be obtained to evaluate intra-articular pathology.

Treatment Treatment is based on the amount of displacement and type of fracture pattern. The main goal in treatment of physeal injuries is to prevent growth disturbances and avoid damage to the physis. Salter-Harris I and II injuries that are nondisplaced can be treated nonoperatively. They require immobilization in either a long leg cast or hip spica cast for a minimum of 6 weeks.2 The duration of the cast and the method for immobilization are determined by the age and size of the patient. Displaced fractures need to be reduced to anatomic alignment. The acceptable amount of displacement is less than 2 mm.2 Reductions generally require general anesthesia. If reduction cannot be obtained or the fracture is unstable, operative fixation may be warranted. Smooth transphyseal pins are used for type I and II injuries. A large metaphyseal fracture fragment in a type II injury can be stabilized with either smooth pins or 4.5-mm or larger cannulated screws. Some physicians advocate bending or burying the pins to avoid bacterial contamination and the risk for a septic joint. Salter-Harris III and IV injuries that are stable and nondisplaced can also be treated nonoperatively using a cast. Weekly follow-up is indicated for the first 2 to 3 weeks to observe for any displacement of the fracture in the cast.

1642 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Figure 23C2-2 Antero posterior (A) and lateral (B) radiographs of a 12-year-old girl with knee pain after a motor vehicle crash. These radiographs demonstrate a Salter-Harris III fracture of the distal femur.

B

A

Fractures with displacement or that are irreducible with closed means require operative fixation. The goal in treatment is to restore joint congruity and align the physis. Percutaneous pins or cannulated screws can be used to obtain fixation (Fig. 23C2-4). These are all intra-articular fractures, so weight-bearing is limited until fracture healing is observed on plain radiographs (Table 23C2-1).

Proximal Tibial Epiphyseal Fractures History and Physical Examination

Treatment Treatment once again is similar to that for distal femoral epiphyses. The goal for these epiphyseal fractures is anatomic reduction to prevent growth disturbances. Nondisplaced and stable Salter-Harris I and II injuries can be treated nonoperatively with the use of cast immobilization for a minimum of 6 weeks.2 Displaced fractures require reduction under anesthesia. Most of the injuries are hyperextension type; thus, flexion usually achieves reduction of the fracture. These injuries are usually immobilized

Fractures of the proximal tibial epiphysis are less common than those of the distal femoral epiphysis. Almost half of proximal tibial injuries occur in sporting activities.17 These injuries are usually the result of hyperextension and valgus forces. Because of the close proximity of the popliteal artery, vascular injuries are a concern with these types of injuries. Neurovascular injury occurs in up to 10% of proximal tibial epiphyseal injuries.3 Many believe that proximal tibial fractures are equivalent to knee dislocations in adults. Physical examination should consist of a thorough evaluation of the neurovascular status of the extremity, including the dorsalis pedis and posterior tibial arterial pulses and function of the peroneal and posterior tibial nerves. Close monitoring for compartment syndrome should also be considered. If there is any abnormality in the vascular status of the limb, a vascular surgery consultation is needed for evaluation for an arteriography.

Imaging Basic imaging includes plain radiographs, anteroposterior and lateral views. Stress radiographs may also be indicated (Fig. 23C2-5). See the earlier section on distal femoral epiphyseal fractures for further imaging studies.

Figure 23C2-3 Computed tomographic scan of the knee demonstrating a Salter-Harris III fracture of the distal femur. The patient has a fracture line that starts intra-articularly and extends into the metaphysis.

Knee 1643 Figure 23C2-4 Anteroposterior (A) and lateral (B) radiographs after operative fixation with two cannulated screws of the Salter-Harris III distal femur fracture.

A

B

in about 20 to 30 degrees of flexion, which helps reduce the risks for displacement and vascular compromise.22 If reduction cannot be sustained or the fracture is irreducible by closed means, operative fixation is required. Smooth, crossed transphyseal pins are used for stable fixation. A Salter-Harris type II injury with a large metaphyseal fragment can be stabilized with cannulated screws. Treatment of Salter-Harris III and IV injuries is the same as for distal femoral epiphyseal fractures of the same type. Toetouch is permitted in the cast once the patient’s symptoms allow (see Table 23C2-1).

Complications The risk for growth deformity remains the number one concern after epiphyseal fractures. This risk is lowest with type I and II injuries and increases with severity of the fracture. There is almost a 100% chance of growth disturbance with type V injuries. In fractures that involve the distal femoral epiphysis, shortening and angular deformity can be common (Box 23C2-7). Leg-length discrepancies of less than 2 cm can be treated nonoperatively. If more than

Return to Sports The time to return to athletic activities is determined by the type of fracture. Patients with Salter-Harris I and II injuries can usually return to sports in 3 to 4 months. Athletes with Salter-Harris III and IV injuries take longer to return to sports, roughly 4 to 6 months.2

TABLE 23C2-1 Treatment Options Type

Nondisplaced

Displaced

I

Cast immobilization for at least 6 wk Cast immobilization for at least 6 wk Cast immobilization for 6 wk

1. Closed reduction with cast immobilization 2. ORIF: smooth pins; cast for 4 wk 1. Closed reduction with cast immobilization 2. ORIF: smooth pins; cast for 4 wk 1. Closed reduction with cast immobilization 2. ORIF: cannulated screws; cast for 4 wk 1. Closed reduction with cast immobilization 2. ORIF: cannulated screws; cast for 4 wk

II III

IV

Cast immobilization for 6 wk

ORIF, open reduction with internal fixation.

Figure 23C2-5 Physeal separation of medial proximal tibia with stress radiographs without joint space widening. (From Edwards P, Grana W: Physeal fractures about the knee. J Am Acad Orthop Surg 3:63-69, 1995.)


BOX 23C2-7 Complications of Knee Fractures

• Leg-length discrepancies • Angular deformity—valgus • Vascular compromise—popliteal artery injury 2 cm, referral to a pediatric orthopaedist for epiphysiodesis or lengthening would be prudent. Angular deformity, especially valgus deformity, can occur after physeal injuries. Valgus deformity after proximal tibial epiphyseal fractures can spontaneously correct up to 3 years after injury if enough growth remains in the child.17 Bony bridges can lead to angular deformities; they can be evaluated using MRI, which is the imaging modality of choice to evaluate for osseous bridge lesions. These lesions can be removed if they occupy less than 50% of the growth plate. Patients should be followed clinically at 6-month intervals to observe leg-length discrepancy and angular deformity until skeletal maturity. They should be followed for up to 2 years after initial injury.2

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l MCL injuries in children are treated similarly to those in adults. l Isolated grade I and II MCL strains are treated nonoperatively. l Grade III MCL tears are also treated nonoperatively, but some surgeons advocate operative reconstruction.

l Fractures of the epiphysis or physis are more common than ligamentous injuries in children. l Stress radiographs may be indicated to rule out physeal injuries. l Fracture treatment revolves around anatomic reduction and stabilization with cast immobilization or open reduction with internal fixation. l Salter-Harris I and II injuries require 3 to 4 months before return to sports. l Salter-Harris III and IV injuries require 4 to 6 months before return to sports. l Leg-length discrepancies and angular deformity are complications of physeal fractures.

S U G G E S T E D

R E A D I N G S

Abel M: Orthopedic Knowledge Update: Pediatrics 3. Rosemont, Ill, American Academy of Orthopedic Surgeons, 2006, pp 281-289. Bertin K, Goble E: Ligament injuries associated with physeal fractures about the knee. Clin Orthop 177:188-195, 1983. Birch J: Instructional Course Lectures: Pediatrics. Rosemont, Ill, American Academy of Orthopedic Surgeons, 2006, pp 121-129. Johnson D, Mair S: Clinical Sports Medicine. Philadelphia, Mosby-Elsevier, 2006, pp 639-650. Jones R, Henley B, Frances P: Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop 213:137-140, 1986. Kannus P, Jarvinen M: Knee ligament injuries in adolescents: Eight year follow up of conservative management. J Bone Joint Surg Br 70:772-776, 1988. Salter R, Harris W: Injuries involving the epiphyseal plate. J Bone Joint Surg 45:587-622, 1963. Zionts L: Fractures around the knee in children. J Am Acad Orthop Surg 10: 345-355, 2002.


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Anterior Cruciate Ligament Injuries 1. Anterior Cruciate Ligament Injuries in the Adult Nicholas J. Honkamp, Wei Shen, Nnamdi Okeke, Mario Ferretti, and Freddie H. Fu

ANATOMY AND BIOMECHANICS Anatomy The anterior cruciate ligament (ACL) originates on the medial wall of the lateral femoral condyle. It courses anteriorly and medially across the knee joint and inserts into the tibial articular surface. It consists of two functional bundles, the anteromedial (AM) bundle and the posterolateral

(PL) bundle, named for their tibial insertion sites.1-3 The primary role of the ACL is to provide primary anteroposterior stability and secondary rotatory stability to the knee joint. Microscopically, the ligament is primarily composed of longitudinally arranged collagen fibrils. The diameter of these fibrils ranges from 20 to 170 μm with the diameter being largest in the distal region decreasing proximally. The percentage of total cross-sectional area occupied by collagen fibers remains significantly unchanged along the

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A

B

Figure 23D1-1 Sagittal plane (A) and oblique coronal plane (B) magnetic resonance imaging of the knee show the two bundles of the anterior cruciate ligament, the anteromedial (AM) and the posterolateral (PL) bundles.

length of the ligament. Multiple type III collagen–positive fibrils form a collagen fiber that is bundled together and ensheathed by a thin layer of connective tissue named the endotendineum. The bundled fibers and endotendineum make up what is called the subfascicular unit. Subfasciculi are collected in another connective tissue layer called the epitendineum, a much thicker layer than the endotendineum. This unit is named the fasciculus, the primary collagen unit of the ligament. The ligament is surrounded by the paratenon, which blends in with the epitendineum.4 The ends of the ligament deviate from this architecture and instead resemble fibrocartilage. This portion of the ligament includes oval-shaped cells, surrounded by a metachromatic extracellular matrix, that lay amongst the collagen fibrils.5 The blood supply to the ACL is primarily the middle genicular artery, a branch of the popliteal artery. It pierces

Figure 23D1-2 An arthroscopic view shows the two functional bundles of the anterior cruciate ligament, the anteromedial (AM) bundle and the posterolateral (PL) bundle. LFC, lateral femoral condyle.

the posterior capsule at the level of the intercondylar notch and courses along the posterior surface of the ACL within the synovial membrane surrounding the ligament. This synovial membrane originates at the posterior inlet of the intercondylar notch of the femur and extends distally to the tibial attachment of the ACL. Along the dorsal surface of the ACL, the middle genicular artery gives off ligamentous branches. The largest ligamentous branch, the tibial intercondylar artery, reaches the ACL at its proximal end and bifurcates just proximal to the tibial spine to supply both tibial condyles.6 The ligamentous branches form a periligamentous plexus, indicated as the source of profuse effusion and hemarthrosis typically seen after injury to the ACL. Blood vessels from the plexus penetrate the ligament horizontally and anastomose with a longitudinally oriented interligamentous network. Other sources of blood supply to the ACL are the inferior medial and lateral genicular arteries originating from the posterior surface of the popliteal artery.7 The innervation of the ACL comes from the posterior articular nerve, a branch of the tibial nerve in the popliteal fossa. It follows the path of the middle genicular artery piercing the posterior capsule and forms the popliteal plexus that tracks along the synovial lining and periligamentous vessels of the ligament.6 Although these appear to be primarily vasomotor, there are fibers in the intrafascicular spaces of the ligament that are similar in size to pain fibers.5,8 Furthermore, mechanoreceptors have been described on the surface of the ACL with their long axes running parallel with the ligament. The receptors themselves are housed at the insertion sites, primarily the femoral insertion site. These receptors may have proprioceptive qualities; however, there remains some uncertainty as to their exact function.9,10 There have been several fetal, cadaveric, arthroscopic, and radiographic studies detailing the gross anatomy of the ACL (Figs. 23D1-1 to 23D1-3).1-3,11-14 Fu and coworkers11 have shown that during early fetal development, the ACL is observed to consist of two distinct bundles, the AM and PL bundles. Fetal histologic examination of the ACL observed a septum of connective tissue separating the two bundles


LFC

AM PL

A

B

Figure 23D1-3 A, Fetal knee joint displaying two distinguishable bundles of the anterior cruciate ligament (ACL), the anteromedial (AM) bundle and the posterolateral (PL) bundle. B, On histologic examination of the fetal ACL, a septum (arrow) that separates the AM and PL bundles can be observed. LFC, lateral femoral condyle.

(see Fig. 23D1-3). The position and length of the bundles vary with changing angles of knee flexion and extension (Fig. 23D1-4). The selective recruitment of ACL fibers is partially the result of the changing length of the fibers with tension. As the fibers are recruited, the ligament has been shown to elongate by up to 3 mm with extension.15 From 0 to 30 degrees of flexion, the AM bundle shortens from its baseline length. With continued flexion from 30 to 70 degrees, the AM bundle lengthens back to its baseline length. Beyond 70 degrees of flexion, the bundle continues to elongate, beyond the baseline length, until it reaches maximal strain at about 120 degrees of flexion. The PL bundle is at maximal length and maximal strain when the knee is at full extension. As the knee is flexed, the PL bundle shortens, achieving minimal strain at about 120 degrees. At full extension, the bundles are parallel, and the femoral attachments sites are oriented vertically. With 90 degrees of knee flexion, the femoral PL attachment moves anteriorly, aligning the attachment sites horizontally. This motion creates

a situation in which the ACL bundles cross each other as the knee goes from extension into flexion. As mentioned earlier, the ACL has attachments on both the femur and the tibia. The specific locations of these attachments also play an important role in the selective recruitment of the collagen bands. This is due to the large area of each attachment site that allows various portions of the ligament to tighten at various degrees of knee flexion. The femoral attachment site is located on the posteromedial surface of the intercondylar notch on the lateral femoral condyle. The attachment site is circular, spanning an area of about 113 mm2. The tibial attachment site is located about 15 mm behind the anterior border of the tibial articular surface, medial to the attachment of the anterior horn of the lateral meniscus. This attachment is more oval, covering an area of about 136 mm2.2 For comparison, the cross-sectional area of the ACL mid-substance averages about 40 mm2. The femoral attachment sites of both bundles are often accompanied by bony landmarks. Arthroscopic and cadaveric studies (unpublished data) have shown two bony landmarks known as the cruciate ridge and the bundle ridge.11 The cruciate ridge runs proximal to distal, and it has been observed that no ACL fibers are anterior to this ridge. The bundle ridge runs anterior to posterior between the femoral insertion of the AM and PL bundles. This ridge is seen with careful dissection of the femoral ACL insertion site that maintains the bony anatomy of the intercondylar notch of the femoral condyle (Fig. 23D1-5). These two bony ridges can be used as useful landmarks in ACL reconstruction.

Biomechanics

Figure 23D1-4 In full extension, the femoral insertion sites of the anteromedial (AM, red) and posterolateral (PL, yellow) bundles of the anterior cruciate ligament are vertical. In 90 degrees of knee flexion, the insertion sites are horizontal. The fibers of the two bundles are parallel in extension and cross each other as the knee is flexed.

The main function of the ACL is restraint of anteroposterior translation of the tibia relative to the femur.16,17 It also acts as a secondary restraint to tibial rotation and valgus or varus stress. Age is an important factor in the strength of the ACL; typically, older ACLs fail with lower loads than do younger ACLs.18,19 With passive range knee extension, the ACL experiences forces of about 100 N, whereas walking produces about 400 N of force. Activities involving

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Figure 23D1-5 Arthroscopic view of the intercondylar notch. The cruciate ridge is above the femoral insertion sites of the anteromedial (AM) and posterolateral (PL) bundles, whereas the bundle ridge separates them.

acceleration, deceleration, or cutting maneuvers can produce up to 1700 N of force on the ACL.20 The ACL has a maximal tensile load of 2160 ± 157 N and a stiffness of 242 ± 28 N/mm.18 It is able to withstand strain of roughly 20% before failing. Furthermore, the ACL works in concert with many other anatomic structures in and around the knee joint that complement the function of the ACL to pro vide joint stability and limit pathologic knee motion.21-23 Thus, the ACL must experience an abnormal load to exceed failure capacity and sustain injury. Important variables that influence ACL strain are the position of the knee and the dynamic interaction of muscle activity. As shown by Beynnon and colleagues, increasing knee extension increases strain on the ACL.24 Restoration of anteroposterior translational stability alone does not correlate with subjective evaluations of knee stability. This suggests that rotational stability is an important function of the ACL and is a key to adequate knee stability.25 The cadaveric study of 10 knees by Gabriel and associates26 was an analysis of a combined rotatory load of 10 Nm (Newton-meter) valgus and 5 Nm internal tibial torque at 15 and 30 degrees of flexion. For the PL bundle, an in situ force of 21 N was recorded at 15 degrees and 14 N at 30 degrees. For the AM bundle, the in situ forces were 30 N and 35 N, respectively. This shows that at these angles, both the AM and PL bundles contribute not only to anteroposterior stability but also to rotational stability of the knee. Cadaveric biomechanical studies have shown that singlebundle ACL reconstruction is most successful in restoring anteroposterior knee stability but is insufficient in controlling combined rotatory loads of internal tibial and valgus torque.27 Yagi and associates28 performed a study comparing a single-bundle reconstruction with the femoral tunnel placed at the 11- or 1-o’clock position with anatomic double-bundle ACL reconstruction. This study concluded that

double-bundle ACL reconstruction is better able to resist anterior tibial translation at full extension and 30 degrees of flexion compared with the single-bundle technique. Furthermore, when a rotatory torque was applied at 15 and 30 degrees of flexion, the double-bundle ACL reconstruction had a response closer to that of the intact ACL compared with the single-bundle technique. Yamamoto and coworkers29 also did a comparison of the double-bundle ACL reconstruction to single-bundle reconstruction, with the femoral tunnel being placed at about the 10-o’clock position for the right knee. They reported that the doublebundle anatomic reconstruction better restored the anterior tibial translation at 60 and 90 degrees of flexion when compared with the single-bundle technique. Mae and associates30 duplicated similar results in their work using a two-socket quadrupled hamstring graft when tested by use of robotics. Another study performed by Tashman and coworkers31 looked at the in vivo kinematics of normal knees and knees subjected to single-bundle reconstruction. Subjects with a normal ACL were compared with a group of patients who underwent single-bundle ACL reconstruction to evaluate anteroposterior translation and knee rotation during downhill jogging. It was discovered that patients who underwent single-bundle ACL reconstruction had fully restored anteroposterior translation but increased tibial rotation as compared with subjects with a normal ACL during treadmill running. These studies indicate that double-bundle ACL reconstruction may be the best reparative technique for restoring the normal kinematics of the knee joint.

BASIC SCIENCE OF THE ANTERIOR CRUCIATE LIGAMENT Biologic Response to Anterior Cruciate Ligament Injury The ACL functions in unison with other anatomic structures in the knee to limit anterior translation and maintain knee joint stability. However, when injury does occur, it is often found that the complementary structures are also damaged or are insufficient to maintain the function of the lost ligament.21-23,32,33 Furthermore, when the ACL sustains injury or becomes deficient, other structures within the knee joint are at risk for injury, such as the menisci and the chondral surfaces.34-36 Typically, injury to extra-articular ligaments leads to the formation of local hematoma, which organizes into a fibrinogen mesh where inflammatory cells settle to mediate the natural inflammatory response. As the inflammation wanes, granulation tissue forms and reorganizes into fibrous tissue. The formation of fibrous scar tissue restores function to the ligament.37 The ACL, however, is intraarticular. The ACL is encased in only a thin envelope of synovial lining, unlike other extra-articular ligaments such as the medial collateral ligament (MCL) that have strong soft tissue encasement. When the ACL sustains injury, its synovial lining is compromised as well. Bleeding from this injury dissipates throughout the joint space and is unable to organize into fibrous tissue. Thus, the formation of fibrous scar tissue never occurs, and the ligament


remains functionally incompetent. When the synovial lining remains intact, which often occurs in partial ligament injuries, blood clot formation occurs that initiates scar formation.38,39 Other factors that may be influencing the lack of healing seen in the ACL injuries include the cytokine profile of the intra-articular space. After injury, proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-α are elevated, whereas protective anti-inflammatory cytokines like interleukin receptor antagonist protein are decreased. Such a hostile cytokine environment is thought to contribute to the poor healing observed in the ACL and may have long-term implications in the development of osteoarthritis.40 Despite current knowledge of the healing differences between intra-articular and extra-articular ligaments, much remains unclear. In comparing extra-articular ligaments such as the MCL with intra-articular ligaments such as the anterior cruciate, the cruciate ligament fibroblasts have a significantly higher production of extracellular matrix and collagenous proteins than the collateral ligament fibroblasts.41,42 However, under conditions of inflammation, the fibroblasts of the cruciate ligament exhibit lower mobility than those of the medial collateral.43 Furthermore, migration of the cells in the cruciate ligament is slower in comparison to the MCL.44 More work in vivo and in vitro is clearly needed in understanding and characterizing the healing response in ligament tissue.

Biology of Anterior Cruciate Ligament Graft Reconstruction The poor healing of the ACL, combined with the risk for subsequent injury to the other supporting structures, has treatment implications. With the ligament unable to heal on its own, reconstructive surgery is often performed wherein tendon grafts are transplanted to replace the deficient ligaments. After transplantation, biologic modifications occur to incorporate the grafts into the host knee. Initially, the tendon graft is subjected to the process of inflammation and avascular necrosis. After the donor fibroblasts have died, revascularization of the remaining graft tissue occurs. Inflammation and revascularization is seen within 20 days after implantation but takes 3 to 6 months for revascularization to finalize. Next, migration and repopulation of the graft by host fibroblasts occur. This is reported to be complete within 4 to 6 weeks at which time no donor fibroblasts are detectable. Lastly, there is gradual remodeling of the graft and remodification of the collagenous structure as the collagen realigns longitudinally along the graft in a similar fashion to the normal cruciate ligament.45,46 This collagen remodeling and realignment of the graft can be seen on histologic evaluation at 6 weeks after transplantation and can continue for up to 6 months.37 The transplanted graft has the ability to develop and adapt to mechanical demands. However, it never fully resembles the structure of the original graft tendon tissue or the native cruciate ligament it replaced. The ultrastructure of the ligament, the size of the fibrils, and the concentrations of the extracellular matrix differ significantly from the original tissue.37,47

EPIDEMIOLOGY Injury of the ACL accounts for roughly 40% to 50% of all ligamentous knee injuries. Injury to the cruciate ligament is even more common in the young athletic population. In the general population, 70% of injuries that occur are secondary to sports activity.48 Among the activities related to ACL injury, skiing and soccer are ranked as the highestrisk activities for cruciate injury. Women display a higher propensity to ACL injury compared with men in most sports, including basketball, volleyball, and soccer.49 Before advances in reconstructive surgery, many of these injuries would limit sports. Currently, cruciate ligament reconstruction is allowing for the return to sports activity for most patients. Although results vary, many return to sports activity after about 6 months when given appropriate postoperative therapy. Recognition of the high prevalence of ACL injury in the sporting population will assist in prompt diagnosis and treatment as well as reduce time lost to injury.

CLASSIFICATION There is no standardized classification system widely used in the evaluation of ACL injuries. We prefer to divide patients into those with multiple ligamentous injuries, including an ACL injury, and those with isolated ACL injuries. For those with isolated ACL injuries, we attempt to determine whether the injury is a partial versus a complete tear. We subdivide partial injuries by which bundles are involved, as we commonly perform ACL single-bundle reconstruction and augmentation surgery in those cases in which one bundle remains functionally intact and the other bundle is torn. Although a further subclassification, which includes any associated chondral or meniscal pathology, is noteworthy, we do not formally separate these injuries into different sub-categories.

EVALUATION Clinical Presentation and History A thorough patient history is the initial step to diagnose and treat ACL injuries. Obtaining a complete history of the injury will direct the physical examination toward a complete and accurate diagnosis. Mechanism of injury, initial symptoms, previous injuries, time since injury, and any late sequelae, including reinjuries, are all pertinent information to obtain while taking a presenting patient’s history. Mechanism of injury can be crucial in the proper diagnosis of injury. Unfortunately, most of the time, patients are unable to recall precisely the events or mechanisms of injury.50,51 When this situation arises, it is often helpful to inquire about witness accounts and, if possible, video footage of the injurious event. Often in sports injuries, a coach, personal trainer, or teammate may be able to give an account of the events. Among the more common mechanisms of injury are low-energy injuries that occur during athletic activities. These types of injuries include direct contact injuries and those secondary to indirect noncontact mechanisms such

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as sudden deceleration or rotational maneuvers. Direct contact injuries often result in hyperextension or valgus stress on the knee, resulting in cruciate ligament injury. Of the two types, noncontact injury is the most common, with only about one third of patients detailing a contact mechanism of injury.52 High-impact or high-energy injuries such as motor vehicle crashes less commonly cause cruciate ligament injuries. With high-energy mechanisms, patients often present with concurrent injuries, including musculoskeletal, pelvic, abdominal, spine, and head injuries. In such cases, a thorough history and physical examination is highly important to assess and treat these associated injuries. The initial symptoms and sensations at the time of injury are also very important in determining a diagnosis. Patients are often able to recall common sensations such as popping or tearing at the time of injury; these represent some of the most common initial complaints of cruciate ligament injury.51,53 Other symptoms that a patient may complain about include the inability to bear weight on the injured leg and instability or the sensation of the knee “giving out.” Attention should be given to the ability to continue with competitive activity because many athletes are unable to participate after sustaining an acute injury.54 Post-traumatic swelling of the knee joint is another indicator of ligament injury. Swelling is the physical manifestation of hemarthrosis following disruption of the ligament’s blood supply. This event can be seen within 12 hours after injury.51,55 All of the aforementioned symptoms are indicative of injury to the ACL; however, they are not exclusive to the cruciate ligament because they may occur with injury to other anatomic structures in the knee such as the MCL, the menisci, the patella, or the posterior cruciate ligament (PCL). Conversely, absence of symptoms or signs such as a hemarthrosis does not exclude a diagnosis of ACL injury. In documenting a complete history, activities of daily living are important pieces of patient information to collect. Such facts include activity level, job requirements, sports activity, and future plans of activity. These factors weigh heavily in making treatment decisions. Surgically, such factors may dictate the choice of graft, postoperative rehabilitation speed, as well as surgical timing.

Physical Examination and Testing Physical examination is of monumental importance in diagnosing ACL injuries. Although patient history is useful in indicating ligament injury, the physical examination should be able to establish a definite diagnosis of injury to the cruciate ligament in most cases. Timing of the physical examination must be considered when evaluating an injury. Examinations performed immediately after an injury (before the onset of swelling, pain, and reflex muscle splinting) are more accurate than after the injury response has been initiated. Typically, this can occur only when the examining clinician is present at the time of the injury. If the examination is delayed and the initial symptoms have manifested, the patient may be difficult to evaluate, decreasing the accuracy of the examination. In these situations, it is best to repeat the examination in a few days. The initial step in examination is observation of the knee, including the presence of malalignment or swelling.

Malalignment can be indicative of a fracture or a sign of knee dislocation, both of which may require urgent medical attention. Depending on the time frame of the examination, an effusion may be detectable. This often appears about 4 hours after injury and may not be present with immediate examination of an injured knee. Therefore, a lack of an effusion is not an indication to exclude cruciate ligament injury. Furthermore, the severity of the injury may affect the presence of an effusion as well. With more severe injuries that injure a greater portion of the knee and the surrounding tissues, the consequential effusion may have several pathways to diffuse from the primary site of injury. After inspection, manual palpation of both knee joints is performed. Accurate assessment begins with palpation of the unaffected knee provided the injury is unilateral. Doing so will provide the examiner with a referential baseline with which to compare the injured limb. It also has the secondary benefit of familiarizing the patient with the examination procedure and thus relaxing the patient and preventing guarding, which can limit examination findings. The ACL is itself unable to be palpated, but palpation still plays an important role in cruciate ligament injury evaluation. Palpation is useful in detecting the presence of an effusion that may have been missed on inspection. It also serves to quantify the degree of effusion if present. Palpation is also a good examination tool to detect injury to surrounding knee structures. Medial and lateral joint line tenderness may indicate concomitant meniscal or chondral injury. Other structures to palpate include the medial and lateral collateral ligaments and their insertion sights. Functional testing of the knee should then be performed. This includes both active and passive range of motion testing to check for loss of motion. Various factors may cause loss of motion, including pain in the knee, a large effusion, an incompetent extensor mechanism, or a mechanical block. Effusions may be aspirated to alleviate pain and improve motion. Examining the aspirate can provide further clinical clues by confirming the presence of hemarthrosis, which can be indicative of ligament injury, or the presence of fat globules in the fluid, which indicates a fracture within the knee. If there is a mechanical block, the differential diagnosis should include meniscal tears, ruptured ACL obstruction, or loose body. Use of other diagnostic tools, such as radiographs or magnetic resonance imaging (MRI), may be needed to fully discern the cause of the obstruction. Stability testing of the knee should follow next. Standard practice should include testing of not only anterior stability but also posterior, varus, valgus, and rotational stability. Anterior stability testing usually employs the use of the Lachman test. The Lachman test is performed while the knee is flexed at 20 to 30 degrees (often bolstered with a thigh support). In this position, a manual anterior force is applied to the proximal tibia while the distal femur is stabilized with the opposite hand. The anterior laxity is assessed in the degree of anterior translation of the tibia relative to the femur and in the firmness of the end point at which translation is halted. From patient to patient, there is natural variance of normal laxity within the joint. Therefore, in assessing anterior stability of an injured individual, there is no absolute degree indicative of disease; rather,


a comparison is made between the injured and the contralateral normal knee. The degree of translation is categorized in grades of laxity. Grade I laxity describes 1 to 5 mm of increased anterior translation. Grade II laxity is 6 to 10 mm, and grade III is more than 10 mm of translation when compared with the opposite, uninjured knee.56 In addition to the Lachman test, arthrometers have been employed to provide objective instrumented laxity measures of ACL laxity. The KT-1000 (MEDmetric, San Diego, CA) is the mostly commonly cited device. Although not replacing the function of the Lachman test, arthrometric examination does provide some advantages over the manual examination, including the assessment of large patients when the manual examination can be limited owing to lack of control of a large limb. In similar fashion to the Lachman test, KT-1000 testing is performed with thigh support placing the limb in 20 to 30 degrees of knee flexion. A footrest is included with lateral supports to prevent external rotation of the tibia, maintaining a neutral rotation of both limbs (an issue to be aware of when performing the Lachman test). The device is aligned with the joint line, and positioned with a sensor pad on the patella and tibial tubercle. Two Velcro straps attached to the arthrometer are used to fasten the device in position vertically along the lower limb. Before zero point calibration through trial runs, the patient is asked to relax the thigh muscles; it is best to have the patient resting in the supine position. A vertical anterior force is applied with the use of a handle, and measurements of translation are made with 15, 20, and 30 pounds (67, 89, and 134 N, respectively) of force on the tibia. At each force level, the device emits an audible tone denoting the force threshold for measurement. Additional testing with the KT-1000 includes the maximal manual pull test. This is performed by applying an anterior force on the proximal posterior tibia, much like the Lachman and recording the maximal measurement displayed on the arthrometer. This device is used on both the injured and normal knee for comparison. Accuracy is a key concern when employing the use of either the Lachman test or the KT-1000 to assess laxity. With the Lachman test, the knee must be maintained in a neutral alignment while performing the examination. It has been shown that internal or external rotation decreases the degree of anterior translation, yielding a false-negative reading and potentially masking true injury.20 Other factors to consider include the presence of a large effusion or muscle splinting, which limits anterior translation as well. PCL incompetence often can mislead an examiner to overestimate anterior translation. This occurs when an insufficient PCL allows for posterior sag of the tibia. If unnoticed, the tibia would appear to translate anteriorly a greater distance, giving a false-positive result. Accuracy of the KT-1000 is affected by a variety of issues. Among these include user error, such as malalignment of the arthrometer along the tibia or joint line and improper application of anterior force. Relaxation of the quadriceps is also important in ensuring accuracy of arthrometric measures. Patient apprehension or pain may make relaxation of the thigh muscle impossible when performing the KT-1000 examination; however, it is essential in obtaining correct information about the state of the ACL.

The anterior drawer test is another examination technique used to evaluate anterior translation of the tibia. The knee is placed in 90 degrees of flexion, and the foot is held in place throughout the examination. Next, manual application of an anterior force is performed on the posterior proximal tibia. Measurement of the observed translation is graded like that of the Lachman test. The Lachman test is a more sensitive physical examination test than the anterior drawer test and therefore is used more frequently in the clinical examination. The pivot shift test is another clinical examination test to measure instability in the knee secondary to ACL injury. The test begins with the knee in full extension, and the patient is asked to relax the musculature of the limb being tested. A valgus stress is placed on the tibia, while an axial load and internal rotation are simultaneously applied. The knee is then slowly flexed with these applied forces. During this motion, the lateral side of the plateau subluxates to a greater extent than the medial side.57 With further flexion, the lateral tibia reduces, producing the pivot shift. This test is graded on the degree of subluxation and reduction of the lateral compartment of the knee, with grade 0 having no detectable shift, grade I having the tibia in a smooth glide during reduction, grade II having an abrupt reduction, and grade III having the tibia momentarily lock in the subluxated position before reduction. The sensitivity of this examination has shown to be highly dependent on patient apprehension, with its highest accuracy performed with the patient under anesthesia.54 Accuracy of the examination is influenced by injury to other structures in the knee as well, such as meniscal injuries and MCL injuries, which tend to decrease a detectable shift, leading to a misdiagnosis of ACL injury.

Imaging Radiographic studies of patients presenting for evaluation of ACL injury are often complementary in the primary diagnosis of ligament injury. A thorough history and physical examination of the knee can usually provide all the information to accurately diagnose ACL deficiency. However, there are benefits to performing radiographic imaging studies that can affect treatment and rehabilitation. Plain radiographic imaging plays a primary role in the exclusion of associated injuries in the evaluation of the ACL. Such associated injuries include lateral capsular avulsions (known as Segond’s fractures)58 and tibial eminence avulsion fractures seen in younger patients or those with osteopenia. Plain films can also alert the physician to the presence of loose bodies, proximal and distal knee fractures, degenerative disease, and osteophyte formation in chronic ACL-deficient knees.59,60 MRI is a highly useful tool for confirming the diagnosis of ACL disease. It is highly specific and sensitive and is able to provide information on the other intra-articular structures in the knee as well as evaluate both bundles of the native ACL. Fu and coworkers have published studies detailing the visualization of both bundles using MRI.11-13 They demonstrated use of viewing planes that follow the natural course of the ligament to improve the visualization of the AM and PL bundles (see Fig. 23D1-1B). The ability to visualize the individual bundles provides important

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information for surgical reconstruction of an incompetent cruciate ligament, especially when the double bundle reconstruction technique is employed for treatment. The presence of a chondral injury or bone bruise on MRI is highly indicative of ACL injury. About 80% of ligament injuries are accompanied by a bone bruise.61,62 These lesions are commonly located in the lateral tibial plateau and lateral femoral condyle. They are the result of abnormal impaction of the articular surfaces after ACL injury as the lateral compartment subluxates anteriorly. The presence of a bone bruise may also affect rehabilitation, leading to prolonged recovery of range of motion and stability, as was shown by the work of Johnson and coworkers.63

TREATMENT CONSIDERATIONS Gender Issues Female athletes have a fourfold to sixfold greater incidence of ACL injuries compared with male athletes participating in the same cutting and landing sports.64 When combined with an exponential increase in high school and collegiate sports participation among females in the past 30 years,65,66 the number of ACL injuries in female athletes has skyrocketed. The reasons for this gender disparity in ACL injuries are likely multifactorial. Several theories have been published to explain this disparity, and they can generally be divided into anatomic, hormonal, neuromuscular, and biomechanical differences. Anatomic differences include static standing knee alignment, notch width differences, joint laxity, foot alignment, and body mass index. Women have a relatively wider pelvis, which can lead to an increased Q angle. Some authors have linked an increased Q angle to increased ACL injury rates,67-69 whereas others have not.70 Because Q angle is generally a measurement of the patellofemoral joint and not knee valgus, other factors may be contributing to these mixed results.71 A smaller femoral notch width, even when corrected for bone width (so-called notch width index), has been show by some authors to increase the risk for ACL injury independent of gender,72-75 whereas others have noted no difference in notch width between genders nor an association between notch width and injury.70 Increased joint laxity is more commonly found in female athletes, and this increased laxity affects both sagittal plane (ACL) and coronal plane (MCL) motion.74,76,77 Such coupled anterior and valgus loading of the knee is a common mechanism for an ACL injury. Increased joint laxity in women can also be found in the foot, whereas increased foot pronation (“navicular drop”) is a predictor of anterior tibial translation, which may further strain the ACL.78,79 Increased ACL injury risk appears in girls typically around age 12 years, which coincides with a natural increase in body mass index (BMI). Uhorchak and associates74 and Buehler-Yund80 both found body mass index to be a significant risk factor for knee injury. The influence of hormonal changes during the female menstrual cycle and its potential effects on ACL injuries has generated significant controversy. Although some

s tudies have confirmed increased ACL injury risk during the ovulatory or postovulatory (early luteal) phases,81,82 others have not found any relationship between cycle phase and injury risk.83 A recent meta-analysis of nine prospective cohort studies on the topic found that six of the studies failed to show any relationship between cycle phase and anterior knee laxity, whereas the remaining three showed increased knee laxity during the ovulatory and early luteal phases (days 10 to 14 in a standard 28-day cycle).84 Oral contraceptives may have a role in decreasing the risk during this period.81 Neuromuscular and biomechanical differences also exist between male and female athletes. ACL injuries occur most commonly during periods of high dynamic loading of the knee joint, when muscular forces are unable to sufficiently dampen joint loads such that the passive ligamentous restraints are subjected to threshold failure loads. The gender difference in neuromuscular and subsequent biomechanical forces across the female knee joint significantly affects dynamic knee stability.85-87 Female athletes show increased activation of the quadriceps relative to the hamstrings (Q/H ratio)88,89 as well as decreased ratio of firing of medial to lateral quadriceps and hamstrings.88,90 Combined, these imbalances cause anterior tibial translation and valgus, which directly loads the ACL. The neuromuscular differences in female athletes have prompted research into neuromuscular interventional training programs in females in an effort to decrease the risk for knee injuries in general and ACL injuries in particular. A recent meta-analysis by Hewett and coworkers70 examined six published interventions targeted toward ACL injury prevention in female athletes. Four of the six significantly reduced knee injury incidence, and three of the six significantly reduced ACL injury incidence in female athletes. In evaluating those studies that successfully reduced ACL injuries among female athletes, plyometric training, combined with biomechanical analysis, and technique training were common components. Furthermore, training sessions should be performed more than 1 time per week, and the duration of training should be a minimum of 6 weeks in length.

The Older Patient The health benefits of improved physical fitness are readily accepted. This has led to a recent increase in the activity level of patients older than 40 years. More sports-related injuries, including ACL injuries, are being seen in this group. Traditionally, patients older than 40 years were treated nonoperatively after ACL injury.91 It has been demonstrated, however, that a significant portion of these patients have episodes of instability despite activity modification and progressive degenerative changes.91,92 Clearly, patients older than 35 years do benefit from reconstruction of the ACL and can expect results comparable with those in groups of younger patients.93-96 The ACL deficiency must be addressed in the early stages after injury, however, before chronic degenerative changes occur. Results of ACL reconstruction in older patients with long-term, chronic ACL deficiency are not as predictable. Patients older than 40 years willing to modify their activities can do well with an ACL-deficient knee, but we recommend

1652 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 23D1-1 Clinical Studies of Partial Anterior Cruciate Ligament (ACL) Tears Study

N

Follow-Up (yr)

Age (yr)

Isolated Partial Tear

Exclusion Criteria

Lysholm Score

Activity Rate of Return

ACL Insufficient during Follow-up

McDaniel, 1976101 Odensten et al, 1985104 Kannus & Jarvinen, 198792

9

1.3

20

6

>75% tear

N/A

N/A

17%

21

5.8

25.5

6

N/A

95(84-100)

N/A

14%

41

8

32

10

N/A

90(17-100)

N/A

N/A

Sandberg & Balkfors, 1987105 Noyes et al, 1989103 Buckley et al, 198999

29

3

26

29

N/A

94 (mean)

21%

62%

32

5

21.4

15

>75% tear

N/A

21%

38%

25

4.1

25

12

>75% tear

60%

Fruensgaard & Johannesen, 1989100 Sommerlath et al, 1992106 Bak et al, 199798 Messner & Maletius, 1999102

41

1.5

29

18

N/A

21

12

29

0

60% G/E 44% (Feagin-Blake score) 92(69-100) stable 50% knees; 84(45-100) unstable knees 93 32%

56

5.3

27

56

>75% tear

86(52-100)

30%

23%

22

240

29

0

>50% tear

95(71-100)

14/22 after rehab, 7/22 at 12 yr f/u 5/22 at 20 yr f/u

N/A

ACL reconstruction for those patients who wish to remain active, particularly if they wish to remain involved with high-risk activities, and for those patients who are “physiologically” young. This subset of patients has done well in our experience after ACL reconstruction; however, this group represents a skewed population, consisting of the most active and motivated of all middle-aged patients. Older patients do present with both medical and nonmedical issues that may not be seen in the younger population and must be taken into account in planning an ACL reconstruction. Medically, there may be associated health concerns requiring appropriate evaluation and coordination with primary care physicians or internists. There are often more stringent personal or professional responsibilities, which may have an impact on the timing of surgery and the ability to rehabilitate the knee. In an effort to reduce operative morbidity and enhance recovery, the use of allograft has gained popularity. Recent follow-up studies have shown allograft ACL reconstruction to be comparable to autograft in this older population.94,96

Partial Tears What constitutes the diagnosis of a partial ACL tear is controversial. Some have chosen to define a partial tear on the basis of the physical examination findings, whereas others have based the diagnosis on findings at arthroscopy. The incidence of partial tears ranges from 10% to 28% of all ACL injuries.97 In our experience, the incidence tends to

Radiographic Follow-up

15% of grade II ACL injuries had degenerative joint disease

44% 9%

3 of 12 had degenerative joint disease progression; 9 of 12 were stable

be toward the lower end of this range. Although the natural history of complete ACL ruptures has been well defined, patients with partial ACL tears have a less predictable clinical course. A review of the literature on the natural history of nonoperatively treated, isolated, arthroscopically confirmed partial ACL tears is shown in Table 23D1-1.92,98-106 Critical differences such as the degree of chondral and meniscal pathology, the type of rehabilitation, presence of symptomatic instability, and the lack of long-term radiographic follow-up make broad conclusions difficult to determine. The diagnosis of partial ACL tears can be challenging. Findings on clinical examination, including Lachman and anterior drawer testing, can be subtle. We use a combination of history, physical examination findings, KT-2000 arthrometer testing, and findings on MRI. The two-bundle concept of the ACL anatomy is well documented.107 Partial ACL tears involving the PL bundle, which has a large contribution to rotatory stability, often manifest as increases in pivot shift testing; similarly, partial ACL tears involving the AM bundle, which has a large contribution to sagittal plane stability, often manifest as increases in Lachman or anterior drawer testing.108 Liu and colleagues have shown, with KT-2000 arthrometer testing of partial tears, that mild to moderate injuries (one half to full tear of a single bundle) produce only small changes in the anterior tibial translation at different force levels.109 Additionally, a normal KT does not preclude the presence of a partial ACL injury.

Knee 1653

TABLE 23D1-2 Mediolateral Distribution of Meniscal Tears in the Acutely Injured Anterior Cruciate Ligament (ACL)

Author DeHaven McDaniel Noyes Woods Indelicato Cerabona McCarroll Henning Warren Hirshman Sgaglione Shelbourne Shelbourne Sherman Paletta (skiers) Paletta (nonskiers) Keene Sgaglione Spindler Ihara Overall

Incidence of Meniscal Tears in Acute ACL Injuries (%)

No. of Injured Menisci

Medial (%)

Lateral (%)

65 82 72 50 77 46 75 NA 65 53 60 NA 67 45 41

56 10 40 64 40 50 18 76 — 127 43 32 286 27 33

37 50 37 53 65 56 67 55 50 39 44 13 42 70 24

63 50 63 47 35 44 33 45 50 61 56 87 58 30 76

63

54

52

48

81 73 68 NA

57 24 50 40 1127 (total)

40 46 40 25 44

60 54 60 75 56

Medial vs. Lateral Distribution

From Bellabarba C, Bush-Joseph CA, Bach BR Jr: Patterns of meniscal injury in the anterior cruciate–deficient knee: A review of the literature. Am J Orthop 26:18-23, 1997.

TABLE 23D1-3 Mediolateral Distribution of Meniscal Tears in Chronic Anterior Cruciate Ligament (ACL) Insufficiency

Author Warren McDaniel Noyes Woods Indelicato Fowler Warren Aglietti Kornblatt McCarroll Finsterbush Henning Hirshman Irvine Keene* Keene† Sgaglione Satku Overall

Incidence of Medial vs. Lateral Meniscal Tears Distribution in Chronic ACL No. of Injured Injuries (%) Menisci Medial (%) Lateral (%) 98 86 92 88 91 73 — — 82 100 65 — 76 86 — 89 100 58

107 27 17 135 65 38 34 110 36 6 23 111 119 127 54 02 22 61 1184 (total)

87 81 59 64 69 50 76 84 75 67 74 71 90 44 59 58 59 74 70

13 19 41 36 31 50 24 16 25 33 26 29 10 56 41 42 41 26 30

*Less than 12 months after injury. †More than 12 months after injury. From Bellabarba C, Bush-Joseph CA, Bach BR Jr: Patterns of meniscal injury in the anterior cruciate–deficient knee: A review of the literature. Am J Orthop 26:18-23, 1997.

Associated Injuries We find that reviewing the MRI with an experienced musculoskeletal radiologist is often helpful in correctly diagnosing a partial ACL tear. Standard MRI cuts have variable sensitivity in diagnosing partial ACL tears, ranging from 0.4 to 0.75.110 The addition of oblique sagittal and coronal MRI has been shown to increase the diagnostic accuracy.111 The finding of a residual straight and tight ACL fiber seen on at least one image, a focal increase in ACL signal intensity, and the absence of a bone bruise are signs suggestive of a partial ACL tear.112,113 When the diagnosis is confirmed, the treatment of partial ACL tears is still difficult. Age, activity level, degree of laxity, associated injuries, and the presence of symptomatic instability are all important factors to consider. Patients compliant with a postinjury rehabilitation protocol emphasizing hamstring strengthening, brace wear, and activity modification may respond favorably to nonoperative treatment. Other patients not willing or able to mentally and physically cope with such a program may be better served with reconstructive surgery. As our knowledge of ACL double-bundle anatomy has increased, we have performed single-bundle reconstructions in those patients found to have single-bundle ACL tears (AM or PL bundle) with the remaining bundle functionally intact. In our last 360 patients operated on for ACL injury, we have performed 16 single-bundle augmentation reconstructions.

The association of ACL tears with injuries to other structures of the knee has long been recognized.114-116 O’Donoghue115,116 coined the phrase “the unhappy triad” in referring to the association of ACL injury with MCL and medial meniscal tears. More recently, it has been noted that lateral meniscal tears are more commonly seen in association with combined ACL and MCL injuries.117-119 Bellabarba and coworkers120 performed an extensive review of meniscal injuries associated with acute and chronic ACL insufficiency (Tables 23D1-2 and 23D1-3). They found a 41% to 81% incidence of meniscal tears in acute ACL injuries; 56% were lateral tears, and 44% were medial tears. In chronic ACL-deficient knees, the rate of associated meniscal injury ranged from 58% to 100%. In this population, medial meniscal tears were more common, representing 70% of all meniscal injuries. Special consideration should be given in evaluating the meniscus in patients with concurrent ACL tears because this combination frequently changes management and prognosis. Prospective studies have shown that MRI is capable of both high sensitivity and specificity (>90% each) in the detection of meniscal tears in ACL stable knees.121 However, the accuracy of meniscal tears by MRI drops significantly in the context of a concurrent ACL tear (Table 23D1-4).121-124 Many of these tears involve the peripheral portion of the posterior body and horn of the lateral

1654 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 23D1-4 Sensitivity and Specificity of Magnetic Resonance Imaging in Context of Anterior Cruciate Ligament (ACL) Tear

Sensitivity in MM Tears Sensitivity in LM Tears Study

ACL Intact

ACL Torn ACL Intact

ACL Torn

DeSmet & Graf, 1993121 Jee et al, 2004122 Rubin et al, 1998124 Justice & Quinn, 1995123

0.97

0.88

0.94

0.69*

N/A 0.98 0.97

1 0.84* 0.92

N/A 0.9 0.84

0.62* 0.83 0.77

TABLE 23D1-5 Treatment Factors Associated with Meniscal Tears

Factors Associated with Healed Meniscal Tears

Factors Associated with Nonhealing Meniscal Tears

Lateral meniscal tears Partial-thickness tears

Medial meniscal tears Ability to lock meniscus arthroscopically Rim width > 4 mm Radial tears

Rim width < 4 mm Concurrent anterior cruciate ligament reconstruction Vertical longitudinal tears

Meniscal body tears

*P < .05 LM, lateral meniscus; MM, medial meniscus.

meniscus; surgeons should pay particular attention to this area during the diagnostic arthroscopic examination. Because the importance of the meniscus in knee stability,125,126 load transmission,127,128 and the prevention of long-term arthrosis has been proved,129,130 the need for meniscal preservation is essential. If meniscal repair is not possible, partial meniscectomy should be chosen with care taken to leave an intact outer rim of meniscus. Meniscal repairs done in conjunction with ACL reconstruction have a higher rate of healing.131,132 Reasons for this include the beneficial effects of a hemarthrosis and fibrin clot formation which aid in repair,133,134 the protective effect of a competent ACL on decreasing the mechanical forces imposed on the meniscus,130 and the nondegenerative nature of the meniscal tears seen in associated acute ACL injuries (versus the degenerative meniscal changes seen in meniscal tears with intact ACLs).135 Longitudinal tears less than 10 mm or partial-thickness tears of the lateral meniscus have been shown to have a high rate of healing and a low propensity for development of symptoms; these tears have been shown to do well with conservative treatment and concurrent ACL reconstruction.136,137 The same has not been true of the medial meniscus tears, which have been shown both clinically and on second-look arthroscopic examinations to have a high propensity for nonhealing or progression with conservative treatment.136-138 Therefore, we aggressively treat all medial meniscal tears at the time of ACL reconstruction. Partial lateral meniscus tears we treat conservatively, with full-thickness lateral tears treated surgically depending on multiple factors (Table 23D1-5). MCL injuries are often found in association with ACL injury. Ninety percent of all knee ligament injuries in young and active individuals are ACL, MCL, or combined ACL and MCL injuries.139 Isolated MCL injuries are generally regarded to heal with nonoperative treatment.140,141 The treatment, however, of combined high-grade MCL and complete ACL injuries has been controversial. Many patients present with low-grade MCL strains and complete ACL injuries and are treated with ACL reconstruction only. In the presence of a severe MCL injury, concern exists that the reconstructed ACL may see increased forces and that the nonreconstructed MCL will not heal properly in such an environment. However, evidence favoring the nonoperative treatment of MCL injuries in combined ACL and MCL injuries comes from animal studies142,143; however,

animal studies do show that repaired MCLs may have higher ultimate strengths than unrepaired MCLs.144,145 Adequate healing of the nonoperatively treated MCL in the context of ACL reconstruction, however, has been shown in multiple retrospective studies.146-149 Additionally, prospective studies have documented the good outcomes in patients treated with ACL reconstruction and nonoperative bracing of the MCL.150,151 The one randomized, prospective study comparing ACL reconstruction with operative versus nonoperative treatment of combined ACL and grade III MCL injuries found no difference between the two groups.152 Concern exists regarding the risk for arthrofibrosis in the setting of a multiligament (ACL and MCL) injured knee in which acute operative treatment is undertaken. We do not delay surgery a set time after injury to avoid arthrofibrosis; instead, we routinely wait until the patient has attained full extension and has achieved flexion to 120 degrees and until the majority of the acute hemarthrosis has resolved (typically 5 to 10 days).

Natural History For fair comparisons to be drawn on the effects of ACL reconstruction versus conservative treatment in ACL injuries, knowledge of the natural history of the ACL-deficient knee is required. Unfortunately, no large prospective trials on the natural history of ACL-deficient knees have been adequately done. With the available studies done at present, there is a general consensus among practicing orthopaedic surgeons that chronic ACL deficiency can lead to chronic functional instability, which may increase the risk for meniscal or chondral injury. It is clear from the literature that the primary complaint of ACL-deficient patients is recurrent episodes of givingway.15,153 It is such recurrent episodes that lead to less than 20% of patients returning to their preinjury level of activity.153-155 These recurrent episodes of instability also place these patients at increased risk for new and recurrent meniscal and chondral injuries, with such injuries leading to the development of further intra-articular damage153,154,156,157 and ultimately osteoarthritis of the knee.158,159 Although some studies have shown no increased rates of osteoarthritis in conservatively treated ACL-deficient knees as compared with uninjured knees,160,161 studies with greater than 10 years of follow-up have shown greatly increased rates in ACL-deficient knees.154,159,162 It appears that at least 10 to 15 years are needed for such radiographic changes to occur. Levy and associates estimated the incidence of

Knee 1655

meniscal tears in patients with unreconstructed ACL injuries at 40% by 1 year, 60% by 5 years, and 80% by 10 years after the initial ACL disruption.163 This is likely accelerated in young, active patients who attempt to return to high-level activity. Nebelung and associates showed that 35 years after ACL injury treated conservatively in a group of former East German Olympic athletes, 18 of 19 patients required at least partial meniscectomy, and 10 of those 19 patients had already undergone total knee replacement secondary to severe osteoarthritis.164 However, a subgroup of patients is able to compensate for their ACL deficiency and do well with nonoperative treatment. Multiple studies have attempted to define factors that would prospectively identify this subgroup of patients.165-168 Such an identification system would both spare those patients from surgery who would do well with nonoperative treatment and identify those patients who, treated conservatively, are at risk for further reinjury, which ACL reconstructive surgery could help avoid. Such factors have included the number of preinjury International Knee Documentation Committee (IKDC) level I or II activities (cutting and jumping activities), KT-1000 arthrometer manual maximal injured minus normal displacement difference exceeding 5 to 7 mm, inability to perform a onelegged hop test, and an inability to regain normal gait parameters by 40 days after injury.165-168 Although age at the time of injury has not been consistently proved an accurate predictor in identification of this subgroup, age by itself is correlated with increased activity levels that include cutting and jumping activities. Thus, older patients have been shown to be more likely to successfully adapt their activities to avoid recurrent instability episodes.91

TREATMENT OPTIONS Nonoperative Treatment As stated in the previous section, ACL reconstruction is recommended in patients who either are young, are active in high-level sports involving cutting or pivoting, or whose physical examination reveals greatly increased knee laxity. The goal of ACL reconstruction is to return functional stability to the knee to provide for a return to full activities as well as to prevent any further injury to meniscal or chondral surfaces that can lead to early-onset osteoarthritis. Advances in the surgical technique, anesthetic and pain management, and postoperative rehabilitation have reduced morbidity and increased functional outcomes in ACL reconstruction. With these advances, the use of conservative treatment for ACL injuries has fallen out of favor for patients in the aforementioned groups. Older and more sedentary patients may do well with conservative treatment that includes aggressive quadriceps and hamstring strengthening.91 However, even in this subgroup, some patients may continue to experience recurrent episodes of functional instability. Thus, the most important part of this decision process involves a thorough discussion with the patient regarding reasonable functional outcomes with each treatment and the activity modifications and chance of success that accompany operative versus conservative treatment.

Operative Management Early surgical treatment of ACL injury involved attempts at primary repair.3,169 Early reports were thought to be promising in returning stability and increasing patient function170,171; however, intermediate (5 years) and longterm follow-up (15 years or more) studies documented poor subjective, objective physical examination, and radiographic results.172-174 Attempts at improving these results focused on augmentation procedures, both intra-articular and extra-articular, that commonly used hamstring tendons or the iliotibial band. Initial follow-up studies showed improvements in knee stability, return of function, and a decreased rate of revision surgery.175,176 Although these results were consistently better than primary repair, longer term follow-up studies again showed deteriorating results as compared with more modern autogenous reconstruction techniques that began to appear.172,175,177 Thus, both primary repair and augmentation procedures fell from favor. With continued medical and technologic advances, the use of prosthetic ligament reconstruction devices became popular in the 1980s. Carbon fiber,178 polylactic acid (PLA)–coated carbon fiber,179 and polytetrafluoroethylene (PTFE)180 were all introduced during this period. The most popular device, the Kennedy ligament augmentation device (LAD)181 introduced in 1980, was a flat 6-mm diamond-braided polypropylene device. Justification for its popularity centered on its ability to provide protection and load-sharing to the biologic reconstructive tissue during the time of its transient phase of weakness and degeneration in the early postoperative period.181 Other touted advantages for augmentation and stand-alone LADs included decreased donor site morbidity, faster rehabilitation, and stronger structural grafts.182 Early results of LADs used in primary repair and augmentation cases were encouraging, particularly in purely soft tissue ACL graft reconstructions.183,184 However, further studies showed complication rates ranging up to 63%, including persistent effusions and reactive synovitis,185 delayed maturation of the autogenous graft,186 and infection.182,185,187 Because of these complications and the lack of any definitive data showing significant improvements with the use of LADs,172,186,188,189 their overall use has greatly decreased. In addition, advances in autograft and allograft tissues and improvements in graft placement and fixation have rendered the previous theoretical advantages of LADs obsolete. Advances in ACL reconstructive surgery have continued to occur with improvements in arthroscopic technology, equipment, and surgeon skill. A gradual transition has occurred from open reconstructive procedures, to an arthroscopic two-incision technique, to an arthroscopic one-incision technique. Multiple advances have led to an increase in our understanding and success in ACL reconstruction surgery. These include a better understanding of the appropriate timing of surgery as well as graft selection and subsequent harvesting. Additional biomechanical and animal research has also provided more detailed explanations of the anatomic structure of the ACL and which has led to improvements in ACL tunnel placement, tensioning, and fixation. Each of these areas is discussed in detail in the sections to follow.


Timing of Surgery There has been ample debate surrounding the ideal timing of ACL reconstruction surgery. Beginning in the early 1980s, ACL reconstructions were often done acutely within the first week after injury. As results of postoperative complications including arthrofibrosis began to appear in the literature, a common belief was that a delay in surgery would help minimize this complication. Arthrofibrosis is the most common postoperative complication after ACL reconstruction,190 and a loss of motion (particularly terminal extension) can be more debilitating than instability. A prospective cohort study by Kocher and colleagues191 on the determinants of patient satisfaction after ACL reconstruction showed that stiffness is one of the most common subjective complaints given by patients with poor postoperative outcomes. Use of the available literature to help resolve this issue, however, is difficult because of varying definitions surrounding acute versus chronic reconstruction and loss of motion parameters. Additionally, most studies are retrospective and suffer from bias and confounding variables that make accurate conclusions difficult to determine. Thus, studies have found increased rates of arthrofibrosis from early ACL reconstruction,192-195 whereas others have found early reconstruction to be safe.196,197 More recently, the determination of whether it is safe to proceed with ACL reconstruction has shifted from a measurement of the absolute time interval after injury to a measurement of the amount of inflammation and swelling present in the knee. Articles by both Shelbourne and colleagues198 and Mayr and associates190 have supported this view, as patients with excellent preoperative range of motion, minimal swelling, good leg control, and an appropriate mental state have had good postoperative outcomes regardless of the time period after injury. Our own experience supports this as we routinely use range-of-motion, swelling, knee irritability and pain, and quadriceps control as our determining factors for the readiness of the knee for surgery. To facilitate this process, we occasionally aspirate larger knee effusions, use compression knee braces, and start physical therapy and electrical stimulation of the

quadriceps muscle preoperatively. Aggressive postoperative rehabilitation has also been shown to decrease the rates of arthrofibrosis after surgery.193,194

Graft Selection The optimal graft material for ACL reconstruction remains an area of active debate. Although advances in ACL reconstruction have improved the success rate up to 90% in some cases with regard to stability and patient satisfaction,199 the ideal graft material to obtain these results has varied from surgeon to surgeon. The ideal graft should have structural properties similar to the native ACL that are present at implantation and persist throughout the “ligamentization” process of graft incorporation. Additionally, the graft should allow secure fixation, good biologic incorporation, and minimal donor site morbidity.200 Autograft ACL graft options include bone–patellar tendon–bone (BPTB), quadriceps tendon, and quadrupled semitendinosus and gracilis hamstring (HS) tendon. Allograft options include quadriceps, Achilles, tibialis anterior or posterior, BPTB, and HS. Because of its relative ease of harvest, its comparable structural properties to that of the native ACL,201,202 rigid fixation,202 bone-to-bone healing,37,201,202 and favorable track record,203-205 the autograft BPTB has historically been the graft of choice and is considered the gold standard against which other grafts are compared. Multiple factors are involved in a surgeon’s ACL reconstruction graft choice and include the biomechanical properties, biologic incorporation, associated donor site complications, graft tensioning issues, graft fixation options, and clinical outcome.

Biomechanical Properties The biomechanical properties of the common ACL grafts, including autograft BPTB, are compared in Table 23D1-6.19,20,202,206,207 A few important points deserve mentioning when evaluating biomechanical data on ACL grafts in the literature. Both native ACLs and potential graft choices should always be tested with both the graft and the subjected forces aligned in the anatomic position.

TABLE 23D1-6 Graft Choices for Anterior Cruciate Ligament (ACL) Reconstruction Surgery Graft

Tensile Load (N)

Stiffness (N/mm)

Cross-sectional Area

Native ACL

2160

242

44

BPTB (10 mm)

2977

620

35

Quadruple hamstring Quad Tendon

4090

776

53

2352

463

62

Biologic Healing

Morbidity

Fixation

Outcomes/ Return to Play

Autograft Bone to bone (6 wk)

Extremity Interference weakness, screw kneeling pain Soft tissue healing Flexion weakness Variable (10-12 wk) Combination Similar to BPTB Interference bone to bone and screw soft tissue

4-6 mo Slight subjective laxity, 6 mo Limited data

Allograft BPTB (10 mm)

Similar to BPTB Similar to BPTB autograft autograft

BPTB, bone–patellar tendon–bone.

Similar to BPTB Bone to bone autograft (6 wk)

None

Interference screw

>6 mo, limited data

Knee 1657

Woo and colleagues208 showed that testing in the anatomic position greatly affected the ultimate load and stiffness data obtained; additionally, these same researchers found a substantial age-related decrease in the properties of the native ACL,208 which may also apply to cryopreserved allograft tissue. Because of such differences in the donor age, graft size, and specific biomechanical testing used, it is very difficult to compare studies. An additional factor in previous studies dealing with allografts was the use of sterilizing radiation (>3.0 mrad) or the use of ethylene oxide, both of which significantly weakened the grafts.209-211 Current cryopreservation techniques quoted in more recent studies do not have this weakening effect.210,212,213

Graft Healing Biologic graft healing encompasses both the graft attachment site healing as well as the healing process of ligamentization or graft revascularization and incorporation. Attachment site healing in grafts containing bone, particularly autografts, closely resembles fracture healing with graft bone–to–host bone healing occurring within 6 weeks.214 Purely soft tissue grafts typically take 8 to 12 weeks to heal into host bone.215 The process of graft revascularization and incorporation proceeds through well-defined phases starting with an in flammatory phase during which the graft undergoes degeneration.215-218 The donor fibroblasts undergo cell death, and the remaining biologic material serves as a scaffold for host cell fibroblast migration, which occurs with host revascularization during the second phase of incorporation. Graft strength and stiffness greatly decrease (up to 80%) during this phase, which lasts from about day 20 to 3 to 6 months after surgery.217 The final phase involves collagen maturation as the graft approaches but does not reach its original strength at implantation. Although both allografts and autografts proceed through the same phases of incorporation, allografts are thought to proceed at a slower rate,218,219 leading to a potentially increased rupture rate.220,221 There are no randomized, controlled trials comparing the outcomes of ACL reconstructions using allografts versus autografts. Allografts have been proposed to have less perioperative and postoperative morbidity than autografts.222 However, a study by Saddemi and associates did not find any difference in perioperative or postoperative morbidity between the two grafts.223,224 Although numerous articles have been published concerning the results of ACL reconstruction with allografts, most are retrospective case series with varying surgical techniques and graft types, which makes comparisons to autografts difficult.225-230 A small number of these studies support the notion of delayed allograft incorporation leading to laxity and failure,65,220,221 but most studies have shown no increased rate of graft rupture or increased laxity as compared with autograft.225-232

Donor Site Complications and Graft Harvest Although donor site complications are infrequently reported overall, most of the complications arise from autograft BPTB grafts. These include patellar fractures,233 patellar tendon

ruptures,234 localized numbness, and tendonitis.214 Generally, the dimensions of the bone blocks are 25 mm in length by 10 mm in width. Although larger bone blocks significantly increase the stress across the remaining patella,235 there are reportedly no differences between trapezoidal, square, or circular bone plugs.235,236 The effect of bone grafting of the defect is a difficult issue to resolve because of the statistical numbers needed237 but has not been shown to be of any statistical benefit.238,239 Patellar tendon rupture is rare,240 but care should be taken to identify the middle third of the tendon when harvesting. Closure of the patellar tendon after harvest may cause shortening of the tendon.241 We prefer to close the paratenon, which may help in healing of the tendon defect and avoid scarring to the overlying skin.239,242 Anterior knee pain after BPTB harvest has been reported to occur in up to 50% of cases,243 but a direct correlation to BPTB harvest is being refuted. The source of this pain may be multifactorial; the incidence of postoperative knee pain has been decreasing in more recent studies because of earlier rehabilitation, avoidance of immobilization, and emphasis on recovery of motion and strength.201,244,245 Autograft HS harvest may injure a superficial branch of the saphenous nerve.223 Problems associated with quadriceps tendon autograft harvest are more infrequent, resulting in part from fewer nervous structures in the incision area and the denser bone present in the proximal patella.214 Allograft use has increased during the past 20 years.246 Purported reasons for this increase include decreased morbidity and operative time, preservation of the extensor and flexor mechanisms, availability of specific graft sizes, improved cosmesis, and a reliable source of graft material in multiligament injuries or revision cases in which autograft choices are limited.221,226,227,247 In contrast, concerns have been raised about slow graft incorporation (see previous section), tunnel enlargement,230 and the risk for disease transmission.214 The risk for disease transmission remains a serious concern. There have been two cases of disease transmission of hepatitis C in 1991 and one case of human immunodeficiency virus (HIV) transmission in 1985, all from BPTB allografts.248,249 Many of these problems have been decreased or eliminated because of improved donor screening and testing procedures employing polymerase chain reaction (PCR) testing, which has significantly decreased the window of vulnerability between host infection and the detection of antibodies during screening procedures. The American Association of Tissue Banks frequently revises their recommended guidelines and currently recommends screens for HIV, hepatitis B and C, syphilis, and human T-cell lymphotropic virus, as well as blood and tissue cultures for bacterial infection. Despite this, two separate patients in 2000 receiving BPTB allografts from a common donor both developed Pseudomonas aeruginosa septic joint infections, with bacterial testing showing both strains to have an identical genotype.250 Additionally, a patient died in 2001 of Clostridium sordellii septic shock after receiving an infected osteochondral knee allograft.251

Graft Tension Appropriate graft tensioning during ACL reconstruction surgery remains a difficult quantifiable task. The concept that adequate tension is necessary to restore adequate


anteroposterior stability at the time of ACL reconstruction, whereas too much tension may lead to graft stretching, fixation failure, and capture of the knee is easy to understand. However, there are multiple variables that affect graft tensioning, including the knee flexion angle and rotational position of the knee during tensioning and the specific graft type used. These variables make drawing conclusions across multiple studies difficult. Cadaveric and finite element modeling studies on the effects of initial graft tension on knee stability have been done using both HS252 and BPTB.253 These recommend tensioning the grafts between 40 and 60 N of force near full extension. Another conflicting variable is that most surgeons manually tension their grafts, and this applied force can vary significantly254 such that reproducibility becomes a significant issue. Prospective, randomized controlled trials evaluating the potential effects of different tensioning levels and their clinical and functional effects have been done. Three studies255-257 were completed on patients receiving BPTB grafts, and one study258 was completed on patients receiving four-strand HS grafts. In the studies by van Kampen and associates256 and Yoshiya and colleagues257 using BPTB grafts, they did not find any significant differences on clinical or functional outcomes between patients whose grafts were tensioned at 20 versus 40 N or 25 versus 50 N, respectively. Nicholas and coworkers255 compared groups tensioned at 45 versus 90 N and found that, in the 45 N group, 23% of the subjects had side-to side differences in knee laxity greater than 5 mm, compared with 0% in the 90 N group. No other clinical or functional differences were found. Yasuda and colleagues258 in a similar study using four-strand HS grafts, found a significant correlation between higher initial tension applied at the time of fixation and normal anteroposterior knee laxity measurements at the time of final follow-up. Again, no other differences in clinical or functional results were found. Questions have been raised regarding the fact that the difference in the two tension levels was not of sufficient magnitude to create differences in knee laxity measurements at baseline in those BPTB studies showing no difference in laxity.259 It is also possible that the loss in tension is the result of friction between the bone block and the tibial tunnel in BPTB grafts,259,260 from wrapping of the graft around an interference screw in soft tissue grafts260 and from postoperative cyclic loading.260,261 A lack of preloading the graft before implantation, which would help eliminate the natural viscoelasticity of soft tissue grafts, has also been suggested as a reason for loss of graft tension. A primate study by Graf and colleagues262 showed that preconditioning can reduce acute tension loss in BPTB grafts. However, a randomized, controlled trial by Ejerhed and colleagues263 compared preconditioning with no preconditioning in BPTB grafts and found no differences in knee laxity, clinical outcome, or activity level. Similarly, Nurmi and associates,264 in an experimental study, questioned the reasonableness of preconditioning soft tissue grafts in ACL reconstruction. Studies by Schatzmann and colleagues265 and Arnold and coworkers261 showed that a large number of cycles (>100 cycles) or high tension (75 to 80 N) were needed to reach a steady viscoelastic state, perhaps explaining why no effect of preconditioning was found in previous studies.

Recommendations regarding tension are still not universally agreed on. From the aforementioned studies, it appears that application of higher tensions (up to 90 N) with the knee near or at full extension may reduce anteroposterior knee laxity. However, the effect that such tensioning has on the tibiofemoral contact stresses is unknown and requires further biomechanical and clinical study. The effects of preconditioning on ultimate ligament tension also requires further study.

Initial Fixation and Strength Rigid fixation of the ACL graft at the time of implantation is considered one of the most important factors determining the long-term success of ACL reconstruction. The strength of the initial graft fixation is the weak leak during the initial 6- to 12 week period during which healing of the graft to host bone occurs.214 Biomechanical testing of ligament reconstruction fixation devices has been widely performed in the laboratory using various materials, including testing machines and different fixation devices. This allows better comparisons across different fixation devices and even across different mechanical studies. The most commonly reported biomechanical measure has been ultimate load to failure. Although it is an important measure of the ultimate load the graft can withstand during a catastrophic event such as a fall, it does not give information about how the graft construct (graft plus fixation) responds to the more common submaximal repetitive loading cycles that are experienced during aggressive postoperative rehabilitation programs.266 Thus, cyclical loading and stiffness profiles have become more common biomechanical measures reported to address this question. Most loads seen by an ACL graft during early rehabilitation are likely 200 N or less, with a maximum between 400 and 500 N.267,268 Although the literature surrounding graft fixation constructs is extensive, more attention has been focused on the more problematic fixation on the tibial side. Reasons for increased tibial fixation problems include the decreased bone quality of the tibial metaphysis, the increased force on the ACL graft in the parallel tibial tunnel compared with the nonparallel femoral tunnel, difficulty in securing and tensioning a four-strand hamstring graft, and the fact that tibial inference screw fixation is inserted counter to the direction of tension on the graft.269-271 It is also helpful to be aware of certain variables and differences that exist across various biomechanical publications when evaluating the literature. Particularly as it pertains to soft tissue fixation in the tibia, these cross-study variables include differences in specimen bone density, the geometry of implanted hardware or screws, hardware material differences, screw length and width differences, and the manner in which tunnels are drilled. Finally, owing to the scarcity of human bone and tissue, many studies are done using nonhuman tissues such as porcine or bovine specimens, which may have noticeable differences when compared with human bone and tissue. More studies are commonly reporting specimen bone mineral density (BMD) because increased BMD has been linked to an increase in fixation strength.269,272,273 BMD is higher in animal (particularly porcine) than in human

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TABLE 23D1-7 Bone–Patellar Tendon-Bone Biomechanical Fixation Studies Study

Fixation Type

Specimen

Test

Scheffler et al, 2002279

Stainless steel interference screw (8 × 25 mm)

Human

Caborn et al, 1997286

Biointerference screw (7 × 25 mm)

Human

Titanium alloy interference screw (7 × 25 mm) 2 staples with bone block in tibial groove Stainless steel interference screw (9 mm)

Human

Femur-tibia complex; anterior tibial displacement Femur with tensile load 20 mm/min

Biodegradable interference screw (9 mm)

Human

Interference screw (9 × 25 mm, outside-in technique) Interference screw (7 × 25 mm, endoscopic technique) Suture tied over buttons Staple 6.5 mm screw

Human

Gerich et al, 1997290 Johnson & van Dyk, 1996287

Steiner et al, 1994289

Kurosaka et al, 1987291

Load to Failure (N)

Stiffness (N/mm)

384

66

Cyclic Testing

Mode of Failure

Stepwise increase 20 N; laxity increase 3.4 mm

Tibial graft pullout with (n = 3) and without (n = 5) bone block fracture Femoral fixation; ligament-bone separation Fracture tibial bone block; ligament-bone separation Slippage of bone block in tibial groove

552.5

N/A

558

N/A

Human

Tibia

588

86

N/A

Human

Femoral cortex removed; force in line with tunnel Femoral cortex removed; force in line with tunnel Femur-tibia complex

436

N/A

Tendon/cortical bone graft pull-out from femur

565

N/A

Failure associated with cortical and cancellous bone of graft Bone plug slippage past interference screw; usually tibial

423

46

N/A

Human

Femur-tibia complex

588

33

N/A

Human

Tibia/femur not specified

248.2

12.8

N/A

128.5 214.8

10.8 23.5

N/A N/A

Human Human

tibia,273-275 such that more optimistic results may be obtained when different fixation methods are tested on porcine specimens only. Screw geometry, specifically screw diameter and length, is also related to fixation strength. Although increasing screw size reportedly increases fixation strength,276 screw length has shown an even more important positive correlation to fixation strength.276,277 The screw material, metal or bioabsorbable, can also be responsible for cross-study differences, with biomechanical data on bioabsorbable screws at least equal to the data on metal screws.272,278,279 The ratio of the screw diameter to that of the tunnel diameter also varies across studies. Although intuitively a better match would seem to improve fixation, studies have shown no significant differences when the gap between the two is equal to or less than 2 mm.280,281 Finally, using tibial dilators to compact the soft cancellous bone in the proximal tibia during creation of the tibial tunnel has been variably done in clinical and biomechanical studies. Contrary to intuitive thinking, this has not been shown to have a significant effect on fixation strength.275,282-284 The most commonly used grafts are autograft BPTB and HS grafts and, to a lesser extent, their allograft counterparts. Their mechanical fixation to host bone can be categorized as either direct fixation (interference screws, staples, spiked washers), which compresses the graft against the host bone, or indirect fixation (cross-pin, screw

Avulsion fracture at tendon insertion

and post, EndoButton), which suspends the graft within a bony tunnel.266 For BPTB grafts, the most commonly performed and reported fixation is direct fixation using interference screws on both the tibial and femoral sides (Table 23D1-7). Because of its direct fixation of bone against bone,266 its aperture or juxta-articular fixation,285 and its favorable biomechanical profile,286-289 it has been the workhorse of BPTB graft fixation. Owing to concerns about screw divergence and graft injury during insertion, other options have been tested, including staple290,291 and press fit292,293 techniques. Less biomechanically secure constructs include suture post and button fixation (see Table 23D1-7).279,291,294 Soft tissue graft fixation on the femoral side has multiple options, with no clearly superior option (Table 23D1-8). Because of their ease of insertion with no additional incisions, both the EndoButton and interference screws are popular choices. Kousa and colleagues295 found that the bone mulch screw had the most favorable biomechanical profile, whereas To and associates296 favored cross-pin fixation. Scheffler and coworkers279 showed favorable results in their femur-graft-tibia model with bioscrew interference fixation. Soft tissue graft fixation on the more problematic tibial side also has multiple options (Table 23D1-9). Although multiple fixation devices had ultimate fixation strengths above 500 N, the WasherLoc and Intrafix devices had the

1660 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 23D1-8 Anterior Cruciate Ligament Soft Tissue Graft Biomechanical Fixation Studies: Femoral Side Study

Fixation Type

Specimen

Load to Failure (LFT) (N)

Test

Stiffness (N/mm)

Cyclic Testing (mm)

1086, 781

79

After 1500 Cycles (50-200 N), Displacement in mm 3.9 mm

1112, 925 589, 565 546, 534 868, 768 794, 842 430

115 66 68 77 96 23

2.2 4 3.9 3.7 3.2 N/A

312 1126 242

25 225

N/A N/A

LTF, LTF after Cyclic Loading Kousa et al, 2003295

To et al, 1999296


Endobutton CL

Porcine

Bone mulch screw Bioscrew RCI screw Rigid fix SmartScrew ACL Endobutton CL Human Mitek anchor Cross-pin RCI interference screw (7 mm)

Human

Femur; force along axis of drill hole

Femur; pull in line of tunnel

Femur

Bioabsorbable interference screw

Mode of Failure

Suture loop knot failure Migration of anchor Pin failure Graft pulled out around screw (13/16 specimens) Graft and screw pulled out from femoral tunnel (3/16)

341

TABLE 23D1-9 Soft Tissue Anterior Cruciate Ligament Graft Biomechanical Fixation Studies: Tibial Side Study

Fixation Type

Specimen

Kousa et al, 2003272

Magen et al, 1999273

Load to Failure (LTF) (N)

Tibia: pull in line of tunnel

Coleridge & Amis, 2004297


Test

RCI screw Delta screw Intrafix bicortical screw WasherLoc Intrafix Tapered bioabsorbable screw (35 mm)

Bovine

Human

Metal interference screw (9 × 25 mm) WasherLoc Tandem washers

Cyclic Testing (mm)

Mode of Failure

N/A

N/A N/A N/A N/A N/A N/A N/A

491 641 543 770 946 796

N/A N/A N/A N/A N/A 49.2

1000 cycles 70-220 N slippage (mm) 1.3 1.15 0.69 1.17 0.88 N/A

647

64.5

N/A

N/A N/A

975,917

87

After 1500 cycles (50-200 N); displacement in mm 3.2

769,675 1321, 1309 612,567 471,423

69 223 91 61

4.2 1.5 4.1 4.7

N/A N/A N/A N/A

665,694 Yield load in place of LTF (N)

115

N/A N/A

350

340

3.8 Stepwise increase by 50 N; displacement at 250 and 500 N mm) 1.80, 3.67

905 768

506 318

0.55, 1.95 0.30, 0.86

N/A N/A

LTF, LTF after cyclic loading

WasherLoc Spiked washers Intrafix Bioscrew Titanium interference screw (8 × 25 mm) Bioscrew (8 × 25 mm)


Stiffness (N/mm)

Tibia: pull in line of tunnel Porcine

Human


N/A

N/A

Knee 1661

more favorable data when comparing stiffness and displacement during cyclic loading.272-274,297

CLINICAL OUTCOMES The choice of ACL graft and technique available to the orthopaedic surgeon consists of dozens of choices with hundreds of articles expressing opinions and outcome data. Most of these articles are retrospective case series of a single graft, with several potential sources of bias and no adequate comparison group. There are articles describing comparisons between the two most common grafts, autograft BPTB and HS, but each article is statistically limited in its ability to draw strong conclusions because of limited sample size.65,203-205,298-309 In an effort to increase statistical power and provide orthopaedic surgeons with statistically stronger data on which to make their decisions, meta-analyses have been done.199,200,310 A meta-analysis is a technique to statistically combine or integrate the results of several independent clinical trials to increase statistical power. In addition to meta-analyses, an emphasis has been placed on performing more randomized controlled trials (RCTs) of ACL reconstruction using BPTB versus HS grafts. Such RCTs help to limit any confounding variables or biases that limit the ability of non-RCTs to draw statistically powerful and meaningful conclusions regarding graft choice and operative technique. In a similar vein, meta-analyses199,200,310 and systematic review311 of the available RCTs have more recently been completed. A systematic review presents data on several studies in a tabular form, which allows the reader to draw comparisons and conclusions regarding the data present in multiple studies. A large meta-analysis of the available articles published on ACL reconstruction with BPTB versus HS grafts was done by Freedman and colleagues199 in 2003. Their meta-analysis inclusion criteria were broad, including retrospective and uncontrolled studies as well as studies involving only one type of reconstruction with varying rehabilitation protocols. It reported on 1348 patients culled from 21 and 13 studies, respectively, involving BPTB or HS ACL reconstructions. They found that BPTB ACL reconstruction was associated with a statistically significant decreased rate of failure and laxity and provided patients with a more stable knee. Hamstring ACL reconstruction was found to have a significantly decreased incidence of anterior knee pain and rate of arthrofibrosis requiring manipulation or lysis of adhesions. Yunes and associates310 performed a more restricted meta-analysis involving only prospective, semirandomized studies. It consisted of four studies comprising 424 patients. Their findings were somewhat similar to those of Freedman and colleagues199 in that BPTB reconstructions were found to give a statistically more stable knee with regard to KT-2000 and pivot shift objective testing. Additionally, they found that BPTB had an 18% increased chance of returning to preinjury levels than HS grafts. Remaining variables, including range of motion, failure and complication rates, and Lachman testing, showed no statistical difference between the two groups. No data were obtained on anterior knee pain or quadriceps weakness because of limitations in the available studies.

Multiple RCTs, comparing BPTB and HS ACL reconstructions, have been published since 2000. Spindler and colleagues311 and Goldblatt and coworkers200 performed a systematic review and meta-analysis, respectively, on these trials in an effort to improve our understanding. Spindler and colleagues311 included nine RCTs in their systematic review. Because this was not a meta-analysis, data were presented in tabular form only. They found slightly increased laxity in HS reconstructions in three of seven studies, but no differences in graft failure, functional scores, or activity levels between the two groups. They also found more kneeling pain in BPTB groups in all four of the studies that reported this outcome; however, only one of nine studies reported an increased incidence of anterior knee pain in the BPTB groups. Goldblatt and coworkers200 performed a comprehensive meta-analysis of randomized or controlled trials, which included 11 studies comprising 1039 patients. Inclusion criteria were identical rehabilitation protocols within each study, a minimal 2-year follow-up, and the presence of both subjective and objective outcomes data. Outcomes favoring BPTB (P 3 mm Flexion Loss > 5 deg Rupture Decreased Activity Pivot-Shift > 0 Lachman > 0 Complications Meniscus Surgery Pivot-shift >= 2 KT > 5 mm IKDC B+C+D Swelling IKDC C+D IKDC D Anterior knee pain Extension loss > 0 deg Extension loss > 5 deg

6 3 3 4 6 4 8 7 5 4 7 3 4 3 5 4 5 3 5

Favors HT

Favors BPTB

P value .22 .37 .01 .04 .46 .12 .09 .06 .79 .75 .83 .84 .71 .97 .68 .68 .12 .13 .06

624 286 182 446 597 340 761 713 530 451 672 182 450 286 516 450 367 186 406 0.2

0.5

1 2 Relative Risk

5

Figure 23D1-6 Summary of risk ratios for various outcomes measures: hamstring versus patellar tendon autograft in anterior cruciate ligament reconstruction. BPTB, Bone patellar tendon bone; HT, Hamstring tendon; IKDC, International Knee Documentation Committee. Redrawn from Goldblatt JP, Fitzsimmons SE, Balk E et al: Reconstruction of the anterior cruciate ligament: Meta-analysis of patellar tendon versus hamstring tendon autograft. Arthroscopy 21[7]:791-803, 2005.

in patients with tunnels greater than 2 mm from the anatomic insertion site as defined by radiographs. Significant room for improvement in tunnel position likely exists. Kohn and coworkers,314 in an analysis of cadaveric knees that had undergone BPTB reconstructions, showed only 50% excellent and 75% acceptable tunnel position on the femoral and tibial sides. Malpositioned tunnel placement continues to be one of the most common reasons for revision ACL reconstruction.315,316 Thus, although single-bundle reconstruction techniques are capable of providing good or excellent outcomes in up to 90% of our patients,205,302 significant room for improvement exists. Despite recent data that moving the femoral tunnel down the face of the femur to a more horizontal position better restores both anteroposterior and rotational stability to the knee,317 recent authors have

noted persistent instability with functional testing and degenerative radiographic changes after single-bundle reconstruction.31,318-321 Tashman and associates have used a stereoradiographic system to evaluate the threedimensional kinematics of reconstructed and intact knee. Their findings suggested that single-bundle ACL reconstruction failed to restore normal rotational knee kinematics during dynamic loading.31 Newer techniques involving re-creation of both functional bundles of the ACL, the AM and PL, have recently been published; clinical as well as biomechanical studies involving double-bundle ACL reconstruction have shown promise in restoring more normal stability to the knee.28,29,108,322-326 This anatomic double-bundle reconstruction may provide us with a technique to further improve the success rates of ACL reconstruction.

Authors’ Preferred Method Positioning and Arthroscopic Setup

The correct limb to be operated is identified and marked by the surgeon. The patient is placed in a supine position on the operative table. The contralateral leg is placed in an abducted position with the knee and hip slightly flexed in a well-�� padded leg holder, and the leg is secured in position with an elastic bandage (Fig. 23D1-7). The operative knee is examined under anesthesia with Lachman, anterior and posterior drawer, varus-valgus, and pivot shift testing. The examination allows assessment of the extent of the ACL injury. If a partial tear of the

ACL is considered, the arthroscopic examination will confirm the diagnosis. After examination, a pneumatic tourniquet is applied around the upper thigh of the operative leg. The limb is exsanguinated by elevation for 3 minutes, and the tourniquet is insufflated to 300 to 400 mmHg depending of the size of the patient. The foot of the table is flexed, and the operative leg is placed in the leg holder. The use of the leg holder allows the knee to be positioned at 90 degrees of flexion with a range of motion from full extension to 120 degrees of flexion (see Fig. 23D1-7). The operative leg is aseptically prepared and draped.

Knee 1663

Authors’ Preferred Method—cont’d needle is inserted medially and distally to the AM portal just above the meniscus. The spinal needle needs to reach the medial wall of the lateral femoral condyle, at the origin of the footprint of the PL bundle. Once the needle is correctly placed, the AAM portal is made with a No. 11 blade. The AAM portal allows better visualization of the tibial and femoral ACL footprints and will also be used as a working portal during the surgical procedure. A diagnostic arthroscopy is completed, including inspection of the suprapatellar pouch, patellofemoral joint, medial and lateral gutters, and medial and lateral compartments. Special attention is given to the menisci and chondral surfaces. Usually, full-thickness longitudinal and bucket handle meniscal tears in the red-red and red-white zones are repaired using an inside-out technique. Partial-thickness and stable tears less than 10 mm in length are not surgically treated. Outerbridge grade II and III chondral lesions may be treated with the use of a cartilage thermal device. Unstable cartilage lesions and Outerbridge grade IV lesions may be treated by débridement and microfracture. Figure 23D1-7 A knee holder is used to keep the operative knee stable during the surgery. It also allows good range of motion of the knee during the surgery.

Diagnostic Arthroscopy

Arthroscopy is performed to diagnose and treat any associated injuries. The correct portal positions are critical to obtain optimal intra-articular visualization and to manage the arthroscopic instrumentation. We use the standard anterolateral (AL) and AM portals, as well as an accessory anteromedial portal (AAM) (Fig. 23D1-8). The AL portal is close to the inferior border of the patella. The AM portal is placed medial to the patellar tendon, slightly lower than the AL portal. To establish the AAM portal, the arthroscope is placed into the standard AM portal, and an 18-gauge spinal

Figure 23D1-8 Surgical incisions for anterior cruciate ligament surgery: anterolateral portal (LP), anteromedial portal (MP), accessory medial portal (AMP), and tibial incision.

Insertion Site Marking

The ACL rupture pattern is evaluated during the diagnostic arthroscopy, as are the native footprints of the AM and PL bundles on the tibial plateau (Fig. 23D1-9) and lateral wall of the intercondylar notch (Figs. 23D1-10 and 23D1-11). When identified, the tibial and femoral footprints of each bundle are marked by a thermal device (ArthroCare Corporation, Sunnyvale, Calif). The PL tibial footprint is located in the center of a triangle formed by the posterior root of the lateral meniscus, the PCL, and the AM bundle of the ACL (see Fig. 23D1-9). The AM tibial footprint is located anteromedial to the PL tibial footprint. The tibial ACL stumps are left intact to preserve their proprioceptive and vascular

Figure 23D1-9 The oval anteromedial (AM) and circular posterolateral (PL) tibial insertions are marked with a thermal device. Tunnel guidewires have been placed in the center of the AM and PL bundle tibial insertion sites. The center of the PL bundle is 3 to 5 mm from the posterior aspect of the triangle formed by the posterior cruciate ligament (PCL), lateral meniscus posterior root, and AM bundle insertion site. LFC, lateral femoral condyle. Continued


Authors’ Preferred Method—cont’d rupture pattern and bony anatomy are easier to visualize in acute than in chronic ACL injuries. Thus, a thorough understanding of the double-bundle ACL anatomy is essential to identify and mark the correct insertional footprints. Graft Preparation

Figure 23D1-10 With the knee in 90 degrees of flexion, the posterolateral (PL) bundle insertion is marked on the femoral side with a thermal device. Care is taken to preserve the superior border of the ACL fibers, which serve as the upper limit for tunnel placement. AM, anteromedial bundle.

contributions. On the femoral side, the ACL bundle origins are located under a bony landmark called resident’s ridge. It is important to note that in most cases, there is a clear change in the topography between the AM and PL femoral insertions, forming a bony landmark between the AM and PL bundle femoral origins called the cruciate ridge. The cruciate ridge and the change in the ACL femoral topography make location of the AM and PL bundles on the femur easier (see Fig. 23D1-5) We do not perform a notchplasty because it destroys the bony landmarks and the topography of the ACL femoral anatomy. It is important to note that the

Figure 23D1-11 Similar to the marking of the posterolateral (PL) bundle insertion, the anteromedial (AM) insertion on the femoral side is marked with a thermal device. The anterior cruciate ligament remnant is preserved to serve as the reference for tunnel placement.

While the diagnostic arthroscopy and insertion site marking are being performed, the grafts are being prepared on the back table by an assistant. Typically, we use two separate tibialis anterior or tibialis posterior tendon allografts. However, HS autograft may also be used. The allografts are removed from the −80° C freezer and thawed in a warm saline solution. Usually, the allograft is 24 to 30 cm in length, and we fold each tendon graft to obtain 12 to 15 cm doublestranded grafts (Fig. 23D1-12). First, the tendon allografts are trimmed, and the diameters of the double-stranded grafts are adjusted. Typically, the tendon grafts are trimmed such that the diameter of the double-stranded AM graft is 8 mm and that of the double-stranded PL graft is 7 mm. However, the diameters of the graft may be adjusted depending on the size of the patient. The ends of the grafts are sutured using a baseball stitch with No. 2 Ti-Cron sutures. An EndoButton CL (Smith & Nephew, Andover, Mass) is used to loop each graft and obtain a double-stranded graft. The length of the EndoButton loop is chosen according to the measured length of the femoral tunnels. It is important to know the available EndoButton loop lengths (15 to 40 mm in 5 mm increments). The exact length of the EndoButton loop is chosen after measuring the femoral tunnel length. Tunnel Placement

The PL femoral tunnel is drilled first. A Steadman awl is used to create a small hole in the center of the PL bundle femoral insertion to facilitate the placement of a 3.2-mm guidewire that is inserted through the AAM portal (Fig. 23D1-13). The tip of the guidewire is placed on the small hole and malleted into position. Once the tip of the guidewire is placed in the

Figure 23D1-12 Grafts were prepared on the back table by an assistant.

Knee 1665


Figure 23D1-13 A Steadman awl is used to mark the desired femoral anteromedial (AM) and posterolateral (PL) positions for guide pins. This also makes it easier for the guide pins to be inserted into the chosen spot.

correct position, the femoral PL tunnel is drilled with an acorn drill that is inserted over the guidewire. It is important to note that during the entire procedure to create a PL femoral tunnel, the knee is positioned at 90 degrees of flexion, which brings the PL bundle footprint anteriorly. The PL femoral tunnel is drilled to a depth of 25 mm (Fig. 23D1-14). The far cortex is breached with a 4.5-mm EndoButton drill, and the depth gauge is used to measure the distance to the far cortex. When the total length to the far cortex is longer than 38 mm, the PL femoral tunnel is drilled to a depth of 30 mm. To obtain the correct length of the EndoButton loop, 6 mm is added to the difference between the total length (TL) and the length of the graft femoral tunnel (GL). Thus, the formula is length of the EndoButton loop = (TL − GL) + 6. For example, when a 38-mm tunnel is drilled to the far cortex and the graft femoral tunnel is drilled to 30 mm, the

Figure 23D1-14 Posterolateral (PL) femoral tunnel is drilled through the accessory anteromedial portal.

f ollowing calculation is performed: EndoButton loop length = (38 − 30) + 6. In this example, the EndoButton length is 14 mm. Because 14 mm is not available, the 15-mm EndoButton loop is chosen. Always the approximation is done to the higher number to ensure that the EndoButton will be able to flip and achieve appropriate cortical fixation. To create the two tibial tunnels, a 4-cm skin incision is made over the AM surface of the tibia at the level of the tibial tubercle. The PL tibial tunnel is the first to be drilled. The elbow ACL tibial drill guide is set at 45 degrees, and the tip of the drill guide is placed intra-articularly on the tibial footprint of the PL bundle previously marked. On the tibial cortex, an osteoperiosteal flap is detached, and the tibial drill starts just anterior to the superficial MCL fibers. Once the tibial drill guide is set, a 3.2-mm guidewire is passed into the stump of the PL tibial footprint (Fig. 23D1-15). The AM

Figure 23D1-15 Different views of the tibial guide pins from lateral portal (left) and medial (right) portal. Both portals provide good views on the tibial side. However, the medial portal is superior in observing the lateral wall of the intercondylar notch. Continued



Figure 23D1-16 Overhead and lateral pictures demonstrate the orientation of anteromedial (AM) and posterolateral (PL) tibial tunnel dilators. The tibial tunnels were both drilled with the drill guide set at 45 degrees.

tibial tunnel is drilled with the elbow ACL tibial drill guide set at 45 degrees, and the tip of the drill guide is placed on the tibial footprint of the AM tunnel previously marked. On the tibial cortex, the starting point for the AM bundle is placed anterior, lateral, and proximal from the PL starting point, under the osteoperiosteal flap detached previously (Fig. 23D1-16). After the elbow ACL tibial drill guide is placed in the desired position, a 3.2-mm guidewire is passed into the stump of the AM tibial footprint (see Fig. 23D1-15). When both tibial guidewires are in place, the two tibial tunnels are drilled using a cannulated drill. Usually, the diameter of PL and AM tunnels are 7 and 8 mm, respectively. The femoral AM tunnel is the last tunnel to be drilled. During the AM tunnel drilling, it is important to flex and hold the knee to about 120 degrees. A transtibial technique as used for a single-bundle ACL reconstruction is our first choice to create the AM femoral tunnel. However, in some cases, the transtibial technique cannot reach the center of the AM bundle previously marked. Then, we can try to reach the center of the AM femoral footprint through the PL tibial tunnel. Using this approach, the AM graft needs to be trimmed to a 7-mm diameter. In cases in which the center of the AM femoral footprint is not reached through either the PL or AM tibial tunnels, we use the AAM portal to reach the center of AM bundle (Fig. 23D1-17). Using this approach, the total length of the femoral tunnel is shorter, and caution is needed to avoid compromising the cortical integrity of the lateral femoral condyle with the 8-mm drill. When the tip of the guidewire is placed in a correct position, the guidewire is malleted into position, and an acorn drill is inserted over the guidewire. The AM femoral tunnel is drilled to a depth of 35 to 40 mm when it is done through a transtibial approach. In cases in which the AM femoral tunnel is performed through the AAM portal, it is drilled to a depth of 25 to 30 mm (Fig. 23D1-18). The far cortex of the AM femoral tunnel is breached with a 4.5-mm EndoButton

drill, and the depth gauge is used to measure the distance to the far cortex. The length of the EndoButton loop is chosen in a similar fashion to the PL tunnel drilling. Graft Placement and Fixation The first graft to be passed is the PL graft (Fig. 23D1-19). A beath pin with a long-looped suture attached to the eyelet is passed through the AAM portal and out through the PL femoral tunnel. The looped suture is visualized within

Figure 23D1-17 Creation of the anteromedial (AM) femoral tunnel through either the accessory medial portal (AMP) or the tibial posterolateral (PL) tunnel results in anatomic placement of the AM bundle. Attempts at creating the AM femoral tunnel through the AM tibial tunnel may sometimes result in placement of the AM graft superior to the upper limit of the native AM bundle (gray area). Thus, the femoral tunnel should be drilled independent of the tibial tunnels.

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Figure 23D1-18 The anteromedial (AM) and posterolateral (PL) femoral tunnels have been created in the anatomic position. LFC, lateral femoral condyle.

Figure 23D1-20 Final result of anatomic double-bundle anterior cruciate ligament (ACL) reconstruction. Note that the upper border of the ACL remnant can still be visualized after passing the grafts. AM, anteromedial bundle; PL, posterolateral bundle.

the joint and retrieved with an arthroscopic suture grasper through the PL tibial tunnel. The Ti-Cron sutures of the graft are passed through the looped suture, and the graft is passed in a retrograde fashion up the tibia and femur. After the graft is successfully passed, the EndoButton is flipped for femoral fixation. The AM graft is passed using the trans tibial technique when the tunnel was created transtibially or through the AAM portal when the tunnel was created through the AAM portal, using the same technique as in the PL bundle graft passage. The EndoButton is flipped in a similar fashion to establish AM bundle femoral fixation. When the AM femoral tunnel is drilled through the PL

tibial tunnel, it is important to pass the suture of the AM graft through the PL tibial tunnel and retrieve it through the AM tibial tunnel before performing the PL graft passage (Fig. 23D1-20). After passing the grafts, the knee is moved in full range of motion, and the grafts are observed under scope to exclude the possibility of ACL or PCL impingement (Fig. 23D1-21). Preconditioning of the grafts is performed by flexing and extending the knee through a range of motion from 0 to 120 degrees about 20 to 30 times. On the tibial side, we prefer to use a Calaxo bioabsorbable screw (Smith & Nephew, Andover, Mass). A 7 × 25-mm screw is used in the PL tibial tunnel, and an 8 × 25-mm screw is used in the AM

Figure 23D1-19 The posterolateral (PL) graft is passed first, followed by the anteromedial (AM) graft. When the knee is in flexion, the AM and the PL bundles show a crossing pattern.

Figure 23D1-21 The posterior cruciate ligament (PCL) triangle that is formed by the anterior cruciate ligament (ACL), the PCL, and the roof of the intercondylar notch is shown. PCL impingement is rarely seen even without notchplasty. Continued


Authors’ Preferred Method tibial tunnel. The graft fixation is performed with the knee in 0 degrees of flexion for the PL bundle graft and at 60 degrees of flexion for the AM graft (Fig. 23D1-22). During fixation, maximal tension is applied to the sutures, and the screws are properly placed. The remaining graft left protruding from the tibial tunnel is removed. Arthroscopic inspection is performed to observe the intra-articular graft tension. The use of the AAM portal to drill AM femoral tunnel may lead to a short femoral tunnel, and the far cortex may be compromised by the use of an 8-mm drill, making EndoButton fixation impossible. In this case, a lateral incision is made, and postfixation of the EndoButton loop is performed using a 4.5-mm diameter screw.

Closure

The osteoperiosteal flaps overlying the tibial drill holes are closed with a 0-0 absorbable suture. The subcutaneous layer is closed with an interrupted 2-0 absorbable suture, and the skin with a running subcuticular 3-0 absorbable suture. We do not inject Bupivacaine intra-articularly, to avoid possible cell toxicity. The peripheral nerve block typically provides anesthesia for about 24 hours. We do not use drains. The wound is covered by Steri-Strips, dry sterile gauze, Kerlix roll, a cryotherapy pad, and finally a Cryocuff. We put the knee in a hinged knee brace, locked in full extension.

Figure 23D1-22 Anteromedial bundle graft passage and fixation at 60 degrees of knee flexion. The posterolateral bundle has been passed first and fixed in full extension.

POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Rehabilitation The optimal rehabilitation program after ACL reconstruction has changed considerably over the past 20 years because of advancements in surgical techniques, graft selection, and fixation methods, as well as an improved understanding of the biology and biomechanics of the knee. Accelerated rehabilitation programs, which permit early range of motion, immediate weight-bearing, and early return to sport, have become the accepted standard and have helped the patient to return to a normal and complete level of function in the shortest time possible without compromising the integrity of the surgically reconstructed knee. However, prospective randomized controlled trials are still needed to prove this trend, as well as further research into the biology of graft healing, the appropriate limits of graft strain, and the effects of functional activities on graft stability.

Open and Closed Kinetic Chain Exercise One of the major goals of postoperative rehabilitation is to restore the range of motion of the knee joint, without compromising the integrity and function of the ACL graft. Generally, in the early rehabilitation program, closed kinematic chain (CKC) exercises are safer than the openor kinematic chain (OKC) exercises because research has suggested that CKC exercises apply less anteriorly directed forces on the tibia,327-329 increase tibiofemoral compressive forces,330,331 increase co-contraction of the hamstrings,328,332 mimic functional activities more closely than OKC exercises,329,333 and reduce the incidence of patellofemoral complications, especially at low knee flexion angles.329,333 A variety of different definitions of CKC and OKC exercises are used in the literature. Briefly, CKC exercises are defined as those in which the foot is in contact with a solid surface (Fig. 23D1-23). Ground reaction force is transmitted to all of the joints in the lower extremity, and muscles spanning all of the joints of the lower extremity are used. Examples of CKC exercises are the squat and leg press. In contrast, OKC exercises are defined as those in which the foot is not in contact with a solid surface

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Figure 23D1-23 Leg press machine. Patient is doing a closed chain exercise.

(Fig. 23D1-24). Thus, one segment of the limb is stabilized while the other segment moves freely, and only the muscles spanning the knee are required to perform the exercise. An example of OKC exercise is the leg extension machine. However, many activities cannot be clearly classified as CKC or OKC. Daily activities like walking, stair climbing, and jumping are combinations of OKC and CKC movements. Understanding the mechanics of different activities and their impact on the healing ACL graft is the key to the success of ACL surgery rehabilitation. Several studies have reported that OKC exercises generate significantly greater anterior tibial translations in the ACL-deficient knee than CKC exercises. Jonsson and colleagues reported a 1.9-mm average increase of anteriorly directed tibial displacement in the ACL-deficient knee during the active knee extension exercise (OKC) when the knee was near extension (15 to 10 degrees), whereas no increase was recorded during the step-up exercise (CKC).334 Using analytic models, Escamilla and associates determined that

Figure 23D1-24 Straight leg raise. Patient is doing an open chain exercise.

the mean peak force on the ACL was 158 N during the OKC exercise when the knee was at 15 degrees of flexion, whereas it was not loaded during the CKC exercises.329 However, incorporating accurate three-dimensional geometry of the knee and the material properties of different tissues into the analytic model is needed in the future to accurately mimic the loading environment on the ACL graft. Attention has also been paid to the direct measurements of ACL strains when OKC and CKC exercises are performed (Table 23D1-10) because excessive strains could permanently stretch out or fail the tissue. Using the differential variable reluctance transducer, Beynnon and associates52 showed that consistent distinction between CKC and OKC activities was not found, although both exercises resulted in increased strain values in the ACL, with squatting showing slightly higher strain values than knee extension. This finding suggests that certain CKC activities, such as squatting, may not be as safe as we believed, particularly at low flexion angles. However, CKC exercises did show an advantage in that increasing resistance did not lead to an increased strain in the ACL, whereas it did during OKC exercises.

TABLE 23D1-10 Rank Comparison of Peak Anterior Cruciate Ligament Strain Measured during Commonly Prescribed Rehabilitation Exercises* Rehabilitation Exercise Isometric quadriceps contraction at 15 degrees (30 Nm of extension torque) (OKC) Squatting with sport cord (CKC) Active flexion-extension of the knee with 45-N weight boot (OKC) Lachman test (150 N of anterior shear load; 30-degree flexion) Squatting (CKC) Active flexion-extension (no weight boot) of the knee (OKC) Simultaneous quadriceps and hamstring contraction at 15 degrees (OKC) Isometric quadriceps contraction at 30 degrees (30-Nm extension torque) (OKC) Stair climbing (CKC) Leg press at 20-degree flexion (40% body weight) (CKC) Lunge (CKC) Stationary bicycling (CKC) Isometric hamstring contraction at 15 degrees (to 10 Nm flexion torque) (OKC) Simultaneous quadriceps and hamstring contraction at 30 degrees (OKC) Isometric quadriceps contraction at 60 degrees (30-Nm extension torque) (OKC) Isometric quadriceps contraction at 90 degrees (30-Nm extension torque) (OKC) Simultaneous quadriceps and hamstring contraction at 60 degrees, 90 degrees (OKC) Isometric hamstring contraction at 30, 60, and 90 degrees (10 Nm flexion torque) (OKC)

Peak Strain (%) 4.4 (0.6) 4.0 (0.6) 3.8 (0.5) 3.7 (0.8) 3.6 (0.5) 2.8 (0.8) 2.8 (0.9) 2.7 (0.5) 2.7 (1.2) 2.1 (0.5) 1.9 (0.5) 1.7 (0.7) 0.6 (0.9) 0.4 (0.5) 0.0 0.0 0.0 0.0

*Mean ± standard error. CKC, closed kinetic chain; OKC, open kinetic chain. From Fleming BC, Oksendahl H, Beynnon BD: Open- or closed-kinetic chain exercises after anterior cruciate ligament reconstruction? Exerc Sport Sci Rev 33(3):134-140, 2005.


The effects of OKC and CKC exercises on functional outcome have been evaluated in three independent prospective randomized clinical trials.5,10,14 Bynum and coworkers found that the mean side-to-side difference in knee laxity of the OKC group (3.3 mm) was significantly greater than that of the CKC group (1.6 mm) 19 months after surgery. The CKC group also returned to sport earlier than the OKC group. However, the two rehabilitation protocols have some differences in the levels of resistance and the progression of exercise, which may account for the better outcomes of the CKC group. Mikkelsen and associates335 randomized the patients into two rehabilitation programs. One group used CKC exercises for 24 weeks, and the other used the same CKC rehabilitation program with the addition of OKC exercises (isokinetic quad strengthening) from weeks 6 to 24. Interesting, significantly higher quadriceps torque was observed in the later group. The authors suggested that certain OKC exercises may be beneficial. However, the improvement may simply be due to the addition of exercises, independent of the type of exercise added. Nonetheless, the addition of the OKC exercises in this time frame did not produce a negative outcome. In another study, Morrissey and Hooper found that there are no clinically significant differences in the functional improvement resulting from the choice of OKC and CKC exercises in the early period of rehabilitation.333 However, this report may be limited because of the short rehabilitation program (2 to 6 weeks after surgery). In summary, the CKC exercises appear to protect the graft and help restore knee functions by different mechanisms. CKC exercises generate low anterior shear force and tibial displacement through most of the flexion range, increase tibiofemoral compressive forces, and reduce the incidence of patellofemoral complications. Additionally, in vivo strain data supported the notion that the ACL is a primary restraint to anteroposterior translation of the knee, and that knee hamstring co-contractions reduce ACL strains relative to isolated contractions of the quadriceps and gastrocnemius muscles. However, in the prospective randomized clinical trials that were designed to evaluate the effectiveness of OKC and CKC exercises in helping graft healing and restoring knee functions, contradictory conclusions were drawn, suggesting that the difference of OKC and CKC exercises may not be clinically significant and that additional prospective randomized clinical trials must be performed to determine the optimal time and combination to introduce these exercises. The key of ACL surgery rehabilitation is to use activities that minimize graft strain and put the ACL at the lowest risk for development of laxity.

REHABILITATION CONSIDERATIONS Pain and Effusion Pain and swelling are common after any surgical procedure. They cause reflex inhibition of muscle activity and therefore should be controlled appropriately to facilitate early range of motion and strengthening activities. The RICE principle, including rest, ice, compression, and elevation,

remains the standard of care in reducing pain and swelling. Narcotic and anti-inflammatory pain medications are commonly prescribed in the acute postoperative setting. Muscle activities like quad sets and ankle pumps can help to reduce swelling by improving venous return. Electrical muscle stimulation of the quadriceps is also used to promote muscle activity before the return of voluntary muscle control.

Cryotherapy Cryotherapy is a common treatment modality after orthopedic surgery procedures. The forms of cryotherapy include ice packs, ice baths, and continuous flow cooling devices. The beneficial effects of cryotherapy are obtained through lowering joint temperature.336,337 Low temperature can help to lower the metabolism, reduce inflammation, and induce vasoconstriction, which, in turn, contributes to less tissue swelling, less pain, and less hemarthrosis.336,338 A recent meta-analysis including seven randomized clinical trials showed that postoperative drainage (P = .23) and range of motion (P = .25) were not significantly different between cryotherapy and control groups. However, cryotherapy was associated with significantly lower postoperative pain (P = .02).339 It was considered an inexpensive, easy to use way to reduce pain, inflammation, and effusion after knee surgery. Complications such as superficial frostbite and neurapraxia are rarely seen and can be prevented by avoiding prolonged placement of the cold source directly on the skin.

Motion Loss of motion is one of the most common complications after ACL reconstruction. The most common causes of this complication include arthrofibrosis, cyclops syndrome, and inappropriate graft placement or tensioning.340 It may lead to symptoms like anterior knee pain, abnormal gait, muscle atrophy, and early degenerative changess of the joint.340-342 Usually, the loss of extension is more commonly seen and more poorly tolerated than the loss of flexion.341 With the evolvement of rehabilitation concepts and the improvement of surgical technique, range of motion problems after ACL reconstruction have been minimized. Aggressive postoperative rehabilitation protocols are being used to restore the knee motion. The goal is to achieve full extension right after the surgery and regain 10 degrees of flexion per day. By 7 to 10 days after surgery, the knee should achieve 90 degrees of flexion. Bracing in slight hyperextension has been proposed as an easy way to ensure full knee extension.343 Early passive and active range of motion is augmented by the use of a continuous passive motion machine. Prevention is the key to achieving range of motion. It is suggested that control of pain and swelling, early reactivation of the quadriceps musculature, patellar mobilization, and early return to weight-bearing contribute to the return of motion. In comparison, postoperative immobilization may slow down the process and increase the need for manipulations to regain motion.344 It is worth noting that graft positioning is an important factor in regaining range of motion. If tunnel placement of the ACL graft is incorrect, it may limit knee flexion. With

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the growing popularity of double-bundle ACL reconstruction, some argue that it may cause ACL and PCL impingement and lead to loss of motion.345 This emphasizes the importance of correct tunnel positioning. If the tunnels are positioned anatomically and the normal anatomy is closely restored, range of motion should not be a concern in performing this type of surgery.326

Weight-Bearing Weight-bearing was prohibited in earlier rehabilitation protocols because of concern over graft laxity and failure. With the development of surgical technique and the knowledge that immediate rehabilitation produces no adverse reactions, a trend toward immediate weight-bearing in the postoperative setting has evolved.346 Additionally, early weight-bearing may help to improve cartilage nutrition, reduce disuse osteopenia, and hasten quadriceps recovery. In a prospective randomized trial performed by Tyler and colleagues,347 immediate weight-bearing was compared with delayed weight-bearing for 2 weeks after ACL reconstruction with a central third BPTB autograft. At a mean follow-up of 7.3 months, no differences were observed between the two rehabilitation protocols in terms of range of motion, vastus medialis oblique function, and anteroposterior knee laxity (clinical examination and KT-1000). However, the immediate weight-bearing group showed a decreased incidence of anterior knee pain. The findings indicate that immediate weight-bearing after ACL reconstruction may be beneficial by lowering the incidence of anterior knee pain, whereas it does not apply excessive loads on the graft or its fixation. Accelerated rehabilitation protocols usually begin with tolerated weight-bearing immediately after surgery with a progression to full weightbearing without crutches by 10 to 14 days.

Muscle Training Issues The early initiation of muscle training is very important in the prevention of muscle atrophy and weakness. Muscle activation and strengthening, including voluntary exercises, electrical muscle stimulation, and biofeedback, should be started before surgery as well as immediately after surgery. Electrical stimulation can help to initiate muscle activation when reflex inhibition can not be overcome in patients who are suffering severe pain and swelling. Biofeedback is helpful in enhancing the force of muscle contraction. Quadriceps muscle strength is correlated with good outcomes after ACL reconstruction. Strengthening of the quadriceps is the focus of many rehabilitation programs. However, achieving the appropriate hamstring-to-quadriceps ratio may provide even better protection for the ACL. The role of the hamstring muscles is to flex the knee joint, increase joint compression, and pull the tibia backward through a posterior shear force at tibial flexion angles greater than 20 degrees. Thus, hamstring contraction decreases ACL strain.348,349 Baratta and colleagues350 suggested that with reduced hamstring antagonist activity, the risk for injury is increased. However, no correlation could be found between hamstring strength and functional tests.351 Little attention has been paid to the gastrocnemius muscle, although some authors have demonstrated its functional importance for knee stability.328,352

Endurance training should be included in the rehabilitation program because fatigue affects not only the muscle contraction strength but also the electromechanical response time and rate of muscle force generation.353,354 Fatigue is also associated with decreased knee proprioception and increased joint laxity compared with baseline values.355,356 It has been shown to alter motor control strategies in recreational athletes, which may increase anterior tibial shear force, strain on the ACL, and risk for injury in both female and male subjects.357

Electrical Muscle Stimulation and Biofeedback Electrical muscle stimulation is used as an adjunct to voluntary exercises in an effort to recover muscle strength after ACL reconstruction. The effectiveness of this method is controversial in the literature. Sisk and colleagues358 claimed there was no significant difference in muscle strength as a result of electrical stimulation. Halkjaer-Kristensen and Ingemann-Hansen359 noted that isometric exercise and electrical stimulation were both ineffective in preventing muscular atrophy. However, Morrissey and colleagues360 reported that application of electrical stimulation alone is more effective than voluntary exercises. This controversy is due in part to the use of different electrical stimulation protocols, including parameters like frequency, intensity and impulse width, duration, and the number of electrodes and their placement. Snyder-Mackler and colleagues361 performed a randomized controlled trial of rehabilitation after ACL reconstruction with either a semitendinosus tendon combined with a ligament augmentation device or a central third BPTB preparation. Patients were randomized to undergo rehabilitation with neuromuscular electrical stimulation and volitional exercises or with volitional exercises alone. Eight weeks after surgery, patients were evaluated for their gait and thigh muscle strength. The incorporation of neuromuscular electrical stimulation into volitional exercises had resulted in more near-normal gait parameters and stronger quadriceps muscles. Later, Snyder-Mackler and colleagues362 reported the results of a multicenter randomized controlled trial of rehabilitation after ACL reconstruction with different graft materials and surgical techniques. The patients were assigned to treatments with high-intensity neuromuscular electrical stimulation, high-level volitional exercises, low-intensity neuromuscular electrical stimulation, or combined high- and low-intensity neuromuscular electrical stimulation. The 4-week follow-up results revealed that high-intensity neuromuscular electrical stimulation combined with volitional exercises was better at restoring extensor strength compared with volitional exercises alone. Biofeedback is a principle that is widely used in muscle rehabilitation and strengthening programs. The principle of electromyographic biofeedback is that the patient has a visual or auditory representation of the quality of muscle contraction. The patient then tries to enhance the level of the visual or auditory output by contracting the muscle group in or over which the electromyogram electrodes have been placed. Biofeedback is more effective than electrical stimulation in facilitating recovery of peak torque of quadriceps after ACL reconstruction.363 The combination


of biofeedback and exercises is better than exercise alone in recovery of quadriceps function after ACL reconstruction,364 and better than exercise alone in quadriceps strengthening in normal subjects.365

Proprioception Proprioception is defined as the culmination of all neural inputs originating from joints, tendons, muscles, and associated deep tissue proprioceptors. These inputs are projected to the central nervous system for processing and ultimately result in the regulation of reflexes and motor control.366 Mechanoreceptors are specialized nerves located in skin, joints, tendon, ligament, and skeletal muscle. They serve as transducers to convert mechanical signals into afferent nerve signals, providing position sense and conscious awareness by initiating reflexes to stabilize joints and maintain stance. ACL deficiency results in an unstable knee. However, several authors have demonstrated that restoring mechanical stability alone (ACL reconstruction) does not guarantee functional stability.367,368 Anatomic and histologic studies have demonstrated the presence of proprioceptive mechanoreceptors in the fibers of the ACL.367,369 In addition, with forced increases in anterior tibial translation, muscle responses, including increases in hamstring activation and inhibition of quadriceps activity, were observed.370,371 It has been suggested that the ACL serves a sensory and proprioceptive role, in addition to its role as a mechanical stabilizer.367,368 Lephart and coworkers9 suggested that altered proprioception may reduce the effectiveness of protecting the knee and may predispose the ACL to repetitive microtrauma and ultimately failure. Proprioception was also shown to be positively related to the function of the ACL-injured knee.372 After ACL reconstruction, patients continue to have deficits in proprioception and neuromuscular joint control for at least 6 months and as long as 1 year after surgery.373,374 Thus, it is important to incorporate beginning, intermediate, and advanced proprioceptive training exercises throughout the postoperative rehabilitation protocol.375 Studies376,377 have shown proprioceptive deficits in both limbs of patients with unilateral ACL deficiency, indicating that clinicians should not use the contralateral limb as a control when assessing proprioceptive parameters. Another important issue of proprioception is the difference between genders. Females possess greater deficits in proprioception after injury or ACL reconstruction. This is further discussed in under “Gender Issues.”

Bracing Two forms of braces, rehabilitation braces and functional braces, are used to protect the graft in the rehabilitation of ACL reconstruction. Rehabilitation braces are used in the early postoperative period, and functional braces are used when the patient returns to strenuous activity. There appears to be a consensus that the use of a rehabilitation brace results in fewer problems than no bracing during the early stage of rehabilitation, including less pain, less swelling, and lower prevalence of hemarthrosis and wound drainage. Three independent randomized controlled

t rials378-380 suggested, however, that rehabilitation bracing does not have a long-term effect on clinical outcome, range of knee motion, subjective outcome, anteroposterior knee laxity, activity level, or function. In addition, rehabilitation bracing was found to be helpful in preventing potential loss of extension range of motion. Two randomized controlled trials343,381 showed that the application of a rehabilitation brace in full extension or hyperextension during the early postoperative stage was effective in recovering full extension of the operative knee and that the stability of the graft was not compromised. The role of functional knee bracing in ACL reconstructions is controversial. Two randomized controlled trials382,383 did not show evidence of benefit by using functional braces after ACL reconstruction. However, biomechanical studies of functional ACL bracing suggest that some functional knee braces do increase mechanical stability under low loading conditions.52,384 In a recent cohort study,385 ACL reconstructed skiers without a functional brace were estimated to be almost 3 times more likely to sustain a subsequent knee injury.

Rehabilitation Protocol after Anterior Cruciate Ligament Reconstruction The rehabilitation protocol for ACL reconstruction has changed dramatically during the past several years. Instead of conservative rehabilitation with limitation of range of motion, delayed weight-bearing (8 to 10 weeks), and delayed return to sports (9 to 12 months), current ACL reconstruction rehabilitation protocols emphasize immediate range of motion, immediate weight-bearing, and earlier return to sports (4 to 6 months). Although there may be slight differences between protocols used in different practices, most are based on the same basic principles. Because of improvements in surgical technique and accelerated rehabilitation protocols, most recent ACL reconstruction outcome studies have achieved a 90% success rate in terms of restoring knee stability, patient satisfaction, and return to full athletic activity.199 The optimal graft material remains controversial. Autografts including the patellar, hamstring, and quadriceps tendons, and allografts including the quadriceps, patellar, Achilles, hamstring, anterior and posterior tibialis tendons and the fascia lata, are the main options. Although each graft choice has its unique features, no evidence has been provided that we need different rehabilitation protocols to match different graft choices. Comparison studies of allografts versus autografts226,386 and BPTB graft versus HS graft302,387,388 have demonstrated few differences in outcomes with similar accelerated rehabilitation protocols. Our rehabilitation protocol for ACL reconstruction is listed as an example of current trend. This protocol is used in all of our ACL reconstruction patients, regardless of the choice of graft and single-bundle versus double-bundle technique (Box 23D1-1).

Rehabilitation of Associated Injuries Meniscal damage frequently occurs at the time of an ACL injury. The frequent association of repairable tears with a torn ACL adds concerns about the influence of an

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Box 23D1-1 Anterior Cruciate Ligament Reconstruction and Rehabilitation Protocol Stage 1 Begin immediately after surgery through about 6 weeks. Goals 1. Protect graft fixation. 2. Minimize effects of immobilization. 3. Control inflammation. 4. Achieve full extension and flexion range of motion. 5. Educate patient on rehabilitation progression. Therapeutic Exercises 1. Heel slides 2. Quadriceps sets 3. Patellar immobilization 4. Non–weight-bearing gastroc-soleus stretches; hamstring stretches begin at 4 weeks 5. Straight leg raises in all planes with brace in full extension until quadriceps strength is sufficient to prevent extension lag 6. Quadriceps isometrics at 60 and 90 degrees Stage 2 Begin 6 weeks after surgery and extend to about 8 weeks. Goals 1. Restore normal gait. 2. Maintain full extension, progress with flexion range of motion. 3. Protect graft fixation. Therapeutic Exercises 1. Wall slides 0 to 45 degrees 2. Four-way hip machine 3. Stationary bike 4. Closed-chain terminal extension with resistance tubing or weight machine 5. Toe raises 6. Balance exercises 7. Hamstring curls 8. Aquatic therapy with emphasis on normalization of gait 9. Continue hamstring stretches, progress to weight-bearing gastroc-soleus stretches Stage 3 Begin 8 weeks after surgery and extend through about 6 months.

a ccelerated rehabilitation program on meniscal healing rates. Barber and Click suggested that no modification of an ACL reconstruction accelerated rehabilitation program is needed for meniscus repairs performed in conjunction with the reconstruction.131 Mariani and colleagues also showed that no deleterious effects were observed in patients undergoing ACL reconstruction and concomitant meniscus repair.389 Bone bruises and chondral lesions are also often seen with ACL injury. Little has been reported on the rehabilitation of these concomitant injuries.

Goals 1. Achieve full range of motion. 2. Improve strength, endurance, and proprioception of the lower extremity to prepare for functional activities. Therapeutic Exercises 1. Continued flexibility exercises as appropriate for patient 2. Stairmaster (begin with short steps, avoid hyperextension) 3. Nordic Track 4. Advanced closed-chain strengthening (one-leg squats, leg press 0 to 50 degrees, step-ups begin at 2 inches, etc. 5. Progress proprioception activities (slide board, use of ball with balance activities, etc.) 6. Progress aquatic therapy to include pool running, swimming (no breaststroke) Stage 4 Begin 6 months after surgery and extend through about 9 months. Goal 1. Achieve progress in strength, power, and proprioception to prepare for return to functional activities. Therapeutic Exercises 1. Continue to progress with flexibility and strengthening program. 2. Initiate plyometric program as appropriate for patient’s functional goals. 3. Achieve functional progression, including walking and jogging progression; forward and backward running at half, three fourths, and full speed; cutting; crossover; and carioca exercises, among others. 4. Initiate sport-specific drills as appropriate for patient. Stage 5 Begin 9 months after surgery. Goals 1. Safe return to athletics 2. Maintenance of strength, endurance, proprioception 3. Patient education with regard to possible limitations Therapeutic Exercises 1. Gradual return to sports participation 2. Maintenance program for strength and endurance

Functional Training During the past several years, restoring proprioception, dynamic stability, and neuromuscular control has been gradually incorporated into the rehabilitation programs of ACL reconstruction patients. They have a critical effect on the prevention of knee reinjuries. In addition, these drills are usually fun and take some of the focus away from the knee, thereby helping to maintain the patient’s motivation during physical therapy.


Basic proprioceptive exercises such as joint repositioning, CKC weight-shifting, and minisquats are usually started during the second postoperative week, when the pain and swelling associated with surgery subsides and the patient regains quadriceps control. As proprioception is advanced, drills to encourage agonist-antagonist muscle coactivation during functional activities should be incorporated. Dynamic stabilization drills, including single-leg stance on flat ground and unstable surfaces, cone-stepping, and lateral lunge drills, usually begin during the first 2 to 3 weeks. These drills help to enhance dynamic stability and facilitate gait normalization.390 Plyometric jumping drills are also used to facilitate dynamic stabilization and neuromuscular control of the knee joint. By producing a maximal concentric contraction following a rapid eccentric loading on the muscle, plyometric training is used to train the lower extremity to avoid injury by producing and dissipating forces.391,392 Another aspect of rehabilitation regarding neuromuscular control is the enhancement of muscle endurance. Bicycle, elliptical machines, stair climbing, and slide boards are highly repetitive and low-resistance drills that are safe to be used for long durations to strengthen the muscles and to train the muscles to perform against fatigue. When performed toward the end of a treatment session, these drills can challenge the neuromuscular control of the knee joint when the dynamic stabilizers have been adequately fatigued.390 Sport-specific drills should be added slowly at the late stage of rehabilitation to ensure the safety of the graft. The intention of sport-specific training is to simulate the functional activities associated with sports and facilitate the return to the previous level of sports activities. It also helps to prevent injury by training the neuromuscular system to perform in a reflexive pattern. It is worth noting that neuromuscular control at the knee is supported by the entire lower extremity and the core muscles. Therefore, exercises to enhance total body strength, flexibility, endurance, and neuromuscular control must not be neglected.

Functional Testing To measure the functional status of the knee, a variety of tests have been used. Noyes and colleagues393 developed a battery of functional tests consisting of the single hop for distance, the triple hop for distance, the crossover hop for distance, and the 6-min timed hop. Besides these commonly used functional tests, the vertical jump, the crossover hop for distance, and the figure-eight hop have also been proposed. Because no single test can evaluate the dynamic function of the knee adequately, a series of functional tests is usually used in combination to test knee function. Papannagari and associates394 measured the kinematics of reconstructed and the intact contralateral knees 3 months after surgery using a dual-orthogonal fluoroscopic system while the subjects performed a single-leg weight-bearing lunge. There was a significant increase in

anterior translation of the reconstructed knee compared with the intact knee at full extension and 15 degrees of flexion. Meanwhile, the anterior laxity of the reconstructed knee as measured with the arthrometer was similar to that of the intact contralateral knee. This suggested that future ACL reconstruction should aim at restoring the function of the knee under physiologic loading conditions. Researchers have noted persistent instability with functional testing and degenerative radiographic changes after single-bundle ACL reconstruction.31,167 Single-bundle ACL surgery and biomechanical studies of ACL reconstruction have focused on restoring anterior stability in response to anterior tibial loads. However, knee joint kinematics are not restored under functional loading conditions and are at least partly responsible for the development of degenerative changes.31,395-397 Double-bundle ACL reconstruction more closely restores the normal anatomy of ACL and may be the future of ACL reconstruction.398 Its efficacy of restoring normal knee kinematics needs to be evaluated by functional tests. In addition, current functional tests are typically performed under nonfatigued test conditions in both the clinical and scientific settings. The ability of these tests to assess whether a patient has regained lower extremity function after ACL reconstruction is therefore limited. Augustsson and Thomee399 developed a single-leg hop test performed under standardized, fatigued conditions and have examined its reliability. They suggested that functional testing should be performed both under nonfatigued and fatigued test conditions to evaluate the ACL reconstructed knee comprehensively.400

Criteria for Return to Play The decision of when to permit a patient to return fully to unrestricted activities and sports is empirical in most cases because there is poor correlation of functional testing, clinical testing, and subjective testing methods in evaluating a patient after ACL reconstruction (Table 23D1-11). In a retrospective study, Glasgow and colleagues401 found no difference in sagittal translation or graft failure in patients who returned to sports activities before or after 6 months after surgery. Shelbourne and Davis.402 observed that some of their patients participated in sporting activities against their advice 3 months after surgery. Measurements of sagittal translation before and after sports participation revealed increased translation in only 2% of the patients. Although unnecessary delay of returning to unrestricted activities should be avoided, a premature return is dangerous and can jeopardize the graft. The use of multiple criteria, including the return of range of motion, muscle strength and balance, static stability as measured by KT1000, and dynamic stability as measured by functional testing, is necessary in determining the clearance for a patient to return to full activity. Unfortunately, many practicing orthopaedists simply make their decision based on time instead of these criteria.

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TABLE 23D1-11 Review of Recent Literature for Returning to Play after Anterior Cruciate Ligament Reconstruction Study

Method

Weight-Bearing

Brace

Exercises

Running, Drills

Return to Play

Aglietti et al, 1997403 Anderson et al, 2001203

Hamstring vs. patellar tendon Hamstring vs. patellar tendon

PWB day 3, FWB at 8 wk 25% × 1 week, 50% week 2, full week 3

7 days

4 mo

7-8 mo

Day 1

12 wk

6-7 mo

Aune et al, 2001299 Beynnon et al, 2002301

Hamstring vs. patellar tendon Two-strand hamstring vs. patellar tendon

Full immediately

Knee immobilized 4 wk Knee immobilized after surgery; functional at 3 wks None

CCE and bike at 2 wk 7 days

6 wk

6 mo

Run at half speed 12 wk, full speed 4 mo

6-8 mo

Ejerhed et al, 2003303

Hamstring vs. patellar tendon

Full immediately

Running at 3 mo

6 mo

Running at 10 wk

9 mo

As tolerated

6-8 mo

TTWB × 3 wk

Hinged brace locked at 10 degrees flexion for 1 wk, then motion allowed on day 7 in brace, used as necessary at 5 wk None CCE immediately, full extension with load at 6 wk None CCE × 6 mo, bike 3 wk Postoperative brace CPM × 1 wk, early in full extension for hydrotherapy PT, 10 degrees of extension ext lock for hamstring None OCE 4 wk

8-10 wk

4 mo

Conserve: PWB at 2 wk, full at 4 wk

Hinged brace for 12 wk

Conserve: ROM at 1 wk, isokinetic at 8 wk

Conserve: sports activity at 6 mo

Conserve: 12 m o

Accelerated: ROM immediate, CCE at 2-3 wk CCE 7-10 days

Accelerated: swimming 5-6 wk

Accelerated: 6-9 m o

Jogging at 6 wk

6 mo

TTWB × 3 wk, then WBAT

Feller & Webster, Hamstring vs. WBAT 2003305 patellar tendon Gobbi et al, Quadrupled bone– WBAT 2003404 semitendinosus vs. patellar tendon Howell & Taylor, Hamstring 1996405 Majima et al, Hamstring, 2002406 accelerated vs. conservative

Accelerated: WBAT immediate

Pinczewski et al, 2002407 Rose et al, 2004408 Shaieb et al, 2002308

Hamstring vs. patella tendon Hamstring vs. patellar tendon Hamstring vs. patellar tendon

WBAT

None

Full at day 1 WBAT at 1 wk

Hinged postoperative brace for 6 wk Not stated

Shelbourne & Davis, 1999402

Patellar tendon

WBAT

Functional brace

CPM × 4 days, Drills at 7 wk, CCE at 3 wk running at 12 wk ROM at 1 week, Running at 2 mo CCE and bike at 2-3 wk Active-assisted 5-6 wk flexion at 7-10 days

6 mo 5-6 mo 2-6 mo

CCE, closed chain exercises; CPM, continuous positive motion; FWB, full weight-bearing; OCE, open chain exercises; PT, physical therapy; PWB, partial weightbearing; ROM, range of motion; TTWB, toe touch weight bearing; WBAT, weight bearing as tolerated. From Cascio BM, Culp L, Cosgarea AJ: Return to play after anterior cruciate ligament reconstruction. Clin Sports Med 23(3):395-408, 2004.

C l

r i t i c a l

P

o i n t s

he ACL is an intra-articular ligament that consists of T two functional bundles, the AM bundle and the PL bundle, named for their tibial insertion sites. l The insertion site orientation and the position and the length of the ACL bundles vary with changing angles of knee flexion and extension. In full extension, both bundles are in parallel and act as anteroposterior stabilizers of the knee joint. In flexion, the bundles cross one another, and the PL bundle functions in rotational stabilization of the knee. l Biomechanical studies have shown that single-bundle reconstruction cannot restore normal knee kinematics. Double-bundle ACL reconstruction closely restores normal ACL anatomy and knee kinematics.

l Females have an increased risk for ACL rupture beginning at about age 12 years. The reasons are multifactorial and may include a decreased notch width index, hormonal differences, and altered neuromuscular firing patterns that help create increased anterior and valgus moments about the knee. l There is no rigid upper age limit on ACL reconstruction. Symptoms such as recurrent instability, active lifestyle, and the ability to comply with postoperative guidelines are important aspects to consider. l Partial ACL tears, often of a single ACL bundle, are being diagnosed with increasing frequency. A combination of physical examination and MRI findings is helpful in making the diagnosis. l The MCL and lateral meniscus are commonly injured concurrently with an ACL tear. Medial meniscal injuries are more common in chronic ACL tears.

1676 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� l The natural history of an ACL-deficient knee in an active or young patient is often one of progressive meniscal and chondral degeneration, which may lead to early-onset arthrosis. l Multiple ACL graft and fixation options exist for ACL reconstruction. Both HS and BPTB autografts have performed well in follow-up studies. l Although the results of ACL reconstruction are generally good, there is no evidence to date that ACL reconstruction can prevent knee arthrosis. As more research is completed, the use of an anatomic double-bundle ACL reconstruction may help improve ACL outcomes.

S U G G E S T E D

Buoncristiani AM, Tjoumakaris FP, Starman JS, et al: Anatomic double-bundle anterior cruciate ligament reconstruction. Arthroscopy 22(9):1000-1006, 2006. Chhabra A, Starman JS, Ferretti M, et al: Anatomic, radiographic, biomechanical, and kinematic evaluation of the ACL and its two functional bundles. J Bone Joint Surg Am 88(Suppl 4):2-10, 2006. Fu FH, Bennett CH, Lattermann C, Ma B: Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med 27:821-830, 1999. Girgis FG, Marshall JL, Monajem A: The cruciate ligaments of the knee joint: Anatomical, functional and experimental analysis. Clin Orthop 106:216-231, 1975. Goldblatt JP, Fitzsimmons SE, Balk E, et al: Reconstruction of the anterior cruciate ligament: Meta-analysis of patellar tendon versus hamstring tendon autograft. Arthroscopy 21(7):791-803, 2005. Hewett T, Ford K, Myer G: Anterior cruciate ligament injuries in female athletes. Part 2: A meta-analysis of neuromuscular interventions aimed at injury prevention. Am J Sports Med 34:490-498, 2006. 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 32(8):1986-1995, 2004.

R E A D I N G S

Arnoczky SP: Anatomy of the anterior cruciate ligament. Clin Orthop 172:19-25, 1983. Beynnon, BD, Johnson RJ, Abate JA, et al: Treatment of anterior cruciate ligament injuries: Part 1. Am J Sports Med 33:1579-1602, 2005. Beynnon, BD, Johnson RJ, Abate JA, et al: Treatment of anterior cruciate ligament injuries: Part 2. Am J Sports Med 33:1751-1767, 2005.

R e f erences Please see www.expertconsult.com

S e c t i o n

D

Anterior Cruciate Ligament Injuries 2. Anterior Cruciate Ligament Injuries in the Child Nicholas J. Honkamp, Wei Shen, and Freddie H. Fu

The past 2 decades have seen a significant increase in the number of anterior cruciate ligament (ACL) tears in adolescents. Most of these injuries involve either a midsubstance ACL tear or a tibial spine avulsion fracture that contains the ACL attachment. Femoral ACL avulsion fractures are rare. Central to this increase is the explosion of athletic participation in both male and female adolescents in sports commonly associated with ACL injuries such as soccer, basketball, skiing, and football. Coincident with this increased participation level is the improved diagnostic capabilities of the physician using magnetic resonance imaging (MRI), instrumented laxity measuring devices, and arthroscopy. Although the treatment of tibial spine avulsion fractures is generally agreed on, the management of midsubstance ACL tears is still a matter of debate. The potential for skeletal growth postoperatively presents unique problems when surgical treatment is considered. Nonoperative management with bracing and rehabilitation has been the traditional approach, but more recent reports document poor functional results and a high incidence of further injury to the menisci and joint surfaces. Extra-articular reconstructive procedures are nonanatomic, and their long-term

results are unknown. For these reasons, intra-articular reconstruction has been proposed. ACL reconstruction with transtibial and transfemoral tunnels, transtibial and over the top femoral placement, and nontunnel techniques has been reported. Recent studies simulating these procedures in growing animals have had mixed results, with some finding few growth disturbances and others frequent and severe angular and length deformities. These studies suggest that tunnel size, graft choice, tunnel fill, and graft tension all play a role in skeletal growth after reconstruction. The current review seeks to critically appraise the literature to date and construct an analysis of the current techniques and their reported results.

INCIDENCE Clanton reported the earliest review of the literature in 1979, citing less than 1% incidence of knee ligament injuries in all knee injuries reported in patients younger than 14 years.1 DeLee and Curtiss in 1983 reported an incidence of 1% in children aged 14 years or younger with knee injuries.2 More recent reports puts the figure at

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3.3% to 3.4%.3,4 Interestingly, Kellenberger and associates5 reported an 80% incidence of tibial spine avulsions in children aged 12 years or younger, compared with a 90% incidence of intrasubstance ACL tears in children 12 years or older. Thus, an age of about 12 to 14 years may serve as a rough defining zone between possible avulsion fractures and intrasubstance ACL tears. As children age into late adolescence, the relative weakness of the proximal tibial physes relative to the ACL diminishes because the closing physes no longer represent the weak link in the knee joint support system.

MECHANISM OF INJURY, HISTORY, AND PHYSICAL EXAMINATION ACL injuries in children, like those of an adult, are usually caused by a quadriceps active, noncontact valgus injury. A fall off a bike with the use of a planted foot to help break the fall is a frequent mechanism.6-8 Like adults, most children present with a knee hemarthroses in the acute case, or recurrent effusions and instability in the chronic ACLdeficient patient. Often, an audible sound can be heard with an ACL injury. A reluctance to bear weight or return to activities and loss of range of motion are also common. Children represent a unique population in that congenital or physiologic states should always be considered in the differential diagnosis. Thus, the practice of examining the contralateral limb in an adult patient takes on special importance in the child. What may present as an ACLdeficient knee may in actuality be physiologic laxity or congenital absence of the ACL. Examining other joints in the lower or upper extremities may also help confirm excessive laxity or ligament absence. The standard tests of knee laxity, including the Lachman, anterior and posterior drawer, and pivot shift tests, should all be elicited. Often, guarding and swelling are present to a degree that ligamentous examination may be difficult or impossible. Re-examination in 1 to 2 weeks may then be helpful. Additional attention in the physical examination should be paid to patellar instability or subluxation represented by a positive apprehension test, increased Q angle, hindfoot valgus, or foot pronation. Referred pain from the hip may occur with congenital pelvic deformities or slipped capital femoral epiphysis. Infection should always be included in the differential diagnosis in a child as well. Plain film radiography should always be obtained before more advanced imaging. Anteroposterior, lateral, and patellar views should be obtained to look for periarticular fractures, avulsions, osteochondral damage, and congenital or developmental abnormalities.

Assessment of Skeletal Maturity Numerous methods have been used to assess skeletal maturity in adolescents. The most common, devised by Tanner,9 physiologic signs of development, including the presence of menarche, breast tissue, and pubic hair in females and the development of the testes and penis and pubic hair in males. Other methods to assess skeletal maturity include anteroposterior and lateral radiographs

of the knee, assessment of bone age using radiographs of the hand, Risser staging of iliac crest ossification, presence or absence of an adolescent growth spurt, and comparison of the patient’s height to that of older siblings and parents.3

TIBIAL EMINENCE FRACTURES Fractures of the tibial eminence occur because of a chondroepiphyseal avulsion of the ACL insertion on the anteromedial tibial eminence.10,11 Meyers and McKeever described a classification system for avulsion fractures based on the elevation and rotation of the eminence fragment.7 Type I fractures have minimal or no displacement, and type II fractures have anterior hinging of one third to one half of the tibial eminence. Type IIIA fractures are completely displaced from the fracture bed, and type IIIB fractures demonstrate rotational malalignment (Fig. 23D2-1). Zaricznyj added a type IV to Meyers and McKeever’s fracture classification in 1977.12 He described seven comminuted tibial eminence fractures that he described as type IV. Additional knee injuries should also be sought during the evaluation of a child with a tibial eminence fracture, including meniscal tears, meniscal entrapment within the fracture (most commonly medial), and associated collateral ligament injuries.

Treatment Type I fractures are universally treated nonoperatively with immobilization owing to their nondisplaced nature. Type II fractures can often be successfully treated with closed reduction and immobilization with or without associated aspiration of the hemarthrosis to allow for improved extension. Although some authors believe that immobilization in full extension helps reduce the avulsion fragment through direct compression from the lateral femoral condyle,8,13,14 it has been shown that the ACL functionally lengthens in the last 20 degrees of extension.15 Thus, data support treatment of type II fractures with knee immobilization in approximately 15 to 20 degrees of flexion for 4 to 6 weeks, which places the least strain on the ACL–avulsion fragment complex.16-19 In whatever position the knee is ultimately immobilized, fragment reduction should be confirmed with radiographic methods. Often, soft tissue interposition consisting of menisci or cartilage prevents the eminence fragment from anatomically seating in its bed. Kocher and colleagues20 found that 65% of type III fractures and 26% of type II fractures had entrapment of the anterior horn of the meniscus, most commonly medial. This has been confirmed by other authors as well, particularly in type III fractures.21,22 Additionally, plain radiographs may underestimate the extent of the fracture when cartilage composes a large proportion of its volume.23 Because of these findings, many authors have advocated direct inspection through open or arthroscopic means of all type III fractures and any type II fracture that does not reduce anatomically on radiographs.20,23 With either method, the fracture fragment and its associated bony bed should be débrided of any clot or debris, and any associated meniscochondral entrapment should be released. Fracture fixation has been commonly obtained


A

B

C

Figure 23D2-1 Meyers and McKeever classification of tibial eminence fractures in children. A, Type I is a nondisplaced fracture. B, Type II is a displaced fracture that is hinged posteriorly. C: Type III fractures are completely displaced.

with suture,22,24,25 wire,26 or screw fixation.6,8,14,27,28 Comminuted type IV fractures may be best managed with suture fixation through the soft tissue insertion of the ACL fibers. Transepiphyseal fixation is not recommended because of the risk for anterior growth arrest and hyperextension deformity.29 Follow-up studies of type III fractures using cannulated screw fixation have all found good functional outcomes despite persistent laxity. Kocher and coworkers28 reviewed their results in six patients at minimal 2-year follow-up. They found mean postoperative Lysholm and Tegner scores of 99.5 and 8.7, respectively. One patient had a grade A Lachman (normal) test, three had grade B (nearly normal), and two had grade C (abnormal). Instrumented knee laxity showed side-to-side differences of greater than 3 mm in four of six patients. Smith and colleagues30 found subjective instability symptoms in only 2 of 13 patients, but 87% had a positive Lachman test. Reynders and associates31 found similar results of good subjective stability with documented objective knee laxity in their 26 patients treated with an intrafocal screw and spiked washer. Davies and coworkers32 used a cannulated Acutrak screw in their four pediatric cases, with all patients returning to their preinjury exercise status.

Larger studies comprising all three types of tibial eminence fractures treated with a variety of fixation methods (closed reduction with or without aspiration, arthroscopic reduction and casting, suture fixation, screw fixation) have been done by Janarv and colleagues6 and Willis and associates14 Similarly, Janarv and colleagues6 found that 38% of their 61 cases had pathological knee laxity that was not related to subjective knee function. Willis and associates14 found clinical signs of anterior instability in 64% and instrumented laxity in 74% of their 50 patients. However, most of these patients had no subjective complaints. Persistent anterior knee laxity despite anatomic or near anatomic reduction and healing of the tibial spine avulsion fractures in children is likely related to some interstitial stretch injury to the ACL at the time of the fracture. In a primate study, Noyes and colleagues10 found frequent elongation and disruption of ligament architecture despite gross ligament continuity in experimentally produced tibial spine fractures at both slow and fast loading rates. Another potential complication of either operative or nonoperative treatment is loss of terminal knee extension.7,8 This can be caused by either hypertrophy of the tibial spine secondary to hyperemia or residual displacement and can lead to a bony block to full extension.

Authors’ Preferred Method The goal of any treatment approach should be anatomic reduction of the fracture fragment. Type I fractures may be treated with cast treatment near full extension for 4 to 6 weeks. Type II fractures should undergo attempted closed

reduction in extension under anesthesia with radiographic evaluation. Because of the high rate of meniscal entrapment or other debris causing a block to anatomic reduction, we advise arthroscopic or open treatment of any type II fracture

knee 1679


A

B

Figure 23D2-2 Anteroposterior (A) and lateral (B) radiographs of a type III tibial eminence fracture.

Figure 23D2-3 Sagittal magnetic resonance imaging section showing a type III tibial eminence fracture.

MIDSUBSTANCE ANTERIOR CRUCIATE LIGAMENT TEARS Nonsurgical Treatment Because of the perceived rarity of the injury, as well as fear of damaging open physes, much of the initial published literature discussed nonoperative treatment. The distal femur and proximal tibia is a key growth center in the longitudinal

that does not anatomically reduce in extension. We recommend open or arthroscopic treatment of all type III fractures (Figs. 23D2-2 and 23D2-3). Fixation may be obtained with any cannulated screw device or with heavy suture (1-0 or 2-0 nonabsorbable) placed through the base of the ACL attachment. The suture technique is especially useful in cases in which the bony component is small or fragmented. We bring the sutures out in a transepiphyseal fashion and tie them over a bony bridge. We often use an ACL-aiming guide for creation of our epiphyseal tunnels (Fig. 23D2-4). Care should be taken to ensure that all hardware and bone tunnels be placed in an extraphyseal location and that the reduction is confirmed visually and radiographically. Range of motion and strengthening exercises may then be started on a gradual basis, usually 2 to 4 weeks after surgery, depending on the strength of fixation. Return to activities is allowed between 3 and 4 months after fixation if there is evidence of radiographic healing and clinical stability of the knee.

Figure 23D2-4 The use of an anterior cruciate ligament– aiming guide to help direct the epiphyseal placement of the tibial tunnels for fixation.

growth of the leg, accounting for about 65% of longitudinal growth of the leg. Concern over causing premature growth plate damage and subsequent closure or angular deformity dictated that early treatment be nonoperative. Bracing, quadriceps and hamstring strengthening, and activity modification were cornerstones of early treatment. Chick and Jackson,33 in 1978, presented one of the first series on partial or complete ACL ruptures managed nonoperatively in young adults. In their series of 30 patients


with an average age of 20 years, symptoms of knee instability, intermittent effusion and stiffness, and mild sclerotic changes on radiographs were noted. A similar series by Fetto and Marshall34 in 1979 involving more than 200 young adult patients with ACL tears noted “a progressive deterioration and dysfunction” of the knee joint. Hawkins and associates,35 in 1986, described 40 ACLdeficient patients, with an average age of 20 years, treated nonoperatively. Thirty-five of 40 rated their knee as fair or poor, and 12 of 40 considered it a liability. These studies on young adults demonstrate that recurrent instability due to nonoperative treatment of ACL injuries can often lead to increased incidence of meniscal and articular cartilage damage. Attention to the long-term outcomes of nonoperative ACL injury began to focus on the adolescent population in the 1980s and early 1990s. Numerous studies documented low satisfaction rates, low knee function scores, high rates of meniscal pathology, and poor return to sport and recreational activities. In a 1988 paper, McCarroll and associates4 reported on 16 patients with torn ACLs, with an average age of 13 years, treated conservatively with bracing and rehabilitation. Nine of 16 gave up their sport because of continued instability. Of the 7 patients who continued playing their sport, all had recurrent “giving way” episodes, and 3 had serious reinjuries to their affected knee. Kannus and Jarvinen36 reported on 32 adolescent patients with partial or complete knee ligament injuries treated by cast immobilization. Partial ligament injuries had good to excellent results. However, the 4 patients with complete ACL ruptures and longer term followup had decreased knee scores, definitive radiographic evidence of post-traumatic arthritis, and decreased strength. Angel and Hall37 reported on 22 patients with ACL tears treated conservatively. In their average 51-month follow-up, 41% had meniscal pathology, and no patients with complete ACL tears were able to return to sports. Graf and associates38 and Mizuta and Kubota39 both reported on adolescents with complete ACL tears treated with bracing and hamstring and quadriceps strengthening. All their patients ultimately failed bracing with recurrent instability and pain. Sixteen of their 20 patients treated strictly nonoperatively suffered meniscal tears. Although the numerous authors cited previously found poor results with nonoperative treatment, one recent study did find acceptable results with delayed nonoperative treatment. Woods and colleagues compared 13 patients (average age, 13.8 years) who underwent delayed surgical reconstructive treatment of the ACL-deficient knee once they had reached skeletal maturity to a group of skeletally mature adolescents who underwent the same arthroscopically assisted ACL reconstruction with a bone–patellar tendon–bone (BPTB) graft. They showed no significant differences between the groups in additional intra-articular knee injuries. Before reconstruction, the skeletally immature patients were given specific rehabilitation exercises, strictly forbidden from participating in vigorous team sports involving cutting or twisting activities, excused from gym class, and given a noncustom (“off the shelf”) knee brace.

Surgical Treatment Primary Anterior Cruciate Ligament Repair Similar results were also found when primary repair of a torn ACL was attempted in an adolescent. Two series2,40 dealing strictly with adolescents found that 7 of 11 patients had unstable knees, and the authors did not advocate further use of this procedure. An additional study41 including both pediatric and adult ACL injuries treated with primary repair or a synthetic ligament repair found lower levels of activity and increased episodes of instability. Difficulties relating to primary repair stem from interruption of the blood supply as well as exposure to the knee joint synovial fluid. Tearing of the ACL severs its main blood supply from the middle genicular artery. Additionally, this injury often damages the ligament’s synovial sheath, which further destroys its blood supply and exposes it to the harsh and limited nutritional supply of the synovium and joint fluid. The adolescent ACL injury thus represents a difficult problem. This population is not amenable to dependable activity modification and subjects their knee joints to high functional levels. Benefits gained by not violating the physeal growth plates and limiting growth arrest and angular deformities are mitigated by the increased rate of meniscal and cartilage damage that can similarly curtail future functional capabilities through the development of early degenerative joint disease. Additionally, the psychosocial drawbacks of limited recreational and sporting activities in the adolescent managed with activity modification must be considered.

Extra-articular Reconstruction As nonoperative and primary repair procedures reported suboptimal results, extra-articular reconstruction became more widely reported. These procedures, while avoiding the physes, provide some increased stability. The types of reconstructions have varied, as have their results. Various modifications of an iliotibial (IT) band tenodesis have been performed.4,38 These procedures take a portion of the IT band left attached distally, secure it to the lateral femur proximally, place it from posterior to anterior through the femoral notch, and tack it to the proximal tibia distally. Less than half of the reported patients in these series treated with this procedure have remained free of instability. Micheli and colleagues42 used both an intra-articular and extra-articular repair with the IT band with improved results in 10 prepubescent patients. Kocher and associates43 used a combined intra-articular and extraarticular IT band graft in 42 patients in Tanner stage 1 or 2 and reported excellent midterm results at a mean of 5.3 years. Similarly, some surgeons44,45 have devised intra- and extra-articular reconstructions using the gracilis and semitendinosus tendons on the medial aspect of the knee, or reconstructions through the epiphyseal portion of bone.46 These reconstructions avoid violating the physes by placing the grafts in various positions, including through epiphyseal drill holes above the physes, grooved troughs on the tibia and femur, or threaded positions under the menisci.

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Although these studies have shown some positive results, the data are hindered by low numbers and varied outcomes measures. In addition, varied skeletal ages and follow-up periods make comparisons difficult. For instance, some patients returned to lesser levels of competitive sport, whereas others returned with bracing or other precautions not specified.

Transphyseal Anterior Cruciate Ligament Reconstructions—Animal Studies Although transphyseal drill holes are the gold standard of adult ACL reconstruction because of their anatomic placement of ligament grafts and their superior fixation, drilling across an open physis is still controversial. In an attempt to more accurately assess the risk for transphyseal drilling leading to premature physeal closure in adolescents, numerous animal studies have been reported. Earlier animal studies demonstrated that a hole drilled across an open growth plate will fill with bone and subsequently result in a physeal bar formation and at least partial physeal fusion.47 A smooth pin placed across an active growth plate and left in place will prevent the formation of a physeal bar. This is the rationale for the frequent use of smooth pins in the treatment of various conditions involving the fractures through the growth plates of children, including the distal tibia and distal humerus. Stadelmaier and associates47 used skeletally immature dogs to show that a semitendinosus graft placed across the femoral and tibial growth plates also prevented the formation of a bony bridge. Factors such as the size and location of the drill hole have been shown to be important in determining the extent of physeal damage. Makela and colleagues48 used New Zealand white rabbits to show that drilling the equivalent of 7% or more of the cross-sectional physeal growth plate resulted in significantly higher rates of shortening and angular deformities. Janarv and associates,49 using similar animals, confirmed these results and concluded that drilling 7% to 9% of the physeal cross-sectional area resulted in growth disturbance, whereas no retardation was seen in injuries of 4% to 5%. Guzzanti and coworkers50 used white rabbits to show that physeal drilling of 3% to 4% of the cross-sectional area of the femur and tibia caused 3 of 21 tibias to develop shortening or valgus angulation, whereas no leg-length discrepancies (LLDs) were found in any of the 21 femurs analyzed. Although an untensioned graft, like those used in the aforementioned studies, may help prevent physeal bar formation, human ACL reconstructions involve use of a tensioned graft to provide normal ligamentous tension and adequate postoperative stability. The Heuter-Volkmann principle asserts that although certain amounts of compression and tension can stimulate physeal bone growth, supraphysiologic forces (like a tensioned graft) may cause physeal bar formation and premature physeal closure. Studies by Houle and colleagues51 and Edwards and coworkers52 suggest a relationship between tensioned ACL grafts across either dog or rabbit tibial and femoral physes and significant shortening and angular deformities. Again, the tibia seemed more sensitive to the effects of physeal drilling.

In summary, the animal data do offer some support to limiting physeal damage to less than 7% to 8% of the crosssectional area of the physes. It is estimated that an 8-mm drill hole used in an ACL repair in a 12-year-old patient destroys 3% to 4% of the physis. Drill holes placed more perpendicular to the physes damage less cross-sectional area and are preferred. Placement of tensioned grafts, particularly across the tibia, appears to increase the chance of angular deformities.

Transphyseal Anterior Cruciate Ligament Reconstructions—Human Studies Some authors have used similar-sized drills with 8-mm drill holes to place allograft or autograft ACL reconstructions in a transphyseal position across the tibia, while placing the graft behind and posterior to the lateral femoral condyle in an over-the-top position on the femur. Studies by Lo and colleagues,53 Andrew and associates,54 and Bisson and coworkers55 used this procedure and reported moderate success in 22 patients. Generally, these patients were 13 years or older and had follow-ups ranging from 39 to 88 months. Three patients had LLDs greater than 5 mm, with 18 of 22 patients rating their outcome as good or excellent. There were two re-tears, and 3 patients were unable to return to their preinjury activities. The failure of nonoperative treatment, combined with the mixed results and lack of long-term follow-up of extraarticular procedures, has led several authors to recommend operative treatment. Particularly in the older (13 to 14 years and older) adolescent, drilling of the tibia and femur has gained in popularity as more reported studies are published. Lipscomb and colleagues56 reported in 1986 the technique of ACL reconstruction using a transphyseal tibial tunnel and a femoral tunnel placed distal to the femoral physes in the distal femoral epiphysis. They reported on 24 patients aged 12 to 15 years treated with the aforementioned reconstruction supplemented with an IT band tenodesis. Sixteen patients reported their knee as “normal,” and 8 as “improved.” Twenty-three of 24 patients had good or excellent objective results. However, 5 patients had LLDs of 6 to 10 mm, and 2 patients had LLDs of 13 mm and 20 mm. In McCarroll’s landmark 1988 series,4 he also included 14 patients treated with autologous BPTB reconstructions using tibial and femoral transphyseal drill holes. All 14 returned to their previous sports. There were no growth abnormalities reported, and the average passive anterior drawer sign was 1.7 mm. Two additional studies by Edwards and colleagues57 and Pressman and coworkers58 showed encouraging results with transphyseal tibial and femoral tunnels. Pressman58 compared this intra-articular, transphyseal technique with nonoperative and primary repair techniques. The transphyseal technique demonstrated significantly better objective knee outcomes scores, and no LLD greater than 1 cm. Edwards57 evaluated 20 patients, average age 13.7 years, with hamstring or BPTB transphyseal autografts. Nineteen patients returned to their previous sport, and 15 rated their function as excellent. Two patients with poor results suffered re-tears within 1 year of operation, whereas


2 additional patients with poor results had excessive anterior translation and stretching of their graft. Additionally, 3 patients had greater than 5 mm LLD, all of which were asymptomatic. As more studies with ACL reconstruction using transphyseal drilling were published, more attention began to be focused on accurate measuring of LLD, rates of ACL reinjury, and size and placement of the graft. McCarroll and colleagues59 published a follow-up series in 1994 including 60 patients, average age 14.2 years, with a mean follow-up of 4.2 years. Again, transphyseal tibial and femoral tunnels were used (diameter not reported). No LLDs or angular deformities were reported using plain radiographs and manual measurements. Average postoperative growth measured 2.3 cm. Three patients tore the ACL graft longer than 2 years after surgery, whereas 4 patients tore their opposite ACL during the follow-up period. Aronowitz and associates60 published a series on 19 patients treated with Achilles tendon allograft placed through both physes. Average age was 13.4 years, and average follow-up was 25 months. The authors used 9- to 10-mm drill holes, and measured leg lengths postoperatively with scanograms. All patients were satisfied with their repair, and 16 of 19 returned to their sport. Average leg length discrepancy was −1.2 mm on the

perative side. In 2002, Fuchs and colleagues61 reported o on 10 patients treated with BPTB graft. Average age was 13.2 years. At an average of 40 months of followup, 9 rated their result as excellent and 1 as good. Average postoperative growth was 10 cm, and none had a significant LLD by clinical examination or by patient complaint. Overall, transphyseal reconstruction using hamstring, patellar tendon, or Achilles grafts offers an anatomic reconstruction with good clinical results and a low incidence of LLD. Overwhelmingly, these studies have focused on children 13 to 14 years old and older. Care was taken to place only the soft tissue graft across the physes, and drill holes less than 8 to 10 mm were used. Taking these precautions, growth disturbances can still occur. A case report of a 14-year-old boy with 9-mm transphyseal tunnels demonstrated a significant distal femur valgus deformity.62 It was attributed to a cannulated screw placed across the distal femoral physes as well as bone plugs placed across both physes. Kocher and colleagues, in a study based on a survey of experts in the management of pediatric ACL injuries, reported 15 patients who had growth disturbances including varus and valgus deformities, tibial recurvatum, and LLDs.63 Physeal hardware complications were the biggest contributing factor.

Authors’ Preferred Method It is our practice to manage pediatric patients with wide open physes with hamstring autografts placed in a transphyseal tibial location and over-the-top position on the femur. We use a more centrally placed tibial tunnel, typically 6 to 7 mm in diameter. We place only soft tissue across the physes, use suture and post fixation, and ensure that our post fixation is well away from the physes (Fig. 23D2-5).

A

In those patients with closing growth plates and less than 2-year growth remaining, we will typically use a hamstring autograft reconstruction utilizing transphyseal tibial and femoral tunnels. Fixation options include screw and post, EndoButton, staples, or interference screws away from the physes. We use our standard postoperative ACL rehabilitation protocol.

B

Figure 23D2-5 Postoperative anteroposterior (A) and lateral (B) radiographs of a transtibial or over-the-top femur anterior cruciate ligament reconstruction on a skeletally immature patient using staple fixation placed well away from the physes.

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C

r i t i c a l

P

S U G G E S T E D

o i n t s

l The increased number of pediatric ACL injuries reflects the increased participation seen in youth sports. l Most injuries represent midsubstance ACL tears or tibial avulsion fractures. Femoral avulsion fractures of the ACL attachment are rare. The cut-off age for midsubstance versus avulsion fractures is about 12 to 14 years of age. l Physical examination of a pediatric patient with a suspected ACL injury should focus on ligamentous instability, patellar instability, and referred pain from the hip. Comparison to the contralateral extremity is critical to rule out ligamentous laxity or congenital absence of the ACL. l Meyers and McKeever described a classification system for avulsion fractures based on the elevation and rotation of the eminence fragment. Type I fractures have minimal or no displacement, and type II fractures have anterior hinging of one third to one half of the tibial eminence. Type IIIA fractures are completely displaced from the fracture bed, and type IIIB fractures demonstrate rotational malalignment. l Type I fractures can be managed with cast immobilization in 20 degrees of flexion. Type II fractures can be managed with cast immobilization if an anatomic reduction can be maintained. Type III fractures are generally treated operatively. l Treatment of pediatric midsubstance ACL tears is controversial. Nonoperative treatment, however, has led to recurrent instability, pain, and new meniscal and chondral injuries in a high percentage of patients. l Operative treatment of pediatric ACL tears, however, is also controversial. Options include extra-articular reconstructions, intra-articular reconstructions, and combined intra-articular and extra-articular reconstructions. No specific technique has demonstrated superiority. l Recently, the most popular techniques have included transphyseal tibial tunnels with an over-the-top femoral placement and transphyseal tibial and femoral tunnels with soft tissue grafts in patients nearing skeletal maturity.

R E A D I N G S

Aronowitz ER, Ganley TJ, Goode JR, et al: Anterior cruciate ligament reconstruction in adolescents with open physes. Am J Sports Med 28(2):168-175, 2000. Bales CP, Guettler JH, Moorman CT 3rd: Anterior cruciate ligament injuries in children with open physes: Evolving strategies of treatment. Am J Sports Med 32(8):1978-1985, 2004. Fehnel DJ, Johnson R: Anterior cruciate injuries in the skeletally immature athlete: A review of treatment outcomes. Sports Med 29(1):51-63, 2000. Graf BK, Lange RH, Fujisaki CK, et al: Anterior cruciate ligament tears in skeletally immature patients: Meniscal pathology at presentation and after attempted conservative treatment. Arthroscopy 8(2):229-233, 1992. Kocher MS, Foreman ES, Micheli LJ: Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy 19(10):1085-1090, 2003. Kocher MS, Garg S, Micheli LJ: Physeal sparing reconstruction of the anterior cruciate ligament in skeletally immature prepubescent children and adolescents. J Bone Joint Surg Am 87(11):2371-2379, 2005. Kocher MS, Micheli LJ, Gerbino P, et al: Tibial eminence fractures in children: Prevalence of meniscal entrapment. Am J Sports Med 31(3):404-407, 2003. Kocher MS, Saxon HS, Hovis WD, Hawkins RJ: Management and complications of anterior cruciate ligament injuries in skeletally immature patients: Survey of the Herodicus Society and the ACL Study Group. J Pediatr Orthop 22(4): 452-457, 2002. Mah JY, Adili A, Otsuka NY, Ogilvie R: Follow-up study of arthroscopic reduction and fixation of type III tibial-eminence fractures. J Pediatr Orthop 18(4): 475-477, 1998. Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 52(8):1677-1684, 1970.


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Posterior Cruciate Ligament Injuries 1. Posterior Cruciate Ligament Injuries in the Adult Nicholas J. Honkamp, Anil S. Ranawat, and Christopher D. Harner

The past decade has seen a renewed interest in the posterior cruciate ligament (PCL) as numerous studies have reported on its anatomy, biomechanics, and various reconstruction techniques. Despite this, our knowledge of the PCL still lags behind that of other knee ligamentous structures, particularly the anterior cruciate ligament (ACL). The more infrequent nature of PCL injury, lack of familiarity with its injury

and treatment, increased surgical risks, and poor results of early surgical treatment are all factors that have led to this disparity in knowledge. However, with advances in basic science knowledge pertaining to the PCL and improved awareness and imaging modalities, PCL injuries are being more accurately diagnosed and treated. This has led to more focus on the various treatment options and their results.


Likewise, multiligament injuries are also being more increasingly recognized, particularly injuries to the PCL and posterolateral corner (PLC). These injuries can occur from athletics but are more commonly related to trauma. Accurate recognition of all injured ligaments is critical because the prognoses of multiligament injuries are more than those of isolated PCL injuries. This chapter reviews the relevant anatomy, biomechanics, physical examination and radiographic diagnostics, treatment, and outcomes data on PCL injury.

23 mm

19 mm

Level of adductor tubercle

RELEVANT ANATOMY To accurately diagnose and treat PCL injuries, a thorough knowledge of the anatomy and biomechanics of the PCL is mandatory. Although easily visualized during arthroscopy, the PCL is technically an extra-articular structure. Synovium that reflects from the posterior capsule surrounds its anterior, medial, and lateral sides, whereas the posterior border of the PCL is intimately associated with the capsule and periosteum.1,2 The PCL averages in length between 32 and 38 mm and has a cross-sectional area at its midsubstance of 31.2 mm2, which is about 1.5 times larger than the ACL.1,3,4 Knowledge of the intra-articular length is critical for the selection of an appropriate graft in reconstruction. The femoral and tibial insertion sites are about 3 times larger than the cross-sectional area at the midsubstance level of the ligament.4,5 The fibers of the PCL attach in a lateral to medial direction on the tibia at a fovea about 1.0 to 1.5 cm below the joint line (Fig. 23E1-1). On the femoral side, the PCL fibers attach adjacent to the anterior cartilage margin of the medial femoral condyle in an anteroposterior direction on the femur (Figs. 23E1-2 and 23E1-3). There are three main components to the PCL: the anterolateral (AL) bundle, the posteromedial (PM) bundle, and the meniscofemoral ligaments.4,6 These components each have unique bony insertions as well as anatomic and biomechanical properties (Figs. 23E1-4 and 23E1-5).4 The AL bundle is about 2 times larger in cross-sectional area than the PM bundle, and its stiffness and ultimate strength are about 150% of the PM bundle.1,2,4 Tension in the two bundles varies depending on the degree of knee flexion. With the knee in extension, the PM bundle is aligned in a proximal to distal direction and is taut. The PM bundle

Anterior cruciate

32 mm 9 mm Figure 23E1-2 The broad complex origin of the posterior cruciate ligament is in the form of a semicircle on the medial femoral condyle.

slackens as the knee flexes, with its fibers passing between the medial femoral condyle sidewall and the AL bundle.4,7 With deep knee flexion, the PM bundle moves anterior and away from the tibial plateau such that they become taut again in deep knee flexion (Fig. 23E1-6).2,7 The AL bundle is slack in the extended knee and thus appears curved when viewed on magnetic resonance imaging (MRI) in the sagittal plane. With knee flexion, this bundle becomes taut.4,7 The varying width of the ligament, its complex insertional site anatomy, and its nonisometric tensioning patterns all combine to make isometric reconstruction of the ligament difficult.

Posterior cruciate ligament in extension

Posterior cruciate 13 mm

Figure 23E1-1 The posterior cruciate ligament inserts in a central fovea on the tibia about 1.5 cm below the joint line.

Figure 23E1-3 The fibers of the posterior cruciate ligament attach in an anterior-to-posterior direction on the femur and a medial-to-lateral direction on the tibia. (Redrawn from Girgis FG, Marshall JL, Monajem A: The cruciate ligaments of the knee joint: Anatomical, functional and experimental analysis. Clin Orthop 106:216-231, 1975.)

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AL PM

AL PM

Figure 23E1-4 The anatomic position of the anterolateral (AL) and posteromedial (PM) bundles of the posterior cruciate ligament. (From Harner CD, Höher J: Current concepts: Evaluation and treatment of the posterior cruciate ligament injuries. Am J Sports Med 26:471-482, 1998.)

The anterior and posterior meniscofemoral ligaments (MFLs) of Humphrey and Wrisberg, respectively, are the third component of the PCL complex. These ligaments arise from the posterior horn of the lateral meniscus and sandwich the PCL anteriorly and posteriorly, respectively (Fig. 23E1-7). A recent review of the literature found that 93% of knees had at least one MFL and about half had both.8 Because their attachment is to the mobile lateral meniscus, it is possible for the PCL to be ruptured but the MFLs to be intact. Because of their anatomic locations, their relative strength, and their ability to resist posterior drawer forces, they may act as a splint to keep a ruptured PCL in position while it heals.7,9 Although not intimately associated anatomically with the PCL, the PLC structures of the knee are commonly injured together with the PCL. Thus, knowledge of their anatomy is relevant to the PCL. Various names have been attributed to structures comprising the PLC, greatly contributing to the confusion surrounding this area of the knee. Two recent cadaveric studies have helped define this anatomic area.10,11 The main constituents of the PLC are the popliteus ligament, the popliteofibular ligament (PFL), and the lateral collateral ligament (LCL).12-14 The arcuate and fabellofibular ligaments are variably present.15,16 The LCL and capsule are tight in full knee extension and slacken as the knee flexes. In contrast, the popliteofibular ligament complex (popliteus and PFL) is isometric and stabilizes the knee at all angles of flexion.17 These structures are ideally situated to resist tibial external rotation and, to a lesser degree, posterior tibial translation, whereas the LCL primarily restricts varus.12-14

Posteromedial bundle attaches to side wall of notch

Anterolateral bundle attaches to roof of notch

Artificial split between bundles

Posterior-oblique fibers

Posteromedial bundle overlays anterolateral Figure 23E1-5 Posterolateral view of the left knee showing double-bundle architecture of native posterior cruciate ligament. (From Amis AA, Gupte CM, Bull AMJ, Edwards A: Anatomy of the posterior cruciate ligament and the meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc 14[3]:257-263, 2006.)


A

B

Figure 23E1-6 Sagittal cross section of the left knee. A, In full extension, the anterolateral bundle (dashed arrow) is slack, whereas the posteromedial bundle (solid arrow) is taut. B, In 90 degrees of flexion, the anterolateral bundle is taut, and the posteromedial bundle is slack. (From Amis AA, Gupte CM, Bull AMJ, Edwards A: Anatomy of the posterior cruciate ligament and the meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc 14[3]:257-263, 2006.)

Blood Supply and Innervation The vascular supply of the knee and the cruciate ligaments has been well described.18,19 The popliteal artery gives rise to five branches that supply blood to the knee joint: the superior and inferior geniculate arteries (both with medial and lateral branches) and the middle geniculate artery (Fig. 23E1-8). The middle geniculate artery penetrates the posterior capsule of the knee, providing the major blood supply to the cruciate ligaments, synovial membrane, and posterior capsule itself. Furthermore, the synovial sleeve covering the PCL is well vascularized and is a major contributor to the blood supply of the ligament.18,19 The distal portion of the PCL also receives a portion of its blood supply from capsular vessels originating from the inferior geniculate and popliteal arteries.

The PCL and its synovial sleeve are supplied by nerve fibers from the popliteal plexus. This plexus receives contributions from the posterior articular nerve (prominent branch of posterior tibial nerve) and from the terminal portions of the obturator nerve.20 Golgi tendon organlike structures have been observed near ligament origins beneath the synovial sheath and are thought to have a proprioceptive function in the knee.20,21 Katonis and associates22 have identified Ruffini’s corpuscles (pressure receptors), Vater-Pacini corpuscles (velocity receptors), and free nerve endings (pain receptors) in a histologic study of mechanoreceptors in the PCL. These studies indicate that disruption of the PCL alters not only the knee kinematics but also the afferent signals to the central nervous system.23

Anterior cruciate ligament Anterior meniscofemoral ligament (ligament of Humphry)

Posterior meniscofemoral ligament (ligament of Wrisberg)

Posterior horn of lateral meniscus

Posterior cruciate ligament

Figure 23E1-7 The meniscofemoral ligaments (Humphry’s and Wrisberg’s) arise from the posterior horn of the lateral meniscus and insert anteriorly and posteriorly to the posterior cruciate ligament, respectively, on the medial femoral condyle.

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Popliteal artery

Superior medial genicular artery

Superior lateral genicular artery

Middle geniculate artery Inferior lateral genicular artery Inferior medial genicular artery

Figure 23E1-8 The vascular supply to the knee joint is through the superior and inferior medial and lateral geniculate arteries. The middle geniculate artery pierces the posterior capsule and is the main vascular supply to the cruciate ligaments.

Ligament Biomechanics The tensile strength of the PCL has varied across multiple investigators from 739 to 1627 N.4,24-26 This variation is explained partially by the fact that the individual PCL fibers act at different flexion angles and at different directions such that a uniaxial test of the whole ligament is not an accurate estimate of its strength. Thus, these numbers are likely underestimations.27 Additionally, age has been shown to be a significant factor in the strength of ligamentous tissue.28,29 As stated earlier, the PCL is composed of three functional components, the AL and PM bundles and the MFLs of Wrisberg and Humphrey.1 The AL bundle is considerably larger in cross-sectional area (about 43 mm2 versus 10 mm2) and strength (1620 N versus 258 N) than the PM bundle.30 The mean strength of the MFLs averages 300 N, roughly equivalent to the PM bundle (Table 23E1-1). The PLC structures have garnered increased attention during the past decade as their anatomy has been clearly defined and their intimate relationship with the PCL in TABLE 23E1-1 Biomechanical Size and Strength of

the Three Major Components of the Posterior Cruciate Ligament Mean Strength Anterolateral bundle Posteromedial bundle Meniscofemoral ligaments

1620 N 258 N 300 N (each)

Cross-Sectional Area mm2

43 10 mm2 Variable

controlling knee movements has been elucidated. As the knee moves from extension to flexion, there is a coupled external tibial rotation owing to the greater mobility of the lateral compartment.31,32 Although the PCL functions as the dominant restraint to posterior tibial translation with increasing flexion, none of its three functional components are the primary restraint to posterior tibial translation at full extension or to external tibial rotation at any knee flexion angle.33 The importance of these secondary stabilizers, notably the PLC, in helping to control posterior tibial translation as well as functioning as the primary restraint to external tibial rotation has been a major research milestone during the past decade. Perhaps the most notable structure among the PLC is the popliteus complex. The popliteus complex consists of the popliteus muscle-tendon unit and the ligamentous connections from the tendon to the fibula, tibia, and meniscus, known as the popliteofibular ligament and popliteotibial and popliteomeniscal fascicles, respectively.10-15 As these structures cradle the posterolateral aspect of the knee, they tighten in full extension (providing the main restraint to posterior tibial translation at extension) and tibial external rotation at all flexion angles. The popliteus muscle itself provides both static and dynamic stability through its tendinous insertion into the lateral femoral condyle and its muscular pull, respectively.14,34,35 It is important to note that although the LCL is part of the PLC, the LCL functions independently of the PLC. The LCL provides varus stability and does not assist the PLC structures in preventing posterior tibial translation. Thus, varus and posterior or posterolateral instability should be evaluated separately.36,37 Finally, hamstring and quadriceps muscle actions provide dynamic stability to help reduce loads on the PCL.38,39 The synergistic relationship between the PCL and PLC in limiting posterior translation and external rotation is well established. Combined sectioning of both structures results in significantly increased laxity as compared with sectioning of either structure alone (Table 23E1-2).5,12,14 Studies have shown that isolated sectioning of the PLC or the PCL increased posterior tibial translation up to

TABLE 23E1-2 Kinematic Changes in Response to

Isolated and Combined Injury of the Posterior Cruciate Ligament and Posterolateral Structures under a Posterior Drawer Test* Injury

PCL

PCL-PLS

PLS

Isolated

Posterior translation (90 degrees) External rotation (30 degrees) Varus

2+ 1+ 1+

0 1+ 1+

Combined (PCL and PLS)

Posterior translation (90 degrees) External rotation (30 degrees) Varus

3+ 2+ 2+

*Values indicate the amount of knee laxity as described by knee classification systems. PCL, posterior cruciate ligament; PLS, posterolateral structures. From Boynton MD, Tietjens BR: Long-term followup of the untreated isolated posterior cruciate ligament-deficient knee. Am J Sports Med 24:306-310, 1996.


12 mm at full extension and 90 degrees of flexion, respectively. When both structures were sectioned, laxity at each position increased up to 25 mm.12,13 Similarly, the absence of one structure significantly increases the stress in the remaining structure. Vogrin and colleagues showed that the in situ force in the PCL increases 2 to 6 times that of the normal knee in response to an external rotation torque in the presence of PLC deficiency.40 The converse (increased stress seen in the PLC structures in the PCLdeficient knee in response to posterior drawer force) is also true. Thus, failure to recognize and reconstruct both structures in the setting of a combined PLC and PCL injury can result in persistent joint laxity and early failure when one structure is reconstructed.41,42 A biomechanical study by Sekiya and associates42 proved that by addressing both structures in a combined injury, more normal knee kinematics was restored. Because of its larger area and strength, the historical approach to PCL reconstruction has centered on replacing the larger anterolateral bundle. Multiple studies, however, have shown that this reconstructive technique fails to reproduce normal knee biomechanics.43-46 In single-bundle PCL reconstructions, the anterolateral bundle is commonly fixed at 90 degrees of knee flexion, where the PCL is the primary restraint to posterior tibial translation. Doing so, however, only restores knee kinematics at middle to high flexion angles but leaves residual laxity at knee flexion angles near extension.47 Conversely, fixation of a singlebundle AL graft near full extension increases the likelihood of graft failure and loss of flexion due to overconstraining the knee joint.47,48 It has been shown that adjusting the insertion site of the femoral bundle more strongly influences graft tension and overall posterior tibial translation than adjusting the tibial insertion site.49-53 This is due to the rotational movement of the femoral condyle relative to the more fixed tibial insertion site during knee motion.52,53 Grood and colleagues52 and Sidles and associates53 have noted that the shallow-deep (proximal-distal) location of the tunnel in the femoral notch has the greatest effect on the tension in the PCL bundle grafts. The most ideal position for a single-bundle femoral tunnel remains unanswered. Multiple authors have looked for an isometric point, but few fibers of the native PCL are isometric.54 Efforts to place the graft in this location have not restored stability, particularly at higher flexion angles.50,55 Other authors have advocated a nonisometric femoral attachment located shallow (distal) within the femoral notch when viewed at 90 degrees of flexion.50,54,56 This has shown improved stability but still does not replicate the native PCL biomechanics.50 To more closely reproduce the anatomy and tensioning patterns of the intact PCL, double-bundle PCL reconstructions were developed. The results of these are discussed later.

the incidence in trauma or sporting activity cohorts is much higher. Fanelli and associates,58,59 in a prospective analysis on patients presenting to a regional trauma center with acute hemarthrosis of the knee, found that 56.5% of these patients were trauma victims, whereas 32.9% were sports related. In this population, isolated PCL ruptures were rare, with 96.5% of the PCL injuries involving multiligamentous injuries. In a more sports focused cohort, Schulz and colleagues60 found an athletic cause in 40% of their 587 patients with PCL insufficiency. Thus, motor vehicle crashes and sports-related trauma are the most commonly cited causes of PCL injury.58-63 The exact incidence and distribution of PCL injuries among specific sports is less well known. Sports involving contact, such as football, baseball, skiing, and soccer, are more frequently associated with PCL injury.60,64-68 The retrospective sports-specific incidence of PCL injury for hockey, soccer, handball, wrestling, and rugby has been found to range between 1% and 4%.64,66,69,70 Ligamentous disruption of the PCL, unlike injury to the ACL, is most often the result of external forces. The classic “dashboard” injury (i.e., extrinsic force) occurs from a posteriorly directed force on the anterior aspect of the proximal tibia with the knee in a flexed position (Fig. 23E1-9).71 Similarly, an athlete who falls on a flexed knee with the foot in plantar flexion is at risk for a PCL injury.43 In contrast, if the foot is in dorsiflexion, the force is transmitted more through the patella and distal femur, protecting the PCL from injury (Fig. 23E1-10). Noncontact injuries to the PCL have also been reported in the literature. The most common mechanism for isolated PCL injuries in athletes was forced hyperflexion of the knee as reported by Fowler and Messieh.65 These injuries often resulted in only partial tearing of the PCL, leaving the posteromedial fibers intact. Another mechanism is knee hyperextension, which is often combined with either a varus or valgus force resulting in a combined ligamentous injury with a much more guarded prognosis.

EVALUATION Clinical Presentation and History The incidence of PCL injuries varies significantly across different study populations. The reported incidence in the general population has been found to be 3%.57 However,

Figure 23E1-9 Posterior cruciate ligament injuries are most frequently the result of a blow to the front of the flexed knee.

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B

A

Figure 23E1-10 A, Falling on a flexed knee with the foot in a dorsiflexed position spares injury to the posterior cruciate ligament (PCL) by transmitting the force to the patellofemoral joint. B, Landing with the foot plantar flexed injures the PCL as the posteriorly directed force is applied to the tibial tubercle. C, Hyperflexion of the knee without a direct blow is a common mechanism of PCL injury in athletes.

C

Injuries to the PCL can be classified according to severity (grade I to grade III), timing (acute versus chronic), and associated injuries (isolated versus combined). These variables have significant implications for outcomes of patients and thus are an important consideration in making treatment decisions. Isolated injuries to the PCL can be classified into partial (grade I or grade II) and complete (grade III) tears. In most cases, this is done clinically and corresponds to the laxity in the PCL, as measured by the step-off between the medial tibial plateau and the medial femoral condyle with the posterior drawer test. Stress radiography has also been show to corroborate these findings.72 Isolated grade III or complete PCL tears can occur, but they are frequently associated with other ligament injuries and, in particular, injury to the PLC.36 Distinguishing between the isolated and combined PCL injuries is critical because the prognosis for and treatment of these injuries are vastly different. Isolated injuries, in general, may be treated nonoperatively and have a good to excellent prognosis.65,67,73,74 Combined ligament injuries involving the PCL have a more guarded prognosis, however. Superior results may be possible in this group with early surgical intervention rather than with conservative treatment.36,63 Although the distinction between acute and chronic injury is somewhat arbitrary, it has important ramifications, especially in the treatment of combined ligamentous injuries. These cases frequently involve injury to the PLC, and surgical treatment in the acute phase (i.e., before 3 weeks) allows primary repair of the PLC. After 3 weeks, significant scar formation limits the success of primary repair and typically commits the surgeon to waiting a full 3 months to allow completion of the healing response before surgical reconstruction can be implemented. Furthermore, chronic injuries may become associated with significant pericapsular stretching (secondary to posterior and posterolateral tibial subluxation), resulting in secondary rotational instability or the development of arthrosis. In these cases, it

may be difficult to determine the extent of the initial injury as well as to devise the optimal treatment plan. Finally, combined PCL injuries are commonly associated with fractures as well as with injuries to vessels, nerves, and other soft tissue structures. An occult knee dislocation should be suspected when examination reveals disruption of both the ACL and the PCL or any three-ligament injury. Although the integrity of the popliteal vessel and peroneal nerve must be assessed in any significant knee injury, their function must be particularly scrutinized in this situation because the incidence of injury ranges from 15% to 49%.36,71,75-79 If a knee dislocation is suspected, a low threshold for appropriate vascular studies and monitoring is recommended.

Physical Examination and Testing Patients with injuries to the PCL may present for evaluation in a variety of different scenarios. Injuries may range from a seemingly benign fall on the athletic field to severe trauma after a motor vehicle crash. Evaluation of the injured knee begins with obtaining a detailed history, trying to delineate the mechanism of injury, its severity, and possible associated injuries. The more acutely traumatized the knee, the more difficult it will be to examine. Unlike patients with isolated ACL injuries, those with acute, isolated PCL injuries do not typically report hearing or feeling a “pop.” Although many suspect a knee injury, patients do not typically relate a sense of instability. They may note mild to moderate swelling, accompanying stiffness, and occasionally mild knee pain. The pain may be located posteriorly, and they may lack 10 to 20 degrees of knee flexion.63 Conversely, patients with combined ligament injuries are rarely asymptomatic. After the initial swelling from the acute injury has resolved, individuals with PCL and PLC injuries may complain of pain and instability of the knee. This is especially true in patients


with varus alignment, who may develop varus recurvatum thrust during gait.80 Dysesthesias or weakness of the foot dorsiflexors and evertors may also be present if an associated injury occurred to the peroneal nerve. Chronic injuries to the PCL and PLC can cause disability ranging from almost no functional impairments to severe limitations during activities of daily living.65,67,81-85 Furthermore, patients who are symptomatic frequently report pain as their predominant complaint.81-83,85-87 Other patients with chronic PCL tears, however, may complain more of disability than instability, with walking on inclines or ramps being most problematic.43 In general, patients with chronic, isolated injuries to either the PCL or PLC tend to function at higher levels than do patients with combined ligamentous injuries.81,88 The resultant posterior subluxation, increased adduction moment, and medial concentration of the joint reaction force may contribute to the development of arthrosis. Whether the severity corresponds to the degree of abnormal translation is still controversial.81,84 A thorough knee examination is essential and should follow the sequence of observation, evaluation of range of motion, palpation, and ligamentous examination followed by specialized testing. In the acute setting, contusions about the anterior tibia and popliteal ecchymosis may be noted. Assessment for meniscal damage or other ligamentous injury aside from the PCL and PLC should routinely be performed. Special care must be undertaken in evaluating the ACL in the setting of a PCL-insufficient knee. Although less frequent, the posteromedial corner (PMC) can also be injured, and its integrity should also be documented. The noninvolved knee must be examined first to determine the normal relationship of the tibia to the femur because the tibia will be subluxated posteriorly in the injured knee. After this is corrected in the injured knee, standard anterior drawer and Lachman’s tests can be performed. Significant translation of more than 10 mm in the sagittal plane suggests injury to both cruciate ligaments.36 Despite increased awareness of PCL, PLC, and PMC injuries, they are still frequently not recognized at the initial evaluation.

Posterior Drawer Test The most accurate clinical test for assessment of PCL integrity is the posterior drawer test (Fig. 23E1-11).43,61 The patient is placed supine, and the knee is flexed to 90 degrees while a posteriorly directed force is placed on the proximal tibia. This test can be performed with the tibia in neutral, external, and internal rotation. In cases of isolated PCL tears, there is a decrease in posterior tibial translation with internal tibial rotation. The MCL and posterior oblique ligament contribute to this secondary restraint.89,90 The extent of translation is evaluated by noting the change in the distance of step-off between the medial tibial plateau and the medial femoral condyle. Equally important during this test is to assess the quality of the end point. The plateau is normally positioned about 1 cm anterior to the condyle but can vary, making examination of the contralateral knee essential. PCL injury can be graded with respect to the amount of laxity determined by this test. Grade I is consistent with excessive posterior translation but maintenance of an

Figure 23E1-11 Assessing the tibial step-off before performing the posterior drawer examination. (Adapted from Miller MD, Harner CD, Koshiwaguchi S: Acute posterior cruciate ligament injuries. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery, vol 1. Baltimore, Williams & Wilkins, 1994.)

anterior step-off. Grade II is classified as a 5- to 10-mm translation corresponding to the plateau’s being displaced flush to the level of but not posterior to the condyle. Both of these grades represent partial tears of the PCL. More than 10 mm of translation constitutes a grade III injury, with the plateau displaced posterior to the condyle, and is consistent with a complete tear of the PCL. The degree of sagittal translation should also be assessed with the knee flexed 30 degrees. A slight increase in translation at 30 degrees and not at 90 degrees of flexion may indicate a PLC injury; increased sagittal translation at both 30 degrees and 90 degrees, with maximal translation at 90 degrees of knee flexion, is consistent with a PCL injury (see Table 23E1-2).

Posterior Sag Test (Godfrey’s Test) The posterior sag test may provide additional information in evaluation of the PCL. The hip and knee are flexed to 90 degrees. With a complete PCL tear, the pull of gravity will displace the tibia posterior to the femur while the examiner supports the weight of the limb by the foot (Fig. 23E1-12).

knee 1691

External Rotation of the Tibia (Dial Test)

Figure 23E1-12 A positive Godfrey’s test. (Adapted from Miller MD, Harner CD, Koshiwaguchi S: Acute posterior cruciate ligament injuries. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery, vol 1. Baltimore, Williams & Wilkins, 1994.)

Quadriceps Active Test The quadriceps active test can also aid in the diagnosis of complete ruptures. For this test, the knee is placed at 60 degrees of flexion. While the examiner holds pressure on the foot, the patient is asked to contract the quadriceps isometrically. In the presence of a complete tear of the PCL (grade III), the patient will achieve dynamic reduction of the posteriorly displaced tibia (Fig. 23E1-13).

Proper evaluation of the PLC can be difficult with the tibia subluxated posteriorly as in a grade III PCL injury, so reducing the tibia to neutral is essential before testing for PLC injury.61,91-93 Testing is best performed with the patient positioned prone or supine, while an external rotation force is applied to both feet with the knee positioned at 30 degrees and then 90 degrees of flexion. The degree of external rotation is measured by comparing the medial border of the foot with the axis of the femur. Because wide variability of external rotation is possible at these positions, it is essential to compare the results with the contralateral side.94,95 More than a 10-degree difference is considered abnormal.96 The popliteus complex portion of the PLC is the primary restraint to external rotation at all degrees of knee flexion, but its effect is maximal at 30 degrees. An increase of 10 degrees or more of external rotation at 30 degrees of knee flexion, but not at 90 degrees, is considered diagnostic of an isolated PLC injury.97 Conversely, the PCL is the secondary restraint to external rotation when the knee is at 90 degrees of flexion.12,52,95 Thus, an isolated PCL injury should have increased external rotation at only 90 degrees, whereas increased external rotation at both 30 and 90 degrees of knee flexion suggests a combined PCL and PLC injury (see Table 23E1-2). The recognition of this posterolateral instability component is essential clinically because it may significantly affect the treatment of associated ligamentous instability.

Posteromedial Pivot Test The integrity of the posteromedial corner can be tested using the PM pivot test.98 This test evaluates the integrity of the PCL, MCL, and posterior oblique ligament. A positive test result occurs when the knee shifts anteriorly as it is extended to about 20 degrees while a varus, compression, and internal rotation stress is applied to the tibia.

Figure 23E1-13 The quadriceps active drawer test. In the presence of a complete tear of the posterior cruciate ligament, dynamic reduction of the posteriorly displaced tibia will be achieved.


varus opening at full extension, a combined injury of the PLC, PCL, and ACL may be present.12-14,95,96,100

Gait and Limb Alignment The evaluation of gait and limb alignment is particularly important for those with chronic injury of the PLC. Compared with the medial side of the knee, the articular anatomy of the lateral side is inherently less stable.31,32,94 In patients with chronic PLC insufficiency, the dynamic stabilizers of the lateral knee are not functioning optimally. This may lead to excessive posterolateral rotation and varus opening (or thrust) in the stance phase of gait.101 Therefore, it is critical to evaluate lower limb alignment in patients with chronic PLC instability. In the presence of varus alignment and a lateral thrust, a valgus (opening or closing) proximal tibial osteotomy is necessary to correct the alignment because soft tissue reconstructions alone will fail.102,103 Similarly, a patient with chronic PCL deficiency and a primary varus alignment will be more susceptible to posterolateral injury. Thus, to plan successful treatment of the patient with multiple ligamentous knee injuries, the examiner must determine the extent of injury to all ligaments involved, namely, the PCL, the PMC, the popliteus complex, and the LCL, as well as the primary alignment of the limb.

Imaging Studies Radiography Figure 23E1-14 The reverse pivot shift test starts with the knee in flexion. The posteriorly subluxed lateral tibial plateau reduces as the knee is brought into extension. (Adapted from Miller MD, Harner CD, Koshiwaguchi S: Acute posterior cruciate ligament injuries. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery, vol 1. Baltimore, Williams & Wilkins, 1994.)

Reverse Pivot Shift Test This test can be performed by passively extending the knee from 90 degrees of flexion with the foot externally rotated and a valgus force applied to the tibia. A positive result is observed when the posteriorly subluxated lateral tibial plateau abruptly reduces at 20 to 30 degrees of flexion (Fig. 23E1-14).99 Other tests, such as the external rotation recurvatum, the posterolateral drawer, and the posterolateral Lachman’s test, can further aid in diagnosis of the extent of injury to the PCL and PLC but are more difficult to perform reproducibly and to interpret.

Collateral Ligament Examination Varus and valgus stress tests are important in assessment of the integrity of the LCL portion of the PLC. These should be performed with the knee in full extension and in 30 degrees of flexion. Isolated PCL injury does not significantly affect varus or valgus stability. Increased varus opening at 30 degrees of knee flexion indicates an injury to the LCL and possibly the popliteus complex. Additional slight increased opening at full extension is consistent with injuries to both of these structures. If there is a large degree of

Our standard knee series includes bilateral standing anteroposterior and flexion 45 degrees weight-bearing, as well as Merchant’s patellar and lateral radiographs. These films should be carefully scrutinized for subtle posterior tibial subluxation (which may be the only radiographic finding in isolated PCL injuries), avulsion fractures, joint space narrowing, and slope of the proximal tibia. The plain radiographs must also be closely evaluated for any evidence of avulsion fractures involving the PCL, fibular head, and Gerdy’s tubercle. These bony avulsion injuries, when recognized acutely, may be repaired primarily with superior results compared with late reconstruction.104 Hall and Hochman105 described a medial Segond’s fracture that represents a medial capsular avulsion in PCL injuries. Furthermore, failure to recognize fractures of the tibial tubercle can be a particular problem. The unopposed pull of the hamstrings causes posterior tibial subluxation, which can become fixed within a short time, requiring open reduction. In addition, long-leg cassette views are critical to evaluate overall lower extremity alignment, particularly varus, in chronic or revision cases. Stress radiographs and contralateral views, although not routine, may be helpful in some situations.106 Hewett and associates106 retrospectively evaluated 21 patients with partial or complete PCL tears with both stress radiology and KT-1000 measurements. They concluded that stress radiographs were more accurate than KT-1000 measurements in diagnosing PCL tears. Most have concluded that greater than 8 mm posterior displacement on stress radiographs indicates a complete PCL tear, whereas greater than 12 mm indicates injury to secondary structures.72,106,107

knee 1693

We agree with Schulz and colleagues,72,107 however, that stress radiography may be influenced by multiple factors, including tibial rotation and tissue compliance, such that physical examination by an experienced clinician is as sensitive as stress radiography.

Magnetic Resonance Imaging MRI has become the diagnostic study of choice in evaluation of the knee with a presumed PCL injury. This study is 96% to 100% sensitive in detecting acute tears of the PCL and can also determine the precise location of the tear, with implications for treatment.95,108-110 For example, the femoral “peel-off” injury is particularly amenable to primary repair.111,112 The normal PCL appears dark on T1- and T2-weighted sequences and is curvilinear in appearance. However, chronic tears of the PCL can heal and assume the aforementioned curvilinear appearance; thus, MRIs for chronic PCL tears are much less sensitive, and the appearance of a normal shape of the ligament should not be used as a criterion for a normal PCL.63,113,114 There is some data to support the use of MRI as a prognostic sign of PCL healing.114 MRI is also necessary to assess the menisci, articular surfaces, and other ligaments of the knee, which also have relevance to treatment and prognosis.115 Bone bruises are common in PCL injuries; however, their location can vary within the knee, unlike the uniform appearance of ACL bone bruises.116 MRI of the PLC of the knee has consistently improved. With the help of different imaging techniques and the addition of a coronal oblique technique, the sensitivity of visualizing and accurately diagnosing injuries to the PLC can exceed 80%.117,118

Bone Scanning A bone scan may prove helpful in the evaluation and management of chronic PCL injuries. Patients with these injuries are predisposed to early medial and patellofemoral compartment chondrosis.43,73,119 In the setting of an isolated PCL-deficient knee with medial or patellofemoral compartment pain and normal radiographs, a bone scan to assess these compartments may be helpful. If there is increased uptake, surgical intervention may be beneficial.87 If there is no increased uptake, a continued nonoperative approach is our treatment of choice.

TREATMENT OPTIONS Controversy still exists with respect to the indications for nonoperative versus surgical intervention, techniques of reconstruction, and methods of rehabilitation for the PCL-injured knee. The relatively infrequent occurrence of this injury has unfortunately led to clinical studies with small sample sizes and short-term follow-up. The limited understanding of the PCL and associated injuries has additionally resulted in studies that are frequently a collection of differing patterns of PCL injury—acute, chronic, isolated, combined, partial, and complete—and also lack welldefined indications for surgical management. Most series do not include control groups, combine primary repair and multiple reconstructive techniques, and use different

outcome measures. Because of this, it has been difficult to compare results of different operative techniques and approaches. The following section focuses on a review of the pertinent literature followed by a discussion of current treatment recommendations. We conclude with a presentation of our approach to the management of the PCL-injured knee.

Review of Nonoperative Treatment and Natural History of Isolated Posterior Cruciate Ligament Deficiency Among orthopaedic surgeons, the treatment of isolated PCL injuries continues to be an area of active debate. This debate will likely continue until prospective, randomized trials are done to compare different methods of treatment. Currently, most studies are retrospective in nature and use various outcome measurements, which makes comparisons difficult. To date, there have been four published prospective studies on nonoperative management for isolated PCL injuries (Table 23E1-3). Many authors have found good results with nonoperative treatment of isolated PCL injuries that would indicate a more benign natural history. Dandy and Pusey83 treated 20 patients with persistent knee symptoms due to unrecognized, isolated PCL injury. At 7.2 years of follow-up, 18 of the 20 had a good functional result. The authors thought that the subjective results, objective evaluation findings, and functional capacity without operative intervention were adequate and did not warrant surgical reconstruction or repair. Parolie and Bergfeld67 observed 25 patients with isolated PCL tears resulting from sporting injuries. At a minimum of 2 years of follow-up, 80% were satisfied with their knee function, and 68% returned to their previous level of activity. They also noted that those with unsatisfactory results tended to have diminished quadriceps strength compared with those with successful results. Torg and colleagues87 observed 14 patients with isolated PCL injuries and 29 patients with combined PCL injuries for more than 6 years and concluded that the patients with isolated injuries remained without symptoms and did not require subsequent reconstruction. Other authors have found similar outcomes, but did find some deterioration in outcome with time. Boynton and Tietjens120 observed 30 patients with isolated PCLdeficient knees for an average of 13.2 years and found that the prognosis varies. Eight (21%) of the original 38 patients had surgery for subsequent meniscal tears. Among the 30 patients with isolated PCL-deficient knees with normal menisci, 24 (81%) had at least occasional pain, and 17 (56%) had at least occasional swelling. Keller and colleagues73 observed 40 patients with isolated PCL injuries for an average of 6 years. In this shorter interval, 90% still complained of pain, 65% stated that the knee limited their activity, and 43% reported difficulty with walking. Four prospective studies have been reported on the natural history of isolated PCL injuries. In 1987, Fowler and Messieh65 published their results on 13 patients followed for a mean of 2.6 years. Subjective and functional ratings were all good; when assessed objectively, however, only 3 rated good and 10 fair. Shino and associates68 followed

Study

Design

No. of Patients

Laxity

Follow-Up Outcome Age (yr) (yr) Assessment

Functional Score

Shelbourne Pro et al, 1999121

68

Grade I, 25; grade I.5, 13; grade II, 30

25.2

5.4

83.4 (Lysholm) 84.2 (Noyes) 5.7 (Tegner)

Boynton & Tietjens, 1996120

Retro

30

28.7

13.2

N/A

76/100 (used own scale)

Torg et al, 198687 Keller et al, 199373

Retro

14

Grade I, 5; grade II, 15; grade III, 10 N/A

29

5.7

N/A

Retro

40

33

6

N/A

Shino et al, 199568

Pro

13

Grade I, 24; grade II, 13; grade III, 3 All grade II or III

N/A

4.25

N/A

5 Excellent; 7 good; 1 fair; 1 poor Noyes grade I average, 81; grade II average, 72; grade III, 58 IKDC: 3 normal, 5 nearly normal, 5 abnormal

Fowler & Messieh, 198765

Pro

13

N/A

22

2.6

Hughston criteria: 3 good, 0 fair, 10 poor

Dandy & Pusey, 198283

Retro

20

N/A

31

7.2

Parolie & Bergfeld, 198667

Retro

25

N/A

24.7

6.2

Hughston criteria: 0 good, 8 fair, 12 poor 80% satisfied (scale not specified)

Correlation to DJD

Correlation to Functional Score

Comments

No correlation with laxity, time Positive correlation with quadriceps strength and improved scores Positive Trend (P = .08) correlation for time, positive with time correlation with laxity (P = .037) and decreased scores N/A No correlation with laxity Positive Positive correlation correlation with between laxity and time time to decreased scores No correlation No correlation with time

50% same level, 63/68 had same or 33% lower less PCL laxity at level, 17% follow-up changed sports

Hughston criteria: 13 good

N/A

N/A

All returned to “previous activity”

Hughston criteria: 5 good, 11 fair, 4 poor

No correlation

N/A

N/A

N/A

No correlation

Positive correlation between improved scores and quadriceps strength

68% same level, N/A 16% lower level, 16% no return to sport

DJD, degenerative joint disease; IKDC, International Knee Documentation Committee; Pro, prospective; Retro, retrospective.

Positive trend with time (P = .07)

Return to Sport

26% same level, Prognosis 37% lower extremely varied; level, 37% 8 had meniscal changed sports injuries N/A N/A

11/13 returned to same level

36/40 had knee pain, 26/40 had decreased activity level All 22 original subjects underwent arthroscopy: 5 had lateral meniscus tears, 11 had chondral damage All 13 subjects underwent arthroscopy: 2 had meniscal tears, 4 had chondral lesions 18/20 had good functional result


TABLE 23E1-3 Natural History of Isolated Posterior Cruciate Ligament Injuries Treated Nonoperatively

knee 1695

15 patients for an average of 4.25 years. Eleven of 15 returned to sports at their preinjury level, and 14 patients remained symptom free. Shelbourne and colleagues121 followed 133 patients with isolated PCL injuries for an average of 5.4 years. More than half of these patients were able to return to their preinjury level of activity, and no correlation was found between grade of laxity and radiographic change. Shelbourne and Muthukaruppan122 performed a longer term follow-up of this patient cohort with a modified Noyes survey and the International Knee Documentation Committee (IKDC) subjective knee survey at a mean time of 7.8 and 8.8 years, respectively. Of the 146 patients who had at least four modified Noyes subjective surveys, 40% scored consistently excellent, 10% consistently good, 6% consistently fair, and 2% consistently poor. Furthermore, 16% of these patients had consistently improving scores, 12% had consistently decreasing scores, and 14% had inconsistent scores. Of the 67 patients who scored less than 85 points in the first 2 years after injury, only 34 had a score of less than 85 points at their most recent survey. In summary, numerous investigators have shown that isolated acute PCL injuries (grade I to grade III) do relatively well with conservative treatment. Most patients in these studies, however, had grade II PCL laxity or less. The relatively benign course of these injuries is most likely due to the integrity of the secondary restraints and various portions of the PCL remaining intact.36 Accordingly, Fontboté and associates123 have shown that patients with grade II PCL laxity demonstrate minimal biomechanical and neuromuscular differences despite significant clinical laxity. Although these studies varied with respect to injury mechanism, extent of the PCL injury, physical therapy protocol, and evaluation of outcome and time of follow-up, they do suggest that most patients with PCL-injured knees will do relatively well with conservative care. Even though nonoperative treatment appears to give relatively good results, these patients do not have a normal outcome in all series reported, especially for grade III injuries. The natural history of the PCL-deficient knee leads to increased contact pressures in both the medial and patellofemoral compartments.124-126 The pathomechanics of the PCL-injured knee is unique in comparison to other ligamentous knee injuries (Fig. 23E1-15). As a result of the excessive posterior tibial translation, abnormal wear occurs, and pain rather than instability becomes the major symptomatic issue. We agree with Logan and associates126 that a PCL injury is analogous to a medial meniscus resection in that the PCL injury leads to a fixed anterior subluxation of the medial femoral condyle, which overloads the medial knee compartment. Patients with PCL-deficient knees treated nonoperatively have a high incidence of acute chondral injury and late chondrosis43,73,119,120 (involving the medial femoral condyle and patellofemoral joint) as well as acute and chronic meniscal tears.68,120,127 It has been shown that acutely, 52% of 61 acute PCL-injured patients had chondral injury noted at arthroscopy,128 whereas patients with chronic PCL deficient knees have a variable progression of articular degeneration and symptoms over time. Geissler and Whipple127 studied groups of both acute and chronic PCL-deficient patients. In the acute group,

2) Tibiofemoral contact shifts anteriorly

X

• Posterior horn medial meniscus unloaded • Increase wear of articular cartilage

3) Force in the PLS

1) Posterior tibial translation Figure 23E1-15 Pathomechanics of articular wear secondary to altered tibiofemoral contact forces in the chronically posterior cruciate ligament-deficient knee. PLS, posterior lateral structures.

12% had chondral defects, and 27% had meniscal tears. In the chronic group, 49% had chondral defects (most commonly medial) and 36% had meniscal tears (most commonly medial). These findings are likely to be the result of increased contact pressure that occurs after PCL disruption.124-126 The problem is that investigators have been unable to consistently identify prognostic factors to help predict outcomes of patients. Surprisingly, objective instability and time from injury have correlated poorly with final outcome and radiographic degenerative changes in most studies. Therefore, we, like Shelbourne and associates, believe that in patients with isolated grade II laxity of the PCL, a PCL reconstruction that improves laxity only to grade I may not achieve any better result than nonoperative treatment.122,129 However, in order to prevent the progressive decline associated with the natural history of many grade III injuries, we have adopted a more aggressive approach for these injury patterns.

Review of the Literature on Operative Treatment Avulsion Fractures Involving the Posterior Cruciate Ligament Avulsion fractures of the PCL are relatively rare injuries. When isolated and nondisplaced, these fractures have been effectively managed with a brief period of immobilization. Most would agree, however, that displaced avulsions should undergo operative management.74,130-132 Although several reports do not differentiate between isolated and combined injury patterns, surgical management of tibial avulsion fractures has been fairly successful. In independent studies, both Lee133 and McMaster74 were the first to report good results with this type of treatment. After treating 13 avulsion fractures, Trickey132 noted better results in the surgical compared with the nonsurgical group. Torisu130 treated 21 patients with tibial avulsion fractures with cast immobilization for nondisplaced fractures and early internal fixation for displaced fractures. At an average of 4 years of follow-up, all of the patients had good or excellent results.


Isolated Posterior Cruciate Ligament Injuries As shown previously, there is an emerging consensus that isolated grade III PCL injuries are not as benign in the long term as previously thought.88 Therefore, many surgeons have elected to proceed with PCL reconstruction in patients with isolated grade III (tibia subluxated posterior to femoral condyles, >10 mm displacement) injuries. In most of the studies published on these patients,42,71,134-141 the indications for treatment are persistent knee instability with continued knee pain. The initial results of contemporary reconstruction of the PCL were first described by Clancy and associates43 in 1983. Since that time, multiple studies have been published on the results of PCL reconstruction. This section focuses on those studies involving isolated PCL injuries that underwent reconstruction using contemporary techniques. There are multiple series published on PCL reconstruction done on patients with isolated high-grade (majority grade III) PCL injuries (Table 23E1-4).43,134-143 Several important points are notable from these studies. In studies by Sekiya and associates,142 Wang and coworkers,141 and Mariani and colleagues,139 acute reconstructions had significantly better outcome measures than chronic reconstructions, whereas the study by Deehan and associates136 did not find such a correlation. This conclusion may relate to more articular degeneration that is present in patients with chronic posterior tibial subluxation, which effectively unloads the medial meniscus, as mentioned earlier. Second, no specific graft type has shown superiority in PCL reconstructions135,140,143,144; both autograft and allograft hamstring, patellar tendon, Achilles tendon, and quad tendon have all been used. Third, most patients continued to have residual posterior laxity when compared with their contralateral leg, with many patients improving only one grade in laxity. The somewhat inconsistent results and residual laxity noted after arthroscopic single-bundle PCL reconstruction have been attributed to several potential technical issues. These issues include the use of a transtibial versus tibial inlay method, single- versus double-bundle reconstruction, and the various graft fixation options. Most PCL reconstruction techniques employ a transtibial technique. In posterior cruciate reconstructions using a transtibial technique, the PCL graft must make an acute turn at the posterior opening of the tibial tunnel. This so-called killer turn has been suspected of leading to graft abrasion with subsequent thinning of the graft and eventual graft rupture or excessive laxity.145-147 Thus, the residual posterior knee laxity observed clinically after traditional transtibial PCL reconstruction techniques may be related to this acute turn. Therefore, the tibial inlay technique was introduced by Jakob and Ruegsegger148 and by Berg149 to overcome this perceived disadvantage. The main attraction of the tibial inlay technique is the direct fixation that can be achieved at the tibial attachment site, as well as obviating the killer turn and allowing graft tendon length adjustment. Biomechanical cadaveric studies have been performed to test this hypothesis. Bergfeld and associates150 showed that the inlay technique resulted in less posterior tibial translation with less graft degradation than did the transtibial

technique. This increased rate of graft thinning and degradation was also seen in a later cyclic loading study by Markolf and associates.151 However, the authors of the later subsequent studies152-155 did not find any significant increase in the in situ graft forces, graft laxity, or graft rupture in comparing either technique. Margheritini and coworkers153 argued that the evaluation of cyclic wear in the nonviable grafts used during these cadaveric studies does not account for the biologic remodeling that occurs in vivo, and thus makes such findings clinically less applicable. Retrospective studies comparing transtibial versus tibial inlay138,140 patients did not show any significant differences in subjective outcome or knee laxity measurements (Table 23E1-5). Thus, although the tibial inlay technique may have some biomechanical advantages when tested in a cadaveric model, these advantages have yet to be identified in clinical studies. Another controversy surrounding PCL reconstruction is the debate between single- and double-bundle techniques. Double-bundle PCL reconstructions were introduced to more closely reproduce the anatomy and biomechanical properties of the intact PCL. Biomechanical studies in our laboratory and others have shown that the two bundles demonstrate some reciprocal tightening during knee range of motion.156,157 Additionally, both bundles are active in reducing posterior tibial translation and external tibial rotation, reinforcing the notion that both are required for normal knee kinematics.157 Multiple biomechanical studies have been performed comparing single- versus doublebundle PCL reconstruction (Table 23E1-6).45,46,54,158,159 Four of the five studies have shown that double-bundle PCL reconstructions achieve similar or improved knee biomechanics when compared with single-bundle reconstructions.45,46,54,159 In reviewing these studies, as well as single-bundle biomechanical studies,46,48,50,55,56 a few important points are worth noting. Graft fixation and tensioning patterns differ across studies, which may affect results. Also, despite efforts at replicating the anatomic femoral insertion sites of the PCL bundles, considerable variation exists in the placement of tunnels at these sites across the four studies. The deep-shallow (proximal-distal) attachment location on the femur appears to greatly determine the flexion angle where the graft will be functional. More shallow grafts tense as the knee is flexed, whereas deeper grafts slacken as the knee is flexed. Double-bundle grafts with both grafts placed in deeper (proximal) locations within the notch risk loss of stability in deeper knee flexion angles. A combination of shallow and deep locations produces a reciprocal tightening pattern across the full range of motion. Two clinical studies have compared the outcomes of single- versus double-bundle PCL reconstruction (see Table 23E1-6). Houe and Jorgensen160 used a patellar tendon graft with one femoral tunnel versus a hamstring graft using two femoral tunnels. They evaluated 16 patients at a mean follow-up of 35 months and found no significant differences in Lysholm score, activity level, or graft laxity between the two reconstruction types. Wang and associates161 found similar results in their 35 patients using hamstring grafts in either a single- or double-bundle configuration. They found no significant difference in ligament laxity, functional score, or radiographic changes between

TABLE 23E1-4 Results of Isolated Posterior Cruciate Ligament Reconstructions Study

No. of Patients Age (yr)

Followup (yr)

Sekiya et al, 2005142 Retrospective

21

38

Chan et al, 2006134 Prospective

20

29

Chen et al, 2002135 Retrospective

Graft Type

5.9

5 acute, 16 chronic; all grade III

Achilles allograft

3.3

Unknown; average Quadrupled time 4 mo; all hamstring grade III autograft

A (quad A: 29; tendon): 22; B:27 B (hamstring tendon): 27

A: 2.5; B: 2.2

Mariani et al, 1997139 Retrospective

24

26

2.2

Jung et al, 2004137 Retrospective

12

29

Wang et al, 2003141 Retrospective

30

Deehan et al, 2003136 Prospective

27

Ahn et al, 2005143 Retrospective

Group I Group (hamstring I: 30 autograft): Group 18; group II: 31 II (Achilles allograft): 18

Surgical Tech

Fixation

Subjective utcome O

Transtibial

Tibia: screw and IKDC knee washer; femur: function: 57% metal IS N/NN, 43% A/SA; IKDC activity level: 62% N/NN, 38% A/SA

Transtibial

Tibia: bio IS + screw and washer; femur: bio IS + washer

A:12 acute, 10 A: quad Transtibial chronic; B: 16 tendon acute, 11 chronic; autograft; all grade III B: quadrupled hamstring autograft All chronic Patellar Transtibial tendon autograft

Tibia: A: suture and post; B: screw and washer; femur: A: metal IS; B: screw and washer Tibia and femur: metal IS

4.3

Unknown; average Patellar time, 5.4 mo; tendon range, 1-10 mo autograft

Tibial inlay

Femur: IS; tibia: screw and washer

32

3.3

13 acute, 17 chronic; all grade III

Mixed

Transtibial

Femur: IS; tibia: screw and post

27

3.3

All chronic (16 patients 4-12 mo after injury, 11 patients > 1 yr); grade II and III injuries All chronic; group I: 11 grade II, 7 grade III; group II, 10 grade II, 8 grade III

Hamstring autograft

Transtibial

Femur: IS; tibia: IS

Hamstring autograft and Achilles allograft

Transtibial

Femur: IS and screw and washer; tibia: IS and screw and washer

Group I: 2.9 Group II: 2.3

*Instrumented laxity as determined by stress radiographs. A, abnormal; bio, biologic; IS, interference screw; KT, KT-1000 testing; N, normal; NN, nearly normal, SA, severely abnormal.

Instrumented Laxity*

Posterior Drawer

Miscellaneous

KT posterior IKDC Acute/subacute drawer: 4.5 mm, grading group had KT side-side acute/ significantly difference: subacute: better IKDC and 1.96 mm 75% KT-1000 than N/NN; chronic group chronic: 40% N/NN Lysholm: 93; Average Grade I, 16; 18/20 showed Tegner: 6.3; postoperative grade II, 3; no radiographic IKDC activity KT posterior grade III, 1 deterioration; level: 85% drawer: 3.8 mm 3 patients had N/NN stiffness Lysholm: A: Average N/A 1 patient in 90.63; B: 91.44; postoperative each group had IKDC overall KT posterior stiffness; 86% rating: A: 18 drawer: group A and N/NN, 4 A/SA; A: 3.72 mm, 92% group B B: 22 N/NN, 5 B: 4.11 mm had normal A/SA radiographs Lysholm: 94; KT side-side N/A Significant differences: 6, Tegner: 5.4; correlation mm; 13, IKDC rating: 19 0-2 between poor 3.5 mm; 3, 6-10 N/NN, 5 A/SA results and more mm; 2, >10 mm chronic injuries OAK score: 92.5; Stress x-rays: 3.4 N/A 7 excellent, 4 mm side-side good; IKDC: difference; 11/11 were KT side-side N/NN difference, 1.8 mm Lysholm: 92 (24 N/A Grade I: 16; Significant excellent/good, grade II: 12; correlation 6 fair/poor); grade III: 3 between poor Tegner: 4.5 results and more chronic injuries Lysholm: 94; KT side-side Grade 0/I, No correlation IKDC: 25 N/ difference 23; grade between time NN, 2 A/SA < 2mm: 17 II, 1 from injury to patients; 3-4 surgery and mm, 6 patients outcome

Lysholm group I: Telos stress 90; group 2, 85; radiograph IKDC group I: posterior 16 N/NN, 2 displacement: A; group 2: 14 group I, 2.2 N/NN, 3 A, mm; group II, 1 SA 2.0 mm

N/A

No difference in outcome between the two groups

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Chronicity/Grade

Study

No. of Patients

Age (yr)

Follow-up (yr)

Chronicity/ Grade

Graft Type

Seon & Song, Group A A: 29.1; 2006140 (transtibial): B: 29.4 Retrospective 21; group B (tibial inlay): 22

A: 2.6; B: 3.0

All chronic; all grade II or greater

MacGillivray, Group I 2006138 (transtibial):13 Retrospective Group II (tibial inlay):7

Group I: 6.3; group II: 4.8

All chronic; Mixed group I: 5 grade II, 8 grade III; group II: 3 grade II, 4 grade III

Group I: 29; group II: 31

A: hamstring autograft; B: patellar tendon autograft

Surgical Technique

Fixation

Subjective Outcome

Instrumented Laxity*

Posterior Drawer

Miscellaneous

A: transtibial; Tibia: A: bio Lysholm: A: Telos A: 19 normal/ No significant B: tibial IS; B: screw 91.3; B: 92.8; side-side grade I; differences inlay and washer; Tegner: A: difference: 2 grade II; B: 20 between the femur: A: 5.6; B: 6.1 A: 3.7 mm; normal/grade I; two anchor B: 3.3 mm 2 grade II screw; B: bio IS screw Group I: Tibia: I: IS; Lysholm: KT posterior Group I: Neither method transtibial; II: screw/ group I: 81; drawer: 3 grade I, restored group II: washer group II: group I: 6 grade II, anteroposterior tibial inlay Femur: 76; Tegner: 5.9 mm; 4 grade III; stability to the I: IS, II: IS group I: 6; group II: group II: knee group II: 6 5.5 mm 3 grade I, 3 grade II, 1 grade III

*Instrumented laxity as determined by stress radiographs. A, abnormal; bio, biologic; IS, interference screw; KT, KT-1000 testing; N, normal; NN, nearly normal, SA, severely abnormal.


TABLE 23E1-5 Results of Isolated Posterior Cruciate Ligament Reconstruction: Transtibial versus Inlay

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TABLE 23E1-6 Biomechanical Results of Single-Bundle versus Double-Bundle Posterior Cruciate Ligament Reconstructions Study

Graft Type and Configuration

Manneo et al, Patellar tendon; Y type (2 200054 tibial ends, 1 femoral end)

Graft Locations

Tensioning

Single-bundle All graft fixed at set reconstruction: proximal flexion angle to restore shallow (S1), distal normal posterior tibial shallow (S2), distal deep translation (D); double-bundle reconstruction: S1 and S2, S1 and D

Results S1 and S2 restored laxity within 2 mm of normal. D did not control laxity above 45 degrees of flexion. Both S1/S2 and S1/D double-bundle reconstructions controlled laxity with both bundles of S1/S2 configuration tight in flexion and the bundles in the S1/D configuration tight in a reciprocal fashion

Race & Amis, Patellar tendon; Y type, 18 Single-bundle 199846 mm graft for double-bundle reconstruction: isometric grafts; single 10-mm graft single bundle, single AL for single bundle bundle; double-bundle reconstruction: anatomic AL and PM bundles

All grafts fixed at 60 degrees of flexion

Isometric single bundle graft overconstrained knee in extension and underconstrained in flexion. AL singlebundle graft lax from 90 to 130 degrees of flexion. Only double-bundle graft restored normal knee laxity

Harner et al, 200045

Increased posterior tibial translation at all flexion angles in single-bundle reconstruction, with in situ forces up to 44 N lower than intact ligament. No difference in posterior translation or in situ forces in double-bundle reconstructions compared with intact knee

10-mm Achilles for AL bundle; 7-8 mm doubled semitendinosus for PM bundle; one or two femoral tunnels, one tibial tunnel

Single-bundle reconstruction: AL bundle; double-bundle reconstruction: anatomic AL and PM bundles

AL graft fixed with 134-N posterior load at 60 degrees of flexion. PM graft fixed at full extension

Bergfeld et al, Half Achilles for AL bundle; 2005158 half Achilles split into Y type graft for double bundle; one or two femoral tunnels, tibial inlay

Single-bundle reconstruction: AL bundle; double-bundle reconstruction: anatomic AL and PM bundles

AL graft fixed with Both the single- and double-bundle 40-N anterior drawer techniques closely reproduced the force at 90 degrees of stability as compared with the intact flexion. For doubleknee. Trend for double-bundle construct bundle reconstruction, to overtighten knee from 30 to 60 AL and PM bundles degrees, and for single-bundle construct tensioned at 90 and to allow more translation between 10 and 30 degrees, respectively 90 degrees

Markolf et al, Y-shaped patellar tendon Single-bundle 2006159 graft; 11-mm AL and 8-mm reconstruction: AL PM bundles bundle; double-bundle reconstruction: PM bundles with wide and narrow bone bridge between the AL and PM bundles

AL graft tensioned at Double-bundle graft with PM tunnel with 90 degrees of flexion to wide bone bridge that is tensioned to restore laxity of intact 10 N best restored knee laxity to that of knee within ±1 mm. the normal knee at the expense of slightly Each different PM increased graft forces bundle tensioned at 30 degrees of flexion with either 10 or 30 N

AL, anterolateral; PM, posteromedial.

the two groups at a minimum of 2 years’ follow-up. An additional study by Nyland and coworkers162 found that, in patients with complete PCL deficiency and grade I and II posterolateral corner instability, a double-bundle PCL reconstruction alone restored knee stability better than a single-bundle reconstruction. In a similar effort to maintain the normal double-bundle anatomy of the PCL, an augmentation procedure can be performed when only one bundle of the PCL is injured. In our experience, this can occur in up to one third of our acute or chronic PCL cases. Often the posteromedial bundle of the PCL remains relatively intact, whereas the anterolateral bundle is torn. In this case, we perform a single-bundle augmentation of the AL bundle. Various techniques of augmentation, typically with retainment of the PM bundle and reconstruction of the AL bundle, have been described elsewhere with good results.163-166 In addition, there is evidence that the retained intact ligament may help avoid graft abrasion at the killer turn in transtibial techniques, and the original fibers and augmented fibers may heal together, forming one ligament.167

Another potential source of laxity is the choice of graft and subsequent fixation. Most of the fixation techniques used for PCL reconstruction were originally developed for ACL reconstruction and were adapted for use in PCL reconstruction.144 Because of the different insertional geometries and size of the two ligaments, biomechanical differences exist between the ACL and PCL,168 and requirements for graft fixation in PCL reconstruction may vary significantly from those of the ACL. There is little in the published literature on the biomechanics of PCL fixation devices.169,170 A recent survey of knee surgeons in the Herodicus Society membership found the Achilles tendon allograft to be the most popular graft choice in both acute and chronic reconstructions.171 The same study found that inference screw fixation was used by nearly 70% of surgeons for femoral fixation, whereas interference screw, screw and post, and other devices were used for tibial fixation.171 A final potential source of laxity is the position of the knee at the time of fixation. Most authors have recommended fixation at 90 degrees of knee flexion with an


applied anterior drawer force applied to the knee.36,47,48 This position reflects the dominant role of the PCL in knee stability at this flexion angle as well as the concern in AL single-bundle reconstructions that tensioning the graft at angles closer to full extension risks overconstraining the knee. Accordingly, 55% of those surveyed in the Herodicus Society tensioned their grafts near 90 degrees of knee flexion.171 Definitive answers to all of the aforementioned questions concerning PCL reconstruction outcomes, however, will likely not be answered conclusively until prospective, randomized biomechanical and clinical trials comparing various techniques are conducted.

Combined Posterior Cruciate Ligament Injuries Although PCL injuries can occur in isolation, an increasing number are being recognized as occurring as part of a combined ligament injury pattern and have been treated operatively.172-175 A common injury pattern, which will be the focus of this section, involves damage to the PCL and the structures of the PLC.175,176 In cases of combined posterior and posterolateral instabilities, laboratory results have shown that isolated reconstruction of the PCL only leads to excessive stresses on the PCL graft with subsequent failure.34,39 Biomechanical and clinical studies have shown that the addition of a PLC reconstruction improves the stability of the knee in the setting of a concurrent PCL reconstruction.42,177,178 Various techniques of both PCL and posterolateral reconstruction exist, as detailed in previous sections of this book. Fanelli and associates44 and Noyes and colleagues103 presented some of the earliest reconstructive results of combined PCL and PLC injuries. Noyes and colleagues103 described a proximal advancement of the LCL and PLC in patients with definitive but lax lateral and posterolateral structures with good results. Fanelli and associates44 treated 21 patients with the use of a biceps tenodesis procedure and concurrent PCL allograft or autograft reconstruction. The results showed improvement in preoperative and postoperative Lysholm and Tegner scores, from 51.8 to 90.9 and 2.2 to 5.1, respectively, at minimal 24-month follow-up. In a larger study of 41 patients with PCL and PLC injuries followed for 2 to 10 years, Fanelli and Edson179 found similarly good results. Using Achilles allograft for the PCL reconstruction and a combination of biceps tenodesis and PLC advancement for the PLC reconstruction, they found postoperative Lysholm and Tegner scores of 91.7 and 4.9, respectively. Reflecting the complex injury pattern and the significant surgical reconstruction required for such injuries, however, other studies have found inferior results.180,181 Khanduja and colleagues180 in a follow-up study of 19 patients with 2 to 9 year followup, found that their Lysholm and Tegner scores increased from 41.2 to 76.5 and 2.6 to 6.4, respectively, from preoperatively to postoperatively. They used mainly Achilles allograft for their PCL reconstruction and a Larson-type tenodesis for their PLC reconstruction. They noted that although knee function significantly improved, patients did not have complete knee stability. Similarly, Wang and associates181 followed 25 patients for an average of

2.3 years. Their technique included various allografts for the PCL and the use of iliotibial and biceps tenodesis reconstructions of the popliteus tendon and popliteofibular ligament with or without LCL advancement. They noted 68% satisfactory and 32% unsatisfactory results using the Lysholm scores. Complete restoration of ligament stability was observed in 44% of knees.

Weighing the Evidence Despite some inconsistencies in the literature, most surgeons agree that the treatment of peel-off injuries of the PCL should consist of acute primary repair. Direct repair or reconstruction is also the preferred technique of most orthopaedic surgeons for the treatment of combined PCL injuries (particularly PCL-PLC and PCL-ACL-PLC). In such multiligamentous injury cases, reconstructions are typically done using AL single-bundle reconstruction techniques. Isolated injuries continue to generate a fair amount of debate. However, most surgeons treat isolated, acute grade I and II injuries conservatively with limited activities with or without extension bracing for 4 to 6 weeks, followed by muscle (particularly quadriceps) strengthening. Additionally, many surgeons now recommend conservative treatment of acute, isolated grade III PCL injuries that consists of 4 weeks of full-time extension bracing to prevent posterior tibial subluxation and allow healing of the PCL. However, because operative techniques have advanced, some surgeons may elect to proceed with primary reconstruction of the PCL. This is particularly true in the young or athletic patient. Multiple viable options exist concerning specific graft choices, fixation techniques, and inlay versus transtibial graft placement. With the available literature, there is no clear consensus on these topics. Currently, more reconstructions are done using single-bundle PCL reconstruction techniques, although evidence suggesting superior biomechanical results with double-bundle reconstruction may favor this technique in the future. More clinical studies of double-bundle PCL reconstruction and, more specifically, randomized trials comparing single- versus double-bundle PCL reconstruction are needed. For chronic PCL injuries, clear treatment recommendations are lacking. Most surgeons would elect to treat chronic grade I and II PCL injuries with conservative treatment consisting of quadriceps strengthening and activity modification. In patients who fail such conservative treatment and demonstrate minimal to no chondral damage, PCL reconstruction using either single- or double-bundle techniques is generally recommended. In chronic cases with varus knee alignment and chondral damage in the medial and patellofemoral compartments, interest is gaining in biplanar tibial osteotomies. Biplanar osteotomies in these patients convert the varus knee into neutral or slight valgus alignment while increasing the tibial slope to help reduce the chronic posterior tibial sag. For chronic multiligamentous injuries, surgery to reconstruct the PCL is generally recommended. In such cases, the magnitude of the injury and any previous surgeries often makes stiffness a bigger issue. In such cases, the need for concomitant ACL or collateral reconstruction, or both, needs to be assessed on a case-by-case basis.

knee 1701

Authors’ Preferred Method The treatment algorithm for PCL injuries is multifactorial and steadily evolving. Treatment must be tailored to specific characteristics of the patient and injury. Although the timing, grade, location, and extent of associated injuries are important prognostic factors that must be considered, the patient’s age, occupation, comorbidities, and expectations regarding return to play are equally important in the decision-making process. Algorithms have been developed to aid the physician in treating these difficult problems, but it is important to consider the specific characteristics of each patient before pursuing a specific treatment (Figs. 23E1-16 and 23E1-17). Isolated injuries, in general, may be treated nonoperatively with an excellent prognosis.65,67,73,82,83,87,121,182 Combined injuries have a more guarded prognosis. Better results are possible in this group with early surgical intervention rather than with conservative treatment.36,80,86,92 Isolated Acute Posterior Cruciate Ligament Injury

Like most surgeons, we believe that acute, isolated grade I and grade II PCL injuries usually do not require surgical intervention.65,67,73,82,83,87,121 The outcome of these injuries is most likely related to the remaining integrity of the PCL (single-bundle injury), other secondary restraints (meniscofemoral ligaments), and the intrinsic healing capabilities of the PCL. Partial injuries of the PCL are more likely to heal than the ACL owing to its large size and better blood supply.36,121 For any PCL injury, the specific injury pattern of the PCL should be identified, which includes isolated AL

or PM bundle injuries versus both bundle injuries as well as damage to the meniscofemoral ligaments. With grade I and grade II injuries, the PLC structures are usually intact, and the tibia does not significantly sag at any knee flexion angle. The natural posterior slope of the tibia is protective at preventing further posterior subluxation. The initial treatment is focused on maintaining reduction of the tibia on the femur with intermittent extension bracing for 2 to 4 weeks. We protect their weight-bearing, advance range of motion as tolerated, and focus on quadriceps strengthening. In our experience, most patients are able to return to sports within 2 to 6 weeks after the injury. In acute grade III injuries, the rehabilitative course is not as predictable and frequently requires a longer time. This has pushed our focus to more early surgical interventions in younger athletic patients. A high index of suspicion is necessary to rule out any significant associated PLC or posteromedial side injuries. We recommend 2 to 4 weeks of immobilization in full extension. This will minimize the posterior-displacing effect of both gravity and the hamstrings on the tibia and will allow minor PLC injuries, if present, to heal with less stress.183,184 After the period of immobilization, the mainstay of rehabilitation is quadriceps strengthening to counteract posterior tibial subluxation.183,185,186 Quadriceps sets, straight leg raises, mini flexion squats, and partial weight-bearing with crutches are initiated as measures to help reduce the tibia on the femur.4,36,65,67,68,102,121,122,187-192 About 1 month after the injury, motion exercises are started, and weight-bearing is progressed. Functional exercises follow, such as biking and stair climbing as well as leg presses and knee extensions. After

Acute PCL Injury

“Combined” • PLC (+/- LCL) • MCL and medial side injury • ACL (+/- collaterals) (knee dislocation)

“Isolated”

Grade I or II

III

Nonoperative • quadriceps therapy • 2-4 week extension immobilization • gradual return to activity

Is patient young, athletic or avulsion injury?

No

Nonoperative • 4 weeks of full extension • Avoid posterior tibial subluxation • quadriceps therapy • limited activity

Operative • Surgery peformed < 2 weeks, acute repair of collateral injuries • Single bundle reconstruction for dislocated knee • Single bundle augmentation for grade II PCL

Yes Operative • ORIF avulsion • Single bundle augmentation • Possible, double-bundle reconstruction

Figure 23E1-16 Treatment algorithm for acute injuries of the posterior cruciate ligament (PCL). ACL, anterior cruciate ligament; LCL, lateral collateral ligament; MCL, medial collateral ligament; ORIF, open reduction, internal fixation. Continued


Authors’ Preferred Method— �c �� o n t ’� d � Chronic PCL Injury

“Combined” • PLC (+/- LCL) • MCL and medial side injury • ACL (+/- collaterals) (knee dislocation)

“Isolated”

Grade I or II

III Malalignment?

Nonoperative • quadriceps therapy • activity modification

Symptomatic pain or instability? Yes

No Nonoperative • quadriceps therapy • activity modification Operative • Double-bundle reconstruction • Occasionally, singlebundle augmentation

Yes

No

Malalignment? No

Yes

Operative • Biplanar osteotomy • Staged reconstructions for combined injuries

Operative • Reconstruct all injured components, especially PLC • Double-bundle reconstruction • Single-bundle augmentation if Grade II PCL

Figure 23E1-17 Treatment algorithm for chronic injuries of the posterior cruciate ligament (PCL). ACL, anterior cruciate ligament; LCL, lateral collateral ligament; MCL, medial collateral ligament.

grade III injuries, it takes up to 3 months before the athlete is able to return to sport. PCL functional braces may be used but have not been effective in our experience. Unfortunately, some patients do not respond to nonoperative therapy. These athletes become increasingly symptomatic and are unable to return to sport without some type of surgical intervention. Because of the failure of nonoperative treatment, we are more inclined to operate on young, athletic patients with acute isolated grade III PCL injuries.73,82,120 A PCL avulsion injury is a unique isolated PCL injury with its own treatment algorithm. Although most PCL injuries requiring surgical treatment are best suited for reconstruction versus repair, PCL avulsion injuries are best treated with primary repair typically resulting in favorable outcome.74,104,130-132,193 PCL avulsion most commonly occurs on the femoral side of the ligament, but it can also occur on the tibial side, where it is usually associated with a large bone fragment. One must be careful in this setting because of the potential for postoperative stiffness. With these types of injuries, we have found that it is best to delay surgery for 1 to 2 weeks to allow swelling to resolve and to keep the knee immobilized in full extension. The femoral and tibial avulsions are approached through an anteromedial arthrotomy and a standard or modified posterior knee approach, respectively.194 They can then be fixed with either screws or sutures through drill holes, depending on the presence and size of the bone fragment.37,45,111,195,196 Likewise, if

an avulsion injury to the ACL is also present, it is treated in a similar fashion.196,197 Isolated Chronic Posterior Cruciate Ligament Injury

Most chronic, isolated grade I and grade II tears will similarly respond well to physical therapy. On occasion, some grade II injuries will develop persistent symptoms of intermittent swelling and pain. In these situations, we find it helpful to proceed with both radiographic and scintigraphic evaluation of the joint to assess the status of the joint compartments. If the studies, most notably the bone scan, are consistent with significant medial uptake with osseous malalignment, we recommend an osteotomy. Reconstructions in these settings are usually avoided because current techniques have not been consistent in restoring the knee to normal function.89,158,151-155,198-200 In our experience, patients with isolated, chronic, grade III deficiencies have a mixed postinjury course. Reconstruction is recommended for all patients who become symptomatic despite maximizing physical therapy intervention, especially if the compartments of the knee are still well preserved. In these cases, current surgical techniques can potentially provide enough stability to diminish the persistent posterior instability or pain from the medial or patellofemoral compartment. In our opinion, patients with persistent

knee 1703

Authors’ Preferred Method— �c �� o n t ’� d � symptoms after adequate therapy for an isolated grade III PCL injury are likely to have occult concomitant ligamentous injury, particularly involving the PLC.12,41,81,95,201,202 Depending on the severity, this particular combination of injuries can lead to disability ranging from minimal functional alterations to profound limitations in daily activities.16,80,203-207 We therefore recommend a PLC reconstruction in conjunction with the PCL reconstruction. When a coexistent PLC injury is overlooked, surgical treatment of the PCL may have a higher risk for failure.40,41 In addition, for chronic injuries, it is essential to assess the entire limb for asymmetric varus alignment and, even more important, the presence of a dynamic varus thrust with gait.81,92,208-212 Soft tissue reconstructions alone for ligamentous deficiencies with malalignment will more likely fail over time.102,208,213 Although there are no long-term studies documenting its effectiveness, many authors believe the single most reliable procedure for correcting varus malalignment is a high tibial osteotomy.102,208,213 Corrections can also be biplanar to manipulate and accentuate the native posterior slope in the PCL-deficient knee.189,214,215 Another emerging subset of PCL-injured patients includes those with chronic PCL injuries and associated medial compartment arthrosis. As detailed earlier, patients with chronic PCL injuries often have chronically subluxated tibias, which effectively unloads the medial meniscus and functionally results in a postmeniscectomy knee.36,216 Often these patients have early articular cartilage wear (despite an intact meniscus) and have begun to drift into varus alignment with or without an associated PLC deficiency. These patients often complain more of pain in the medial and patellofemoral compartments than instability symptoms. Their PLC injuries may have been diagnosed and treated conservatively, or overlooked because the patient was able to cope adequately with their PCL insufficiency. It is often with activities that these patients will experience their worst symptoms of pain and knee swelling. Patients with early to moderate medial and patellofemoral arthrosis typically do not respond well to isolated PCL reconstruction. During the past 5 years, we have begun addressing this problem by correcting the alignment of the knee that contributes to the pathology. We have used a biplanar osteotomy to reduce contact forces in the medial compartment by decreasing varus and increasing the posterior slope of the tibia. Radiographic studies have previously reported the relationship between tibial slope and tibial translation.217 Several investigators have noted a similar concept for ACL with varus.218,219 In those cases, the posterior tibial slope is decreased with a combined osteotomy and ACL reconstruction. Cadaveric studies have demonstrated that increasing posterior tibial slope shifts the resting position of the tibia anteriorly, thereby offsetting posterior tibial sag associated with PCL deficiency.189,215,220 In a similar fashion, a slight correction into valgus will help correct any associated varus or PLC deficiency. Such anteromedial opening wedge high tibial osteotomies have been described for the treatment of the PCL-deficient knee.221

Combined Posterior Cruciate Ligament Injury

Most patients with combined injuries benefit from surgery.58,81,85-87,91,206,222-224 These patients are at high risk for persistent and progressive functional instability, and surgical treatment has given a more predictable outcome. Early and accurate diagnoses of all concomitant ligamentous injuries is essential. Numerous injury patterns exist, most commonly, PCL injury with an associated PLC injury. It is important to differentiate PLC injuries that include the LCL from those that do not include the LCL. Other common injury patterns include PCL injuries with concomitant PLC and ACL injuries. These injuries fall under knee dislocations. The appropriate vascular work-up is essential before any reconstructive procedure. Finally, the least common pattern is PCL injury with an MCL or posteromedial injury. In this acute setting, we recommend combined PCL reconstruction and simultaneous repair or reconstruction of all associated, complete ligamentous injuries followed by early motion. If peripheral meniscal tears, capsular avulsions, and ostechondral injuries are encountered, they are also repaired primarily. This treatment approach subjects the patient to fewer operations, decreases concern for late instability, and limits the possibility of postoperative stiffness. Combined PCL and PLC injury is one of the most complex treatment problems encountered in the management of knee ligament injuries. When both the PCL and PLC are ruptured, substantial posterior translation, external rotation, and varus opening can be present at differing angles of knee flexion.81 This combination creates a complex surgical dilemma.100 With several patterns of injury possible, it is difficult to have one surgical plan. It is essential that this injury be appropriately identified because if it is mistaken for an isolated PCL injury and treated nonsurgically, posterior and posterolateral instability will invariably persist.36,37,41,47,58,59,225 Treatment of the acute PLC injury is generally more successful than that of the chronic injury; therefore, acute surgical intervention is recommended for combined PCL and PLC injury.36,63,81,86,88,91,95,187,202,205,206 The timing for surgical treatment of the injured PLC is critical; acute repairs consistently give more favorable results than does reconstruction of chronic injuries.63,81,88,95,187,202,208 Primary repair has also met with better results if undertaken within the first 2 weeks.84,92 Primary repairs are best done for avulsion injuries. Although midsubstance repairs of the LCL can be performed, we tend to supplement the repair of intrasubstance tears with a graft reconstruction. This is done because of less consistent healing of the LCL as well as the limited success in treating chronic insufficiency of the LCL if it were to occur. Attempts at surgical repair beyond the acute time frame (3 to 4 weeks) are frequently disappointing both in localizing discrete anatomic structures and in finding any sturdy tissue to repair. Accordingly, surgical options for chronic injuries are reconstructions rather than repairs. Many reconstructive techniques have been described, but none has consistently shown better results than acute repair. Continued


Authors’ Preferred Method— �c �� o n t ’� d � The treatment of chronic, combined injuries differs from that of the acute disruptions. Beyond 2 weeks from injury, pericapsular scarring becomes significant, and primary repairs are not possible, particularly for the collateral ligaments and avulsion injuries of the cruciates. This occurrence typically commits the surgeon to waiting up to 3 months to allow completion of the healing response before effective treatment can be implemented. In addition, these chronic injuries may become associated with significant capsular stretching, leading to a more extensive rotational instability pattern, persistent subluxation, or the development of arthrosis. This could cause substantial difficulty in determining the extent of the injury as well as the optimal treatment plan. Surgical intervention for these injuries in the chronic setting requires simultaneous reconstruction of the PCL and PLC. As with any chronic grade III PCL injuries, the limb must be assessed for malalignment and a varus thrust gait. Any PCL and PLC reconstruction in this setting will have a significant risk for failure because of chronic repetitive stretching of the reconstruction with time.81,205,207,226 If there is significant deformity, a high tibial biplanar osteotomy may be performed in conjunction with PLC reconstruction, although we favor performing a staged operation because the osteotomy alone may alleviate the patient’s symptoms, avoiding further surgical intervention.92,95 Unlike the PLC, the medial side traditionally has a greater opportunity to heal conservatively. However, in the PCLdeficient knee, we have a low threshold to surgically address the medial side if significant instability exists. Avulsions or intrasubstance tears of the medial collateral ligament may be directly repaired and are best performed acutely when the quality of tissue is robust.227-231 Usually, significant (grade III) medial-sided injuries can be localized to the femoral or tibial sides with the use of radiographic imaging. These can be treated with a posterior oblique ligament advancement or on rare occasion graft reconstruction.229,230,232-235 The specific technical details for the repair or reconstruction of complex, combined injuries are beyond the scope of this chapter. Instead, we focus our discussion mainly on the reconstruction of the PCL, including single-bundle, double-bundle, and augmentation techniques. We also discuss the treatment of associated PLC injuries because they are the most commonly disrupted structures in combined PCL injuries.12,41,44,59,80,81,88,91,92,95,96,103,206 We have also found them to be injured to varying degrees in most chronic PCL injuries. Rationale

Our surgical approach is dictated by identifying all the injured structures and surgically addressing each structure based on our understanding of the basic science, insertional anatomy, and the patient’s characteristics or preferences. To ensure optimal surgical outcome, the surgeon must be familiar with and capable of performing a repair, reconstruction, or augmentation of the PCL and any other associated cruciate, collateral, and capsular structures. For any PCL injury, specific injury patterns including the AL bundle or PM bundle, or

both, must be recognized. This is typically determined by the information obtained from the preoperative examination, the imaging studies, the examination under anesthesia (EUA) and finally arthroscopic evaluation. The EUA is most valuable because it determines the grade of PCL injury and identifies other potentially injured ligamentous structures. Surgery in these cases should be performed in a semielective setting with a skilled operating room staff. In addition, because of the proximity of the vessels to the tibial PCL graft placement, a vascular surgeon should be immediately available. Current reconstructive options include arthroscopic single-bundle or double-bundle techniques as well as arthroscopic and open tibial inlay procedures.36,63,88,187,188,208,236 Various combination of these techniques have also been employed. Most recently, we have begun augmentation procedures, in which we attempt to preserve any intact PCL structures and augment only damaged tissue. We believe, however, that none of these options can effectively reproduce all the components of the PCL complex. The single-bundle technique was developed to reconstruct the anterolateral bundle because of its larger size and greater biomechanical properties.4,6,7,33,46,48,50,205,237 In an attempt to place the graft in the anatomic position of the native anterolateral bundle, a single tibial and femoral tunnel is used. We occasionally use this technique in performing acute PCL reconstructions, especially if it is part of a combined injury pattern.196 Because biomechanical data suggest that the addition of a second bundle significantly decreases posterior tibial translation, the double-bundle technique has become our preferred procedure over the traditional single-bundle technique.45,46,238-240 Although the tibial inlay procedure is favored by some surgeons, we think this approach is technically demanding and requires a prone or lateral decubitus position, adding operative time and becoming particularly burdensome in attempting repair of a combined ligament injury.149,208 At this time, tibial fixation variation has not been shown to affect the behavior of the graft significantly, and so the theoretical benefits may not outweigh the technical demands of this technique.149,152-155,241,242 A variety of tissues and fixation devices have been used for reconstruction. As with the ACL, we feel that proper placement is more critical than graft type or fixation technique. Autologous tissues typically used today include ipsilateral or contralateral bone–patellar tendon–bone, hamstring, iliotibial band, and central quadriceps tendon grafts. Bone– patellar tendon–bone, Achilles tendon, and soft tissue (anterior tibialis) are the most commonly used allograft tissues. We now favor soft tissue tendon anterior tibialis allograft because of its high tensile strength, ease of passage and fixation, and lack of donor site morbidity. Additional benefits of this graft include its exceptional size and length, making it versatile compared with other graft options. Multiple methods of fixation exist, including EndoButton, (Smith & Nephew Endoscopy, Andover, Mass), cortical screws and washers, and staples. No single technique is universally accepted. The treating surgeon should be familiar with several of these options so that the final choice can depend on the surgical situation.

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Authors’ Preferred Method— �c �� o n t ’� d � The rationale for our present techniques is based on the anatomy and biomechanics of the PCL. Not all PCL injuries are the same. Different injury patterns will dictate different techniques. As stated earlier, EUA, MRI, and arthroscopic findings, combined with individual patient characteristics, are all critical for a successful reconstruction. Currently, we use three different arthroscopic transtibial techniques, which are all variations based on PCL insertion site anatomy. Our indications for AL single-bundle reconstruction is an acutely injured knee or a multiligamentous knee. The indications for augmentation are evolving but include mostly acute but some chronic cases, in which there is preservation of function in one of the remaining bundles of PCL. Finally, our indications for double-bundle reconstructions are chronic grade III with either PLC or PM-sided injuries, revision, and rarely acute injuries. Stated another way, for most acute injuries, a singlebundle (AL) reconstruction or augmentation is performed (see Fig. 23E1-16). For chronic injuries, either a singlebundle augmentation or a double-bundle reconstruction with or without collateral surgery is performed. If there is significant malalignment, an opening wedge biplanar high tibial osteotomy is performed (see Fig. 23E1-17). Operative Technique: Single-Bundle Reconstruction, Single-Bundle Augmentation, and Double-Bundle Reconstruction

When performing PCL surgery, our patient is positioned supine in 90 degrees of flexion without use of a tourniquet. A detailed examination under anesthesia is performed first. After an EUA is performed and the imaging and office notes reviewed, standard arthroscopic assessment of the knee joint is performed to confirm the extent of the injury and to assist with the repair or reconstructive procedure whenever possible. If the operation is performed in the acute setting, the potential for fluid extravasation should be carefully considered. In this case, we recommend using gravity flow rather than a fluid pump, and the surgeon should frequently assess the calf pressure. If increased calf pressure is noted during the case, the arthroscopic procedure should be immediately abandoned. If warranted, we have a low threshold to extend any of our lateral tibial incisions and perform a fasciotomy of any involved compartments in the leg. First, our attention is turned to the ACL and the tibiofemoral compartments to assess any secondary signs of associated injury patterns. Only after this is done is our attention turned to the PCL and its injury pattern. After confirmation of the PCL injury pattern, a decision is made if an augmentation procedure is possible, remembering that tissue may appear normal but can have significant interstitial injury. MRI data can also be helpful in making this decision. Once the exact procedure is determined, the remnants of the PCL insertions are débrided with the use of a posteromedial as well as standard anterior portals. A 70-degree scope is critical to accurately view the tibial insertion, and care must be taken to avoid injury to the closely situated neurovascular structures. A tibial tunnel is then created from the anteromedial tibia and directed posteriorly to the native PCL tibial attachment (Fig. 23E1-18). The correct position is critical

and should be checked with intraoperative radiographs after the guidewire is placed. If a single-bundle or augmentation procedure is performed, care is taken to place the single guidewire in the appropriate insertion site. If a double-bundle reconstruction is performed, two guidewires are placed and confirmed radiographically, with the AL guidewire being more lateral and distal and with the PM guidewire more medial and proximal (Fig. 23E1-19). The starting point for the two tibial tunnels can either be divergent (one medial, one lateral) or stacked (Fig. 23E1-20). We use both fluo roscopy and arthroscopic guidance to drill the tibial tunnels, and we usually start with power and finish by hand. After the tibial tunnels are completed, attention is focused on creating the femoral tunnels. The lateral portal is enlarged, and the knee is hyperflexed to drill the femoral tunnel (Fig. 23E1-21). The femoral insertion site anatomy is identified, and the appropriate tunnel is marked for a single-bundle reconstruction, singlebundle augmentation, or double-bundle reconstruction. If an augmentation procedure is being performed, care is taken to preserve any remaining functional PCL tissue. Most commonly, the PM and MFLs are preserved and augmented with a single-bundle AL reconstruction (Fig. 23E1-22). We most commonly use anterior tibialis allograft tendons. This tissue is looped over a 40-50 Endoloop (EndoButton may or may not be removed depending on fixation) to make a two-stranded construct with whipstitches in both free ends with 2 nonabsorbable suture. These grafts are then passed anterograde through the tibial tunnel and subsequently retrograde into the femur. One or two grafts are used depending on whether an augmentation, single-bundle reconstruction, or double-bundle reconstruction is being performed. The grafts are first fixed on the femoral side with either EndoButtons or posts through an Endoloop and then cycled repeatedly. Depending on the reconstruction, the anterolateral bundle is tensioned at 90 degrees and then fixed with a

Figure 23E1-18 Posterior cruciate ligament tibial guidewire placement and drilling. (Adapted from Miller MD, Harner CD, Koshiwaguchi S: Acute posterior cruciate ligament injuries. In Fu FH, Harner CD, Vince KG [eds]: Knee Surgery, vol 1. Baltimore, Williams & Wilkins, 1994.) Continued


Authors’ Preferred Method— �c �� o n t ’� d �

AL PM

PM AL

Figure 23E1-21 External view of femoral drilling with camera in medial portal and drill in lateral portal with the knee hyperflexed.

Posterior Cruciate Ligament and Posterolateral Corner: Acute and Chronic Figure 23E1-19 The ideal femoral and tibial tunnel positions for a double-bundle posterior cruciate ligament reconstruction. AL, anterolateral bundle; PM, posteromedial bundle.

post and a washer on the tibia, and the posteromedial bundle is tensioned at 30 degrees of flexion and secured in a similar fashion over a post (Fig. 23E1-23). If additional collateral or meniscal surgery is being performed, tibial fixation is withheld until these procedures are done.

Figure 23E1-20 A double-bundle posterior cruciate ligament reconstruction with one stacked tibial tunnel.

The treatment of combined acute PCL and PLC injuries is centered on recognizing the injury pattern, as well as its extent and grade. This is followed by immediate, direct anatomic repair of all PLC ligamentous injuries, preferably within the first 2 weeks. Depending on the quality of the tissue or type of injury, repair or reconstructive techniques may be used. First, attention is turned to the PCL reconstruction. If there is functional PCL tissue remaining and the injury grade is only grade II, we favor an augmentation technique. In most cases, however, we perform doublebundle reconstructions because these are commonly grade III injuries. Double-bundle reconstructions begin with proper identification of the AL and PM tibial insertion sites. After the tibial tunnels have been completed, attention turns to the femoral tunnel insertion sites. They are marked with an awl, and then guidewires are placed through the anterolateral portals and are drilled and dilated with the knee in hyperflexion (Fig. 23E1-24). As with single-bundle reconstructions, soft tissue anterior tibialis allograft tendons are looped over a 40-50 Endoloop, making a two-stranded construct with whipstitches in both free ends. For double-bundle reconstructions, two grafts are then passed anterograde through the tibial tunnel and subsequently retrograde into the femur. Our preferred graft is an anterior tibialis allograft, but if an Achilles tendon allograft is used, it is used for the anterolateral tunnel while an anterior tibialis tendon is used for the posteromedial tunnel (Fig. 23E1-25). The grafts are first fixed on the femoral side with either EndoButtons or posts through an Endoloop and then cycled repeatedly. Final tibial fixation is deferred until the PLC is addressed.

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B

A

Figure 23E1-22 Positioning of femoral tunnels for anterolateral (AL) bundle augmentation. A, Injury to the AL bundle with an intact posteromedial bundle (PM) bundle and meniscofemoral ligaments. B, AL bundle reconstruction with tibialis anterior allograft and preservation of intact PM bundle.

Our approach to PLC begins with a lateral “hockey-stick” incision paralleling the posterior edge of the iliotibial band, which is then split, exposing the deep structures of the LCL anteriorly and the lateral head of the gastrocnemius muscle and underlying popliteus complex more posteriorly. Special

A

attention is given to identifying the injured structures. When the posterolateral structures, including the LCL, are avulsed off their femoral attachments with preservation of the popliteus tendon, direct repair of these structures by internal fixation, or suture anchors is recommended. On

B

Figure 23E1-23 Radiographs after single bundle anterolateral augmentation. A, Anteroposterior radiograph. B, Lateral radiograph. Continued



A

B

Figure 23E1-24 Positioning of femoral tunnels for double-bundle reconstruction. A, Femoral tunnel position for anterolateral and posteromedial bundles. Note that the anterolateral bundle is more anterior. B, Double-bundle reconstruction with tibialis anterior allografts.

ccasion, there is interstitial tearing of the LCL, mandato ing concomitant reconstruction (Fig. 23E1-26).243,244 For this, either bone–patellar tendon–bone or Achilles tendon allograft is used. The LCL can be detached and elevated from its distal insertion, and the allograft bone block is then fixed vertically into the fibular head by interference screw fixation distally, respecting the proper insertional anatomy. Fluoroscopic guidance is used to properly position this tunnel.10 A blind femoral tunnel is then made, and the Achilles tendon allograft is tensioned proximally over a post, interference screw, or suture anchors. The native LCL can

then be tensioned both proximal and distal to the graft and then directly sutured to the midsubstance of the Achilles allograft to reinforce the reconstruction. The extent of injury to the popliteus and, more important, its attachments to the fibula through the popliteofibular ligament must then be visualized. The popliteofibular ligament is now recognized as a significant component of the popliteus complex, particularly as a static stabilizer.14,95 We, therefore, believe that this step is the most crucial to the overall success or failure of the procedure. When this tendon is avulsed off its tibial or femoral insertion, appropriate

1

2

1 2

A

B

Figure 23E1-25 Graft placement. A, The tibialis anterior or Achilles tendon allograft for the anterolateral bundle (inset, 1) and a second tibialis anterior for the posteromedial bundle (inset, 2) are passed in anterograde fashion through the tibial tunnel. B, Grafts are then fixed to corresponding femoral tunnels. (Adapted From Petrie RS, Harner CD: Double bundle posterior cruciate ligament reconstruction technique: University of Pittsburgh approach. Op Tech Sports Med 7:118-126, 1999.)

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A

B

Figure 23E1-26 Lateral collateral ligament (LCL) reconstruction with bone–patellar tendon–bone or Achilles tendon allograft. A, The torn or stretched LCL is elevated from its fibular insertion, and the allograft is fixed in a tunnel in the proximal fibula using an interference screw. The tensioned graft is then fixed to the lateral epicondyle using multiple suture anchors or with a post on the medial side. B, The native LCL is tensioned and sutured to the graft. (Adapted from Cole BJ, Harner CD: The multiple ligament injured knee. Clin Sports Med 18:241-262, 1999.)

tension with anatomic restoration of the popliteofibular ligament is possible. The popliteus can be easily repaired with internal fixation, suture anchors, or a blind tunnel to its femoral insertion. The popliteofibular ligament can be repaired to its fibular attachments with similar fixation. Tension is applied with the knee in 20 to 30 degrees of flexion during the final fixation. If the popliteus tendon tissue cannot be repaired by this approach, reconstruction is indicated as with a chronic injury. Final PCL tibial fixation is then performed. The reconstructed anterolateral bundle is tensioned at 90 degrees and then fixed with a post and a washer on the tibia. Subsequently, the posteromedial bundle is tensioned at 30 degrees of flexion and then secured in a similar fashion over a post (Fig. 23E1-27). Chronic cases of posterolateral instability demonstrate tissue redundancy and excessive scarring posterior to the LCL, and identification of the particular structures of the popliteus complex is difficult. Many techniques have been recommended, including arcuate ligament advancement, biceps tenodesis, and popliteofibular ligament reconstruction with allograft or autograft tissue, but no consensus exists on which is the best procedure.11,86,100,103,203,245,246 In this situation, we currently recommend anatomic reconstruction of the popliteofibular ligament and, if necessary, the LCL. The PCL is reconstructed using a double-bundle technique and then attention is then focused on the reconstruction of the PLC. With use of the same approach to the lateral knee, the LCL is identified; if it is part of the injury pattern, it is reconstructed as described previously. If the LCL is intact, our attention turns to the PFL. A PFL reconstruction is then performed with anterior tibialis allograft with either

soft tissue fixation around the biceps tendon or more rigid fixation with a second fibular tunnel. An oblique anteriorto-posterior tunnel oriented similarly to the course of the ligament is then created in the proximal fibula. A proximal, blind femoral tunnel is then created at the anatomic insertion site of the popliteus tendon anterior to the femoral epicondyle in its anatomic “saddle.” The popliteus is mobilized and then advanced with a prepared anterior tibialis allograft into the blind femoral tunnel. The anterior tibialis graft is then passed under the iliotibial band and LCL into the proximal, posterior fibular tunnel opening and out the distal, anterior opening. The knee is then placed in 30 degrees of flexion, in which final posterolateral stabilization is performed. Fixation at the femoral side is stabilized over a post or button tied over the medial cortex through a separate skin incision. The knee is maintained in 20 to 30 degrees of flexion with neutral to slight internal rotation of the foot as the graft is tensioned and secured in the fibular tunnel with an interference screw and the remaining portion of the graft is sutured to the iliotibial band. This is then followed by final PCL tibial fixation as described previously (Fig. 23E1-28). Postoperatively, the patients follow PLC protocol modification of the PCL reconstruction protocol. Immediately after the operation, the injured limb is placed in a wellpadded hinged knee brace locked in extension. This should be performed with care to avoid any posterior translation of the tibia while it is applied. Immobilization in extension enables the knee joint to remain reduced and minimizes the effects of gravity and hamstring forces that create posterior tibial sag, thus allowing the collateral ligament repair or reconstruction a chance to heal.36,247,248 Continued



A

B

Figure 23E1-27 Radiographs after double-bundle posterior cruciate ligament (PCL) reconstruction with repair of femoralsided PLC. A, Anteroposterior radiograph. B, Lateral radiograph.

A

B

Figure 23E1-28 Radiographs after double-bundle posterior cruciate ligament (PCL) reconstruction with popliteofibular ligament reconstruction for chronic grade III PCL and posterolateral corner. A, Anteroposterior radiograph. B, Lateral radiograph.

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POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Postoperative Prescription The PCL rehabilitation protocol is, in general, slower than that for isolated ACL reconstruction. Reconstructions of PCL and PLC combined injuries are progressed even slower with crutch use continued for 12 versus 8 weeks to allow the lateral soft tissue repair or reconstruction to heal without undue tension. Our postoperative PCL rehabilitation program is broken down into four phases: (1) 0 to 4 weeks, (2) 1 to 3 months, (3) 3 to 9 months, and (4) 9 to 12 months.36,88 Supervised physical therapy takes place for about 3 to 5 months after surgery.

Phase 1 A hinged knee brace is maintained in full extension for the first postoperative week and is then unlocked for range of motion exercises. These exercises are performed with the assistance of a physical therapist who applies an anterior drawer force to the proximal tibia as the patient flexes the knee. The anterior force is important in preventing posterior tibial sag. During this time, the patient is allowed to bear weight as tolerated on the limb with the brace locked in full extension. Crutches should be used for ambulation during the first 6 to 8 weeks. For combined PCL and PLC reconstruction, the brace is locked in full extension at all times for a total of 4 weeks, and crutches are required for 12 weeks. Quadriceps exercises are the mainstay of rehabilitation and are begun in the form of quadriceps sets and straight leg raises starting the first postoperative day. Therapeutic exercises include wall slides (0 to 45 degrees), which are closed chain to take advantage of native sagittal slope of the tibia and its tendency to keep the tibia anterior.189 Active hamstring exercises are avoided because of the potential for the muscles to subluxate the tibia posteriorly and stress the reconstruction. Range of motion is gradually increased but not to exceed 90 degrees during this phase.

Phase 2 This phase begins 4 weeks after surgery and lasts 8 weeks. The goals are to allow the healing of the soft tissue reconstruction to bone, which takes 6 to 8 weeks, and the return of normal motion and gait. The brace is unlocked between 4 and 6 weeks after surgery for controlled gait training only. It is then unlocked for all activities during the 6- to 8-week period. Crutches and the brace are removed after 8 weeks if the patient exhibits good quadriceps strength and control, full knee extension, knee flexion of 90 to 100 degrees, and normal gait pattern. If the PLC was also reconstructed, the brace and crutches are continued for a total of 12 weeks after surgery. At 4 weeks, therapeutic exercises still include wall slides (0 to 45 degrees), which are gradually progressed to mini squats. At 8 weeks, a stationary bike is added with the heel forward on the pedal and the seat slightly higher than normal. Pool therapy is

also begun focusing on normal heel-to-toe gait pattern pool. Finally, balance and proprioception exercises such as single leg stances are introduced.

Phase 3 Phase 3 extends from 3 to 9 months after surgery. The patient is expected to achieve full pain-free range of motion, normal gait, and good quadriceps strength and should have no patellofemoral complaints. Obtaining the last 10 to 15 degrees of flexion may take up to 5 months. Exercises are advanced to jogging in the pool and walking on the treadmill. Closed chain kinetic exercises are continued throughout this period to improve functional strength and proprioception. Quadriceps strength and hamstring flexibility need to be maximized and maintained.

Phase 4 This period extends from about 9 to 12 months after surgery. The goal during this time is the gradual return to work and athletic participation as well as the maintenance of strength and endurance. This may involve sports-specific training, work hardening, or job restructuring as needed. Education is essential to provide the patient with a clear understanding of the possible limitations. Therapeutic exercises include cross-country ski machines, slide board, running and cutting skills, and jumping and plyometrics.

Outcomes Measurements There has been a growing interest in patient-orientated outcomes and evidence-based medicine (EBM). EBM is the conscientious, explicit, and judicious use of the current best evidence in making decisions about the care of the individual patient.249 The World Health Organization released the International Classification of Function, a model of functioning that provided a framework for identifying meaningful clinical outcomes.250 This has led to the International Knee Documentation Committee (IKDC) and the American Orthopedic Society for Sports Medicine to develop the IKDC Subjective Knee Form, a kneespecific health-related quality-of-life instrument that is appropriate for measuring symptoms, function, and sports activity for individuals with a variety of knee conditions, including ligamentous and meniscal injuries, patellofemoral pain, articular cartilage lesions, and arthritis.251 This instrument has been demonstrated to be reliable, valid, and responsive.252-254 This instrument is a common currency form and does not differentiate by age or sex. Recently, a Cochrane Collaboration of Systematic Reviews of 2005 did a meta-analysis of all randomized and quasi-randomized clinical papers on PCL treatment.255 Although 286 studies were found, none fit the inclusion criteria for randomized controlled studies. The study found only numerous relevant observational studies. It concluded that the lack of randomized controlled trials reflects the relative infrequency of these injuries and possibly the absence of a culture to perform multicenter randomized controlled trials. The study also concluded, based on observational data, that isolated PCL injuries may be treated conservatively with a good prognosis, and PCL


injuries with other multiligament injuries are more likely to be treated surgically but have a more guarded prognosis because these are more extensive injuries.

Potential Complications Complications in the management of PCL injuries can be related to the initial injury, nonoperative treatment, intraoperative complications, or postoperative management. Complications related to the initial injury are usually related to multiligamentous knee injuries and not isolated PCL injuries. Neurovascular injuries occur in about 30% of knee dislocations243,256 (range, 15% to 49%).36,71,75-79 Complications from nonoperative management can include residual laxity, stiffness, knee pain, degenerative joint disease of the medial compartment and patellofemoral compartments, heterotopic ossification, and reflex sympathetic dystrophy.257-259 All these complications are more likely in multiligamentous knee injuries than in isolated PCL injuries. In addition, any one of these can also develop in operatively managed PCL injuries. Intraoperative complications of PCL surgery represent a unique component of PCL injuries and include neurovascular injuries, medial femoral condyle osteonecrosis, compartment syndrome, and tourniquet complications. Although compartment syndrome and tourniquet problems do happen, they are usually considered more likely in multiligamentous knee injuries. Neurovascular injuries, specifically popliteal artery injuries, are relatively unique to PCL surgery because of the proximity of the popliteal artery. Popliteal artery and tibial nerve injuries, although uncommon, are possible with both the inlay and transtibial techniques. In a recent cadaveric study, the popliteal artery is about 29.1 mm from the midportion of the PCL and 9.7 mm from the proximal PCL fovea.260 In another study, it was shown that the mean sagittal and coronal distances were 7.6 and 7.2 mm, respectively, and these distances increase with greater knee flexion angles up to 100 degrees.261 Other cadaveric studies have shown the safe posteromedial approach for a tibial inlay. In one study, the closest any screw was to the popliteal artery was 21.1 mm.262 There is anatomic variation of the popliteal artery, and it has been found to pass medial to or within the medial head of the gastrocnemius,263 so it is recommended that the popliteus be subperiosteally dissected off the tibia. Injuries have been reported when the surgeon strays out of the appropriate plane when doing inlay surgery. For transtibial techniques, neurovascular injuries have been documented in case reports as either lacerations or thrombus formation.264,265 Fanelli has described the posteromedial incision as both a working portal and safety incision.265a This incision allows for adequate visualization and protection of neurovascular structures, and helps reduce compartment syndrome by acting as an outflow portal. In addition to the popliteal and tibial nerve, if PLC surgery is being performed, the peroneal nerve is at risk and should always be identified and protected. Other potential intraoperative complications include medial femoral condyle osteonecrosis and tibial fracture. Osteonecrosis is likely related to drilling femoral tunnels too close to the articular surface and damaging the single nutrient artery to the condyle.266,267

Common complications diagnosed in the postoperative course of PCL injuries include arthrofibrosis, anterior knee pain, and residual laxity. Most motion loss for PCL reconstruction is in flexion as opposed to extension. Causes of flexion loss include suprapatellar adhesions; improper tunnel placement; improper graft tensioning; multiple concurrent ligament procedures, especially open medial sided surgery; poor physical therapy compliance; and the nonisometric nature of PCL reconstructions.258 These can be treated with a manipulation or arthroscopic lysis of adhesion. Manipulation rates may be as high as 10% to 15% in the multiple-injury knee, whereas other series show a mean 10-degree terminal flexion loss.44,268,269 On the opposite spectrum, residual laxity is also quite common. In many cases, PCL reconstructions gradually loosen to grade I or II laxity. The reasons for this are multifactorial as well and include malalignment, missed concomitant injuries, and technical errors. Although most patients can tolerate some degree of residual laxity, reconstructed knees with grade III instability are failures and need to be revised. In a recent review of PCL surgical failures, the modes of failure were documented.270 The most common problem was PLC deficiency (40%), improper graft tunnel placement (33%), associated varus malalignment (31%), and primary suture repair (25%). Residual laxity may also pre sent as anterior knee pain as a result of the posterior sag and increased patellofemoral forces. Other causes of anterior knee pain include harvest morbidities, symptomatic hardware, and postoperative synovitis.

Criteria for Return to Play Using our four-phase PCL rehabilitation program, our criteria for return to play are quite predictable. Patients must exhibit full, pain-free range of motion, understanding that it is not unusual for flexion to be lacking 10 to 15 degrees up to 5 months after surgery. They must also have a normal gait pattern with normal to near-normal quadriceps control and appropriate hamstring flexibility. In addition, they should have no patellofemoral or soft tissue complaints. Finally, they need appropriate endurance and proprioception from sport-specific training. This usually takes 9 to 12 months depending on associated injuries. We do not require brace therapy for return to play, but occasionally, athletes are more comfortable with a functional brace when they first return to sport. C l

r i t i c a l

P

o i n t s

nderstand the insertional anatomy of the three major comU ponents of the PCL: AL bundle, PM bundle, and MFLs. l Understand the anatomy of the posterolateral corner complex, including the LCL, popliteus, popliteofibular ligament, biceps femoris, and iliotibial band. l Understand the biomechanics of the PCL and PLC in terms of their synergistic actions. The PCL is the primary stabilizer to posterior tibial translation at 90 degrees of knee flexion and is the secondary stabilizer to external rotation. The PLC is the primary stabilizer to tibial external rotation at 30 degrees of knee flexion and is the secondary stabilizer to posterior tibial translation.

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l Accurately determine what knee structures are injured by physical examination. In particular, be able to evaluate and document injuries to the PLC, LCL, and PCL. l Understand the natural history of isolated PCL injuries (grades I to III) as well as combined PCL and PLC injuries, including PCL deficiency and associated patellofemoral and medial compartment arthrosis. l Understand the various techniques of PCL reconstruction, including single- versus double-bundle reconstruction, tibial versus transtibial inlay, PCL augmentation, and graft choices, fixation types, and tensioning patterns.

S U G G E S T E D

Harner CD, Vogrin TM, Höher J, et al: Biomechanical analysis of a posterior cruciate ligament reconstruction: Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med 28(1):32-39, 2000. LaPrade RF, Ly TV, Wentorf FA, Engebretsen L. et al: The posterolateral attachments of the knee: A qualitative and quantitative morphologic analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral gastrocnemius tendon. Am J Sports Med 31(6):854-860, 2003. Mariani PP, Becker R, Rihn J, Margheritini F: Surgical treatment of posterior cruciate ligament and posterolateral corner injuries: An anatomical, biomechanical and clinical review. Knee 10(4):311-324, 2003. Shelbourne K, Muthukaruppan Y: Subjective results of nonoperatively treated, acute, isolated posterior cruciate ligament injuries. Arthroscopy 21:457-461, 2005. Vogrin TM, Hoher J, Aroen A, et al: Effects of sectioning the posterolateral structures on knee kinematics and in situ forces in the posterior cruciate ligament. Knee Surg Sports Traumatol Arthrosc 8(2):93-98, 2000. Woo SL, Vogrin TM, Abramowitch SD: Healing and repair of ligament injuries in the knee. J Am Acad Orthop Surg 8(6):364-372, 2000.

R E A D I N G S

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 11(5):271-281, 2003. Amis AA, Gupte CM, Bull AMJ, Edwards A: Anatomy of the posterior cruciate ligament and the meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc 14(3):257-263, 2006. Fontbote C, Sell TC, Laudner KG, et al: Neuromuscular and biomechanical adaptations of patients with isolated deficiency of the posterior cruciate ligament. Am J Sports Med 33:982-989, 2005. Harner CD, Baek GN, Vogrin TM, et al: Quantitative analysis of human cruciate ligament insertions. Arthroscopy 15(7):741-749, 1999.


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Posterior Cruciate Ligament Injuries 2. Posterior Cruciate Ligament Injuries in the Child Nicholas J. Honkamp, Anil Ranawat, and Christopher D. Harner

Knee injuries in children are generally less frequent than in adults. However, with the progressive increase in the number of young people participating in organized sports at younger ages, physicians are seeing knee injuries occurring more frequently.1,2 It has been estimated that more than 30 million children and adolescents in the United States now participate in organized athletics.3 Sports participation is beginning at earlier ages with greater frequency of participation and higher intensity. Furthermore, this increased intensity and participation of elite or highly skilled preadolescent athletes in competitive sporting programs have also been implicated in the growing frequency of knee injuries.4 The level of commitment and the intensity of training

required to reach this level of athletic prowess put the skeletally immature knee at considerable risk. In pediatric athletes, the knee and ankle are at greatest risk for injury.3,5 Cutting sports such as football, soccer, basketball, and volleyball represent the highest-risk sports for knee injury.6,7 Causes other than sporting events include traffic accidents and recreational activities, with more injuries occurring during the afternoon when children have more free time.2 Acute ligamentous injury to the knee and, in particular, to the cruciate ligaments in children is being diagnosed more frequently.8,9 This observation has been attributed to a better understanding of and greater clinical suspicion


for ligamentous tears as well as to our ability to diagnose these injuries with improved imaging and arthroscopic techniques.8,10

ANATOMY OF THE YOUNG ATHLETE AND ASSOCIATED KNEE INJURIES Children present unique challenges related to their different physical and physiologic characteristics; children are not merely small adults. Such differences include their larger heads in relation to their bodies, less developed motor coordination, increased incidence of falls and accidents including traffic accidents, and their intense physical activity during play and sports.2,3 There are important physiologic and biomechanical differences that relate specifically to the pediatric knee.2 The presence of open cartilaginous growth plates, increased bone porosity and pliability, unique musculotendinous apophyseal insertions, and growing articular cartilage lead to a different spectrum of injuries in children and adolescents than in adults. In addition, the child is lighter and has a lower center of gravity, shorter lever arms, and decreased muscle strength, thereby considerably reducing the magnitude of forces generated across the lower extremities. These factors, combined with the relatively greater strength of the ligaments compared with the physes, generally protect the pediatric knee from ligamentous injury. Unfortunately, however, growing articular cartilage has been shown to be more susceptible to injury, in both clinical and biomechanical studies, than mature cartilage.11 Knee injuries in children may involve the ligaments, the extensor mechanism, the menisci, the articular cartilage and subchondral bone, the epiphysis, and adjacent structures. The age of the athlete and the anatomic insertion of the ligament (i.e., metaphyseal versus epiphyseal) will determine whether physeal or ligamentous injury occurs (Fig. 23E2-1). Physeal and ligamentous injuries occur with relatively equal frequency in children between 7 and 11 years of age, whereas younger children are more likely to sustain metaphyseal fractures.12 Teenagers sustain ligament injuries with low-energy trauma and physeal fractures with high-energy trauma.12,13 In general, the physis is more likely to be injured during times of rapid growth (i.e., peak height velocity during puberty). Multiple reports have been published dealing with the evaluation and diagnosis of acute knee injuries with associated effusions in children and adolescents.10,14 In general, most (75% or more) involve injuries to the anterior cruciate ligament (ACL), medial or lateral menisci, and osteochondral surfaces. Less frequent causes include collateral ligament and posterior cruciate ligament (PCL) injuries.2,10,14

POSTERIOR CRUCIATE LIGAMENT INJURY The PCL is widely recognized as the primary restraint to posterior tibial translation and is a secondary restraint to external rotation. Although ligamentous disruptions of the ACL are being reported with increasing frequency in the

Femoral epiphyseal plate Fibular collateral ligament Lateral capsular ligament

Fibular epiphyseal plate

Tibial collateral ligament

Medial capsular ligament Tibial epiphyseal plate

Figure 23E2-1 The attachment of the cruciate ligaments occurs within the epiphysis of the femur and the tibia. The medial collateral ligament is the only ligament to cross the tibial physeal plate. Because of the ligaments’ relationship to the physeal plates and their relative strength, stress concentrates at the growth plates, producing physeal injury rather than ligament failure.

pediatric population,8,15 PCL injuries in this age group are extremely uncommon. A thorough review of the literature reveals only sporadic case reports of PCL injuries in the skeletally immature knee.3,16-28 Most of the reports of PCL injuries in children involve avulsions from either the tibial or the femoral attachments, with femoral avulsions being more common. The femoral attachment of the PCL has been reported to be the weakest at the chondro-osseous junction.23,27 Because this attachment site has not yet ossified, avulsion from the femur may not be appreciated on plain radiographs. This has important ramifications for treatment because the physician must be aware of this pattern of avulsion injury (with adjacent periosteum or perichondrium), which is amenable to a successful primary repair if recognized early.

Mechanism of Injury Three mechanisms have been proposed for ligamentous disruption of the PCL: (1) direct pretibial trauma, (2) hyperflexion, and (3) hyperextension (Fig. 23E2-2). Pretibial trauma (i.e., a posteriorly directed blow on the anterior aspect of the proximal tibia) is a commonly cited cause of PCL injury. For example, an athlete falling on a flexed knee with the foot in plantar flexion is at risk for tearing the PCL. If the foot is dorsiflexed, however, the force is transmitted proximally through the patella and the distal femur, thereby protecting the PCL from injury.29 Noncontact injuries, such as forced hyperflexion, have been reported to be the most common isolated PCL injuries in athletes.30 These injuries often result in only partial tearing of the PCL, with the posteromedial fibers remaining intact. Hyperextension injuries are often combined with varus or valgus forces to result in multiligament disruptions, which have a much more guarded prognosis.

knee 1715

A

B

C

Figure 23E2-2 Three mechanisms of posterior cruciate ligament injury. A, Direct pretibial trauma. B, Forced hyperflexion. C, Hyperextension. (From Miller MD, Harner CD, Koshiwaguchi S: Acute posterior cruciate ligament injuries. In Fu FH, Harner CD, Vince KG (eds): Knee Surgery, vol 1. Baltimore, Williams & Wilkins, 1994.)

Classification PCL injuries in both children and adults can be classified according to severity (grades I to III), timing (acute versus chronic), and presence of associated injuries (isolated versus combined).31 These variables have significant implications for patient outcome and thus are important to consider when making treatment decisions. Isolated injuries to the PCL can be classified as partial (grades I or II) or complete (grade III) tears. In most cases, this is done clinically and corresponds to the laxity in the PCL, as measured by the step-off between the medial tibial plateau and the medial femoral condyle. Isolated grade III injuries or complete PCL tears can occur, but they are frequently associated with other ligament injuries, in particular injury to the posterolateral structures. Distinguishing between isolated and combined PCL injuries is critical because the prognosis and treatment of these injuries are vastly different (see Chapter 23E1 on adult PCL injuries).

Evaluation An accurate and detailed history and physical examination are essential to arriving at the correct diagnosis and formulating an appropriate treatment plan. Those physicians who deal frequently with children know the difficulty of accurately diagnosing pediatric musculoskeletal conditions. Young patients may not remember the mechanism of injury or may have difficulty describing it and the details of their associated joint complaints. Their symptoms are frequently vague and generalized. In general, they may limit the accuracy of the knee history and physical examination through a lack of cooperation or inconsistent history and physical examination findings.32-35 Children younger than 6 to 7 years of age are usually unable to localize pain reliably. Their manifestation of a knee disorder may be a limp or refusal to walk.11 Coaches or parents may provide helpful information, but often the injury occurs when the child is unsupervised. Thus, the accuracy of preoperative knee diagnoses varies with the patient age, with the lowest percentages occurring in the preadolescent age group (18% to 55%) and improved percentages

occurring in the adolescent age group (44% to 70%).36-39 This makes a good physical examination even more important, which can be difficult if the child is frightened or in pain. It is very important to gain the child’s trust before proceeding with the examination and to remember that pain from hip injuries may be referred to the medial aspect of the knee as a result of the common sensory supply by the obturator nerve. Evaluation of the injured knee begins with obtaining a detailed history, trying to delineate the mechanism of injury, its severity, and possible associated injuries. Patients with PCL injuries may present for evaluation in a variety of different scenarios. Injuries may range from a seemingly benign fall on the athletic field to severe trauma caused by a motor vehicle crash. The more acutely traumatized the knee, the more difficult it will be to examine it. Unlike patients with isolated ACL injuries, those with acute isolated PCL injuries do not typically report hearing or feeling a “pop.” Although many suspect a knee injury, patients do not typically relate a sense of instability. They may note mild to moderate swelling, accompanying stiffness, and occasionally mild knee pain. The examination of the acutely injured knee begins with evaluation of the neurovascular status, followed by observation of the knee for its resting position and the presence and location of any ecchymosis. The examiner must differentiate between intra-articular effusion and extra-articular swelling. Acute hemarthrosis after trauma to the skeletally immature knee alerts the clinician to a significant intraarticular injury. As mentioned earlier, the most likely diagnoses in such cases include ACL, meniscal, or osteochondral injuries. All important anatomic structures of the knee should be palpated sequentially, leaving those areas most likely to be tender (according to the suspected diagnosis) until last. Stress maneuvers to test ligament integrity in the mediolateral and anteroposterior planes may be performed gently. Comparison with the noninjured extremity is crucial because of the physiologic laxity present in many children. If there is significant tenderness over a growth plate, it may be prudent to obtain radiographs before stressing the knee,


which might displace a fracture. Finally, range of motion of both the knee and the hip (to rule out primary hip disease) is checked near the end of the examination once the patient’s trust has been gained and the rest of the examination has been completed. In any child with ligamentous instability of the knee, congenital absence of the cruciates should be considered. The most common associated causes include proximal femoral focal deficiency, fibular hemimelia, congenital dislocation of the knee, and ball-and-socket ankle. Congenital absence of the cruciates may be an isolated finding40; however, radiographs may show flattening of the tibial eminence or a shallow intercondylar notch.40,41 Finally, hemophilia must be also be considered in the differential diagnosis of a child presenting with hemarthrosis and a history of no or minimal trauma.42

Imaging Imaging studies play an important role in the diagnosis of PCL injuries in children. Plain radiographs may detect avulsion fractures of the femoral and tibial attachments of the PCL. As previously mentioned, the attachment site may not yet have ossified; thus, avulsion of the PCL (especially from the femur) may not be appreciated on plain films. The only clue may be a slight irregularity at the femoral or tibial attachment, which could easily be missed unless the radiographs are carefully scrutinized.43 Before the widespread availability and use of magnetic resonance imaging (MRI), knee arthroscopy was used as a diagnostic and therapeutic tool.10,38,44,45 Unfortunately, multiple authors reported that a significant number of arthroscopies yielded normal results, thus exposing patients to unnecessary surgery.36,38 MRI is extremely useful for evaluating PCL injuries in the skeletally immature knee. It can accurately differentiate between intrasubstance and “peel-off” injuries and can determine whether there is any associated chondral or meniscal disease.31 However, MRI should not be considered a substitute for a thorough history and physical examination. Two recent studies have compared the radiologist’s interpretation of MRI diagnosis and clinical diagnosis of the treating physician (without knowledge of the MRI result) to that of the findings at the time of the diagnostic arthroscopy.46,47 Stanitski47 found that the clinical examination was more accurate than the MRI, whereas Kocher and colleagues46 found no significant differences between clinical examination and the findings on MRI with respect to agreement with the arthroscopic findings. Luhmann and coworkers48 found that the more accurate diagnoses were obtained when the treating physician who performed the physical examination also reviewed the MRI personally. Thus, a history and physical examination, as well as judicious use and personal review of MRI results, are the best method for arriving at a correct diagnosis.

Natural History Owing to the rarity of PCL injury in children and the limited short-term follow-up that has been reported in the literature, the consequences of PCL deficiency in

the skeletally immature knee (with or without treatment) remain unknown. Unfortunately, the literature regarding adult PCL injuries is not extremely helpful because most of the studies are retrospective, combining both isolated and multiligamentous injuries, and do not stratify the outcome according to the degree of instability. There is a general consensus that PCL injuries (especially grade III) are not as benign as previously thought over the long term.31 Patients with chronic PCL injuries experience a variable progression of articular degeneration and symptoms over time. A high incidence of late chondrosis29,49 (involving the medial femoral condyle and the patellofemoral joint) and meniscal tears50 has been noted in adult patients treated nonoperatively. These findings are likely the result of the increased contact pressure that occurs in these compartments after PCL disruption.51,52 The fact that growing articular cartilage is more susceptible to injury than mature articular cartilage is particularly worrisome.11 The problem to date has been that investigators have been unable to identify prognostic factors consistently to help predict patient outcome after PCL injury. It should also be noted that the long-term outcome after nonsurgical treatment of ACL injuries in the skeletally immature has been poor with respect to return to sports and long-term sequelae.53-55

Treatment Rationale The treatment of acute PCL injuries in children is dependent on both the pattern of ligamentous injury and whether there is any associated meniscal or chondral disease. The full extent of the injury must be determined before formulation of a treatment plan because the site of injury (avulsion or midsubstance), its grade (partial or complete), and the presence of associated injuries greatly influence the treatment algorithm. Furthermore, both the child and the parents must be actively involved in the decision-making process. The expectations of both the patient and the family, as well as the maturity of the patient and his or her commitment to rehabilitation, must be taken into consideration before embarking on any surgical intervention.

Avulsion Injuries PCL avulsions (soft tissue or bony) from the femur or the tibia should be repaired primarily. If the child suffered a hyperflexion injury, an avulsion should be suspected; this can be confirmed with MRI of the knee. Arthroscopy and examination with the patient under anesthesia remain the most accurate means of determining the extent of the child’s injury, however, because partial ligament tears can be difficult to distinguish, even with MRI, in the skeletally immature knee.11 Furthermore, arthroscopy will confirm the location of PCL disruption and the feasibility of repair as well as assist in evaluating the menisci and the chondral surfaces for injury. Meniscal repair should be attempted whenever possible, and PCL avulsions from the femur or the tibia should be repaired primarily with transosseous (intraepiphyseal) sutures through drill holes or, for bony

knee 1717

Bunnell suture in PCL

PCL

A

B

C

Figure 23E2-3 A, Posterior cruciate ligament (PCL) avulsion from the femur repaired with a Bunnell-type stitch through the femoral epiphysis. B, PCL avulsion from the tibia repaired with a Bunnell-type stitch through the tibial epiphysis. C, PCL bony avulsion repaired with an intraepiphyseal screw.

avulsions, with either screw or transosseous suture fixation (Fig. 23E2-3).

Midsubstance Injuries Isolated midsubstance cruciate tears are generally not repaired in children because the outcome has not been proved to be any better than in adults.16 Permanent plastic deformation and early degeneration of the ligament may contribute to failure of the repair. Although transphyseal ACL reconstructions with soft tissue grafts (i.e., hamstring) are being performed at some centers,56-58 PCL reconstruction in the skeletally immature knee may be contraindicated. Animal studies have shown that the tibial physis can be very sensitive to transphyseal drilling.59,60 The tibial tunnel in PCL reconstruction crosses the physis peripherally, in comparison with the more central location of an ACL tunnel, thereby theoretically posing a greater risk for physeal injury or closure. Conservative treatment is currently recommended for skeletally immature patients with an isolated grade III midsubstance PCL tear. A recent study has suggested that interstitial tears of the PCL may have some propensity to heal with closed management, particularly those with less than 8 mm of posterior displacement on stress radiographs.61 Initial treatment should include immobilization of the knee in extension with anterior translation to reduce posterior sag. Restoration of range of motion and quadriceps and hamstring strength starts at 4 to 6 weeks. The patients must be followed annually. If functional instability or pain develops, or if radiographs or bone scans are notable for early signs of arthrosis, reconstruction of the PCL can be performed after growth is completed.

Multiligament Injuries In the presence of multiligament injuries, the collateral ligaments are repaired surgically along with any associated meniscal disease. In this scenario, attempting to repair a midsubstance tear of the PCL with suturing may be indicated if there is significant growth remaining. If the resultant posterior laxity is clinically significant, a PCL reconstruction can be performed in the future. In cases in which physeal growth is limited (1 cm

Mild Moderate Severe

From American Medical Association: Standard nomenclature of athletic injuries. Chicago, American Medical Association, 1966.

c ontralateral side at both 30 degrees and 90 degrees of knee flexion. While observing the tibial tubercle, an increase of 10 to 15 degrees of external rotation at 30 degrees of flexion, compared with the uninvolved side, is indicative of an injury to the PLC.16 The knee is then flexed to 90 degrees, and the test is repeated. In an isolated injury to the posterolateral knee, external rotation will now decrease, compared with 30 degrees, due in part to an intact PCL.16 However, if external rotation increases at 90 degrees, a combined injury to the PLC and PCL is suspected.16

Posterolateral Drawer Test The posterolateral drawer test assesses posterolateral stability by comparing the amount of external tibial rotation and posterior tibial translation, relative to the lateral femoral condyle (Fig. 23F-11).48 The knee is flexed to 80 degrees and the hip to 45 degrees. The patient’s foot is stabilized by the examiner in the seated position. A posterior drawer test is then performed in external, neutral, and internal rotation, while observing the relationship of the anterior tibia with respect to the distal aspect of femoral condyles. Increased posterior translation in external rotation signifies injury to the posterolateral and popliteus complex. Conversely, a positive test in neutral or internal rotation is consistent with injury to the PCL. Sensitivity for PLC injuries with this test ranges from 70% to 75%.42,44,46

Reverse Pivot Shift Test This test can be considered a dynamic variant of the posterolateral drawer test,52 and several methods have been described (see Fig. 23F-11). Most commonly, the involved knee is flexed from 60 to 90 degrees. While applying a valgus stress to the knee with the foot in external rotation, the knee is slowly extended. In the patient with posterolateral instability, the tibia is subluxated posteriorly while in the initial flexed position. With extension, the tibia reduces with a tactile shift. This action is thought to result from the iliotibial band changing from a flexor to an extensor at 25 to 30 degrees of knee flexion.11 This test should be


Visualize tibial tubercle rotation

Externally rotate ankle

A

B

Figure 23F-10 A and B, Dial test. Increased external rotation clinically is assessed with the dial test demonstrating isolated posterolateral corner injuries. An external rotation force is applied to the knee while the knee is placed in 30 degrees of flexion. The amount of external rotation is qualitatively measured by observing for differences in rotation of the tibial tubercles between the injured (arrow) and normal contralateral limb. (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York: Thieme, 2006, p 82.)

distinguished from the true pivot shift test, in which the knee is started in extension, and the anterior subluxation of the tibia is reduced as the knee is taken into flexion. The reverse pivot shift test has been shown to have a high falsepositive rate, and up to 35% of uninjured patients can have a positive test when examined under anesthesia.53

Finally, a complete examination should include motor and sensory testing, especially along the common peroneal nerve distribution.

Posterior Tibial Translation

Radiographs

Posterior tibial translation can also be used in the examination process. Performed at both 30 and 90 degrees of knee flexion, the position of the anterior tibia relative to the femoral condyles is assessed following a posteriorly directed force to the proximal tibia. In isolated PCL injuries, there is a loss of the normal anterior tibial step-off at 90 degrees of flexion.16 Conversely, isolated PLC injuries elicit increases in posterior translation only at 30 degrees. Combined PCL and PLC injuries result in increased posterior tibial translation at both 30 and 90 degrees of knee flexion, which is usually greater than or equal to 12 mm.

Radiographic evaluation for cases of posterolateral instability should include anteroposterior weight-bearing views in both flexion and extension, a lateral of the injured knee, and patellofemoral views of both knees.55 Although radiographs are often normal in cases of posterolateral instability, several entities may be evident. Medial compartment arthrosis, Segond’s fracture, an arcuate avulsion fracture from the fibular head, and avulsion fractures of Gerdy’s tubercle are several examples.26,43,49 Other associated injuries, such as tibial plateau fractures, tibiofemoral dislocation, PCL avulsions, or tibial spine fractures, may also be evident. In a patient with chronic posterolateral instability, patellofemoral or tibiofemoral degenerative changes can be observed. Commonly, the medial compartment is most often affected, showing joint space narrowing, tibial osteophytes, and subchondral sclerosis of the tibial plateau. In this situation, standing alignment radiographs are used to evaluate for varus malalignment.11 Finally, stress radiography can be a valuable tool for determining the degree and direction of ligament laxity (Fig. 23F-12).56,57 Bilateral valgus and varus stress radiographs emphasize side-toside variations in medial or lateral joint space widening, whereas radiographs with applied anterior and posterior forces to the proximal tibia can quantitate cruciate ligament integrity.

Other Tests Other tests exist for examining the posterolateral knee, as do combinations of several previously described techniques. Shelbourne and colleagues described a similar test to the reverse pivot shift, coined the dynamic shift test.54 With the hip flexed to 90 degrees, the flexed knee is slowly extended. The combination of gravity and hamstring pull keep the tibia subluxed posteriorly until about 20 degrees. When the tibia reduces, a clunk, or dynamic shift, is elicited. In addition to specific tests for posterolateral knee injury, it is important to include Lachman’s test to assess for increased anterior tibial translation and, thus, integrity of the ACL.

IMAGING

knee 1729

hip and knee at 70˚angle

Tibial subluxation posterolaterally

A

hip and knee at 30˚angle

B

C

Tibia self-reduces at this point

D

Figure 23F-11 A and B, Reverse pivot shift test. A, The knee is flexed to between 70 and 90 degrees, and the foot is externally rotated. This results in a posterolateral subluxation of the tibia on the femur. B, The knee is then extended with a reduction of the posterolaterally subluxed tibia on the femur at about 30 degrees. C and D, Posterolateral drawer test. The knee is flexed to 90 degrees and the foot is externally rotated 15 degrees. A gentle posterolateral rotation force is applied to the knee and the amount of posterolateral rotation on the femur is qualitatively measured compared with the normal contralateral knee. C, Neutral position. D, Posterolateral drawer applied demonstrating increased posterolateral rotation.


A

B

Figure 23F-12 Radiograph of normal knee (A) with normal lateral compartment opening with varus stress. Radiograph of contralateral abnormal knee (B) with increased lateral compartment opening with varus stress at 30 degrees of knee flexion demonstrating a posterolateral corner injury.

Magnetic Resonance Imaging MRI is useful in both the acute and chronic settings for evaluation of the posterolateral knee, especially given the complex anatomy of the lateral and posterolateral knee (Figs. 23F-13 to 23F-15).26,58-60 In the acutely injured and painful extremity, MRI may be the most comprehensive imaging tool for assessing the entire knee joint. Information obtained from the MRI is essential for preoperative planning because structures such as the fibular collateral ligament, popliteus muscle-tendon complex, biceps tendon complex, and lateral capsular attachments can be predictably identified.59 Associated injuries to the meniscus, articular cartilage, and cruciate ligaments can also be identified.

A

In addition to the standard coronal, sagittal, and axial imaging sequences, thin-slice (2-mm) proton density coronal oblique images that include the complete fibular head and styloid are extremely valuable for evaluating the fibular collateral ligament and popliteus tendon.26 High-quality MRI (1.5 Tesla or higher) is preferred because less powerful magnets make delineation of injury difficult.

Arthroscopy The intra-articular assessment of the PLC can be an adjunct for knee evaluation, and its utility has been shown in a prospective case series.61 The posterolateral structures

B

Figure 23F-13 Magnetic resonance imaging appearance of the superficial and deep layers of the iliotibial band and fabellofibular ligament. A, Normal superficial and deep layers (coronal view, right knee). B, Avulsion of iliotibial band off Gerdy’s tubercle (coronal view, left knee).

knee 1731

A

B

Figure 23F-14 A, Magnetic resonance imaging appearance of a normal fabellofibular ligament (white arrow) and normal popliteofibular ligament (black arrow). B, Abnormal appearance of an chronically, attenuated popliteofibular ligament (white arrow).

whose injury can be identified by arthroscopy include the meniscofemoral and meniscotibial portions of the midthird lateral capsular ligament, the femoral attachment of the popliteus tendon, the popliteomeniscal fascicles, and the coronary ligament to the posterior lateral meniscus.

Excessive lateral compartment laxity can be elicited by noting a “drive-through” sign when a varus stress is applied to the knee (Fig. 23F-16).61 This is represented by more than 1 cm of lateral joint line opening.61 In addition, arthroscopy allows further visualization of meniscal and articular cartilage as well as the cruciate ligaments. However, the examiner must be aware and judicious with fluid management to avoid the possibility of fluid extravasation in the acutely injured or capsular-deficient knee.

TREATMENT Grades I and II Posterolateral Knee Injuries Isolated Injury A

B

C

D

Figure 23F-15 Magnetic resonance imaging appearance of the fibular collateral ligament and popliteus insertion. A, Coronal view of normal fibular collateral ligament (right knee). B, Coronal view of normal femoral insertion of the popliteus (right knee). C, Coronal view of tearing of the popliteus tendon origin (black arrow) and fibular collateral ligament (left knee). D, Sagittal view of a popliteus muscle belly edema from an acute popliteus musculotendinosus junction injury (right knee).

Isolated grade I and II PLC injuries are frequently missed in the acute setting, making natural history studies difficult to perform. Fortunately, isolated acute grade I and II knee injuries are almost always treated nonsurgically,62 especially if they have initial valgus alignment.46 Patients are initially immobilized in full knee extension for 3 weeks to allow the injured tissues to heal, then range of motion is gradually introduced. Mild injuries are allowed to bear weight in extension, whereas more severe injuries may require 6 weeks of protected weight-bearing. A functional rehabilitation program is started 6 weeks after injury, emphasizing endurance exercises and quadriceps strengthening, whereas aggressive hamstring work is restricted. Patients with chronic symptomatic posterolateral instability after grade I or II injuries may be treated with a medial compartment unloader brace to determine whether they have improvement in subjective symptoms. Additionally, bilateral varus stress radiographs can quantify the amount of varus laxity present. If patients exhibit varus laxity and subjective improvement in symptoms with a medial compartment unloader brace, they may benefit from a posterolateral knee reconstructive procedure or a proximal tibial osteotomy if they are in varus alignment.5


A

B

Figure 23F-16 Arthroscopic views of lateral compartment. A, Drive-through sign in lateral compartment in a patient with an anterior cruciate ligament, posterior cruciate ligament, and posterolateral corner injury. B, Popliteus tendon avulsion off of the femur (arrow).

Concomitant Cruciate Ligament Injury

Concomitant Cruciate Ligament Injury

Combined ACL or PCL tears with grade I or II PLC injuries need to be critically evaluated for the amount of instability present. LaPrade has recommended that the cruciate ligament tear causing instability be reconstructed and that grade I or II PLC injuries be treated nonoperatively.5 Stress radiographs are helpful in assessing the amount of instability. Increased varus instability places a large amount of stress on the ACL reconstruction graft, whereas increased varus laxity combined with posterolateral rotatory instability places undue stress on a PCL reconstructive graft. This has been known to cause chronic laxity and even failure of the reconstructed cruciate ligament grafts.17,32,33,63

Combined ACL or PCL injuries and grade III PLC injuries are probably best treated surgically in the acute setting after the swelling has subsided. It is recommended to leave a 6- to 7-cm skin bridge between the anterior incision for a cruciate ligament reconstruction procedure and the PLC approach. All the following repairs and reconstructions, whether performed acutely or chronically, use a common surgical approach (see “Authors’ Preferred Method”).

Grade III Posterolateral Knee Injuries

In the acute setting, the treatment of femoral-based PLC knee injuries may include the popliteus tendon or FCL femoral recess procedures as originally described by Hughston.5,15,25 Recent modifications have been noted.5,64 After the surgical exposure of the PLC, the avulsed ends of the FCL or the popliteus tendon are whip-stitched with 2-0 nonabsorbable suture. After sufficient length of the FCL or popliteus is verified, a cruciate ligament guide is used to place an eyelet-tipped pin through the exact attachment site of the FCL or popliteus tendon (Fig. 23F-17). The pin exits medially on the femur proximal to the medial epicondyle and adductor tubercle region; this angulation avoids passing the suture or graft through the intercondylar notch. A horizontal incision is made proximal to the course of the medial patellofemoral ligament and along the distal border of the vastus medialis obliquus muscle. The vastus medialis obliquus muscle is retracted proximally to allow the passing sutures and surgical button to be tied deep to the muscle fibers. A 5- or 6-mm cannulated reamer is placed over the eyelet-tipped pin laterally and reamed to a depth of 1 cm. The passing sutures are placed in the eyelet-tipped pin and are pulled out medially. With the knee in full extension, care is taken to ensure that the avulsed structure is pulled into the tunnel. Finally, the

Isolated Injury In contrast to grade II PLC injuries, grade III PLC injuries have a low probability of healing nonoperatively, and surgical treatment is often needed to allow the best outcome.37 Ligamentous repairs and reconstructions aim to provide varus and posterolateral stability. Interestingly, acute repairs have been shown to lead to improved outcomes when compared with the results of chronic reconstructive procedures.46 In fact, the International Society of Arthroscopy, Knee Surgery, and Orthopaedic Sports Medicine (ISAKOS) has recommended that these surgical procedures be performed within the first 2 weeks after a PLC injury. Significant scar planes develop within 3 weeks of injury that may complicate the surgical exposure of the iliotibial band, biceps femoris, and common peroneal nerve. Additionally, 3 weeks after injury, the posterolateral knee structures do not hold sutures well, which makes rehabilitation techniques using early range of motion protocols more difficult. It is important to note that multitrauma patients and those with severe skin problems may benefit from delayed surgery.

Repair Techniques Advancement or Recession of the Posterolateral Corner

knee 1733 Eyelet-tipped pin enters at popliteus tendon attachment site and exits medially (proximal to medial epicondyle and adductor tubercle region)

Cannulated reamer (to depth of 1 cm)

Figure 23F-18 Lateral capsular repair to bone with suture anchors just distal to articular margin (lateral view, right knee).

Passing sutures through end of avulsed popliteus tendon Figure 23F-17 Popliteus tendon recess procedure. The torn popliteus is whip-stitched. A cannulated reamer is used to drill over an eyelet-tipped guide pin. The guide pin is used to pull the sutures medially and then they are tied over a button on the medial femur. Finally, the popliteus tendon is recessed into the femoral socket. A similar procedure is performed for the fibular collateral ligament. (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York, Thieme, 2006, p 157.)

The coronary ligament is accessed through the second fascial incision. The lateral gastrocnemius is retracted posteriorly; this approach protects the neurovascular bundle and allows visualization of the coronary ligament (Fig. 23F-19). Multiple sutures are passed through the popliteal aponeurosis into the substance of the lateral meniscus and down into the distal tibial attachment site of the coronary ligament. The sutures are then tied with the knee in flexion. The results of repairs of intrasubstance tears of the popliteus and FCL have faired poorly; therefore, these tears are traditionally treated with reconstruction procedures.

Reconstruction Techniques: Overview

passing sutures are fed through a button medially and tied down over the cortex, pulling the avulsed structure into the recess hole. Additionally, suture anchors can be used to reattach the lateral gastrocnemius tendon and portions of the posterior and lateral capsule to their anatomic femoral attachment sites (Fig. 23F-18). Significant gapping occurs when attempts are made to repair the FCL or popliteus to the femur with suture anchors, and thus it is recommended instead to use the recess procedure for these structures. Interestingly, a recent nonrandomized study comparing acute PLC repair to reconstruction found a higher failure rate among patients who underwent a repair.65

PLC reconstructive techniques have recently been broken down into nonanatomic and anatomic techniques. All these techniques may be used to reconstruct an acute or a chronic PLC-deficient knee. The nonanatomic techniques include biceps femoris tenodesis,66,67 Larson technique,68 and Stannard’s modified two-tailed technique.69 The reconstructions all involve creating restraints from either the fibular head or the PLC of the tibia to the lateral femoral epicondylar region. Re-creating the ligament length relationships of the lateral knee in proper isometric positions attempts to create a mechanical advantage and thus resist varus and posterolateral tibial rotations. Recently, an anatomic reconstruction has also been described by LaPrade.19

Intrasubstance Posterolateral Corner Repair

Reconstruction Techniques: Nonanatomic

Intrasubstance injuries to the popliteomeniscal fascicles and coronary ligament to the lateral meniscus may be repaired directly. Direct suture repair of the anteroinferior and posterosuperior popliteomeniscal fascicles is made to the popliteus tendon through the mid-third capsular arthrotomy. The structures are repaired in a direct horizontal mattress technique with nonabsorbable 0-0 suture; this technique allows early range of motion rehabilitation protocols.

Biceps Tenodesis Clancy popularized the biceps tenodesis procedure to repair and augment intrasubstance injuries to the FCL and the PFL; however, the surgeon must ensure that the long head of the biceps tendon is completely intact (Fig. 23F-20). The tenodesis involves transferring the biceps femoris tendon to the anterior aspect of the lateral femoral

1734 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Figure 23F-19 Coronary ligament repair of the lateral meniscus performed between the lateral gastrocnemius tendon and soleus muscle (lateral view, right knee). PCL, posterior cruciate ligament; PFL, popliteofibular ligament. (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York, Thieme, 2006, p 159.)

Biceps femoris

PCL

Coronary ligament PFL

Lateral gastrocnemius Popliteus

Common peroneal nerve Soleus

epicondyle. This procedure attempts to replace the FCL and the PFL through its attachments to the posterolateral capsule complex. Wascher and colleagues determined that a point of fixation 1 cm anterior to the FCL attachment is needed to significantly reduce external tibial rotation and varus laxity.70 After the standard surgical approach, the peroneal nerve is dissected free from the posterior margin of the biceps, and the biceps tendon is released from the lateral gastrocnemius muscle tendon unit. A vessel loop is placed around the nerve, and any attachments of the nerve to the biceps muscle tendon unit are freed. The nerve is traced distally into its entry point in the anterior compartment musculature. If there is constriction of the nerve at this location, it must be released. The inferior aspect of the iliotibial band is freed from its intermuscular septal attachments to allow the biceps tendon and muscle belly to be brought up beneath it. The lateral epicondyle is exposed by incising the iliotibial band and dissected free of soft tissue, exposing the superior aspect of the FCL. A 1-cm wide and 3-cm long trough is made at the upper portion of the lateral femoral condyle. A 3.2-mm hole is drilled just superior to the lateral femoral epicondyle and is directed medially and slightly proximally into the medial femoral condyle, avoiding any tunnels that may have been created for cruciate ligament reconstruction. A 6.5-mm screw with a spiked soft tissue washer is placed at that location. The distal 7 to 8 cm of biceps muscle is resected away from the tendon; otherwise, fixation of the tendon to the lateral femoral condylar trough is impossible because of the interposition of the muscle. The biceps tendon with its posterolateral capsular attachments is brought

proximally and looped over the fixation device; then the knee is passed through a range of motion ensuring that the point of fixation does not interfere with an adequate range of motion. The graft is secured by advancing the screw and washer to the cortex. In an attempt to avoid sacrificing the important biceps tendon function, variations of the biceps tenodesis have been developed using only a portion of the biceps tendon. Generally, a central slip of the tendon that involves about 50% of the cross-sectional diameter is created and left attached at the fibular head. The free end is routed beneath the posterior-most fibers of the biceps tendon at the fibular head, and then advanced to the point of attachment on the femur; this creates a band of tissue approximately in the position of the PFL that can resist posterolateral rotations as well as varus rotations. Importantly, procedures that do not tenodese the total biceps tendon do not provide for retensioning of the posterolateral capsular complex.

Modified Two-Tailed Technique Stannard has described the modified two-tailed technique using a tibialis anterior or posterior allograft (Fig. 23F-21).65 The three critical components of the deep layer of the PLC are reconstructed: the popliteus, the popliteofibular ligament, and the FCL. After a standard surgical approach, a 5-mm hole is drilled from anterior to posterior through the lateral tibia. The posterior hole approximates the position of the popliteus as it crosses along the posterior tibia. The tibial tunnel is tapped with a 7-mm tap. The allograft is sized to 5 mm and passed into the tunnel

knee 1735

B

A

Lateral gastrocnemius muscle

Trough Fibular collateral ligament

Resected 2-inch short head biceps muscle

Short head Long head biceps muscle biceps tendon

C

Lateral gastrocnemius tendon

Common biceps tendon

D Trough

Fibular collateral ligament Common biceps tendon

E

F

Figure 23F-20 Posterolateral reconstruction using biceps femoris tendon (Clancy). A, Common peroneal nerve is carefully dissected; biceps femoris muscle is freed from attachments to the lateral gastrocnemius. B, Femoral origin of the fibular collateral ligament. C, Insertions of the common biceps tendon into the arcuate complex posteriorly and insertion around the fibular collateral ligament. D, Trough is made in the upper third of the lateral femoral epicondyle. E, Biceps femoris tendon is brought anteriorly to the trough in the epicondyle. F, AO cancellous screw and washer are placed inferior to the tendon and tightened. (Adapted from Clancy WG Jr: Repair and reconstruction of the posterior cruciate ligament. In Chapman MW [ed]: Operative Orthopaedics. Philadelphia, JB Lippincott, 1988.)

1736 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Passing sutures

FCL Popliteus tendon graft

Figure 23F-21 The modified two-tailed reconstruction of the posterolateral corner with tibialis anterior autograft. Tibial fixation is accomplished with a bioabsorbable screw. Femoral fixation with a 6.5 cancellous screw and ligament washer. (Adapted from Stannard JP, Brown SL, Farris RC, et al: The posterolateral corner of the knee: Repair versus reconstruction. Am J Sports Med 33[6]:881-888, 2005.)

from posterior to anterior. The graft is fixed with a 7-mm bioabsorbable ligament screw. A second 5-mm hole is then drilled through the proximal fibula from anterolateral to posteromedial. The isometric point on the lateral femoral condyle is then located. The “isometric point” is located just superior to where the FCL and popliteus cross on the lateral femoral condyle. A 4.5-mm bicortical screw going from lateral to medial is placed in the lateral femoral condyle with a spiked ligament washer. The surrounding bone is decorticated to facilitate allograft healing between the attachments of the FCL and popliteus. The graft is then passed from the posterior tibia up and around the screw in the lateral femoral condyle, back down to and through the fibular tunnel, and then back up to the screw and washer. The graft is tensioned with the foot internally rotated and the knee flexed 40 to 60 degrees. The free end of the graft is anchored primarily by the spiked ligament washer but is supplemented with a 2-0 suture.

Reconstruction Techniques: Anatomic Reconstruction of the Popliteus Acute reconstruction of the popliteus tendon can be performed with an autograft or allograft hamstring tendon (Fig. 23F-22). Harvesting of the hamstring tendons has been previously described.5 The semitendinosus tendon is preferred because it is the thicker of the two hamstring tendons; additionally, harvesting the semitendinosus is less likely to injure the saphenous nerve. After the semitendinosus tendon is harvested and tubularized with a 2-0 or 5-0 suture, a 25- to 30-mm deep femoral tunnel is drilled into the anatomic origin of the popliteus.71 A lateral interference screw or a medial surgical button is used

Gerdy’s tubercle

Figure 23F-22 Acute popliteus tendon reconstruction with a hamstring graft. The hamstring graft is pulled into the femoral socket and fixed with a bioabsorbable screw, wrapped around the musculotendinous junction of the popliteus complex, and pulled anteriorly through the tibial tunnel. The graft is fixed in place with a screw and staple. FCL, fibular collateral ligament. (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York, Thieme, 2006, p 161.)

to fix the graft to the femur. Next, the posterolateral sulcus of the tibia is identified at the musculotendinous junction of the popliteus. An eyelet-tipped guide pin is drilled from anterior to posterior in the tibia, using a cruciate ligament guide, exiting at the posterolateral sulcus. The entry point for the anterior tibia is placed just medial and distal to Gerdy’s tubercle. A posterior retractor is placed to protect the posterior neurovascular bundle during the procedure. A 7- to 8-mm reamer is used to fashion the tibial tunnel from anterior to posterior. The graft is then passed distally through the popliteus hiatus between the gastrocnemius and soleus muscles; then the graft is pulled anteriorly from its posterior entry point. The knee is placed in 60 degrees of flexion and neutral rotation while the graft is fixed to the tibia with an interference screw and a bone staple for backup fixation.

Reconstruction of the Fibular Collateral Ligament An FCL reconstruction with autogenous and allograft hamstring tendons has been described.5 The FCL graft is tubularized with a 2-0 or 5-0 suture. An eyelet-tipped pin is then inserted into the anatomic femoral attachment of the FCL. A 7-mm reamer is used to drill a 20- to 25-mm tunnel. The tunnel is then tapped, and the graft is passed into the femur and fixed with an interference screw. A second tunnel is then drilled starting at the lateral aspect of the fibular head at the attachment site of the FCL and exiting through the posterior aspect of the fibular styloid. Care is taken to avoid the attachment site of the popliteofibular ligament. A 6- or 7-mm cannulated reamer is used to drill the tunnels. The graft is then passed under the superficial iliotibial band and the lateral aponeurosis to the long head

knee 1737

of the biceps femoris. The graft is then passed through the fibular tunnel and pulled back upon itself up to the lateral epicondyle (Fig. 23F-23). The knee is placed in 30 degrees of knee flexion and neutral rotation while a valgus force is applied to decrease any varus opening. An interference screw is then placed into the fibular head to secure the graft. The graft is then tied back on itself by passing it through a split in the biceps at the lateral fibular location with 0-0 Vicryl suture. If both the FCL and popliteus are torn in their midsubstance, a direct anatomic reconstruction with an Achilles tendon allograft is performed similar to the technique for the anatomic chronic reconstruction described later in the chapter.

Figure 23F-23 Fibular collateral ligament hamstring autograft reconstruction. The graft is fixed in the femoral tunnel with a bioabsorbable screw. The graft passes under the superficial iliotibial band and the lateral aponeurotic layer of the long head of the biceps femoris. The fibular tunnel is placed through the anatomic attachment site laterally and exits posteriorly to avoid the popliteofibular ligament insertion. The graft is tied upon itself, after fibular tunnel fixation is performed with a bioabsorbable screw (left knee).

Authors’ Preferred Method Anatomic Posterolateral Corner Reconstruction

Preoperative planning. Preoperative planning for reconstruction of the PLC is essential (Table 23F-3). The senior author (RFL) does not use a leg holder. Instead, a sandbag is taped at the foot of the bed to allow for about 70 degrees of knee flexion. A sandbag is also commonly placed under the patient’s hip so that the knee will balance at 70 degrees and not require an assistant to actively hold it in that position. This allows the assistant to concentrate on appropriate

TABLE 23F-3 Authors’ Preferred Surgical Technique Preparation

Instrumentation

Setup

Transtibial or transfemoral anterior and posterior cruciate ligament guide system Beath passing pins with eyelets Cannulated 7- and 9-mm reamers, bioabsorbable interference screws Adsen tipped hemostat for peroneal nerve neurolysis and fine dissection Soft tissue staple fixation system

No leg holder necessary Sandbag taped to bed to allow for 70 degrees of knee flexion Bump under hip to allow for neutral position of knee Standard orthopaedic soft tissue retractors Achilles tendon allograft ≥23 cm long with calcaneus bone plug

From LaPrade FR: Posterolateral knee injuries: Anatomy, evaluation, and treatment. New York, Thieme, 2006.

r etraction throughout the procedure. The patient is placed supine with the operative leg prepared and draped free. The equipment necessary for the posterolateral reconstruction includes standard cruciate ligament reconstruction instruments. Cannulated drill guides are used for guide pin positioning during tunnel placement. Eyelet-tipped passing pins are also used to pass sutures and to ream over during tunnel placement. Cannulated metal and bioabsorbable screws are used for graft fixation, as are small bone staples when secondary fixation is deemed necessary. The Achilles tendon allograft that is used should be at least 23 cm long to ensure that it will be long enough to pass through the course of the reconstructive technique. Surgical exposure of the PLC. A lateral hockey-stick skin incision is used unless previous skin incisions need to be incorporated (Fig. 23F-24A). The incision is drawn with a surgical marker while the knee is in 70 degrees of flexion. It starts 7 to 8 cm proximal to the knee joint at the lateral intermuscular septum, traverses centrally over Gerdy’s tubercle, and extends distally 3 to 4 cm over the anterior compartment of the leg. The knee is then extended to verify that the incision is roughly a straight line in full extension. After the skin incision is made, the subcutaneous tissues are dissected to expose the superficial layer of the iliotibial band. A posteriorly based skin flap is developed using meticulous dissection along this layer until the long head of the biceps femoris is reached. At this point, a common peroneal neurolysis is performed. The common peroneal nerve is typically identified posterior and medial to the long head of the biceps (see Fig. 23F-24B). It is imperative to know the location of the nerve throughout the case and to ensure that it is free of any Continued



A

B

Figure 23F-24 Posterolateral corner approach. A, Marking of surgical incision. B, Peroneal nerve neurolysis performed posterior to the long head of the biceps femoris.

tension. In chronic injuries, the nerve is usually identifiable by direct palpation. If there is scar tissue present that makes identification of the nerve more difficult, the nerve may need to be identified proximally where it crosses posteriorly under the long head of the biceps tendon. After the neurolysis has been completed, a small Penrose drain is placed around it to allow it to be gently retracted from the surgical field. The superficial layer of the iliotibial band is then incised in line with its fibers from the supracondylar process of the femur proximally to Gerdy’s tubercle distally. This fascial incision is retracted to expose the femoral attachments of the fibular collateral ligament, the popliteus tendon, and the mid-third lateral capsular ligament (see Fig. 23F-3B). Next, a vertical arthrotomy is made through the meniscofemoral

portion of the mid-third lateral capsular ligament. This incision is about 1 cm anterior to, and parallel with, the fibular shaft when the knee is flexed to 70 degrees. This incision makes accessible the popliteus origin on the femur, the popliteomeniscal fascicles, and the lateral meniscus. A second fascial incision is made just posterior and parallel to the long head of the biceps femoris concurrent with the peroneal nerve neurolysis. The interval between the lateral head of the gastrocnemius and soleus is then developed by blunt dissection, providing access to the posteromedial aspect of the fibular styloid and the posterolateral aspect of the tibia (Fig. 23F-25). Palpation of the posterolateral aspect of the tibial plateau through this interval allows for identification of the posterior popliteal sulcus, located at

Figure 23F-25 Surgical approach to the posterolateral corner. Through the interval between the lateral gastrocnemius and soleus muscle, one can Biceps femoris palpate tears of the popliteofibular ligament (PFL), the popliteus tendon, and the posterior cruciate ligament (retracted) (PCL) at its attachment on the PCL facet on the posterior aspect of the tibia (lateral view, right knee). FCL, fibular collateral ligament. (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York, Thieme, 2006, p 148.) FCL PCL

PFL

Lateral gastrocnemius (retracted) Popliteus Soleus Common peroneal nerve (retracted)

knee 1739


A

B

Figure 23F-26 A, Split Achilles tendon allograft. B, Tubularization of split Achilles tendon allograft.

the musculotendinous junction of the popliteus. The popliteofibular ligament’s attachment site on the posteromedial down-slope of the fibular styloid is usually identified through this second fascial incision.19 If necessary, a third fascial incision may be made between the posterior border of the iliotibial tract and the anterior aspect of the short head of the biceps femoris. Graft preparation. Tendon grafts are prepared by splitting a calcaneus and Achilles tendon allograft into two equal portions parallel with the fibers of the tendon (Fig. 23F-26). The tendons must be at least 23 cm in length to complete the reconstruction in most patients. The bone blocks of the grafts are fashioned to fit 9 × 20-mm tunnels for the femoral attachments. Two drill holes are made in the bone blocks to hold sutures necessary for graft passage. The tendinous ends of the grafts are tubularized using a whipstitch. Fixation technique. Four bone tunnels are used in the reconstruction: two femoral, one tibial, and one fibular tunnel (Fig. 23F-27). A 7-mm tunnel is made through the fibular head from the attachment site of the fibular collateral ligament, on

the lateral aspect of the fibular head, to the attachment site of the popliteofibular ligament on the posteromedial downslope of the fibular styloid. The attachment site of the fibular collateral ligament is found by entering the bursa between the long head of the biceps femoris and the fibular collateral ligament (see Fig. 23F-3A). The tibial tunnel is created using a cannulated aiming guide placed on the posterior popliteal sulcus at the level of the musculotendinous junction of the popliteus. A guidewire is drilled in the anteroposterior direction from the distal medial aspect of Gerdy’s tubercle to the posterior popliteal tibial sulcus (see Fig. 23F-3C). It is important to leave a bony roof under the articular cartilage in the tibial tunnel. A 9-mm reamer is then passed over the guidewire from anterior to posterior to prepare the tunnel. The anatomic femoral attachments of the popliteus and fibular collateral ligament are once again identified. Two large Beath pins are then drilled parallel across the femur from the attachment sites, exiting proximal and medial to the medial epicondyle and adductor tubercle. It is important to measure the distance between the two Beath pins to verify

FCL- femur

FCL- femur

PLT- femur PFL/PLTtibia

PLT- femur

PFL/PLT -tibia FCL- fibula

PFL- fibula

A

B

FCL- fibula

Figure 23F-27 Fibular, tibial, and femoral tunnel placement for an anatomic posterolateral knee reconstruction. A, Lateral view. B, Posterior view. FCL, fibular collateral ligament; PLT, popliteus tendon; PFL, popliteofibular ligament. (Adapted from LaPrade RF, Johansen S, Wentorf FA, et al: An analysis of an anatomical posterolateral knee reconstruction: An in vitro biomechanical study and development of a surgical technique. Am J Sports Med 32[6]:1405-1414, 2004.) Continued



FCL PLT

PLT PFL

FCL

A

B

Figure 23F-28 The anatomic posterolateral knee reconstruction procedure. A, Lateral view, right knee. B, Posterior view, right knee. PLT, popliteus tendon; FCL, fibular collateral ligament; PFL, popliteofibular ligament. (Adapted from LaPrade RF, Johansen S, Wentorf FA, et al: An analysis of an anatomical posterolateral knee reconstruction: An in vitro biomechanical study and development of a surgical technique. Am J Sports Med 32[6]:1405-1414, 2004.)

that the attachment sites have been correctly identified. This distance should be about 18.5 mm. With the aid of the Beath pins, the two tunnels are then reamed, and the bone plugs are pulled into their respective holes in the femur by suture passage. The bone plugs are then secured with cannulated titanium interference screws. The graft fixed in the popliteus attachment on the femur is used to reconstruct the popliteus tendon. The free end of the graft is passed distally and medially through the popliteal

A

hiatus, reaching the posterolateral aspect of the lateral tibial plateau. The graft is passed through the tibial tunnel from posterior to anterior. The second graft, from the fibular collateral ligament attachment on the femur, is used to reconstruct the fibular collateral ligament and the popliteofibular ligament. It is passed deep to the superficial layer of the ITB and anterior arm of the long head of the biceps femoris, following the path of the native fibular collateral ligament. The graft is then passed through the fibular head from lateral to posteromedial. The knee is flexed to 30 degrees, and a slight valgus stress is applied to reduce any lateral compartment gapping. The graft is then pulled tight and fixed to the fibular head with a bioabsorbable interference screw, thus reconstructing the fibular collateral ligament. The remaining portion of the fibular collateral ligament graft is then passed from posterior to anterior through the tibial tunnel, reconstructing the popliteofibular ligament. With the knee flexed to 60 degrees and in neutral rotation, the popliteofibular ligament and popliteus tendon are secured using a bioabsorbable interference screw placed in the anterior tibial tunnel. These grafts are then reinforced using a staple over the free tendon ends on the anterior tibia. An examination under anesthesia is then performed to confirm that the grafts are securely fixed and functioning to prevent any varus, external rotation, or posterolateral rotation of the tibia on the femur (Figs. 23F-28 and 23F-29). When stability of the knee has been verified, wound closure is performed. The anterior arm of the long head of the biceps femoris is reattached to the fibula, attempting to reconstitute the biceps bursa. The lateral capsular arthrotomy is closed with horizontal mattress 0-0 absorbable sutures. The iliotibial band incision is also closed with 0-0 absorbable sutures. Copious irrigation is performed, and the subcutaneous tissue is closed with either 0-0 or 2-0 absorbable sutures. The skin is closed with a subcuticular nonabsorbable suture with a pullout stitch. Steri-Strips are loosely applied, followed by nonadherent dressings, circumferential cast padding, and a knee immobilizer (Box 23F-2).

B

Figure 23F-29 Anatomic posterolateral reconstruction procedure. A, Lateral view, left knee. B, Posterior view, left knee. FCL, fibular collateral ligament; PFL, popliteofibular ligament. (Adapted from LaPrade RF, Johansen S, Wentorf FA, et al: An analysis of an anatomical posterolateral knee reconstruction: An in vitro biomechanical study and development of a surgical technique. Am J Sports Med 32[6]:1405-1414, 2004.)

knee 1741

Authors’ Preferred Method—cont’d Box 23F-2 Surgical Pearls and Pitfalls Surgical Pearls

• A 1-cm horizontal incision through the anterior arm of

the long head of the biceps facilitates identification of the fibular collateral ligament. • A suture placed into the fibular collateral ligament, through the biceps bursa, facilitates identification of its course and potentially its femoral attachment site. • Placement of the transfemoral eyelet pins should aim through the anatomic attachment sites of the popliteus tendon and fibular collateral ligament laterally to slightly proximal and anterior to the adductor tubercle on the anteromedial aspect of the knee. • The entry site anteriorly for the tibial reconstructive tunnel should be just distal and medial to Gerdy’s tubercle along its flat spot; lateral to this, the tibia downslopes at the anterior compartment and it is difficult to place in a proper tunnel and obtain fixation. • The initial part of the surgical procedure may be performed without a tourniquet; the initial surgical approach, identification of the fibular collateral ligament through the biceps bursa, the common peroneal nerve neurolysis,

and identification and reaming of the fibular head and tibial tunnels may be done with minimal bleeding. Surgical Pitfalls not place the fibular head tunnel too proximal. It may not preserve a good cortical rim of bone at the superior aspect of the fibular tunnel. • Drilling the tibial tunnel too distal at its exit site on the posterolateral tibia could result in a horizontal popliteofibular ligament graft. The tibial tunnel posteriorly should exit 8 to 10 mm proximal from the exit site of the fibular head tunnel. Therefore, the fibular head tunnel should be reamed first, to serve as a reference guide, before drilling the tibial tunnel. • Placing the transfemoral eyelet pins too parallel to the joint may result in the passing sutures going through the intercondylar notch or the guide pins hitting a posterior cruciate ligament femoral tunnel. • Not tubularizing the reconstructive grafts accurately at their ends may result in them bunching up when attempting to pass them through the fibular or tibial tunnels.

• Do

Adapted from LaPrade RF: Posterolateral knee injuries: Anatomy, evaluation, and treatment. New York, Thieme, 2006.

POSTOPERATIVE REHABILITATION, OUTCOMES, AND COMPLICATIONS Postoperative Rehabilitation The postoperative protocol for these injuries can vary depending on the surgical technique, whether the injury is acute or chronic, the presence of associated ligamentous injuries, and the overall health status of the patient. In the acute setting for repair or reconstruction of the PLC, the authors’ preferred rehabilitation protocols are similar.5 The patients are kept non–weight-bearing for 6 weeks. An immobilizer is used to maintain full extension for 1 to 2 weeks, followed by gentle increases in range of motion. Straight leg raises and quadriceps exercises are instituted while the immobilizer is in place (Fig. 23F-30). Open chain hamstring exercises are avoided for 4 months to eliminate hamstring contraction and subsequent stress to the repair site. After 6 weeks, patients are allowed a slow and progressive increase in weight-bearing, weaning from crutches, and light work on an exercise bike. Closed chain leg presses are started, using one fourth of their body weight and limiting knee flexion to 70 degrees. At 3 months, increased activity and jogging are allowed, along with increasing weight with leg presses and increased resistance on the exercise bike. Four months after surgery, patients undergo knee stability evaluation and functional capacity testing for determination of return to play or full activity. In the situation of acute,

combined PLC and cruciate injury, the surgical rehabilitation protocol is generally guided by the PLC injury for the first 6 weeks, followed by attention to specific needs based on the type of cruciate reconstruction. In the chronic posterolateral injury, the authors prefer to reconstruct the fibular collateral ligament, popliteus tendon, and the popliteofibular ligament.5,11 It is imperative that during the early postoperative rehabilitation period, extra stress is not placed on these grafts by knee motions that could lead to stretching and subsequent failure. Thus, the rehabilitation process focuses on developing strong

Figure 23F-30 Nonoperative management. Patient in knee immobilizer performing straight leg raise.

1742 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 23F-4 Postoperative Rehabilitation Protocol for

the Chronic Posterolateral Knee Reconstruction Procedure Recovery Time

Rehabilitation Process

Early postoperative period

Knee immobilizer at all times, other than working on range of motion (ROM) No weight-bearing for 6 wk Avoid tibial external rotation, no hamstring exercise for 4 mo Elevation for control of swelling Quad sets hourly and straight leg raises 4-5 times/ day in immobilizer Gentle ROM 4 times/day out of immobilizer Goal: 90 degrees of knee flexion by 2 wk Increase ROM and quad strengthening Achieve full knee extension and maintain Increase flexion past 90 degrees Initiate weight-bearing, wean from crutches when limp has resolved Begin low-impact closed chain exercise Continue quad sets and straight leg raises Exercise bike once flexion of 105 to 110 degrees obtained; start with 5 min daily with low resistance and advance as tolerated Goals: full range of motion, normal gait pattern Increase in functional strength program Goals: improved quad strength/function, increased endurance, improved coordination/proprioception Walking program: 20 to 30 min daily Biking: increase resistance as tolerated, 3-5 times/ wk for 20 min Step-ups: place operative knee on step and step up, increase repetitions as tolerated Continue maintenance exercise program 3-5 times/wk Strive for maximal strength to operative extremity No competition or pivot sports until cleared by surgeon

Weeks 1 to 2

Weeks 3 to 6 Weeks 7 to 12

Weeks 13 to 16 Months 4 to 6

Months 7 and later

musculature support around the knee to protect the reconstruction during early recovery as well as during normal activity in the future (Table 23F-4).5

Potential Complications As with any operation, PLC surgery has potential complications. Risk for infection and wound breakdown are worrisome complications, especially in the setting of an acute injury or open knee dislocation.5 Surgical planning includes time for soft tissue recovery and resolution of swelling before operative intervention. In the chronic instability patient, previous surgical scars may be present, and surgical approaches should be altered to incorporate these incisions to minimize skin devascularization. Common peroneal injury can occur if careful surgical technique and dissection are not employed. However, between 15% and 29% of posterolateral knee injuries have associated peroneal nerve injury.29,43,46 Thus, it is important to perform a thorough motor and sensory examination of this nerve before surgical intervention so that proper documentation of nerve status is completed preoperatively and a baseline is established. Postoperative arthrofibrosis may occur, especially in the setting of acute PLC surgery and concomitant medial

Figure 23F-31 Anteroposterior standing varus thrust radiograph demonstrating varus laxity after posterolateral corner repair (right knee). (Adapted from LaPrade RF: Treatment of posterolateral knee injuries. In Gumpert E [ed]: Posterolateral Knee Injuries: Anatomy, Evaluation, and Treatment. New York, Thieme, 2006, p 88.)

c ollateral ligament injury.5 Deep venous thrombosis, chro nic pain, and symptomatic hardware may also occur. Additionally, recurrent laxity or instability has been reported (Fig. 23F-31). This can hopefully be avoided by proper preoperative evaluation and diagnosis of associated ligamentous injuries, proper graft and tunnel placement, and appropriate immobilization and rehabilitation protocols following surgical repair.

Return to Play The timing for return to play varies depending on the acute or chronic nature of the original injury and subsequent repair versus reconstruction (Box 23F-3). Surgical technique and associated ligamentous injuries also factor into the length of convalescence. Following acute surgical repair and reconstruction of the PLC, some high-level intercollegiate athletes have returned to full participation 4 months after surgery.5 All these patients had a return of normal knee range of motion, strength, and stability before return to play. In the chronic or combined ligament reconstruction setting, time for return to play may not occur until 6 or 9 months after surgery.5,47,72 Box 23F-3 Return to Play Criteria

•�� Near maximal strength compared with uninvolved limb •�� Full range of motion •�� No instability •�� No pain or swelling with activity •�� No limp •�� Complete sport-specific or functional tests

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Although the timing for return to play is based on multi ple factors, the criteria for return to play can be generalized (see Box 23F-3). First, the patient should have regained normal range of motion and strength compared with the uninvolved side. Maximal strength of the quadriceps and hamstring complexes is essential. Well-placed and functional grafts can stretch out over time if one relies on graft integrity for knee stability rather than having appropriately rehabilitated musculature. In addition, the patient should be without a limp, resultant swelling or pain, or symptoms of instability with activity and sport participation. These criteria can be accurately assessed by performing functional or sport-specific tests that challenge the patient through maneuvers and drills with similar duration and intensity that their particular sport requires.

EVIDENCE-BASED MEDICINE Incidence Injuries to the posterolateral aspect of the knee occur less frequently than injuries to the cruciate ligaments or medial aspect of the knee. The overall incidence of knee ligament injuries is about 1 per 1000 patients per year.73 DeLee and associates retrospectively reviewed 735 knee ligament injuries from 1971 through 1977.42 They found that 12 patients (1.6%) had acute isolated posterolateral knee injuries, whereas 32 (44%) other patients had posterolateral injuries with associated cruciate ligament tears. This resulted in a total incidence of 5.8%. In a consecutive MRI series of 481 knees, Miller and coworkers reported a 6% incidence in 30 patients with posterolateral knee injuries.74 The difficulty in diagnosing posterolateral injuries has led authors to believe that the overall incidence of these injuries has been undetected or underreported.41,42,46,75 Fanelli and Edson reported on a consecutive group of 222 patients with a knee hemarthrosis in a tertiary trauma center, with 28.4% having posterolateral injuries.76 Within this group of 222 patients, 85 had PCL tears, of which 53 (62%) had concurrent posterolateral injuries. Also, 148 of the 222 patients had ACL tears, and 18 (12%) had concurrent posterolateral injuries. LaPrade and colleagues reported on a group of 100 consecutive ACL reconstructions with an 11% incidence of concurrent posterolateral instability.25 In summary, the incidence of posterolateral injuries appears to be between 5.8% and 11%, with up to 28.4% in a tertiary trauma setting. This is in agreement with the belief of most authors that the true incidence of posterolateral knee injuries has been underreported. Hopefully, improved awareness of these injuries and better clinical acumen in diagnosing them will provide future studies with more accurate data.

Cause of Graft Failure Undetected or untreated injuries to the PLC have been identified as a cause of failure of anterior and PCL reconstructions.77-79 Noyes and colleagues reported on a consecutive series of 41 patients with ACL tears, genu varus alignment, and posterolateral instability.79 Of the

41 patients, 15 had a combined total of 19 previous ACL reconstructions that failed. They believed that most of the failures were due to unrecognized posterolateral instability. Noyes and Barber-Westin also reported that between 1990 and 1996, 18 (30%) of 57 patients who underwent revision ACL reconstruction with bone–patellar tendon–bone autografts had untreated or unrecognized posterolateral injuries, apparently contributing to graft failure from the index reconstruction.77 LaPrade and coworkers used a selective ligament cutting technique to determine whether untreated injuries of the posterolateral structures of the knee contribute to increased force on an ACL reconstruction graft, thus potentially leading to graft failure.17 The force on the ACL graft during varus loading at both 0 and 30 degrees of knee flexion was significantly higher after cutting the FCL. The increase in graft force remained significant with additional sequential cutting of the popliteofibular ligament and popliteus tendon. Harner and colleagues evaluated a PCL reconstruction in isolated and combined injury models using a roboticuniversal force-moment sensor testing system.32 In the isolated injury model, reconstruction reduced posterior tibial translation to within 1.5 mm of the intact knee at 30 degrees and 2.4 mm at 90 degrees of knee flexion with a 134-N posterior tibial load applied to the knee. In the combined injury model, posterior tibial translation was increased by 6.0 mm at 30 degrees and 4.6 mm at 90 degrees for the PCL reconstruction compared with the intact knee. Also, external rotation increased up to 14 degrees, and varus rotation increased up to 7 degrees. In situ forces in the PCL graft also increased significantly (22% to 150%) for all loading conditions when the posterolateral structures were cut. Another study by LaPrade and colleagues analyzed untreated posterolateral knee injuries with PCL reconstruction.33 A significant increase in force on the PCL graft was seen when the popliteofibular ligament, popliteus tendon, and fibular collateral ligament were cut compared with intact posterolateral structures when both a varus moment and external rotation torque at 30, 60, and 90 degrees of knee flexion was applied.

Functional Limitations Many authors believe that most patients with PCL tears and functional instability with activity have associated posterolateral rotatory instability of the knee.76 Kannus observed that patients with posterolateral injuries have a higher incidence of osteoarthritis over time.37 Twenty-three patients were followed who had been treated nonoperatively for a grade II or III sprain of the posterolateral complex. At an average of 8 years after the injury, the 11 patients with a grade II sprain had an excellent or good result as assessed with standardized scales. Nine were asymptomatic; however, all had residual laxity. The 12 patients with a grade III sprain had much worse results, with average scores of either fair or poor. Six of the 12 patients with a grade III injury had post-traumatic arthritis on radiographic evaluation, whereas none of the patients with grade II injuries had any radiographic evidence of arthritic changes. A biomechanical study by Skyhar and colleagues used Fuji pressuresensitive film to observe the articular contact pressures in


10 cadaveric knees before and after sequential sectioning of the PCL and the posterolateral complex (the posterolateral capsule, the popliteus muscle and tendon, and the fibular collateral ligament).38 Patellofemoral pressures and quadriceps load were most significantly elevated after combined sectioning of the PCL and the posterolateral complex. Medial compartment pressure was significantly elevated after sectioning of the PCL. They concluded that patients with combined PCL and posterolateral injuries need to be informed about the increased risk for osteoarthritis of these compartments if their injuries were not treated.

Treatment Options For grade I and grade II injuries, nonoperative treatment is almost always recommended.62 Baker and associates observed 13 patients treated nonoperatively who were believed to have isolated grade I PLC injuries.46 All 13 were noted to have returned to their full preinjury level of activity. It is well documented that grade III posterolateral injuries have a low likelihood of healing, and operative treatment is necessary to ensure the best clinical outcome possible.7,37 Furthermore, the results of an acute repair are much better than repair or reconstruction of chronic injuries.42,44,78 However, Stannard and colleagues recently reported a nonrandomized study comparing acute PLC repair to acute reconstruction.69 Fifty-six patients with 57 PLC injuries had a minimum 24-month follow-up. Acute primary repair was performed on 35 patients, with 22 successful outcomes and 13 (37%) failures. Primary reconstructions were performed on 22 patients, with 20 successful outcomes and 2 (9%) failures. They concluded that repair followed by early motion rehabilitation was significantly inferior compared with reconstruction using the modified two-tailed technique.

SPECIAL CONSIDERATIONS Skeletally Immature Patients The basic anatomy and biomechanics of the lateral and posterolateral corners of the knee is described earlier in this chapter. The knee capsule, ligaments, and cartilaginous structure of the knee first appear as an undifferenti ated blastema cell mass at about 5 weeks’ gestation. By week 7 of embryonic development, the individual structures can be identified. PLC knee injuries are rare in skeletally immature populations; however, physeal fractures are more common. Stress radiographs can be extremely helpful in this population.

Chronic Reconstructions The first step in assessing chronic PLC instability involves assessing the patient’s alignment. It has been well documented that failure to correct concomitant genu varum results in failed operative repair or reconstruction of chronic posterolateral injuries.25,79 Varus alignment and the resulting lateral thrust with foot strike place excessive

tension on the repaired or reconstructed lateral structures. Thus, it is vital to correct any genu varus alignment of the lower extremity before any soft tissue reconstructions of the PLC of the knee. Once again, a medial compartment unloader brace may be beneficial in determining who will have improved stability with a proximal tibial osteotomy.

Proximal Tibial Opening Wedge Osteotomy for Genu Varus and Chronic Posterior Cruciate Ligament Instability Preoperatively, long-leg anteroposterior films are obtained to determine the mechanical axis of the lower extremity. If the mechanical axis falls medial to the medial tibial spine, a proximal tibial osteotomy is recommended. If concurrent ACL instability is noted, it is recommended that the sagittal slope be tilted anteriorly to address this laxity pattern (Fig. 23F-32). Conversely, for patients with a concomitant PCL tear and chronic PLC instability, an increase in the posterior tibial slope is recommended. In patients with genu recurvatum, it is thought that increasing the sagittal slope of the tibia posteriorly increases stability. In pure chronic grade III PLC injuries, a pure valgus opening wedge osteotomy is recommended.

Proximal Tibial Osteotomy Technique A standard surgical incision is made vertically on the tibia medially between the tibial tubercle and the posterior border of the tibia to a point just distal to the midportion of the tibial tubercle. The incision is made directly down to bone to avoid skin flap formation. A small periosteal elevator is used to perform a subperiosteal dissection anteriorly under the deep infrapatellar bursa and patellar tendon just proximal to the tibial tubercle. A small Z-retractor is then placed into this location to identify where to make the proximal tibial anterior cut. Posteriorly, a subperiosteal dissection of the tibial collateral ligament and popliteus off the proximal tibia is performed. A radiolucent retractor is placed posteriorly to protect the neurovascular bundle during the subsequent portions of the procedure. Fluoroscopy is used to confirm the placement of two guidewires parallel to the joint line starting just distal to the flare of the proximal medial tibia (Fig. 23F-33A). The slope of the guidewires should attempt to replicate the desired sagittal slope of the proximal tibia after the osteotomy is completed. Initially, an oscillating saw performs the osteotomy. Secondarily, osteotomes are used to complete the osteotomy anteriorly and posteriorly (see Fig. 23F-33B). The lateral-most 1 cm of the tibia should be preserved as the osteotomy is hinged from this location. A spreader device is then slowly inserted into the defect, and the osteotomy is gradually opened to the desired correction. Care is taken to prevent propagation of the osteotomy either into the lateral cortex or the intra-articular portion of the lateral compartment. If the lateral cortex becomes compromised, a bone staple is placed laterally to provide stability. A plate is then used to secure the osteotomy. With concomitant ACL insufficiency, the plate is placed as far posterior as needed to decrease the slope of the proximal tibia so that the anterior tibial cortex acts as a hinge with the lateral cortex. Conversely, PCL insufficiency requires the

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A

B

C

D

F

E Figure 23F-32 Chronic combined posterior cruciate ligament and posterolateral corner ligament injury with varus malalignment. A, Preoperative clinical photograph of knee at 90 degrees of flexion without stress. B, Preoperative clinical photograph of a 3+ posterior drawer. C, Preoperative bent knee stress radiograph demonstrating increased posterior sag consistent with a posterior cruciate ligament injury. D, Preoperative varus stress radiograph consistent with a posterolateral corner ligament injury. E, Preoperative longleg radiograph demonstrating varus malalignment. F, Preoperative lateral radiograph demonstrating the patient’s natural posterior tibial slope.

plate to be placed more anteriorly. Standard screw fixation is performed, filling the most proximal and distal holes first, then filling the central holes. An allograft or autograft cancellous bone graft is placed into the osteotomy site. Excess bone graft is removed to minimize the chance of drainage postoperatively (see Fig. 23F-33C and D). The periosteum is closed over the plate followed by subcutaneous

and then skin tissue. Postoperatively, quadriceps sets are frequently performed in a knee immobilizer. The immobilizer is removed 4 times daily to work on range of motion. By 2 weeks after surgery, a goal of 90 degrees of range of motion is usually met. The patient is kept non–weightbearing in a knee immobilizer for 8 weeks. If consolidation of trabecular bone on the lateral portion of the osteotomy


A

B

C

D

E

F

Figure 23F-33 Opening wedge proximal tibial osteotomy. A, Fluoroscopic (anteroposterior) view demonstrating that the guide pin is parallel to the joint line before performing the proximal tibial osteotomy. B, Completed proximal tibial osteotomy with cut placed strategically to increase the posterior slope. C, Proximal tibial opening wedge osteotomy with spreader device in place. D and E, Anteroposterior and lateral fluoroscopic image demonstrating completed proximal tibial osteotomy with anteriorly placed osteotomy plate and bone graft. Posterior tibial slope has been increased in order to decrease the posterior drawer. F, Immediate postoperative clinical photograph demonstrating minimal posterior drawer after sagittal plane correction with opening wedge osteotomy.

is seen, the patient is gradually allowed to increase their weight-bearing from 25% initially, increasing by 25% weekly, to full by 3 months after surgery. After 6 months, standing long-leg radiographs are obtained to confirm corrective coronal and sagittal plane alignment and to determine whether a second-stage reconstruction is necessary. It is important to note that the osteotomy site must be

completely healed before proceeding to the second-stage reconstruction, which is typically 8 to 9 months after the osteotomy. The hardware is removed at the time of cruciate and PLC reconstructions. Multiple anatomic and nonanatomic techniques have been described; the choice of technique should be based on the injury pattern and surgeon preference.

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C

r i t i c a l

P

S U G G E S T E D

o i n t s

l

I mportant structures include the FCL, popliteus muscletendon complex, and PFL. l The PLC structures provide varus, external rotational, and posterior stability to the knee. l PLC injuries are underdiagnosed; therefore, high suspicion and thorough examination are critical. l PLC injuries are often associated with concomitant injuries (e.g., ACL, PCL injuries). l Untreated PLC injuries result in increased failure rates of ACL and PCL reconstruction and poorer outcomes. l Malalignment must be addressed before or in conjunction with PLC reconstruction. l Acute treatment has improved outcomes compared with chronic treatment. l Reconstruction procedures have improved outcomes compared with primary repair procedures.

R E A D I N G S

Harner CD, Vogrin TM, Hoher J, et al: Biomechanical analysis of a posterior cruciate ligament reconstruction: Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med 28:32-39, 2000. Hughston JC, Andrews JR, Cross MJ, et al: Classification of knee ligament instabilities. Part II: The lateral compartment. J Bone Joint Surg Am 58:173-179, 1976. Kannus P: Non-operative treatment of grade II and III sprains of the lateral ligament compartment of the knee. Am J Sports Med 17:83-88, 1989. LaPrade RF: Arthroscopic evaluation of the lateral compartment of knees with grade 3 posterolateral complex knee injuries. Am J Sports Med 25:596-602, 1997. LaPrade RF: Posterolateral knee injuries: Anatomy, evaluation, and treatment. New York, Thieme, 2006. LaPrade RF, Gilbert TJ, Bollom TS, et al: The magnetic resonance imaging appearance of individual structures of the posterolateral knee: A prospective study of normal knees and knees with surgically verified grade III injuries. Am J Sports Med 28:191-199, 2000. Noyes FR, Barber-Westin SD: Surgical restoration to treat chronic deficiency of the posterolateral complex and cruciate ligaments of the knee joint. Am J Sports Med 24:415-426, 1996. Skyhar MJ, Warren RF, Ortiz GJ, et al: The effects of sectioning of the posterior cruciate ligament and the posterolateral complex on the articular contact pressures within the knee. J Bone Joint Surg Am 75:694-699, 1993.


S e c t i o n

G

Multiple Ligament Knee Injuries Gregory C. Fanelli, Justin D. Harris, Daniel J. Tomaszewski, John T. Riehl, Craig J. Edson, and Kristin N. Reinheimer

Knee dislocations are true orthopaedic emergencies. They can result from high-energy trauma in addition to lowenergy mechanisms. The observed incidence of these injuries is relatively low (less than 1 in 100,000 of all hospital admissions).1 However, this number is likely underrepresentative of the true incidence because many knee injuries spontaneously reduce and do not demonstrate radiographic evidence of dislocation at initial presentation. Most knee dislocations involve tears of the central pivot, including both the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL) along with one or both of the collateral ligaments. In addition to ligamentous injuries, significant capsular and meniscal injury can be present. Fractures and extraneous trauma are not uncommon. Vascular and nervous injuries occur relatively frequently in the multiple ligament–injured knee. They must be evaluated promptly and comprehensively. A detailed neurovascular examination is essential both before and after reduction. Historically, nonoperative treatment consisting of immobilization was deemed acceptable in most instances. With the advent of current arthroscopic techniques of multiple ligament reconstruction, nonoperative treatment is frequently limited to patients with very low functional demands.

RELEVANT ANATOMY AND BIOMECHANICS The knee is primarily a ginglymus (hinge) joint that allows some rotation of the tibia on the femur. Normal range of motion is from 0 degrees of extension to roughly 140 degrees of flexion. Internal and external rotation are typically 10 degrees in either direction, and external rotation allows “locking” of the knee joint in full extension. Stability of the knee is maintained in part by the bony articulation between the femoral condyles and the tibial plateau. Medial and lateral menisci increase the contact surfaces and thus increase static stability to the joint.

Osseous Anatomy The osseous anatomy of the knee consists of the primary articulations of the distal femur, the proximal tibia, and the patella. The distal femur is divided into medial and lateral condyles. The size of the condyles is asymmetric, with the medial condyle projecting more distally and the lateral condyle projecting more anteriorly. The condyles are separated by the trochlear groove, which makes up the patellofemoral articulation.2


The tibial plateau has an approximate 10-degree posterior slope. The medial plateau is slightly concave, whereas the lateral plateau has a more rounded appearance. Although the tibial plateau is somewhat flattened relative to the curved distal femur, congruency is maintained within the knee as the menisci help to increase conformity within the tibiofemoral articulation. The tibial spines separate the medial and lateral plateaus and serve as attachments for the menisci and cruciate ligaments. The patella is the largest sesamoid bone in the body and serves as a fulcrum for the extensor mechanism as well as providing a protective surface for the anterior aspect of the knee.

Ligamentous Anatomy The most significant ligamentous stabilizers of the knee include the ACL, PCL, medial collateral ligament (MCL), and lateral collateral ligament (LCL). In addition, the posteromedial and posterolateral corners (PLCs) of the knee are important structures that also contribute to knee stability. The ACL originates on the posteromedial lateral femoral condyle and courses anteriorly and distally to insert anterior and between the intercondylar eminences on the tibial plateau. The ACL consists of two anatomic bundles. The anteromedial bundle is taut in flexion, whereas the posterolateral bundle is more convex and tight in extension.3 The ACL is typically 30 to 38 mm in length and 10 to 12 mm width. It is an intra-articular structure, yet it has its own synovial membrane. It receives its blood supply from the middle geniculate artery and is innervated by the posterior articular nerve.4 The primary function of the ACL is to resist anterior translation of the tibia relative to the distal femur, but it also serves as a secondary adjunct to varus and valgus stability in full extension. The PCL has a broad femoral origin on the posterolateral aspect of the medial femoral condyle and inserts centrally on the posterior tibial plateau. It is an intra-articular structure but is also encompassed by its own synovial sheath. The anterolateral bundle of the PCL is tight in flexion, whereas the posteromedial bundle receives more tension in extension.5 These bundles are supplemented by the posterior meniscofemoral ligaments. The average length of the PCL is 38 mm, and its width is 13 mm.6 The vascularity of the PCL is supplied by the middle geniculate artery, and it is innervated by nerve fibers from the popliteal plexus from the tibial and obturator nerves.7 The PCL resists posterior translation of the tibia and is a secondary restraint to tibial external rotation. The MCL and the posteromedial corner are the primary restraints to valgus stress in the knee. The anatomy of the medial side of the knee has been described by Warren and Marshall8 in terms of layers. The most superficial layer is the sartorial fascia. The second layer consists of the superficial MCL. The deep MCL and the medial joint capsule are found in layer three. Alternatively, the medial side of the knee can be divided into thirds from anterior to posterior. The anterior third consists of capsular ligaments covered by the extensor retinaculum. The middle third contains the superficial and deep

MCL. The posteromedial corner occupies the posterior third and includes the posterior oblique ligament, the oblique popliteal ligament, and the termination of the semimembranosus. The superficial MCL is the primary restraint to valgus stress of the knee at 30 degrees of knee flexion. Its origin is on the medial epicondyle of the distal femur, and it inserts just posterior to the insertion of the pes anserinus. The posterior oblique ligament, semimembranosus, and oblique popliteal ligament resist valgus stress in full extension as well as anteromedial rotatory instability. The lateral side of the knee has also been divided into layers.9 The most superficial layer consists of the iliotibial band and the biceps femoris. The peroneal nerve lies deep to the biceps at the level of the distal femoral condyle. The middle layer consists of the patellar retinaculum anteriorly and the patellofemoral ligaments posteriorly. The deep layer, layer three, consists of the LCL, popliteal tendon, popliteofibular ligament, fabellofibular ligament, arcuate ligament, and lateral joint capsule. The LCL is the primary restraint to varus stress with the knee in 30 degrees of flexion. It originates on the lateral femoral condyle, just superior and posterior to the axis of motion. It attaches on the fibular head. The remaining structures in layer III make up the PLC. The PLC provides static support to resist posterior translation of the tibia as well as external rotation and varus angulation.

Neurovascular Anatomy A detailed understanding of the neurovascular anatomy of the knee is critical if one is going to treat patients with knee injuries. The neurovascular bundle within the pop liteal fossa is at great risk in knee dislocations because of a few anatomic features. The popliteal fossa is bordered by the biceps femoris tendon at its superior lateral border, the semimembranosus muscle superomedially, and the two heads of the gastrocnemius muscle inferiorly. Within the popliteal fossa, the popliteal artery and vein are separated by a thin layer of fat from the underlying posterior joint capsule. Crossing through the popliteal fossa, from superficial to deep, are the posterior tibial nerve, the popliteal vein, and popliteal artery. With the knee in full extension, the popliteal fascia is tensioned, making palpation of the popliteal artery difficult. Proximally, the popliteal artery emerges from the adductor hiatus and is tethered to this fibrous tunnel. Distally, the popliteal artery is also relatively immobile as it enters another fibrous canal deep to the soleus. These two somewhat immobile points leave the popliteal artery vulnerable to injury when the knee is dislocated. Superior, inferior, and middle geniculate branches branch off of the popliteal artery but are unable to maintain adequate collateral circulation in the event of a vascular injury. As the sciatic nerve emerges into the popliteal space from between and deep to the long head of the biceps and the semitendinosus muscles, it divides into the tibial and common peroneal nerves at a variable level. After dividing, the common peroneal nerve continues along the lower edge of the biceps toward the fibula, crossing superficially to the lateral head of the gastrocnemius.

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The tibial nerve continues down the middle of the popliteal fossa and gives off muscular branches to the plantaris and gastrocnemius muscles. The common peroneal nerve then courses distally around the fibular head to innervate the anterior and lateral compartments of the lower leg.

CLASSIFICATION Numerous classification systems exist to describe knee dislocations. The most commonly used method is by describing the direction of displacement of the proximal tibia relative to the distal femur. However, this system does not account for spontaneously reduced dislocations and may fail to recognize other variations of the multiple ligament–injured knee. Additional characteristics that may help to classify a knee dislocation include the mechanism of injury, the presence or absence of open wounds, the degree of displacement, and the status of the neurovascular structures. In practice, all these characteristics are helpful in the classification of the multiple ligament–injured knee and can assist in determining optimal treatment. The directional classification of knee dislocations is based on the position of the tibia relative to the distal femur. Anterior dislocations occur following a hyperextension injury greater than 30 degrees and are the most common directional dislocation. Posterior knee dislocations occur in 25% of all knee dislocations and typically result from a posteriorly directed force applied to the proximal tibia. Lateral, medial, and rotatory dislocations have also been described.10 High-energy dislocations typically follow motor vehicle collisions and falls from height. Low-energy injuries typically refer to those that occur during athletic activities.11 An ultralow-energy dislocation has been described in morbidly obese patients who sustain severe ligamentous injury following seemingly trivial trauma.12 An anatomic classification system was created by Schenck (Table 23G-1), in which these injuries are classified based on the specific structures about the knee that are compromised. This system describes the ligamentous injury pattern and uses the letter C to designate a circulatory injury, whereas the letter N indicates neurologic injury. It has been used by some authors to direct treatment and predict outcome.13

TABLE 23G-1 Schenck Anatomic Classification of Knee Dislocations Type

Description

KD-I KD-II

Dislocation with intact posterior cruciate ligament Dislocation with complete bicruciate disruption, collaterals intact Complete bicruciate disruption with one collateral disrupted Complete bicruciate dislocation with both collaterals disrupted Dislocation with periarticular fracture Associated vascular injury Associated neurologic injury

KD-III KD-IV KD-V C N

EVALUATION Clinical Presentation and History Knee dislocations, resulting in multiple ligament injuries, are seen in as few as 0.001% of all patients receiving attention for orthopaedic injury.1,14,15 Despite a relatively low annual incidence, a thorough evaluation and comprehensive physical examination are essential because the diagnosis is often missed in the setting of multi-injury trauma. Two common mechanisms of injury have been identified. Sporting injuries often represent a lower energy mechanism, and patients can often present with an isolated knee injury. In contrast, high-energy trauma involving motor vehicles can present a very different picture. Many times, a multiple ligament–injured knee can be overlooked as extremity trauma takes a back seat to more pressing, life-threatening injuries. There is also a subset of patients whose knee dislocations may spontaneously reduce before formal orthopaedic evaluation. The direction of the force vector applied to the knee determines the ultimate position of the dislocation as well as the structures that become injured. Anterior dislocation of the proximal tibia relative to the distal femur typically results from hyperextension of the knee. A posteriorly directed force, such as seen in a dashboard injury, results in posterior dislocation of the tibia. Pure varus or valgus stresses lend to lateral or medial dislocations, respectively. Combined forces can lead to rotational dislocation. In any case, patients with a plausible mechanism and knee pain should have a complete and through knee examination. A high index of suspicion for neurovascular insult is essential.

Physical Examination and Testing Evaluation of the knee with multiple ligament involvement mandates a systematic approach in order to accurately identify all potential injuries. A comprehensive musculoskeletal and neurovascular examination supplemented with appropriate ancillary studies helps the physician formulate a treatment plan. A knee dislocation represents the most dramatic example of the multiple ligament–injured knee. Obvious deformity may be present and a grossly dislocated knee is unlikely to escape diagnosis. However, dislocations that have spontaneously reduced may present more subtly. Complete disruption of two or more knee ligaments should alert the clinician to the possibility of a spontaneously reduced knee dislocation.16 Without proper evaluation and treatment, considerable adverse sequelae and morbidity may result. A thorough history, including mechanism and position of the limb at the time of injury may provide clues to possible ligamentous involvement. Any manipulation of the limb before the patient’s arrival in the emergency department should be noted. A detailed secondary survey should be conducted to assess the other extremities for signs of trauma. The contralateral lower extremity can also be used as a control to compare side-to-side differences with the injured knee with regard to ligament integrity and neurovascular status.


Examination begins with simple inspection (Fig. 23G-1). Resting limb posture should be noted. The presence of lacerations, deformity, skin dimpling, swelling, ecchymosis, and peripheral skin color changes can all provide valuable clues to the mechanism and severity of injury and can potentially affect management. For instance, a “dimple sign” about the anteromedial surface of the knee has been associated with the medial femoral condyle being incarcerated within the medial joint capsule. This injury may be irreducible by closed means and may necessitate immediate open reduction in the operating room to prevent skin necrosis. Likewise, a traumatic arthrotomy, if present, should be identified quickly because open knee dislocations portend a particularly poor outcome. Complete neurovascular examination is the most essential aspect of the initial evaluation. A detailed sensory and motor examination is often difficult to perform in a polytrauma patient. Integrity of the tibial and peroneal nerves should be evaluated and documented. This serves mostly as a baseline for comparison when serial neurovascular examinations prove necessary. More important is the continuity and function of the popliteal artery. The incidence of vascular injury in patients with knee dislocations has been estimated to be anywhere from 16% to 64%.14,17 The popliteal artery is particularly vulnerable because it is relatively tethered between the adductor hiatus and the gastrocnemius-soleus arch. Active hemorrhage, expanding hematoma, and a bruit in the popliteal fossa are all signs of a vascular injury. Two discrete injury patterns to the popliteal artery have been described. Stretching of the popliteal artery, as is often seen with knee hyperextension and anterior dislocation, results in intimal injury. This patient may have a well-perfused limb with intact peripheral pulses. The only sign of injury may be a reduced palpable pulse or Doppler signal compared with the contralateral limb. This is a worrisome injury. The vessel can develop late thrombosis, which can threaten the viability of the entire lower limb if not found promptly. Faithful serial vascular examinations are mandatory. The other described injury pattern involves direct contusion or transection of the artery as is seen with

posterior knee dislocations.10 This injury should be evaluated emergently by a vascular surgeon. Under no circumstances do the presence of pulses rule out arterial injury. The remainder of the physical examination involves evaluation of all extremities with particular attention to the affected knee. Gross deformity or bony crepitus should be noted. Testing the integrity of the major knee ligaments is often difficult in the acute trauma setting. A comprehensive examination generally requires conscious sedation or general anesthesia. A stabilized Lachman’s test, in which the examiner places his or her thigh under the affected knee, allows for a reasonably comfortable and accurate evaluation of anterior and posterior end points. Gross varus or valgus laxity in full extension implies disruption of a collateral ligament, one or both cruciates, and associated capsular injury. Varus or valgus laxity in 30 degrees of flexion better isolates the lateral and medial collateral ligaments, respectively (Fig. 23G-2).

Figure 23G-1 Patient with bilateral multiple ligament– injured knees. Contusions indicate the possibility of knee ligament injury.

Figure 23G-2 Severe valgus laxity in full extension indicating combined posterior and anterior cruciate ligament medial-sided complete tears.

Associated Injuries As stated, knee dislocations often occur in the setting of high-energy trauma. As such, a comprehensive primary and secondary trauma survey are necessary to rule out internal injury as well as injury to the remainder of the axial and appendicular skeleton. Any or all of the four major ligaments about the knee as well as the posteromedial and PLCs can be compromised. Additionally, vascular and neurologic injuries are common. Furthermore, osseous injuries to the distal femur, proximal tibia, patella, and proximal fibula are occasionally associated with knee dislocations. Meniscal tears and osteochondral injuries can also occur.

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Vascular Injuries Vascular injury following a knee dislocation is not uncommon. The estimated incidence in the literature is anywhere from 16% to 64%,14,17 with most studies citing a 32% incidence.10 As mentioned, popliteal artery trauma can occur by direct rupture or intimal tear. Both can lead to disastrous consequences if there is a delay in diagnosis or treatment. Because the popliteal artery is an end artery to the leg, with minimal collateral circulation provided by the geniculate system, any compromise to the point of prolonged obstruction often leads to ischemia and eventual amputation. Furthermore, the popliteal vein is responsible for most of the venous outflow from the knee. Injury to this structure also compromises the viability of the lower limb. As stated previously, one cannot assume the absence of vascular injury simply because pulses are present. Serial vascular examinations are mandatory because intimal flaps can often present as delayed thrombus formation. Additionally, the absence of pulses implies an arterial injury and cannot be attributed to vascular spasm. Failure to recognize an arterial injury can lead to disastrous outcomes. The diagnosis of vascular injury is a clinical one. Any signs of limb ischemia should be taken seriously. The physical examination includes assessment of the pulses by palpation with comparison with the contralateral limb. Doppler ultrasound and ankle-brachial indices (ABIs) are indicated if pulse status is questionable. Distal perfusion, as well as motor and sensory function, should be documented. All these variables need to be reassessed on a frequent basis to evaluate for signs of vascular deterioration. If at any point asymmetry exists between the two lower extremities, urgent vascular studies are indicated. Difficulty ensuring vascularity clinically has always been well documented in numerous reports of knee dislocations.10,17-20 Misdiagnosis of vascularity and subsequent delay in arterial repair based on palpable peripheral pulses or capillary refill has been reported.18 Consequently, numerous authors advocate liberal or mandatory angiographic studies in patients with documented knee dislocations regardless of physical examination findings.21-24 Proponents of this philosophy have emphasized the risks for a missed arterial injury, including muscle ischemia and potential limb amputation. Late vascular compromise has been cited despite normal physical findings following closed reduction.19 The role of routine arteriography has undergone scrutiny in the recent literature and is quite controversial. Several authors have proposed using angiography only in patients who present with diminished or absent pulses and closely observing those with normal, symmetrical pulses.25-28 A recent prospective study compared the use of arteriography in patients with hard clinical signs of vascular injury with serial physical examinations in those without such signs. Physical examination alone yielded a 100% negative predictive value. The authors concluded that an invasive vascular study is not warranted in the absence of hard signs of vascular injury.28 Klineberg and associates29 retrospectively reviewed 57 knee dislocations and discovered that no patients who presented with normal vascular status on physical examination had a vascular injury as determined by

angiography or by clinical follow-up assessment. Stannard and coworkers30 prospectively evaluated 134 consecutive patients who had sustained a multiligamentous knee injury. Only patients with abnormal physical examination findings underwent arteriography. Ten patients had an abnormal physical examination, and arteriography confirmed nine vascular injuries. No cases of vascular injury were found in patients with normal examination findings. The value of the ABI has recently been evaluated as a means to diagnose arterial injury after knee dislocation. In a study by Mills and colleagues,31 38 patients were prospectively evaluated with ABIs after knee dislocations. Only patients whose ABI was lower than 0.90 underwent arteriography. Of the 38 patients, 11 (29%) had an ABI lower than 0.90. All 11 had an arterial injury requiring surgical intervention. None of the patients with an ABI greater than 0.90 experienced vascular compromise. The sensitivity, specificity, and positive predictive value of an ABI lower than 0.90 were 100%. Duplex ultrasonography has also been proposed as a safer, cheaper, and less invasive method of evaluating the popliteal vasculature. Results have been favorable showing a 98% accuracy of detecting extremity vascular trauma.32 Advocates state that ultrasonography offers yet another safeguard against missing a potentially disastrous injury.33 Opponents argue that ultrasounds are operator dependent, cannot account for distorted anatomy surrounding the knee following dislocation, and present an intrinsic delay because a technician must be present to complete the study.28 Less controversy exists regarding management of patients with hard signs of limb ischemia. Arteriography is not indicated in cases with an obviously ischemic limb because there is a danger in delaying revascularization. Many authors contend that arteriographic studies supply little additional information because the location of the lesion is readily predictable.10 Arteriography may be useful if more than one level of injury exists. This can often be accomplished with an intraoperative angiogram before surgical exploration. Angiography is clearly indicated in patients with abnormal or asymmetric vascularity following a knee dislocation in the absence of cold ischemia. It is also useful in those that have had a change in their vascular status following serial physical examinations. Any patient diagnosed with a vascular injury needs emergent vascular surgery consultation, and intervention. Delay in diagnosis or treatment jeopardizes limb viability.

Nerve Injuries Nerve injury can be quite common following dislocation of the knee. The orthopaedic literature estimates the incidence of nerve injury to be anywhere from 20% to 30%.1,1820,34,35 Although tibial nerve injuries have been reported,36 most nerve trauma involves the peroneal nerve. A common theme in peroneal nerve injuries is concomitant injury to the LCL and PLC. The tibial and peroneal nerves are less tightly tethered than the popliteal artery, which explains why they may be less prone to injury. Most injuries are the result of a stretch neurapraxia rather than laceration or frank transection. Recovery of nerve function is unpredictable with most series reporting no recovery in more than


50% of injuries.14,34,37,38 It is essential to distinguish nerve injury from stocking paresthesias that may be indicative of a developing compartment syndrome. Multiple anatomic factors contribute to the propensity of peroneal nerve injury during knee dislocation. Studies have shown that the peroneal nerve has only 0.5 cm of excursion at the fibular head during knee motion.39 Additionally, there is a significantly smaller ratio of epineural tissue to axonal tissue in the peroneal nerve compared with other peripheral nerves making it prone to stretch injuries (Fig. 23G-3).40 Most series report that peroneal nerve continuity is usually maintained after knee dislocations. Reports of traumatic rupture, however, have been described.39,41,42 A diffuse zone of injury is typically encountered at the time of exploration, which correlates with the poor results seen after observation of complete nerve palsies.14,34,37,38 Evaluation of a potential nerve injury mandates a detailed history and physical examination. Motor function, paresthesias, and sensory loss must be documented initially and with serial examinations. Common peroneal nerve injury is the most frequent nerve injury seen following knee dislocations, followed by tibial nerve injury. Motor improvement can often be seen initially because motor grades are typically reduced after dislocations secondary to pain. Delayed neurologic deterioration is often related to swelling, hematoma, or direct compression from a splint or a cast. Electromyography (EMG) and nerve conduction studies can often be beneficial in determining the status of the motor axons in the peroneal nerve. Electromyographic changes that include fibrillation potentials, positive sharp waves, and absence of activity on voluntary effort indicate axon disruption. These changes do not typically appear for 2 to 4 weeks after injury, so EMG is not indicated in the acute setting. A neuropraxic lesion is present if there are no signs of denervation on EMG more than 3 weeks from the initial injury. Serial electromyography can be useful in following nerve recovery and regeneration. There are few reports on long-term treatment of peroneal nerve injury associated with knee dislocation. Management options include observation, neurolysis, primary repair, and

Figure 23G-3 Forced varus dislocation causing severe stretch and attenuation of peroneal nerve. The injury was permanent and required tendon transfers to restore ankle dorsiflexion.

neuroma excision and grafting. Goitz and Tomaino43 presented an excellent review of the management of peroneal nerve injuries associated with knee dislocations. Based on the current literature, the authors recommended observation of incomplete nerve palsies with reasonable anticipation of recovery. Partial or complete ruptures should be referred to an appropriate microsurgeon within 3 months. In cases in which a tension-free primary repair of a complete transection can be performed, consideration should be given to acute anastomosis. The patient can then be kept in a knee immobilizer for 3 weeks, at which time ligamentous reconstruction can be undertaken. This will allow for an uninterrupted postoperative rehabilitation. If the nerve is thought to be in continuity, electrodiagnostic studies should be performed at 6 weeks and 3 months. If no evidence of reinnervation is found by 3 months, consideration should be given to open exploration and neurolysis. If intraoperative nerve action potentials are absent over a small portion of the nerve, consideration can be given to excision of the affected portion with interposition of a cable graft.

Osseous Injuries Bony injuries about the knee may be seen in as many as 60% of all knee dislocations (Fig. 23G-4).20 Characteristic ligamentous and tendinous avulsions are common. These include Segond’s fractures, fibular head avulsions, and cruciate avulsions. These should be treated primarily as ligamentous injuries as opposed to major fractures that are seen in true fracture-dislocations of the knee. Major fractures of the tibial plateau and distal femur are not uncommonly associated with multiligamentous injury.

Figure 23G-4 Segmental tibia fracture accompanying ipsilateral knee dislocation.

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Figure 23G-5 Significant lateral joint line opening on anteroposterior radiograph secondary to anterior and posterior cruciate ligament lateral-sided tears sustained during knee dislocation.

A comprehensive treatment plan is essential because fracture-dislocations certainly add an element of complexity to their treatment. It is essential to recognize that these high-energy fractures result in marked joint instability and are associated with a high risk for soft tissue and neurovascular compromise. Spanning external fixation is often a useful adjunct to assist in temporary stabilization of these injuries in anticipation of delayed bony and ligamentous reconstruction.

Imaging Imaging begins with anteroposterior and lateral radiographs in orthogonal planes before any manipulation. Although a frank dislocation is relatively easy to identify, a spontaneously reduced dislocation may be more surreptitious. One may only appreciate subtle asymmetry or widening of the joint, or the aforementioned bony injuries (Fig. 23G-5). Repeat radiographs are mandatory to confirm joint reduction if applicable. If there is any concern about the integrity of the popliteal artery, arteriography should be used (Fig. 23G-6). It remains the gold standard for assessment of intimal injury. Some centers have used magnetic resonance angiography (MRA) in the evaluation of possible vascular injury associated with knee dislocation. In addition to being less invasive, it avoids the potential for contrast reactions and arterial punctures. More information is needed before MRA supplants direct arteriography as the first-line vascular study in this patient population. After the acute management of the dislocated knee, magnetic resonance imaging (MRI) of the affected knee may be obtained to identify injury to the menisci, articular cartilage, ligaments, and some neurovascular structures. This study is of vital importance to ascertain the complete

Figure 23G-6 Arteriogram demonstrating intact popliteal artery system after knee dislocation.

nature of the injury. Numerous studies verify the high sensitivity and accuracy of MRI in this particular setting.44 MRI has become a routine imaging modality for preoperative evaluation and planning.

TREATMENT OPTIONS Nonoperative Direct comparison of treatment algorithms regarding the multiligamentous knee injury is nearly impossible. The orthopaedic literature can be difficult to interpret because these injuries can be quite heterogeneous and often result from a variety of mechanisms. The presence or absence of a neurovascular injury will have a direct correlation with patient outcome. Timing of surgery, surgical technique, and postoperative protocols can vastly differ among treating surgeons. All these factors make it difficult to identify clinical differences and statistical significance when comparing one treatment protocol to another. Until recent decades, most knee dislocations were traditionally managed conservatively with immobilization for several months.38,45 Various authors reported reasonable results after nonoperative treatment of this devastating injury.17,19 In 1991, Almekinders and Logan46 reported a retrospective review of their series of knee dislocations treated both operatively and nonoperatively. Nearly all had functional limitations. Both groups developed similar degenerative changes. The group treated operatively, however, had better motion (129 degrees versus 108 degrees of flexion) and superior ligamentous stability.


Figure 23G-7 Spanning external fixation applied to severely unstable knee after ultralow-energy knee dislocation. Note the delta frame configuration necessary to achieve adequate stability.

Today, few indications for nonoperative treatment of the multiligamentous knee injury persist. Critically ill patients who are unable to tolerate a surgical procedure or comply with a postoperative protocol may be candidates for nonoperative management. Patients with grossly contaminated wounds and significant soft tissue injury about the surgical site should be considered carefully before any attempt at ligament reconstruction. Lastly, elderly patients with low functional demand and high operative risk may be best treated conservatively.11 The most basic method of nonoperative management is a long-leg or cylinder cast. A long-leg brace with the knee locked in extension may also suffice. A brace is useful when access to wounds about the knee is needed and in critically ill patients who may be prone to extreme fluid shifts and peripheral edema. In some instances, a knee-spanning external fixator may be practical (Fig. 23G-7). It may provide more stability than a brace while allowing access to the knee. Regardless of the type of nonsurgical management, frequent radiographs should be obtained to verify continued reduction of the knee.

Operative As stated earlier, there is great variability in the indications and technique used in the management of multiple ligament injured knees. In addition, many published studies are observational or in the form of a single author’s retrospective review. The literature, while flawed to some degree, still represents our best tool to mold a reasonable and effective treatment algorithm. Many early reports of surgical treatment were made based on the technique of formal arthrotomy and direct repair of the ligaments. One small review found similar results in conservative treatment and direct suture repair.34 Another article47 compared early versus late direct repair of torn ligamentous structures in 13 of 17 patients. They determined that patients treated with early repair fared better than those with repairs done in a delayed fashion. This study supported surgical management of the

islocated knee and introduced the idea that long-term d benefits exist if ligamentous stability can be achieved in the knee. Since the early 1990s, arthroscopically assisted ACL and PCL reconstruction has gained popularity. Several factors have allowed this technique to thrive: (1) improved availability, procurement, sterilization, and storage of allograft tissue; (2) improved arthroscopic instrumentation; (3) better graft fixation methods; (4) improved surgical technique; and (5) improved understanding of the ligamentous anatomy and biomechanics of the knee. The literature is now becoming rife with evidence supporting this surgical approach to multiple ligament–injured knees.15,48-52 Timing of intervention varies greatly based on individual patient considerations. These patients have quite often sustained severe multisystem trauma. Life-threatening injuries obviously take precedence. That being said, open dislocations and dislocations associated with vascular injury are relative surgical emergencies because these represent limb-threatening conditions. These two situations call for provisional stabilization with external fixation combined with either irrigation and débridement in the case of an open knee injury or vascular repair or bypass in the setting of vascular insult. Our preferred surgical tactic is described later in the text.

Weighing the Evidence As stated previously, strategies for the management of knee dislocations have been varied and controversial.53-55 Over time, conservative management of these injuries has been associated with residual instability and poor long-term outcomes.38,56 Most experienced knee surgeons now recommend operative treatment of all compromised ligamentous, capsular, and meniscal structures.1,46,47 Controversy exists regarding operative technique, surgical timing, graft selection, and rehabilitation. The debate over the management of these complex injuries is for the most part due to inconsistent treatment protocols, small and poorly defined patient populations, and a variety of surgical techniques described in the literature.

Nonoperative versus Operative Treatment Multiple comparisons of operative and nonoperative treatment exist in the literature.54,57 A recent retrospective review by Richter and colleagues revealed that operative treatment was superior to conservative management in patients who had sustained traumatic knee dislocations.58 Patients treated operatively had either bicruciate repair or reconstruction using autograft tissue. Rehabilitation protocols varied based on the specific type of cruciate intervention. Patients treated nonoperatively were immobilized for 6 weeks in either a long-leg cast or an external fixator. At an average 8.2-year follow-up, the mean Lysholm and Tegner scores were significantly higher in the surgical group. Patients younger than 40 years of age, who had sports injuries, and who had functional rehabilitation rather than immobilization had better results. In an effort to end the controversy between nonoperative and operative treatment, Dedmond and Almekinders performed a metaanalysis literature review.59 The authors extracted raw data

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from several other studies so that 206 knee dislocations were evaluated. Seventy-four of these injuries were treated nonoperatively, whereas 132 were treated operatively. The average Lysholm knee score for the surgical group was 85.2, and it was 66.5 for the nonoperative group. These results were quite similar to Montgomery and coworkers’ earlier review.60

Surgical Timing The optimal timing of operative intervention is another controversial issue in the literature. Acute surgical intervention avoids excessive scarring of the collateral ligaments, making primary repair less technically demanding, yet in some studies has been shown to have a higher incidence of motion loss at final follow-up.55,61 In the absence of an absolute surgical indication, most authors recommend delaying operative treatment for 1 to 3 weeks. This allows for a period of vascular monitoring in addition to minimizing swelling and allowing capsular injuries to heal, which may permit an arthroscopic reconstruction. The literature differentiates between acute and chronic reconstructions at the 3-week time frame. Acute primary repair of the PLC is nearly universally recommended. Medial-sided injuries are more controversial. Shelbourne and associates61 have recommended nonoperative treatment for MCL and lowgrade PCL injuries with delayed ACL reconstruction if patient symptoms and activity level dictate. They reported satisfactory results in nine patients treated in this manner and believed that the arthrofibrosis potentially associated with concurrent ACL reconstruction and MCL repair could be avoided. Their patients had an average extension loss of 3 degrees and flexion loss of 15 degrees. Fanelli and associates62 also showed successful bracing of low-grade MCL injuries followed by delayed central pivot reconstruction. In this series, there was no difference in postoperative Lysholm scores between those patients treated acutely and those treated in a delayed fashion. In contrast to the two previous studies, most series have reported better results in patients treated with acute ligamentous reconstruction. Noyes and Barber-Westin51 reviewed the results in 11 patients who had undergone allograft bicruciate and PLC reconstruction. Seven patients were treated acutely, whereas 4 patients were treated in a chronic setting. The patients who had undergone delayed reconstruction had lower overall ratings and more subjective difficulties during activity than did patients in the acutely treated cohort. Wascher and colleagues56 reported on 13 patients who underwent ACL and PCL reconstruction using allograft tissue. Nine patients were treated acutely. Better results were noted in those patients treated within 3 weeks of injury. A recent retrospective review by Harner and coworkers63 confirmed that patients treated in an acute fashion have better postoperative results. Nineteen of 31 patients in their series were treated with acute surgical reconstruction with allograft tissue. All knee rating scores were significantly better in the group treated with early surgery. There was no difference in final range of motion between the acutely and chronically treated cohorts. Laxity tests were consistently improved in both groups, but results were more predictable in the acutely treated patients.

Graft Selection Graft selection remains a matter of surgeon preference. Many authors have reported using allograft tissue in treating multiligamentous knee injuries.15,56,64,65 Reduced donorsite morbidity and shorter operative times are advantages of using allograft tissue. Fanelli and colleagues62 reviewed 20 bicruciate ligament reconstructions, in which 14 PCL reconstructions and 4 ACL reconstructions were performed with allograft tissue. After comparing KT-1000 results, the authors concluded that the autografts and allografts were equivalent. Cole and Harner reported only one graft failure out of 60 allograft cruciate reconstructions in a series of 31 patients.64 Ohkoshi and associates66 reviewed 13 knees that had been treated in a staged fashion with all autograft tissue. All patients underwent acute PCL reconstruction using contralateral hamstring tendons. Three months after surgery, the knees were reassessed, and any residual laxity was treated with delayed reconstruction. Anterior cruciate injuries were addressed using ipsilateral hamstring or patellar tendon autografts. Medial structures were reconstructed using ipsilateral semitendinosus, and lateral-sided injuries were augmented using autogenous biceps tendon. Average range of motion was 0 to 139.5 degrees of flexion. No collateral instability was noted at final follow-up, and average anteroposterior laxity was 2.3 mm.

Posterior Cruciate Ligament Reconstruction Significant refinements in PCL reconstruction have been developed recently as authors have begun to appreciate its importance in knee stability following multiligamentous injury. Controversies surrounding transtibial versus tibial inlay and single- versus double-bundle reconstruction continue. At the present time, no randomized prospective studies exist comparing various PCL reconstruction techniques in this particular patient population. Advocates of single-bundle transtibial PCL reconstruction cite multiple studies justifying its use.56,63,67,68 In both Harner’s and Fanelli’s series, all patients treated with this technique had grade I laxity or better on posterior drawer testing at final follow-up. The tibial inlay technique has been developed as a way to avoid the “killer turn.” Biomechanical studies have shown less graft abrasion and pretension with this method of PCL reconstruction.69,70 Recent studies have shown good clinical outcomes with the tibial inlay technique.71,72 In addition to the transtibial tunnel versus tibial inlay debate, controversy exists regarding single- versus doublebundle reconstruction. Normal PCL function is more accurately reproduced in biomechanical studies with a double-bundle technique.73,74 Single-bundle reconstructions have shown good clinical results for both transtibial62,63,75,76 and tibial inlay techniques.77 Double-bundle techniques are being developed, and early clinical results are promising.72,78-81 Stannard and colleagues72 were the first to report on double-bundle tibial inlay PCL reconstruction in the multiple ligament–injured knee. Allograft Achilles tendon was used in 29 patients with 30 knee dislocations to treat PCL insufficiency. All patients had concomitant PLC injuries, and 29 of 30 knees had ACL tears.


At 2-year follow-up, PCL stability was grade 0 in 24 of 30 knees and grade I in the remaining 6. Cooper and Stewart71 performed single-bundle tibial inlay PCL reconstruction in 44 patients with multiligamentous involvement. At final follow-up of 39 months, all patients were improved subjectively. Patients with full-thickness chondral defects had significantly worse outcomes. Posterior stability was reconstituted in all patients.

REHABILITATION Stiffness and recurrent instability are two of the most common complications following operative treatment of multiligamentous knee injuries. Long-term immobilization usually imparts improved stability at the expense of motion. Early motion and aggressive rehabilitation lead to improved function, yet risk failure of ligament reconstructions. No true randomized study exists comparing early functional rehabilitation with prolonged immobilization following these injuries. Obviously, a delicate balance must be achieved between motion and stability to achieve optimal results. Shelbourne and associates11 had noted problems with stiffness following bicruciate ligament reconstruction. They modified their technique to include early PCL reconstruction with PLC repair. ACL reconstruction was performed on a delayed basis if necessary. Early active motion and continuous passive motion were used to optimize function. In their initial study, all patients treated in this fashion achieved excellent range of motion. Noyes reported results on 11 bicruciate ligament reconstructions treated with early protected postoperative motion.51 For the first 4 weeks after surgery, patients began active-assisted range of motion from 10 to 90 degrees, 6 to 8 times a day. Between therapy sessions, the knee was

immobilized in full extension in a split cylinder cast. Full weight-bearing was allowed after 3 months. Nearly 5 years after surgery, the average knee range of motion was normal in 9 of 11 patients. One patient had a 5-degree loss of both flexion and extension, whereas a second patient reached only 100 degrees of knee flexion. Failure rates of PCL and ACL reconstruction were 18% and 9%, respectively. Nearly half of the patients in this series required surgical manipulation during their postoperative rehabilitation, and 2 patients were treated for motion loss with arthroscopic débridement of adhesions. Recent literature has focused on attempts to maintain early motion while minimizing shear forces on reconstructed grafts. Fitzpatrick and associates82 performed a cadaveric study in which knee stability was assessed biomechanically using an articulated external fixator. Anterior and posterior tibial translation was significantly decreased at 30 and 90 degrees of flexion, respectively, after application of the fixator to the cruciate-deficient knee. The theoretical advantage of this device would be to allow early range of motion in the immediate postoperative period while limiting posterior shear forces on the freshly reconstructed central pivot grafts. Stannard and colleagues83 performed a functional outcome study in which 40 patients with 43 knee dislocations were evaluated. Group A consisted of 12 patients who underwent multiligamentous knee reconstruction followed by placement of a hinged-knee external fixator. Group B included 27 knees that underwent an identical surgical and rehabilitation protocol with the exception that a brace was used in lieu of the hinged fixator. At an average 2-year follow-up, the ligament failure rates were 7% in group A and 29% in group B. No differences were noted in range of motion between the groups. Further study is needed to determine the optimal rehabilitation protocol in these patients.

Authors’ Preferred Method Fanelli Sports Injury Clinic Experience

Surgical Timing

Our practice is at a tertiary care regional trauma center. There is a 38% incidence of PCL tears in acute knee injuries, with 45% of these PCL-injured knees being combined ACL and PCL tears.75,84 Careful assessment, evaluation, and treatment of vascular injuries is essential in these acute multiple ligament–injured knees. There is an 11% incidence of vascular injury associated with these acute multiple ligament–injured knees at our center.19 Our preferred approach to combined ACL and PCL injuries is arthroscopic ACL and PCL reconstruction using the transtibial tunnel technique, with collateral and capsular ligament surgery as indicated.85 Not all cases are amenable to the arthroscopic approach, and the operating surgeon must assess each case individually. Surgical timing is dependent on vascular status, reduction stability, skin condition, systemic injuries, open versus closed knee injury, meniscus and articular surface injuries, other orthopaedic injuries, and the collateral and capsular ligaments involved.

Some ACL, PCL, and MCL injuries can be treated with brace treatment of the MCL followed by arthroscopic combined ACL and PCL reconstruction 4 to 6 weeks after healing of the MCL. Other cases may require repair or reconstruction of the medial structures and must be assessed on an individual basis. Combined ACL, PCL, and posterolateral injuries should be surgically addressed as early as is safely possible. ACL, PCL, and posterolateral repair and reconstruction performed between 2 and 3 weeks after injury allows healing of capsular tissues to permit an arthroscopic approach, and still permits primary repair of injured posterolateral structures. Open multiple ligament knee injuries and dislocations may require staged procedures. The collateral and capsular structures are repaired after thorough irrigation and dé bridement, and the combined ACL and PCL reconstruction is performed at a later date after wound healing has occurred.

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Figure 23G-8 Severe soft tissue injury in a patient with bilateral open knee dislocations. Skin issues are the most frequent surgical timing modifiers that cause delay of surgical reconstructions in multiple ligament–injured knees.

Care must be taken in all cases of delayed reconstruction that the tibiofemoral joint reduction is maintained. The surgical timing guidelines outlined previously should be considered in the context of the individual patient. Many patients with multiple ligament injuries of the knee are severely injured multiple-trauma patients with multisystem injuries. Modifiers to the ideal timing protocols outlined earlier include the vascular status of the involved extremity, reduction stability, skin condition, open or closed injury, and other orthopaedic and systemic injuries (Fig. 23G-8). These additional considerations may cause the knee ligament surgery to be performed earlier or later than desired. We have previously reported excellent results with delayed reconstruction in the multiple ligament–injured knee.49,62 Graft Selection

The ideal graft material should be strong, provide secure fixation, be easy to pass, be readily available, and have low donor site morbidity. Our preferred graft for the PCL is an Achilles tendon allograft for the anterolateral bundle and a tibialis anterior allograft for the posteromedial bundle. We prefer Achilles tendon allograft or other allograft for the ACL reconstruction. The preferred graft material for the PLC is allograft tissue.86 Cases requiring MCL and posteromedial corner surgery may have primary repair or reconstruction, or a combination of both. Our preferred method for MCL and posteromedial reconstructions is a primary repair and posteromedial capsular advancement with allograft augmentation as needed. Surgical Approach

Our preferred surgical approach is a single-stage arthroscopic combined ACL and PCL reconstruction using the transtibial tunnel technique with collateral and capsular ligament surgery as indicated. The PLC is repaired and then augmented with a split biceps tendon transfer, biceps tendon transfer, semitendinosus free graft, or allograft tissue. Acute medial injuries not amenable to brace treatment undergo

Figure 23G-9 The surgical leg is draped free for multiple ligament reconstruction. A lateral post is used for stability. No leg holder is used. The fully extended operating table supports the well leg.

primary repair, and posteromedial capsular shift and allograft reconstruction as indicated. The operating surgeon must be prepared to convert to a dry arthroscopic procedure or to an open procedure if fluid extravasation becomes a problem. Surgical Technique

The principles of reconstruction in the multiple ligament– injured knee are identification and treatment of all pathology, accurate tunnel placement, anatomic graft insertion sites, use of strong graft material, secure graft fixation, and a deliberate postoperative rehabilitation program. The patient is positioned supine on the operating room table. The surgical leg hangs over the side of the operating table, and the well leg is supported by the fully extended operating table. A lateral post is used for control of the surgical leg. We do not use a leg holder (Fig. 23G-9). The surgery is done under tourniquet control unless prior arterial or venous repair contraindicates the use of a tourniquet. Fluid inflow is by gravity. We do not use an arthroscopic fluid pump. Allograft tissue is prepared, and arthroscopic instruments are placed with the inflow in the superior lateral portal, arthroscope in the inferior lateral patellar portal, and instruments in the inferior medial patellar portal. An accessory extracapsular extra-articular posteromedial safety incision is used to protect the neurovascular structures and to confirm the accuracy of tibial tunnel placement (Fig. 23G-10). The notchplasty is performed first and consists of ACL and PCL stump débridement, bone removal, and contouring of the medial wall of the lateral femoral condyle and the intercondylar roof. This allows visualization of the over-the-top position and prevents ACL graft impingement throughout the full range of motion. Specially curved Arthrotek (Biomet Sports Medicine, Warsaw, Ind) PCL instruments are used to elevate the capsule from the posterior aspect of the tibia (Fig. 23G-11). Continued



A

B

C

Figure 23G-10 A-C, The 1- to 2-cm extracapsular posterior medial safety incision allows the surgeon’s finger to protect the neurovascular structures and confirm the position of instruments on the posterior aspect of the proximal tibia. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

The PCL tibial and femoral tunnels are created with the help of the Arthrotek Fanelli PCL/ACL drill guide (Fig. 23G-12). The transtibial PCL tunnel is positioned from the anteromedial aspect of the proximal tibia 1 cm below the tibial tubercle to exit in the inferior lateral aspect of the PCL anatomic insertion site. The PCL femoral tunnel originates externally between the medial femoral epicondyle and the medial femoral condylar articular surface to emerge through

Figure 23G-11 Specially curved posterior cruciate ligament (PCL) reconstruction instruments used to elevate the capsule from the posterior aspect of the tibial ridge during PCL reconstruction. Posterior capsular elevation is critical in transtibial tunnel PCL reconstruction because it facilitates accurate PCL tibial tunnel placement and subsequent graft passage. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

the center of the stump of the anterolateral bundle of the PCL. The PCL graft is positioned and anchored on the femoral side, followed by PCL graft tensioning and tibial fixation (Fig. 23G-13). The ACL tunnels are created using the single-incision technique. The tibial tunnel begins externally at a point 1 cm proximal to the tibial tubercle on the anteromedial surface of the proximal tibia to emerge through the center of the stump of the ACL tibial footprint. The femoral tunnel is positioned next to the over-the-top position on the medial wall of the lateral femoral condyle near the ACL anatomic insertion site. The tunnel is created to leave a 1- to 2-mm posterior cortical wall so that interference fixation can be used. The ACL graft is positioned and anchored on the femoral side, followed by ACL graft tensioning and tibial fixation (Fig. 23G-14). Posterolateral reconstruction with the free-graft figureof-eight technique uses semitendinosus autograft or allograft, Achilles tendon allograft, or other soft tissue allograft material. A curvilinear incision is made in the lateral aspect of the knee extending from the lateral femoral epicondyle to the interval between Gerdy’s tubercle and the fibular head. The fibular head is exposed, and a tunnel is created in an anterior-to-posterior direction at the area of maximal fibular diameter. The tunnel is created by passing a guide pin followed by a cannulated drill, usually 7 mm in diameter. The peroneal nerve is protected during tunnel creation and throughout the procedure. The free tendon graft is then

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Figure 23G-12 The Arthrotek Fanelli posterior cruciate ligament (PCL) and anterior cruciate ligament (ACL) drill guide system is used to precisely create both the PCL femoral and tibial tunnels and the ACL single-incision technique and double-incision technique tunnels. The drill guide is positioned for the PCL tibial tunnel so that a guidewire enters the anteromedial aspect of the proximal tibia about 1 cm below the tibial tubercle, at a point midway between the posteromedial border of the tibia and the tibial crest anteriorly. The guidewire exits in the inferior lateral aspect of the PCL tibial anatomic insertion site. The guide is positioned for the PCL femoral tunnel so that the guidewire enters the medial aspect of the medial femoral condyle midway between the medial femoral condyle articular margin and the medial epicondyle, at least 2 cm proximal to the medial femoral condyle distal articular surface (joint line). The guidewire exits through the center of the stump of the anterolateral bundle of the PCL. The drill guide is positioned for the single-incision endoscopic ACL technique so that the guidewire enters the anteromedial surface of the proximal tibia about 1 cm proximal to the tibial tubercle at a point midway between the posteromedial border of the tibia and the tibial crest anteriorly. The guidewire exits through the center of the stump of the tibial ACL insertion. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

passed through the fibular head drill hole. An incision is then made in the iliotibial band in line with the fibers directly overlying the lateral femoral epicondyle. The graft material is passed medial to the iliotibial band, and the limbs of the graft are crossed to form a figure-eight. A drill hole is made 1 cm anterior to the fibular collateral ligament femoral insertion. A longitudinal incision is made in the lateral capsule just posterior to the fibular collateral ligament. The graft material is passed medial to the iliotibial band and secured to the lateral femoral epicondylar region with a screw and spiked ligament washer at the previously mentioned point. The posterolateral capsule that had been previously incised is then shifted and sewn into the strut of figure-eight graft tissue material to eliminate posterolateral capsular redundancy. The anterior and posterior limbs of the figure-eight graft material are sewn to each other to reinforce and tighten the construct. The procedures described are intended to eliminate posterolateral and varus rotational instability. Certain cases require reconstruction of the popliteus tendon using an additional graft passed through a transosseous drill hole through the proximal lateral tibia (Fig. 23G-15).

Figure 23G-13 Drawing demonstrates doublebundle double femoral tunnel posterior cruciate ligament reconstruction. Note primary fixation with resorbable interference screws and backup fixation with ligament fixation buttons and screw and spiked ligament washer. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

Posteromedial and medial reconstructions are performed through a medial hockey-stick incision (Fig. 23G-16). Care is taken to maintain adequate skin bridges between incisions. The superficial MCL is exposed, and a longitudinal incision is made just posterior to the posterior border of the MCL. Care is taken not to damage the medial meniscus during the capsular incision. The interval between the posteromedial capsule and medial meniscus is developed. The posteromedial capsule is shifted anterosuperiorly. The medial meniscus

Figure 23G-14 Anterior cruciate ligament reconstruction using the single-incision endoscopic technique. Drawing shows completed combined posterior and anterior cruciate ligament reconstruction. Note primary fixation with resorbable interference screws and backup fixation with ligament fixation buttons and screws and spiked ligament washers. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.) Continued



A

A

B

Figure 23G-15 A, Surgical technique for posterolateral and lateral reconstruction using allograft or autograft figureof-eight reconstruction combined with posterolateral capsular shift and primary repair of injured structures, as indicated. This surgical procedure reproduces the function of the popliteofibular ligament and the lateral collateral ligament and eliminates posterolateral capsular redundancy. B, Reconstruction of the popliteus tendon in cases in which that reconstruction is indicated. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

is repaired to the new capsular position, and the shifted capsule is sewn into the MCL. When superficial MCL reconstruction is indicated, this is performed with allograft tissue or semitendinosus autograft. This graft material is attached at the anatomic insertion sites of the superficial MCL on the femur and tibia. The posteromedial capsular advancement is performed and sewn into the newly reconstructed MCL (see Table 23G-1).

B

Figure 23G-16 A and B, Surgical treatment of medial side injuries. Severe medial side injuries are successfully treated with primary repair using suture anchor technique combined with medial collateral ligament (MCL) reconstruction using allograft tissue and the posteromedial capsular shift procedure. The allograft can anatomically reconstruct the superficial MCL. The allograft is secured to the anatomic insertion sites of the superficial MCL using screws and spiked ligament washers. The posteromedial capsule can then be secured to the allograft tissue to eliminate posteromedial capsular laxity. This technique addresses all components of the medial side instability. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

the tibia is internally rotated, slight valgus force is applied to the knee, and final tensioning and fixation of the PLC is achieved. Reconstruction and tensioning of the MCL and posteromedial corner are performed after the ACL, PCL, and PLC reconstructions are completed, and are done in 30 degrees of knee flexion (Table 23G-2). Technical Hints

The posteromedial safety incision protects the neurovascular structures, confirms accurate tibial tunnel placement, and allows the surgical procedure to be done at an accelerated pace. The single-incision ACL reconstruction technique

Graft Tensioning and Fixation

The PCL is reconstructed first, followed by the ACL, followed by the posterolateral complex and medial side (Box 23G-1). The Arthrotek tensioning boot is used for tensioning the ACL and PCL reconstructions (Fig. 23G-17). Tension is placed on the PCL graft distally, and the knee is cycled through a full range of motion to allow pretensioning and settling of the graft. The knee is placed in 70 to 90 degrees of flexion, the Arthrotek tensioning boot is tensioned to 20 pounds to restore the normal tibial step-off, and fixation is achieved on the tibial side of the PCL graft with a screw and spiked ligament washer and an Arthrotek Bio-Core bioabsorbable interference screw. The knee is maintained at 30 degrees of flexion, the Arthrotek tensioning boot is tensioned to 20 pounds with tension on the ACL graft, and final fixation is achieved of the ACL graft with an Arthrotek Bio-Core bioabsorbable interference screw and a Biomet Sports Medicine ligament fixation button or spiked ligament washer back-up fixation. The knee is then placed in 30 degrees of flexion,

Box 23G-1 Order of Anterior Cruciate Ligament, Posterior Cruciate Ligament, Posterolateral Corner, and Medial Collateral Ligament Reconstruction 1. Posterior cruciate ligament tibial tunnel 2. Posterior cruciate ligament femoral tunnel 3. Posterior cruciate ligament graft passage and femoral fixation 4. Anterior cruciate ligament tibial tunnel 5. Anterior cruciate ligament femoral tunnel 6. Anterior cruciate ligament graft passage and femoral fixation 7. Posterolateral corner repair and reconstruction 8. Medial-sided repair and reconstruction

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A

B

Figure 23G-17 The knee ligament-tensioning boot (A) is used to precisely tension posterior cruciate ligament (PCL) and anterior cruciate ligament (ACL) grafts. During PCL reconstruction, the tensioning device is attached to the tibial end of the graft and the torque wrench ratchet set to 20 pounds. This restores the anatomic tibial step-off. The knee is cycled through full flexionextension cycles, and with the knee at about 70 degrees of flexion, final PCL tibial fixation is achieved with an Arthrotek Bio-Core bioabsorbable interference screw and with a screw and spiked ligament washer for backup fixation. The tensioning device is applied to the ACL graft, set to 20 pounds, and the graft is tensioned with the knee in 70 degrees of flexion (B). Final ACL fixation is achieved with Arthrotek Bio-Core bioabsorbable interference screws and with spiked ligament washer or ligament fixation button backup fixation. The mechanical tensioning boot ensures consistent graft tensioning and eliminates graft advancement during interference screw insertion. It also restores the anatomic tibial step-off during PCL graft tensioning and applies a posterior drawer force during ACL graft tensioning. (Courtesy of Biomet Sports Medicine, Warsaw, Ind.)

prevents lateral cortex crowding and eliminates multiple through-and-through drill holes in the distal femur, reducing stress riser effect. It is important to be aware of the two tibial tunnel directions and to have a 1-cm bone bridge between the PCL and ACL tibial tunnels. This will reduce the possibility of fracture. We have found it useful to use primary and back-up fixation. Primary fixation is with resorbable interference screws, and back-up fixation is performed with a screw and spiked ligament washer or Arthrotek ligament fixation button. Secure fixation is critical to the success of this surgical procedure (see Fig. 23G-14).

TABLE 23G-2 Order of Tensioning and Final Fixation Structure

Tensioning Position

Posterior cruciate ligament

70 to 90 degrees of knee flexion while restoring normal tibial step-off and neutral rotation 30 degrees of knee flexion while maintaining normal tibial step-off and neutral rotation 30 degrees of knee flexion while internal rotation and anterior translation are applied to the proximal tibia 30 degrees of knee flexion after posterior cruciate ligament, posterolateral corner, and anterior cruciate ligament tensioning and fixation have been performed

Anterior cruciate ligament Posterolateral corner

Medial collateral ligament

Results without the Arthrotek Graft Tensioning Boot

We previously published the results of our arthroscopically assisted combined ACL and PCL, and PCL and posterolateral complex, reconstructions using the reconstructive technique described in this chapter.49,62,67,68,87 Our most recently published 2- to 10-year results of combined ACL and PCL reconstructions without the Arthrotek graft tensioning boot are presented here.67 This study presented the 2- to 10-year (24- to 120-month) results of 35 arthroscopically assisted combined ACL and PCL reconstructions evaluated before and after surgery using Lysholm, Tegner, and Hospital for Special Surgery knee ligament rating scales, KT-1000 arthrometer testing, stress radiography, and physical examination. This study population included 26 males and 9 females with 19 acute and 16 chronic knee injuries. Ligament injuries included 19 ACL, PCL, and posterolateral instabilities, 9 ACL, PCL, and MCL instabilities, 6 ACL, PCL, posterolateral, and MCL instabilities, and 1 ACL and PCL instability. All knees had grade III preoperative ACL and PCL laxity and were assessed before and after surgery with arthrometer testing, three different knee ligament rating scales, stress radiography, and physical examination. Arthroscopically assisted combined ACL and PCL reconstructions were performed using the single-incision endoscopic ACL technique and the single femoral tunnel, single-bundle transtibial tunnel PCL technique. PCLs were reconstructed with allograft Achilles tendon (26 knees), autograft bone-tendon-bone Continued


Authors’ Preferred Method—cont’d (BTB; 7 knees), and autograft semitendinosus and gracilis (2 knees). ACLs were reconstructed with autograft BTB (16 knees), allograft BTB (12 knees), Achilles tendon allograft (6 knees), and autograft semitendinosus and gracilis (1 knee). MCL injuries were treated with bracing or open reconstruction. Posterolateral instability was treated with biceps femoris tendon transfer, with or without primary repair, and posterolateral capsular shift procedures as indicated. No Arthrotek graft tensioning boot was used in this series of patients. Postoperative physical examination results revealed normal posterior drawer and tibial step-off in 16 of 35 (46%) knees. Normal Lachman’s test and pivot shift tests in 33 of 35 (94%) knees. Posterolateral stability was restored to normal in 6 of 25 (24%) knees, and tighter than the normal knee in 19 of 25 (76%) knees evaluated with the external rotation thigh-foot angle test. The 30-degree varus stress testing was normal in 22 of 25 (88%) knees, and grade I laxity in 3 of 25 (12%) knees. The 30-degree valgus stress testing was normal in 7 of 7 (100%) surgically treated MCL tears and was normal in 7 of 8 (87.5%) brace-treated knees. Postoperative KT-1000 arthrometer tests of mean side-to-side differences showed 2.7 mm (PCL screen), 2.6 mm (corrected posterior), and 1.0 mm (corrected anterior) measurements, a statistically significant improvement from preoperative status (P = .001). Postoperative stress radiographic side-to-side difference measurements at 90 degrees of knee flexion and 32 pounds of posteriorly directed proximal force were 0 to 3 mm in 11 of 21 (52.3%), 4 to 5 mm in 5 of 21 (23.8%), and 6 to 10 mm in 4 of 21 (19%) knees. Postoperative Lysholm, Tegner, and Hospital for Special Surgery knee ligament rating scale mean values were 91.2, 5.3, and 86.8, respectively, demonstrating a statistically significant improvement from preoperative status (P = .001). No Arthrotek graft tensioning boot was used in this series of patients. The conclusions drawn from the study were that combined ACL and PCL instabilities could be successfully treated with arthroscopic reconstruction and the appropriate collateral ligament surgery. Statistically significant improvement was noted from the preoperative condition at 2- to 10-year follow-up using objective parameters of knee ligament rating scales, arthrometer testing, stress radiography, and physical examination. Postoperatively, these knees are not normal, but they are functionally stable. Continuing technical improvements will most likely improve future results. Results with the Arthrotek Graft Tensioning Boot

These new data present the 2-year follow-up results of 15 arthroscopically assisted ACL and PCL reconstructions using the Arthrotek graft tensioning boot.76 This study group consists of 11 chronic and 4 acute injuries. These

FUTURE DIRECTIONS We have now converted to performing the double-bundle, double femoral tunnel PCL reconstruction surgical technique because there is convincing basic science data

injury patterns included 6 ACL, PCL, and PLC injuries; 4 ACL, PCL, and MCL injuries; and 5 ACL, PCL, PLC, and MCL injuries. The Arthrotek tensioning boot was used during the procedures as in the surgical technique described previously. All knees had grade III preoperative ACL and PCL laxity and were assessed before and after surgery using Lysholm, Tegner, and Hospital for Special Surgery knee ligament rating scales, KT-1000 arthrometer testing, stress radiography, and physical examination. Arthroscopically assisted combined ACL and PCL reconstructions were performed using the single-incision endoscopic ACL technique, and the single femoral tunnel, single-bundle transtibial tunnel PCL technique. PCLs were reconstructed with allograft Achilles tendon in all 15 knees. ACLs were reconstructed with Achilles tendon allograft in all 15 knees. MCL injuries were treated surgically using primary repair, posteromedial capsular shift, and allograft augmentation as indicated. Posterolateral instability was treated with allograft semitendinosus free graft, with or without primary repair, and posterolateral capsular shift procedures as indicated. The Arthrotek graft tensioning boot was used in this series of patients. Postreconstruction physical examination results revealed normal posterior drawer and tibial-step off in 13 of 15 (86.6%) knees. Normal Lachman’s test in 13 of 15 (86.6%) knees and normal pivot shift tests in 14 of 15 (93.3%) knees. Posterolateral stability was restored to normal in all knees with posterolateral instability when evaluated with the external rotation thigh-foot angle test (9 knees equal to the normal knee, and 2 knees tighter than the normal knee). Thirty-degree varus stress testing was restored to normal in all 11 knees with posterolateral lateral instability. Thirty- and zero-degree valgus stress testing was restored to normal in all 9 knees with medial side laxity. Postoperative KT-1000 arthrometer testing mean side-to-side difference measurements were 1.6 mm (range, 3 to 7 mm) for the PCL screen, 1.6 mm (range, 4.5 to 9 mm) for the corrected posterior, and 0.5 mm (range, 2.5 to 6 mm) for the corrected anterior measurements, a significant improvement from preoperative status. Postoperative stress radiographic side-to-side difference measurements measured at 90 degrees of knee flexion and 32 pounds of posteriorly directed proximal force using the Telos stress radiography device were 0 to 3 mm in 10 of 15 knees (66.7%), 4 mm in 4 of 15 knees (26.7%), and 7 mm in 1 of 15 knees (6.67%). Postoperative Lysholm, Tegner, and Hospital of Special Surgery knee ligament rating scale mean values were 86.7 (range, 69 to 95), 4.5 (range, 2 to 7), and 85.3 (range, 65 to 93), respectively, demonstrating a significant improvement from preoperative status. The study group demonstrates the efficacy and success of using a mechanical graft-tensioning device (Arthrotek graft tensioning boot) in single-bundle, single femoral tunnel arthroscopic PCL reconstruction.

supporting the efficacy of this procedure.73 This doublebundle, double femoral tunnel technique more closely approximates the anatomic insertion site of the native PCL and should theoretically provide improved results (Fig. 23G-18). Our clinical results with 15- to 36-month

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Figure 23G-18 Intraoperative photograph demonstrating placement of an Achilles tendon allograft reconstructing the anterolateral bundle of the posterior cruciate ligament (PCL) and a tibialis anterior allograft reconstructing the posteromedial bundle of the PCL. Note how the double-bundle double femoral tunnel PCL reconstruction more closely fills the femoral anatomic insertion site of the posterior cruciate ligament. ACL reconstruction was performed with an Achilles tendon allograft. (Courtesy of Gregory C. Fanelli, MD.)

follow-up of 66 consecutive PCL-based multiple ligament knee reconstructions, however, showed no significant difference between double- and single-bundle PCL reconstruction results evaluated with Telos stress radiography, KT-1000 arthrometer testing, and Tegner, Lysholm, and Hospital for Special Surgery knee ligament rating scales. Both the single- and double-bundle groups had a mean of less than 3 mm side-to-side difference on stress radiography and arthrometer testing. This indicated restoration of normal side-to-side difference measurements for the PCL reconstructions using both the single-bundle and doublebundle surgical techniques. Another area of interest is the incorporation of the Musculoskeletal Transplant Foundation (Edison, NJ) Cascade System autologous platelet rich fibrin matrix into the grafts used in the cruciate and collateral ligament reconstructive procedures (Fig. 23G-19). There are several studies indicating favorable effects on the ligament graft tissue and the clinical results.88-90 We have demonstrated favorable initial clinical results with respect to graft incorporation, wound healing, and early stability; however, there is no long-term follow-up as of this writing.

POSTOPERATIVE PRESCRIPTION The postoperative protocol (Box 23G-2) following multiple ligament reconstruction is typically divided into four specific phases. Phase I consists of the first 6 postoperative weeks. The emphasis during phase I is on graft protection. Immediately postoperatively, patients are placed in a long-leg hinged knee brace locked in full extension. Cryotherapy is used to minimize postoperative swelling. The patient is mobilized with physical therapy, with non– weight-bearing instructions applied to the operative limb. Following discharge from the hospital, outpatient physical therapy is instituted, with emphasis placed on quadriceps strengthening through isometrics and low-intensity

Figure 23G-19 A platelet-rich fibrin matrix clot created by the Musculoskeletal Transplant Foundation Cascade System is incorporated into the lateral posterolateral reconstruction to potentially enhance graft incorporation and wound healing. (Courtesy of Gregory C. Fanelli, MD.)

electric stimulation. During weeks 4 through 6, flexion exercises are allowed from 0 to 90 degrees. Patellar mobilization, gentle hamstring and gastrocnemius stretching, and “foot pump” exercises are also used. Phase II begins during the seventh postoperative week. The brace is unlocked to allow full flexion and may be removed at night. Weight-bearing is initiated at this time as well and is increased in a progressive fashion until the patient is bearing full weight by postoperative week 10. Active and passive range-of-motion exercises are initiated, albeit guardedly to avoid excessive posterior shear forces on the PCL. Once the patient is fully weight-bearing, closed kinetic chain exercises are instituted. These exercises are restricted to a range from 60 degrees to full extension to contain tibiofemoral shearing and patellofemoral compressive forces. Balance and proprioception training activities are also initiated as part of phase II rehabilitation. Open chain flexion and extension exercises are avoided during this time. Between the 10th and 12th postoperative weeks, the hinged knee brace is discontinued. A functional brace may be used at this time to assist with varus and valgus stability. Knee flexion should approach 120 degrees during the third phase of rehabilitation. A lack of the last 10 to 15 degrees of knee flexion is not uncommon but rarely results in any functional limitation. If active flexion of 90 degrees has not been reached by postoperative week 12, manipulation under anesthesia with or without arthroscopic débridement may be considered. During the fourth through sixth postoperative months, closed chain strengthening exercises are advanced. Aerobic conditioning exercises are also initiated at this time. As rehabilitation progresses, open chain exercises and straight-line jogging can commence. At the end of the sixth postoperative month, isokinetic assessments are obtained. Quadriceps and hamstrings deficits of 20% or less are desired before the patient is allowed to begin sport-specific activities. Phase IV of the multiple ligament–injured knee rehabilitation protocol occurs during the 7th through 12th


Box 23G-2 Multiple Ligament Reconstruction Rehabilitation Phase I: 0 to 6 weeks Goals

• Graft protection • Maintain patellar mobility • Maintain quadriceps tone • Maintain full passive extension • Control pain and swelling Program

• Non–weight-bearing ambulation with crutches • Brace locked in full extension • Cryotherapy • Quadriceps sets • Patellar mobilization • Ankle pumps and stretching exercises • Active range of motion from 0 to 90 degrees from weeks 4 to 6

Phase II: 6 to 12 weeks Goals

• Initiate weight-bearing • Increase knee flexion • Maintain quadriceps tone • Improve proprioception • Avoid isolated quadriceps and hamstring contraction Program • Progress to full weight-bearing over the next 4 weeks • Open brace to full flexion • Prone hangs • Passive flexion exercises • Closed chain strengthening

postoperative months. Return to sports or heavy labor is predicated on the absence of swelling with minimal to no pain. Strength and functional tests should be within 90% of the contralateral uninjured side. Patients return to clinic 1 year after the initial postoperative date. A complete physical examination is performed along with stress radiographs, arthrometric testing, and completion of ligament rating forms. The functional brace is continued for sports or rigorous activities for an additional 6 months. Patients continue to return on a yearly basis so that long-term effectiveness and patient satisfaction can be assessed.

POTENTIAL COMPLICATIONS Complications involving multiligamentous knee injuries are seen rather frequently, and great care must be employed to minimize their incidence and significance. Accurate diagnosis, appropriate surgical timing, and structured rehabilitation are all essential to avoid complications. In the initial management of these injuries, a detailed neurovascular examination is paramount. Failure to recognize injury to the popliteal artery or vein can lead to loss of limb. In cases in which the vascular status of the leg is in question, further diagnostic tests should be obtained.

• Stationary bicycle • Hip strengthening and continued proprioceptive retraining

• Discontinue hinged brace by week 12 Phase III: 4 to 6 months Goals

• Maximize flexion and maintain full extension • Improve quadriceps and hamstring strength • Improve functional skills • Improve cardiovascular endurance Program

• Progressive closed chain strengthening • Single leg proprioception exercises • Isolated quadriceps and hamstring exercises with increasing resistance

• Straight-line jogging followed by sprinting • Fit for anterior/posterior cruciate ligament brace • Begin agility drills in brace • Sport-specific drills • Isokinetic testing at end of phase III Phase IV: 7 to 12 months Program

• Assess functional strength via single-leg hop • Return to sports when the following criteria are met

o

o

o

o

inimal to no pain M Isokinetic and functional tests within 10% of the uninvolved side Successful completion of sport specific drills Anterior/posterior cruciate ligament functional brace

Delay in revascularization must be avoided. Focusing on the potential limb-threatening vascular injuries remains the first step in avoiding serious complications of these injuries. Failure to recognize the severity of the injury complex can also lead to an inadequate treatment plan and worse outcomes. MRI should be used early to supplement physical examination findings in order to identify all compromised ligamentous structures. Specific perioperative complications following multiple ligament knee reconstructions include iatrogenic neurovascular injury, compartment syndrome, fluid extravasation, and wound problems. In patients with vascular injury, vascular repair needs to be among the first treatments rendered. During definitive ligament reconstruction, the vascular repair must be protected. Excessive manipulation of the knee may place a vascular anastomosis under tension. It is ideal to have the vascular surgeon that performed the aforementioned revascularization available, in case the vascular repair fails. The highest potential for iatrogenic vascular injury exits during posterior cruciate reconstruction. The posteromedial safety incision is described earlier and is extremely useful in protecting the popliteal artery and tibial nerve during PCL surgery.62 Passage of the guide pin for the

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t ibial tunnel should be done under direct visualization using the arthroscope or fluoroscopic imaging. Hand drilling of the posterior cortex of the tibial tunnel is also effective in reducing the risk for penetration into the neurovascular structures. The common peroneal and tibial nerves are also at significant risk during these multiligamentous reconstructions. In many cases, some degree of nerve injury exists preoperatively. Great care must be employed to avoid further trauma to the nervous structures. Lateral-sided injuries are often associated with injury to the common peroneal nerve. During open reconstruction of the PLC, the nerve must be identified and protected at all times. It is at significant risk when drilling tunnels in and around the fibular head and when using the biceps tendon as part of the ligamentous reconstruction. The tibial nerve is most at risk for injury during PCL tibial tunnel preparation. It should be protected in a similar manner as that of the popliteal artery. Compartment syndrome of the leg can be a potentially disastrous complication of knee dislocations. It can occur early after the initial injury, or it may manifest in a delayed fashion, especially in cases of revascularization following a period of lower leg ischemia. Additionally, fluid extravasation during arthroscopy can create an iatrogenic compartment syndrome if capsular structures have not healed sufficiently to allow an arthroscopic approach.91 One must be prepared to convert to open central pivot reconstructions in these specific cases. High pump pressures should be avoided. Postoperative infection and wound dehiscence are also potential complications in these cases. Multiple incisions are usually required to perform these procedures. Adequate skin bridges must be maintained to avoid skin necrosis. Open injuries should be thoroughly débrided and irrigated in an operative setting. Undue tension on surgical incisions creates potential for delayed wound healing. Delaying surgery for a short time to allow improvement in the quality of the soft tissue envelope before definitive surgery is ideal.92 Stiffness and recurrent laxity and instability are the two primary long-term complications patients experience following operative treatment of the dislocated knee. A fine balance exits between creating a stiff, stable knee and a supple knee with functional laxity. A review of the literature indicates that stiffness is the primary complication found in patients treated with operative ligament repair and reconstruction.15,34,57,59 However, the few series that have compared operative and nonoperative treatment have recommended surgical treatment despite this known complication.20,51,60,64,93 To minimize postoperative stiffness, some authors have suggested a short delay between the initial injury and definitive ligamentous reconstruction.55,61 Three weeks has been suggested as an optimal time to allow the early post-traumatic inflammatory process to subside before adding a second postsurgical insult to the knee. Benefits of this approach are that capsular injuries are allowed to begin to heal which may allow for arthroscopic intervention. The negative aspect is that primary repair of the PLC structures is more optimal at an earlier time frame. Delay creates secondary scarring, which can force one to proceed with PLC reconstruction.

Recurrent or persistent ligamentous laxity is seen much less frequently in treating the multiple ligament–injured knee because early, aggressive surgical treatment has become more commonplace. However, residual posterior sag of the tibia is not uncommon. Failure to address collateral or corner injuries often leads to functional instability and potential failure of the central pivot reconstructions. Prolonged delay to surgery has been shown to have worse long-term outcomes secondary to increased laxity as well as an increased number of articular cartilage and meniscal injuries. Avoiding complications in the treatment of the multiple ligament–injured knee depends on early recognition and treatment of all potential neurovascular complications. Complete diagnosis of all injured structures needs to be followed by careful preoperative planning and surgical timing. Neurovascular structures must be protected at the time of ligamentous reconstruction. A detailed rehabilitation program must be employed and followed. Stiffness and arthrofibrosis remain a complex issue that should be addressed promptly for optimal results.

CRITERIA FOR RETURN TO PLAY Return to athletic activities or heavy labor is predicated on multiple factors. It is considered at about the seventh postoperative month. Swelling should be absent, and pain should be at a minimum. Isokinetic strength and functional testing should be within 90% of the contralateral, uninjured side. Patients are fitted with a functional combined instability brace. The brace is recommended for strenuous activity for an additional 12 months. It is important to counsel patients that a return to their previous level of function and activity may not be attainable following these potentially devastating injuries.

CONCLUSIONS AND SUMMARY Multiple ligament injuries of the knee are complex injuries requiring a systematic approach to evaluation and treatment. Gentle reduction, along with documentation and treatment of vascular injuries, is a primary concern in the acute dislocated and multiple ligament–injured knee. Arthroscopically assisted combined ACL and PCL reconstruction with appropriate collateral ligament surgery is a reproducible procedure. Knee stability is improved postoperatively when evaluated with knee ligament rating scales, arthrometer testing, and stress radiographic analysis. Acute MCL tears, when combined with ACL and PCL tears, may in certain cases be treated with bracing. PLC injuries, combined with ACL and PCL tears, are best treated with primary repair as indicated, combined with reconstruction using a post of strong autograft or allograft tissue. Surgical timing depends on the ligaments injured, the vascular status of the extremity, reduction stability, additional injuries, and the overall health of the patient. We prefer the use of allograft tissue for reconstruction in these cases because of the strength of these large grafts and the absence of donor site morbidity. Our most recent study group demonstrates the efficacy and success of using a mechanical graft-tensioning device (Arthrotek graft tensioning boot) in single-bundle, single femoral tunnel arthroscopic PCL reconstruction.


C

r i t i c a l

P

o i n t s

l

nee dislocations result from violent trauma and are K orthopaedic emergencies. l Vascular injury is common (32%) and must be diagnosed and treated promptly. l Absolute surgical indications include vascular injury, open injuries, and irreducible dislocations. l Surgical timing is dictated by the ligaments injured, the vascular status of the extremity, reduction stability, additional injuries, and the overall health of the patient. l Surgical delay of 2 to 3 weeks helps minimize the risk for postoperative stiffness. l Better surgical results are achieved with anatomic repair and reconstruction of all compromised structures. l Fluid extravasation may preclude an arthroscopic approach to ligament reconstruction. l Specialized instruments and the posteromedial safety incision can help minimize the risk for iatrogenic trauma during PCL reconstruction. l A dedicated rehabilitation program is essential to maximize function and stability. l Stiffness is the most common complication, and manipulation under anesthesia may be needed to maximize results.

S U G G E S T E D

R E A D I N G S

Cole BJ, Harner CD: The multiple ligament injured knee. Clin Sports Med 18: 241-262, 1999. Fanelli GC (ed): Posterior Cruciate Ligament Injuries: A Practical Guide to Management. New York, Springer-Verlag, 2001. Fanelli GC (ed): The Multiple Ligament Injured Knee: A Practical Guide to Management. New York, Springer-Verlag, 2004. Fanelli GC: Rationale and surgical technique for PCL and multiple knee ligament reconstruction. Arthrotek, Inc. Surgical Technique Manual No. Y-BMT979/071506/K, 2006. Fanelli GC, Edson CJ: Arthroscopically assisted combined ACL/PCL reconstruction: 2-10 Year follow-up. Arthroscopy 18:703-714, 2002. Fanelli GC, Edson CJ, Orcutt DR, et al: Treatment of combined anterior cruciateposterior cruciate ligament-medial-lateral side knee injuries. J Knee Surg 18: 240-248, 2005. Good L, Johnson RJ: The dislocated knee. J Am Acad Orthop Surg 3:284-292, 1995. Green A, Allen BL: Vascular injuries associated with dislocation of the knee. J Bone Joint Surg [Am] 59:236-239, 1977. Shelbourne KD, Wilckens JH, Mollabashy A, et al: Arthrofibrosis in acute anterior cruciate ligament reconstruction: The effect of timing of reconstruction and rehabilitation. Am J Sports Med 19:332-336, 1991. Sisto DJ, Warren RF: Complete knee dislocation: A follow-up study of operative treatment. Clin Orthop 198:94-101, 1985.

R efere n ces Please see www.expertconsult.com

S e c t i o n

H

Osteochondritis Dissecans C. Thomas Vangsness Jr. The etiology of osteochondritis dissecans (OCD) remains unclear, and all treatment algorithms are anecdotal in nature without evidence-based medicine.1,2 OCD was originally thought to be an inflammatory problem and initially was named osteochondritis. The disease was formally termed OCD by Koenig3,4 to explain the late problems of loose bodies in the joint. Although not necessarily an inflammatory process, the term OCD has persisted in the literature.5

CLASSIFICATION A uniformly accepted classification system for the anatomic changes seen with OCD has not been established. OCD has been classified by bone maturity: 1. Juvenile lesions have open distal femoral physes. 2. Adolescents have closing distal femoral physes. 3. Adults have fully closed distal femoral physes.

Historically, the classification of OCD has been made from plain radiographs to define the lesion size and location. Most radiologic classification systems attempt to determine the presence and stability of any loose fragments. Whether we use conventional tomography, computed tomography (CT) with or without arthrography, standard arthrography, scintigraphy, or magnetic resonance imaging (MRI) with or without dye, none of these is ideal. Berndt and Harty6 originally described four stages of lesions on plain radiographs of talar OCD, which has since been applied to the knee. Stage I shows a small area of compression of the subchondral bone. Stage II is a partially detached osteochondral fragment. Stage III is a completely detached fragment that remains in the crater of origin, and stage IV shows complete detachment and a loose body. Cahill and Berg7 divided the knee radiograph into 15 distinct zones (Fig. 23H-1). The zones are numbered 1 to 5 from medial to lateral and essentially divided by the notch of the knee. Each compartment is divided in half. In

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TABLE 23H-2 Magnetic Resonance Imaging

Classification of Knee Osteochondritis Dissecans

5

4

3

2

Blumensaat’s line

1 A B

C

Stage

Description

1 2

Small change of signal without clear margins of fragment Osteochondral fragment with clear margins but without fluid between fragment and underlying bone Fluid is visible partially between fragment and underlying bone. Fluid is completely surrounding the fragment, but the fragment is still in situ. Fragment is completely detached and displaced (loose body).

3 4 5

B

A

Figure 23H-1 Alphanumeric zone classification of knee osteochondritis dissecans lesions. Anteroposterior (A) and lateral (B) views of the knee demonstrate the 15 regions. The five numbered zones on the anteroposterior view are divided centrally by the notch (zone 3). The lettered zones on the lateral view are divided by Blumensaat’s line anteriorly and the posterior cortical line. The half-moon–shaped shaded area in each view of the distal femur represents an old lesion. (Redrawn from Cahill BR, Berg BC: 99m-Technetium phosphate compound joint scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles. Am J Sports Med 11:329-335, 1983.)

the lateral radiograph, Blumensaat’s line divides the knee into areas A, B, and C. This classification system applies to adult knees. Milgram8 has documented the radiographic characteristics of OCD around the femoral condyles. Fragmentation and collapse, along with increased separation, was noted with a sclerotic base around the femoral defect and a radiolucent crescentic zone. Barrie9 outlined the components of fragmentation in the pathogenesis of OCD. The classification system for juvenile OCD is based on technetium-99m phosphate scintigraphy findings (Table 23H-1). The scan’s activity is related to the plain radiograph.7,10 Zero is normal, and stage I demonstrates a small change on radiography, but no increased activity on bone scan. Stage II shows an increased uptake in the lesion, but not in the adjacent femoral condyle. Stage III shows an increased uptake in both the lesion and the adjacent femoral condyle. Stage IV demonstrates involvement in both the femoral lesion and the adjacent tibial surface. Stages III and IV are thought to be more systemic OCD TABLE 23H-1 Bone Scan Classification of Juvenile Osteochondritis Dissecans Stage

Description

0 I

Normal radiographic and scintigraphic appearance The lesion is visible on plain radiographs, but bone scans reveal normal findings. The scan reveals increased uptake in the area of the lesion. In addition, there is increased isotope uptake in the entire femoral condyle. In addition, there is uptake in the tibial plateau opposite the lesion.

II III IV

lesions. Paletta and colleagues11-13 noted that patients with open physeal plates and increased activity on bone scan had improved healing compared with older patients with closed growth plates. MRI has been used to develop a better understanding of these lesions (Table 23H-2). MRI techniques have limitations in detecting articular cartilage changes in OCD. MRIs have been classified with the lesions containing fluid behind them as partially detached.14 High signal intensity on T2-weighted images can help distinguish a break in the articular cartilage surface. Gadolinium as a contrast material has also been used to predict the stability of these OCD lesions.14 Future pulsing sequences with and without contrast will help delineate and explain the OCD process.15 Arthroscopy has improved our understanding of the diagnosis and management of OCD. Chondral lesions that have an intact articular cartilage are called closed lesions. Open lesions can be partial or complete depending on the involvement of the articular cartilage. Cartilage stability can be partial or complete depending on the probing at the time of surgery. Mesgarzadeh and associates16 used conventional radiography, bone scintigraphy, and MRI to assess the mechanical stability of OCD in the femoral condyles. Arthroscopy examination showed lesions to be grossly loose when lesions were large (>0.8 cm3) or associated with broad sclerotic margins (especially >3 mm thick) on routine radiographs. Significant accumulation of bone-seeking radionuclides during the flow, blood-pool, and late phase of radionuclide examination generally indicated a loose fragment. MRI showing fluid at the interface of the fragment and the bone also correlated with loose fragments. The density of the fragment was not a useful indicator of stable or unstable lesions.

EPIDEMIOLOGY The peak prevalence of juvenile OCD is noted during the preteen years, and OCD is thought to be rare among children younger than 10 years. The adolescent OCD is estimated to be between 0.2% and 0.3% based on knee radiographs and 1.2% based on knee arthroscopy studies.6,17 The highest risk occurs in patients aged 10 to 15 years. Male-to-female ratios have been quoted in the literature as between 2:1 and 5:3. Twenty to 25% of the cases are bilateral.18,19 OCD usually involves the lateral portion of the medial condyle in three fourths of the cases (Fig 23H-2).20,21 Posterior portions of the femoral


A

B

C

D

Figure 23H-3 Osteochondritis dissecans of the patella.

E Figure 23H-2 Location of osteochondritis dissecans of the femoral condyles. Medial condyle: classic, 69% (A); extended classic, 6% (B); inferocentral, 10% (C). Lateral condyle: inferocentral, 13% (D); anterior, 2% (E). (Redrawn from Aichroth P: Osteochondritis dissecans of the knee. J Bone Joint Surg Br 53:440-447, 1971.)

c ondyles and the tibial plateau can be affected. Patellar lesions can occur 5% to 10% of the time and are usually located in the inferior medial area (Fig. 23H-3).22-24 The femoral trochlea region for OCD is rare (Fig. 23H-4).25

ETIOLOGY The literature defines three major areas of etiology: constitutional-hereditary, vascular, and traumatic. Repetitive or persistent microtrauma to a vulnerable area appears to be the major etiologic source.1,26 Many predispositions to OCD lesions have been suggested in the literature.27,28 OCD has been found in a variety of inherited conditions including dwarfism, tibia vara, Legg-Calvé-Perthes disease, and Stickler’s syndrome.29 OCD has been suggested to represent a variation of epiphyseal dysplasia.27 Ultimately, genetic inheritance will most likely be proved over time to be multifactorial in nature. Authors have looked at the pathophysiology between osteonecrosis and OCD.19 An analogy has been made to a sequestrum. Studies have shown detached OCD lesions with no histopathophysiologic evidence of osteonecrosis.30 A limited uptake of tetracycline and radionuclide has been noted in OCD lesions.31 Traumatic injury has been reported in up to 40% of patients with OCD providing evidence for the traumatic origin of OCD lesions.32 It is also been thought that the tibial spine eminence may create shearing effects to the lateral aspect in the medial knee condyle, creating increased contact forces.33,34

NATURAL HISTORY Outcomes in the literature have looked at patient maturity as the major predictive determinant of outcome. Younger patients have a high healing potential, although adolescent improvement is still unpredictable.19,33,35,36 About 50% of these lesions tend to heal. In the mature group, the rate of healing is decreased, depending on the location and size of the lesion. Degenerative joint disease can become the long-term final outcome of OCD.37 Specific outcomes depend on the origin of the OCD and the size, location, and specific status of the articular cartilage lesion.38 It must be emphasized that no randomized clinical trials exist to elucidate the natural history of this disease process. A large multicenter review of the European Pediatric Orthopaedic Society (500 knees, 318 juveniles, 191 adults)29 provided several important conclusions: A stable fragment had a better prognosis, and pain and swelling were not

Figure 23H-4 Osteochondritis dissecans of the femur.

Knee 1769 Juvenile (open physis)

Radiographs

Adult (closed physis)

Stable

Stable

Physical examination


Stable

Stable

MRI

Unstable

MRI

Stable

Stable

Not positive

Bone scan

Malalignment

Positive

No

Activity restriction (3 mo)

Yes

Osteotomy

• Impending physeal closure • Clinical signs of instability • Expanding lesion on plain films

Arthroscopy

Stable

Unstable reducible

Unstable with fragmentation or osteolysis

Transchondral drilling

Fixation graft

Fixation and graft

Treat symptomatically

Unstable and chondral damage

Fixation and graft, chondrocyte transplant, or osteochondral graft

Figure 23H-5 Treatment algorithm for osteochondritis dissecans of the knee.

good indicators of loosening. Radiography and CT were not useful in predicting loosening of the fragment. Sclerosis on plain films gave a poor response to drilling treatments. A lesion larger than 2 cm in diameter gave a worse prognosis, and when there was loosening of the fragment, surgical results were better than nonsurgical results. Classically defined anatomic lesions had a better prognosis. An adult onset of symptoms had more abnormal findings after the treatment period, and more than one in five of those with open physeal plates had abnormal knee radiographs an average of 3 years after treatment.

CLINICAL TREATMENT Crawford and Safran39 presented a treatment algorithm for knee OCD (Fig. 23H-5). Early clinical diagnosis and treatment are critical to optimize patient outcomes. The literature recommends plain radiographs of the knee, including anteroposterior, lateral, notch, and skyline radiographs followed by an MRI. Sometimes an MRI with contrast will further clarify the classification of the lesion. Bone scans can also provide bone activity information.


Nonoperative Management In juvenile and adolescent lesions with open physeal plates, the natural history of stable OCD lesions is generally favorable, and nonoperative treatment is appropriate.40,41 Activity levels must be decreased with consideration for immobilization. The length of this immobilization and duration of limited activity are uncertain. Continuous passive motion for the common OCD can be considered. The side effects of prolonged immobilization must be considered, including ongoing joint stiffness, muscle atrophy, and potential cartilage degeneration. Partial weight-bearing issues with this conservative protocol have not been established. Repeat MRIs with intra-articular contrast can be considered, although the best timing of these scans has not been established. Older patients with an OCD lesion have a less certain course, and mechanical symptoms, fragment loosening, and detachment should be monitored with plain radiographs or sequential MRI examinations with or without contrast.

Operative Management Cahill42 reported a 50% success rate of nonoperative management of juvenile and adolescent OCD. Juvenile OCD lesions can undergo an arthroscopic examination and drilling.13 Epiphyseal drilling with or without articular cartilage penetration aims to promote vascular channels for potential healing.2 Retrograde drilling is also an acceptable technique, although technically more difficult. Adult OCD must be observed for potential loose bodies. If adult OCD lesions are unstable or there are loose bodies, surgical intervention is appropriate.43 The maintenance of the articular cartilage surface is important and may necessitate repair of the unstable fragments or the osteochondral defect. Inadequate healing is associated with nonclassic OCD lesions, multiple lesions, or underlying medical conditions such as smoking. Débridement of the fibrous tissue and drilling of the sclerotic subchondral base of the OCD lesion is recommended.44 An autologous bone graft can be placed in the crater before reduction and fixation. Screws have also been used successfully to fix larger fragments.4,28,45-47 The recent use of bioabsorbable screws and pins helps avoid a second surgery to remove hardware.48 Loosening and failure of bioabsorbable screws have been reported in the literature.49,50 If the OCD lesion is too small, has fragmentation, or has inadequate bony backing (less than 2 mm of bone), the surgeon may be forced to simply remove the OCD piece.51,52 To promote filling of the defect, drilling, abrasion arthroplasty, and microfracture methods can be used to recruit pluripotential cells from the marrow elements.53,54 Autologous osteochondral plugs can be obtained from neighboring regions of the knee to fill the defect in the skeletally mature patient.55,56 Autologous chondrocyte implantation (ACI) has been used to treat larger femoral defects. In the skeletally mature patient, a bone graft can be placed into the base of the crater followed by the ACI procedure.13,57,58 Staged and planned defect reconstruction with fresh osteoarticular allografts is difficult in terms of the logistics of obtaining and processing this fresh graft.26,59-61 Good results have been published, although long-term results are not available.43 Regardless of the chosen surgical technique

applied to knee OCD lesions, long-term evidence-based literature does not exist.

CONCLUSION The etiology and natural history of OCD continues to be uncertain. The effect of skeletal maturity has been emphasized. With newer diagnostic techniques and newer MRI pulsing sequences, a better understanding of the biology of these lesions over time will be learned. The long-term problems are pain and arthritis in the knee, and patient education needs to be emphasized, although it difficult because of the relative infrequency with which OCD occurs. Longterm randomized clinical trials need to be done. C

r i t i c a l

P

o i n t s

l OCD is a disease originating in the subchondral bone with late secondary problems involving the articular cartilage surface. l Clinical manifestations are variable and relate to the site of involvement and stage of the disease. l Genetics probably play a role, and knee trauma is a common cause. l Classifications are made from radiographs and MRIs. l Treatment protocols depend on the age, location of disease, and stage of the disease process. l There are no published randomized clinical trials to provide good evidence-based medicine to specifically delineate treatment regimens. l A uniformly accepted classification system has not been established. Classification of OCD has been made from plain radiographs to define the lesion size and location. l The peak prevalence of juvenile OCD is noted during the preteen years, with the highest risk appearing between patients aged 10 to 15 years. Juvenile OCD lesions can undergo an arthroscopic examination and drilling. l Older patients with an OCD lesion have a less certain course, and mechanical symptoms, fragment loosening, and detachment should be monitored with plain radiographs or sequential MRI examinations with or without contrast. l If adult OCD lesions are unstable or there are loose bodies, surgical intervention is appropriate. Maintenance of the articular cartilage surface is important.

S U G G E S T E D

R E A D I N G S

Aichroth P: Osteochondritis dissecans of the knee: A clinical survey. J Bone Joint Surg Br 53:440-447, 1971. Bentley G, Biant LC, Carrington RW, et al: A prospective, randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. J Bone Joint Surg Br 85:223-230, 2003. Cepero S, Ullot R, Sastre S: Osteochondritis of the femoral condyles in children and adolescents: Our experience over the last 28 years. J Pediatr Orthop B 14(1): 24-29, 2005. Flynn JM, Kocher MS, Ganley TJ: Osteochondritis dissecans of the knee. J Pediatr Orthop 24(4):434-443, 2004. Garrett JC: Osteochondritis dissecans. Clin Sports Med 10:569-593, 1991. Hefti F, Beguiristain J, Krauspe R: Osteochondritis dissecans: A multicenter study of the European Pediatric Orthopedic Society. J Pediatric Orthop B 8:231-245, 1999. Hui JH, Chen F, Thambyah A, Lee EH: Treatment of chondral lesions in advanced osteochondritis dissecans: A comparative study of the efficacy of chondrocytes, mesenchymal stem cells, periosteal graft, and mosaicplasty (osteochondral autograft) in animal models. J Pediatr Orthop 24(4):427-433, 2004.

Knee 1771 Kocher MS, Tucker R, Ganley TJ, Flynn JM: Management of osteochondritis dissecans of the knee: Current concepts review. Am J Sports Med 34:1181-1191, 2006. Makino A, Muscolo DL, Puigdevall M, et al: Arthroscopic fixation of osteochondritis dissecans of the knee: Clinical, magnetic resonance imaging, and arthroscopic follow-up. Am J Sports Med 33(10):1499-1504, 2005. Murray JR, Chitnavis J, Dixon P, et al: Osteochondritis dissecans of the knee: Longterm clinical outcome following arthroscopic debridement. Knee 14:94-98, 2007. Ronga M, Zappala G, Cherubino M, et al: Osteochondritis dissecans of the entire femoral trochlea. Am J Sports Med 34(9):1508-1511, 2006.

Twyman RS, Desai K, Aichroth PM: Osteochondritis dissecans of the knee: A longterm study. J Bone Joint Surg Br 73:461-464, 1991. Uematsu K, Habata T, Hasegawa Y, et al: Osteochondritis dissecans of the knee: Long-term results of excision of the osteochondral fragment. Knee 12(3): 205-208, 2005.


S e c t i o n

I

Articular Cartilage Lesion Andreas H. Gomoll, Adam Yanke, and Brian J. Cole Damage to the articular cartilage comprises a spectrum of disease entities ranging from single, focal chondral defects to more advanced osteoarthritis disease, the latter of which is not discussed in this chapter. Left untreated, articular cartilage lesions have no spontaneous repair potential. Therefore, various techniques have evolved to stimulate defect repair or overtly replace these defects. Conventional techniques, such as abrasion arthroplasty, drilling, or microfracture, attempt to fill the defect with a fibrocartilaginous scar produced by marrow-derived pluripotent stem cells. This tissue, however, is of lesser biologic and mechanical quality than hyaline cartilage. More recently developed techniques, such as autologous chondrocyte implantation (ACI) and matrix autologous chondrocyte implantation (MACI), achieve a tissue that more closely resembles the original hyaline cartilage but are expensive and involve sophisticated and prolonged rehabilitation. This chapter provides a concise overview of current techniques for cartilage repair, presents new developments in this evolving area, and subsequently discusses the authors’ preferred techniques in more detail.

RELEVANT ANATOMY AND BIOMECHANICS Partial-thickness chondral lesions do not penetrate the subchondral bone and are therefore avascular, do not heal, and may enlarge over time. Full-thickness defects, especially with injury to the underlying vascular bone, have the potential to fill with a fibrocartilaginous scar formed by cells invading from the marrow cavity. The resulting tissue, however, is predominantly composed of type I collagen, resulting in inferior mechanical properties compared with the type II collagen-rich hyaline cartilage. Long implicated in the subsequent development of osteoarthritis, focal chondral defects result from various causes. Patients are about evenly split in reporting a traumatic versus an insidious onset of symptoms; athletic

activities are the most common inciting event associated with the diagnosis of a chondral lesions.1 Traumatic events and developmental causes such as osteochondritis dissecans (OCD) predominate in younger age groups. For example, traumatic hemarthroses in young athletes with knee injuries are associated with chondral defects in up to 10% of cases2; patellar dislocation is strongly associated with damage to the articular surface, with chondral defects of the patella see in up to 95% of patients3; the incidence of OCD is estimated at 30 to 60 cases per 100,000 people.4 Several large studies have found high-grade chondral lesions (Outerbridge grades III and IV) in 5% to 11% of younger patients (1.5 cm Exposed subchondral bone

More than half the cartilage depth, and: A. Not to the calcified layer B. To the calcified layer C. To the subchondral bone D. Blisters Osteochondral lesion violating the subchondral plate A. Superficial B. Deep

CLASSIFICATION

ICRS, International Cartilage Repair Society.

with osteotomies popularized this technique for the treatment of osteoarthritis with comparatively large correction angles.10 The population treated for chondral defects today, however, is predominantly athletic and does not tolerate large degrees of overcorrection. When performed concurrently with cartilage repair, osteotomy around the knee should restore the mechanical axis to at least neutral alignment. Even

Normal

ICRS Grade 1 Nearly Normal

A

in patients with early joint space narrowing, overcorrection of the mechanical axis should be limited to 2 degrees or less. Ligamentous insufficiency, most commonly of the ACL, increases shear forces in the knee joint, predisposes the joint to further injury, and thus contributes to chondral damage. Any patient undergoing cartilage repair should therefore be carefully evaluated for instability, which can be corrected in a staged or concomitant fashion. Meniscal insufficiency, such as after subtotal meniscectomy, increases contact stresses by up to 300% in the respective compartment and is associated with the development of osteoarthritis.11 In carefully selected patients with meniscal insufficiency, meniscal allograft transplantation can provide pain relief and improved function. The ideal candidate for allograft transplantation has a history of prior total or subtotal meniscectomy with refractory, activity-related pain localized to the involved compartment. Following meniscal allograft transplantation, good to excellent results are achieved in nearly 85% of cases, and patients demonstrate a measurable decrease in pain and increase in activity level.12

B

Earlier classification schemes were mainly descriptive in nature and have largely been abandoned. Newer systems have evolved to classify chondral defects based on size and depth to establish a universal language among clinicians and researchers, and to ideally provide a correlation of lesion grade with clinical outcome. Currently, the most commonly used classifications are the Outerbridge13 and International Cartilage Repair Society systems (Table 23I-1; Fig. 23I-1).14

ICRS Grade 2 Abnormal

ICRS Grade 3 Severely Abnormal

ICRS Grade 4 Severely Abnormal

A

B

A

C

D

B

Figure 23I-1 International Cartilage Repair Society classification of chondral defects. (See Table 23I-1 for further explanation of grades.)

Knee 1773

Figure 23I-2 Computed tomographic arthrogram demonstrating an osteochondritis dissecans lesion in the medial femoral condyle. The defect was previously treated with arthroscopic fixation using multiple screws.

EVALUATION Clinical Presentation and History Patients often present with a history of knee injury, or prior surgical procedures such as meniscectomy or ACL reconstruction. They report activity-related knee pain and swelling, especially with impact activities such as running. Often, the pain localizes to the affected compartment, and occasionally synovitis develops, resulting in diffuse pain. Larger defects can be associated with mechanical symptoms, profound crepitus, popping, and giving-way.

Physical Examination and Testing Depending on the acuity of symptoms, typical physical examination findings include an antalgic gait, soft tissue swelling and joint effusion, quadriceps atrophy, tenderness with palpation of the joint line and femoral condyle, and occasionally, mild varus or valgus laxity due to loss of cartilage or meniscal substance. With the exception of very advanced cases, or in large lesions with loose bodies, motion is generally preserved. It is important to evaluate limb alignment and ligamentous stability because any deficiencies should be treated in either staged or concomitant procedures.

Imaging Radiographic work-up should include a standard weightbearing anteroposterior (AP) view in extension, posteroanterior (PA) view in 45 degrees of flexion (Rosenberg view), flexion lateral view, and axial view of the patellofemoral joint (Merchant or skyline view). Double-stance, weightbearing, long-leg radiographs are obtained to quantify lower extremity alignment to determine whether corrective osteotomy is required. Computed tomography (CT) is used infrequently, unless the lesion also affects the subchondral bone, such

Figure 23I-3 Sagittal magnetic resonance image showing a focal chondral defect (arrow) with associated marrow edema of the subchondral bone. Fat-saturated proton density fast-spin echo sequence.

as in osteochondritis dissecans (OCD) or traumatic osteochondral defects. Here, CT, especially when combined with arthrography, can be very helpful to delineate the exact dimensions of the defect more precisely and to assess bone healing (Fig. 23I-2). Another application for CT is in the evaluation of patellofemoral cartilage lesions, where it allows calculation of the tibial tubercle to trochlear groove (TT-TG) distance. This parameter is an alternative to using the quadriceps angle and is important when considering a tibial tubercle osteotomy or anteromedialization. Magnetic resonance imaging (MRI) assessment of the articular surface (Fig. 23I-3) has received increased attention because of newly developed protocols for cartilagespecific high-resolution imaging and contrast enhancement with intravenous and intra-articular gadolinium. Delayed gadolinium-enhanced MRI of cartilage is a new imaging protocol that provides an assessment of the glycosaminoglycan content of cartilage (Fig. 23I-4).15 It represents a useful tool for noninvasive follow-up evaluation after cartilage repair techniques such as ACI. Although arthroscopy remains the gold standard for assessing articular injury, sensitivities and specificities approaching 90% have been reported with MRI protocols using a 1.5-Tesla magnet.16-19 Furthermore, MRI provides additional information on the ligamentous and meniscal structures, which, if compromised, would require staged or concomitant treatment.

TREATMENT OPTIONS Nonoperative Treatment Nonoperative treatment options for cartilage defects can be separated into physical measures and pharmacologic treatment, which is further subdivided into oral and injectable agents. Physical measures include weight loss, exercise, and bracing. Obesity has been established as an independent

�rthopaedic �� S �ports �� Medicine �� 1774 DeLee & Drez’s� O 1.46e+003

1.17e+003

879

586

293

0

Figure 23I-4 Color-coded delayed gadolinium-enhanced magnetic resonance imaging of cartilage allows assessment of the glycosaminoglycan content of a defect after cartilage repair, here after autologous chondrocyte implantation. (Courtesy of Dr. Tom Minas.)

risk factor for symptomatic arthritis of the knee, with odds ratios between 3 and 10,20 and weight loss of as little as 10 lb has been shown to decrease symptomatic arthritis by as much as 50%.21 Quadriceps weakness has been implicated in the development of symptomatic knee arthritis,22 and a strengthening program is thought to improve pain and function. Although mild to moderate levels of activity are thought to be beneficial, high- and elite-level activities, especially those of impact and torsion, contribute to symptomatic arthritis of the hip and knee.23 Bracing is frequently prescribed by orthopaedic surgeons to either stabilize a ligament-deficient knee or unload a compartment in unicompartmental arthritis of the knee. Functional bracing of ACL-deficient knees serves to decrease the risk for reinjury.24 Unloader braces have been demonstrated to significantly decrease symptoms and improve quality of life in unicompartmental knee arthritis.25 Pharmacologic treatment of knee arthritis includes oral agents such as acetaminophen, nonsteroidal antiinflammatory drugs (NSAIDs), and neutraceuticals such as chondroitin sulfate and glucosamine. Acetaminophen and NSAIDs have long been the mainstay of treatment for many musculoskeletal disorders. The risks for severe liver damage with acetaminophen overdose and for cardiovascular and gastrointestinal complications with NSAID use should be discussed with the patient. More recently, several trials have demonstrated the efficacy of chondroitin sulfate and glucosamine for the treatment of arthritic hip and knee pain with improvements in pain and function of about 50%,26 although there is high variability in the quality of individual preparations. Injectables, including steroids and viscosupplementation, represent a more invasive but viable option if oral treatment fails to improve symptoms. Steroid injection has been proved beneficial in numerous trials, with pain relief of 30% to 50%, which is usually only temporary and is strongest in the first 4 weeks.27 Viscosupplementation with hyaluronic acid provides similar levels of, but longer lasting, pain relief.28

Operative Treatment Conventional Cartilage Repair Techniques Before the development of modern bioengineering techniques, orthopaedists were restricted to procedures that aimed to palliate the effects of chondral lesions or attempted to stimulate a healing response initiated from the subchondral bone resulting in the formation of fibrocartilage to fill the defect. Simple arthroscopic lavage and débridement of arthritic joints has been used since the 1940s29 in an effort to reduce symptoms resulting from loose bodies and cartilage flaps. Although lavage alone has not been found to be effective, in combination with débridement, it can result in adequate pain reduction in slightly more than half of patients.30,31 The goal of débridement of chondral defects is to remove any loose flaps of articular cartilage and to create a defect shouldered by a stable rim of intact cartilage leading to reduced mechanical stresses in the defect bed. Currently, its use is limited to the treatment of small, incidental lesions found during arthroscopy, or for larger and usually more diffuse arthritic lesions in an attempt to delay the need for more invasive procedures such as total joint replacement. Marrow stimulation techniques (MSTs), such as drilling, abrasion arthroplasty, and predominantly, microfracture, attempt to induce a reparative response. This is achieved by perforation of the subchondral bone after radical débridement of damaged cartilage and removal of the tidemark “calcified” zone to enhance the integration of repair tissue. Perforation of the subchondral bone results in the extravasation of blood and marrow elements with formation of a blood clot in the defect. Over time, this blood clot, and the primitive mesenchymal cells contained within, differentiates into fibrocartilaginous repair tissue that fills the defect. Unlike hyaline cartilage, this fibrocartilage largely consists of type I collagen and exhibits inferior wear characteristics. Postoperatively, MSTs require extended periods of relative non–weight-bearing for 6 weeks or longer as well as the use of continuous passive motion (CPM) for up to 6 hours per day to enhance maturation of the repair tissue. Even though MSTs result in reparative tissue with inferior wear characteristics, treatment of smaller defects (12 mo Overall, 87% improvement, 13% failures (defined as lack of improvement or objective graft failure) Average, 5.6 yr 91% good or excellent results; 93% patient satisfaction Average, 47 mo 96% good or excellent results; 60% return to athletic activity levels equal to or greater than before injury Average, 46.4 mo 71% good or excellent results

ACL, anterior cruciate ligament; OCD, osteochondritis dissecans.

Autologous Chondrocyte Implantation

Osteochondral Autograft Transplantation

Several long-term studies have reported good to excellent results in 70% to 80% of patients after ACI for the treatment of chondral lesions in the knee (Table 23I-2). The results of ACI compare favorably with other forms of treatment, such as débridement,46 microfracture,47 mosaicplasty,48 and osteochondral autograft transfer.49 Patch hypertrophy resulting in mechanical symptoms such as clicking and popping occurs in up to 15% to 20% of patients, typically 7 to 9 months after the procedure,50 and can be addressed with arthroscopic débridement of the hypertrophic tissue.

Patients treated with osteochondral autograft transplantation experienced good to excellent results in about 90% of condylar lesions, 80% of tibial defects, and 70% of trochlear lesions.51 The treatment of patellar defects remains controversial, with some groups reporting almost universal failure in this location.48

Osteochondral Allograft Transplantation Following osteochondral allograft transplantation, good to excellent results are achieved in nearly 85% of cases, and patients demonstrate a measurable decrease in pain and increase in activity level (Table 23I-3).

TABLE 23I-3 Results of Osteochondral Allograft Transplantation for Chondral Defects in the Knee Study 198957

Meyers et al, Garrett, 199458 Ghazavi, 199759 Chu et al, 199960 Aubin et al, 200161 Shasha et al, 200362

No. of Patients

Mean Age (yr)

Location*

Mean Follow-Up

Results

39 17 123 55 60 65

38 20 35 35 27 N/A

F, T, P F F, T, P F, T, P F T

3.6 yr 3.5 yr 7.5 yr 75 mo 10 yr 12 yr

78% success, 22% failure 94% success 85% success 76% good or excellent, 16% failure 84% good or excellent, 20% failure Kaplan-Meier survival rate: 5 yr—95%; 10 yr, 80%; 15 yr, 65% 20 yr, 46%

*Defect location: F, femur; T, tibia; P, patella.

Authors’ Preferred Method We have developed a comprehensive treatment a lgorithm (Fig. 23I-5) based on defect size and location that takes into consideration the patient’s activity and demand level. 52 Four commonly used techniques that have yielded excellent results in our experience are discussed here.

Microfracture

Microfracture is most commonly performed as an allarthroscopic procedure, and the set-up and patient positioning follow that of routine knee arthroscopy. In very posterior defects, the patient should be positioned so that knee hyperflexion can be achieved. Continued


Authors’ Preferred Method—cont’d Lesion Location#

Femoral Condyle

Patellofemoral

Malalignment

Meniscal Deficiency

Rehabilitation

Ligament Insufficiency

Patellofemoral Alignment

Size

Size

< 2-3 cm2

≥ 2-3 cm2

< 2-3 cm2

Microfracture ++ 1˚ OC Autograft ++ ACI OC Allograft

+/+/++ ++

Low Demand Microfracture ++ ACI/AMZ* +/OC Autograft/AMZ* OC Allograft/AMZ*

OC Autograft ++ 2˚ ACI +/OC Allograft

++ ++

ACI/AMZ* ++ OC Autograft/AMZ* + High Demand OC Allograft/AMZ* +

≥ 2-3 cm2

++ +/+ ++ ++

Figure 23I-5 Treatment algorithm for isolated femoral and patellofemoral focal chondral lesions. For condylar lesions, comorbidities of ligament instability, meniscal deficiency, and malalignment must be assessed and corrected if needed. For trochlear and patellar lesions, patellofemoral alignment must be evaluated to select the proper degree of anteromedialization. ACI, autologous chondrocyte implantation; AMZ, anteromedialization tibial tubercle osteotomy; OC, osteochondral; #, assumes minimal bone loss; *, AMZ is often performed for lateral and central patellofemoral lesions and is of questionable benefit for medially located patellofemoral lesions. (Redrawn from Alford JW, Cole BJ: Cartilage restoration, part 2: Techniques, outcomes, and future directions. Am J Sports Med 33[3]:443-460, 2005.)

Approach and defect preparation. After routine iagnostic arthroscopy, the chondral defect is débrided d with a motorized shaver in forward or reverse, and a curet is used to achieve stable vertical shoulders. The débridement includes the calcified cartilage layer and should not violate the subchondral bone. Occasionally, accessory portals have to be created depending on the exact defect size and location. Microfracture. After thorough débridement, multiple holes are created in the subchondral bone with a microfracture awl (Fig. 23I-6A). In an effort to remain perpendicular to the chondral surface, it may be necessary to rotate the articular surface in line with the awl or create accessory portals. It is important to preserve the integrity of the subchondral bone, which can be violated if holes are not spaced wide enough and thus connect or become confluent. Ideally, the micro fracture holes should be spaced about 3 to 4 mm apart, resulting in 3 to 4 holes per cm2. Stability of the transition zone between surrounding cartilage and regenerate fibrocartilage

can be improved by placing holes directly adjacent to the defect shoulders. After completion of the microfracture, pump pressure is lowered, and bleeding should be observed from all holes (see Fig. 23I-6B). Closure. Arthroscopy portals are closed with interrupted sutures. The patient should be counseled that occasionally joint aspiration may become necessary because of persistent bleeding from the treated defect. Autologous Chondrocyte Implantation

After arthroscopic cartilage biopsy and culture, a process that usually takes about 6 weeks, the cell suspension is shipped to the surgical facility. The patient is positioned supine on a standard operating table with a thigh tourniquet. Especially in very posterior lesions of the femoral condyle, a leg positioning device is helpful to stabilize the knee in hyperflexion. The lower leg is prepared into the field to just above the ankle to allow harvesting of the periosteal patch.

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A

B

Figure 23I-6 A, Arthroscopic image showing a full-thickness chondral defect on the tibial plateau. Multiple pick holes are created with the microfracture awl. B, Bleeding is observed from the pick holes after the tourniquet has been released and the arthroscopic fluid pressure has been lowered.

Approach. For single lesions of the femoral condyles, a limited medial or, less commonly, lateral parapatellar arthrotomy is used (Fig. 23I-7A). Adequate exposure is critical, and it may become necessary to mobilize the meniscus by incising the coronary ligament and taking down the intermeniscal ligament, with subsequent repair at the end of the procedure. Correct placement of retractors is crucial, especially in limited incisions. A bent Hohmann or Z-retractor placed into the intercondylar notch is helpful to displace the patella to the contralateral side. A Z- or rake retractor is helpful to control the peripheral soft tissues. For multiple defects, a standard medial parapatellar arthrotomy is performed with lateral subluxation or dislocation of the patella. Defect preparation. Meticulous preparation of the lesion is critical for the success of the procedure. The defect must be cleaned of all degenerated tissue to achieve a stable rim of healthy cartilage with vertical shoulders. This is performed by first outlining the defect with a scalpel incision down to the subchondral plate, taking as much of the surrounding cartilage to remove all unstable or undermined areas. However, if this would transform a contained into an uncontained lesion, it is advisable to leave a small rim of degenerated cartilage to sew to rather than using bone tunnels or suture anchors. The defect is then thoroughly débrided with small ring or conventional curets while maintaining an intact subchondral plate to minimize bleeding, which results in migration of a mixed stem cell population from the marrow cavity into the chondral defect. If the subchondral plate is sclerotic, such as in chronic defects, partially healed OCD lesions, or after prior microfracture, we prefer to carefully thin out the sclerotic bone with a fine bur and cold irrigation. Minor bleeding from the subchondral bone is controlled with thrombin- or epinephrine-soaked sponges or, rarely, a needle-tipped electrocautery device in the cutting mode. After the defect is prepared, it is templated using glove paper, which is oversized by about 2 mm in both length and width because there is shrinkage of the periosteum as it is procured. Periosteal harvest. The most accessible site for procurement of the periosteal patch is the proximal medial tibia.

Either the arthrotomy is extended distally or a second incision is made located centrally over the anteromedial surface of the proximal tibia starting 3 to 5 cm inferior to the pes anserine insertion. The subcutaneous fat is incised superficially, and further dissection with Metzenbaum scissors exposes the tibial periosteum. The template is used to outline the periosteum, which is incised using a fresh No. 15 blade and mobilized with a small, sharp periosteal elevator. The patch should be gently removed from its bony bed to avoid tearing; the periosteum is pulled upward with nontoothed microforceps as it is gently removed from the tibia with a gentle pushing motion of the periosteal elevator (see Fig. 23I-7B). After the patch has been harvested, it should be spread out on a moist sponge to avoid desiccation and shrinkage. If a tourniquet has been used, it can be deflated at this point for the remainder of the procedure. Patch fixation. The periosteal patch is retrieved from the back table and placed over the defect, with the cambium layer facing the defect. The periosteum is gently unfolded and stretched with nontoothed forceps; an obviously oversized patch can be trimmed back carefully at this time, preserving a small rim of 1 to 2 mm. Suturing is performed with 6-0 Vicryl on a P-1 cutting needle immersed in mineral oil or glycerin for better handling. The sutures are placed through the periosteum and then the articular cartilage, exiting about 3 mm away from the defect edge, everting the periosteal edge slightly to provide a better seal against the defect wall. The knots are tied on the patch side to remain below the level of the adjacent cartilage. Interrupted sutures are initially placed on each side of the patch (3, 6, 9 and 12 o’clock), adjusting the tension of the patch after each suture and trimming the periosteum as needed to obtain a patch that is neither too loose as to sag into the defect, nor so tight that it would cut out of the sutures. Thereafter, additional sutures are placed in-between to circumferentially close the gaps. An opening wide enough to accept an angiocatheter is left in the most superior aspect of the defect to inject the chondrocytes. Water tightness of the suture line is first tested by slowly injecting saline into the covered defect with a tuberculin syringe and plastic 18-gauge angiocatheter. Continued


Authors’ Preferred Method—cont’d Figure 23I-7 A, A large chondral defect has been outlined on the weight-bearing femoral condyle. B, Periosteum is being harvested from the proximal tibia: fine, toothless pickups keep tension on the patch, which is freed from the bone with a sharp periosteal elevator. C, The periosteal patch has been sutured in place and the suture-line waterproofed with fibrin glue.

A

B

Any leakage should be addressed with additional sutures or fibrin glue as needed. Lastly, the saline is reaspirated to prepare the defect for implantation. Chondrocyte implantation. The cells are now resuspended and sterilely aspirated from the transport tubes with a tuberculin syringe through an 18-gauge or larger needle because smaller gauge needles can damage the cells. The needle is then removed and replaced with a flexible, plastic 18-gauge, 2-inch angiocatheter. The angiocatheter is introduced into the defect through the residual opening of the periosteal patch. As the angiocatheter is slowly withdrawn, cells are injected until the defect is filled with fluid. One or two additional sutures and fibrin glue are then used to close the injection site (see Fig. 23I-7C). Wound closure. We minimize the use of intra-articular drains to avoid damage to the periosteal patch. When drains are used, it should be without suction and with care to position the tubing away from the defect. The wound is closed in layers, and a soft dressing is applied to the knee. Prophylactic intravenous antibiotics are used for 24 hours after surgery.

C

Osteochondral Autograft Transplantation

Osteochondral autograft transplantation can be performed through either an arthroscopic or open approach (Fig. 23I-8A), based on the exact defect size and location and surgeon’s preference. Frequently, we assess the defect arthroscopically, followed by harvesting of the autograft from the trochlear ridge through a small, 1.5- to 2-cm parapatellar incision. We believe that a mini-open, rather than arthroscopic, approach allows better curvature matching of the donor to the recipient site. This is especially true for the donor site, which is typically difficult to access through an all-arthroscopic approach. Several proprietary systems are available, and the surgeon should follow the guidelines of the respective system used. We describe the general technique here, without reference to individual systems. Approach and defect preparation. The lesion is evaluated through routine knee arthroscopy. Needle localization with an 18-gauge spinal needle aids in the creation of accessory portals that allow perpendicular orientation of the

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A

C harvesting tube to the articular surface. Occasionally, a central, transpatellar tendon approach is required. In this case, the patellar tendon should be split in line with its fibers and repaired at the end of the procedure. An appropriately sized defect harvesting tube is selected, and dependent on the size of the lesion, one or more recipient holes are created, thus removing the chondral defect along with about 8 to 10 mm of subchondral bone. This is best performed under tourniquet to improve visualization. Graft harvest. Again, an accessory portal is used, or more frequently, we recommend a small, 1.5- to 2-cm incision after needle localization. Common donor locations include the intercondylar notch and medial and lateral trochlea. We prefer to harvest from the medial trochlea or close to the sulcus terminalis in the lateral femoral condyle because of lower patellofemoral contact stresses in that region.35 The corresponding, slightly oversized graft harvesting chisel is selected and placed perpendicular to the articular surface. With a mallet, it is advanced to a depth of about 8 to 10 mm; the harvester is then twisted or toggled and retrieved with the graft. This process is repeated until the required number of osteochondral plugs has been harvested. The donor site can be

B

Figure 23I-8 A, A trochlear defect from a nail gun injury has been exposed through an arthrotomy (the patient also required autologous chondrocyte implantation to the patella). B, The graft has been advanced slightly out of the harvesting chisel to allow trimming to the correct length. C, An osteochondral cylinder has been transferred from the lateral trochlea to the more centrally located defect. The harvest site has been back-filled with a synthetic plug.

left untreated, or filled with synthetic graft, such as the TruFit back-fill plug (OBI, San Antonio, Tex) or similar material. Graft placement. The depth of the recipient site is measured to ensure that the defect is about 1 mm deeper than the length of the graft. The graft is then advanced within the harvesting tube so that the end is just visible (see Fig. 23I-8B). The harvester is introduced into the joint and oriented perpendicularly to the articular surface, and the graft is slowly advanced into the recipient site. Subsequently, the harvester is removed, and the graft is fully seated and made flush by gentle pressure with an oversized tamp. It is preferable to slightly recess the graft rather than leaving it proud (see Fig. 23I-8C). Closure. The arthroscopic portals are closed with interrupted sutures. A mini-arthrotomy should be closed in layers, including the joint capsule and retinaculum. Osteochondral Allograft Transplantation

Similar to ACI, osteochondral allograft transplantation is performed through an arthrotomy sized to be consistent with the location and extent of the lesion. The patient Continued



A

B

C

D

E

F

Figure 23I-9 A, A large chondral defect of the weight-bearing femoral condyle is inspected through a limited, peripatellar approach. B, A guide pin has been introduced perpendicularly into the defect and is being overdrilled with an appropriately sized reamer. C, The prepared defect after reaming to a depth of about 6 to 8 mm. D, Selecting the appropriate harvest site on the fresh allograft hemicondyle. E, Allograft cylinder before trimming to the appropriate depth, which has been marked out for each quadrant. F, The transplant has been introduced into the recipient site. Press-fit fixation is usually sufficient but can be augmented with resorbable pins.

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Authors’ Preferred Method—cont’d is positioned supine on a standard operating room table. A leg positioning device can be helpful for very posterior lesions that require hyperflexion of the knee. The most commonly used technique is the press-fit plug or mega-OATS technique; several proprietary systems have been developed to facilitate graft sizing and preparation. Approach. Most commonly, an anterior midline incision is made from the proximal pole of the patella to the tibial tubercle, but medial or lateral paramedian incisions can be used as well. The incision is carried down to the capsule; then full-thickness skin flaps are raised to create a mobile window. A medial or lateral peripatellar capsulotomy is performed from the superior pole of the patellar to the tibial tubercle. Recently, more limited incisions such as the subvastus or midvastus approaches have gained popularity, and the authors feel that these approaches allow for accelerated postoperative quadriceps rehabilitation. The patella is retracted with either a Z-retractor or bent Hohmann retractor placed into the notch. We have found it helpful to release the fat pad, and dissect the anterior meniscal horn from the capsule to allow for better exposure, especially with small incisions. Defect preparation. Once the lesion is exposed, the abnormal cartilage is identified (Fig. 23I-9A). It is of utmost importance to reconstruct the normal geometry of the articular surface with the donor graft. A cylindrical sizing guide is placed over the defect to determine the

POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Rehabilitation Tables 23I-4 to 23I-6 describe our postoperative rehabilitation protocols after microfracture and osteochondral autograft and allograft transplantation. The rehab protocol after ACI (Table 23I-7) is divided into three phases, based on the slow maturation of the repair tissue, which at the same time has to be protected from overloading and stimulated to encourage tissue maturation. The three phases of the healing process are the proliferative (fill) phase, the transitional (integration) phase, and the remodeling (hardening) phase, each of which can accommodate increasing amounts of load. During the initial proliferative phase, protection of the graft is paramount, and the patient is limited to touchdown weight-bearing for 6 weeks. During this phase, patients also use a CPM machine for 6 to 8 hours per day to reduce the likelihood of adhesions and aid in maturation of the transplant. This initial period is followed by the transitional stage in which patients advance to full weight-bearing over the course of several weeks. Additional exercises are prescribed based on the specific

ptimal plug diameter, and a guide pin is drilled through o the sizing guide to a depth of 2 to 3 cm. A 6- to 8-mm deep recipient socket is created with a cannulated reamer (see Fig. 23I-9B and C), and the exact depth of the cylindrical defect is measured in all four quadrants. Multiple drill holes are created in the floor of the defect to improve blood supply. Graft preparation. The appropriate donor site is then identified on the allograft condyle (see Fig. 23I-9D), which is secured in the workstation, and a mark is made at the 12-o’clock position to aid in orientation. A bushing of appropriate diameter is selected and set to the angle required to match the contour of the recipient site. The donor harvester is passed through the proximal graft housing and drilled through the entire depth of the donor condyle. After extracting the graft from the donor harvester, the four quadrants of the graft are marked (see Fig. 23I-9E) and trimmed down to match the depths previously recorded from the recipient site. It is helpful to slightly bevel the edges of the graft to facilitate insertion and avoid excessive impaction pressures. Graft insertion. The recipient site is now prepared for insertion with a calibrated dilator, and the graft is press-fit with manual pressure and gentle tapping (see Fig. 23I-9F). It is preferable to recess the graft slightly rather than leaving it proud. Absorbable pins may be used for supplemental fixation.

l ocation and type of the defect. During the final remodeling phase that begins about 3 months after transplantation, the joint is increasingly loaded with strengthening and impact-loading activities. A full return to high-impact and pivoting activities should be delayed for at least 12 months until near-complete graft maturation has been achieved. Complete maturation is not expected until 12 to 24 months.

Outcomes Measures Commonly used outcomes measures include functional scores, such as the Lysholm score, Tegner activity, and International Knee documentation Committee rating systems, as well as health surveys, including the SF-12 or SF-36. Other measures include subjective parameters such as patient satisfaction, and objective ones such as range of motion, swelling, quadriceps atrophy, radiographic joint space narrowing, and others.

Complications General complications inherent to knee surgery are infection and stiffness, which are more common with open than arthroscopic procedures. Nerve damage after knee surgery usually takes the form of injury to the infrapatellar branch of the saphenous nerve, resulting in a numb area over the


TABLE 23I-4 Rehabilitation Protocol for Microfractures Phase

Weight-Bearing

Brace

Range of Motion

Therapeutic Exercise

Microfracture of the Femoral Condyle

I (0-8 wk)

Touchdown weight-bearing (20-30%) for the first 6-8 weeks.

None

II (8-12 wk)

Gradual return to full weight-bearing Full with a normalized gait pattern.

None

CPM: use is for 6-8 hours per day. Set Passive stretching/exercise for the at a rate of 1 cycle/minute, advancing first 6-8 weeks, quad/hamstring 10 degrees daily. Begin at a level of isometrics. flexion that is comfortable for the patient. Advance to full flexion as tolerated. Gain full and pain free. Progressive active strengthening

None

Full and pain free.

III (6-9 mo)

Return to full activities, including cutting, turning, and jumping.

Microfracture of the Patellofemoral Articulation

I (0-8 wk)

Weight-bearing as tolerated

II (8-12 wk)

Full

Locked 0-40 degrees CPM: use is for 6-8 hr per day. Set at of flexion for a rate of 1 cycle/min, ranging from weight-bearing 0-40 degrees None Gain full and pain free

III (≥12 wk)

Full

None

Full and pain free

Passive stretching and exercise for the first 6-8 wk; quad and hamstring isometrics Begin closed chain activities, emphasizing a patellofemoral program Return to full activities, including cutting, turning, and jumping

CPM, continuous passive motion.

TABLE 23I-5 Rehabilitation Protocol for Osteochondral Autograft Transplantation Phase

Weight-Bearing

Brace

Range of Motion

Therapeutic Exercise

I (0-6 wk)

Non–weight-bearing

0-6 wk: CPM is used for 6-8 hr/day. Begin at 0-40 degrees, increasing 5-10 degrees/day per patient comfort. Patient should gain 100 degrees by week 6.

Passive and active-assisted ROM to tolerance; patella and tibiofibular joint mobilizers (grades I and II); stationary bike for ROM; quad, hamstring, adduction, and gluteal sets; hamstring stretches; hip strengthening; SLRs; ankle pumps

II (6-8 wk)

Progress to full weight-bearing

0-1 wk: Locked in full extension (removed for CPM and exercises) 2-4 wk: Gradually open brace in 20-degree increments as quad control is gained; discontinue use of brace when quads can control SLR without an extension lag None

Gradually increase flexion. Patient should have 130 degrees of flexion.

III (8-12 wk)

Full with a normalized gait pattern

Gait training; scar and patellar mobilizers; quad and hamstring strengthening; begin closed chain activites (wall sits, shuttle, mini squats, toe raises); begin unilateral stance activities Advance phase II activities

None

Full and pain free

CPM, continuous passive motion; ROM, range of motion; SLR, straight leg raises.

TABLE 23I-6 Rehabilitation Protocol for Osteochondral Allograft Transplantation Phase

Weight-Bearing

Brace

I (0-6 wk)

Non–weight-bearing

II (6-8 wk)

Partial weight-bearing (25%)

0-1 wk: Locked in full extension 0-6 wk: CPM is used for (removed for CPM and exercises) 6-8 hr per day. Begin at 2-4 wk: Gradually open brace in 0-40 degrees, increasing 20-degree increments as quad 5-10 degrees/day per control is gained; discontinue use patient comfort. Patient of brace when quads can control should gain 100 degrees SLR without an extension lag by week 6. None Gradually increase flexion. Patient should have 130 degrees of flexion.

III (8-12 wk) Gradually return to full weight-bearing IV (12 wk to 6 mo)

None

Full with a normalized None gait pattern

CPM, continuous passive motion; ROM, range of motion; SLR, straight leg raise.

Range of Motion

Progress to full and pain free. Full and pain free.

Therapeutic Exercise Passive and active-assisted ROM to tolerance; patella and tibiofibular joint mobilizers (grades I and II); quad, hamstring, and gluteal sets; hamstring stretches; hip strengthening; SLRs Scar and patellar mobilizers; quad and hamstring strengthening; stationary bike for ROM; continue to advance lower extremity strengthening activites Gait training; begin closed chain activites (wall sits, shuttle, mini squats, toe raises); begin unilateral stance activities Advance phase III activities

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TABLE 23I-7 Rehabilitation Protocol for Implantations Phase

Weight- Bearing

Brace

Range of Motion

Therapeutic Exercise*

0-2 wk: Quad sets, SLR, hamstring isometrics—complete exercises in brace if quad control is inadequate. 2-6 wk: Begin progressive closed chain exercises. †6-10 wk: Progress bilateral closed chain strengthening, begin open chain knee strengthening. 10-12 wk: Progress closed chain exercises using resistance less than patient’s body weight, progress to unilateral closed chain exercises, begin balance activities. Advance bilateral and unilateral closed chain exercises with emphasis on concentric and eccentric control. Continue with biking, Stairmaster, and treadmill; progress balance activities. Advance strength training, initiate light plyometrics and jogging. Start 2-min walk/2-min jog. Emphasize sportspecific training. Continue strength training. Emphasize single-leg loading. Begin a progressive running and agility program. Highimpact activities (e.g., basketball, tennis) may begin at 16 mo if pain free.

Femoral Condyle Autologous Chondrocyte Implantation

I (0-12 wk)

0-2 wk: Non–weightbearing 2-4 wk: Partial weightbearing (30-40 lb) 4-6 wk: Progress to use of one crutch 6-12 wk: Progress to full weight-bearing

0-2 wk: Locked in full extension (removed for CPM and exercise) 2-4 wk: Gradually open brace 20 degrees at a time as quad control is gained. Discontinue use of brace when quads can control SLR without an extension lag.

0-4 wk: CPM: use in 2-hr increments for 6-8 hr/day at 1 cycle/min. Begin at 0-30 degrees, increasing 5-10 degrees/day per patient comfort. Patient should gain at least 90 degrees by week 4 and 120 to 130 degrees by week 6.

II (3-6 mo)


None

Full active range of motion

III (6- 9 mo)


None

Full and pain free

IV (9-18 mo)


None

Full and pain free

Patellofemoral Autologous Chondrocyte Implantation‡

I (0-12 wk)

0-2 wk: Non– weight-bearing 2-4 wk: partial weightbearing (30-40 lb) 4-8 wk: Continue with partial weight-bearing. Progress to use of one crutch. 8-12 wk: Progress to full weight-bearing and discard crutches.

0-2 wk: Locked in full extension, removed only for CPM and exercise 2-4 wk: Locked in full extension with weightbearing 4-6 wk: Begin to open 20 to 30 degrees with ambulation. Discontinue use after 6 weeks.

0-4 wk: CPM: use in 2-hr increments for 6-8 hr/day. Begin at 0-30 degrees—1 cycle/min; after week 3, increase flexion by 5-10 degrees/day. 6-8 wk: Gain 0-90 degrees 8 wk: Gain 0-120 degrees

II (3-6 mo)


None

Full range of motion

III (6-9 mo)


None

Full and pain free

IV (9-18 mo)


None

Full and pain free

1-4 wk: Quad sets, SLR, hamstring isometrics—complete exercises in brace if quad control is inadequate. 4-10 wk: Begin isometric closed chain exercises. At 6-10 wk, may begin weight-shifting activities with involved leg extended if full weight-bearing. At 8 wk, begin balance activities and stationary bike with light resistance. 10-12 wk: Hamstring strengthening, Thera-Band 0-30 degrees resistance, light open chain knee isometrics Begin treadmill walking at a slow to moderate pace, progress balance and proprioceptive activities. Initiate sport cord lateral drills. Advance closed chain strengthening. Initiate unilateral closed chain exercises. Progress to fast walking and backward walking on treadmill (initiate incline at 8-10 mo), initiate light plyometric activity. Continue strength training—emphasize single-leg loading, begin a progressive running and agility program. High-impact activities may begin at 16 mo if pain-free.

*If pain or swelling occurs with any activities, they must be modified to decrease symptoms. †Respect chondrocyte graft site with closed chain activities: If anterior, avoid loading in full extension, if posterior, avoid loading in full flexion > 45 degrees. ‡Most trochlear and patellar defect repairs are performed in combination with a distal realignment. Weight-bearing is restricted for the first 4 to 6 weeks to protect the bony portion of the distal realignment during healing. May consider patellofemoral taping or stabilizing brace if improper patella tracking stresses implantation. Postoperative stiffness in flexion following trochlear or patellar implantation is not uncommon, and patients are encouraged to achieve 90 degrees of flexion at least 3 times a day out of brace after their first postoperative visit (days 7-10). CPM, continuous passive motion; SLR, straight leg raise.


lateral aspect of the knee. Rarely, nerve damage can result from direct injury to the peroneal nerve, or indirect, tourniquet-related injury to the sciatic and tibial nerves. Specific risks associated with individual procedures are graft detachment or delamination after ACI, and subchondral collapse or nonunion after osteochondral allograft transplantation.

Criteria for Return to Play Most cartilage repair procedures require extensive post operative rehabilitation and delayed return to athletic activities. As a general rule, the operated extremity should be relatively pain free, and without residual stiffness, swelling or muscle atrophy before a return to play can be considered. More important than these general guidelines, however, cartilage repair requires a protracted healing period that frequently extends long after the previously mentioned criteria have been met. This is not apparent to outside observation by the patients, who therefore will have to be frequently reminded of their restrictions. Return to play is individualized based on the specific procedure and sport; participation in high-impact and pivoting activities such as basketball and soccer is delayed for 9 to 12 months, whereas impact-free activities such as stationary biking can be considered as early as 8 to 12 weeks after surgery.

C

r i t i c a l

P

o i n t s

l Careful preoperative assessment of number, size, and location of cartilage lesions is critical to successfully plan a cartilage repair procedure. A low threshold for a diagnostic arthroscopy should be maintained if imaging cannot provide a conclusive answer. l Cartilage defects are frequently caused by, or made more symptomatic because of, associated pathology, such as malalignment or meniscal deficiency. This pathology has to be correctly identified and addressed in a staged or concurrent manner. l Bone length radiographs are a necessity to evaluate alignment and to plan for concurrent osteotomy if needed. l A frank preoperative dialogue with the patient and family is needed to discuss the complex nature of the procedure, the long rehabilitation required, and the expected results. Patients often present with unrealistic expectations leading to less than optimal satisfaction rates. l Most cartilage repair procedures are time sensitive; fresh osteochondral allografts and autologous cultured chondrocytes have a limited shelf life of only a few days, and cannot be frozen. A discussion with the operating room staff and receiving is necessary to ensure correct delivery and handling of the grafts. The patient needs to be aware that the surgical date cannot be moved once the process has started.

Special Populations Historically, cartilage repair procedures have been limited to the younger patient. However, our aging population wants to remain active longer and is less willing to accept the limitations of joint replacements. Therefore, chronologic age older than 50 years as a contraindication to cartilage repair is being revisited. Adolescents with open growth plates require special consideration. Osteochondral allograft transplantation has to be considered carefully in order not to injure the physeal plate. Also, the osteotomies performed concurrently to cartilage repair procedures, especially in the patellofemoral joint, are often contraindicated in the growing child. Inflammatory arthritis remains a contraindication to cartilage repair, except in the rare case in which it is burnt out and the lesions are focal and contained. Congenital malformation, such as multiple epiphyseal dysplasia, can occasionally be successfully addressed with osteochondral allograft transplantation.

S U G G E S T E D

R E A D I N G S

Alford JW, Cole BJ: Cartilage restoration, part 1: Basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med 33(2):295-306, 2005. Alford JW, Cole BJ: Cartilage restoration, part 2: Techniques, outcomes, and future directions. Am J Sports Med 33(3):443-460, 2005. Cole BJ, Schumacher HR: Injectable corticosteroids in modern practice. J Am Acad Orthop Surg 13(1):37-46, 2005. Farr J, Lewis P, Cole B: Articular cartilage: Patient evaluation and surgical decision making. J Knee Surg 17(4):219-228, 2004. Gomoll AH, Minas T, Farr J, Cole BJ: Treatment of chondral defects in the patellofemoral joint. J Knee Surg 19(4):285-295, 2006. Hangody L, Rathonyi GK, Duska Z, et al: Autologous osteochondral mosaicplasty: Surgical technique. J Bone Joint Surg Am 186(Suppl):65-72, 2004. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation. Clin Sports Med 18(1):13-44, 1999. Steadman JR, Briggs KK, Rodrigo JJ, et al: Outcomes of microfracture for traumatic chondral defects of the knee: Average 11-year follow-up. Arthroscopy 19(5): 477-484, 2003.


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J

Knee Replacement in Aging Athletes Mark J. Billante and David R. Diduch

A painful arthritic knee in a young patient can be a challenge for today’s orthopaedist. Nonoperative treatment, such as anti-inflammatory medication, physical therapy, injections, lifestyle modification, and bracing, often provides only limited and temporary relief. Operative options include arthroscopic débridement, proximal tibial osteotomy, arthrodesis, and unicompartmental or total knee replacement. Most patients are not willing to accept the functional limitations of a knee arthrodesis. Proximal tibial osteotomies have good short-term results, but do not predictably relieve pain in the long term.1-4 Unicompartmental knee replacement is an option for patients with single compartment osteoarthritis and angulation of the knee, but frequently degenerative changes are not limited to one compartment. Knee replacement is an excellent option for treatment of both osteoarthritis and rheumatoid arthritis in elderly patients. The literature clearly demonstrates both predictable pain relief and improved function.5-16 People in the United States are living longer than ever. As the average age of our population increases, so does the prevalence of arthritic joints. With changing demographics, our outlook regarding total knee replacement is also changing. The senior citizens of today are no longer content to be less active in their “golden years”; they want to maintain their active lifestyle after joint replacement, placing additional stresses on prosthesis and surgeon alike. The excellent results seen with total knee replacement in older patients have helped expand the indications to include arthritis in younger patients. Total knee replacement has been shown to be successful in treating younger patients as well.7,17-19 Yet, concerns about the durability of prostheses with regard to loosening and wear debris generated by more active patients still exists. Currently, many of the recommendations regarding recreational and sporting activity after knee replacement are based on personal and consensual opinion. This chapter reviews the current literature regarding sports participation after knee replacement while highlighting clinical evaluation, surgical techniques, and future directions for treatment in this difficult patient population.

CURRENT LITERATURE REVIEW REGARDING SPORTS AFTER KNEE ARTHROPLASTY Few studies specifically address recommendations regarding athletic activity and sports participation after knee arthroplasty. Those that do are frequently based on surgeon

advice and experience rather than concrete data. Prospective randomized studies are not available and would likely be impractical for this patient population. Few physicians could tell their patients they have been randomized into the group that jogs 3 times a week, or conversely tell a tennis player he or she has been randomized to the sedentary group and cannot resume tennis after surgery. Physicians therefore are left somewhere between good advice and hard evidence. The following section reviews the current pertinent literature and provides recommendations based on the best available information to date. Physicians and patients must balance the beneficial and deleterious effects of activity after knee arthroplasty. Inactivity can lead to reduced aerobic fitness, loss of coordination and postural reflexes, loss of muscle mass, and osteoporosis, whereas physical fitness and exercise reduce mortality, anxiety, and depression, and improve muscle coordination, strength, and bone density.20 Ries and colleagues found benefits in cardiovascular fitness after hip and knee arthroplasty. Significant improvements were seen in exercise duration, maximal workload, and peak oxygen consumption after 2 years. They concluded that joint replacements enable patients to increase their activities and improve their physical fitness.21,22 Conversely, other studies have shown increased activity to be associated with increased wear of the prosthesis. Schmalzried and coworkers reported that up to 500,000 submicron particles are released with each step after total knee replacement. The particles can initiate a cascade of processes that eventually lead to periprosthetic osteolysis and loosening.23,24 Schmalzried also showed that wear is a function of use. He found that wear was related more to activity than age of the patient. Lavernia and colleagues found a positive correlation between activity level, length of implantation, and wear rates at an average of 74 months.25 Implant loosening is another important consideration after knee arthroplasty. Athletic activity may increase the stress on implant fixation in compression, tension, rotation, and shear. Mallon and Callaghan found that radiolucent lines occurred in 79% of cemented total knee arthroplasties (TKAs), 45% of uncemented TKAs, and 54% of TKAs when the groups were combined in patients who played golf a minimum of 3 times per week.26,27 They also found that the occurrence of radiolucent lines and the incidence of pain during and after play were higher for patients with TKA than total hip arthroplasty. However, Diduch and coworkers reported on TKA in young, active patients and found that 9% had radiolucent lines that were present immediately postoperatively and did not progress over the course of the study.28 None of the patients in the study underwent revision surgery due


to femoral or tibial component loosening. To date, there has not been a definitive study demonstrating a causative relationship between activity and implant loosening. Healy and associates surveyed 58 members of the Knee Society regarding their recommendations for athletics and sports participation after knee replacement.29 They recommended low-impact aerobics, stationary bicycling, bowling, croquet, ballroom dancing, jazz dancing, square dancing, golf, horseshoes, shooting, shuffleboard, swimming, and walking. Road bicycling, canoeing, hiking, rowing, cross-country skiing, stationary skiing, speed walking, tennis, and weight machines were recommended if the patient previously participated in these activities. In general, high-impact activities were not recommended. These activities included high-impact aerobics, baseball, softball, basketball, football, gymnastics, handball, hockey, jogging, lacrosse, racquetball, squash, rock climbing, soccer, singles tennis, and volleyball. No conclusions were made regarding fencing, rollerblading, downhill skiing, and weightlifting. Healy also emphasized delaying return to recreational or athletic activity until quadriceps and hamstrings were sufficiently rehabilitated. Healy felt surgeons should educate patients regarding risks associated with higher levels of activity but ultimately let the patient decide what activities to participate in postoperatively. Kuster used six criteria to provide more “scientifically” based guidelines regarding activity after total joint replacement.30 These criteria included wear of total joint replacements, joint load and moments during sports activities, activity and fixation of the prosthesis, recreation versus exercise, and the difference between total hip arthroplasty and TKA. Ultimately, he recommended that patients should remain physically active after joint replacement for general health, prevention of cardiac problems, improvement of bone quality, and enhanced prosthesis fixation. Fitness should be maintained by low-impact aerobic activities such as swimming, cycling, walking, or aqua aerobics. Patients who wished to continue participation in sports with higher joint loads such as skiing, tennis, and hiking should do so only on a recreational basis.31 Kuster noted that knee designs show much smaller stress levels near extension than in flexion for the same load.32 Activities such as hiking or jogging have high joint loads between 40 and 60 degrees of knee flexion, when many knee designs are not conforming.33 This may lead to very high polyethylene inlay stress. Hence, regular jogging or hiking with intense downhill walking produces a large overloaded area with the danger of delamination and polyethylene destruction for many modern knee designs. Mont and associates compared clinical and radiographic outcomes for 50 patients who engaged in high-impact activities such as golf, skiing, tennis, cycling, or jogging at a minimum of 4 years after TKA, to an age-matched cohort of 50 sedentary patients.34 At a mean follow-up of 7 years, there were two revisions and one clinical failure in each group, with no progressive radiolucencies reported. High-impact activities conferred no difference in outcomes in the study. The authors also evaluated 30 total knee replacements in patients younger than 50 years in a separate study. At a mean of 7 years’ follow-up, they reported good or excellent clinical and radiographic outcomes in 29 of 30 patients. Mont and associates also studied patients who played tennis after

TKA. Forty-six knee replacements in 33 patients were reviewed. Two of 46 (4%) knees required revision surgery due to polyethylene wear at 8 and 11 years.35 Diduch and colleagues investigated 103 TKAs in patients younger than 55 years.28 They found that patients had an increase in their Tegner scores from 1.3 preoperatively to 3.5 postoperatively. This improvement reflects a change from sedentary desk-type work with limited walking on even ground to an occupation that involves light labor, such as nursing or truck driving, and some recreational activities, such as cycling, cross-country skiing, or swimming. The Tegner score improved postoperatively in all but two patients who had no change in the score. Thus, no patient had deterioration of functional status after knee replacement. Additionally, 19 patients (24%) had a score of at least 5 points, indicating regular participation in activities such as tennis, downhill skiing, cycling, or strenuous farm or construction work. Despite the patients’ active lifestyles, loosening that necessitated revision was not a problem in their series. The survivorship estimate, with revision of the femoral or tibial component as the end point, was 94% at 18 years. The only aseptic revision involved a 22-year-old patient, who participated in football, baseball, basketball, and softball and was employed as a firefighter. The revision, 7 years postoperatively, revealed wear of a relatively thin, carbon-fiber–reinforced polyethylene spacer without loosening of the tibial tray. Accelerated wear of carbonfiber–reinforced polyethylene has been well documented, and this material is no longer recommended for use in knee replacements.36,37 The literature is particularly sparse regarding sports after unicompartmental knee replacement, with only one recent article directly addressing the issue. Fisher and colleagues reported on 42 patients who had a unicompartmental knee replacement using the Oxford prosthesis at an average follow-up of 18 months.38 They reported that 93% of patients successfully returned to their regular sporting activities following surgery. These sports included swimming, golf, dancing, cycling, hiking, jogging, and squash.

RECOMMENDATIONS REGARDING SPORTS AFTER KNEE ARTHROPLASTY Remaining physically active after joint replacement is beneficial for maintenance of general health, prevention of cardiac problems, and improvement of bone quality. Ideally, regular exercise should be limited to low-impact activities such as swimming, cycling, water aerobics, or walking. Patients who want to continue sports such as skiing, hiking, and tennis can do so on a recreational basis. Patients should also be made aware of joint-load–reducing measures such as using ski poles during hiking, skiing on flatter slopes, and avoiding icy conditions. Diagonal instead of skating techniques can be used while cross-country skiing. Cycling with low loads, higher frequencies, and increased seat height is beneficial. It may be unwise to take up new technically demanding sports after knee replacement such as skiing, hiking, mountain biking, horse riding, or tennis. The joint loads and risk for injury are higher for these activities in unskilled individuals.30 However, if patients

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Box 23J-1 Recommended Sporting Activities after Knee Arthroplasty Recommended/Allowed Low-impact aerobics Stationary bicycling Golf Walking Speed walking Swimming Elliptical machines Ski machines Rowing Weight machines Bowling Dancing Horseback riding Hiking Cross-country skiing Allowed with Previous Experience Road bicycling Singles, doubles tennis Racquetball Squash Downhill skiing Ice skating Not Recommended Football Basketball Baseball Hockey Soccer Lacrosse Rock climbing Volleyball Gymnastics Jogging Handball

participated in these sports before surgery, it is safe to resume them postoperatively (Box 23J-1). It is important to reiterate that there is a lack of a definitive consensus regarding sporting activity after knee arthroplasty in the literature. Healy’s article is the closest paper to a consensus, but it is based on survey results of Knee Society members rather than definitive data.29 We concur with the recommendations seen in most papers that encourage low-impact activities for maintenance of general health and fitness while avoiding high-impact activities that would place dangerous levels of stress on the prosthesis. However, we permit lateral movement activities such as skiing or racquet sports because there has not been a definitive study proving these sports to be detrimental in the survivorship of TKA. There does appear to be consensus in recommending against jogging, running, and jumping sports. As physicians, we can facilitate discussion of appropriate postoperative activities and encourage patients to use common sense when choosing what sports to participate in after surgery.

CLINICAL EVALUATION History A complete history and physical examination is necessary in order to avoid missing other potential sources of knee pain. Inconsistent findings at the knee should alert the examiner to evaluate the patient for alternative diagnoses such as referred pain from the hip or back. Most patients report knee pain exacerbated by activity, relieved by rest, and associated with varying degrees of swelling. The swelling may be intermittent or constant in nature. Pain localized to one compartment is common early in the disease process, as opposed to diffuse knee pain that suggests multiple compartment involvement and more advanced arthritis. Rest pain is also more common in advanced osteoarthritis or osteonecrosis. Pain with stair climbing, prolonged sitting, or squatting suggests patellofemoral involvement. Mechanical symptoms such as intermittent locking or catching may be related to articular surface irregularity, loose bodies, or meniscal pathology, which is common secondary to osteoarthritis. Pain and instability may both be present when arthritis and ligamentous insufficiency coexist. It is important to differentiate instability due to pain, effusion, and quadriceps inhibition from true ligamentous insufficiency, which may or may not be associated with pain. Responses to previous treatments such as nonsteroidal anti-inflammatory drugs (NSAIDs), therapy, injections, bracing, osteotomy, or arthroscopic débridement are helpful to direct further management. A frank discussion regarding patient expectations should also occur. Older patients may be content with limited activity, as long as they are pain free. In contrast, younger or more active patients may find the same activity levels to be severely disabling. The Internet has enabled patients to become educated about their diagnosis and treatment options. Time spent with patients answering questions, discussing treatment options in detail, and differentiating good and bad information can facilitate realistic expectations for surgeon and patient alike. Having pamphlets or websites for patients to review at their own pace is also helpful.

Physical Examination A complete examination of the knee is essential. Special attention should be paid to previous incisions on the knee, joint line tenderness, patellar tenderness and crepitus, varus and valgus deformities, and ligamentous stability. In addition, body habitus, range of motion, flexion contractures, and extension lags should be noted. The back and ipsilateral hip and ankle should be examined for abnormalities, including decreased range of motion. Distal pulses, sensation, and strength should also be evaluated.

Diagnostic Imaging A standard radiography series includes a standing posteroanterior (PA) view of both knees in 45 degrees of flexion, a lateral view, and a sunrise view of the affected knee. The


that will not worsen their pain is helpful. Exercise that includes high-impact activity such as jumping and running should be avoided. Running on treadmills, stair-climbing machines, and leg extension exercises put added pressure on the patellofemoral joint and can exacerbate symptoms. Low-impact activities such as swimming and bicycling are excellent recommendations. Elliptical machines, stationary bikes, and leg press exercises are good for quadriceps strengthening without excessive loading of the patellofemoral joint. Limiting stair-climbing and squatting activities can also reduce pain in patients with patellofemoral arthritis. If possible, patients also should be encouraged to modify their work responsibilities to those that are physically less demanding. Adaptations at home such as raising the level of a chair or toilet seat can be beneficial for those with chronic symptomatic knee arthritis.

Therapy A

B

Figure 23J-1 A, Medial compartment narrowing demonstrated on a weight-bearing anteroposterior radiograph. B, A posteroanterior view with 45 degrees of flexion weightbearing in the same patient demonstrates advanced arthritic changes.

45-degree PA view can demonstrate subtle loss of joint space, especially in the lateral compartment, which is indicative of early chondrosis. Frequently, the 30- to 60-degree flexion zone has the earliest loss of cartilage and is easily overlooked on full extension radiographs (Fig. 23J-1). Because the 45-degree PA view provides an excellent view of the notch, changes that suggest chronic anterior cruciate ligament (ACL) deficiency can be seen, such as hypertrophy of the tibial spines and narrowing of the notch itself. Changes common after meniscectomy (joint space narrowing, flattening of the femoral condyles, and osteophyte formation along the periphery of the tibia) are more apparent with this view. If joint space narrowing is minimal, magnetic resonance imaging (MRI) of the knee can help identify meniscal pathology or other intra-articular abnormalities. MRI can also identify more rare pathologic processes such as avascular necrosis, spontaneous osteonecrosis of the knee, and neoplastic bone lesions. Degenerative meniscal tears often are present concurrently with osteoarthritis. The surgeon must keep in mind that the arthritis is the primary process involved and treat the patient accordingly. In most cases, if joint space narrowing is present on the 45-degree PA view, MRI is unnecessary.

TREATMENT OPTIONS Lifestyle Modifications Obesity is a known risk factor for osteoarthritis, and losing weight decreases the risk for developing and exacerbating osteoarthritis.39 Educating patients about exercise options

Range of motion exercises reduce or prevent contractures. A flexion contracture results in increased patellofemoral contact stresses during standing and walking, which can exacerbate arthritic symptoms. Periarticular muscle strengthening helps stabilize the knee and can reduce knee symptoms. Cross-training and flexibility are important components of a complete rehabilitation program. Modalities such as heat, ultrasound, hydrotherapy, and cryotherapy are thought to work by reflex-mediated pathways involving free nerve endings, vasodilation, and other mechanisms. Duration and frequency of these modalities should be adjusted to optimize results and minimize symptoms.

Bracing and Support Devices Even though knee sleeves do not alter joint reaction forces or alignment, they can provide a sense of stability through enhanced proprioception. Patients with unicompartmental arthritis can be fitted with an “unloader” brace. The device provides a three-point bending force, with one force applied at the center of the knee and two opposing forces applied proximal and distal to the knee joint. This reduces joint reactive forces in the affected compartment. Prospective studies with valgus bracing for medial compartment arthritis reported a 50% decrease in the number of patients complaining of pain with activities of daily living after brace wear for an average of 7 hours a day, 5 days a week.40 A recent study demonstrated that “off the shelf” and custom braces were both beneficial with regard to pain relief and stiffness in patients with medial compartment arthritis; however, additional relief was gained with custom braces.41 Bracing also has limitations. Cost ($800 to $1000) and the cumbersome nature of the brace may limit usefulness of this treatment option. The best candidate for brace treatment has unicompartmental arthritis with at least a partially correctable, mild deformity and minimal patellofemoral symptoms. Using a cane in the contralateral hand is an effective way to reduce symptoms by relieving force on the affected knee. Canes should reach the top of the greater trochanter of a patient wearing shoes. Unfortunately, patients are often reluctant to use supportive devices in the long term owing to perceptions of lost independence.

Knee 1791

Patients often view pain relief as the most important goal of treatment. For this reason, acetaminophen is an accepted first-line analgesic agent for treatment of osteoarthritis despite lacking anti-inflammatory action. Furthermore, its favorable side-effect profile makes it an option for patients unable to tolerate traditional NSAIDs because of gastric toxicity. The recommended dosing is 650 mg every 4 to 6 hours as needed, to a maximal dosage of 4000 mg per day. A dose of 1000 mg 3 to 4 times daily is usually sufficient. Use within recommended dose levels is rarely associated with renal toxicity or hepatotoxicity, but routine laboratory work should be done for patients with long-term use.42

lacebo-controlled trials suggest that glucosamine is effip cacious in managing osteoarthritis without toxicity or side effects.44 Chondroitin sulfate is a glycosaminoglycan found in articular cartilage that is important for binding collagen fibrils. It has protective effects due to competitive inhibition of the degradative enzymes that lead to cartilage breakdown. Chondroitin sulfate also inhibits thrombus formation, which can occur in periarticular tissues and limit subchondral and synovial blood flow. About 70% of the oral dose is absorbed in the gut. Clinical studies showed effective pain relief and increased function without toxicity or side effects.45 Glucosamine and chondroitin sulfate have synergistic actions when taken together. Concurrent use appears to result in a net increase in the amount of normal cartilage matrix, potentially slowing progression of osteoarthritis.46

Nonsteroidal Anti-inflammatory Medications

Corticosteroid Injections

NSAIDs have been the preferred oral medication for the treatment of the swollen and painful arthritic knee because of their analgesic and anti-inflammatory actions. There are multiple preparations on the market without definitive studies demonstrating superior efficacy of one preparation over another. Generally, they act by reversibly inhibiting the cyclooxygenase (COX) side of arachidonic acid metabolism, thereby blocking production of proinflammatory agents, such as prostaglandins and leukotrienes. Unfortunately, the beneficial effects of prostaglandins are also inhibited, such as the protective effects on the gastric mucosal lining, renal blood flow, and sodium balance. Their most common side effect is dyspepsia. Other potential side effects include gastrointestinal ulcers, hepatotoxicity, renal toxicity, and cardiac failure. These effects are dose related and more severe in older patients with prolonged elimination. Contraindications to NSAIDs include a history of gastrointestinal disease, hepatic disease, renal disease, or concurrent anticoagulation therapy. Patients on prolonged NSAID therapy should be monitored closely for side effects by the orthopaedist or primary care physician. Recent scrutiny of selective COX-2 inhibitors has brought their role in treatment of arthritis into question. These drugs were developed to treat pain and inflammation while reducing the risk for serious gastrointestinal side effects seen with other nonselective NSAIDs. Several questions remain about the safety advantage of COX-2 inhibitors including whether they actually lower the risk for serious gastrointestinal events and whether their potential gastrointestinal advantage is negated by an increased risk for thromboembolic complications. Clinical trials are currently under way to help answer these questions. Until the results of these trials are known, COX-2 inhibitors should be used with caution, especially in patients with established or increased risk for cardiovascular disease.

Corticosteroid injections are helpful in patients who have failed first-line anti-inflammatory therapy or who have contraindications to use of acetaminophen or NSAIDs. An intra-articular injection is a potent anti-inflammatory agent with minimal risk for systemic effects or complications, although diabetic patients should be counseled that their blood glucose level will likely rise after receiving the injection. Crystalline corticosteroids can induce a corticosteroid-crystal synovitis or poststeroid flare, but this is rare and usually self-limited. Injections provide variable relief, lasting from a few days to 6 months or longer, particularly in the absence of mechanical symptoms. Steroid injections should be limited to a maximum of three per year because they can cause articular cartilage softening and erosion. Complications include skin pigmentation changes and subcutaneous fat atrophy when delivered in the subcutaneous space. Contraindications include suspected septic joint and recent fracture or trauma.

Medical Management and Injections Acetaminophen

Glucosamine and Chondroitin Sulfate Glucosamine provides the building blocks for the chondral matrix production normally produced by chondrocytes from glucose metabolism. When taken orally as a salt, 87% of the dose is absorbed in the gut and primarily processed through renal excretion, with lesser amounts processed by the liver.43 The results of randomized, double-blinded,

Viscosupplementation Injectable hyaluronic acid, or “viscosupplementation,” is available as a series of three to five weekly injections for treatment of symptomatic osteoarthritis. The injections supplement the reduced concentrations of hyaluronic acid found in the joints of patients with osteoarthritis. Viscosupplementation provides improved “elastoviscosity,” enabling the synovial fluid to be more effective in absorbing joint loads and lubricating articular surfaces. Enhanced endogenous hyaluronic acid synthesis by synovial cells, proteoglycan synthesis by chondrocytes, anti-inflammatory effects, and analgesic effects on nociceptive pain receptors are additional benefits. Any appreciable effusion should be aspirated before injection. Local anesthetic should not be combined with the hyaluronic acid other than infiltration into the skin for local anesthesia. Complications include hypersensitivity to hyaluronic acid preparations and severe postinjection inflammation occurring in 1% of patients. Newer compounds made with recombinant methods appear to reduce this occurrence. Contraindications include patients with a known hypersensitivity to hyaluronic acid preparations and those with skin diseases or infections in the area of injection.


Cost is a consideration with viscosupplementation. Currently, a series of injections costs between $500 and $1000 for the medication and injection procedure fees.

Operative Treatment Options Arthroscopy Proinflammatory cytokines are released by degenerating articular cartilage and synovium in osteoarthritis. These cytokines cause chondrocytes to release lytic factors that cause breakdown of proteoglycans and type II collagen. One of the benefits of arthroscopic treatment is lavage of these factors out of the knee. Edelson and colleagues found that lavage alone had good or excellent results in 86% of their patients at 1 year and in 81% at 2 years using the Hospital for Special Surgery Scale.47 Jackson and Rouse compared the results of lavage alone versus lavage combined with débridement. 48 Of the 65 patients treated with lavage alone, 80% showed initial improvement, but only 45% maintained that improvement at final follow-up. Of the 137 patients treated with lavage plus débridement, 88% showed initial improvement with 68% maintaining improvement at final followup. Others like Gibson and associates found no statistically significant improvement with either method even in the short term.49 Because of these mixed results, the efficacy of arthroscopic treatment of osteoarthritis is controversial. Patients who get the most benefit from arthroscopic débridement are those who present with a history of mechanical symptoms, symptoms of short duration (10 mm increased anterior displacement involved knee) and associated medial or lateral ligament deficiency is present. Consider when meniscus repair is performed. Athletically active patient desiring best knee possible for return to sports activities. Expect adaptive shortening FCL in most patients after valgus-producing osteotomy. At HTO, avoid disrupting proximal tibiofibular joint, which would allow proximal migration and laxity of posterolateral structures. Patients usually have increased lateral joint opening of 8 mm at the intercondylar notch (12 mm or more at periphery), have increased external rotation of 10 to 15 degrees, and require posterolateral reconstruction at time of ACL reconstruction. Combined posterolateral reconstruction and ACL reconstruction are always performed together to limit hyperextension and varus rotations.

Modified from Noyes FR, Barber-Westin SD, Hewett TE: High tibial osteotomy and ligament reconstruction for varus angulated anterior cruciate ligament–deficient knees. Am J Sports Med 28:282-296, 2000.


a four-strand semitendinosus–gracilis tendon autograft. We avoid allografts for ACL reconstructions in revision knees whenever possible because of the higher failure rates of these grafts compared with autografts.46,48,49 If an allograft is required and the knee demonstrates marked anterior displacement indicating involvement of the secondary ligament restraints, consideration may be given to also performing an iliotibial band extra-articular Loseetype procedure.49

Contraindications In general, HTO is avoided in knees that demonstrate a 15 × 15 mm2 area or more of exposed bone on both the tibial and femoral surfaces. There are knees in which the area of exposed bone may be slightly greater that are considered candidates; however, as a general rule, articular cartilage should be present over the majority of the joint surfaces. Major concavity of the medial tibial plateau with loss of bone stock is a contraindication to HTO. Knees that demonstrate (on standing 45-degree posteroanterior radiographs50) no remaining joint space in the medial compartment are not candidates. An arthroscopic procedure is done just before HTO to assess the amount of remaining articular cartilage and remove symptomatic meniscus fragments and other tissues. An absolute contraindication for a medial opening wedge osteotomy is the use of nicotine products in any form. The complication of a nonunion is not worth the risk, and a minimum of 8 weeks of abstinence before surgery should be insisted. The patient is warned that there may still be an increased risk for healing problems. A relative contraindication is body weight greater than 200 lb (91 kg). Although there may be some patients in whom HTO is indicated who weigh up to 225 lb (102 kg), this operation is avoided in patients with a higher body weight because the beneficial effect of unloading the medial compartment will not be achieved. A relative contraindication is increased medial slope to the affected medial tibial plateau in the coronal plane. This finding indicates that it will not be possible to significantly unload the medial compartment with an HTO, and the knee will remain with all of the weight-bearing confined to the medial compartment. This problem can be tested before surgery on examination of the knee joint with the standard varus-valgus stability tests at 20 to 30 degrees of knee flexion. In these knees with advanced medial arthrosis, there is no neutral point in which there is simultaneous contact of the medial and lateral compartments. The tibia goes into a “teeter-totter” state, with contact alternating between the medial or lateral compartment and obvious separation of the noncontacted compartment because of bone loss. Marked patellofemoral symptoms contraindicate HTO. The finding of asymptomatic articular cartilage changes to the patellofemoral joint is not a contraindication to HTO because clinicians have noted that the end result in terms of longevity of the HTO is dependent on the symptomatic medial tibiofemoral compartment.1,51 An abnormal patella infera or alta position contraindicates an opening or closing wedge osteotomy, respectively, because these procedures would further decrease or elevate the patella position.

WEIGHING THE EVIDENCE The survival rates reported after osteotomies are shown in Table 23K-7. Although conversion to total knee arthroplasty (TKA) is uniformly used as an end point for survival of HTO, some investigators also incorporate a low overall Hospital for Special Surgery (HSS) knee rating score, patient dissatisfaction, or the presence of pain in patients who declined TKA as additional end points. The highest long-term survival rate for closing wedge osteotomy was reported by Koshino and colleagues, who followed 75 knees from 15 to 28 years postoperatively.52 At the final follow-up examination, 93.2% of the patients had not converted to total or unicompartmental knee arthroplasty or complained of moderate to severe knee pain. The authors attributed the success of the procedure to the achievement of 10 degrees of anatomic valgus, avoidance of a flexion contracture, and incorporation of a patellofemoral decompressive procedure in patients with preexisting patellofemoral degeneration. Other closing wedge osteotomy studies show more modest survival rates 10 and 15 years after surgery. The 10-year survival rates range from 51% to 78%, with an average rate of 64% when Koshino and colleagues’ series is excluded.51,53-56 The investigations of Naudie and coworkers55 and Billings and associates had the lowest 10-year survival rates of 51% and 53%, respectively. Naudie and coworkers reported that the probability of survival increased in patients who were younger than 50 years of age at the time of the HTO and who had preoperative knee flexion greater than 120 degrees.55 Billings and associates54 failed to find a statistically significant association between survival rates and patient age, amount of valgus correction achieved, or postoperative complications. More recent studies from Sprenger and Doerzbacher56 and Aglietti and associates53 reported more favorable results 10 years after surgery, with survival rates of 74% and 78%, respectively. Fifteen-year survival rates of closing wedge osteotomy, provided to date by only a few authors, range from 39% to 57%.53,55-57 Aglietti and associates reported that male gender and preoperative quadriceps strength correlated with a long-term survival rate of 57%.53 Sprenger and Doerzbacher determined that the survivability of HTO (56% at 15 years) was related to the achievement of 8 to 16 degrees of valgus measured 1 year postoperatively.56 Naudie and associates reported the probability of survival decreased in patients older than 50 years, or in whom a previous arthroscopic débridement, presence of a lateral tibial thrust, preoperative knee flexion less than 120 degrees, or delayed union or nonunion postoperatively was present.55 Huang and coworkers identified only preoperative varus malalignment as predictive of survivability of HTO.57 Knees with 9 degrees or less of varus had a 10-year survival rate of 93%, whereas those with more than 9 degrees of varus had a 10-year survival rate of only 56%. Fewer data are available regarding survival rates following opening wedge osteotomy. Three studies reported 84%,58 89%,59 and 94%60 survival rates 5 years after surgery. After 10 years, survival rates are available from only two investigations: 63% in Weale and colleagues’ series of 73 cases,59 and 85% from Hernigou and Ma’s series of 203 knees.60 Weale and colleagues hypothesized that

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TABLE 23K-7 Survival Rates after High Tibial Osteotomy

Study Huang,

200557

Koshino, 200452

Sterett, 200458 Aglietti, 200353 Sprenger,

200356

Weale, 200159

Type of Osteotomy

N, Patient Age (Range)

End Points for Survival Analysis

Closing wedge Closing wedge

93, 57 yr (38-73) 75, 59 yr (46-73)

Opening wedge Closing wedge Closing wedge

38, 51 yr (34-79) 91, 58 yr (36-69) 76, 69 yr (47-81)

Opening wedge

76, 54 yr (36-70)

1. TKA 2. Patient dissatisfaction 1. TKA or unicompartmental arthroplasty 2. Moderate pain at final follow-up >15 yr postoperatively 1. TKA 2. Revision HTO 1. TKA 2. HSS score < 70 1. TKA 2. HSS score < 70 3. Patient dissatisfaction 1. TKA 2. Waiting for TKA 3. Postoperative sepsis precluded revision TKA

Hernigou, 200160 Opening wedge Billings, 200054 Closing wedge Naudie, 199955 Closing wedge Coventry, 199351 Closing wedge

215, 61 yr (48-72) 64, 49 yr (23-69) 106, 55 yr (16-76) 87, 63 yr (41-79)

Insall, 198461a

95, 60 yr (30-83)

Closing wedge

Survival Rates after Surgery 5 Years

10 Years

15 Years

Correlations with Survival Rate

94.6%

87%

75.2%

97.8%

96.2%

93.2%

Preoperative tibiofemoral alignment (9 degrees varus) None

84%

NA

NA

None

96%

78%

57%

86%

74%

56%

Alignment at healing, muscle strength, male gender Alignment at 1 yr after surgery

88.8%

63%

NA

None

94%

85%

68%

None

TKA

85%

53%

NA

None

TKA

73%

51%

39%

1. TKA 87% 2. Moderate or severe pain in patients who declined TKA Survival rate not calculated, but 23% revised to TKA

66%

NA

Body weight, delayed or nonunion, age, preop flexion Body weight, alignment at 1 yr after surgery HSS excellent to good results: 2 yr—97%, 5 yrs—85%, 9 yrs—37%. Alignment did not correlate with results; passage of time determined result.

HSS, Hospital for Special Surgery rating system; NA, not available; TKA, total knee arthroplasty.

rogression of arthrosis in the medial compartment correp lated with HTO failure.59 Hernigou and Ma did not comment on factors that could have affected the survival rates in their investigation. These authors provided the only 15-year survival rate published at the time of writing of opening wedge osteotomy of 68%. The ability of HTO to alleviate pain has been demonstrated in many studies53,61-65; however, the longevity of pain relief correlates with the length of follow-up achieved postoperatively. Unfortunately, several investigators did not separately assess pain when determining clinical outcome but only provided final rating scores from knee rating systems such as the Lysholm, Hospital for Special Surgery, WOMAC, and the American Knee Society.54,58,61,66-68 Aglietti and associates followed 61 patients clinically from 10 to 21 years after surgery and reported that 79% had no or only mild knee pain.53 Koshino and colleagues reported in a small series of 18 patients that all had relief of pain on follow-up evaluations ranging from 38 to 114 months postoperatively.61 Only 9 patients had more than 7 years of follow-up in this investigation. Rinonapoli and coworkers followed 60 knees from 10 to 21 years after surgery and reported that pain at rest was absent in 55%, mild in 18%, moderate in 22%, and severe in 5%.65 Pain on

walking was absent or mild in 55%, moderate in 27%, and severe in 18%. Satisfactory pain relief has been reported in most studies that followed knees that had HTO and ACL reconstruction (either concomitant or staged). Williams and associates followed 25 ACL-deficient varus-angulated knees from 24 to 106 months after surgery.69 Thirteen of these knees were treated with a combined HTO and ACL reconstruction, and 12 had only an HTO. At follow-up, 84% had no pain with vigorous activity. Dejour and associates performed a combined HTO and ACL patellar tendon autograft reconstruction in 44 knees.70 At follow-up, which ranged from 1 to 11 years postoperatively, 66% had no pain or pain only after vigorous activity. Functional limitations with daily activities such as walking and stair climbing are typically reported in most patients before HTO. In addition, few patients are able to participate in even light sports activities without experiencing noteworthy symptoms. After surgery, the ability to walk an unlimited distance or more than 1 km is an important measure of daily function. Koshino and associates reported that 94% of 75 knees could walk more than 1 km without pain at 15 to 28 years after a closing wedge HTO.52 A more modest finding was reported by


Pfahler and associates, who found that 57% of 62 knees followed 6 to 14 years after surgery could walk more than 1 hour.64 Koshino and associates described a small series of 21 patients who received an opening wedge osteotomy followed 38 to 114 months after surgery. At the most recent follow-up examination, 89% reported the ability to walk

an unlimited distance without limitations.61 The American Knee Society walking score improved from a preoperative mean of 19 ± 5.4 points to 46.7 ± 7.3 points at follow-up (P 20 mm Hg

From Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 18(1):35-40, 1990.

(Table 24B-1) are used to confirm the presence of CECS in the involved compartments.

TREATMENT OPTIONS Initial management is generally nonoperative, consisting of a period of rest and removal of the inciting physical activity. Patient education and activity modification are the mainstays of conservative management. Nonoperative treatments such as physical therapy, anti-inflammatory agents, and orthotics play an important role in the management of many causes of exercise-induced leg pain; however, they usually are not effective in the management of CECS. Proper pre-exercise warm-up and stretching programs may be beneficial. During symptomatic periods, icing and a short course of anti-inflammatory medication may be used. The initial phase of treatment should include relative rest from the inciting activity, stretching, antiinflammatory agents, physical therapy, correction of training errors, and corrective foot orthotics. Before return to activity, both extrinsic and intrinsic factors must be addressed and corrected if possible. Extrinsic factors that may be altered include the running surface, shoe design, and the training program. Stretching and strengthening exercises and orthoses may be used to address intrinsic factors inherent to muscle balance or limb alignment. Other biomechanical factors identified may also be addressed before return to activity as a means of altering the forces going through the involved compartment. Because adequate response to conservative measures may be difficult to obtain reliably, operative treatment should be employed if the athlete fails to respond to a rehabilita tion program of 3 to 6 months’ duration and wishes to continue with the activity associated with the CECS.9,17-19,42,44 Treatment is with fasciotomy, with or without fasciectomy, and resection of any fascial bands. Addressing areas of muscle herniation is also indicated for a com plete release. Open and percutaneous techniques have been described, and current trends are for limited incision techniques with rapid return to weight-bearing, motion, and resumption of activity. The symptomatic compartments should be addressed by surgical release. Previously, those individuals with anterior symptoms had anterior and lateral compartments released. Schepsis and colleagues45 found that, in patients with complaints isolated to the anterior compartment, isolated release of the anterior compartment produced results equal to a combined anterior and lateral compartment release. We now recommend addressing only those compartments that are symptomatic with positive pressure measurement.

Leg 1861

WEIGHING THE EVIDENCE There are no controlled trials in the literature comparing operative and nonoperative treatment of CECS and no studies comparing the different surgical procedures. Most surgical procedures report a high rate of satisfaction and return to unlimited physical activity, with 60% to 100% rates of relief.43,45-54 De Fijter and associates reported a 96% return to unlimited exercise in 118 military personnel following a percutaneous fasciotomy, with an average followup of 62 months.47 Raikin and colleagues reported bilateral simultaneous releases in 16 patients; 16 months after surgery, 13 patients were pain free, whereas 3 had continued mild but improved pain, and all returned to sports an average of 10.7 weeks after surgery.52 Moushine and coworkers reported 18 consecutive athletes treated with a two-incision fasciotomy technique, all of whom returned to full sporting activity at the 2-year follow-up, with average return to sporting activity of 25 days.51 Howard and colleagues reported slightly less favorable results of 68% pain relief, but when stratified by compartment, patients with anterior release had 81% relief, whereas posterior release yielded 50% relief.49 Slimmon and associates also had less favorable outcomes using a single-incision technique.54 They reported 60% good or excellent results in patients undergoing a single

operation, with 58% of patients exercising at a lower level than before the development of symptoms. Hutchinson and coworkers demonstrated incomplete releases with a single-incision technique,55 which may account for the less favorable outcomes. Schepsis and colleagues looked at the practice of releasing only the pressure-positive compartments or also releasing adjacent compartments.45 They found that release of only the involved anterior compartment and releasing both the anterior and lateral compartments yielded identical results, but that release of both compartments resulted in an average 3 weeks’ longer return to sports (11.4 versus 8.1 weeks). In conclusion, minimally invasive, percutaneous, and single- and double-incision techniques are all currently used. There is evidence that single-incision techniques yield inferior results54 compared with double-incision techniques. In general, there is a high rate of satisfactory outcome and return to sporting activities and a relatively low complication rate with surgical treatment of CECS. With accurate diagnosis of CECS, excellent results can be achieved if the procedure is performed properly. When a diagnosis of CECS has been made, the patient wishes to undergo surgical treatment, and modification of activity is unacceptable to the patient, fasciotomy of the affected compartments may be recommended.

A u t h o r s ’ P r e f e r r e d M e t h o d Anterior and Lateral Compartment Release

We prefer to use a double-incision technique similar to that described by Rorabeck and colleagues.53 The anterior intermuscular septum is usually superficially located and centered between the palpable anterior border of the tibia and the lateral border of the fibula. Two longitudinal incisions, 2 to 3 cm long, are centered over the intermuscular septum (IMS) at the junctions of the proximal and middle, and middle and distal, thirds of the leg (Fig. 24B-3). They are

carried down full-thickness to the muscle fascia. The IMS and superficial peroneal nerve can be easily identified. Using finger dissection, the plane is developed between the muscle fascia and subcutaneous fatty tissues from the knee to the ankle. One channel is made over each compartment to avoid making a large subcutaneous space and to minimize the occurrence of a seroma. The superficial peroneal nerve and any branches are visualized through the distal incision (Fig. 24B-4) and are protected throughout the

Figure 24B-3 Skin markings for anterior and lateral compartment double-incision technique. Incisions are placed along the intermuscular septum, located about midway between the subcutaneous anterior border of the tibia and the subcutaneous lateral border of the fibula. The distal incision is centered over the exit of the superficial peroneal nerve, about 10 cm from the ankle joint line. The proximal incision is centered 10 cm distal to the proximal fibula.

Figure 24B-4 Superficial peroneal nerve in the distal incision. Continued



Figure 24B-5 Fascial incisions for anterior and lateral compartment releases. Note the intermuscular raphe between the incisions.

Figure 24B-6 Fasciotomy is performed using long Metzenbaum scissors in a push-cut fashion. The nerve is visualized directly and protected in the distal incision.

procedure. The nerve is released if its exit from the fascia is felt to be tight. A small longitudinal incision is then made into the anterior and lateral fascia 1 cm on either side of the IMS at both incisions (Fig. 24B-5). From the proximal incision, the anterior and lateral compartment fasciotomy is carried proximally (Fig. 24B-6). We prefer to use 8- and 12-inch Metzenbaum scissors, but a fasciotome may also be used. The distal incision is then used to carry the fasciotomies distally to the level of the superior extensor retinaculum. Using either proximal or distal incisions, the fasciotomies are connected. The advantages of the doubleincision technique are that it gives easier access to the anterior and lateral compartment fascia adjacent to the IMS and confirmation of a complete fasciotomy. We strongly recommend when using this technique not to proceed with the fasciotomy until you have separated the subcutaneous tissue from the fascia. This decreases the risk for injury to the subcutaneous structures, and it makes passage of the instrument much easier and allows distal inspection to confirm complete fasciotomy.

must be complete because it also represents the proximal confluence of the flexor hallucis longus and flexor digitorum longus (FDL) fascia. This releases the deep posterior compartment. A Bristow is then used to release the tibialis posterior muscle off the tibia, completing the release of the tibialis posterior compartment (Fig. 24B-8). We have found this technique effective to release the deep posterior compartments. Remaining on the posterior aspect of the tibia throughout the release ensures safety of the posterior tibial neurovascular bundle, which is posterior to the tibialis posterior and FDL. Verification of an adequate release by digital examination is of the utmost importance. Following the anterior or posterior releases, the tourniquet is released, and hemostasis is obtained. The subcutaneous tissues are closed, and the skin is sutured using a subcuticular stitch. A sterile dressing and a compression bandage are applied to both legs. As mentioned, most patients have bilateral symptoms and hence undergo bilateral procedures. Patients with anterior and posterior symptoms have both compartments released.

Posterior Compartment Release

We use a single-incision technique for the release of the superficial and deep posterior compartments. The incision is located 1 cm posterior to the posterior subcutaneous border of the tibia. It is centered at the level of the distal gastrocnemius curve and is 8 to 10 cm long (Fig. 24B-7). The long saphenous nerve and vein are usually in the center of the field and are easily identified on the posteromedial border of the tibia. Proximally, the flexor digitorum longus occupies this position. A small vertical incision is made at the osseofascial junction, and then, using Metzenbaum scissors and staying directly on the posterior border of the tibia, the fascia is released to the level of the tibialis posterior tendon. The surgeon’s finger should follow the instrument to ensure a complete release. The release is then taken proximally. The soleus will be encountered in the proximal one third of the tibia at the soleus bridge. Release of this stout structure

Figure 24B-7 Skin marking for posterior compartment releases. A 10-cm incision is located along the posteromedial subcutaneous border of the tibia, centered at the distal insertion of the gastrocnemius muscle.

Leg 1863

A

B

Figure 24B-8 A and B, Fascial incisions for posterior compartment releases. The muscle fascia is taken directly off of the posteromedial border of the tibia.

POSTOPERATIVE PRESCRIPTION, OUTCOMES MEASUREMENT, AND POTENTIAL COMPLICATIONS Weight-bearing is initiated immediately after surgery, with crutches discontinued as tolerated. Early passive and active range of motion exercises are implemented postoperatively to prevent postoperative fascial scarring.8,17,18,20 During the first 2 days, patients follow a RICE (rest, ice, compression, and elevation) protocol as well as anterior and posterior stretching (toe pointing) 3 to 5 times per day. From the third day to the 2-week follow-up visit, patients perform aggressive anterior and posterior compartment stretches 3 times per day and increase the walking distance. Once they are weaned from crutches, nonimpact activities such as hydrotherapy, stationary cycling, and elliptical training are begun. After 2 weeks, the wounds are checked, and a formal physical therapy regimen of stretching and functional return to sport-specific activity is begun. When strength and control of the ankle and foot are regained, functional training can begin, usually by 4 to 6 weeks. At that point, running may be implemented, with speed and agility drills added during the eighth week.17,18,20 By 8 to 12 weeks after surgery, athletes typically return to full participation in sports. Complications reported have included hematoma or seroma formation (9%), superficial peroneal nerve injury (2%), anterior ankle pain (5%), and recurrence of symptoms (2%).47 A recently published study in the vascular surgery literature highlighted the function of the muscles and their compartments in the return of fluids in the dependent limb and raised the concern of venous insufficiency after fascial release, but there have not been any documented cases to date with clinically significant findings.56

CRITERIA FOR RETURN TO PLAY Objective criteria for return to play following fascial release for CECS do not exist. The return to play is based on satisfactory completion of the progression outlined in the preceding section. The athlete should be nearly pain free, have demonstrated acceptable strength and endurance, and be able to replicate the demands of practice and play in the therapy sessions. Return to full athletic activities should be accomplished by 8 to 12 weeks after surgical intervention. C

r i t i c a l

P

o i n t s

l History on presentation is the most important part of the

l

l l

clinical examination for sifting through the differential diagnosis. The onset of symptoms will be at a consistently reproducible point in the exercise routine and will be relieved only by rest. Double-incision techniques are favored laterally to allow dissection and visualization of the superficial peroneal nerve to avoid injury. Dissection between the subcutaneous tissues and fascia is performed bluntly using the fingers. For anterior and lateral releases, separate channels are formed for each compartment instead of making one large pocket over the entire anterolateral portion of the leg. The superficial peroneal nerve exits the lateral compartment fascia 11 cm from the distal tip of the fibula. The distal incision should be centered at this point to allow for direct visualization and protection of the nerve. Early range of motion exercises and weight-bearing are encouraged postoperatively to avoid secondary scarring after the fasciotomy. Crutch use is as needed and is generally discontinued within 1 week after surgery.


S U G G E S T E D

R E A D I N G S

Mavor GE: The anterior tibial syndrome. J Bone Joint Surg Br 38B(2):513-517, 1956. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 18(1):35-40, 1990. Rorabeck CH, Bourne RB, Fowler PJ: The surgical treatment of exertional compartment syndrome in athletes. J Bone Joint Surg Am 65(9):1245-1251, 1983.

Styf J, Korner L, Suurkula M: Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. J Bone Joint Surg Br 69(2):301-305, 1987.


C H A P T E R

25

Foot and Ankle S ect i o n

A

Biomechanics Andrew Haskell and Roger A. Mann

ANKLE JOINT The ankle joint allows sagittal plane motion of 20 degrees of dorsiflexion and 50 degrees of plantar flexion; however, there is a great deal of variability among individuals. The ankle joint is not a simple hinge joint, but rather the trochlear surface of the talus is a section from a cone whose apex is based medially (Fig. 25A-2).4 The talus is stabilized within the ankle mortise by bony and soft tissue restraints. The congruity of the ankle mortise leads to considerable inherent bony stability.5,6 Ligament support includes the deltoid ligament medially7 and three separate ligamentous bands laterally: the anterior and posterior talofibular ligaments and the calcaneofibular ligament.8 The anterior talofibular ligament is taut with the ankle joint in plantar flexion, when it is in line with the fibula; and the calcaneofibular ligament is taut with the ankle joint in dorsiflexion, when the ligament is in line with the fibula 250 Body Weight (%)

This section discusses the biomechanical linkage of the joints of the foot and ankle and their effects on the lower extremity. The ankle joint, subtalar joint, transverse tarsal joint, and metatarsophalangeal joints are uniquely interrelated so that function in one reliably alters the mechanics of the others. The foot and ankle complex initially helps absorb the impact of ground contact and later in stance provides the body with a stable platform from which to function. During walking, the toes are lifted from the floor, but in athletics, forceful push-off facilitates rapid acceleration and deceleration, direction changes, and jumping. Dysfunction of the foot and ankle complex may result in an altered gait pattern, degradation of athletic performance, and compensatory changes in the knee and hip joints. The ankle and subtalar joint complex function as a universal joint, linking pelvic, thigh, and leg rotation to hindfoot motion and longitudinal arch stability. This allows the ankle joints to compensate for some degree of dysfunction in the hindfoot, and vice versa. Athletics, however, requires maximal performance from these systems, and dysfunction of ankle and foot mechanics often leads to pain, injury, and loss of performance. Athletics is distinguished from normal walking by the stresses applied to the joints. The stresses can be repetitive, as in a long distance runner, or impulsive, as occurs in the pushoff foot of a shot-putter. The vertical force involved in running is 2 to 2.5 times body weight compared with 1.2 times body weight in walking,1 and can be higher for many sports with extreme push-off, such as a football lineman engaged in blocking or a basketball player engaged in rapid accelerating and jumping activities (Fig. 25A-1). The nature of these forces depends on the activity and includes vertical force, fore-and-aft shear, side-to-side shear, and torque forces. These forces are measured in a variety of ways, including force plate analysis or thin film pressure transducers placed in a shoe.2 The foot and ankle complex must be supple enough to absorb impact and rigid enough to transmit muscle forces, or injuries such as sprains, strains, stress fractures, and fascial tears may result. Athletic training can help to attenuate these forces and minimize the risk for injury.3

Walking Running

200 150 100 50

0

25

50

75

100

Time (% Stance Phase) Figure 25A-1 Comparison of vertical ground reaction force for walking (blue line) compared with jogging (red line). The horizontal axis is scaled as a percentage of total time in stance phase for walking (0.6 sec) and running (0.24 sec). The vertical axis is shown as a percentage of body weight. (From Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007.)

1865


Figure 25A-2 The trochlear surface of the talus is a section from a cone. The apex of the cone is directed medially, and the open end is directed laterally. (From Stiehl JB [ed]: Inman’s Joints of the Ankle, 2nd ed. Baltimore, Williams & Wilkins, 1991.)

(Fig. 25A-3).4 The anterior talofibular ligament is injured most frequently during ankle sprains, in part because the ankle has less intrinsic bony stability in plantar flexion when this ligament is under tension.9 Isolated injuries to the calcaneofibular ligament are less frequent, although they often occur in conjunction with anterior talofibular sprains. Dorsiflexion and plantar flexion occur at the ankle joint during gait. At heel strike, the dorsiflexed ankle rapidly plantar flexes. This ends at foot flat, after which progressive

A

B

dorsiflexion occurs. Dorsiflexion reaches a maximum at 40% of the walking cycle, when plantar flexion begins as the heel rises, and continues until toe-off, when dorsiflexion occurs again during the swing phase (Fig. 25A-4). The force applied across the ankle joint during walking has been measured at about 4.5 times body weight.10 This maximal stress occurs just before and just after the onset of plantar flexion of the ankle joint. If this force were extrapolated to running, in which the ground reaction force is over double that of walking, we would see stress across the ankle joint that approaches 10 times body weight. Muscle control of the ankle joint can be divided into the anterior and posterior compartments. The anterior compartment consists of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. The posterior compartment consists of the gastrocnemius-soleus group, tibialis posterior, flexor digitorum longus, and flexor hallucis longus. The lateral compartment, consisting of the peroneus longus and brevis, functions with the posterior compartment. During normal walking, the anterior compartment muscles become active late in the stance phase and in the swing phase to bring about dorsiflexion of the ankle joint by a concentric (shortening) contraction (see Fig. 25A-4).11 This muscle group remains active after heel strike to control the rapid plantar flexion of the ankle joint that occurs by an eccentric (lengthening) contraction. This eccentric contraction during plantar flexion helps to dissipate the forces on the limb at initial ground contact. The anterior compartment becomes electrically silent by foot flat. The posterior compartment muscles are active after foot flat (15% to 20% of gait cycle), during which time the ankle joint is undergoing dorsiflexion, and they remain active until about halfway through the cycle, at which time about 50% to 60% of ankle joint plantar flexion has occurred.12 This muscle group initially undergoes an eccentric contraction controlling forward movement of the tibia over the foot, then a concentric contraction when plantar flexion begins. The electrical activity of the posterior calf group ceases before full plantar flexion has occurred, indicating that the last portion of plantar flexion is a passive phenomenon.

C

Figure 25A-3 Calcaneofibular (a) and anterior talofibular (b) ligaments. A, In plantar flexion, the anterior talofibular ligament is in line with the fibula, thereby providing most of the support to the lateral aspect of the ankle joint. B, When the ankle is in neutral position, both the anterior talofibular and the calcaneofibular ligaments support the joint. The obliquely placed structure depicts the axis of the subtalar joint. It should be noted that the calcaneofibular ligament parallels the axis. C, When the ankle joint is in dorsiflexion, the calcaneofibular ligament is in line with the fibula and supports the lateral aspect of the joint. (A to C, From Stiehl JB [ed]: Inman’s Joints of the Ankle, 2nd ed. Baltimore, Williams & Wilkins, 1991.)

Foot and Ankle 1867

As the speed of gait increases to steady running and sprinting, several changes occur. The ankle joint starts in slight dorsiflexion and, at heel strike, rather than the ankle plantar flexing to a foot flat position, the ankle remains dorsiflexed (see Fig. 25A-4). The tibia moves forward, and the foot flat position is achieved. As running speed increases, the magnitude of the motion increases, the stance phase is reduced significantly, and the period of double limb support gives way to a period lacking limb support. The electrical activity of the anterior compartment still begins late in stance and continues through swing, but it now lasts through about the first third of the stance phase. The posterior calf muscles show a significant change in their activity in that they become active late in swing phase and remain active until about halfway through ankle joint plantar flexion.13 This increased activity in the posterior calf musculature probably results in increased stability of the ankle joint at the time of initial ground contact. 30

SUBTALAR JOINT The subtalar joint is a complex joint that permits inversion and eversion. The axis of the subtalar joint is variable but is about 42 degrees to the horizontal plane and passes from medial to lateral at about 16 degrees (Fig. 25A-5).10,14 Measurement of subtalar joint movement during walking and running is difficult and is based on many assumptions. Although the overall pattern of motion appears to be consistent, the magnitude of motion is variable.15 The range of motion of the subtalar joint in its pure form, inversion and eversion, is 30 degrees of inversion and 15 degrees of eversion, with considerable variability among people. To measure this motion accurately, it is important to start with the calcaneus in line with the tibia. The subtalar joint is less constrained than the ankle, being stabilized primarily by the joint configuration and the interosseous ligament.16,17 This joint is stable when the

PLANTAR FLEXION-DORSIFLEXION RUN

Toe-off

20 dorsiflexion 10

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0 10 plantar flexion 20 30

gastrocnemius-soleus anterior tibial

30 20 dorsiflexion 10 degrees

JOG

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0

0.1

0.2 0.3

0.4

0.5 0.6 sec.

0.7 0.8

0.9

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Figure 25A-4 Ankle joint range of motion for walking, jogging, and running. The muscle function of the anterior and posterior compartment is noted on the bottom of the graph. (Redrawn from Mann RA: Biomechanics of running. In American Academy of Orthopaedic Surgeons: Symposium on the Foot and Leg in Running Sports. St. Louis, CV Mosby, 1982.)


tala Sub is ax

NT

69°

r

OF OI IS R J X A LA TA UB

x = 23°

S

21°

4°

47°

x = 41°

Horiz. plane

B

A

Figure 25A-5 Variations in the subtalar joint axes. In the horizontal plane (A), the axis approximates 45 degrees and (B) passes about 23 degrees medial to the midline. (A and B, Adapted from Isman RE, Inman VT: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10:97, 1969.)

long axis of the tibia passes medial to the obliquely placed subtalar joint axis. In the normal foot, subtalar joint eversion ceases with weight-bearing owing to the configuration of the joint surfaces and the interosseous ligament. When the weight-bearing line is lateral to the subtalar joint axis, inversion stability depends on lateral ligament support and active muscle function. The subtalar joint has been likened to an oblique hinge that functions to translate motion between the transverse tarsal joint distally and the ankle joint and leg proximally (Fig. 25A-6).18,19 This linkage is important for energy dissipation at heel strike. At the time of initial ground contact during walking, the slightly inverted subtalar joint

A

B

Figure 25A-6 Mitered hinge effect of subtalar joint. The joint acts as a mitered hinge, converting motion in the calcaneus below into the tibia above and, conversely, from the tibia above into the calcaneus below. (A and B, Redrawn from Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007.)

ndergoes rapid eversion, the tibia undergoes internal u rotation, the transverse tarsal joints become supple, and the medial longitudinal arch flattens (Fig. 25A-7). These are passive energy-absorbing mechanisms. In a person with flatfoot and increased eversion of the subtalar joint (Fig. 25A-8), an increased amount of tibial internal rotation may occur, which can affect the knee, patellofemoral, or hip joint in selected cases. An orthotic device that supports the longitudinal arch with medial heel posting may restrict subtalar joint rotation and decrease the internal rotation of the lower extremity, possibly resolving knee or hip pain. This linkage is also important for efficient energy transfer during heel rise and toe-off. After the initial eversion, the subtalar joint undergoes progressive inversion, which reaches a maximum at toe-off, when eversion begins again. This movement increases the stability of the transverse tarsal joints and medial longitudinal arch, stiffening the foot and allowing it to act as a rigid extension of the leg. Although the initial eversion is passive, the inversion that follows appears to be both passive and active. The inversion results from an external rotation torque from the lower extremity above, which is transmitted across the ankle joint and is translated by the subtalar joint into inversion. The plantar aponeurosis mechanism and the oblique metatarsal break enhance the inversion, as described later. The muscle function around the subtalar joint can be appreciated best by looking at the muscles in relation to the subtalar joint axis (Fig. 25A-9). Muscles medial to the axis are invertors, muscles lateral to it are evertors, and the function of the muscles on the axis is determined by the position of the subtalar joint. The main invertors are the tibialis posterior and the gastrocnemius-soleus complex, and the main evertor is the peroneus brevis and, to a much lesser extent, the peroneus longus, which is mainly a plantar flexor of the first metatarsal. The tibialis anterior lies on the subtalar

Foot and Ankle 1869

A

joint axis and has little influence on the subtalar joint, although it is the only functioning muscle at heel strike and, as such, besides controlling plantar flexion of the ankle joint, may resist eversion at the subtalar joint. The inversion that occurs during the last half of stance is due to the passive mechanisms noted previously, along with the input from the gastrocnemius-soleus complex and the posterior tibialis. The patient who lacks posterior tibial tendon function cannot initiate standing on tiptoe but can maintain the position when it is achieved. It can be concluded that posterior tibial tendon function is necessary to initiate inversion, and the gastrocnemius-soleus complex is necessary to maintain it. As noted in the discussion of ankle function, with running, the posterior calf muscles become active late in swing phase and remain active through most of stance (see Fig. 25A-4). Besides providing stability to the ankle joint, these muscles probably bring about some inversion of the subtalar joint before initial ground contact.

B

TRANSVERSE TARSAL JOINT C

D

Figure 25A-7 Model demonstrating flattening and elevation of the longitudinal arch. A and B, Flattening of the longitudinal arch occurs at the time of heel strike with eversion of the calcaneus and internal rotation of the tibia. C and D, Elevation and stabilization of the longitudinal arch are associated with the outward rotation of the tibia, causing inversion of the calcaneus and locking of the transverse tarsal joint. (Redrawn from Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007.)

The transverse tarsal joint, consisting of the talonavicular and calcaneocuboid joints, lies distal to the subtalar joint and is influenced strongly by it.20 The motion of the transverse tarsal joint is that of adduction and abduction and is measured with the calcaneus in neutral position and the forefoot parallel to the floor. Normal motion is about 20 degrees of adduction and 10 degrees of abduction. The main support of the joint is ligamentous, but its stability is derived from subtalar joint inversion without much direct muscle control. The axes of the transverse tarsal joint are aligned such that when the calcaneus is in an everted position, the axes are parallel, permitting more motion to occur around this joint system. During normal walking, this occurs at heel strike, creating a flexible foot to absorb the energy of impact. When the calcaneus is inverted, the axes of the transverse tarsal joint are nonparallel, creating a stable joint system (Fig. 25A-10).20 This occurs at heel rise and toe-off, creating a rigid foot to effectively lengthen the limb and assist in propulsion during running.

SUBTALAR ROTATION HEEL STRIKE

TOE-OFF

HEEL STRIKE

10

NORMAL FOOT

0 INVERSION 10 EVERSION

FLAT FOOT

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30

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PERCENT OF WALK CYCLE Figure 25A-8 Graph of subtalar joint motion in the normal individual and in a flatfooted individual. (Redrawn with permission from data in Wright DG, Desai ME, Henderson BS: Action of the subtalar and ankle joint complex during the stance phase of walking. J Bone Joint Surg Am 46:361, 1964.)

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Tib. ant.

Ext. hal. longus Ext. dig. longus

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xis

Tib. post F. dig. longus F. hal. longus

Peroneus long Peroneus brevis

T. calcaneus

A

Plantar flexors

B

Figure 25A-9 A, The location and the types of rotation that occur about the ankle and the subtalar axes. B, The relationship of the various extrinsic muscles about the subtalar and ankle joint axes. Ext. dig. longus, extensor digitorum longus; Ext. hal. longus, extensor hallucis longus; F. dig. longus, flexor digitorum longus; F. hal. longus, flexor hallucis longus; T. calcaneus, tibialis calcaneus. (Redrawn from Haskell A, Mann RA: Biomechanics of the foot. In American Academy of Orthopaedic Surgeons: Atlas of Orthoses and Assistive Devices. Philadelphia, Elsevier, 2008.)

EVERSION

INVERSION TN

TN

C

C C

The windlass mechanism describes the function of the plantar aponeurosis during gait. The plantar aponeurosis arises from the tubercle of the calcaneus and inserts into the base of the proximal phalanges (Fig. 25A-11). After heel rise, the metatarsophalangeal joints dorsiflex, tightening the plantar aponeurosis. This depresses the metatarsal heads, elevates and stabilizes the longitudinal arch, and helps to bring the calcaneus into an inverted position (Fig. 25A-12).21 The inverted calcaneus causes the transverse tarsal joint axes to diverge, helping to stabilize the midfoot at toe-off. The oblique metatarsal break is created by the lateral slope formed by the metatarsophalangeal joints two through five (Fig. 25A-13).18 This oblique line creates a cam-like action as the body weight is brought over the metatarsal heads, further enhancing external rotation of the lower extremity and inversion of the calcaneus.

joint motions are enhanced further by the function of the plantar aponeurosis, the transverse metatarsal break, and the muscles of the leg and foot. It is this linked series of movements that enables the athlete to absorb the forces of impact, yet create a rigid platform from which to push off. These joint linkages are essential for high-performance function of the lower extremity. If one of these linkages

C

WINDLASS MECHANISM AND METATARSAL BREAK

LINKAGE OF THE FOOT AND ANKLE The functions of the ankle joint, subtalar joint, transverse tarsal joint, and plantar aponeurosis have been examined and their interdependence described. The linkage between these joints should be emphasized further. The terms pronation and supination describe a coordinated series of movements of the foot and ankle that facilitate its two main functions during gait, namely, energy absorption at impact and energy transfer during stance (Table 25A-1). These

Figure 25A-10 The function of the transverse tarsal joint as described by Elftman. When the calcaneus is in eversion, the resultant axes of the talonavicular (TN) and calcaneocuboid (CC) joints are parallel or congruent. When the subtalar joint is in an inverted position, the axes are incongruent, giving increased stability to the midfoot. (Redrawn from Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007.)

Foot and Ankle 1871

Flexor tendon

Capsule

Plantar pads

Plantar pad Plantar aponeurosis

C

Lateral

Medial

A D

B Figure 25A-11 Plantar aponeurosis. A, Cross section. B, The plantar aponeurosis originates from the tubercle of the calcaneus and passes forward to insert into the base of the proximal phalanges. The aponeurosis divides, permitting the long flexor tendon to pass distally. C, Components of the plantar pad and its insertion into the base of the proximal phalanx. D, Extension of the toes draws the plantar pad over the metatarsal head, pushing it into plantar flexion. (From Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007, p 24.)

within the system fails to function properly, stress is placed on the joints proximal and distal to it. Although we speak of ankle joint dorsiflexion and plantar flexion, only about half of this motion comes from the ankle joint; the remainder comes from the movement occurring within the subtalar and transverse tarsal joints.22 If there is diminished motion of the ankle joint, perhaps from an anterior impingement,

ME

TA BR TARS EA AL K

x= 62°

53.5°

72.5°

Figure 25A-12 The function of the plantar aponeurosis. The brown outline shows the medial column with the foot at rest. The red figure shows the medial column with the first ray dorsiflexed. Note that dorsiflexion of the metatarsophalangeal joints tightens the plantar aponeurosis, which results in depression of the metatarsal heads, elevation and shortening of the longitudinal arch, inversion of the calcaneus, and elevation of the calcaneal pitch.

Figure 25A-13 The metatarsal break passes obliquely at an angle of about 62 degrees to the long axis of the foot. (Adapted from Isman RE, Inman VT: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10:97, 1969.)


TABLE 25A-1 Comparison of Foot Characteristics Based on Foot Position

Foot Position Characteristic

Pronation

Supination

Joint position

Ankle dorsiflexion Subtalar eversion Transverse tarsal abduction Supple Heel strike Energy absorption

Ankle plantar flexion Subtalar inversion Transverse tarsal adduction Rigid Foot flat to toe-off Energy transfer to ground

Arch stiffness Gait cycle Function

degenerative changes within the joint, or fusion, the subtalar and transverse tarsal joints compensate for the lost motion. If there are degenerative changes within the subtalar or transverse tarsal joints, any loss of ankle joint motion is magnified. This compensatory increase in motion of the neighboring joints often leads to pain, loss of function, and degenerative changes over time.23 Moving distally, if the motion in the subtalar joint is restricted, its ability to translate rotation proximally and distally is impaired, placing increased stress on the ankle and transverse tarsal joints. Talocalcaneal coalition can lead to a spastic peroneal flatfoot or ball-in-socket ankle because of the effect of lack of subtalar motion. The degree of ankle joint dorsiflexion and plantar flexion also is affected, and the ankle can become arthritic from the abnormal stresses.24 Impairment of the transverse tarsal joint impairs subtalar joint motion because for subtalar motion to occur, rotation must occur around the talonavicular joint as well as the calcaneocuboid joint. If an isolated arthrodesis of the talonavicular or calcaneocuboid joint is carried out, most subtalar joint motion is lost.25 When performing an arthrodesis around the hindfoot, sparing the talonavicular joint when appropriate usually leaves the patients with a more functional foot. The metatarsophalangeal joints also are affected by loss of motion. First metatarsophalangeal joint dorsiflexion is lost in hallux rigidus, a degenerative arthritis of the first metatarsophalangeal joint. This leads to a compensatory external rotation of the foot during gait to relieve the stress across the involved area. This compensation, in turn, can affect the alignment of the lower extremity. The theory behind orthotic use for many conditions involving the foot, ankle, knee, hip, and back is the effect it has on this linkage system within the lower extremity. Soft orthoses and compliant shoe material help absorb the impact of initial ground contact. For individuals engaged in repetitive sports, such as long-distance running, a material that helps absorb some of this impact could be beneficial if the athlete is having problems related to impact, such as heel pain, metatarsalgia, or shin splints. However, softer material paradoxically can lead to greater vertical impact when landing from jumps in an attempt to improve balance and stability.26 On a more sophisticated level, the use of a medial heel wedge, whether in the shoe or within an orthotic device, may have some influence on the rotation of the subtalar joint.27 Because at the time of initial ground contact rapid eversion

of the subtalar joint and flattening of the longitudinal arch occur, a buildup of material along the medial arch that prevents some of this rotation from occurring, in theory, would decrease the amount of internal rotation being transmitted to the lower extremity, affecting the ankle, knee, and hip. From a clinical standpoint, some patients appear to benefit from an orthotic device, although the benefit may be in part psychological.28 A runner with chronic knee pain may be helped by an orthotic device that limits eversion of the calcaneus, which, in turn, diminishes internal rotation of the tibia and affects the patellofemoral joint. Reliable data to support this theory are lacking.

C

r i t i c a l

P

o i n t s

At heel strike, the foot and ankle help absorb the force of

l

contact with the ground. l During the heel rise and toe-off phases of gate, the foot becomes more rigid, providing a stable platform for the body. l The subtalar joint links motion of the leg and foot such that eversion of the hindfoot causes internal rotation of the tibia at heel strike, and external rotation of the tibia causes inversion of the hindfoot at heel rise. l Eversion of the hindfoot unlocks the transverse tarsal joints, making the foot supple; inversion of the hindfoot locks the transverse tarsal joints, making the foot more rigid. l The muscles of the leg and foot contract both concentrically and eccentrically during the gait cycle to control the rate of ankle plantar flexion and dorsiflexion during walking and to provide stability during running. l Athletics increases the normal stresses on the foot and ankle and can lead to acute or overuse injuries.

S U G G E S T E D

R E A D I N G S

Elftman H: The transverse tarsal joint and its control. Clin Orthop 16:41, 1960. Gross ML, Davlin LB, Evanski PM: Effectiveness of orthotic shoe inserts in the long-distance runner. Am J Sports Med 19:409, 1991. Hicks JH: The mechanics of the foot: II. The plantar aponeurosis and the arch. J Anat 88:25, 1954. Isman RE, Inman VT: Anthropometric studies of the human foot and ankle. Bull Prosthet Res 10:97, 1969. Mann RA, Beaman DN, Horton GA: Isolated subtalar arthrodesis. Foot Ankle Int 19:511, 1998. Mann RA, Haskell A: Biomechanics of the foot and ankle. In Coughlin MJ, Mann RA, Saltzman CL (eds): Surgery of the Foot and Ankle, 8th ed. Philadelphia, Mosby, 2007. Nilsson J, Thorstensson A, Halbertsma J: Changes in leg movements and muscle activity with speed of locomotion and mode of progression in humans. Acta Physiol Scand 123:457, 1985. Tochigi Y, Amendola A, Rudert MJ, et al: The role of the interosseous talocalcaneal ligament in subtalar joint stability. Foot Ankle Int 25:588, 2004. Tochigi Y, Rudert MJ, Saltzman CL, et al: Contribution of articular geometry to ankle stabilization. J Bone Joint Surg Am 88:2704, 2006. Wülker N, Stukenborg C, Savory KM, et al: Hindfoot motion after isolated and combined arthrodeses: Measurements in anatomic specimens. Foot Ankle Int 21:921, 2000.


Foot and Ankle 1873

S ect i o n

B

Sports Shoes and Orthoses Andrew H. Borom and Thomas O. Clanton

There should be little surprise that an entire section of one chapter would be devoted to a discussion of sports shoes. The athletic shoewear industry has grown to such an extent that it has reached one of the pinnacles of achievement in our society—the front cover of Sports Illustrated (Fig. 25B-1).1 With this achievement, both increasing recognition from Wall Street investors and harsh criticism alleging consumer exploitation surfaced.2-4 Sports shoes became “high tech” and rode a wave of advertising to become a status symbol.4,5 Among today’s youth, the “right” shoe may vary from week to week. Athletic shoe sales rose to approach $8 billion in 1998, with fully half of that total brought in by the top two athletic shoe manufacturers. Not surprisingly, the top retailer of athletic shoes spent more on promotions and advertisements (some $163.2 million) than the next nine producers combined.6 Major shoewear manufacturers have paid six-figure salaries to high-profile athletes and coaches to endorse their products.4,7 Financial benefits from shoe contracts have become a major consideration for college athletic programs and their coaches.7 In this distorted environment, it is often difficult to wade through the hype to discover the contributions of merit in shoewear technology. This section attempts to do just that. A foundation of relatively stable information is provided to guide the reader through this subject despite the constant changes fueled by fashion trends and advertising gimmickry as well as scientific research. To understand where we are and where we are headed, some historical perspective is necessary.

A more ancient type of shoe was a hide shoe made by folding the skin or hide of a beast around the foot. This is the forerunner of what we call a moccasin, a term derived from the Algonquin Indians and introduced into English literature in 1612 by John Smith’s “Map of Virginia.”10 Examples of this form of shoe come from excavations in Denmark of early Bronze Age oak-log coffins dating to about 1000 bc.10 Although earlier examples do not appear to have been preserved, one can assume that the early hunters of the Stone and Ice Ages must have been capable of seeing the advantages of covering the foot for protection. What could be more logical than using the hide of their prey to provide a suitable foot covering? Rock carvings have provided evidence that these hide shoes were secured to the foot by lashing them around the instep and arch.10 Cave paintings found in Spain dating to 15,000 bc depict boots made of animal skin and fur.11 More recent descriptions of shoemaking from animal hides are provided in the works of Xenophon, Niebuhr, and

HISTORY The history of sports shoes parallels the history of shoewear itself. According to legend, shoes were originally designed after an Arab chief dismounted from his camel onto a thorn and declared that all the earth would be covered with leather. Seeing the error in this logic, the chief’s main advisor decided to make something that would cover just the feet. Although this makes a good story, it has not been supported by the discovery of shoes in the Fertile Crescent.8 Indeed, the earliest footwear was discovered in south central Oregon in 1932 by anthropologist Luther Cressman—a sandal made from sagebrush bark (Fig. 25B-2).8,9 This find dates back 10,000 years to pre-Columbian times, but design features indicate a much earlier origin. It supports the notion that the shoe’s primary function is to protect the sole from the hazards of the environment.

Figure 25B-1 Sports Illustrated cover indicating the notoriety of sports shoes. (Illustration by Julian Allen. From Sports Illustrated, vol 72, May 14, 1990.)


Figure 25B-2 Earliest existing footwear, dating back some 10,000 years. It is made from sagebrush bark and was found in south central Oregon by anthropologist Luther Cressman in 1932. (Photograph by Steve Bonini. Courtesy of University of Oregon Museum of Natural History and State Museum of Anthropology.)

inkerton.12-14 Examples of the bear paw used as a shoe P are seen in Figure 25B-3 from the Musée de l’Homme in Paris.10 This bear paw with claws attached could be considered the first shoe with cleats. A later development in shoewear and the second broad type of shoe is made of two components, an upper and a sole.10 These are joined together at the lower edge of the foot. The appearance of this shoe occurs in Roman times, when a hide shoe reinforced by an extra piece of sole material was used.11 Furthermore, during this time, the insole appears as a layer added for comfort and protection against chafing. These design features were a product of necessity owing to the abuse to which soldiers’ feet were subjected. Similarly, modern design features were generated to protect the athletes’ feet, particularly those involved in distance running. Because early humans were largely dependent on hunting, one can postulate that the earliest footwear was used in running. With civilization’s advancement and socialization, shoes took on symbolic functions.11 Papyrus sandals for religious ceremonies and jeweled sandals for high-fashion gatherings have been discovered in the burial holdings of Egyptian pharaohs.15 Although these have little to do with sports shoes, they do foreshadow the current specialization, trendy colors, and designs incorporated into athletic shoewear construction. Competitors in the early Greek games competed barefoot according to early drawings found on vases of that period (Fig. 25B-4).9 Inasmuch as shoemaking was a well-developed trade by this time, it appears that early athletes eschewed comfort for the presumed benefits of barefoot performance, that is, less weight, better feel for the surface, and improved traction. Robbins and Waked revived interest in barefoot running with their hypothesis that the excessive cushioning found in modern shoewear prevents appropriate sensory feedback and results in a “pseudoneurotrophic” effect.16

Figure 25B-3 Example of the bear paw shoe. (Courtesy of the Musee de l’Homme in Paris.)

Figure 25B-4 Competitors in the early Greek games competed barefoot, according to early drawings found on vases from that period. (Courtesy of the Metropolitan Museum of Art, Rogers Fund, 1914.)

Foot and Ankle 1875

The sensibility of the plantar foot is a key reason that gymnasts and dancers perform with bare or minimally shod feet. While an individual is running, plantar tactile reflexes and the intrinsic shock absorption system of the body complement one another and result in behavior modification to control load magnitude. Specifically, humans dramatically reduce impact force by altering knee and hip flexion at ground contact.16 A series of studies by Robbins and coworkers have proposed that cushioned shoes lead to negligible decreases in load because subjects decrease flexion to accommodate the instability produced by softer surfaces.15,16 A recent study demonstrated that subjects presented with a “deceptive” advertisement of the ability of a surface to cushion impact led individuals to increase the ground reaction force of a barefoot footfall when compared with a “warning” and “neutral” message. This was despite the fact that the surface was covered with an identical thickness of ethyl-vinyl acetate surfacing material.17 Although the notion that “deceptive” advertising can lead to potentially harmful behavior associated with shoewear is intriguing in light of the enormous sums spent on advertisements by shoe companies, noted authorities on running and running shoes have not been impressed with this theory of the importance of sensory feedback.18 They point out that biomechanical abnormalities such as excessive pronation, excessive Q angle at the knee, forefoot varus, and so on are the primary causes of running injuries, not a lack of sensory feedback. Furthermore, it is only with shoewear adaptations that these abnormalities can be corrected, according to these experts.18 Ironically, one of the editors of Runner’s World magazine recorded his shoewear experience over a 20-year period in a shoe diary and noted that a 5-year period of barefoot running was his healthiest period.9 There is even a Web site now that promotes the benefits of shoeless running: www.runningbarefoot.com.19 Although it is clear that Western-style shoes have contributed to many of the foot ills of modern society such as bunions, corns, calluses, and neuromas,20,21 there is circumstantial evidence to suggest that improvements in running shoe construction have reduced the prevalence of Achilles tendinitis and allowed greater numbers of average citizens to participate in the sport of distance running.9 Tracing the history of the running shoe is an enlightening look at the shoe industry itself, at the role of sports in society, and at the international trade competition surrounding sport and its premier athletes. The most thorough sources of information in this area are The Running Shoe Book, written in 1980 by Peter Cavanagh, and The Complete Book of Athletic Footwear, written by Melvyn Cheskin in 1987.9,22 Both trace the evolution of running shoes through the footraces of 16th-century fairs and the pedestrian races of the later 1800s to modern-day track and field competition. Important landmarks in this history can be picked out along the way. The turnshoe construction technique was firmly established by the 12th century. It allowed a shoe to be made with the seams on the outside and the smooth material inside next to the foot. The shoe was turned inside out to produce the finished product.9,22 By the 14th century, shoe construction had incorporated small strips of leather called welts to allow a replaceable outsole to be added to the upper.23 Since the 14th century,

shoemaking has been fairly standardized, with shoes consisting of the following: 1. Two parts: upper and lower 2. Four processes: cutting, fitting, lasting, and bottoming 3. Eight tools: knife, awl, needle, pinchers, last, hammer, lapstone, and stirrup24 With the Industrial Revolution, the craft of shoemaking went from an in-home trade to a model of manufacturing method with the use of machines and mass production. Entire books have discussed the significance of this method to the development of industry in the United States.25,26 Leather was the mainstay of shoemaking throughout this period and continued as such into the 1900s. A change in shoemaking and the origin of the sneaker were presaged by the first patent, granted in 1832, for attaching rubber to the sole of the shoe. Unfortunately, the material was too unstable and lacked durability.11 In 1839, Charles Goodyear’s vulcanization process turned rubber into a usable material, but it was more than 100 years before rubber replaced leather as the most desirable outsole material for running shoes.9 Cavanagh cites the development of the Spencer shoe, a spiked shoe found in England’s Northampton Museum, as the 1865 precursor of modern track shoes (Fig. 25B-5).9 This shoe shows the separation of running shoes into a line separate from street shoes, although a spiked shoe used for cricket was patented in England in 1861. Spiked shoes were used in the short races popular in that day. Longer distances became popular in the latter part of the 19th century. Races around circular tracks for 144 straight hours became a spectator event imbued with international flavor. These pedestrians, as the participants were called, wore high-top leather boots and thick wool socks reminiscent of combat boots used in the military. Although pedestrian races faded in popularity, long-distance racing gained an audience,

Figure 25B-5 The Spencer shoe, a spiked shoe found in England’s Northampton Museum, was the 1865 precursor to modern track shoes. (Courtesy of the Northampton Museum, Northampton, England.)


and the Olympics were reborn in Athens, Greece, in 1896. A marathon was included as a race of 40 km to commemorate the legend of Pheidippides. Cavanagh marks this Olympic race as the impetus for development of the distance shoe, or training shoe, we use today.9 The popularity of the marathon prompted the Spalding Company to introduce a long-distance shoe for the general public in 1909.9 Three shoes were advertised, two being high-tops (Fig. 25B-6). They had leather uppers and rubber soles and were priced at $5 to $8. A retired shoemaker named Richings began custom making a shoe for distance runners near the 1930s that predated the custom shoewear used by elite athletes of our day.9 By the early 1900s, production of running shoes was in full swing, and the 1915 Spalding catalog advertised shoes for sprinting, middle-distance running, jumping, and pole-vaulting (Fig. 25B-7).22 Competition entered the scene at about the same time when Sears Roebuck entered the catalog shoe sales market and began the continuing controversy over who makes the best running shoe.22 Endorsements by famous athletes were seen much earlier, but notable shoes were the Kiki Cuyler, Jr., basketball shoe and the Chuck Taylor AllStar shoe. We continue to see society’s ongoing enchantment with famous athletes and their shoewear, as evidenced by the incredible popularity of the “Air Jordan” and “Bo Knows” campaigns of the Nike shoe company in the late

1980s and early 1990s. Despite recent cuts in advertising budgets for most of the major shoe manufacturers,27 the fact that basketball shoe sales alone are responsible for as much as 25% of total athletic shoe revenue28 ensures that certain National Basketball Association stars will expand their talent into marketing. A shoe designed for sports alone did not come into existence until the latter half of the 19th century. Croquet was a popular recreation during the Victorian period, and a croquet sandal appeared during this time.11 Known as the sneaker, it was in use by the 1860s and had a fabric upper, a rubber sole, and laces.9,11,29 Further sports development in the late 1800s spawned the need for durable but lightweight shoes with variable traction requirements depending on the playing surface. Wilcox provides several illustrations of these specialized sports shoes of the late 1800s in his book, The Mode in Footwear (Fig. 25B-8).29 From these developments, we can trace the roots of the multibillion-dollar sports shoe industry and can conclude that the protection of our feet and fashionable design have always been important concerns of humankind. From this foundation, an explosion occurred in sports-specific footwear that has provided us with today’s shoes for basketball, rock climbing, tennis, snowboarding, soccer, gymnastics, fishing, rollerblading, skating, jumping, sprinting, and so forth (Fig. 25B-9).

Figure 25B-6 Long-distance shoes introduced by the Spalding Company for the general public in 1909. (From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.)

Figure 25B-7 Page from the 1915 Spalding catalog advertising shoes for sprinting, middle-distance running, jumping, and pole-vaulting. (From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.)

Foot and Ankle 1877

ANATOMY OF THE SPORTS SHOE Just as the anatomy of the human body is the basis on which the surgeon’s skill rests, the anatomy of the sports shoe is critical to those who must understand athletes and their injuries. Although the process of shoe manufacturing has evolved into a multibillion-dollar industry, the basic shoe remains the same. This section first looks at the anatomy of the basic sports shoe and then discusses the shoe features unique to particular sports. The actual manufacturing process is discussed briefly.

Most of what has been written about athletic footwear has concentrated on shoes designed for the runner. Therefore, the prototype shoe for this section is the running shoe, and shoes for other sports are described in similar terms with specific modifications. Figure 25B-10 illustrates the components of the shoe. For the sake of simplicity, the shoe can be broken down into two basic components: the upper and the bottom. The upper covers the foot, whereas the bottom cushions it and provides the interface between the foot and the surface. These two basic components are then subdivided into

Man’s summer sport shoe, Balmoral style, white canvas with leather 1879

Polo ankle boot (today called Chukkar or Jodhpur) 1850s

Gentleman’s riding boot 1850s Man’s buckled hunting boot, gaiter style, leather and cloth, protruding rubber insertion in heel 1850s

Man’s gymnastic shoe, eyelets halfway, hooks to top, calf or canvas 1890s

Man’s hunting shoe in Blucher style with toebox and tongue of heavy calf 1885

Sports shoe worn hunting, striped fabric and leather 1850s

Football player’s shoe, veal calf and leather thongs 1912

Cyclist’s boot of calf or canvas and leather 1910

Figure 25B-8 Illustrations of specialized sports shoes of the late 1800s. (Adapted from Wilcox RT: The Mode in Footwear. New York, Charles Scribner and Sons, 1948.)


Figure 25B-9 Photograph from typical shoe store with wall of sport-specific shoes in all varieties. (Photograph by Andrew Borom.)

their various parts. The upper is composed of toe box, toe cap, vamp, quarter, saddle or arch bandage, eyelet stay, eyelets, throat, tongue, collar, Achilles tendon protector, heel counter, foxing, forefoot and rearfoot stabilizers, and lining. The bottom consists of sockliner or insole, insole board, midsole, wedge, and outer sole. Although some of these names differ from those used in traditional shoemaking, the actual construction of a sports shoe does not vary remarkably from the traditional shoe manufacturing process (see Glossary in Box 25B-1).

To understand the shoe itself, it is necessary to review the steps by which the shoe is made. Integral to this process is the last (from the Old English laesk, meaning sole or footprint), which acts as an artificial foot form.22,30 This allows the shoe upper to be created in the proper shape, size, and dimensions. Important measurements with respect to the last are the toe pitch or toe spring, the girth, and the heel height or pitch (Fig. 25B-11).22,31 The variation in toe spring and heel height can affect the movement of the foot by improving or impairing the rocker action of the foot during gait.31 Shape is also a critical consideration in analyzing the form for the last of a shoe. This shape can be either straight-lasted or curve-lasted depending on the amount of inward curve built into the last. Because most feet have a slight inward curve, the curved type of last provides better comfort and fit for most feet. The curved last allows the most shoe flexibility and is particularly well suited to the athlete with a highly arched or cavus foot. When the last is straighter, it translates into better medial support for the foot and is best suited to the flatter foot or to the person with an overpronated foot. Figure 25B-12 depicts the difference between straight and curved lasts. Sports shoe manufacturers use a curve of about 7 degrees in a curved last.22 Variations exist now as slightly curved and semicurved lasts. As we examine the last, the next consideration is the shape of the toe box. The various alternatives are depicted in Figure 25B-13.22 It is clear that this feature has an important bearing on fit and comfort. The best example of this is the need for the athlete with clawing in the toes or even a single hammer toe to have a toe box of sufficient height to prevent chafing. Text continued on p 1886.

Tongue Achilles tendon Collar protector Lining Throat Eyelet Eyelet stay Vamp Toebox

Heel counter (under foxing) Upper

Foxing Sock liner or insole Rearfoot stabilizer Midsole with wedge

Bottom

Outsole Rearfoot stabilizer

A

Quarter Stabilizing straps

Toecap

B Lining Sock liner or insole

Heel counter

C

Wedge

Outsole

Midsole

Insole board

Figure 25B-10 Illustrations of athletic shoes. A, Overview of external appearance. B, Separation of shoe into component parts. C, Sectional view of interior of shoe.

Foot and Ankle 1879

Box 25B-1 Glossary of Foot and Shoe Terminology* Abduction: To move away from the midline of the body. Achilles notch: A depression cut into the back of the heel collar to provide a secure fit and prevent irritation of the Achilles tendon. Adduct: To move toward the midline of the body. Adduction: Moving a part toward the midline of the body. Adhesive (cement): Substance capable of holding materials together by surface attachment. Air: First introduced in 1979, Nike’s cushioning concept of encapsulated air units in the midsole isn’t actually air, it’s Freon. Depending on the model, the air units may be in the heel or forefoot, or both. Air ball: An air-pressurized ball imbedded in the heel of HiTec Badwater models for additional shock absorption. Anatomical: Pertaining to the structure of the body. Anatomical last: A stabilizing footbed contoured in such a way that the heel sits down in the midsole, rather than resting atop a flat platform. Developed and used extensively by Turntec. Anatomy: The study of the structure of the body and the relationships between its parts. Anterior: Front portion. Anterior heel: Type of metatarsal bar, also known as Denver bar or Denver heel; the apex coincides with the posterior edge under the posterior half of the metatarsal shafts. ARC: Avia’s stabilizing system, which is made of plastic in one of two configurations. Placed in the rearfoot, the “fingers” of the ARC spread out on impact to absorb shock and stabilize the foot. Arch bandage: Reinforcing strips of fabric stitched inside the shoe on the medial and lateral quarters. Arch cushion (cookie): Support pad for the medial arch of the foot. Asymmetric: In shoemaking this applies to lasts and patterns that have uneven shapes, the right side different from the left. ATP (heel horn): Extended padding at the back heel collar to protect the Achilles tendon (Achilles Tendon Protector). Autoclave: Vessel or oven in which chemical reaction or cooking takes place under pressure such as in the vulcanizing construction method. Axis: A reference line for making measurements. Ground reaction forces are usually evaluated relative to a set of three orthogonal axes: vertical, longitudinal (direction of motion), and transverse (right angle to direction of motion). Backpart (rear foot): Portion of the last extending rearward from the break of the joint to the back of the last. Backpart width: The width of the heel end measured parallel to the heel featherline plane at a specified distance from the heel point. Bal (Balmoral): Front-laced shoe in which the meeting of the quarters and the vamp is stitched or continuous at the distal end of the throat. Bal is the abbreviation of Balmoral, the Scottish castle where this style was first introduced. Ball: Widest part of the sole, at the metatarsal head. Ball girth: Circumference measure around the last encompassing the first to the fifth metatarsal area.

Bar, comma: Comma-shaped bar wedged laterally and posteriorly, also known as Hauser. Bar, Denver: See Anterior heel. Bar, Jones: Metatarsal bar placed between the inner sole and outer sole. Bar, Mayo: Metatarsal bar with the anterior edge curved to approximate the position of the metatarsal heads. Bar, metatarsal: Rubber, leather, or synthetic bar applied transversely across the bottom of the sole, with the apex immediately posterior to the metatarsal heads. Bar, rocker: Sole bar having its apex beneath the metatarsal shafts causing rocking instead of flexing action. Bar, Thomas: Narrow metatarsal bar with abrupt anterior and posterior drop-offs. Bar, transverse: See Bar, metatarsal. Base plane: The plane to which the last in its proper attitude is referenced for the purpose of defining certain terms. Bias cut: Cut away upswept heel. Bilateral: Affecting both right and left sides. Biomechanics: The study of the internal and external forces acting on the human body and the effects produced by these forces. Blind eyelet: A metal or plastic eyelet concealed beneath the top surface of the shoe leaving only a small, rimless hole. Blown rubber: The lightest kind of rubber outsole material. As the outsoles are manufactured, air is injected into the rubber to lighten and soften the outsole. Few outsoles today are made with full blown rubber because it lacks durability, but many outsoles have blown rubber in the forefoot and midfoot for lightness and a harder carbon rubber in the high-wear area of the heel. Blucher: Front-laced shoe in which the quarters are not attached distally to the vamp, giving more allowance at the throat and instep in fitting. Opposite of bal style. Front quarters or tabs are stitched over the vamp for a short distance at the throat. Board last: One of three ways shoes are constructed. A fully board-lasted shoe is constructed by gluing the upper to fiberboard before it is attached to the midsole. Board lasting promotes stability and provides a good platform for orthotics but lacks flexibility. Few new models are fully board lasted. (See combination last and slip last for information about the more common types of last.) Boot, high top: High quarter shoe in which the quarters cover the malleoli. Bottom: The sole up to the breast of the heel. On a wedge sole, the term covers the complete sole. Bottom filler: Material that fills the cavity between the outer and inner soles. Bottoming: The operation of attaching the completed sole to the upper. Bottoming out: When the midsole material has worn out and is too soft relative to a runner’s size, it compresses too quickly, which results in compromised shock absorption and support. Box toe: Hardener used to maintain shape of front toe area. Continued


Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Break: Flex point or path; creasing formed at the vamp when the shoe is dorsiflexed. Breastline: An arbitrary line defining the forward boundary of the heel seat. Breathability: The ability of a material to absorb and ventilate foot moisture; not to be confused with porous. Bumper: Rubber toe strip attached over front toe area. Calfskin leather: Leather made from the skin of calves. Cantilever: A concave outsole design in which the outer edges flare out on impact to dissipate shock. Used extensively by Avia. Carbon rubber: The most durable kind of rubber outsole material. It’s a solid rubber with a carbon additive that makes the material stronger. If an outsole is not full carbon rubber, it probably has a carbon-rubber heel pad. Celluloid: A thermoplastic material. Cellulose: Natural polymeric. Cement process: Construction stuck-on bottoming method. Center of pressure: An outsole design in which the middle area is bordered by an elevated tread pattern along the outer rim to promote stable footing. This also makes for a lighter shoe by exposing the midsole and eliminating unnecessary outsole material in the center. Used in some Nike, Diadora, New Balance, Hi-Tec, Avia, and Adidas models. Certified pedorthist: One who is certified by the Board for Certification in Pedorthics (BCP). Chainstitch: Sewing method used for stitching uppers to soles. Chukka: Three-quarter Blucher boot with two or three eyelets or a strap with a buckle. Circular vamp: Design vamp extended from toe to heel breast. Coefficient of friction: A number between 0 and 1 indicating the slip resistance of a material such as a shoe sole on a particular surface. The greater the value, the less likely any slipping. Collar: Top line of the shoe quarters. Many are padded. Narrow strip of material stitched around the proximal edge of the quarter. Combination last: Last with wider forepart and narrow heel fitting. Indicates the shoe is board lasted in the rearfoot for stability, but slip lasted in the forefoot to promote flexibility. Remove the sock liner of your shoe; if it is combination lasted, you will find a fiberboard in the rearfoot and stitching in the front. The last deviates from standard proportions, usually to accommodate feet with narrow heels. Compaction: Permanent flattening and deformation of sole material (bottoming out). Composition: Scraps that are pulverized, compressed, and held with a binder to form a sheet material for insoles, midsoles, heel bases, and other components. Compression deflection: The amount of deformation observed in a material after it has been subjected to a compressive or impact load. Compression mold: Shaping materials by heat and pressure.

Compression set: The amount of permanent deformation observed in an unloaded material following a single or multiple load application. Conformability: Ability of a material to mold itself to the shape of the foot. Contact face: The surface brought into contact with another surface or object. Contoured midsoles: Similar to anatomic lasts, contoured midsoles are shaped to the foot. This promotes stability. Contour insoles: Foam insoles capable of retaining pressure pattern of the foot. Cookie: Arch pad in shoe; wafer-shaped longitudinal arch support. Copolymer: A natural or synthetic compound. Cordovan: Leather not made from hide or skin but from a ligament-like shell found under the buttocks of animals such as the horse, mule, and zebra. Often referred to as a “shell” and tanned in a burgundy (cordovan) color. Cork: Made from the bark of the cork tree, which may be combined with other materials. Available in various forms such as sheet cork, natural cork, cushion cork. Different names are given to the cork according to the binders used. Corrective shoe: Shoe with special features designed to help correct some type of foot disorder. The term has been displaced by other terms such as a prescription shoe or a modified shoe. Corset, ankle: Reinforcement to preserve the shape of the quarter’s counter. Laced fabric within the shoe intended to retain the hindfoot on the inner sole. Counter, long lateral: Counter extended anteriorly beyond the breastline on the lateral side. Counter, long medial: Counter extended anteriorly beyond the breastline on the medial side. Counter (pocket): See Heel counter. Crepe rubber: Natural rubber soling material; latex rubber compounded for use as soles and heels. Crest, toe: Convex cushion under the plantar phalangealsulcus. Curved last: Refers to the shape of a shoe. Curve-lasted shoes are shaped somewhat like a banana and offer less medial (inner) support but greater foot mobility. Generally, curved-lasted shoes are for biomechanically efficient, faster runners who want a responsive shoe. Cushioning: The ability to absorb shock. Because a runner generates a force of about 3 times the body weight on impact, this is a crucial shoe characteristic. Cushioning is primarily a function of the midsole. Custom shoes: Shoes made to the customer’s specifications. Dellinger web: Embedded into the midsole of some Adidas models, the Dellinger web is a fabric that maintains the durability of the midsole. Designed by University of Oregon coach Bill Dellinger. Denier: Weight of synthetic fibers (measure of fineness). Density: Weight per unit volume of a substance. The measure of the firmness of the midsole material. Many shoes have midsoles of varying densities. For example, a two-density EVA midsole will usually have the firmest material (designated by a darker color) on the medial side to control pronation.

Foot and Ankle 1881

Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Derby: Design quarters overlapping vamp and tongue. Design: Pattern or cut of upper. Die cutting: Cutting of upper or sole materials with metal dies. Differential loading: The application of forces of varying magnitudes. Dip construction: Direct injection process. Distal: Part farthest from the central portion of the body. Dorsal: Top of foot, the upper surface of the foot. Dorsiflexion: Moving the toes up toward the distal end of the foot toward the leg. Doubler: Interlining placed between the vamp and vamp lining for additional reinforcement; interfacing between upper material and lining. Drop-off: Anterior vertical edge of a metatarsal. Duo process: Method of upper assembly construction by cementing instead of stitching edge. Durometer scale: A method of determining material hardness on a scale of 0 to 100, with lower readings indicating softness. Dutchman: Lateral sole wedge. DVP: Direct vulcanizing process. Elasticized material: Resilient fabric used for goring in panels and inserts for shoe uppers. Elastomer: Term used for synthetic rubber. Electrodynograph: An instrumentation system consisting of individual sensors to measure pressure at selected locations on the bottom of the foot. Electromyography: The measurement of the electrical activity associated with muscular contractions. Elevation: Material added to the entire sole or heel. Elvalite: A new foam developed by DuPont that’s being used as a midsole material in some Reebok models. Elvalite has the cushioned feel of EVA but is more durable. Elvaloy: Resin modifier added to PVC. Embossing: Depressing a specific pattern in leather or fabrics. EVA: Ethylene vinyl acetate (EVA) is the most common midsole foam used in running shoes. Compressionmolded EVA is heated and compressed into the shape of the midsole. It is light, resilient, and has good cushioning properties. Nearly every running-shoe company uses EVA in at least some of its midsoles. Eversion: Turning out the plantar aspect of the foot from the midline of the body. Evert: To turn out the plantar aspect of the foot so that it faces away from the midline of the body. Exercise physiology: The study of the effects of exercise on the biochemical function of the body and its parts. Expanded vinyl: Soft, nonbreathable PVC (stretchy base) material (as opposed to nonexpanded vinyl: harder, nonbreathable [rigid base] material). Extended eyestay: A design wherein the eyestay is extended to form the toe cap. External: Outer part; lateral. External heel counter: A rigid, plastic collar that wraps around the heel of the shoe for support and to control pronation.

Eyelets: Holes for lacing (blind) with metal reinforcements or eyelet hooks. Eyestay: Reinforcement around lacing holes. Fabric: Woven or nonwoven flexible material. Feather edge: Last bottom profile. Finish: Coating on leather or synthetic material. Finishing: End of manufacturing process. Flanging: The edge where the upper is turned outside for attachment to outsole or midsole. Flare: Widened heel or sole base. Flared heel: Wider flanged heel for landing. Flex: To bend. Flex grooves: Strategically placed ridges in the midsole of the forefoot that make the shoe more flexible at toe-off. Flexibility: A shoe’s ability to bend; the rigidity of the shoe bottom composite usually evaluated in the forefoot region of the shoe. Flex path (break): Girth area at the main metatarsal of foot, which must flex as foot pushes off from ground. Flexion energy: The energy required to bend a shoe or object through a flexion cycle. Flow molding: The construction method of molding PVCcoated materials as an exact replica of original uppers. Footbridge: A stability device. As used by Nike in the Air Structure and Air Span II, the footbridge is molded into the midsole across the rearfoot. Reebok uses a footbridge in its Ventilator, but it’s placed under the arch on the medial side. Asics uses a variation of the footbridge in the Gel-MC. Footframe: An extension on top of the midsole or an additional piece that cradles the foot for added support and prevents the foot from rolling over. Force: A pushing or pulling effect that produces motion or deformation of an object or material. Forefoot stability strap: A leather or plastic overlay on both sides of the ball area of the shoe that reinforces the upper and offers stability and support. Forepart: Area of foot from the ball to the toe; portion of the last extending from the ball to the toe. Forepart centerline: The best line of symmetry of the forepart bottom pattern. Frontal plane: The vertical plane that passes through the body dividing into a front and a back half. Functional anatomy: The study of the effects of body structure on performance. Functional shoe: Shoe designed to serve a specific purpose. Gait laboratory: A testing lab equipped with specialized equipment for the study of walking and running. Gel: The primary cushioning system used by Asics in all of its performance shoes. It is a pad of silicone in the midsole, which, depending on the model, is found in the heel or the forefoot, or both. Geometric last: Last using a geometric rather than the traditional arithmetic grading system. Intended for better shoe fit and to facilitate automated manufacturing. Girth: Circumferential dimension measured around the last; widest part of the last. Continued


Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Goniometer: An instrument used to measure angles. It can be employed to evaluate motions of the joints, particularly the knee and ankle joints. Goodyear welt: Construction method of stitching uppers to sole; shoemaking process in which the joining of the upper, inner sole, and outer sole is accomplished with a welt. Goring: Elastic fabric inserted in the front or sides of an upper, the expansion of which allows a larger opening to insert the foot. Grade increment: The change per size and shoe width of any last dimension. Grade rate: The ratio of the change in girth per size to the change in length per size. Grading: Method used by designers to size original patterns. Heel breast: Anterior margin of heel; front face of the heel or anterior portion at the shank. Heel counter: A firm, usually plastic cup that is encased in the upper and surrounds the heel. It controls excessive rearfoot motion. It may be notched to accommodate the Achilles tendon. Heel counter pocket: Rearpart upper material pocket containing heel stiffening material. Heel curve: A side-view profile of the back end of the last from the top of the last to the heel seat or featherline. Heel curve angle: Angle between the heel featherline plane and heel point 2½ inches (63 mm) up from the heel point intersecting the heel curve. Heel elevation: Modification measured in a vertical line at the center of the heel; the vertical distance between the base plane and the heel point is the heel elevation. Heel featherline: A line that defines the heel seat shape. Heel height: Vertical measurement from the plantar surface to the heel seat at the anterior surface of the heel, usually in increments of eighths of an inch. 1. Spring heel, 3⁄8 to 6⁄7 inch; heel base lies under the outer sole eliminating a definite heel breast. 2. Flat heel, 6⁄8 to 10⁄8 inches. 3. Military heel, 10⁄8 to 13⁄8 inches. 4. Cuban heel, 13⁄8 to 14⁄8 inches. 5. Wedge heel, 4⁄8 to 14⁄8 inches; slopes upward from ball to posterior heel. Heel pad: Resilient material to cushion or raise the heel. Heel pitch: Slant at the posterior aspect of the heel; amount of rise at back of last when last is held level. Heel plug: Found in multidensity outsoles, where the most durable rubber is placed in the high-wear area of the heel. Heel point: The rearmost point of the heel featherline. Heel seat: Area of the shoe upon which the foot rests; the bottom surface of the heel end of the last from the breast line back. Heel seat width: The greatest width of the heel seat measured from featherline to featherline perpendicular to the heel centerline. Heel, Thomas: Heel with anteriorly curved medial border. High cut: Over the ankle shoe design.

Horizontal plane: See Transverse plane. Hytrel: A resilient and durable polymer plastic developed by DuPont and used for a variety of shoe components by several companies. It’s most commonly used as forefoot support straps. IMP (injection): Injection molding process form of shoe construction (see also Lasting insole). Inflare: Asymmetric inward swing of last shape; last or shoe whose forepart provides more medial than lateral surface area. Injection molded: Shoe construction whereby a heatsoftened plastic is injected into a mold, then compressed against the mating surface of a concentric mold and allowed to cool and harden. Inlay: Prefabricated removable material upon which the foot directly rests inside the shoe. In some shoes, the inlay is an integral design component. Inner sole: Material conforming to the size and shape of the last bottom upon which the foot rests (see also Insole). Insert: A type of orthosis, although the term has been used interchangeably in some circles with inlays and insoles to designate an off-the-shelf device placed inside the shoe. The Health Care Financing Agency defines it as a total contact, multiple-density, removable inlay that is directly molded to the patient’s foot or a model of the patient’s foot and that is made of a suitable material with regard to the patient’s condition. Inserts: Metal threaded retainers for spikes or studs. Insole: Integral design component (layer) of the shoe that is the shoe’s structural anchor to which is attached the upper, toe box, heel counter, linings, and/or welting. Instep: Medial inside arch area of the shoe. Instep: Portion of the upper over the midfoot. Instep girth: The dimension around a last passing through the instep point. Interface: The surface forming the common boundary between two bodies or spaces. Internal: Inner part; medial. Inversion: Turning the plantar aspect of the foot in toward the midline of the body. Invert: To turn in the plantar aspect of the foot so that it faces the body’s midline. Ionic cushioning: Pillars of polyurethane in the midsole used by Saucony to add durability. Ionomer resins: A family of thermoplastic resins. Iron: Dimension used for measuring sole thickness, 1⁄48-inch; thus a 6-iron sole is 1⁄8-inch thick. Isoprene: Fundamental rubber molecule. Joint girth: The greatest dimension around the last passing through the break joint. Kinematics: The science of pure or abstract motion. Kinetic energy: Energy associated with motion. Lace locks: Plastic devices on the upper that maintain tension on the laces. Lace stay: Portion of the upper containing eyelets for lacing. Lace-to-toe: Low- or high-quarter shoe laced to the toe; a design in which the eyestay is extended down to the toe box area.

Foot and Ankle 1883

Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Last: Three-dimensional facsimile of the foot; model approximating the shape and size of the weight-bearing foot, made of wood or plastic, over which a shoe is formed. The shape of the last determines the shape of the shoe. The straighter the last, the greater the medial support. Generally, faster, lighter runners who need less support prefer curved-lasted (or semicurved) shoes. Runners who need maximal medial support and those who overpronate opt for straight or slightly curved shoes. Last bottom centerline: A line defined by the toe and heel point. Last bottom featherline: A line that defines the bottom shape of the last (last bottom pattern). Last bottom width: The width across the ball area of the last bottom at its widest point. Lasting: Fitting and shaping of the upper to the last. Lasting allowance: Extra material on shoe patterns to fit around and under the bottom edge of the last. Lasting insole: An insole used to attach an upper to an insole before bottoming; the bottom surface of the upper. Lasting margin: See Lasting allowance. Last joint break: Point located at the intersection of the shank and the forepart, tangent to heel point and perpendicular to last centerline. Last systems: Methods of sizing last dimensions: Arithmetic, Geometric, Dynametic, Europoint. Lateral: Outer side of the foot or limb; the side away from the midline of the body. Leather: Material created by tanning a hide or skin. Length: Dimension on the center of the last bottom from toe point to heel point. Levy mold: Full-length inlay that conforms to contour of the plantar foot. Lightweight trainer: A training shoe that weighs less than 10 ounces. It can be used for training or racing, but it’s not as durable or supportive as most training shoes. Lining: The inside backing material for uppers. Lockstitch: A method of sewing the upper to the bottom. Long heel girth: The dimension around a last passing through the instep and heel featherline point. Long heel plate: A sheet metal bottom surface extending from the heel to midway of the shank area. Longitudinal arch: Curvature of hind and midfoot. Longitudinal force: The force generated in the direction of motion by a walker or runner during foot contact and related to the slip characteristics of a shoe. Also referred to as the anteroposterior force. Low cut: Below the ankle shoe design. McKay: A shoe construction method that uses tacks and a stitched sole; the upper is tacked, stapled, or cemented, and the sole is attached with chainstitches. MCR: Microcellular rubber. Medial: The side closest to the midline of the body; inside area of the foot. Memory: The speed and extent to which a material recovers to its original shape after load compression. Mesh: Woven or knitted nylon material for uppers.

Metatarsal pad: A soft wedge of material placed under the ball of the foot to add shock absorption and comfort for forefoot strikers. Metatarsals: The long bones of the foot between the toes and ankle. Midsole: The layer of material between the upper and outsole. It’s the most important component of the shoe because it provides most of the cushioning. The midsole is usually made of EVA or polyurethane or some combination of the two. Moccasin: A method of construction whereby the upper is placed under the last and extended up and around to form the quarter and vamp. Modification: Alteration, change, or addition. Mold, mould: That which is shaped, molded, or formed; a cavity used to shape plastic or rubber by pressure and heat. Molded shoe: Shoe made from a model of the foot. Monk strap: Shoe with a wide buckled strap across the instep. Motion analysis: The analysis of total or partial body movements for the purpose of better understanding how the body functions. The analysis is usually done in conjunction with high-speed filming and computers. Motion control devices: Materials and designs that control the inward rolling (overpronation) of the foot. Nap: The surface pile or layer of textile fabric. Negative heel: Heel with plantar surface lower than the ball of the shoe. Neoprene: Synthetic, rubber-like material, very durable, used for outsoles, heels, and other components; oilresistant; an elastomer, polychloroprene. Neutral position: The most efficient functional position for the foot producing the least amount of stress on the joints, ligaments and tendons. Open toe: Shoe design with no front center seam. Orthopaedic shoe: Shoe designed with features to accommodate or reposition foot abnormalities. Orthosis: Corrective device that is used to protect, support, or improve function of parts of the body that move. Outflare: Last or shoe whose forepart provides more lateral than medial surface area. Outsole: Bottom, ground-contacting portion of the shoe; the black material on the bottom of the shoe that strikes the ground. Carbon rubber is the most common outsole material because it is firm and resilient. Blown rubber has a more cushioned feel but is less durable. Oxford: A shoe design with a laced, low-cut shoe; low quarter-laced shoe. Pad: A device placed inside a shoe to provide support or relieve pressure from a specific location such as a longitudinal arch pad or a metatarsal pad. They are made of various materials and come in a variety of shapes and sizes. Pattern: The cut-out pieces making up the design of the upper. Pedorthics: Allied health profession concerned with the design, manufacture, fit, and modification of footwear and related appliances. Continued


Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Pedorthist: Practitioner of pedorthics. Phylon: A foam similar to EVA and the name of the midsole material that Nike uses in several models. Hi-Tec also uses Phylon in one model. Pivot point: The rotation area on sole under ball of foot. Plantar: The bottom or sole of the foot. Plantar flexion: The downward movement of the toes or distal end of the foot away from the leg. Plastic: Synthetic material or human-made polymeric substance, excluding rubber. Platform: Elevated sole. Polyethylene: A thermoplastic material or ethylene. Polymer: A molecular compound, natural or synthetic. Polypropylene: A tough lightweight plastic. Polystyrene: A transparent thermoplastic. Polyurethane: A synthetic rubber that’s a common midsole material. It is firmer, heavier, and more durable than EVA, but it’s not as cushioned. Polyurethane is often used with EVA in many popular models, such as the Nike Air Pegasus, Avia 2200, and New Balance 997, with the polyurethane in the rearfoot for firmness and durability and the EVA in the forefoot for flexibility. Polyurethane resins: A family of resins from which polyurethane is produced. Polyvinyl: A semirigid plastic used for some heel counters. Polyvinyl acetate: A thermoplastic material. Polyvinyl chloride: Thermoplastic material with various applications such as soles and heels and as a coating for uppers and linings. Porous: Material having pores. Posterior: Behind, back. Posting: The use of a firmer material (usually midsole material) to slow foot motion in the rear or middle of the midsole. Posting is usually used to limit overpronation. Potential energy: Energy associated with position. Prefabricated: A sole unit built from more than one layer. Prescription: Legal order, requesting specific treatment, signed by a medical doctor, podiatrist, or osteopath. Prescription shoe: Footwear prescribed by a medical practitioner, either stock or custom-made. Prewelt construction: Shoe construction in which the upper and welt are joined by chainstitches, the insole and upper are cemented, and the outer sole is lockstitched to the welt. Pronation: A complex multijoint action of the foot that is usually estimated from the inward rotation of the heel relative to the leg producing the inward rolling motion that takes place in the foot and ankle joint following footstrike during running; a triplane motion of the foot or part of the foot that consists of simultaneous movements: abduction, dorsiflexion, and eversion; basically, a movement away from the midline of the body, up and out; lowering the medial foot arch; the opposite of supination. Nearly all runners pronate to some degree, or should. If the foot rolls too far inward, however, injuries can result. Overpronation, or the extreme inward roll of the foot, places a strain on tendons and ligaments.

Proportional last: Last with geometric, rather than arithmetic, grading that conforms better to proportional size increments. Prosthetic foot: An imitation foot closely resembling the shape, texture, flexibility, and weight of a human foot. Used in testing procedures. Proximal: Closest to a reference point such as the center of the body. PU: Polyurethane (cellular plastic). Pump: Low-cut shoe not built above the vamp line and usually held onto the foot without fastenings. Push rod: A rod that functions in conjunction with a cam to open or close valves. PVC: Polyvinyl chloride (plastic material). Quarter: Posterior aspect of the upper; the major pattern piece making up the sides of the upper. Rearfoot stability: The ability of the shoe to control foot pronation during the initial 40% to 50% of the support phase. Resiliency: The ability to regain quickly the original shape (return energy rebound). Resin: Solid organic products of natural or synthetic origin. Ridge: A well-defined intersection of the wall and the conical section of the forepart. Rigid shank: Firm, stiff, inflexible area of the shoe between the heel breast and ball. Rocker bar: See Bar, rocker. Rocker bottom: See Bar, rocker. Rubber: An elastomer or natural rubber compound; resilient natural or synthetic material. Running machine: A piece of equipment, used to test shoe characteristics, that simulates the actions of running on a shoe. Sagittal plane: The vertical plane that passes through the body from back to front dividing it into a left and right half. Seam: Sewing that joins together pieces of the upper. Semi cut: A design cut just on or over the ankle. (Also called three-quarter cut.) Shank: The reinforcement under the arch between the heel and the sole; the bottom area of the last between the breastline and the joint break. Shank piece: Rigid reinforcement of the shank. Shank plug: A metal piece inserted in the shank in order to clinch metal shank fasting staple. Shearing force: A force that causes or tends to cause two parts of a body to slide relative to each other. Shoe size: Prewalkers: 3000-4 Big boys: 5½-11 Infants: 1-8 Growing girls: 3�� ½�� -10 Children: 8�� ½�� -12 Men: 6�� ½�� -16 Misses: 12�� ½�� -4 Ladies: 4-13 Youths: 12�� ½�� -4 Boys: 3�� ½�� -6

Foot and Ankle 1885

Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Silicone: A slippery polymeric material used in treating shoes for water repellency. Skive: The thinning down of edges of leather or poromeric material; to cut in thin layers or to a fine edge. Slip last: The most flexible type of shoe construction. With a slip-lasted shoe, the upper is stitched together like a moccasin and glued to the midsole. Slip lasting allows for a better fit. Lasting method whereby a closed upper is formed before being stretched over the last. Sneaker: The American name for vulcanized, canvas rubber shoe. Sockliner: The material (regularly called an insole) inserted between the foot and lasting insole next to the foot; material covering the dorsal surface of the inner sole. Sole: Bottom or ground contact area of footwear. Sole leather: Heavy leather, usually cattle hide that is dryfinished and used for outer soles. Speed lacing: A lacing method that uses D-rings. Splint, Denis-Browne: Rigid bar between both shoes used to abduct the feet. Splint, Friedman-counter: Flexible strip attached to both counters; used to limit internal rotation. Split: The flesh or the underside of the leather hide after the grain side has been removed. Split leather: See Sole leather. Stability: The ability of the shoe to keep the foot moving in a forward direction, rather than allowing for excessive side-to-side movement. Stabilizer: An ingredient used in formulating elastomers and synthetics. Standard deviation: A standard measure of dispersion of a frequency distribution around the average value. A distribution is typically made up of 3 standard deviations on either side of the average value. Stitchdown: A method of sewing the uppers to the bottom. Straight last: A last that is relatively straight on the medial side to add stability. The straighter the last, the greater the medial support. 1. Form for constructing a shoe that can be worn on either foot. 2. Form for constructing a shoe in which the medial border approximates a straight line. Studs: Large knobs protruding from the sole. Suction cups: Indentations on the outsole that provide traction on smooth surfaces. Supination: A triplane motion of the foot or part of the foot that consists of simultaneous movements: adduction, plantar flexion, and inversion; basically, a movement toward the midline of the body, down and in; elevation of the medial foot arch; the opposite of pronation. Oversupination occurs when the foot remains on its outside edge after heel strike instead of pronating. A true oversupinating foot underpronates or does not pronate at all, so it does not absorb shock well. It is a rare condition, occurring in less than 1% of the running population. Symmetrical: In shoemaking, this applies to lasts or patterns that have even sides, the right side the same as the left side. Synthetic: Something resulting from synthesis rather than occurring naturally; a product (as drug or plastic) of chemical synthesis.

Tanning: Process of converting raw hides and skins into leather by a combination of chemical and mechanical means. Tensile strength: The pulling force expressed in measuring leathers or fabrics; the resistance of a material to being pulled apart. Terminal wear condition: A condition in which the outsole of a shoe is worn completely through to the midsole or underlying material. Thermoplastic: Material capable of being repeatedly softened by heat and hardened by cooling; a type of rigid, durable plastic used for most heel counters. Thomas bar: See Bar, Thomas. Throat: Entrance of the shoe where normally the vamp and quarters meet; the topline of the vamp in front of the instep. Throat opening: The distance in a straight line from the vamp point to the back seam tuck. Toe box: Reinforcement used to retain the original contour of the toe and guard the foot against trauma or abrasion. Toe cap: An additional protective device on the frontal toe area. Toe recede: The slope of the top surface of the last extending from the toe point to the point of full toe thickness. Toe spring: The vertical distance between the base plane and the toe point of a last having the desired heel elevation; the vertical distance between the ground and the toe point giving the shoe frontal pitch. Tongue: A layer of upper material that protects the top part of the foot from pressure from the laces. Some tongues on Asics shoes are now split to allow the foot to expand. Tongue guide: The tag or slit in the tongue through which the laces are slotted to hold the tongue in place (lace keeper). Top line: The open area of the shoe around the ankle. Torque: A force that causes or tends to cause rotation of an object about an axis. The torque (also called moment) is the result of the magnitude of the force, its direction, and distance from the axis of rotation. Torsion: The stress caused by twisting a material. Torsional rigidity: The amount of stiffness in the shank and waist of a shoe. Torsion system: The flagship technology of Adidas. It’s a system designed to allow the forefoot and rearfoot to move independently of each other to encourage freedom of movement. Shoes designed with the Torsion system have a groove cut into the midsole where the foot bends naturally during the running gait. The Torsion Bar is a Kevlar strip embedded lengthwise into the midsole to control excessive twisting of the foot. TPR: Thermoplastic rubber. Traction: The amount of friction or resistance to slip between a shoe outsole and the contact surface. Transverse arch: Curvature of metatarsal heads. Transverse force: The force generated at a right angle to the direction of motion by a walker or runner during foot contact and most closely related to rearfoot stability. Also referred to as the mediolateral force. Continued


Box 25B-1 Glossary of Foot and Shoe Terminology—cont’d Transverse plane: The horizontal plane that passes through the body from side to side and back to front dividing it into an upper and lower half. Tread: The soling configuration of the outsole. Treadmill: A rotary machine-driven belt that allows subjects to run in a confined space. Treadpoint: Point of the bottom forepart of last or shoe in contact with the treading surface. Tricot: Knitted fabric commonly used for linings in women’s shoes. Unit sole: The bottom unit with sole and heel portions molded together as a single piece. Universal last: A standard last used by sports shoemakers for all width fittings. Upper: The material making up the “top” part of the shoe. Urethane: Plastic used for uppers, soles, top lifts, and other components; commonly known as polyurethane. Urethane: A resin combination with polymers. U-throat: A lacing eyestay pattern at the front of the shoe. Vamp: Forepart of the upper. The top or front part of the upper over the toe and lacing area. Vamp length or depth: The distance measured along the toe profile from the vamp tack to the toe point. Vamp tack: An arbitrary point on top of a last forepart marked by a tack, measured from the toe. Vegetable tanning: Tanning that uses plant or vegetable materials; uses materials derived from plant life such as oak, chestnut, quebracho, myrobalans, or divi-divi. Velcro: Nylon hook and loop tape fastener that clings on contact. Vertical force: The force perpendicular to a level surface. The dominant force generated by a walker or runner during foot contact and most closely related to the shock absorption characteristics of a shoe. Vinyl: A PVC material that’s available in expanding and nonexpanding types.

Vulcanize: A method of shoemaking in which the rubber sole and/or foxing is cured by heat after attaching to the upper; bonding of the outer sole to the upper from a sole mold in which the soft rubber molds to the shoe, then is allowed to cool and harden. Common in footwear such as sneakers. Waist: Section of the last or shoe between the ball and instep. Waist girth: The smallest dimension around a last between the joint girth and the instep girth. Wall: Straight sides around the periphery of the forepart of certain style lasts. Water repellent: Shoes treated so that they will shed water. Waterproof: Shoes treated so that water cannot penetrate. Wear tester: A piece of equipment used to evaluate the resistance of the outsole of a shoe to abrasion. Wedge: Tapered leather, rubber, or other material used to elevate one side of the sole or heel; replaces the heel. Wedge angle: The angle between the heel featherline plane and the base plane, with the last positioned on the base plane. Wedging: Insertion of wedges inside the shoe or on the sole or heel. Weighted shaft: A shaft with a weighted end that is used to impact shoes or material. Welt: A narrow strip around the outside of the sole, stitched between the upper and the sole. Width: Measurement of circumference around the ball of the foot; a coded method for shoe girth sizing. Width sizing: Most running shoes are available in just one width; a few selected models are offered in two. New Balance is the only company that offers its shoes in several widths. For men: from AA to EEEE. For women: AA to EE. Wing tip: The design of the toe cap. ZO2: A Turntec feature; it is a silicone pad that is used for cushioning in the insole.

*This glossary has been compiled from: An A to Z guide to shoe terminology. Runner’s World, 25:48-49, 1990; Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987, pp 163-245; Prescription Footwear Association/Board for Certification in Pedorthics: 1992/93 Desk Reference and Directory. Columbia, Md, Prescription Footwear Association, 1992, pp 65-78; and Janisse D (ed): Introduction to Pedorthics. Columbia, Md, Pedorthic Footwear Association, 1998.

In the evolution of shoewear, the last was originally chiseled out of stone.31 Later models were whittled from wood. A machine used in shaping gunstocks was converted to make lathes and led to the first lastmaking plant in Lynn, Massachusetts, in 1820.31 Today most lasts are made from plastic, a process developed by the Sterling Last Corporation in 1969.31 Metal lasts are used when direct- or injectionmolded soles are attached to the upper because the heat used in this process is poorly tolerated by wood or plastic.22 The dimensions of lasts are based on the average measurements of the segment of the population to whom the shoe will be marketed (e.g., men or women).9,22 In the past, women’s shoes were based on scaled-down versions of lasts derived from the male foot anatomy. Recent investigations have noted several structural differences between the male and the female foot. Specifically, the female foot typically has a narrower Achilles tendon, a narrower heel in relation

to the forefoot, and a foot that is narrower in general than its male counterpart.32 In addition to these dimensional discrepancies, women have proportionately shorter leg length to total body height than do men, necessitating more foot strikes per distance covered. Because of their smaller feet, the heel-to-toe gait cycle is completed more quickly. Consequently, the cumulative ground reaction force is increased in the female runner, particularly in elite women runners, who tend to be midfoot strikers.33 The repetitive nature of running causes these factors to be magnified tremendously over the life of a typical athletic or running shoe. Until recently, women’s shoe manufacturers typically scaled down all key internal dimensions of a male athletic shoe in fixed proportion. This practice, termed scaling or grading, persists today. Fortunately, most major athletic shoe companies now have divisions devoted to female athletic footwear, and many have developed lasts based on the anatomy

Foot and Ankle 1887

Toe spring

Heel height

Girth

Narrow round

Oval

Pitch Figure 25B-11 Important measurements with respect to the last are toe pitch or toe spring, girth, and heel height or pitch. (Adapted from Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987; and Stacoff A, Luethi SM: Special aspects of shoe construction and foot anatomy. In Nigg BM: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics, 1986; Copyright © 1986 by Benno M. Nigg.)

of the female foot.32 Now, the last is divided and measured in ways that more closely duplicate the average shape of the foot, and a method exists for custom-making a last and producing a shoe to individual specifications. This is frequently done for elite athletes and particularly for athletes in certain sports such as figure skating. It is considered cost ineffective and unnecessary for the general public.22 The divisions and measurements used for the last are shown in Figure 25B-14.22 Individualized lasts are made from an outline of the weight-bearing foot, a weightbearing impression (to determine pressure distribution), a profile showing the height of the big toe and the instep contour, measurements of overall width and length, and specific girth measurements. Girth measurements are made from (1) the joint—around the metatarsophalangeal joints, (2) the waist—the smallest circumference behind the metatarsophalangeal joints, (3) the instep—the smallest circum ference around the arch, (4) the long heel girth—the circumference from the lower edge of the heel around the instep, (5) the short heel girth—the circumference from the lower edge of the heel around the ankle at the lowest crease line, and (6) the ankle—the circumference around the malleoli that is used in high-top shoes and boots.9,22 The process of lastmaking has achieved some level of automation with respect to the upper, for which computer technology has been used more effectively. Computer-aided design

Oxford

Oval round

Natural shape

High/wide

High

High/round

Figure 25B-13 Various alternatives for the shape of the toe box. (From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.)

and manufacturing processes produce three-dimensional designs for the upper and allow direct transference of this information into automated methods of pattern grading and cutting.22 This reduces the work of a formerly laborintensive operation and foreshadows further innovations in computer-assisted production of sports shoes. Figure 25B-10 illustrates shoe parts.

Specific Shoe Parts: Upper The upper of the shoe is the material that covers the foot. As such, the most important consideration is the specific material used and its relationship to the purposes for which the shoe is purchased. A shoe with a nylon mesh upper is far from ideal for a cold-weather hiking boot, and thick leather is, by the same token, less than ideal for a running shoe in warm climates. These material considerations are discussed in a later section.

Toe Box The front part of the shoe upper is crucial to the health of the toes. Adequate depth is necessary to prevent chafing of the skin over the bony prominences at the interphalangeal joints. Reinforcements of the toe box in the form of stiffeners can vary from being nonexistent in running shoes to being quite stiff in hockey skates or hiking boots. An inserted stiffener protects the toes and prevents the collapse of the upper material onto the toes. Its disadvantages are added weight and stiffness.

Toe Cap Straight

Semicurved

Curved

Figure 25B-12 Illustration of the difference between straight, semicurved, and curved last shoe.

The addition of material called foxing to the front of the shoe protects the toes and increases the durability of the toe box. The toe cap is usually an isolated component in running shoes and is made of suede or rubber stripping.


Shank

Fore part

Heel seat

Bottom view

Heel curve or rake

Side view Instep Comb Waist

Short heel girth

Back part Long heel girth

Ball/girth Toe width Toe recess

Shank Fore part

Cuboid allowance

Last division and measurements Figure 25B-14 The divisions and measurements used with the last. (From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.)

Vamp One of the 16 to 20 pieces of material forming the upper of a shoe is called the vamp. It is the piece (or two pieces) of material forming the front part of the upper and sewn to the eyestays and quarters. Most shoes use a single piece of material for the vamp to eliminate a seam in the toe box area. The vamp is sewn to the quarters at the midfoot level, and these seams are usually hidden by the various trademark stripings of different companies. Split-vamp construction has been popularized as a method allowing better shoe fit for some individuals. It splits the vamp

into two separate pieces with separate lacing systems (Fig. 25B-15).

Quarter This is the other major piece of material composing the upper. Two pieces form the sides of the shoe and conform to the midfoot and arch area of the foot. In shoes designed for side-to-side movement, the vamp and quarter are usually reinforced by extra material (usually leather) called the saddle or arch bandage.

Eyelet Stay and Eyelets

Figure 25B-15 Split vamp shoe with two separate pieces on the upper with separate lacing systems. (Photograph by Thomas O. Clanton.)

The eyelet stay reinforces the holes or eyelets used for lacing. It can be incorporated into the reinforcing material of the saddle and provides additional support for the forefoot and midfoot. Holes are replaced with plastic or metal rings or hooks in some athletic footwear to allow quicker or more forceful lacing. Many athletic shoes have extra eyelets for individualization of a snug but comfortable fit. Widening the reinforcing layer and the eyelets has allowed variable-width lacing to accommodate some of the width sizing difficulties seen in sports shoes. Variable-width or dual-lacing systems can be used with conventional or nontraditional lacing patterns to accommodate variations in foot size, bone spurs, nerve irritation, or other problems. Widely placed eyelets allow the laces to pull the quarter tighter for narrow feet, and narrowly placed eyelets are better suited to a wider foot (Fig. 25B-16).32

Foot and Ankle 1889

control. The size of the heel counter and the quality of the material vary between shoes.

Forefoot and Rearfoot External Stabilizers (Footframe) A

B

C

D

Material is used as a reinforcing component to cup the rearfoot or forefoot of the shoe for greater stability. This is a molded material that may or may not be an integral part of the midsole.

Lining This is the material that acts as the inside backing for the material of the upper. It must be smooth and nonirritating because it is in direct contact with the foot. E

F

G

Figure 25B-16 Examples of lacing patterns for use in certain forefoot conditions. A, Variable-width lacing used for wide foot. B, Variable-width lacing used for narrow foot. C, Independent lacing system using two separate laces. D, Crisscross lacing pattern designed to avoid area of dorsal prominence or pain. E, Lacing pattern useful in highly arched foot so that laces never cross over the top of the foot. F, Lacing pattern designed to pull the toe box up to relieve pressure on the toes. G, Crisscross and loop lacing system used to hold the foot snugly in the heel of the shoe to treat or prevent heel blisters or chafing. (Redrawn from Frey C: Foot health and shoewear for women. Clin Orthop 372:32-44, 2000.)

Specific Shoe Parts: Bottom The bottom, or sole, of the shoe is important in protecting the foot from the environment. Therefore, it requires materials that are both comfortable and durable. In modern athletic footwear, these two features are accomplished by using multiple components.

Sockliner or Insole

The portion of the upper that extends under the laces is called the tongue. It may be padded to reduce irritation to the dorsum of the foot. The tongue is often slit in a way that allows the laces to anchor the tongue and prevent it from sliding laterally.

This material cushions the foot and is the layer between the foot and the bottom of the shoe. Various materials have been used for this layer and are discussed in the next section. Most sports shoes come with removable sockliners to allow them to be replaced when they are worn out or when a corrective orthosis is necessary. The insole reduces friction and provides some degree of shock absorption. It also absorbs perspiration and can provide some canting or control of overpronation. The capability of this material to mold to the shape of the foot can be a source of additional comfort and control.

Collar

Insole Board

The collar forms the uppermost part of the quarters and is the part through which the foot enters the shoe. When excessively stiff or high, the collar can irritate the hindfoot or ankle malleoli. It often has extra padding.

The cellulose fiberboard to which the upper is attached in the conventional lasting process is called the insole board; hence the term board-lasted. This process provides the greatest stability, as opposed to slip lasting, which has no insole board under the sockliner, and leads to improved comfort and flexibility. The intermediate option is combination lasting, in which there is an insole board in the hindfoot with stitching in the forefoot where it has been slip lasted (Fig. 25B-17).

Tongue

Achilles Tendon Protector The extended area on the back of the shoe acts as a pull tab and protection for the Achilles tendon. It should be both molded and padded well to prevent irritation of this area. The high tab design that caused irritation of the Achilles tendon has been replaced by a “bunny-ear” design with a dip in the center.34 The cutaway should be wide enough to prevent friction on the sides of the Achilles tendon.

Heel Counter This reinforcement to the upper of the shoe is located in the heel area. It is a stiffened material of fiberboard or plastic that is molded to the heel and provides greater rearfoot

Midsole Known as the heart of the running shoe, the midsole is sandwiched between the upper and the outsole of the shoe and provides the bulk of shock absorption. With the wedge, this component also produces the desired heel lift, rocker action, and toe spring. Through the use of canting and variable hardness, the midsole can control foot motion. With the use of anatomic contouring, even greater stability and comfort can be achieved. Variations in the materials used add another dimension to what the midsole can do for the foot.


C

B

A

Figure 25B-17 Examples of different lasting methods for running shoes. A, Slip-lasted shoe. B, Board-lasted shoe. C, Combination-lasted shoe. (Photographs by Thomas O. Clanton.)

Many of the more significant and recent design advances have occurred through alteration of the midsole.35 These modifications are seen as significant enough by the manufacturers that they are frequently incorporated in the name or advertising campaigns of the various shoe products (Table 25B-1). One particular midsole modification has even contributed to the most recognizable nickname of one of the greatest basketball players of all time—Michael “Air” Jordan.

TABLE 25B-1 Materials Encapsulated in Midsole Cushioning Designs Shoe Manufacturer

Trade Name

Material and Design

Asics Avia

Gel Arc

Brooks

Hydroflow

Converse

He:01

Etonic

Soft Cell

New Balance

ENCAP

Nike Puma Reebok Reebok

Air

Silicone resin in a pad DuPont Hytrel in polyurethane Silicone fluid in a twochambered plastic bladder Helium gas in polyurethane and nylon Combined gel and ambient air Ethylene vinyl acetate core in polyurethane shell Freon gas in polyurethane Honeycomb pads Honeycomb pads Pads connected by tubing, which allows air flow during stride

Hexalite DMX

Compiled from Heil B: Running shoe design and selection related to lower limb biomechanics. Physiotherapy 78:406-417, 1992; Frey C: Footwear and stress factures. Clin Sports Med 16:249-257, 1997; and shoe product brochures and the Web sites of the named shoe manufacturers.

Outsole This is the bottom layer of the shoe that makes contact with the ground. The outsole can be constructed with different materials, patterns, colors, and densities. These factors, excluding color variations, can be used to modify the shoe’s stability, flexibility, comfort, and shock absorption. These features are discussed in greater detail later in this chapter.

MATERIALS USED IN SHOES AND SHOE INSERTS The petroleum industry has affected many areas of society, including shoe construction. Traditional materials such as leather, rubber, and cotton (canvas) still have their place, but the search for lighter, more durable, more shock-absorbing materials has led to the development of complex foams with high-tech names such as Elvalite, Hexalite, Hydroflow, Hytrel, Kevlar, Millithane, Phylon, and ZO2.22,36-40 Technologic developments in the field of materials science have progressed at such a rate that it is virtually impossible for the athletic shoe salesperson, the equipment manager, or the sports medicine specialist (much less the average runner) to maintain a current working knowledge in this area. A comprehensive discussion of materials science and the various materials of shoe construction is beyond the scope of this textbook and beyond the attention span of either the author or the reader. Therefore, this section is designed to educate the reader on the fundamentals while providing resources for those interested in further research.

Polymer Science, in Brief The history of polymer science has been summarized succinctly by Cheskin, although he differs with the Encyclopaedia Britannica about some dates.22 Various landmarks are listed in Table 25B-2.

Foot and Ankle 1891

TABLE 25B-2 History of Polymer Science 1493-1496 1615 1735 1835 1839 1860 1862 1869 1879 1909 1920s 1921 1922 1928 1931 1935 1937 1939 1940s

Christopher Columbus notes Indians playing with balls made from gum of a tree during his second voyage— rubber discovered by Western man Spaniard describes the use of tree milk in Indian footwear and cloaks French geographical team to South America describes “caoutchou” as the condensed juice of the Hevea tree Preparation of vinyl chloride Discovery of vulcanization process for rubber by Charles Goodyear Basic component of rubber discovered and named isoprene First plastic produced by English chemist Alexander Parkes, called Parkesine and later Xylonite. It was a nitrocellulose softened by vegetable oil and camphor. Plasticizing effect of camphor recognized by John Wesley Hyatt; cellulose nitrate patent for celluloid introduced French chemist Bonchardat introduces process of heatcracking rubber. Heat and pressure patent for phenolic resins introduced by Backebrend (Bakelite) Discovery of foam rubber made by confining gaseous bubbles within the rubber First injection molding machine produced and automated by polymerization German chemist Studinger writes that rubber is a chain of isoprene units. This provided theoretical background for polymerization. DuPont begins laboratory study of polymers leading to “superpolyamide” or nylon. Polychloroprene (Neoprene) first marketed commercially Germany produces synthetic rubber: Buna S from styrene butadiene, Buna N from nitrate butadiene Polyurethanes produced British invention of polyethylene Redox process for low-temperature polymerization introduced in Germany to provide more uniform product.

Rubber and Plastic Technology for the Outsole and Midsole Rubber is an organic substance that is a primary component of most athletic footwear. It can be obtained in nature as the milky latex produced by tropical and subtropical trees, or it can be manufactured synthetically.41,42 Natural rubber has the empirical formula C5H8, as assigned by Michael Faraday in 1826.43 The synthetic rubber most commonly used in outsoles is styrene-butadiene rubber.22,43 Styrene’s empirical formula is C8H8, whereas butadiene’s is C4H6.43,44 Different properties of styrene-butadiene rubber can be created by altering the ratio of these two substances or by

varying other elements within the manufacturing process. The addition of carbon black as a filler in the final curing process improves the elasticity and tensile strength of rubber, resulting in improved durability.43 According to the Encyclopaedia Britannica, plastics are “synthetic materials that are capable of being formed into usable products by heating, milling, molding and similar processes. The term is derived from the Greek plastikos, ‘to form.’”45 They have come into increasing use in the shoewear industry in large part as a result of their ability to soften but not melt when heated, which allows for a change in shape without a loss of cohesiveness or mechanical properties and allows for processing into a stable new form on cooling. These synthetics include a vast array of materials that have properties of diverse usefulness. They can be grouped into thermoplastic or thermosetting varieties,46 the basics of which are outlined in Table 25B-3. Regardless of their type, plastics are dependent on the process of polymerization for their existence. This is the process whereby two or more molecules are joined into chains or networks of repeating units (the monomer).45 In an effort to increase the shock absorbency of hard rubber soles, gaseous bubbles were introduced into liquid rubber in a process that produced foam rubber in the 1920s.43 When the structure of the material has openings to environmental air (like a sponge), the material is defined as open-cell foam. Closed-cell foams differ in that their structure is not open to environmental air.47 This cellular construction provides cushioning as a result of the compressibility of the cellular structure as well as the encapsulated gas. Repetitive impact stress can cause a breakdown in the foam material owing to compaction of the foam cell structure. This can occur in as little as 1 hour in some open-cell, lightweight foams. This effect has been studied in running shoes and indicates a loss of 25% of the initial shock absorption after just 50 miles and a loss of more than 40% after 250 to 500 miles, according to machine testing.48 Most experienced runners do not change shoes during this mileage range because it may be reached within 1 month of purchasing the shoe and there may be little external appearance of wear. This type of breakdown has stimulated a search for new and improved polymers for the midsole as well as alternative cushioning systems. Polyurethanes are one of the most versatile groups of synthetic rubber polymers.22,41 They are produced by the polymerization process, in which diisocyanates react with polyols (multiple OH groups) into polyesters or polyethers.45 A liquid catalyst or resin hardener is used to initiate the chemical process. In liquid or semiliquid form, the polyurethane rubber can then be cast, mixed, milled, or vulcanized. Variations in the process can result in materials with

TABLE 25B-3 Synthetic Material Properties Group

Properties

Examples

Thermoplastic

Soft when heated Hard when cooled Heating and reheating repeatable (heat labile) Shaped by heating Retains shape when cooled Once set, process not repeatable (heat stable)

Ethylene vinyl acetate, polyvinyl chloride, polyethylene Polypropylene, some polyurethanes

Thermosetting

Melamine, phenolic and furan resins, aminoplastics, alkyds, epoxy resins Polyesters, silicones, most polyurethanes


a wide range of properties, ranging from hard plastics to soft foams with consequent differences in rigidity and flexibility. Polyurethanes can be either thermoplastic or thermoset resins. Because of their versatility, these compounds have become an integral part of the athletic footwear industry with uses as both midsoles and outsoles. Relatively lightweight and quite durable, polyurethane can be injectionmolded into specific shapes or used as a flat sheet. This allows it to be processed into multistudded athletic shoes and intricately patterned running shoe outsoles.49 Companies continue to support research and development departments to find the ultimate polyurethane for cushioning and durability without sacrificing additional weight.38,39 Ethylene vinyl acetate (EVA) is a copolymer made from ethylene and vinyl acetate in a high-pressure addition polymerization process.22 It is used most commonly as a foam produced by dispersal of gaseous bubbles within the liquid plastic. With a density less than that of polyurethane, it is lighter and less expensive while providing good resiliency and cushioning properties.13,50 It can be adjusted to provide varying hardness, and this has been incorporated into “dualdensity” and “tridensity” midsoles.30,38,39 The harder foam usually has a darker color to denote this difference for the educated consumer. When placed in certain key areas of the midsole, these firmer midsole components can theoretically add control features to the shoe. Because EVA has a tendency to deform with repetitive stress, a process of compression molding is often added, using a combination of heat and pressure to improve the memory and the durability of this foam.30 The competitiveness between shoewear manufacturers and the expanding field of polymer science are irrepressible stimuli to advances in the materials used in athletic shoewear. New forms of lightweight and durable polyurethane have already been introduced and are gradually replacing EVA midsoles in the more expensive running shoe lines.38-40,50 In nonrunning shoes, in which wear and weight are less important, polyurethane midsoles and outsoles are already quite common.51-53 Foams made from new polymers are being introduced with such rapidity that it is hard to keep them all straight. Shoewear companies traditionally attach proprietary names to their technologically based cushioning systems and materials, and it can be difficult to obtain relevant background information. The introduction of air encapsulation in 1979 by Nike signaled a new era in shock absorption technology. Despite early problems with instability, other companies rapidly adopted this encapsulation using other materials (see Table 25B-1). Encapsulation of a cushioning material such as air or gel avoids or delays the compaction seen with traditional midsole foams, thus improving a shoe’s durability.35,54-57 Whether such innovations prevent injuries remains open to speculation, but one can be certain that the athletic shoewear industry will continue to merge science and technology with marketing to give us more sophisticated names and polished promotions.

Heel Counter Materials The next shoe region in which materials play an integral role is the heel counter. The increasing attention placed on rearfoot stability by research resulted in the incorporation

of more rigid materials into the heel cup of the shoe. Originally, the heel counter was found only in the running shoes made by the Dassler brothers at Adidas and Puma and consisted of a fiberboard construction.9 The fiberboard lost its stiffness with repetitive wear and constant moisture, leading to the use of more durable plastics. Today, molded plastics take the place of sheet plastic to provide better fit. Heel counters are made from a variety of synthetics, including polyethylene, polyvinyl chloride, and other thermoplastic materials.22,30,39 The stability of the heel counter is enhanced by foxing, external stabilizers, or footframes made of leather or synthetic materials.

Upper Materials Leather remains the most commonly used material in general shoewear construction, particularly for the upper.47,58 It has gradually been replaced in many athletic shoes, in which synthetics provide certain specialty features such as better breathability or reduced weight.22 Leather comes from the skin of an animal and goes through a tanning process to fix the proteins in the skin and eliminate components that would promote degradation. This process can be varied to affect the properties and texture of the finished product. Two layers of the skin are available for use in shoemaking once the skin has been split (Fig. 25B-18).22,47 This process reduces the thickness of the material and changes its properties, the inner split being softer but tending to fray more readily. Leather’s usefulness is apparent from its universal applicability to footwear construction since ancient times. It has the ability to adapt to the shape of the foot and maintain the altered configuration. Leather transmits perspiration (“breathes”) and can be treated to resist or repel water.22,58 Tensile strength is outstanding (up to 4 tons per square inch), flexibility is excellent, and puncture and abrasion resistance is superior.22 The tanning process, along with the finishing and dyeing of the leather, can accentuate one or all of these properties. The disadvantages of leather are its deformability under stress, its tendency to crack when successively moistened and dried, its weight, and cost variations. Nylon-weave uppers are made from polyamide resin fibers woven together into a taffeta and doubled or interfaced with a thin foam or tricot lining.22 In the assembly process, these layers are “flamed,” or heat-bonded. This bonds the laminates together, resulting in a material more flexible and absorbent than if the layers were glued.34 The variables in this composition process are the exact material

Grain side or outer split Full thickness of leather

ain it gr Top spl knife Chamois or sp lit s ue Flesh side or inner split de

Figure 25B-18 Splitting of leather into two layers of skin for use in shoemaking. (Redrawn from Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987; and Philps JW: The Functional Foot Orthosis. New York, Churchill Livingstone, 1990.)

Foot and Ankle 1893

used in the thread, the size of the thread, the number of threads in the bundles, and the number and orientation of the bundles going lengthwise and widthwise (Fig. 25B-19).9 The closeness of the weave affects the mechanical properties of the fabric. The nylon weave of a taffeta upper has good durability, softness, and flexibility and is lightweight, making it a superior replacement for leather in many athletic shoes.9,22 Nylon mesh is made from the same nylon threads, but in a knitted rather than a woven process (Fig. 25B-20).9 This knitted process adds space within the strands without compromising strength. Thus, the breathability of the upper is improved. It can be used as a single-, double- or triplemesh knit. Increasing the denier of the thread adds body and strength to the fabric. Whether used in mesh or woven form, the nylon upper is generally combined with a thin foam and a tricot lining for improved fit and comfort.22 Other synthetic materials are finding their way into athletic shoe uppers, including Gore-Tex (W. L. Gore and Associates, Elkton, Md).30 Thermoplastic vinyl has uses in golf shoes in coated or laminated applications to leather or fabric. Slush- and dip-molded uppers of thermoplastic materials are used in recreational ice skates and certain waterproof footwear, whereas injection-molded thermoset plastic is the norm for ski boots.22 Depending on the shoe’s intended use, the shoewear manufacturer can provide a full range of breathability, extending from complete breathability up to complete insulation and waterproofing. The upper can be easily or barely deformable. Weight can be varied over a wide range, and the foot can be protected minimally or maximally.

Inlays, Inserts, Insoles, and Orthoses Since ancient times, it has been known that the addition of leaves, moss, or animal skin to the inside of the shoe could provide cushioning for the foot and protection from environmental stresses.10 For soldiers on long marches, this extra protection might mean the difference between life and death. For modern-day runners and athletes, this

Figure 25B-19 Nylon-weave uppers made from fibers woven together into a taffeta. (Redrawn from Cavanagh PR: The Running Shoe Book. Mountain View, Calif, Anderson World, 1980.)

cushioning is intended to protect the most readily identifiable weak link in the kinetic chain. Many athletes would provide testimonial support for the merits of their orthotic devices or inserts in preventing injury or enhancing performance. Although it has been more difficult to document these beneficial effects objectively,31,59,60 scientific evidence of the shock absorption properties of the various materials used in these devices does exist.54,57,61,62 This section provides some acceptable definitions to help make sense of this confusing area and then describes some of the materials used. The following section discusses their biomechanical properties. Because of the confusion that surrounds this area, we have chosen to use the definitions of terms accepted by the Pedorthic Footwear Association.63 The insole is the integral design component (layer) of the shoe that is the shoe’s structural anchor to which is attached the upper, toe box, heel counter, linings, and welting. The inlay is a prefabricated removable material upon which the foot directly rests inside the shoe. In some shoes, the inlay is an integral design component. The insert is a type of orthosis, although the term has been used interchangeably with inlays and insoles in some circles to designate an off-the-shelf device placed inside the shoe. For the purpose of this chapter, we use the definition for an insert supplied by the Health Care Financing Agency: a total contact, multiple density, removable inlay that is directly molded to the patient’s foot or a model of the patient’s foot and that is made of a suitable material with regard to the patient’s condition. An orthosis (or orthotic device) is a device that is used to protect, support, or improve function of parts of the body that move. A common error is to use the adjective orthotic as a noun. A pad is a device placed inside a shoe to provide support or relieve pressure from a specific location such as a longitudinal arch pad or a metatarsal pad. Pads are made of various materials and come in a variety of shapes and sizes. Inlays and inserts can be made from a single material or a composite of several materials. The most commonly used materials are leather, cork, foam, felt, and plastic.41 Based on the previous definitions, inlays are “off-the-shelf,” whereas inserts are “custom made.” The latter can be subdivided into

Figure 25B-20 Nylon mesh made from threads with a knitted rather than a woven process. (Redrawn from Cavanagh PR: The Running Shoe Book. Mountain View, Calif, Anderson World, 1980.)


those made from a casting of the foot and those made from an impression of the foot (Fig. 25B-21).41,47,64 These can be formulated in a weight-bearing, partial weight-bearing, or non–weight-bearing fashion. A recent trend in orthosis manufacture uses digital foot scanners, obviating the need for a negative mold of the foot. A topographic reading of the plantar foot is obtained using laser scanning, digitized force-plate gait and pressure analysis, or digital analysis of multiple air pegs. These manufacturing devices employ computer-assisted design in the final conversion of data to orthosis.65-68 The devices, which are at present quite expensive, largely rely on the subtalar neutral position as a starting point for data collection. The subtalar neutral position has been variously defined as the position from which there is equal inversion and eversion range of motion, the position from which there is twice as much inversion as eversion, or the position from which the talar head is most fully covered by the tarsal navicular when palpating the foot. It is unclear how much a small variation in this point affects readings and ultimately function. Adequate data in the form of prospective, randomized, controlled studies comparing the use of orthoses manufactured with these systems and inserts made with traditional methods are lacking. There are no data confirming their superiority or justifying their cost.69 Given the uncertainty surrounding the multitude of theories guiding orthotic prescriptions, it would be helpful to have some scientific support for the ability of foot orthoses to accomplish their stated objective. For general classification purposes, inserts can be further divided into accommodative or functional varieties. Accommodative devices are those that are designed with a primary goal of conforming to the individual’s anatomy, whereas functional devices are designed with the primary goal of controlling an individual’s anatomic function, such

as providing support or stability, or assisting ambulation.47,63,70 Different materials can be used for these purposes, leading to an additional subdivision into rigid, semirigid, and soft, in which the material becomes the critical factor. As discussed previously, the materials used in shoes, and now in orthotic devices, can be either natural or synthetic.41 The most commonly used natural materials are leather, rubber, cork, metal, and felt. Synthetics include plastics and foams (both closed and open cell), which can be manufactured with varying qualities of hardness, density, durability, and moldability. The following paragraphs consider the advantages and disadvantages of these materials.

Natural Materials Leather is extremely durable and conforms well to the contours of the foot. It is readily available, is tolerated well by the skin, and combines well with other materials as a composite.41,58 On the negative side, leather is relatively expensive and provides very little shock absorption.47 Rubber has been discussed in the preceding section. It provides good shock absorption with durability but is heavy, and its qualities vary considerably according to the exact process used in its production.41,42 Rubber foams are made by the addition of chemical additives or air. Closedcell foam rubbers are more stable and durable.47 Cork is a lightweight cushioning material made from the outer bark of a tree.71 Although it does not work well when in direct contact with the skin, it is usually used in combination with leather and has a good history of use as an insert. Synthetic forms of cork are now used. Although cork was the material used in the first formal shoe insert in the 18th century,72 it has fallen into disfavor because of its mediocre shock and shear absorption capacities in comparison with some of the newer products.

Synthetic Materials

Figure 25B-21 Foam box used for taking an impression of a foot to make a custom-made orthosis. (Photograph by Andrew Borom.)

Among synthetic materials, there are a wide variety of plastics and foams that have been used in the fashioning of orthoses, inlays, inserts, pads, and insoles. Included in this group are various synthetic rubbers, polyolefins, thermoplastics, thermosetting materials, viscoelastic materials, polyurethane foams, and certain copolymers and composites.41,47,54,64 Because many of these have been described previously, the present discussion is confined to materials in common use that have not been previously described. Styrene-butadiene rubber is a synthetic rubber that has found considerable applicability in orthotic devices both as a basic shell and as a posting material.41 Neoprene is a special rubber made of polychloroprene and is primarily known for its use as an inlay or insole material in the form of a closed-cell foam commonly known as Spenco or as an open-cell foam called Lynco (Table 25B-4).41,54,73 It functions well to reduce friction and attenuate shock but is somewhat hot (particularly in the closed-cell form). The polyolefins consist of polyethylenes, polypropylenes, and their copolymers.41,74 When fabricated as foam, these materials fill a multitude of uses. Because of the modifications available in the manufacturing process, it is possible to vary the mechanical properties of the material over

Foot and Ankle 1895

TABLE 25B-4 Neoprene Foams

TABLE 25B-6 Polyurethane Foams

Name

Qualities

Company

Name

Qualities

Company

Spenco

Closed cell, nylon cover Open cell

Spenco Medical Corp Waco, Tex Apex Foot Products, Englewood, NJ

PPT

Open cell, single density Open cell, single density

Langer Biomechanics Group, Deer Park, NY Rogers Corp, East Woodstock, Conn Force 10-Polymer Dynamics, Allentown, Pa UCO International, Prospect Heights, Ill UCO International, Prospect Heights, Ill

Lynco

Poron Axidyne OVA-FLEX

a wide range. Therefore, these foams can be constructed as flexible, semirigid, or rigid orthoses. Table 25B-5 lists some of the trade names for polyethylene foams that are in common use along with their manufacturers.41 Thermoplastic materials are materials that become malleable when heated and hold the set configuration when cooled. They allow reheating for further remodeling.45,46 Polyvinyl chloride (PVC) is one example of such a material. As a plastic, PVC is frequently found in the heel counter of athletic shoes. Polyethylene thermoplastics are one of the most commonly used orthotic materials because they can be fashioned to conform to the patient’s foot and maintain this position under weight-bearing stress.41 The material is relatively stable yet possesses adequate flexibility and strength. Depending on the manufacturing process, the polyethylene thermoplastic can have a low, medium, high, or ultrahigh density. For orthoses, ultrahigh-density polyethylene is most commonly used. Trade names for these products include Ortholen, Subortholen, and Vitrathene.41,47 Thermosetting materials differ from thermoplastics in that they can be molded after heating, but once set, they do not allow repetition of this process. Therefore, they are heat stable.46 The material can be processed into either a plastic or foam and is used in both forms. The most common thermosetting resins are phenolics, furan resins, aminoplastics, alkyds, allyls, epoxy resins, polyurethanes, some polyesters, and silicones.45 The original thermosetting material was a combination of phenol and formaldehyde (Bakelite) formed by high pressure and high temperature.45,46 The physical properties of these plastics can be varied by altering the filler material.46 Polyurethanes can be either a thermosetting resin or a thermoplastic.45 Their principal application is in the form of an open-cell or closed-cell foam. There are a variety of trade names for these products (Table 25B-6). The materials come in various densities and thicknesses, and their mechanical properties are described later in this section.

TABLE 25B-5 Polyethylene Foams Name

Qualities

Company

Plastazote

Three densities

Pelite

Three densities

Aliplast Berkezote

Four densities Medium density

UCOlite

Medium density

UCOplast 10

Very firm

Apex Foot Products, Englewood, NJ Durr-Fillauer Medical Inc., Chattanooga, Tenn AliMed Corp., Dedham, Mass Foot & Ankle Orthopaedic, Bedford Hills, NY UCO International, Prospect Heights, Ill UCO International, Prospect Heights, Ill

OVA-FIT

Low to medium density Medium density

Viscoelastic materials are materials that combine the mechanical properties of a viscous fluid and an elastic solid. When subjected to a constant deformation or load, their response varies in relationship to the time of application.75 This is an important mechanical property that is also exhibited by tissues of the human body. The viscoelastic nature of a material allows both the storage and dissipation of mechanical energy.59 This would seem to be a desirable quality in an inlay or insert, leading to the claims of manufacturers that it is the perfect material for shock attenuation in running or jumping. Because the time required for stress relaxation to take place is a critical factor in functional shock absorption, however, one cannot assume that these claims are entirely accurate. The trade names for the most commonly used viscoelastic orthoses are given in Table 25B-7. Copolymers are substances formed by a process of co polymerization wherein two unlike molecules are united in either a randomly or regularly alternating sequence within a chain.74 An example of this is the nylon acrylic resin Rohadur, which is made from methylmethacrylate and acrylonitrile.41 It is heat moldable and rigid and is primarily used as a functional orthosis. According to Levitz and coauthors, this material was developed in Germany in the 1950s and sold in the form of resin pellets. The different companies that marketed the product for orthopaedic use turned the pellets into sheets of resin.41 When the original material was discovered to be possibly carcinogenic, it was reformulated and is now a clear mahogany-colored plastic. It is widely used in making orthoses and comes in sheets varying from 2 to 5 mm in thickness. It is one of the most rigid materials available.47 Although each of these materials can be found among the various orthotic devices on the market today, each has specific advantages and disadvantages. One foam may have excellent cushioning properties yet be inordinately heavy or hot, and one plastic may be very strong and stable while being difficult to work (Table 25B-8). For this reason, the use of composite orthoses has emerged to combine the properties of two different materials to their best advantage.

TABLE 25B-7 Viscoelastic Materials Name

Company

Sorbothane Viscolas

Sorbothane Inc., Kent, Ohio Chattanooga Corp., Chattanooga, Tenn

1896 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25B-9 Proposed Concept for Inserts and Orthoses

TABLE 25B-8 Copolymer Foams Trade Name

Qualities

Manufacturer

Polyolefin Foams

Evazote

Closed cell EVA material

Apex Foot Products, Englewood, NJ

Open cell

Apex Foot Products, Englewood, NJ

Polyvinyl Chloride Foam

S.T.S.

The ideal orthosis is moldable to the foot, durable, lightweight, effective in maintaining the proper foot position, and capable of eliminating detrimental stress. Because it appears that no one material can combine all these properties, we can expect an increase in the types and complexities of these composites.

BIOMECHANICAL ASPECTS OF SHOES AND ORTHOSES An understanding of biomechanics as it applies to athletic shoes and the use of orthotic devices requires some understanding of gait and the history of its study, which dates back to the time of Aristotle. Cavanagh has reviewed this history in his book Biomechanics of Distance Running, wherein he points out the influence of such men as Leonardo da Vinci, Isaac Newton, Giovanni Borelli, the Weber brothers, Etienne Jules Marey, Vierordt, Braune and Fischer, Eadweard Muybridge, A. V. Hill, Wallace Fenn, Nicholas Bernstein, Herbert Elftman, O. Boje, and Rodolfo Margaria.76 Contemporary workers in this field include Barry Bates, David Brody, Peter Cavanagh, Tom Clarke, Ed Frederick, John Hagy, Harry Hlavac, Verne Inmann, Stan James, Roger Mann, Benno Nigg, Merton Root, Don Slocum, Thomas Sgarlato, John Weed, and others. It would take an entire chapter to review the contributions of these men—hence the interested reader is referred to their original works, the references from Mann’s section on biomechanics, and the preceding section on the causes of injury to the foot and ankle. Without the contributions of these individuals, there would be no foundation on which we could base further research. Whether one is talking about shoes or orthoses or a combination of these, from a biomechanical standpoint, one is primarily concentrating on (1) the effect of shoes or orthoses on reducing the forces present at foot strike, (2) their ability to improve functional motion within the foot, and (3) their efficacy in preventing or treating pathologic conditions in the lower extremity. Although it is known that certain other biomechanical parameters such as running economy and speed can be altered by shoes and orthoses, these factors are not discussed in any depth in this section. Nigg reviewed the available literature and combined this with nearly 2 decades of his own investigations in the field of shoewear research to formulate a new concept for inserts and orthoses. Although the interested reader is referred to this excellent review for details, the Human Performance

Situation-Dependent Variables

Subject-Dependent Variables

A force signal acts as an input variable on the shoe, based on the chosen movement.

The soft tissue and mechanoreceptors on the plantar surface of the foot act as a third filter. The shoe acts as a first filter for The filtered information is the force input signal. detected by the central nervous system, which provides a subjectspecific dynamic response. The insert or orthosis acts as a The subject performs the second filter for the force input movement task at hand. signal. From Nigg BM, Nurse MA, Stefanyshyn DJ: Shoe inserts and orthotics for sport and physical activities. Med Sci Sports Exerc 31(Suppl 7):S424-S428, 1999.

Laboratory in Calgary proposes that the traditional view of the ability of orthoses or inserts to align the skeleton is not supported in the available literature. Rather, the concept that an orthosis or insert functions most effectively if it minimizes muscle work is advanced by these investigators.77 The basics of this proposed concept are found in Table 25B-9. The situation-dependent variables can be influenced by the shoe, insert, orthosis, or selection of the movement task, whereas the subject-dependent variables, by definition, vary from individual to individual. If this proposal is accepted, the authors suggest that it is possible to conclude the following regarding orthoses: • The skeleton has a preferred path for a given movement task (e.g., running). • If an intervention supports the preferred movement path, muscle activity is decreased. Interference with the preferred path increases muscle activity. • An optimal insert or orthosis decreases muscle activity. • An optimal insert feels comfortable owing to decreased muscle activity with resultant decreased fatigue. • With an optimal insert, performance should increase in association with decreased muscle activity and fatigue. This proposal is clearly innovative and controversial because it is unsupported by adequate experimental evidence. Further research matching subject and insert characteristics to identify the optimal solution for insert and orthosis fitting will, it is hoped, fill this evidence gap.77 As mentioned previously, the functional orthosis is fabricated based on a specific biomechanical theory. It usually uses the “subtalar neutral” position as the starting point. This theoretically aligns the hindfoot with the forefoot and allows the foot to function in its most biomechanically advantageous position. The functional orthosis changes the position of the foot with respect to the weight-bearing surface. The accommodative orthosis, in contrast, brings the surface up to meet the foot in its steady-state position in an effort to improve weight distribution and alleviate symptoms. The accommodative device must be fabricated from a material that will mold easily to the surface of the foot because one of its primary purposes is to accommodate deformities. In contrast, the functional orthosis must be rigid enough to maintain the foot in the position chosen

Foot and Ankle 1897

for maximal function. This makes it apparent why plastic is usually selected for the functional device and a polyethylene or polyurethane foam is more commonly the choice if accommodation is the goal.

Shock Absorption Loading of the athlete’s body during sports activities has been implicated as a significant causal factor in pain and injury.78-81 The study of this relationship is an essential element in the field of sports biomechanics.76,82,83 Numerous works have been published on the biomechanics of walking and running,83-90 and a like number have documented the forces acting on the foot during various activities.79,88-97 Measurement of the pressure under the foot during gait dates back to 1882 with the work of Beely, who used crude manual methods. Since then, measurement of load has progressed to the use of force plates with the aid of piezoelectric transducers or strain gauge technology with computer analysis.97,98 The vertical force component produces skeletal transients beginning at heel strike or foot strike, and these have been theorized to produce injury through their resultant shock and shear waves.99-104 Experimental support for this analysis was provided by the finding that osteoarthritis developed in the joints of sheep housed on concrete.105,106 The association between chronic repetitive trauma, exercise, and arthritis has been the source of considerable controversy.107-110 Although controlled studies have failed to demonstrate a clear relationship between osteoarthritis and the loads generated in sports such as running (in otherwise healthy participants),109-114 this relationship has nevertheless served as an important catalyst for the athletic shoe industry to improve the shock absorption qualities of shoes. Although increasing cushioning in shoewear seems intuitively appealing as a method to diminish shock transmission to the skeleton, Robbins and coworkers have produced a sizeable volume of work outlining the potentially detrimental effects of soft materials in shoes.17,115-118 Robbins and Hanna proposed that shoewear creates a pseudoneurotrophic condition that eliminates the plantar tactile response from the human system designed to minimize impact loading through alteration of musculoskeletal response.119 It has been demonstrated that although certain interface materials reduce vertical impact from inanimate objects dropped on them, human landing paradoxically increases these forces.120 Gymnasts landing on a 10-cm thick mat demonstrated a 20% increase in vertical impact compared with a rigid surface.121 Behavioral modifications that can either amplify or reduce vertical impact include variation in amplitude of hip and knee flexion.122 Bending at these joints is decreased when landing on soft surfaces. This stiff-legged landing serves to heighten impact, whereas landing on hard surfaces results in increased hip and knee flexion to absorb energy.121 Stability is part of this equation. When soft materials are placed beneath the plantar surface of individuals on a force platform, stability declines as measured by increased sway.123 Human balance improves when placed on thin, stiff surfaces.124,125 To accommodate these factors, humans adopt landing strategies to deal with the landing surface. Decreased hip and knee flexion is used momentarily to increase stability by

compressing the interface material.121 Robbins and Waked examined ground reaction force in 12 men without disability using a 4.5-cm foot fall onto a force platform covered with one of four materials.121 Vertical impact was inversely related to surface stiffness, with the softest surface producing the greatest impact. They concluded that balance and vertical impact are closely related and hypothesized that landing on a soft surface is accompanied by an attempt to render it more stable by compressing the material, decreasing its thickness and increasing its stiffness. Although recognizing the impracticality of barefoot activity, they propose that currently available athletic shoes are too soft and thick and recommend redesign.121 In a further study by the same investigators, a “deceptive” advertising message associated with an EVA-covered platform was shown to produce higher vertical impact forces than the identical platform with a preceding “neutral” or “warning” message.17 Although this theory has not been universally accepted, there is evidence that shoe manufacturers are incorporating thinner midsole shoes into their product lines, with the purported advantage of “more speed and stability.”55 Despite this opposing viewpoint, there are scientific data to support the incorporation of elements of cushioning for the reduction of certain overuse injuries.

Experimental Work Available independent data on laboratory testing of various materials used in shoes and orthotic devices are somewhat limited compared with other areas of research in the fields of sports medicine, orthopaedics, and podiatry. In one of the earliest studies of this kind, Brodsky and coworkers studied the effects of repeated compression and the effects of repeated shear and compression on the behavior of five commonly used materials for shoe inserts.54 They also determined the force-attenuation properties of the new and used materials. The materials tested were Plastazote (Apex Foot Products, South Hackensack, NJ), Pelite (DurrFillauer Medical Inc., Chattanooga, Tenn), PPT (Langer Biomechanics Group, Inc., Deer Park, NY), Sorbothane (Sorbothane, Inc., Kent, Ohio), and Spenco (Spenco Medical Corp., Waco, Tex). To test compression, the authors used an Instrom testing machine and subjected the materials to cyclic loads. The greatest degree of compression was seen with the soft-grade Plastazote, which went from an original thickness of 6.6 mm to 4.55 mm after 5000 cycles. Lesser amounts of compression were seen with mediumgrade Pelite, Spenco, and Sorbothane, and the least change was found with PPT. In the same study, the authors also looked at the resilience of the different materials. Resilience is a measure of a material’s ability to resume its original shape after having been distorted. This is an important property in an insole or orthotic device. The resilience of the above materials was determined by remeasuring their thickness after a period of rest. Both Plastazote and Pelite showed good rebound in thickness after a 12-hour rest, which allowed a return to 6.0 mm for the Plastazote (a 70% return). Unfortunately, after rebound takes place, accelerated compression occurs when the material is again subjected to the same stress. Some of the results of this study are displayed in Table 25B-10.54

1898 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25B-10 Maximum Loss in Thickness Expressed as Percentage of Original Thickness after 10,000 Cycles Material

Compression (%)

Shear Compression (%)

Plastazote (soft) Pelite (medium) Spenco Sorbothane PPT

55 15 15 3 0

45 16 3.6 10.2 0

From Brodsky JW, Kourosh S, Stills M, et al: Objective evaluation of insert material for diabetic and athletic footwear. Foot Ankle 9:111-116, 1988. © American Orthopaedic Foot and Ankle Society.

Foto and Birke recently investigated resilience for the most commonly prescribed multidensity material combinations used in manufacturing orthotic devices. Dynamic strain, or the material’s percent deformation per cycle, as well as strain loss (or compression set), reflective of the material’s permanent deformation, was measured for each of four combinations of materials. Cyclic loading to 10,000 and 100,000 cycles demonstrated marked differences in the temporary and permanent deformation of the various combinations. Although the materials tested are more commonly used in the treatment of diabetic plantar pressure problems, the authors point out that an ideal pressurerelieving orthosis should demonstrate a dynamic strain of 50% or better at 350 kPa of pressure and that compression set should be minimal. Excessive compression set corresponds to losses in posting, pressure relief, or accommodation of deformity.55 Furthermore, composite material performance is affected by the overall thickness as well as the ratio of the individual materials. The forces on the foot during walking, running, and other sports activities are rarely only compressive in nature. Therefore, a more physiologic test measures how these materials withstand both shear and compression. This process was examined in the study by Brodsky using a special jig designed for this purpose.54 The highest degree of change in thickness was again seen in Plastazote with a lesser amount of change in the samples of Pelite and Sorbothane, minimal change in Spenco, and essentially no change in PPT. Rebound was again noted in the materials after a period of rest. One interesting finding was that although Plastazote and PPT showed similar results in both the compression and the shear-compression tests, a notable difference was evident between the Spenco and the Sorbothane. Spenco tended to resist shear better than compression, whereas Sorbothane showed a better resistance to compression than shear.54 From the standpoint of the patient and the clinician, the most pertinent information concerning a given insole material is how much reduction in force it affords, that is, how much of the force that is transmitted is actually experienced by the foot? Bench research confirms that all materials (Plastazote, Pelite, PPT, Spenco, UCOlite, ZDEL, and Sorbothane) reduce the force transmitted to the load cell protected by these materials by 10% to 60%.54,57,126-128 Nigg and colleagues, in a review of the literature, examined the available data on shock absorptive insert materials

and concluded that the typical reduction of impact loading is in the 10% to 20% range. They questioned whether these small reductions are capable of reducing injury, and suggest that material alteration of inserts may produce an effect through adjustments in the muscular response of the locomotor system.77 The ability of different materials to accomplish shock absorption can change depending on the amount of force involved and the study methodology, with the exception of Sorbothane, which transmits the highest forces over the entire range.54,57 In contrast, an in vivo study of British Royal Marine recruits evaluating in-shoe pressures found Sorbothane to be significantly better in attenuating peak pressure at heel strike for both marching (23% decrease) and running (27% decrease).62 All materials demonstrate a reduction in shock absorbency after cyclic stress (a phenomenon known as stress relaxation), although this reduction is considerably more apparent in the softer grades of polyethylene foams such as Plastazote, which can lose more than 50% of its shock absorbency after 25,000 cycles.54,126 The actual amount of cushioning contributed by a given material varies according to several factors that have significant implications for their applicability to sports. In general, greater cushioning occurs with increasing thickness of the material, but this also increases weight and affects the stability, comfort, and flexibility of the device or the shoe. Furthermore, it has been shown that softer shoes may allow increased pronation compared with shoes with a firm midsole, for example, and this could produce rather than prevent certain types of injuries.129-131 As stated earlier in this chapter, the correlation between laboratory testing conditions and the physiologic situation in the athlete may be rather poor.120,130-137 Such factors as the size of the missile head used in the impact tests, the shape of the head, and the height from which the missile is dropped can all affect the results of the tests.134 Other factors influencing load magnitude include running velocity, joint kinematics, running strategy, choice of surface, and pattern of foot contact.23,72,50,93,130,132-135,138-140 Therefore, one must be cautious in interpreting test results and include in the equation the data gained from experience and clinical trials.

Clinical Work The clinical influence of improved shock absorption provided by shoes and inserts is reviewed to some extent in Chapter 25C. Other studies dealing with the effect of cushioning on injury and pain are discussed here. Stress fractures are an obvious example of an injury for which one would expect to see a reduction in incidence with the use of improved cushioning in shoes or with shockabsorbing insoles. Unfortunately, studies of stress fractures in military recruits have shown inconclusive results. Milgrom and colleagues studied the effect of a semirigid, composite orthotic device on the incidence of stress fractures in Israeli Army recruits.141 There was a reduction in the incidence of femoral stress fractures, but the effect on tibial and metatarsal fractures was insignificant. In fact, the average number of stress fractures per recruit was identical in both groups of recruits, those with the orthotic device and those without. In a subsequent study, Milgrom and coworkers prospectively randomized 390 recruits to

Foot and Ankle 1899 Prospective study n=131 Avg. 30 km/wk Nigg et al., 1995

Relative injury frequency 40 Percent

30 20 10 0

A

F Low 25% 605–1018

Mid 50% 1019–1378

High 25% 1379–2000

(N)

40 Percent

30 20 10 Loading rate

0

B

Low 25% 0.8–47.2

Mid 50% 47.3–79.1

High 25% 79.2–97.4 (N/s)

Figure 25B-22 Relative injury frequency for groups with (A) high-, medium-, and low-impact force peaks, and (B) high-, medium-, and low-maximal loading rate. (Redrawn from Nigg BM, Kahn A, Fisher V, Stefanyshyn D: Effect of shoe insert construction on foot and leg movement. Med Sci Sports Exerc 30:550-555, 1998.)

train in either standard issue military boots or a modified basketball shoe. The latter group sustained significantly fewer metatarsal stress fractures and overuse injuries of the foot. Prevention was limited, however, to injuries related to vertical impact loading. In particular, tibial stress fractures were not prevented because they are the result of bending stress. The overall incidence of lower extremity overuse injuries was likewise unaffected.142 Milgrom and associates prospectively examined stress fracture incidence in Israeli army recruits fitted with either a soft or semirigid custom-

made functional orthosis, and compared them with a group who wore no biomechanical orthosis. All recruits trained in a modified infantry boot whose sole design resembled a basketball shoe. Although their data appeared to suggest a protective benefit in the soft orthosis group, more than half of the subjects failed to complete the study. The leading cause of failure to complete the study was dissatisfaction with the orthosis, although the soft orthoses were better tolerated than the semirigid variety.62 In a separate study, Nigg prospectively followed 131 runners for 6 months. Although no difference in injury frequency was seen for subjects with low-, medium- or high-impact force peaks, those runners with a high loading rate sustained roughly 50% fewer injuries than those with a low loading rate (Fig. 25B-22).143 Gardner and coworkers found no reduction in stress fractures with the use of a viscoelastic insole placed in the shoes of military recruits.144 Another element of shock absorption relates to foot pressure and involves proper distribution of load. Locally concentrated forces can cause pathologic lesions such as intractable plantar keratoses, corns, and in the diabetic population, ulceration. Additionally, comfort may be affected by concentration of local pressure. Plantar pressure assessment has played a key role in the management of diabetic patients with neuropathy.145-149 Running shoes, by virtue of their design, have been used to better distribute plantar pressures in this patient population in the hopes of avoiding ulceration.147 Shoewear that reduces peak plantar pressure can do so either by reducing the force or by increasing the area over which the force is distributed. The ability of an insole or insert to distribute peak pressures and cushion the plantar foot, although related to the composition and thickness of the insert material, seems more dependent on the plantar tissue thickness.150 Although the footwear industry is known to evaluate inshoe pressure, this information (like so much else in the athletic shoe industry) is considered proprietary and is not available to the scientific community.146 Although pressure assessment does not seem necessary or practical in the normal population, Figure 25B-23 demonstrates the

Peak pressure = 177 kPa at great toe

No contact on medial longitudinal arch

Peak pressure = 53 kPa at great toe

Minimal contact on medial longitudinal arch Peak pressure =146 kPa at heel

Peak pressure = 181 kPa at heel

A

Contact area = 131 cm2

B

Contact area = 144 cm2

Figure 25B-23 Example of peak pressure measurements comparing different shoes. A, Shoe with limited cushioning properties. B, Shoe with improved cushioning properties. (Redrawn from Mueller MJ: Application of plantar pressure assessment in footwear and insert design. J Orthop Sports Phys Ther 29:747-755, 1999.)


ability of a moderately priced running shoe to distribute pressure more effectively over its plantar surface than an inexpensive sports shoe.146 Considering the amassed results of bench and clinical studies, there is considerably less correlation than one would expect for the hypothesis that shock attenuation reduces injury. At best it would appear that improvement in a shoe’s shock-attenuating characteristics can decrease vertical impact-related lower extremity injuries and can change the pattern, but not the overall incidence, of overuse injury.

Alignment and Control As noted in the chapter sections on the causes of injury to the knee, lower leg, and foot and ankle, there is a suspected association between positional abnormalities in the feet and injuries occurring in other areas. As more attention is focused on sports and their attendant injuries, many workers have sought an explanation for the causes of these injuries and a method of treatment that would allow continued participation in sports. The running shoe industry has capitalized on this proposed association between injuries and the feet and has developed entire shoe lines as well as specific shoe features based on the idea of providing improved “control” for the foot. Biomechanical theories have provided the rationale for this development as well as a method of treatment using prescription orthoses. The concept is that there is an ideal functional position for the various articulations of the lower extremity. Theoretically, when the foot is in a properly balanced position (achieved by having the subtalar joint in a neutral position), the foot has the greatest ability to adapt to the stresses placed on it in weight-bearing. In this subtalar neutral position, the maximal amount of inversion and eversion is available and can be used to dissipate the forces of weight-bearing and to transfer load properly to other areas of the lower extremity. Alignment has particular implications for problems about the knee because pronation through the subtalar joint results in internal rotation of the tibia. Excessive pronation has therefore been implicated as a causal factor in anterior knee pain,151-157 iliotibial band syndrome,139,151,155-158 pes anserinus bursitis,155 and popliteal tendinitis (see Chapter 25C).151,155,159 The problems attributed to excessive pronation have not been limited to the knee. In the leg, ankle, and foot, excessive pronation has been associated with posterior tibial tendinitis,151,153,156,160-162 overuse syndromes in runners,153,163 medial tibial stress syndrome,162,164 tarsal tunnel syndrome,165,166 cuboid syndrome,167,168 plantar fasciitis,153,156,169 Achilles tendinitis,129,151,153,162 metatarsalgia,162 and stress fractures.170,171 From this listing of virtually every known medical condition affecting the lower leg, it should become obvious to the astute reader that excessive pronation is a seemingly disastrous condition for the athlete. As such, it is natural to expect a plethora of laboratory and clinical studies offering scientific confirmation of the relationship between excessive pronation or rearfoot instability and these pathologic conditions. Unfortunately, the few studies that have addressed this question have failed to provide a conclusive answer.

Although most studies that have been done on the use of rearfoot control features and orthotic devices have focused on the advantages of these features in the treatment of the pronated foot, shoe features and orthotic devices have also been used to treat the opposite foot condition—the cavus or highly arched foot. As discussed in Chapter 25A, the cavus foot type tends to be more rigid and has less available motion to dissipate the forces of weight-bearing. Consequently, it is the cavus foot that has been implicated in the production of plantar fasciitis,151,163,169,172,173 stress fractures,170,171,174 and medial tibial stress syndrome.162 Because the cavus foot is generally more rigid and is commonly associated with a plantar flexed first ray and a varus hindfoot, orthotic support is designed to alleviate these problems. A less rigid orthosis is preferable to provide improved shock absorption and allow some degree of flexibility. Although reports have found that up to 75% of patients who have pronation-related problems benefit from the use of an orthotic device, there has been a considerably less favorable response to the use of orthoses in the cavus foot population.153,175-177 Clinical experience has been the source of most of the evidence supporting the use of orthotic devices for the treatment of a variety of conditions that plague the athlete, particularly the runner. Although much of the scientific and anatomic basis for the use of orthoses can be traced to the work of Manter,178,179 Elftman,178,180-182 Hicks,183,184 Close,185-187 and Inman,43,45,188 it has primarily been orthotists and podiatrists who have experimented with various shapes and materials in an effort to develop a practical approach to the prescription of orthoses. The field of orthotic prescriptions has a pseudoscientific aura. This is created by many factors: erudite yet ambiguous terminology, seemingly contradictory theories, failure to establish what constitutes the normal foot (much less the abnormal), lack of recognition of normal anatomic variation, confusing concepts of what is compensated and what is not, and limited use of the scientific method in establishing the criteria for employment of orthoses and evaluation of their usefulness.31,70,189-195 Faced with this conundrum, it is valuable to reflect on the former foundational work while viewing current shoe and orthotic research with a combination of skepticism and open-mindedness. One can then investigate the available experimental and clinical work, which either supports or refutes the scientific basis for prescribing orthoses or using particular modifications in athletic shoewear.

Experimental Work Studies concerned with control of alignment and maintenance of rearfoot stability must begin by determining an acceptable indication of foot pronation.196 Because pronation is a complicated triplane movement, it is difficult to quantify this movement with currently available techniques. Therefore, it has been generally agreed in the research community to use the degree of calcaneal eversion (valgus) as the indicator of pronation.189,197,198 By using heel eversion alone, the associated abduction and dorsiflexion are discounted.179 Nevertheless, this appears to be the most practical method and the one that has gained acceptance. Measurement is done by observing the subject from a posterior viewpoint using reference markers on the lower

Foot and Ankle 1901

7°

Supinated

–11°

Neutral

Pronated

Shoe with midsole

Shoe without midsole

Bare foot

Figure 25B-24 Position of reference markers on the lower leg to define its axis and a second set of markers on the calcaneus to denote its position in kinematic analysis of gait. (Redrawn from Sport Research Review. Beaverton, Ore, Nike Sport Research Laboratory, Nov/Dec 1989.)

Figure 25B-25 Depiction of the effect of shoewear in increasing pronation from the barefoot condition. (Redrawn from Sport Research Review. Beaverton, Ore, Nike Sport Research Laboratory, Nov/Dec 1989.)

leg to define its axis and a second set of markers on the calcaneus to denote its position (Fig. 25B-24). Gait analysis is then performed using high-speed film cinematography, video cameras, or optoelectronic systems to visualize the markers during each phase of gait.199 The marker positions can then be plotted using anatomic landmarks and sent to a computer for analysis. This is the process of digitalization, from which are derived the specific angles exhibited at specific points in time in the gait cycle. In the cinematographic system originally used, the manual plotting and calculations needed for each frame of film made this an incredibly time-consuming and laborious method subject to a certain degree of human error. Kinematic analysis provides information on a number of variables including initial Achilles tendon angle, maximal Achilles tendon angle, initial pronation, total pronation, initial pronation velocity, and so on.95 By employing a video system, one can use a video processor to analyze the film and eliminate part of the tedious process of manual plotting. In the more sophisticated optoelectronic systems, the markers are actually infrared light-emitting diodes and are filmed by infrared-sensing cameras, thereby allowing further automation of the kinematic analysis.197 Regardless of the visualization method used, certain important factors must be taken into consideration. Sampling must be performed at a rate that is at least twice the frequency of the movement being analyzed, requiring a minimal rate of 200 Hz for rearfoot movement.199 The accuracy of the data collection system must be ensured both by the equipment manufacturer and by the on-site testing facility. Calibration, marker-to-marker distance testing, optimization of the collection environment, and meticulous attention to detail are just some of the factors necessary to ensure validity in kinematic testing.199 For example, the markers can be placed using either a relative method, wherein four markers are arbitrarily placed on the posterior foot or shoe and the posterior calf, or an absolute method, which uses standard anatomic landmarks. Furthermore, it should be remembered that testing is done in

a variety of conditions including different test subjects, different speeds from walking to sprinting, different surfaces ranging from treadmill to various over-ground conditions, in shoed and shoeless conditions, in varying types of shoewear, and in shoes with or without orthoses.189 This background is necessary to understand some of the information provided by the studies on rearfoot control. Although it is easy to see how a determination of rearfoot position could be performed in the barefoot runner, an obvious problem exists when the heel is hidden inside a shoe.200 How does one determine the proper position for the markers? This question has been answered by studies that have used a window in the heel of the shoe to allow visualization of the calcaneus position.196 One such study reported by Nigg analyzed measurements using one type of shoe in three test subjects with three trials per subject. A 2- to 3-degree shift was noted between the subject’s heel and the shoe itself.95 Because this shift was systematic, it was not believed to invalidate the test method. In a more recent study, Stacoff placed intracortical bone pins into volunteers to monitor movement coupling between shoe, calcaneus, and tibia. Apart from the difficulty of recruiting volunteers for this type of invasive monitoring, they observed considerable individual differences in coupling between these areas and suggested that we have yet to unravel the details of this complex interaction.201 Shoes and shoe design characteristics can have considerable effect on the kinematics of the foot in running and other sports activities including rearfoot control. Some of this effect is simply the result of displacement of the foot away from the contact surface by the shoe. It has been shown by several investigators that the Achilles tendon angle is decreased in the shoeless condition.189,197,200 The total rearfoot movement and rate of pronation are also reduced in the barefoot runner.95,189,197,200,202 This suggests that wearing shoes increases not only pronation but also other temporally related variables.189,197 This effect of shoewear is demonstrated in Figure 25B-25.


The shoe design variables that have been investigated most thoroughly with respect to kinematic effect include sole hardness, heel height, use of a heel flare, width of the midsole, and torsional flexibility.189,197 Sole hardness is measured in terms of durometer, a 25 shore A durometer sole being considerably softer than a 45 shore A durometer sole. Clarke and associates showed that the softer the sole, the greater the degree of maximal pronation and total rearfoot movement.129 A similar study by Nigg found exactly the opposite result, the softer sole having less total pronation.95 A later study by Nigg and colleagues confirmed their previous results, and further elaborated that the total foot eversion was roughly double for hard versus soft inserts.143 The harder inserts allowed for more individual variation of movement and did not force a preset movement pattern to the foot. Despite significant interindividual variance, the subjects with a flexible foot were more likely to have diminished tibial rotation. This study concluded that individual variation must be taken into account when matching feet to inserts. Because other factors such as overall shoe stiffness, shoe construction techniques, and variations in sole geometry can have significant effects on the kinematic function of the foot, it is easy to surmise how different results can be forthcoming from different laboratories when performing similar tests.189 Potential confusion in test results also occurs in the relationship of heel height to rearfoot control variables. Bates and coworkers found that raising the heel height in relation to the forefoot could reduce both maximal pronation and the period of pronation.200 Stacoff and Kaelin analyzed the effect of heel height over the range from 18 to 43 mm and found the same effect in the range from 23 to 33 mm but the opposite effect on pronation at the upper and lower ends of heel height.203 To cap things off, Clarke and associates discovered no significant effect of varying heel heights between 10 and 30 mm.129 It is apparent that there are inconsistencies in the studies generating dissimilar results and adding to an already confusing picture. With the introduction of the New Balance 305 Interval shoe in 1975, a new variable appeared in the shoe-foot control equation.9 The flared heel, seen originally in this shoe, was added primarily to improve the stability of the shoe by widening the base of support when the foot was on the ground. Following the principle that “if a little bit is good, then more will be better,” Nike introduced a shoe in the late 1970s that had a full 1-inch lateral heel flare. Unfortunately, a negative byproduct was quickly perceived in the increasing incidence of lateral knee pain that occurred with this shoe.9 Nigg and Morlock discovered the underlying problem with the flared heel in a scientific study of 14 runners reported in 1987.156 Using three shoes identical except in their degree of lateral heel flare, the authors noted increased initial pronation with wider flare but no difference in total pronation or impact forces at heel strike. Increasing the lateral heel flare increases the lever arm on the axis of motion across the subtalar joint, resulting in earlier initiation of a pronating movement, greater rearfoot angulatory velocity, and an increased initial Achilles tendon (touchdown) angle. A similar study by Nigg and Bahlsen confirmed this result but indicated that heel flare was less important when a softer midsole was used.204 This study supported the earlier work of Cavanagh on a

rounded heel design by demonstrating a reduction of more than 15% in the time of peak force with use of this modification.189,204 Two shoe design characteristics that have been introduced recently are related to midsole width and torsional flexibility. Both have been supported by shoe companies—Nike promoting the wider midsole and Adidas promoting running shoes with greater torsional flexibility.40,196,205 According to the results provided by the Nike Sports Research Laboratory, reductions in maximal pronation and maximal pronation velocity can be obtained by increasing sole width to about 90 mm.197 Torsional flexibility is a new concept related to evaluating the foot in three dimensions rather than by the traditional twoplane analysis of rearfoot inversion and eversion. Work by Stacoff and colleagues has demonstrated that large torsional movement occurs between the forefoot and hindfoot in the barefoot state.202 This three-dimensional linkage between the forefoot and hindfoot is mediated through the tarsometatarsal (Lisfranc’s) and transverse tarsal (Chopart’s) joints and in a shoe can be influenced by shoe sole construction factors. Shoe soles that are stiff in the longitudinal direction restrict the torsional movement normally produced when the forefoot adapts to the ground. Adidas has taken this concept and developed an entire line of running shoes with “a unique construction that controls the natural torsion, or twisting of the foot.”205 They also claim “the foot moves as nature intended it to. The natural twisting of the front part of the foot is controlled so that it no longer strains joints and tendons. Performance greatly improves, whereas injury and muscle strain are substantially diminished.”205 This seems to be an exaggerated claim for a shoe design feature that affects a foot movement that itself is not entirely understood, much less how it is changed by the shoe design and how that relates to other kinematic values. More time and research will be necessary to establish the importance of such factors as shoe width and torsional flexibility because they appear to be mutually exclusive based on examination of the shoes produced with this technology (Fig. 25B-26). The fabrication of orthotic devices to control rearfoot stability, thereby treating various disorders of the lower extremity, has a rather short history. In 1962, Rose presented one of the earliest studies on the ability of a positionmodifying device (the Schwartz meniscus) within the shoe to alter the rotation of the lower leg.206 Sheehan, writing in the Preface to The Foot Book by Harry Hlavac, traced the origin of biomechanical therapy to the early 1970s and the development of sports podiatry.207 He theorized that the increasing problem with anterior knee pain in runners was the key to the development of orthotic devices for the foot. The ability of a shoe insert to provide benefit when a surgical solution was not forthcoming led to “the ascendancy of orthopedic medicine.”207 Ascend it did, as orthoses for sports scaled new heights in cost, in numbers, and in varieties of conditions for which they were recommended. At present, many athletes and coaches think that the orthotic device is standard athletic equipment. Athletes come to the clinician with one sort of complaint or another and a self-made diagnosis requesting “orthotics.” In this environment, it is critical that individuals involved in the

Foot and Ankle 1903

Figure 25B-26 Example of wide versus narrow midsole widths used in the Nike (right) and Adidas (left) running shoes. (Photograph by Thomas O. Clanton.)

field of sports medicine understand not only the biomechanical principles behind the use of orthotic devices but also the relevant literature from gait laboratory studies. As in the evaluation of shoewear, kinematic analysis of various parameters is essential to the documentation of

it was Nigg who first determined the effect of shoe inserts on gait using film analysis.31 Nigg’s study concluded that a properly functioning insert should change gait characteristics toward values consistent with those of normal feet. Cavanagh and colleagues presented a paper at the 1978 meeting of the American Orthopaedic Society for Sports Medicine in Lake Placid, New York that showed a reduction in maximal pronation and maximal velocity of pronation in runners who used a properly placed felt shoe pad as a medial support.189 Nigg and associates reported in 1986 on the use of various conditions and positions (from no support to anterior to posterior positions) for medial supports within the shoe, demonstrating that placing the pad (elastic cork in this instance) more posterior reduced initial pronation and maximal pronation to a lesser extent (Fig. 25B-27).208 Taunton and coworkers found a similar reduction in maximal pronation with the use of an orthosis.209 These studies support the ability of an orthosis to affect kinematic parameters. Further work in this area was provided by Smith and colleagues, who studied 11 well-trained runners using soft or semirigid orthoses while running on a treadmill at a 6- and 7-minute mile pace.210,211 They found that calcaneal eversion was reduced in their subjects, who had an average rearfoot varus posting of 4.2 degrees. This reduced maximal pronation from a mean of 11.3 degrees in controls to 10.5 degrees for the soft orthosis to 10.1 degrees for the semirigid device, only a 1% change. Maximal velocity of pronation was reduced from a mean of 540 degrees per second in controls to 430 degrees per second for the soft orthosis to 464 degrees per second for the semirigid group, an 11% change. Although the reduction in maximal pronation is quite small compared with the expected result for this amount of posting, the reduction in pronation velocity may play a larger role in symptomatic relief provided by orthoses—an effect that can be achieved as adequately by the less expensive soft orthosis as by the semirigid orthosis. Although these studies further augment the role of

Changes in Angles Degrees

15

2

∆βpro = maximal Achilles tendon angle

10

3

Lateral

∆β10 = initial penetration

4

5

5

Medial

∆γ10 = initial change of rearfoot angle

3 4 5 Bare With 2 foot out Anterior Posterior Figure 25B-27 Graphic demonstration that placing an insert more posteriorly reduces initial pronation and maximal pronation. (From Nigg BM: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics, 1986. Copyright © 1986 by Benno M. Nigg.)

orthotic effects on gait. According to Stacoff and Luethi,


rthoses in adjusting kinematic variables, other authors o have had results that are less supportive. One of the most widely recognized studies of foot orthoses and their effect on gait is that done by Bates and associates in 1979.163 This study failed to confirm a significant reduction in maximal pronation with a custom-molded orthotic device compared with shoes in six symptomatic runners. The study compared its results with control values obtained in a previous study of 10 asymptomatic runners.200 Their results also suggested that an increased velocity of pronation occurred with the orthotic device in contrast to the findings of the previously mentioned studies. Rodgers and LeVeau produced a similar study using 29 runners fitted with custom-made semirigid orthoses made from polypropylene.212 Subjects ran in their own shoes on an outdoor track and were filmed with 16-mm film at 120 frames per second. Runners completed three randomly sequenced runs in the following conditions: (1) barefoot, (2) shoe without orthosis, and (3) shoe with orthosis. Values obtained for maximal pronation, angulatory velocity of pronation, and time spent in pronation were not significantly different among the three conditions. There was, however, a trend toward decreased maximal pronation and time in pronation in the shoe with orthosis group. Smith and colleagues pointed out some of the flaws in the various studies related to inadequate control of confounding variables such as type of shoe, type of orthosis, and physical measurements of test subjects.211 Given the number of variables that are being analyzed in these gait studies of running, there should be little surprise that some discrepancies exist. More studies will be necessary to determine which of the variables is important in relation to the clinical situation and the prevention or treatment of injuries. Progress in this field would proceed at a more rapid rate if there could be some universal agreement on terminology, methods of measurement, normal values, and sharing of information without commercial self-interest.

Clinical Work Although there is a widespread belief in sports medicine circles that biomechanical abnormalities are a significant causal factor in lower extremity injuries, clinical studies have had paradoxical results. The military formerly believed that the pronated flat foot was more susceptible to injury, but recent work has disproved this belief. DeVan and Carlton suggested as early as 1954 that stress fractures of the metatarsals were equally common among pronated, normal, and cavus foot types.213 Bensel214 and Gilbert and Johnson215 reached the same conclusion from their research. Further confirmation of this conclusion has come from the Israeli Army study of 295 recruits, which indicated that the low-arched foot might even protect against the development of stress fractures.174 The overall incidence of stress fractures in their study was 39.6% in recruits with a high arch, 31.3% in those with average arch height, and 10% in those with a low arch. It is important to note that in these studies, the criteria for defining arch height were subjective, and determinations were made in a non–weight-bearing position. A continuation of the Israeli Army study was reported in 1989 with a more quantitative determination of the

TABLE 25B-11 Risk Factors in Running Injuries Characteristics of Runners

Characteristics of Running

Characteristics of Running Environment

Age Gender Structural abnormalities Body build Experience Individual susceptibility Past injury

Distance Speed Stability of pattern Form Stretching, weighttraining, warm-up and cool-down

Terrain Surface Climate Time of day Shoes

From Powell KE, Kohl HW, Caspersen CJ, et al: An epidemiological perspective on the causes of running injuries. Physician Sportmed 14:100-114, 1986.

longitudinal arch based on radiographic analysis.171 This study reported a higher number of metatarsal stress fractures in recruits with low arches, whereas the incidence of femoral and tibial fractures in these recruits was less than that in those who had a higher arch. This result seemingly contradicts the findings of the previous studies. It should be noted that both of the Israeli Army studies excluded those with marked pes cavus or pes planus from the outset. A subsequent Israeli Army study examined the use of custom soft or semirigid functional orthoses and suggested a benefit in reducing stress fractures; however, fewer than half the recruits completed the study using their assigned orthoses (25% dropped out because of dissatisfaction with the orthosis). Nearly 50% of the arriving recruits were already using orthoses (30% custom-made).62 All of this adds further confounding variables complicating interpretation of the various clinical studies and extrapolation of an association between biomechanical parameters and symptomatology. Among runners, it is evident that a number of risk factors have been implicated in the production of injuries (Table 25B-11).216-218 Because so much emphasis is placed on the relationship between overpronation and injury, it is natural to expect confirmation of this in the epidemiologic surveys of running injuries. One of the first studies to focus attention on the role of pronation in runners was that of James and colleagues in 1978.153 They reported a 58% incidence of pronation in 180 patients evaluated for a variety of complaints. It is important to note that one cannot draw the conclusion that most injured runners have pronated feet because there is no way of determining the overall incidence of pronation in the running population. Despite this fact, it is our opinion that this study was instrumental in focusing the attention of sports medicine specialists on the role of alignment in sports injuries. Unfortunately (or perhaps fortunately for the overpronator), no such relationship has been clearly determined in epidemiologically valid studies.217 One of the most comprehensive studies of running injuries is the Ontario cohort study, which included 1680 runners. Anthropometric measurements including femoral neck anteversion, pelvic obliquity, knee and patella alignment, rearfoot valgus, pes cavus and pes planus, somatotype, and running shoewear pattern were made in 1000 of these runners. The study concluded that “none of the anthropometric variables measured was

Foot and Ankle 1905

TABLE 25B-12 Effectiveness of Orthoses

Diagnosis

No. of Patients (%)

Percentage Improved with Orthosis

Posterior tibial syndrome Pes planovalgum Metatarsalgia Plantar fasciitis Calcaneal spur Iliotibial band tendinitis Cavus foot Leg-length inequality Chondromalacia patellae Achilles tendinitis Miscellaneous Total

55 (27.5) 23 (11.5) 30 (15) 20 (10) 18 (91) 14 (7) 13 (6.5) 10 (5) 6 (3) 4 (2) 7 (3.5) 200 (100)

77 90 87 81 66 25 NA NA NA NA

NA, not available. From D’Ambrosia RD: Orthotic devices in running injuries Clin Sports Med 4:611-618, 1985.

s ignificantly related to risk.”218 The most consistent risk factor for a running-related injury is weekly training mileage, and this has been proved in study after study.216-220 When weekly distance reaches 64 km or 40 miles per week, the risk for injury increases by 3 times.216,218 Additionally, no correlation has been shown between shoe characteristics (e.g., varus wedge or waffle sole) or shoe expense and injury reduction in these studies.144,218,221 Given all this information, what role does rearfoot stability provided by shoes or orthoses play in the prevention or treatment of athletic injury? Although the scientific approach of systematically establishing a basis for the use of orthoses has failed, there does appear to be some practical basis for prescribing orthoses to injured athletes. Seventy-eight percent of the injured runners in the oft-quoted series of James and colleagues reported some benefit from the use of either rigid or flexible orthoses.153 D’Ambrosia subdivided patients by diagnosis and analyzed the numbers who benefited from the use of an orthosis. The subgroup with pes planovalgus had the most benefit (90% of patients), whereas the subgroup with pes cavus had the least benefit (25% of patients) (Table 25B-12).175 Another study from the Louisiana State University Medical Center Runner’s Clinic reported a 72% improvement in symptoms with the use of orthoses, although these were prescribed for only 10% of their total patient population.222 Blake and Denton surveyed 180 patients and reported that 70% claimed that they were “definitely helped” by treatment with functional foot orthoses.223 Donatelli and coworkers used a similar questionnaire survey of patients to document a 90% relief of pain in patients treated with semirigid orthoses alone.224 A recent multicenter study compared custom-made and prefabricated orthoses in the treatment of plantar fasciitis. Patients were treated with stretching alone or stretching with one of four different orthoses, three of which were prefabricated and one of which was custom-fitted. Stretching alone produced improvement in 72%, whereas those who combined stretching with a silicone heel cup showed the most improvement (95%). Subjects who stretched and used a custom orthosis improved only 68% of the time.

Stretching alone or combined with a prefabricated inlay of any of the types tested was significantly more likely to lead to improvement than use of a custom orthosis with stretching.225 Santilli and Candela found that 100% of 40 athletes complaining of metatarsalgia were relieved of symptoms by a custom-molded polyurethane insert that enabled them to resume sports within 3 weeks.226 Kelly and Winson found that a prefabricated foam inlay with the ability to individualize the placement of the metatarsal support was more effective in relieving metatarsalgia than a prefabricated silicone orthosis, which could not be “semi-customized.”145 A study by Gross and associates reported that 75% of 347 long-distance runners had complete resolution of or great improvement in their symptoms with various types of orthoses (mostly flexible).176 Similar success rates of 70% to 90% have been reported by other clinics using orthotic prescriptions for various athletic injuries.31,176 Based on this evidence that orthoses can improve symptoms and generate documentable alterations in defined kinematic variables, one would assume that a positive attitude exists supporting their continued use. The inconsistency is that “different schools of applying inserts seem to have equal success despite the fact that their inserts look quite different.”31 Support for the value of expensive running shoes (incorporating some of the same principles as orthoses) to treat injuries or symptoms is harder to generate.221 Injury rates for runners have shown no decrease during the past 3 decades of improved shoewear technology, although many factors are at work in this statistic.9,216-218,220,221,227-229 These include the entry of the less physically fit into, and an aging of, the running population. Comparative studies of injury rates in runners have been performed for two separate periods by the University of British Columbia Sports Medicine Clinic.227,228 The results indicate a reduction in foot and ankle injuries in the more recently studied group but an increase in knee injuries. This finding begs the question originally proposed by Cavanagh of whether the increasing technology applied to shoewear has actually contributed to this change.9 The work of the Human Performance Group in Quebec appears to substantiate the idea that increasingly well-cushioned and controlled athletic footwear has tended to produce injuries rather than protect the athlete from them.115-119,229 Perhaps an enterprising shoe company will spend part of its advertising budget on a cooperative study with a runners’ clinic to produce a study that will help answer the question of whether these technologic advancements are helping or hurting. Realistically, the number of variables involved presents an almost insurmountable barrier to epidemiologically valid studies of this nature. Although much has been accomplished in this field in a relatively short time, there are still many unanswered questions and ample opportunities for the inquisitive researcher.

Energy Return Although several shoe companies either state or imply the ability of their products to return energy to the athlete, little support exists for this in the scientific literature.77,230,231 Any shoe that would return energy of a beneficial nature to its user would need to return this energy at the correct location, time, and frequency. Unfortunately, materials


used to increase shock absorption tend to be poor for energy return.232,233 Additionally, the location of maximal possible energy storage (the rearfoot) is not ideal for use of any returned energy.231,233 Nigg and Segesser have demonstrated that running with running shoes actually requires 3% to 5% more energy than running barefoot.231 They have calculated that the maximal amount of returnable energy from shoewear is less than 1%, which is not even sufficient to overcome the energy requirement of accelerating the shoe itself, or to make up the additional vertical movement added by the shoe.231 Consequently, claims of a shoe’s ability to improve or alter performance through return of energy to its wearer should be viewed with skepticism. It appears that energy considerations may be better met through limitation of energy loss.233 Stefanyshyn and Nigg examined the effect of increased bending stiffness in the midsole, through insertion of a carbon-fiber plate, on jump height and loss of energy through the metatarsophalangeal joint.233 They surmised that stiffening the metatarsophalangeal joint would decrease the amount of energy lost and increase jumping performance. The former was indeed the case for both running and jumping, and vertical jump height was increased by 1.7 cm in the stiffest shoe tested. No comment was made on the potential for increased risk for injury to the Achilles tendon complex, as has been suggested in stiff-soled designs.34

Friction and Torque This aspect of shoewear is thoroughly covered in Chapter 25C and will not be repeated here. Obviously, shoe design features carry major significance in this area. Nigg and Segesser suggested that frictional loads on the human body are of greater importance in the production of sportsrelated pain and injuries than impact loads.234 The interested reader is referred to the previously noted chapter for a discussion of friction and torque related to athletic shoewear.

PROPER FIT AND SHOE PURCHASE DECISIONS Although biomechanical abnormalities have caught the attention of both the athlete and the sports medicine practitioner in recent years, these problems are much less likely

to be the source of day-in and day-out problems compared with the difficulties created by poorly fitting shoes. It is the poorly fitted shoe that creates such commonplace annoyances as blisters, ingrown toenails, certain forms of calluses, metatarsalgia, nerve compression syndromes, “black toes,” corns, and a variety of other unnecessary ills. Most of these conditions are preventable with a working knowledge of shoe-fitting techniques. The most classic case of a footwear-related problem is the bunion. Although there are certainly individuals who have an anatomic predisposition to develop this condition, it has become evident from accumulated scientific research that the improperly fitted shoe is of major significance in the causes of bunions, or hallux valgus. Hoffman’s study of barefooted peoples demonstrated “progressive characteristic deformation and inhibition of function” in people who wore shoes compared with those who remained shoeless.235 Kato and Watanabe pointed out the relationship between the development of hallux valgus as a clinical entity in Japan and the introduction of the Western-style shoe to replace the traditional geta sandal.21 Other studies have reached similar conclusions, but this has had little effect on the shoe manufacturing industry or the consuming public, who continue to believe that the dainty foot is the most attractive foot. Shoe fit is governed primarily by sizing systems used in the manufacturing process. The English system, originated in 1324, was based on the length of barleycorns (one barleycorn equals 1⁄3 inch).22,74 Today there are numerous systems of sizing in use around the world, making it difficult to fit the foot based on size alone. The most common systems are the English, the American standard, the Continental sizing, and the centimeter systems.22 When determining the proper size to try at the shoe store, it is traditional to use a device such as the Brannock, the Ritz, or the Scholl to size the foot. These devices measure the overall length of the foot, the position of the metatarsal break (related to arch length and toe length) and the girth or width of the foot. The latter is designated by a letter in most circumstances, with AAA being the most narrow, C and D being standard medium widths, and EEE being the widest.22 This form of width sizing is relatively standard and corresponds to various last width standards as seen in Table 25B-13 and Figure 25B-28. In athletic shoewear, it is uncommon to find width sizing available. The New Balance Company has made width sizing a relatively successful marketing strategy in the

TABLE 25B-13 Last Width Standards (Generally Accepted) American Men’s 8A 8B 8C 8D 8E 8EE 8EEE

9A 9B 9C 9D 9E 9EE

10A 10B 10C 10D 10E

Inches (cm) 8½ 8¾ 9 91⁄8 9¼ 9½ 9¾

(21.6) (22.2) (22.9) (23.2) (22.5) (24.1) (24.8)

Inches (cm) 8 ⁄16 815⁄16 91⁄8 93⁄8 97⁄16 911⁄16 10 11

(22.1) (22.7) (23.2) (23.8) (24.0) (24.6) (25.4)

From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.

Widths Available AAAAA AAAA AAA AA

A B C D

E EE EE EEE EEEE

Foot and Ankle 1907 International Size-Scale Comparison Chart 15

16

14

15

11

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13

9

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1 7

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32 31

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8 7 6

27 26

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2 1 13 12

22 21 20

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8 7 6 5

16 15 14

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2 1 0

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49 48 47 46 45 44 43 42 41 40 39 38 37 36 35 34 33 32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17 16 15 14 13 12 11 10 9 8 7 6 5 4 3 2 1

32 31 30 29 28 27 26 25

13½ 12½

24

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10 9 8 7 6 5 4 3 2 1 Approx Age

Metric Scale

French Sizes

Japanese Sizes

Boston Sizes

American Custom Sizes

American Standard Sizes

English Sizes

Inches

American Ladies Sizes

Figure 25B-28 International size scale comparison chart. (From Cheskin MP: The Complete Handbook of Athletic Footwear. New York, Fairchild Publications, 1987.)


F

C A

B

D

E

A — Ball girth B — Waist girth C — Instep girth D — Long heel girth E — Short heel girth F — Heel-toe length Figure 25B-29 Right and left feet with different shapes and shoe fit requirements. (Photograph by Thomas O. Clanton.)

running shoe market. At present, most athletic shoes are made on a standard D last for men and a C last for women. Adjustability for width is often incorporated into the lacing system. A variety of lacing strategies can be used to accommodate a range of temporary or permanent foot shape considerations, and these are demonstrated in Figure 25B-16.32 Additionally, newer, round “laceroni” shoelaces have found their way into shoes. These slide more easily than flat laces when used with the newer loop and web eyelet designs. Pressure is thus more evenly distributed on the dorsal foot than with flat laces, and problems with kinking are minimized. Nevertheless, these lace designs have the slight disadvantage of untying more easily.56 Although women’s shoes are made on a narrower last than men’s, many athletic women have a foot shape more like a man’s and therefore are more properly fitted by the use of a man’s shoe. The manufacturing process has a major impact on how the shoe fits, specifically with regard to the exact last that is used. Different manufacturers use different lasts, which naturally affect the size and fit of the shoe and cause the discrepancies seen in the fit of the same size shoes from different companies. It is for this reason that when an athlete finds one particular make and model of shoe that is satisfactory, he or she will not vary from it except in extraordinary circumstances. This has led to such practices as a famous athlete endorsing a particular company’s shoes while wearing the shoe of a different company, or having his shoes modified by a logo change to resemble the shoes being endorsed.22 Clearly, the proper fitting of the shoe is indispensable to maximal performance in the eyes of many sports participants. Because fit and comfort are so critical, it would seem that the popular shoe surveys would try to determine how to achieve proper fit for the benefit of their readership. Evidently, this is a matter of individual preference and is not quantifiable in the same sense that shock absorption and pronation control can be analyzed. There are too many variables among individuals and even major differences between right and left feet in the same individual (Fig. 25B-29). Comfort and fit are a matter of individual

Figure 25B-30 Measurements used in proper fitting of a shoe include the ball girth, the waist girth, the instep girth, the long heel girth, the short heel girth, and the heel-to-toe length or stick length. (Redrawn from Cavanagh PR: The Running Shoe Book. Mountain View, Calif, Anderson World, 1980.)

preference—some people like a snug fit, whereas others like a more loosely fitting shoe; some like the feel that a soft insole provides, whereas others do not like this sensation; and some like the feel of a higher heel, and others cannot tolerate this. In our own dealings with patients, it has become evident that although we can make suggestions based on reasonable empirical considerations, it is impossible for us to predict with accuracy which shoe a specific patient with a specific foot type will select as the most comfortable. It should be apparent from the earlier discussion that much of what goes into the fit and comfort of the shoe is derived from the lastmaking process (see the earlier section entitled “Anatomy of the Sports Shoe”). Six measurements are taken into consideration in this process: the ball girth, the waist girth, the instep girth, the long heel girth, the short heel girth, and the heel-to-toe length or stick length (Fig. 25B-30).22 Other important specifications are the toe spring, the heel breast, the heel height, and the heel pitch.22,31 These measurements are then used by the lastmaker to turn a piece of unfinished rock maple or other wood into the finished last. The variability of design produces endless possibilities for fit. Stacoff and Luethi calculated that if 20 different elements in shoewear construction were varied by five systematic steps, more than 95 trillion test shoes would be produced.31 Traditionally, a great deal of craftsmanship has gone into the area of lastmaking. Now, with computer technology, standardization has been introduced that will ideally lead to better fit and greater comfort. In determining the proper fit of a pair of shoes, it is commonly believed that the shoe may be somewhat uncomfortable on the first fitting but can then be “broken in” over time. Conversely, it is often thought that the shoe that feels comfortable in the store the first time will then fit comfortably for the rest of its natural life. Unfortunately, both of these concepts are subject to error. For these reasons, it is important to approach thoughtfully the purchase or fitting

Foot and Ankle 1909

Figure 25B-32 Demonstration of the “pinch” test. The individual stands in the shoe bearing weight while the examiner pinches a small amount of material in the upper between the thumb and index finger across the forefoot of the shoe. (Photograph by Thomas O. Clanton.) Figure 25B-31 Demonstration of proper fitting of a shoe for length. Between half width and a full width of the examiner’s thumb can be placed between the end of the longest toe and the end of the shoe. (Photograph by Thomas O. Clanton.)

of a pair of athletic shoes. The decision to purchase a particular shoe should be based on the quality of construction (brand name may or may not be a factor in this). One should avoid buying a shoe simply because it is made by a specific company or endorsed by a certain athlete. Many universities and professional sports teams receive shoes at considerable discounts or even have them donated for the publicity derived by the shoe company. In this situation, it is not uncommon to encounter fitting problems in certain athletes who simply do not have a foot that fits well into the selected shoe. Also, some athletes’ feet require shoes with greater stiffness or other specific characteristics that are not available in the offered shoes. Rather than forcing athletes to adjust to the shoe for the sake of conformity, it is preferable to let them participate in the selection of a shoe that they know will fit well and that will allow them to perform to the best of their ability. Although this is seldom possible in intercollegiate or professional sports, the sports medicine specialist should be sensitive to the relationship between poorly fitting shoes and certain complaints of the athlete as well as the need to switch to a more supportive shoe when appropriate. There are three basic determinations to be made in the fitting of shoes. One must first ascertain that the length is correct. This can be guided by the “rule of thumb” test performed by pressing on the end of the shoe while the wearer is applying full weight. There should be between half and a full width of the examiner’s thumb between the end of the longest toe and the end of the shoe (Fig. 25B-31).

It is essential to note that for many people, the second toe is longer than the great toe. Another important test for length is to have the athlete kick the plantar forefoot into the ground as he would in a sudden stop. If the toes jam uncomfortably into the end of the shoe, the shoe will not last long, the toes will suffer, or the shoe will be shelved. It is wise to do this test before the shoe is purchased. The next step in the fitting process is to determine proper width. The “pinch” test helps with this. The individual stands in the shoe while the examiner tries to pinch a small amount of material in the upper between the thumb and index finger across the forefoot of the shoe (Fig. 25B-32). The final test is a determination of the flex point of the shoe in relation to the metatarsal break of the foot. If the shoe does not have the proper degree of flexibility in the appropriate location, one can expect problems (Fig. 25B-33). In the past, the flexibility test was one of the common tests used by Runner’s World in their annual shoe survey.9 The shoe was bent through a 40-degree range, and the force required to do this was measured with a strain gauge. It has been assumed that the less force required, the better, because this is force that must be generated by the runner. There is a fallacy with this assumption, however. It has become evident in shoes designed for artificial surfaces that the overly flexible shoe can predispose the wearer to sprains of the metatarsophalangeal joints, such as turf toe (see Chapter 25C for further details).236 Furthermore, certain athletes may have underlying problems such as hallux rigidus or plantar fasciitis that are aggravated by the overly flexible shoe. Joseph, in a study from the 1930s, found that the average male needs only 30 degrees of flexibility in the first metatarsophalangeal joint for normal walking and that the stiffer soled shoe provided better support for

1910 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25B-14 Ten Points of Proper Shoe Fit A

B C

A

1. Sizes vary among shoe brands and styles. Don’t select shoes by the size marked inside the shoe. Judge the shoe by how it fits your foot. 2. Select a shoe shape that conforms as nearly as possible to the shape of your foot. 3. Have your feet measured regularly. The size of your feet changes as you grow older. 4. Have both feet measured. Most people have one foot larger than the other. Fit to the largest foot. 5. Fit at the end of the day when your feet are largest. 6. Stand during the fitting process and check that there is adequate space (3⁄8 to ½ inch) for your longest toe at the end of each shoe. 7. Make sure that ball of your foot fits comfortably into the widest part (ball pocket) of the shoe. 8. Don’t purchase shoes that feel too tight, expecting them to “stretch” to fit. 9. Your heel should fit comfortably in the shoe with a minimal amount of slippage. 10. Walk in the shoe to make sure it feels right! (Fashionable shoes CAN be comfortable!) From American Orthopaedic Foot and Ankle Society, National Shoe Retailers Association, and Pedorthic Footwear Association: 10 Points of Proper Shoe Fit.

B

1

2

Figure 25B-33 Demonstration of differences in metatarsal break point seen in feet of the same length and how this affects shoe fit. A, Both feet have the same overall length (line A) but different heel-to-ball lengths (lines B and C). B, Improper fit of the heel-to-ball length can create functional problems in the shoe. Point 1 represents the center of rotation of the first metatarsophalangeal joint, and point 2 represents the flexion point of the shoe. (From Prescription Footwear Association: Reference Guide and Directory to Pedorthic Practice. Columbia, Md, 1988.)

the foot.237 The findings documented in the earlier section on “Energy Return” also support increased stiffness in the shoe’s sole. One can quickly realize that all the answers are not available on this aspect of comfort and fit. This is one of the many areas in which a great deal of individual variability exists in both objective and subjective factors. A number of other considerations should be taken into account in the shoe selection process and are mentioned only briefly here. As noted earlier, the shape of the shoe is determined by the last, and this shape can be divided into either straight or curved forms (see Fig. 25B-12). The straight last provides greater support along the medial aspect of the foot and is better suited to the athlete who has a lower arch or who tends to overpronate. Cheskin also recommends the straight-lasted shoe for the athlete who participates in activities demanding slower and more controlled movements, whereas the curved last is better for faster movements.22 The curved last is generally better for the individual who has an adducted foot or a cavus foot. In purchasing shoes, one should try to mimic the conditions under which they will be worn as much as possible. Because feet tend to swell at the end of the day or after

vigorous activity, this should be taken into consideration. In most individuals, one foot is larger than the other or has certain anatomic features that mandate greater emphasis in the fitting process. One generally uses a specific sock in specific shoes, and it is important to remember this in the fitting process. Also, one’s shoe size does not remain static over the years. A recent survey by the Women’s Footwear Council of the American Orthopaedic Foot and Ankle Society found that women’s feet increase in size in a relatively consistent fashion from the second to the sixth decade of life.20 Even in the same manufacturer, there can be variations within the same labeled size for different shoes. Despite the fact that in the United States alone, there are an estimated 1.2 billion pairs of shoes sold annually by some 200,000 salespeople employed by more than 50,000 shoe stores or departments, fewer than one fourth of Americans can recall the last time they had their feet sized. It is estimated that nearly three fourths of Americans wear shoes that fit improperly, with the leading offenders being shoes that are too narrow or too short.238 To help combat the seemingly bewildering task of finding a pair of shoes that fit well, the American Orthopaedic Foot and Ankle Society, in combination with the National Shoe Retailers Association and the Pedorthic Footwear Association, has summarized many of the points contained in the preceding paragraphs and compiled a brochure outlining the “10 Points of Proper Shoe Fit” (Table 25B-14). The quality of production is not always the same for every shoe even within the same product line. The purchaser should pay close attention to the construction of the shoe in the fitting process. There may be a bad seam or an improperly applied layer that will affect fit and comfort. The type of material used in the construction of the shoe upper is also of interest because it affects the conformability of the shoe as well as its breathability. The temperature

Foot and Ankle 1911

and humidity perceived by the foot are related to this latter property and are a factor in the shoe’s comfort. One should appreciate the knowledge required of the athletic equipment manager or skilled salesperson in selecting the correct shoe for individuals who have markedly varying feet and participate in numerous athletic endeavors. For this reason, it is helpful if the manager or salesperson has personal experience with athletic shoes as well as some book knowledge and apprenticeship training along with a desire for a satisfied athlete-customer. It is quite common for those involved in the care of athletes, particularly runners, to be asked for suggestions about the best running shoe, tennis shoe, skating boot, and so on. From the foregoing discussion, it should be obvious that there is no one shoe that can fulfill all the criteria necessary to be the ideal shoe for all individuals. We have seen shoes used in sports progress from a rather simplistic design to a design that involves more computers and researchers than many fields of medicine. By the same token, the price has achieved similar emphasis, and we see teenagers getting summer jobs in order to purchase $150 basketball shoes, only to keep them in the closet for fear of having them stolen.60 There is no question that a decision about which shoe to wear or to recommend is very important to an industry that pays six-figure salaries to college coaches and offers multimillion-dollar contracts to high-profile professional athletes. Nevertheless, it is this climate of commercialism and competitiveness that has produced dramatic achievements in the athletic shoewear industry during the past 20 years. No doubt even the least expensive shoes are a far cry from the technologically unsophisticated shoes worn by our forefathers. It is unnecessary to reach the conclusion that one must wear the shoe with the latest gimmick or the highest price tag to achieve one’s maximal performance or to avoid serious injury. For the most part, all the well-known companies in the athletic shoe industry make a high-quality product and have high- and low-end options. In selecting a shoe, one must remember that price can be used only as a very general guide to the quality and functional usefulness of a shoe. Once a running shoe, for example, reaches the $50 level, it usually incorporates all the principal components that are critical to satisfactory performance in such a shoe. Also, the price of the shoe is

directly proportional to the amount of advertising used to market that shoe. Interestingly, there is usually another shoe of virtually identical quality available at a lower price from the same manufacturer. The consumer should always consider that shoe manufacturers might provide misleading information to the consumer. For example, a 1991 survey by Running magazine asked manufacturers to provide information regarding the type of runner for whom their shoes were designed. Of 171 models of shoes, including spikes as well as running and general athletic shoes, 26% were purported to be for both pronators and supinators, 36% claimed an advantage for both the high-arched and flat-footed individual, and amazingly, two shoes in the survey claimed benefit for every distance, foot type, heel-strike pattern, and surface mentioned.34

SUMMARY Knowledge of athletic shoes, pads, inlays, inserts, and orthoses has become important in the field of sports medicine for many reasons. This knowledge is essential not only from the standpoint of treating and preventing injuries but also to halt the propagation of misleading information and avoid unnecessary expense. Athletic shoewear is essential for the protection of the athlete’s foot, but this protection must extend to the athlete as a whole. With a brief historical perspective and knowledge of the construction of shoes and orthoses, individuals can better understand the factors involved in this protection. These factors include shock absorption, stability, friction and torque, and proper fit. Their specific contributions to athletic performance, comfort, and injury risk remain incompletely elucidated despite numerous laboratory and clinical studies. It is hoped that this chapter not only has stimulated increased awareness of the role of athletic shoes and orthoses in the field of sports medicine but also has pointed out the need for further research.



S e c t i o n

C

Ligament Injuries 1. Ligament Injuries of the Foot and Ankle in Adult Athletes Melissa D. Koenig

The foot and ankle serve as a constant interface with our environment. This unique collection of tissues, each with a variety of specialized functions, allows efficient, upright stance and locomotion. Injury to the foot and ankle ligaments results in varying degrees of impairment and associated disability. Athletic ability, regardless of competitive level, is dependent on foot and ankle function. Diagnosis and treatment of foot and ankle ligament injuries are dependent on a complete understanding of foot and ankle anatomy and biomechanics (Fig. 25C1-1). An excellent review of foot and ankle biomechanics is presented within the first section of this chapter (see Chapter 25A, Biomechanics). The diagnosis and treatment of common ligament injuries to the ankle and foot in the adult athlete are reviewed in the following sections.

INJURY TO THE ANKLE LIGAMENTS In the following section, ankle ligament injuries are arbitrarily divided into lateral ankle sprain, medial ankle sprain, ankle syndesmosis sprain, and dislocation of the ankle without fracture. The division is artificial in that many ankle sprains represent a combination of ligament injuries. Ankle ligament injury associated with malleolar fracture is not discussed as a separate topic. An anatomic division of the ankle ligaments is presented in Table 25C1-1 for the purpose of completeness and discussion.

Lateral Ankle Sprain Lateral ankle sprain represents one of the most common injuries in the athletic population.1 Inversion of the plantar flexed ankle is the accepted mechanism of injury for lateral ankle sprain (Fig. 25C1-2). Stretching or tearing of the lateral ankle ligaments leads to inversion instability, a condition that may present in an acute or chronic setting. The highest incidence of injury is localized to the lateral ankle ligaments but may also include the subtalar joint. Among the lateral ankle ligaments, the most commonly injured structure is the anterior talofibular ligament (ATFL). Among cadets at West Point, one third sustained one or more inversion injuries during their 4-year placement.1 Among high school students, ankle injuries are estimated to occur in 1 of every 17 participants per season; 85% of these injuries are ankle sprains.2

Gerber and associates prospectively evaluated cadets at West Point over a 2-month period.3 Football, soccer, jogging, and basketball were the activities most often associated with ankle sprain. Among high school athletes, ankles sprains are most common among men’s and women’s basketball players, followed by participants in football and women’s cross-country.2 A varsity high school basketball survey revealed that 70% of players had a history of ankle sprain.4 Ankle sprain is the most common soccer injury (17% of injuries in senior division men’s soccer), with a cumulative incidence of 27% over an 8-year period.5 Lateral ankle injuries were the injury most commonly associated with disruption of training among runners in one study.6 Commonly cited risk factors associated with lateral ankle injury include generalized ligamentous laxity, inappropriate shoewear, irregular playing surface, and cutting activity. Glick and colleagues reported that preexisting laxity of the lateral ankle ligaments, in the form of increased talar tilt on stress radiograph, is a significant risk factor.7 Furthermore, Thacker and coworkers completed a review of the literature and determined that a history of previous lateral ankle sprain is the most commonly cited risk factor for ankle sprain.8 Although hypermobility, generalized joint laxity, and previous ligament injury should intuitively qualify as significant risk factors for lateral ankle injury, Baumhauer and associates published a contrary conclusion.9 They completed a prospective study of joint laxity, foot and ankle alignment, ankle ligament stability, and isokinetic strength as risk factors for inversion ankle injuries. Among 145 college-aged athletes, 15 injuries were reported during a single intercollegiate season (lacrosse, soccer, and field hockey). No significant differences were found between the injured and uninjured groups with regard to the stated risk factors.

Relevant Anatomy Normal Anatomy The talus articulates with the tibia and fibula to form the ankle joint (talocrural joint). The clinical range of motion is variable but usually ranges from 0 to 10 degrees of dorsiflexion and 40 to 50 degrees of plantar flexion. The empirical axis of the joint is somewhat oblique such that plantar flexion and dorsiflexion produce concomitant internal and external rotation of the foot relative to the leg. The rotational movements are translated through the subtalar joint

Foot and Ankle 1913

Inferior extensor retinaculum

Posterior talofibular ligament

Anterior inferior tibiofibular ligament Anterior talofibular ligament Lateral talocalcaneal ligament Interosseous talocalcaneal ligament Cervical ligament

Calcaneofibular ligament

Bifurcate ligament

A

Superficial Deltoid Ligament

Deep Portion Deltoid Ligament

Tibiocalcaneal ligament Tibionavicular ligament Superficial tibiotalar ligament

B

Anterior inferior tibiofibular ligament Anterior talofibular ligament Calcaneofibular ligament

Posterior tibiotalar ligament

Spring ligament

Posterior inferior tibiofibular ligament Deltoid Deltoid ligament ligament

Posterior talofibular ligament Calcaneofibular ligament

Cervical ligament

C

D

Figure 25C1-1 Compendium of the foot and ankle ligaments. A, Lateral view of the foot and ankle demonstrating the anterior talofibular ligament, calcaneofibular ligament, posterior talofibular ligament, anterior-inferior tibiofibular ligament, lateral talocalcaneal ligament, inferior extensor retinaculum, interosseous talocalcaneal ligament, cervical ligament, and bifurcate ligament. B, Medial view of the foot and ankle demonstrating the superficial deltoid ligament, including the tibionavicular, spring ligament, tibiocalcaneal, and superficial tibiotalar components. C, Anterior view of the ankle and hindfoot demonstrating the deltoid ligament with its superficial and deep components, the anterior-inferior tibiofibular ligament, the cervical ligament, the anterior talofibular ligament, and the calcaneofibular ligament. D, Posterior view of the ankle and hindfoot demonstrating the deltoid ligament with its superficial and deep components, the posterior-inferior tibiofibular ligament, the posterior talofibular ligament, and the calcaneofibular ligament.

and the remainder of the foot to produce supination and pronation during the gait cycle. Inman noted that the anterior margin of the talar dome is wider than the posterior margin by an average of 2.4 mm.10 The implication of this differential width is the stability imparted to the ankle joint during ankle dorsiflexion,

along with the relative instability associated with ankle plantar flexion. The functional stability of the ankle is the product of its soft tissue support. The ankle capsule is reinforced by several groups of ligamentous structures. The lateral ligamentous complex includes the ATFL, the calcaneofibular


TABLE 25C1-1 Ankle Ligament Groups Lateral ankle ligaments Medial ankle ligaments

Ankle syndesmosis

Anterior talofibular ligament (ATFL) Calcaneofibular ligament (CFL) Posterior talofibular ligament (PTFL) Superficial deltoid (tibionavicular ligament, tibiospring ligament, and superficial tibiotalar ligament) Deep deltoid (deep anterior tibiotalar ligament and deep posterior tibiotalar ligament) Anterior-inferior tibiofibular ligament (AITFL), posterior-inferior tibiofibular ligament (PITFL), distal interosseous ligament (IOL)

ligament (CFL), and the posterior talofibular ligament (PTFL) (Fig. 25C1-3). The ATFL originates from the anterior aspect of the distal fibula and inserts onto the talar body just anterior to the articular facet. It measures 5 mm in width and 12 mm in length.11 Its fibers blend with the anterior lateral capsule of the ankle. The CFL originates from the anterior border of the distal lateral malleolus and courses medially, posteriorly, and inferiorly to its insertion on the calcaneus. Its fibers blend with the peroneal tendon sheath. Typically a cordlike structure 4 to 6 mm in diameter and 2 to 3 cm long, the CFL is directed 10 to 45 degrees posterior to the line of the longitudinal axis of the fibula.11 The PTFL originates from the posterior border of the fibula and inserts at the posterior lateral aspect of the talus; it is 6 mm in diameter and 9 mm in length.11 The PTFL blends with the posterior ankle capsule. The position of the talus relative to the long axis of the leg is important for determination of the function of the lateral ankle ligaments (Fig. 25C1-4).10 At a position of neutral dorsiflexion, the ATFL is perpendicular to the axis

Anterior talofibular ligament

of the tibia, and the CFL is oriented parallel to the tibia.12 In this position, the CFL provides resistance to inversion stress or varus tilt of the talus. If, however, the talus is plantar flexed (the most common position for lateral ankle inversion injuries), the ATFL is parallel and the CFL is perpendicular to the axis of the tibia. Therefore, with the foot in the most common position for lateral ankle ligament injury, the ATFL is placed in the precarious situation of providing resistance to inversion stress.13 Colville and colleagues used 10 cadaveric ankles to measure strain in the lateral ankle ligaments with the ankle moving from dorsiflexion to plantar flexion.14 The ATFL strain increased with increasing degrees of plantar flexion, internal rotation, and inversion. Conversely, the CFL strain increased with increasing degrees of dorsiflexion and internal rotation. The authors concluded that the ATFL and the CFL work in tandem to provide lateral ankle stability throughout the entire range of ankle motion.

Anatomy and Biomechanics The biomechanical characteristics of the ankle ligaments are such that failure (rupture) is due to increasing load as opposed to twisting or shearing.15 Isolated testing of the individual ankle ligaments demonstrates that the ATFL is the first to fail and the deep deltoid ligament is the last to fail.15 The ATFL is considered the weakest lateral ankle ligament.16-18 Lateral ankle ligament failure is typically midsubstance rupture or a talar avulsion.15 Isolated division of the three lateral ankle ligaments yields predictable results.12,19-24 Division of the ATFL allows increased talar tilt with the ankle in a plantar flexed position, but not in a neutral dorsiflexion position. Division of the CFL allows increased subtalar motion in a neutral dorsiflexion position, but the ankle remains stable in a plantar flexed position. Division of both the ATFL and the CFL results in an unstable ankle. Division of the PTFL allows increased ankle dorsiflexion but does not impart lateral ankle instability. The stabilizing effect of each of the lateral ankle ligaments is dependent on the position of the talus at the time of the applied stress. Stormont and coworkers further advanced the method of ligament testing through the addition of physiologic loads with fixed axial rotation to the sequential ligament

Posterior talofibular ligament

Anterior talofibular ligament


Figure 25C1-2 Inversion of the plantar flexed ankle is the mechanism of injury for lateral ankle sprain associated with a tear of the anterior talofibular ligament.

Figure 25C1-3 The lateral ligamentous complex of the ankle consists of the anterior talofibular ligament, calcaneofibular ligament, and posterior talofibular ligament.

Foot and Ankle 1915

ATFL ATFL

CFL

CFL

A

B

Figure 25C1-4 A, At a position of neutral dorsiflexion, the anterior talofibular ligament (ATFL) is perpendicular to the axis of the tibia, and the calcaneofibular ligament (CFL) is oriented parallel to the tibia. In this position, the CFL provides resistance to inversion stress or varus tilt of the talus. B, If, however, the talus is plantar flexed (the most common position for lateral ankle inversion injuries), the ATFL is parallel and the CFL is perpendicular to the axis of the tibia, and the ATFL provides resistance to inversion stress or varus tilt of the talus.

sectioning protocol.25 Inversion stability was provided by the CFL and the ATFL in the unloaded ankle and entirely by the articular surface in the loaded ankle. Eversion stability was provided by the deltoid in the unloaded ankle and entirely by the articular surface in the loaded ankle. The stabilizing effect of the articular cartilage as described earlier (physiologic load and fixed axial rotation) does not represent the in vivo situation. Remember, normal gait and foot and ankle motion are associated with internal and external rotation of the tibia.10 Kinematic experiments by Cass and Settles placed axial loads on the ankle while allowing axial rotation.26 Computed tomography (CT) was used to evaluate the ankle subjected to an inversion stress. Interestingly, the talar tilt did not change with isolated section of the ATFL or the CFL. Division of both ATFL and the CFL produced an average of 20.6 degrees of talar tilt. The authors concluded that ankle joint stability is provided by the lateral ankle ligaments and not by the ankle articular surfaces. Broström described the ligamentous lesions found during the surgical exploration of 105 recent ankle sprains.27 The ATFL was the most commonly injured structure. The ATFL was completely torn as an isolated injury in 65 cases and as an associated injury in an additional 25 patients. The CFL was the second most commonly injured ligament; it was completely or partially torn as an associated injury in 23 patients. The most common combination of ligamentous injuries was a complete tear of the ATFL and a partial or complete tear of the CFL as described in 20 patients.

Complete ligament tears were noted to occur with concomitant rupture of the adjacent joint capsule. Broström observed that with the talus in a reduced position, the torn ends of the capsule and ligament remained well apposed in most cases. Broström further noted that a tear of the CFL was always associated with a tear of the adjacent peroneal tendon sheath, an observation that is key to ankle arthrography (Table 25C1-2). The advent of magnetic resonance imaging (MRI) has allowed a more detailed evaluation of ligamentous injuries, beyond that provided and limited by surgical exposure. Tochigi and colleagues performed MRI on 24 patients with acute inversion injury of the ankle.28 They detected 23 ATFL, 15 CFL, 11 PTFL, 8 deltoid ligament, 13 interosseous talocalcaneal ligament, and 12 cervical ligament injuries. In addition to the loss of stability imparted to the ankle by ligament rupture, an interruption of normal neural processes has been documented. The disruption of capsular mechanoreceptors29 and the subsequent loss of afferent nerve function and ankle motor coordination may further contribute to the development of chronic instability.30 This loss of function is addressed directly by proprioceptive and coordinated motion rehabilitation. The most significant problem associated with acute lateral ankle sprain is the predisposition to development of chronic instability. The natural history of untreated chronic lateral ankle instability is loss of function and progressive osteoarthritic changes around the ankle.31-33

TABLE 25C1-2 Distribution of Ligament Injury after Inversion Injury Study 196540

Broström, Brunner & Gaechter, 199134 Povacz et al, 199868

Diagnostic Method

No.

ATFL (%)

ATFL + CFL (%)

Arthrography Surgery Surgery

239 180 73

152 (64) 52 (29) 29 (40)

40 (17) 101 (56) 42 (58)

ATFL + CFL + PTFL (%)

2(3)

CFL (%)

AITFL (%)

Deltoid (%)

0 (0) 27 (15)

25 (10)

6 (2.5)

AITFL, anterior-inferior tibiofibular ligament; ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament; PTFL, posterior talofibular ligament.


Clinical Evaluation

History

Although rupture of the lateral ankle ligaments is appropriately considered when a plantar flexion–inversion injury is evaluated, it is imperative that the examination not be limited to these structures. An inversion foot or ankle injury is approached as a constellation of possible injuries, including ATFL sprain, CFL sprain, syndesmosis sprain, deltoid sprain, subtalar sprain (chronic insufficiency of the lateral hindfoot associated with subtalar instability isolated or combined with lateral ankle ligament instability has been shown to occur in up to two thirds of patients34), subtalar coalition, bifurcate ligament sprain, peroneal tendon instability, peroneal tendon tear, lateral malleolus fracture, talar dome osteochondral injury, anterior process of the calcaneus fracture, and fracture of the base of the fifth metatarsal. Although classification systems abound, no single system is routinely used in the literature. Sprains can be considered from the perspective of graded ligament injury, as suggested by the American Medical Association35 and O’Donoghue.36 Injuries are graded based on stretch, partial tear, or complete rupture of the ligament, as is noted in Table 25C1-3. Additional information with regard to associated ligamentous injuries is noted. Grading lateral ankle injuries is much more of a gestalt process than a scientific endeavor. It is not important for the physician to differentiate a grade I from a grade II injury, but the physician should be able to discern a grade I from a grade III injury, or an isolated ATFL injury from an ATFL injury associated with rupture of the syndesmosis. Jackson and associates have established a functional classification system that hinges on the ability of the patient to walk with no limp (mild), walk with a limp (moderate), or not walk (severe).1 The degree of injury was related to a return to full activity in 8, 15, and 19 days for mild, moderate, and severe sprains, respectively.

Relevant historical information includes previous ankle injury, the mechanism of injury, the ability of the patient to continue to play or bear weight, and current symptoms. Severe lateral ankle sprains are associated with a history of inversion injury with a characteristic “pop.” Acute pain and swelling develop quickly, and frequently the athlete is unable to continue playing.

Physical Examination Examination of the patient includes evaluation of the entire extremity. Inspection of the leg, ankle, and foot may reveal swelling, ecchymosis, blister formation, or gross deformity. A vascular and sensory assessment is always performed. The region is palpated systematically with attention to pain over ligamentous, bony, or tendinous structures. Tenderness at the ATFL and the CFL is particularly important to note. Muscle testing is assessed for strength and pain during activation. Motion around the foot and ankle is always assessed with the patient seated and relaxed. The knees are flexed and the feet allowed to fall into an equinus position. The leg is gently grasped while the heel is held in a neutral position and the ankle brought to a right angle or neutral dorsiflexion. From this position, maximal dorsiflexion and plantar flexion are observed in both passive and active modes and compared with the uninjured side. Stress testing is a useful clinical tool that provides a portion of the diagnostic data needed for grading ankle sprains. Stress testing alone is not adequate for reproducible diagnosis of lateral ankle ligament injuries.37,38 Ankle stability is evaluated by several stress tests. The anterior drawer test is used to demonstrate the integrity of the ATFL (Fig. 25C1-5). The patient is seated, and

TABLE 25C1-3 Grading System for Ankle Ligament Injury Acute Grade

Anatomic Injury

Historical Findings

Examination Findings

I

Stretching of the ATFL

II

Partial tearing of the ATFL

Mild swelling, mild ATFL tenderness, stable ankle Moderate swelling, moderate ATFL tenderness, stable ankle

III

Complete rupture of the ATFL

Inversion injury, subacute pain and swelling, continuous athletic activity Inversion injury, acute pain and swelling, inability to continue athletic activity, painful gait Inversion injury with associated “pop,” acute severe pain and swelling, inability to walk

Severe swelling, severe ATFL tenderness, unstable ankle

Subclassification CFL injury

ATFL and CFL injury

Chronic instability

Persistent laxity at lateral ankle ligaments

Medial ankle injury

Deltoid ligament—complete or partial disruption AITFL, PITFL, and IOL injury

Syndesmosis injury Subtalar injury

CFL, interosseous talocalcaneal ligament, cervical ligament

Mechanism related to ankle dorsiflexion Recurrent ankle sprains, “giving way,”30,75 apprehension and anxiety related to the ankle Abduction or eversion mechanism, pain over the medial ankle External rotation mechanism, pain over the ankle syndesmosis Frequent “ankle sprains,” sinus tarsi pain, difficulty on uneven ground

Additional tenderness at CFL, increased varus tilt of the talar dome Swelling and tenderness at lateral ankle ligaments associated with recurrent injury; ankle instability despite grade of injury Swelling and tenderness over deltoid, valgus instability Swelling and tenderness over syndesmosis, pain at syndesmosis with squeeze test177 or forced external rotation176 Increased subtalar range of motion, sinus tarsi tenderness

AITFL, anterior-inferior tibiofibular ligament; ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament; IOL, distal interosseous ligament; PITFL, posteriorinferior tibiofibular ligament.

Foot and Ankle 1917

A

B

Figure 25C1-5 A and B, The anterior drawer test of the ankle. Note the skin dimple consistent with a positive test.

the flexed leg hangs off of the table. The examiner stabilizes the distal tibia with one hand while the other hand grasps the heel behind and pulls the foot forward to produce forward translation. The test is performed with the ankle in both neutral and plantar flexion positions. The results are compared with those of the contralateral ankle, and the test is repeated as required. A few millimeters of translation is normal. With a complete ATFL tear, the talus subluxates anteriorly and a dimple appears over the anterolateral joint due to suction. A portable ankle ligament arthrometer may be used in conjunction with manual testing to improve the accuracy and reliability of the test.39 Testing is occasionally uncomfortable, particularly in the acute setting. False-negative results may be caused by involuntary guarding or pain response. Local anesthesia

A

increases the accuracy of the anterior drawer test (when performed with a mechanical testing device).37 Broström noted that clinical instability was almost never present among arthrographically proven, acute, nonanesthetized ankle ligament ruptures.40 After spinal anesthesia was established, all ankles with a proven ATFL rupture demonstrated a positive anterior drawer sign. Broström went on to report in a separate publication that the anterior drawer test without any form of anesthesia was useful in diagnosing persistent (chronic) tears of the ATFL.41 The results of the anterior drawer test are also influenced by the thickness of the fat pad at the posterior calcaneal tuberosity and by ligamentous laxity.42 The talar tilt test is performed with the patient seated (Fig. 25C1-6). The leg is secured with the examiner’s open hand,

B

Figure 25C1-6 A and B, The talar tilt (inversion stress) test of the ankle.


the heel is grasped from behind with the opposite hand, and a varus or inversion force is placed in an effort to produce talar tilt. The results are compared with those of the contralateral ankle, and the test is repeated as required. The test is performed with the ankle in both neutral and plantar flexion positions. Stressing the ankle in neutral dorsiflexion differentially tests the function of the CFL, whereas stressing a plantar flexed talus tests the ATFL.12 Increased inversion of the calcaneus may represent ankle or subtalar instability.34 Varus tilt to a limited degree is probably normal.43 The high incidence of bifurcate ligament sprain warrants a brief discussion with regard to its presentation. Broström noted clinical evidence of bifurcate ligament injury in 18.6% of patients with acute ankle sprains and 3.7% of patients with confirmed lateral ankle ligament ruptures.40 Bifurcate ligament injury is characterized by diffuse lateral hindfoot and midfoot swelling with associated ecchymosis. Tenderness tends to localize to the course of the bifurcate ligament, which is distinct from the course of the ATFL. The ankle and midfoot remain stable. Pain is easily reproduced with forced inversion of the plantar flexed foot. Broström noted that the differentiation between lateral ankle ligament injury and bifurcate ligament injury was best achieved by eliciting indirect tenderness.40 He suggested manipulation of the heel to produce lateral ankle pain and stabilization of the heel with simultaneous forced forefoot motion to produce bifurcate pain.

Imaging Radiographs Radiographs in the anteroposterior, mortise, and lateral projections are required for ankle evaluation. Weight-bearing radiographs better reproduce physiologic loading, but they are not always obtainable in the acute phase owing to pain. The radiographs are evaluated with regard to malleolar fracture, physeal fracture, osteochondral fracture, and avulsion fracture. Alignment and translational abnormalities are also noted, particularly at the syndesmosis and the medial ankle joint space. (See “Ankle Syndesmosis Sprain” and “Medial Ankle Sprain,” later.) During surgical exploration of 60 chronic ankle sprains, Broström noted 5 cases (8%) with anterior lateral talar osteochondritis dissecans.44 Anderson and Lecocq reported a 22% incidence of osteochondral lesions in a mixed series of 27 cases of single and recurrent lateral ankle injuries.13 The lesions were located at the lateral talus in 5 patients and at the medial talus in 1 patient. The presence of a subfibular ossicle may be indicative of acute or chronic injury to the ATFL,45 or it may be a normal variant (os subfibulare). Broström noted that avulsion of bone fragments is an uncommon pathologic finding after an acute ankle sprain.40 He further noted that patients who sustained an avulsion fracture were more likely to be older and female.

acute lateral ankle ligament injury.1,34 Accuracy is compromised by pain response, peroneal spasm,46 variable stress technique, and lack of control data in the case of a previously injured contralateral ankle. The use of a local anesthetic injection may eliminate some of these variables and result in more accurate stress radiographs. The talar tilt stress radiograph is an anteroposterior view of the ankle taken while an inversion force is applied. The stress can be performed manually or with commercially available devices that provide standardized and quantitative applied stress. The degree of tilt is determined by measuring the angular divergence between the distal tibial articular surface and the talar dome (Fig. 25C1-7). Stress radiographs have been described with the foot in dorsiflexion, neutral, and plantar flexion with the knee flexed or straight. The literature offers no consensus with regard to normal and pathologic findings in radiographic stress tests. Bonnin reported radiographic data demonstrating 4 degrees of varus tilt in 10% to 15% of noninjured ankles.47 Hughes evaluated varus stress radiographs of both ankles in 90 injured and 90 noninjured patients and concluded that 6 degrees of increased talar tilt represents the transition from “normal to abnormal” talar tilt.48 Rubin and Whitten published data analyzing the range of talar tilt present in stress radiographs of 152 normal ankles.38 About 56% of the noninjured ankles in their study had talar tilts of 3 to 23 degrees. However, only 2 ankles measured more than 20 degrees, and only 6 had more than 15 degrees of talar tilt. Seligson and associates used mechanical devices to obtain controlled stress radiographs of 25 functionally normal ankles.49 The talar tilt in these asymptomatic ankles varied from 0 to 18 degrees. The anterior translation as seen on the lateral stress radiograph never exceeded 3 mm. Cox and Hewes performed stress radiographs on 404 ankles of patients with no history of previous ankle injury.50

Stress Radiographs The bilateral stress radiograph is used to quantify anterior talar translation and varus tilt of the talus. Stress radiographs are not routinely necessary for the evaluation of

Figure 25C1-7 The talar tilt (inversion) stress radiograph. The talar tilt angle refers to the angle between two lines drawn to the tibial plafond and the talar dome.

Foot and Ankle 1919

Manual stress was applied to the plantar flexed ankle for an anteroposterior radiograph. No talar tilt was detected in 365 (90.3%) of the ankles, 1 to 5 degrees of talar tilt was detected in 32 ankles (7.9%), and greater than 5 degrees of talar tilt was detected in only 7 ankles (1.7%). Glasgow and colleagues suggested the importance of a lateral stress radiograph.21 They cited the prevalence of ATFL ruptures and the associated anterior instability. The anterior drawer stress radiograph is a lateral radiograph taken while an anterior displacement stress is applied to the ankle with the foot in gentle plantar flexion. The degree of translation is determined by measuring the shortest distance between the talar dome and the posterior margin of the tibial articular surface (Fig. 25C1-8).51 Numerous studies have found a range of translation between 2 and 9 mm, with most less than 4 mm. With more than 5 mm of anterior translation, most consider this a positive test consistent with ATFL rupture.

A

C

Other Imaging Arthrography The unpredictable effect of patient guarding during stress radiography is overcome by the use of ankle arthrography.52,53 This method is relatively simple. Contrast material is injected into the acutely injured ankle, preferably with fluoroscopic guidance, and radiographs are obtained in various projections with attention to areas of extravasation. A false-negative result from an early capsular seal is possible. The procedure has been used much less since the increased availability of MRI. Broström and colleagues performed arthrography of 321 fresh ankle sprains.54 Extra-articular leakage occurred in 239 cases (74%). Surgical exploration was performed in 99 of these cases and in an additional 6 cases that did not demonstrate leakage. The authors concluded that

B

Figure 25C1-8 A, The anterior drawer stress radiograph. Anterior talar displacement (in millimeters) is recorded by measuring the shortest distance from the most posterior articular surface of the tibia to the talar dome. B, The anterior drawer stress radiograph with no anterior talar displacement, negative test. C, The anterior drawer stress radiograph with increased anterior talar displacement, positive test.


a rthrography was useful within the first 7 days of an acute ankle sprain. Leakage of contrast into the peroneal tendon sheath correlated with tear of the CFL. Leakage in front of the lateral malleolus correlated with ATFL rupture. Leakage in front of the syndesmosis correlated with complete rupture of the syndesmosis. Leakage at the medial malleolus correlated with partial deltoid rupture. The presence of extra-articular contrast in the flexor hallucis longus (FHL) and flexor digitorum longus (FDL) tendon sheaths, as well as the posterior facet of the subtalar joint, was not diagnostic. Peroneal sheath injection (tenography), as described by Black and associates, is useful in discerning injury of the CFL.53 Contrast leakage from the sheath or passage into the ankle joint suggests CFL disruption.

Magnetic Resonance Imaging MRI is a useful method for evaluation of acute, subacute, and chronic lateral ankle ligament injuries (Fig. 25C1-9).55 Associated injuries to the talar dome, subchondral bone, and peroneal tendons, as well as the interosseous and cervical ligaments of the subtalar joint, are visualized.28 MRI also reveals tarsal coalition. Rijke and colleagues used a dedicated knee coil and axial images of the neutral and plantar flexed ankle to describe various ligament injuries.55 Complete disruption, partial disruption, and laxity were all visualized. Additionally, hemorrhage and soft tissue swelling were indicative of an acute injury. The high sensitivity associated with MRI mandates that images be carefully correlated with clinical findings. Its accuracy, lack of ionizing radiation, noninvasiveness, decreasing cost, and increasing availability suggest that MRI is the imaging modality of choice when a definitive diagnosis with objective documentation is important.

Therapeutic Options Nonsurgical treatment is the primary choice of management for most lateral ankle sprains, no matter how severe. All acute injuries are treated with the RICE (Rest, Ice, Compression, Elevation) method and protected weightbearing. The amount of rest required after an acute ankle sprain is determined by several factors. Many studies have reviewed the effect of cold application to the injured extremity. Cold therapy is an effective, inexpensive, and easy-to-use modality for the treatment of acute musculoskeletal injury. Appropriately applied cold therapy decreases both pain perception and the biochemical reactions that produce inflammation, and produces vasoconstriction with a concomitant reduction in soft tissue swelling and bleeding. Hocutt and coworkers demonstrated the importance of using cold therapy (ice whirlpool or ice pack for 15 minutes 1 to 3 times a day) in the treatment of acute ankle sprains.56 Furthermore, the group demonstrated a faster recovery associated with early cold therapy (within the initial 36 hours after an ankle sprain) compared with delayed cold therapy or early heat therapy. Compression is typically provided in the form of an elastic bandage but may involve casting, splinting, pneumatic orthosis, or mechanical compression devices.57

Elevation of the ankle helps to reduce swelling and pain. Elevating the extremity above the level of the heart should be emphasized. Any decrease in height will reduce the pressure that edema must overcome before being mobilized out of the acutely swollen tissues surrounding the ankle.

Grade I and Grade II Lateral Ankle Ligament Injuries Treatment of mild and moderate ankle sprains is symptomatic, with an emphasis on recovery of range of motion, strength, and coordination. The detailed rehabilitation program is outlined here. A nonrigid functional ankle brace, such as a lace-up brace, or a semirigid pneumatic ankle brace is used during all phases of recovery.

Grade III Lateral Ankle Ligament Injuries Several reliable treatment methods are available for complete lateral ankle ligament injuries. Treatment methods include early mobilization, cast immobilization, and surgical repair. Injection of anesthetics or corticosteroids into the acutely sprained ankle is never indicated.1,58 Aspiration of the joint hematoma and injection of hyaluronidase did not produce improved outcomes in one study.59 The ankle is supported by the use of a variety of methods, including a nonwalking cast, a walking cast, a removable cast boot, a semirigid pneumatic ankle brace, a nonrigid functional ankle brace, and various ankle taping methods. Various immobilization methods are summarized in Table 25C1-4.

Cast Immobilization Practically speaking, casting has a useful role when limited to the initial 2 to 3 weeks after acute injury. Application of a short leg cast allows a rapid return to work activities and early discontinuation of crutch walking. Published reports discuss casting periods as long as 6 weeks. Prolonged immobilization is not recommended. In fact, Jackson and colleagues suspect that the use of a cast for moderate and severe ankle sprains simply delays recovery for the number of days that the cast is used.1 Complete immobilization is provided with a short leg cast. The assumption is that casting allows the ruptured ends of the lateral ankle ligaments to heal in a nearanatomic position. Various cast positions have been advocated in an effort to reapproximate the torn ligament ends. Smith and Reischl suggested 5 to 15 degrees of dorsiflexion based on fresh cadaveric models.4,60 Slight eversion is also a common suggestion.61 As soon as the swelling and pain remit, a functional rehabilitation program is instituted with a semirigid pneumatic ankle brace. Drez and coworkers used a more protracted immobilization method to treat 39 patients with first-time, combined ATFL and CFL injuries.61 All cases were evaluated by stress radiography before and after treatment. The protocol included 7 to 10 days in an everted splint and 6 weeks in an everted walking cast, followed by ankle rehabilitation and a 1-month delay in return to athletic activity. A 79.5% success rate was obtained as determined by a

Foot and Ankle 1921

ATFL

ITCL talus

talus

talus fibula

calcaneus

PTFL

tibia

CL

tibia

talus talus

DTL fibula

talus

calcaneus calcaneus

calcaneus

CFL

A

talus talus

talus ATFL

fibula

CFL calcaneus

PTFL

fibula

tibia CL ITCL

talus

DTL talus

calcaneus

talus

calcaneus

calcaneus

B Figure 25C1-9 A, Magnetic resonance imaging key for the normal ankle. B, Magnetic resonance imaging key for the injured ankle. ATFL, anterior talofibular ligament; CFL, calcaneofibular ligament. (Redrawn from Tochigi Y, Yoshinaga K, Wada Y, Moriya H: Acute inversion injury of the ankle: Magnetic resonance imaging and clinical outcomes. Foot Ankle Int 19:730-734, 1998.)

repeat talar tilt stress radiograph with 5 degrees or less angulation compared with the uninjured ankle. Eiff and associates used a prospective study to compare early mobilization and immobilization for the treatment of first-time lateral ankle sprains.62 The early mobilization group was treated with an elastic wrap for 48 hours followed by application of a semirigid pneumatic brace and a common rehabilitation program. The immobilization

group was treated with a non–weight-bearing plaster splint for 10 days followed by a common rehabilitation program. Both methods produced excellent results at 1-year follow-up with low rates for residual symptoms (5%) and reinjury (8%). A semirigid pneumatic ankle brace (Air-Stirrup, Aircast, Inc., Summit, NJ) has shown proven results with advantages that include cost-effective treatment, the capacity for


TABLE 25C1-4 Immobilization Methods for Foot and Ankle Injuries Immobilization Method

Common Application

Advantage

Disadvantage

Short-leg nonwalking cast

Initial treatment for severe ankle and midfoot sprains; definitive treatment of stable syndesmosis and Lisfranc injuries Initial treatment for severe ankle and moderate foot sprains

Excellent protection for all foot injuries and most ankle injuries; effective edema management

Poor rotational control for ankle syndesmosis; rapid deconditioning; inconvenient for dressing, showering, and sleeping Poor rotational control for the ankle syndesmosis; rapid deconditioning; inconvenient for dressing, showering, and sleeping

Short-leg walking cast

Removable cast boot (3D Walker, Bledsoe Boot [Bledsoe Brace Systems, Grand Prairie, Tex], CAM boot)

Initial treatment for moderate ankle and foot sprains

Semirigid pneumatic ankle brace (Air-Stirrup, Aircast, Summit, NJ)

Functional treatment for hindfoot and ankle injuries at various recovery phases, including acute ankle sprains,51,58,63,66,72 prevention of recurrent ankle sprains159,162-164

Nonrigid functional ankle brace (lace-up or Velcro closures)

Functional treatment for hindfoot and ankle injuries at various recovery phases, including chronic injuries

Ankle and foot taping

Functional treatment for foot and ankle injuries at various recovery phases, including chronic injuries

independent rehabilitation, an early return to function, and predictable results (Fig. 25C1-10).63 The semirigid orthosis is lined by opposing dual air cells; the system produces a milking action that actively reduces ankle edema. Several experimental studies have demonstrated the brace’s effectiveness in reducing ankle inversion.23,64,65

A

Excellent protection for most foot and ankle injuries; improved ability to bear weight; continuous rehabilitation provided; self-applied device Removable protection for ankle and foot injuries; improved ability to bear weight; continuous rehabilitation provided; self-applied device Rigid support for hindfoot and ankle injuries—allows ankle range of motion, allows continued athletic participation, facilitates resolution of edema (air cell systems)58; self-applied device; device used within shoe; low cost Nonrigid support for hindfoot and ankle injuries—allows ankle range of motion, allows continued athletic participation; self-applied device; device used within shoe Custom-applied support for foot and ankle injuries; provides resistance to inversion,64 provides biofeedback,70 allows continued athletic participation

No rotational control through ankle; poor edema control; athletic participation restricted No rotational control through ankle; bulky within shoe

No rotational control through ankle

Rapid loosening with time-limited effectiveness159; requires trained personnel for application; high cost over the course of a season158

Early Mobilization Early mobilization, or functional treatment, is the current favored treatment method. Treatment and rehabilitation are directed without the use of rigid cast immobilization. After the acute pain and swelling remit (after about

B

Figure 25C1-10 A, Semirigid pneumatic ankle brace. B, Lace-up ankle brace.

Foot and Ankle 1923

48 hours), weight-bearing to tolerance is encouraged, and a rehabilitation program is instituted. This method specifically avoids immobilization, which many believe simply prolongs the recovery period. A semirigid pneumatic ankle brace, walking boot, or taping is used throughout the rehabilitation period. Konradsen and colleagues used a prospective, randomized study to evaluate the effectiveness of early mobilization compared with total immobilization for complete lateral ankle ligament injuries.51 Early mobilization allowed an earlier return to work and resumption of athletic activity. The 1-year follow-up was similar for both groups. Klein and coworkers used a randomized study to evaluate the same methods.66 Patients treated with a pneumatic ankle brace fared better than those treated with a short leg cast for 6 weeks. Stress radiographs did not significantly differ after treatment. Sommer and Schreiber used a prospective, randomized study to compare plaster cast immobilization (for 3 weeks followed by a pneumatic ankle splint), early mobilization with a pneumatic ankle brace, and early mobilization with an Unna boot for the treatment of stress radiograph-documented lateral ankle ligament ruptures.67 They reported lower direct cost and improved stability in the mobilization groups. A recent study to evaluate the effectiveness of early mobilization was published by Povacz and associates in 1998.68 The group performed a randomized prospective study of 146 adults with acute lateral ankle sprains diagnosed by clinical findings and stress radiographs. The treatment was either immediate operative repair followed by 6-week immobilization in a short leg cast or placement of an ankle orthosis for 6 weeks. Nonoperative treatment produced subjective and objective results comparable to those associated with operative treatment. The nonoperative treatment was also associated with a significantly shorter recovery period.

Surgical Repair Surgical management of the acute unstable lateral ankle sprain remains controversial. Several authors have recommended primary surgical repair for severe injury or injury in the high-demand athlete (Fig. 25C1-11).41,69-72 Kaikkonen

and colleagues reported excellent and good results at a 6- to 8-year follow-up after primary repair of acute lateral ligament rupture.73 No operative complications occurred. Others have reported favorable, reproducible results with primary repair of acute ruptures.11,41,74 Most physicians currently agree that the role of surgery in the acute setting is very small. Rare circumstances, such as open injuries, large avulsion fractures, and frank dislocation may warrant acute lateral ligament repair. Some authors have reported on adverse outcomes with acute surgical treatment. Freeman compared strapping and early mobilization, immobilization with plaster for 6 weeks, and ligament repair with immobilization for the treatment of complete lateral ankle ligament ruptures.75 The periods of disability were 12, 22, and 26 weeks for patients in the early mobilization, immobilization, and ligament repair groups, respectively. Ligament repair produced the greatest number of complaints at 1-year follow-up, including the only cases with residual loss of motion. Freeman suggested early mobilization as the treatment of choice for lateral ankle ligament ruptures. Broström used a prospective study to compare the use of primary surgical repair followed by 3 weeks of plaster immobilization (95 cases), 3 weeks of plaster immobilization alone (82 cases), and strapping with early mobilization (104 cases).41 Although surgical repair provided excellent results, including a low (3%) residual symptomatic instability rate, Broström went on to suggest that primary surgical repair should not be the routine treatment for acute ruptures. He cited the protracted postoperative recovery, the risk for infection, the risk for painful scar formation, and the success of late lateral ankle ligament reconstruction. Evans and coworkers recognized the discrepancy in immobilization periods and performed a prospective, randomized trial with 3 weeks of immobilization in a plaster cast with or without surgical repair of the acute lateral ankle ligament rupture.76 An independent 2-year follow-up concluded that surgical repair yielded similar radiographic results (stress radiographs) and slightly worse functional results. Twice as many patients in the operative group were forced to give up athletic activity. Loss of subtalar inversion and surgical complications were also cited as disadvantages of primary repair of acute injury.

Superficial peroneal nerve

Oblique incision Sural nerve

A

B

C

D

Figure 25C1-11 Surgical technique for primary lateral ankle ligament reconstruction. A, A short oblique incision is made at the anterior margin of the distal fibula. B, Blunt subcutaneous dissection is performed, with care taken to protect the superficial peroneal nerve and the sural nerve. C, The anterior lateral capsule is exposed, and the anterior talofibular ligament, calcaneofibular ligament, and capsular tears identified. D, The tears are approximated and repaired with absorbable suture.


Repair of acute injury produces results similar to those associated with delayed reconstruction. Because most patients respond to nonsurgical management, primary repair offers few advantages. Today, operative repair of the complete, acute lateral ankle ligament injury is very infrequent.58 Most authors favor nonsurgical treatment for acute ruptures.41,75,77,78

Technique: Primary Lateral Ankle Ligament Repair 1. The procedure is performed with the patient under general anesthesia. The patient is supine with a wellpadded proximal tourniquet and a soft bump placed beneath the ipsilateral hemipelvis. 2. An image intensifier is used to obtain bilateral varus tilt and anterior drawer stress views. Brodén’s stress views are also obtained, if indicated. 3. Arthroscopy of the ankle is performed if clinical presentation or imaging suggests intra-articular disease. 4. The extremity is exsanguinated, and the tourniquet is inflated. A bump is placed under the leg to prevent anterior translation of the talus. 5. A short oblique incision is made at the anterior margin of the distal fibula. This incision incorporates the lateral arthroscopy portal. 6. Blunt subcutaneous dissection is performed, with care taken to protect the superficial peroneal nerve and the sural nerve. 7. The anterior lateral capsule is exposed, and the ATFL, the CFL, and capsular tears are identified. The ankle joint is inspected for chondral or osteochondral fragments. The joint is copiously irrigated. The peroneal sheath is evaluated for tears. 8. The tears are approximated and repaired with absorbable suture. All sutures are placed and then tied from posterior to anterior with the ankle held in neutral dorsiflexion and slight eversion. Avulsion fractures are repaired directly to the fibula or talus. 9. The wound is closed in layers, and a short leg splint is applied. At 10 days, the incision is inspected, and a short leg weight-bearing cast or walking boot is applied. Four to 6 weeks after surgery, the patient is transitioned to an ankle brace. A guided rehabilitation program is instituted and monitored. Patients may actively dorsiflex and evert the foot with inversion limited to neutral. Progressive stretching, strengthening, and proprioception exercises are instituted 6 to 8 weeks after surgery. A semirigid pneumatic ankle brace is used for 6 months after surgery.

Chronic Lateral Ankle Ligament Instability The chronic or recurrent lateral ankle sprain is associated with apprehension, discomfort, swelling, muscular weakness, tenderness, and loss of coordination.30,44 Instability may be overt or subtle and has been described as a “giving way” of the ankle.30 Significant disability is noted, particularly if the patient runs on uneven or loose surfaces. Objective instability of the ankle joint is defined by patient symptoms and positive stress radiographic findings. The condition develops after acute injury in up to 20% of patients.41,77,79

A related condition is functional lateral ankle instability, defined by frequent sprains, difficulty running on uneven surfaces, and difficulty jumping and cutting. Freeman reported this sensation in 21 of 42 patients 1 year after initial lateral ankle ligament rupture.80 Increased varus tilt on stress radiograph, was present in only 6 of these cases. Hansen and coworkers noted a similar lack of agreement between clinical symptoms and persistent talar tilt.81 Brand and colleagues reported a 10% prevalence of functional lateral ankle instability among 1300 Naval Academy freshmen.82 Functional instability may be related to previous ankle sprain, chronic lateral ankle instability, or peroneal weakness.

Rehabilitation without Surgery Successful resolution of chronic lateral ankle instability is possible without surgical stabilization.44,83,84 Patients with chronic, recurrent injuries are treated with a rehabilitation program, and their activity levels are reduced. Functional ankle bracing is continued throughout the treatment period. The key points of rehabilitation are motor strength (particularly of the peroneal muscles), proprioception, and coordination.

Surgical Treatment Patients with chronic injuries that remain symptomatic after a supervised rehabilitation program are candidates for surgical management. Radiographic criteria include talar tilt greater than 15 degrees (or a side-to-side difference of more than 10 degrees) and anterior drawer translation greater than 5 mm (or a side-to-side difference of more than 3 mm). A multitude of procedures have been used for lateral ankle ligament reconstruction, many with reasonable success. In 1932, Nilsonne described a procedure for stabilization of the lateral ankle.85 He repaired a chronic CFL rupture and reinforced the repair with a peroneus brevis tenodesis. Evans86-88 and Watson-Jones84,89 modified the tenodesis. A further modification in the form of an augmentation procedure was proposed by Elmslie90 and refined by Chrisman and Snook.91 The Evans procedure is a transposition of the entire peroneus brevis tendon through the distal fibula (Fig. 25C1-12). Evans recognized the tenodesis resulted in the loss of subtalar inversion after this procedure.87 The Watson-Jones procedure reconstructs the lateral ankle ligaments with a peroneus brevis tenodesis configured to replace the course of the ATFL (Fig. 25C1-13).84,89 The classic method uses the entire peroneus brevis tendon.92 The procedure does not reproduce the anatomic orientation of the CFL. Because the tenodesis of the peroneus brevis lies at a right angle to the subtalar joint empirical axis, loss of subtalar motion is to be expected.10 The Watson-Jones procedure has been modified to spare the function of the peroneus brevis tendon with the use of a split peroneus longus tendon graft,33,93 a complete peroneus longus tendon graft,94 a split peroneus brevis tendon graft,33,95 a plantaris tenodesis,96 a free plantaris tendon graft,34,97 and a split Achilles tenodesis.98,99 Using the split peroneus longus modification of the Watson-Jones procedure, Barbari and associates reported

Foot and Ankle 1925

Peroneus longus

Peroneus brevis Figure 25C1-12 The Evans procedure.

excellent or improved outcomes in 39 of 42 ankles (Fig. 25C1-14).93 Problematic issues include loss of ankle dorsiflexion and subtalar inversion. Brunner and Gaechter completed a retrospective comparison of the split peroneus brevis modification with the free plantaris tendon graft modification of the WatsonJones procedure.34 This study demonstrated slightly more favorable results with the plantaris tendon graft. Increased patient satisfaction and fewer reoperations were noted. The free plantaris graft modification is a more anatomic approach to addressing lateral ligament failure, particularly of the CFL. This procedure preserves the function of the peroneus brevis while sacrificing the vestigial100 plantaris. In 1934, Elmslie described the use of a fascia lata graft passed through drill holes to re-create and augment the ATFL and the CFL.90 The idea of re-creating the anatomic

Figure 25C1-13 The Watson-Jones procedure.

Figure 25C1-14 The Barbari modification of the WatsonJones procedure. (Redrawn from Barbari SG, Brevig K, Egge T: Reconstruction of the lateral ligamentous structures of the ankle with a modified Watson-Jones procedure. Foot Ankle 7:362-368, 1987.)

configuration of the ATFL and CFL was adopted by Windfeld.101 He used the entire peroneus brevis to perform a modified Watson-Jones repair. The peroneus brevis tendon was passed through the fibula from front to back and sewn to the remnants of the ATFL at the talus and the CFL at the calcaneus. The procedure limited the graft to local tissue and attempted to reconstruct both lateral ligaments. In 1969, Chrisman and Snook modified the Elmslie repair by using a split peroneus brevis tendon, instead of a strip of fascia lata, to reconstruct the ATFL and the CFL (Fig. 25C1-15).91 The 2-year follow-up of seven patients confirmed a successful return to strenuous athletic activity in all participants. Although moderate loss of subtalar motion occurred, it was not problematic. In 1985, the same authors published a long-term follow-up (average followup, 10 years).102 Of the 48 ankles evaluated, 43 had attained excellent and good outcomes. Of the 3 patients with fair and

Figure 25C1-15 The Chrisman-Snook procedure.


poor results, all had sustained subsequent severe trauma, and one had suffered from generalized ligamentous laxity. Other complications included sural nerve injuries and an asymptomatic loss of inversion. Riegler reported the 2-year follow-up of 11 young athletes after a Chrisman and Snook reconstruction.103 Ten patients returned to their primary athletic activity. All patients lost inversion of the subtalar joint compared with the uninvolved side. Savastano and Lowe published similar results.104 Among 10 ankles treated with a Chrisman and Snook reconstruction, 9 obtained satisfactory results despite limited subtalar inversion. Colville and coworkers performed a biomechanical comparison of the Evans, Watson-Jones, and Chrisman and Snook reconstructions.105 It was determined that each procedure stabilized the ankle but also produced limited subtalar inversion. Colville and Grondel described an anatomic split peroneus brevis lateral ankle reconstruction.106 This procedure reproduces the anatomic orientation of the ATFL and the CFL. The peroneus tendon function appears to remain intact; furthermore, the anatomic approach preserves subtalar function (80% of nonoperated hindfoot inversion). Mechanical stability was verified with stress radiographs in all 17 patients. Minor difficulties with aching and swelling persisted at the 42-month average follow-up. The authors advocate the technique for patients with inadequate local tissue for anatomic reconstruction, generalized hypermobility, and previously failed reconstructive techniques. Paterson and associates described an anatomic reconstruction of the ATFL with a semitendinosus autograft.107 The average 24-month follow-up suggests that the reconstruction is useful for instability not associated with the subtalar joint. Kin-Com dynamometer testing revealed no significant loss of knee flexion strength. Anderson and Lecocq reported a successful delayed repair of the ATFL and CFL with simple plication.13 Broström advocated a similar approach (Fig. 25C1-16).44 His report of successful delayed lateral ankle ligament repair remains significant. Sixty patients with chronic symptoms after lateral ankle sprain were treated with end-to-end ligament repair or advancement of the torn end of the ATFL into the anterior border of the fibula. In 3 of these cases, the repair was fortified with a flap of the lateral talocalcaneal ligament. Average follow-up was 2.9 years. Forty-three patients were completely asymptomatic. Only 3 patients (5%) complained of severe or moderately severe symptoms. Forty-six of the 56 patients who were re-examined were “normal.” Abnormal findings included positive anterior drawer sign (4), impaired mobility (2), tenderness (5), and soft tissue induration (4). Broström’s technique has several advantages over tenodesis and augmentation methods. The technique accomplishes anatomic restoration and maintains joint mobility, it is relatively simple, and it is less morbid with regard to the use of peroneal tendon grafts and length of incision. Other authors have obtained similar good results.108 Gould and associates recommended modification of the Broström technique.109 They removed the intervening scar from the ATFL, repaired the ligament, and supplemented the repair with both a flap from the lateral talocalcaneal ligament and an advancement of the inferior extensor retinaculum (Fig. 25C1-17). Late repair was

A

B Figure 25C1-16 The repair of a chronic lateral ankle ligament rupture as described by Broström. A, Chronic anterior talofibular ligament (ATFL) rupture and direct repair. B, Chronic ATFL rupture with insufficient tissue for simple direct repair and reconstruction using ATFL repair with advancement of the flap of the lateral talocalcaneal ligament into the fibula. (Redrawn from Broström L: Sprained ankles. VI. Surgical treatment of “chronic” ligament ruptures. Acta Chir Scand 132:551-565, 1966.)

erformed on 50 patients. The anterior translation of the p talus was reduced to 2 mm or less, and talar tilt to less than 12 degrees. All patients returned to athletic activity. A rating scale based on activity, stability, mobility, swelling, and overall satisfaction revealed that all patients scored between 8 and 10 of 10 possible points. The inferior extensor retinaculum is composed of two layers, superficial and deep to the extensor tendons. Harper concluded that the superficial layer of the inferior extensor retinaculum remains a constant, substantial tissue, suitable for lateral ankle and subtalar joint reconstructions, as proposed by Gould and associates.109,110 Biomechanical testing with cadaveric ankle has proved the efficacy of the Broström repair in restoring ankle stability while maintaining ankle and subtalar range of motion.111 Others have used the Gould modification of the Broström repair with consistent reproducible stabilization and return to athletic activity.112 Harper further modified the Gould modification by using a flap fashioned from the superficial layer of the inferior extensor retinaculum (Fig. 25C1-18).113 When a Broström repair is performed, identification of the torn ligament ends is often difficult, if not impossible. To bypass this difficulty, Karlsson and colleagues used division and imbrication of the attenuated ATFL and CFL.114 They reported good to excellent results in 132 of 153 ankles available for follow-up (mean, 6 years). Reconstruction of both the ATFL and the CFL produced better results than did isolated reconstruction of the ATFL. Most patients with unsatisfactory results were noted to have generalized hypermobility, longstanding lateral ankle instability, or a history of previous ankle reconstruction.

Foot and Ankle 1927

Anterior talofibular lig.

Calcaneofibular lig.

A

Lateral malleolus

Lateral malleolus

Lateral talocalcaneal lig. sutured to lat. malleolus

Extensor retinaculum reinforcement

B

Figure 25C1-17 Gould modification of the Broström technique. After repair of the anterior talofibular or calcaneofibular ligament, reinforcements with the lateral talocalcaneal ligament (A) and extensor retinaculum (B) are made.

Karlsson and coworkers performed 60 lateral ankle ligament reconstructions with a modification of the Broström repair.115 These authors advanced the ATFL and the CFL into a 4 × 4-mm bone trough at the anterior aspect of the distal fibula. The remaining periosteal flap was repaired over the ATFL. Good or excellent results were obtained in 53 (88%) of the patients. Unsatisfactory results were associated with generalized ligamentous laxity or longstanding instability. Despite the many surgical options, ankle stabilization is effective and produces good or excellent results in more than 91% of chronic lateral ankle ligament instability cases.116,117 Radiographic stability does not always correlate with clinical outcome. Patients with early signs of osteoarthritis may experience progressive arthrosis despite stabilization. Persistent instability leads to osteoarthritis of the ankle joint.31-33 Ankle arthroscopy at the time of lateral ankle ligament reconstruction provides the surgeon with an opportunity for a more thorough evaluation of the ankle joint. Komenda and Ferkel suggest the use of ankle arthroscopy before lateral ankle ligament stabilization for treatment of loose bodies, osteochondral lesions of the talus, and ankle Anterior talofibular ligament

lnferior extensor retinaculum

A

pain unrelated to instability.118 They also suggest the procedure for evaluation of ATFL integrity and suitability of local tissue for reconstruction. Patients should be carefully evaluated for severe ankle or hindfoot cavovarus. A calcaneal osteotomy may need to be performed in conjunction with lateral ligament repair to prevent failure of the procedure. Patients with failed lateral ankle reconstruction due to re-rupture are placed into rehabilitation and fitted with an orthosis. Repair of the acute injury is a reasonable alternative to functional treatment. Persistent instability can be treated with a repeat Broström repair with the Gould modification, or an anatomic reconstruction with local tissue or a free tendon graft.119 Technique: Lateral Ankle Ligament Reconstruction with a Gould Modification of the Broström Repair

1. The procedure is performed with the patient under general anesthesia. The patient is supine with a wellpadded proximal tourniquet and a soft bump placed beneath the ipsilateral hemipelvis.

Anterior talofibular ligament Calcaneofibular ligament

lnferior extensor retinaculum


B

Figure 25C1-18 Harper modification of the Gould modification of the Broström technique. A flap from the inferior extensor retinaculum is mobilized and sutured to the lateral fibula. (Redrawn from Harper MC: Modification of the Gould modification of the Broström ankle repair. Foot Ankle Int 19:788, 1998.)


2. An image intensifier is used to obtain bilateral varus tilt and anterior drawer stress views. Brodén’s stress views are also obtained, if indicated. 3. Arthroscopy of the ankle is performed if clinical presentation or imaging suggests intra-articular disease. 4. The extremity is exsanguinated, and the tourniquet is inflated. A bump is placed under the leg distally to prevent anterior translation of the talus. 5. A short oblique incision is made at the anterior margin of the distal fibula. The incision incorporates the lateral arthroscopy portal if used. 6. Blunt subcutaneous dissection is performed, with care taken to protect the superficial peroneal nerve and the sural nerve. The extensor retinaculum is identified and tagged. 7. The anterior lateral capsule is exposed, and the ATFL and the CFL are identified. The capsule is incised just distal to the origin of the ATFL and the CFL, and the ankle joint is inspected. 8. The anterior margin of the fibula is exposed by subperiosteal elevation of the proximal capsule. The anterior fibula is decorticated, and three to five tunnels are created with a small K-wire. The capsule with the ATFL and the CFL is secured with multiple nonabsorbable braided sutures. The sutures are passed through the tunnels, and the capsule is advanced onto the decorticated margin of the fibula with the ankle held in dorsiflexion and eversion. The lateral periosteal sleeve and the proximal capsule are repaired over the advanced ligament. This repair can also be performed with suture anchors in the fibula or by soft tissue imbrication. 9. The superficial layer of the extensor retinaculum is secured with suture and advanced to the anterior fibula. This provides significant subtalar stability. 10. The wound is closed in layers, and a short leg splint is applied in slight eversion. At 10 days, the incision is inspected, and a short leg weight-bearing cast is applied. Four weeks after surgery, a rehabilitation program is instituted and monitored. A removable cast boot or a semirigid pneumatic ankle brace is used for an additional 4 to 6 weeks. The repair is further protected during subsequent athletic activity with an ankle brace for 6 months after surgery.

addition to orthotic devices, an elastic sock is available for a dditional mobilization of edema (Fig. 25C1-19). In the acute phase, the athlete’s pain and inflammation are addressed with rest, cold therapy, and whirlpool. A trial of electrical stimulation may be considered. Ankle and subtalar joint passive and active range of motion are re-established with inversion limited to neutral for 6 weeks. Isometrics around the ankle and subtalar joints is initiated as pain allows. Weight-bearing to tolerance is encouraged. Once the acute pain subsides, flexibility is addressed in all planes. An inclined board is a useful adjunct to gastrocnemiussoleus and Achilles stretching (Fig. 25C1-20). Strengthening is initiated with towel scrunches (Fig. 25C1-21), toe pickup activities, manual resistive inversion and eversion, elastic bands (Fig. 25C1-22), seated toe and ankle dorsiflexion with progression to standing, and seated supination-pronation with progression to standing. Closed chain activities are gradually introduced, including one-leg balance and sport-specific activities on a trampoline, as well as use of the biomechanical ankle platform system (BAPS) (Fig. 25C1-23). Aerobic fitness is maintained with cross-training activities such as water running (Fig. 25C1-24) and cycling. Heat therapy, such as the application of warm packs, is a useful modality before the therapy session. It reduces pain and spasms and thus facilitates increased range of motion. Cold therapy, compression, and elevation are used after each therapy session to reduce inflammation. As the athlete returns to sport, protective bracing, range of motion, and strength activities are continued from the subacute phase. Walking and running activities are allowed to progress within the limits of a pain-free schedule. Once running activity is mastered, a monitored plyometric

Rehabilitation after Surgery Tissue injury initiates a predictable and sequential series of events known as the healing response. The response is typically divided into three phases with arbitrary and overlapping time lines.120 The initial phase is the inflammatory phase, which includes the first through the third day following injury. The second phase is a proliferative phase of tissue repair that extends from day 3 to day 20. The final phase is a remodeling phase that proceeds after day 9. To a certain degree, rehabilitation follows the phases of the healing response in an effort to reduce the undesirable effects of inflammation (i.e., pain, swelling, loss of function) while simultaneously promoting tissue repair and functional recovery. For rehabilitation of the ankle, emphasis is placed throughout the protocol on ankle and subtalar flexibility, motor function, and coordination.30 The ankle is supported by a semirigid pneumatic ankle brace. In

Figure 25C1-19 Elastic sock used for foot and ankle edema mobilization and control.

Foot and Ankle 1929

Osteochondral Lesion

Figure 25C1-20 Gastrocnemius-soleus and Achilles stretching is facilitated with an inclined board.

( cutting) program is introduced with progressive difficulty. Schedules are carefully controlled to avoid reinjury during these activities.

Associated Injuries If a lateral ankle ligament injury is suspected either by the reported mechanism of injury (inversion mechanism) or by the initial physical findings (lateral ankle or hindfoot swelling), a multitude of diagnoses must be considered. These may present as isolated findings or as concomitant injuries. Evaluation begins with a detailed history and physical examination with particular attention to the ankle and hindfoot.

Anderson and Lecocq reported a 22% incidence of osteochondral lesions in a mixed series of 27 cases of single and recurrent lateral ankle injuries.13 These lesions were located at the lateral talus in five patients and at the medial talus in one patient. Meyer and associates reported the successful use of CT in the evaluation of the chronically painful ankle after ankle sprain.121 These scans demonstrated intra-articular or juxta-articular bony fragments in 13 of 31 patients. The fragments were located in the anterolateral or lateral aspect of the ankle or subtalar joints in 12 of the 13 patients. Recurrent lateral ankle instability is associated with repetitive shear and compression forces across the ankle articular surface. Taga and colleagues used ankle arthroscopy to evaluate chondral lesions before lateral ankle ligament reconstruction in 31 patients.122 Articular cartilage damage was seen in 89% of the acute ankle injuries and 95% of the chronic ankle injuries. They determined that cartilage damage most frequently was located at the anteromedial tibial articular surface. Furthermore, lesions tended to worsen with regard to depth of injury as the period of ankle instability lengthened. The location and severity of the cartilage damage as seen with the arthroscope correlated with clinical findings. The significance of the treated and untreated chondral lesions associated with a previously unstable ankle remains unknown. Komenda and Ferkel also used ankle arthroscopy to evaluate ankles before lateral ankle ligament reconstruction for chronic instability in 54 patients.118 Intra-articular disease, such as loose bodies, synovitis, and osteophytes, was seen in 93% of the ankles. Osteochondral lesions of the talus or chondromalacia, or both, were found in 25% of patients. Options for treating osteochondral injuries include conservative and surgical approaches. Nonsurgical treatment includes rehabilitation, bracing, oral anti-inflammatory medications, and intra-articular steroid injection. When these treatments fail, surgery is considered. Various techniques, including arthroscopy with débridement, drilling, microfracture, internal fixation, and cartilage transfer, are used. Rehabilitation depends on the procedure performed.

Bone Bruise

Figure 25C1-21 Towel scrunches. The towel is gathered beneath the foot with active toe motion. The activity begins in a seated position and progresses to standing.

With the advent of MRI, subtle injuries to the subchondral bone are easily imaged. Mink and Deutsch described a bone bruise as a traumatic, nonlinear marrow lesion localized to the subchondral bone, typically represented by a T1-weighted signal loss and a T2-weighted signal intensity.123 The natural history of bone bruise is not completely understood and remains controversial. Isolated bone bruise subsequent to knee injury has a predictable and benign course.124 Lahm and coworkers reported no arthroscopic changes (and no clinical sequelae) related to bone bruise associated with various knee injuries.125 Conversely, Johnson and associates identified arthroscopic (e.g., softening, fissuring, and fracture) and histologic (e.g., chondrocyte and osteocyte necrosis) changes that suggested significant damage to the cartilage overlying bone bruise associated with anterior cruciate ligament disruption.126


A

B

Figure 25C1-22 Elastic band exercises. The Thera-Band is posted on a table leg and is used to provide resistance as the foot is exercised. A, Elastic band exercises for resisted inversion. B, Elastic band exercises for resisted eversion.

A

C

B

Figure 25C1-23 Closed chain activities. A, One-leg balance on a trampoline. B, Sport-specific activity (throwing) on a trampoline. C, Biomechanical ankle platform system.

Foot and Ankle 1931

Ant. inferior tibiofibular lig. Distal Fascicle

Figure 25C1-24 Water running for cross-training after foot or ankle injury.

Nishimura and colleagues and Labovitz and Schweitzer suggested that the bone bruise is an indicator of concomitant ligamentous injury to the ankle and that the pattern and location of the lesion correlate with a specific mechanism of injury.127,128 Alanen and coworkers used a prospective study to establish a 27% incidence of bone bruise (i.e., microtrabecular fracture) after ankle inversion injury.129 Ninety-five patients with otherwise normal radiographs were imaged. No clinical significance was related to the occurrence of the bone bruise.

Anterior Lateral Ankle Impingement Chronic anterior lateral ankle pain after an inversion ankle injury is a well-recognized entity. Bassett and associates described a distal fascicle of the anterior-inferior tibiofibular ligament; the structure was found in 10 of 11 cadaveric specimens130 (Fig. 25C1-25). Impingement of the fascicle against the talar dome occurs with ankle dorsiflexion between 9 and 17 degrees. The clinical component of the study identified abrasion of the talar articular cartilage in five of the seven patients. Resection of the fascicle was curative and did not increase ankle instability. A meniscoid lesion of the anterior lateral ankle has also been described (Fig. 25C1-26).131 Hamilton reported finding entrapment of the capsule between the talus and the lateral malleolus during the surgical management of two of three acute, high-grade, lateral ankle sprains.72 He speculated that the capsular interposition might provide the substrate for the classic meniscoid lesion. Chronic anterior lateral ankle pain is treated with an aggressive 6-week course of physical therapy and bracing to eliminate subtle instability. Oral anti-inflammatory and cortisone injection therapy may also be used. Patients who fail conservative management are treated with ankle arthroscopy and débridement of the anterolateral lesion (meniscoid lesion), if present.

Peroneal Tendon Instability Peroneal tendon instability is an entity that may be associated with lateral ankle instability. The condition may be secondary to an inversion ankle injury.13 It may produce

Calcaneofibular lig.

Ant. talofibular lig.

Figure 25C1-25 The distal fascicle of the anterior-inferior tibiofibular ligament is normally parallel and distal to the main ligament and separated from it by a fibrofatty septum. Inset,: After an inversion sprain of the ankle, the distal fascicle may impinge on the anterolateral aspect of the talus. (Redrawn from Bassett FH, Gates HS, Billys JB, et al: Talar impingement by the anteroinferior tibiofibular ligament: A cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am 72:55-59, 1990.)

functional ankle instability caused by the subluxation of the peroneal tendons. Chronic subluxation or frank dislocation of the peroneal tendons may also produce degenerative tears of the peroneus brevis tendon. The peroneus brevis and longus muscles form individual tendons that pass behind the lateral malleolus to turn anteriorly toward their respective insertions at the base of the fifth metatarsal and the base of the first metatarsal. At the level of the lateral malleolus, the tendon of the peroneus brevis remains anterior to the peroneus longus. The tendons are retained within the peroneal groove by the superior peroneal retinaculum (SPR).132 The SPR originates from the periosteum on the posterolateral ridge of the fibula.133 The peroneal groove is a shallow bony groove134 deepened by a fibrocartilaginous ridge. The mechanism of injury for an acute dislocation is related to a sudden, forceful, passive dorsiflexion of the inverted foot combined with reflex contraction of the peroneal tendons.135-137 As has been stated previously, chronic subluxation may also be related to chronic lateral ankle instability.138 The injury produces a variety of pathologic features, which include elevation of the SPR off the lateral border of the fibula with concomitant dissection of the tendons beneath the lateral fibular periosteum, tear of the SPR, or fracture of the posterolateral margin of the fibula. The anatomic classification of peroneal tendon instability, as described by Oden, is based on the location of SPR disruption.139 Chronic subluxation of the peroneus brevis tendon onto the posterolateral border of the fibula has been implicated in the development of longitudinal tears of the peroneus brevis tendon.140,141 Longitudinal tear of the peroneal tendons has also been described after acute and chronic lateral ankle inversion injury.142,143 Acute peroneal tendon dislocation produces pain over the course of the peroneal tendons as well as along the lateral border of the fibula. The patient may recall a pop at the time of injury. Often, the patient is


A

B

Figure 25C1-26 The “meniscoid lesion” associated with chronic anterior lateral ankle pain after lateral ankle ligament injury. A, Arthroscopic image of an anterior-lateral meniscoid lesion as seen from the medial portal. The lateral talofibular and talotibial joint space is occupied by the lesion. B, Arthroscopic image of the ankle after complete resection of the meniscoid lesion.

capable of providing a vivid description of dislocation. The tendon may or may not spontaneously reduce. A careful examination of the acute injury confirms swelling and tenderness posterior to the lateral malleolus.135,136,144-146 Active dorsiflexion of the foot from a plantar flexed and everted position may produce apprehension, subluxation, or dislocation (Fig. 25C1-27). Dislocation is not always actively elicited. Lateral ankle ligament stability is also assessed as part of a comprehensive examination. As with all lateral ankle injuries, routine radiographs are obtained. Fracture of the posterolateral margin of the fibula is a rare finding but indicates SPR disruption. MRI is the best imaging modality to evaluate peroneal disease, including tenosynovitis, partial or complete peroneal tendon rupture, peroneal tendon subluxation or dislocation, integrity of the SPR, and the competency of lateral ankle ligaments and internal derangement of the ankle and subtalar joints. A single, acute dislocation of the peroneal tendons is treated with an initial course of immobilization. A short leg cast is applied, and the patient is allowed to bear weight as tolerated. At 6 weeks, the stability of the peroneal tendons

A

is verified. An ankle rehabilitation program is instituted with an emphasis on peroneal strength and proprioception. Casting is aborted if the patient detects peroneal instability within the cast. Patients with recurrent or chronic dislocation do not respond to nonsurgical treatment methods.136,144,146-152 For these patients, surgical reconstruction is required. Surgical treatment includes exploration, tendon repair or tenodesis, peroneal groove deepening, and superior peroneal retinaculum reconstruction, as dictated by surgical findings. Technique: Deepening of the Peroneal Groove and Imbrication of the Superior Peroneal Retinaculum

1. The procedure is performed with the patient under general anesthesia. The patient is supine with a wellpadded proximal tourniquet and a soft bump placed beneath the ipsilateral hemipelvis. 2. A curvilinear incision is made over the course of the peroneal tendons. The initial exposure can be limited to 4 cm, with most of the incision proximal to the tip of the lateral malleolus. Care is taken to protect the sural nerve at the distal aspect of the incision.

B

Figure 25C1-27 A, Reduced peroneal tendons. B, Dislocated peroneal tendons as foot is dorsiflexed and everted.

Foot and Ankle 1933

3. The SPR is exposed and instability of the peroneal tendons verified by manipulation of the foot and ankle. The SPR, identified as a thickening in the sheath, and synovial sheath are sharply divided in line with the posterior border of the lateral malleolus. Exposure is completed by systematic synovectomy and tenolysis of the peroneal tendons. The peroneus brevis muscle that lies within the peroneal groove is resected off of the tendon. 4. Partial longitudinal tears involving less than 50% of the peroneal tendons are débrided and repaired with running sutures. 5. A shallow peroneal groove is deepened through a threesided, medially based osteoperiosteal flap. After a portion of the underlying cancellous bone is removed, the flap is replaced. Alternatively, the flap is resected and the underlying cancellous bone smoothed with bone wax. 6. The SPR is repaired and advanced onto the posterior lateral aspect of the fibula. This is typically accomplished through multiple drill holes using an absorbable suture. 7. The wound is closed in layers and a short leg splint applied in slight plantar flexion and eversion. At 10 days, the incision is inspected and a short leg weight-bearing cast applied for 4 weeks. Patients are then transitioned to a removable boot for 6 more weeks, and a rehabilitation program is instituted. An ankle brace is used for an additional 4 to 6 months. Activities are gradually resumed as the athlete regains full range of motion and strength.

Nerve Palsy The superficial peroneal nerve is susceptible to tension injury after inversion ankle injury. Patients complain of numbness at the dorsal foot or pain of the fascial hiatus radiating distally. Careful physical examination confirms loss of sensation on the dorsal foot. Pain may be reproduced with percussion of the superficial peroneal nerve, particularly at the crural fascia hiatus, or with passive plantar flexion and inversion of the foot. Differential injection of local anesthetic is also used to establish the diagnosis. Treatment is symptomatic but must include conservative management for the ankle instability. Johnston and Howell reported seven cases of superficial peroneal nerve neuropathy associated with inversion ankle injury.153 Five of the patients were also diagnosed with reflex sympathetic dystrophy. Surgical exploration revealed several abnormalities, including a distal exit from the crural fascia, scar, anomalous nerve, and a vessel leash. Nitz and colleagues performed electrodiagnostic testing on 60 consecutive patients with severe ankle sprains.154 The group of patients with medial and lateral ligament injuries (30) included 5 patients with peroneal and 3 patients with posterior tibial injuries. The group of patients with medial, lateral, and syndesmosis ligament injuries (36) included 31 patients with peroneal and 30 patients with posterior tibial injuries. Traction injury to the peroneal and tibial nerves at the bifurcation of the sciatic nerve is one possible mechanism of injury. Electrodiagnostic studies are used for documentation at presentation and follow-up. Sensory deficits do not require intervention. Motor deficits may require bracing with an ankle foot orthosis. Spontaneous recovery is typical.

Subtalar Sprain Meyer and coworkers performed ankle stress radiographs and subtalar joint arthrography on 40 patients with acute inversion sprains.155 They classified the injuries based on the extent of lateral ankle ligament and subtalar ligament injury. Thirty-two (80%) of the patients sustained injury to both the lateral ankle and the subtalar joint. Six patients with negative stress ankle radiographs had positive subtalar arthrograms. Subtalar joint sprain and subtalar instability are discussed in detail in the following foot section.

Subtalar Coalition Recurrent ankle sprain is not an uncommon presentation for the 10- to 14-year-old athlete with tarsal coalition. Lateral hindfoot pain, recurrent sprains, flatfoot, and decreased subtalar motion all point to talocalcaneal or calcaneonavicular coalition. The entity is diagnosed with oblique radiographs, CT, or MRI. Treatment is symptomatic initially with orthoses. Persistent symptoms require excision or occasionally hindfoot arthrodesis.

Bifurcate Ligament Sprain Injury to the bifurcate ligament or the anterior process of the calcaneus is associated with a plantar flexion–inversion mechanism (see Figs. 25C1-1, 25C1-48, and 25C1-49). The injury is often associated with, or mistaken for, a concomitant lateral ankle sprain. Diagnosis is clinical, but MRI confirmation may be obtained. Treatment is symptomatic with foot and ankle rehabilitation and is occasionally protracted owing to persistent symptoms. This injury is also reviewed in great detail in the foot section.

Tibiofibular Synostosis Heterotopic ossification of the interosseous ligament occasionally is noted after disruption of the syndesmosis (Fig. 25C1-28). Whiteside and associates identified six patients, all professional athletes, with tibiofibular synostosis and a history of inversion and internal rotation injuries.156 The authors’ experiences suggest excision for cases of persistent pain and limited dorsiflexion. Recurrence occurred in two of three cases. In my experience, the presence of ossification of the interosseous ligament or complete synostosis does not appear to be associated with a poor outcome (among patients with syndesmosis injury, not isolated lateral ankle injury). Certainly, a poorly reduced syndesmosis with an associated synostosis presents a need for excision of the synostosis and anatomic reduction.

Fifth Metatarsal Base Fracture The base of the fifth metatarsal is also susceptible to injury after a plantar flexion–inversion mechanism. The associated lateral hindfoot swelling and tenderness are distal and inferior to the ATFL. The diagnosis is confirmed with


Chronic lateral ankle instability produces a variable amount of impairment. The treating physician should emphasize a comprehensive and well-supervised rehabilitation program to prevent recurrent instability. Until ankle stability is achieved, a nonrigid or semirigid ankle brace is used to support the ankle. If significant improvement is not demonstrated within 6 weeks, I use a Broström procedure as modified by Gould to reconstruct the ATFL and the CFL. Intraoperative imaging is used to obtain bilateral stress views of the ankles to document instability. Arthroscopy of the ankle is used before stabilization, if indicated by clinical examination (e.g., anterolateral tenderness, talar dome tenderness) or MRI findings (e.g., osteochondral lesion of the talus, loose body).

Return-to-Play Criteria

Figure 25C1-28 Ossification of the syndesmosis in a former collegiate football player.

routine foot radiographs. Treatment is generally supportive with immobilization in a cast, walking boot, or stiffsoled shoe for 4 to 6 weeks.

Author’s Preferred Method Injury to the lateral ankle requires an individualized a pproach. Treatment must balance the needs of the athlete with the available professional support and facilities. High school, collegiate, and professional athletes are treated according to an accelerated schedule. These athletes are fortunate enough to have professional trainers for daily monitoring and treatment. Trainers and their staff are also able to provide ongoing ankle taping for practice and competition. Acute grade I and grade II sprains are treated with a supervised physical therapy program. Medical antiinflammatory therapy and cold therapy are used to reduce swelling and pain. Cast immobilization is avoided. A semirigid pneumatic ankle brace is used throughout the rehabilitation period and well into the return-to-sports phase. High-grade (grade III) lateral ankle sprains are treated with a brief 3- to 7-day period of weight-bearing to tolerance in a removable boot or a cast. The most comprehensive approach avoids casting and focuses on a supervised physical therapy program, including modalities (e.g., cold therapy, compression, electrical stimulation) for swelling and pain control. A semirigid pneumatic ankle brace is used throughout the rehabilitation period and well into the return-to-sports phase, typically 4 to 6 months.

Recovery of function after a lateral ankle sprain follows a logical sequence of events. Once the initial pain and swelling subside, coordination and strengthening activities are emphasized. Gradually, the patient is able to return to walking, running, and cutting programs. I return patients to sport once they master sport-specific drills with minimal discomfort. A semirigid pneumatic ankle brace or taping is used to prevent recurrent injury. Prevention of recurrence and new injuries has received much attention in the literature. Key components of prevention include strength conditioning, coordination, proprioception, stretching, and external support. Taping of the ankle is perhaps the most widely used prophylactic method.157 Rovere and colleagues published a retrospective analysis of taping, and the laced ankle stabilizer that confirmed that taping was much less effective in the prevention of new and recurrent ankle injuries among collegiate football players.158 Taping appears to be limited by time-related loosening.159,160 Glick and coworkers studied the effect of tape on six ankles with significant (>5 degrees) talar tilt.7 Each subject performed 20 minutes of exercise. Only one of the six ankles remained firmly supported by the ankle tape. Walsh and Blackburn acknowledge the time-related loosening associated with ankle taping.161 They contend that the method continues to play a supportive role, perhaps limited to restricting the extremes of motion. They recommend taping against the skin and secondarily around the shoe (football). They emphasize that tape, in any amount or configuration, is not a substitute for rehabilitation. Although taping is inexpensive on a per-use basis, significant cost is associated with long-term application by trained personnel.158 Hamill and colleagues suggested the use of a semirigid pneumatic orthosis for the prevention of recurrent lateral ankle sprains; they cite a reduction in mediolateral excursion force and velocity in an experimental setting.162 Decreased inversion, based on angular displacement, has also been demonstrated.163 Soccer players with and without a history of lateral ankle sprains were randomly assigned by Surve and associates to use a semirigid pneumatic ankle brace (Sport Stirrup, Aircast, Inc., Summit, NJ).164 The orthosis reduced

Foot and Ankle 1935

the incidence of lateral ankle sprains in the group with a history of previous ankle injury but not in the group without such a history. Thacker and colleagues completed a review of 113 studies and concluded that supervised rehabilitation must be completed before resumption of running or practice.8 Furthermore, these authors recommended the use of an orthosis for 6 months after a severe lateral ankle sprain. A sobering study completed by Gerber and associates clearly illustrates the long-term disability associated with ankle sprain.3 This prospective observational study of 104 West Point cadets confirmed that 95% of the cadets had returned to athletic activity by the 6-week follow-up. At the time of the 6-month follow-up, all cadets had returned to athletic activity, but 40% remained symptomatic. The persistent dysfunction was related neither to the grade of sprain nor the presence of joint laxity. In summary, athletes return to sport after recovery of pain-free ankle motion, strength, and protective reflexes. The athlete must complete sport-specific drills with a high degree of confidence and comfort. Most important, the ankle is braced until functional and anatomic stability are achieved.

Medial Ankle Sprain Isolated injury to the deltoid ligament is rare. Staples reviewed 110 cases of deltoid injury.165 Deltoid rupture without associated ankle fracture was noted in only 10 cases. Of these 10 cases, 5 were isolated to the deltoid, 3 were associated with syndesmosis injury, and 2 were associated with anterior capsule injury.

Relevant Anatomy The deltoid ligament consists of superficial and deep components (Fig. 25C1-29).166,167 The superficial deltoid ligament originates from the anterior portion of the medial malleolus and spreads out to insert on the navicular, talus, and calcaneus. The superficial deltoid includes four parts—the tibionavicular ligament, the tibiospring ligament, the tibiocalcaneal ligament, and the superficial tibiotalar ligament. The deep deltoid ligament includes two parts—the deep anterior tibiotalar ligament and the deep posterior tibiotalar ligament. It is a short, thick ligament that traverses from the intercollicular groove onto the medial talus and blends with the medial capsule of the ankle joint. The biomechanical characteristics of the ankle ligaments are such that failure (rupture) is due to increasing load as opposed to twisting or shearing.15 Isolated testing of the individual ankle ligaments demonstrates that the ATFL is the first to fail and the deep deltoid ligament is the last to fail.15 The deltoid ligament functions to limit abduction. It is a strong structure that requires significant force to cause rupture. Siegler and colleagues tested 20 fresh cadaveric ankles.18 Based on increasing ultimate load, components of the deltoid were ordered from weakest to strongest as follows: the tibiocalcaneal ligament, the tibionavicular ligament, the tibiospring ligament, and the posterior tibiotalar ligament.

Superficial portion deltoid ligament

Deep portion deltoid ligament

Spring ligament Sustentaculum tali Figure 25C1-29 The superficial and deep layers of the deltoid ligament. (Redrawn from Close JR: Some applications of the functional anatomy of the ankle joint. J Bone Joint Surg Am 38:761781, 1956.)

Close has demonstrated the importance of the medial ligaments in maintaining a normal medial clear space, that is, a normal intermalleolar distance.166 He provided a detailed anatomic description but no data to support his conclusions. Earll and coworkers conducted a cadaveric study to assess the importance of the deltoid ligament relative to talocrural contact and pressure.168 Division of the tibiocalcaneal fibers of the superficial deltoid resulted in significant decreased contact area (maximum, 43%) and an associated increase in contact pressure (maximum, 30%). Division of the other components of the deltoid resulted in insignificant changes in joint contact. Kjærsgaard-Andersen and associates used a cadaveric model to study the effect of isolated division of the tibiocalcaneal ligament.169 They reported a maximal median increase in tibiotalocalcaneal abduction of 6.1 degrees and a corresponding maximal median increase in talocalcaneal abduction of 3.6 degrees. The authors concluded that the tibiocalcaneal ligament is an important stabilizer of the medial hindfoot. Rasmussen and colleagues used a cadaveric model to study the effect of isolated division of the deltoid ligament with a device that allowed recording of rotatory movements in two planes.170 The tibiocalcaneal ligament (superficial deltoid) and the intermediate tibiotalar ligament (deep deltoid) provided resistance to abduction of the talus. The deltoid also provided significant resistance to external rotation of the talus.

Clinical Evaluation Isolated deltoid rupture is a rare injury, usually associated with a traumatic mechanism of injury. Most deltoid ruptures are associated with ankle fractures. Ankle fractures associated with a pure deltoid rupture typically involve the posterior deep tibiotalar ligament.171 Evaluation of the medial ankle sprain is designed to elicit information that allows classification of the injury. Various classifications have been described, but graded ligament injury, as suggested by the American Medical Association35 and by O’Donoghue,36 is sufficient. Injuries


are graded based on stretch (grade I), partial tear (grade II), or complete rupture of the ligament (grade III). Additional information with regard to associated ligamentous injuries is noted.

History Information relevant to previous ankle injury, the mechanism of injury, the ability of the patient to continue to play or walk, and current complaints represent the salient historical points. The patient frequently reports feeling a pop in the medial ankle with associated pain and swelling.

Incisura fibularis

1 cm

Physical Examination It is imperative that the examination not be limited to the medial ankle ligaments. Inspection of the leg, ankle, and foot may reveal swelling, ecchymosis, blister formation, or gross deformity. A vascular and sensory assessment is performed, followed by palpation of the entire leg, ankle, and foot. Tenderness at the deltoid and surrounding area is particularly important to note. Attention is paid to symptoms in other areas that could indicate ankle fracture, lateral ligament sprain, syndesmotic injury, combined proximal fibular fracture (Maisonneuve pattern), or proximal tibiofibular joint injury. Motion about the foot and ankle is determined with the patient seated and relaxed. The knees are flexed and the feet allowed to fall into an equinus position. Ankle and subtalar range of motion is documented and motor function graded. Stress testing is a useful clinical and radiographic tool that provides a portion of the diagnostic data required for grading ankle sprains. The anterior drawer test and the varus talar tilt test are used to demonstrate the integrity of the ATFL and the CFL. A valgus talar tilt test is used to evaluate the integrity of the deltoid. The test is performed in both ankle neutral and plantar flexion positions. Valgus stress is applied to the talus through the hindfoot, and a comparison is made between injured and noninjured ankles. Testing is occasionally uncomfortable, particularly in the acute setting. False-negative results may be caused by involuntary guarding or pain response. The ankle can be injected with local anesthetic to facilitate a better examination. The chronic or recurrent medial ankle sprain is associated with functional or mechanical medial instability, apprehension, discomfort, swelling, and tenderness over the deltoid. This clinically manifests as a valgus and pronation deformity that many patients can correct by contracting the posterior tibialis muscle.

Imaging Radiographs Radiographs in the anteroposterior, mortise, and lateral projections are required for ankle evaluation. Weightbearing radiographs are used in an effort to reproduce physiologic loading.

0.5 cm Medial joint space width

Syndesmosis width Displacement of distal fibula

Figure 25C1-30 Techniques of measuring the lateral displacement of the lateral malleolus (mortise view) and the width of the syndesmosis (mortise view) and medial joint space (anteroposterior view). (Redrawn from Harper MC: The deltoid ligament: An evaluation of need for surgical repair. Clin Orthop 226:156-168, 1988.)

Radiographs are evaluated with regard to malleolar fracture, physeal fracture, osteochondral fracture, avulsion fracture, and deltoid ossification. Alignment and translation deformity are also inspected, particularly at the syndesmosis and the medial ankle joint space (Figs. 25C1-30 and 25C1-31). An increased medial clear space suggests complete rupture of both components of the deltoid.166 Radiographs are frequently normal with partial ligament injuries.

Stress Radiographs Valgus talocrural instability may occur after deltoid disruption.172 The bilateral stress radiograph is used to quantify valgus tilt of the talus. The valgus tilt stress radiograph is similar to the clinical test but is performed during an anteroposterior radiograph. The degree of tilt is determined by measuring the angular divergence between the distal tibial articular surface and the talar dome. Leith and associates performed valgus stress radiography on 32 previously uninjured patients.173 This examination was performed on both ankles in a neutral position with and without valgus stress. The authors demonstrated that 91% of the ankles had less than 2 degrees and that the remaining 9% of the ankles had between 2 and 3 degrees of valgus tilt. They suggest that an ankle with a valgus tilt greater than 2 degrees has a high probability of deltoid injury. The external rotation stress radiograph is also used to evaluate associated syndesmosis injury. This test is described in the section on “Ankle Syndesmosis Sprain.”

Foot and Ankle 1937 Anteroposterior View

A

B

B

C

A = Lateral border of posterior tibial malleolus B = Medial border of fibula C = Lateral border anterior tibial tubercle

B

A B

C

B

A Syndesmosis A (6 mm or 42% of fibular width)

Figure 25C1-31 Syndesmotic radiographic criteria. A, The syndesmosis clear space as depicted on the anteroposterior view and by coronal section. The tibiofibular clear space is the distance between the lateral border of the posterior tibial malleolus (point A) and the medial border of the fibula (point B) on the anteroposterior radiograph. This space is normally less than 6 mm.187 B, The syndesmosis overlap as seen on the anteroposterior view and by coronal section. The tibiofibular overlap is the distance between the medial border of the fibula (point B) and the lateral border of the anterior tibial prominence (point C) on the anteroposterior radiograph. This space is normally greater than 6 mm, or 42% of the fibular width.187 (Redrawn from Stiehl JB: Complex ankle fracture dislocations with syndesmosis diastasis. Orthop Rev 14:499-507, 1990.)

Arthrography The unpredictable effect of patient guarding during stress radiography is overcome by the use of ankle arthrography.52,53 This method is relatively simple and can provide objective evidence of deltoid disruption. Contrast material is injected into the acutely injured ankle, preferably with fluoroscopic guidance, and radiographs are obtained in various projections with attention to areas of extravasation. A false-negative result from an early capsular seal is possible. The procedure has been largely replaced by the use of MRI.

Magnetic Resonance Imaging MRI is a useful method for evaluation of acute, subacute, and chronic ankle ligament injuries.55 Deltoid disruption, partial or complete, is demonstrated by fiber disruption, edema, and associated injuries to the surrounding soft tissue and bone (see Fig. 25C1-9). Visualization of the deltoid ligament requires careful attention to the position of the foot during the test. On coronal images, the tibionavicular and anterior tibiotalar components are best seen with the foot in plantar flexion, whereas the tibiocalcaneal and posterior tibiotalar portions are visualized with the foot in dorsiflexion.174

Therapeutic Options The treatment of this injury depends on the severity of disruption and associated injuries. All acute injuries are treated with the RICE method followed by gentle range of motion and protected weight-bearing. Many studies have reviewed the effect of cold application to the injured extremity. Cold therapy is an effective, inexpensive, and easy-to-use modality for the treatment of

acute musculoskeletal injury. Appropriately applied cold therapy decreases pain perception, decreases the biochemical reactions that produce inflammation, and produces vasoconstriction with a concomitant reduction in soft tissue swelling and bleeding. Compression is typically provided in the form of an elastic bandage but may also include casting, splinting, pneumatic orthosis, or mechanical compression devices.57 Elevation of the ankle helps to reduce swelling and pain. The ankle is supported by a variety of methods, including the use of a nonwalking cast, a walking cast, a removable cast boot, a semirigid pneumatic ankle brace, a nonrigid functional ankle brace, or various ankle taping methods. Various immobilization methods are summarized in Table 25C1-4.

Grade I Medial Ankle Sprains Treatment is symptomatic with an emphasis on recovery of range of motion, strength, and coordination. A structured ankle rehabilitation program remains an important part of treatment. A nonrigid functional ankle brace, such as a lace-up brace, or a semirigid pneumatic ankle brace is used during all phases of the recovery. Return to competition is usually delayed when compared with lateral ankle sprains.

Grade II and Grade III Medial Ankle Sprain Complete immobilization is provided with a short leg walking cast or boot. Weight-bearing to tolerance is encouraged. The assumption is that immobilization allows the ruptured ends of the medial ankle ligaments to heal in a near-anatomic position. Immobilization is continued for 6 to 8 weeks depending on resolution of swelling,


t enderness, and instability. A comprehensive ankle rehabilitation program is used along with a semirigid pneumatic orthosis for up to 6 months from the date of injury. Surgical treatment is rarely necessary and is reserved for patients with a persistent valgus tilt or in whom the medial clear space is not reduced.165,175 Technique: Repair of Medial Ankle Ligaments

Author’s Preferred Method of Treatment Completely isolated deltoid injuries are rare. Occasionally, an athlete presents with a high-grade lesion with predominantly medial symptoms. In this instance, I prefer to use a short leg cast or walking boot for 4 to 6 weeks in an effort to promote anatomic healing of the deltoid fibers. A comprehensive, supervised physical therapy program then follows. An ankle brace is used throughout the rehabilitation period and well into the return to sports phase. Medical anti-inflammatory therapy is provided to reduce swelling and pain. Chronic medial ankle instability is rare. The clinical and radiographic work-up must be meticulously done before a medial reconstruction is undertaken. Partial tears and ossicles associated with the anterior colliculus can be a common source of dysfunction. Isolated removal and local repair can provide relief.

1. A longitudinal incision is created over the medial malleolus and extended to the talonavicular joint. 2. Both the superficial and deep components of the deltoid ligament are inspected as are the adjacent posterior tibial and flexor digitorum tendons. 3. The ankle joint is inspected for articular surface lesions and loose bodies. This can be done arthroscopically before the open procedure if desired. 4. Anatomic repair of the deep fibers is completed before repair of the superficial fibers. Nonabsorbable sutures are used. In cases of complete avulsion from the medial malleolus, a suture anchor can be used. 5. The incision is closed in a layered fashion, and a splint is applied. At 10 days, the patient is placed into a short leg cast. Patients are not allowed to bear weight for 4 weeks after surgery. At that point, the patient is transitioned into a walking boot and allowed to progress to full weight-bearing over 4 weeks. An ankle rehabilitation program with emphasis on range of motion, strengthening, and proprioception is started. The athlete continues to wear an ankle brace during sports for 6 months after surgery.

Recovery follows a logical sequence of events. Once the initial pain and swelling subside, coordination and strengthening activities are emphasized. Gradually, the patient is able to return to walking, running, and cutting programs. Patients are returned to sport once they master sportspecific drills. A semirigid pneumatic ankle brace or taping accelerates the schedule.

Chronic Medial Ankle Sprain and Instability

Ankle Syndesmosis Sprain

Occasionally, a medial ankle sprain produces a chronic deltoid insufficiency or medial ankle pain. Difficulty with push-off may also be noted. Careful review of the initial treatment program may suggest the need for an aggressive and well-supervised rehabilitation program along with a semirigid pneumatic orthosis. If it is believed that the rehabilitation was adequate, further imaging with stress radiographs and MRI is obtained to better delineate the condition. An ossicle within the anterior deltoid may produce medial symptoms without clinical instability. Symptomatic anterior deltoid ossicles are surgically débrided, followed by postdébridement valgus stress radiographs. Sympto matic medial ligament insufficiency is most easily treated with local repair and imbrication of the deltoid. Advancement of the deltoid to the medial malleolus may be facilitated through drill holes or with suture anchors. If the local tissues are inadequate for a direct repair, a reconstruction can be performed. Autograft or allograft material is placed from the tibia to the talus or navicular. This technique can be combined with spring ligament repair or reconstruction if that ligament is attenuated as well.

Injury to the ankle syndesmosis, or a high ankle sprain, is most common in collision sports.176 Injury to the syndesmosis results in more impairment to the athlete when compared with lateral ankle sprains. Boytim and colleagues reported 98 ankle injuries among the players of a professional football team over a 6-year period.176 Twenty-eight significant lateral ankle sprains and 15 syndesmosis sprains were reported. The players with syndesmosis sprains missed more games and more practices and used more treatments than players with lateral ankle sprains. Hopkinson and coworkers retrospectively reviewed 1344 ankle sprains that occurred over a 41-month period at the U.S. Military Academy.177 Fifteen of these patients (1.1%) were diagnosed with syndesmosis sprain. A subsequent prospective study at the same institution revealed that syndesmosis sprains accounted for 17% of ankle sprains over a 2-month period.3

Rehabilitation A detailed rehabilitation program is outlined in the section on lateral ankle ligament injury. Ankle and subtalar flexibility, motor function, and coordination30 are emphasized throughout the protocol.

Return-to-Play Criteria

Relevant Anatomy The interosseus membrane connects the tibia to the fibula. At the level of the ankle, three defined ligaments are present: the anterior-inferior tibiofibular ligament (AITFL), the posterior-inferior tibiofibular ligament (PITFL), and the interosseous ligament (IOL) (Fig. 25C1-32). The AITFL courses from the anterodistal fibula to the anterolateral (Tillaux-Chaput) tubercle of the tibia. The AITFL is the most commonly injured ligament in syndesmotic sprains and can result in symptomatic impingement in some cases.

Foot and Ankle 1939

IOL

IOL

Syndesmotic ligaments AITFL ATFL

PITFL

DL

PTFL DL

A

Syndesmotic ligaments

CFL

B

Figure 25C1-32 A, The tibiofibular syndesmosis from the front—anterior-inferior tibiofibular ligament (AITFL), anterior talofibular ligament (ATFL), and deltoid ligament (DL). B, The tibiofibular syndesmosis from the back—posterior inferior tibiofibular ligament (PITFL), distal interosseous ligament (IOL), posterior talofibular ligament (PTFL), calcaneofibular ligament (CFL), deltoid ligament (DL).

The PITFL is composed of the deep transverse t ibiofibular ligament and a superficial portion. The two components form a strong yet elastic structure, which usually fails last in syndesmotic injury. The IOL connects the tibia to the fibula about 0.5 to 2.0 cm above the plafond. Proximally, it continues as the interosseus membrane, which provides little additional strength to the syndesmotic ligaments. The syndesmosis, along with the deltoid ligament, maintains the critical anatomic relationship between the tibia and the talus. Ramsey and Hamilton used a carbon black transference technique to clearly demonstrate that lateral displacement of the talus results in an incremental decrease in contact area with each millimeter of translation.178 The first millimeter of lateral translation produced an average 42% reduction in contact area between the tibia and the talus. Failure to reduce the ankle syndesmosis and the associated lateral talar translation greatly increases the risk for post-traumatic ankle arthritis (Fig. 25C1-33). Anatomic dissection by Close revealed that division of the syndesmosis and of the interosseous ligament produces minimal widening of the intermalleolar distance.166 Only after the deltoid ligaments are divided does the syndesmosis separate. His conclusion is that significant trauma to the ankle must occur for the ankle mortise to appear wide. Broström described the ligamentous lesions found during the surgical exploration of 105 recent ankle sprains.27 The ATFL was the most commonly injured structure. The ATFL was completely torn as an isolated injury in 65 cases and as an associated injury in an additional 25 patients. The CFL was the second most commonly injured ligament. It was completely or partially torn as an associated injury in 23 patients. The AITFL was completely torn in 6 cases. No incomplete ruptures were noted. Five of these injuries occurred at midsubstance, and 1 involved an avulsion fracture off the anterior tibia. The torn ends of the ligament remained well apposed. External rotation of the talus produced up to 5 mm of diastasis in 5 cases and 1 to 2 mm in the sixth case. The mechanism of injury is thought to be external rotation, although researchers have been unable to reliably

reproduce syndesmosis sprain without fracture. An external rotation force first disrupts the AITFL, followed by the IOL, but usually spares the PITFL. Increased force can lead to spiral fractures of the proximal fibula (Maisonneuve fracture). In 1968, Lovell described the case of a 13-year-old tobogganner who sustained a forced external rotation injury to the ankle.179 The patient presented with a fixed external rotation foot deformity that was associated with a posterior dislocation of the fibula perched behind the lateral tibia. Closed reduction and casting produced an excellent result. Boytim and associates suggested two specific mechanisms of injury in the professional football player.176 The first is direct force applied to the posterior leg of a downed player whose foot is in an externally rotated position. The

Figure 25C1-33 Post-traumatic ankle arthritis subsequent to an incompletely reduced ankle syndesmosis and lateral talar translation. Note the wide syndesmosis and medial joint space width, the narrow superior joint space, and the lateral subchondral cyst formation.


second is an external rotation force at the knee while the foot is firmly planted. Fritschy evaluated 10 world-class slalom skiers with syndesmosis injuries.180 He speculated that a common mechanism of forced external rotation of the talus against the fibula produced all of their injuries. A retrospective review by Hopkinson and colleagues failed to establish a consistent mechanism of injury among athletes of different sports with syndesmosis sprain.177

Clinical Evaluation Sprains can be considered from the simplistic perspective of graded ligament injury, as suggested by the American Medical Association35 and by O’Donoghue.36 Injuries are graded based on stretch (grade I), partial tear (grade II), or complete rupture (grade III) of the AITFL. Additional information with regard to associated ligamentous or bony injuries is noted. Edwards and DeLee described a classification system for ankle diastasis without fracture (grade III sprain) based on the presence of radiographic diastasis with and without stress.181 A latent syndesmosis injury appeared normal on an unstressed radiograph and abnormal or widened on external rotation stress mortise radiograph. A frank syndesmotic injury was seen as a widened syndesmosis on unstressed radiographs. The frank injuries were further divided into four types: type I, lateral fibular subluxation without plastic deformity of the fibula; type II, lateral fibular subluxation with plastic deformity of the fibula; type III, posterior subluxation of the fibula behind the lateral tibia; and type IV, superior dislocation of the talus between the tibia and fibula with diastasis and no fibula fracture.

to a former chief athletic trainer at the U.S. Military Academy. The test is performed by compression of the midleg from posterior lateral to anterior medial. Pain produced at the AITFL suggests injury to the same, as long as fracture, contusion, and compartment syndrome are not present. The authors retrospectively reviewed eight patients with syndesmosis sprains; all were noted to have a positive squeeze test at initial evaluation. A separate biomechanical analysis of the squeeze test demonstrated that the squeeze test produced reproducible separation of the fibula and tibia.183 Boytim and associates described an external rotation stress test (Fig. 25C1-35).176 The patient is seated and relaxed with the hip and knee flexed and the foot and ankle held in a neutral position. The knee is maintained in a forward-facing position while a gentle but firm external rotation force is applied to the foot. Pain reproduced at the anterior syndesmosis is diagnostic of a syndesmosis injury. A secondary test is the direct eversion maneuver (Fig. 25C1-36).184 The maneuver is accomplished with the patient in a seated and relaxed position. The examiner gently secures the leg and foot as a direct eversion or abduction force is applied across the ankle. Increased translation compared with the contralateral ankle is a positive result.

Imaging Radiographs The radiographic examination includes weight-bearing views of the ankle, orthogonal views of the leg, and, when indicated, a computed tomographic scan of the syndesmosis (see Figs. 25C1-30 and 25C1-31).185,186

History Information relevant to previous ankle injury, the mechanism of injury, the ability of the patient to continue to play or walk, and current complaints represent the salient historical points. Syndesmosis injury is suggested by a mechanism of forced external rotation of the foot.

Physical Examination The examination is systematic and includes careful palpation along the entire interosseous ligament and the fibula. Fracture of the fibula at all levels must be considered. Although dislocation of the proximal tibiofibular joint is rare,182 it must also be considered when proximal leg symptoms are present. Local tenderness at the AITFL or along the interosseous ligament suggests a syndesmosis sprain. There may be tenderness over the deltoid ligament, usually with an associated abduction force at the time of injury. Ankle range of motion is carefully assessed. Also, lateral ankle stability is determined with performance of the anterior drawer and talar tilt tests. One must never forget that pain out of proportion to the injury is a finding consistent with acute compartment syndrome. Hopkinson and coworkers described a squeeze test used to identify syndesmosis ruptures at the time of initial presentation (Fig. 25C1-34).177 The squeeze test was attributed

Figure 25C1-34 The squeeze test.177 Syndesmosis injury is suspected when compression of the midleg produces pain at the ankle syndesmosis.

Foot and Ankle 1941

B

A

Figure 25C1-35 The external rotation stress test of the syndesmosis. (A, Redrawn from Boytim MJ, Fischer DA, Neumann L: Syndesmotic ankle sprains. Am J Sports Med 19:294-298, 1991.)

Harper and Keller used 12 cadaveric legs to establish radiographic criteria for a normal syndesmosis.187 Plastic spacers with 1-mm increments were used to produce the diastases. With the use of standard anteroposterior and mortise radiographs, it was determined that the “clear space” on either view is normally less than 6 mm. This was in fact the most reliable parameter for evaluating the integrity of the syndesmosis. The normal overlap between the fibula and the anterior process of the tibia

A

is greater than 6 mm, or 42% of the width of the fibula on the anteroposterior view, or greater than 1 mm on the mortise view. Ostrum and colleagues used a more specific approach to the question of radiographic diastasis.188 The authors included 40 female and 40 male normal volunteers to establish normal values. Their first finding was a distinct difference between the sexes. To bypass the sex variation, they suggested sexspecific absolute values or non–sex-specific ratios.

B

Figure 25C1-36 A, The direct eversion maneuver is accomplished with the patient in a seated and relaxed position. The examiner gently secures the leg and foot as a direct eversion or abduction force is applied across the ankle. Increased translation compared with the contralateral ankle is a positive result. B, A positive stress radiograph showing increased translation. (A, Redrawn from Stiehl JB: Complex ankle fracture dislocations with syndesmotic diastasis. Orthop Rev 19:499-507, 1990.)


Late radiographs after a syndesmosis rupture may reveal varying degrees of interosseous ligament calcification. Hopkinson and associates retrospectively reviewed radiographs of 10 patients with syndesmosis sprains, as diagnosed by a positive squeeze test at initial evaluation.177 Radiographs for nine of the patients demonstrated heterotopic calcification. At an average of 20 months after injury, all ankles were asymptomatic. Taylor and colleagues reported finding heterotopic ossification on 11 of 22 follow-up radiographs after syndesmosis sprain sustained during football (diagnosed by tenderness at the syndesmosis).189 No player developed frank synostosis. The lower incidence of heterotopic ossification, as compared with the Hopkinson report, may be related to the method of diagnosis (squeeze test versus local tenderness). Patients with heterotopic ossification experienced a delayed recovery (i.e., 32 days without heterotopic ossification, 43 days with heterotopic ossification). The authors suggested a correlation between severity of injury and the formation of heterotopic ossification. Patients with heterotopic ossification also were more likely to experience recurrent inversion ankle sprains.

Stress Radiographs When routine radiographs are normal and there is a concern for a latent syndesmotic injury, stress radiographs are obtained. Radiographs are taken with application of an external rotation and abduction force through the ankle. Xenos and coworkers performed an experimental study with 25 cadaveric ankles.190 Each ankle was tested under a constant external rotation torque. After sequential division of the syndesmosis and subsequent repair, the authors concluded that the lateral external rotation stress radiograph is superior to the mortise stress radiograph for the detection of syndesmosis injury.

acute syndesmosis injury. Among 27 patients, the imaging was 100% sensitive and 71% specific.191

Computed Tomographic Scan Computed tomographic scans are able to obtain images in the axial, sagittal, and coronal planes. These images can be reconstructed to create a detailed three-dimensional representation of the relationship of the tibia to the fibula. Ebraheim and coworkers demonstrated the superiority of CT over plan radiographs in detecting syndesmotic disruption.192 They used a cadaveric model and plastic spacers to demonstrate the inability of routine radiographs and CT to identify 1-mm diastases at the syndesmosis. Computed tomographic scans identified 2- and 3-mm diastases. Routine radiographs failed to identify 2-mm and 50% of the 3-mm diastases.

Magnetic Resonance Imaging MRI is a useful method for evaluation of syndesmosis injuries. Its accuracy, lack of ionizing radiation, noninvasiveness, decreasing cost, and increasing availability suggest that MRI is the imaging modality of choice for the ankle joint. Ligament discontinuity, wavy ligament contour, and the inability to image the ligament are all findings consistent with a syndesmosis injury. The high sensitivity associated with MRI mandates that images be carefully correlated with clinical findings (Fig. 25C1-37A).

Therapeutic Options All acute injuries are treated with the RICE method and non–weight-bearing until definitive diagnosis is established.

Isolated Grade I and Grade II Syndesmosis Sprains

Before the development of MRI, arthrography was commonly used to document injury to the syndesmosis. After injection of contrast material into the ankle, a positive test showed dye leakage more than 1 cm superior to the plafond. Broström and associates performed arthrography of 321 fresh ankle sprains.54 Extra-articular leakage occurred in 239 cases (74%). Surgical exploration was performed in 99 of these cases and in an additional 6 cases that did not demonstrate leakage. The authors concluded that arthrography was useful within the first 7 days of an acute ankle sprain. Leakage of contrast into the peroneal tendon sheath correlated with tear of the CFL. Leakage in front of the lateral malleolus correlated with ATFL rupture. Leakage in front of the syndesmosis correlated with complete rupture of the syndesmosis. Leakage at the medial malleolus correlated with partial deltoid rupture.

After the acute pain and swelling remit (within 72 hours), weight-bearing to tolerance is encouraged, and a rehabilitation program is instituted. Treatment is symptomatic with an emphasis on recovery of range of motion, strength, and coordination. A semirigid pneumatic ankle brace or taping is used throughout the rehabilitation period. Taping is applied with an effort to restrict or reduce external rotation. While facing the athlete, the trainer applies the tape from lateral to medial. Gerber and coworkers prospectively evaluated 96 West Point cadets with acute ankle sprains.3 Sixteen of these injuries were primarily syndesmosis sprains treated with early mobilization. Regardless of grade of injury, patients with syndesmosis sprains were most likely to experience an unacceptable outcome at 6 months’ follow-up. The authors speculated that lack of accurate evaluation, underestimation of extent of injury, and incomplete rehabilitation may account for the poor results among patients with syndesmosis sprains.

Nuclear Imaging

Isolated Grade III Syndesmosis Injuries

Radionuclide imaging of the acute syndesmosis injury without fracture is not a common practice. Marymont and colleagues used radionuclide imaging 1 to 2 weeks after

Treatment of the complete syndesmosis disruption is based on displacement and stability. Latent injuries as described by Edwards and DeLee181 may be treated with a

Arthrography

Foot and Ankle 1943

A

B

Figure 25C1-37 A, Magnetic resonance image demonstrating complete tear of AITFL and partial tear of PITFL. B, Open treatment of syndesmotic rupture.

protracted course of non–weight-bearing in a short leg cast or a removable cast boot. Non–weight-bearing status is maintained for 6 to 10 weeks depending on the resolution of local tenderness and pain with provocative maneuvers. Nonoperative treatment is recommended only for isolated, stable injuries. If the injury is associated with medial bony or ligamentous injury, internal fixation is suggested.

A

B

Frank injuries with a displaced or widened syndesmosis require closed reduction and internal fixation or open reduction and internal fixation (Fig. 25C1-38). The adequacy of the reduction is based on radiographs of the noninjured ankle. Based on the evaluation of 34 ankle fractures, Leeds and Ehrlich concluded that the poorly reduced tibiofibular diastasis predisposed the patient to a poor outcome and

C

Figure 25C1-38 Syndesmosis rupture. A, Anteroposterior injury radiograph. B, Internal fixation with fully threaded 4.5-mm screw. C, Anteroposterior radiograph after screw removal.


osteoarthrosis.193 Reduction of the syndesmosis to within 2 mm of the contralateral side correlated with good subjective and objective results at an average follow-up of 4 years. Published recommendations for syndesmosis screw removal vary from as early as 6 weeks194 to nonremoval. Most authors maintain screws for a minimum of 12 weeks after surgery. Harper reported syndesmosis failure following removal of syndesmosis screw fixation 6 and 8 weeks after insertion.195 The syndesmotic screw eventually loosens and does allow at least some motion at the distal tibiofibular joint.195-197 Grath noted in his comprehensive treatise that the removal or nonremoval of a syndesmotic screw does not produce detrimental effects.198 Thordarson and associates acknowledged the disadvantages of permanent screw fixation to include prominent painful hardware, disruption of normal biomechanical relationships at the syndesmosis, screw fracture, need for a second operative procedure if removal is selected, stress shielding of bone, and interference with MRI and CT.199 To obviate the need for permanent hardware, the group tested 4.5-mm polylactide (PLA) screws against 4.5-mm stainless steel screws in a cadaveric model. They concluded that the PLA screws were of sufficient strength to maintain fixation and allow healing of the syndesmosis.

to prevent over-reduction of the mortise and subsequent loss of ankle dorsiflexion (see Fig. 25C1-38B). 7. The wound is closed in layers and a short leg splint applied. At 10 days, the incision is inspected and the patient is transitioned to a short leg cast or removable boot. Patients are prevented from bearing weight for a minimum of 4 weeks. After 4 weeks, a rehabilitation program is instituted and monitored. Partial weightbearing is allowed after 4 to 6 weeks and progressed to full by 8 to 12 weeks. The fixation is removed 3 months after surgery, before resumption of athletic activity is permitted. The patient continues for 6 months with an ankle brace during rehabilitation and sports activities.

Unusual Syndesmosis Injuries

Surgical Repair

Olerud reported a single case of posterior dislocation of the fibula (Edwards and DeLee type III) and subluxated talus associated with a violent supination and external rotation mechanism of injury.201 This patient was successfully treated with primary open reduction and syndesmotic screw placement. Edwards and DeLee used a fibular osteotomy to reduce lateral displacement of the fibula associated with plastic deformity of the fibula (Edwards and DeLee type II).181 The procedure was successfully used on two patients with this unusual injury.

Technique: Closed or Open Reduction and Internal Fixation of the Ankle Syndesmosis (see Fig 25C1-37B)

Chronic Syndesmosis Sprains

1. The procedure is performed with the patient under general anesthesia. The patient is supine with a wellpadded proximal tourniquet and a soft bump placed beneath the ipsilateral hemipelvis. 2. An image intensifier is used to attempt closed reduction of the syndesmosis. If reduction is not satisfactory, an open reduction is performed. 3. The extremity is exsanguinated and the tourniquet inflated. A linear incision is placed over the tibiofibular space about 2 to 3 cm above the plafond. Care is taken to protect the lateral branch of the superficial peroneal nerve as it courses over the syndesmosis. 4. The syndesmosis is exposed, and tearing of the AITFL is noted. The tear is approximated and repaired with absorbable suture. Avulsion fractures are repaired directly to the fibula or tibia. Open reduction is accomplished by débridement of the distal tibiofibular articulation. Reduction is performed and held with a large forceps on the tibia and fibula. 5. If reduction of the medial joint space remains incomplete, a medial ankle arthrotomy and a deltoid ligament repair are performed. Sutures are placed but are not tied until the syndesmosis is satisfactorily reduced and stabilized. 6. The syndesmosis repair is then protected by placement of one or two 3.5- or 4.5-mm screws. These screws are placed 2 cm200 above the ankle joint line with the ankle in a neutral dorsiflexion position. The fixation is directed from the relatively posterior fibula into the more anterior tibia. Three or four cortices are captured with the screw. A nonlag technique is used in an effort

Little literature exists on how to optimally treat chronic syndesmosis injuries. Reconstruction requires scar débridement from the syndesmosis and ankle joint. Reduction is held with large clamps while a tendon graft is placed through drill holes in the fibula and tibia to recreate the AITFL. Trans-syndesmotic fixation is placed to protect the reconstruction, and the medial deltoid ligament is repaired or reconstructed. Some authors have advocated arthroscopic treatment of chronic syndesmotic injuries.202 Patients who underwent resection of the torn portion of the interosseus ligament and chondroplasty reported improvement in postoperative pain, swelling, stiffness, and activity level. The authors also reported normalization of the external rotation stress test. Although the authors did not perform transsyndesmotic fixation, it can be done in conjunction with this procedure to stabilize the syndesmosis. Katznelson and coworkers used a distal tibiofibular arthrodesis to treat chronic syndesmosis ruptures.203 All five ruptures were the sequelae of injuries initially diagnosed as lateral ankle ligament sprains. All five patients obtained excellent results at the time of final follow-up. The report did not discuss return to athletic activity, nor was the time to follow-up noted.

Rehabilitation Treatment of patients with low-grade syndesmosis sprains is symptomatic, with bracing and a rehabilitation program as outlined previously. Rehabilitation for postoperative syndesmosis injuries is effectively delayed by 4 to 6 weeks.

Foot and Ankle 1945

Non–weight-bearing status is maintained for 6 to 8 weeks, followed by progression to full weight-bearing by 12 weeks. Ankle and subtalar flexibility, motor function, and coordination30 are emphasized throughout the protocol. The ankle is supported with an ankle brace during later rehabilitation and return to sports for 6 months postoperatively. In addition to the ankle brace, an elastic sock is available for mobilization of edema (see Fig. 25C1-19).

Author’s Preferred Method of Treatment I treat acute syndesmosis injury not associated with fracture with the RICE method and non–weight-bearing until the definitive diagnosis is established. Isolated grade I or II syndesmosis injuries are allowed to begin weight-bearing to tolerance after the acute pain and swelling remit. Treatment is symptomatic with an emphasis on recovery of range of motion, strength, and coordination. Patients frequently benefit from the support of a walking boot shortly after injury. They are later transitioned into a supportive ankle brace. I use the Edwards and DeLee classification system for grade III sprains.181 This system is based on the presence of radiographic diastasis with and without stress. A latent syndesmosis injury appears normal on an unstressed radiograph and abnormal or widened on external rotation stress mortise radiograph. A frank injury is seen as a widened syndesmosis on unstressed radiographs. Patients with latent injuries do not need surgery if the reduction of the fibula is anatomic on CT or MRI. Patients are not allowed to bear weight for at least 4 to 6 weeks. Sequential radiographs are used to monitor alignment. Patients are transitioned to a walking boot and are allowed to progressively start bearing weight after 6 weeks. Frank injuries require closed or open reduction and screw fixation. Rehabilitation is similar to that described for stable latent injuries. Screw fixation is removed 3 to 4 months postoperatively before resumption of full athletic activity is permitted.

Return-to-Play Criteria Recovery follows a logical sequence of events. Once the initial pain and swelling subside, coordination and strengthening activities are emphasized. Gradually, the patient is able to return to walking, running, and cutting programs. Patients are returned to sport once they master sport-specific drills. A semirigid pneumatic ankle brace is maintained during this time. Fritschy evaluated 10 world-class slalom skiers with syndesmosis injuries.180 The unexpected finding was that all skiers returned to their original level of competition, but the time to return ranged between 18 months and 12 years. Gerber and colleagues completed a prospective observational study of 96 West Point cadets with ankle sprains, including 16 syndesmosis sprains.3 All patients were treated with a functional rehabilitation program. At the time of the 6-week and 6-month follow-up examinations, grade I syndesmosis sprains were associated with worse outcomes

compared with all ankle sprains, including grade II and III syndesmosis sprains.

Ankle Dislocation without Fracture Dislocation of the ankle joint is typically associated with major or minor bony injuries. Dislocation without associated fracture is rare.

Relevant Anatomy The ankle joint ligamentous support is described in detail earlier. The stability of the ankle joint is such that ankle dislocation without associated malleolar fracture is uncommon. Wilson and coworkers reviewed the literature and found 14 cases of ankle dislocation without fracture.204 Most of these injuries were associated with falls or direct trauma. The authors further described two cases. The first was a posterior dislocation of the ankle and the second an upward dislocation of the ankle associated with a wide diastasis of the distal tibiofibular joint.

Clinical Evaluation History Dislocation of the ankle joint with or without fracture produces dramatic pain and deformity. The patient may report spontaneous reduction, or reduction on the field may be noted by the patient or a trainer. Reduction produces significant relief of pain. Information relevant to previous ankle and subtalar injury, the mechanism of injury, and current complaints represent the salient historical points.

Physical Examination Examination of the patient includes evaluation of the entire extremity. Inspection of the leg, ankle, and foot may reveal swelling, ecchymosis, blister formation, or gross deformity. A vascular and sensory assessment is performed, followed by a palpation of the entire leg, ankle, and foot.

Imaging Radiographs Radiographs of a dislocated ankle are typically dramatic (Fig. 25C1-39). Three standard views are reviewed, and a lack of talocrural continuity is diagnostic for an ankle dislocation. Radiographs taken after a formal reduction or after spontaneous reduction are less dramatic but nonetheless must be obtained and carefully scrutinized for malleolar fractures, talar fractures, and osteochondral fractures (Fig. 25C1-40). Subsequent radiographs are obtained to ensure anatomic reduction and to monitor heterotopic ossification.

Magnetic Resonance Imaging MRI is useful for delineation of ligamentous injury after ankle dislocation. The ligament remnants are occasionally imaged and may suggest continued nonoperative management. Osteochondral injury is also assessed.


with primary open reduction and syndesmotic screw placement.

Rehabilitation The rehabilitation phase begins as soon as the ankle is deemed stable. The program focuses on reducing swelling and re-establishing range of motion. After completing rehabilitation, the athlete is gradually returned to progressive activity. An ankle brace is used to provide additional support and biofeedback.

Author’s Preferred Method of Treatment Figure 25C1-39 Ankle dislocation without fracture.

Therapeutic Options This injury is usually identified on the field. Reduction brings about tremendous pain relief and reduces ongoing swelling and damage to nerves, vessels, and articular cartilage. Once the patient presents to the hospital, a complete examination is performed before reduction. General anesthesia is recommended, but early reduction with intravenous sedation may be possible.204 If anatomic reduction is not possible, open reduction is required. If at the time of reduction, the ankle remains unstable, internal or external fixation is required. A tibiofibular diastasis associated with a syndesmosis rupture must also be reduced and stabilized (see previous section). Olerud reported a single case of a posterior dislocation of the fibula and subluxated talus in association with a violent supination and external rotation mechanism of injury.201 This patient was successfully treated

A

After radiographic documentation is obtained, a closed reduction is performed with the patient under conscious sedation or general anesthesia. The stability of the reduction is ideally simultaneously determined. Immobilization and complete radiographic studies, including CT or MRI, are obtained after reduction. The length of immobilization is determined by postreduction stability. Ideally, a non–weight-bearing cast is used for 4 weeks. This is followed by application of a removable cast boot for an additional 4 to 6 weeks of weight-bearing to tolerance and initial rehabilitation. A semirigid pneumatic orthosis is used for up to 6 months after the injury. Emphasis is placed on reducing swelling and improving range of motion, strength, and proprioception.

Return-to-Play Criteria The patient must be prepared for an unpredictable return to competitive activity. Many pitfalls await the patient. The most significant is persistent stiffness. Return to play is allowed only after range of motion has been re-established and local tenderness and swelling have resolved.

B

Figure 25C1-40 A, Ankle dislocation with fracture at the tip of the lateral malleolus. B, Ankle dislocation with fracture at the medial tuberosity of the talus (different case).

Foot and Ankle 1947

c

d

b

a

e

Talus c

d b

a

ATFL

CFL

Calcaneus

A

CL

IOL

Figure 25C1-41 Anterolateral ligamentous structures of the subtalar joint—anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), cervical ligament (CL), and interosseous talocalcaneal ligament (IOL). (Redrawn from Meyer JM, Garcia J, Hoffmeyer P, Fritschy D: The subtalar sprain: A roentgenographic study. Clin Orthop 226:169-173, 1988.)

INJURY TO THE FOOT LIGAMENTS In the following section, subtalar sprain, subtalar dislocation, bifurcate sprain, and Lisfranc sprain are reviewed. First metatarsophalangeal joint sprain, also called turf toe, is reviewed in a separate section within this chapter (see Chapter 25H). The incidence of injury to the foot ligaments is certainly lower than that to the ankle ligaments. The cause of injury is reviewed in great detail in a separate section within this chapter (see Chapter 25J).

Subtalar Sprain Recently, more attention has been directed at the subtalar joint as a source of pathology. Subtalar joint injury varies from a mild subtalar sprain to a complete subtalar and talonavicular dislocation without fracture. Subtalar joint sprain is most commonly associated with a lateral ankle sprain. The injury less frequently presents as an isolated entity that produces persistent pain and instability after inversion injury to the foot and ankle.205

Relevant Anatomy and Biomechanics A review of hindfoot bony anatomy and function facilitates understanding of the ligamentous anatomy in this region. The talus articulates with the calcaneus through the subtalar joint, which is composed of anterior, middle, and posterior facets. The most important of these articulations is the posterior facet.206 The oblique empirical joint axis of the posterior facet converts rotatory movement from the leg to the foot. Internal rotation of the leg produces (by means of the oblique empirical axis) eversion of the calcaneus,

B

Figure 25C1-42 A, Ligaments of the sinus tarsi: a, lateral retinacular root; b, intermediate retinacular root; c, medial retinacular root; d, cervical ligament; e, interosseous ligament. B, Calcaneal attachments of the ligaments of the sinus tarsi. (Redrawn from Harper MC: Lateral ligamentous support of the subtalar joint. Foot Ankle 11:354-358, 1991.)

which, in turn, places the foot in a supple configuration (pronation). External rotation of the leg produces the opposite effect of calcaneal inversion and increased foot rigidity (supination). Failure of the hindfoot to move through this natural motion reduces the effectiveness of the foot as a mechanical shock absorber and as a rigid lever for propulsion. Subtalar motion is a complex three-plane motion that includes motion in the sagittal, frontal, and axial planes.207-209 The clinical range of motion as described by Sarrafian includes 25 to 30 degrees of inversion and 5 to 10 degrees of eversion.210 The determination of clinical range of motion is imperfect at best owing to the obliquity of the joint, its association with other joints, and the soft tissues surrounding the joint. Pearce and Buckley found a threefold overestimation of the clinical range of motion compared with the motion determined by CT.211 Stability of the subtalar joint is accomplished through bony configuration and ligamentous orientation. Bony stability is greatest with the calcaneus everted, a position that allows the greatest degree of posterior facet contact and congruity.210 Lateral subtalar joint stability is provided by a group of lateral ligamentous structures. Harper reviewed the anatomic literature and compiled data from 10 cadaveric dissections.110 Based on Harper’s work, the lateral ligaments of the subtalar joint are divided into three layers— superficial, intermediate, and deep (Figs. 25C1-41 and 25C1-42; Table 25C1-5). The inferior extensor retinaculum is composed of two layers—superficial and deep to the extensor tendons. Harper concluded that the superficial layer of the inferior extensor retinaculum remains a constant, substantial tissue, suitable for lateral ankle and subtalar joint reconstructions, as proposed by Gould and associates.109 Magnusson highlighted the importance of the talocalcaneal interosseous ligament, the ankle ligaments, and the


TABLE 25C1-5 Lateral Ligamentous Support of the Sinus Tarsi

Superficial layer Intermediate layer Deep layer

Lateral root of the inferior extensor retinaculum Lateral talocalcaneal ligament Calcaneofibular ligament Intermediate root of the inferior extensor retinaculum Cervical ligament Medial root of the inferior extensor retinaculum Interosseous talocalcaneal ligament

5 mm

From Harper MC: Lateral ligamentous support of the subtalar joint. Foot Ankle 11:354-358, 1991.

A medial and lateral malleoli for the restriction of extreme supination and pronation.212 Smith, after empirically determining the axis of the subtalar joint, demonstrated that the cervical ligament limits inversion and the interosseous ligament limits eversion of the calcaneus across the subtalar joint.213 In 1968, Laurin and colleagues completed anatomic studies that demonstrated the importance of the CFL in maintaining subtalar stability.23 This group sequentially divided the ATFL and the CFL (along with the lateral talocalcaneal ligament) before taking stress radiographs. Isolated division of the ATFL produced primarily talocrural instability, and isolated division of the CFL produced primarily talocalcaneal instability (lateral joint opening). The group further speculated that the mechanism of subtalar joint sprain (isolated CFL injury) is forced inversion of the foot below a dorsiflexed ankle. Chrisman and Snook also used a cadaveric model to demonstrate that subtalar instability occurs after section of both the CFL and part of the lateral talocalcaneal complex.91 Kjærsgaard-Andersen and coworkers, also using a cadaveric model, obtained measurements continuously through the ankle range of motion with a constant adduction force across the tibiotalocalcaneal joint complex.214 Isolated division of the CFL resulted in increased hindfoot adduction through the talocalcaneal joint, as opposed to the talocrural joint. This incremental difference was maximal at 5 degrees of ankle dorsiflexion. The clinical application, as suggested by the authors, is to place the ankle in slight dorsiflexion during stress testing of the ankle and subtalar joints. A second cadaveric study by Kjærsgaard-Andersen and associates revealed that the CFL provides significant rotatory stability to the talocalcaneal joint.215 External rotation after isolated division of the CFL increased up to 5.4 degrees at the tibiotalocalcaneal complex and up to 2.9 degrees at the talocalcaneal complex. The authors concluded that the CFL is the primary restraint to hindfoot external rotation. Heilman and colleagues used 10 fresh cadaveric ankles to demonstrate that the CFL tightens with supination and dorsiflexion.216 Selective division of the CFL produced 5 degrees of lateral opening across the posterior facet of the subtalar joint. Division of the lateral subtalar capsule added no further instability to

B

C

Figure 25C1-43 Stability of the subtalar joint after serial ligament sectioning. A, Brodén’s view of the subtalar joint, intact ligaments. B, Brodén’s view of the subtalar joint, after sectioning of the calcaneofibular ligament (CFL). C, Brodén’s view of the subtalar joint, after sectioning of the CFL, capsule, and interosseous ligament. (Redrawn from Heilmen AE, Braly G, Bishop JO, et al: An anatomic study of subtalar instability. Foot Ankle 10:224-228, 1990.)

the joint. Finally, division of the interosseous ligament completely destabilized the joint, leading to dislocation (Fig. 25C1-43). A third experimental study by Kjærsgaard-Andersen and coworkers demonstrated that isolated division of the cervi cal or interosseous ligament resulted in relatively minor increases in three-plane joint motion.208 These authors concluded that the resulting instability was significant despite the small angular changes. Furthermore, injury to either ligament may be related to the sinus tarsi syndrome or talocalcaneal instability. Knudson and associates used a cadaveric model to specifically study the effect of interosseous ligament division.209 Measurements taken before and after interosseous ligament sectioning suggested that the interosseous ligament provides significant subtalar joint support, particularly in supination. The exact cause of subtalar instability remains unsolved. Several factors, including local bony and ligamentous anatomy, contribute to this entity. Treating this condition requires an understanding of the anatomy and biomechanics of this region.

Clinical Evaluation As has been stated previously, sprains are frequently evaluated by graded ligament injury, as suggested by the American Medical Association35 and by O’Donoghue.36 Acute injuries are graded based on stretch (grade I), partial tear (grade II), or complete rupture (grade III) of the subtalar capsule or supporting ligaments, including the CFL, the interosseus ligament, and the cervical ligament. A grade III tear is suggested by a clinical history of severe deformity or swelling, examination consistent with gross subtalar instability, or MRI demonstrating ligamentous disruption. The clinical evaluation provides additional information with regard to associated ligamentous injuries, especially of the lateral ankle.

Foot and Ankle 1949

History History alone is usually insufficient to distinguish between subtalar and lateral ankle instability. Information relevant to previous ankle and subtalar injury, the mechanism of injury, the ability of the patient to continue to play or walk, and current complaints are important to obtain. Severe subtalar sprains are associated with a history of inversion injury with a characteristic pop; acute pain, swelling, or deformity; and the inability to continue activity. After the acute event, patients may report recurrent instability with walking, running, and sports. They frequently report difficulty on uneven surfaces. Lateral pain in the region of the sinus tarsi may be present.

135° 45°

45°

A

B

Figure 25C1-44 Clinical examination of the subtalar joint is facilitated by placement of the empirical subtalar joint axis horizontal with the ground. A, Place the foot in 45 degrees of equinus. B, Examine the patient prone with the knee flexed 135 degrees. (Redrawn from Inman VT: The Joints of the Ankle. Baltimore, Williams & Wilkins, 1976, p 108.)

Physical Examination The differential diagnosis of an inversion foot or ankle injury includes ATFL sprain, CFL sprain, syndesmosis sprain, deltoid sprain, subtalar sprain, subtalar coalition, bifurcate ligament sprain, peroneal tendon instability, peroneal tendon tear, lateral malleolus fracture, talar dome osteochondral injury, anterior calcaneus process fracture, and fracture of the base of the fifth metatarsal. Chronic insufficiency of the lateral hindfoot associated with subtalar instability isolated or combined with lateral ankle ligament instability has been shown to occur in up to two thirds of patients.34 Examination of the patient includes evaluation of the entire extremity. Inspection of the leg, ankle, and foot may reveal swelling, ecchymosis, blister formation, or gross deformity. A vascular and sensory assessment is documented, followed by a palpation of the entire leg, ankle, and foot. Tenderness at the sinus tarsi, the ATFL, and the CFL is particularly important to note. Clinical examination of the subtalar joint is difficult to complete owing to the complex nature of subtalar motion and its association with leg, ankle, and foot motion.217 Evaluation of motion is determined by gently grasping the leg while the ankle is held at a right angle or in a neutral dorsiflexion position. With the widest part of the talus engaged into the ankle mortise, adduction of the heel is more likely to represent motion through the talocalcaneal joint rather than the talocrural joint. From a neutral position (heel vertical), maximal passive inversion and eversion are measured. An alternative method is placement of the empirical subtalar joint axis horizontal with the ground by allowing the foot to fall into 45 degrees of equinus, or by examining the patient prone with the knee flexed 135 degrees (Fig. 25C1-44).10 Gross clinical instability is consistent with a grade III sprain.

Imaging Radiographs Radiographic demonstration of the subtalar joint is difficult.218 Brodén described an oblique view of the foot designed to produce tangential images of the posterior facet of the subtalar joint (Fig. 25C1-45).219 The view is obtained with the foot in 45 degrees of internal rotation and the beam centered on the sinus tarsi and angled

posteriorly (by 10, 20, 30, or 40 degrees). The images are carefully inspected with attention to small fractures, nonconcentric joint alignment, loose body, and arthrosis.

Stress Radiographs Several methods for stress radiography of the subtalar joint have been described. Stress radiography of the ankle joint to quantify the extent of concomitant ankle instability is recommended and described previously. The ankle talar tilt test is dependent on the contralateral ankle for control measurements. Varus tilt of the ankle, to a limited degree, is probably normal. Increased inversion of the calcaneus may represent talocrural (ankle) or talocalcaneal (subtalar) instability.34 Radiographic data suggest that 4 degrees of varus tilt occurs in 10% to 15% of noninjured ankles.47 Varus stress radiographs of both ankles in 90 injured and 90 normal ankles revealed that 6 degrees of increased tilt represents the transition from “normal to abnormal” tilt.48 The subtalar varus tilt test is performed with the ankle in a neutral position.214 A Brodén view of the posterior facet

BRODÉN I PROJECTION FOOT POSITION limb internally rotated 45° ankle dorsiflexed 90°

CENTRAL RAY centered 2-3 cm distal and anterior to lateral malleolus four pictures, 10°, 20°, 30°, and 40° off the perpendicular Figure 25C1-45 Brodén’s oblique view of the foot designed to produce tangential images of the posterior facet of the subtalar joint. The view is obtained with the foot in 45 degrees of internal rotation and the beam centered on the sinus tarsi and angled posteriorly (10, 20, 30, or 40 degrees).


of the subtalar joint is obtained as a varus stress is applied to the subtalar joint. Angular divergence or lateral opening at the posterior facet is compared with the contralateral foot for quantification of instability. A relatively new method is the forced manual dorsiflexion-supination stress lateral radiograph described by Ishii and colleagues.220 The true lateral ankle radiograph is used to establish the position of the lateral talar process relative to the posterior facet of the calcaneus. Clinical and cadaveric experiments indicate that this method is useful for detecting subtalar instability. Stress radiographs can be performed in the office with a mini C-arm or in the operating room. A 40-degree Brodén view is obtained with inversion stress applied to both the calcaneus and the fifth metatarsal head laterally while the medial distal tibia is stabilized. Heilman and associates described a 5-mm separation between the talus and the calcaneus as indicative of subtalar instability.221 The reliability of the stress Brodén view has been challenged by other authors. Harper completed a review of ankle and subtalar stress radiographs in 14 injured extremities, the contralateral noninjured extremities, and 18 additional asymptomatic extremities.222 Lateral opening of the subtalar joint, as seen on the Brodén stress view, did not significantly differ between the injured and the uninjured contralateral extremity. Furthermore, results from the asymptomatic extremities revealed subtalar articular divergence between 0 and 20 degrees, with an average of 9 degrees. Similar findings using fluoroscopic methods have also been reported.223

Arthrography Subtalar arthrography for evaluation of acute injury to the CFL or the interosseous ligament remains a useful technique. Meyer and coworkers performed ankle stress radiographs and subtalar joint arthrography in 40 patients with acute inversion sprains.155 They classified the injuries based on the extent of lateral ankle ligament and subtalar ligament injury. Thirty-two (80%) of the patients sustained injury to both the lateral ankle and the subtalar joint. Six patients with negative stress ankle radiographs had positive subtalar arthrograms. Sugimoto and associates recommend using an image intensifier to obtain anteroposterior, lateral, and 45-degree oblique views of the subtalar joint.224 Extravasation of contrast into the peroneal sheath or ankle joint suggests CFL rupture; leakage into the sinus tarsi suggests interosseous ligament or anterior capsule of the posterior facet joint rupture. The authors also noted that this method is not limited by the lack of availability and the cost associated with MRI.

Computed Tomography The inability of the stress Brodén view to provide useful screening for subtalar instability was confirmed by van Hellemondt and colleagues.225 Using helical CT, the authors demonstrated no significant difference in subtalar tilt between a group of patients with suspected subtalar instability and the contralateral asymptomatic extremities. The authors suspect that translation produces the tilt seen on routine stress radiographs, as opposed to true divergence of the talus and calcaneus. It is interesting to note

that CT did isolate four cases of fibrous middle facet coalition and a large calcaneal cyst. Finely cut CT is also useful in the evaluation of high-grade sprains to rule out associated fractures.

Magnetic Resonance Imaging MRI is useful for the diagnosis of acute and chronic ankle and subtalar ligamentous injury28 and their sequelae (see Fig. 25C1-9). With proper imaging, MRI can identify injuries to the cervical and interosseus ligaments. High sensitivity mandates that images be carefully correlated with clinical findings. MRI is also useful for identification of tarsal coalition.

Therapeutic Options All acute injuries are treated with the RICE method, as detailed earlier. Patients with high-grade injuries are immobilized and protected from bearing weight until the acute symptoms resolve.

Grade I and Grade II Subtalar Sprains Low-grade sprains are treated with early mobilization. Patients are allowed to bear weight to tolerance, and a rehabilitation program is instituted. Treatment is symptomatic, with an emphasis on recovery of foot and ankle range of motion, strength, and proprioception. A removable fracture boot is used during the initial recovery period, followed by use of a semirigid pneumatic ankle brace.

Grade III Subtalar Sprains High-grade injuries, as determined by clinical findings, are treated with 3 weeks of immobilization in a short leg cast. Patients may bear weight as tolerated. Once clinical stability is achieved, a comprehensive foot and ankle rehabilitation program is instituted. A removable fracture boot is used during the second 3-week period, followed by the use of a semirigid pneumatic ankle brace.

Chronic Subtalar Instability The Broström anatomic ligament reconstruction with the Gould modification reliably addresses lateral ankle and subtalar instability. The lateral capsular imbrication or advancement must extend to include the CFL as well as the ATFL. Imbrication of the extensor retinaculum to the lateral fibula effectively limits excessive subtalar motion. Historical procedures using tendon graft or transfer to reconstruct the lateral ligaments also stabilize the subtalar joint. Elmslie’s original technique using a piece of fascia lata to reconstruct the lateral ankle also constrained the subtalar joint. Chrisman and Snook’s technique split the peroneal brevis and rerouted it to stabilize the ankle and subtalar joints. This nonanatomic reconstruction can overly constrain the subtalar joint. Newer techniques attempt to reconstruct the joints in a more anatomic manner. Kato demonstrated that conservative management designed to prevent anterior translation of the calcaneus relative to the talus was effective for most patients.226

Foot and Ankle 1951

B 3 2 A

1

Figure 25C1-46 Interosseous ligament reconstruction as described by Schon has the advantage of an anatomic reconstruction. (Redrawn from Schon LC, Clanton TO, Baxter DE: Reconstruction of subtalar instability: A review. Foot Ankle 11:324, 1991.)

Fourteen patients underwent reconstruction of the interosseus ligament with an Achilles tendon graft augmented by cervical and lateral ligament reconstruction. Because the reconstruction was performed near the center of rotation, subtalar motion was not limited (the publication did not provide data to substantiate this finding). All patients reported excellent outcomes. Schon and coworkers reviewed several tendon transfers used for lateral ankle stabilization that also have utility for subtalar stabilization.227 Stabilization with a tendon transfer is suggested in cases of severe injury, generalized ligamentous laxity, and previous failed reconstruction. Interosseous ligament reconstruction, as described by Schon, has the advantage of an anatomic reconstruction (Fig. 25C1-46). The anatomic configuration ensures preservation of ankle and subtalar motion. The authors recommend its use for mild subtalar instability.

Rehabilitation With nonoperative treatment, tissue injury initiates a predictable and sequential series of events known as the healing response. This response is typically divided into three phases with arbitrary and overlapping time lines.120 The initial phase is the inflammatory phase and includes the first through third days after injury. The second phase is a proliferative phase of tissue repair that extends from day 3 to day 20. The final phase is a remodeling phase that proceeds after day 9. To a certain degree, rehabilitation follows the phases of the healing response in an effort to reduce the undesirable effects of inflammation (e.g., pain, swelling, loss of function) while simultaneously promoting tissue repair and functional recovery. The emphasis of rehabilitation is placed on ankle, subtalar, midfoot, and forefoot flexibility, motor function, and coordination.30 The hindfoot is supported by a functional ankle brace or various taping methods. An elastic sock is available for additional mobilization of edema (see Fig. 25C1-19).

The pain and inflammation associated with the first few days following subtalar joint sprain are addressed with rest, cold therapy, and whirlpool. A trial of electrical stimulation may be considered for nonbony injuries. Foot and ankle passive and active range of motion are re-established. Isometrics may be initiated as pain allows. Once the acute pain subsides, flexibility is addressed in all planes. An inclined board facilitates stretching the gastrocnemius-soleus complex (see Fig. 25C1-20). Strengthening is initiated with towel scrunches (see Fig. 25C1-21), toe pick-up activities, manual resistive inversion and eversion, elastic bands (see Fig. 25C1-22), seated toe and ankle dorsiflexion with progression to standing, and seated supination-pronation with progression to standing. Closed chain activities are gradually introduced, including one-leg balance, sports-specific activities on a trampoline, and use of the BAPS (see Fig. 25C1-23). Aerobic fitness is maintained with cross-training activities such as water running (see Fig. 25C1-24) and cycling. Heat therapy, such as the application of warm packs, is a useful modality before the therapy session. It reduces pain and spasms and thus facilitates increased range of motion. Cold therapy, compression, and elevation are used after each therapy session to reduce inflammation. Patients are allowed to progress to walking and running activities within the limits of a pain-free schedule. Once running activity is mastered, a monitored plyometric program is introduced with progression of difficulty. Schedules are carefully controlled to avoid reinjury.

Associated Injury Sinus Tarsi Syndrome O’Connor described a sinus tarsi syndrome as persistent pain at the sinus tarsi that follows a lateral ankle sprain.228 Others have noted the syndrome to follow as a sequela of subtalar instability.208 Taillard and associates noted that, in addition to pain over the sinus tarsi, patients with sinus tarsi syndrome complain of lateral ankle instability (Table 25C1-6).229 The cause of the condition is poorly understood and few diagnostic criteria exist. O’Connor speculated that the condition was related to fat pad scarring.228 The diagnosis was made in 45 patients, 14 of whom were treated with sinus tarsi débridement, a procedure that included resection of the fat pad and the superficial ligaments at the floor of the sinus tarsi. Complete relief was noted in 9 patients and partial relief in the remaining 5. Brown performed the O’Connor operation on 11 patients with sinus tarsi syndrome.230 Ten patients reported significant relief. A single patient with early signs of talar osteoarthritis did not improve. Meyer and Lagier presented four cases of sinus tarsi syndrome, all successfully treated by curettage of the sinus tarsi contents.231 Histologic findings from the small series indicated fibrous scar formation consistent with a traumatic cause. Two of the patients were treated with simultaneous subtalar arthrodesis, and one was treated with repair of a ruptured CFL. Parisien and Vangsness described the use of subtalar joint arthroscopy for evaluation of the posterior facet and its anterior recess.232 Parisien used this technique to rule


TABLE 25C1-6 Clinical Signs of Sinus Tarsi Syndrome History of foot or ankle inversion sprain Subjective instability Tenderness Ankle stability Anesthetic injection to the sinus tarsi Radiographic findings Arthrography (subtalar) Magnetic resonance imaging

Laboratory testing (rule out systemic inflammatory process)

Yes Yes Localized to the sinus tarsi Yes/no Temporary symptomatic improvement Normal Loss of sinus tarsi filling Rupture of interosseous ligament or cervical ligament; bone edema, soft tissue swelling, or fibrosis at sinus tarsi

Data from references 155, 228, and 229.

out intra-articular disease, to perform biopsy of synovium, and to release periarticular adhesions in three patients with post-traumatic hindfoot pain.233 A diagnostic approach to chronic sinus tarsi pain includes routine and stress radiographs to rule out ankle and subtalar instability as well as MRI to rule out contiguous arthrosis and ganglion formation. Local injection of anesthetic and corticosteroid is most important for diagnosis and initial empirical treatment. Ankle bracing and foot and ankle rehabilitation are used as adjunctive treatments. Occasionally, sinus tarsi exploration and débridement are performed either by open method or arthroscopically. When indicated, open débridement begins with an incision over the sinus tarsi. Care is taken to avoid the lateral branch of the superficial peroneal nerve. The inferior extensor retinaculum is reflected distally along with the extensor digitorum brevis muscle. The capsule of the subtalar joint is incised. The joint is inspected for chondral injury and osteophytes, which are addressed as needed. Fibrofatty tissue is resected from the sinus tarsi, but the ligaments are kept intact. The wound is closed in a layered fashion with attention to reattachment of the extensor digitorum brevis. Patients are placed in a splint postoperatively. After 10 days, the patient is placed into a weight-bearing short-leg cast for 4 more weeks.

Author’s Preferred Method of Treatment Low-grade subtalar sprains are treated with a semirigid pneumatic orthosis, weight-bearing to tolerance, and early rehabilitation of the foot. Most of these injuries are associated with a lateral ankle sprain, and treatment is dictated by the ankle injury. High-grade injuries, as suggested by a clinical history of severe deformity or swelling, examination consistent with gross subtalar instability, or MRI demonstrating ligamentous disruption, are placed in non–weight-bearing short leg casts for 3 weeks. This is followed by application of a removable cast boot for an additional 3 weeks of bearing weight to tolerance. A comprehensive rehabilitation program follows, with an emphasis placed on reducing swelling and improving range of motion, strength, and proprioception.

Return-to-Play Criteria Recovery follows a logical sequence of events. Once the initial pain and swelling subside, coordination and strengthening activities are emphasized. Gradually, the patient is able to return to walking, running, and cutting programs. A semirigid pneumatic brace (see Fig. 25C1-10) or taping accelerates the schedule. Patients are returned to sport once they have mastered sport-specific drills.

Subtalar Dislocation Subtalar joint dislocation varies from isolated subtalar and talonavicular dislocation to dislocation associated with talar, calcaneal, or navicular fractures. The injury is unusual during athletic participation; it most commonly is associated with high-energy mechanisms. Grantham reported five case of medial subtalar dislocation, all with an inversion mechanism of injury.234 Four of these patients sustained the injury while playing basketball. Dendrinos and coworkers reported a single case of subtalar dislocation without fracture in a professional basketball player.235 DeLee and Curtis identified 17 subtalar dislocations in a 7-year period.236 The direction of the dislocation was anterior, lateral, and medial, for 1, 4, and 12 patients, respectively. Four of the medial dislocations were associated with an inversion mechanism of injury; each patient attained full subtalar range of motion and was asymptomatic at the last follow-up. Avascular necrosis did not occur. Christiensen and associates noted arthrosis in each of 17 patients with a fracture-dislocation of the subtalar joint and 6 of 13 patients with isolated dislocation of the subtalar joint.237

Relevant Anatomy A review of hindfoot bony and ligamentous anatomy is presented in the preceding section (see “Subtalar Sprain”). The subtalar joint is stable in an everted position. This suggests that lateral dislocations are more likely to be associated with higher degrees of trauma, fractures, and less favorable outcomes.217,237,238

Clinical Evaluation History Patients with subtalar joint dislocation present with a history of acute and severe pain associated with obvious hindfoot deformity.

Physical Examination After trauma protocols are followed, the extremity is carefully examined (Fig. 25C1-47). Open injuries are documented along with the neurologic and vascular status of the extremity.

Imaging Radiographs Routine radiographs of the foot and ankle in orthogonal views confirm the preliminary diagnosis. Repeat

Foot and Ankle 1953

Author’s Preferred Method of Treatment

Figure 25C1-47 Subtalar dislocation.

Subtalar dislocations, both related and unrelated to athletic activity, warrant significant attention at the outset. Historical information to determine the mechanism of injury is paramount. Trauma protocols are followed as indicated. After radiographic documentation is obtained, a closed reduction is performed with the patient under conscious sedation or general anesthesia. The stability of the reduction is assessed at the time of reduction. Complete radiographic studies, including CT, are obtained after reduction. The length of immobilization is determined by postreduction stability. A stable reduction is immobilized initially in a non–weight-bearing cast for 2 weeks. This is followed by application of another short leg cast or removable fracture boot for an additional 4 to 6 weeks. Patients are encouraged to bear weight as tolerated. Initial rehabilitation emphasizes swelling reduction and improved range of motion, strength, and proprioception.

r adiographs with anteroposterior, oblique, Brodén,219 and lateral projections, as well as CT, are required before definitive and complete diagnosis is determined.

Therapeutic Options Subtalar dislocation without fracture is treated expediently with closed reduction. Reduction is required for decompression of neurovascular structures and should not be delayed without appropriate reason. General anesthesia is probably more predictable and is less likely to produce associated injury to the foot. The knee is flexed in an effort to relax the gastrocnemius muscle.217 Relocation is performed by accentuation and then reversal of the deformity along with traction applied through the foot. As has been noted earlier, repeat and complete radiographs and CT are required for verification of subtalar joint reduction and assessment of associated fractures. After reduction of isolated subtalar joint dislocations is performed, the joint is usually stable. With a stable joint, immobilization for 4 to 8 weeks is indicated. DeLee and Curtis suggest 3 weeks of immobilization, immediate toe range of motion, and early subtalar range of motion. Recurrent dislocation did not occur in any of the 17 subtalar dislocations in the series.236 Dendrinos and colleagues reported a single case of subtalar dislocation without fracture in a professional basketball player.235 The patient was treated with closed reduction. After 5 years of continued professional play, the same foot suffered an almost identical subtalar dislocation. The recurrence was attributed to coincidence.

Rehabilitation After a period of immobilization, a comprehensive foot and ankle rehabilitation program (as described earlier in the section, “Subtalar Sprain”) is instituted for maximal recovery of hindfoot function. Continued subtalar support is provided by a semirigid pneumatic orthosis.

Return-to-Play Criteria After completing short-term rehabilitation, the athlete is gradually returned to progressive activity. An ankle brace is used to provide additional support and biofeedback. Return to play is allowed only after local tenderness and swelling have resolved.

Bifurcate Sprain Injuries to the bifurcate ligament typically result from forceful inversion and plantar flexion of the foot. This results in either bifurcate ligament sprain or an avulsion fracture of the anterior process of the calcaneus. Broström noted clinical evidence of bifurcate ligament injury in 18.6% of patients with acute ankle sprains and 3.7% of patients with confirmed lateral ankle ligament ruptures.40 Backmann and Johnson considered bifurcate ligament rupture to be a common injury.239 Søndergaard reported a 24% incidence of bifurcate or talonavicular sprain among patients presenting with an acute ankle or foot inversion sprain.240 An additional 9% of patients were noted to have a combination of bifurcate and talonavicular ligament and lateral talocrural ligament injuries.

Relevant Anatomy The bifurcate ligament is a short, stout ligament that originates from the anterior process of the calcaneus, divides into two arms, and inserts onto the navicular and cuboid (Fig. 25C1-48; see Fig. 25C1-1).206 The origin is contiguous with the superior aspect of the calcaneal facet of the calcaneocuboid joint. The origin of the ligament is routinely visualized during the lateral approach to the sinus tarsi for triple arthrodesis. The ligament is distal and anterior to the inferior tip of the fibula, and superior and proximal to the base of the fifth metatarsal.


Physical Examination Anterior inferior tibiofibular ligament Anterior talofibular ligament

Bifurcate ligament Figure 25C1-48 Schematic drawing demonstrating the bifurcate ligament.

Physical examination confirms diffuse lateral hindfoot and midfoot swelling with associated ecchymosis. Tenderness tends to localize to the course of the bifurcate ligament, an area that is distinct from the course of the ATFL. The ankle and midfoot remain stable. Pain is easily reproduced with forced inversion of the plantar flexed foot. Broström noted that the differentiation between lateral ankle ligament injury and bifurcate ligament injury was best achieved by eliciting indirect tenderness.40 He suggested manipulation of the heel to produce lateral ankle pain and stabilization of the heel with simultaneous forced forefoot motion to produce bifurcate pain.

Imaging Radiographs

Clinical Evaluation Sprains can be classified according to the perspective of graded ligament injury, as suggested by the American Medical Association35 and by O’Donoghue.36 Acute injuries are graded based on stretch (grade I), partial tear (grade II), or complete rupture (grade III) of the bifurcate ligament. Additional information with regard to associated ligamentous injuries, especially at the lateral ankle, is noted.

History A bifurcate ligament sprain or an avulsion fracture of the anterior process of the calcaneus must be considered when a patient presents with a suspected ankle sprain. The plantar flexion inversion mechanism associated with injury to the ATFL is the same mechanism as that responsible for the bifurcate ligament sprain. The patient often recalls a pop or snap followed by swelling and ecchymosis. The patient’s ability to continue play after the acute injury is variable.

A

Routine radiographs, including anteroposterior, lateral, and oblique views of the foot and ankle, are obtained. A pure bifurcate ligament sprain is not associated with bony injury; however, an avulsion fracture of the anterior process of the calcaneus is confirmed with the lateral radiograph (Fig. 25C1-49). The size of the fragment may vary from a fine calcified body to a significant portion of the anterior process and the contiguous calcaneocuboid facet.

Computed Tomography Computed tomography is the preferred method for assessing avulsion fractures, but it is not particularly useful for evaluating an isolated bifurcate ligament sprain.

Magnetic Resonance Imaging Isolated bifurcate ligament injury is not routinely imaged by MRI. A sprain is confirmed by edema within or adjacent to the ligament as well as by increased marrow signal at the anterior process of the calcaneus.

B

Figure 25C1-49 A, Avulsion fracture of the anterior process of the calcaneus. The triangular fragment is either intra-articular or extra-articular and varies in size. B, Magnetic resonance image demonstrating increased signal within the bifurcate ligament consistent with sprain.

Foot and Ankle 1955

Therapeutic Options Acute bifurcate sprains are treated with the RICE method followed by gentle range of motion and protected weightbearing. The hindfoot is supported by the use of a variety of methods, including a splint, a walking cast, a removable boot, a functional ankle brace, or various taping methods. Chronic bifurcate sprains are treated with a range of motion program and reduced activity levels. Intralesional and intra-articular (calcaneocuboid) steroids are placed, under fluoroscopic guidance, with the patient either in the sports medicine practitioner’s office or in a radiology suite. Operative treatment is rare for bifurcate ligament injuries. Large, displaced, intra-articular anterior process fractures are treated with open reduction and internal fixation through a sinus tarsi approach. The extensor digitorum brevis muscle is elevated and the fragment reduced and provisionally pinned. Fixation is accomplished with a small or mini-fragment screw. For symptomatic nonunions, the same approach is used, with the addition of local bone graft. Unfortunately, most bony nonunions are not amenable to open reduction with internal fixation owing to their small size. Excision is a reasonable option, but it does not yield the immediate relief that both patient and surgeon expect. Therefore, excision of a symptomatic nonunion is considered only after 6 to 12 months of rehabilitation.

Rehabilitation Emphasis throughout the protocol is placed on rehabilitation of the foot and ankle and on subtalar flexibility, motor function, and coordination.30 The foot is supported by a functional ankle brace or various taping methods. An elastic sock is available for additional mobilization of edema (see Fig. 25C1-19). In the acute phase, the athlete’s pain and inflammation are addressed with rest, cold therapy, and whirlpool. A trial of electrical stimulation may be considered for nonbony injuries. Foot and ankle passive and active range of motion are re-established. Isometrics may be initiated as pain allows. Once the acute pain subsides, flexibility is addressed in all planes. An inclined board is a useful adjunct to gastrocnemius-soleus and Achilles stretching (see Fig. 25C1-20). Strengthening is initiated with towel scrunches (see Fig. 25C1-21), toe pick-up activities, manual resistive inversion and eversion, elastic bands (see Fig. 25C1-22), seated toe and ankle dorsiflexion with progression to standing, and seated supination-pronation with progression to standing. Closed chain activities are gradually introduced (see Fig. 25C1-23), including one-leg balance, sport-specific activities on a trampoline, and use of the BAPS. Aerobic fitness is maintained with cross-training activities such as water running (see Fig. 25C1-24) and cycling. Heat therapy, such as the application of warm packs, is a useful modality before the therapy session. It reduces pain and spasms and thus facilitates increased range of motion. Cold therapy, compression, and elevation are used after each therapy session to reduce inflammation. As patients prepare to return to sports, walking and running activities are progressed within the limits of a pain-free

schedule. Once running activity is mastered, a monitored, plyometric and cutting program is introduced. Schedules are carefully controlled to avoid reinjury. Søndergaard and coworkers reviewed the results of treatment for 162 midtarsal sprains (bifurcate ligament or talonavicular ligament, or both) and 161 talocrural sprains and concluded that the two injuries produce similar outcomes.240 Both groups returned to preinjury athletic activity at an average of 21 days.

Author’s Preferred Method Bifurcate ligament sprains are initially treated with a short removable fracture boot. Patients are allowed to bear weight as tolerated. Early rehabilitation of the foot and ankle follows. Occasionally, I place a less athletic patient in a short leg walking cast in an effort to improve pain control and allow increased levels of independent activity. Injuries associated with small anterior process fractures are treated as severe sprains. Delayed union or nonunion is unlikely and is even less likely to remain symptomatic. Large, intra-articular fractures are treated with a short leg cast and weight-bearing to tolerance. Displaced fractures are treated surgically with internal fixation. Chronic pain related to nonunion or malunion is treated conservatively for a minimum of 6 to 12 months. If a small fragment remains symptomatic, it is excised. Attempted union of larger fragments requires open treatment with internal fixation and bone grafting.

Return-to-Play Criteria Recovery follows a logical sequence of events. Once the initial pain and swelling subside, coordination and strengthening activities are emphasized. Gradually, the patient is able to return to walking, running, and cutting programs. A protective brace or taping accelerates the schedule. Patients are returned to sport once they master sport-specific drills.

Lisfranc Sprain Much of the literature discussing injury to the Lisfranc joint complex is in association with severe high-energy fracture-dislocations. The poor outcome among these patients is well known by orthopaedic surgeons. Subtle Lisfranc injuries can occur during athletic activity and can be challenging to diagnose. Curtis and associates described 19 such injuries associated with athletic activity.241 The most common activity was basketball, followed by running. Meyer noted 24 midfoot sprains among university football players between 1987 and 1991.242 The incidence was calculated at 4% of football players per year. Shapiro and colleagues identified nine injuries to the Lisfranc ligament associated with collegiate gymnastics (four), collegiate football (three), collegiate pole vault (one), and recreational tennis (one).243


Relevant Anatomy The midfoot is a stable configuration of five bones (navicular, cuboid, medial cuneiform, middle cuneiform, and lateral cuneiform) joined together in a complex system of multifaceted, relatively immobile joints (Fig. 25C1-50). The tarsometatarsal articulation between the midfoot and the metatarsals is known as the Lisfranc joint. The second metatarsal cuneiform joint is the most stable of the entire complex. Two factors contributing to the second metatarsal cuneiform joint stability include a recessed bony configuration (keystone) and a strong plantar ligament connecting the base of the second metatarsal to the medial cuneiform (Lisfranc’s ligament). A significant amount of force is required to produce fracture-dislocation. The mechanism of injury is either direct crushing or indirect loading of the fixed forefoot.244 Wiley reviewed 20 cases of Lisfranc injury and identified direct and indirect mechanisms of injury.245 The indirect mechanisms of injury were acute abduction of the forefoot (most common) and forced plantar flexion of the forefoot. Forced dorsiflexion of the forefoot may occur as the result of landing from a jump, continued forward motion on a planted forefoot, a fall from a height, or a brake pedal injury. Curtis and coworkers described the mechanism of injury to include plantar flexion and rotation with or without abduction of the forefoot.241 Meyer and associates determined a mechanism of injury from 16 football players with midfoot sprains.242 Eight players reported an indirect twisting mechanism; six players reported contact to the heel of a plantar flexed forefoot; two players reported a crush injury to the dorsum of the foot. Shapiro and colleagues identified a consistent mechanism in nine athletes who sustained a Lisfranc injury.243 Each athlete placed full weight onto the first ray with the foot in an externally rotated and pronated position. The resulting injury includes tearing of a relatively weak dorsal capsular structure, tearing of the strong plantar ligament between the medial cuneiform and the base of the second metatarsal, and to a varying degree, fracture of chondral and bony structures on both sides of the joint. Subsequent to the displacement that occurs at the time of

injury, the joint complex either returns to a nondisplaced state or remains displaced owing to the interposition of the capsule and osteochondral fragments.

Clinical Evaluation Sprains can be classified according to ligament injury, as suggested by the American Medical Association35 and by O’Donoghue.36 Acute injuries are graded based on stretch (grade I), partial tear (grade II), or complete rupture (grade III) of the Lisfranc capsule and supporting ligaments, including the Lisfranc ligament. Stable injuries, including grade I and II sprains, are not associated with displacement or deformity. Unstable injuries, grade III sprains, vary between nondisplaced injuries and frank fracture-dislocations. Nunley and Vertullo have proposed a classification system for athletic midfoot injuries. Stage I represents a ligament sprain with no diastasis or loss of arch height on a weight-bearing radiograph. Stage II injuries have diastasis of 1 to 5 mm between the first and second metatarsals without arch height loss. Stage III injuries are associated with diastasis and loss of arch height as defined by a decrease or reversal in the distance between the plantar medial cuneiform base and the fifth metatarsal base on a weight-bearing lateral foot radiograph.246

History Typically, the athlete can recall a specific mechanism of injury. The injury is associated with a pop or snap followed by pain, swelling, and ecchymosis localized to the midfoot. Some patients are able to bear weight with pain, but are unable to run, jump, or continue to play after the acute injury. After a severe injury, weight-bearing is very painful and unlikely. Pain localized to the midfoot should raise suspicion for a subtle Lisfranc injury.

Physical Examination Physical examination confirms diffuse midfoot swelling with associated ecchymosis. Sensory and vascular examination with particular attention to the deep peroneal nerve and the dorsalis pedis artery is documented. Stability is tested in the sagittal plane (dorsiflexion and plantar flexion) by securing the midfoot with one hand and grasping the first metatarsal with the other hand. A dorsiflexion force is applied; when compared with the opposite midfoot, pain and increased mobility are abnormal findings. Frontal plane stability is demonstrated by applying an adduction or abduction force across the Lisfranc joint. Myerson and colleagues described a passive pronationabduction test to evaluate the stability of the joint complex (Fig. 25C1-51).247-249 This maneuver elicits pain and reproduces the patient’s symptoms.

Imaging Figure 25C1-50 The Lisfranc articulation with its ligamentous attachments. Note the recessed second tarsometatarsal joint and the Lisfranc ligament in place of the first-second intermetatarsal ligament.

Radiographs The bilateral standing anteroposterior radiograph provides critical information used to help classify the injury. Additionally, weight-bearing lateral and oblique views of

Foot and Ankle 1957

with a poor outcome.250 The authors also studied 20 normal volunteers. With the use of the standing lateral radiograph, the distance between the plantar aspect of the medial cuneiform was related to the plantar aspect of the fifth metatarsal base. In all normal subjects, the medial cuneiform was higher than the fifth metatarsal base.

Stress Radiographs

Figure 25C1-51 Frontal plane stability at the Lisfranc joint is demonstrated by application of a passive pronation-abduction. (Redrawn from Komenda GA, Meyerson MS, Biddinger KR: Results of arthrodesis of the tarsometatarsal joints after traumatic injury. J Bone Joint Surg Am 78:1668, 1996.)

the foot are obtained. A diastasis between the bases of the first and second metatarsals suggests an unstable injury. A small fragment of bone, called the fleck sign, represents an avulsion fracture of the Lisfranc ligament from the base of the second metatarsal (Fig. 25C1-52). The medial border of the second metatarsal should be parallel to the medial edge of the middle cuneiform on the anteroposterior view. The medial border of the fourth metatarsal should align with the medial border of the cuboid on the oblique radiograph. Dorsal displacement of the metatarsal bases is best assessed on the weight-bearing lateral projection. Faciszewski and associates reviewed 15 cases of subtle injury of the Lisfranc joint and determined that flattening of the longitudinal arch correlated with a poor outcome, whereas persistent diastasis up to 5 mm did not correlate

A

In cases with strong clinical signs and normal radiographs, stress films can help elicit subtle widening.251 The procedure can be performed in the office after injection of local anesthetic into the region or in the operating room with the patient under general anesthesia. Both pronation-abduction and supinationadduction forces are applied to the forefoot, and widening or instability of the tarsometatarsal articulation is noted.

Computed Tomography Further imaging with CT allows for a more detailed analysis. Alignment, displacement, and subtle osseous injury are best evaluated with fine-cut CT (see Fig. 25C1-52).

Magnetic Resonance Imaging MRI is occasionally used to identify the hemorrhage and edema associated with acute ligamentous injury or to differentiate complete and partial tears.252

Therapeutic Options All acute injuries are treated with the RICE method, as described earlier. Patients are immobilized and prevented from bearing weight until a definitive diagnosis is

B

Figure 25C1-52 A diastasis and occasionally a bone fragment between the first and second metatarsal bases suggest injury to the Lisfranc joint. A, Lisfranc injury as seen on routine standing radiograph. B, Lisfranc injury as seen on computed tomography.


e stablished. Subsequent treatment is predicated on the stability of the Lisfranc complex.

Grade I Lisfranc Sprain These injuries are immobilized in a short leg cast and kept from bearing weight for 4 to 6 weeks. On verification of stability by clinical and radiographic examination, patients are transitioned to a walking boot, and weight-bearing to tolerance is encouraged. A rehabilitation program is instituted, with an emphasis on recovery of foot and ankle range of motion, strength, and coordination. As healing progresses, the boot is discontinued, and a steel or fiber carbon shoe insert is used to reduce bending forces at the midfoot. Supportive tape or custom-molded orthotics may decrease the time before return to athletic activity. If pain persists or the patient is unable to return to competition, operative management is considered.

Grade II Lisfranc Sprain As previously described, this group includes injuries with 2 to 5 mm of displacement. There is some disagreement about whether these injuries can be addressed through closed reduction and internal fixation instead of open treatment. Those that favor this technique use large reduction forceps and fluoroscopy to guide reduction before screw placement. Other authors advocate open treatment described next.

Grade III Lisfranc Sprain Unstable nondisplaced injuries, as verified by radiographs and CT, are treated with open reduction and internal fixation. Weight-bearing is delayed for 8 to 12 weeks after surgery. Routine screw removal remains controversial, but generally does not occur until 12 to 16 weeks after surgery. Meyer and colleagues reported no untoward effect associated with small, persistent diastasis between the first and second metatarsal bases after a midfoot sprain in a collegiate football player.242 Aitken and Poulson244 and Brunet and Wiley253 found that persistent subluxation or malalignment caused little functional disability. Others contend that anatomic reduction and stable fixation remain paramount.251,254-258 Nondisplaced injury or anatomic reduction does not prevent poor outcome. Resch and Stenström completed a review of 45 consecutive tarsometatarsal injuries, with an average 5-year follow-up.257 They noted that 3 of the 11 patients with nondisplaced tarsometatarsal injuries (50 years of age) and younger (8 degrees) • Fifth metatarsal lateral bowing • Pes planus

metatarsal osteotomy roomy toe box

• Return to sport expected 4 to 6 months after surgery

sal head

Foot and Ankle 2133 Figure 25H-90 A, Enlarged metatarsal head. B, The 4-5 intermetatarsal angle and metatarsophalangeal 5 angle. C, Increased 4-5 intermetatarsal angle. D, Lateral angulation of the distal fifth metatarsal. (A, C, and D, © M. J. Coughlin. Used by permission.)

Metatarsal phalangeal-5 angle

4–5 intermetatarsal angle

A

C

B

D

Classification

Evaluation

Three types of deformity have been described (Box 25H-48).286 Coughlin295 further reported the frequency of occurrence of each type of deformity. Coughlin noted a type 1 deformity in 27% of cases, type II in 23% of cases, and type III in 50% of cases.

Clinical Presentation and History The major subjective complaints of an athlete are pain and irritation caused by friction between the underlying bony abnormality and restricting footwear. Patients complain


Box 25H-48 Classification of Bunionette Deformities

Box 25H-50 Treatment Options for Bunionette

Type I: Enlargement of the metatarsal head or lateral exostosis Type II: Abnormal lateral bend of the fifth metatarsal with a normal 4,5 intermetatarsal angle (23%) Type III: Increased 4,5 intermetatarsal angle (>8 degrees [50%])

• Shoe modifications • Callus shaving • Orthotics

of swelling, pain with shoes, and callus formation over the deformity (Box 25H-49).

Nonoperative

Operative

• Lateral condylectomy • Metatarsal head resection • Distal metatarsal osteotomy • Diaphyseal osteotomy • Proximal fifth metatarsal osteotomy • Fifth ray resection

Physical Examination On clinical evaluation, the examiner inspects the lat eral eminence and lateral border of the foot for an inflamed bursa,284,287,296 a plantar keratosis,284,297,298 a lateral keratosis,299 or a combined plantar lateral kera tosis.282,299 Diebold and Bejjani299 noted that two thirds of the patients in their series had significant pes planus. Diebold and Bejjani299 also noted that one third of the patients had a plantar lesion, and half had a lateral kera totic lesion. Force plate studies or imprints that evaluate the pressure concentration on the plantar aspect of the foot are helpful in the analysis of a plantar keratosis (see Box 25H-49). A bunionette can develop in combination with a hallux valgus deformity. An increased 1-2 intermetatarsal angle combined with an increased 4-5 intermetatarsal angle results in a wide or splay foot abnormality.280,284,290,300,301

Imaging Radiographic evaluation includes standing anteroposterior and lateral radiographs. The 4-5 intermetatarsal angle and the MTP-5 angle are measured on standing anteroposte rior radiographs (see Box 25H-49).

Treatment Options Nonoperative Treatment Most bunionette deformities respond well to nonopera tive measures. Constricting footwear is often a signifi cant cause of symptoms in the athlete. Pain, swelling, and

Box 25H-49 Typical Findings in Bunionette Deformities

• Pain

and irritation over the lateral aspect of the fifth metatarsal head • Plantar or lateral keratosis formation • Elevated 4,5 intermetatarsal angle or metatarsophalan geal 5 angle

chronic irritation over the lateral bursa of the fifth meta tarsal head are reduced significantly by the use of properly fitted shoes.280,283,285,294,296,302 Padding of the prominent metatarsal head283,294 and shaving of the hypertrophic cal lus will relieve symptoms. An orthotic device can control pronation and secondarily can reduce discomfort over the prominent fifth metatarsal head (Box 25H-50).

Operative Treatment Surgical treatment of a bunionette is indicated for defor mities that continue to cause symptoms despite appropriate nonoperative measures. Numerous operative techniques have been proposed for surgical correction of a sympto matic bunionette deformity (see Box 25H-50). Lateral condylectomy is considered when an isolated enlargement of the fifth metatarsal head of lateral condyle occurs (Box 25H-51; Figs. 25H-91 and 25H-92). Failure of

Box 25H-51 Lateral Condylectomy

• Center a longitudinal skin incision over the lateral con dyle of the fifth metatarsal.

• Protect the dorsal cutaneous nerve of the fifth toe. • Create an inverted L-type capsular incision by

de taching the dorsal and proximal capsular attachments, allowing exposure of the fifth metatarsal head (see Fig. 25H-91). • Distract the fifth metatarsophalangeal (MTP) joint and release the medial capsule. • Resect the lateral eminence with an osteotome or sagittal saw (see Fig. 25H-92A). • Close the MTP capsule by suturing it to the dorsal peri osteum and to the abductor digiti quinti proximally (see Fig. 25H-92B). • If necessary, place a suture through a drill hole in the fifth metatarsal metaphysic dorsal and lateral to ensure a stable capsular closure and prevent recurrence or lateral subluxation of the MTP joint.

Foot and Ankle 2135 L-shaped capsule incision

Box 25H-52 Distal Metatarsal Osteotomy Types

• Distal chevron osteotomy • Distal oblique osteotomy • Crescentic osteotomy • Transverse distal osteotomy • Distal closing wedge osteotomy Abductor digiti quinti

Capsule

Figure 25H-91 An L-shaped capsular incision is used to expose the fifth metatarsal head.

lateral condylectomy as a treatment of the bunionette defor mity has led to the development of more extensive resec tion procedures. Excision of the fifth metatarsal head,303 resection of the distal half of the metatarsal,298 and fifth ray resection304 all have been used to treat a bunionette defor mity but are not appropriate in the initial treatment of the symptomatic athlete. These procedures are used as salvage procedures for infection, ulceration, or severe deformity. Less radical operative procedures that preserve foot or toe function are preferred in athletes. Many different distal fifth metatarsal osteotomy tech niques have been described for treating the sympto matic bunionette (Box 25H-52). Hohmann305 originally described a transverse osteotomy of the metatarsal neck, although the lack of stability of this procedure increases the risk for a transfer lesion or a malunion. Kaplan and associates282 used a distal closing wedge osteotomy inter nally fixed with 2-mm Kirschner wire. These authors282 suggested the use of internal fixation because they believed that a distal osteotomy is unstable and can rotate postop eratively with loss of correction. Most frequently, a distal oblique, crescentic, or chev ron osteotomy is considered. A distal oblique osteo tomy300,301,306 is performed from distal lateral to proximal

medial (Box 25H-53; Figs. 25H-93 to 25H-95). Haber and Kraft284 used a distal crescentic osteotomy. These authors did not use internal fixation and reported delayed healing and excessive callus formation at the osteotomy site. An alternative procedure is resection of the prominent lateral condyle in combination with a distal chevron osteotomy. Throckmorton and Bradlee287 performed a transverse chevron-type osteotomy without fixation, relying on this stable osteotomy shape to hold the postoperative position (Box 25H-54; Fig. 25H-96). Boyer and DeOrio307 describe fixation of the chevron osteotomy with a bioabsorbable pin. Recently, several minimally invasive techniques have been reported in the literature with good results.308,309 The indications for a diaphyseal fifth metatarsal oste otomy are a bunionette deformity associated with either an increased 4-5 intermetatarsal angle or lateral bowing of the distal metatarsal. MTP joint realignment with a lateral eminence resection is performed simultaneously if neces sary (Box 25H-55; Fig. 25H-97). A diaphyseal metatarsal osteotomy has been used to correct a bunionette defor mity.295,310 Voutey288 carried out a transverse osteotomy in the diaphysis but described problems with rotation, angulation, and pseudarthrosis. Yancey292 used a double transverse closing wedge osteotomy in the diaphyseal region to correct a bunionette deformity characterized by lateral angulation of the fifth metatarsal. Gerbert and colleagues311 recommended use of a biplane osteotomy

Medial capsular release

A

B

Figure 25H-92 A, The lateral eminence is resected, and a medial capsulotomy is performed. B, Lateral capsular reefing may be reinforced by a drill hole through the lateral metaphysis of the fifth metatarsal.


eminence.

cephalad direction to create an elevating effect on the dis tal fragment, then the fragment is rotated (Fig. 25H-98). Proximal osteotomies are associated with a higher inci dence of nonunion secondary to potential injury to the blood supply to the fifth metatarsal.299,312

capsular incision (see Fig. 25H-91)


Box 25H-53 Distal Oblique Osteotomy

• Make a midlateral longitudinal incision over the lateral • Release the proximal and dorsal capsule using an L-type • Release the abductor digiti quinti and resect the lateral

eminence with an osteotome or sagittal saw (see Fig. 25H-93A) • Create the oblique osteotomy of the metaphyseal neck using either a saw or osteotome (see Fig. 25H-93A). The osteotomy is oriented in a proximal lateral to distal medial direction. • Displace the distal fragment medially on the metatarsal and impact the bone on the proximal fragment (see Fig. 25H-93B and C). (The osteotomy can be fixed with a Kirschner wire [see Fig. 25H-94B]).

for a combined plantar lateral keratotic lesion to displace the distal fragment in a medial direction. Mann294 and Coughlin295,310 used an oblique diaphyseal fifth metatarsal osteotomy to treat diffuse keratotic lesions on either the plantar or plantar lateral aspects of the fifth metatarsal. The oblique orientation of the metatarsal osteotomy per mits a dorsal medial translation of the metatarsal as the dis tal fragment is rotated. Internal fixation was recommended with either a small fragment screw or wire loop or a Kirsch ner wire. Mann294 did not realign the fifth MTP joint with this procedure, and no results were reported, although one case of nonunion was noted. Coughlin310 modified Mann’s oblique diaphyseal osteotomy by performing a fifth MTP joint realignment and lateral eminence resection (see Box 25H-55). The fifth MTP medial capsular structures are not released because release might impair the circulation to the fifth metatarsal head. If a combination plantar lateral keratosis is present, the oblique osteotomy is oriented in a

A

B

C

Figure 25H-93 A, Distal oblique osteotomy coupled with lateral eminence resection. B, Resection of fifth metatarsal metaphysis with distal oblique osteotomy. C, Impaction of osteotomy site.

Kitaoka and Holiday313 reported on 21 feet that had undergone a lateral condylar resection. These authors313 concluded that a minimal correction was achieved with the procedure, although it did relieve symptoms. As Kelikian285 noted, “at best a lateral condylectomy is a temporizing measure like simple exostectomy on the medial side of the foot; in time, deformity will recur.” The only indication for a lateral condylectomy is an enlarged lateral condyle. Symptomatic relief often follows a condylectomy alone; however, a distal metatarsal osteotomy achieves greater correction of the deformity. Kitaoka and Leventen314 reported an average of 5 degrees of correction of the 4-5 intermetatarsal angle and a diminished forefoot width of 4 mm with 87% patient satisfaction after distal oblique osteotomy. Sponsel,301 who advocated an oblique distal osteotomy, noted an 11% delayed union rate, and Keating and coworkers300 reported 75% of patients to have transfer lesions with a 12% recur rence rate. Pontious and colleagues315 reported a much

A

B

Figure 25H-94 A, Preoperative radiograph shows severe bunionette deformity. B, After distal oblique osteotomy with internal fixation. (Courtesy of H. Zollinger-Kies, Zurich, Switzerland.)

Foot and Ankle 2137

A

B

Figure 25H-95 A and B, Preoperative and postoperative radiographs of distal oblique osteotomy. (A and B, © M. J. Coughlin. Used by permission.)

higher rate of success in oblique osteotomies that were internally fixed (see Fig. 25H-94). Throckmorton and Bradlee287 and others283,316,317 reported high levels of good and excellent results with the chevron osteotomy. Kitaoka and associates317 reported

Box 25H-54 Distal Chevron Osteotomy

• Make a midlateral longitudinal incision over the lateral eminence.

• Release the proximal and dorsal capsule using an L-type capsular incision (see Fig. 25H-91).

• Avoid soft tissue stripping to avoid vascular insult to the

distal metatarsal fragment. about 2 mm of the lateral eminence with an osteotome or a sagittal saw. • Mark the apex of the osteotomy with a drill hole in the midportion of the metatarsal. • Create a horizontal chevron osteotomy with a sagittal saw. The osteotomy is based proximally with an angle of 60 degrees (see Fig. 25H-96A) and oriented in a lateralto-medial direction. • Displace the distal fragment about 2 to 3 mm in a medial direction and impacted onto the proximal phalanx (see Fig. 25H-96B). • Use Kirschner wire fixation when necessary. • Remove any remaining prominent bone in the metaphy seal region of the fifth metatarsal with a sagittal saw. • Reef the lateral capsule to the abductor digiti quinti or the dorsal periosteum of the fifth metatarsal. If necessary, reattach the capsule through drill holes on the dorsal aspect of the metaphysis.

• Remove

the 4-5 intermetatarsal angle was reduced an average of 2.6 degrees, and the MTP-5 angle was reduced an average of 8 degrees with a chevron osteotomy. Moran and Claridge318 stressed that there was a low margin of error with this oste otomy and that there was a high risk for either recurrence or overcorrection. As a result, these authors encouraged the use of Kirschner wire stabilization of the osteotomy site. Coughlin295 reported on 30 feet that had undergone a midshaft diaphyseal metatarsal osteotomy. All went on to successful union. The average 4-5 intermetatarsal angle was reduced 10 degrees, and the MTP-5 angle was reduced 16 degrees. No transfer lesions developed, and a 93% patient satisfaction rate was reported. The average foot width was reduced 6 mm. Midshaft osteotomies do not appear to have an increased nonunion rate. Vienne and colleagues319 reported good or excellent results in 97% of their series of patients with diaphyseal osteotomies for bunionette correction. In this study, the 4-5 intermetatarsal angle was reduced from an average of 10 degrees preopera tively to 1 degree postoperatively. Shereff and associates312 noted that more proximally positioned osteotomies are at increased risk for delayed healing as a result of interruption of the interosseous and extraosseous blood supply to the proximal fifth metatarsal (Fig. 25H-99). Salvage procedures are less desirable in the athletic popu lation. Although McKeever298 reported a high level of suc cess in his series of 60 cases of metatarsal head resection, no criteria for postoperative evaluation were included. Kitaoka and Holiday320 reported on a small series and noted that 82% had fair or poor results, including the complications of severe shortening, transfer metatarsalgia, stiffness, and continuing symptoms. Dorris and Mandel321 reported malalignment of the fifth toe in 59% of patients, and Addante and col leagues322 reported malalignment and wound problems after metatarsal head resection and silicone implant arthroplasty.

�rthopaedic �� S �ports �� Medicine �� 2138 DeLee & Drez’s� O Figure 25H-96 A, Lateral view of a fifth metatarsal chevron osteotomy. B, Anteroposterior view after chevron osteotomy.

A

B


Box 25H-55 Oblique Diaphyseal Osteotomy

• Make a midlateral longitudinal incision is from the base

of the fifth metatarsal to the middle of the proximal phalanx (see Fig. 25H-97A). • Carry the dissection down to the fifth metatarsal shaft. • Protect the dorsal cutaneous nerve and retract the abductor digiti quinti in a plantar direction to expose the diaphysis of the fifth metatarsal. • Create an L-type capsular incision (see Fig. 25H-91) to expose the lateral eminence. • Remove the lateral eminence with a sagittal saw or osteotome. • Perform the resection in a line parallel with the metatarsal shaft. • Make a direct horizontal osteotomy in a dorsal proximal– to–plantar distal plane (see Fig. 25H-97B). • Drill the fixation holes before final displacement of the osteotomy site. • Drill a gliding hole in the dorsal distal fragment and create a tapped fixation hole in the proximal plantar fragment. • Complete the osteotomy and rotate the distal fragment medially (see Fig. 25H-97C). • Fix the osteotomy with either a small fragment compres sion screw or two minifragment compression screws. • Repair the fifth MTP joint capsule and bring the fifth toe into proper alignment (see Fig. 25H-97D and E). • Approximate the abductor digiti quinti and the MTP capsule. If necessary, reattach the capsule through drill holes on the dorsal aspect of the metaphysis.

Conservative management of a symptomatic bunionette in cludes the use of padding, shaving of keratotic lesions, and roomy footwear. In many cases, an athlete can continue sports activities with the use of orthotic devices or pads. Development of chronic bursal thickening, blistering, and symptomatic keratoses leads to operative treatment in certain patients. Because of the risk for transfer lesions, recurrence of deformity and malunion, delayed union, or nonunion of osteotomy sites, surgical intervention should be delayed until a patient experiences significant difficulty in sports activities. Surgical versatility in the treatment of a bunionette de formity is important. Attention to the underlying pathol ogy helps to determine whether a condylectomy with a distal soft tissue repair, a distal metatarsal osteotomy, or a diaphyseal biplane osteotomy offers the best treatment for the symptomatic bunionette deformity in the athlete. Analysis of the physical findings including examination of the plantar aspect of the foot for the presence of keratotic lesions helps to differentiate the type of bunionette present and the appropriate treatment. Evaluation of radiographs is necessary to analyze the nature of the deformity. When an enlarged fifth metatarsal head or medial emi nence is present (with or without a pronated foot or fifth ray), lateral condylectomy with MTP joint realignment or distal metatarsal osteotomy is the treatment of choice. The presence of a pure lateral keratotic lesion makes a chevron osteotomy preferable because of the stability of this osteotomy. Kirschner wire fixation often helps to stabilize the osteotomy site. When a plantar lateral keratotic lesion is present (with or without an increased 4-5 intermetatarsal angle or lateral deviation), a distal oblique osteotomy as described by Kitaoka and Leventen314 or a diaphyseal biplane osteotomy is considered. When there is an abnormally wide 4-5 intermetatarsal angle or when lateral deviation of the distal fifth metatarsal is present, a diaphyseal biplane osteotomy affords an excellent means of correction. Although there is some disagreement about the need for internal fixation after a fifth metatarsal osteotomy,315 the development of delayed union, malunion, nonunion, or transfer lesions in patients in whom floating osteotomies have been performed indicates a need for internal fixation.

Foot and Ankle 2139

A

C B

D

E

Figure 25H-97 A, Incision for a fifth metatarsal diaphyseal osteotomy. B, The horizontal osteotomy is performed from a proximal-dorsal to a plantar distal site. C, The osteotomy is rotated. D, Preoperative radiograph. E, Postoperative radiograph after oblique osteotomy. (D and E, © M. J. Coughlin. Used by permission.)

Postoperative Prescription, Outcomes Measurement, and Potential Complications Although recovery from bunionette surgery usually is rel atively rapid, conservative methods often are used either to alleviate symptoms or to help postpone surgery until

the off-season. Postoperatively, the foot is wrapped in a soft gauze and tape dressing, and the patient ambulates in a postoperative shoe. Sutures are removed 2 weeks after surgery. Pins are removed at 6 weeks, and the toe is taped in the proper alignment for 4 more weeks. A below-knee cast can be used if the surgeon is concerned about fixa tion or the reliability of the patient. Weight-bearing in


A

90°

Saw blade 90°

20° Saw blade

12mm

B

C

Figure 25H-98 A, To achieve elevation of the fifth metatarsal head, the saw is oriented in a cephalad direction, and the osteotomy site is rotated. B, Schema illustrating effect of horizontal osteotomy. With the saw blade oriented in a lateral-to-medial direction, the osteotomy site is rotated and does not elevate the distal metatarsal. C, Schema illustrating effect of oblique osteotomy. With the saw blade oriented in a medial-to-lateral but also superior direction, as the osteotomy site is rotated, the distal fragment is elevated. (B and C, Adapted from Lutter L: Atlas of Adult Foot and Ankle Surgery. St. Louis, Mosby, 1997, pp 110-111.)

a postoperative shoe usually is carried out by having the patient bear more weight on the inner aspect of the foot at first. By 3 weeks, a plantigrade stance and gait pattern are encouraged. Recurrence of deformity is the most common com plication after lateral condylectomy (Fig. 25H-100).

A

B

ccasionally, fifth MTP joint realignment is complicated O by joint subluxation or dislocation (Fig. 25H-101). An adequate capsular joint repair helps to avoid this complica tion. Any dissection in this area can result in injury to the lateral cutaneous nerve to the fifth toe (a branch of the sural nerve), leading to numbness or formation of neuroma.

C

Figure 25H-99 A, Preoperative radiograph shows moderate bunionette deformity. B, After proximal fifth metatarsal osteotomy. C, Symptomatic nonunion after proximal osteotomy. This osteotomy took about 12 months to heal and prevented the patient from participating in high school athletics for that season. (From Mann RA, Coughlin MJ [eds]: Surgery of the Foot and Ankle, 6th ed. St. Louis, Mosby, 1993.)

Foot and Ankle 2141

A

B

C

Figure 25H-100 A, Radiograph shows type 1 bunionette deformity with a large metatarsal head. B, After lateral condylectomy. C, Recurrence 3 years after lateral condylectomy.

Dorsal angulation with development of an IPK or trans fer lesion beneath the fourth metatarsal head is a reported complication of distal metatarsal osteotomy. Delayed union or nonunion has been observed as well. The use of internal fixation reduces the incidence of malunion and nonunion after fifth metatarsal osteotomies. An oblique diaphyseal osteotomy can also be complicated by malunion, delayed union, nonunion, or transfer metatarsalgia.

Criteria for Return to Play Return to athletic activities is expected earlier after a lat eral condylectomy or MTP joint realignment than after a fifth metatarsal osteotomy. After a lateral condylec tomy, usually aggressive walking can be initiated 4 weeks

after surgery, with running after 6 weeks. After a distal osteotomy, aggressive walking is initiated at 8 weeks, and if no complications are encountered, jogging and running can be started progressively between 10 and 12 weeks postoperatively. Diaphyseal osteotomies require slightly longer healing time. In these cases, aggressive walking is initiated between 8 and 10 weeks and progressive run ning after 12 weeks. If there is clinical concern of incom plete healing of the osteotomy, progression of activity should be delayed. Roomy footwear with an adequate toe box is more comfortable during initiation of athletic activities.

C

Figure 25H-101 Dislocated metatarsophalangeal joint after simple condylectomy.

r i t i c a l

P

o i n t s

ost conditions of the forefoot are successfully treated l M nonoperatively in athletes. l When athletes with forefoot deformity (hallux valgus or lesser toe deformity) have pain associated with shoewear, modification of shoes by stretching constricting areas or relieving pressure areas can relieve the athlete’s symp toms completely. l Choosing appropriate orthotics or shoes for an athlete depends on careful examination and recognition of subtle malalignment that may be contributing to symp toms. l When choosing operative treatment, the surgical procedure(s) must address all anatomic abnormalities present. l Athletes should expect up to 3 to 6 months until full return to sport after most forefoot surgeries, espe cially when deformity correction through osteotomy is required.


S U G G E S T E D

R E A D I N G S

Anderson RB: Turf toe injuries of the hallux metatarsophalangeal joint. Tech Foot Ankle Surg 1(2):102-111, 2002. Baxter DE: Treatment of bunion deformity in the athlete. Orthop Clin North Am 25(1):33-39, 1994. Boyer ML, DeOrio JK: Transfer of the flexor digitorum longus for the correction of lesser-toe deformities. Foot Ankle Int 28(4):422-430, 2007. Campbell D: Chevron osteotomy for bunionette deformity. Foot Ankle Int 2:355-356, 1982. Coughlin MJ: Hallux valgus in the athlete. Sports Med Arthrosc Rev 2:326-340, 1994. Coughlin MJ: Operative repair of the mallet toe deformity [erratum appears in Foot Ankle Int 16(4):241, 1995]. Foot Ankle Int 16(3):109-116, 1995.

Coughlin MJ: Second metatarsophalangeal joint instability in the athlete. Foot An kle 14(6):309-319, 1993. Coughlin MJ: Sesamoid pain: Causes and surgical treatment. Instr Course Lect 39:23-35, 1990. Coughlin MJ, Dorris J, Polk E: Operative repair of the fixed hammertoe deformity. Foot Ankle Int 21(2):94-104, 2000. Mann RA, Mann JA: Keratotic disorders of the plantar skin. J Bone Joint Surg Am 85(5):938-955, 2003.


S e c t i o n

I

Osteochondroses and Related Problems of the Foot and Ankle S. Terry Canale and David R. Richardson

OVERVIEW OF OSTEOCHONDROSIS The term osteochondrosis has been applied to more than 50 eponymic entities to describe a variety of conditions characterized by abnormal endochondral ossification of physeal growth. Osteochondrosis is the singular term and is used to describe a noninfectious disease process involving the growth or ossification centers in children that begins as a degeneration or osteonecrosis followed by regenera tion or recalcification. Because normal endochondral ossi fication does not always present a uniform radiographic pattern, the differentiation of osteochondrosis from nor mal growth often is difficult. The etiology of osteochondrosis is complex and has been described as traumatic, constitutional, idiopathic, and hered itary. Most authors now believe that multiple factors are responsible for these changes. For example, excessive physi cal demands during athletic activity may incite osteochondral

changes in growing bone made vulnerable by constitutional factors. Once the process has begun, repetitive trauma or pressure may prolong recovery or contribute to deformity. All osteochondroses heal, but treatment may be required to relieve pain or prevent residual deformity, especially in osteochondroses around the foot and ankle in athletes. The osteochondroses have been classified according to etiology, anatomic location, and type of growth center, but none has had much practical application. In a clinically ori ented classification, Siffert1 divided the osteochondroses into three basic groups: articular, nonarticular, and phy seal (Table 25I-1). Mintz and colleagues2 described a clas sification based on the magnetic resonance imaging (MRI) appearance of the lesion (Table 25I-2). Osteochondroses of specific locations also have been further classified, and these specialized classification systems are discussed with the specific osteochondroses. According to the Siffert classification, osteochondro ses involving the foot and ankle generally are articular or

TABLE 25I-1 Clinical Classification of Osteochondrosis Type

Involvement (Example)

Characteristics

Treatment

Articular

Primary: articular and epiphyseal cartilage and subadjacent endochondral ossification (Freiberg disease) Secondary: articular and epiphyseal cartilage as consequence of osteonecrosis of adjacent bone (Legg-Calvé-Perthes disease, Köhler disease) Tendon attachment (Osgood-Schlatter disease) Ligament attachment (vertebral ring, epicondyle) Impact sites (Sever disease, Iselin disease) Long bones (tibia vara) Vertebrae (Scheuermann disease)

Degenerative arthritis, pain, limitation of motion

Minimize epiphyseal deformity Encourage joint congruity

Local pain with activity, local tenderness, adolescents, self-limited

Individualized Allow rapid, safe return to activity while minimizing sequelae

Nonarticular Physeal

Modified from Siffert RS: Classification of the osteochondroses. Clin Orthop 158:10-18, 1981

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TABLE 25I-2 Magnetic Resonance Imaging Classification of Osteochondrosis Grade

Magnetic Resonance Imaging Appearance

0 1 2 3 4 5

Normal cartilage Abnormal signal but intact Fibrillation or fissures not extending to bone Flap present or bone exposed Loose undisplaced fragment Displaced fragment

Metatarsal head (Freiberg)

Data from Mintz DN, Tashjian GS, Connell DA, et al: Osteochondral lesions of the talus: A new magnetic resonance grading system with arthroscopic correlation. Arthroscopy 19:353-359, 2003

nonarticular. Articular osteochondroses, such as Freiberg and Köhler diseases, may result in degenerative arthritis, pain, and limitation of motion, and treatment should be aimed at minimizing epiphyseal deformity and maximizing joint con gruity. Nonarticular osteochondroses, such as Sever disease of the calcaneus and Iselin disease of the base of the fifth metatarsal, cause local pain with activity and local tender ness, usually occur in adolescents, and are self-limited con ditions. Treatment of any osteochondritic condition must be individualized to allow the athlete a rapid, safe return to activity and to minimize sequelae of the condition.

OSTEOCHONDROSES OF THE FOOT AND ANKLE Although a number of osteochondritic conditions in the foot and ankle have been described, most are rare and usually asymptomatic. The most common osteochondroses in the foot and ankle that cause symptoms and require treatment affect the talus, calcaneus, navicular, cuneiforms, metatar sals, and sesamoids (Fig. 25I-1). Because an osteochondro sis may have its onset in childhood or adolescence and not become evident until adulthood, it is difficult to divide these conditions into clear-cut adult and pediatric categories.

Osteochondral Lesions of the Talus Konig,3 in 1888, first used the term osteochondritis dissecans to describe loose bodies in the knee joint, theorizing that they were caused by spontaneous necrosis of bone. In 1922, Kappis4 noted the similarity of lesions of the ankle to those in the knee and referred to osteochondritis dis secans of the ankle. In 1932, Rendu5 suggested that osteo chondritic lesions represented traumatic intra-articular fractures, and the primarily traumatic etiology of osteo chondral lesions of the talus (OLT) has been supported by numerous authors.6-12

Relevant Anatomy and Biomechanics The talus is a uniquely shaped bone divided into three ana tomic regions: dome, neck, and head. The talar dome artic ulates with the tibia and fibula on its superior, medial, and lateral surfaces to form the ankle joint. Inferiorly, it articu lates with the posterior facet of the calcaneus and, along with the inferior surfaces of the head and neck of the talus,

Cuneiforms (Buschke)

Navicular (Köhler)

Fifth metatarsal base (Iselin)

Talus (Koenig, Kappus)

Calcaneus (Sever) Figure 25I-1 Common sites of osteochondrosis in the foot. The specific form of disease is mentioned in parentheses.

forms the subtalar joint. It plays a key role in ankle motion and in supporting the axial load during weight-bearing. Because it lacks muscular or tendinous insertions, indirect perfusion of the talar dome is limited; injury to the artery of the tarsal canal, a branch of the posterior tibial artery, disrupts the main intraosseous blood supply to the central two thirds of the talar dome. In addition, about 60% of the talar dome is covered with hyaline cartilage, further reduc ing its vascular supply and reparative capacity.13 Boyd and Knight14 showed that the tibiotalar articulation is subjected to more load per unit area than any other joint in the body, and Millington and coworkers15 demonstrated that more force than previously thought is placed at the talar shoulders where osteochondral lesions typically occur. Several authors16-20 have hypothesized that even minimal talar displacement can result in medial stress concentration in the tibiotalar joint and lead to cartilage damage. Berndt and Harty21 proposed two possible mechanisms for osteochondral fractures of the talus: (1) compressive injury to a dorsiflexed and inverted ankle (direct tibiotalar impact) that crushes the subchondral bone of the lateral talar dome, with or without overlying cartilage damage; and (2) inversion and external rotation forces on a plantar flexed ankle that can produce osteochondral injuries to the medial surface of the talus. O’Farrell and Costello22 also described a combination of inversion and plantar flexion as a mechanism of injury for medial talar lesions. Other mechanisms have been described, including impaction of the talar dome against


the lateral malleolus (causing lateral dome lesions) or against the posterior tibial lip (causing medial defects).21,23,24 Ankle sprains have been identified as the most common injuries leading to OLT.25-28 In ankle sprains that involve a plantar flexed foot forcibly supinating and injuring the anterior talofibular ligament, the plantar flexed foot and talus subluxate or dislocate, and the posteromedial corner of the talus strikes the tibial plafond, causing a chondral bruise, chondral cracks, shearing off of the corner of the talus with intact chondral attachments, or a complete frac ture of the corner of the talus. Lateral lesions usually are located anterior or central on the talar dome. Also, they are shallower and more wafer shaped than medial lesions, possibly because of a more tangential force vector that results in shearing-type forces. Medial lesions are central and posterior as well as deeper and cup shaped because the combination of inversion, plantar flexion, and external rotation forces causing the posteromedial talar dome to impact the tibial articular sur face has a relatively more perpendicular force vector.21,29

Classification The classification of Berndt and Harty, based on radio graphic findings, remains a useful system for describing osteochondral lesions of the talus. However, more recent classification systems reflect advances in technology, such as computed tomography (CT),30 MRI,31 and ankle arthroscopy,32,33 (Table 25I-3) and may contribute to a more accurate prognosis. Raikin and colleagues34 divided the talar dome articular surface into nine zones in a grid configuration: zone 1 was the most anterior and medial, zone 3 was anterior and lat eral, zone 7 was the most posterior and medial, and zone 9 was the most posterior and lateral (Fig. 25I-2). From MRI examinations of 424 ankles with reported osteochondral talar lesions, they recorded the frequency of involvement and size of lesion for each zone. The medial talar dome was more fre quently involved (62%) than the lateral talar dome (34%); in the anteroposterior direction, the midtalar dome was much more frequently involved (80%) than the anterior (6%) or posterior (14) thirds; zone 4 (medial and mid) was most fre quently involved (53%), with zone 6 second (26%). Lesions in the medial third of the talar dome were significantly larger and deeper than those in the lateral talar dome.

Evaluation Clinical Presentation and History In patients with acute injuries, the ankle and foot usually are swollen and painful, which can limit the specificity of physi cal examination. Patients with chronic injuries generally complain of mechanical symptoms, such as locking or giving way, or a feeling of instability of the ankle joint, in addition to pain and persistent swelling. Pain may occur only with certain ankle movements during sport or strenuous activity. An OLT should be considered in any patient who pre sents with a history of a “persistent ankle sprain.” Eighty percent of patients with traumatic OLT have a history of a seemingly benign ankle sprain. Taga and associates35 found cartilage lesions in 89% of acutely injured ankles and in

95% of ankles with chronic injuries. They concluded that the longer the time from initial injury, the more severe the associated cartilage lesions. They suggested that these car tilage lesions are the primary cause of persistent pain in patients with chronic ankle instability. Studies have found cartilage damage in up to 66% of ankles with lateral liga ment injuries and 98% of ankles with deltoid ligament injuries.36,37 No correlation has been found between the amount of cartilage damage and the severity of lateral liga ment injury.36 In contrast, Komenda and Ferkel26 found chondral injuries in only 25% of 55 unstable ankles.

Physical Examination and Testing The ankle and foot, especially, should be palpated to iden tify locations of tenderness; the medial and lateral cor ners of the talar dome should be palpated with the ankle maximally plantar flexed. A careful neurovascular examina tion is essential. Range of motion in the involved foot and ankle should be compared with that of the contralateral extremity. Stability of the ankle should be evaluated with an anterior drawer test with the ankle plantar flexed and dorsi flexed and with inversion and eversion stress testing. Other soft tissue or bony causes should be ruled out (Box 25I-1).

Imaging Oblique and plantar flexed radiographic views that avoid tibial overlap generally show the lesion more clearly than plain films. If radiographs are suggestive but not diagnostic of OLT, technetium-99m bone scanning can help identify localized bony pathology. If an OLT is suggested by either radiograph or bone scan, CT or MRI, or both, can provide more definitive information. Axial and sagittal CT cuts can help determine the location of the lesion (anterior, medial, or posterior) as well as its depth and size (Fig. 25I-3). MRI is useful for both preoperative evaluation and postopera tive follow-up. Anderson and colleagues38 demonstrated that low signal intensity in T1-weighted images is an early and definitive sign of even stage I lesions. A high signal rim between the osteochondral fragment and the talar bed is considered indicative of instability of the fragment, with the presence of joint fluid or fibrous granulation tissue as a result of the mobility of these fragments. It has been noted that the diameter of the lesion measured on MRI was significantly larger than indicated on radiographs,39 an important factor in preoperative planning. We recommend MRI evaluation to detect changes that provide information about detachment and viability of the fragment and help make the decision to preserve or to excise the fragment (Fig. 25I-4). MRI also may allow more appropriate treat ment because it delineates the lesion more accurately than either radiography or CT.40 OLTs that have a high signal rim on T2-weighted images are most likely unstable.41 In a study of 22 ankles with OLT, Higashiyama and associates42 found that the low and high signal rims present before sur gery disappeared in 100% and 77% of ankles, respectively. A decrease in or disappearance of the signal rim correlated well with clinical results: no patient in whom the signal rim persisted had a good result. It has been suggested that heli cal CT, MRI, and diagnostic arthroscopy are significantly better than history, physical examination, and standard

Foot and Ankle 2145

TABLE 25I-3 Classification of Osteochondral Lesions of the Talus Radiographic Classification*

Stage

Radiographic Finding

I IIa IIb III IV V

Small area of compression of subchondral bone Partially detached osteochondral fragment Subchondral cyst on magnetic resonance imaging38 Completely detached osteochondral fragment remaining in the crater Displaced osteochondral fragment Radiolucent lesions on computed tomography scan43

Computed Tomography Classification�

Stage

Computed Tomography Appearance

I IIa IIb III IV

Cystic lesion of talar dome with intact roof Cystic lesion with communication to talar dome surface Open articular surface lesion with overlying nondisplaced fragment Nondisplaced lesion with lucency Displaced osteochondral fragment

Magnetic Resonance Imaging and Arthroscopy Classification� Cartilage

Grade

Magnetic Resonance and Arthroscopy Appearance

A B

Viable and intact Breached and nonviable

Bone

Stage

Magnetic Resonance and Arthroscopy Appearance

1 2 3 4

Subchondral compression or bone bruise that appears as high signal on T2-weighted images Subchondral cysts not seen acutely, develop from stage 1 lesions Partially separated or detached fragments in situ Displaced fragments

Arthroscopic Classification§

Grade

Arthroscopic Appearance

I II III

Intact, firm, shiny articular cartilage Intact but soft articular cartilage Frayed articular cartilage

Arthroscopic Classification¶

Grade

Arthroscopic Finding

A B C D E F

Articular cartilage is smooth and intact but may be soft or ballottable Articular cartilage has a rough surface Articular cartilage has fibrillations or fissures Articular cartilage with a flap or exposed bone Loose, nondisplaced osteochondral fragment Displaced osteochondral fragment

*Data from Berndt AL, Harty M: Transchondral fracture of the talus. J Bone Joint Surg Am 41:988-1029, 1959. †Data from Ferkel RD, Sgaglione NA: Arthroscopic treatment of osteochondral lesions of the talus: Long-term results. Orthop Trans 17:1011, 1993. ‡Data from Taranow WS, Bisignani GA, Towers JD, et al: Retrograde drilling of osteochondral fragments of the talar dome. Foot Ankle Int 20:474-480, 1999 §Data from Pritsch M, Horoshovski H, Farine I: Arthroscopic treatment of osteochondral lesions of the talus. J Bone Joint Surg Am 68:862-865, 1986. ¶Data from Cheng MS, Ferkel RD, Applegate GR: Osteochondral lesions of the talus: A radiologic and surgical comparison. In Ferkel RD, Whipple TL, Burst SE (eds): Arthroscopic Surgery: The Foot and Ankle. Philadelphia, Lippincott-Raven, 1996.

radiography for detecting or excluding OLT. Diagnostic arthroscopy does not perform better than helical CT and MRI.40 In general, arthroscopy should not be used as the initial method for diagnosing OLT.

Treatment Options Nonoperative Nonoperative treatment may be attempted for CT stage I or II lesions and for stage III lesions in skeletally imma ture patients. Nonoperative treatment of acute OLT

enerally involves an initial period of non–weight-bearing g with cast immobilization, followed by progressive weightbearing and mobilization to full ambulation by 12 to 16 weeks. The recommended duration of nonoperative treatment is varied, with some authors recommending 6 months7 and others6 up to 12 months before opera tive treatment is chosen. Based on the results of nonop erative treatment of 35 chronic cystic OLT, Shearer and colleagues43 concluded that (1) nonoperative manage ment of chronic cystic OLT is a viable option with little or no risk for developing significant osteoarthritis; (2) most lesions remain radiographically stable; (3) there is


Box 25I-1 D ifferential Diagnosis of Osteochondral Lesions of the Talus

• Syndesmosis injury • Ankle soft tissue impingement lesions • Complex regional pain syndrome type I • Degenerative arthrosis • Occult talar fractures • Lateral ankle instability • Tarsal coalition • Peroneal tendon subluxation or tendinitis • Subtalar dysfunction Lavage, Débridement, and Excision

Small, chronic, symptomatic lesions may benefit from arthroscopic lavage and débridement by removing catabolic cytokines and loose bodies from the ankle, which can be the source of mechanical symptoms. However, adding curettage and drilling has been associated with better results.12,48 Figure 25I-2 Anatomic nine-zone grid scheme on the talar dome: nine equal surface area zones, with zones 1, 4, and 7 positioned on the medial talus and zones 1, 2, and 3 positioned anteriorly. (From Raikin SM, Elias I, Zoga AC, et al: Osteochondral lesions of the talus: Localization and morphologic data from 424 patients using a novel anatomical grid scheme. Foot Ankle Int 28:154-161, 2007.)

poor correlation between changes in lesion size and clini cal outcome, although the few patients with lesions that decrease significantly in size tend to do well, and those with lesions that increase significantly in size tend to do poorly; (4) the development of mild radiographic changes of osteoarthritis does not correlate with clinical outcome; (5) the general course of chronic cystic OLT is benign, with more than half of patients improving to good or excellent results with nonoperative management; (6) lat eral lesions tend to do better than medial ones; and (7) adult-onset lesions tend to do better than juvenile-onset lesions. Alexander and Lichtman44 suggested that a delay in treatment does not affect outcome; however, more recent studies have questioned this.45-47 Lesions present ing more than 1 year after injury or the onset of symptoms may have a poorer prognosis.45 Also, radiographic results are improved when the interval between injury and opera tive treatment is reduced.45,47 This indicates that early diagnosis and treatment are advisable.

Operative Options for open or arthroscopic treatment of OLT gen erally are based on one of three specific goals: (1) stimulat ing the bone marrow by débridement or drilling, with or without loose body removal; (2) securing the lesion to the talar dome so that it will heal in place; or (3) stimulating the development of hyaline cartilage. Techniques include excision, drilling, and curettage, alone or in combination; internal fixation with screws, Kirschner wires, or bioab sorbable devices; cancellous bone grafting; osteochondral autograft or allograft procedures; and autologous chondro cyte implantation or transplantation.

Curettage, Drilling, and Microfracture

Marrow-inducing reparative techniques, such as abrasion, drilling, and microfracture, aim to stimulate chondropro genitor cells within the underlying marrow. These stem cells populate the fibrin clot in the talar defect and produce a fibrocartilaginous matrix composed of chondroblasts, chondrocytes, fibrocytes, and an unorganized matrix that protects the surface from excessive loading. The dis advantage of these reparative techniques is the weaker mechanical properties of the fibrocartilage matrix, which lacks the normal biomechanical and viscoelastic character istics of normal tissue. Arthroscopic results appear superior to open procedures.48 Internal Fixation

Fixation devices include permanent or bioabsorbable low-profile pins, nails, or headless screws. Acute OLTs do markedly better after fixation than do chronic lesions. Lesions need to be larger than 8 mm to allow secure internal fixation. Restoration of Articular Hyaline Cartilage

Restorative techniques usually are recommended for defects larger than 2 cm2. These techniques can include autologous chondrocyte implantation (ACI), matrix or membrane ACI (MACI), collagen-covered autologous chondrocyte implantation (CACI), arthroscopic allograft or autograft (AAP) with platelet-rich plasma (PRP) implan tation, osteochondral autograft, osteochondral autologous transfer system (OATS) and mosaicplasty, fresh osteochon dral graft, stem cell–mediated implants, and scaffolds. Osteochondral autografting procedures such as OATS and mosaicplasty require the harvest of grafts from a donor site, such as the lateral supracondylar ridge or intercondy lar notch of the femur, for insertion into the OLT. These techniques generally are used for moderate to large grade III or IV lesions. Concerns about donor site morbidity have prompted graft harvest from sites other than the dis tal femur, including the anterior talar dome, and the use of allografts.

Foot and Ankle 2147

A

B

C

Figure 25I-3 A, Posteromedial osteochondral lesion of the talus (arrow). B, Coronal plane CT image. C, Axial plane CT image. (From Richardson DR: Ankle injuries. In Canale ST, Beaty JH [eds]): Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Fresh-frozen allografts (mega-OATS procedure) have been used for large osteochondral lesions in the knee, but seldom in the talus. Gross and colleagues49 listed as their indication for this procedure a lesion at least 1 cm in diameter and 5 mm deep that could not be internally fixed. Chondrocyte viability is a primary concern, and it is essential that the graft be harvested within 24 hours of the donor’s death and be stored at 4° C for less than 5 days. A benefit of using an ipsilateral talar allograft is the ability to harvest from a similar area as the defect and thus have a closely matched graft. Autologous Chondrocyte Implantation or Transplantation

ACI involves harvesting 200 to 300 mg of autologous chon drocytes from the distal femur, growing the cells in vitro for 2 to 5 weeks, then implanting them into the defect. An autologous periosteal flap is harvested and sewn over the implanted cells and sealed with fibrin glue. A “sandwich” procedure has been described for lesions with concomitant bone loss.50 The bony defect is grafted and covered with a periosteal patch with its cambium side facing the cartilage. A second periosteal patch with its cambium side facing the bone is sewn over the first patch to create a space for the

Figure 25I-4 Magnetic resonance imaging appearance of stage IV osteochondral lesion of the talus.

cells. ACI is best suited for large and well-contained stage III or IV defects, large lesions with extensive subchondral cystic changes, and lesions in which previous operative treatment has failed. According to Ferkel and Hommen,51 the ideal patient for ACI is between 15 and 55 years old and has no malalignment, degenerative joint disease, or instability of the joint. The procedure is contraindicated in bipolar (kissing) lesions that involve both the tibia and the talus.51,52 Because of concerns about donor-site mor bidity after harvest from the distal femur,53,54 other donor sites have been suggested. Giannini and associates55 used detached osteochondral fragments as a source of cells.

Weighing the Evidence Most of the literature about OLT consists of case series (level IV evidence) or case reports (level V evidence). For some of the newer techniques, numbers are too small and follow-up too short to make definitive recommendations. Shearer and colleagues43 reviewed the results of nonsurgical management of 35 OLTs and concluded that nonsurgical management of chronic cystic (stage 5) OLT is a viable option with little or no risk for development of osteoarthritis. Their clinical results were good or excellent in 54%, fair in 17%, and poor in 29%. A meta-analysis of 14 studies with a total of 201 patients showed only a 45% success rate of nonsurgical treatment of grades I and II and medial grade II OLTs, and nonoperative treatment of chronic lesions had a success rate of 56%.48 The highest success rate was obtained with excision, curettage, and drill ing (85%), followed by excision and curettage (78%) and curettage alone (38%). Shelton and Pedowitz56 reported just 25% satisfactory results after nonoperative treatment of grade II and III lesions. Gobbi and coworkers,57 in a randomized trial comparing chondroplasty, microfracture, and OATS in 33 patients, found no significant differences in clinical results among the three methods. However, each treatment group con tained a small number of patients, and three different sur geons were involved in the surgeries. Individual studies of various treatment methods have reported good results.

2148 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Lavage, Débridement, and Excision

In the meta-analysis by Verhagen and coworkers,48 exci sion alone had an overall success rate of 38%, with a range of 30% to 100% in individual studies. Excision and curettage had a success rate of 76% (range, 53% to 100%). Arthroscopic procedures had a higher success rate (84%) than did open procedures (63%). Savva and associ ates58 described repeat arthroscopic débridement in 12 of 215 patients who had arthroscopic treatment of OLT; at an average 6-year follow-up, results were good in all 12, and 8 had returned to their preinjury levels of sports. Curettage and Drilling or Microfracture, Bone Grafting

Good to excellent results after drilling have been reported in 28% to 93% of patients. Ferkel and colleagues51 reported 72% excellent or good results in 64 patients, Taranow and coworkers59 reported an 81% success rate in 16 patients with retrograde drilling, and Becher and Thermann60 reported 83% excellent and good results and 17% satisfactory results in 30 patients at an average follow-up of 2 years after micro fracture. To determine whether the presence of a subchon dral cyst affected the results of arthroscopic microfracture or abrasion arthroplasty, Han and colleagues61 compared the results in 20 defects with cysts to those in 18 defects without cysts and found no differences in the clinical results. They concluded that small cystic lesions can be successfully treated by arthroscopic microfracture or abrasion arthroplasty. Autogenous Cancellous Bone Grafting

Saxena and Eakin62 compared the results of microfracture procedures in 26 patients to those after bone grafting in 20 patients. Overall, 96% of patients had excellent or good results, and there was no difference between the groups in the percentages of those who returned to sports. Bone grafting, however, required a longer time to return to activity than did microfracture in high-demand patients, but the two groups had similar postoperative American Orthopaedic Foot and Ankle Society (AOFAS) scores. Regardless of treatment type, patients with anterolateral lesions had the fastest returns to activity and the highest AOFAS scores. Draper and Fallat63 compared the results of 14 patients treated with bone graft ing with those of 17 patients treated with curettage and drill ing. At almost 5-year follow-up, those with bone grafting had better range of motion and less pain. Kolker and colleagues,64 however, reported that 6 of 13 patients required further surgery after open antegrade autologous bone grafting and concluded that autologous bone grafting alone should not be used as primary treatment for patients with symptomatic advanced OLT and deficient or absent overlying cartilage.

Osteochondral Autografts (Osteochondral Autologous Transfer System, Mosaicplasty)

Scranton and associates65 reported 90% good to excel lent results in 50 patients with type V OLT at an average 3-year follow-up after osteochondral autograft transplan tation using a single, arthroscopically harvested graft from the distal femur. Thirty-two of their 50 patients (64%) had at least one previous operation that failed to relieve symp toms. Hangody and collegues66 described good to excellent results in 34 of 36 patients 2 to 7 years after mosaicplasty. Kreuz and coworkers67 used mosaicplasty procedures for the treatment of 35 OLTs after failure of arthroscopic excision, curettage, and drilling. The osteochondral graft was harvested from the ipsilateral talar facet, and a mal leolar or tibial wedge osteotomy was used to access central or posterior lesions. Although there were no nonunions of the osteotomies, patients with small osteochondral lesions accessible through an anterior approach without additional osteotomy had the best results. Osteochondral Allografts

Although several studies have reported good results with this technique in the knee, there are few reports of its use in the ankle. Gross and associates49 reported that six of nine allografts remained in situ with a mean sur vival rate of 11 years; three patients required arthrodesis because of graft resorption and fragmentation. Kim and colleagues68 used tibiotalar osteochondral shell autografts in seven patients; at 10-year average follow-up, only four had excellent or good results. Complications included graft fragmentation, poor graft fit, graft subluxation, and nonunion. Autogenous Chondrocyte Implantation or Transplantation

Koulalis and colleagues69 reported excellent to good results at 17 months’ follow-up in all 8 of their patients treated with ACI, and Whittaker and associates70 described ACI in 10 patients, 9 of whom were “pleased” or “extremely pleased” with their results at 4-year follow-up; however, 1 year after surgery, Lysholm knee scores had returned to preoperative levels in only 3 patients, suggesting donorsite morbidity in the other 7. Baums and coworkers52 reported 12 patients with ACI of the talus for defects that averaged 2.3 cm2. At about 5 years’ follow-up, 7 had excellent results, 4 had good results, and 1 had a satisfac tory result. The AOFAS mean score improved from 43.5 before surgery to 85.5 after surgery. Patients who had been involved in competitive sports were able to return to their full activity levels.

Author’s Preferred Method For a stage I or II OLT, non–weight-bearing in a cast or boot is first tried for 6 to 10 weeks, depending on the size of the lesion. If this fails to relieve symptoms, arthroscopic excision, curettage, and microfracture or drilling is done. In a skeletally immature patient with a stage III OLT, a trial of conservative treatment is warranted before surgical treat ment. For stage III or IV OLT in skeletally mature patients,

arthroscopic microfracture or drilling is the first choice and has obtained good results in about 90% of our patients (Fig. 25I-5). The use of a noninvasive ankle distractor (Fig. 25I-6) will help with visualization of posterior lesions. If this option fails to relieve symptoms, an osteochondral autograft (lesion < 1.5 cm2) (Table 25I-4) or allograft (lesion >1.5 cm2) is used.

Foot and Ankle 2149


A

B

C

D

Figure 25I-5 A, Stage IV osteochondral lesion of the talus. B, Arthroscopic view of displaced osteochondral fragment. C, Arthroscopic excision and drilling. D, Note vascular channels created in defect.

Technique of Arthroscopic Drilling, xcision, or Pinning of OLT E

• View anterolateral lesions through an anteromedial por

Figure 25I-6 Noninvasive ankle distraction for ankle arthroscopy. (From Richardson DR: Ankle injuries. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

tal, with instrumentation for drilling, excision, or pinning inserted through an anterolateral portal, changing portals as necessary for optimal viewing and fixation. • Posteromedial lesions can be more difficult to view and treat. With noninvasive distraction and use of a small, 2.7-mm scope in the anterolateral portal, most postero medial lesions can be treated through anteromedial and posterolateral portals. • Use a small, curved curet or curved microfracture awl to make perforations in the subchondral bone. • If needed, make a small bony trough on the anteromedial tibia to improve access to posterior lesions. • If the lesion still is not accessible, use a guide to place a Kirschner wire through the medial malleolus for drilling of the lesion (Fig. 25I-7). • A malleolar osteotomy may be required for pinning of larger lesions. • Other helpful instruments are an open-end curet, a small 2.7-mm full-radius resector, and a small 2.7-mm bur. Continued


Authors’ Preferred Method—cont’d TABLE 25I-4 Authors’ Preferred Treatment of OLT MRI Stage


Primary Operative Treatment

After Failed Primary Procedure

I or II

Cast or boot: non–weight-bearing for 6-10 weeks depending on size; ankle brace for 3 months

Arthroscopic excision, curettage, microfracture/drilling

III

Cast or boot: Acute injury (< 10 weeks) skeletally immature: non-weight-bearing for 6-10 weeks Skeletally mature or chronic injury: proceed to operative treatment No role for conservative treatment

Minimally damaged surface: arthroscopic transtalar drilling Damaged surface: microfracture/drilling

Damaged surface < 1.5 cm2, osteochondral autograft transport; > 1.5 cm2, osteochondral allograft As above

IV

V

Cast or boot: weight bearing as tolerated for 6-10 weeks; ankle brace for 6 months

Minimally damaged surface: If < 1 cm2, arthroscopic transtalar drilling; If > 1 cm2, internal fixation Damaged surface: microfracture or drilling Minimally damaged surface: arthroscopic transtalar drilling + bone graft Damaged surface: microfracture or drilling

Technique of Osteochondral Autograft or Allograft Transplantation

• With

the patient under general anesthesia, prepare the affected lower extremity from the ankle to the knee. Examine the ankle arthroscopically to further delineate the chondral lesion. • Harvesters are made for lesions 5 to 11 mm (larger sizes also are available). • Approach lateral lesions through an anterior sagittal incision and perform a medial malleolar osteotomy for medial lesions. Rarely, a lateral malleolar osteotomy will be needed to access posterolateral lesions. • Use a commercially available recipient sizer and harvester to create a recipient hole for the donor osteochondral plug. Extract the plug to a depth of 10 mm (Fig. 25I-8A and B). Place the harvester perpendicular for dome lesions (see Fig. 25I-8C) and at 45 degrees for talar shoulder lesions.

As above

Cyst < 1.5 cm: as above + bone graft Cyst > 1.5 cm: bulk allograft

• Drill

multiple holes into the subchondral bone of the r ecipient hole (see Fig. 25I-8D). • Obtain a graft from the ipsilateral knee, arthroscopically from the medial femoral condyle, or from the lateral femoral condyle through a small incision (see Fig. 25I-8E and F). For talar shoulder lesions, obtain a graft from the lateral trochlea. • Use the specially designed donor harvester to obtain osteochondral grafts that measure 5 to 11 mm in diam eter and 10 to 12 mm in depth (slightly deeper than the recipient hole). • Insert the cylindrical grafts carefully into the recipient hole using the designed extruder or collared pin through the donor harvester (see Fig. 25I-8G and H). • Do not remove the OATS harvester before completion of full graft extrusion. Do not allow the harvester to deviate from the insertion angle. Either of these may cause frac ture of the donor core.

Anteromedial OLT

Transmalleolar portal

Kirschner wire

Anterolateral portal

A

Anteromedial port

B

Anteromedial OLT

Figure 25I-7 A, Transmalleolar drilling of osteochondral lesion using a guide. The scope is in the anterolateral portal, and inflow is through the posterolateral portal. B, Holes are drilled through the medial malleolus into the talus down to areas of bleeding bone. (From Ferkel RD: Arthroscopy of ankle and foot. In Mann RA, Coughlin MJ [eds]: Surgery of the Foot and Ankle, 8th ed. Philadelphia, Elsevier, 2006.)

Foot and Ankle 2151


A

D

B

E

C

F

Figure 25I-8 Osteochondral autograft and allograft transplantation. A, Trial sizer for harvester. B, Recipient harvester. C, Plug 10 to 12 mm deep is removed from recipient site. D, Multiple holes are drilled at the base of the lesion. E, Autograft is obtained from the femoral condyle with a donor harvester (for talar shoulder lesions, graft is obtained from corner of trochlea). F, Donor graft in harvester.

• Use the sizer-tamp to gently tamp the core flush with the

surrounding cartilage. • Test range of motion of the ankle to ensure that the graft is well seated and secured. • Close the incision and secure the osteotomy in the usual fashion (see Fig. 25I-8I). Place one drain in the knee and

apply a compressive dressing to the ankle. Apply a poste rior splint with strips. For very large lesions, allografts can be harvested from an ipsilateral donor talus (see Fig. 25I-8J).

Continued



I G

H

J

Figure 25I-8—cont’d G and H, Graft is placed in recipient hole. I, Malleolar osteotomy is secured with two partially threaded cancellous screws (holes are predrilled before osteotomy). J, For large defects, allografts can be taken from donor talus. (From Richardson DR: Ankle injuries. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008; courtesy of Dr. Robert Anderson, Charlotte, NC.)

Postoperative Prescription, Outcomes Measurement, and Potential Complications Postoperative Prescription After arthroscopic excision, curettage, and drilling, the patient is non–weight-bearing in a boot for 4 weeks, then progresses to weight-bearing in the boot in physical therapy. Active motion is begun at 12 days after surgery. After inter nal fixation or OATS, the patient is non–weight-bearing in a cast for 8 weeks, then progresses to weight-bearing in a boot for 4 weeks in physical therapy. A brace is then worn during a gradual return to activities as symptoms dictate.

Outcomes Measures Clinical outcomes measures include pain relief, ankle sta bility, and ankle motion.

Potential Complications The most common complication is continued pain. Repeat MRI evaluation or second-look arthroscopy (Fig. 25I-9) is reasonable if pain persists after 4 months. We have had several patients with continued pain after osteochondral grafting of an OLT; all had complete or significant relief of symptoms after arthroscopic débridement of the graft. Other potential complications are wound infection and neural injury, most often to the superficial peroneal nerve.

Criteria for Return to Play • Minimal or no symptoms, minimal swelling • Participating in physical therapy out of boot • After internal fixation, OATS, or cartilage replacement, a brace must be worn while participating in sports for 6 months after the procedure.

Foot and Ankle 2153

26 with microfracture and 20 with autogenous bone graft ing. Results were excellent or good in 44 (96%) of the 46 lesions, and the average time to return to sports activity was 17 weeks. The return to activity was significantly lon ger in the bone graft group (20 weeks) than in the micro fracture group (15 weeks); return to sports was faster after arthroscopic treatment (16 weeks) than after arthrotomy (17.5 weeks), but there was no difference in postoperative AOFAS scores. Patients with anterolateral lesions had the fastest return to sports and the highest AOFAS scores.

Osteochondral Lesions of the Distal Tibia

Figure 25I-9 Second-look arthroscopy 15 months after osteochondral autologous transfer system (OATS) procedure shows good incorporation of the osseous portion of the graft, but incomplete incorporation of the cartilage. Repeat arthroscopy was done because of impingement symptoms, which resolved after surgery.

Special Populations Skeletally Immature Patients The literature concerning the treatment of OLT in skel etally immature patients is scarce, and treatment recom mendations usually are based on the Berndt and Harty classification: nonoperative treatment for stages I and II and medial stage III lesions and operative treatment for lateral stage III and stage IV lesions. Higuera and associ ates71 reported excellent or good results in 18 of 19 patients, and Kumai and colleagues45 reported good results in 10 of 11 with nonoperative treatment. In the series of Letts and associates,72 13 of 24 children initially treated non operatively required operative treatment. More recently, Perumal and associates73 concluded that few OLTs in skeletally immature patients heal with 6 months of nonop erative treatment. In their 31 patients (mean age 12 years), after 6 months of nonoperative treatment only 5 (16%) had complete clinical and radiographic healing, 24 (77%) had persistent lesions on radiographs, and 2 had severe pain. Of the 13 who subsequently had operative treatment, 11 healed clinically and radiographically within 12 months; the other 2 had persistent lesions on radiographs but no clinical symptoms. In their compilation of the literature reporting operative treatment of OLT in 48 children, Letts and colleagues72 found excellent or good results in 34 (71%), fair results in 12 (25%), and poor results in 2 (4%). In the only comparison of outcomes of surgery for OLT in adults and adolescents, Bruns and Rosenbach74 found that adolescents had better long-term outcomes than adults, regardless of the severity of the lesion.

High-Level Athletes Although a number of treatment methods have been shown to be successful in treating OLT in young, active patients, the ability to return to high-level athletic activ ity has not been well-documented. Saxena and Eakin,62 in a series of 44 athletic patients with 46 OLTs, treated

Osteochondral lesions of the distal tibia are much less com mon than those of the talus, and there is little informa tion in the literature about their etiology, natural history, or treatment. It appears that they, like talar lesions, are primarily caused by trauma. “Mirror image” or “kissing” lesions of the talus and distal tibia have been described.75 In one of the largest series of osteochondral lesions of the distal tibia,76 11 of 17 patients recalled an inversion injury to the ankle. Symptoms may include pain, stiffness, swelling, locking, and instability. Radiographs usually are not help ful, but MRI and CT can identify the lesion (Fig. 25I-10). Treatment is similar to that of osteochondral lesions of the talus: débridement and curettage of the lesion, abrasion of the defect to subchondral bone, and drilling or micro fracture of the subchondral bone. Mologne and Ferkel76 reported excellent or good results in 14 of 17 patients an average of 44 months after débridement, curettage, abra sion, and drilling or microfracture. If this is unsuccessful, a retrograde osteochondral autograft or allograft trans fer procedure can be done77,78; instrumentation has been developed to make this easier.

OTHER LESIONS THAT CAN MIMIC ANKLE SPRAINS Injuries of the ligaments around the ankle joint are com mon in athletic individuals, accounting for the highest percentage of injuries in epidemiologic studies of sports injuries,79-83 regardless of the sport, level of participation, or age or sex of the participants. Usually, these injuries are diagnosed promptly and treated appropriately; however, continued ankle pain or instability should raise suspicion of some other entity. Conditions that can be misdiagnosed as ankle sprains include fractures, neoplasms, impingement syndromes, and coalitions of the tarsal bones. Delayed or incorrect diagnosis can result in prolonged disability.

Fractures of the Talus and Calcaneus Fractures of the talar and calcaneal processes can be mis taken for ankle sprains (Table 25I-5). Misdiagnosis or delayed diagnosis of these injuries can lead to nonunion, which can cause ankle pain that limits athletic activity. Missed lateral talar process fractures were found in about 1% of 1500 patients initially diagnosed with lateral ankle sprains84; in a series of 25 anterior calcaneal process frac tures, 7 (28%) were initially diagnosed as anterior talo fibular ligament sprains.85 In 20 patients with avulsion


A

C

B

Figure 25I-10 Osteochondral lesion of the distal tibia in a female collegiate basketball player. A, Coronal fat-suppressed magnetic resonance imaging. B, Axial computed tomography (CT) shows posterior-central lesion and small subchondral cysts. C, Sagittal CT shows depth of the defect. (From Mologne TS, Ferkel RD: Arthroscopic treatment of osteochondral lesions of the distal tibia. Foot Ankle Int 28:865-872, 2007.)

fractures of the posterior talus that were all initially diag nosed as ankle sprains, the average number of physician visits before correct diagnosis was about 6, and 1 patient was seen 17 times.86 Clark and coworkers87 reviewed ankle radiographs of 1153 patients with acute ankle trauma and determined that an ankle effusion of 13 mm or more had a positive predictive value of 82% for occult fracture.

Relevant Anatomy and Biomechanics The lateral talar process is an osseous protuberance that articulates superolaterally with the fibula and helps to stabilize the ankle mortise. Inferomedially, it articulates with the calcaneus to form the lateral portion of the sub talar joint. The posterior process of the talus is made up of the lateral and medial tubercles. The lateral tubercle is the larger of the two and serves as the attachment of the posterior talocalcaneal and posterior talofibular ligaments. The posterior third of the deltoid ligament attaches on the medial tubercle. The undersurface of both tubercles

forms the posterior fourth of the subtalar joint. An acces sory bone, the os trigonum, often is present posterior to the lateral tubercle and can be confused with a fracture of the lateral tubercle. Fractures of the lateral tubercle of the posterior process can be caused by hyper–plantar flexion or inversion, whereas those of the medial tubercle usually are caused by dorsiflexion and pronation injuries because the medial tubercle is avulsed by the deltoid ligament.

Evaluation and Classification Most fractures of the talar and calcaneal processes result in pain, tenderness, or swelling in specific locations (see Table 25I-5) that help distinguish them from ankle sprains and from each other. Patients with fractures of the anterior calcaneal process usually report a sudden twist of the ankle with immedi ate pain on the outer aspect of the midportion of the foot and discomfort with weight-bearing. Pain and tenderness are located in the region of the sinus tarsi, with maximal

TABLE 25I-5 Talar and Calcaneal Process Fractures That Can Mimic Ankle Sprains Fracture

Mechanism


Radiograph

Lateral talar process

Inversion + dorsiflexion

Mortise view Lateral view

Posterior talar process (lateral tubercle)

Hyper–plantar flexion (compression fracture) or inversion (avulsion fracture)

Posterior talar process (medial tubercle)

Dorsiflexion, pronation

Anterior calcaneal process

Inversion + plantar flexion (avulsion fracture); dorsiflexion (compression fracture)

Point tenderness anterior and inferior to lateral malleolus (over lateral process); pain with plantar flexion, dorsiflexion, subtalar joint motion Tenderness to deep palpation anterior to Achilles tendon, over posterolateral talus; plantar flexion may produce pain; swelling in posterolateral ankle Tenderness to deep palpation between medial malleolus and Achilles tendon; swelling posterior to medial malleolus and anterior to Achilles tendon Point tenderness over calcaneocuboid joint (about 1 cm inferior and 3 to 4 cm anterior to lateral malleolus)

Lateral view

Oblique view (foot in 40 degrees of external rotation) Lateral view Lateral oblique view

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TABLE 25I-6 Classification of Calcaneal Anterior and Lateral Talar Process Fractures

Classification of Calcaneal Anterior Process Fractures

Type I Type II Type III

Nondisplaced tip avulsion Displaced avulsion fracture not involving the calcaneocuboid articulation Displaced, larger fragments involving the calcaneocuboid joint

Classification of Lateral Talar Process Fractures

Type A Type B Type C

Small, minimally displaced, extra-articular avulsion Medium-sized fracture involving only the talocalcaneal articular surface Larger fracture involving both talocalcaneal and talofibular articulations

tenderness 2 cm anterior and 1 cm inferior to the anterior talofibular ligament, which helps distinguish this lesion from a lateral ankle sprain. Avulsion fractures of the ante rior calcaneal process are best seen on a lateral oblique projection, whereas compression fractures are best seen on a lateral view of the hindfoot. Anterior calcaneal process fractures often are associated with other ankle pathology, including tarsal coalitions, ankle sprains, and bifurcate lig ament abnormalities. In a review of 1479 foot and ankle MRI studies, Petrover and associates88 found 15 fractures of the anterior process (1%), only 2 of which had no associ ated abnormality. Fractures of the anterior calcaneal proc ess generally are classified according to displacement and involvement of the calcaneocuboid joint (Table 25I-6).85 Fractures of the posterior process of the talus most often involve the lateral tubercle (Fig. 25I-11). Lateral tubercle factures can be caused by hyper–plantar flexion (compres sion) or inversion (avulsion) and have been associated with football and rugby kicking, which places the ankle in a forced plantar flexed position. Pain may be exacerbated by plantar flexion or, because of the proximity of the flexor hal lucis longus tendon, by dorsiflexion of the hallux. In almost

50% of ankles, the os trigonum (fused or separate) is just posterior to the lateral tubercle of the posterior talar proc ess and may be mistaken for a fracture. Differentiation of a fracture of the lateral tubercle from a nonunited second ary ossification center is best made on a lateral radiograph. An acute fracture is suggested by a rough, irregular corti cal surface along the line of separation, whereas a normal os trigonum has a smooth and rounded cortical surface. These fractures also can be classified according to size, dis placement, and joint involvement (see Table 25I-6). Fractures of the medial tubercle generally are caused by dorsiflexion-pronation injuries that cause avulsion of the medial tubercle by the deltoid ligament. They usually result in a tender, firm mass posterior to the medial mal leolus, with no ankle instability or limitation of motion. These fractures are difficult to see on routine radiographs, and CT or MRI may be necessary to confirm the diagnosis. Ebraheim and colleagues,89 in a cadaver study, determined that the 30-degree external rotation view of the ankle is most likely to show this injury. Fractures of the entire posterior process (both tubercles) have been described but are rare. Fractures of the lateral talar process, the “snowboarder’s fracture,” are relatively infrequent but should be suspected in patients who complain of lateral ankle pain after an inversion or dorsiflexion injury. From 33% to 41% of these injuries are missed on initial examination.84,90-92 Point tenderness over the lateral talar process should prompt CT evaluation. Von Knoch and associates93 found that 14 of 16 displaced or unstable lateral process fractures were associated with severe concomitant hindfoot injuries. A morphologic classification of these fractures has been described94: type I, chip fracture; type II, large fragment; type III, comminuted.

Treatment Nonoperative treatment generally is sufficient for acute process and tubercle fractures with small (2 mm) fragments with significant articular involvement.90,91 Valderrabano and colleagues97 developed a treatment algorithm based on the fracture type (McCrory-Bladin94 classification) (Fig. 25I-12). Operative treatment may con sist of open reduction and internal fixation of large frag ments, primary excision of severely comminuted fractures, or delayed excision of chronic nonunions.


Figure 25I-11 Lateral radiograph shows fracture of the lateral tubercle of the posterior talar process (arrow). (From Judd DB, Kim DH: Foot fractures frequently misdiagnosed as ankle sprains. Am Fam Physician 66:785-794, 2002.)

Because of the relatively infrequent occurrence of these process and tubercle fractures, there is little evidence in the literature on which to base treatment recommendations. Most studies include only a small number of patients or are isolated case reports. In one of the larger series of ante rior calcaneal process fractures (25 fractures), all 18 treated

2156 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Fracture Type McCrory-Bladin Classification

Fracture Displacement

Type I Chip

Type II Large Fragment

Type III Comminuted

Primary Therapy

Secondary Therapy (if necessary)

Nonoperative Nondisplaced ORIF

Débridement

Displaced Débridement

Figure 25I-12 Treatment algorithm for fractures of the lateral talar process. (Redrawn from Valderrabano V, Perren T, Ryf C, et al: Snowboarder’s talus fracture: Treatment outcome of 20 cases after 3.5 years. Am J Sports Med 33:871-880, 2005.)

nonoperatively had good results, whereas 5 of 7 treated with excision had good results.85 The worst outcomes were in patients with the longest delays in diagnosis and treatment. Medial talar process fractures generally are reported to do well with nonoperative treatment, if diagnosed and treated promptly.98,99 Although Giuffrida and colleagues100 reported that five of six medial process fractures required arthrodesis after nonoperative treatment, the fractures in their series were all associated with high-energy medial subtalar dislocations. Lateral talar process fractures appear to do less well with nonoperative treatment. In a series of 23 lateral talar process fractures in snowboarders,93 7 minimally displaced fractures were treated nonoperatively, and 16 displaced or unstable fractures were treated with open reduction and internal fixation. Fifteen of the patients (10 treated opera tively and 5 treated nonoperatively) regained their prein jury levels of athletic activity. The 6 operatively treated patients who failed to regain preinjury participation levels all had severe associated injuries of the ankle or hindfoot. At 3.5-year follow-up of 20 lateral talar process fractures,97 the AOFAS scores were higher in the 14 treated with open reduction and internal fixation (ORIF) (97 points) than in the 6 treated nonoperatively (85 points); all 14 patients treated with ORIF regained their preinjury levels of sport, whereas only 2 of the 6 treated nonoperatively did so.

Authors’ Preferred Method Most fractures of the calcaneus and talus that mimic an kle sprains heal with cast immobilization, and this is our preferred treatment unless displacement or comminution is severe or the fracture fragment is large. ORIF is indicat ed for noncomminuted, displaced fractures because large, displaced, articular fragments, if unreduced, have a high risk for nonunion. For displaced intra-articular process and tubercle fractures, especially those of the lateral talar process, that are too comminuted for internal fixation, pri mary excision allows early mobilization without the risk for painful nonunion.

Postoperative Prescription, Outcomes Measurements, and Potential Complications A short leg walking cast is applied over a compression dressing after ORIF and worn for 3 weeks, after which the dressing is removed, and a weight-bearing cast or brace is worn for another 3 weeks. After primary excision, immobi lization usually consists of 2 to 3 weeks in a weight-bearing cast or removable boot. Full weight-bearing is allowed when radiographic healing of the fracture is evident. Phys ical therapy is instituted for muscular strengthening, pro prioception, balance, and sport-specific functions. The primary clinical outcome measures are pain relief, joint motion, and return to activity. The AOFAS hindfoot score can be used for functional evaluation. Radiographs or CT scans evaluate healing. The most frequent complications after process and tubercle fractures of the hindfoot are chronic pain and the development of arthritis. Symptomatic nonunion is likely if these fractures are not diagnosed and treated promptly. Late excision of the un-united fragment can improve symp toms,96,101-103 but results appear to deteriorate the longer the interval between nonunion and excision.85,101

Criteria for Return to Play Return to play depends on both the fracture and the ath lete. Motivated athletes generally can return to sports when fracture healing is documented and normal strength and motion have been regained. A range of motion equal to the uninjured ankle and 85% of contralateral strength should be obtained before returning to sport.

Impingement Syndromes The term ankle impingement encompasses a wide variety of soft tissue and bony conditions around the ankle that can cause chronic pain and decreased motion and limit athletic activity. Various forms of mechanical impingement can be caused by synovial proliferation, bone spur formation, or ligamentous scarring and hypertrophy. Impingement gen erally is described as anterolateral, anterior, or posterior. Combined anterior and posterior impingement also has been described.104

Foot and Ankle 2157

A

B

Figure 25I-13 Anterior impingement syndrome. A, Magnetic resonance image shows osteophyte on distal tibia. B, Radiograph after excision of osteophyte. (From Richardson DR: Ankle injuries. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Evaluation Anterior impingement probably is the most common of the impingement syndromes and occurs most often in bal let dancers and football, basketball, and soccer players. The first symptom is pain that begins as a vague discomfort and becomes sharper and more localized to the front of the ankle and usually is exacerbated by cutting or pivoting maneuvers. Physical examination finds tenderness between the anterior tibial tendon and the medial malleolus, which is exacerbated with dorsiflexion and relieved with plantar flexion. With the ankle plantar flexed, exostoses can be pal pated on the superior surface of the talar neck. Imaging studies show a beak-like prominence at the anterior rim of the tibial plafond, usually associated with a corresponding area of the opposed margin of the talus proximal to the talar neck, within the anterior ankle joint capsule (Fig. 25I-13). These osteophytes can impinge on each other, and soft tissues can become entrapped between them. Anterior impingement has been classified into four grades to indi cate severity (Fig. 25I-14).105 Two distinctive impingement lesions in the anterior talus have been described: a localized “divot” that accepts the growing tibial spur during dorsi flexion, prevents the formation of an osteophyte on the anterior talar neck, and allows unimpeded dorsiflexion106; and a “tram track” lesion, formed when a prominent osteo phyte carves a longitudinal trough in the articular surface of the talar dome.107 Anterolateral impingement is believed to be caused by relatively minor inversion injuries of the ankle and to occur after about 3% of ankle sprains.108 Tearing of the anterolateral soft tissues and ligaments, without substan tial associated mechanical instability, followed by repeated microtrauma can result in hypertrophy of the synovial tissue and fibrosis in the anterolateral ankle gutter, causing pain and mechanical impingement. Several studies109-113 have suggested that a contributing factor may be hypertrophy of an accessory fascicle of the anterior tibiofibular ligament (Bassett ligament) (Fig. 25I-15). Most patients complain of chronic vague pain over the anterolateral ankle, exacerbated by cutting or pivoting maneuvers, and physical examina tion identifies tenderness along the lateral gutter and the anterior tibiofibular ligament. Maximal dorsiflexion and deep palpation to the anterolateral corner of the ankle joint

reproduces the pain. The “charger” stance, with the patient bearing weight, flexing the knee, and keeping the heel flat on the ground (Fig. 25I-16), also produces pain in this cor ner of the ankle.114 Impaired proprioception also has been identified in patients with anterolateral impingement. Anteromedial impingement is an uncommon cause of chronic ankle pain that also is associated with an inversion mechanism that injures the lateral and medial ankle liga ments. A meniscoid lesion or a thickened anterior tibio talar portion of the deltoid ligament may impinge on the

A

B

C

D

Figure 25I-14 Classification of anterior impingement. A, Grade I: synovial impingement, spur ≤3 mm. B, Grade II: osteochondral reaction exostosis, spur >3 mm. C, Grade III: severe exostosis with or without fragmentation, secondary spur on talus. D, Grade IV: pantalocrural osteoarthrotic destruction. (Redrawn from Ferkel RD, Scranton PE: Current concepts review: Arthroscopy of the ankle and foot. J Bone Joint Surg Am 75: 1233-1242, 1993.)


Anterior inferior tibiofibular ligament

Distal fascicle

Calcaneofibular ligament Anterior talofibular ligament

A

B

Figure 25I-15 A, Distal fascicle of the anterior inferior tibiofibular ligament is parallel and distal to the anterior tibiofibular ligament proper and is separated from it by a fibrofatty septum. B, With dorsiflexion of the ankle, the distal fascicle may impinge on the anterolateral aspect of the talus. (From Bassett FH 3rd, Gates HS 3rd, Billys JB, et al: Talar impingement by the anteroinferior tibiofibular ligament. J Bone Joint Surg Am 72:55-59, 1990.)

anteromedial corner of the talus during dorsiflexion of the ankle, resulting in osteophyte formation or a chondral lesion, or both. Posterior impingement has been described as os trigo num syndrome, talar compression syndrome, and posterior block of the ankle and has been extensively described in ballet dancers as well as in gymnasts, soccer players, and down-hill runners.110,111,115,116 The mechanism of injury has been compared with a nutcracker because the posterior talus and surrounding soft tissues are compressed between the tibia and the calcaneus during plantar flexion of the foot.117 Bony causes of posterior impingement include the os trigonum (an accessory ossicle of the lateral talar tuber cle that persists in as many as 7% of adults), the Stieda process (an elongated lateral talar tubercle), a prominent posterior calcaneal process, and loose bodies (Table 25I-7). Soft tissue factors can include synovitis of the flexor hallucis longus tendon sheath, the posterior synovial recess of the subtalar and tibiotalar joints, and the posterior intermal leolar ligament. Pain is worse with forced plantar flexion and with push-off maneuvers. Posteromedial impingement occurs after severe ankle inversion injury that damages the deep posterior fibers of the medial deltoid ligament. Chronic inflammation and hypertrophy of the ligament result in fibrotic scar tissue that can be trapped between the medial wall of the talus and the posterior margin of the medial malleolus. Figure 25I-16 “Charger” stance causes pain in the anterolateral corner of the ankle in patients with anterolateral impingement. (From Hyer CF, Buchanan MM, Philbin TM, et al: Ankle arthroscopy. In ElAttrache NS, Harner CD, Mirzayan R, Sekiya JK [eds]: Surgical Techniques in Sports Medicine. Philadelphia, Lippincott Williams & Wilkins, 2007.)

Treatment Options: Weighing the Evidence Initial treatment of any impingement lesion should be nonoperative, including restriction of activity, orthoses, nonsteroidal anti-inflammatory drugs (NSAIDs), and

Foot and Ankle 2159

TABLE 25I-7 Etiology of Posterior Ankle Impingement Syndrome Pathology

Example

Trigonal process Synchondrosis injury True compression Flexor hallucis longus dysfunction Tibiotalar pathology

Fracture (acute or chronic)

Osteochondritis Fracture Subtalar pathology Arthritis Other Prominent calcaneus posterior process Combined

Tenosynovitis Posterior capsuloligamentous injury Osteochondritis Calcified inflammatory tissue Flexor hallucis longus tenosynovitis and synchondrosis injury

From Maquirriain J: Posterior ankle impingement syndrome. J Am Acad Orthop Surg 13:365-371, 2005.

possibly cortisone injection. If nonoperative methods are unsuccessful at relieving pain and mechanical symptoms, arthroscopic débridement of soft tissue lesions or excision of bony lesions, or both, is successful in most patients. In two of the larger series of anterolateral lesions,118,119 includ ing 64 lesions, 58 (91%) had excellent or good results, 4 had fair results, and 2 had poor results after arthroscopic treatment. At a mean follow-up of 6 years after arthros copy, 40 (70%) of 57 patients with anterior lesions had resumed sports, 21 of them playing soccer.120 Results were good in all patients who had no preoperative osteoarthritis (OA), in 73% of those with grade I OA, and in only 29% of ankles with grade II OA. Posterior arthroscopy also can be used for excision of an os trigonum, tenolysis, loose body removal, spur excision, and débridement of OLT.121 Two studies each reported that 14 of 15 patients returned to their preinjury levels of sports after posterior arthros copy.121,122 Henderson and La Valette104 described anterior arthroscopic and open posterior treatment for com bined anterior and posterior impingement in 62 patients; 47 (81%) had excellent or good outcomes, 9 (15.5%) had fair outcomes, and 2 (3.5%) had poor outcomes.

Authors’ Preferred Method If nonoperative measures do not relieve symptoms, arthros copy is indicated for excision, débridement, decompression, or synovectomy. Large exostoses may require open arthrot omy for excision. Arthroscopic treatment of ankle impingement begins with a careful inspection of all structures that may be con tributing factors (Table 25I-8). Standard anteromedial and anterolateral ankle portals are used (Fig. 25I-17). Technique of Arthroscopic Treatment of Ankle Impingement

• With the patient under general anesthesia, apply and in flate a thigh tourniquet. • Insert a needle just medial to the anterior tibial tendon and distend the ankle joint with 15 to 20 mL of saline.

TABLE 25I-8 Ankle Impingement Syndromes: Arthroscopic Examination Medial Portal

Lateral Portal

Medial gutter Medial malleolus Deep fibers of deltoid ligament

Lateral gutter Lateral malleolus Anteroinferior talofibular ligament Anterior joint line, anterior tibia Talar dome Medial malleolus Medial gutter

Anterior joint line, anterior tibia Talar dome Tibiofibular joint, ligaments Lateral gutter

From Hyer CF, Buchanan MM, Philbin TM, et al: Ankle arthroscopy. In ElAttrache NS, Harner CD, Mirzayan R, Sekiya JK (eds): Surgical Techniques in Sports Medicine. Philadelphia, Lippincott Williams & Wilkins, 2007.

• Make a small longitudinal incision to allow insertion of a

2.7-mm or 4.0-mm, 30-degree angle arthroscope through an anteromedial portal just medial to the anterior tibial tendon. Take care to pass the arthroscope across the an terior aspect of the joint and not across the dome of the talus. • Make a separate anterolateral portal just lateral to the peroneus tertius tendon to allow inflow and outflow of saline. Be aware of the superficial peroneal nerve in this area. Instruments and the arthroscope can be switched to either portal as necessary. • Fully examine the ankle with the use of a noninvasive ankle distraction device as necessary (see Fig. 25I-6). Distraction may need to be removed to identify and gain access to large anterior osteophytes, especially on the talus, because distraction may cause the anterior capsule to tighten. • Use a pressure irrigation system with a 3.5-mm full-radius resector to clear the anterior synovium and define the an terior tibial and superior talar bony spurs. • Use a 3-mm bur to remove the spurs, resecting them back to the level of normal cartilage. • Smooth off the tibial surface with a 3.5-mm full-radius resector. • Carry out a similar procedure on the superior neck of the talus. • Again, examine the whole ankle by passing the arthroscope gently over the dome of the talus. This can be accom plished with the use of manual distraction in mid–plantar flexion or with a commercially available noninvasive ankle distraction device. • After irrigation, place 20 mL of 0.25% bupivacaine into the joint, suture the incision, and apply a compression dressing. Continued



A

B

Figure 25I-17 Ankle arthroscopy portals. A, Anteromedial portal site. B, Anterolateral portal site. (From Phillips BB: Arthroscopy of the lower extremity. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

If synovitis is found, typically along the anterior joint line and in the medial and lateral ankle gutters, an arthro scopic resector is used to remove the hypertrophic synovitis. Débridement begins in the medial gutter, then the anterior joint line, and finally the lateral gutter. Switching portals is necessary for complete débridement. Hypertrophy of the anterior tibiofibular ligament, which appears as a whitish, thick, scar-like lesion, is resected and débrided. For anterior bony impingement, the anterior ankle cap sule is carefully reflected and elevated superiorly off the anterior tibia and inferiorly off the talar neck. An arthro scopic bur is used to remove the exostoses on the tibia and talus. It is important to make sure the bur is facing bone to avoid damage to the soft tissues, especially the anterior neu rovascular bundle. A trough can be made with a 3-mm bur about 1 mm proximal and parallel to the anterior edge of the tibia. This trough is taken down to subchondral bone to the level of surrounding normal cartilage, and an arthroscopic bone biter is used to remove the bony spur. This allows more control of the bur with less risk for damage to the articular surface than may occur with an arthroscopic shaver.123 If the exostoses are large, open excision may be preferable through an anteromedial incision and arthrotomy. Tibial osteophytes typically are located laterally and the talar osteophytes medi ally. They can be easily removed with an osteotome. Posterior synovectomy can be done arthroscopically through a posterolateral portal (Fig. 25I-18). For excision of posterior bony impingement, we usually prefer an open, pos terolateral approach. The interval between the Achilles ten don and peroneal tendons is developed, with care to protect the sural nerve. The os trigonum is removed with subperio steal dissection. The lateral tubercle of the posterior process

of the talus (Stieda process) is removed with a curved oste otome or rongeur to ensure that the posterior talar surface is flush with the posterior tibial surface. If decompression of the flexor hallucis longus is indicated, a posteromedial approach can be developed along the tarsal tunnel.

Figure 25I-18 Posterior portal site for ankle arthroscopy. (From Phillips BB: Arthroscopy of the lower extremity. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Foot and Ankle 2161

Figure 25I-19 CT shows medial facet tarsal coalition of talus and calcaneus.

Postoperative Prescription, Potential Complications, and Criteria for Return to Play After ankle arthroscopy, weight-bearing to tolerance, with or without crutches, usually is allowed the first week after sur gery. Then a progressive program of strengthening, range of motion, and functional agility is begun. Generally, return to competitive sports is possible by about 6 weeks after surgery when the patient is pain free and range of motion and strength are comparable to the unaffected ankle. The most frequent complication of ankle arthroscopy is temporary numbness or tenderness at a portal site caused by local nerve dam age. Osteophytes may recur, especially in athletes who have recurrent supination trauma or repeated forceful dorsiflexion of the ankle, but these are not always symptomatic.120

Tarsal Coalition Particularly in children and adolescents, there is an asso ciation between frequent ankle sprains and tarsal coalitions, including fibrous (syndesmosis), cartilaginous (synchondro sis), and bony (synostosis) coalitions. Although the frequency of tarsal coalition has long been estimated at 1%, more recent information indicates a frequency of 11%, possibly because of

A

Figure 25I-21 Pigmented villonodular synovitis eroding into superior portion of the talar neck caused symptoms of ankle sprain in young athlete.

more frequent identification by MRI.124 Patients may com plain of mild deep pain and limited range of motion, usually after a traumatic ankle sprain that “just never seems to get better.” Often symptoms are relieved by rest and aggravated by prolonged or heavy activity, suggestive of ankle ligament injury.125 Radiographs or CT scans can confirm the diagnosis (Fig. 25I-19). If nonoperative measures, such as bracing or casting and NSAIDs, fail to relieve symptoms, open or arthroscopic excision of the coalition is indicated.126 After coalition excision, a removable boot usually is worn for about 6 weeks, and strengthening and flexibility exercises are done.

Neoplasms Neoplasms such as osteoid osteoma, eosinophilic granu loma (Fig. 25I-20), and pigmented villonodular synovitis (Fig. 25I-21) can mimic ankle sprain. Neoplasms of the ankle can mimic a number of ankle conditions, including chronic sprains, anterior impingement, stress fracture, osteomyelitis, and osteonecrosis. Appropriate treatment of these lesions often is delayed because of misdiagnosis; one

B

Figure 25I-20 Eosinophilic granuloma may cause symptoms of ankle sprain. A, Lesion in head and neck of talus. B, After excision and bone grafting.


study reported a 2.5-year delay in the diagnosis of osteoid osteomas in five patients,127 and another reported a delay of more than 3 years in one patient.128 A typical feature of osteoid osteoma is pain that worsens at night and is relieved by aspirin, but this may not be present in all patients with osteoid osteomas. Treatment of osteoid osteomas usually is en bloc excision or curettage of the nidus. Successful arthroscopic treatment of osteoid osteomas of the ankle has been described,128-131 which allows an earlier return to activ ity (2 to 3 months after surgery) than open procedures.

OTHER APOPHYSITIS, OSTEOCHONDRITIS, AND DEVELOPMENTAL ANOMALIES OF THE FOOT THAT CAN CAUSE DISABILITY IN ATHLETES Calcaneal Apophysitis (Sever Disease) First described by J. W. Sever132 in 1912, calcaneal apophy sitis (Sever disease) is a common cause of heel pain, espe cially during running, that most often occurs in children who are engaged in activities such as basketball and soccer. The calcaneal apophysis appears as an independent center of ossification in boys aged 9 to10 years and ossifies around the age of 17 years; in girls, this occurs earlier. The average age at presentation is 11 years in boys and 8 years in girls. Sever disease is 2 to 3 times more common in boys, and 60% of patients have bilateral involvement. Aptly described by Sever as an “inflammation of the calcaneal apophysis result ing in the clinical symptoms of pain at the posterior heel, mild swelling, and difficulty with walking,” the condition often causes a child to walk with an antalgic gait. The heel pad and posterior aspect of the heel are tender, but swelling usually is minimal. Pain is located at the most distal portion of the heel pad and along the posterior aspect of the heel up to the most distal portion of the Achilles tendon. The heel cord itself is not especially tight. Ogden and associates133 suggested that this entity should be called Sever injury rather than Sever disease because MRI evidence indicated that the true pathogenesis is a stress microfracture related to chronic repetitive microtrauma. The stress microfractures were found in the metaphysis of the body of the calcaneus adjacent to, but not directly involving, the apophysis. Radiographs are not essential to the diagnosis but can rule out other conditions, such as fracture, infection, or neoplasm. They may show a sclerotic and fragmented calcaneal apophysitis (Fig. 25I-22), but the radiographic appearance usually is normal. The necessity of curtailing the activity that incites pain is controversial. Because they consider this condition a chronic, repetitive injury to metaphyseal bone, some have suggested that temporary discontinuation of the activity is essential. Most patients are able to return to normal sports activity after 2 months of rest; in only the most severe cases is immobili zation necessary.134,135 Conversely, Weiner and associates136 reviewed the records of 227 patients with Sever disease and concluded that activity restriction is unnecessary; they recom mended an in-shoe orthosis, no limits on physical activity, with 4 to 6 weeks of casting for persistent symptoms.

Figure 25I-22 Increased sclerosis and fragmentation of calcaneal apophysis (Sever disease).

Osteochondrosis of the Tarsal Navicular (Köhler Disease) First described by Köhler137 in 1908, osteochondrosis of the tarsal navicular is a relatively uncommon cause of pain and limp in children. Like Sever disease, boys are more commonly affected than girls; however, the age of onset is younger, 5 years in boys and 4 years in girls. Thirty-three percent of patients have bilateral involvement. Tenderness in the area of the tarsal navicular is the most consistent phys ical finding. The radiographic findings are variable degrees of sclerosis, flattening, and irregular rarefaction of the navic ular (Alka-Seltzer-on-end appearance) (Fig. 25I-23). Loss of the trabecular pattern and fragmentation also are common. Other bones of the foot usually are normal. Köhler dis ease is self-limiting, and the final outcome is not affected by treatment. Short-leg walking cast immobilization for 6 to 8 weeks has been reported to result in faster resolution of symptoms than conservative treatment.138

Accessory Navicular The accessory navicular is a separate ossification center for the tuberosity of the navicular that is present in about 14% of all feet, but most of these are asymptomatic and even tually fuse with the navicular.139,140 In some individuals, however, the accessory navicular can be a source of medial foot pain. The accessory navicular may exist as a separate ossicle within the posterior tibial tendon (type I), may form a synchondrosis with the navicular (type II), or may fuse with the navicular and create a cornuate navicular (type III) (Fig. 25I-24). Often the posterior tibial tendon inserts onto the accessory navicular instead of onto the tuberosity of the navicular, which has been suggested to alter the pull of the tendon and cause a flatfoot deformity. Symptoms are most common when the accessory navicular forms a synchon drosis with the navicular (type II). Symptoms usually begin

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B

Figure 25I-23 A and B, Increased sclerosis and narrowing (Alka-Seltzer-on-end appearance) of the navicular (Köhler disease) in a young athlete with complaints of pain in the medial midfoot area.

A

A

D

B

C

Figure 25I-24 Accessory navicular. A and B, Type I. C and D, Type II. (Redrawn from MacNicol MJ, Voutsinas S: Surgical treatment of the symptomatic accessory navicular. J Bone Joint Surg Br 66:218-226, 1984.)


B

A

C

D

Figure 25I-25 A and B, Bilateral accessory navicular. Note “opening up” of metatarsal cuboid-cuneiform articulation, suggesting flattening of the longitudinal arch. C and D, Note sag at talonavicular joint in left foot (C) compared with right foot (D). (From Murphy GA: Pes planus. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

in adolescence and are made worse by activity and weightbearing. In adults, the onset of pain usually is acute after an eversion injury or other foot trauma. Pain is localized over the prominence of the accessory navicular and at the medial arch of the foot. A painful bursa may be present over the navicular prominence. Standard anteroposterior and lat eral views of the foot (Fig. 25I-25), along with a 45-degree eversion oblique view, usually are sufficient for diagnosis, but bone scanning and MRI can be helpful if the diag nosis is in question.141 Initial treatment of a symptomatic accessory navicular is nonoperative and directed at reliev ing pressure at the painful medial prominence and reduc ing inflammation. The classic operative treatment for an accessory navicular that does not respond to nonoperative measures is removal of the ossicle (Kidner procedure142), which generally gives good results.143,144 The benefits of

t ransposition of the posterior tibial tendon to the plantar aspect of the navicular are questionable.140,145-147 Percuta neous drilling of the accessory navicular to induce or accel erate fusion was reported to obtain excellent or good results in 30 of 31 feet.148 Percutaneous placement of one or two 3.5-mm or 4.0-mm cannulated screws across the synchon drosis has been recommended in athletes 14 to 30 years of age who have symptoms consistent with synchondrotic stress fracture.149 Malicky and associates150 described open fusion between the ossicle and navicular bone: after excision of the synchondrosis and the adjacent subchondral bone, one or two 2.7-mm or 3.5-mm lag screws are inserted to “arthodese” the bones together. They recommended this procedure in adults with large, painful accessory navicular bones because it leaves the posterior tibial tendon attach ment intact and provides a more reliable healing surface.

Authors’ Preferred Method Initial treatment is nonoperative and can include physi cal therapy aimed at controlling coexisting tendinitis and strengthening the posterior tibial tendon, molded orthoses, shoe modifications, and cast immobilization. If symptoms

persist, we prefer simple excision of the accessory navicu lar. It is important to excise enough of the prominence to create a surface that is flush with the medial border of the midfoot.

Foot and Ankle 2165


A

C

B Figure 25I-26 Excision of accessory navicular. A, Incision. B, Exposure of the posterior tibial tendon. C, Removal of accessory navicular. (From Murphy GA: Pes planus. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Technique of Excision of Accessory avicular N

• Beginning 1 to 1.5 cm inferior and distal to the tip of the medial malleolus, curve the skin incision slightly dorsal ward, peaking at the medial prominence of the accessory navicular and sloping distally to the base of the first meta tarsal (Fig. 25I-26A). • Ligate the plantar communicating branches of the saphe nous system and identify the posterior tibial tendon as it approaches the accessory navicular (see Fig. 25I-26B). • Identify the dorsal and plantar margins of the tendon 2 cm proximal to the accessory navicular, and expose

the tendon distally, ending at the bone. This exposes the entire tendon without disturbing the part extending plantarward toward its multiple insertions. • Use sharp dissection to shell the accessory navicular from the posterior tibial tendon (see Fig. 25I-26C). Return to Sport

After operative treatment, a short-leg cast is worn for 6 weeks. Range of motion exercises are begun after cast removal, and return to competition usually can be accomplished within 8 to 10 weeks.


Osteochondrosis of the Cuneiform Osteochondrosis of the cuneiform (Buschke disease) is rare, with few reports in the literature. Repetitive trauma with insult to the developing osseous tissue is believed to be responsible for this osteochondrosis, especially in the pronated foot in which continuous pressure is placed on the medial side of the foot and the medial cuneiform. Of the 19 patients described in the English literature, 18 were boys; 12 were 5 or 6 years old, and the youngest was 2 years old.151,152 Pain and limping usually are pres ent, but the lesion can be asymptomatic. Pain occasionally can be elicited by gentle pressure over the medial cunei form, and mild swelling rarely is present. Radiographs usu ally show a sclerotic, fragmented medial cuneiform (Fig. 25I-27). Osteochondrosis of the medial cuneiform has been associated with other tarsal bone lesions in most patients and is almost always bilateral. Treatment is nonoperative and includes control of the foot pronation and reduction of pain with rest and medial arch supports.

Osteochondrosis of the Metatarsal Head (Freiberg Disease) First described by Freiberg153 in 1914, osteochondrosis or osteonecrosis of the metatarsal head is most common in adolescent athletes who perform on their toes in either sprinting or jumping activities. It is more common in girls than in boys, making it the only osteochondrosis with a female predilection. The second, followed by the third, metatarsal head is most commonly involved. Fewer than 10% of patients have bilateral involvement. The patho genesis is unknown, but Gauthier and Elbaz154 found that patients with longer second metatarsals and excessive plantar pressure under the second metatarsal head had no significantly higher risk. These findings would appear to call into question mechanical stress being the sole or even the primary cause of Freiberg disease. The primary complaint often is a vague forefoot pain that is worsened by activity and weight-bearing and relieved with rest. The

Figure 25I-27 Increased sclerosis and fragmentation of the first cuneiform (Buschke disease) in a child who complained of pain in the medial midfoot area.

pain usually is worse at extremes of motion, with pain under and around the involved metatarsophalangeal joint. Palpation may identify swelling and slightly increased temperature. The initial process of pain and synovitis is followed by radiographic findings of sclerosis, resorption of the subchondral plate, fracture, collapse, and fragmen tation. Secondary degenerative changes and remodeling then occur in the flattened metatarsal head (Fig. 25I-28). Several staging systems have been developed to corre late physical and radiographic findings with treatment (Fig. 25I-29 and Table 25I-9), but their reliability is still unproved.

Treatment Options Initial treatment is nonoperative, including metatarsal relief pads, restriction of running and jumping activities, and occasionally a short-leg walking cast worn for 6 to 12 weeks until acute symptoms are resolved. A number of operative procedures have been described for persistent symptoms, including débridement, synovectomy, drilling, osteotomy, interpositional arthroplasty, and joint replacement. Dor sal wedge or dorsiflexion osteotomy (Fig. 25I-30) has been used successfully for all stages of the disease,154-157 although the range of motion of the MTP joint is decreased. More recent innovations include the use of absorbable pins for fixation of the osteotomy, which obviates the need for a second operation for implant removal; arthroscopic tech niques for synovectomy and drilling158,159; and osteochon dral plug transplantation.158,160 Carro and coworkers160 recommended an age-based approach to the treatment of Freiberg disease, beginning with arthroscopic synovectomy and débridement, followed by open or arthroscopic osteo chondral transplantation in late adolescence and adulthood, and an arthroscopic Keller procedure (with or without interpositional arthroplasty) for more severe involvement in late adulthood. However, in our experience, resection of the base of the proximal phalanx or the metatarsal head should be avoided to avoid transfer metatarsalgia or hallux valgus caused by instability of the second digit.

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A

B

A

B

C

D

C Figure 25I-28 Freiberg infarction. A and B, Note flattening of second metatarsal head. C, Note marrow edema of second metatarsal.

Authors’ Preferred Method Initial treatment is nonoperative, including restriction of sports activities and short-term cast-with-toe-plate immobilization. After acute symptoms resolve, metatarsal pads inserted proximal to the MTP joint are used during running and sports. Operative treatment is indicated for persistent symptoms. For adolescents and young adults, joint débridement and removal of loose bodies usually are sufficient, and return to sports generally is possible in 6 to 8 weeks. More extensive surgery (dorsiflexion or metatar sal shortening osteotomy) is reserved for older patients with late-stage involvement.

E Figure 25I-29 Levels of progression of Freiberg disease. A, Early fracture of subchondral epiphysis. B, Early collapse of dorsal central portion of metatarsal with flattening of articular surface. C, Further flattening of metatarsal head with continued collapse of central portion of articular surface with medial and lateral projections; plantar articular cartilage remains intact. D, Loose bodies form from fractures of lateral projections and separation of central articular fragment. E, End-stage degenerative arthrosis with marked flattening of the metatarsal head and joint space narrowing. (Redrawn from Katcherian DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69-81, 1994.)

Iselin Disease Iselin disease is a traction apophysitis of the base of the fifth metatarsal that occurs in late childhood or early adolescence at the time of the appearance of the proximal apophysis of the tuberosity of the fifth metatarsal.161 This secondary ossification center is a small, shell-shaped fleck of bone ori ented slightly obliquely with respect to the metatarsal shaft and located on the lateral plantar aspect of the tuberosity (Fig. 25I-31). It usually is not visible on anteroposterior or lateral radiographs but can be seen on an oblique view. Symptoms include tenderness over a prominent proximal fifth metatarsal and pain over the lateral aspect of the foot with weight-bearing. Participation in sports that require

2168 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25I-9 Staging and Classification Systems for Freiberg Disease Katcherian

Smillie

Gauthier/Elbaz

Thompson/Hamilton

Description

Radiographs

Level A

Stage I

Stage 0 + 1

Type 1

Level B

Stage II

Stage 2

Type 2

Radiographs normal; bone scan may detect Radiographs may show slight widening of joint, sclerosis of epiphysis, collapse and flattening of articular surface

Level C

Stage III

Stage 2

Type 2

Earliest form; fissure in epiphysis Progression of subchondral fracture with bone resorption; collapse of dorsal central portion of metatarsal head and alteration of articular surface Further deformation and collapse of central portion of head

Level D

Stage IV

Stage 3

Type 3

Level E

Stage V

Stage 4

Type 3

Fracture and separation of central portion and peripheral projections of involved metatarsal head resulting in loose bodies Advanced arthrosis secondary to progressive flattening and deformity of metatarsal head

Progressive flattening of metatarsal head with osteolysis and collapse; zone of rarefaction around sclerotic bone as healing and revascularization take place; premature physeal closure may be present Fragmentation of epiphysis, early joint narrowing, multiple loose bodies

Joint space narrowing, hypertrophy of metatarsal head, irregularity of base of proximal phalanx with osteophyte formation

MT, metatarsal. Modified from Katcherian DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69-81, 1994.

r unning, jumping, and cutting, which cause inversion stresses on the forefoot, is a common factor.162,163 The affected area over the tuberosity is larger than that on the noninvolved side, with soft tissue edema and local erythema. The area is tender to palpation at the insertion of the peroneus brevis, and resisted eversion and extreme plantar flexion and dor siflexion of the foot elicit pain. Oblique radiographs show enlargement of the apophysis and often fragmentation of

this secondary ossification center (Fig. 25I-32) and widen ing of the cartilaginous-osseous junction. Technetium-99m bone scanning shows increased uptake over the apophysis. Failure of the apophysis to fuse with the metatarsal (Fig. 25I-33) can cause symptoms into adulthood. Os vesalia num, a sesamoid in the peroneus brevis (Fig. 25I-34), must be distinguished from Iselin disease, and the nonunited apophysis should not be mistaken for a fracture.

Figure 25I-30 Dorsal closing wedge osteotomy and crosspinning for Freiberg infarction. (Redrawn from Chao KH, Lee CH, Lin LC: Surgery for symptomatic Freiberg’s disease: Extraarticular dorsal closing wedge osteotomy in 13 patients followed for 2 to 4 years. Acta Orthop Scand 70:483-486, 1999.)

Figure 25I-31 Fragmentation of secondary ossification center (Iselin disease) in a young athlete who complained of pain and swelling over the base of the fifth metatarsal.

Foot and Ankle 2169

Os vesalianum

Iselin disease

Figure 25I-32 Enlargement and fragment of epiphysis in Iselin disease. (From Canale ST: Osteochondrosis or epiphysitis and other miscellaneous affections. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Authors’ Preferred Method Treatment of Iselin disease is always nonoperative and in cludes limitation of activity, ice, and NSAIDs. If symptoms persist or are severe, a brief period of cast immobilization can be helpful. After resolution of acute symptoms, stretch ing exercises and range of motion exercises for the ankle and subtalar joints on a wobble board are initiated. Return to competition is allowed when discomfort is tolerable after activity. Plantar arch strapping or an arch support system placed in the shoe to elevate and relieve stress on the fifth metatarsal may allow athletic activity without pain.

Figure 25I-33 Nonunion of fifth metatarsal as a result of Iselin disease. (From Canale ST: Osteochondrosis or epiphysitis and other miscellaneous affections. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Figure 25I-34 Os vesalianum must be distinguished from Iselin disease. (From Canale ST: Osteochondrosis or epiphysitis and other miscellaneous affections. In Canale ST, Beaty JH [eds]: Campbell’s Operative Orthopaedics, 11th ed. Philadelphia, Elsevier, 2008.)

Osteochondritis of the Sesamoids Although small, seemingly insignificant bones of the foot, the sesamoids can cause disabling pain in an athlete. Galen, in 180 ad, named these small bones the sesamoids because of their resemblance to flat, oval sesame seeds. During the seventh or eighth week of embryonic develop ment, both sesamoid bones of the hallux appear as islands of undifferentiated connective tissue between the first metatarsal heads. The fibular (lateral) sesamoid is present slightly sooner than the tibial (medial) sesamoid. Ossifica tion begins at about 8 or 9 years of age in girls and 10 or 11 years of age in boys. There may be two or more centers of ossification, with the tibial sesamoid being bipartite at skeletal maturity in about 10% to 15% of the population; the fibular sesamoid rarely is bipartite.164-166 The two hal lucal sesamoids are embedded in the tendons of the short flexor of the hallux and are held together by the intersesa moid ligament and the plantar plate, which inserts on the base of the proximal phalanx of the hallux (Fig. 25I-35). The sesamoids function to absorb weight-bearing pressure, reduce friction, and protect tendons. They are important to the dynamic function of the hallux and act as a fulcrum to increase the mechanical force of the flexor hallucis bre vis tendon. The sesamoid complex normally transmits as much as 50% of body weight and during push-off may transmit loads of more than 300% of body weight.167 Osteochondritis of the hallucal sesamoids is most com mon in young women but has been reported in nearly all age and gender groups from adolescence through adult hood.164 Osteochondritis may occur as a primary patho logic entity or may be a late stage of repetitive stress injury involving osteonecrosis (Fig. 25I-36). Trauma is believed


Flexor brevis Abductor Anterior sesamoidal ligament

Medial sesamoid

Flexor hallucis longus

Figure 25I-35 Anatomy of the sesamoids. (Redrawn from Leventen EO: Sesamoid disorders and treatment: An update. Clin Orthop 269:236-240, 1991.)

to the most frequent cause, but osteonecrosis with sub sequent regeneration and excessive calcification may be present. The diagnosis of sesamoid injury constitutes a spectrum of abnormality rather than an isolated injury.165 Depending on the stage at which the patient is first seen, the diagnosis may range from bursitis over the tibial sesa moid to the vague entity sesamoiditis, which encompasses both osteochondrosis and osteochondritis. In later stages, the diagnosis may include stress fracture, traumatic or degenerative arthritis, and chondromalacia. Hematoge nous osteomyelitis of the sesamoid also should be included in the differential diagnosis, and sesamoid periostitis may occur in athletes with one of the rheumatoid variants, such as psoriasis, Reiter syndrome, and ankylosing spondylitis. Typically, patients have pain and tenderness to palpation over the involved sesamoid, without swelling or erythema that would indicate infection or bursitis. An axial radio graph or CT may show an enlarged or deformed sesamoid with irregular areas of increased bone density, mottling, and fragmentation.168 Comparison views of the opposite foot are helpful to distinguish a bipartite sesamoid from a fracture.

A

Authors’ Preferred Method Initial treatment is nonoperative, including NSAIDs, activity modification, and full-length shoe orthoses with a metatarsal pad and a relief beneath the first metatarsal pad. If no relief is obtained, a period of cast immobilization is tried. Persistent symptoms are an indication for sesamoid excision. Only the symptomatic sesamoid should be excised because of the likelihood of creating an intrinsic minus cock-up (hallux extensus) deformity with excision of both sesamoids. Even excision of a single sesamoid may result in hallux varus deformity, exacerbation of hallux valgus, or overload of the metatarsal head. Removal of both sesa moids results in about a 30% decrease in flexion strength of the hallux.169,170 Return to athletic activity usually is possible at 6 weeks after excision of one of the sesamoids; competitive sports are not allowed for 12 weeks after exci sion of both sesamoids.

B

Figure 25I-36 A, Osteochondrosis of the tibial (medial) sesamoid in a runner. B, Note fragmentation of sesamoid.

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r i t i c a l

P

S U G G E S T E D

o i n t s

l Important differences exist related to the mechanism of injury for medial and lateral talar dome lesions, and these must be recognized and considered in choosing treatment methods. l Most OLT, including posterior ones, can be treated arthroscopically, but accessory portals often are required. l The shorter the interval between the diagnosis of MRI stage II and IV OLT and operative treatment, the better the results. l OLT and fractures of the talar and calcaneal processes can be mistaken for ankle sprains and should be suspected when there is an inability to bear weight on the foot and ankle, severe swelling, or continued pain 3 to 4 weeks after “ankle sprain.” l Small, minimally displaced fractures of the talar and cal caneal processes usually can be successfully treated non operatively, but larger fragments (>1 cm) or displaced fragments (>2 mm) generally require open reduction and internal fixation. l Ankle impingement syndromes usually occur after an inver sion ankle injury or repetitive ankle flexion to extremes (e.g., sprinters, ballet dancers) and can be caused by bony lesions (i.e., osteophytes, os trigonum, Stieda process) or soft-tissue lesions (i.e., thickened ATFL [Basset ligament], deltoid ligament injury, tenosynovitis, meniscoid lesion). l Pain with palpation and dorsiflexion suggests anterior impingement (most common), whereas pain with forced plantar flexion is indicative of posterior impingement. l Initial treatment of ankle impingement is nonoperative; if symptoms persist, arthroscopic treatment (débridement, synovectomy, excision, decompression) is successful in 90% to 95% of patients. l Sever, Köhler, Buschke, Freiberg, and Iselin diseases; accessory navicular; and osteochondritis of the sesamoids are all relatively rare conditions that may be confused with traumatic injury; initial treatment is always nonoperative, which is successful in most patients.

R E A D I N G S

Baums MH, Heidrich G, Schultz W, et al: Autologous chondrocyte transplanta tion for treating cartilage defects of the talus. J Bone Joint Surg Am 88:303-308, 2006. Dedmond BT, Cory JW, McBryde A Jr: The hallucal sesamoid complex. J Am Acad Orthop Surg 14:745-753, 2006. Gobbi A, Francisco RA, Lubowitz JH, et al: Osteochondral lesions of the talus: Randomized controlled trial comparing chondroplasty, microfracture, and osteo chondral autograft transplantation. Arthroscopy 22:1085-1092, 2006. Hassan AH: Treatment of anterolateral impingements of the ankle joint by arthros copy. Knee Surg Sports Traumatol Arthrosc 15:1150-1154, 2007. Kopp FJ, Marcus RE: Clinical outcome of surgical treatment of the symptomatic accessory navicular. Foot Ankle Int 25:27-30, 2004. Kreuz PC, Steinwachs M, Erggelet C, et al: Mosaicplasty with autogenous talar autograft for osteochondral lesions of the talus after failed primary arthroscopic management: A prospective study with a 4-year follow-up. Am J Sports Med 34:55-63, 2006. Perumal V, Wall E, Babekir N: Juvenile osteochondritis of the talus. J Pediatr Orthop 27:821-825, 2007. Verhagen RA, Struijs PA, Bossuvt PM, van Dijk CN: Systematic review of treat ment strategies for osteochondral defects of the talar dome. Foot Ankle Clin 8:233-242, 2003. Watson AD: Ankle instability and impingement. Foot Ankle Clin 12:177-195, 2007.


S e c t i o n

J

Etiology of Injury to the Foot and Ankle Christopher B. Hirose, Thomas O. Clanton, and Robert M. Wood The etiology of injury to the foot and ankle is of utmost importance in sports medicine. The capacity to recognize the injury-causing conditions and the ability to control them may help prevent these same injuries. Research has shown that when etiologic factors are addressed, it is pos sible to decrease injury rates significantly.1-3 This chapter reviews predisposing conditions for injury of the foot and ankle and the variables that may have a protective value. The primary areas of importance are

(1) joint flexibility, (2) shoewear, and (3) the quality of the playing surface. Injury variables can be divided into intrinsic and extrin sic factors.4-6 Intrinsic factors include both an athlete’s indi vidual physical and personality characteristics. The physical characteristics include age, sex, genotype, somatotype, strength, speed, agility, coordination, fitness, flexibility, malalignment, muscle composition, previous injury, and residual structural inadequacies.4,5,7-35


Personality characteristics such as extroversion, anxiety level, conscientiousness, self-confidence, determination, responsiveness to coaching, discipline, dependency, sensi tivity, and others may play a role in whether an individual is injury prone.4,17,26,36-41 The contribution of these variables constitutes the individual athlete’s intrinsic risk for injury. Extrinsic factors include the kind of sports activity, the training methods, the knowledge and skill of the coach, the level of competition, the environmental conditions, the type of shoewear used, the playing surfaces, and the equip ment.4,5,8-10,18,22,26-28,32,42-58 There is, and always has been, an inherent risk for injury associated with athletic endeavors. The kind of athletic activity can further be separated into high, medium, or low risk for foot and ankle injuries (Box 25J-1).59-61 In addition, each sport poses a different risk to a particular body part. For example, running carries a low risk for shoulder injuries but a high risk for foot or knee injuries. Conversely, swim ming may pose a high risk for shoulder injuries but a low risk for foot and ankle injuries. Certain other variables play a role in the risk for injury, including playing time, level of competition, the movements required, equipment used, individual versus team play, the level of fitness, and the enforcement of the rules and regulations.60,62,63 Collins and colleagues examined athletes at 100 U.S. high schools and found that nationally 6.4% of all high school sports–related injuries were related to breaking of the rules of the sport.64 Practice methods also have a definite impact on injury statistics.10,45,65,66 In competitive running, training tech niques such as high-mileage workouts, excessive use of plyometrics, and interval work have been implicated in the incidence of overuse problems.6,67-69 Certain factors fre quently lead to overstress: (1) when unprepared athletes are asked to cross-train with long-distance running for such sports as swimming, basketball, or volleyball; (2) when ath letes are out of shape because it is early in the season; and (3) when it is the transition period between seasons when a player shifts from one sport to another without recognizing the different stresses introduced by the variation in perfor mance requirements, shoes, and playing surfaces involved. Running programs that involve excessive mileage or, more commonly, “too much too soon” are responsible for stress fractures or other overuse syndromes.8,28 Taunton and coworkers found that being active for less than 8.5 years was positively associated with injury in both sexes for tibial stress syndrome; and women with a body mass index of less than 21 kg/m2 were at a significantly higher risk for tibial stress fractures.70 A lack of stress adaptation frequently results in overload problems and injury. Other training techniques may increase an athlete’s risk for injury. Plyometric training is promoted to improve jumping ability and speed71; however, such exercises as bench jumping and bounding can overload the system.72 This is particularly true when stress accommodation is not allowed and when shoes and surfaces are inappropriate for these activities. Stress tolerance varies widely from individual to indi vidual. This must be recognized in the design of preseason, in-season, and off-season training programs. Unnecessary exposure to injury can be attributed to coaching meth ods. Uncontrolled scrimmages and excessive contact work increase injury rates in football.10 Gymnasts who perform complex maneuvers without adequate spotting

Box 25J-1 High-, Medium-, and Low-Risk Sports for Foot and Ankle Injury High Risk

• Ballet • Basketball • Dance • Ice skating • Mountaineering • Running • Skateboarding • Snowboarding • Soccer Medium Risk

• Aerobics • Baseball • Football • Gymnastics • Ice hockey • Lacrosse • Racquetball, squash • Roller skating • Rugby • Tennis • Volleyball • Water-skiing Low Risk

• Archery • Boating • Bowing • Cycling • Equestrian • Fishing • Golf • Parachuting • Rodeo • Skiing • Weight training • Wrestling Adapted from Sports Injuries. Accident Facts. Report of the National Safety Council, 1990, p 88; and from Table 26-1 in Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA (eds): Surgery of the Foot and Ankle, 7th ed. St. Louis, Mosby, 1999.

or preparation have a higher risk for injury.22 Baseball and softball players who practice sliding into fixed bases are unnecessarily exposed to foot and ankle trauma (Fig. 25J-1).47,48 Finally, the “no pain, no gain” coaching philos ophy can pressure an athlete to return to play after an injury without adequate rehabilitation and increase the potential for injury: an ankle syndesmosis injury treated functionally as a typical lateral ankle sprain can worsen considerably. In these times of astronomical salaries for professional ath letes, there is increasing emphasis on players returning to sport after injury in the shortest amount of time possible. The environment may affect injury risk: weather con ditions can alter the playing surface, the shoes worn, the interface characteristics between shoe and surface, and the attitudes of players and coaches. The complex interplay

Foot and Ankle 2173

A

C

B

Figure 25J-1 A, Potential for injury created by sliding into a fixed base. B, A 15-year-old boy who injured his ankle sliding into second base. C, Distal fibula fracture of 15-year-old male baseball player. (A, Photograph courtesy of Rice University Sports Information Office; B, photograph by Christopher B. Hirose.)

between extrinsic and intrinsic elements makes statistical analysis difficult from a precise epidemiologic perspective. As scientists, we must recognize that injury statistics are only as good as the integrity of the investigator, the statisti cal methods, and the research design.73-76 The use of performance-enhancing drugs and nutri tional supplements has been rearing its ugly head for more than a century.77,78 In 1886, Arthur Linton, a 24-year-old Welsh cyclist, died during a race from Bordeaux to Paris. He was believed to have taken the stimulant trimethyl. Shortly thereafter, Charles Edouard Brown-Séquard, in

1889, extracted testosterone in dogs and injected himself with the extract, claiming that it made him feel younger. From 1940 to 1945, the Germans tested anabolic steroids in prisoners, and Hitler himself may have used them. Some believe his behavior late in life exhibited the characteris tics of steroid use: aggressiveness and violent behavior with bouts of depression and suicidal ideation. In 1954, the Soviet weightlifting team dominated the sport, and their team doctors revealed the use of injected testosterone. At the 1976 Montreal Olympics, the East German women’s swim team dominated with 11 of 13 individual gold medals,


setting 8 world records in the process. Much later, the German team coaches admitted to steroid use. Based on the lawsuits filed in German court, it is believed that up to 2000 of the East German athletes who have used anabolic steroids are now suffering from serious health problems, including liver tumors, heart disease, testicular and breast cancer, infertility, eating disorders, depression, and birth defects. The list of world-famous athletes who used, or are accused of using, performance enhancing drugs continues to grow: Canadian sprinter Ben Johnson, NFL defensive end Lyle Alzado, baseball’s 1996 National League MVP winner Ken Caminiti (who died of a heart attack at age 41 years), Major Leaguers Barry Bonds and Jose Canseco, Tour de France Winner Floyd Landis, Sydney Olym pic Champion Marion Jones—who had her five medals stripped by the International Olympic committee, and most recently Roger “The Rocket” Clemens.78 Unfortu nately, with the desire to win, sometimes at all costs, this list of famous athletes may continue to grow. Quite clearly, there are negative effects associated with the use of per formance-enhancing drugs. They are illegal, constitute an unfair advantage, and place the athlete at an unnecessary and serious risk.77,79,80 Injury risk is a natural and accepted part of sports par ticipation. Different sports with different performance factors naturally provide varying degrees of exposure to injury.26,60 The broad categories of analysis in the injury equation are intrinsic and extrinsic factors. For the foot and ankle, the primary areas of importance are joint flexibility, shoewear, and the quality of the playing surface. These can be related to a classification of sports activities based on six basic motions: (1) stance, (2) walking, (3) running, (4) jumping, (5) throwing, and (6) kicking.22,81 Running, jumping, and kicking seemingly pose the greatest risk for injury to the foot and ankle. By using these types of categorization and classification, combined with scien tific analysis of biomechanical stresses, it may be possible to analyze injury potential more accurately and to design effective prevention strategies.

INCIDENCE Injuries to the lower extremities account for most sports injuries.82 Between 55% and 90% of all sports injuries occur from the hip region down to the toe.83 Running, jump ing, and kicking sports are associated with injuries to the foot and ankle. When combined with cutting and sliding maneuvers, the injury statistics increase dramatically. It has been suggested that the sprained ankle is the single most common injury in sports, and many ankle sprains go unreported and untreated (Fig. 25J-2).84-89 Nevertheless, epidemiologic analysis of sports injuries occurring around the world indicates an overwhelming preponderance of injuries to the lower extremities, and most of these are sprains, strains, and contusions.46,84,86,87,89-96 Studies of sports-related injuries in the running and jumping sports have suggested an incidence of injury of 10% to 15% for the ankle and 3% to 15% for the foot.86,90,92,93,96 In their study of more than 12,000 injuries occurring in 19 different sports in a university sports clinic, Garrick and Requa found that 25% of these injuries involved the foot and ankle.86 Patients participating in running, tennis, and

Figure 25J-2 Ankle ligamentous examination at the University of Texas. (Photograph by Thomas O. Clanton.)

dance were seen most frequently in this clinic setting. Kan nus and colleagues reported on the injuries seen in their European sports medicine clinic, where the most common sports were soccer, running, and orienteering.92 Ankle injuries accounted for 9% of the visits to the clinic during a 6-month period. Achilles tendon problems and heel pain accounted for another 7%. DeHaven and Lintner, from the University of Rochester Section of Sports Medicine, sur veyed injuries seen over a 7-year period, including patients from unorganized sports all the way through the profes sional level.90 Of the 3431 cases studied, 12% involved the ankle, and 3% involved the foot. The three sports most commonly producing injury in this clinical setting were football, basketball, and soccer. In 1980, Zaricznyj and associates reported a thorough analysis of the causes and severity of sports injuries in a population of school chil dren from elementary through high school.96 This study documented all injuries in a population of 25,512 school children. Of these, 11.4% occurred to the ankle. The foot and toes were injured in 6%. A thorough analysis of the incidence of injury in different sports reveals the magnitude of the problem. Soccer claims anywhere from 40 to 120 million participants worldwide and about 13 to 16 million in the United States.97,98 It has an injury rate of 22% to the ankle and 8% to the foot.82 Football involves an estimated 17,400,000 participants in the United States.98 The overall likelihood of player injury in football has been estimated to be anywhere from 10% to 80% of participants. Combining these numbers with the estimated injury rate to the foot and ankle of 15% to 25%, the total injuries to the foot and ankle in football in this country range from a low of about 261,000 to a high of 3,480,000. 9,99-103 The estimated injury rates for the foot and ankle in other sports are listed in Table 25J-1. When combined with esti mates of participation numbers in those sports,98 the magni tude of the athletic injury problem to the foot and ankle and the need for better prevention become evident. Whether the sport is a team or individual sport, organized or unorganized, professional or nonprofessional does not appear to make a major difference in the types of foot and ankle injuries that occur and has only a minor influence on the overall injury rate. This suggests that the intrinsic movements and extrinsic load characteristics of the foot and ankle required by sports participation involve a certain basic risk for injury.

Foot and Ankle 2175

TABLE 25J-1 Injury Rates Calculated for the Foot and Ankle in Various Sports from a Review of the Literature Sport/Study

Skill Level

Ankle Injury (%)

Foot Injury (%)

Recreational Recreational

12 11

5 18

Professional and nonprofessional Review of literature

17

22

14

15

Professional

19

4

Professional Professional High school

19 18 31

4 6 8

N/A Club

F&A F&A

8 14

Various levels Student

17 22

15 15

Top class Top class

F&A F&A

13 6

Aerobics

Rothenberger Garrick

Sohl

Basketball

Zelisko Henry Moretz

Dance (general)

Washington Rovere Equestrian

Bermhang Bixby-Hammett

Meyers

Blyth Culpepper DeLee Zemper

High school High school High school College

Canale

Ferkel Perlik

Cottlieb Walter Temple Marti Brown Smith

Johnson Blitzer Dowling Pino

Professional Amateur

2 3

3 2

Squash/racquetball

Club High school

21 10

3 8

Tennis

Amateur High school College Professional Junior

0 0 7 0 4

0 0 10 0 1

College College

15 14

4 4

N/A N/A

41 40

8 35

Military

7

0.3

Parachuting

Petras

N/A 2

College/club

8

2

Recreational Recreational N/A N/A

19 15 26 30

11 16 26 10

National males Age 14-19 yr

8 29

8 8

Various Youth

9 F&A

N/A 8

USSA

8

N/A

Recreational

26

3

Swedish senior male division Various Amateur leagues (France)

17

12

36 20

8 N/A

Recreational N/A

21 20

2 7

Elite

11

9

National amateur

18

6

N/A

4

15

Elite, Olympic

2

0

College Olympic College High school

10 10 4 3.8/100 wrestlers

3 0 0

Soccer

Ekstrand Nilson Bareger-Vachon

Berson Soderstrom Winge Volleyball

Schafle Water skiing

Hummel Weight training

Mountaineering

McLennan Tomczak

10 8

Freestyle

College

Lacrosse

Muller Nelson

College N/A

Skiing Downhill

2 4 2 4 AE = 0.25 2

Ice hockey

Park

1

Running

15 11 18 16 AE = 1 11

Gymnastics

Sutherland

6

Rugby

Golf

Caine Garrick

College

Snowboarding

Football

McCarroll McCarroll

Foot Injury (%)

Ice skating

Cycling

Davis Kiburz

Ankle Injury (%)

Rodeo

Micheli

Baseball

Garfinkel

Skill Level

Roller skating

Ballet

Garricki

Sport/Study

Kulund Wrestling

Roy Lok Snook Requa

AE, number of injuries per athletic exposure; F&A, foot and ankle; N/A, not available; USSA, United States Ski Association. From Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA (eds): Surgery of the Foot and Ankle, 7th ed. St Louis, Mosby, 1999, pp 1093-1094.


FLEXIBILITY AND STIFFNESS Flexibility is one of the components of physical fitness that has been judged to be critical for injury-free perfor mance.104,105 Its effect on injury to the foot and ankle has been discussed primarily in relation to (1) ankle joint stiff ness affecting the incidence of ankle sprains and (2) flatfeet or hyperpronated feet as a source of injury or pain.

Definitions Flexibility is the range of motion commonly present in a joint or group of joints that allows normal and unimpaired function.106,107 It can be subdivided into static and dynamic flexibility. Static flexibility is the maximal range of motion that a joint can achieve with an externally applied force, such as gravity. Dynamic flexibility is the range of motion that an athlete can produce and the speed at which he or she can produce it. Dynamic flexibility is important in high-velocity movement sports such as throwing, sprint ing, or jumping.104,107 Having excellent static flexibility does not mean that one possesses excellent dynamic flex ibility. Beighton and coworkers noted that articular range of motion is a spectrum, where one end of the spectrum includes considerable joint laxity.108 When flexibility exceeds the normal range of movement in multiple joints, an individual is considered loose-jointed or hypermobile. Hypermobility has been shown to have multiple inheri tance patterns and can occur in both benign and patho logic forms.109-113 Box 25J-2 shows characteristics of joint mobility patterns and changes with age and gender and ethnicity. Stiffness is the physical measurement of a reduced range of motion of a joint or a group of joints. The loss of flex ibility during rapid growth in children causes both mus cle tendon imbalance and increased apophyseal traction. Resultant overuse injuries include traction apophysitis and tendinitis. Sever’s disease is a common cause of heel pain in adolescents. Little discussion in the medical literature centered on hypermobility until it was proposed as a heritable cause of joint problems by Finkelstein in 1916.114 Connective tissue diseases such as Ehlers-Danlos syndrome, Marfan syndrome, Larsen’s syndrome, Down syndrome, hyperly sinemia, homocystinuria, and osteogenesis imperfecta are

Box 25J-2 Flexibility Generalizations

• Inherited characteristic • Individual variability • Joint specific • Females more flexible then males • Decreases with age • Can be acquired through training • Strength training does not necessarily reduce flexibility • Little relationship with body proportion or limb length • Little relationship with injury rate Data from references 13, 107, 108, 116, 118, 121, 126, and 127.

known to be associated with joint hypermobility and resul tant subluxation and dislocation of joints, although this rarely affects the foot and ankle joints.111,115-117 Hypermobility is a trademark of certain sports such as diving, gymnastics, and ballet. Ballet dancers are par ticularly noted for excessive motion in their spine, hips, and ankles.118 To a certain degree, individuals with these traits of flexibility are selected through the intense train ing that is required in competitive dancing. It seems that inherited hypermobility gives these individuals an advan tage during the training years.118 There is also a nega tive side: studies have shown that hypermobile dancers have a higher incidence of injuries than those who are not hypermobile.65,119 Although Nicholas cited hypermobility as a causative factor in ligamentous injuries in athletes in 1970,120 this relationship was not confirmed in follow-up studies.38,121-123 The connection between hypermobility, particularly when it is familial, and dislocation of one or more joints is rela tively well established, but it has not included the other joints of the foot and ankle.116,121 The occurrence of joint effusions in the knees and ankles in the absence of trauma or other known inciting causes was attributed to hypermo bility by Sutro in 1947.124 Additionally, there have been some reports suggesting an association between hypermo bility and osteoarthritis.116,118,121,125 Although the presence of flatfeet is frequently included among the characteristic findings of individuals who are hypermobile, it is quite clear that not all individuals with flatfeet are hypermo bile.126,127 There is considerably less evidence implicating hypermobility with other pathologic conditions of the foot and ankle. Criteria for the diagnosis of hypermobility were first proposed by Carter and Wilkinson128 and later modified by Beighton and colleagues.108 The tests com monly used include (1) passive thumb apposition to touch the forearm, (2) passive little finger hyperextension of more than 90 degrees, (3) elbow hyperextension of more than 10 degrees, (4) knee hyperextension of more than 10 degrees, and (5) forward flexion of the trunk with the knees straight and the palms of the hands resting flat on the floor (Fig. 25J-3). Hypermobility is diagnosed in individuals who can perform three or more of these tests.117 The distinction between hypermobility, or laxity, and instability is an important one. Hypermobility is normal movement carried beyond the range found in most indi viduals. This hypermobility is primarily a function of the stiffness within the muscles, ligaments, and tendons cou pled with the bony configuration of the joint. Instability is a symptom-producing phenomenon that is related to the ligamentous and bony integrity of joint as well as compres sive joint forces and neuromuscular control mechanisms and their opposition to the forces of shear, distraction, and angulation. Instability may be further subdivided into functional and mechanical instability. The idea of functional instability as proposed by Freeman is “… the occurrence of recurrent joint insta bility and the sensation of joint instability due to the contributions of any neuromuscular deficits.”1,129 Such deficits would primarily be related to injury to the joint mechanoreceptors and afferent nerves resulting in combi nations of impaired balance, reduced joint position sense,

Foot and Ankle 2177

A

B

C

Figure 25J-3 Tests for hypermobility. A, Passive thumb apposition to touch forearm. B, Passive little finger hyperextension. C, Forward flexion of the trunk so that palms rest on the floor. (Photographs by Christopher B. Hirose.)

and slower firing of the peroneal muscles in response to inversion stress. Mechanical stability, in contrast, is defined as “laxity of a joint due to structural damage to ligamentous tis sues which support the joint.”129 Structural damage also includes damage to the bony support of the joint. This type of instability is not always evident on physical exami nation. The varus stress test applied to the ankle to pro duce a talar tilt demonstrating lateral ligamentous injury at the ankle can be difficult to interpret in patients who have increased subtalar motion. Adding to the difficulty of such an assessment, as of this writing, there are no scientifically based anatomic and biomechanical definitions that are uni versally accepted.

Historical Perspective on Flexibility Hypermobility is often seen in athletes and may be more frequently symptomatic than in the nonathletic population. This is likely due to the added stress of sports participa tion. According to Grahame, Hippocrates first mentioned hypermobility as a source of difficulty for athletes as early as the 4th century bc.116 The importance of flexibility in athletic performance and the prevention of injury are of rather recent ori gin according to Corbin.107 The immobility caused by wartime injuries, together with the epidemic of polio myelitis, instigated research efforts in this field in the past century. Cureton emphasized flexibility as an important component of physical fitness as early as 1941 after his work with swimmers during the 1932 Olympic games.130,131 Kraus’ work led to the formation of the President’s Council on Physical Fitness and Sports and fostered much of the subsequent research on flexibil ity.107 In a classic work, DeVries proved the value of passive stretching in improving flexibility.132,133 Further more, the work of Salter and associates in Toronto has shed new light on the importance of maintaining flex ibility and motion postoperatively in patients who have undergone musculoskeletal procedures. The benefits of continuous passive motion to the joints and to the

s urrounding musculotendinous and ligamentous struc tures are well established.134-136 Although the natural inclination and the accepted teaching for many years in the fields of sports medicine and exercise physiology has been that stretching is a preventive measure for athletic injury, there is little conclusive epi demiologic evidence to support this idea, and studies have been contradictory and inconclusive.45,137,138 Two welldesigned studies of running-related injuries failed to show a significant relationship between stretching or its absence and the frequency of injury.32,51 Conversely, a study of mil itary basic trainees showed a reduction in overuse injures with an effective hamstring flexibility program.139 Research from Duke University has provided scientific ground work on the preventive aspects of stretching and warm-up periods by showing that greater tension is required to rup ture a muscle that has been stretched.140,141 There is the possibility that a degree of tightness protects against injury when joints are stressed. This implies that stretching beyond a certain point may reduce the load-sharing ability of the musculotendinous units or the capsuloligamentous com plex, which are responsible for joint stability.137 Ingraham believes that the current evidence suggests that stretching and increasing the range of motion beyond function are not beneficial and may actually cause injury and decrease performance.142 If this is indeed the case, excessive stretch ing or hypermobility could result in increased stress on the ligaments, bone, and cartilage at the joint, leading to injury or arthritis.141,143,144 This may be the situation when ballet dancers force ankle plantar flexion to such an extent that it creates posterior impingement symptoms and reactive bone formation (Fig. 25J-4).65,119,145-147 The balance between adequate and excessive stretching is further demonstrated in studies of runners. Research has shown that during level running a great deal of energy is stored in the muscle-tendon unit.13,148 Several laborato ries have shown that less flexible individuals use less oxy gen to cover the same distance while running at the same speed than more flexible individuals.149 This interesting fact may explain why runners as a group are relatively inflexible unless specific stretching exercises are pursued.


A

B

Figure 25J-4 A, Computed tomographic scan demonstrating bony posterior impingement. B, Excised bony fragment. (Photographs by Christopher B. Hirose.)

The importance of muscle stiffness in athletic injury remains an area for continued study because there is no scientifically based program for flexibility training with statistically reproducible results in lowering injury rates or improving performance.13 In summary, there appears to be an optimal range of motion for each individual and for each of his or her joints that may be sport specific. Warming up and stretching to obtain or maintain this range may or may not prevent

Sagittal plane Frontal plane

Horizontal plane

injury, but stretching beyond this range is potentially harm ful. Certain sports require a particular range of motion and flexibility. Athletic activity and the competitive process tend to select naturally those who can attain the movement criteria with the most efficiency and without a subsequent increase in injury rate.150

Joint Motion We define joint motion based on the position of the human body in relation to the three cardinal planes: the sagittal, frontal, and horizontal planes (Fig. 25J-5 and Table 25J-2).151 This system considers pronation and supination as a triplane motion. Pronation consists of eversion, abduction, and dorsiflexion, and supination consists of inversion, adduc tion, and plantar flexion.151,152 It is apparent that motion in almost all joints and specifically in the ankle, subtalar, and transverse tarsal joints is actually a triplane motion to one degree or another.152-156 As an example, dorsiflexion of the ankle produces some degree of foot abduction as well as external rotation. Similarly, plantar flexion produces some adduction and internal rotation. There are different norms for range of motion of the ankle, subtalar, and first metatarsophalangeal joints (Tables 25J-3 to 25J-5). This is due to the degree of ana tomic constraints around these joints for each individual. A review of the literature shows that the average ankle range of motion is calculated as 53 degrees, with average dorsiflexion equaling 18 degrees and average plantar flexion

TABLE 25J-2 Terminology Used for Motion, Instability, and Deformity Plane

Motion

Position

Deformity

Sagittal

Dorsiflexion Plantar flexion Inversion Eversion Adduction Abduction Pronation Supination

Dorsiflexed Plantar flexed Inverted Everted Adducted Abducted Pronated Supinated

Calcaneus Equinus Varus Valgus Adductus Abductus Pronatus Supinatus

Frontal Figure 25J-5 The cardinal planes of motion. (Redrawn with permission from Women in Sports. Sport Research Review. Beaverton, Ore, Nike Sport Research Laboratory, Mar/Apr, 1990; and Oatis C: Biomechanics of the foot and ankle under static conditions. Phys Ther 68:1815-1821, 1988.)

Transverse Triplane description

Foot and Ankle 2179

TABLE 25J-5 First Metatarsophalangeal Joint Motion

TABLE 25J-3 Ankle Joint Motion*

Study

Method

Dorsiflexion (Extension) (degrees)

AAOS159 Bonnin406 Boone and Azen158 Sammarco175 WB NWB Weseley169

NS NS A

20 10 to 20 12.6 ± 4.4

50 70 25 to 35 35 to 55 56.2 ± 6.1 66.8 ± 5.5

P P P

21 ± 7.21 23 ± 7.5 0 to 10 (max 23)

23 ± 8 23 ± 9 26 to 35 (min 10) (max 51)

44 ± 7.6 46 ± 8.25 26 to 45 (min 51) (max 84)

13 to 33

23 to 56

36 to 89

24.9 ± 3.0 20

28.5 ± 7.5 53.4 ± 5.25 40 60

Lundberg155 Review/ NS summary Personal study NS AMA407 A or P

Plantar Flexion (degrees)

Study Total (degrees)

*When a range is given, it signifies the range of greater concentration. A, active; NS, not specified; NWB, non-weight-bearing; P, passive; WB, weight-bearing.

equaling 35 degrees.155-159 Variability in ankle motion mea surements is introduced depending on the methodology of measurement: radiographic or clinical using flexometry, goniometry, or electrogoniometry; selection of land marks; and measurement of specific tibiotalar movement or combined ankle-foot motion.155 Timing with regard to a warm-up period and geographic consideration may also be important.160-162 As one moves distally, range of motion of the joints of the foot and ankle becomes increasingly difficult to measure objectively. This is particularly true of subtalar motion, for which numerous methods of measurement have been described. No consensus for normal motion has been reached (Fig. 25J-6; see Table 25J-4). This absence of a consensus creates considerable difficulty when trying to determine whether or not subtalar instability exists.163 It is clear that there is intersubject variability in measur ing subtalar motion. At the current state of knowledge, subtalar motion is generally described as movement in the frontal plane of 10 to 59 degrees, with an average of 24 degrees.164,165

AAOS157 AMA407 Sammarco175 Joseph176

Standing

16 Clanton173

Dorsiflexion (degrees)

Plantar Flexion (degrees)

70 50 90

45 30 30

Active

Total

51 (40 to 100) 72.3 ± 12.4

74

23 (3 to 43) 35.0 ± 10.2

Transverse tarsal joint motion plays an important role in lower extremity kinematics. Its instability has been described as medial swivel syndrome.166,167 There has even been one report of surgical treatment of patients with trans verse tarsal joint instability.168 Average motion in the trans verse tarsal joint depends on the position of the hindfoot, or subtalar joint. As the subtalar joint undergoes eversion early in the gait cycle, the axes of the transverse tarsal joint are aligned so that they become parallel in this everted position of the heel, and this permits increased motion. This is about 22 degrees.153 Conversely, when the heel is inverted as occurs near the end of stance phase, the axes of the transverse tarsal joint become more divergent and less mobile, averaging 8 degrees of motion.153 This fact is important when assessing range of motion about the tib iotalar joint. If range of motion of the tibiotalar joint is tested with the hindfoot in an everted position, one gets a falsely increased range of motion due to a combination of motion through the tibiotalar joint and transverse tarsal joint. With the heel inverted, a truer measure of tibiotalar

TABLE 25J-4 Subtalar Joint Motion Study AAOS157

Inman154

Sammarco175 DeLee408 McMaster409 Brantigan410 James251 Milgrom411

Inversion (degrees)

Eversion (degrees)

Arc (degrees)

5 — 20 — 25 — 23 ± 6

5 — 5 — 5 — 8±4

10 44 ± 7 25 35 30 38 ± 6 31 ± 7

Method

R

L

ASOS Cailiet James

2.0 ± 7.4 21.4 ± 5.4 18.4 ± 5.2

31.2 ± 7.7 3.9 ± 4.1 21.6 ± 5.5 3.4 ± 3.1 18.4 ± 5.2 6.4 ± 3.7

R

L

4.0 ± 4.2 3.2 ± 3.3 6.7 ± 4.2

25–30°

A

0°

B

5–10°

C

Figure 25J-6 Method of measuring subtalar motion with patient prone and knee flexed. A, Neutral position at 0 degrees on goniometer. B, Inversion. C, Eversion. (Redrawn with permission from American Academy of Orthopaedic Surgeons: Joint Motion-Method of Measuring and Recording. Chicago, American Academy of Orthopaedic Surgeons, 1965; and Oatis C: Biomechanics of the foot and ankle under static conditions. Phys Ther 68:1815-1821, 1988.)


joint motion can be obtained because a minimal amount of motion is taking place through the transverse tarsal joint. Large variations in motion exist in this region, and this makes the job of defining separate motions for the talo navicular and calcaneocuboid joints difficult.155 The lit erature indicates that 13 to 15 degrees of dorsiflexion or plantar flexion movement occurs in the midfoot.169 Motion in the tarsal-metatarsal joints is also a triplane motion, but it occurs primarily in a single plane.153,156 This is most obvious in the first and fifth ray, where we describe dorsiflexion and plantar flexion movement. With dorsiflex ion of the first ray, however, some degree of abduction and external rotation occurs, and with plantar flexion, there is adduction and internal rotation.170 Some believe that the first ray, like the transverse tarsal joint, has a locking mechanism. Perez and colleagues have demonstrated that the frontal plane position of the first ray affects the sagit tal plane motion.55 An everted position, compared with an inverted position, has the least mobility in the sagittal plane. Average dorsiflexion and plantar flexion in the first through fifth tarsal-metatarsal joints are 3.5, 0.6, 1.6, 9.6, and 10.2 degrees, respectively.171 The triplane motion of supi nation and pronation was also described as 1.5, 1.2, 2.6, 11.1, and 9.0 degrees, respectively. This motion is used to advantage in the Lapidus procedure for treating hallux val gus and metatarsus primus varus in the hypermobile foot. Translational movements are abnormal in this area, and excessive forces are a cause of pathologic conditions rang ing from stress fractures at the base of the second metatarsal to mild diastasis between the first and second metatarsals

(Fig. 25J-7) and on to the more severe forms of Lisfranc’s fracture-dislocation (Fig. 25J-8). The normal range of motion in the first metatarsopha langeal joint is quite variable (Fig. 25J-9). According to Joseph, the average range of motion is 51 degrees of active dorsiflexion and 74 degrees of active plus passive dorsi flexion using the axis of the first metatarsal as the neutral line.172-174 The natural position for this joint in the standing posture is 16 degrees of dorsiflexion. Active plantar flexion varies between 23 degrees and 45 degrees.172-174 In per forming these measurements, some variability occurs from the positioning of the ankle and subtalar joints. Motion is reduced when the ankle is in dorsiflexion and the subtalar joint is inverted. Motion is also reduced with advancing age.172 When maximal dorsiflexion is reached in the first metatarsophalangeal joint, the normal gliding motion of the proximal phalanx on the metatarsal head ceases, and impingement can occur between the proximal phalangeal base and the first metatarsal head.175 This may be a source of some of the problems seen in turf toe injury as well as hallux rigidus. First metatarsophalangeal joint dorsiflexion is important because of its relationship to gait and to stabil ity of the skin of the metatarsal pad.176 Motion in the lesser metatarsophalangeal joints and interphalangeal joints has been studied less thoroughly. Joseph’s study included motion at the interphalangeal joint of the great toe. Average motion was 31 degrees of total extension and 46 degrees of active plantar flexion. Recorded norms for lesser metatarsophalangeal joint motion has a wide range from 40 degrees to 90 degrees of dorsiflexion

Figure 25J-7 A, Non–weight-bearing radiograph with small fleck sign near the base of the second metatarsal. B, Weight-bearing radiograph with subtle diastasis. (Photographs by Christopher B. Hirose.)

A

B

Foot and Ankle 2181 Figure 25J-8 A, Photograph of a swollen midfoot and forefoot in a patient with a Lisfranc injury. B, Radiograph of diastasis and fracture of the second metatarsal. (Photographs by Christopher B. Hirose.)

A

B

and from 35 degrees to 50 degrees of plantar flexion.157,175 Excessive movement or stress to the lesser metatarsopha langeal joints can be a rare source of disease. Isolated syno vitis and instability of the lesser metatarsophalangeal joints, however, are becoming increasingly recognized as a source of forefoot pain in patients, including athletes.177,178 Inter phalangeal joint motion in the lesser toes is even less well

defined, with 0 degrees being the standard for extension and 35 to 40 degrees for plantar flexion.157 Loss of motion in these interphalangeal joints rarely creates symptoms unless there is a fixed flexion deformity, such as a hammer toe or mallet toe (Fig. 25J-10). Knowledge of the normal range of motion allows one to determine the etiology of specific injuries to athletes, while Figure 25J-9 Variability of first metatarsal phalangeal joint dorsiflexion. (Photographs by Christopher B. Hirose.)

A

B


Figure 25J-10 Proximal interphalangeal joint flexion. (Photograph by Christopher B. Hirose.)

being mindful that a considerable degree of variation exists that obscures a precise cause-and-effect relationship.

Etiologic Role of Flexibility With a more scientific understanding of joint motion and flexibility, we will examine foot and ankle injuries related to flexibility or its absence. Turf toe injuries provide one of the best examples of disease related to loss of flexibility. It was initially believed that turf toe injuries were related to lack of flexibility in the first metatarsophalangeal joint.179 We might expect a greater frequency of hyperexten sion injuries in athletes who have less natural dorsiflexion motion in the first metatarsophalangeal joint. All research to date, however, has failed to confirm an etiologic relation ship between the loss of dorsiflexion of the first metatarsal phalangeal joint and turf toe injuries.173,174,180,181 An initial first metatarsal phalangeal joint injury can cause long-term morbidity, and hallux rigidus and hallux valgus are two specific long-term sequelae.173,182 In hallux rigidus, a loss of motion occurs in the first metatarsophalangeal joint that produces pain (Fig. 25J-11).183 Lack of flexibility in the lesser metatarsophalangeal joints or interphalangeal joints is rarely linked with inju ries or pathologic conditions in athletes. The loss of inter phalangeal joint motion is a key component in mallet toes, hammer toes, and claw toes, and flexibility exercises

are often advocated in the treatment of these conditions. A lack of flexibility in such toes can result in painful calluses at the tips of the toes and painful corns over the dorsum of the interphalangeal joints. A lack of dorsiflexion in a lesser metatarsophalangeal joint can be a source of pain and disability, particularly when this involves the second toe. There is usually an iatrogenic or post-traumatic cause. Conversely, increased motion appears to be a factor in conditions involving the second metatarsophalangeal joint, including transient synovitis, crossover second toe, and subluxation and dislo cation of the second toe.177,178,184 Flexibility studies on the relation of these conditions to injury of the lesser metatar sophalangeal joints are sparse. Hypermobility of the first ray has been implicated as a source of problems in the foot such as stress fractures, but confirmatory studies using accepted statistical techniques are lacking.185,186 Simkin and colleagues have suggested an asso ciation between low arches and metatarsal stress fractures.187 Gross and Bunch measured stresses in 21 distance runners and found that the greatest force occurred under the first and second metatarsal heads.188 Using the model of the meta tarsals as proximally attached rigid cantilevers, the authors showed that the greatest bending strain and shear force occurred in the second metatarsal, where stress fractures are most common. These two studies provide circumstantial evidence that increased first ray flexibility is an anatomic fac tor in stress fractures of the second metatarsal shaft. Studies of the length of the metatarsals in dancers and risk for second metatarsal stress fractures note contradictory and inconclusive findings.189-192 Some believe that a longer second metatarsal predisposes dancers to an increase risk for second metatarsal stress fracture193-195 because a long second metatarsal is believed to be the recipient of added stress, especially in the en pointe position.196 Others note no association between the relatively long second metatar sal and increased risk for stress fracture.191,197 We may expect that the best source of a direct link between the lack of flexibility and injury would come from the ankle because of the high frequency of ankle injuries in sport. The tight Achilles tendon has been blamed for numer ous conditions, including bunions,198 turf toe,181 midfoot strain or plantar fasciitis,199-201 ankle sprains,202 Achilles tendinitis,68 calf strains,203,204 and hyperpronation.205-207

Figure 25J-11 Hallux rigidus. (Photograph by Christopher B. Hirose.)

Foot and Ankle 2183

Although there are numerous studies, evidence remains scarce for a causal relationship. Walsh and Blackburn sug gested heel cord stretching as a preventive maneuver to decrease the incidence of ankle sprains, but they reported no results from this program.202 Mahieu and colleagues determined that increased ankle dorsiflexion excursion and reduced plantar flexion strength may be linked with Achil les tendon overuse injuries.208 The strength of the plantar flexors and amount of dorsiflexion excursion were identi fied as significant predictors of an Achilles tendon overuse injury. A plantar flexor strength lower than 50 Nm and dorsiflexion range of motion higher than 9.0 degrees were possible thresholds for developing an Achilles tendon over use injury.208 It seems somewhat paradoxical that on the one hand, the athletic trainer works hard to improve the athlete’s flexibility at the ankle, and on the other hand, the trainer tapes or braces the ankle before practice or games to restrict motion. Hyperpronation has been blamed for many problems known to runners.205-207 Many runners come to their local orthopaedist, podiatrist, or running shoe salesperson with the self-made diagnosis of “pronated feet” and ask for a shoe or an orthotic device to cure their shin splints, knee pain, or arch pain. Running shoes have been made and marketed spe cifically for pronated feet or for the supinated, rigid, cavus foot.209-211 The complex movements in the foot and ankle associated with pronation produce a more flexible foot at the time of weight transfer. This can produce problems in one of two ways. First, the normal foot212,213 goes through 6 to 10 degrees of subtalar eversion in the frontal plane during gait, and the flatfoot or pronated foot may have 12 to 15 degrees of motion.214-217 This increased motion will produce a cor responding increase in transverse plane motion.218 Second, the speed with which the rearfoot angle changes seems to be important.219,220 The pronated foot goes through the avail able pronation range more quickly, and this force results in increased load transmission.214,221 Both of these movements are important components of load absorption in running. In addition, the duration of foot pronation may also have a protective effect on tibial stress fractures. In the cavus foot, there is more rigidity in the joints of the foot.219,222 This means that loads are not dampened as effectively, and higher stress is applied at each level, which can become symptomatic. So far, treatment has centered on the use of orthotic devices, but their success in the ath lete with a cavus foot is limited.207,222-224 As with all areas of science, studies of the etiology of foot and ankle injuries produce more and more questions. Because of the interrelationship of many factors and the extent of individual variability, it has been difficult to impose the proper degree of control in open systems and in vivo studies to come to solid conclusions. Current studies have not provided a reliable prediction of the influence of the pronated or cavus foot on the risk for injury.28,187,215,225-229 A 1999 study from the Mayo Clinic looked at the effect of foot structure and range of motion on musculoskeletal overuse injuries.230 The study group was a well-defined cohort of 449 naval trainees. They were tracked prospec tively for injuries throughout training. The risk factors that predisposed trainees to overuse injuries in this study were dynamic pes planus, pes cavus, restricted ankle dorsi flexion, and increased hindfoot inversion.

SHOEWEAR-RELATED INJURY Although the role of flexibility in sports injuries of the foot and ankle remains somewhat unclear, more evidence exists implicating shoewear and playing surfaces. The intimate relationship between these two makes separation into indi vidual components difficult. Many studies of sports inju ries look at these in a combined manner as the shoe-surface interface.231-238 The shoe can be a factor in athletic inju ries in other ways, such as improper fit, lack of cushion ing, inadequate support, and abnormal force generation. For this reason, shoewear and playing surfaces have been included as separate etiologic factors here, but the reader should maintain an awareness of their interdependency.

History Barefoot participation in sports was the norm in ancient times. Perhaps the first recorded injury in shod feet was noted by the Greeks.61 Today, shoes can cause problems for athletes in so many ways, one has to wonder whether it might be better for athletes to participate without shoes. An advantage to barefoot play can be seen in young chil dren who remove their shoes to race. More recently, Zola Budd and Abebe Bikila achieved Olympic fame without shoes (Fig. 25J-12). The symptom-free nature of peoples who trod without shoewear (regardless of their degree of pes planus or pes cavus) also makes one question the true value of modern shoewear.239-242 Numerous studies have demonstrated that the least amount of pronation occurs during barefoot run ning.214,220,243,244 This finding stimulates an inquiry into the

Figure 25J-12 Zola Budd running in 1984 Olympic 3000-meter race against Mary Decker. (© 1991 David Madison.)


role of pronation in injury and whether a shoe designed for overpronators is protective. Robbins and colleagues cham pioned the role of sensory feedback from the plantar surface of the foot in modifying load and protecting the runner from stress-related injury.245-247 They suggested that this important system is impaired by modern footwear, creating a “pseudo-neuropathic” condition. In support of this, they note that studies have shown no trend toward a reduction in injury from the use of modern athletic footwear. DeWit and colleagues looked at the biomechanics of the stance phase during barefoot and shod running.248 Barefoot running is characterized by a significantly larger external loading rate and a flatter foot placement at touchdown. This flatter foot placement correlates with lower peak heel pressures. It was postulated that runners adopt this altered foot placement position in order to limit the local pressure beneath the heel. Divert and colleagues studied the biomechanics of barefoot compared with shod runners.209 Barefoot runners showed lower contact and flight time and lower passive peak than shod. They concluded that barefoot running leads to a reduction of impact peak in order to reduce the high mechanical stress occurring during repetitive steps. They then studied why athletes have a higher oxygen consump tion and lower net efficiency when running shod compared with running barefoot. Many believe that this effect is due to the additional mass of the shoe, and their results show that there is a significant mass effect and increasing oxygen consumption. However, stride frequency, vertical stiffness, leg stiffness, and mechanical work were significantly higher in barefoot condition. The lower net efficiency reported in shod running may also be due to the impact-dampen ing properties of the shoe as the foot strikes the ground.249 Even though these studies suggest that shoes have no pro tective effect, most athletes still use shoes for competition and daily life. We explore a critical analysis of shoes in this chapter and discover how they fall short in their role as pro tective equipment for the sports participant.

factors.251 Nineteen percent of the 180 runners in their series were treated by a change or modification in shoewear. Lysholm and Wiklander studied 60 runners with 55 injuries during a 1-year period.252 Surface or shoe problems were the primary sources of injury in 3 cases and one of multiple factors in 10 others. Inferior footwear was the etiologic fac tor blamed in 34 of 318 injuries in soccer players. Football has provided the best perspective on shoewear and its relationship to knee and ankle injuries. Torg and Quedenfeld published an extensive study in 1971 relating the incidence and severity of knee and ankle injuries to shoe type and cleat length in Philadelphia high school foot ball players.253 Rates of injury to the ankle were reduced from 0.08 per team per game to 0.01 per team per game by switching from conventional cleated football shoes to soccer-style shoes with multiple shorter cleats. This result was substantiated by the work of Mueller and Blyth, who noted a reduction in knee and ankle injuries by resurfacing the playing field (30.5% reduction), changing from regular cleats to soccer shoes (22.3% reduction), or making both changes (46% reduction).254 Although these studies do not consider such shoe-related problems as cleating-induced contusions or lacerations or turf toe, they do provide a framework for studying the role of shoes in sports injury.

Mechanical Factors Shoe Fit

The exact incidence of injury attributable to athletes’ shoes is unknown, but several studies have included shoes as a sep arate factor in injury rates.250 James and colleagues included shoes and surfaces as one of three categories under cause of injury in runners in addition to training errors and anatomic

The most obvious problem with shoes that plagues the shod people of the world regardless of whether they are athletes is the proper fit. Even the smallest problem with fit can prevent athletes from performing to the best of their capabilities. For example, a web corn can become so pain ful that each step is agony. Metatarsalgia can result from a shoe that is too tight across the forefoot. Similarly, a narrow shoe often aggravates a Morton’s neuroma (Fig. 25J-13). The black toe of long-distance runners can be a sequela of improper shoe fit. Toe deformities such as ham mer toes, claw toes, and overlapping fifth toes may become symptomatic in athletes whose shoes have toe boxes that are either too narrow or of insufficient depth. Calluses and blis ters are inherent in most sports participation (Fig. 25J-14). Improperly fitted shoes that rub the skin excessively or allow the foot to move or slide disproportionately in the

Figure 25J-13 Morton’s neuroma excised from the third web space. (Photograph by Christopher B. Hirose.)

Figure 25J-14 Calluses in a long-distance runner. (Photograph by Christopher B. Hirose.)

Incidence

Foot and Ankle 2185

shoe enhance the frequency of calluses and blisters. Other irritants include the insole edge, penetrating cleats, promi nent seams, and orthotic device edges.

Cushioning The importance that cushioning protects athletes from injury has been promoted largely by the running shoe industry and those whose research it supports.255 The run ning literature has seen a proliferation of articles address ing impact forces, shoe cushioning, shock absorption, and the effects of various alterations in shoe construction. The logical assumptions have been that load on the human body is directly attributable to impact forces at foot strike and that these forces are naturally altered by the cushioning properties of the shoe.243,255-258 These assumptions fos ter the belief that changing the shoe’s material properties (e.g., midsole thickness) can influence impact load, thereby changing rates of injury. Impact forces are a critical feature in the etiology of sports-related pain and injury whether acute or chronic.27 The bionegative effects of impact loads are evident from the damage produced to articular cartilage by high-impact loads.259,260 Radin and coworkers showed that deleterious changes occurred in the biochemical and biomechani cal properties of articular cartilage of sheep walking con stantly on concrete as opposed to those walking on wooden chips.259,260 Impact force and shock wave transmission play a role in the etiology of experimentally induced osteoar thritis.261,262 Shock-absorbing insoles in the boots of South African military recruits produced a 9% reduction in their incidence of overuse injuries.263 In addition, the German armed forces studied the properties of cushioned insoles. The aim was to assess metatarsal head loading in combat boots with respect to the prevention of metatarsal stress fractures comparing cushioned with standard conventional insoles. The cushioned insoles were superior to the con ventional insoles with respect to the plantar pressure dis tribution.264 These studies support the belief that impact loads are an etiologic factor in certain injuries, but care ful analysis leaves the impression that this load plays a less than consequential role. Ground reaction forces are the primary external force acting on the human body during running.27,265-268 These

forces increase as running velocity increases. Higher ground reaction forces are seen in the progression from walking to jogging to sprinting to jumping. Estimates vary from 1.2 times body weight (BW) for walking to 2.5 times BW for jogging. Sprinting increases load by 3 to 6 times BW, whereas jumping multiplies this force by 6 to 8 times BW27 (Table 25J-6). Impact force amplitude is reduced when soft materials are used in the shoe or running surface.269 This reduction is achieved by increasing the deceleration dis tance of the foot. Calculations of impact peaks can be made from the following equation: Fmax = Fxi = v fm,

where Fmax is the maximal force occurring in the vertical direction (Fxi) and is proportional to velocity (v), the mass of the body (m), and the spring constant for that body (f). From this equation it is apparent that impact velocity has the greatest influence on vertical load. It is also reduced by reducing the mass (e.g., body weight) or by reducing the spring constant (e.g., knee flexion angle).246,270-272 As an etiologic factor in injury, shock absorption has not proved to be the critical factor that advertising would lead us to believe. Although changing from a new shoe with good cushioning properties to an old shoe lacking these properties can produce injury, an injury may come from changing to a newer shoe as well. It may be that change itself is the critical factor in an injury that occurs during a repetitive activity. Reinschmidt and Nigg have noted that for running shoes, at least, pronation control and cushioning are still considered the key concepts for injury prevention despite the fact that conclusive clinical and epidemiologic evidence is missing for these design strategies.273 In addi tion, recent running shoe research has suggested that cush ioning may not be related to injuries and that cushioning during the impact phase of running may be more related to aspects like comfort and muscle fatigue. A more recent study refuted the shock-absorbing qualities of insoles in injury prevention. This study was a randomized con trolled trial of 1205 Royal Air Force recruits to assess the differences, if any, in the efficacy of two commonly avail able shock-absorbing insoles. Similar rates of lower limb injuries were observed for all insoles (shock-absorbing and non–shock-absorbing) in the trial.274

TABLE 25J-6 Variations in Ground Reaction Force from Walking to Jogging to Sprinting to Jumping Study

Movement

Velocity (m/sec)

Footwear

Fmax (N)

Fmax (BW)

Cavanagh, 1981 Cavanagh, 1981 Clarke, 1982 Frederick, 1981 Frederick, 1981 Cavanagh, 1980 Frederick, 1981 Nigg, 1981 Nigg, 1978 Nigg, 1981

Walking heel-toe Walking heel-toe Running heel-toe Running heel-toe Running heel-toe Running heel-toe Running heel-toe Running heel-toe Running jump Running jump

1.3 1.3 2.7 3.4 3.8 4.5 4.5 5.5 6.0 8.0

Barefoot Casual shoes Running shoe Barefoot Barefoot Running shoe Barefoot Running shoe Spikes Spikes

— — — 1365 1590 — 1963 2350 4000 5500

0.6 0.3 2.8 2.0 2.3 2.2 2.9 3.6 5.3 7.9

BW, body weight; N, Newtons. From Nigg BM: Biomechanical aspects of running. In Nigg BM (ed): Biomechanics of Running Shoes. Champaign. III, Human Kinetics, 1986, p 21. Copyright 1986 by Benno M. Nigg.


Energy Absorbed N-m

14

A

Machine Testing Runner A Runner B Test System

12 10 8 6 4 10

Energy Absorbed N-m

One case example for the role of poor cushioning is that of a 26-year-old runner who sustained bilateral stress frac tures of the fibulae after he changed from his usual pair to an older pair of shoes for a 14-km race.275 Instrom testing of the original running shoe and the ipsilateral older shoe demonstrated that the original running shoe had twice as much energy absorption and 5 times the deformation as the older pair. Although lack of shock absorption is the pos tulated cause of injury in the aforementioned case, other factors might have played a role as well. These include the change itself, the altered muscle activity causing increased bending moments on the fibula, increased muscle activity resulting in muscle fatigue and loss of the protective func tion of the muscle, and variations in foot geometry leading to increased pronation.275-283 Cook and coworkers have demonstrated by mechani cal testing and in vivo experimentation that different shoe models vary by as much as 33% in shock-absorbing char acteristics, and all show significant decreases with mile age.284,285 Initial shock absorption values were reduced by 60% or more after 250 to 500 miles of machine-tested running. Other variables that reduced shock absorption were environmental conditions, such as moisture con tent of the shoe (e.g., perspiration or rain) and hardness of the testing surface (e.g., asphalt versus grass). Some run ning authorities have suggested that running shoes may have time-related life spans. The longevity of the shoe is related to the mileage run and usually falls in the 500- to 1000-mile range (Fig. 25J-15).243 One study examined heel pad stresses during heel strike with simulated wear of the ethylene vinyl acetate foam commonly found in modern sport shoes. Heel pad stresses were consistently increased when the ethylene vinyl acetate thickness was decreased, suggesting that the age of the shoe affects the viscoelastic properties of the shoe.286 Whittle looked at transient impulses beneath the foot and how they are generated and attenuated.287 He found that there is a “shock-wave” that passes up the limb that may lead to degenerative joint disease. Limb position ing, materials used in shoe construction, and the use of orthoses can alter these forces. In addition, the intrinsic shock absorption system of the body produces behavior modification to control load magnitude. Impact forces are dramatically reduced by increasing knee and hip flexion at ground contact.288 Several studies have proposed that cushioned shoes lead to negligible decreases in load because subjects decrease flexion to accommodate the instability produced by softer surfaces.12,288-290 In reality, the human body accommodates load using complex strategies, and the material used for cushioning in shoes is most likely a very small element in this shock absorption system. Milani and colleagues’ study supports this hypothesis.291 The percep tual ratings of eight identical running shoes with a rela tively close range of midsole stiffness was examined. Their findings suggest that the body’s sensory systems differenti ate well between impacts of different frequency content, and that subjects adapt their running style to avoid high heel impacts.291 Experimental results do not universally confirm that a lack of shock absorption is the major cause of injury.225,292,293 Softer materials of inadequate thickness have a tendency to reach maximal compressibility and then transmit greater

8

6

4 0

B

In vivo Testing Runner A Runner B Test System

100

200

300

400

500

Miles

Figure 25J-15 Life span of running shoes related to mileage as demonstrated by reduction in retention of initial shock absorption with increasing mileage run in the shoes. A, Machine testing. B, In vivo testing. (Redrawn with permission from Cook SD, Kester MA, Brunet ME: Shock absorption characteristics of running shoes. Am J Sports Med 13:248-253, 1985.)

amounts of load.220 To reduce impact forces, material thickness must be of sufficient height to prevent maximal compressibility. In one study, however, a change in mid sole hardness from soft to hard did not alter the impact force peaks measured in 14 test subjects at four different running velocities.294 These results appear to be related to the variation in the point of application on the foot of the ground reaction force. Harder materials impose a larger lever arm in the force equation by moving the effective point of application farther lateral from the subtalar joint axis. This produces an increase in both initial pronation and initial pronation velocity, corresponding to an increase in deceleration distance over time and a resulting decrease in the impact force.269,294 The foot-shoe-surface interac tion is so complex that investigators are still debating the proper methodology for testing it. There are dramatic differences between machine testing and subject testing, between internal forces and external forces, and between subjects as well as in the same subject under varying test conditions.220,225,292,295-298 Bates and coworkers have even shown that the same test in the same runner can produce

Foot and Ankle 2187

different results between trials.225,295 With all these con founding data, it is hardly surprising that investigators in this field frequently disagree and have occasionally pro duced contradictory results. In the final analysis, the question remains whether the cushioning provided by the shoe is a critical factor in the etiology of injury in the athlete. The sport shoe industry and its related research have concentrated heavily on improving the shock-absorbing characteristics of its shoes. We have seen a plethora of innovative cushioning designs such as air soles, gel shoes, variable density and encapsulated soles, and soles that will automatically vary cushioning according to the runner’s weight or speed. As remarkable as these designs are, there is still no universally accepted scientific study that proves better cushioning in the shoe lowers the incidence of injury in runners. Robbins and Waked noted that deceptive advertising creates a false sense of security with users of expensive athletic shoes, inducing attenua tion of impact-moderating behavior, increased impact, and injury.299 In conclusion, it can be stated that a lack of cushioning may be a factor in producing injury but prob ably not to the degree to which some researchers and shoe manufacturers might lead us to believe.

Shoe Control For the running shoe, control or support is primarily inter preted in the context of rearfoot control. This is defined as the shoe’s ability to limit the amount or rate of pronation occurring through the subtalar joint at heel strike.214 A less well-defined component of shoe support is its control of take-off supination, which occurs at the lateral forefoot during toe-off.220 Foot support also consists of the rela tive flexibility of the shoe, most often measured as forefoot flexibility, which allows the shoe to bend at the metatarsal phalangeal joints.243 Greater flexibility has been consid ered desirable, but shoe flexibility can be a major factor in turf toe injuries.179,234 Conversely, stiffening the sole in the area of the metatarsophalangeal joint may decrease energy loss and improve performance.300 Control of movement in the sagittal plane by the shoe remains a subject for further investigation. Support for lateral motion and medial and lateral shear is a concern in court shoes: tennis, basketball, and aerobic shoes.301-305 Lateral stability, torsional flexibility, cushion ing, and traction control appear to be important design strategies to decrease the risk for injury.273 The support provided for the ankle by high-top shoes has been an important consideration in preventing injury, particularly in basketball and football (Fig. 25J-16).305-310 Brizuela and associates examined the performance of basketball shoes with increased ankle support compared with a shoe with no ankle support.311 The high support shoes resulted in higher forefoot impact forces and lower shock transmission to the tibia. The use of high support shoes also resulted in lower ranges of eversion and higher ranges of inversion for the ankle on landing. In the motor performance tests, the high support shoes reduced the height jumped and increased the time to complete the running course compared with low support shoes. This study underlines the importance of designing shoes that will maximize performance with out compromising safety. Johnson and associates tested

Figure 25J-16 Examples of a current high-top and low-top athletic shoe. (Photographs by Christopher B. Hirose.)

torsional stiffness of high-top football shoes using a special chair and measurement apparatus and found that high-top shoes were 50% stiffer than low-cut models.307 Theoreti cally, the high-top shoe should stimulate the propriocep tive feedback mechanism, resulting in greater sensitization of the peroneal muscles and improved stability for the ankle.312 Potential negatives induced by the high-top shoe include the reduction in load carried by the collateral liga ments of the ankle and the limitation in subtalar motion restricting the foot’s ability to adapt to surface irregularities. Handoll and colleagues believe that the protective effect of high-top shoes still remains to be established.313 They stud ied various interventions, including external ankle supports in the form of a semirigid orthosis, air-cast braces, high-top shoes, ankle disk training, taping, muscle stretching, boot inserts, and controlled rehabilitation. The main finding was a significant reduction in the number of ankle sprains in people allocated external ankle support and no statisti cal difference in those athletes wearing high-top shoes.313 Although some evidence supports the ability of high-top shoes to lower the rate of injury to the ankle,280,314,315 other studies have found no difference in ankle sprain incidence related to shoe type.316-318 In related work, the effect of ankle bracing and taping on athletic performance and injury prevention remains unclear despite numerous stud ies.315,319-325 Control characteristics are essential elements in modern sports shoes designed for prevention of injury, but not all features are beneficial. Rearfoot stability provided by the athletic shoe has become a critical ingredient in managing the overuse prob lems attributed to overpronation (Fig. 25J-17).326,327 Run ning shoes are designed to accomplish this control. Included are such creative concepts as cantilever soles with imbed ded plastic stability devices, plastic torsion bars, composite plates, gel pods, air chambers, progressive-rate polymer columns, variable-density-foam midsole platforms, metal springs buried inside the heel, and even magnetic impactsensing systems, materials of variable hardness in areas of the midsole, thermoplastic heel counters, heel flares, external stabilizers, and combination lasts. The impor tance attributed to rearfoot control is derived from the

2188 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� Figure 25J-17 Rear foot stability provided by athletic shoewear. Illustration of two runners switching between their commonly used shoes without control features and shoes with special control features provided in the laboratory. (Redrawn with permission from Nigg BM, Bahlsen AH, Denoth J, et al: Factors influencing kinetic and kinematic variables in running. In Nigg BM [ed]: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics Publishers, 1986, p 157. © 1986 by Benno M. Nigg.)

Subject A Right leg

21°

Without

assumption that overpronation produces injuries in run ners. This assumption has been extrapolated from studies of runners beginning with the classic study by James and colleagues.251 Fifty-eight percent of those injured were classified as pronators on biomechanical examination.251,328 The ability of the shoe or an orthosis to control excessive pronation is supported by the work of Bates and associates, Cavanagh, Nigg and Morlock, and Smith and coworkers (Fig. 25J-18).243,329-331 Take-off supination has been blamed for Achilles ten don strain and reduced performance.220 Take-off supina tion corresponds to the take-off angle, which should be close to 180 degrees. Angles between 160 and 170 degrees are indicative of increased take-off supination. Interest ingly, take-off supination is seldom seen in people engaged in barefoot running and is primarily a product of shoewear. It is unaffected by midsole hardness and running velocity but is heightened by additional medial support, especially when such support is located more posterior in the shoe. Nigg and coworkers have shown that geometric solutions are possible by adding lateral forefoot support or midsole

Subject B Right leg

12°

12°

31°

With Without Running heel-toe. 4 m/s

With

grooves.220 Little clinical information is available to sup port or refute this concept in shoe control.332 The next category to be assessed in the etiology of ath letic injury is shoe flexibility. This quality can be assessed by the amount of force necessary to flex the shoe’s forefoot 40 to 50 degrees.333,334 According to Ryan, the running shoe should be “moderately flexible” to allow proper foot mechanics.335 A shoe with greater flexibility is typically preferred by runners and is even advocated for those with rigid cavus feet. More convincing clinical and experimental evidence exists to implicate excessive flexibility of shoes in causing football injuries. In 1964, artificial grass was introduced, and a flexible sole soccer shoe replaced the traditional stiff, cleated football shoe.179,234 A new symptom complex appeared that was attributed to the use of these more flex ible shoes on the harder surface, which was nicknamed turf toe.234 Two cases of turf toe were found in track ath letes whose sprains occurred while wearing flexible racing spikes.179 Further characterization of this injury has made turf toe a well-defined clinical entity and has incriminated

Foot and Ankle 2189

Change of the rearfoot angle of the calcaneus

��10

8 Medial Degrees

6 Lateral 4

2

2 3 4 5

Figure 25J-18 Shoe control of excessive pronation as demonstrated by change in rearfoot angle (Δγ10) resulting from systematic alterations in location of medial support (positions 2 to 5) in the running shoe compared with support while barefoot and in shoe without support. (Redrawn with permission from Nigg BM, Bahlsen AH, Denoth J, et al: Factors influencing kinetic and kinematic variables in running. In Nigg BM [ed]: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics Publishers, 1986, p 152. © 1986 by Benno M. Nigg.)

0 1 2 3 4 5 Barefoot Shoe Anterior . . . . . . . . . . Posterior without support Shoe condition and position of medial support

overly flexible shoewear conclusively in its etiology (Fig. 25J-19).173,179-181 To their credit, shoewear manufacturers have responded by either stiffening the forefoot or provid ing shoe inserts to stiffen the forefoot.336 These examples support the view that the shoe flexibility plays a critical role in the etiology of injuries to the forefoot.

Orthotics Is the runner with a hyperpronating foot truly more sus ceptible to injury? Does a rigid orthosis holding the foot in a subtalar neutral position reduce the likelihood of injury? What role do orthoses have in injury reduc tion or production? Further evidence corroborating the effect of pronation control is provided by the results of treatment of injury by the use of orthoses, which led to

improvement and resumption of training in 70% to 90% of those treated.152,337-339 Nigg believes that there is some evidence that orthotics reduce movement-related inju ries, but that the orthotic functions as a second filter of force input, the first being the shoe and the third being the athlete’s foot.340 An orthotic can optimally function by simply reducing muscle activity, increasing comfort, and ideally increasing performance. Nigg and associates looked at the effect of shoe insert construction on foot and leg movement.341 They found that the changes resulting from the use of all inserts in total shoe eversion, total foot eversion, and total internal tibial rotation were smaller than 1 degree when compared with the no-insert condi tion. Also, they found that the soft insert construction was more restrictive than the harder inserts. They concluded that it is important to match specific feet and shoe inserts

Figure 25J-19 Variability of the forefoot stiffness of two different running shoes. (Photographs by Christopher B. Hirose.)

A

B


optimally. Kulcu and colleagues studied over-the-counter insoles and gait patterns with those who have a flexible flatfoot.342 They concluded that over-the-counter insoles have no beneficial effect in normalizing forces acting on the foot and on the entire lower extremity. Crosbie and Burns studied orthotics in those with pes cavus deformi ties and found that the mechanisms by which orthotic intervention is effective in improving pain and function in painful, idiopathic pes cavus remain unclear and equivo cal.343 In addition, Krivickas studied overuse injuries and bony alignment of the extremities and noted that although malalignment of the lower extremities is frequently cited as predisposing to knee extensor mechanism overuse injuries and foot injuries, orthotics do not have any effect on knee alignment, and although they can alter subtalar joint align ment, the clinical benefit of this remains unclear.20 Despite the improvements in rearfoot control offered by current athletic shoewear, it has been difficult to relate this to any evidence for reduction in incidence of running injuries.

Cleats and Sole Modifications Traction is a crucial ingredient in efficient performance in all sports and is related to the design features of ath letic shoewear. It can also be influenced by the playing surface and by the weight of the participant. Factors to be considered in the analysis of traction related to shoewear include the outsole materials used, the sole pattern, and the presence of cleats as well as their size and configuration. Load related to traction is studied primarily with regard to torque and friction.138,231,238,333,344 Outsoles are the bottom-most layer of the shoe that has direct contact with the ground. The most frequently used materials are carbon rubber, styrene butadiene rubber, ethylene vinyl acetate, and polyurethane.345,346 In general, if the material is harder, its durability is greater. Traction considerations must encompass the interaction of these materials with a variety of playing surfaces and conditions,

including the artificial surfaces used indoors and outdoors as well as the amount of moisture or dust on the field or court.347 Major differences occur in the coefficients of static and sliding friction for various shoe-surface combinations (Table 25J-7).348 Torque is the component of traction that is measured as the tendency of a force to rotate an object around an axis. It correlates with the static coefficient of friction. Laboratory experiments have established large differences in torque between different shoe-surface combinations, as illustrated in Figure 25J-20.348 Rheinstein and colleagues performed similar experiments supporting this difference in torque as related to outsole material, outsole hardeners, player weight, and playing surface.347 They found greater maximal torques with the softer outsoles combined with artificial and clean hardwood flooring in heavier players. Rubber-soled shoes demonstrated much more sensitivity to dust than the polyurethane soles when analyzed for loss of traction. This research has considerable implications in sports medicine because higher torque means higher load transmission to the body and an increased potential for injury. Alternatively, lack of traction implies sliding, slipping, falling, and poor performance. Where is the proper balance? This question may be unanswerable but deserves attention. Outersole tread design has developed from the flat rub ber of the traditional canvas tennis shoe of yesteryear to the high-technology multiple-patterned sole we see in running shoes and court shoes today (Fig. 25J-21).345,349 These tread designs theoretically alter the mechanical properties of the shoe by enhancing performance or pre venting injury by determining the flexion path for the shoe, the proper break point, and the pivot point, as well as by affecting traction and shock absorption.346 The tread design has been used in marketing certain running shoes, including the original Nike waffle sole (Fig. 25J-22). The tread design can clearly alter the traction characteristics of the shoe, but its relationship to foot function and injury prevention remains unproved.

TABLE 25J-7 Friction Coefficients for Several Floor Combinations Tested under Laboratory Conditions Surface Shoe

Carpet

Synthetic Granular

PVC

Sand

Asphalt

1.05-1.15

0.95-1.05

1.00-1.20

0.40-0.60

0.70-0.80

0.95-1.05

0.80-0.95

0.80-0.90

0.30-0.55

0.60-0.75

0.50-0.60

0.75-0.90

0.40-0.50

0.30-0.50

0.65-0.75

1.15-1.25

1.05-1.15

1.00-1.10

0.50-0.60

0.70-0.80

105-1.15

0.95-1.05

0.80-0.90

0.40-0.60

0.70-0.80

0.60-0.70

0.80-0.90

0.40-0.50

0.40-0.50

0.75-0.85

Sliding Friction Coefficients

All-around shoe Little profile All-around shoe Treaded Profile Tennis shoe Indoor No profile Static Friction Coefficients

All-around shoe Little profile Jogging shoe Treaded Profile Tennis shoe Indoor No profile PVC, pol�� yvinyl c�� hloride.

Maximum Torque (Nm)

Foot and Ankle 2191

40 Mean

Standard deviation

30

la y C

t al As ph

ra ss G

r tif gr icia as l s Te nn is

oo In d

Ar

O

ut do

or

20

Surface Figure 25J-20 Mean values and standard deviations for maximal torque for 12 subjects on seven surfaces in eight different shoes. (Redrawn with permission from Nigg BM, Denoth J, Keir B, et al: Load sport shoes and playing surfaces. In Frederick EC [ed]: Sport Shoes and Playing Surfaces. Champaign, Ill, Human Kinetics Publishers, 1984, p 12. © Nike, Inc.)

Efficiency of movement is an important factor in ath letic performance, and proper traction ensures that internal forces generated by the body’s muscles are efficiently con verted into movement. A natural byproduct of this relation ship was the introduction of cleats to the outsole of the shoe to improve traction. Introduced about 100 years ago for sports, they have been a source of controversy ever since. Rule changes in sports banned pointed cleats and placed size

limits on cleats. The polemics continued with the concept that foot fixation was a leading cause of injury of the ankle and knee in sports.346,350,351 Dr. Daniel Hanley of Bowdoin College championed this attack on rigid cleating, particu larly in the heel area, after he observed the incidence of sig nificant noncontact injuries to the knee at Bowdoin.345,351,352 Cleat modifications followed, including plastic heel disks,237 lower profile oval cleats,345 soccer cleats,353 and cleats attached to a rotating turntable (Fig. 25J-23),245,350 as well as cleats with a circular design for artificial grass, the Tanel 360 (Fig. 25J-24).354,355 This design concept theoretically allows pivoting with adequate traction but without the problem of foot fixation. Queen and colleagues examined the effect of different cleat plate configurations on plantar pressure. 356 They noted significant differences in forefoot loading pat terns among cleat types, but no definitive conclusions were drawn in regard to injuries. Research has documented the relationship between cleats and sports injuries. Rowe studied the effect of different shoes and cleats on knee and ankle injuries in the New York State Public High School Athletic Association during the 1967 and 1968 seasons.353 He found a reduction in injuries with the use of a low-cut disk heel shoe com pared with low- and high-top shoes with heel cleats and an even more substantial reduction with short soccer-type cleats used by athletes playing on natural grass. Although Rowe’s findings were not subjected to statistical verifica tion, ankle injuries were reduced from a high of 77 per 100,000 hours of participation to 34 per 100,000 by changing from the low-cut conventional heel to the soccer shoe. Rates of injury with the soccer shoe were lower than those seen with either type of high-top shoe. Torg and Queden feld found a similar reduction in ankle injuries from 0.45 per team per game with conventional cleats to 0.23 per team per game with a soccer-type shoe.253 Cameron and Davis found

A

B

C

D

Figure 25J-21 Different tread designs: A, Track shoe. B, Football cleats. C, Baseball spikes. D, Running shoe. (Photograph by Christopher B. Hirose.)


A

B

Figure 25J-22 The original Nike Waffle shoe. (© Nike, Inc.: www.nike.com.)

a progressive reduction in ankle injuries from 8.46% with a cleated shoe to 7.69% with a heel plate to 5.64% with a soc cer shoe to 3.00% with their swivel shoe design.350 An exhaustive study of injuries in North Carolina high school football players by Mueller and Blyth emphasized the critical role of the playing surface in evaluating the role of cleats.254 They reported a reduction in knee and ankle injuries from 14.8% to 11.5% by changing from tra ditional cleats to soccer-type shoes on properly maintained fields. Bonstingl and colleagues concluded that there was a positive relationship between torque and injury.357,358 The highest torque occurred with a conventional foot ball shoe, which contained seven ¾-inch high cleats. A substantial reduction in torque occurs in circular pat tern outsole design (e.g., the original Tanel 360 shoe). Other studies have confirmed these differences in friction and torque between various outersoles, cleats, and playing

Figure 25J-23 Dr. Bruce Cameron’s swivel shoe alternative cleat design. (Photograph by Thomas O. Clanton.)

surfaces.231,233,344,357,359 This is one of the most obvi ous areas in which basic science and clinical research in the field of sports medicine have had an impact on sports equipment designed to prevent injury.

PLAYING SURFACES AND INJURY Of all the etiologic factors involved in foot and ankle inju ries, the playing surface may be the most important and, at the same time, the least understood. If it is true that load on the human body is the common ground for discover ing clues to the causes of athletic injury, the influence of forces and moments intrinsic to the surface of play must be critically analyzed.348,360 Traditional sports surfaces have been composed of natural materials: wooden basketball courts, clay and grass tennis courts, cinder tracks, grass and dirt baseball diamonds, and natural grass football and soc cer fields. With advancing technology, there was a move to replace these with more durable low-maintenance syn thetic surfaces. Although such surfaces had some attractive advantages, they were not universally accepted and were subjected to quick criticism that followed their short-lived popularity. Sports surfaces should accomplish three functions: (1) protection, (2) performance, and (3) maintenance.293 The first is concerned with the protection of the athlete from excessive forces and injury. The sports perfor mance function relates to the optimization of the athletic experience through the qualities of the surface. Mainte nance refers to the durability and conservation of the sur face and preserving the former two qualities. The task of reviewing all sports surfaces is overwhelming, considering that wrestling mats, gymnastic beams, ice-skating rinks, and snow-packed slalom courses could all be included. To

Foot and Ankle 2193

Figure 25J-24 Alternative cleating patterns in the Tanel 360 football shoe. (Photograph courtesy of Tanel Corporation.)

gain some understanding of this broad topic, we divide surfaces into indoor and outdoor surfaces and into natural and synthetic surfaces. There is some overlap between sur faces in sports, and multiple uses are the rule in most sports facilities. As the characteristics of a particular surface used in one sport are delineated, the reader is reminded that the surface characteristics are applicable in other sports, but that protective, technical, and performance characteristics may vary among sports, types of athletes, shoewear, and environmental situations.

History Since ancient times, humans have competed athleti cally. The surface chosen was that which occurred natu rally, most commonly grazed fields and dirt areas freed of rocks and obstacles. As culture progressed, so did the playing fields, and stadiums were created for competition in ancient Greece. Improvements in these outdoor facili ties were accomplished by maintaining the fields, using developments in soil and grass technology, crowning to improve drainage, and limiting play to allow the surface to recover. It was not until 1964 that synthetic grass, pro duced by Monsanto, was introduced and installed on the playing field at Moses Brown School in Providence, Rhode Island.51,361,362 Developed as a substitute for grass in a place where its natural growth was difficult, this artificial surface created little impact until the 1960s. On April 9, 1965, the “eighth wonder of the world,” the Astrodome, was com pleted amid much hype in a city known for space-age tech nology: Houston, Texas.363 A special grass was developed to grow inside the Astrodome: Tifway 419 Bermuda.363 Even the foundation soil required a unique design. Unfor tunately, when the clear Lucite roof panels were darkened to eliminate glare and lost fly balls, the grass withered, and management scrambled to find a suitable substitute. The

following year, the natural grass was replaced by Monsan to’s synthetic grass, and this became known as AstroTurf. Now, grass playing fields in natural and custom-installed varieties compete with synthetic surfaces.364 Entire publi cations advise facility managers in the most intricate detail of how to maintain playing fields.32 The debate about which is the better surface has involved both the public and the scientific community, and more than 50 articles have appeared without a summary conclusion.51,57,160,360,365-371 Perhaps the key deficiency in these studies is their poor control of other key factors in the turf equation such as the shoe, field maintenance, and weather. Synthetic grass manufacturers have been forced to make improvements in their fibers, mats, underpads, and drainage systems, and advocates of natural grass have used modern methods to introduce advances of their own. As long as prevention of injury is a prime concern in these advances, both the indi vidual athlete and society as a whole will benefit. This same revolutionary process has occurred in other outdoor surface sports, such as tennis and track. Ten nis originated from a French handball game called jeu de paume at about the 13th century and was played in court yards over a fringed net.372 Major Walter Wingfield of North Wales invented a game in 1873 from which modern outdoor tennis has evolved. Its popularity spread so rapidly that the All England Croquet Club added the name Lawn Tennis to its title and sponsored the first championship in 1877. As the name indicates, grass was the original surface used for play. As the popularity of tennis increased, other playing surfaces were needed to allow winter play and to bypass the problems inherent in growing a playing field. In 1909, Claude Brown introduced the clay court. Although these surfaces remain popular, new court surfaces have flourished to such a degree that modern tennis has the widest choice of playing surface of any major sport (Table 25J-8). Only recently have the surface characteristics of


Glare

Initial Cost per Court Including Base* (1992) prices

Maintenance

Avg. Time before Resurfacing

Resurfacing Cost (1992) prices)

Surface Hardness

Fast dry

No

No

14,000-18,000†

Daily and yearly

Annual

1000-3000

Soft

With subirrigation Clay

No

Generally

24,000-26,000 9,000-11,000

Daily and yearly

5 yr

Top dressing 1000-1500

Soft

Grass

No

no

15,000-17,000

Daily and yearly

Indefinite

Varies

Soft

Sand-filled synthetic turf‡

Yes

no

25,000-30,000

Daily and yearly

Indefinite

N/A

Soft

Porous concrete

Yes

yes

27,000-31,000

Minor

Indefinite

N/A

Hard

Court Type

Repairs May Be Costly

TABLE 25J-8 Chart Comparing Various Tennis Court Surfaces

Porous

Nonporous Noncushioned

Concrete post-tensioned Concrete reinforced

Yes

No (if colored)

22,000-25,000

Very minor

5 yr (if colored)

3000-3500

Hard

Yes

No (if colored)

19,000-21,000

Very minor

5 yr (if colored)

3000-3500

Hard

Asphalt plant mix (colored)

No

No

16,000-18,000

Very minor

5 yr

2500-3000

Hard

Emulsified asphalt mix

No

No

19,000-21,000

Very minor

5 yr

3000-3500

Hard

Asphalt penetration macadam

No

No

15,000-17,000

Very minor

5 yr

3000-3500

Hard

Nonporous Cushioned

Asphalt bound system (colored) Liquid applied synthetic

No

No

19,000-23,000

Very minor

5 yr

2500-3500

Soft

Yes

Possible

30,000-40,000

Very minor

5-10 yr

2500-3500

Soft

Textile§ Modular§ Removable§

No No No

No No No

25,000-28,000 22,000-26,000 25,00-30,000

Very minor Very minor Very minor

Varies Varies Varies

Varies Varies Varies

Soft Soft Soft

*Prices vary regionally, do not include site preparation or fencing, and will be somewhat reduced when building or resurfacing batteries of courts. †Including sprinkler system. ‡Damaged areas may be readily repaired. §Including base construction and structurally sound surface. Reprinted from Tennis Courts 1992-1993 with the permission of the United States Tennis Association, 707 Alexander Road, Princeton, NJ 08540.

Cushioned Surface

Durable

Court Speed Adjustable

Lines Affect Ball Bounce

Yes, slightly

Yes

Yes

Yes

Yes if tapes

No

No‡

Yes

Short if damp court

Yes

Varies

Slow

Yes

Yes

Yes

Yes

No

No‡

Yes

Moderately long

Yes

Green

Slow

Yes

Out only

Yes

Yes

Yes if tapes No

Yes

No

Short

Yes

Green, red

Fast

No

Yes

Yes

Yes

No

Yes

Yes

Short

Yes

Concrete

Fast

No

Out only

No

No

No

No

Hard objects can damage Hard objects can damage Yes

Controllable

Yes

Variety

Fast

No

Yes

No

No

No

No

Yes

Yes

Variety

Fast

No

Yes

No

No

No

No

Yes

Yes

Variety

Fast

No

Yes

No

No

No

No

Yes

Yes

Variety

Fast

No

Yes

No

No

No

No

Yes

Yes

Variety

Fast

No

Yes

No

No

No

No

Yes

Yes

Yes

Variety

Fast

No

Yes

No

No

No

Yes

Yes

Yes

No if glossy finish, yes if gritty finish Yes Yes Yes

Variety

Fast

No

Yes

No

No

No

Yes

Yes

Yes

Variety Green, red Variety

Fast Fast Fast

No No No

In only Yes In only

N/A Yes N/A

No Yes No

No No No

Yes Yes Minor

Yes Yes Yes

No Yes No

Long if glossy finish, medium if gritty finish Long if glossy finish, medium if gritty finish

Long if glossy finish, short if gritty finish Varies shortest to longest Short Medium to short Varies shortest to longest

No if glossy finish

Slide Surface

Fast

Surface OK In & Out

Green, red

Ball Discolored

Drying Time After Rain

Yes

Ball Spin Effective

Short if damp court

Ball Skid Length

Colors

Surface Cool on Hot Day

Foot and Ankle 2195

No


these courts been subjected to laboratory and subject tests in an attempt to establish their safety. Track and field is unquestionably the oldest form of organized sports activity, dating back 3500 years to ancient Greece. The religious festival at Olympia featur ing this activity became an event of such proportions that the Greeks dated events with reference to the year of the Olympiad.373,374 Records dating back to 776 bc indicate that a race covering 192 m took place on a track about 32 m wide.374 These early contests were held on grass, and later races took place on public thoroughfares. Improvements in track design led to the use of cinders and a mixture of cinders and clay by the late 1800s. Syn thetic surfaces began to appear in the 1960s with the pro duction of a prototype track by the 3M Corporation for Macalester College in 1965.361 The synthetic track gained wide appeal after its use in the 1968 Olympics in Mexico City, where numerous records were set. Although ath letes have long known the difference between “fast tracks” and “slow tracks,” it remained for McMahon and Greene from Harvard to produce a track engineered to optimize running speed.375-378 This was an indoor track that theo retically and practically enhanced speed by about 2% (or 5 seconds per mile), and the physics have since been incor porated into outdoor track surfacing technology. Although the cinder track has been virtually eliminated from elite competition, its value in reducing injuries remains clear, and some schools have preserved cinder tracks for use in training. Tracks for elite competition are generally made from rubber or synthetic materials such as polyurethane. Corporate research and development departments work ing in conjunction with bioengineers at universities in locations as far apart as Calgary, Zurich, Rome, and Boston design these surfaces to maximize performance and reduce injury potential.379 The origin of the movement of sports events from out doors to inside can also be traced to ancient Greece. The name gymnasium is derived from the Greek word meaning “school for naked exercise.”380 Exercise was an integral part of Greek society, but the gymnasium also served as a public facility for the training of male athletes to par ticipate in the aforementioned public games. From its beginning as a room that served as a gathering place for exercise, the gymnasium grew in proportion to accom modate baths, dressing quarters, rooms for specialized purposes, and larger areas for contests and spectators.380 The first modern gymnasium opened in Copenhagen in 1799.381 Pestalozzi, Ling, and Spiess stimulated further development, and groups such as the Young Men’s Chris tian Association and the Young Men’s Hebrew Associa tion included physical exercise in their activities in the mid-1800s. The international Young Men’s Christian Association training school in Springfield, Massachusetts was the site where James Naismith introduced the new game of basketball to the world in 1891.382 Wooden floors became the traditional gymnasium surface and continued to predominate for basketball courts as well as for other indoor courts and dance studios. Contemporary surfaces have been said to have advantages ranging from improved durability to noise reduction to better use of space, but seldom have their supporters argued for improved safety. In the study of sports surfaces, whether indoor or out

door, it is evident that many factors affect the safety value of the surface. These include not only the visible surface and the top finish but also, and equally important, the undersurface.

Injury Incidence Although there is consensus that sports surfaces play a crit ical role in causing athletic injuries, it has been quite dif ficult to establish the incidence of injury in a sport that can be attributed solely to the playing surface. Even in the area of traditional grass football fields, there have been stud ies that have suggested differences in incidence of injury from field to field, although the surface material is the same. The 1992 study by Powell and Schootman is one of the best-controlled studies demonstrating that football players were at significantly higher risk for knee ligament injury when playing on AstroTurf as compared with natu ral grass.383 Unfortunately, their study does not address injuries outside the knee. A study of North Carolina foot ball players conducted by Mueller and Blyth254 showed that a reduction in the injury rate resulted simply from resurfacing and maintaining the game and practice fields. Injury rates plummeted from 29.3% on unresurfaced fields in 1969 to 14.8% on resurfaced fields in 1972, a 30% reduction. Poor field conditions were considered a factor in 8 of 34 soccer injuries in the paper by Sullivan,95 in 14 of 18 outdoor soccer injuries in Hoff and Martin’s series,46 and in 62 of 318 injuries in the Swedish study of Ekstrand and Gillquist.91 These studies draw attention to the play ing field and its importance and the need for further work on proper playing surfaces and their maintenance to reduce injury rates in sports. FieldTurf was developed to duplicate the playing characteristics of natural grass. Mey ers and associates studied the differences in injuries of high school football players between the two surfaces and found that the types of injuries were different between the two surfaces. The natural grass surface produced more head and neural traumas and ligamentous injuries. The Field Turf produced more injuries during higher temperatures, muscle-related trauma, and epidermal injuries.384 Studies of injuries and injury rates in sports ranging from dance189,385 to ice hockey386,387 to tennis388 have mentioned the sport’s surface as a factor. For example, Pasanen and colleagues studied the injury risk in pivoting indoor sports between artificial floors and wooden floors.389 They found that the risk for a traumatic injury in pivoting indoors sports is two-fold higher on artificial floors when compared with wooden floors, largely due to a higher shoe-surface friction level. Although the surface is frequently named as a source of problems in runners, there have been no studies that have unequivocally confirmed this.28 The Ontario cohort study found no association between running surface and injury, whereas the companion study from South Caro lina showed a statistically meaningful relationship only for females running on concrete.228 In baseball, if the base is included as a part of the play ing field surface, several studies can be cited indicating that this is the primary factor in ankle injuries in baseball and softball. Janda and coworkers found that 71% of the recreational softball injuries in their study were related to sliding into bases.47 A follow-up to this study showed the

Foot and Ankle 2197

MECHANICAL FACTORS Regardless of the surface, the underlying question to be answered is how the surface affects load in the individual participant.298,348 For this purpose, attention has been focused on certain material properties of the sports sur face such as hardness and friction together with perfor mance properties such as energy loss or resilience. Nigg has reviewed the methods by which a playing surface may be characterized and specified some of the tests that are important in determining these properties.394

Hardness One of the most obvious differences between surfaces detected by casual observation as well as by sophisticated testing is the relative hardness or softness. Hardness is related to the ground reaction force. In conformity with Newton’s first law (for every action there is an equal and opposite reaction), the vertical reaction force responds to the vertical force component applied by the individual at foot strike. Its amplitude is affected by the shock-absorbing qualities of the surface to which the force is applied. The time needed for force absorption and reaction is the key to the amplitude of the reaction force and relates to the com pliance of the surface material. Hard materials deform less than soft materials during identical impact testing condi tions: a well-maintained grass lawn is softer than a concrete sidewalk. When impact occurs between an object such as a leg and a surface such as grass or concrete, it is the surface hardness that limits the time of impact while increasing the amplitude of the reaction force (Fig. 25J-25). Kerdok and colleagues built experimental platforms with adjustable stiffness to examine the leg stiffness and metabolic cost of the athlete.395 The 12.5-fold decrease in surface stiffness resulted in a 12% decrease in the runner’s metabolic rate

Surface A (Hard)

Reaction force N

implications of an injury-prevention method such as the use of a breakaway base on these surface-related injuries.48 Janda and associates estimated that breakaway bases could reduce the incidence of serious injury in softball by 96% and result in a $2 billion per year savings in acute medical care costs.390 In the area of children’s playground injuries, statis tics suggest that falls to the ground account for 60% of playground equipment injuries, yet barely half of day care playground equipment is installed on impact-absorbing surfaces.246,391 Impact studies of five types of loose-fill playground surfaces at a variety of drop heights, mate rial depths, and conditions suggested that shredded rub ber was the best performer, and there was little difference between sand, wood fibers, and wood chips; and pea gravel had the worst performance, making it a poor choice for playground surfacing.392 A separate study supported these findings: children sustained significantly more inju ries in playgrounds with concrete surfaces than in those with bark or rubberized surfaces. Playgrounds with rub ber surfaces had the lowest rate of injury, with a risk half that of bark and a fifth of that of concrete. Rubberized impact-absorbing surfaces are safer than bark.393 Certainly the playing surface is an important consideration in the prevention of injury.

Surface B (Soft)

Time of impact msec Figure 25J-25 Example of relationship between time of impact and type of surface. Hard surface (A) has a short time of impact but a high reaction force, whereas soft surface (B) has a longer time of impact and a lower reaction force.

and a 29% increase in their leg stiffness. They concluded that an increased energy rebound from the compliant surfaces studied contributes to the enhanced running economy. It takes little imagination to determine that sports participation on a soft surface such as a gymnastics mat carries less risk for certain impact-related injuries than a similar activity performed on a wooden floor. By the same token, athletes running on shock-absorbing gymnastics mats compared with a tuned track would set few records.378 From these mundane examples, we can conclude that there are some opposing factors confronting us in this analysis. Although a harder surface may provide a better surface for performance needs in certain sports, it may create simulta neously an increased exposure to injury. This fact appears to be borne out most obviously by synthetic tracks. Hardness is the resistance generated by a material during deformation in response to an externally applied force.348,396 In the study of various materials, their behav ior is described by means of a stress-strain curve or stressdeformation diagram. The plastic or elastic behavior of a material is determined by the remaining deformation once the acting force is removed. When the deformation persists, the material is described as plastic, and when the material returns to its original shape, it is elastic. A sports surface may be further characterized as being either area elastic or point elastic.397 Owing to their high bending strength, area elastic surfaces distribute forces over a wide area. Point elastic surfaces have low bending strength and therefore deform only in a very confined area (Fig. 25J-26). This fact has implications for both performance and health. From the clinical standpoint, there is a widespread belief that harder surfaces are associated with a higher incidence of injury for any given activity. This conclusion seems obvious, but it is difficult to support scientifically. Such conditions as shin splints, stress fractures, tibial stress syndrome, turf toe, bursitis, arthritis, and even acute frac tures have been associated with the higher loads imparted by surfaces with limited compliance. Bowers and Martin


producing initial decelerations as high as 80 G force (G) is a primary etiologic factor.400 The relationship between surface hardness and stress fractures has been mentioned in several studies.72,159,188,280-282,401 With this as background, it is apparent that surface hardness is important in the study of athletic injury, although its relative contribution among the interrelated factors is imprecise.

Friction

Point Elasticity

Area Elasticity

Figure 25J-26 Example of point elastic surface and area elastic surface. (Redrawn with permission from Denoth J: Indoor athletic playing surfaces—floor vs. shoe. In Segesser B, Pförringer W [eds]: The Shoe in Sport. Chicago, Year Book Medical Publishers, 1989, pp 65-69.)

demonstrated the existence of reduced shock-absorbing characteristics in 5-year-old AstroTurf compared with new AstroTurf, describing this as “clearly detrimental to player safety.”398 Unfortunately, they did not show a clear relationship between this lack of impact absorption and an increase in either acute or chronic injuries. Larson and Osternig399 reported one of the few clinical studies implicating surface hardness as a source of specific athletic injury in 1974. In a survey of Pacific-8 Conference ath letic trainers after the 1973 football season, they showed that the incidence of prepatellar and olecranon bursitis was increased on artificial grass compared with natural grass and attributed this increase to the hard underlying subbase. Anecdotally, considerable evidence of problems with harder playing surfaces exists because players commonly complain of aching feet and legs after standing and practic ing on older synthetic fields. The injury most frequently associated with sports par ticipation on artificial grass is turf toe.179,181,234 This injury is a sprain of the first metatarsophalangeal joint that has been inextricably linked to the artificial playing surface. Turf toe is a distinct clinical entity related to the combina tion of a relatively flexible shoe and a hard artificial sur face.234 Despite the weight of clinical evidence pointing to the relationship between turf toe and the artificial surface, little statistical support exists implicating surface hardness as a major factor. The injury does indeed occur on natural grass and probably has more to do with the flexibility of the shoe and frictional characteristics of the surface than its hardness. Impact forces, skeletal transient forces, and excess load produced by hard surfaces have been emphasized as etiologic factors in many other conditions ranging from osteoarthritis to shin splints to stress fractures. Statistical verification of this relationship, however, remains absent. An increased incidence of tibial periostitis, Achilles tendi nitis, Achilles tendon rupture, and muscle rupture are pos tulated to be the result of hard surface synthetic tracks.53 Haberl and Prokop have related these conditions to what they call Tartan syndrome and propose that surface hardness

Without friction, human locomotion would be impossible. The frictional properties of the surface are the second crit ical mechanical factor of sport surfaces related to sports performance and injury. Whereas hardness is defined by a high vertical stiffness, friction relates to horizontal stiff ness. The static coefficient of friction (μ) is the inherent property of the two contacting materials. It can be calcu lated from the equation μ = F/W, where W is the weight of the object being moved over a surface and F is the force required to move the object.344,402 This equation applies to smooth, uniform surfaces, but not to the shoe-turf inter face. Therefore, a similar term has been described as the release coefficient (r). It is expressed as r = F/W, where W is the weight in the shoe and F is the force necessary to release the shoe-turf interface when engaged.344 The difficulties imposed by reduced friction are well known to the novice ice skater. High friction between the shoe and the surface translates into good traction for the athlete and improved performance. Unfortunately, this factor also means greater load on the body, which may exceed physi ologic limits. Therefore, a trade-off exists between perfor mance-enhancing qualities and safety considerations. Friction can be viewed in several ways that are impor tant to sports biomechanics. There are two types of fric tion to be considered: static and kinetic.403 Static friction is the resistance to movement between two objects that are not moving relative to each other. It is a surface property of the contact surfaces. Kinetic friction occurs when two objects are moving relative to each other, rub together, and typically slow down one or both of the objects. Friction can also be viewed in terms of horizontal or rotational fric tion.348,393,403 Functionally, the former corresponds to the force resisting the foot sliding or moving sideways, whereas rotational friction relates to torque generated in activities such as turning. Torque is considered one of the primary etiologic factors in injuries to the knee and ankle.231,357

Energy Loss A separate but equally important property apart from hardness is the energy loss that occurs when a material is loaded. This property varies over a wide range from sur face to surface and carries major implications in the field of sports biomechanics. As depicted in Figure 25J-27, materials can exhibit similar elastic behaviors on the stress and strain diagram and yet have very different responses to the effects of loading and unloading. In this figure, material A shows no loss of mechanical energy, whereas material B depicts a loss of mechanical energy equivalent to the shaded area. This energy loss is not a true mate rial property because it depends on the loading rate and other variables. When a material has the quality of variable

Foot and Ankle 2199

Material 2

Stress

Stress

Material 1

Deformation

Figure 25J-27 Differences in response of materials to loading and unloading despite similar elastic behavior. (Redrawn with permission from Denoth J: Load on the locomotor system and modelling. In Nigg BM [ed]: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics Publishers, 1986, p 96. © 1986 by Benno M. Nigg.)

deformation dependent on velocity of deformation, it is described as viscoelastic. If energy applied to a surface is lost in the surface deformation, performance may suffer.378 Surfaces that deform to greater degrees are called compliant and result in increased contact time. This is the means by which cushioning occurs. By increasing the time of colli sion, the force between the colliding bodies is decreased. The final property of importance in athletic performance on a given surface is its resilience. High resilience indicates that the energy stored in the surface owing to its stiffness is returned to the athlete. This has implications for enhanc ing performance as well as lessening fatigue.378,397

Experimental Work Because of a presumed association with injuries, fric tional properties of various sport surfaces and athletic shoes have been the subject of studies by several authors. Torg and Quedenfeld published pioneering work in the field of sports medicine in 1971 aimed at reducing injury rates by targeting the shoe-surface interface.253 The study was done on grass and concentrated on the relationship between the number and size of shoe cleats and the inci dence and severity of knee injuries in high school football players. This investigation showed a reduction in ankle injuries from 72 to 36 and in ankle fractures from 13 to 7 by changing from a traditional seven-cleated football shoe to a multicleated soccer shoe. Continuing this study, Torg and colleagues performed laboratory studies to determine the torque necessary to release an engaged shoe-surface interface.236,237 Twelve shoes and nine surface condi tions were tested for a total of 108 release coefficients. These are shown in Tables 25J-9 and 25J-10. Coefficient differences of 0.05 were determined to be significant. The release coefficients ranged from a high of 0.55 ± 0.06, with a conventional seven-cleated football shoe on dry grass, to a low of 0.20 ± 0.02, with a conventional shoe that had an uncleated disk heel (Bowdoin modification) on dry Polyturf. The use of wet versus dry conditions was based on the study by Bramwell and colleagues in 1972, which

s uggested that fewer injuries were sustained on wet syn thetic fields than dry synthetic fields.404 From their study, Torg and coworkers concluded that the release coefficient varies with (1) the number, length, and diameter of the cleats; (2) the type of surface—natural or artificial; (3) the condition of the surface—wet or dry; and (4) the outsole material of the shoe—polyurethane or soft rubber. They classified shoes as safe for a particular surface when the release coefficient was 0.31 or below. Cawley and colleagues recently studied nine shoes by three manufacturers, which were characterized as turf, court, molded cleat, or traditional cleat and tested on both natural grass and synthetic turf.405 They found that the cleated shoes (both traditional and molded) generated the highest frictional and torsional resistance on the grass surface when compared with the other categories of shoes. Grass generated higher peak moments than turf for the cleated shoes. These results demonstrate the considerable differences between laboratory and physiologic conditions and that the increase in frictional resistance is nonlinear with increasing loads. Stanitski and associates determined the static coefficient of 16 different shoe-surface combinations.402 They used a drag test of a size 13 shoe with a 25-pound load pulled both with and against the grain, across various sections of football fields. Their results are shown in Table 25J-11. The coefficient of friction ranged from a high of l.54 for a Riddell At-31 (standard last, leather upper, molded plas tic sole, 203⁄8-inch conical cleats) on Polyturf to a low of 0.92 for the Puma 1430 (“soft last,” molded rubber sole, 233⁄8-inch cylindrical cleats with central indentations) on Tartan Turf and grass fields. These investigators found no grain effect and “essentially no change” when the surface was wet. Bowers and Martin continued the study of cleat-surface friction, adding the new parameter of a new versus a worn synthetic surface.233 The cleats from two different shoes were studied. One cleat was evaluated in both a slightly worn and a very worn state. Three similar shoes were mounted in a triangular pattern on a platform weighted from 2 to

2200 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25J-9 Results of Torque Testing in 12 Shoes for Nine Surface Conditions Release Coefficients Shoe

Grass

Grass Wet

AstroTurf

Astroturf Wet

Tartan Turf

Tartan Turf Wet

Poly Turf

Group I 0.55 ± 0.06 0.35 ± 0.03 0.34 ± 0.03 0.29 ± 0.3 Group II 0.44 ± 0.04 0.31 ± 0.03 0.32 ± 0.02 0.26 ± 0.02 Group III 0.37 ± 0.04 0.26 ± 0.02 0.26 ± 0.03 0.20 ± 0.02 Group IV 0.36 ± 0.03 0.32 ± 0.04 0.41 ± 0.03 0.26 ± 0.03 0.34 ± 0.03 0.23 ± 0.02 0.33 ± 0.02 Group V 0.28 ± 0.03 0.27 ± 0.03 0.29 ± 0.03 0.29 ± 0.03 0.27 ± 0.03 0.24 ± 0.02 0.26 ± 0.02 Group VI 0.40 ± 0.01 0.36 ± 01 0.41 ± 0.02 Group VII 0.45 ± 0.04 0.37 ± 0.02 0.45 ± 0.02 Shoes in groups I-V have plastic or polyurethane soles. Shoes in groups VI-VII have rubber soles. Group I: Conventional 7-posted football shoe, ¾-inch cleat length, 3⁄8-inch tip diameter, plastic sole Group II: Conventional 7-posted football shoe, ½-inch cleat length, 3⁄8-inch tip diameter, polyurethane sole Group III: Conventional shoe with five ¾-inch cleats, 3⁄8-inch tip diameter, Bowdoin heel, polyurethane sole Group IV: Soccer style, 15 cleats with 3⁄8-inch tip diameter, polyurethane sole Group V: Soccer style, 15 cleats with ½-inch tip diameter, polyurethane sole Group VI: Soccer style, 12 cleats (ten 3⁄8-inch length and two ½-inch length), ½-inch tip diameter, rubber sole Group VII: Soccer style, 49 to 121 cleats (3⁄8-inch or 5⁄16 -inch length), ½-inch tip diameter to pointed tips, rubber sole

Poly Turf Wet

0.23 ± 0.02 0.23 ± 0.02

From Torg JS, Quedenfeld TC, Landau S: The shoe-surface interface and its relationship to football knee injuries. J Sports Med 2:261-269, 1974.

14 pounds that was pulled across the new or worn turf. This study showed 16% more friction against the grain of a 5-year-old AstroTurf field when wet and 22% more fric tion when dry (Fig. 25J-28). From this study, the authors provided a formula for calculating coefficients of friction for individual shoes and surfaces that increased linearly with the number of cleats. They suggested that changes in friction altered player performance (e.g., smaller slip angles on wet turf) and that increasing friction could pro duce “foot lock” and result in increased injuries. Bonstingl and coworkers expanded the study of shoes and surfaces by looking at dynamic torque for 11 shoe types on four dry turf samples at two different player weights.357 They used the swivel shoe of Cameron’s design, five styles of multicleated soccer shoes, four styles of noncleated basket ball shoes, and a conventional football shoe for grass (seven ¾-inch plastic screw-on cleats with metal tips). The four surfaces were AstroTurf, Tartan Turf, Polyturf, and grass. The two player weights used for the normal force were 170 pounds (77 kg) and 200 pounds (91 kg). All combinations were tested for both toe stance and foot stance positions. They found that all shoes except the swivel shoe developed about 70% more torque in foot stance than in toe stance

and that the higher player weight resulted in more torque. The conventional shoe tested on grass had among the high est torque. Although noncleated shoes generally had less torque for all playing surfaces, this was not absolutely true for all surfaces. This study proved that torque applied to an athlete’s leg depends on (1) the type and outsole design of the shoe, (2) the playing surface, (3) the player weight being supported, and (4) the foot stance assumed. Culpepper and Niemann continued the study of the shoe-turf interface in 1983 by looking at the release coef ficient for torque in several shoe-surface combinations.344 They tested five different soccer-style shoes of variable cleat number and configurations on old and new Polyturf and new AstroTurf under wet and dry conditions. Loads rang ing from 10 to 90 pounds were transferred down a metal shaft to a prosthetic foot on which the different shoes were mounted (Fig. 25J-29). The release coefficient of torque was calculated for 30 different conditions (Table 25J-12). The authors found that although a specific shoe did vary in its release coefficient ranking on different surfaces, a shoe that had a low coefficient on one surface under one condition was generally lower on all three surfaces whether wet or dry, whereas a shoe that ranked higher did so for all conditions.

TABLE 25J-10 Relationship of Shoe-Turf Interface

Release Coefficient to Incidence of Football Knee Injuries Release Coefficient

0.60— 0.50— 0.40— 0.30— 0.20— 0.10—

Not safe Probably safe Probably safe Safe

TABLE 25J-11 Friction Coefficients for Various Surfaces and Shoes

0.49

0.31

From Torg JS, Quedenfeld TC, Landau S: The shoe-surface interface and its relationship to football knee injuries. J Sports Med 2:261-269, 1974.

Coefficient of Sliding Friction Surface Shoe

Poly Turf

Astro Turf

Tartan Turf

Grass

A B C D

1.49 1.54 1.33 1.38

1.34 1.31 1.23 1.16

1.42 1.16 1.13 0.92

1.23 1.21 1.07 0.92

From Stanitski CL, McMaster JH, Ferguson RJ: Synthetic turf and grass: A comparative study. J Sports Med 2:22-26, 1974.

Foot and Ankle 2201

A

B

C

D

Figure 25J-28 AstroTurf evolution. A, Original AstroTurf (new) in its 1966 design with long nylon ribbon. B, Original AstroTurf showing its grain effect. C, Newer AstroTurf 8. D, Weave pattern of AstroTurf designed to prevent a grain effect. (Photographs by Thomas O. Clanton.)

Another study of both static friction and torque appeared in 1983, when Van Gheluwe and colleagues tested nine different shoes on three varieties of artificial turf in both the toe stance and foot stance positions.238 In their analy sis, the authors demonstrated higher values for friction and torque for AstroTurf compared with the other surfaces (AstroTurf scored highest in 22 of 36, or 61%, of the test conditions). They attributed this result to the nylon fiber of AstroTurf compared with the polypropylene fiber used in the other surfaces. This confirmed the work of Bonst ingl and colleagues; however, the results violate the law of physics for dry friction, which predicts the linear relation ship for friction between two surfaces. This contradiction is significant when interpreting the results of other studies that have assumed this linear relationship. Andreasson and coworkers in Sweden published a more detailed study in 1986 evaluating torque and friction in a dynamic mode on an artificial surface.231 This was the first study to specifically add dynamic torque by using a rotat ing disk on which the surface was applied to simulate speed from walking to running. Twenty-five different shoes were tested, including running shoes, tennis shoes, soccer shoes for artificial turf, and soccer shoes for natural turf. Torque in toe stance varied from a low of less than 10 Nm for one of the running shoes and one of the multicleated soccer shoes to a high of more than 50 Nm for another multi cleated soccer shoe placed against the grain of the Poligrass

Artificial leg

Surface being tested

Rotation

Force plate Figure 25J-29 Example of device for testing torque. (Redrawn with permission from Physical Tests. Sport Research Review. Beaverton, Ore, Nike Sport Research Laboratory, Jan/Feb, 1990; and Van Gheluwe B, Deporte E, Hebbelinck M: Frictional forces and torques of soccer shoes on artificial turf. In Nigg BM, Kerr BA [eds]: Biomechanical Aspects of Sport Shoes and Playing Surfaces. Calgary, University of Calgary Press, 1983, pp 161-168.)


TABLE 25J-12 Release Coefficients of 30 Shoe-Surface Combinations New Poly Turf Dry

Wet

0.27 ± 0.01 0.35 ± 0.03 0.21 ± 0.01 0.32 ± 0.03 0.28 ± 0.01

0.21 ± 0.01 0.29 ± 0.01 0.23 ± 0.01 0.24 ± 0.01 0.29 ± 0.01

Shoe A B C D E

Old Poly Turf Dry

New Astro Turf Wet

0.24 ± 0.02 0.33 ± 0.05 0.29 ± 0.05 0.32 ± 0.02 0.30 ± 0.01

Dry

0.24 ± 0.02 0.31 ± 0.01 0.00 ± 0.01 0.31 ± 0.01 0.25 ± 0.02

Wet

0.19 ± 0.01 0.38 ± 0.03 0.19 ± 0.01 0.34 ± 0.03 0.26 ± 0.01

0.24 ± 0.01 0.35 ± 0.02 0.22 ± 0.02 0.26 ± 0.01 0.28 ± 0.01

Date from Culpepper MI, Niemann KMW: An investigation of the shoe-turf interface using different types of shoes on Poly-turf and Astro-turf: Torque and release coefficients. Alabama J Med Sci 20:387-390, 1983.

test surface. The authors showed that the frictional force is independent of speed between 1 and 5 m/second, but this is below the 7 to 10 m/second speeds that occur in modern football and soccer. Torque was generally lower for shoes with polypropylene outsoles compared with polyurethane and rubber-like soles. Nigg and Segesser reported in 1988 on the variation in friction related to a change in load.360 They found when studying the six different surfaces considered for the Toronto SkyDome playing surface that the static coef ficient of friction changed from lows of 1.13 for 280 N normal loads to highs of 3.48 for 769 N loads (Table 25J13).360 The tested surfaces ranked differently for the two load conditions. This result indicates the complexity of using material tests for choosing a playing surface because the individuals playing vary by a factor of 2 or more in weight and generate forces that may be well beyond those studied to date in laboratory tests.400 Just as there are differences between natural and artifi cial grass that affect the frictional properties of the play ing surface, similar differences have been known for other sport surfaces. Rheinstein and colleagues looked at static drag and dynamic torque characteristics of different shoes on two basketball surfaces (Fig. 25J-30).347 The three playing surfaces tested were clean hardwood, dusty hard wood, and clean artificial flooring (Tartan indoor surface manufactured by the 3M Corporation). Polyurethane soles produce less torque than the elastomer outsoles for all weight, floor, and surface condition parameters. Torque also decreased with increasing sole hardness for the elasto mer outsoles on the clean hardwood and artificial surface. As expected, greater player weight increased torque, and dust on the hardwood flooring cut torque almost in half. The polyurethane soles were considerably less affected by dust than the elastomer outsoles. One would expect that high friction and torque could overload the athlete and

result in injury. These findings have obvious implications for performance as well as prevention of injury in sports medicine. Nigg and associates measured the coefficients of static and sliding friction in 1980 for five different surfaces and three styles of shoewear.348 The dynamic, or sliding, coefficient of friction ranged from a low of 0.3 on sand (clay) with an indoor tennis shoe or a treaded jogging shoe to a high of 1.20 on a polyvinylchloride floor with an allaround shoe (see Table 25J-7). Nigg expanded on this work in 1986 and has used these studies to emphasize the dominant role of the playing surface on the translational friction coefficient, although he acknowledged the open question of whether the structure or material, or both, are most responsible for the result.218 In a separate study, Nigg and colleagues measured torque for 12 subjects rotating 180 degrees on one leg on seven different sport surfaces and with eight different types of shoes.303 Mean values for the different surfaces are shown in Figure 25J-20. The range varied from 20 Nm to 38 Nm, the highest torque being found on artificial grass. In an expanded study using average torque for five tested surfaces (10 Nm to 20 Nm) and average torque for 10 tested shoes (13 Nm to 18 Nm), Nigg proposed that torque was shoe and surface codependent to a greater degree than translational friction.218 In attempting to correlate the material tests for translational friction with the subject tests for rotational friction, Yeadon and Nigg found no relationship.397 This study demonstrates the dif ficulty of combining material and subject tests, as occurs also in tests of impact load, in which the subject’s response to a test condition may alter the result.394 Synthetic playing surfaces with rubber or sand infill are now used on many athletic fields such as soccer, football and rugby. Although these surfaces may come closer to the mechanical characteristics of a true grass playing surface

TABLE 25J-13 Variation in Static Coefficient of Friction for Translation with Variation in Vertical Load Using Football Shoes on Six Different Playing Surfaces (A through F)

Static Coefficient of Friction (Translational) Load (Vertical) (N)

A

B

C

D

E

F

280 769

1.13 3.15

1.42 2.90

1.30 2.57

1.30 2.57

1.56 3.48

1.51 3.15

From Nigg BM, Segesser B: The influence of playing surfaces on the load on the locomotor system and on football and tennis injuries. Sports Med 5:375-385, 1988.

Foot and Ankle 2203 a Ø (3.00 ± 0.10) mm b Ø (1.25 ± 0.15) mm 0.04 c 2.50 + – 0.01 mm d Ø (0.79 ± 0.01) mm r Ø (0.10 ± 0.01) mm f Ø (16.0 ± 2.50) mm

(

Shore A a b

c

)

Shore D a b

30° ± 1°

c

35° ± 0.25°

r d f

f

Figure 25J-30 Methods for measuring shore hardness. (Redrawn with permission from Denoth J: Load on the locomotor system and modelling. In Nigg BM [ed]: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics Publishers, 1986, p 97. © 1986 by Benno M. Nigg.)

than the older turf designs, their potential effects on lower extremity biomechanics and related injury rates necessitate further study. With the continued introduction of different playing surfaces, the relentless study the shoe-surface interaction can only help improve athlete safety. It does, however, raise some interesting questions. Does this put schools that can not afford multiple types of player surfaces at a measurable disadvantage? Does it put athletes at greater risk for injury when they are not afforded the best playing surface for a given game condition? Does the use of a shoe on surfaces for which it is not designed carry liability exposure for the school? Does there exist a shoe or surface that is “the best” for a particular sport?

Clinical Relevance In 1980, Nigg and associates reported the results of a ret rospective study of tennis injuries using a questionnaire.348 Using one tennis player during one 6-month season as a sin gle case, they analyzed 2481 cases to determine the relation ship between injury and playing surface. The foot and ankle were the most commonly affected area when ankle joint, Achilles tendon, heel, and sole cases were combined (Fig. 25J-31). The authors factored in the variation and frequency of play for the different surfaces by determining the relative frequency of pain per hour per week (Table 25J-14).360 Their data showed that the lowest frequency of injury occurred on clay and synthetic clay surfaces, and a lower frequency

Number of Cases with Pain

400

300

200

100

0

Back

Groin

Hip

Knee

Calf

Ankle Achilles Heel Joint Tendon Area of Involvement

Sole

Other

Figure 25J-31 Number of cases of tennis players with back and lower extremity pain by area of involvement. (Redrawn with permission from Nigg BM, Segesser B: The influence of playing surfaces on the load on the locomotor system and on football and tennis injuries. Sports Med 5:375-385, 1988.)

2204 DeLee & Drez’s� O �rthopaedic �� S �ports �� Medicine �� TABLE 25J-14 Frequency and Relative Frequency of Pain in Tennis Players Related to Six Different Playing Surfaces Surface

Frequency of Pain (%)

Relative Frequency (%/hr/wk)

Clay Synthetic sand Synthetic Surface Asphalt Felt carpet Synthetic grill

2.2 3.0 10.7 14.5 14.8 18.0

0.5 1.6 3.0 3.9 4.8 3.8

From Nigg BM, Segesser B: The influence of playing surfaces on the load on the locomotor system and on football and tennis injuries. Sports Med 5:75-385, 1988.

of pain occurred on asphalt or concrete than on carpet or synthetic grill. Using this information, Nigg and Segesser speculated that the compliance of a surface is less important in tennis injuries than its frictional properties.360 Studies of the frictional properties of track surfaces have also yielded interesting insight on performance and injury. Stucke and colleagues pointed out the importance of static friction coefficients for starting efficiency in running events.403 When the static coefficient of friction is small, shorter steps and less body lean are used. The authors mea sured the static coefficient of friction for starting, stopping, and turning during 100 trials using five subjects wearing the same shoe type. They found that the cinder track had an intermediate value between 0.65 and l.72, compared with the synthetic outdoor surfaces’ values of 0.8 to 2.22 and the synthetic indoor surface values of 0.54 to 1.47 (Fig. 25J-32). This study emphasizes the variability between surfaces by pointing out that an artificial surface does not automatically indicate a surface with greater frictional stresses. Automatic changes in movement technique are influenced by the variation in surface friction properties. The authors speculated that the use of surfaces of varying frictional properties during training and competition is disadvantageous because of the time necessary to perfect a repertoire of movement skills to meet the requirements

1.0

Stopping

0.6

µSTAT

0.4

0.2

0.2 A

2.5

Starting

B Cinder Ground Artificial Surface Surface

0

Turning

�STAT

2.0

0.6

0.4

0

This discussion of the etiologic factors involved in the foot and ankle injuries should introduce the concepts nec essary to understand the injuries discussed in the other sections in this chapter. It is only after one understands the underlying causes of a problem that solutions are forthcoming. In the foot and ankle, as in no other area of the body, there is a direct interaction between anatomy and the environment—between the foot and ankle and

0.8

µSTAT

µ*DYN

SUMMARY

�[cm]

µ

0.8

µSTAT

1.0

of different sport surfaces. This conclusion begs the ques tion of whether it is preferable to train on one surface (e.g., natural grass) to reduce injury exposure when contests will be held on a different surface (e.g., artificial grass), or to train on the same surface on which the contest will be conducted with scheduled training in a sequence of gradu ated stress to allow proper adaptation by the body. When frictional properties of a surface are too low, slip ping can occur, and injuries may result.360 When the fric tional resistance is too high, the load transference to the body may exceed its range of tolerance, resulting in injury. An optimal range between excessive frictional overload and lack of traction exists to prevent injury. Nigg has suggested optimal ranges for the coefficient of translational friction for various sports.360 He based his recommendations on both objective and subjective assessments, and the range was always between 0.5 and 0.7. Stussi and colleagues calculated the coefficients of static friction to be 0.6 and sliding friction to be 0.5 for clay; values on fabric courts approached 1.0.305 Ankle strain is reduced, according to Stussi and colleagues, during braking maneuvers on sandy courts. They acknowl edged that greater performance demands might require increasing coefficients of friction and suggested that more stable shoewear (e.g., with improved ankle support) might allow the player to tolerate the greater strain of the higher friction surfaces. Owing to the epidemiologic flaws in the study of tennis injuries by Nigg and coworkers,360 the final answer on the relationship between the frictional properties of playing surfaces and athletic injuries has not been deter mined, but the stage is certainly set for such a study.

1.0

A

B Cinder Ground Artificial Surface Surface

0

A B Cinder Ground Artificial Surface Surface

Figure 25J-32 Variation in coefficient of friction between three different track surfaces for starting, stopping, and turning. μ, coefficient of friction for translation; η, coefficient of friction for rotation; DYN, dynamic; STAT, static. (Redrawn with permission from Stucke H, Baudzus W, Baumann W: On friction characteristics of playing surfaces. In Frederick EC [ed]: Sport Shoes and Playing Surfaces. Champaign, Ill, Human Kinetics Publishers, 1984, pp 91-96. © Nike, Inc.)

Foot and Ankle 2205

s hoewear, and between shoewear and the playing surface. As the reader investigates the specific injuries and patho logic conditions that beset athletes in sports, he or she should keep in mind the individual nature of these injuries and their potential risk factors. When causes are discov ered, prevention is only a step behind. C

r i t i c a l

P

o i n t s

l It is our job as physicians to act as educators for coaches, therapists, and athletic trainers so that they understand the benefit of returning an athlete to sport participation at the appropriate time after injury. Likewise, we should point out the risks involved when criteria for return to competition are ignored. l Warming up and stretching to obtain or maintain this range may or may not prevent injury, but stretching beyond this range is potentially harmful. l The role of flexibility in foot and ankle injuries is unclear. l A lack of cushioning may be a factor in producing injury but probably not to the degree to which some researchers and shoe manufacturers might lead us to believe. l There is more evidence supporting the link between shoe wear control and injury incidence than that of shoewear cushioning. l The compliance of a surface may be less important in injuries than the frictional properties of a surface. l The optimal ranges for the coefficient of translational fric tion for a playing surfaces is likely between 0.5 and 0.7.

S U G G E S T E D

R E A D I N G S

Botrè F, Pavan A: Enhancement drugs and the athlete. Neurol Clin 26:149-167, 2008. Caplan A, Carlson B, Faulkner J, et al: Skeletal muscle. In Woo SL-Y, Buckwalter JA (eds): Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill, American Academy of Orthopaedic Surgeons, 1988, pp 213-291. Clanton TO: Athletic injuries to the soft tissues of the foot and ankle. In Coughlin MJ, Mann RA (eds): Surgery of the Foot and Ankle, 7th ed. St Louis, Mosby, 1999. Divert C, Mornieux G, Baur H, et al: Mechanical comparison of barefoot and shod running. Int J Sports Med 26:593-598, 2005. Hamilton WG: Foot and ankle injuries in dancers. Clin Sports Med 7:143-173, 1988. Inman VT: The Joints of the Ankle, 2nd ed. Baltimore, Williams & Wilkins, 1991. Mann RA, Baxter DE, Lutter LD: Running symposium. Foot Ankle 1:190-224, 1981. Nigg BM: Biomechanics of Running Shoes. Champaign, Ill, Human Kinetics Books, 1986. Schwartz RP, Heath AL, Misiek W: The influence of the shoe on gait. J Bone Joint Surg 17:406-418, 1935. Torg JS: Athletic footwear and orthotic appliances. Clin Sports Med 1:157-175, 1982.


A p p e n d i x

Sports Medicine Terminology Dean C. Taylor, Robert A. Arciero, Donald T. Kirkendall, and William E. Garrett, Jr.

The purpose of this appendix is to define commonly used sports medicine terms and to establish a basis for standardized orthopaedic sports medicine terminology. The language must be understandable for patients, health care professionals, the media, orthopaedic surgeons, and sports medicine specialists. If we want to communicate our ideas to others, we need to do so in a comprehensible way. If the language we use is ambiguous, confusing, contradictory, inconsistent, or filled with nonwords (as it often is), our communication is ineffective, misleading, and potentially problematic. The bases for the presentation of the material in this chapter are not our own opinions or pet peeves. We have solicited suggestions from experts (editors of major orthopaedic journals and established medical editors) to assist in improving the language of sports medicine. We have attempted to synthesize the collective wisdom of sports medicine organizations to help develop consensus when possible. We hope that this chapter can serve as a starting point for standardizing sports medicine terminology and lead to further refinement of our unique language. The importance of using consistent and proper terms helps research findings to be more accessible and understandable to the audience. But more importantly, misuse of the language can affect patient care. Physicians in the same group using different definitions of terms could compromise patient care when interacting on a common patient. This could also extend to health care support such as nurses, nurse practitioners, physician assistants, physical therapists, athletic trainers, and more. This chapter is divided into two segments: commonly accepted sports medicine terminology and some special topics along with sports medicine classification systems. We point out common misuses of terminology. In situations in which there are good arguments for consensus, we argue for the acceptance of the terminology or the classifications. If there is conflicting usage, we point out the strengths, the weaknesses, or the limitations.

SPORTS MEDICINE TERMINOLOGY Sports medicine terminology is a highly descriptive mix of athletic, lay, and medical language. It is filled with athletic terms, such as jumper’s knee, tennis elbow, skier’s thumb, and footballer’s ankle, and common terms, such as shoulder separation and hip pointer. The language is colorful and has developed over time as prominent athletes, media personnel, trainers, and physicians have added their own terms, or

misuse of terms, to the mix. This rich and vivid language can also be confusing because many terms are used improperly or have developed different meanings over time. For example, the media routinely confuses strain and sprain. Or how does a dislocation differ from a frank dislocation? What is a nonfrank dislocation and what is the “line” to be crossed when identifying a dislocation as frank, and do all physicians understand where this line is? How about stomach versus abdomen? Does a patient place his or her hand on the stomach or the abdomen? Unless there is an incision to reach into, it’s probably the abdomen. Where is the line separating the lower abdomen from the groin? These may seem to be nonsense examples, but such misuse of terms is what leads to confusion and miscommunication. Medical professionals are aware that humans have upper and lower extremities, not arms and legs. The upper extremity contains the arm and the forearm. The lower extremity contains the thigh and leg. Table APP-1 lists some definitions of commonly used sports medicine terms, some of which can be misleading. It may be difficult to eliminate these terms from our sports medicine language, but their elimination is necessary if we are to improve our ability to communicate consistently. For example, how can one explain to a medical student that a jumping athlete with tenderness of the proximal patellar tendon has a localized degenerative process, not an inflammatory process, when the terminology we use to describe the condition is “patellar tendinitis”? Maffulli and associates1 have discussed this common incorrect usage of the term tendinitis. To try to develop an international consensus on describing tendon problems, the Magellan Orthopaedic Society, the alumni society for the international sports medicine traveling fellowships, considered this terminology problem. The Society decided that most overuse tendon problems are associated with noninflammatory degenerative-type changes in the tendon, which histologically should be called tendinosis. Inflammation around a tendon is more commonly tenosynovitis, such as in de Quervain’s or Achilles tenosynovitis. Because tendinitis, tenosynovitis, and tendinosis are all histologic diagnoses, however, these terms should not be used for the clinical diagnosis of an overuse tendon problem. Rather, the term tendinopathy is a better descriptor for the clinical diagnosis (see Table APP-1). This distinction may seem insignificant to some people, but when terminology interferes with accurately teaching students, residents, and patients, it is a real problem because our language loses clarity. Another problem is the use of terms or phrases in the wrong context. Frequently, strain—an injury to a muscle— is incorrectly used to describe a sprain—an injury to a 2207


TABLE APP-1 Definitions of Commonly Used Sports Medicine Terms Abrasion—a worn-away area of skin Arm—the part of the upper extremity between the shoulder and the elbow, sometimes used incorrectly in place of “forearm” Arthritis—inflammation of a joint (commonly used to describe arthrosis) Arthrosis—degeneration of a joint Bursitis—inflammation of a bursa Cartilage—the tissue covering the articular surface of bones Chondromalacia—softening of articular cartilage; frequently used incorrectly for patellofemoral pain before operative inspection of the patellar articular cartilage Cramp—a painful spasmodic muscle contraction Dislocation—displacement of the bones of a joint from their normal position; usually implies loss of articulation of the joint surfaces that are normally in apposition Forearm—the part of the upper extremity between the elbow and the wrist Instability—a condition of increased joint motion due to ligament injury; a symptom Laceration—an open wound, commonly referred to as a “cut” Laxity—looseness or slackness, usually when describing the character of a ligament; may be used when describing a normal or an abnormal ligament; a sign Leg—the part of the lower extremity between the knee and the ankle, sometimes used incorrectly in place of “thigh” Lower extremity—thigh + leg + ankle + foot Meniscus—within the knee, a crescent or crescent-shaped tissue of fibrous cartilage Operation—an act performed by a surgeon; a surgical procedure Radiograph (or roentgenogram)—the image produced by passing x-rays through the body onto specially sensitized film Sprain—injury to a ligament secondary to excessive load (sometimes used incorrectly to describe a muscle-tendon unit injury) Strain—injury to a muscle-tendon unit secondary to excessive contractile or stretching load (sometimes used incorrectly to describe a ligament injury) Subluxation—a partial dislocation Surgery—the branch of medicine that treats injuries, diseases, and deformities by manual or operative methods, or conceptually, the work performed by a surgeon (often used incorrectly in place of “operation”) Tendinitis—inflammation of a tendon Tendinopathy—disease process of a tendon Tendinosis—degeneration of a tendon Tenosynovitis—inflammation of a tendon sheath Thigh—the part of the lower extremity between the hip and knee Upper extremity—the arm + forearm + wrist + hand X-ray (or roentgen ray)—the actual electromagnetic radiation used to make radiographs (commonly used as a synonym to radiograph)

ligament—and vice versa. Incidence and prevalence are other terms that are sometimes incorrectly interchanged. Two examples of the meanings of inappropriately used words being accepted and ingrained in our use are “arthritis” and “x-ray.” Arthritis is often used incorrectly to describe a degenerative joint; the term arthrosis may be the accurate term. X-ray is commonly used instead of the accurate term radiograph to refer to the image made by radiography. We use these terms so frequently on a day-to-day basis that the incorrect meanings have become accepted. This acceptance then becomes a problem when we are communicating with newcomers to the sports medicine language and in formal writing and presentations. The correct terminology is defined in Table APP-1. Surgery is another word that is frequently used incorrectly in place of “operation,” as in “The knee surgery we performed on the patient yesterday was a success.” Surgery is defined as a field of medicine or the concept of the work performed by a surgeon, not an actual surgical procedure. An operation is the act performed by the surgeon. “The knee operation we performed…” is the correct usage. Many times, commonly used terminology has evolved because a certain term may be easier to use than more accurate language. These terms are not incorrect but can be misleading. For example, it may be difficult to explain to a patient how someone who does not play tennis can develop tennis elbow. In these cases, it is important to know the synonyms. The common usage is unlikely to

isappear, but it is necessary to know the accurate termid nology to improve understanding and for formal writing or presentation. Some examples of common terms and their associated precise synonyms and definitions are listed in Table APP-2. TABLE APP-2 Commonly Used Sports Medicine Terms Common Term

Precise Term

Break Bruise Burner/stinger Dead arm

Fracture Contusion/ecchymosis Brachial plexus traction injury Condition of transient episodes of upper extremity loss of function, associated with recurrent, transient anterior subluxation34 Syndesmosis ankle sprain Iliac crest contusion or abdominal muscle strain at iliac crest insertion Patellar tendinopathy Muscle strain Nonspecific term for leg pain; usually implies a condition of overuse; specific conditions (stress reaction, stress fracture, tendinopathy, exertional compartment syndrome, and the like) should be used as diagnosis Acromioclavicular sprain Ulnar collateral ligament sprain of thumb metacarpophalangeal joint Lateral epicondylar tendinopathy

High ankle sprain Hip pointer Jumper’s knee Muscle pull Shin splints

Shoulder separation Skier’s/gamekeeper’s thumb Tennis elbow

Appendix 2209

TABLE APP-3 Nonwords Commonly Used in Sports Medicine

TABLE APP-4 Commonly Misused Plural Forms of Singular Words

Nonword

Correct Word

Singular

Plural

Allograph Crepitence Patulent Sublux

Allograft Crepitus/crepitation Patulous Subluxate or subluxation

Bacterium Basis Criterion Curriculum Datum Fungus Maximum Medium Patella Septum Sequela

Bacteria Bases Criteria Curricula Data Fungi Maxima Media Patellae Septa Sequelae

Other words that are used in a questionable context include the -logy words, such as pathology, morphology, and symptomatology. The -logy suffix comes from the Greek logos, meaning work or reason, and refers to the science or study of the subject designated by the stem to which it is affixed.2 Thus, the traditional meaning of the word pathology is the science or study of disease processes. Morphology refers to the science of the forms and structure of organisms2 and symptomatology to the science of disease symptoms. Common usage has led to other definitions for these -logy words. A secondary meaning of pathology has become “the structural and functional manifestations of disease”2; for morphology, “the form and structure of a particular organism, organ or part”2; and for symptomatology, “the combined symptoms of a disease.”2 For example, orthopaedists frequently refer to intra-articular pathology when describing abnormalities in a joint or the appearance of a meniscal tear. These forms of common usage have become accepted in presentations and verbal communication but are not accepted by some journal editors. In addition, our communication will be easier if we can keep our language as simple as possible. Therefore, we would recommend using the -logy words in their more traditional meanings. The common form of pathology could be replaced with words such as injury, lesion, finding, or damage. Similarly, shape, appearance, structure, or form can replace morphology, and symptoms can be used instead of symptomatology. Methods should be used consistently, not methodology, when referring to “the methods we used in our study.” Suffer is a word that is commonly used inappropriately, as in “a patient suffered a tibia fracture.” This is more common in the lay media but is still present in medical writing and presentations. Inasmuch as the extent of suffering associated with injuries is often unknown and difficult to quantify, it is better to use the word sustain to denote an injury, as in “a patient sustained a tibia fracture.” Some nouns in sports medicine are now being used as verbs. Examples include scope or arthroscope (“we arthroscoped his knee”), biopsy (“we biopsied the lesion”), and radiograph or x-ray as described previously (“we x-rayed his leg”). These usages are common in sports medicine, but not acceptable. The use of nouns as new verbs should be avoided in formal presentations or writing. We can offer numerous other similar instances. Consider gender versus sex. Inanimate objects have gender in languages like Spanish, French, and others, whereas sex is biologic. The proper term for males and females is sex, but most editors will ask that the word gender be used. We also use many nonwords in sports medicine. At worst, this can make us look unintelligent and can lead to

poor communication, especially with those for whom English may be a second language. At best, these terms sometimes become so ingrained in usage that they are adopted as accepted words. Some of the nonwords are listed in Table APP-3. Several common terms are incorrectly used in the plural form. For example, the phrase, “The data is shown in Figure 1,” should be stated as, “The data are shown in Figure 1.” Table APP-4 provides some commonly misused plural forms of singular words. Some terms remain controversial, and no consensus on usage exists. For example, the patellar ligament or the ligamentum patellae fits the strict definition of a ligament in that it connects two bones, the patella and the tibia; however, as an extension of the quadriceps muscle group, it functionally acts as a tendon, the connection between a muscle and a bone, and can also be called the patellar tendon. Both usages are accepted and understood, but there is no consensus among orthopaedic journals. We use “patellar tendon” because the patella is a large sesamoid, and the collagen that extends distally from the patella acts as a tendon to extend the knee when the quadriceps muscle group contracts. Similarly, the flexor hallucis longus tendon extends distally from the plantar sesamoid bones to the head of the first metatarsal.

SPORTS MEDICINE CLASSIFICATION SYSTEMS We create classification systems to improve our ability to communicate both clinically and in research. We also use the classifications to help decide courses of action when presented with a clinical problem. A few classification systems are widely accepted, make sense, and contribute to the understanding of a process. Rockwood’s classification3 of acromioclavicular joint sprains is an example of a classification that is well accepted in North America. Seddon’s classification4 of nerve injuries (neurapraxia, axonotmesis, neurotmesis) is also well accepted because the terms describe the extent of injury and are easy to understand and remember. Most of our classification systems are plagued by the existence of other competing classification systems, by lack of acceptance, or by varied interpretation of the grading. These problems create a significant communication


dilemma. When multiple classification systems are in place, using them is equivalent to a situation in which everyone is speaking different languages and no one knows which languages the others are speaking. For example, using the Hughston classification,5 a grade II medial collateral ligament knee sprain has no medial joint space opening with valgus stress at 30 degrees of flexion, but using Fetto and Marshall’s classification6 a grade II injury is “unstable… with a firm end point if chronic and soft if acute.” If different classifications are used, understanding is impaired. Even if there is only one system that is not widely accepted, it can be used to communicate only with those who understand and use the system. For example, if an English-speaking physician is trying to describe a LaugeHanson supination-eversion type IV ankle fracture to another English-speaking physician who does not know the Lauge-Hanson classification, communication will be as effective as if one of them were speaking a foreign language. If we are trying to expand education and understanding, it is not effective to have a language with limited acceptance. Perhaps the worst situation is when a classification system exists that has different interpretations so that one individual may have a completely different idea of what another is intending to communicate. This situation is common in communications about articular cartilage lesions. These lesions are usually graded I to IV based on Outerbridge’s classification of chondromalacia patellae7; however, there have been several modifications of the Outerbridge classification, and these modified grading schemes are now applied to articular cartilage lesions throughout the knee and in other joints. As a result, in a lecture on cartilage injury, a grade II lesion may mean many different things to an audience, rendering the use of all the classifications ineffective. The fact that there is confusion regarding classification systems is well recognized. In a 1997 questionnaire sent to the Herodicus Society members, 97% believed that there was confusion in grading of knee ligament injuries (Richard J. Hawkins, MD, personal communication). Even though the Society’s members recognized that there was no agreement regarding grading injuries, 82% still used some type of classification. Although we need classification systems to communicate, many of the ones we have now are inadequate.

General Lack of Consensus Regarding Grading and Measurement Most classification systems in orthopaedic surgery and sports medicine have three grades: I/II/III, 1/2/3, or 1+/2+/3+. (What the “+” means in grading is unclear, but it has become a common part of the sports medicine language. One might think “1+” is greater than “1” but not quite “2.” If so, what is “3+”?) The three-level method of grading is simple and easily understood. It generally provides information about the magnitude of injury or measurement. In medicine, these classifications are widely recognized to represent adjectives such as mild/moderate/severe, small/medium/large, or little/moderate/big.

Therefore, there is usually understanding, though inexact, when general grading scales are used. Communication could be greatly improved, however, if descriptive words instead of numbers were used to classify. In the story of Goldilocks, it is much better to talk about a papa bear, a momma bear, and a baby bear instead of a type III, type II, and type I bear. Similarly, it is easier to describe a nerve injury as neurapraxia, axonotmesis, or neurotmesis instead of type I, II, or III. In efforts to make the classification systems more exact, authors have applied quantitative values to the gradations. Differences of opinion have led to different classification systems based on differing magnitudes of the measurements used to define the classification grades. As a result, we find several different classifications in place and are unable to compare one study with another. Because of the many differing classification systems, it might be reasonable to eliminate the grading systems and instead to quantify measurements precisely. The only problem with this concept is that our measurements are so imprecise that comparisons between different examiners have little agreement. The members of the International Knee Documentation Committee clearly illustrated this point. When examining patients with different knee conditions, the International Knee Documentation Committee members differed appreciably in their measurements of translation on Lachman’s test and grading of the pivot shift and reverse pivot shift tests.8 Additionally, there was a wide variability among examiners in how instability tests were performed.9,10 Using different methods for making the same measurement affects the results, thus contributing to the general lack of agreement regarding the measurement values. We have a significant problem in sports medicine if even the experts, such as the International Knee Documentation Committee members, cannot agree on what is measured, how to measure it, or what the results of the measurement are. Partly for this reason, when the Anterior Cruciate Ligament (ACL) Study Group examined the problem of knee classifications in 2000, the members agreed that when examining a knee, a general description of the findings was better than exact millimeter measurements. The group decided that better agreement could be reached in regard to the assessment of whether an ACL was torn and whether a collateral ligament injury was mild, moderate, or severe (grade I, II, or III) than on the millimeter measurements of displacement during a physical examination (Richard J. Hawkins, MD, personal communication). We agree that physical examinations can determine whether there is an injury and generally approximate the extent of injury. Whenever possible, injuries, findings, and examination results for individual cases should be described in common language, and if measurements are reasonably accurate, they can be included in this description. Going back to the example of the three bears, it is much clearer to say that we were chased by an 8-foot (2.4-meter) male bear than by a type III bear, even if the bear in question was only 7 feet 6 inches (2.25 meters tall). More to the point, an articular cartilage lesion is better described as a 2 cm × 2 cm halfthickness lesion than as a type II or III (depending on the classification system used) lesion of the femoral condyle.

Appendix 2211

A

B

C

D

Figure APP-1 Classification of superior labrum injuries. A, Type I, fraying and degeneration of the superior labrum. B, Type II, detachment of the superior labrum and the biceps anchor from the superior glenoid. C, Type III, bucket handle tear of the superior labrum, with the peripheral labrum and the biceps anchor remaining intact. D, Type IV, bucket handle tear of the superior labrum with extension of the tear into the biceps tendon. (From Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990.)

To provide some understanding of the language, the following subsections outline and clarify the qualities and deficiencies of the classification systems that have been created to (1) describe anatomic changes associated with pathologic conditions, (2) define physical examination findings, and (3) grade the extent of an injury.

Classifications Anatomic Changes Associated with Pathologic Conditions Anatomic changes due to injury or disease that are seen repetitively intraoperatively or on imaging studies are often classified for research purposes or to assist in treatment. The following classifications are examples of these grading schemes.

Superior Labral Injuries With the development of shoulder arthroscopy has come the realization that a severe injury to the superior glenoid labrum can be a source of symptoms. Snyder and colleagues11 coined the term SLAP, which has become associated with I

II

superior labral injuries. SLAP stands for superior labrum anterior to posterior. This term is so firmly ingrained in shoulder terminology that it is often used without clarifying the severity of the injury, the precise diagnosis, and a description of loss of function. Hence, the acronym may be confusing for those just learning about shoulder injuries. Snyder and colleagues11 also described the classification of superior labral injuries (Fig. APP-1).

Acromion Shape Bigliani and coworkers12 described various shapes of the acromion that are associated with impingement syndrome of the shoulder (Fig. APP-2). These shapes are usually defined on a suprascapular outlet view radiograph. Obtaining a good outlet view can be difficult, and the shape of the acromion can vary depending on the angle of the x-ray beam. Therefore, as in any classification system, there can be variability in the measurements.

Radiographic Changes of the Knee In 1948, Fairbank13 outlined radiographic changes associated with previous meniscectomy (Table APP-5). These radiographic findings have come to be known as Fairbank’s changes and are telltale signs of arthrosis that can follow

III

TABLE APP-5 Fairbank’s Changes Marginal ridge Femoral condyle flattening

Figure APP-2 Classification of acromion shapes. I, Flat acromion from posterior to anterior. II, Anterior acromion has an inferior curve relative to the remainder of the acromion slope. III, Anterior acromion has an acute angle, or “hooked” shape, relative to the remainder of the acromion slope. (From O’Brien SS, Allen AA, Fealy S, et al: Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In Rockwood CA, Matsen FA [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 45.)

Joint space narrowing

Ridge or osteophyte formation at the margin of the outer aspect of the femoral condyle Flattening of the femoral condyle’s normally concave curvature as visualized on an anteroposterior radiograph Narrowing of the space between the femoral condyle and the tibial plateau; usually best defined on an anteroposterior radiograph with the patient bearing weight. An anteroposterior radiograph taken with the patient bearing weight and the knee flexed 45 degrees is often helpful in demonstrating joint space narrowing and has come to be known as the Rosenberg view33


TABLE APP-6 Modified Outerbridge Classification of Articular Cartilage Lesions Grade I Grade II Grade III Grade IV

Cartilage softening and swelling Fragmentation and fissuring, ≤1-cm diameter area Fragmentation and fissuring, >1-cm diameter area Erosion of cartilage to bone

partial or complete meniscectomy. Fairbank’s changes are now commonly used to describe any radiographic evidence of arthrosis of the knee.

Articular Cartilage Lesions In 1961, Outerbridge7 published his classification of articular cartilage lesions associated with chondromalacia patellae. This classification has subsequently been used to classify articular cartilage lesions in general throughout the knee and in other joints. Furthermore, the Outerbridge classification has been modified based on arthroscopic findings. The grading criteria of the Outerbridge classification have been modified and misquoted in various articles on cartilage injury. Others have attempted to use grading scales based on lesion depth,14 shape,15 and a combination of measures.16,17 Noyes and Stabler17 have reviewed many of the classification systems in their article describing their system. Unless there is a clear definition of the classification system being used to describe a lesion, there will be confusion. We propose that for simplicity’s sake and for general understanding, the appearance of individual cartilage lesions be described by size, depth, and location; for example, a 1.5 cm × 2.0 cm partial-thickness lesion of the medial femoral condyle. When classifying a series of lesions in a research study, it is important that the classification be clearly defined. We suggest the Outerbridge classification for general research use when grading cartilage lesions because it is the original scale for cartilage injury, is widely accepted, and remains the best-known grading scale. The only modification that we make is changing the cutoff between grades II and III from 1⁄2 inch to 1 cm, owing to the conversion to the metric system after the publication of the original article (Table APP-6). In research, if the Outerbridge classification is not used, the classification that is used should be well described and defined. Recently, the International Cartilage Repair Society has developed a rating scale to assess articular cartilage lesions. Although use of this scale is increasing, inter-rater and intrarater reliability data are lacking.

Classification of Physical Examination Findings Physical examination findings are frequently classified into different gradations, especially in the evaluation of ligaments and the translational or rotational changes that may result from injury. Noyes and colleagues18 have provided clear definitions for much of the terminology that is used to document examination findings. Quantitative physical examination measurements should be described as translations or rotations, and not as the amount of “laxity” in

TABLE APP-7 General Grading of Translation/Joint Opening for Ligament Testing 1-5 mm >5 mm and 2-cm translation)

Humeral head translation up to, but not over, the glenoid rim Humeral head translation over the glenoid rim with spontaneous reduction Humeral head translation over the glenoid rim without spontaneous reduction (“locked out”)

III

ASES grading scale can also be applied to inferior translation of the humerus when evaluating the sulcus sign. The grading results are reported for each shoulder in isolation and not in comparison with the contralateral shoulder. In 1990, Hawkins and Bokor23 proposed a four-level grading system for glenohumeral translation (Fig. APP-3). In 1998, they subsequently modified this grading scale (Table APP-9),22 and it was then used as part of the American GRADE

GLENOHUMERAL TRANSLATION

CLINICAL

Trace Small amount of humeral head translation

I

Humeral head rides up the glenoid slope but not over the rim

II

Humeral head rides up and over the glenoid rim Reduces when stress removed

III

Humeral head rides up and over the glenoid rim Remains dislocated on removal of stress

Figure APP-3 Diagram of grades of translation of the humeral head in the glenoid fossa during the load and shift test. (From Hawkins RJ, Bokor DJ: Clinical evaluation of shoulder problems. In Rockwood CA Jr, FA Matsen 3rd [eds]: The Shoulder, vol 1, 1st ed. Philadelphia, WB Saunders, 1990. pp 149-177.)

2 3

Shoulder and Elbow Surgeons evaluation. Subsequently, McFarland and colleagues24 and Bach and associates25 have described great inter-rater and intrarater variability when using the ASES grading scale. One of the reasons for this variability is that grading by tactile appreciation of translation short of subluxation (as in the original grading scale) is easier to identify than millimeters of translation (as used in the ASES scale).24 In fact, there is a 0.3 greater reliability if the grading of translation is based on whether the humeral head translates over either the anterior or posterior glenoid rim.25 McFarland and coworkers also suggested that the lowest grades (trace and 1 in the first edition of the book or 0 and 1 in the second edition) be combined.24 When grades 0 (or trace) and 1 are combined, the intra-and inter-rater reliability is improved. Therefore, we would recommend using the classification system of Hawkins and Bokor, as modified by McFarland and coworkers,24 for reporting glenohumeral translation (see Table APP-9). Inferior translation has been measured most commonly using an inferior traction force applied to the upper extremity, as described in the sulcus sign by Neer and Foster.26 Bahk and colleagues27 pointed out that the sulcus sign usually is graded as I (2 cm). An alternative for describing the sulcus sign when measuring the amount of inferior translation is to simply use centimeters, which may be a more accurate method to communicate.

Anterior Cruciate Ligament The diagnosis of an ACL injury is largely based on two physical examination techniques: Lachman’s test and the pivot shift test. Lachman’s test can be based on manual examination, an instrumented examination, or radiographic analysis. The measurement in millimeters is usually the difference between the measurements in the injured knee and in the normal contralateral knee. Different grades have been described. We recommend the use of a three-grade scale based on grading described by the AMA (see Table APP-7).19 Additionally, the end point is graded as A-firm end point, or B-soft, or not a well-defined end point. Compared with the normal knee, a knee with 8 mm of increased anterior translation with a soft end point would be a grade IIB Lachman. The pivot shift has had numerous descriptions and different grading schemes. Owing to varying degrees of the pivot shift phenomenon, we have used a grading system (Table APP-10) based on the classification of Bach and associates.25 The one deficiency of this grading scheme is that a 2+ pivot shift encompasses a wide range of findings;


TABLE APP-10 Pivot Shift Test Grade

Description

I

Mild, also known as pivot glide, slight subluxation with test, but no “jump” or “shift” Moderate, obvious jump or clunk with reduction of tibia Severe, marked clunk; tibia may remain subluxated unless reduction maneuver is employed

II III

TABLE APP-11 American Medical Association Ligament Injury Classification Grade

Description

I

Mild, minor tearing of ligament fibers; no demonstrable increase in translation on examination Moderate, partial tear of ligament without complete disruption; slight to moderate increased translation on examination Severe, complete tear of the ligament; marked increase in translation on examination

II III

however, this system does allow the examiner to assign different grades based on the magnitude of abnormal examination findings.

Posterior Cruciate Ligament The primary test for evaluating the posterior cruciate ligament is the posterior drawer test. Traditionally, the posterior drawer test has been graded similarly to other ligament tests (see Table APP-7). Posterior tibial translation so that the anterior tibia is flush with the femoral condyles has generally been considered to be 10 mm of posterior translation, or the dividing point between a 2+ or 3+ posterior drawer findings. Obviously, patient size varies so that the flush position does not always equate to 10 mm of posterior translation. To improve the understanding of posterior drawer measurement, the “thumb sign” has been introduced. The examiner performs the thumb sign test by sliding his or her thumbs off the femoral condyles onto the tibial plateau. The test is graded as anterior, flush, or posterior depending on the position of the anterior tibial plateau relative to the femoral condyles. The consensus of the ACL Study Group was that the thumb sign was a better assessment than millimeters of posterior tibial translation in documenting the posterior drawer findings.

Collateral Ligaments of the Knee The integrity of the knee collateral ligaments is assessed by applying a valgus (MCL) or varus (fibular collateral ligament) rotational stress to the knee positioned in 30 degrees of flexion. The amount of opening in millimeters of the medial or the lateral joint space is measured and is compared with the normal contralateral knee or is considered an isolated examination. The amount of opening is classified using the AMA grading scale (see Table APP-7) or by documenting the measurement in millimeters. Based on the ACL Study Group consensus, using the 1+, 2+, and 3+ grades may be the best way to communicate, especially because measuring joint space opening is not reproducible to within 1 or 2 mm.

CLASSIFICATION SYSTEMS USED TO DESCRIBE SPORTS INJURIES General Ligament

Ligament injuries are generally graded on three levels based on the AMA guidelines (Table APP-11).19 This classification can be confusing because there are also three

grades for measuring translation on the physical examination, as discussed in the previous section. Some authors use these translational changes to classify the extent of injury. This usage results in conflicting classifications and confusion because they are not the same. For example, a grade I MCL injury of the knee will have no increased medial knee opening to valgus stress, but a grade II injury may have 1+ or 2+ medial joint opening to valgus stress. Additionally, some authors use their own grading scales for ligament injuries. The lack of uniformity is the biggest communication problem in grading the severity of ligament injuries.

Muscle Strains Currently, there is no good classification for muscle strain injuries. Unlike ligament injuries, partial disruption of a muscle-tendon unit is difficult to assess with mechanical testing; using a scale similar to the ligament injury classification, therefore, is not exact. The physical examination findings that can be assessed in a strain are tenderness, muscle strength, swelling, ecchymosis, and the presence of a defect in the muscle-tendon unit. Based on these findings, muscle strain injuries can be classified as interstitial strains, intramuscular strains, partial ruptures, or complete ruptures (Table APP-12). Interstitial injury without disruption of blood vessels or muscle fibers is the mildest form of strain. There may be mild to moderate tenderness and mild strength loss, but no swelling, ecchymosis, or defect with an interstitial strain. Intramuscular injuries are the next highest level of severity in muscle strains. In intramuscular strains, there is enough tensile force to cause limited muscle fiber and capillary disruption. The injury is usually localized adjacent to a muscle-tendon junction, where, because of the fiber disruption, there is swelling and possibly ecchymosis. Tenderness and weakness may be moderate to severe, but there is no palpable defect at the injury site.

TABLE APP-12 Classification of Muscle Strain Injuries Injury Type

Swelling/Ecchymosis

Defect

Interstitial strain Intramuscular strain Partial rupture Complete rupture

Absent Present Present Present

Absent Absent Present, incomplete Present, complete loss of continuity

Appendix 2215

Figure APP-4 The five degrees of nerve injury based on the Sunderland classification of peripheral nerve injuries. 1, Neurapraxia equivalent with conduction block. 2, Axonotmesis equivalent with intact endoneurium resulting in wallerian degeneration. 3, Loss of nerve fiber continuity; perineurium and epineurium intact. 4, Loss of nerve fascicle continuity; only epineurium intact. 5, Complete nerve transection. (From Sunderland S: Nerve Injuries and Their Repair: A Critical Appraisal. Edinburgh, Churchill Livingstone, 1991, p 222.)

In partial muscle ruptures, there is a palpable defect, and tenderness, weakness, and swelling may be more severe than in intramuscular strains. In complete muscle ruptures, there is a disruption of all muscle fibers and total loss of function of the muscle injured. Complete ruptures are uncommon injuries.

Nerve Injuries Based on his extensive experience treating peripheral nerve injuries during World War II, Seddon4 classified nerve injuries as neurapraxia, axonotmesis, or neurotmesis. Neurapraxia is defined as a “failure of conduction in a nerve in the absence of structural changes, due to blunt injury, compression or ischemia; return of function normally ensues.”2 Axonotmesis is a “nerve injury characterized by disruption of the axon and myelin sheath but with preservation of the connective tissue fragments, resulting in degeneration of the axon distal to the injury site; regeneration of the axon is spontaneous and of good quality.”2 Neurotmesis is a “partial or complete severance of a nerve, with disruption of the axon and its myelin sheath

and the connective tissue elements; regeneration does not occur.”2 Sunderland28 classified nerve injuries into five types (Fig. APP-4). Types I and II are neurapraxia and axonotmesis, respectively. Types III to V represent increasing severity of nerve injury to complete transection. Both classifications are used and well known. Seddon’s classification probably has the greatest acceptance among all orthopaedists because of its descriptive nature and because it is simple and easy to understand. Sunderland’s classification may be better accepted among hand surgeons and neurosurgeons because it provides additional clarification that can be helpful in deciding between treatment alternatives.

Specific Injury Classifications Acromioclavicular Joint Injuries Rockwood3 has presented a classification for acromioclavicular joint injuries that is well accepted and commonly used. This classification is shown in Table APP-13.


TABLE APP-13 Classification of Acromioclavicular Joint Sprains Type I Type II

Type III Type IV

Type V

Type VI

Acromioclavicular (AC) ligament sprain only; interstitial without evidence of injury to the AC joint on radiographs AC ligament disruption without injury to the coracoclavicular (CC) ligaments; widening of the AC space on radiographs with minimal increase in the CC distance Disruption of the AC and CC ligaments; increase in CC distance on radiographs Ligaments injured as in type III with posterior translation of the lateral clavicle relative to the acromion with displacement of the clavicle into or through the trapezius muscle; posterior translation of the clavicle is seen on the axillary lateral radiograph Ligaments injured as in type III with detachment of the deltoid and the trapezius from the lateral clavicle; marked increase in the coracoclavicular separation, CC space 100% to 300% of normal Ligaments injured as in type III with inferior translation of the lateral clavicle; clavicle is inferior to the acromion and coracoid on radiographs

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

Medial Collateral Ligament Several grading schemes exist for MCL injuries, and as a result, there is confusion when trying to compare studies on these injuries. Many use the AMA’s nomenclature for damage to the ligament as a basis for injury classification. Others use the instability classification of 1+, 2+, and 3+ for grades I, II, and III. Hughston5 clearly outlined how study results can differ because of differences in classification systems used. He compared several studies with his own work and found that each study had a different definition for a grade III MCL sprain. Hughston’s classification is similar to the AMA’s; however, his interpretation is that only grade III injuries can have medial opening to valgus stress. Hughston further subdivides grade III injuries by the extent of medial opening: 1+, 2+, or 3+. Others have interpreted that grade II may have increased opening of the medial joint space consistent with a partial tear (1+ or 2+ opening). As Hughston5 demonstrated, our understanding of the best way to treat MCL injuries is impaired by the use of various classifications. We recommend the use of the AMA system owing to its simplicity and the overall awareness of the classification. Based on physical examination findings, grade I (interstitial) injuries have no increased medial opening to valgus stress, grade II (partial injuries) have 1+ or 2+ opening, and grade III (complete tears) have 3+ opening. We recommend that authors clearly define their classifications and that readers understand that many classifications exist so that the data are properly presented and interpreted.

Fibular Collateral Ligament The grading of fibular collateral ligament injuries usually follows the standard I, II, and III scheme for ligament injuries. Instability is usually graded based on amount of

lateral joint-line opening to varus stress with the knee in 30 degrees of flexion. Again, some authors use the instability grading as injury grading, which results in confusion and inability to compare studies. We recommend the use of the AMA guidelines for ligament injury, as described for MCL injuries.

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

Ankle Sprains Ankle sprains are usually separated into medial, lateral, and syndesmosis types. Grading of ankle sprains using the AMA classification can be difficult because many times, more than one ligament is involved. As a result, a “mild, moderate, or severe” grading scheme is usually employed to document the severity of injury. The West Point Ankle Grading System29 (Table APP-14) provides guidelines for grade I, II, and III injuries.

Concussive Injury Although brain injury is not an orthopaedic issue, recognizing and reporting these injuries is an important aspect of caring for athletes involved in contact and collision sports. There are few injuries as polarizing or more confusing than a concussion injury. The earlier comments on the grading of injury are magnified here because of the lack of agreement on the definition of injury and the lack of standardization of terms. There are two primary concerns regarding a concussive head injury. First is recognizing that an injury has occurred. Second is when to allow a player to return to play (beyond the scope of this chapter). Recognition of the injury is a function of the definition of the injury. The Concussion in Sport group offers this lengthy definition: “(1) Concussion may be caused by a direct blow to the head, face, neck, or elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head. (2) Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. (3) Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury. (4) Concussion results in a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. (5) Concussion is typically associated with grossly normal structural neuroimaging studies.”30

Appendix 2217

TABLE APP-14 West Point Ankle Grading System Criteria

Grade I

Grade II

Grade III

Evidence of instability Reaction to manual ligament stress testing Localization of tenderness Lateral sprains

None Mild to moderate discomfort

None or slight Moderate to intense discomfort

Definite No pain or intense discomfort

Mild to moderate over ATaFL only Deltoid only Distal syndesmosis only

Intense over ATaFL + CFL + PTaFL Deltoid Distal syndesmosis and proximally > 4 cm Complete tear of ligaments involved Impossible

Well-localized Slight Positive squeeze or external rotation stress test

Moderate to intense over ATaFL + CFL Deltoid Distal syndesmosis and proximally ≤ 4 cm Partial tear, partial macroscopic disruption to ligaments involved Difficult or impossible without supportive device (i.e., brace, tape, cane) ± Localized Significant Positive squeeze and external rotation stress tests

Radiograph—no mortise widening Minimal edema superior and anterior to lateral malleolus

Radiograph—no mortise widening Moderate edema superior and anterior to lateral malleolus

Medial sprains Syndesmosis sprains Suspected disorder Weight-bearing capability Edema, ecchymosis Syndesmosis sprains Special tests

Stretch to ligaments involved without macroscopic disruption Full or partial without significant pain

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

ATaFL, anterior talofibular ligament; CFL, calcaneal fibular ligament; PTaFL, posterior talofibular ligament. Modified from Gerber JP, Williams GN, Scoville CR, et al: Persistent disability associated with ankle sprains: A prospective examination of an athletic population. Foot Ankle Int 19:655, 1998.

After recognizing that an injury has occurred, many health care professionals will attempt to grade the severity of injury. Table APP-15 shows three popular grading schemes (out of well over a dozen recognized scales). With most grading scales, each higher grade suggests a more serious injury to a specific location, such as in grading ligament injuries. In general, the higher the grade of injury, the more challenging the prognosis. As the previous definition states, this is a functional, not a structural, injury, and the presence or length of loss of consciousness is not prognostic of outcome. Thus, using loss of consciousness or memory loss or other features as criteria for injury severity is problematic. Many physicians who deal with concussive injury prefer not to use a grading system. They prefer simply to describe the injury as “concussion with 30 min

3 (Severe)

LOC > 5 min, or PTA > 24 hr

No LOC Confusion No amnesia No LOC Confusion Amnesia LOC

No LOC Symptoms < 15 min No LOC Symptoms > 15 min Any LOC Brief vs. prolonged

*American Academy of Neurology. LOC, loss of consciousness; PTA, post-traumatic amnesia.

clear consensus on which scale is best. Assigning a grade to a concussion injury can be very confusing to patients and health care colleagues alike. Until the definitive grading scale is defined and validated, grading of concussion injury probably should be avoided.

BASIC STATISTICAL TERMS The language of statistics can be as confusing to orthopaedic surgeons as the language of medicine is to the lay public. In a profession whose advances are a result of research, however, proper understanding of some statistical terms is important to making decisions about the quality of research and whether results are meaningful to any particular physician’s practice. A statistics course is far beyond the scope of this chapter, but some basic statistical terms that are used on a regular basis require an understanding for communication between professionals and patients alike.

Reliability and Validity The fundamental definition of reliability is the degree of consistency with which an instrument or rater measures a variable.31 Within this definition are multiple levels of reliability. For example, one of the most common types of reliability is test-retest reliability (or intrarater reliability). A test is said to be reliable if measurements taken today and tomorrow by the same rater are similar. Another aspect of reliability is objectivity. Do two (or more) raters get the same results when administering a test? For example, do two different surgeons rate a manual muscle or range of motion or other clinical test the same? This is sometimes called inter-rater reliability. Other aspects of reliability are


internal consistency and split-half reliability that are critical for questionnaire development. The definition of validity is multifaceted. The most commonly applied definition is the degree to which an instrument measures what it is supposed to measure. In research, studies are designed to allow reasonable interpretations of the data based on controls (interval validity), definitions (construct validity), analysis (statistical validity), and generalizations (external validity).31 Researchers need the company of a statistician to help with the design and analysis of a project to ensure all the nuances of the research process are satisfied.

Samples and Populations Research (especially clinical research) attempts to make some generalization about a population. Thus, the population needs to be defined at the outset of a project. A population is the entire set of cases or units the study attempts to generalize, and a sample is a subset of the population under study.31 Selecting the sample from a defined population requires special procedures to ensure a representative group of cases.

Dependent and Independent Variables In almost all research projects, there is a variable of interest and a variable modified to affect the variable of interest. The dependent variable is assumed to depend on or be caused by another variable. The independent variable is the variable presumed to cause or determine a dependent variable, or the variable manipulated or controlled by the researcher.31 For example, a paper is about outcomes after patellar ligament versus hamstring grafts for ACL rupture. The independent variable is graft (hamstrings versus patellar ligament), and the dependent variable is outcome.

Power Power is the ability of a statistical procedure to find a significant difference that really exists.31 In planning a project, the researchers need to consider what difference is important, the inherent variability in the measurements, and the planned level of significance. When all this is known, the appropriate number of cases to detect the desired difference can be studied. This is probably the most commonly requested service of a statistician in the planning stages of a project.

Clinical versus Statistical Significance A paper shows that there is a 0.8-degree difference in range of motion between two groups and that this difference is statistically significant. The question the reader might ask is whether this difference is of any practical significance and whether the reader’s methods are sensitive enough to detect such a small difference. One way that clinical significance is reported is by the use of confidence intervals. The clinician can more easily determine whether the detected difference is sufficient enough to warrant a change in practice. Part of the issue is the use of the word significant. To avoid confusion in medicine and research, the use of the

word significant should be reserved for statistical reporting and not be used as a synonym for important, critical, distinctive, or other similar terms.

EPIDEMIOLOGY TERMS Epidemiology is a special class of statistics that deals with the incidence, distribution, and control of disease in a population. The basic concepts are, whether one is aware of it or not, a common feature of dealing with colleagues and patients. Many basic epidemiologic statistics are based on the simple 2 × 2 table (Table APP-16) that asks, in this case, if a diagnostic procedure actually does find the existence of a clinical condition.

Sensitivity versus Specificity These are generally used to describe the utility of a test. Sensitivity is the fraction of true positives detected by a test (in Table APP-15, that would be a/a + c). Specificity is the fraction of true negatives detected by a test (as d/b + d). Assume that a test has a sensitivity of about 70% and a specificity of 95%. This means that about 70% of people with the condition will have a positive test (the remaining 30% will have a false-negative test) and that 95% of people without the condition will have a negative test (the remaining 5% will have a false-positive test).

Relative Risk and Odds Ratio Relative risk (routinely abbreviated as RR) estimates the degree of an association between exposure to a condition and the likelihood of developing the condition in the exposed group relative to those not exposed.32 In general, the relative risk is computed for prospective, randomized clinical trials, or cohort studies. Change the rows in Table APP-16 to Exposure to some risk and the columns to Outcome. RR is calculated as [a/(a + b)]/[c/(c + d)]. Consider prior ankle injury as a risk for subsequent injury. A sample of athletes has their records reviewed for injury history and then followed over the course of some predefined duration. Exposure would be prior ankle sprain (yes/no), and the outcome would be a new sprain (yes/no). At the end of the study, if the calculated relative risk were 4.5, this would mean an athlete with a prior ankle sprain is 4.5 times as likely to suffer another sprain than the player with no prior ankle sprain. A relative risk of 1.0 means the rates of disease in the exposed and unexposed groups are similar. An RR of more than 1.0 is a positive association (a prior ankle sprain is associated with a subsequent ankle sprain), and an RR of less than 1.0 is a negative association (greater flexibility is associated with fewer strain injuries). The odds ratio is a special case of relative risk and is usually used in retrospective or case-control studies.31 Table APP-16 The Basic 2×2 Table Disease present? Yes Test positive? Yes Test positive? No

a c

Disease present? No b d

Appendix 2219

Prevalence versus Incidence Prevalence is the proportion of individuals in a population with the particular condition at a specific point in time (as of today, how many residents of a nursing home have osteoporosis?). Incidence is the number of new cases that develop in a population during a defined time interval (how many new cases of osteoporosis are diagnosed in this nursing home over a 3-year period?).31


I n d e x

Note: Page numbers followed by f refer to figures; page numbers followed by t refer to tables; page numbers followed by b refer to boxes.

A A band, 4f, 5, 6f, 13f, 208f A priori power analysis, 111 ABCDE mnemonic, 517, 519–520, 521f Abdomen on-field injury to, 526–527 pain in, 1451, 1452f preparticipation examination of, 512 Abdominal bracing, in core training, 280, 280f Abductor digiti quinti, nerve to, 2044, 2044f, 2045f entrapment of, 2044, 2044f, 2059–2060, 2060f release of, 2052 Abductor pollicis longus tendon, injury to, 30 Ablation procedures, in sudden death prevention, 170 Abrasion, 201–202 Abrasion procedure, arthroscopic, 52–53 Abscess, 387–388, 387f methicillin-resistant Staphylococcus aureus in, 395–397, 396b, 396f subperiosteal, 587, 589f Accessory lateral collateral ligament, 1301–1302, 1303f Accessory navicular, 1963, 1963f, 2162–2165, 2163f–2164f excision of, 2165, 2165f injury to, 2022–2023, 2024f Accuracy, 100, 108, 109f Acebutolol, 160t Acetabular labrum anatomy of, 1452–1453, 1453f tears of, 1470–1471, 1470f in children, 469, 470f magnetic resonance imaging in, 581–582 Acetabulum abnormal femoral head contact with, 1471–1472, 1471f–1472f anatomy of, 1452–1453, 1453f, 1500 chondral injury of, 1472 fracture of, 1464 Acetaminophen, in osteoarthritis, 1791 Acetylcholine, 353 Achilles tendon, 1997–2011 anatomy of, 1997, 2031 augmented end-to-end repair of, 2006t, 2007–2008, 2008f end-to-end repair of, 2006, 2006t, 2010–2011, 2010f–2011f examination of, 629–630 excision of, 2000 flexor hallucis longus reconstruction of, 2000, 2039f–2040f, 2041 imaging of, 630 inflammation of, 30 injury to, 1997–2002 anatomic considerations in, 1997 classification of, 29 evaluation of, 1998 flexibility and, 2182–2183 magnetic resonance imaging in, 563, 565f

Achilles tendon (Continued) nonoperative treatment of, 1998–1999 operative treatment of, 1999–2002 overuse, 29–30, 628–630, 1975, 1997, 2000–2001 playing surface and, 2198 rehabilitation after, 2001 magnetic resonance imaging of, 563, 565f, 2034, 2034f overuse injury of, 29–30, 628–630, 1975, 1997, 2000–2001 percutaneous repair of, 2008–2009 peritendinitis of, 30, 563, 1975, 1997, 2000, 2001 reconstruction of, 2000, 2039f–2040f, 2041 in retrocalcaneal bursitis, 2030, 2034, 2034f, 2036–2037 rupture of, 2002–2011 evaluation of, 2002–2004, 2003f external fixation in, 2009 imaging in, 2003–2004, 2003f needle test in, 2003 neglected, 2009 nonoperative treatment of, 2004–2005, 2004t operative treatment of, 2004–2011, 2004t, 2005f, 2006t, 2007f–2008f, 2010f–2011f percutaneous treatment of, 2008–2009 Thompson’s test in, 2003 stretching exercise for, 1999 three-tissue bundle suture repair of, 2006–2007, 2006t, 2007f ACL. See Anterior cruciate ligament (ACL) Acne, 205, 415 Acne mechanica, 202 Acromioclavicular joint anatomy of, 769, 769f, 826–828, 826f–827f, 831f arthrosis of, 829–830 biomechanics of, 826–828 dislocation of. See Acromioclavicular joint injury innervation of, 831f intra-articular fracture of, 854–855 kinematics of, 775–776, 776f, 828, 828f osteoarthritis of, 956, 959f osteophyte of, 956, 959f palpation of, 996, 997f pediatric anatomy of, 783, 783f biomechanics of, 786–787, 787f radiography of, 835–836 anteroposterior view for, 835–836, 949 normal, 835–836 posteroanterior, 949 stress view in, 835, 837f Stryker notch view in, 835, 838f, 949 Zanca view for, 835, 836f, 854 resection of, SLAP lesion and, 1024 Acromioclavicular joint injury, 826–856 anatomy in, 826–828, 826f, 827f classification of, 828, 829f, 830b, 2215, 2216t

Volume 1: pages 1 to 1156; Volume 2: pages 1157 to 2220.

Acromioclavicular joint injury (Continued) coracoid fracture with, 880, 882, 882f, 883f, 884 evaluation of, 828–836 cross-arm adduction test in, 830, 832f imaging in, 835–836, 836f–�� 838f O’Brien’s test in, 830, 832f Paxinos’ test in, 830 radiography in, 831b, 833f–834f, 835–836, 836f–838f glenoid neck fracture with, 863, 865b, 865f mechanism of, 828, 830f pain pattern in, 828–829, 831f pediatric and adolescent, 855–856, 855f physical examination in, 828–834, 831b, 831f, 832f radiography in, 831b, 833f–834f, 835–836, 836f–838f, 949 return to play for, 854, 854t treatment of, 836–845 acromioclavicular ligament repair in, 840, 841f, 846–851, 847f–853f arthroscopic, 844 biceps transfer in, 840–841, 841f in children, 856 complications of, 851–853 coracoclavicular ligament reconstruction in, 842, 843f, 846–851, 847f–853f coracoclavicular ligament repair in, 841, 841f coracoclavicular ligament transfer in, 841–842 distal clavicle resection in, 842–844, 843f, 843t dynamic muscle transfer in, 840–841, 841f modified Weaver-Dunn procedure with augmentation in, 842 nonoperative, 838–840, 839f–840f, 844–845 operative, 838t, 840–846, 845f–846f osteolysis after, 853 pain after, 853 pin-related complications of, 851–852 return to play after, 854, 854t type I, 829f, 830b, 831, 833t type II, 829f, 830b, 831, 833f, 833t type III, 829f, 830b, 831–832, 833t, 834f type IV, 829f, 830b, 832, 833t, 834f type V, 829f, 830b, 832, 833t, 835f, 847f type VI, 829f, 830b, 833, 833t Acromioclavicular ligaments, 775, 776f, 826–827, 826f, 827f injury to. See Acromioclavicular joint injury repair of, 840, 841f, 846–851, 847f–853f Acromion accessory ossification center of, 781, 781f, 859, 860f, 955–956, 958f unfused, 781, 781f anatomy of, 859, 990, 990f, 992f, 1034t down-sloping of, 955, 957f enthesophyte of, 955, 958f fracture of, 866–867, 867b classification of, 867b

ii

Index

Acromion (Continued) magnetic resonance imaging of, 866f radiography of, 861, 861f, 866f return to play after, 873 stress, 867 treatment of, 866–867, 867f, 873f magnetic resonance imaging of, 955–956, 956f, 957f, 959b ossification centers of, 859, 860f type I, 955, 956f, 959b, 2211, 2211f type II, 955, 956f, 959b, 2211, 2211f type III, 955, 956f, 959b, 2211, 2211f Acromioplasty, 1008–1009 Actigraph, 451 Actin, 4, 5t Acute anterior cervical spinal cord injury, 674, 678 Acute lymphocytic leukemia, foot in, 1974 Acute mountain sickness, 504 Acyclovir, in herpes gladiatorum, 197 Adapalene, in acne, 205 Addison’s disease, 77t Adductor brevis, 1454t, 1455f, 1485 strain of, 1460–1461, 1490–1493 in adolescents, 1493 complications of, 1493 evaluation of, 1490–1491, 1490b, 1491f prevention of, 1492b return to play after, 1493, 1493b treatment of, 1491–1492, 1491b–1492b, 1492t Adductor canal syndrome, 1496b, 1497–1499 return to play after, 1498, 1498b treatment of, 1497–1498, 1498b, 1498f Adductor longus, 1454t, 1455f, 1485 strain of, 1460–1461, 1490–1493 in adolescents, 1493 complications of, 1493 evaluation of, 1490–1491, 1490b, 1491f prevention of, 1492b return to play after, 1493, 1493b treatment of, 1491–1492, 1491b–1492b, 1492t Adductor magnus, 1454t, 1455f, 1485 strain of, 1460–1461, 1490–1493 in adolescents, 1493 complications of, 1493 evaluation of, 1490–1491, 1490b, 1491f prevention of, 1492b return to play after, 1493, 1493b treatment of, 1491–1492, 1491b–�� 1492b, 1492t Adenosine triphosphate, in energy metabolism, 210, 210f Adhesive capsulitis, 1094–1103 athroscopic release in, 1096–1102 anterior capsule in, 1098, 1099f–1100f bursectomy in, 1100, 1102f complications of, 1103, 1103b contraindications to, 1096–1097, 1097b indications for, 1096, 1097b inferior capsule in, 1099–1100, 1101f joint entry for, 1097–1098, 1097f–1098f physical therapy after, 1102, 1103b repeat, 1103 results of, 1103 rotator interval in, 1098, 1098f subacromial space in, 1100, 1102f closed manipulation in, 1095–1096 evaluation of, 1095, 1095b in female athlete, 489–490, 490t imaging in, 967, 967t, 968f, 1095 methylprednisolone in, 1096, 1103b nonoperative treatment of, 1095, 1095b open release in, 1096 pathoanatomy of, 1094 patient history in, 1095, 1095b

Adhesive capsulitis (Continued) physical examination in, 1095 treatment of, 1095–1096, 1095b. See also Adhesive capsulitis, arthroscopic release in Adolescents. See Children/adolescents Adrenal gland, exercise effects on, 217–218, 217t α-Adrenergic receptor agonists in complex regional pain syndrome, 365 in hypertension, 160t, 161 β-Adrenergic receptor agonists, in exercise-induced bronchospasm, 181 α-Adrenergic receptor antagonists in complex regional pain syndrome, 363t in hypertension, 160t, 161 β-Adrenergic receptor antagonists in complex regional pain syndrome, 363t, 365 in hypertension, 159, 160t in sudden death prevention, 170 Adrenocorticotropic hormone, exercise effects on, 217, 217t Adson’s test in thoracic outlet syndrome, 1131, 1132f in vascular injury, 1138, 1138f Advanced dynamic training, in shoulder rehabilitation, 244–246, 245f–248f AED. See Automatic external defibrillator Aerobic exercise, 400 caffeine effects on, 421 Aeromonas hydrophila infection, 397, 398t Age/aging ACL injury and, 1651–1652 allograft properties and, 38 articular cartilage changes with, 40 bone changes with, 72, 78 immune function and, 148 osteochondral repair and, 52 tendon changes with, 25, 30 thermal balance and, 499 Aggrecan, 44 throwing-related accumulation in, 1215 Aggression, anabolic-androgenic steroids and, 417 Airway assessment in cervical spine injury, 667, 668f emergency, 519, 520t, 520f–521f Akin procedure, 2070, 2072b, 2072f–2073f, 2076, 2078f Albright’s disease, 73t Albuterol, in exercise-induced bronchospasm, 182 Alcohol matrixectomy, 2099–2100 Alcohol use/abuse, 401, 424–425 in hypertension, 159t Aldosterone, exercise effects on, 217, 217t Alendronate, in complex regional pain syndrome, 363t, 365 Alertness drug enhancement of, 451–452, 452t impairment of, 453 Alertness zones, 454, 455f performance and, 454–456, 455f Alkaline phosphatase, 74t–76t, 77t serum, in elbow heterotopic ossification, 1292 Allen’s test, 1320–1321, 1321f, 1357, 1359 Allergy, anaphylactic response in, 530 Allodynia, 356t in complex regional pain syndrome, 354, 356 Allograft(s), 137–145. See also Graft(s) donor screening for, 138–139 historical perspective on, 137–138 infection risk with, 141–142 ligamentous, 38, 142–143


Allograft(s) (Continued) meniscal, 143–144, 1620–1622, 1621f osteochondral, 144–145 glenohumeral joint, 1111, 1111f, 1115, 1115f knee, 1775, 1777, 1777t, 1781–1783, 1782f, 1784t talus, 2146–2148, 2150–2152, 2150t, 2151f–2152f, 2153 procurement of, 138–139 sterilization of, 139 storage of, 140–141 ALPSA (anterior labroligamentous periosteal sleeve avulsion) lesion, 974, 974f Altitude. See High altitude AMBRI (atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift) syndrome, 616 Amenorrhea, 478, 478f American Association of Tissue Banks, 137–139 American Heart Association, preparticipation examination recommendations of, 508, 509, 512t Amino acids, supplemental, 405, 409 Amitriptyline, in complex regional pain syndrome, 362, 363t Amlodipine, 160t Anabolic-androgenic steroids acne and, 415 adverse effects of, 415–417 athletic performance and, 414–415 body image disorders with, 417 cardiac effects of, 416 in children/adolescents, 467–468 complications of, 413–414 doses of, 415 efficacy of, 414 estrogen-related side effects of, 415–416 female use of, 412 hepatic effects of, 416–417 historical perspective on, 411–414 legal regulation of, 413 mechanism of action of, 414–415 musculoskeletal effects of, 415–416 opioid abuse and, 417 psychiatric effects of, 417 testicular effects of, 416 testing for, 413 Anaerobic exercise, 399–400 Analytical research, 107–108 Anaphylaxis, exercise-induced, 205, 530 Ancylostoma braziliense infection, 201 Androgen(s), 414. See also Anabolic-androgenic steroids adverse effects of, 415–417 athletic performance and, 414–415 mechanism of action of, 414 Androstenedione, 418 Aneurysm popliteal artery, 1838, 1844 throwing-related, 1226 Aneurysmal bone cyst, 983–984 Angiography in axillary artery injury, 1139, 1139f in hypothenar hammer syndrome, 1357, 1357f in knee dislocation, 1751, 1753f in popliteal artery entrapment, 1840, 1842, 1843f, 1844f in thoracic outlet syndrome, 1133 Angiotensin-converting enzyme inhibitors, in hypertension, 159, 160t Angiotensin receptor blockers, in hypertension, 159, 160t Anisocoria, preparticipation examination for, 509

Index Ankle. See also Foot (feet); Subtalar joint; Talus anatomy of, 338, 1865, 1866f arthroscopy of, 127, 127f in impingement, 2159–2160, 2159t, 2160f indications for, 127 normal anatomy on, 127, 127f portals for, 127, 127f positioning for, 127 biomechanics of, 1865–1867, 1865f–1867f, 2178–2179, 2178f, 2178t–2179t bone bruise of, 1929, 1931 brace for, 340, 1921–1922, 1921t, 1922f dislocation of. See also Ankle sprain with fracture, 1945, 1946f without fracture, 1945–1946, 1946f return to play after, 1946 foot linkage of, 1870–1872, 1872t fracture of dislocation with, 1945, 1946f pediatric, 597, 598f, 1964–1969 evaluation of, 1964 outcome of, 1966–1969, 1967t, 1968f, 1969f Salter-Harris type I, 1965, 1965f Salter-Harris type II, 1965, 1965f, 1968f Salter-Harris type III, 1965, 1965f, 1966f Salter-Harris type IV, 1965f, 1966, 1967f, 1969f stress, 2017–2018, 2017f�� –�� 2020f. See also Foot (feet), stress fracture of inferior extensor retinaculum of, 338 injury/instability of, 338–341, 1870–1873. See also Ankle sprain bracing in, 340 diagnosis of, 339 incidence of, 2174–2175, 2175t intra-articular pathology and, 339 mechanism of, 338–339 medial, 339 operative treatment of, 340–341 playing surface and, 2192–2204. See also Playing surface prevention of, 340 shoewear and, 2183–2192. See also Shoes, injury and taping in, 340 treatment of, 339–341 ligaments of, 338, 1912–1914, 1913f, 1914t, 1915f, 1935, 1935f, 1938–1940, 1939f. See also specific ligaments biomechanics of, 1914–1915, 1915t, 1935 injury to. See Ankle sprain magnetic resonance imaging of, 571, 573, 574f magnetic resonance imaging arthrography of, 537 motion of, 1912, 2178–2179, 2178f, 2178t, 2179t muscle function at, 1867, 1869, 1870f osteochondral lesions of, 2142–2153, 2142t. See also Osteochondrosis (osteochondroses), talar rehabilitation of. See Ankle rehabilitation stress fracture of, 2017–2018, 2017f–�� 2020f. See also Foot (feet), stress fracture of taping of, 340, 1934 tendons of. See Achilles tendon; Flexor hallucis longus tendon; Peroneus brevis tendon; Peroneus longus tendon; Tibial tendon Ankle brace, 340, 1921–1922, 1921t, 1922f Ankle-brachial index in knee dislocation, 1751 in popliteal artery entrapment, 1839

Ankle impingement, 2156–2161 anterior, 2157, 2157f anterolateral, 1931, 1931f–1932f, 2157, 2158f meniscoid lesion and, 1931, 1932f anteromedial, 2157–2158 evaluation of, 2157–2158, 2157f, 2158f, 2159t posterior, 2160, 2161t posteromedial, 2160 return to play after, 2161 treatment of, 2158–2160, 2159t, 2160f Ankle rehabilitation after bifurcate sprain, 1955 after dislocation, 1946 after lateral sprain, 1928–1929, 1928f–1929f, 1930f, 1931 after subtalar dislocation, 1953 after subtalar sprain, 1951 after syndesmosis sprain, 1944–1945 therapeutic exercise for, 272–276 eccentric training in, 275–276, 276f evertor muscle training in, 275 gastrosoleus training in, 273, 275f neuromuscular control training in, 273, 275, 275f neuromuscular training in, 273, 274f proprioceptive training in, 273, 275, 275f, 298 single-leg training in, 273, 275f Ankle sprain, 338–341, 1912–1974 in children/adolescents, 1963, 1964f grading of, 2216, 2217t high (syndesmosis), 1938–1945 anatomy of, 1938–1940, 1939f arthrography in, 1942 chronic, 1944 computed tomography in, 1942 direct eversion maneuver in, 1940, 1941f evaluation of, 1940, 1940f, 1941f external rotation stress test in, 1940, 1941f grade I, 1940, 1942, 1945 grade II, 1940, 1942, 1945 grade III, 1940, 1942–1944, 1943f, 1945 history in, 1940 latent, 1940 magnetic resonance imaging in, 1942, 1943f physical examination in, 1940, 1940f, 1941f radiography in, 1940–1942 radionuclide imaging in, 1942 rehabilitation for, 1944–1945 return to play after, 1945 squeeze test in, 1940, 1940f stress radiography in, 1942 treatment of, 1942–1944, 1943f lateral, 1912–1935 anatomy of, 1914–1915 anterior drawer stress radiography in, 1919, 1919f anterior drawer test in, 1916–1917, 1917f anterior lateral ankle impingement and, 1931, 1931f, 1932f arthrography in, 1919–1920 bifurcate ligament sprain and, 1918, 1933 biomechanics of, 1914–1915, 1915t bone bruise and, 1929, 1931 Broström procedure in, 1926–1928, 1927f Chrisman-Snook procedure in, 1925–1926, 1925f chronic (recurrent), 1924–1929, 1934 rehabilitation for, 1924 surgical treatment of, 1924–1928, 1925f, 1926f, 1927f


iii

Ankle sprain (Continued) classification of, 1916, 1916t cold therapy in, 1920 distribution of, 1915, 1915t evaluation of, 1916–1918, 1916t Evans procedure in, 1924 fifth metatarsal base fracture and, 1933–1934 grade I, 1916, 1916t, 1920, 1934 grade II, 1916, 1916t, 1920, 1934 grade III, 1916, 1916t, 1920, 1934 history of, 1916 magnetic resonance imaging in, 1920, 1921f mechanism of, 1913, 1914f nerve palsy and, 1933 neural features of, 1915 osteochondral lesion and, 1929 peroneal tendon instability and, 1931–1933, 1932f physical examination in, 1916–1918, 1917f prevention of, 1934–1935 radiography in, 1918–1919, 1918f–1919f rehabilitation for, 1928–1929, 1928f, 1929f, 1930f, 1931f return to play after, 1934–1935 risk factors for, 1912 stress radiography in, 1918–1919, 1918f stress testing in, 1916 subtalar coalition and, 1933 talar tilt test in, 1917–1918, 1917f taping in, 1934 tibiofibular synostosis and, 1933, 1934f treatment of, 1920–1925, 1934 brace in, 1920, 1921–1922, 1922f cast immobilization in, 1920–1922, 1922t early mobilization in, 1922–1923 surgical, 1923–1924, 1923f untreated, 1915 Watson-Jones procedure in, 1924–1925, 1925f magnetic resonance imaging of, 571, 573, 574f, 1920, 1921f, 1937, 1942, 1943f medial, 339, 1935–1938 anatomy of, 1935, 1936f arthrography in, 1937 evaluation of, 1935–1936 grade I, 1937 grade II, 1937–1938 grade III, 1937–1938 history in, 1936 magnetic resonance imaging in, 1937 mechanism of, 1935 physical examination in, 1936 radiography in, 1936–1937, 1936f–1937f rehabilitation after, 1938 return to play after, 1938 treatment of, 1937–1938 vs. neoplasm, 2161–2162, 2161f prevention of, 338–341 talar osteochondral lesions and, 2144 vs. tarsal coalition, 2161, 2161f Ankle syndesmosis sprain. See Ankle sprain, high (syndesmosis) Anterior circumflex humeral artery, 1071–1072, 1072f Anterior cruciate ligament (ACL), 1644–1683. See also Anterior cruciate ligament (ACL) injury; Anterior cruciate ligament (ACL) reconstruction; Knee rehabilitation anatomy of, 1644–1646, 1645f–1648f, 1748 attachments of, 1644, 1646, 1646f biomechanics of, 1646–1647 during active range of motion, 1586, 1586f anteromedial bundle in, 1584, 1585–1586

iv

Index

Anterior cruciate ligament (ACL) (Continued) in arthroscopic meniscectomy, 1585–1586 autograft-related, 1584 during flexor-extensor exercises, 1586–1587 force measurements in, 1581–1582, 1585 gender and, 1584 with internal rotation, 1583, 1583f during isometric quadriceps contraction, 1586 during kinetic change exercises, 1586 during leg extension exercises, 1587 load-elongation curve in, 1583–1584, 1583f meniscectomy and, 1585–1586, 1590–1591 observational studies of, 1581 posterolateral bundle in, 1584 stabilizing function in, 1584–1588 strain measurements in, 1582, 1586–1588, 1586f, 1587t in weight-bearing flexion, 1585 blood supply to, 1645 collagen of, 1644–1645 fetal, 1645–1646, 1646f innervation of, 1645 insertion of, 1582 ligament unloading exercises for, 222–224, 223t loading of, 93f, 94–95, 1583–1584, 1583f exercise-related, 222t rehabilitative exercise effects on, 221–222, 222t squat exercise effects on, 223, 223t, 224, 224f, 263 stabilizing function of, 1584–1588 stair climbing effects on, 223t, 224 stationary cycling effects on, 223, 223t Anterior cruciate ligament (ACL) injury, 1644–1683 anterior drawer test in, 1650 biologic response to, 1647–1648 classification of, 1648, 2216 clinical presentation of, 1648–1649 cytokines in, 1648 epidemiology of, 1648 female athlete, 483–485 etiology of, 333–334 incidence of, 333 ligament reconstruction for, 485, 486t–487t mechanism of, 485, 488t prevention of, 333–334, 485, 487b risk factors for, 484–485, 484b functional testing in, 1649, 1652, 1674 history in, 1648–1649 KT-100 arthrometry in, 1650, 1652 Lachman test in, 1585–1586, 1649–1650, 2213 magnetic resonance imaging in, 553, 557f, 569, 571f, 572f, 1650–1651, 1653–1654, 1654t malalignment in, 1649 mechanism of, 1648–1649 medial collateral ligament injury with, 1632–1633, 1633f, 1634–1635, 1634f, 1635f, 1636, 1653, 1654 meniscal injury with, 1653–1654, 1653t epidemiology of, 1601 rehabilitation for, 1672–1673 treatment of, 1605–1606, 1654, 1654t meniscectomy and, 1590–1591 natural history of, 1654–1655 palpation examination in, 1649 partial, 1652–1653, 1652t pediatric, 1679–1683 iliotibial band tenodesis in, 1680

Anterior cruciate ligament (ACL) injury (Continued) incidence of, 1676–1677 nonoperative treatment of, 1679–1680 operative treatment of, 1680–1682, 1682f physical examination in, 1677 tibial eminence fracture with, 1677–1679, 1678f, 1679f physical examination in, 1649–1650 pivot shift test in, 1650, 2213–2214, 2214t posterolateral corner injury with, 1732, 1743 proprioceptive function after, 294. See also Knee rehabilitation, proprioceptive exercises in radiography in, 1650 swelling in, 1649 treatment of, 1655. See also Anterior cruciate ligament (ACL) reconstruction age and, 1651–1652 gender and, 1651 nonoperative, 1655 varus angulation with, 1801–1803, 1802t, 1803f clinical presentation of, 1803–1804 evaluation of, 1803–1814, 1805f, 1806t gait analysis in, 1808–1809, 1809f, 1810f, 1811f imaging and calculations in, 1809–1814, 1811f, 1812f, 1813f, 1814f, 1814t, 1815t physical examination in, 1804–1808, 1805f, 1806t, 1807f, 1808f treatment of, 1814–1835. See also High tibial osteotomy Anterior cruciate ligament (ACL) reconstruction, 1655–1676 arthroscopic examination for, 1662–1663, 1663f biology of, 1648 in children, 1681–1683, 1682f graft for, 38, 1656–1661, 1656t allograft, 142–143, 1656–1657, 1656t autograft, 37–38, 1584, 1656–1657, 1656t biology of, 1648 biomechanical properties of, 1584, 1656–1657 bone–anterior cruciate ligament–bone allograft in, 38 bone–patellar tendon–bone autograft, 37–38, 1584, 1656–1657, 1656t, 1659, 1659t, 1661, 1662f disease transmission with, 1657 donor site complications with, 1657 fixation of, 1658–1660, 1659t, 1660t, 1666–1668, 1667f, 1668f healing of, 1657 infection of, 391–393, 392t, 393t outcomes of, 1661–1662, 1662t placement of, 1666–1668, 1667f, 1668f preparation of, 1664, 1664f removal of, 393, 393b selection of, 1656, 1656t synthetic, 1655 tension of, 1657–1658 xenograft in, 38 insertion site marking for, 1663–1664, 1663f, 1664f in knee dislocation, 1758, 1759f ligament augmentation device for, 1655 medial collateral ligament injury repair with, 1632–1633, 1633f, 1634–1635, 1634f, 1635f, 1636 meniscal repair with, 1605–1606 outcomes of, 1661–1662, 1662f positioning for, 1662, 1663f


Anterior cruciate ligament (ACL) reconstruction (Continued) posterolateral corner injury and, 1743 rehabilitation after, 1668–1676, 1669t. See also Knee rehabilitation biofeedback in, 1671–1672 bracing in, 1672 cryotherapy in, 1670 electrical stimulation in, 230–233, 231f, 232f, 233f, 234f, 1671 functional testing in, 1674 kinetic chain exercise in, 1668–1670, 1669f muscle training in, 1671, 1674 proprioceptive training in, 1672, 1674 protocol for, 1672, 1673b range of motion in, 1670–1671 return-to-play plyometric training in, 300–321 contraindications to, 303 criteria for, 301–303, 302f glossary for, 324–330 stage I (dynamic stabilization and strengthening), 303–307, 304f, 305f, 306f, 322 stage II (functional strength), 307–312, 308f, 309f, 310f, 311f, 312f, 322–323 stage III (power development), 312–316, 313f, 314f, 316f, 323 stage IV (sport performance), 316–320, 317f, 318f, 319f, 320f, 324 RICE in, 1670 strain measurements for, 1586–1588, 1586f, 1587t unloading exercises in, 222–224, 223t weight-bearing in, 1671 return to play after, 301–303, 302f, 320–321, 1674, 1675t giving away and, 301 IKDC subjective rating and, 301 screw for, 1659 strain gauge analysis after, 1586f, 1587–1588 tibial osteotomy with, 1792, 1814–1816, 1815t, 1833, 1835. See also High tibial osteotomy results of, 1817, 1825–1830, 1828f, 1829f timing of, 1656 tunnel placement for, 1664–1666, 1665f, 1666f, 1667f Anterior drawer stress radiography, in lateral ankle sprain, 1919, 1919f Anterior drawer test in anterior cruciate ligament injury, 1650 in lateral ankle sprain, 1916–1917, 1917f in medial ankle sprain, 1936 in medial collateral ligament injury, 1629, 1630t Anterior interosseous nerve syndrome, 1317, 1317f Anteromedial tibial tuberosity transfer, in patellar dislocation, 1567 Antibiotics, 386–387 in erythrasma, 194t, 196 in folliculitis, 194, 194t, 195 in impetigo, 194, 194t in Lyme disease, 155 in septic olecranon bursitis, 1213 Anticoagulation physiologic, 372, 373f prophylactic, 378–384, 379t–381t in venous thromboembolism, 384–385, 384t Anticonvulsants, 188–189 cognitive effects of, 190, 191t in complex regional pain syndrome, 363t after head injury, 661

Index Antidepressants, in complex regional pain syndrome, 362, 363t Antidiuretic hormone, exercise effects on, 217, 217t Antihypertensive drugs, 158–161, 160t Antithrombin III, 372, 373f deficiency of, 372, 374t Anulus fibrosus, 717. See also Intervertebral disk biomechanics of, 718 tear in, 740–741 Aorta coarctation of, 158 rupture of, 167 Aortic insufficiency, 158 Apley’s test, 1601–1602 Apnea definition of, 448 sleep, 448–449 Apophysitis calcaneal, 1973–1974, 1974f, 2053–2054, 2143f, 2162, 2162f fifth metatarsal, 2167–2169, 2168f–2169f iliac, 1475 tibial tubercle, 599, 1526f, 1527–1529 Apprehension test in glenohumeral joint instability, 914, 915f, 939, 939f, 941 in patellar dislocation, 1538, 1539f, 1558 in rotator cuff disorders, 996, 999f in SLAP lesion, 1025 Arcuate ligament, 1585, 1588–1589, 1723 Arginine, 408, 421 Arginine α-ketoglutarate, 421 Arm. See also Elbow; Glenohumeral joint; Wrist anatomy of. See also specific structures muscular, 1157–1158, 1158f, 1160f–1161f neurovascular, 1157, 1159–1161, 1160f–1161f osseous. See Humerus; Radius; Ulna Arm curls, 88f, 213, 213f, 252, 252f Arrhythmias, inhalant-related, 430 Arrhythmogenic right ventricular cardiomyopathy, 166, 167f Arteriography. See Angiography Artery, 371f. See also specific arteries Arthritis degenerative. See Osteoarthritis patellofemoral, in female athlete, 489 pediatric inflammatory, 602–603, 602f septic, 602 rheumatoid. See Rheumatoid arthritis Arthrodesis first metatarsophalangeal joint, 2075 lunotriquetral, 1331, 1331f in sternoclavicular joint dislocation treatment, 810 triple, in posterior tibial tendon injury, 1980 Arthrofibrosis after high tibial osteotomy, 1832 knee rehabilitation and, 225 Arthrography, 535–537. See also Computed tomography (CT) arthrography; Magnetic resonance arthrography (MRA) ankle, 537 in high (syndesmosis) sprain, 1942 in lateral sprain, 1919–1920 in medial sprain, 1937 in subtalar sprain, 1950 hip, 536–537 knee, 536, 537f shoulder, 535–536, 536f, 949–950, 949f, 1000 wrist, 536

Arthropathy capsulorrhaphy, 1104b, 1105–1106, 1105t, 1114 dislocation, 1104–1105, 1104b Arthroplasty elbow for arthrosis, 1278 in distal humeral fracture nonunion, 1258 heterotopic ossification after, 1290, 1291f hip, 1499–1512 anatomy for, 1500–1502 approaches to, 1505 bearings for, 1505–1506 biomechanical aspects of, 1501–1502 high-offset femoral component in, 1502 minimally invasive, 1505 return to play after, 1507–1508, 1508t stability with, 1502 technique of, 1508–1512, 1509f, 1510f, 1511f, 1512f infection with, 394–395, 394f, 394t interphalangeal, 2121–2122, 2123b, 2123f–2124f knee, 1787–1801 athletic activity after, 1787–1789, 1789b clinical evaluation for, 1789–1790 imaging for, 1789–1790, 1790f mobile-bearing prostheses in, 1797–1798 vs. nonoperative treatment, 1790–1792 patient history and, 1789 physical examination in, 1789 quadriceps rupture with, 1521 total, 1794–1797, 1795t, 1796f, 1797f bearing surfaces in, 1800 gender-specific, 1799 high-flexion, 1798–1799, 1798f, 1799f indications for, 1794 minimally invasive, 1799–1800, 1800f prior proximal tibial osteotomy and, 1792 results of, 1795, 1795t unicompartmental, 1792–1794, 1793f metatarsal head, 2124, 2130f shoulder in fracture, 1046, 1048f in instability arthropathy, 1114 in osteoarthritis, 1110, 1113–1114, 1113f, 1114f, 1115–1118, 1116f, 1116t, 1117f, 1118f in rheumatoid arthritis, 1114 simulation of, 1151, 1153, 1153f–1155f Arthroscopy, 121–131 in acromioclavicular joint reconstruction, 844 ankle, 127, 127f in impingement, 2159–2160, 2159t, 2160f indications for, 127 normal anatomy on, 127, 127f portals for, 127, 127f positioning for, 127 in biceps tendon evaluation, 1009–1010 complications of, 122–124 deep vein thrombosis with, 123–124, 124b, 383–384, 383t elbow, 129–130, 129f in capitellar osteochondritis dissecans, 1243–1244, 1243f, 1245f in heterotopic ossification, 1296–1297 indications for, 129 in lateral epicondylitis, 1203–1204 normal anatomy on, 130, 130f in olecranon bursitis, 1212 portals for, 129–130, 129f positioning for, 129 in recurrent instability, 1307–1310, 1309f in valgus extension overload, 1224–1225


Arthroscopy (Continued) equipment for, 121–122, 122f, 123f complications with, 123 sterilization of, 121 hip, 125–126, 126f, 1473–1474, 1473t, 1474f in acetabular labral tears, 1470, 1470f complications of, 1474 in femoroacetabular impingement, 1472 indications for, 125–126, 1473, 1473t in ligamentum teres rupture, 1473, 1473f in loose body removal, 1472, 1472f normal anatomy on, 126, 126f portals for, 126, 126f positioning for, 126 technique of, 1473–1474, 1474f image interpretation in, 122, 122f intra-articular injury with, 122–123 irrigation during, 122, 123f knee, 124–125, 124f, 125f in abrasion procedure, 53 in anterior cruciate ligament reconstruction, 1662–1668, 1663f, 1664f, 1665f, 1666f, 1667f. See also Anterior cruciate ligament (ACL) reconstruction in arthritis, 1792 deep vein thrombosis with, 123–124, 124b indications for, 124 in medial collateral ligament injury, 1632–1633, 1633f, 1634–1635, 1634f, 1635f in meniscal injury, 1602–1603, 1606, 1606f, 1618 normal anatomy on, 125, 125f in patellar dislocation, 1545, 1570–1572 portals for, 124–125, 125f positioning for, 124, 124f in posterior cruciate ligament and posterolateral corner injury, 1706–1710, 1707f in posterior cruciate ligament reconstruction, 1705, 1706f, 1707f in posterolateral corner injury, 1706–1710, 1707f, 1730–1731, 1732f in varus malalignment, 1808, 1808f pediatric in elbow injury, 468 in hip injury, 469, 470f in shoulder instability, 468, 469f in tibial spine fracture, 469, 472f in wrist injury, 468, 470f positioning for, 122 in scapulothoracic bursectomy, 890–891, 891f shoulder, 127–129, 128f, 1147–1151 in adhesive capsulitis, 1096–1102, 1097f–1102f, 1103b in anterior glenohumeral joint instability, 919–923, 921f–923f, 927–929 in anterior labral repair, 1151, 1152f in glenohumeral joint osteoarthritis, 1110–1111, 1115, 1115f, 1118, 1118t–1119t in glenoid detachment, 1220, 1220f indications for, 127 knot tying for, 1147, 1148f learning methods for, 1147, 1149f in multidirectional glenohumeral joint instability, 930–931, 930f normal anatomy on, 128–129, 129f portals for, 128, 128f positioning for, 127–128, 128f in posterior glenohumeral joint instability treatment, 924–926, 926f–927f in rotator cuff repair, 1009–1010, 1149, 1150f, 1151, 1218–1219, 1219f

vi

Index

Arthroscopy (Continued) in SLAP lesion, 1025, 1026–1031, 1027f–1031f suite for, 121 tourniquet effect during, 123 wrist, 130–131, 130f, 1430–1450 in children, 468, 470f in chondral lesions, 1447–1449, 1448f distal radioulnar joint portals for, 1434–1435 in dorsal ganglion cyst, 1444–1445, 1445f equipment for, 1430–1431, 1431f indications for, 130, 1430 in ligament instability, 1434, 1434t, 1442–1443, 1443f in ligament tears, 1442–1443, 1443f in loose bodies, 1447 normal anatomy on, 131, 131f in ostectomy, 1449–1450 portals for, 130–131, 130f, 1431–1435, 1431f 1-2, 1431, 1431f 3-4, 1431–1433, 1431f, 1432f 4-5, 1431f, 1433, 1433f 6-R, 1431f, 1433, 1433f 6-U, 1431f, 1433 distal radioulnar joint, 1434–1435 radial midcarpal, 1434, 1434f, 1434t scaphoid trapezium trapezoid, 1434, 1435f ulnar midcarpal, 1434 volar, 1434 positioning for, 130 in proximal row carpectomy, 1449–1450 radial midcarpal portal for, 1434, 1434f, 1434t in radial styloidectomy, 1449 scaphoid trapezium trapezoid portal for, 1434, 1435f in scapholunate ligament injury, 1325 in synovectomy, 1443–1444 in triangular fibrocartilage complex tears, 1435–1442. See also at Triangular fibrocartilage complex (TFCC) tears ulnar midcarpal portal for, 1434 in ulnar styloid impaction syndrome, 1445–1447, 1446f volar portal for, 1434 Arthrosis acromioclavicular joint, 829–830 elbow joint, 1278 glenohumeral joint, 929 Arthrotek tensioning boot, 1760, 1761f, 1762 Articular cartilage. See Cartilage, articular Artificial turf, 1210 Ascorbic acid (vitamin C) deficiency of, 72–73, 73t requirements for, 406b Askin’s tumor, 610 Aspiration (needle) of cyst, 585 in olecranon bursitis, 1248, 1248f Aspirin, in venous thromboembolism prevention, 378–384, 381t Asthma. See Bronchospasm Atenolol in complex regional pain syndrome, 363t in hypertension, 160t Athlete-ready position, 313f, 325 Athlete’s foot, 1964 Athletic pubalgia, 1463–1464 vs. adductor strain, 1490 Athletic trainer, 530 Atlanto-dens interval, 694, 695f in Down syndrome, 705, 707b

Atlanto-occipital fusion, 693 Atlanto-occipital instability, in children/ adolescents, 704–705, 705f Atlantoaxial complex, 677f Atlantoaxial instability, 514t, 677, 677f, 694, 695 in children/adolescents, 705, 707f Atlantoaxial subluxation, rotary, in children/ adolescents, 706–707, 708f Atlas (C1) fracture of, 677, 677f, 678f, 695–696, 705, 706f occipitalization of, 711 posterior arch absence in, 711, 711f ATPase, in muscle contraction, 8–9, 9f Atrophy, in complex regional pain syndrome, 358 Aura, with seizure, 186 Autograft(s). See also Graft(s) in anterior cruciate ligament reconstruction, 37–38, 1584, 1656–1657, 1656t, 1659, 1659t, 1661, 1662f articular cartilage, 53–54 bone, 81, 83t ligament, 36–38 fascia lata, 37 iliotibial band, 37 patellar tendon, 37 semitendinosus tendon, 37–38 osteochondral in knee, 1775, 1777, 1780–1781, 1781f in talus, 2146–2147, 2148, 2150–2152, 2150t, 2151f–2152f, 2153 periosteum, 53–54 Automatic external defibrillator, in sudden death, 171–172, 171t Autonomic nervous system, 353 in complex regional pain syndrome, 353–355, 354f, 356–357, 357f, 360–361 Avascular necrosis, 73, 77 femoral head, 1466–1467, 1467b, 1467t in children, 1476–1477 slipped capital femoral epiphysis and, 1476 histology of, 77 humeral head, 1049, 1105t, 1106–1107, 1107f arthroscopic treatment of, 1110–1111 magnetic resonance imaging of, 984, 985f physeal injury and, 1085 sesamoid, 2089 Avulsion fracture anterior process of calcaneus, 1954, 1954f, 2153–2156, 2154t, 2155t hip and pelvis, 553, 555, 1474–1475, 1475f, 1489 iliac spine, 553, 556f, 1475 imaging of, 553, 555, 556f, 557, 557f ischial, 1489, 1489f lesser humeral tuberosity, 1175–1176 lesser trochanter, 1475 rib, 895–896, 896f Axial load test in glenohumeral joint instability, 914–915 in rotator cuff disorders, 996, 999f Axillary artery anatomy of, 911–912, 1036f, 1071–1072, 1072f arteriography of, 1139, 1139f injury to, 1140–1141, 1141f anterior shoulder dislocation and, 1139–1140, 1140f, 1141f Axillary nerve anatomy of, 912, 1034, 1036b, 1036f, 1161f evaluation of, 1036–1037, 1038f


Axillary nerve (Continued) injury to in glenohumeral joint instability, 933, 934f paralabral cyst and, 980, 980t in proximal humeral fracture, 1049 quadrilateral space compression of, 1142 Axillary vein, effort thrombosis of, 1130, 1134, 1141–1142 Axis (C2), fracture of, 678, 694, 696, 707–708 Axis of rotation, 1190, 1191f Azoospermia, anabolic-androgenic steroids and, 416

B Back pain. See Low back pain Back squat, shoulder injury and, 249 Bagging, 430 Balance training, single-leg, in knee rehabilitation, 271 Ball exercises, in trunk stabilization, 342t, 345, 347–348 Band good morning exercise, 316f, 325 Band walking exercise, 258, 259f Bankart lesion, 616, 912, 933, 934f. See also Glenohumeral joint instability, anterior arthroscopic treatment of, 919–923, 920f, 921f–923f in children, 468, 470f, 940–941, 940f, 941f magnetic resonance arthrography of, 973–974, 973f, 974t magnetic resonance imaging of, 969, 969f, 973 radiography of, 968–969 reverse, 936, 942, 942f, 974t arthroscopic treatment of, 924–926, 926f–927f, 942, 942f in children, 942, 942f magnetic resonance arthrography of, 975, 975f variants of, 974, 974f, 974t Barefoot running, 1874–1875, 1874f, 2183–2184, 2183f Baseball. See also Overhead throwing circadian rhythms and, 457 pediatric. See also Little Leaguer’s elbow; Little Leaguer’s shoulder humeral fracture in, 1068, 1070f Baseball finger, 1388, 1420–1422, 1420f, 1421f Basketball, jet lag and, 458 Bathing, epilepsy and, 192 Battle’s sign, 525 Bayes’ network, 114 Bayonet sign, 1554 Bean bucket wrist and forearm training, 255, 255f Bear paw shoe, 1874, 1874f Behavior, anabolic-androgenic steroid effects on, 417 Behind-the-neck training, shoulder injury and, 248–249 Benazepril, 160t Bench press, shoulder injury and, 247–248, 248f Benign rolandic epilepsy, 187 Bennett’s fracture, 1402–1403, 1402f, 1403f, 1411, 1412 Bent leg side bridge exercise, in core training, 284, 284f Benzodiazepines, in complex regional pain syndrome, 363t, 364 Betazolol, 160t Bethesda Guidelines, in sudden death prevention, 169, 170t Bias, research, 100

Index Biceps brachii anatomy of, 858, 858f, 859f, 1157–1158, 1158f, 1160f pediatric, 785 long head of, tendon of. See Biceps tendon short head of, transfer of, 840–841, 841f Biceps curl, 88f, 213, 213f, 252, 252f Biceps femoris, 1485, 1485f, 1721–1722. See also Hamstring muscles Biceps load test, in SLAP lesion, 1025t Biceps tendon anatomy of, 771–772, 911, 989, 990, 991f, 992, 992f, 1018, 1018f arthroscopic evaluation of, 1009–1010 biomechanics of, 992, 992f, 1019–1021, 1019f, 1020b, 1021f detachment of. See SLAP (superior labrum, anterior to posterior) lesion distal rupture of, 1167–1170 classification of, 1168, 1168t evaluation of, 1168 imaging of, 1168, 1169f rehabilitation after, 1169–1170, 1170t treatment of, 1168–1170 fraying of, 1220 histology of, 1018, 1018f hourglass, 981, 982f magnetic resonance imaging of, 980–983, 981f, 982f pediatric, 790 popeye deformity of, 1165, 1166f rupture of, 1165–1167, 1166f, 1167t scapular attachment of, 858, 858f subluxation/dislocation of, 772, 981–983, 982t, 1009 evaluation of, 997 superior labral attachment of, 1018, 1018f tears of, 981, 992 clinical manifestations of, 996, 996f, 997, 1000f magnetic resonance imaging in, 566, 568f Biceps tenodesis, 1733–1734, 1736f Bicipital groove, 771–772, 1034t palpation of, 996, 997f Bifurcate ligament, 1913f, 1953, 1954f Bifurcate sprain, 1918, 1933, 1953–1955 calcaneal fracture and, 1954, 1954f evaluation of, 1954, 1954f rehabilitation for, 1955 return to play after, 1955 treatment of, 1955 Biglycan, 44 Binge drinking, 424–425 Biofeedback, 224–225, 233, 234f in anterior cruciate ligament rehabilitation, 1671–1672 in muscle atrophy, 224–225 with stretching exercises, 292f, 293 Biological rhythms. See Chronobiology Biomechanics, 85–96. See also at specific joints and structures angular kinematics in, 90, 91f degrees of freedom in, 89 dynamics in, 87, 89–93 force vectors in, 86, 90f free-body diagrams in, 87, 88f joint contact forces in, 87 joint motions in, 90, 93f kinematics in, 87, 90, 91f kinetics in, 90–91 linear kinematics in, 90, 91f loading-related, 93–95, 93f–95f mechanical properties in, 93–95, 93f–�� 95f moment/torque vectors in, 86 Newton’s laws in, 86–87, 89t, 92–93

Biomechanics (Continued) relative motion in, 89–90 scalars of, 86 statics of, 86–87 structural properties in, 93, 94f units of measurement in, 85, 85t vectors of, 86 viscoelasticity in, 95–96, 95f Biomechanics of Distance Running (Cavanagh), 1896 Biopsy, CT-guided, 585, 586f Bioscaffolds, in tendon healing, 28 Bipartite patella, 1574 Bipartite scaphoid, 1366 Bipartite sesamoid, 2028, 2029f, 2088 Bird dog exercise, in core training, 282–283, 283f Bisoprolol, 160t Bisphosphonates in complex regional pain syndrome, 363t, 365 in tibial stress fracture, 1854 Bitter orange, 409 Black heel, 202, 202f Blackburne-Peel ratio, for patella height, 1523, 1523f, 1539, 1541f Bleeding. See Hematoma; Hemorrhage Bleeding disorder, 514t Blinding, statistical, 100, 104–105 Blisters, foot, 1964 shoe fit and, 2184–2185 Blood alcohol concentration of, 424, 449–450 venous stasis of, 371. See also Thrombosis Blood flow in complex regional pain syndrome, 361, 365 exercise effects on, 219–220 Blood pressure classification of, 156, 157t exercise effect on, 219–220, 220t measurement of, 157, 157b preparticipation examination for, 512, 513 Blount’s disease, 599 Blumensaat line, 1539, 1541f Body Blade training, in shoulder rehabilitation, 245, 246f Body clock. See Chronobiology Body image disorders, anabolic-androgenic steroids and, 417 Boils, 194–195, 194t Bone(s), 65–70. See also at specific bones age-related changes in, 72, 78 anabolic-androgenic steroid effects on, 416 biomechanics of, 77–78 blood supply of, 69, 69f, 70f calcification of, 67, 68f calcitonin effects on, 71, 71t calcium of, 70, 71t cancellous (spongy, trabecular), 65, 66f remodeling of, 68 cells of, 65–67, 67t cortical (compact), 65, 66f, 67t remodeling of, 68, 68f corticosteroid effects on, 72 cyst of radiography in, 552, 553f unicameral, 606, 606f fracture through, 552, 553f, 606, 606f, 1085, 1086f death of. See Avascular necrosis density of decrease in, 72–73 in female athlete, 478, 481 development of, 587–588, 588f ectopic. See Heterotopic ossification


vii

Bone(s) (Continued) endochondral, formation of, 78 estrogen effects on, 72 formation of, 78 distraction-induced, 81–82, 83f endochondral, 78 intramembranous, 78 growth factors of, 79–80 growth hormone effects on, 72 healthy, 406 infection of. See Osteomyelitis injury to. See Fracture(s) and at specific bones intramembranous, formation of, 78 matrix of, 67, 68f mechanical properties of, 77–78 mineral metabolism of, 67, 70–71, 71t disorders of, 72–73, 73t, 74t–75t, 76t–78t parathyroid hormone effects on, 71, 71t pathologic, 66f phosphate of, 70, 71t physis of, 78, 587–588 proteoglycans of, 67 remodeling of, 67–68, 68f, 79 thyroid hormone effects on, 72 tumor of, 74t, 77t, 547, 547f types of, 65, 66f, 67t vitamin D effects on, 71, 71t Bone bruise, lateral ankle sprain and, 1929, 1931 Bone cyst radiography in, 552, 553f unicameral, 606, 606f fracture through, 1085, 1086f Bone graft, 81, 83t allograft, 81, 83t, 137 autograft, 81, 83t cancellous, 81, 83t cortical, 81, 83t osteoarticular (osteochondral), 81 vascularized, 81 in Kienböck’s disease, 1377 in scaphoid nonunion, 1341–1345, 1342f–1344f Bone marrow, 69–70 Bone mineral density decrease in, 72–73 in female athlete, 478 Bone morphogenetic proteins in fracture healing, 79–80 in heterotopic ossification, 1289 Bone scan. See Radionuclide imaging Bone–anterior cruciate ligament–bone allograft, 38 Bone–patellar tendon–bone autograft, 1584, 1656–1657, 1656t, 1659, 1659t, 1661, 1662f Bony humeral avulsion of glenohumeral ligament (BHAGL) lesion, 555 Borrelia burgdorferi infection, 155–156 BOSU exercises, 305f, 308f, 315f, 325–327 Botox injection, in lateral epicondylitis, 1200 Bounding exercise, 315f, 327, 328 Boutonnière injury/deformity, 1388–1389, 1388f, 1389f pediatric, 1418, 1419f, 1422–1423, 1422f, 1424f pseudo, 1389–1390 treatment of, 1389, 1389f Bowstring sign, 722 Box drop-off exercises, 327 Box step-down exercise, 308f, 324 Boxer’s cast, 1413–1414, 1413f Boxer’s fracture, 1393–1394, 1393f, 1412–1413, 1413f Boxer’s knuckle, 1390

viii

Index

Brace/bracing in ankle instability, 340 in anterior cruciate ligament rehabilitation, 1672 in capitellar osteochondritis dissecans, 1242 in elbow dislocation, 1269 in knee osteoarthritis, 1790 in lateral ankle sprain, 1921–1922, 1921t, 1922f in lateral epicondylitis, 618–619, 618f, 1200–1201, 1201f in patellar dislocation, 1547, 1566 in posterior cruciate ligament rehabilitation, 1711 in tibial stress fracture, 1854 Brachial artery, 1159, 1160f, 1161f Brachial neuritis. See Parsonage-Turner syndrome Brachial plexus anatomy of, 671f, 1034, 1036f injury to, 670–673, 671f prevention of, 673, 673f, 674f Brachialis muscle, 1157–1158, 1158f Brain, 657 injury to. See Head injury Brainstem, 657 Breast cancer of exercise and, 481 radionuclide imaging in, 547, 548f injury to, 479 Breathing, assessment of, 519, 520t, 521f Bridging exercise in anterior cruciate ligament rehabilitation, 308f, 326 in core training, 281–284, 281f–�� 282f, 285f in knee rehabilitation, 258, 258f, 308f, 326 in trunk stabilization, 342t, 344 unilateral, in core training, 281f Bright light therapy in jet lag, 458–459, 458f, 459t in seasonal affective disorder, 444–445 Brisement therapy, in retrocalcaneal bursitis, 2035 Broad jump, 314f, 324–325, 327 Bronchitis, 149–150 Bronchodilators, in exercise-induced bronchospasm, 182 Bronchospasm, exercise-induced, 180–185 clearance for participation and, 513 clinical manifestations of, 181, 181b complications of, 185 definition of, 180, 181t diagnosis of, 181–182, 183f differential diagnosis of, 181, 181b evaluation of, 182 on-field, 526 prevalence of, 180, 181t return to play criteria for, 184f, 185 risk for, 180–181 treatment of, 182–184, 183f nonpharmacologic, 183f, 184 pharmacologic, 182–183, 182t, 183f sideline, 184–185, 184b, 184f Broström procedure, 1926–1928, 1927f Brown-Séquard syndrome, 710 Bucket handle fracture, in child abuse, 595–596, 596f Buford complex, 575, 972, 972f, 1017–1018, 1017f Bulbocavernous reflex, 675 Bulls-eye lesion, in quadriceps strain, 1494, 1495f Bundle ridge, 1646, 1647f Bunion, 1962–1963

Bunionettes, 2132–2142 anatomy of, 2132, 2132b, 2133f in children, 1963 classification of, 2133, 2134b evaluation of, 2133–2134, 2134b imaging in, 2134, 2134b nonoperative treatment of, 2134, 2134b operative treatment of, 2134–2141 care after, 2139–2140, 2140f, 2141f diaphyseal metatarsal osteotomy in, 2135–2136, 2137, 2138b, 2139f, 2140f distal chevron osteotomy in, 1966f, 2135–2136, 2135b, 2137b distal metatarsal osteotomy in, 2135–2136, 2135b distal oblique osteotomy in, 2135–2136, 2135b, 2136b, 2136f, 2137f lateral condylectomy in, 2134–2135, 2134b, 2135f, 2140, 2140f return to play after, 2141 physical examination in, 2134, 2134b Burner syndrome, 670–673, 710–711 vs. acute herniated disk, 704, 711 cervical stenosis and, 671–672 in children/adolescents, 710–711 clearance for participation and, 513 prevention of, 673, 673f vs. spinal cord injury, 524 Burning hands syndrome, 710 Bursa (bursae) infraserratus, 886, 886f, 887b olecranon, 1246–1247 retrocalcaneal, 2031, 2031f, 2032f. See also Retrocalcaneal bursitis scapular, 886, 887b, 887f scapulotrapezial, 886, 887b, 887f subacromial, 990, 991f subscapularis, 771 supraserratus, 886f, 887b trapezoid, 886 Bursectomy olecranon, 1248 in rotator cuff tear repair, 1013 scapulothoracic, 890–891, 891f Bursitis iliopectineal, 1458 iliopsoas, 1457–1458, 1457f ischial, 1457 olecranon, 1209–1212, 1246–1249. See also Olecranon bursitis retrocalcaneal, 2030–2041. See also Retrocalcaneal bursitis scapulothoracic, 889–891, 891f trochanteric, 1455–1457, 1456f Bursography in iliopsoas bursitis, 1457, 1457f in snapping hip syndrome, 1458 Bursoscopy, scapulothoracic, 890–891, 891f Burst fracture atlas, 677, 677f–678f, 705, 706f C4, 681, 681f lumbar spine, 541f, 735, 735f Buschke’s disease, 2143f, 2166, 2166f γ-Butyrolactone, 409

C C protein, 4, 5t Caffeine, 401, 409, 421, 451–452, 453t Calcaneal angle, 2035, 2035f Calcaneal apophysitis (Sever’s disease), 1973–1974, 1974f, 2143f, 2162, 2162f treatment of, 2053–2054 Calcaneal nerve, medial, 2043, 2044f, 2045f


Calcaneocuboid joint biomechanics of, 1869, 1870f impairment of, 1872 Calcaneofibular ligament, 338, 1913–1914, 1913f, 1914f, 1915f biomechanics of, 1865–1866, 1866f injury to. See Ankle sprain, lateral; Subtalar sprain repair of, 1923–1924, 1923f Calcaneus anterior process of, avulsion fracture of, 1954, 1954f, 2153–2156, 2154t, 2155t fracture of, 2153–2156, 2154t, 2155t return to play after, 2156 posterior-superior pain in. See Retrocalcaneal bursitis stress fracture of, 556f, 646, 647f, 2016t, 2019–2020, 2022f Calcification. See also Heterotopic ossification; Myositis ossificans periarticular, 1289 Calcitonin in bone metabolism, 71, 71t in complex regional pain syndrome, 363t, 364–365 Calcium bone, 70, 71t deficiency of, cramps and, 12 in muscle contraction, 208, 209f requirement for, 70, 406, 406b in female athlete, 478, 478t serum, 74t–76t, 77t urinary, 74t–76t Calcium channel blockers in complex regional pain syndrome, 363t, 364 in hypertension, 160t, 161 Calcium hydroxyapatite, 67 Calf raise exercise, in ankle rehabilitation, 273, 275f Call to Action against Underage Drinking, 425 Callus bony, 79, 80f, 81t stratum corneum, 2108. See also Plantar keratoses shoe fit and, 2184–2185, 2184f Calories, requirements for, 402–403 Calorimetry, indirect, 212–213, 212f Campylobacter fetus infection, 397 Cancer, 514t bone, 74t, 77t, 547, 547f breast, 481, 547, 548f oral, smokeless tobacco and, 428 positron emission tomography in, 547 prostate, anabolic-androgenic steroid effects on, 416 Candesartan, 160t Candida infection, 397, 398t Cane, in knee osteoarthritis, 1790 Cannabis use/abuse, 425–426 Capitate anatomy of, 1319–1320, 1319f avascular necrosis of, 1375 fracture of adult, 1348–1349 pediatric, 1368 Capitellum fracture of, 1251, 1251f–1252f fixation of, 1256, 1257f ossification of, 1227–1228 osteochondritis dissecans of. See Osteochondritis dissecans, capitellum osteochondrosis of, 623, 625f, 1238 Capitolunate angle, 1322, 1322f Capsaicin, in complex regional pain syndrome, 364

Index Capsular ligament, 793–794, 793f, 794f Capsular shift procedure, in glenohumeral joint instability, 927, 945 Capsulorrhaphy arthropathy, 1104b, 1105–1106, 1105t, 1114 Captopril, 160t Carbamazepine in complex regional pain syndrome, 363t in epilepsy, 188, 191t Carbohydrate(s) after exercise, 404 before exercise, 404 during exercise, 404 metabolism of, 211 requirement for, 403–404, 403t Carbohydrate loading, 403–404 Carbonated beverage, 401 Cardiac arrest, 526. See also Sudden death Cardiac output, exercise effect on, 219, 219f, 220t Cardiomyopathy anabolic-androgenic steroids and, 416 dilated, 152 hypertrophic, 164–165, 164f, 170 right ventricular, arrhythmogenic, 166, 167f Cardiopulmonary resuscitation equipment for, 517, 518t guidelines for, 520, 520t, 521f Cardiovascular disease, preparticipation examination for, 509, 512, 512t, 514t Cardiovascular system anabolic-androgenic steroid effects on, 416 cocaine effects on, 429 exercise effects on, 218–220 hypothermia effects on, 501 inhalant effects on, 430 marijuana effects on, 426 nicotine effects on, 428 Carpal tunnel syndrome, 626, 1359–1361 clinical manifestations of, 1360 electrodiagnostic study in, 1361 physical examination in, 1360 return to play after, 1361 treatment of, 1360–1361, 1360f Carpometacarpal joint anatomy of, 1386–1387 dislocation of, 534f, 1386–1387, 1387f thumb, dislocation/subluxation of, 1398 Carpometacarpal ligaments, 1320 Carpus. See Wrist Carrying angle, 1190, 1192 Cartilage, articular, 40–55. See also specific joints age-related changes in, 40 biomechanics of, 48 calcified zone of, 41f, 42f, 46 cell-matrix interactions in, 45, 45f chondrocytes of, 41, 41f, 45, 45f, 47f collagen of, 42–43, 43f composition of, 40–42, 41f creep of, 48 deep zone of, 41f, 42f, 46 extracellular matrix of, 41–42, 42f, 45, 45f for graft, 55 regions of, 46–48, 47f fluid of, 41 glycoproteins of, 45 immobilization effects on, 228 injury to, 48–52, 49t. See also at specific joints arthroscopic abrasion for, 52–53 artificial matrix grafts for, 55 blunt trauma, 50–51 cartilage shaving for, 52 chondrocyte implantation for, 55 fracture, 49t, 51–52 grafts for, 53–55

Cartilage, articular (Continued) laceration, 50 matrix, 48, 49–50, 49t proteoglycan effects of, 44 subchondral bone abrasion for, 52–53 surgical treatment of, 52–53 tissue disruption, 49t, 50–51 interterritorial matrix of, 47f, 48 laceration of, 50 magnetic resonance imaging of, 576–582, 578f in children, 592–593 at hip, 581–582 at knee, 579–580, 579f–581f at shoulder, 580–581, 582f, 583f noncollagenous proteins of, 45 pediatric, 592–593 pericellular matrix of, 46, 47f proteoglycans of, 41, 42, 43f, 44–45 loss of, 49, 49t repair of, 48–52, 49t repetitive impact loads on, 50–51 shaving of, 52 stress relaxation of, 48 structure of, 41f–42f, 45–48 superficial zone of, 41f–42f, 46 territorial matrix of, 46, 47f transitional zone of, 41f, 42f, 46 viscoelastic properties of, 48 zones of, 41f, 42f, 46, 579–580 Cartilage graft(s), 53–55 allograft, 54 artificial matrix, 55 autograft, 53–54 perichondrial, 53–54 periosteal, 53–54 Cast/casting in Achilles tendon rupture, 2005 in calcaneal fracture, 2156 in lateral ankle sprain, 1920–1921, 1921t playing, 1362 in proximal humeral physeal fracture, 1076–1077 in talar fracture, 2156 Catecholamines, 353 in complex regional pain syndrome, 354, 354f exercise effects on, 217–218, 217t, 218f receptors for, 353 Caton-Deschamps ratio, 1539, 1541f Cauda equina, 717–718 Cauda equina syndrome, 743 Causalgia. See Complex regional pain syndrome Causation, 100–101 Cavus foot, 1963, 2183 in children/adolescents, 1963 shoe for, 1900 stress fracture and, 1850 Cefazolin, 386, 387t Cefuroxime, 387t Celecoxib, in tendon healing, 29 Cellulitis, 387–388, 387f, 547 Central nervous system, 353 cocaine effects on, 429 in force production, 7 inhalant effects on, 430 injury to. See Cervical spine injury; Head injury; Spinal cord injury Cephalosporins, 386, 387t Cerebellum, 657 Cerebral edema, high-altitude, 504–505 Cerebral palsy, 514t Cerebrospinal fluid (CSF) in head injury, 657 leak of, 525


ix

Cerebrum, 657 Cervical collar, in rotary atlantoaxial subluxation, 707 Cervical cord neurapraxia/quadriplegia, 681–686 developmental stenosis and, 693–694, 710 grade of, 685–686 os odontoideum and, 692, 692f pathophysiology of, 690–691, 691f prevention of, 686–690, 687f–690f recurrence of, 686, 686f stenosis and, 681–686, 683f–�� 685f, 710 Cervical ligament, 1913f Cervical radiculopathy, vs. lateral epicondylitis, 618 Cervical spine. See also Cervical spine injury anterior subluxation of, C3-C4, 678–679, 679f canal:vertebral body ratio in, 694, 694f computed tomography of, 539–541, 540f congenital anomalies of, 711–712, 711f, 712b, 712f facet dislocation of C3-C4, 679, 679f, 707–709 C4-C7, 680, 707–709, 709f fracture of, 675–677. See also Cervical spine injury C1-C3, 677–678, 677f, 678f in children/adolescents, 704–708, 705, 706f C3-C4, 678–679 in children/adolescents, 708–709 C4-C7, 679–681, 680f–682f in children/adolescents, 708–709 return to play after, 696f, 697–698, 697f–�� 698f compression, 680–681, 680f–�� 682f in children/adolescents, 709, 709f instability in, 675–676, 676f management principles in, 675–677, 676f return to play after, 696f, 697–698, 697f, 698f surgical treatment of, 676–677 vertebral body, 680–681, 681f–682f, 697f, 698, 698f fusion of congenital, 693, 693f, 711–712, 712f surgical, 699, 699f, 700f intervertebral disk of herniation of, 674, 698–699, 699f in children/adolescents, 704 injury to, 674, 698–699, 699f rupture of, 674, 678 pediatric. See also Cervical spine injury, pediatric anatomy of, 702–703, 703f congenital anomalies of, 711–712, 712b, 712f pedicles of congenital absence of, 711 fracture of, 678, 707–708 scoliosis of, congenital, 711 sprain of, 673–674 stenosis of, 681–686. See also Cervical cord neurapraxia/quadriplegia developmental, 693–694, 695f, 710 measurement of, 683–686, 683f–685f, 694, 694f ratio method measurement of, 683–686, 683f, 684f, 685f in spear tackler’s spine, 694, 695f, 710 stingers and, 672 subluxation of atlantoaxial, 706–707, 708f C3-C4, 678–679, 679f without fracture, 674

Index

Cervical spine injury, 665–701 in ambulatory patient, 669–670 in diving, 690 emergency management of, 665–669, 691 airway in, 667, 668f facemask removal in, 667, 667f head tilt–jaw lift maneuver in, 667, 668f helmet removal in, 668–669, 670f imaging in, 669 immobilization in, 666–667, 666f jaw thrust maneuver in, 667, 668f logroll in, 666–667, 666f six-plus-person lift in, 667 spine board for, 666–667, 666f transport in, 669, 669f football-related, 665–669, 686–690, 687f, 688f, 689f, 690f airway in, 668f, 670f facemask removal in, 667, 667f helmet removal in, 668–669, 670f immobilization in, 666–667, 667f fracture, 675–677, 676f. See also Cervical spine, fracture of return to sports after, 696f, 697–698, 697f, 698f in hockey, 690 intervertebral disk, 674, 698–699, 699f ligamentous, 696–697 logroll for, 519, 519f, 666–667, 666f lower cervical spine fracture and dislocation, 679–681, 679f, 681f–683f, 696–697 midcervical spine fracture and dislocation, 678–679, 679f, 696–697 nerve root–brachial plexus, 670–673, 671f–674f on-field, 522–524, 524f assessment of, 523–524, 524f pathophysiology of, 690, 690f pediatric, 701–713 airway management in, 703 atlanto-occipital instability, 704–705, 705f atlantoaxial instability, 705, 707b, 707f emergency treatment of, 703 epidemiology of, 702 hangman’s fracture, 707–708 Jefferson fracture, 705, 706f odontoid fracture, 707 rotary atlantoaxial subluxation, 706–707, 708f soft-tissue, 703–704 sports-specific, 702 subaxial fracture, 708–709, 709f personnel training for, 665–666 planning for, 665 prevention of, 686–690, 687f–690f quadriplegia with. See Cervical cord neurapraxia/quadriplegia return to sports after, 691–701 atlanto-occipital fusion and, 693 developmental stenosis and, 693–694, 694f fracture and, 676, 676f, 696f, 697–698, 697f, 698f intervertebral disk injury and, 698–699, 699f Klippel-Feil deformity and, 693, 693f middle and lower spine trauma and, 696–697 odontoid anomalies and, 692, 692f spear tackler’s spine and, 694, 694f spinal fusion and, 699, 699f, 700f upper spine trauma and, 694–696, 695f, 696f spinal stenosis and, 681–686, 683f–686f, 710 spine board for, 665, 666–667, 666f

Cervical spine injury (Continued) sprain, 673–674 subluxation C3-C4, 678–679, 679f without fracture, 674 upper spine fracture and dislocation, 677–678, 677f–679f return to sports and, 694–696, 695f, 696f Cervical spine injury without radiography abnormality, 702, 703, 704 Cervical sprain, 673–674 Chest, flail, 526, 893. See also Rib(s), fracture of Chest radiography in myocarditis, 151 in pulmonary embolism, 376 Chevron procedure, in hallux valgus, 2070, 2073b, 2073f, 2074f, 2076 Chilblains, 203 Child abuse, 595–596, 596f humeral physeal fracture in, 1283 rib fracture in, 894 Children/adolescents, 463–474. See also Female athlete accessory navicular in, 1963, 1963f acromioclavicular injuries in, 855–856, 855f adductor injury in, 1493 anabolic-androgenic steroid use by, 467–468 ankle sprain in, 1963, 1964f anterior cruciate ligament injury in, 1679–1683, 1682f arthroscopy in, 468–473. See also Arthroscopy, pediatric avulsion fracture in at hip, 1474–1475, 1475f, 1489 ischial, 1489, 1489f bone development in, 587–588, 588f, 589f bunion in, 1962–1963 bunionettes in, 1963 calorie requirement for, 402–403 cavus foot in, 1963 cervical spinal cord injury in, 709–711 cervical spine injury in, 701–713. See also Cervical spine injury, pediatric chondroblastoma in, 604f, 605 complex regional pain syndrome in, 367, 369 computed tomography in, 590, 590f congenital cervical spine anomalies in, 711–712, 711f–712f, 712b dehydration in, 465–466 elbow of. See Elbow, pediatric endurance training in, 464 ergogenic drug use by, 412–413 Ewing’s sarcoma in, 607, 609f, 610 femoral shaft stress fracture in, 1481 fibrous dysplasia in, 606, 608f flexibility in, 464–465 fluid requirement for, 402 fracture in ankle, 597, 598f, 1964–1969, 1965f–1969f bucket handle, 596, 596f carpal, 1364–1371. See also at specific bones clavicular, 596, 596f distal femur, 595, 595f femoral shaft, 1481 fifth metatarsal, 1969–1970, 1971f glenoid, 872, 875 hip, 597, 598f, 1474–1475, 1475f, 1489 humeral. See Humeral fracture (distal), pediatric; Humeral fracture (proximal), pediatric imaging of, 593–596, 594f, 595f, 596f, 597f, 598f ischial, 1489, 1489f metatarsal, 1969–1971, 1970f–1971f nonaccidental, 595–596, 596f


Children/adolescents (Continued) patellar, 1576–1577, 1576f radius, 594f, 595, 597 rib, 894 scapular, 872, 875 tibial eminence, 1677–1679, 1678f, 1680f tibial spine, 469, 472f Tillaux, 597, 598f, 1965, 1966f, 1968–1969 toe, 1970, 1971f ulna, 594f, 595f, 597 gender differences in, 476–477, 477t. See also Female athlete giant cell tumor in, 605, 605f glenohumeral joint instability in, 932–946. See also Glenohumeral joint instability, pediatric hamstring injury in, 1489 heat-related injury in, 465–466 hip injury in, 469, 470f, 1474–1477, 1475f, 1476f, 1476t iliac apophysitis in, 1475 imaging in, 587–610. See also at specific imaging modalities juvenile idiopathic arthritis in, 602–603, 602f knee injury in, 469, 471f Legg-Calvé-Perthes disease in, 599, 600f, 1476–1477 magnetic resonance imaging in. See Magnetic resonance imaging (MRI), pediatric nonossifying fibroma in, 605–606, 605f nutrition in, 467 osteochondritis dissecans in. See Osteochondritis dissecans osteochondroma in, 606, 607f osteochondroses in, 599, 599f, 1972–1974, 1973f, 1974f osteoid osteoma in, 603, 603f, 605 osteomyelitis in, 599, 601, 601f–602f osteosarcoma in, 606–607, 608f Panner’s disease in, 623, 625f, 1238 performance-enhancing substance use by, 467–468 peroneal tendon subluxation in, 1963–1964 posterior cruciate ligament injury in, 1713–1718, 1714f–1715f, 1717f psychosocial development of, 466 pump bumps in, 1963 quadriceps contusion in, 1484 quadriceps strain in, 1497 radiography in. See Radiography, pediatric radionuclide imaging in, 591, 591f, 601f–602f, 1230 septic arthritis in, 602 shoulder injury in, 468, 468f shoulder instability in, 468, 469f slipped capital femoral epiphysis in, 597, 598f, 1475–1476, 1476f, 1476t sports participation by, 463 adult involvement in, 466–467 coaches in, 466–467 injury with, 463–464 psychosocial development and, 466 readiness for, 466 strength training in, 465 tarsal coalition in, 1960–1962, 1961f, 1962f thermoregulation in, 465–466 thoracolumbar spine injury in, 754–768. See also Thoracolumbar spine injury, pediatric ultrasonography in, 590, 590f, 592–593 unicameral bone cyst in, 606, 606f wrist injury in, 468, 470f, 1363–1377. See also Wrist injury, pediatric

Index Chitosan, 409 Chloroquine phosphate, in cramps, 12 Chlorothiazide, 160t Chlorthalidone, 160t Chondrocyte(s), 41, 41f matrix interaction with, 45, 45f–46f, 49 proteoglycan synthesis of, 45, 49 tissue-engineered, 1776 Chondrocyte implantation, 55, 1774–1775 matrix techniques with, 1775–1776 rehabilitation after, 1785t results of, 1777, 1777t technique of, 1778–1780, 1780f Chondroitin sulfate, 43f, 44, 409 in knee arthritis, 1774, 1791 Chondrolysis, glenohumeral, 984, 984f, 1105t, 1106 Chondromalacia knee, 579, 580f, 581f sesamoid, 2089 wrist, 1447–1449 Chondromatosis, synovial, 1473 Chondroplasty, abrasion, of wrist, 1448–1449, 1448f Chop-and-lift exercises, in core training, 287, 288f Chrisman-Snook procedure, 1925–1926, 1925f Chromium, requirements for, 406b Chronic exertional compartment syndrome, 14–15, 15f, 650–651, 1857–1863, 1857b anatomy of, 650, 650f, 1858, 1858b, 1858f complications of, 1863 evaluation of, 14, 15f, 1859–1860, 1859f, 1860t pain in, 1858, 1859 return to play after, 1863 treatment of, 14–15, 651, 1860–1863, 1861f–1862f, 1863f Chronic tendinitis syndrome, 29–30 Chronobiology, 441–445, 442f. See also Circadian rhythms; Sleep bright light treatment and, 444–445, 445f circadian rhythms in, 442f, 443–444, 443f, 444f consultation on, 450 seasonal rhythms in, 444 Cigarette smoking, 426–428, 428f Circadian rhythms, 443–444, 443f, 444f cortisol in, 457 definition of, 443, 443f, 444f in depression, 452 dim light melatonin onset in, 457 endogenous, 456–457, 456f hormonal markers of, 457 impairment in, 453 light effect on, 443, 444f markers of, 456–457 performance and, 442, 442f, 457 sleep-wake, 445, 446f, 447f suprachiasmatic nucleus and, 443–444 Circulation, emergency assessment of, 520, 521f Citric acid cycle, 211–212 Citrus aurantium, 409 Clam exercise, in knee rehabilitation, 258, 259f Classification, 2209–2217. See also at specific injuries of injury, 2214–2217, 2214t, 2215f, 2216t, 2217t of pathology-related anatomic changes, 2211–2212, 2211f, 2211t, 2212t of pathology-related physical findings, 2212–2214, 2213f, 2213t, 2214t Claudication neurogenic, 745, 745t vascular, 745, 745t in popliteal artery entrapment, 1837

Clavicle. See also Sternoclavicular joint distal fracture of. See Acromioclavicular joint injury osteolysis of, 854, 855f resection of, 842, 843f acromioclavicular ligament injury and, 844 coracoclavicular ligament reconstruction with, 842, 843f failure of, 844 instability after, 827 without ligament reconstruction, 842–844, 843t medial. See also Sternoclavicular joint dislocation of. See Sternoclavicular joint injury, severe sprain (dislocation) fracture of, 804f, 805f, 824 vs. sternoclavicular dislocation, 804, 804f osteotomy of, 810 physis of, 794, 796f, 811 injury to, 811, 824–825, 824f anterior, 811, 824–825 posterior, 811, 825 return to play after, 825 treatment of, 819 resection of, 810 motion of, 776, 828, 828f pediatric, 780–781, 781f, 783–784, 784f fracture of, 596, 596f Claw hand deformity, 1312, 1312f Claw toe deformity, 2118, 2118t, 2120b, 2129 evaluation of, 2119 operative treatment of, 2121–2125, 2122f Clay shoveler’s fracture, 709 CLEAR mnemonic, 757–758 Clearance for participation, 513–515. See also Preparticipation examination legal aspects of, 531 Cleats, injury and, 2184, 2190–2192, 2195f, 2196f Clindamycin, 387, 387t CLOCK gene, 442 Clomiphene citrate, anabolic-androgenic steroid interaction with, 415–416 Clonazepam, in complex regional pain syndrome, 363t Clonidine in complex regional pain syndrome, 363t, 364, 365 in hypertension, 160t Clothing, in cold environment, 499–500 Clotrimazole, in dermatophyte infection, 200t Coach, 530 Coagulation, 371–372, 373f Cocaine use/abuse, 428–429 marijuana use and, 426 Coccyx, 1451–1452 Codman’s point, palpation of, 996, 997f Cohort study, 101 Cold, common, 149 Cold-induced vasodilation, 500 Cold injury, 203, 498–502, 528–529. See also Hypothermia clothing and, 499–500 drug use and, 499 medical conditions and, 499 physiology of, 498–499 Cold intolerance, in complex regional pain syndrome, 356 Cold therapy. See Cryotherapy Collagen articular cartilage, 42–43, 43f bone, 67, 68f


xi

Collagen (Continued) breakdown of, myoglobin excretion and, 12 implant of, 39 ligament, 32–33, 34, 1644–1645 meniscal, 57, 57t, 58–59, 58f–59f, 1598–1599 physical properties of, 22–23 structure of, 22, 23f tendon, 22–23, 22f, 23f, 23t, 1515, 1517f age-related changes in, 25 corticosteroid effects on, 26–27 exercise-related changes in, 25, 26f immobilization-related changes in, 25–26, 26f NSAID effects on, 27 synthesis of, 27–28 types of, 22, 23t Collagen hydrolysate, 409 Collar cervical, in rotary atlantoaxial subluxation, 707 cowboy, 673, 673f, 674f Collateral ligaments fibular (lateral). See Fibular (lateral) collateral ligament (FCL) first metatarsophalangeal joint, 2064–2065, 2065f, 2082 lateral. See Fibular (lateral) collateral ligament (FCL) medial. See Medial collateral ligament (MCL) metacarpophalangeal joint, 1380 injury to, 1380, 1399–1401, 1400f, 1401f ulnar. See Ulnar collateral ligament (UCL) Common cold, 149 Common peroneal nerve, injury to, 1751–1752, 1752f Commotio cordis, 165, 165f, 526 Compartment(s) increased pressure in, 650. See also Compartment syndrome lower extremity, 650–651, 651f, 1858, 1858b, 1858f pressure measurement in, 14, 650–651, 1860, 1860t Compartment syndrome acute, 14, 527–528 diagnosis of, 14, 1859–1860, 1859f, 1860t exertional, 14–15, 15f, 650–651, 651f, 1857–1863. See also Chronic exertional compartment syndrome lower extremity, 650–651, 651f anatomy of, 1858, 1858b, 1858f classification of, 1858–1859 complications of, 1863 evaluation of, 1859–1860, 1859f, 1860t after knee dislocation treatment, 1765 thigh, 1483–1484 treatment of, 1860–1863, 1861f, 1862f, 1863f with on-field injury, 527–528 pathophysiology of, 14 Pedowitz criteria in, 1860, 1860t upper extremity, flexor-pronator hypertrophy and, 622 Complete Book of Athletic Footwear, The (Cheskin), 1875 Complex regional pain syndrome, 351–369, 353b clinical presentation of, 355–358, 356t definition of, 351, 353b diagnosis of, 352, 353b, 355–356, 358–361 bone scan in, 359 epidural blockade in, 359 hematologic tests in, 358 magnetic resonance imaging in, 359 paravertebral sympathetic ganglion blockade in, 359

xii

Index

Complex regional pain syndrome (Continued) phentolamine testing in, 359–360 radiography in, 358 regional intravenous sympathetic blockade in, 360 spinal blockade in, 359 sudomotor measurement in, 360–361 vasomotor measurement in, 360 motor abnormalities in, 357–358 pathophysiology of, 353–355, 354f patient education on, 369 pediatric, 367, 369 psychological issues in, 358 sensory disturbances in, 356, 356t sudomotor abnormalities in, 355 support groups for, 369 sympathetic dysfunction in, 356–357, 357f terminology for, 351–352, 352b, 352t, 353b treatment of, 361–367, 368, 368f α-adrenergic blockers in, 363t, 365 algorithm for, 368, 368f antidepressants in, 362, 363t benzodiazepines in, 363t, 364 bisphosphonates in, 363t, 364–365 calcitonin in, 363t, 364–365 calcium channel blockers in, 363t, 364 capsaicin in, 364 clonidine in, 365 corticosteroids in, 362 electroconvulsive therapy in, 365 membrane stabilizers in, 363t, 364 neuromodulation techniques in, 366–367 NSAIDs in, 363t, 364 opioids in, 363t, 364 patient education in, 369 pharmacologic, 362–365, 363t physical therapy in, 362 psychotherapy in, 365 surgery in, 367 surgical sympathectomy in, 366 sympatholysis in, 365 trophic changes in, 358 vasomotor abnormalities in, 355 Compression fracture cervical spine, 680–681, 680f–682f in children/adolescents, 709, 709f lumbar spine, 546, 547f thoracic spine, 546, 547f, 734–735, 734f, 755, 755f Compression-rotation test, in SLAP lesion, 1025t Computed arthrotomography, of glenohumeral joint, 950–951 Computed tomography (CT), 533, 539–543 in acromioclavicular joint injury, 834f in avulsion injury, 553 in biceps femoris strain, 16, 17f in bifurcate sprain, 1954 in cervical spine fracture, 698f in deep venous thrombosis, 376 in distal humeral fracture, 1250 in elbow heterotopic ossification, 1292f, 1298, 1298f in femoral neck stress fracture, 554f in femoral osteochondritis dissecans, 1773, 1773f in femoral stress fracture, 1479 in fracture, 552 of glenohumeral joint, 950, 950f in glenohumeral joint instability, 916 in glenoid neck fracture, 861, 862f, 864f in glenoid rim fracture, 868f, 871f helical, 539 in high (syndesmosis) ankle sprain, 1942 in hip arthroplasty, 542, 542f

Computed tomography (CT) (Continued) in hook of hamate fracture, 543, 544f in humeral fracture, 983 image quality in, 539 in infection, 543 of intervertebral disk, 727, 727f in intracranial hemorrhage, 660, 661f in Jefferson fracture, 705, 706f in Lisfranc sprain, 1957, 1957f in lumbar burst fracture, 541, 541f in lumbar isthmic spondylolisthesis, 748–749 of lumbar spine, 727 monitor for, 539, 540f in occult fracture, 552, 557 in odontoid fracture, 540–541, 540f in osteomyelitis, 543 in particle disease, 542, 542f in patellar osteochondritis dissecans, 1531 in patellofemoral disorders, 1564–1565, 1566t pediatric, 590, 590f in avulsion fracture, 599 bone on, 591–592 in fracture, 590f, 597, 598f in proximal humeral physeal fracture, 1074 radiation dose in, 588 of pelvis, 541–542 in popliteus tendon avulsion, 541–542, 542f in proximal humeral fracture, 1038–1039 in rotary atlantoaxial subluxation, 706–707, 708f in shoulder disorders, 543 of spine, 539–541, 540f, 541f in spondylolysis, 761, 762, 763f in sternoclavicular joint injury, 804–805, 805f in stress fracture, 552, 554f in subtalar sprain, 1950 in tarsal coalition, 1961, 1961f, 2161, 2161f in tarsal navicular stress fracture, 646, 646f of thoracic spine, 727 in tibial plateau fracture, 542, 543f in tibial stress fracture, 1853 in tracheal displacement, 821, 821f in trapezium fracture, 1348, 1349f windowing in, 539, 540f Computed tomography (CT) angiography in popliteal artery entrapment, 1839–1840, 1840f in pulmonary embolism, 378, 378f Computed tomography (CT) arthrography in glenohumeral joint osteoarthritis, 1108 of knee, 536, 537f Computed tomography (CT)–myelography in lumbar disk herniation, 743 in lumbar spine stenosis, 746 in thoracic disk herniation, 738 Concussion, 522, 658–662 classification of, 658, 659t, 2216–2217, 2217t clearance for participation and, 513 definition of, 658 evaluation of, 658b, 659–660 grade 1, 658, 659t grade 2, 658, 659t grade 3, 658–659, 659t grading of, 522, 523t, 658–659, 659t imaging in, 660 incidence of, 662 on-field evaluation of, 659–660 return to play after, 513, 522, 523t, 659, 659t seizure and, 660 signs and symptoms of, 658b treatment of, 660 Conditioning, team physician advice on, 516 Conduction, heat loss by, 493, 499


Condylectomy in bunionettes, 2134–2135, 2134b, 2135f, 2140, 2140f in corns, 2116, 2117f, 2124 in intractable plantar keratoses, 2111, 2113f in mallet toe, 2122–2123, 2123f, 2124f Cone ambulation, in knee rehabilitation, 295, 296f Cone reaching, in knee rehabilitation, 296, 297f Confidence interval, 99 Confidentiality, athlete, 531 Confirmation, diagnosis, 110 Congenital anomalies cervical spine, 711–712, 711f, 712b, 712f lumbar spine, 746–747, 747f, 748f odontoid, 692, 692f renal, 712, 712f scaphoid, 1366 sternoclavicular joint, 799, 811 superior peroneal retinaculum, 1991 Conoid ligament, 827 Consciousness, alteration in. See Concussion; Head injury Construct validity, 100 Contact dermatitis, 202, 203f Content validity, 100 Continuous positive airway pressure, in sleep apnea, 448 Contracoup injury, 657, 657f Control group, 101 Contusion abdominal, 526 femoral, 1542, 1543f foot, 1964 groin, 1459–1460 iliac crest, 1459 muscle, 13. See also Quadriceps muscle, contusion of magnetic resonance imaging in, 558 myositis ossificans with, 13–14, 14f, 558 myocardial, 526 pulmonary, 526 quadriceps. See Quadriceps muscle, contusion of renal, 527 thoracic spine, 732–733 Convection, heat loss by, 499 Coracoacromial arch, anatomy of, 990, 990f–991f Coracoacromial ligament, 828 anatomy of, 773–774, 990, 990f magnetic resonance imaging of, 956, 959f resection of, 1009 Coracobrachialis muscle anatomy of, 1158, 1158f scapular attachment of, 858, 858f transfer of, 840–841, 841f Coracoclavicular ligament, 827, 827f injury to. See Acromioclavicular joint injury reconstruction of, 842, 843f, 846–851 approach to, 846, 847f–848f clavicle bone tunnel preparation for, 849–850, 850f–851f closure for, 851 complications of, 851–853 coracoid bone tunnel preparation for, 848, 849f graft-clavicle fixation for, 850–851, 852f, 853f graft-coracoid fixation for, 849, 850f graft preparation for, 847–848, 849f management after, 851–853 repair of, 841, 841f in sternoclavicular joint injury treatment, 824 transfer of, 841–842

Index Coracohumeral distance, 956 Coracohumeral ligament. See also Rotator interval anatomy of, 773, 966 biomechanics of, 788 Coracoid anatomy of, 990, 990f fracture of, 876–885 acromioclavicular dislocation and, 880, 882, 882f, 883f, 884 classification of, 882 computed tomography in, 879, 880f electromyography in, 879 vs. epiphysis, 879, 881f exercises after, 884 glenohumeral dislocation and, 876, 877 mechanism of, 876–877, 877b neurologic injury with, 877, 878, 878f nontraumatic etiologies of, 877 patient history in, 877–878 pattern of, 877, 878f physical examination in, 878 radiography in, 861, 862f, 878–879, 878f, 879f, 880f, 881f stress, 877–878 Stryker notch view for, 861, 862f, 879, 880f, 881f suprascapular nerve involvement in, 880, 882f–883f treatment of, 880–882, 881f–883f, 884b ossification of, 859, 859f, 860f, 879, 881f pediatric, 782 Core training, 277–288, 277t, 289t abdominal bracing in, 280, 280f advanced functional training in, 288 AIR principles in, 279 bridging progression in, 281–282, 281f–282f curl-up progression in, 284–285, 285f gluteal training in, 285–286, 286f lateral flexion progression in, 283–284, 284f latissimus dorsi training in, 286 loading parameters in, 279–280 manual perturbation training in, 286, 287f program design for, 279 quadruped progression in, 282–283, 282f, 283f rhythmic stabilization training in, 286 rotation training in, 286–288, 288f–289f scapular training in, 286, 286f in thoracolumbar spine rehabilitation, 728–730, 730f Corn, 2116, 2117f, 2119 interdigital, 2116, 2118f, 2119, 2124 Coronary artery, anomalies of, 165, 165f, 166f Coronary heart disease, in diabetes mellitus, 175–176 Coronary ligament, 1722 repair of, 1733, 1734f Coronoid fracture of, 1263, 1265f, 1273 anteromedial, 1266, 1270–1271 basal, 1266 classification of, 1264, 1266 operative treatment of, 1266, 1267f–1268f, 1269–1270, 1270f, 1275–1276 tip, 1264, 1266, 1269–1270, 1270f stabilizing effect of, 1192, 1193f Correlation, 100–101 Corticosteroid(s) bone effects of, 72 in cervical fracture, 675, 691 in complex regional pain syndrome, 362 in epilepsy, 190 in exercise-induced bronchospasm, 182

Corticosteroid(s) (Continued) injection of. See Corticosteroid injection in low back pain, 731 pectoralis major rupture and, 902 in tendon healing, 29 Corticosteroid injection in Achilles tendon injury, 1999 in de Quervain’s tenosynovitis, 1355 epidural, 534, 535f, 584, 584f fluoroscopy-guided, 582–584, 584f in knee arthritis, 1774, 1791 in lateral epicondylitis, 618, 1200 in meniscal injury, 1605 in plantar fasciitis, 2048–2049 in retrocalcaneal bursitis, 2035, 2036 in rotator cuff disorders, 1007 tendon, 31 experimental studies of, 26–27 long-term effects of, 26–27 studies of, 26–27 Cortisol exercise effects on, 217, 217t levels of, 457 Corynebacterium minutissimum infection, 194t, 195–196, 196f Costoclavicular ligament, 793, 793f Costoclavicular maneuver, in vascular injury, 1138, 1138f Coumadin, prophylactic, in venous thromboembolism, 378–384, 381t Counterforce brace, in lateral epicondylitis, 618–619, 618f, 1200–1201, 1201f Coup injury, 657, 657f Cowboy collar, 673, 673f, 674f Coxa sultans, 1458–1459 Cramps, 11–12 creatine and, 418 heat, 495–496, 529 Crank test, in SLAP lesion, 1025t Creatine, 408, 418–419 nonresponse to, 418 Creep, 48, 59, 95–96, 95f Crepitus, scapulothoracic, 886–889, 887b, 887f Cricothyroidotomy, needle, 519, 520f Criterion-related validity, 100 Cross-arm adduction test, in acromioclavicular joint injury, 830, 832f Crossing sign, in femoral trochlear dysplasia, 1561, 1561f Cruciate ligaments. See Anterior cruciate ligament (ACL); Posterior cruciate ligament (PCL) Cruciate ridge, 1646, 1647f Crutches, removal of, in knee rehabilitation, 295 Cryopreservation, allograft, 140–141 Cryotherapy, 234–235, 235f in ACL rehabilitation, 1670 in heat illness, 529 in lateral ankle sprain, 1920 in medial ankle sprain, 1937 in retrocalcaneal bursitis, 2035 in thoracolumbar spine injury, 731 CT. See Computed tomography (CT) Cubital tunnel syndrome, 1311–1315 anatomy of, 1312, 1312f etiology of, 1311–1312, 1311f history in, 1312 physical examination in, 1312, 1312f–1313f treatment of, 1312–1315 anterior subcutaneous transposition in, 1313–1314, 1313f–1315f anterior submuscular transposition in, 1314 medial epicondylectomy in, 1314–1315


xiii

Cubital tunnel syndrome (Continued) nonoperative, 1312–1313 operative, 1313–1315, 1313f in situ decompression in, 1313 Cuboid, stress fracture of, 646, 2023 Cullen’s sign, 526 Cumulative incidence, 103 Cuneiform osteochondrosis of, 2166, 2166f stress fracture of, 646, 2023 Curl-up exercise against abdominal brace, 285, 285f beginner’s, 285, 285f in core training, 284–285, 285f Cyclist’s palsy, 1361 Cyst(s) aspiration of, 585 bone aneurysmal, 983–984 radiography in, 552, 553f unicameral, 606, 606f fracture through, 552, 553f, 606, 606f, 1085, 1086f ganglion, suprascapular nerve compression with, 617, 1121, 1121f, 1123 humeral, 983–984 image-guided aspiration of, 585 meniscal, 1613 paralabral, 580–581, 582f, 964–965, 965f, 980, 980t popliteal (Baker’s), 537–538, 538f rotator cuff, 964–965, 964f synovial, suprascapular nerve compression with, 617 ultrasonography of, 537–538, 538f Cytokines in complex regional pain syndrome, 355 in infection, 147

D Dacron prosthesis, in ligament injury treatment, 36 De Quervain’s tenosynovitis, 624–625, 1355, 1356f magnetic resonance imaging in, 569, 570f Dead bug exercise in core training, 285, 285f in trunk stabilization, 342t, 343 Death, sudden. See Sudden death Débridement, arthroscopic in glenohumeral joint, 1110, 1110f, 1115, 1115f in knee, 1774, 1792 in SLAP lesion, 1027, 1028 Decentralization supersensitivity, in complex regional pain syndrome, 355 Decision analysis, 99, 112 Decorin, 44 Deep peroneal nerve, entrapment of, 2061–2062, 2061f Deep venous thrombosis, 370–385 age-related factors in, 373, 375f arthroscopy and, 123–124, 124b, 383–384, 383t evaluation of, 374, 376–378, 376t, 377f high tibial osteotomy and, 1833 treatment of, 378–385, 384t prophylactic, 378–384, 379t, 381t, 382f Defibrillator, implantable, in sudden death prevention, 169–170 Degrees of freedom, 89 Dehydration, 401 in children/adolescents, 465–466 exercise-related, 494–495 hyponatremic, 495

xiv

Index

Dehydroepiandrosterone (DHEA), 414, 417–418 Delayed-onset muscle soreness, 12–13, 13f, 215–216 Delayed union, scaphoid fracture, 1366, 1367f Deltoid ligament, 338, 1913f, 1935, 1935f injury to, 1935–1938, 1936f, 1937f magnetic resonance imaging of, 573 ossicles within, 1938 repair of, 1938 Deltoid muscle anatomy of, 771, 1034, 1035f, 1035t, 1036b, 1063, 1063f pediatric, 784, 785f biomechanics of, 1063 denervation edema of, 965, 965f, 980 humeral attachment of, 1071 neurologic evaluation of, 1036–1037, 1038f rupture of, 1063–1064 clinical evaluation of, 1064 physical examination in, 1064 treatment of, 1064 scapular attachment of, 859f, 886f Dementia pugilistica, 663b Denervation supersensitivity, in complex regional pain syndrome, 355 Dependency, of variables, 100–101 Depression anabolic-androgenic steroids and, 417 bright light therapy in, 444–445, 445f sleep disorders in, 452 Dermatan sulfate, 44 Dermatitis, contact, 202, 203f Dermatologic disorders. See at Skin Dermatophyte infection, 198–200, 198f, 199f, 200f Desipramine, in complex regional pain syndrome, 362, 363t DEXA (dual-energy x-ray absorptiometry), 72 Dexamethasone, iontophoresis for, 234 DHEA (dehydroepiandrosterone), 417–418 Diabetes mellitus, 172–179, 514t coronary heart disease in, 175–176 evaluation of, 175–176, 176b, 179 exercise in, 172–175, 173f–175f glucose regulation in, 174, 174f hyperglycemia in, 175, 175f, 177–178, 177b hypoglycemia in, 174–175, 174b, 177, 177b acute management of, 178–179, 179b insulin in, 176–178, 176t, 177b, 177t, 178f peripheral neuropathy in, 176 pre-participation guidelines in, 179 treatment of, 176–179, 176t, 177b, 177t, 178b, 178f Dial test in posterior cruciate ligament injury, 1691 in posterolateral corner injury, 1727, 1728f Diaphysis, 587–588 Diarrhea, 152, 514t Diet. See also Nutrition fad, 406 in female athlete, 477–479, 478f, 478t, 479b at high altitude, 505 in hypertension, 158, 159t for pediatric athlete, 467 for weight gain, 406, 408b for weight loss, 406, 407b Dietary supplement(s), 406–409. See also specific supplements definition of, 417 ergogenic, 417–422 Dietary Supplement and Health Education Act (1994), 407, 468 Dieter’s Tea, 409 Dihydrotestosterone, 414

Diltiazem in complex regional pain syndrome, 363t in hypertension, 160t Diphosphonates, in heterotopic ossification, 1294 Direct eversion maneuver, in high (syndesmosis) ankle sprain, 1940, 1941f Disability, emergency assessment of, 520, 521f Diskectomy in congenital lumbar stenosis, 748f in lumbar disk herniation, 744, 744f, 751f Diskography percutaneous, 584–585 thoracolumbar, 728 Dislocation. See at specific joints Distraction osteogenesis, 81–82, 83f Diuretics, in hypertension, 158–159, 160t Diving, cervical spine injury in, 690 Doping, 413 Dorsal intercalary segmental instability (DISI), 1322, 1323f Double-bundle posterior cruciate ligament reconstruction, 1705–1706, 1705f–1706f in combined injury, 1706–1710, 1708f, 1709f, 1710f evaluation of, 1696, 1699–1700, 1699t Double-leg jumping exercise, in knee rehabilitation, 296, 298f Double PCL sign, in meniscal injury, 1602, 1603f Down syndrome activity restrictions in, 705, 707b atlanto-occipital instability in, 705, 705f atlantoaxial instability in, 705, 707f Doxazosin, 160t Doxepin, in complex regional pain syndrome, 363t Drawer test anterior in anterior cruciate ligament injury, 1650 in lateral ankle sprain, 1916–1917, 1917f in medial ankle sprain, 1936 in medial collateral ligament injury, 1629, 1630t anterior-posterior, in glenohumeral joint instability, 943–944, 944f posterior, in posterior cruciate ligament injury, 1690, 1690f posterolateral, in posterolateral corner injury, 1727, 1729f Drive-through sign, 1731, 1732f Drop finger (mallet finger), 1388, 1420–1422, 1420f, 1421f Drowning, epilepsy and, 192 Drug(s) alertness-enhancing, 451–452, 453t emergency assessment of, 520, 521f ergogenic, 410–423, 2173–2174. See also Anabolic-androgenic steroids and specific drugs historical perspective on, 410–411 iontophoresis for, 233–234, 235f recreational, 424–431.See also specific drugs tendon effects of, 1516 thermal balance and, 499 Dual-energy x-ray absorptiometry (DEXA), 72 Dumbbell floor press, in shoulder rehabilitation, 247, 248f Dumbbell fly exercise, shoulder injury and, 249 Duncan loop, 135, 135f Durkan’s compression test, 1360 Dusting, 430 Dynamic shift test, in posterolateral corner injury, 1728 Dysesthesia, definition of, 356t


Dyskinesia scapular, 1007 scapulothoracic, 891–892

E Ear, on-field injury to, 525 East German athletes, drug use by, 412 Eating disorders, 478, 478f, 514t Eccentric training, in ankle rehabilitation, 275–276, 276f Ecchymosis, in pectoralis major rupture, 902, 903f ECG. See Electrocardiography (ECG) Echocardiography screening, 168 in sudden death prevention, 168 Eczema, 204, 204f Edema cerebral, high-altitude, 504–505 in complex regional pain syndrome, 355, 356 heat, 530 postexercise, 216 pulmonary, high-altitude, 504 Effort thrombosis axillary vein, 1141–1142 on-field, 527 subclavian vein, 1129, 1131f, 1134 Elastic deformation energy, 94 Elastin ligament, 34 meniscal, 58 tendon, 23 Elbow. See also Olecranon anatomy of, 1301–1303, 1302f–1303f on arthroscopy, 130, 130f normal variants in, 1229 arthroplasty of for arthrosis, 1278 in distal humeral fracture nonunion, 1258 heterotopic ossification after, 1290, 1291f arthroscopy of. See Arthroscopy, elbow arthrosis of, 1278 axis of rotation of, 1190, 1191f biomechanics of, 1189–1197 axis of rotation in, 1190, 1191f carrying angle in, 1190, 1191f, 1192 forces in, 1194–1195, 1196f, 1230 humerus in, 1189, 1189f normal, 1190 radial head in, 1190, 1190f ulna in, 1189–1190, 1189f carrying angle of, 1190, 1192 continuous passive motion of, after fracture treatment, 1277 effusion of, 535f in children, 596–597, 597f entrapment neuropathy at. See Cubital tunnel syndrome; Pronator syndrome; Radial tunnel syndrome forces across, 1194–1195, 1196f, 1230 fracture-dislocation of, 1262–1271, 1304. See also Elbow dislocation evaluation of, 1263–1267, 1264f, 1265f, 1266f–1267f mechanisms of, 1262 operative treatment of, 1263, 1267–1271 in anteromedial coronoid facet fracture, 1270–1271 complications of, 1271 in coronoid tip fracture, 1269–1270, 1270f in radial head fracture, 1269 stability testing in, 1268–1269, 1269f

Index Elbow (Continued) patterns of, 1263 terrible triad, 1259, 1263, 1264f, 1266, 1269 fracture of. See Capitellum, fracture of; Humeral fracture (distal); Olecranon, fracture of; Radial head, fracture of; Radial neck, fracture of golfer’s, 620–621, 1205–1206, 1205f, 1206f heterotopic ossification of. See Heterotopic ossification, elbow instability of postoperative, 1277–1278 recurrent, 1307–1310, 1307f–1310f stages of, 1263 trauma-related, 1262–1271. See also Elbow, fracture-dislocation of; Elbowdislocation ligaments of. See also Radial collateral ligament; Ulnar collateral ligament anatomy of, 1301–1302, 1303f magnetic resonance imaging of, 576, 577f, 578f stabilizing effect of, 1193, 1195f, 1231, 1231f Little Leaguer’s. See Little Leaguer’s elbow miner’s. See Olecranon bursitis motion of, 1190–1192, 1191f extension, 1190, 1191f, 1196f flexion, 1190, 1191f, 1196f functional, 1192 normal, 1190 pronation, 1190 supination, 1190 nursemaid’s, 1301, 1302f, 1303–1305, 1305f ossification of, 1227–1229, 1228f, 1229f, 1279, 1280f osteochondritis dissecans of. See Osteochondritis dissecans, capitellum overuse injury of, 617–624, 618f lateral, 617–619, 618f medial, 619–624, 620f, 624f pediatric dislocation of. See Elbow dislocation, pediatric fracture of, 1279–1288. See also Humeral fracture (distal); Olecranon, fracture of; Radial head, fracture of; Radial neck, fracture of gymnastics-related injury to, 1236 injury to, 468, 469f, 470f, 596–599, 597f, 598f, 623–624, 624f, 1236–1240 gymnastics-related, 1236 lateral, 1238–1239 medial, 1236–1238, 1236f, 1238f posterior, 1239–1240, 1239f tennis-related, 1236 throwing-related, 1221–1225, 1223f, 1225f. See also Little Leaguer’s elbow; Overhead throwing injury, pediatric loose body in, 470f ossification of, 1227–1229, 1228f, 1229f, 1279, 1280f radiography of, 1279–1288 tennis-related injury to, 1236 throwing-related injury to, 1221–1226, 1223f, 1225f. See also Little Leaguer’s elbow; Overhead throwing injury, pediatric rehabilitation of. See Elbow rehabilitation stability of, 1192–1197, 1230–1231 coronoid in, 1192, 1193f intraoperative testing of, 1268–1269, 1269f lateral collateral ligament complex in, 1193, 1195f, 1231 medial collateral ligament in, 1193, 1194f, 1230–1231, 1231f

Elbow (Continued) muscles in, 1194, 1196f olecranon in, 1192, 1192f radial head in, 1192–1193, 1193f stiffness of, differential diagnosis of, 1293 student’s. See Olecranon bursitis tennis. See Epicondylitis, lateral (tennis elbow) terrible triad of, 1259, 1263, 1264f, 1266, 1269 Elbow dislocation, 1262–1271, 1300–1310 anatomy of, 1301–1303, 1302f, 1303f capsuloligamentous injury in, 1263 classification of, 1303–1304, 1303f closed reduction for, 1262, 1304–1305, 1305f, 1306 complications of, 1307–1310, 1307f–1310f coronoid fracture with, 1263, 1265f evaluation of, 1304 external fixation in, 1306, 1306f fracture with. See Elbow, fracture-dislocation of incidence of, 1300 instability after, 1307–1310 lateral collateral ligament reconstruction in, 1308, 1310, 1310f physical examination in, 1307–1308, 1307f, 1308f treatment of, 1308–1310, 1309f mechanisms of, 1262, 1300–1301, 1301f, 1302f nerve injury with, 1263, 1304 nonoperative treatment of, 1262, 1304–1305, 1305f, 1306 olecranon fracture with, 1263–1264, 1266f, 1267f–1268f, 1273 open reduction for, 1305 operative treatment of, 1305–1306, 1306f patterns of, 1263, 1264f–1267f pediatric, 1288, 1300–1310, 1302f classification of, 1303–1304 closed reduction for, 1304–1305, 1305f complications of, 1307–1310, 1307f evaluation of, 1304 incidence of, 1300 mechanism of, 1300–1301, 1301f–1302f post-reduction care in, 1306–1307 surgical treatment of, 1305–1306 treatment of, 1304–1306, 1305f post-reduction care in, 1306–1307 posterior, 1263, 1264f, 1269 rehabilitation after, 1306–1307 return to play after, 1310 stages of, 1263 treatment of, 1304–1306 vascular injury with, 1263, 1304 Elbow rehabilitation, therapeutic exercise for, 250–255 extensor training in, 253–254, 253f flexor training in, 251–253, 252f–253f forearm muscle training in, 254–255, 254f, 255f rhythmic stabilization training in, 255, 255f total arm strengthening in, 251 Elderly people. See Age/aging Electrical stimulation, 229–233 in anterior cruciate ligament rehabilitation, 230–233, 231f–234f, 1671 in complex regional pain syndrome, 366–367 in fracture healing, 80 for functional restoration, 230–233, 231f–234f in pain modulation, 229–230, 230f in swelling, 230, 231f Electrocardiography (ECG) in long Q-T syndrome, 166–167, 167f in myocarditis, 151 in pulmonary embolism, 376


xv

Electrocardiography (ECG) (Continued) screening, 168, 169t in sudden death prevention, 167–169, 169t Electroconvulsive therapy, in complex regional pain syndrome, 365 Electromyography (EMG) of biceps tendon, 1019, 1019f, 1024 in brachial plexus injury, 673 in carpal tunnel syndrome, 1361 in coracoid fracture, 879 in entrapment neuropathy, 1311 in knee dislocation, 1752 in lateral epicondylitis, 1199 in Parsonage-Turner syndrome, 1144 in suprascapular nerve injury, 1122, 1123–1124 in tarsal tunnel syndrome, 2058 in ulnar neuropathy, 623 in valgus instability, 620 Elmslie-Trillant procedure, 1567 Elson’s test, 1389 Embolism, pulmonary. See Pulmonary embolism Embryo, endochondral bone formation in, 78 Emergency. See On-field emergency EMG. See Electromyography (EMG) Emissary vein, 69, 70f Emphysema, subcutaneous, sternoclavicular joint injury and, 821–822, 823f Empty-can exercise, in shoulder rehabilitation, 243–244, 243f, 244f Enalapril, 160t Endomysium, 3, 207, 208f Endorphins antiepileptic effects of, 187 exercise effects on, 217, 217t Endothelium, disruption of, 370, 371f Endurance training in ACL rehabilitation, 1671, 1674 in children/adolescents, 464 in female athlete, 479–480 muscle effects of, 10 Energy exercise-related requirements for, 498 muscle metabolism of, 210–213, 210f sources of, 498 Energy loss/return playing surface and, 2198–2199, 2199f shoe and, 1905–1906 Enthesophyte, of acromion, 955, 958f Enzyme-linked immunosorbent assay, in deep venous thrombosis, 376 Eosinophilic granuloma, 2161, 2161f Ephapse, in complex regional pain syndrome, 353–355, 354f Ephedra, 409 Epicondylitis lateral (tennis elbow), 30, 31, 566, 576, 612, 617–619, 618f, 1197–1205 chair test in, 1199 in children/adolescents, 1236 coffee cup test in, 1199 counterforce brace in, 618, 618f, 1200–1201, 1201f demographics of, 1197 differential diagnosis of, 1199 electromyography in, 1199 evaluation of, 1198–1199 focal hyaline degeneration in, 1198, 1198f hand exercises in, 1200 history in, 1198–1199 magnetic resonance imaging in, 566, 568f, 1199 nonoperative treatment of, 1199–1201, 1200f–1201f

xvi

Index

Epicondylitis (Continued) operative treatment of, 619, 1201–1205 arthroscopic release in, 1203–1204 extra-articular lateral epicondylar release in, 1204–1205, 1204f open release and resection in, 1201–1203, 1202f percutaneous release in, 1203 pathology of, 1197–1198, 1198f physical examination in, 1199 racquet selection and, 1200, 1201f radial nerve compression in, 1199 radiography in, 1199 treatment of, 1199–1205 medial (golfer’s elbow), 566, 620–621, 1205–1206 evaluation of, 1205, 1205f nonoperative treatment of, 1205 operative treatment of, 1205–1206, 1206f Epidemiological terminology, 2218–2219, 2218t Epidural blockade, in complex regional pain syndrome, 359, 366 Epidural corticosteroid injection, 534, 535f Epidural hematoma, 660, 661f Epilepsy, 185–192, 522–523 accidental death and, 187, 192 bathing and, 192 evaluation of, 190–192 exercise effects on, 187–188 historical perspective on, 185–186 immunotherapy in, 190 seizure frequency in, 187–188 surgery in, 190 swimming and, 192 terminology for, 186–187, 186b treatment of, 188–192, 191t vagal nerve stimulator in, 189–190 Epimysium, 3, 207, 208f Epinephrine, 353 exercise effects on, 217–218, 217t, 218f Epiphysis, 587–588, 588f of distal femur, 1638 of medial clavicle, 794, 796f, 811 of proximal humerus, 1069–1070, 1070f of proximal tibia, 1638 Epistaxis, on-field, 525 Epitenon, 20, 21f Eprosartan, in hypertension, 160t Epstein-Barr virus infection, 150–151 Epworth Sleepiness Scale, 450, 450f Ergogenic drugs, 410–423, 2173–2174. See also Anabolic-androgenic steroids and specific drugs historical perspective on, 410–411 ERMI Extensionator, 292, 292f ERMI Flexionator, 225, 225f, 292, 292f Error, statistical, 100, 111 Erysipelothrix rhusiopathiae infection, 397, 398t Erythrasma, 194t, 195–196, 196f Erythropoietin high-altitude effects on, 420, 503 recombinant, 420–421 Essex-Lopresti lesion, 1259, 1260 Estivation, 444 Estrogen, 414 bone effects of, 72 exercise effects on, 217t, 218 Estrogen replacement therapy, in female athlete, 478 Ethics, for team physician, 530–531 Ethylene oxide, in allograft sterilization, 139 Eucapnic voluntary hyperventilation challenge, 182 Evans procedure, 1924, 1925f

Evaporation, heat loss by, 493, 499 Excessive daytime sleepiness, 448–449 Exercise. See Exercise physiology; Rehabilitation; Therapeutic exercise(s) Exercise physiology, 207–220 cardiorespiratory response in, 218–220, 219f, 220t hormonal adaptation in, 217–218, 217t, 218f maximum oxygen uptake in, 218, 219f muscle, 10–11, 208–213, 209f, 210f, 212f. See also Muscle(s) neuromuscular adaptation in, 214–216, 216t respiratory response in, 220 training response in, 213–214, 214t, 215f Exertional compartment syndrome. See Chronic exertional compartment syndrome Exertional myositis, 496 Exertional rhabdomyolysis, 496–497 Exposure. See also Hypothermia emergency assessment of, 520, 521f Extensor carpi radialis brevis tendon, tear of, 1198. See also Epicondylitis, lateral Extensor carpi ulnaris tendinopathy, 1351, 1354–1355 classification of, 1354 clinical manifestations of, 1354 physical examination in, 1354 radiography in, 1354 return to play after, 1354 treatment of, 1354–1355, 1355f Extensor carpi ulnaris tendon inflammation of, 625 subluxation of, 625 Extensor hallucis longus tendon, 2065, 2065f Extensor pollicis longus tendon, injury to, 1401–1402 Extensor training, in elbow rehabilitation, 253–254, 253f External fixation in Achilles tendon rupture, 2009 in knee dislocation, 1754, 1754f External oblique muscle, strain of, 1461 External rotation exercise, in shoulder rehabilitation, 242–243, 242f, 243f External rotation recurvatum test, in posterolateral corner injury, 1726, 1726f External rotation stress test, in high (syndesmosis) ankle sprain, 1940, 1941f Extracorporeal shock-wave therapy in Achilles tendon injury, 1999 in lateral epicondylitis, 1200 in plantar fasciitis, 2049–2050, 2052 in retrocalcaneal bursitis, 2035 Eye(s) loss of, 514t on-field examination of, 525 on-field injury to, 525 raccoon, 525

F Fabellofibular ligament, 1722, 1731f FABERE test, in degenerative hip disease, 1503 Face validity, 100 Facet joint dislocation of C3-C4, 679, 679f, 708–709 C4-C7, 680, 708–709 in low back pain, 741 Factor V Leiden, 372, 374t Factor VIII, increase in, 372, 374t False-negative rate, 108, 109f False-positive rate, 108, 109f


Fas-T-Fix device, in meniscal repair, 1612–1613, 1612f Fascia lata, in sternoclavicular joint dislocation treatment, 810 Fascicle, 3, 4f Fasciectomy, 651 Fasciitis, plantar. See Plantar fasciitis Fasciotomy, 651 in chronic exertional compartment syndrome, 1860–1863, 1861f–1863f in plantar fasciitis, 2050, 2051–2052, 2053 in thigh compartment syndrome, 1483, 1484 Fat body, in female athlete, 476 dietary, metabolism of, 211 Fatigue muscle, 214, 214t nutritional deficits and, 401 seizures with, 187 Fatigue fracture. See Stress fracture Feet. See Foot (feet) Felodipine, 160t Female athlete, 475–491 anatomic parameters in, 476–477, 477t anterior cruciate ligament injury in, 483–485, 484b, 486t–487t, 487b, 488t, 1651 prevention of, 333–334, 485, 487b bone density in, 481 breast cancer in, 481 calcium intake by, 478, 478t conditioning for, 479–480, 480b forefoot problems in, 490–491, 491b frozen shoulder in, 489–490, 490t heart rate in, 476–477 iron deficiency in, 478–479, 479b knee replacement in, 1799 menopause in, 480–481, 481b nutrition in, 477–479, 478f, 478t, 479b patellofemoral arthritis in, 489 patellofemoral dislocation in, 487, 489, 489b patellofemoral joint injury in, 485, 487, 489 patellofemoral pain in, 487 physical examination of, 479 physiologic parameters in, 476–477, 477t pregnancy in, 481–483, 482b shoes for, 490–491, 491b, 1886–1887 shoulder instability in, 489 sport participation by, 475–476, 475f, 475t, 476f stress fracture in, 483, 483b, 483f, 632–633, 1478, 1849–1850, 1851–1852, 1856 Female athlete triad, 478, 478f, 633 Femoral artery, 1453, 1455f, 1514 occlusion of, 1497–1499 Femoral canal, 1463 Femoral condyles, osteochondritis dissecans of. See Osteochondritis dissecans, femoral condyle Femoral epicondylar axis, 1581 Femoral head abnormal acetabular contact with, 1471– 1472, 1471f, 1472f anatomy of, 1452, 1500 avascular necrosis of, 1466–1467, 1467b, 1467t in children, 1476–1477 slipped capital femoral epiphysis and, 1476 blood supply to, 1452, 1501 chondral injury of, 1472 fracture of, 1464 resurfacing procedures for, 1506 Femoral neck fracture of, 1464 stress fracture of, 638–640, 640f, 1465–1466, 1465f

Index Femoral neck (Continued) classification of, 639, 641f complications of, 639 compression-side, 639, 641f, 643f displaced, 639, 642f magnetic resonance imaging in, 554f tension-side, 639, 641f, 642f Femoral nerve, 1453, 1455f entrapment of, 1469 Femoral nerve stretch test in lumbar disk herniation, 743 in thoracolumbar spine injury, 722, 723f Femoral nerve tension sign, in thoracolumbar spine injury, 722 Femoral shaft, stress fracture of, 641, 1477–1481 anatomy of, 1477–1478 in children, 1481 classification of, 1478, 1478t clinical presentation of, 1478 grade of, 1478, 1478t imaging of, 1479, 1479f, 1480f physical examination in, 1478–1479, 1479b return to play after, 1481, 1481t shoewear and, 1898–1899 treatment of, 1479–1481, 1480f Femoral triangle, 1453 Femoral vein, 1453, 1455f Femoral version, 1500 Femoroacetabular impingement, 1471–1472, 1471f, 1472f, 1503 Femorotibial joint, biomechanics of, 1514–1515 Femur. See also at Femoral contusion of, 1542, 1543f distal. See also Knee anatomy of, 1549–1550, 1550f epiphyseal fracture of, 1641–1642, 1641b, 1641f, 1642f, 1643–1644, 1643f, 1644b epiphyseal ossification of, 587, 588f growth plate of, 1638 stress fracture of, 555f proximal. See also Femoral head; Femoral neck; Hip anatomy of, 1452, 1549, 1549f anteversion of, 1549, 1549f, 1565 torsion of, 1549, 1549f, 1565 version of, 1549, 1549f Femur–anterior cruciate ligament–tibia complex, tensile loading of, 93, 94f Fertility, anabolic-androgenic steroid effects on, 416 Fetal warfarin syndrome, 381, 382f Fever, 514t Fibrin clot augmentation, in meniscal injury, 1608 Fibroblasts ligament, 33–34, 35 tendon, 20, 22, 24, 27 Fibrochondrocytes, of meniscus, 1598–1599 Fibroma, nonossifying, in children, 605–606, 605f Fibronectin ligament, 34 meniscal, 58 Fibula, stress fracture of, 644, 644f, 1849, 2016t, 2018, 2019f Fibular (lateral) collateral ligament (FCL). See also Posterolateral corner anatomy of, 1685, 1719–1720, 1719f, 1720f, 1722f, 1731f, 1748 biomechanics of, 1724 evaluation of, 1692 reconstruction of, 1736–1737, 1737f high tibial osteotomy and, 1815t, 1833, 1834f stabilizing function of, 1588–1589

Field-exercise challenge test, in bronchospasm, 182 Finger(s). See also Thumb boutonnière deformity of, 1388–1389, 1388f, 1389f flexor pulley system injury of, 1392 foreign body of, 538, 539f fracture of, 1393–1398 metacarpal, 1393–1394, 1393f, 1394f, 1395f, 1411–1414, 1411f, 1412f, 1413f phalangeal, 1338, 1394–1398, 1395f, 1396f, 1397f, 1406–1411, 1406f–1410f Jersey, 1390–1392, 1391f pediatric, 1424–1428, 1424f–1427f ligamentous injury of, 1379–1387. See also Carpometacarpal joint; Interphalangeal joint; Metacarpophalangeal joint mallet, 1388, 1420–1422, 1420f, 1421f tendon injury to, 1387–1392, 1388f, 1389f, 1391f trigger, 626 Fingernail injury, 1428, 1428f, 1429f–1430f Fingertip injury, 1428–1430, 1428f, 1429f– 1430f Finkelstein’s test, 1355, 1356f Fisher exact test, 114 Fist test, in femoral stress fracture, 1479 Flail chest, 526, 893. See also Rib(s), fracture of Flake sign, in triceps tendon rupture, 1170– 1171, 1171f Flatfoot acquired, 631, 1981 medial tibial syndrome and, 15 orthotic devices for, 2044, 2046f Flexibility in children/adolescents, 464–465 excessive. See Hypermobility in foot and ankle injury, 2176–2183, 2176b, 2182f of shoes, 1909, 1910f, 2188–2189, 2189f in turf toe, 2182 Flexor carpi radialis tendinitis, 625–626, 1356–1357 Flexor carpi ulnaris tendinitis, 625, 1356–1357 Flexor digitorum longus tendon transfer, 1980 Flexor digitorum profundus tendon avulsion of (Jersey finger), 1390–1391, 1391f neglected, 1391–1392 pediatric, 1424–1428, 1424f–1427f disruption of, 1392 Flexor hallucis brevis tendon, 2065, 2066f Flexor hallucis longus tendon in Achilles tendon reconstruction, 2039f–2040f, 2041 anatomy of, 1984 injury to, 30, 1983–1987 in ballet dancer, 1984, 1985–1987 differential diagnosis of, 1984–1985 evaluation of, 1984–1985 magnetic resonance imaging in, 563, 564f nerve injury with, 1984, 1985 treatment of, 1985–1987, 1986f repair of, 1985–1987 Flexor-pronator injury, 622 Flexor pulley system, disruption of, 1392 Flexor training, in elbow rehabilitation, 251–253, 252f, 253f Floating ribs, 895–896, 896f Floating shoulder, 863, 865f Fluconazole, in dermatophyte infection, 199–200, 200t Fluid(s) for adolescent, 402 articular cartilage, 41


xvii

Fluid(s) (Continued) for children, 402 cold/cool, 401 in cramps, 12 after exercise, 402 before exercise, 401 during exercise, 401 glycerol in, 402 guidelines for, 401, 402t in heat illness prevention, 494 at high altitude, 505 ligament, 34 loss of, 401 for pediatric athlete, 402, 465–466 requirements for, 401–402, 402t types of, 401 Fluoroquinolones, tendinopathy with, 30 Fluoroscopy, 534, 535f computed tomography, 585, 586f in corticosteroid injection, 582–584, 584f in methacrylate cement injection, 585, 585f Folate, requirements for, 406b Folliculitis, 194–195, 194t, 195f, 196f Fondaparinux, in venous thromboembolism prevention, 378–384, 381t Food(s) carbohydrate in, 403, 403t, 404 fat in, 405, 405t glycemic index of, 403, 403t protein in, 405, 405t thermic effects of, 498 Foot (feet). See also Ankle; Hallux; Metatarsal(s); Toe(s) ankle linkage of, 1870–1872, 1872t cavus, 1850, 1900, 1963, 2183 deformity of, patellar stability and, 1550 entrapment neuropathy of, 2057–2063 deep peroneal nerve, 2061–2062, 2061f nerve to abductor digiti quinti, 2059–2060, 2060f posterior tibial nerve, 2057–2059, 2057f, 2058b, 2059f superficial peroneal nerve, 2062–2063, 2062f sural nerve, 2060–2061, 2061f fasciitis of. See Plantar fasciitis in female athlete, 490–491, 491b frostbite of, 203, 203f hyperpronation of, 2183 injury to, 2171–2205. See also specific injuries and conditions environment and, 2173 extrinsic factors in, 2172, 2172t, 2173f flexibility and, 2176–2183, 2176b, 2182f. See also Hypermobility incidence of, 2174–2175, 2175t intrinsic factors in, 2171–2172 overuse, 628–631 performance-enhancing drugs and, 2173–2174 personality and, 2172 playing surface and, 2192–2197. See also Playing surface risk factors in, 2171–2174, 2172t, 2173f shoewear and, 2183–2192. See also Shoes, injury and training techniques and, 2172–2173, 2173f keratosis of. See Plantar keratoses ligament injury in, 1947–1960. See also Bifurcate sprain; Lisfranc sprain; Subtalar sprain; Turf toe osteochondral lesions of, 2142–2171, 2142t, 2143f, 2143t calcaneal, 1973–1974, 1974f, 2054, 2143f, 2162, 2162f

xviii

Index

Foot (feet) (Continued) cuneiform, 2143f, 2166, 2166f fifth metatarsal base, 2143f, 2167–2169, 2168f, 2169f metatarsal head, 599, 1973, 1973f, 2143f, 2166–2167, 2167f, 2168t navicular, 599, 1972–1973, 1973f, 2143f, 2162, 2163f talar, 2143–2153, 2143f. See also Osteochondrosis (osteochondroses), talar overuse injury to, 628–631 pitted keratolysis of, 196, 196f plantar fasciitis of. See Plantar fasciitis plantar keratosis of. See Plantar keratoses retrocalcaneal bursitis of. See Retrocalcaneal bursitis stress fracture of, 646–650, 648f, 2012–2017, 2012t. See also specific fractures age and, 2014 anatomic factors in, 2012–2014 ankle, 2017–2018, 2017f, 2018f, 2019f, 2020f biomechanics of, 2013 diagnosis of, 2014–2015 gender and, 2014 hindfoot and midfoot, 2018–2024, 2021f, 2022f, 2023f history in, 2014 imaging in, 2014–2015, 2015f, 2016f metatarsal, 2024–2030, 2025f, 2026f, 2027f, 2028f physical examination in, 2014 previous surgery and, 2014 risk factors for, 2013–2014 treatment principles in, 2015–2017, 2016t in systemic illness, 1974 tendon injury of. See Achilles tendon; Flexor hallucis longus tendon; Peroneus brevis tendon; Peroneus longus tendon; Tibial tendon Football cervical spine injury in, 665–669, 686–690, 687f, 688f, 689f, 690f airway in, 667, 668f, 670f facemask removal in, 667, 667f helmet removal in, 668–669, 670f immobilization in, 666–667, 667f transport in, 669, 669f jet lag and, 458 pediatric, humeral fracture in, 1068–1069 posterior shoulder dislocation in, 937, 937f spear tackler’s spine and, 694, 695f, 710 sternomanubrial dislocation in, 897, 898f Force at joint, 87 patellofemoral. See Patellofemoral joint reaction force shear, 94f, 95 vector, 86, 90f Forearm training, in elbow rehabilitation, 254–255, 254f, 255f Foreign body, ultrasonography of, 538, 539f Formoterol, in exercise-induced bronchospasm, 182 Fosinopril, 160t Fovea capitis, 1452 Fracture(s). See also Stress fracture acromion, 866–867, 866f, 867b, 867f, 873 ankle, 1964–1969, 1965f, 1966f, 1967f, 1968f, 1969f dislocation with, 1945, 1946f atlas (C1), 677, 677f, 678f, 695–696, 705, 706f avulsion anterior process of calcaneus, 1954, 1954f, 2153–2156, 2154t, 2155t

Fracture(s) (Continued) hip and pelvis, 553, 555, 1474–1475, 1475f, 1489 iliac spine, 553, 556f, 1475 imaging of, 553, 555, 556f, 557, 557f ischial, 1489, 1489f lesser humeral tuberosity, 1175–1176 lesser trochanter, 1475 rib, 895–896, 896f axis (C2), 678, 695–696, 707–709 Bennett’s, 1402–1403, 1402f, 1403f, 1411, 1412 boxer’s, 1393–1394, 1393f, 1412–1413, 1413f bucket handle, in child abuse, 595–596, 596f calcaneal, 2153–2156, 2154t, 2155t capitate, 1348–1349, 1368 cervical spine C1-C3, 677–678, 677f, 678f, 695–696 in children/adolescents, 704–708, 705, 706f C3-C4, 678–679, 696–697 in children/adolescents, 708–709 C4-C7, 679–681, 680f, 681f, 682f, 696f, 697–698, 697f, 698f in children/adolescents, 708–709 compression, 680–681, 680f, 681f, 682f, 683f in children/adolescents, 709, 709f instability in, 675–676, 676f management principles in, 675–677, 676f surgical treatment of, 676–677 vertebral body, 698, 698f in child abuse, 595–596, 596f clay shoveler’s, 709 deep venous thrombosis after, 384 epiphyseal distal femur, 65f, 1641–1642, 1641b, 1641f, 1642f, 1643–1644, 1644b proximal tibia, 1642–1644, 1643f, 1643t, 1644b fatigue. See Stress fracture and at specific bones glenoid neck, 861f, 862–863, 862f, 864f, 865b, 865f hamate, 1340–1347, 1346f, 1347t hangman’s, 678, 707–708 healing of, 78–79, 79t, 80f, 81t blood supply and, 69 callus formation in, 79, 80f, 81t electricity effect on, 80 growth factors in, 79–80 problems of, 80–81, 82f, 83f ultrasound effect on, 80 humeral. See Humeral fracture Jefferson, 677, 677f, 678f, 705, 706f Jones’, 1969–1970, 1971f lumbar spine, 733–736, 733f, 735f lunate, 1350, 1353f, 1370, 1370f march, 1849. See also Tibia, stress fracture of metacarpal, 1393–1394, 1393f, 1394f, 1395f nasal, 525 nonunion of, 80–81, 82f, 83f occult, imaging in, 546, 552, 557 odontoid, 677–678, 678f in children/adolescents, 707 olecranon, 1271–1276. See also Olecranon, fracture of on-field, 525, 527 osteochondral. See Osteochondral fracture osteoporotic imaging of, 546 radionuclide imaging in, 547f treatment of, 585, 585f pars interarticularis, 726, 726f, 755, 756, 756b patellar, 1572–1577, 1574f, 1576f


Fracture(s) (Continued) phalangeal, 1394–1398, 1395f, 1396f, 1397f pisiform, 1350, 1352f, 1370–1371 rib, 525, 893–896, 893t, 895f, 895t, 1187 Rolando, 1403 sacral, 736, 736f scaphoid, 1335–1340, 1335f, 1336f, 1336t, 1338f, 1341f–1344f, 1364–1368, 1365f, 1366f, 1367f Segond’s, 1650 sternum, 896–900, 897f, 898f, 899f stress. See Stress fracture and at specific bones talar, 2153–2156, 2154t, 2155f, 2155t, 2156f thoracic spine, 733–736, 733f, 734f in child/adolescent, 755, 755f trapezium, 1345–1348, 1349f, 1370 triplane, 1966, 1967f, 1968–1969 triquetrum, 1349–1350, 1351f, 1368–1369, 1369f Free-body diagrams, 87, 88f Free fatty acids, caffeine effects on, 421 Free-running rhythm, 443, 444f Freeze drying, of allograft, 140–141 Freiberg’s infraction, 599, 1973, 1973f, 2143f, 2166–2167, 2167f, 2168t treatment of, 2166, 2168f Friction playing surface, 2198, 2204, 2204f shoe-related, 1906 Friction-induced injury cutaneous, 202, 202f, 203f iliotibial band, 560, 562f, 627–628, 629f, 630f Frostbite, 203, 203f, 528 Frostnip, 528 Frozen shoulder. See Adhesive capsulitis Fulcrum test, in femoral stress fracture, 1479 Full-can exercise, in shoulder rehabilitation, 244, 244f Fungal infection, 198–200, 198f, 199f Furunculosis, 194–195, 194t

G Gabapentin in complex regional pain syndrome, 363t, 364 in epilepsy, 189, 191t Gadolinium, 550 Gage’s sign, 1476 Gait, 2012–2013 ankle joint in, 1866–1867, 1867f, 1870–1872, 1872t metatarsal break in, 1870, 1871f orthosis effects on, 1902–1904, 1903f plantar aponeurosis in, 1870, 1871f in posterior cruciate ligament injury, 1692 in recurrent patellar dislocation, 1554–1555 subtalar joint motion in, 1870–1872, 1872t in varus malalignment, 1808–1809, 1809f, 1810f, 1811f windlass mechanism in, 1870, 1871f Gait training, in knee rehabilitation, 295, 296f Game of Shadows (Fainaru-Wada and Williams), 410 Gamekeeper’s thumb, 1399–1401, 1400f, 1415 Gamma irradiation, in allograft sterilization, 139 Ganglion cyst suprascapular nerve compression with, 617, 1121, 1121f, 1123 wrist, 1444–1445, 1445f Ganglionectomy, 1445 Gap junctions, 24 Gap test, in varus malalignment, 1808, 1808f Gardner-Wells tongs, in cervical spine fracture, 675

Index Gastrocnemius muscle antagonist action of, 1586 release of, in popliteal artery entrapment, 1844–1845, 1845f, 1846b, 1846t stretching exercise for, 291, 291f Gastrointestinal system cocaine effects on, 429 preparticipation examination of, 512 Gastrosoleus muscle, strengthening exercises for, 273, 275f Gemellus muscle, 1454t, 1455f Gender. See also Female athlete anterior cruciate ligament biomechanics and, 1584 anterior cruciate ligament injury treatment and, 1651 foot stress fracture and, 2014 knee arthroplasty and, 1799 pediatric/adolescent differences in, 476–477, 477t popliteal artery entrapment and, 1837 proximal humeral fracture and, 1067 strength and, 476 wrist injury and, 1363 Gene therapy, 422–423 in knee cartilage lesions, 1776 Genetic testing, in hypertrophic cardiomyopathy, 165 Genicular artery, 1645 Genie stretch, 290f, 291 Genitourinary system on-field injury to, 526–527 preparticipation examination of, 512 Giant cell tumor, 605, 605f Giardiasis, 152 Gilmore’s groin, 1463–1464 GIRD (glenohumeral internal rotation deficit) disorder, 979–980, 980f Girls. See Female athlete GLAD (glenolabral articular disruption) lesion, 976, 978f Glading, 430 Glasgow Coma Scale, 662t Glenohumeral internal rotation deficit (GIRD) disorder, 979–980, 980f Glenohumeral joint. See also Shoulder anatomy of, 769, 769f, 770–775, 932 bony, 771–772, 771f, 772f capsular, 772–773, 772f, 910 labral, 774 ligamentous, 773–774, 909, 910f muscular, 770–771, 770f. See also Infra spinatus; Subscapularis; Supraspinatus; Teres minor pediatric, 782–783, 783f vascular, 911–912 arthritis of. See Glenohumeral joint osteoarthritis arthrography of, 969 arthrosis of, 929 biomechanics of, 777–778, 787–788, 787f, 788f, 932–933, 990–994. See also Overhead throwing capsule of, 772–773, 772f, 782–783, 783f, 910 chondrolysis of, 984, 984f, 1105t, 1106 computed arthrotomography of, 950–951 computed tomography of, 950, 951f, 969 conventional arthrography of, 949–950, 949f degenerative disease of. See Glenohumeral joint osteoarthritis dislocation of. See Glenohumeral joint instability infection of, 984 instability of. See Glenohumeral joint instability

Glenohumeral joint (Continued) intracapsular pressure of, 774 kinematics of, 777–778, 2212–2213, 2213f, 2213t ligaments of. See Glenohumeral ligament(s) magnetic resonance arthrography of, 953–954 magnetic resonance imaging of, 953, 953t, 960t, 969, 969f, 970f osteoarthritis of. See Glenohumeral joint osteoarthritis pediatric anatomy of, 779–780, 779f, 782–783, 783f biomechanics of, 787–788, 787f, 788f dynamic stability of, 789–790, 790f static stability of, 788–789, 789f radiography of, 915–916, 947–949, 947b, 968–969 anteroposterior view for, 947, 948f, 1037, 1039f–1040f axillary lateral view for, 947–948, 948f, 1038, 1042f Grasbey view for, 947, 948f scapular Y view for, 948–949, 948f, 1037, 1041f Stryker notch view for, 916, 948f, 949 Velpeau axillary view for, 1038, 1042f West Point view for, 916 rheumatoid arthritis of, 1105t, 1106, 1107f arthroplasty in, 1114 arthroscopic treatment of, 1110–1111 rotations of, 769, 770f, 778 stability of, 912, 932–933 active, 774–775, 789–790, 789f passive, 771–774, 771f, 788–789, 789f translations of, 769, 777–778, 2212–2213, 2213f, 2213t ultrasonography of, 951–953, 952f, 953t Glenohumeral joint instability, 616, 769, 909–931 anterior, 914t. See also Glenohumeral joint instability, pediatric, anterior arthroscopic treatment of, 919–923, 920f, 921f–923f, 927–929 Bankart lesion with, 912, 919f–923f capsular laxity with, 912 clinical presentation of, 913–916, 913b complications of, 929–930 magnetic resonance arthrography in, 973–974, 973f, 974f, 974t nonoperative treatment of, 916f, 917–919, 917f, 918f in older patient, 974–975 open stabilization for, 923–924, 928–929 operative treatment of, 917f, 919–924, 920f–923f, 927–929 physical examination in, 914–915, 915f thermal capsulorrhaphy for, 929–930 vascular injury with, 1139–1140, 1140f anterior apprehension test in, 914, 915f, 939, 939f arthropathy with, 1104–1105, 1104b, 1114 arthroscopic anterior stabilization in, 919–923, 920f–923f arthroscopic posterior stabilization in, 924–926, 926f–927f classification of, 913, 919b, 967–968 clinical presentation of, 913–916, 913b, 914t computed tomography in, 543, 916 in female athlete, 489 Jobe’s relocation test in, 914, 915f load and shift test in, 914–915 magnetic resonance arthrography in, 973–975, 973f, 974f, 974t, 975f


xix

Glenohumeral joint instability (Continued) magnetic resonance imaging in, 916, 969, 969f, 970f multidirectional, 616, 913 arthroscopic treatment of, 930–931, 930f magnetic resonance arthrography in, 973 pain pattern in, 913–914 pathoanatomy of, 912–913 pediatric, 468, 469f, 932–946 anterior, 933–936 axillary nerve in, 933, 934f clinical presentation of, 933, 934f imaging in, 934, 935f nonoperative treatment of, 935, 935f, 936f operative treatment of, 935–936 physical examination in, 933, 934f recurrent, 914, 914t, 938–941, 939f, 940f, 941f reduction for, 935, 935f, 936f return to play after, 936 atraumatic, 942–946, 943f, 944f nonoperative treatment of, 945, 945f operative treatment of, 945 return to play after, 946 classification of, 933, 933b incidence of, 933 posterior, 936–938, 937f, 938f recurrent, 941–942, 942f return to play after, 938 physical examination in, 914–915, 915f posterior, 913 arthroscopic treatment of, 924–927, 925f, 926f–927f magnetic resonance arthrography in, 975, 975f open capsular shift procedure for, 927 operative treatment of, 924–927, 926f–927f pediatric, 936–938, 937f, 938f, 941–942, 942f radiography in, 915–916, 968–969, 969b. See also Glenohumeral joint, radiography of recurrent anterior, 914, 914t, 938–941, 939f, 940f, 941f posterior, 941–942, 942f sulcus sign in, 914, 915f treatment of, 916–929, 916f, 917f algorithms for, 916f, 917f arthroscopic anterior stabilization in, 919–923, 920f–923f arthroscopic posterior stabilization in, 924–927, 925f–927f complications of, 929–930 historical perspective on, 912 immobilization in, 917–919 in multidirectional instability, 930–931, 930f nonoperative, 917–919, 917f, 918f operative, 919–927, 920f–923f, 925f–927f reduction in, 916–917, 917f return to play after, 929 unidirectional, 616 vascular injury with, 1139–1140, 1140f, 1141f venous thrombosis with, 1140, 1141f Glenohumeral joint osteoarthritis, 929, 1104–1119 chondrolysis-related, 1104b, 1105t, 1106 classification of, 1104, 1104b, 1108, 1109f computed tomography arthrography in, 1108 evaluation of, 1107–1108 glenoid version in, 1108, 1109f instability-related, 1104b, 1105–1106, 1105t, 1106f, 1114

xx

Index

Glenohumeral joint osteoarthritis (Continued) physical examination in, 1108 post-traumatic, 1104–1105, 1104b, 1105t primary, 1104, 1105f, 1105t radiography of, 1108, 1108f secondary, 1104–1108, 1104b treatment of, 1109–1116 algorithm for, 1115f–1116f arthroplasty in, 1113–1114, 1113f, 1114f, 1115, 1116f rehabilitation after, 1116–1118, 1116t, 1117f, 1118f arthroscopic, 1110–1111, 1115, 1115f complications of, 1118, 1118t, 1119t rehabilitation after, 1116, 1116t arthroscopic débridement in, 1110, 1110f, 1115 biologic resurfacing in, 1112–1113, 1112f glenoidplasty in, 1110 humeral head resurfacing in, 1111–1112, 1112f joint-resurfacing, 1111–1112, 1111f, 1112f joint-sparing, 1110–1111, 1110f nonoperative, 1109–1110 osteochondral allograft in, 1111, 1111f, 1115, 1115f return to play after, 1118, 1118t Glenohumeral ligament(s), 772–773, 772f humeral avulsion of. See also Glenohumeral joint instability, anterior bony, 555 magnetic resonance arthrography in, 978–979, 979f magnetic resonance imaging in, 575, 575f inferior anatomy of, 772f, 773, 774, 789, 789f, 910, 910f, 911f, 911t function of, 911f, 2194 functional loosening of, 1020, 1020f magnetic resonance arthrography of, 575, 575f, 971, 971f magnetic resonance arthrography of, 573, 575, 575f, 971–972, 971f, 972f, 973f middle anatomy of, 772f, 773, 789, 789f, 910, 910f, 911f, 911t, 1017–1018, 1017f cord-like, 1017–1018, 1017f, 1021, 1023f function of, 910, 911f magnetic resonance arthrography of, 971, 972f superior anatomy of, 772f, 773, 788–789, 910, 910f, 911f, 911t, 966, 990, 991f function of, 910, 911f magnetic resonance arthrography of, 971–972, 973f Glenoid. See also Glenoid labrum; Glenoid neck anatomy of, 772, 772f biologic resurfacing of, 1112–1113, 1112f epiphyseal line of, 860f fracture of. Glenoid neck, fracture of in children, 872, 875 classification of, 857, 858f comminuted, 872, 872b computed tomography in, 861, 862f vs. epiphyseal line, 860f intra-articular, 867–872, 868f, 869f, 870f, 871f, 872b radiography of, 861, 861f return to play after, 873, 875 type I (rim), 867–868, 868f, 869f, 870f, 872, 872b, 873–875 type II-V (fossa), 871f, 872, 872b, 873, 874f

Glenoid (Continued) ossification of, 859 posterosuperior impingement of. See Shoulder impingement, internal version of, in glenohumeral joint osteoarthritis, 1108, 1109f Glenoid labrum anatomy of, 774, 909–910, 969–971, 970f, 1016–1019, 1017f normal variations in, 970f, 972, 972f anterior avulsion of. See Bankart lesion anterosuperior, 1017–1018, 1017f biceps tendon insertion on, 1018, 1018f biomechanics of, 1016, 1019–1021 bumper effect of, 1016 cartilage undermining of, 970f, 972 cyst of, 580–581, 582f, 964–965, 965f, 980, 980t histology of, 1017, 1017f, 1018, 1018f inferior, 1017, 1017f magnetic resonance arthrography of, 969–971, 970f sublabral hole and, 1017, 1017f superior, 1016–1017. See also SLAP (superior labrum, anterior to posterior) lesion throwing-related injury to, 1219–1221, 1220f vascularity of, 1018–1019 Glenoid neck, fracture of, 862–863, 862f, 864f, 865b, 865f computed tomography in, 861, 862f, 864f return to play after, 873 treatment of, 873, 874f Glenoidplasty, in osteoarthritis, 1110 Glenolabral articular disruption (GLAD) lesion, 976, 978f Glenopolar angle, 1713 Glucagon exercise effects on, 217t, 218 parenteral, 179 Glucosamine, 409 in knee arthritis, 1774, 1791 Glucose for hypoglycemia, 178–179, 179b metabolism of, during exercise, 173–175, 174f, 174t γ-Glutamyltransferase, in anabolic-androgenic steroid user, 416 Gluteal artery, 1454, 1501 Gluteal muscle raise exercise, in knee rehabilitation, 267, 268f Gluteal nerve, 1454, 1501 Gluteus maximus, 1454t, 1455f neuromuscular activation exercises for, 285–286 Gluteus medius, 1454t, 1455f neuromuscular activation exercises for, 257–258, 258f, 259f, 285–286 Gluteus medius tendon, 567–568 Gluteus minimus, 1454t, 1455f Gluteus minimus tendon, 567–568 Glycemic index, 403, 403t Glycerol for hyperhydration, 402 ingestion of, 402 Glycogen, 211 depletion of, 403 muscle, 400–401 depletion of, 403 repletion of, 403, 403t, 404 Glycolysis, 210–211, 210f aerobic, 211 anaerobic, 211 Glycosaminoglycans immobilization effects on, 228 tendon, 23–24


Godfrey’s test, in posterior cruciate ligament injury, 1690–1691, 1691f Golfer’s elbow, 620–621, 1205–1206, 1205f treatment of, 1205–1206, 1205f, 1206f Gracilis, 1454t, 1455f, 1485 strain of, 1460–1461 Graft(s). See also Allograft(s); Autograft(s) in ACL reconstruction. See Anterior cruciate ligament (ACL) reconstruction, graft for articular cartilage, 53–55. See also Osteochondral allograft/autograft allograft, 54 autograft, 53–54 preservation of, 54 bone, 81, 83t allograft, 81, 83t, 137 autograft, 81, 83t cancellous, 81, 83t cortical, 81, 83t osteoarticular (osteochondral), 81 vascularized, 81 in Kienböck’s disease, 1377 in scaphoid nonunion, 1341–1345, 1342f–1344f ligament, 35–39 allograft, 38, 142–143 autograft, 36–38 Dacron augmentation of, 36 xenograft, 38 meniscal, 63–64 allograft, 64, 143–144 synthetic, 64 nail bed, 1429, 1430f osteochondral allograft, 141, 144–145 in capitellar osteochondritis dissecans, 1244, 1245f tendon, 35–39 in ulnar collateral ligament reconstruction, 1401, 1401f Great toe. See Hallux Great vessels, injury-related compression of, 821, 822f Grey Turner’s sign, 526 Griseofulvin, in dermatophyte infection, 198–199, 200t Groin, contusion of, 1459–1460 Ground reaction force, 86 Growth factors in bone, 67 in fracture healing, 79–80 in knee cartilage lesions, 1776 in muscle injury treatment, 16 in tendon injury treatment, 31 Growth hormone, 419–420 bone effects of, 72 exercise effects on, 217, 217t, 421 Growth plate. See Epiphysis; Physis Guanfacine, in hypertension, 160t Gymnasts elbow disorders in, 1236, 1246 ulnocarpal impingement in, 1376 wrist disorders in, 1375–1376, 1376f Gynecomastia, anabolic-androgenic steroids and, 415

H H band, 6f H zone, 4f, 5 HAGL (humeral avulsion of glenohumeral ligament) lesion, 575, 575f, 978–979, 979f bony, 555

Index Haglund’s deformity, 2030, 2031f. See also Retrocalcaneal bursitis magnetic resonance imaging of, 2034, 2034f treatment of, 2036, 2038, 2038f Hair follicles, bacterial infection of, 194–195, 194t Hallux metatarsophalangeal joint injury of. See Turf toe sesamoids of. See Sesamoid(s) subungual exostosis of, 2105–2107, 2105t, 2106b, 2106f, 2107f Syme amputation of, 2099, 2104f taping of, 2090, 2093f Hallux interphalangeal angle, 2066, 2066t Hallux rigidus, 2182, 2182f Hallux valgus, 2064–2081 anatomy of, 2064–2068, 2064f, 2065f, 2066f, 2066t, 2067f biomechanics of, 2067–2068, 2067f, 2068f classification of, 2068, 2068b distal metatarsal articular angle in, 2066, 2066t, 2072 evaluation of, 2069 hallux interphalangeal angle in, 2066, 2066t hallux valgus angle in, 2066, 2066f, 2066t history in, 2069, 2069b joint congruency in, 2066, 2067f mild, 2069b, 2071f moderate, 2069b, 2071f nonoperative treatment of, 2069–2070 1-2 intermetatarsal angle in, 2066, 2066f, 2066t operative treatment of, 2070–2081, 2070b, 2071f, 2072b, 2079b Akin procedure in, 2070, 2072b, 2072f, 2073f, 2076, 2078f arthrodesis in, 2075 care after, 2080–2081 Chevron procedure in, 2070, 2073b, 2073f, 2074f, 2076 combined multiple first ray osteotomies in, 2071–2072, 2078f, 2079, 2080f complications of, 2081, 2081b distal soft tissue realignment in, 2070, 2074b, 2075f, 2076, 2078, 2079f in high-performance athlete, 2081 Keller procedure in, 2072, 2075 proximal first metatarsal osteotomy in, 2070–2071, 2076b, 2077f, 2078–2079 return to play after, 2081, 2081b salvage procedures in, 2072, 2075–2076 physical examination in, 2069, 2069b radiography in, 2069, 2069b risk factors of, 2064, 2064f sagittal sulcus in, 2068, 2068f sesamoid dysfunction and, 2090 severe, 2069b, 2071f Hallux valgus angle, 2066, 2066f, 2066t Hallux varus after fibular sesamoidectomy, 2093 mild, 2079 moderate, 2079 postoperative, 2078, 2079f sesamoid dysfunction and, 2090 severe, 2079 Halstead’s maneuver, in thoracic outlet syndrome, 1131, 1132f Hamate, anatomy of, 1319–1320, 1319f Hamate fracture adult, 1340, 1345 classification of, 1340 clinical manifestations of, 1340, 1345 computed tomography in, 543, 544f physical examination in, 1345, 1346f

Hamate fracture (Continued) radiography in, 1345, 1346f return to play after, 1348 treatment of, 1345, 1347t pediatric, 1369–1370 Hammer toe deformity, 2117, 2118t evaluation of, 2119–2120, 2119f, 2120b, 2121f nonoperative treatment of, 2121, 2121f operative treatment of, 2121–2125, 2122f, 2123f, 2124b Hamstring curl, 266, 317f, 325, 329–330, 337 Hamstring muscles anatomy of, 1485, 1485f strain of, 1461–1462, 1486–1489 in children/adolescents, 1489 classification of, 1485, 1485t clinical presentation of, 1486 complications of, 1489 imaging of, 1486f, 1487, 1487f magnetic resonance imaging in, 558, 559f mechanisms of, 335, 335f nonoperative treatment of, 1487 operative treatment of, 1488–1489 physical examination in, 1486–1487, 1486b, 1486f prevention of, 336–337, 337f, 337t, 1488–1489 previous, 336 rehabilitation protocol for, 1488, 1488t return to play after, 1489, 1489b risk factors for, 335–336, 336b treatment of, 1487–1489, 1487b stretching exercises for, 289–290, 290f, 292f, 293 Hamstring raise exercise, in knee rehabilitation, 267, 268f Hand injury. See also Finger(s); Thumb; Wrist adult, 1379–1403 biomechanics of, 1379 epidemiology of, 1379 fracture, 1393–1398 metacarpal, 1393–1394, 1393f, 1394f, 1395f phalangeal, 1394–1398, 1395f, 1396f, 1397f ligamentous, 1379–1387. See also Carpometacarpal joint; Interphalangeal joint; Metacarpophalangeal joint management of, 1379 tendon, 1387–1392, 1388f, 1389f, 1391f pediatric, 1404–1430 anatomy of, 1404, 1404f evaluation of, 1404–1405, 1405f fracture, 1405–1414 metacarpal, 1411–1414, 1411f, 1412f, 1413f phalangeal, 1405f, 1406–1411, 1406f–1411f ligamentous, 1414–1420. See also Carpometacarpal joint; Interphalangeal joint; Metacarpophalangeal joint radiography in, 1405 tendon, 1420–1428, 1420f–1422f, 1424f–1427f Hangman’s fracture, 678, 707–708 Hawkins’ sign, 997, 1000f Head injury, 657–663. See also Cervical spine injury concussive, 658–662, 658b, 659t. See also Concussion contracoup, 657, 657f coup, 657, 657f evaluation of, 522, 662t


xxi

Head injury (Continued) Glasgow Coma Scale in, 662t hematoma with, 660–661, 661f hemorrhage in, 660–661, 661f incidence of, 662 on-field, 522–524 prevention of, 662 return to play after, 522, 523t, 659t, 662, 663b risk for, 662, 662b seizure and, 661 treatment of, 660, 662, 662t, 663b Head tilt–jaw lift maneuver, in cervical spine injury, 667, 668f Heart anabolic-androgenic steroid effects on, 416 cocaine effects on, 429 exercise effects on, 218–220 hypothermia effects on, 501 inhalant effects on, 430 nicotine effects on, 428 Heart murmurs, preparticipation examination for, 512 Heart rate exercise effect on, 219, 219f, 220t in female athlete, 476–477 maximal, 219 Heat conductive transfer of, 493, 499 dissipation of, 493, 499 evaporative transfer of, 493, 499 physiologic adaptations to, 493–494 production of, 498–499 radiative transfer of, 493, 499 Heat cramps, 495–496 Heat edema, 530 Heat exhaustion, 494–495, 529 Heat illness/injury, 493–497, 514t, 528, 528f, 529–530 in children/adolescents, 465–466 risk factors for, 494 Heat stroke, 496, 529 Heat syncope, 494, 529–530 Heat therapy, in thoracolumbar spine injury, 731 Heavy-load eccentric training, in Achilles tendon injury, 1999 Heel black, 202, 202f pain in, 2030–2056. See also Plantar fasciitis; Retrocalcaneal bursitis in children, 2037 classification of, 2053 in entrapment neuropathy, 2059–2060 HLA-B27 in, 2047 referred, 2047 in sarcoidosis, 2051 in seronegative spondyloarthritis, 2033–2034, 2047 spur of, 2042–2043, 2042f. See also Plantar fasciitis Heel cups in plantar fasciitis, 2053f in retrocalcaneal bursitis, 2035 Heel lift, in Achilles tendon injury, 1998 Heel pad in retrocalcaneal bursitis, 2037, 2038f for shock absorption, 2052 Heel touch exercise, 308f, 324 Height, in preparticipation examination, 509 Helmet in cervical spine injury, 687, 687f, 689, 689f removal of, in cervical spine injury, 668–669, 670f

xxii

Index

Hematoma epidural, 523, 660, 661f heterotopic ossification treatment and, 1297–1298 intracerebral, 660–661, 661f in osteochondral fracture, 51 rectus sheath, 526 septal, 525 subdural, 660, 661f subungual, 2098 Hemiarthroplasty, shoulder, 1046, 1048f Hemodialysis, cramps during, 12 Hemoglobin A1c, 176–177, 176t Hemorrhage. See also Hematoma intracranial, 659, 660–661, 661f muscle, 17–18, 18f pelvic fracture and, 541 Hemothorax, on-field, 526 Heparin prophylactic, in venous thromboembolism, 378–384, 381t, 382f in venous thromboembolism, 384–385, 384t Hepatitis A virus infection, 154 Hepatitis B virus infection, 154–155 Hepatitis C virus infection, 155 Hepatitis D virus infection, 155 Hepatitis E virus infection, 154–155 Hepatocellular carcinoma, anabolic-androgenic steroids and, 416–417 Hepatomegaly, clearance for participation and, 513 Hernia, 1462–1464 clearance for participation and, 513 femoral, 1463 inguinal, 1462–1463 sports, 1463–1464 Herpes gladiatorum, 197, 197f Herpes labialis, 197, 197f Herpes simplex virus infection, 197, 197f Heterophil antibody test, 150 Heterotopic ossification, 82 elbow, 1289–1300 alkaline phosphatase levels in, 1292 anatomy of, 1290, 1293 anterior, 1290 anterolateral, 1296 anteromedial resection in, 1296–1297 chemoprophylaxis in, 1294, 1297 classification of, 1293–1294 clinical presentation of, 1290 differential diagnosis of, 1293 distal humeral fracture and, 1256 etiology of, 1289 functional classification of, 1293–1294 genetic factors in, 1290 history in, 1290 intra-articular, 1296 magnetic resonance imaging in, 1293 neurologic injury and, 1291 nonoperative treatment of, 1295 operative treatment of, 1295–1297, 1295f, 1298f–1299f complications of, 1297–1298 management after, 1297 pathophysiology of, 1289–1290 physical examination in, 1291–1292 posterolateral, 1290, 1296 posteromedial, 1296 prevention of, 1294–1295, 1297 radiation therapy in, 1294–1295, 1297 radiography in, 1292–1293 radioulnar, 1297 risk factors for, 1290–1291, 1290f–1292f trauma and, 1277, 1290, 1290f–1292f ultrasonography in, 1293

Heterotopic ossification (Continued) hip, 82, 1460 interosseous talocalcaneal ligament, 1933 muscle. See Myositis ossificans after proximal humeral fracture, 1050 proximal radioulnar joint, 1297 radiation in, 82, 1277, 1294–1295, 1297 High altitude, 502–503 adverse effects of, 504–505 cerebral edema at, 504–505 competition at, 503–504 definition of, 502 diet and, 505 fluids and, 505 physical characteristics of, 502 physiologic effects of, 503 pulmonary edema at, 504 simulation of, 504 training at, 220, 504, 505 erythropoietin and, 420 High tibial osteotomy, 1804–1835 arterial injury with, 1832 arthrofibrosis after, 1832 closing wedge, 1821–1824, 1824f–1826f complications of, 1830–1833 outcomes of, 1816–1818, 1817t, 1825–1829, 1828f, 1829f complications of, 1830–1835 contraindications to, 1816 correction wedge determination in, 1810–1811, 1812f, 1813f deep venous thrombosis after, 1833 delayed union after, 1831–1832 gap angle in, 1812, 1813f iliac crest harvest site pain after, 1833 indications for, 1814–1816, 1815t, 1833, 1835 nonunion after, 1831–1832 opening wedge, 1818–1821, 1819f–1823f complications of, 1830–1833 open wedge angle measurement in, 1812–1814, 1813f, 1814f, 1814t, 1815t outcomes of, 1816–1818, 1817t, 1829–1830, 1830f patella infera with, 1832–1833 patellar height measurement in, 1811 peroneal nerve injury with, 1832 rehabilitation after, 1824–1825, 1827t results of, 1816–1818, 1817t return to play after, 1824–1825 teeter effect after, 1830–1831 tibial plateau fracture after, 1832 timing of, 1814–1815, 1815t varus deformity recurrence after, 1831 weight-bearing line ratio in, 1810, 1811f, 1812f High-voltage galvanic stimulation in inflammation, 230, 231f in lateral epicondylitis, 618 Hill-Sachs lesion, 912–913, 920f magnetic resonance arthrography of, 973, 973f radiography of, 968–969 Hindfoot, stress fracture of, 2018–2024, 2021f, 2022f, 2024f Hip. See also Acetabular labrum; Acetabulum; Femur anatomy of, 1452–1453, 1453f arthroplasty of, 1504–1512 anatomy for, 1500–1502 approaches to, 1505 bearings for, 1505–1506 biomechanical aspects of, 1501–1502


Hip (Continued) computed tomography after, 542, 542f high-offset femoral component in, 1502 minimally invasive, 1505 return to play after, 1507–1508, 1507t–1508t stability with, 1502 technique of, 1508–1512, 1509f–1512f arthroscopy of, 1473–1474, 1473t, 1474f. See also Arthroscopy, hip in acetabular labral tears, 1470f indications for, 1473t in ligamentum teres rupture, 1473f in loose body removal, 1472f avulsion fracture of, in children, 1474–1475, 1475f, 1489 blood supply to, 1501 chondral injury of, 1472, 1473t computed tomography–guided biopsy of, 585, 586f degenerative disease of, 1467, 1467b classification of, 1502, 1502b clinical presentation of, 1502–1503 etiology of, 1500 imaging of, 1503 nonoperative treatment of, 1503–1504, 1504b, 1504f operative treatment of. See Hip, arthroplasty of pain in, 1503 physical examination in, 1503 primary, 1500 range of motion testing in, 1503 secondary, 1500 dislocation of, 1464 femoroacetabular impingement at, 1471–1472, 1471f–1472f forces on, 1453 fracture of, 1464–1466, 1465f avulsion, 1474–1475, 1475f in children/adolescents, 597, 598f, 1474–1475, 1475f, 1489 computed tomography of, 542 stress, 1464–1466, 1465f injury to, 1455–1474, 1456b. See also specific injuries bone, 1464–1467, 1465f in children/adolescents, 469, 470f, 1474–1477, 1475f–1476f, 1476t intra-articular, 1469–1474 nerve, 1467–1469 soft tissue, 1455–1464, 1456b innervation of, 1453–1455, 1455f ligaments of, 1452–1453, 1453f loose bodies of, 1472, 1472f magnetic resonance imaging arthrography of, 536–537 muscles about, 1453, 1454t, 1455f, 1500–1501 heterotopic ossification of, 1460 strains of, 1460–1462, 1460t, 1485–1497. See also at specific muscles neonatal, 590, 590f nerve entrapment at, 1467–1469 pain in, 1452f range of motion of, 1452t resurfacing procedures for, 1506–1507 snapping, 1458–1459 stress fracture of, 1464–1466, 1465f synovial disease of, 1473 vasculature of, 1453–1455 Hip abduction exercise, in knee rehabilitation, 258, 258f Hip extension exercise, in knee rehabilitation, 258, 258f, 267

Index Hip hyperextension exercise, in knee rehabilitation, 267 Hip lift, single-leg, in core training, 281 Hip pointer, 1459 Hippocampus, marijuana effects on, 426 HIV infection. See Human immunodeficiency virus (HIV) infection Hockey, cervical spine injury in, 690 Homans’ sign, 374 Hook of hamate fracture. See Hamate fracture Hop test, in femoral stress fracture, 1479 Hopping, single-leg, in knee rehabilitation, 296, 298f, 315f, 329 Horn blower’s sign, in glenohumeral joint osteoarthritis, 1108 Horseback riding, proximal humeral fracture in, 1067–1068, 1068f, 1069 Hot-tub folliculitis, 194–195, 196f Hug exercise, dynamic, 241, 241f Human immunodeficiency virus (HIV) infection, 153–154, 514t allograft transmission of, 141 exercise and, 154 prevention of, 153–154 testing for, 154 Human papillomavirus (HPA) infection, 197–198 Humeral avulsion of glenohumeral ligament (HAGL) lesion, 575, 575f, 978–979, 979f bony, 555 Humeral circumflex artery, 1033–1034, 1034f, 1036f Humeral condyles lateral, fracture of, 1280t, 1284–1285, 1284f medial, fracture of, 1280t, 1286 ossification of, 1228 Humeral epicondyles fracture of, in children, 1238 lateral, fracture of, 1256 pediatric, 1284–1285 medial avulsion fracture of, 1183–1186, 1183b, 1183f, 1184f, 1185f fracture of, 1285–1286, 1286f ossification of, 1228 Humeral fracture (distal), 1250–1258 evaluation of, 1250–1251, 1250f–1252f nonunion of, 1278 operative treatment of, 1251–1256 complications of, 1256, 1258 countersunk threaded screw in, 1255 exposure for, 1251–1253, 1252f extensile lateral exposure in, 1253, 1253f fixation techniques in, 1253–1256, 1253f–1255f, 1257f heterotopic ossification with, 1256 home run screw in, 1254–1255, 1255f implant-related complications of, 1258 locking screw plating in, 1254–1255 metaphyseal comminution and, 1255 nonunion after, 1256, 1258 olecranon osteotomy in, 1252–1253, 1252f orthogonal plating in, 1253–1254, 1253f outcomes of, 1256 parallel plating in, 1254, 1254f, 1255–1256 rehabilitation after, 1277 stiffness after, 1256 triple plating in, 1254, 1254f ulnar nerve injury with, 1256 pediatric, 1280t, 1281–1283 cosmetic deformity after, 1282–1283 lateral condyle, 1280t, 1284–1285, 1284f lateral epicondyle, 1284–1285 medial condyle, 1280t, 1286

Humeral fracture (distal) (Continued) medial epicondyle, 1285–1286, 1286f supracondylar, 596–597, 597f, 1280t, 1281–1283, 1282f T-condylar, 1283 transphyseal, 1283 vascular injury with, 1282 Humeral fracture (proximal), 1033–1056 anatomy of, 1033–1034, 1033f, 1034t classification of, 1035–1036, 1037f clinical evaluation of, 1036–1038 four-part, 1037f, 1048f, 1053–1054 greater tuberosity, 1037f, 1050, 1051f–1052f head-splitting, 1037f, 1053–1056 incidence of, 1035 lesser tuberosity, 1037f, 1050, 1053f, 1175–1176 pediatric, 1090, 1090b mechanism of, 1036 neurovascular examination in, 1036–1037 nonoperative treatment of, 1040 operative treatment of, 1040–1049, 1043b avascular necrosis after, 1049 complications of, 1049–1050 in four-part fracture, 1048f, 1053–1054 humeral head replacement for, 1046, 1048f intramedullary nailing for, 1043, 1045–1046, 1047f in lesser tuberosity fracture, 1050, 1053f locking plates for, 1040–1041, 1043b, 1044f loss of motion after, 1050 malunion after, 1049–1050 myositis ossificans after, 1050 neurovascular injury after, 1049 nonunion after, 1049 open reduction and internal fixation for, 1046–1047 percutaneous reduction and pinning for, 1041–1042, 1043b, 1045f plate fixation for, 1042–1043 rehabilitation after, 1056–1057, 1057f–1058f retrograde Ender nails for, 1043, 1046f return to play after, 1059 suture tension band fixation for, 1043, 1043b in three-part fracture, 1052–1053, 1054f, 1055f–1056f in two-part greater tuberosity fracture, 1050, 1051f–1052f in two-part surgical neck fracture, 1050–1052, 1054f wire fixation for, 1043, 1043b pediatric, 594, 594f, 1066–1093 age and, 1068 baseball and, 1068, 1070f epidemiology of, 1067–1069 epiphyseal, 1172–1175. See also Little Leaguer’s shoulder football and, 1068–1069 gender and, 1067 in high-performance athlete, 1066, 1081, 1081f–1082f horseback riding and, 1067–1068, 1068f, 1069 incidence of, 1067–1069, 1072 lesser tubercle, 1090, 1090b macrotrauma and, 1068, 1069f metaphyseal, 1085–1089, 1089t age and, 1086 anatomic characteristics of, 1085–1086, 1085f, 1086f through bone cyst, 1085, 1086f classification of, 1087


xxiii

Humeral fracture (proximal) (Continued) displaced, 1087, 1088f extra-articular, 1086 greenstick-type, 1085, 1085f, 1087 incidence of, 1086–1087 intramedullary pins for, 1088, 1088f– 1089f muscle forces in, 1085–1086, 1086f nondisplaced, 1087 olecranon traction for, 1087–1088 open reduction for, 1088 percutaneous stabilization for, 1088, 1088f, 1089f radiography in, 1087 remodeling in, 1085, 1087, 1087f, 1088f, 1088 signs and symptoms of, 1087 treatment of, 1087–1089, 1087f–1089f in non–high-performance athlete, 1067 in nonorganized sports, 1067–1068 in organized sports, 1067 patterns of, 1072, 1072b physeal, 779, 780f, 1072–1085, 1089t anatomic characteristics of, 1073 avascular necrosis after, 1085 callus formation in, 1073, 1078f cast for, 1076–1077 classification of, 1074 closed treatment of, 1076–1077, 1077f, 1080, 1081f–1082f complications of, 1084–1085 computed tomography in, 1074 dislocation and, 1085 displacement with, 1073, 1073f, 1074, 1075b, 1075f–1076f fragment displacement with, 1073, 1073f growth arrest after, 1084 in high-performance athlete, 1081, 1081f–1082f incidence of, 1073 intracapsular, 1073 intramedullary nail fixation for, 1078, 1080f ipsilateral injury with, 1074 malunion of, 1082f, 1085 mechanism of, 1074 nerve injury with, 1074 nonskeletal complications of, 1084 open reduction for, 1078–1079, 1081f, 1084 operative treatment of, 1077–1084, 1079f–1082f, 1083f percutaneous fixation for, 1077–1078, 1079f, 1080f periosteum in, 1072 postfracture care in, 1084 radiography in, 1074–1075, 1076f reduction for, 1076–1077, 1078–1079, 1078f, 1081f, 1083–1084, 1083f remodeling after, 1076, 1078f return to play after, 1084 Salter-Harris I, 1073, 1085 Salter-Harris II, 1073, 1075f, 1085 Salter-Harris III, 1073, 1085 Salter-Harris IV, 1073, 1085 signs and symptoms of, 1073–1074 stress, 1070 structural aspects of, 1072–1073, 1073f swelling with, 1073 traction reduction for, 1077 treatment of, 1075–1084, 1083f management after, 1084–1085 nonoperative, 1076–1077, 1077f, 1080, 1081f–1082f operative, 1077–1084, 1079f–1083f

xxiv

Index

Humeral fracture (proximal) (Continued) sequelae of, 1067 sport-specific, 1068–1069, 1069f–1070f stress, 1090–1093. See also Little Leaguer’s shoulder causative factors in, 1091, 1092f imaging of, 1092, 1093f signs and symptoms of, 1091–1092, 1093b treatment of, 1092 treatment of, 1066–1067 physical examination in, 1036–1037, 1038b, 1038f radiography in, 1037–1038, 1038b, 1043f–�� 1046f, 1048f anteroposterior view for, 1037, 1039f–1040f axillary view for, 1038, 1042f lateral view for, 1037–1038, 1041f Velpeau axillary view for, 1038, 1042f return to play after, 1059 soft tissue injury with, 1035 surgical neck, 1037f, 1040, 1044f–1045f, 1050–1052, 1054f three-part, 1037f, 1043, 1046f, 1047f, 1052–1053, 1054f, 1055f–1056f treatment of, 1038t, 1039–1056, 1043b. See also Humeral fracture (proximal), operative treatment of two-part, 1037f, 1040, 1044f–1045f, 1050–1052, 1051f–1052f, 1054f Humeral fracture (shaft), 1176–1183 anatomy of, 1176–1177 biomechanics of, 1176–1177, 1177f classification of, 1177, 1177f complications of, 1182 evaluation of, 1177–1178 imaging of, 1178, 1179f, 1180f, 1180t, 1181f return to play after, 1182 in snowboarders, 1183 stress, 634–635, 1176–1177, 1178–1179, 1180t, 1182 throwing-related, 1226 treatment of, 1162b, 1178–1182, 1179f–1181f, 1182b anterolateral approach for, 1159 medial approach for, 1161 posterior approach for, 1159, 1161 triceps-splitting approach for, 1161 Humeral fracture-dislocation, proximal, 1037f Humeral head, 1034t angulation of, 771–772, 771f articular surface of, 771–772, 771f–772f avascular necrosis of, 1105t, 1106–1107, 1107f arthroscopic treatment of, 1110–1111 magnetic resonance imaging of, 984, 985f physeal injury and, 1085 post-traumatic, 1049 blood supply to, 1033–1034 magnetic resonance imaging of, 983 osteochondral allograft for, 1111, 1111f pediatric, 782 replacement of, 1046, 1048f resurfacing of, 1111–1112, 1112f Humeral tuberosity greater, 1033, 1033f, 1034t lesser, 1033, 1033f, 1034t avulsion fracture of, 1090, 1175–1176 fracture of, 1037f, 1050, 1053f Humeroscapular articulation, 990 Humerus anatomy of, 1157–1158, 1157b, 1158f, 1160f, 1161f developmental, 780, 782, 782f aneurysmal cyst of, 983–984

Humerus (Continued) distal articular surface of, 1189 fracture of. See Humeral fracture (distal) ossification of, 1227–1228, 1228f–1229f supracondylar process of, 1229 fracture of, 596–597, 597f, 1186, 1186f, 1280t, 1281–1283, 1282f proximal anatomy of, 1033, 1033f, 1034t biomechanics of, 1034–1035 blood supply to, 1033–1034, 1034b, 1034f, 1071–1072, 1072f capsular attachments of, 1071, 1071f epiphysis of, 1069–1070, 1070f–1071f injury to, 1173, 1173b. See also Little Leaguer’s shoulder fracture of. See Humeral fracture (proximal) metaphysis of, 971f, 1070–1071, 1071f metastases of, 983, 983f muscle attachments of, 1070–1071, 1071f muscular anatomy of, 1034, 1035f, 1035t nerve supply of, 1034, 1036f pediatric, 782, 782f physis of, 779, 779f, 1070, 1070f closure of, 782, 782f, 1070 shaft of, fracture of. See Humeral fracture (shaft) Humphrey, ligament of, 1597, 1685, 1686f Hyaluronic acid, 43f, 44 in knee osteoarthritis, 1791–1792 Hydralazine, in hypertension, 160t Hydration, 401–402 with creatine use, 418 glycerol in, 402 guidelines for, 401–402, 402t optimization of, 402 Hydrochlorothiazide, 160t Hydrotherapy, after shoulder arthroplasty, 1116t, 1117–1118 β-Hydroxy-β-methylbutyrate, 422 γ-Hydroxybutyrate, 409, 422 Hydroxycitrate, 409 Hyperabduction maneuver, in vascular injury, 1138–1139, 1139f Hyperalgesia, 356t in complex regional pain syndrome, 354, 356 Hypercalcemia, 73t Hypercoagulability, 371–372 primary, 372–374, 374f Hyperesthesia, 356t in complex regional pain syndrome, 356 Hyperglycemia, 175, 175f, 177b, 178 Hyperhomocysteinemia, 374t Hyperhydration, 402 Hypermobility, 2176–2178 criteria for, 2176, 2177f historical perspective on, 2177–2178 vs. instability, 2176–2187 lower extremity injury and, 2182–2183 Hyperparathyroidism, 73t, 74t, 77t Hyperpathia, 356t in complex regional pain syndrome, 356 Hyperplasia, muscle, 214, 214t Hypertension, 156–161 classification of, 156, 157t 158, 157t–158t diagnosis of, 157–�� evaluation of, 158, 161 monitoring of, 161 secondary, 158, 158t treatment of, 158–161, 159t–160t α-adrenergic receptor agonists in, 161 α-adrenergic receptor antagonists in, 160t, 161


Hypertension (Continued) angiotensin-converting enzyme inhibitors in, 159, 160t angiotensin receptor blockers in, 159, 160t β-adrenergic receptor antagonists in, 159, 160t calcium channel blockers in, 160t, 161 combination, 161 diuretics in, 159, 160t white coat, 157 Hyperthermia, 528, 528f, 529–530 Hyperthyroidism, 74t, 77t Hypertrophy, muscle, 214, 214t Hyperventilation, epileptiform discharges with, 187 Hypoalgesia, in complex regional pain syndrome, 356 Hypocalcemia, 73t Hypoesthesia, in complex regional pain syndrome, 356 Hypoglycemia acute management of, 178–179, 179b postexercise, 174–175, 174b, 177–178, 177b Hyponatremia, 402, 495 in heat illness, 529 Hypoparathyroidism, 73t–74t Hypophosphatasia, 73t, 76t–77t Hypopnea, definition of, 448 Hypotension, sternoclavicular joint injury and, 822, 823f Hypothenar hammer syndrome, 1357–1359 clinical manifestations of, 1357 physical examination in, 1357 radiography in, 1357, 1357f return to play after, 1359 treatment of, 1358–1359, 1358f Hypothermia, 500–502, 528–529 cardiovascular effects of, 501 mild, 500–501 moderate, 500–501 neurologic effects of, 500–501 prevention of, 501–502 renal effects of, 501 severe, 500–501 treatment of, 501 Hypothesis, 99, 110–112 alternate, 110 null, 110 Hypoxia high-altitude, 502–503 seizures with, 187

I I band, 4f, 5, 6f, 208f Ice test, in complex regional pain syndrome, 356 Ice therapy. See Cryotherapy Iliac apophysitis, 1475 Iliac crest, 1452 contusions of, 1459 graft harvest–related pain at, 1833 Iliac spine, avulsion fracture of, 556f, 1475 Iliofemoral ligament, 1452, 1453f Ilioinguinal nerve, entrapment of, 1469 Iliopatellar band, 1551, 1552f, 1719 Iliopectineal bursitis, 1458 Iliopsoas, 1454t, 1455f strain of, 1461 Iliopsoas bursitis, 1457–1458, 1457f Iliotibial band anatomy of, 1719 for ligament autograft, 37 stretch for, 291–292, 291f tightness of, 1558

Index Iliotibial band friction syndrome, 627–628, 629f magnetic resonance imaging in, 560, 562f Noble compression test in, 628, 628f Ober’s test in, 628, 629f treatment of, 628, 630f Iliotibial band tenodesis, in pediatric ACL injury, 1680 Ilium, 1452 Imaging. See specific imaging modalities Immobilization, 77t cartilage effects of, 228 in cervical spine injury, 666–667, 666f glycosaminoglycans effects of, 228 tendon effects of, 25–26, 26f, 28 in thoracolumbar spine injury, 720 Immune system cartilage allograft and, 54 exercise effect on, 147–148, 148f, 148t Immunoglobulin A, secretory, exercise effects on, 147, 148t Immunoglobulin G, in Epstein-Barr virus infection, 150 Immunotherapy, in epilepsy, 190 Impetigo, 193–194, 193f–194f, 194t Impingement. See Ankle impingement; Femoroacetabular impingement; Shoulder impingement Impingement test, 998 Implant chondrocyte, 55, 1774–1780, 1777t, 1780f, 1785t collagen, 39 infection with, 394–395, 394f, 394t Implantable defibrillator, in sudden death prevention, 169–170 Incidence, 102, 102t, 103, 2219 Indapamide, in hypertension, 160t Indirect calorimetry, 212–213, 212f Indomethacin in heterotopic ossification, 1294 in tendon healing, 29 Infection, 147–156. See also specific infections allograft transmission of, 141–142, 1657 anterior cruciate ligament graft, 391–393, 393b, 393t, 1657 blood-borne, 153–156 bone. See Osteomyelitis Borrelia burgdorferi, 155–156 cardiac, 151–152 cutaneous, 193–200 bacterial, 193–196, 193f–194f, 194t clearance for participation and, 513 fungal, 198–200, 198f–200f, 200t return-to-play guidelines for, 195t viral, 196–198, 197f–198f epidemiology of, 149 Epstein-Barr virus, 150–151 gastrointestinal, 152 hardware-related, 394–395, 394f, 394t hepatitis, 154–155 human immunodeficiency virus, 153–154 intestinal, 152 after knee dislocation treatment, 1765 pericardial, 152 respiratory, 149–150 return to play after, 150 risk for J-curve theory of, 148, 148f reduction of, 148 shoulder, 389–391, 390f, 391t, 392f Staphylococcus aureus, 395–397, 396b, 396f methicillin-resistant, 193, 194–195, 194t, 195f, 395–397, 396b, 396f prevention of, 396–397

Infection (Continued) superficial, 387–388, 387f, 389f toenail. See Ingrown toenail treatment of, 386–387, 387t unusual, 397–398, 398t urinary tract, 152–153 Infectious mononucleosis, 149, 151 Inference, 99, 112 Inferior lateral genicular artery, 1723 Inferior peroneal retinaculum, 1987 Infertility, anabolic-androgenic steroids and, 416 Inflammation in complex regional pain syndrome, 354–355 cutaneous, 204–205, 204f–205f in delayed-onset muscle soreness, 216 electrical current therapy in, 230, 231f in ligament healing, 34–35 in tendon healing, 27–28 Infrapatellar tendon injury, 560, 561f Infraspinatus anatomy of, 770–771, 770f, 911, 989, 989f, 1035t pediatric, 785, 785f atrophy of, 770 fatty infiltration of, 989, 989f function of, 991 humeral attachment of, 1070–1071, 1071f scapular attachment of, 859f, 886f strengthening exercises for, 242–243, 242f–243f Ingrown toenail, 2096–2104 anatomy of, 2096–2097, 2096b, 2097f classification of, 2097, 2097b evaluation of, 2097–2098, 2098b history in, 2097 imaging in, 2098 nonoperative treatment of, 2098, 2098f–2099f operative treatment of, 2098–2105, 2098b alcohol matrixectomy in, 2099–2100 care after, 2101–2102 complete nail plate avulsion in, 2099, 2101f complete onychectomy in, 2099, 2103f complications of, 2100–2101 partial nail plate avulsion in, 2099, 2100f partial onychectomy in, 2099, 2102f phenol matrixectomy in, 2099–2100, 2105f plastic nail wall reduction in, 2099, 2101f return to play after, 2102–2103, 2105b Syme amputation in, 2099, 2104f physical examination in, 2098, 2098b Inhalant use/abuse, 429–430 Injury, 431–441. See also specific structures and injuries cognitive response to, 436–437 coping skills in, 435–436 depression and, 453 disruptive impact of, 435 emotional nourishment in, 435 in older athlete, 433 prevalence of, 432–433 psychological response to, 431–432, 433–436 three-foci contextual considerations in, 434–435 treatment team in, 436 Innominate bone, 1451–1452 Insall-Salvati ratio, 1522, 1523f, 1539, 1541f in patellar rupture, 1522–1523, 1523f Insomnia, 447–448, 448b Insulin, 176–178, 176t, 177b, 177t, 178f excessive, exercise and, 174–175, 174b exercise effects on, 217t, 218 insufficient, exercise and, 175, 175f physiology of, 173–175, 174f


xxv

Insulin-like growth factor–1, 20, 419–420 Insulin pump, 178, 178b, 178f Intercalary segmental instability dorsal (DISI), 1322, 1323f volar (VISI), 1322, 1324f Interclavicular ligament, 793, 793f International Knee Documentation Committee, subjective rating form of, 301 Interosseous talocalcaneal ligament, 1913f heterotopic ossification of, 1933 reconstruction of, 1951, 1951f Interphalangeal joint distal, dislocation of, 1384, 1386, 1418–1420, 1419f proximal anatomy of, 1381–1382, 1382f dislocation of, 1381–1384 in children, 1417–1418, 1417f–1418f classification of, 1382, 1382f clinical presentation of, 1382 complex dorsal, 1383, 1383f dorsal, 1382–1383, 1417–1418, 1417f, 1418f fracture with, 1383, 1383f–1385f palmar, 1384 treatment of, 1382–1384 type I, 1382 type II, 1383, 1383f type III, 1383, 1383f–1385f volar, 1384, 1386f, 1417–1418, 1417f fracture-dislocation of, 1383, 1383f–1385f fracture-subluxation of, 1383–1384, 1385f sprain of, pediatric, 1414 subluxation of fracture with, 1383–1384, 1385f palmar, 1384 volar, 1384 Interquartile range, 112 Intersection syndrome, 624–625, 1356 Intertubercular groove, pediatric, 783 Interventional procedures, imaging for, 582–586 at peripheral joints, 582–584, 584f at spine, 584–585, 584f–585f Intervertebral disk biomechanics of, 718–719 cervical spine herniation of, 674, 698–699, 699f in children/adolescents, 704 injury to, 674, 698–699, 699f rupture of, 674, 678 lumbar, 717, 718–719. See also Lumbar spine, degenerative disk disease of herniation of, 741–744, 744f, 751f, 752 in children/adolescents, 764–766, 765f, 767–768, 767b thoracic anatomy of, 717, 717f biomechanics of, 718–719 herniation of, 738, 739f, 755–756 Intra-articular disk ligament, 792–793, 792f–793f Intracerebral hematoma, 660–661, 661f Intraclass correlation coefficient, 100, 118 Intracranial hemorrhage, 659, 660–661, 661f Intramedullary nailing in proximal humeral fracture, 1043, 1045–1046, 1047f in proximal metaphyseal humeral fracture, 1088, 1088f–1089f in proximal physeal humeral fracture, 1078, 1080f in tibial stress fracture, 1854–1855 Intubation, endotracheal, 519 Iontophoresis, 233–234, 235f in plantar fasciitis, 2049

xxvi

Index

Irbesartan, in hypertension, 160t Iron deficiency of, in female athlete, 478–479, 479b requirements for, 406b Irrigation, during arthroscopy, 122, 123f Ischial bursitis, 1457 Ischial tuberosity, avulsion fracture of, 1475 Ischiofemoral ligament, 1452, 1453f Ischium, avulsion fracture of, 1489, 1489f Iselin’s disease, 2143f, 2167–2169, 2168f–2169f Isotretinoin, in acne, 205 Isradipine, in hypertension, 160t Itraconazole, in dermatophyte infection, 200t

J J sign, in patella dislocation, 1556 Jaw thrust maneuver, in cervical spine injury, 667, 668f Jefferson fracture, 677, 677f–678f, 705, 706f Jerk test, in glenohumeral joint instability, 941 Jersey finger, 1390–1392 classification of, 1390 neglected, 1391–1392 pediatric, 1424–1428, 1424f–1427f physical examination in, 1390 treatment of, 1391, 1391f Jet lag, 457–460, 458f adjustment avoidance and, 460 bright light exposure and, 458, 458f melatonin and, 459–460 performance and, 460 room light and, 458–459, 459t–460t Jobe’s relocation test in glenohumeral joint instability, 914, 915f, 939, 939f in glenohumeral joint osteoarthritis, 1108 in rotator cuff disorders, 996, 999f Jogger’s foot, 2053 Joint(s). See also specific joints motion at, 90, 93f, 2178–2182, 2178f preparticipation examination of, 512–513 Joint capsule, glenohumeral, 772–773, 772f Joint reaction force, 86, 89f. See also Patellofemoral joint reaction force Jones’ fracture, 1969–1970, 1971f, 2025–2027, 2026f, 2027f Jones (tendon-sling) procedure, 1994–1995, 1994f Juggling, time of day and, 457 Jugular vein, 794, 797f Juices, 401 Jumper’s knee, 30, 31, 626–627, 626f evaluation of, 1518–1519 imaging in, 560, 561f, 1519, 1519f–1520f pathophysiology of, 1515–1518, 1517f–1518t stages of, 1519 treatment of, 1519–1521, 1520f Jumping exercise, double-leg, in knee rehabilitation, 296, 298f Juvenile idiopathic arthritis, 602–603, 602f

K Karolinska Sleepiness Scale, 450 Kehr’s sign, 526 Keller procedure, in hallux valgus, 2072, 2075 Kelly’s bone block procedure, 1993, 1993f Keratan sulfate, 43f, 44 Keratolysis, pitted, 196, 196f Ketamine, in complex regional pain syndrome, 364

Ketoconazole, in dermatophyte infection, 200t Kicking, dynamic analysis of, 90, 91f Kidner’s procedure, 2164, 2165, 2165f Kidneys absence of, 514t congenital anomalies of, 712, 712f hypothermia effects on, 501 on-field injury to, 527 Kienböck’s disease adult, 1350, 1353f pediatric, 1376–1377, 1377b, 1378f Kinematics, 90 acromioclavicular joint, 775–776, 776f, 786–787 angular, 90, 91f glenohumeral joint, 777–778, 787–788, 787f–788f linear, 90, 91f scapulothoracic joint, 776–777, 776f, 787–788, 788f sternoclavicular joint, 775, 775f, 786 Kinetic chain, 221–222 Kinetic chain exercise after ACL reconstruction, 232, 232f, 1668–1670, 1669f, 1669t upper extremity, 232, 232f Kinetic muscle testing, in thoracolumbar spine, 728 Kinetics, 90–91 Kleinman’s shear test, 1330–1331 Klippel-Feil syndrome, 693, 693f, 711–712, 712f Knee. See also Patella anatomy of, 1548–1553, 1579 bony, 1549–1550, 1549f–1550f, 1747–1748 dynamic restraints in, 1548, 1548f lateral, 1718–1723, 1719f–1722f ligamentous, 1551–1553, 1551f–1553t, 1748 medial, 1624–1627, 1624f–1626f, 1638, 1638b posterolateral, 1718–1723, 1722f neurovascular, 1748–1749 posteromedial corner, 1625, 1627f soft tissue, 1550–1553, 1551f static restraints in, 1548, 1548f arthroplasty for. See Knee arthroplasty arthroscopy of. See Arthroscopy, knee biomechanics of, 1579–1596, 1747 bumper model of, 1580 compound hinge model of, 1580, 1581f experimental studies of, 1581 femoral epicondylar axis in, 1581 four-bar cruciate linkage model of, 1580, 1580f ligament, 1581–1589, 1583f, 1586f, 1587t. See also at specific ligaments mathematical model of, 1580 meniscal, 1589–1591. See also at Meniscus (menisci) models of, 1580–1581, 1580f–1581f patellofemoral, 1591–1596, 1592f–1595f rotation, 1579–1580, 1579f shear forces during, 222 three-dimensional tibiofemoral joint model of, 1580–1581 translation, 1579–1580, 1579f cartilage lesions of, 1771–1786 classification of, 1772, 1772t, 2212, 2212t clinical presentation of, 1773 débridement for, 1774 etiology of, 1771–1772 history in, 1773 imaging in, 1773, 1773f–1774f marrow stimulation techniques for, 1774 nonoperative treatment in, 1773–1774


Knee (Continued) operative treatment in, 1774–1786 age and, 1786 algorithm for, 1778f autologous chondrocyte implantation for, 1774–1775, 1777, 1777t, 1778–1780, 1780f, 1785t complications of, 1783 contraindication to, 1786 gene therapy for, 1776 growth factors for, 1776 matrix-associated techniques for, 1775–1776 microfracture for, 1776, 1777–1778, 1779f, 1784t osteochondral allograft transplantation for, 1775, 1777, 1777t, 1781–1783, 1782f, 1784t osteochondral autograft transplantation for, 1775, 1777, 1780–1781, 1781f, 1784t outcomes of, 1783 rehabilitation after, 1783, 1784t–1785t return to play after, 1786 stem cells for, 1776 synthetic plugs for, 1776 tissue-engineered cartilage for, 1776 physical examination in, 1773 chondral lesions of. See Knee, cartilage lesions of chondromalacia of, 579, 580f–581f computed tomography arthrography of, 536, 537f cysts of, 537–538, 538f deep complex of. See Arcuate ligament; Popliteus tendon dislocation of. See Knee dislocation effusion of, in patellar dislocation, 1556 Fairbank’s changes of, 2211–2212, 2211t jumper’s. See Patellar tendinosis ligaments of. See Anterior cruciate ligament (ACL); Fibular (lateral) collateral ligament (FCL); Medial collateral ligament (MCL); Popliteofibular ligament; Posterior cruciate ligament (PCL) magnetic resonance arthrography of, 536 menisci of. See Meniscus (menisci) motions of, 1579–1580, 1579f. See also Knee, biomechanics of multiligament injury to. See Knee dislocation osteochondritis dissecans of. See Osteochondritis dissecans, patellar overuse injury of, 626–628, 626f, 629f pain in, after tibial stress fracture treatment, 1855 physeal fracture of, 595, 595f, 1640–1644, 1640b distal femur, 1641–1642, 1642b, 1642f, 1643f proximal tibia, 1642–1644, 1643f, 1643t popliteal (Baker’s) cyst of, 537–538, 538f posterolateral corner of. See Posterolateral corner proprioceptive function in, 294. See also Knee rehabilitation, proprioceptive exercises in prosthetic. See Knee arthroplasty radiography of, 2211–2212, 2211t rehabilitation of. See Knee rehabilitation replacement of. See Arthroplasty, knee rotation of, 1579–1580, 1579f stretching exercises for, 292–293, 292f translation of, 1579–1580, 1579f ultrasonography of, 537–538, 538f varus-aligned, 1801–1803, 1802t, 1803f. See also Varus malalignment

Index Knee arthroplasty, 1787–1801 athletic activity after, 1787–1789, 1789b clinical evaluation for, 1789–1790 imaging for, 1789–1790, 1790f mobile-bearing prostheses in, 1797–1798 vs. nonoperative treatment, 1790–1792 patient history and, 1789 physical examination in, 1789 quadriceps rupture with, 1521 total, 1794–1797, 1795t–1797f bearing surfaces in, 1800 gender-specific, 1799 high-flexion, 1798–1799, 1798f–1799f indications for, 1794 minimally invasive, 1799–1800, 1800f prior proximal tibial osteotomy and, 1792 results of, 1795, 1795t unicompartmental, 1792–1794, 1793f Knee dislocation, 1747–1764 bony injury with, 1752–1753, 1752f classification of, 1749, 1749t clinical presentation of, 1749 imaging of, 1753, 1753f inspection in, 1750, 1750f Lachman test in, 1750, 1750f nerve injury with, 1751–1752, 1752f neurovascular examination in, 1750 nonoperative treatment of, 1753–1754, 1754f operative treatment of, 1754–1765, 1762b ACL reconstruction in, 1758, 1759f, 1760b Arthrotek tensioning boot in, 1760, 1761f, 1762 without Arthrotek tensioning boot, 1761–1762 compartment syndrome after, 1765 complications of, 1764–1765 fixation technique in, 1760, 1761b graft selection for, 1755, 1757 infection after, 1765 instability after, 1765 nerve injury with, 1764–1765 vs. nonoperative, 1754–1755 platelet-rich fibrin matrix clot in, 1763, 1763f position for, 1757, 1757f posterior cruciate ligament reconstruction in, 1755–1756, 1758, 1759f, 1762–1763, 1763f posterolateral reconstruction in, 1758–1759, 1760f preparation for, 1757, 1758f rehabilitation after, 1756, 1763–1764, 1764b results of, 1761–1762 return to play after, 1765 stiffness after, 1765 timing of, 1755, 1756–1757, 1757f vascular injury with, 1764–1765 physical examination in, 1749–1750, 1750f vascular injury with, 1750, 1751, 1753, 1753f, 1764–1765 Knee rehabilitation, 221–222, 222t adhesions and, 225 arthrofibrosis and, 225 articular cartilage protection in, 225–228, 226f–227f biofeedback in, 224–225, 233, 233f ERMI Flexionator in, 225, 225f gait pattern in, 225 kinetic chain in, 221–222, 222t muscle inhibition and, 224–225 neuromuscular stimulation in, 231, 231f, 232–233, 232f–234f patellar mechanics in, 226–228, 226f–227f patellofemoral joint reaction forces and, 226, 226f, 1595–1596, 1595f proprioceptive exercises in, 294–296

Knee rehabilitation (Continued) cone ambulation, 295, 296f cone reaching, 296, 297f double-leg jumping, 296, 298f lunging, 296, 297f plyoball toss, 294, 294f side-to-side weight shifting, 294–295, 295f single-leg hopping, 296, 298f sports cord lunges, 296, 297f return-to-play phase of, 300–321 criteria for, 301–303, 302f stage I, 303–307, 304f–306f stage II, 307–310, 308f–312f stage III, 312–316, 313f–314f, 316f stage IV, 316–320, 317f–320f return-to-play plyometric training in, 300–321 contraindications to, 303 criteria for, 301–303, 302f glossary for, 324–330 stage I (dynamic stabilization and strengthening), 303–307, 304f–306f, 322 stage II (functional strength), 307–312, 308f–312f, 322–323 stage III (power development), 312–316, 313f–314f, 316f, 323 stage IV (sport performance), 316–320, 317f–320f, 324 therapeutic exercise for, 255–272 ACL loading with, 221–222, 222t ACL strain measurements in, 1586–1588, 1586f, 1587t acute phase of, 255 advanced phase of, 255 band walking, 258, 259f gluteal muscle raise in, 267, 268f gluteal musculature, 257–258, 258f–259f hamstring curls in, 266 hamstring raise in, 267, 268f hip abduction, 258, 258f hip extension in, 258, 258f, 267 hyperextension in, 267 kinetic chain, 1668–1670, 1669f, 1669t leg extension, 227–228, 227f leg press, 227, 227f, 259–260, 260f ligament unloading, 222–224, 223t, 224f lunges in, 264–266, 265f, 266f manual perturbation training in, 270–271, 271f multiplanar squats in, 270, 270f neuromuscular activation, 256–258 neuromuscular control training in, 268–270, 269t, 270f PCL loading with, 221–222, 222t program design for, 255–256 proprioceptive training in, 268–270, 269t, 270f quadriceps, 256–257, 257f quadriceps dominant squatting, 258–263, 260f–263f return-to-activity phase of, 256 Romanian deadlift in, 267–268, 269f single-leg balance training in, 271 single-leg presses in, 263, 264f single-leg Romanian deadlift in, 268, 269f single-leg strength training in, 263–266, 264f–265f single-leg wall squats in, 264, 265f slide board leg curls in, 266–267, 267f sport cord activities in, 271, 272f, 296, 297f squat and reach in, 270, 271f squats in, 258–259, 260–263, 261f–263f stability ball bridges in, 266, 267f stability ball curls in, 266–267, 267f


xxvii

Knee rehabilitation (Continued) step-ups in, 264, 264f straight leg, 267–268 subacute phase of, 255 Total Gym in, 259–260, 260f unstable surface training in, 271, 272f wall squats in, 260, 260f, 264, 265f transcutaneous electrical nerve stimulation in, 229–230, 230f, 233, 233f Knot/knot tying, 135–136, 135f Duncan loop, 135, 135f Nicky’s, 135, 135f Roeder’s, 135, 135f for shoulder arthroscopy, 1147, 1148f for SLAP lesion repair, 1028, 1030–1031, 1030f, 1031f KOH testing, 198, 200f Köhler’s disease, 599, 1972–1973, 1973f, 2143f, 2162, 2163f Krebs’ cycle, 211–212 KT-100 arthrometry in anterior cruciate ligament injury, 1650, 1652 in posterior cruciate ligament injury, 1692–1693 Kyphoplasty, lumbar, 585, 585f Kyphosis, 736–737 classification of, 737 Scheuermann’s, 737 thoracic, 718

L Labetalol, in hypertension, 160t Laceration cartilage, 50 muscle, 11, 11f skin, 201–202 Lachman test in anterior cruciate ligament injury, 1585–1586, 1649–1650, 2213 in knee dislocation, 1750, 1750f in meniscal injury, 1602 Lactate, high-altitude effects on, 503 Lactate threshold, 211, 218 Lactic acid, creatine buffering of, 418 Lamotrigine, in epilepsy, 189, 191t Landau-Kleffner syndrome, 190 Larva migrans, 201, 202f Larynx, on-field injury to, 525 Lasègue’s sign in lumbar disk herniation, 743 in thoracolumbar spine injury, 722 Laser therapy contraindications to, 236 in rehabilitation, 235–236, 236f Lateral collateral ligament. See Fibular (lateral) collateral ligament (FCL) Lateral femoral cutaneous nerve, 1454, 1455f entrapment of, 1469 Lateral flexion progression exercise, in core training, 283–284, 284f Lateral gastrocnemius tendon, 1719f, 1723 Lateral genicular artery, 1723 Lateral patellofemoral ligament, 1552 Lateral pull test, in patellar dislocation, 1557, 1557f Latissimus dorsi muscle, 771 actions of, 907 anatomy of, 907, 1034, 1035t, 1065 pediatric, 785 contusion of, 1065 functional training of, in core training, 286 press-up exercise for, 241, 242f

xxviii

Index

Latissimus dorsi muscle (Continued) rupture of, 907–908, 907b–908b, 1065 scapular attachment of, 859f, 886f strain of, 1065 strengthening exercise for, 1003, 1006f Latissimus dorsi tendon injury, 1065 Learning naps and, 449, 449f sleep deprivation and, 449–450 Left ventricular hypertrophy, athletic participation guidelines for, 161 Leg extension exercise, patellar effects of, 227–228, 227f Leg-length inequality after epiphyseal fracture, 1643–1644 stress fracture and, 632 Leg press exercise in knee rehabilitation, 259–260, 260f patellar effects of, 227, 227f single-leg, in knee rehabilitation, 263, 264f Legal issues, 531 Legg-Calvé-Perthes disease, 599, 600f, 1476–1477 Lennox-Gastaut syndrome, 189 Leptospirosis, 152 Lesser trochanter, avulsion fracture of, 1475 Leukemia, magnetic resonance imaging in, 610 Leukocytes, radiolabeled, in osteomyelitis, 547 Leukoplakia, smokeless tobacco and, 428 Leukotriene modifiers, in exercise-induced bronchospasm, 182 Levator scapulae pediatric, 786, 786f scapular attachment of, 859f, 886f Levetiracetam, in epilepsy, 191t Liability, 531 Lice, 200–201, 201f Lidocaine, in complex regional pain syndrome, 364 Lidocaine injection test, in thoracic outlet syndrome, 1133 Lift-off test, in subscapularis evaluation, 1065 Ligament(s), 32–39. See also specific ligaments cells of, 33–34 collagen of, 32–33, 34 elastin of, 34 fibroblasts of, 35 grading of, 2212, 2212t, 2214, 2214t healing of, 34–39 allografts in, 38, 142–143 autografts in, 36–38 collagen implants in, 39 Dacron augmentation in, 36 grafts in, 35–39 inflammation in, 34–35 remodeling in, 35 tissue engineering in, 39 variables in, 35 xenografts in, 38 insertions of, 33 magnetic resonance imaging of, 569, 571–576 at ankle, 571, 573, 573f at elbow, 576, 577f at knee, 569, 571, 571f–573f at shoulder, 573, 575, 575f at wrist, 575, 575f matrix of, 34 noncollagenous proteins of, 34 proteoglycans of, 34 remodeling of, 35 structure of, 32 types of, 32 water of, 34 Ligament of Testut, 1320, 1432, 1432f Ligament unloading exercise, 222–224, 223t

Ligamentum teres, 1452, 1453 rupture of, 1472–1473, 1473f Light-touch testing, in thoracolumbar spine injury, 722, 722f Linear regression, 113, 113f Link protein, meniscal, 58 Linoleic acid, conjugated, 409 Lisfranc joint, 1956, 1956f. See also Lisfranc sprain computed tomography of, 542–543 fracture-dislocation of, 1955, 2180, 2181f Lisfranc sprain, 1955–1960 anatomy of, 1956, 1956f computed tomography in, 1957, 1957f evaluation of, 1956, 1957f history in, 1956 magnetic resonance imaging in, 1957 physical examination in, 1956, 1957f radiography in, 1956–1957, 1957f rehabilitation after, 1958–1960 return to play after, 1960 treatment of, 1957–1958, 1959f Lisinopril, 160t Little Leaguer’s elbow, 468, 469f, 597, 1234–1235, 1238–1239 clinical manifestations of, 1236, 1236f complications of, 1186 diagnosis of, 1183, 1183b, 1184f–1185f, 1235 history in, 1234–1235 pain in, 1235 past medical history in, 1235 prevention of, 623–624 treatment of, 623, 1183–1185, 1183b, 1184f, 1185f, 1237 Little Leaguer’s shoulder, 468, 468f, 634–635, 635f, 1090–1093, 1172–1175 anatomy of, 1172–1173 classification of, 1173, 1173t complications of, 1175 evaluation of, 1091–1092, 1093b, 1093f, 1173, 1173b, 1174f prevention of, 1175 return to play in, 1175 treatment of, 1092, 1173–1175 Liver anabolic-androgenic steroid effects on, 416–417 on-field injury to, 527 Liver function test, in infectious mononucleosis, 150 Load and shift test in glenohumeral joint instability, 914–915 in rotator cuff disorders, 996, 999f Load-elongation curve, 93, 94f, 95–96, 95f Log-linear analysis, 114 Logistic regression, 113–114, 114f Logroll, 519, 519f in cervical spine injury, 666–667, 666f Long arc quad exercise, in knee rehabilitation, 257 Long QT syndrome, 166–167 β-adrenergic blockers in, 170 Long thoracic nerve anatomy of, 1125, 1125f injury to, 1130–1131, 1130f�� –�� 1131f Loose bodies of elbow, 470f, 621–622 of hip, 1472, 1472f of wrist, 1447 Lordosis, 718 Losartan, 160t Low back pain. See also Lumbar spine, degenerative disk disease of. Thoracolumbar spine injury in athlete, 741 in child/adolescent, 756–757, 757f, 765, 766


Low back pain (Continued) cold therapy in, 731 diagnostic injection in, 731–732, 731t heat therapy in, 731 lumbar spine stabilization in, 728–730, 730f muscle spasm and, 733 muscle strain and, 733 pharmacologic treatment of, 731 trigger point injection in, 732 tumor and, 757, 758f Low-molecular-weight heparin in venous thromboembolism, 384–385, 384t in venous thromboembolism prevention, 378–384, 381t, 382f Lumbar kyphoplasty, 585, 585f Lumbar spine. See also Thoracolumbar spine anatomy of, 717, 724–726, 725f, 754–755 computed tomography of, 541, 541f, 727 degenerative disk disease of, 740–744, 740f annular tear in, 740–741 athletic factors in, 741 in children/adolescents, 764–766, 765f, 767–768, 767b conservative treatment of, 743 evaluation of, 740, 740f, 743 facet joint in, 741 herniation in, 741–744, 744f, 751f, 752 pathophysiology of, 740, 740f return to play and, 744, 744f surgery for, 741, 742f, 744 diskography of, 728 fracture of, 733–736, 733f, 735f burst, 541f, 735, 735f compression, 546, 547f transverse process, 734 injury to. See Thoracolumbar spine injury ligaments of, 717 lordosis of, 718 magnetic resonance imaging of, 727, 727f muscles of, 717 radiography of, 724–726, 725f radionuclide imaging of, 726–727, 726f scoliosis of, 737 spondylolisthesis of degenerative, 747–748, 748t, 752 isthmic, 748–750, 748t, 749f–750f, 752 spondylolysis of, 725, 726f sprain of, 733 stenosis of, 744–748, 744b, 745t, 746f central, 744, 745 congenital, 746–747, 747f–748f conservative treatment of, 746 imaging in, 746 lateral, 744 physical examination in, 746 surgery for, 746, 747f strain of, 733 stress fracture of, 635–636, 636f–637f transverse process fracture of, 734 zygapophyseal joints of, 718, 719f Lumbar spine stabilization, 728–730, 730f Lumbosacral plexus, 1453 Lunate anatomy of, 1319–1320, 1319f dislocation of adult, 1322, 1323f pediatric, 1371 fracture of adult, 1350, 1353f pediatric, 1370, 1370f Lunges, 264–266, 265f, 296, 297f lateral, 266, 266f, 328 reverse, 265 static, 265, 265f walking, 266, 330

Index Lungs exercise effect on, 220 preparticipation examination of, 512, 515t Lunotriquetral arthrodesis, 1331, 1331f Lunotriquetral ligament, 1320 injury to, 1330–1331, 1331f Lyme disease, 155–156 Lymphatics, lower extremity, 1453 Lymphoma, 77t spinal, 757, 758f

M M line, 4f, 5, 6f Ma huang, 409 Macrophages in delayed-onset muscle soreness, 216 exercise effects on, 147, 148t Magnesium deficiency of, 12 requirements for, 406b Magnetic resonance angiography in knee dislocation, 1753 in popliteal artery entrapment, 1840, 1842f in vascular shoulder injury, 1139 Magnetic resonance arthrography (MRA), 550–551, 551f in age-related rotator cuff lesions, 974–975, 975f in ALPSA lesion, 974, 974f of ankle, 537, 551 in Bankart lesion, 973–974, 973f, 974t in biceps tendinopathy, 981, 981f of Buford complex, 972, 972f of elbow, 551 in GLAD lesion, 976, 978f of glenohumeral joint, 949 in glenohumeral joint instability, 969–975, 970f–974f, 974t, 975f of glenohumeral ligaments, 573, 575, 575f of glenoid labrum, 969–971, 970f in glenoid labrum cyst, 580–581, 582f of hip, 536–537, 551 of inferior glenohumeral ligament, 971, 971f of knee, 536, 551 of middle glenohumeral ligament, 971, 972f in multidirectional glenohumeral instability, 973 in post-traumatic anterior glenohumeral instability, 973–974, 973f–974f, 974t in posterosuperior glenoid impingement, 978–979, 979f in rotator cuff tear, 565–566, 567f of shoulder, 535, 536, 536f, 551 in SLAP lesion, 976, 977f of sublabral foramen, 972, 972f of sublabral recess, 970f, 972 of superior glenohumeral ligament, 971–972, 973f of wrist, 536 in wrist injury, 1321 Magnetic resonance imaging (MRI), 533, 547–552 in acetabular labrum tear, 581–582, 1470 of Achilles tendon, 2034, 2034f in Achilles tendon injury, 563, 565f, 630, 2003 in acromioclavicular osteoarthritis, 956, 959f of acromion, 955–956, 956f–957f in adductor strain, 1490–1491, 1491f in adhesive capsulitis, 967, 967t, 968f in ankle dislocation, 1945 in ankle impingement, 2157, 2157f in ankle sprain, 571, 573, 574f, 1920, 1921f, 1937, 1942, 1943f

Magnetic resonance imaging (MRI) (Continued) in anterior cruciate ligament injury, 553, 557f, 569, 571f, 572f, 1650–1651, 1653–1654, 1654t in anterior tibial tendon tear, 560, 562f in avulsion injury, 553, 557f of biceps tendon, 980–983, 981f, 982f in biceps tendon rupture, 1165 in biceps tendon tear, 566, 568f in bifurcate sprain, 1954 in calcaneal stress fracture, 556f, 646, 647f in calcific supraspinatus tendinopathy, 566, 567f in calcific tendinitis, 963, 963f in capitellar osteochondritis dissecans, 1241–1242, 1242f in cartilage injury, 576–582, 578f at hip, 581–582 at knee, 579–580, 579f–581f at shoulder, 580–581, 582f–583f in cervical intervertebral disk injury, 698–699, 699f in chondral defect, 1773, 1773f in chondromalacia, 579, 580f–581f in compartment syndrome, 651, 1859, 1859f in complex regional pain syndrome, 359 contrast agents for, 550–551, 551f of coracoacromial ligament, 956, 959f of coracohumeral distance, 956 in de Quervain’s tenosynovitis, 569, 570f in deltoid denervation atrophy, 965, 965f in denervation edema, 965, 965f, 980 in distal biceps tendon rupture, 1168, 1169f in distal biceps tendon tear, 566, 570f in distal femoral stress fracture, 555f of elbow, 1311 in elbow heterotopic ossification, 1293 fat suppression for, 550 in fatty rotator cuff infiltration, 989, 989f in femoral contusion, 1542, 1543f in femoral neck stress fracture, 554f, 639, 640f, 642f, 1465, 1465f in femoral shaft stress fracture, 1478, 1478t, 1479 in femoroacetabular impingement, 1471, 1472f in flexor hallucis longus tendon rupture, 563, 564f in frozen shoulder, 967, 967t, 968f of glenohumeral joint, 953, 953t, 954, 960t in glenohumeral joint instability, 916, 920f, 925f, 937, 938f in glenohumeral joint osteomyelitis, 984 in glenoid rim fracture, 870f gradient echo, 549 in hamate fracture, 1345, 1346f in hamstring rupture, 557, 558, 559f in hamstring strain, 1486f, 1487, 1487f in high (syndesmosis) ankle sprain, 1942, 1943f in humeral head avascular necrosis, 984, 985f in humeral metastases, 983, 983f in humeral shaft fracture, 1178, 1180f, 1182 in iliotibial band friction syndrome, 560, 562f, 628 image archiving for, 552 image quality in, 551–552 in intra-articular cartilage fragment in shoulder, 581, 583f inversion recovery, 549 in Kienböck’s disease, 1353f in knee arthritis, 1790 in knee dislocation, 1753 in lateral ankle sprain, 1920, 1921f in lateral epicondylitis, 566, 568f, 1199


xxix

Magnetic resonance imaging (MRI) (Continued) in lateral meniscal tear, 579, 579f of lateral meniscus, 1598f in Legg-Calvé-Perthes disease, 599, 600f in ligament injury, 569, 571–576 at ankle, 571, 573, 574f at elbow, 576, 577f at knee, 569, 571, 571f–573f at shoulder, 573, 575, 575f at wrist, 575, 576f in Lisfranc sprain, 1957 in lumbar disk herniation, 743 in lumbar isthmic spondylolisthesis, 749, 749f in lumbar kyphoplasty, 585, 585f of lumbar spine, 727, 727f in lumbar spine stenosis, 746 in malignant fibrous histiocytoma, 557, 560f in medial ankle sprain, 1937 in medial collateral ligament injury, 569, 571, 573f, 1629–1631, 1631f in medial malleolar stress fracture, 644–645, 645f in medial meniscal tear, 579, 580f in medial patellofemoral ligament disruption, 1542, 1542t in meniscal deficiency, 1619, 1619f in meniscal injury, 1601, 1602, 1603f in muscle contusion, 558 in muscle denervation, 558 in muscle injury, 557–558, 559f–560f in muscle strain, 16, 557, 559f in occult fracture, 552, 554f, 557 in olecranon bursitis, 1247 of os acromiale, 955–956, 958f in Osgood-Schlatter disease, 1527 in osteochondral fracture, 578–579, 578f in overhead throwing injury, 1217 in Panner’s disease, 625f in paralabral cyst, 964–965, 965f in Parsonage-Turner syndrome, 1145 in partial-thickness rotator cuff tear, 960–961, 961f in PASTA lesion, 961, 962f in patellar dislocation, 1541, 1542, 1542t, 1565–1566, 1565t–1566t in patellar osteochondritis dissecans, 1531 in patellar tendinopathy, 560, 561f of patellar tendon, 1519, 1519f, 1520f in patellofemoral tracking, 1565 in pectoralis major rupture, 902, 903f, 1060–1061, 1061f, 1163, 1164f pediatric, 590, 593f in avulsion fracture, 599 of bone, 591–592, 593f of cartilage, 593 in chondroblastoma, 604f, 605 in elbow injury, 469f, 1230 in Ewing’s sarcoma, 607, 609f, 610 in fracture, 593–596, 594f, 595f in giant cell tumor, 605, 605f in humeral fracture, 594, 594f in infection, 599, 601–603, 601f, 602f in leukemia, 610 in nonossifying fibroma, 605–606 in osteochondritis dissecans, 471f in osteochondroma, 606, 607f in osteochondroses, 599, 601f in osteoid osteoma, 603, 603f, 605 in osteomyelitis, 601, 601f in osteosarcoma, 606–607, 608f of physis, 592, 593f in posterior cruciate ligament injury, 1716 in slipped capital femoral epiphysis, 597, 598f

xxx

Index

Magnetic resonance imaging (MRI) (Continued) of soft tissues, 593 in thoracolumbar spine evaluation, 761–762 in peroneal brevis tendon tear, 560–561, 563f in peroneal tendinitis, 1989 physics of, 548–549 in pisiform fracture, 1352f in popliteal artery entrapment, 1840, 1841f–1842f in posterior cruciate ligament injury, 569, 572f, 1693 in posterior glenohumeral joint instability, 937, 938f in posterior tibial tendinitis, 1981 in posterior tibial tendon tear, 562, 563f in posterolateral corner injury, 1730, 1730f–1731f proton density images with, 550 pulse sequences for, 549–550 in quadriceps strain, 1494–1495, 1494f–1495f in quadriceps tendinopathy, 560 in quadriceps tendon rupture, 1523, 1524f in radial collateral ligament tear, 576, 577f in radial head fracture, 535f in recurrent anterior glenohumeral joint instability, 940, 940f in rhabdomyolysis, 558 of rotator cuff, 564–566, 566f–568f, 953, 953t, 958–965, 960t in rotator cuff cyst, 964–965, 964f in rotator cuff disorders, 1001, 1001f of rotator interval, 966, 966t, 967f in scaphoid fracture, 552, 554f, 1336, 1336f, 1365 in scaphoid nonunion, 1339–1341, 1341f in scapholunate ligament tear, 575, 576f in SLAP lesion, 581, 583f, 1025, 1026f in soft tissue tumor, 557–558, 560f spatial resolution in, 551–552 spin echo, 549 in spinal lymphoma, 758f in sternoclavicular joint injury, 804 STIR images with, 550 in stress fracture, 552–553, 554f–556f, 633, 634t in subcalcaneal heel pain, 2047 in subperiosteal abscess, 589f in subscapularis tendon tear, 963–964, 964f in subtalar sprain, 1950 in suprascapular nerve injury, 1121–1122, 1121f in supraspinatus fatty atrophy, 963, 963f, 980 in supraspinatus tendinopathy, 960, 960f T1-weighted, 549 T2-weighted, 549–550 in talar osteochondral lesions, 2144–2145, 2145t, 2147f in tendon injury, 558, 560–569 at ankle, 560–563, 562f, 563f, 564f, 565f at elbow, 566–567, 569f, 570f at knee, 560, 561f, 562f at shoulder, 564–566, 566f–568f at wrist, 568–569, 570f in thoracic disk herniation, 738 in thoracic outlet syndrome, 1133 in tibial stress fracture, 1852–1853, 1853f, 2015, 2016f in tibial tendon tear, 562, 563f in Tillaux fracture, 597, 598f in triangular fibrocartilage complex tear, 1436 in trochanteric bursitis, 1456, 1456f in turf toe, 2084, 2084f in ulnar collateral ligament injury, 576, 577f in valgus instability, 620 in wrist injury, 1321

Magnetic resonance neurography, in Parsonage-Turner syndrome, 1145 Magnetic resonance venography, in deep venous thrombosis, 376 Malingerer, 358 Malleolus, medial fracture of, 1969, 1969f stress fracture of, 644–645, 645f, 2016t, 2018, 2020f Mallet finger, 1388, 1420–1422, 1420f operative treatment of, 1420–1422, 1421f pediatric, 1407, 1407f–1408f Mallet thumb, 1401–1402 Mallet toe, 2118–2119, 2118t, 2119f, 2120b, 2128–2129 operative treatment of, 2121–2125, 2123f, 2124f Malocclusion, on-field, 525 Malunion proximal humeral fracture, 1049–1050 proximal physeal humeral fracture, 1082f, 1085 scaphoid fracture, 1368 Manual perturbation training in core training, 286, 287f in knee rehabilitation, 270–271, 271f Manual resistance training, in shoulder rehabilitation, 246, 248f Marathon running immune system effects of, 148 physician staffing of, 171 March fracture, 647 Marfan syndrome, 167 Marijuana use/abuse, 425–426 Marrow stimulation techniques. See also Microfracture in knee cartilage lesions, 1774 Mast cell stabilizers, in exercise-induced bronchospasm, 184 Matrixectomy, in ingrown toenail, 2099, 2101, 2102, 2105f McBride procedure, 2070, 2074b, 2075f, 2076, 2078, 2079f McMurray’s test, in meniscal injury, 1601 Mean, statistical, 112–113, 113f Medial collateral ligament (MCL) allograft with, in ligament injury, 38 anatomy of, 1624–1627, 1624f–1627f, 1748 biomechanics of, 1588–1589, 1625–1626 stabilizing function of, 1588–1589, 1625–1626 Medial collateral ligament (MCL) injury anterior cruciate ligament injury with, 1632–1633, 1633f, 1634–1635, 1634f, 1635f, 1636, 1653, 1654 anterior drawer test in, 1629, 1630t classification of, 1625, 1629t, 2216 complications of, 1637 evaluation of, 1627–1631 grade of, 1629, 1629t, 2214 history in, 1627–1628 magnetic resonance imaging in, 569, 571, 573f, 1629–1631, 1631f nonoperative treatment of, 1631–1632, 1636, 1637 palpation in, 1629 pediatric, 1638–1640 evaluation of, 1638–1639, 1638b grades of, 1639 imaging in, 1640 physical examination in, 1639, 1640b treatment of, 1640, 1640b physical examination in, 1628–1629, 1629t radiography in, 1629, 1630f rehabilitation in, 1636–1637, 1636t


Medial collateral ligament (MCL) injury (Continued) swelling in, 1629 treatment of, 1631–1635, 1633f in grade III injury, 1634–1635, 1634f–1635f nonoperative, 1631–1632, 1636–1637 rehabilitation after, 1636–1637 return to play after, 1637, 1637b valgus stress testing in, 1629, 1630t Medial patellofemoral ligament, 1551, 1551f, 1552 anatomy of, 1534–1536, 1535f, 1551, 1551f in patellar dislocation, 1535–1536, 1536f, 1541–1542, 1542t reconstruction of, 1569–1570, 1571t repair of, 1546 Medial patellomeniscal ligament, 1551, 1551f, 1552 Medial patellotibial ligament, 1551, 1551f, 1552 Medial tibial stress syndrome, 15, 545, 545f, 652, 652t, 1857. See also Chronic exertional compartment syndrome Median, statistical, 112 Median nerve anatomy of, 1159 injury to, 1359–1361 clinical manifestations of, 1360 at elbow, 1317–1318 electrodiagnostic study in, 1361 physical examination in, 1360 in supracondylar fracture, 1282 treatment of, 1360–1361, 1360f Medicolegal issues, 531 Melatonin dim light onset of, 457 in jet lag, 459–460 phase response curve to, 458–459, 459f sleep and, 457 Membrane stabilizers, in complex regional pain syndrome, 363t, 364 Memory declarative, 449 procedural, 449 sleep-related consolidation of, 449–450, 449f Meniscal arrow device, 1611–1612, 1611f Meniscal tear, 56–57, 62–64, 1596–1623 ACL injury and, 1653–1654, 1653t epidemiology of, 1601 rehabilitation for, 1672–1673 treatment of, 1605–1606, 1654, 1654t acute, 1603 Apley’s test in, 1601 arthroscopic examination in, 1602–1603 asymptomatic, 1601 bucket handle, 579, 580f, 1603–1604, 1603f classification of, 1603–1604, 1604f clinical presentation of, 1601 complex, 1604 degenerative, 1603, 1604f double PCL sign in, 1602 epidemiology of, 1600–1601 fascicular, 1613 grade I, 1602 grade II, 1602 grade III, 1602, 1603f historical perspective on, 1596–1597 horizontal, 1604, 1604f Lachman maneuver in, 1602 magnetic resonance imaging in, 579, 579f, 580f, 1602, 1603f McMurray’s test in, 1601 nonoperative treatment of, 1604–1605 oblique, 1604, 1604f

Index Meniscal tear (Continued) operative treatment of, 1605–1615 ACL injury and, 1605–1606, 1654, 1654t all-inside repair in, 1610–1613, 1611f–1612f, 1617 arthroscopic evaluation for, 1606, 1606f biologic enhancement techniques in, 1608 complications of, 1618–1619. See also Meniscus (menisci), deficiency of cyst and, 1613 discoid meniscus and, 1613–1615, 1614f–1615f equipment for, 1606 Fas-T-Fix device in, 1612–1613, 1612f, 1617 fascicular tears and, 1613 fibrin clot augmentation in, 1608 indications for, 1605 inside-out repair in, 1608–1610, 1609f, 1610f outcomes of, 1615–1617 outside-in repair in, 1610, 1611f rehabilitation after, 1618 repair in, 1607–1613 resection in, 1606–1607, 1607f. See also Meniscectomy return to play after, 1618 root avulsion and, 1613 trephination in, 1608 palpation examination in, 1601 patient history in, 1601 physical examination in, 1601–1602 pivot-shift test in, 1602 radial (transverse), 1604, 1604f radiography in, 1602 red-red, 1604 red-white, 1604 squat test in, 1602 terminology for, 1603–1604 vascular, 62–63 vertical/longitudinal, 1603–1604, 1604f white-white, 1604 zone classification of, 1604, 1604f Meniscectomy, 1606–1607, 1607f arthroscopic, 1606–1607, 1607f ACL biomechanics in, 1585–1586 in discoid meniscus, 1615 historical perspective on, 1589 instability after, 1590 load transmission and, 1589 meniscal deficiency after, 1619–1623 allograft transplantation for graft procurement for, 1620–1621 indications for, 1619–1620 outcomes of, 1622 technique of, 1621–1622, 1621f evaluation of, 1619, 1619f osteoarthritis and, 1772 outcomes of, 1615–1617 partial, 1606–1607, 1607f ACL biomechanics in, 1585–1586 biomechanics of, 1589 outcomes of, 1615–1617 Meniscofemoral ligaments, 1597–1598, 1685, 1686f accessory, 1597–1598, 1598f Meniscus (menisci), 56–65. See also Meniscal tear allograft, 1620–1622, 1621f anatomy of, 58–59, 58f–59f, 1597–1599 attachments of, 1597, 1598f tears of, 1613 biomechanics of, 59–61, 60f, 61f–62f, 1589–1591 load transmission and, 1589, 1599–1600

Meniscus (menisci) (Continued) stabilizing function and, 1590–1591, 1600, 1600f blood supply of, 61–62, 1599, 1599f cells of, 57 collagen of, 57, 57t, 58–59, 58f–59f composition of, 57–58, 57t compression of, 60–61, 62f creep of, 59 cysts of, 1613 deficiency of, 1619–1623 allograft transplantation for contraindications to, 1619–1620 graft procurement for, 1620–1621 indications for, 1619–1620 outcomes of, 1622 technique of, 1621–1622, 1621f evaluation of, 1619, 1619f discoid, 1613–1615 classification of, 1613–1614, 1614f examination of, 1614–1615, 1615f resection of, 1615 saucerization of, 1614–1615, 1615f Wrisberg ligament variant in, 1597–1598, 1614 elastin of, 58 embryology of, 1597 extracellular matrix of, 57–58, 57t fibrochondrocytes of, 1598–1599 functions of, 56, 1599–1600 healing of, 62–63 hoop stress in, 60 lateral anatomy of, 1597, 1598f attachments of, 1597, 1598f stabilizing function of, 1591–1592 load transmission through, 1589, 1599–1600 medial anatomy of, 1597, 1598f attachments of, 1597 stabilizing function of, 1590–1591 microstructure of, 1598–1599, 1599f microvasculature of, 1599, 1599f nerve supply of, 62, 1599 noncollagenous proteins of, 58 proteoglycans of, 58, 1599 radial tie fibers of, 59, 59f regeneration of, 63 repair of, 62–64, 1607–1613 all-inside, 1610–1613, 1611f, 1613f in avascular regions, 63–64 Fas-T-Fix device in, 1612–1613, 1612f fibrin clot augmentation with, 1608 grafts in, 63–64, 143–144 inside-out, 1608–1610, 1609f–1610f meniscal arrow device in, 1611–1612, 1611f outcomes of, 1616–1617 outside-in, 1610, 1611f trephination with, 1608 in vascular regions, 62–63 resection of. See Meniscectomy shear properties of, 61, 62f stabilizing function of, 1590–1591, 1600, 1600f stiffness of, 60, 61f, 1600 stress relaxation of, 59 structure of, 58–59, 58f–59f ultrastructure of, 61, 62f viscoelastic properties of, 59–60, 60f, 1600 water of, 57, 57t Menopause breast cancer and, 481 exercise and, 480–481, 481b Menstrual cycle, 445 ACL injury and, 1651


xxxi

Meralgia paresthetica, 1469 Metabolic rate, basal, 498 Metacarpal fracture adult, 1393–1394, 1393f–1395f oblique, 1394, 1395f transverse, 1394, 1395f pediatric, 1411–1414, 1411f–1413f Metacarpophalangeal joint anatomy of, 1380 dislocation of, 1379–1381 in children, 1415–1416, 1416f dorsal, 1380–1381, 1380f, 1381f volar, 1381 ligaments of, 1380 sagittal band rupture over, 1390 sprain of, in children, 1414–1415 thumb, dislocation of, 1398–1399 Metal dermatitis, 202, 203f Metastases, 74t, 77t humeral, 983, 983f radionuclide imaging in, 547, 547f Metatarsal(s) fifth base fracture of, 1933–1934, 2024–2025, 2026f diaphyseal fracture of, 1969–1970, 1971f, 2025–2027, 2026f–2027f stress fracture of, 648, 649f traction apophysitis of, 2167–2169, 2168f–2169f first combined multiple osteotomies in, 2071–2072, 2078f, 2079, 2080f plantar flexion of, 2108, 2109f fracture of, in children, 1969–1971, 1970f–1971f motion of, 2180, 2180f osteotomy of, 2111, 2111b, 2112f–2114f plantar flexion of, 2108, 2109f stress fracture of, 646–648, 648f, 2024–2030 base, 2027, 2028f basilar, 2027 flexibility and, 2182 malunion of, 2024 pediatric, 1970–1971 treatment of, 2016t, 2024–2030 Metatarsal break, 1870, 1871f Metatarsal head, osteochondrosis of, 599, 1973, 1973f, 2166–2167, 2167f, 2168t treatment of, 2166, 2168f Metatarsal osteotomy bunionette treatment with, 2135–2136, 2135b diaphyseal, 2135–2136, 2137, 2138b, 2139f, 2140f distal chevron, 2135–2136, 2135b, 2137b, 2138f distal oblique, 2135–2136, 2135b–2136b, 2136f–2137f hallux valgus treatment with, 2070–2071, 2076b, 2077f, 2078–2079 intractable plantar keratosis treatment with, 2111–2115, 2111b, 2112f–2114f Metatarsal pad, 2110, 2111f, 2121 Metatarsocuneiform joint, first, 2066, 2067f Metatarsophalangeal joint(s) first, 2082f. See also at Hallux anatomy of, 2064–2066, 2065f–2066f, 2081–2082, 2082b, 2180, 2181f arthrodesis of, 2075 biomechanics of, 2082, 2082f congruency of, 2066, 2067f dislocation of, 2084–2085, 2086f injury to. See Turf toe motion of, 2178–2179, 2179t

xxxii

Index

Metatarsophalangeal joint(s) (Continued) sesamoids of. See Sesamoid(s) subluxation of. See Hallux valgus impairment of, 1872 lesser. See also Toe(s), lesser anatomy of, 2115–2116, 2116f arthroplasty of, 2124, 2130f biomechanics of, 2115–2116, 2116f, 2180–2181, 2182f flexibility/inflexibility of, 2182 instability of, 2119, 2120b, 2120f medial deviation of, 2116, 2117f, 2119 treatment of, 2123–2124, 2128f plantar drawer test of, 2119, 2120f radiography of, 2121 release of, 2123–2124, 2125b, 2126f subluxation/dislocation of, 2116, 2119, 2120f treatment of, 2123–2124, 2125b, 2126f–2130f Methacrylate cement, fluoroscopy-guided injection of, 585, 585f Methandrostenolone, 411 Methicillin-resistant Staphylococcus aureus infection, 194–195, 195f, 395–396, 396b Methyldopa, 160t Methylprednisolone, in adhesive capsulitis, 1096, 1103b Metolazone, 160t Metoprolol, 160t Mexiletine, in complex regional pain syndrome, 364 MIBI (methoxyisobutyl isonitrile) perfusion scan, in compartment syndrome, 651 Microfracture, in knee cartilage lesions, 1776, 1777–1778, 1779f, 1784t Micronutrients, requirements for, 405–406, 406b Mile-high effect, 503–504 Milk-alkali syndrome, 77t Milligram test, in thoracolumbar spine injury, 722, 723f Miner’s elbow. See Olecranon bursitis Minoxidil, in hypertension, 160t Moccasin, 1873–1874 Mode, 112 Model building, 113–114 Moexipril, 160t Molluscum contagiosum, 197, 198f Monitored Rehab Systems Cable Column, 233, 233f, 296, 299f Monitored Rehab Systems Functional Squat, 224, 224f, 295–296, 297f Mono-Spot test, 150 Mononucleosis, 149, 151 Monster walk exercise, in knee rehabilitation, 258, 259f Monteggia fracture, 1259, 1260, 1260f, 1273, 1287 Mood anabolic-androgenic steroid effects on, 417 disorders of, sleep disorders and, 452–453 Morning alertness zone, 454, 455f Morningness-Eveningness Scale questionnaire, 456, 456f Morton’s neuroma, 2184, 2184f Moses’ sign, 374 Motion, joint, 90, 93f, 2178–2182, 2178f. See also Range of motion and at specific joints Motor system in complex regional pain syndrome, 357–358 in thoracolumbar spine injury, 722, 722t Motor unit, 209, 214, 216f adaptability of, 9 contractile properties of, 8–9, 9f

Motor unit (Continued) fast-twitch, 8 recruitment of, 8, 9f Hanneman principle of, 209 slow-twitch, 8 Mountain sickness, 504 Mouth leukoplakia of, smokeless tobacco and, 428 on-field injury to, 525 MRI. See Magnetic resonance imaging (MRI) Multiple baseline research design, 105, 105f Multiple endocrine neoplasia, 77t Multiple myeloma, 77t Multiple Sleep Latency Test, 450–451, 451f Muscle(s), 3–20, 207–213. See also specific muscles adaptability of, 9, 10–11, 19 aerobic capacity of, 212–213, 212f ATP-phosphocreatine system of, 210, 210f atrophy of, rehabilitation for, 224–225 carbohydrate metabolism of, 210f, 211 compensatory hypertrophy of, 10 contraction of, 5, 7–10, 8f–9f, 208–210, 209f concentric, 213, 213f eccentric, 213, 213f electrical current reeducation of, 230–233, 231f–233f force generation in, 7–8, 8f–9f isometric, 213 motor unit in, 8–9, 9f sarcoplasmic reticulum in, 5, 7f sliding filament model of, 5 contusion of, 13–14, 14f. See also Contusion cramps in, 11–12 creatine effects on, 418 cross-reinnervation of, 9–10 cross-sectional area of, 3, 5f delayed-onset soreness of, 12–13, 13f, 215–216 endurance training response of, 215, 216t energy metabolism of, 210–213, 210f exercise effects on, 10–11, 213–214, 214t, 215f fat metabolism of, 210f, 211 fatigue of, 19, 214 fibers of, 3, 4f, 5f, 207, 207t. See also Muscle fiber(s) function of, 3 glycolytic system of, 210–211, 210f growth hormone effects on, 419 hemorrhage within, 17–18, 18f hyperplasia of, 10, 214 hypertrophy of, 10, 214 injury to, 11–19. See also specific injuries and disorders response to, 11 intracompartmental pressure of increase in. See Chronic exertional compartment syndrome; Compartment syndrome measurement of, 14, 650–651, 1860, 1860t laceration of, 11, 11f magnetic resonance imaging of, 16, 557–558, 559f, 560f myofibrillar proteins of, 3–5, 5t, 6f, 11 one-joint, 3 oxidative system of, 210f, 211 physiology of, 7–11, 8f–9f protein metabolism of, 210f, 211–212 reflex effects in, 19 resistance training response of, 214–215, 216t sliding filament model of, 5 strain injury of, 15–16. See also at specific muscles active stretch and, 17, 17f


Muscle(s) (Continued) classification of, 1485, 1485t, 2214–2215, 2214t clinical studies of, 15–16, 17f computed tomography of, 16, 17f hemorrhage with, 17–18, 18f laboratory studies of, 16–18, 17f–18f magnetic resonance imaging of, 16, 558, 559f mechanism of, 15 vs. muscle soreness, 15 nondisruptive, 17–18, 18f passive stretch and, 17, 17f prevention of, 16, 19 structural changes with, 15–16, 17f treatment of, 16 stress relaxation of, 18, 19f structure of, 3–7, 4f–7f, 5t, 7t, 207–208, 208f tension-length curve for, 7–8, 8f tetanus of, 7–8, 8f training response of, 213–214, 214t, 215f tumors of, 558, 560f twitch of, 7–8, 8f two-joint, 3 ultrastructure of, 4f, 5, 6f in delayed-onset soreness, 12, 13f viscoelastic properties of, 18, 19f warm-up effects on, 19 Muscle fiber(s), 3, 4f, 5f, 207, 207t in athlete, 7, 10 exercise effects on, 10–11, 209–210 fast-twitch to slow-twitch transition in, 10–11 nuclei of, 5 type I, 5, 6–7, 7t, 207, 207t type II, 5, 6–7, 7t type IIA, 6, 7t, 207, 207t type IIB, 6, 7t, 207, 207t Musculocutaneous nerve, 1034, 1159 Musculotendinous unit, 3, 4f, 20. See also Muscle(s); Tendon(s) Mycobacterium infection, 397, 398, 398t Mycobacterium kansasii infection, 398, 398t Mycobacterium ulcerans infection, 397 Myocardial infarction, anabolic-androgenic steroids and, 416 Myocarditis, 151–152 sudden death and, 165–166, 166f Myocardium anabolic-androgenic steroid effects on, 416 contusion of, 526 inhalant effects on, 430 Myofibrillar proteins, 3–5, 5t Myosin, 3–4, 5t, 6f, 208, 209f ATPase of, 8–9, 9f Myositis, exertional, 496 Myositis ossificans, 13–14, 14f, 82, 1460 adductor, 1493 after proximal humeral fracture, 1050 quadriceps, 1483, 1484b, 1484f, 1495–1496 Myostatin, 422

N Nadolol, 160t Nail plate injury, 1428, 1428f, 1429f–1430f Naps motor skill learning and, 449, 449f power, 453, 454b Natural killer cells, exercise effects on, 147, 148t Naturalistic research, 106–107 Navicular accessory, 1963, 1963f, 1978, 2162–2165, 2163f–2164f

Index Navicular (Continued) excision of, 2165, 2165f injury to, 2022–2023, 2024f stress fracture of, 2016t, 2020–2022, 2023f Near-infrared spectroscopy, in compartment syndrome, 651 Neck on-field injury to, 522–524. See also Cervical spine injury tension of, head injury and, 658 Neck check, 150 Necrosis aseptic. See Avascular necrosis cutaneous, after patellar fracture, 1576 Needle cricothyroidotomy, 519, 520f Needle test, in Achilles tendon rupture, 2003 Neer’s sign, in rotator cuff disorders, 997, 1000f Nerve(s). See also specific nerves afferent, 353 efferent, 353 injury classification for, 2215, 2215f on-field injury to, 527 transection of in complex regional pain syndrome, 354, 354f Nerve conduction study in carpal tunnel syndrome, 1361 in entrapment neuropathy, 1311 in suprascapular nerve injury, 1122–1123 in ulnar neuropathy, 623 Nerve root block, fluoroscopy in, 534, 535f Nerve root injury, cervical, 670–673, 671f Neuralgic amyotrophy. See Parsonage-Turner syndrome Neuritis, brachial. See Parsonage-Turner syndrome Neuroblastoma, 610 Neurologic examination in elbow heterotopic ossification, 1291–1292 preparticipation, 513, 514t–515t in thoracolumbar spine injury, 721–723, 722f, 722t, 723f, 759, 759b in ulnar neuropathy, 622–623 Neurologic injury. See also at specific nerves in lumbar disk herniation, 743 in pediatric thoracolumbar spine injury, 758 Neuroma, Morton’s, 2184, 2184f Neuromodulation therapy, in complex regional pain syndrome, 366–367 Neuromuscular activation exercises in ankle rehabilitation, 273, 274f in core training, 285–286 Neuromuscular control exercises in ankle rehabilitation, 273, 275, 275f–276f in female ACL injury prevention, 334 in knee rehabilitation, 268–271, 269t, 271f Neuromuscular stimulation. See Electrical stimulation Neuropathy. See at specific nerves Newton’s laws first, 89t, 92 second, 89t, 92–93 third, 86–87, 89f, 89t Niacin, requirements for, 406b Nicardipine in complex regional pain syndrome, 363t in hypertension, 160t Nickel dermatitis, 202 Nicky’s knot, 135, 135f Nicotine, 427–428 Nifedipine, in complex regional pain syndrome, 363t, 364 Nisoldipine, 160t Nitric oxide, ergogenic effect of, 421 Noble compression test, 628, 628f

Nocardia infection, 398t Nonossifying fibroma, in children, 605–606, 605f Nonsteroidal anti-inflammatory drugs in complex regional pain syndrome, 363t, 364 in glenohumeral joint osteoarthritis, 1109 in heterotopic ossification, 1294, 1297 in hip degenerative disease, 1504 in knee arthritis, 1774 in knee osteoarthritis, 1791 in lateral epicondylitis, 1200 in olecranon bursitis, 1248–1249 in plantar fasciitis, 2048 in retrocalcaneal bursitis, 2035 in shoulder pain, 1006–1007, 1011 in SLAP lesion, 1026 in tendon disorders, 27, 29, 31 in tibial stress fracture, 1854 Nonunion distal humeral fracture, 1256, 1258, 1278 olecranon fracture, 1276, 1278 proximal humeral fracture, 1049 proximal ulnar fracture, 1276, 1278 radial head fracture, 1278 scaphoid, 1339–1340, 1367–1368 Nordic hamstring lower exercise, 337, 337f, 337t Norepinephrine, 353 exercise effects on, 217–218, 217t, 218f Nose, on-field injury to, 525 Nosebleed, on-field, 525 NS-398, 16 Nuclear medicine. See Radionuclide imaging Nucleus pulposus, 717. See also Intervertebral disk biomechanics of, 719 Nursemaid’s elbow, 1301, 1302f, 1303–1304, 1305, 1305f Nutrient artery, 69, 69f–70f Nutrition, 399–410 bone health and, 406 calorie requirements in, 402–403 carbohydrate requirements in, 403–404, 403t in children/adolescents, 467 fat requirements in, 405, 405t in female athlete, 477–479, 478f, 478t, 479b goals of, 399 hydration in, 401–402, 402t micronutrient requirements in, 405–406, 406b protein requirements in, 404–405, 405t screening form for, 399, 400f sodium requirements in, 402 supplement use and, 406–409, 409b weight management and, 406, 406b, 407b, 408b

O Ober’s test, 628, 629f, 1458, 1558 Obesity, 515t arthritis and, 1773–1774, 1790 O’Brien’s test in acromioclavicular joint injury, 830, 832f in rotator cuff disorders, 997 in SLAP lesion, 915, 1025, 1025t, 1216, 1216f Observational study, 101–103, 101f, 102t–103t Obturator externus, strain of, 1460–1461 Obturator internus, 1454t, 1455f Obturator nerve, entrapment of, 1468 Odds ratio, 2218


xxxiii

Odontoid congenital anomalies of, 692, 692f, 711 fracture of, 677–678, 678f in children/adolescents, 707 computed tomography of, 540–541, 540f Olecranon, 1189–1190, 1189f fracture of, 1271–1276 classification of, 1272–1273, 1272f dislocation with, 1263–1264, 1266f, 1267f–1268f, 1273 evaluation of, 1271–1273, 1272f nonunion of, 1276, 1278 operative treatment of, 1271, 1273–1276 arthrosis after, 1278 complications of, 1276, 1277–1278 heterotopic ossification after, 1277 incision in, 1273 infection after, 1278 instability after, 1277–1278 nonunion after, 1278 rehabilitation after, 1276–1277 tension band wiring in, 1273–1275, 1274f–1275f ulnar nerve injury after, 1277 wound problems after, 1278 pediatric, 1280t, 1286–1287 stress, 1225, 1225f ossification of, 1228 osteophytes of, 1239, 1239f, 1240 resection of, 1192, 1192f Olecranon bursitis, 1209–1212, 1246–1249 acute, 1210–1211 anatomy of, 1209–1210, 1210f, 1246–1247 arthroscopic treatment of, 1212 chronic, 1211–1212, 1211f classification of, 1210–1211 clinical evaluation of, 1247, 1247f crystal-induced, 1247 operative treatment of, 1211–1212, 1248, 1249 radiography of, 1247, 1247f septic, 1212–1213, 1247, 1248–1249 traumatic, 1247 treatment of, 1248–1249, 1248f Olecranon osteotomy, 1252–1253, 1252f Oligospermia, anabolic-androgenic steroids and, 416 Olmesartan, 160t Olympic athletes, drug use by, 410–411, 412–413 Omohyoid, scapular attachment of, 858, 858f–859f, 886f On-field emergency, 516–530 abdominal, 526–527 clavicular, 526 cold-related, 528–529 ear, 525 environmental, 528–530, 528f equipment fort, 517, 518t–519t extremity, 527–528 genitourinary, 526–527 head and neck, 522–524, 523t, 524f heat-related, 528, 528f, 529–530 laryngeal, 525 logroll for, 519, 519f medical bag for, 516–517, 518t–519t musculoskeletal, 527–528 nasal, 525 ocular, 525 oral, 525 pelvic, 526–527 preparation for, 517 primary surgery in, 517, 519–520, 520f, 520t, 521f rib, 525, 526

xxxiv

Index

On-field emergency (Continued) secondary surgery in, 520, 521f thoracic, 525–526 Onychectomy complete, 2099, 2101, 2102, 2103f partial, 2099, 2102f Opioids abuse of, anabolic-androgenic steroid use and, 417 in complex regional pain syndrome, 363t, 364 Oral cancer, smokeless tobacco and, 428 Organ loss, clearance for participation and, 513 Organ transplantation, 515t Orthotic devices. See also Shoes, orthotic devices for for flatfoot, 2044, 2046f injury and, 2189–2190 for intractable plantar keratoses, 2110, 2111f for plantar fasciitis, 2049 for retrocalcaneal bursitis, 2035 for tarsal tunnel syndrome, 2058 Os acromiale, 859, 860f magnetic resonance imaging of, 955–956, 958f unfused, 781, 781f Os calcis, 2031, 2032f fracture of, 2051 ostectomy of, 2000 superior tuberosity of enlargement of, 2031, 2031f. See also Retrocalcaneal bursitis excision of, 2038, 2038f Os odontoideum, 692, 692f, 711 Os peroneum fracture of, 1988 stress fracture of, 2024 Os subfibulare, 1918 Os tibial externum, 1978 Os trigonum, displacement of, 2019, 2021f Os vesalianum, 2168, 2169f Osgood-Schlatter disease, 1526f, 1527–1529 diagnosis of, 1528 etiology of, 1528 imaging in, 599 natural history of, 1528 treatment of, 1529 OssaTron, for plantar fasciitis, 2049–2050 Ossification acromion, 859, 860f appositional, 78 capitellum, 1227–1228 clavicular, 780 coracoid, 859, 859f–860f, 879, 881f distal femur, 587, 588f distal humerus, 1227–1228, 1228f–1229f elbow, 1227–1229, 1228f–1229f, 1279, 1280f glenoid fossa, 859 heterotopic. See Heterotopic ossification humeral condyle, 1228 olecranon, 1228 proximal humerus, 779, 782, 782f proximal radius, 1228 scapular, 781, 781f Osteitis pubis, 1466, 1466f vs. adductor strain, 1490, 1491f Osteoarthritis acromioclavicular joint, 956, 959f glenohumeral joint, 929, 1104–1119. See also Glenohumeral joint osteoarthritis hip, 1467, 1467b classification of, 1502, 1502b clinical presentation of, 1502–1503 etiology of, 1500 imaging of, 1503

Osteoarthritis (Continued) nonoperative treatment of, 1503–1504, 1504b, 1504f operative treatment of. See Arthroplasty, hip pain in, 1503 physical examination in, 1503 primary, 1500 range of motion testing in, 1503 secondary, 1500 knee. See also Knee, cartilage lesions of arthroplasty for. See Arthroplasty, knee arthroscopic treatment of, 1792 bracing in, 1790 evaluation of, 1789–1790 exercises in, 1790 imaging in, 1789–1790, 1790f lifestyle modification in, 1790 medical management of, 1791–1792 meniscectomy and, 1772 osteotomy in, 1792 physical examination in, 1789 posterolateral corner injury and, 1725, 1743–1744 proximal tibial osteotomy in, 1792 support devices in, 1790 sesamoid, 2089 sternoclavicular joint, 811–812, 820 Osteoblasts, 65–66, 78 Osteocalcin serum, 67 urinary, 67 Osteochondral allograft/autograft glenohumeral joint, 1111, 1111f, 1115, 1115f knee, 1775, 1777, 1777t, 1780–1783, 1781f, 1782f, 1784t talus, 2146–2147, 2148, 2150–2152, 2150t, 2151f–2152f, 2153 Osteochondral autologous transfer system, in talar osteochondral lesions, 2146–2147, 2148, 2150–2152, 2151f–2152f Osteochondral fracture, 49t, 51–52 magnetic resonance imaging in, 578–579, 578f Osteochondritis, sesamoid, 2089, 2090, 2092f, 2169–2170, 2170f Osteochondritis dissecans capitellum, 623, 624f, 1238–1239, 1241–1246 arthroscopy in, 1243–1244, 1243f, 1245f classification of, 1241 evaluation of, 1241–1242 grade of, 1241 history in, 1241 imaging in, 1241–1242, 1242f–1243f nonoperative treatment of, 1242 operative treatment of, 1244–1245, 1244f osteochondral grafting in, 1244, 1245f physical examination in, 1241 return to play after, 1244, 1246 treatment of, 1242–1244, 1242f, 1245f femoral condyle, 1766–1771 arthroscopy in, 469, 471f, 1767 classification of, 1766–1767, 1767f, 1767t epidemiology of, 1767–1768, 1768f etiology of, 1768 loose bodies in, 1770 MRI classification of, 1767, 1767t natural history of, 1768–1769 nonoperative treatment of, 1770 scintigraphic classification of, 1767, 1767t treatment of, 1769–1770, 1769f, 1773f zonal classification of, 1766, 1767f femoral trochlea, 1768, 1768f patellar, 1530–1533 diagnosis of, 1531, 1768, 1768f


Osteochondritis dissecans (Continued) etiology of, 1530–1531 natural history of, 1531 vs. osteochondrosis, 1526–1527, 1527f treatment of, 471f, 1531–1533 radiography in, 599, 599f talar, in children/adolescents, 1971–1972 Osteochondroma scapular, 887, 888f subungual, 2105, 2105t Osteochondrosis (osteochondroses), 77, 599, 599f, 1972–1974, 1973f, 1974f, 2153 calcaneal, 1973–1974, 1974f, 2143f, 2162, 2162f capitellar, 623, 625f, 1238 classification of, 2142–2143, 2142t–2143t cuneiform, 2143f, 2166, 2166f distal tibia, 2153, 2154f fifth metatarsal base, 2143f, 2167–2169, 2168f–2169f metatarsal head, 599, 1973, 1973f, 2166–2167, 2167f, 2168t treatment of, 2166, 2168f patellar inferior pole, 599, 1526f, 1529–1530 superior pole, 1530 talar, 2143–2153 anatomy of, 2143–2144 classification of, 2144, 2145t, 2146f evaluation of, 2144, 2146b in high-level athlete, 2153 history in, 2144 imaging in, 2144–2145, 2147f lateral sprain and, 1929 mechanisms of, 2143–2144 nonoperative treatment of, 2145–2146, 2148 operative treatment of, 2146–2147 care after, 2152 complications of, 2152, 2153f drilling in, 2146, 2148, 2149, 2149f–2150f, 2150t internal fixation in, 2146 lavage and débridement in, 2146, 2148 microfracture in, 2146, 2148 osteochondral autograft or allograft in, 2146–2147, 2148, 2150–2152, 2150t, 2151f–2152f, 2153 return to play after, 2152 physical examination in, 2144 tarsal navicular, 599, 1972–1973, 1973f, 2143f, 2162, 2163f tibial tubercle, 599, 1526f, 1527–1529 Osteoclasts, 66–67 Osteocytes, 66, 66f Osteogenesis, distraction, 81–82, 83f Osteogenesis imperfecta, 73 Osteoid osteoma, in children, 603, 603f, 605 Osteolysis, of distal clavicle, 854, 855f Osteoma, osteoid, in children, 603, 603f, 605 Osteomalacia, 72, 73t, 79b Osteomyelitis, 82–84 acute, 82 chronic, 83–84, 84f computed tomography in, 543 of foot, 1974 glenohumeral, 984 hematogenous, acute, 82 multifocal, chronic, 84 positron emission tomography in, 547 radiolabeled leukocyte imaging in, 547 radionuclide imaging in, 547 sclerosing, chronic, 84 spinal, 757, 760f subacute, 84

Index Osteonecrosis. See Avascular necrosis Osteopenia, 73t in female athlete, 478 Osteopetrosis, 73t Osteophyte(s) acromioclavicular joint, 956, 959f elbow, 621–622 olecranon, 52, 1239, 1239f proximal ulna, 1223–1224, 1223f Osteoporosis, 72, 73t in female athlete, 478, 481 periarticular (Sudeck’s atrophy), 358 stress fracture and, 632 Osteotomy medial clavicle, 810 metatarsal bunionette treatment with, 2135–2136, 2135b diaphyseal, 2135–2137, 2138b, 2139f–2140f distal chevron, 2135–2136, 2135b, 2137b, 2138f distal oblique, 2135–2136, 2135b, 2136b, 2136f–2137f hallux valgus treatment with, 2070–2071, 2076b, 2077f, 2078–2079 intractable plantar keratosis treatment with, 2111–2115, 2111b, 2112f–2114f olecranon, 1252–1253, 1252f tibial, 1804–1835. See also High tibial osteotomy in knee arthritis, 1792 in posterior cruciate ligament and posterolateral corner injury, 1744–1747, 1746f trochlear, in dysplasia, 1568–1569 Ovary, absence of, 515t Overhead throwing phases of, 993, 993f, 1091, 1092f, 1214–1215, 1215f in children/adolescents, 623, 624f, 790–791, 790f, 1231–1232, 1232f scapulothoracic motion in, 891 secondary adaptation to, 1215 Overhead throwing injury bursal, 890, 890f elbow, 1221–1226, 1223f, 1225f. See also Overhead throwing injury, pediatric evaluation of, 1215–1217, 1216f–1217f glenoid labrum, 1219–1221, 1220f humeral, 1226 inflammatory, 1218 internal impingement, 986, 987f, 992–993, 1001–1002, 1002f, 1016, 1217, 1218 evaluation of, 1216, 1216f magnetic resonance imaging in, 978–979, 979f nonoperative treatment of, 1010 magnetic resonance imaging in, 1217 neurovascular, 1226 O’Brien active compression test in, 1216, 1216f olecranon fracture, 1225, 1225f pediatric, 1227–1240. See also Little Leaguer’s elbow biomechanics in, 1231–1232, 1232f–1233f epicondylar avulsion fracture and, 1233, 1233f glenohumeral internal rotation deficit and, 1233–1234 in gymnasts, 1236 lateral articular compression and, 1233, 1233f lateral extension overload and, 1234, 1234f medial epicondylar, 1238

Overhead throwing injury (Continued) patterns of, 1232–1234, 1233f–1234f physical examination in, 1229 posterior articular damage and, 1234, 1234f posterior elbow, 1239–1240, 1239f radiography in, 1229–1230, 1230f in tennis players, 1236 ulnar collateral ligament, 1237, 1238f physical examination in, 1216–1217, 1216f, 1217f radiography in, 1217 rib fracture, 895–896, 896f rotator cuff, 1217–1219. See also Rotator cuff disorders; Rotator cuff tear(s) suprascapular nerve, 1221 triceps tendon, 1221, 1226 ulnar collateral ligament, 1221–1224, 1223f ulnar nerve, 1226 valgus extension overload, 621–622, 1224–1225 valgus stability testing in, 1217, 1217f Overuse injury, 29–30, 611–652. See also Chronic exertional compartment syndrome; Stress fracture and specific tendons classification of, 29–30 elbow lateral, 617–619, 618f medial, 619–624, 620f, 624f pediatric, 623–624, 623f–625f extrinsic factors in, 611 foot and ankle, 628–631. See also Achilles tendon iliac, 1475 intrinsic factors in, 611 knee, 626–628, 626f, 629f, 630f. See also Patellar tendinopathy; Patellar tendinosis low back, in adolescent, 766 radionuclide imaging in, 545–546, 545f–547f shoulder, 614–617, 615b. See also Rotator cuff disorders wrist, 624–626 Oxcarbazepine, in epilepsy, 189, 191t Oxidative phosphorylation, 211 Oxygen, uptake of, 212–213, 212f maximum, 218, 219f in children, 464 in female athlete, 476–477 Oxygen therapy, in high-altitude illness, 504

P P value, 110 Paget-Schroetter syndrome, 1129–1130, 1131f, 1134 Paget’s disease, 73t Pain. See also Complex regional pain syndrome back. See Low back pain in compartment syndromes, 14 definition of, 356t in delayed-onset muscle soreness, 12–13 in exertional compartment syndrome, 650 heel. See Heel, pain in knee, after tibial stress fracture treatment, 1855 leg, 1857–1863, 1857b in lumbar disk herniation, 743 sympathetically independent, 351, 360 sympathetically maintained, 351–352, 352f. See also Complex regional pain syndrome diagnosis of, 359–360 terminology for, 338t


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Pain (Continued) in thoracolumbar spine evaluation, 719–720 transcutaneous electrical nerve stimulation for, 229–230, 230f Pain dysfunction syndrome, 351 Pain provocative test, in SLAP lesion, 1025t Pancreas exercise effects on, 217t, 218 on-field injury to, 527 Panner’s disease, 623, 625f, 1238 Paralabral cyst, 964–965, 965f, 980, 980t Parasitic infestations, 200–201, 201f–202f Paratenon, 20, 21f Achilles, 563 Parathyroid hormone, 71, 71t, 77t Pars interarticularis acute fracture of, 755–756, 756b fatigue fracture of (spondylolysis), 635–636, 756, 756b, 762–763 computed tomography in, 546, 546f, 762, 763f radiography in, 635, 636f, 760, 760f radionuclide imaging in, 726, 726f, 761f return to play and, 767, 767b single-photon emission computed tomography in, 546, 546f, 635, 636f, 761, 761f Parsonage-Turner syndrome, 616, 1143–1146 anatomy of, 1143 differential diagnosis of, 1144 electromyography in, 1144 evaluation of, 1144–1145 genetics of, 1143, 1145, 1146 imaging in, 1145 long thoracic nerve in, 1124–1125, 1125f outcomes of, 1145 physical examination in, 1144 return to play and, 1145–1146 treatment of, 1145 Particle disease, 542, 542f PASTA (partial articular-sided supraspinatus tendon avulsion) lesion, 961, 962f Pasteurella multocida infection, 398t Patella, 1513–1576 anatomy of, 1513–1514, 1514f, 1548–1553 bony, 1549–1550, 1549f–1550f, 1573 ligamentous, 1534–1536, 1535f–1548f soft tissue, 1513–1514, 1514f, 1548f, 1550–1553, 1551f–1552f, 1553t vascular, 1573, 1573f ballotable, 1556 biomechanics of, 1514–1515, 1515f contact areas in, 1591–1593, 1592f exercise-related, 226, 226f force transmission in, 1593–1596, 1593f, 1594f–1595f bipartite, 1574 chondral injury of, 1538 contact areas of, 1514, 1515f, 1550, 1550f, 1591–1593, 1592f dislocation of. See Patellar dislocation exercise-related mechanics of, 226, 226f facets of, 1550 force transmission at, 226, 226f, 1593–1596, 1593f–1594f fracture of, 1572–1577 in children, 597, 1576–1577, 1576f classification of, 1573 complications of, 1576 evaluation of, 1573–1574, 1574f lag screw fixation of, 1575 multifragment, 1575 nonoperative treatment of, 1574, 1575f operative treatment of, 1574–1575 radiography in, 1574, 1574f

xxxvi

Index

Patella (Continued) return to play after, 1576 stress, 641–643 gliding movement of, 225, 225f height of Blackburne-Peel ratio for, 1523, 1523f, 1539, 1541f, 1559f, 1560, 1560t Blumensaat line for, 1539, 1541f, 1559, 1559f Caton-Deschamps ratio for, 1539, 1541f, 1559f, 1560, 1560t after high tibial osteotomy, 1832–1833 Insall-Salvati ratio for, 1522, 1523f, 1539, 1541f, 1559f, 1560, 1560t Labelle-Laurin measurement for, 1559–1560, 1559f, 1560t measurement of, 1522–1523, 1523f, 1539, 1541f non–weight-bearing exercise effects on, 226, 227–228, 226f, 227f osteochondral injury of, 1538, 1540f osteochondritis dissecans of, 1530–1533 diagnosis of, 1531, 1768, 1768f etiology of, 1530–1531 natural history of, 1531 vs. osteochondrosis, 1526–1527, 1527f treatment of, 471f, 1531–1533 osteochondrosis of, 1526–1533 inferior pole (Sinding-Larsen-Johansson disease), 599, 1526f, 1529–1530 vs. osteochondritis dissecans, 1526–1527, 1527f proximal pole, 1530 superior pole, 1530 palpation of, 1556–1557, 1556f radiography of, 1558–1564 anteroposterior view for, 1559 axial view for, 1561–1564, 1561t, 1562f, 1563f lateral view for, 1559–1561, 1559f–1560f, 1560t, 1561f Laurin’s view for, 1562, 1563f Merchant’s view for, 1562, 1562f stress, 1564 range of motion of, 1557 Sinding-Larsen-Johansson disease of, 599, 1526f, 1529–1530 stress fracture of, 641–643 subluxation of. See Patellar dislocation sulcus angle of, 1540 tracking of, 1556 abnormal, 1595–1596, 1595f weight-bearing exercise effects on, 226–227, 226f, 227f Wiberg classification of, 1513, 1514f, 1550 Patella alta, 1555, 1555f, 1560 in Osgood-Schlatter disease, 1528 Patella baja, 1555, 1576 Patella infera, 225 high tibial osteotomy and, 1832–1833 Patellar angle, 1528 Patellar dislocation, 1534–1547 apprehension test in, 1538, 1539f arthroscopy in, 1545 chondral injury with, 1538, 1540t clinical presentation of, 1536–1537, 1537f direct mechanism of, 1536–1537, 1537f effusion with, 1556 epidemiology of, 1534, 1534t in female athlete, 480, 487, 489, 489b hemarthrosis in, 1538 iatrogenic, 1545, 1567 imaging in, 1538–1542, 1541f, 1542t, 1543f incidence of, 1534 indirect mechanism of, 1536–1537, 1537f

Patellar dislocation (Continued) joint aspiration in, 1538 lipohemarthrosis in, 1538 mechanisms of, 1536–1537, 1537f, 1552–1553, 1552f medial patellofemoral ligament in, 1535–1536, 1536f, 1541–1542, 1542t, 1546 nonoperative treatment of, 1542–1544, 1544t operative treatment of, 1544–1546, 1544t lateral release in, 1545 medial patellofemoral ligament repair in, 1546 medial retinacular repair in, 1545–1546 rehabilitation after, 1546–1547 osteochondral injury with, 1538, 1540f, 1540t palpation in, 1538 physical examination in, 1538, 1539f recurrent, 1548–1572 apprehension test in, 1558 bayonet sign in, 1554 clinical presentation of, 1553, 1553t computed tomography in, 1564–1565, 1566t foot examination in, 1554 gait examination in, 1554–1555 J sign in, 1556 lateral pull test in, 1557, 1557f lower extremity examination in, 1558 magnetic resonance imaging in, 1565–1566, 1565t–1566t miserable malalignment in, 1554 nonoperative treatment of, 1566 operative treatment of, 1566–1572 arthroscopic, 1570–1572 distal realignment procedures in, 1566–1567 lateral retinacular release or lengthening in, 1567–1568 medial patellofemoral ligament reconstruction in, 1569–1570, 1571t proximal realignment procedures in, 1568 trochlear osteotomy in, 1568–1569 trochleoplasty in, 1568–1569 patella-trochlea compression test in, 1558 patellar glide in, 1558, 1558f patellar tilt in, 1557–1558, 1557f physical examination in, 1553–1558, 1554f–1558f quadriceps angle in, 1553–1554, 1554f radiography in, 1558–1564, 1563f, 1566t anteroposterior, 1559 axial, 1561–1564, 1561t, 1562f, 1564t lateral, 1559–1561, 1559f, 1560f, 1560t, 1561f stress, 1564 sitting examination in, 1555–1556, 1555f–1556f standing examination in, 1554–1555 supine examination in, 1556–1558, 1557f, 1558f tubercle sulcus angle in, 1555, 1556f risk factors for, 1534–1536, 1534b, 1534t Patellar glide, 1558, 1558f Patellar tendinopathy, 560, 561f, 626–627, 1516–1517 metabolic disease and, 1516, 1517b pathophysiology of, 1515–1518, 1517b, 1518t Patellar tendinosis, 30, 31, 626–627, 626f, 1516–1518, 1518t evaluation of, 1518–1519


Patellar tendinosis (Continued) imaging in, 560, 561f, 1519, 1519f–1520f pathophysiology of, 1515–1518, 1517f–1518t stages of, 1519 treatment of, 1519–1521, 1520f Patellar tendon anatomy of, 1514, 1514f autograft with, in ligament injury treatment, 37 bioscaffold effect on, 28 collagen of, 1515, 1516f–1517f drug effects on, 1516 excision of, 1520, 1520f histology of, 1515, 1516f inflammation/degeneration of. See also Patellar tendinopathy; Patellar tendinosis evaluation of, 1518–1519, 1519f imaging in, 1519, 1519f–1520f pathophysiology of, 1515–1518, 1517f–1518f treatment of, 1519–1521, 1520f magnetic resonance imaging of, 1519, 1519f–1520f mechanobiology of, 1516 metabolic disease effects on, 1516, 1517b rabbit, 28 rupture of, 1521–1522, 1522t complications of, 1525 evaluation of, 1522–1523, 1523f–1524f histology of, 1516 treatment of, 1523–1524 Patellar tilt, 1539, 1555, 1557–1558, 1557f Patellofemoral joint. See also Knee; Patella arthritis of, in female athlete, 489 biomechanics of, 1514–1515, 1515f, 1591–1596 contact area in, 1591–1593, 1592f force transmission in, 1593–1596, 1593f–1595f contact regions of, 1591–1593, 1592f instability of. See Patellar dislocation pain in in female athlete, 480, 487 patellofemoral joint reaction force and, 1595, 1595f Patellofemoral joint reaction force, 226, 226f, 1591–1593, 1592f, 1593f with descending stairs, 227 in rehabilitation programs, 1595–1596, 1595f with squatting, 227, 1592–1593, 1592f with walking, 227 Patellofemoral ligaments, 1534–1536, 1535f, 1551–1552, 1551f. See also Lateral patellofemoral ligament; Medial patellofemoral ligament Pathologic fracture, of humeral metaphysis, 1085, 1086f Paxinos’ test, in acromioclavicular joint injury, 830 Pearson’s product-moment correlation, 100, 119 Pectineus, 1485 strain of, 1460–1461 Pectoral nerve, 901 Pectoralis major, 900–907 actions of, 901 anatomy of, 900–901, 901f, 1034, 1035f, 1059–1060, 1059f, 1162 pediatric, 785, 785f biomechanics of, 1162 humeral attachment of, 1071, 1071f innervation of, 901 press-up exercise for, 241, 242f rupture of, 900–907, 1059–1063, 1162–1165 classification of, 901–902, 902t, 1060, 1162, 1162t

Index Pectoralis major (Continued) clinical evaluation of, 1060–1061, 1162–1163 differential diagnosis of, 902 in elderly patients, 1164 evaluation of, 902, 902b, 903f, 1162–1163 magnetic resonance imaging in, 902, 903f, 1060–1061, 1061f, 1163, 1164f mechanism of, 1060 nonoperative treatment of, 903–904, 904t, 1062–1163 operative treatment of, 904–906, 904f, 904t, 906f, 1061–1063, 1062f–1064f, 1163–1165 physical examination in, 1060, 1061f, 1163 radiography in, 902, 1060 rehabilitation after, 1064, 1163–1165, 1164t retraction with, 905 return to play after, 907, 1064 shoulder dislocation and, 902 steroid use and, 902, 1164–1165 suture anchor repair of, 904, 905f, 906 trough repair of, 904, 904f, 906 Pectoralis minor, scapular attachment of, 858, 858f, 886f Pedicles cervical spine, congenital absence of, 711 lumbar spine, in congenital stenosis, 747 Pediculosis capitis, 200–201, 201f Peliosis hepatis, anabolic-androgenic steroids and, 416 Pellegrini-Stieda lesion, 1629, 1630f Pelvic rami, stress fracture of, 1465 Pelvis anatomy of, 1451–1452 avulsion injury of, 541–542, 542f, 553, 555 in children, 599, 1474–1475, 1475f computed tomography of, 541–542, 542f fracture of, 1464 hemorrhage with, 541 functions of, 1452b on-field injury to, 526–527 radiography of, 541 stress fracture of, 638, 1464–1466 Penbutolol, 160t Peptic ulcer disease, 77t Per gene, 442 Performance-enhancing substance use, in children/adolescents, 467–468 Pericarditis, 152 Perichondrium, autograft with, in articular cartilage injury, 53–54 Perilunate dislocation, 1332–1335, 1332f classification of, 1332 clinical manifestations of, 1332 fracture with, 1332, 1333f pediatric, 1371, 1372f, 1373f physical examination in, 1332 radiography in, 1332 return to play after, 1335 treatment of, 1332–1335, 1333f–1334f Perimysium, 3, 207, 208f Perindopril, 160t Periosteum, 69 autograft with, in articular cartilage injury, 53–54 Peripheral neuropathy. See at specific nerves Peripheral vascular resistance, exercise effect on, 219–220, 220t Peritendinitis, 30 Achilles, 30, 563, 1997, 2000–2001 Peritendon, 20, 21f Permethrin in pediculosis capitis, 200 in scabies, 201

Peroneal groove deepening of, 1932–1933, 1993–1994, 1994f tendon subluxation within, 1995–1996 Peroneal nerve common, injury to, 1751–1752, 1752f deep, entrapment of, 2061–2062, 2061f superficial, 15f, 2062, 2063f entrapment of, 2062–2063, 2062f injury to, 1933 tibial osteotomy–related injury to, 1832 Peroneal retinaculum inferior, 1987 superior, 338, 1931, 1987 congenital absence of, 1991 disruption of, 1932 imbrication of, 1932–1933 reconstruction of, 1995 Peroneal tunnel compression test, 1989 Peroneus brevis tendon anatomy of, 1987–1988 injury to, 1987–1988 magnetic resonance imaging of, 560–561, 563f instability of, 1931–1933, 1932f, 1963–1964 subluxation of, 1990–1996 anatomy of, 1990–1991 biomechanics of, 1991 evaluation of, 1991–1992, 1992f nonoperative treatment of, 1992–1993 operative treatment of, 1993–1996, 1993f–1994f treatment of, 1992–1996 tendinitis of, 1988–1990 Peroneus brevis tenodesis, in lateral ankle sprain, 1924–1926, 1925f Peroneus longus, exercise for, 275, 275f–276f Peroneus longus tendon anatomy of, 1987–1988 injury to, 1987–1988 instability of, 1931–1933, 1932f, 1963–1964 magnetic resonance imaging of, 560–561 subluxation of, 1990–1996 anatomy of, 1990–1991 biomechanics of, 1991 evaluation of, 1991–1992, 1992f nonoperative treatment of, 1992–1993 operative treatment of, 1993–1996, 1993f, 1994f treatment of, 1992–1996 tendinitis of, 1988–1990 Perthes’ lesion, 974, 974t Phalangeal fracture adult, 1394–1398, 1395f–1397f anatomy of, 1395 comminuted, 1394, 1395f metaphyseal, 1396, 1396f–1397f oblique, 1396, 1396f transverse metaphyseal, 1396, 1396f– 1397f pediatric, 1406–1411 distal, 1405f, 1406, 1406f–1407f mallet, 1407, 1407f–1408f middle, 1408–1410, 1408f–1410f proximal, 1411 Phalen’s test, 1312, 1360 Pharyngitis, 149 Phenobarbital, in epilepsy, 188, 191t Phenol matrixectomy, 2099–2102, 2105f Phenoxybenzamine, in complex regional pain syndrome, 363t, 365 Phentolamine testing, in complex regional pain syndrome, 359–360 Phenytoin, in epilepsy, 188, 191t Philosophical research, 108


xxxvii

Phosphate bone, 70, 71t serum, 74t–76t Phosphocreatine, in energy metabolism, 210, 210f Phosphorus blood, 77t requirements for, 406b Physical examination. See Preparticipation examination Physical therapy, in complex regional pain syndrome, 362 Physis, 78, 587–588 fracture of, 595, 595f. See also at specific bones imaging of, 591–592, 592f–593f proximal humerus, 779, 779f Pigmented villonodular synovitis, 1473, 2161, 2161f Pindolol, 160t Piriformis, 1454t, 1455f Piriformis syndrome, 1468 Pisiform anatomy of, 1319–1320, 1319f fracture of adult, 1350, 1352f pediatric, 1370–1371 Pitch angle, calcaneal, 2035, 2035f Pitching, 620. See also Overhead throwing phases of, 790–791, 790f, 1091, 1092f in children, 623, 624f, 1232, 1232f–1233f Pitted keratolysis, 196, 196f Pittsburgh sleep quality index, 450 Pituitary gland, exercise effects on, 217, 217t Pivot shift test in anterior cruciate ligament injury, 1650, 2213–2214, 2214t in meniscal injury, 1602 reverse in posterior cruciate ligament injury, 1692, 1692f in posterolateral corner injury, 1727–1728, 1729f in varus malalignment, 1807–1808 Pivot test, posteromedial, 1691 Plantar aponeurosis, 1870, 1871f, 2043–2044, 2043f Plantar digital nerves, 2088–2089, 2089f Plantar drawer test, 2119, 2120f Plantar fasciitis, 631, 2042–2056 anatomic considerations in, 2043–2044, 2043f–2045f biomechanics of, 2044 calcaneal taping in, 2049 corticosteroid injection in, 2048–2049 counterstrain treatment in, 2049 evaluation of, 2044–2046 exostosectomy in, 2051 fasciotomy in, 2051–2052, 2054 heel spur and, 2042–2043, 2042f history in, 2044 iontophoresis in, 2049 magnetic resonance imaging in, 2047 night splints in, 2049 nonoperative treatment of, 2048–2050, 2052–2053, 2053f, 2054–2055 NSAIDs in, 2048 operative treatment of, 2050–2056, 2050b, 2051f os calcis drilling in, 2051 OssaTron in, 2049–2050 physical examination in, 2044–2046 plantar fascia release in, 2051, 2052, 2055–2056, 2055f radiography in, 2046–2047, 2047f radionuclide imaging in, 2046–2047, 2047f

xxxviii

Index

Plantar fasciitis (Continued) return to play after, 2056 shock-wave therapy in, 2049–2050, 2052 Plantar keratoses, 2089, 2089f, 2107–2115, 2107b anatomy of, 2108–2109, 2109b, 2109f–2110f classification of, 2109, 2110b evaluation of, 2109, 2110b history in, 2109 imaging in, 2110 nonoperative treatment of, 2110–2111, 2111f operative treatment of, 2110–2115 care after, 2115 metatarsal osteotomy in, 2111–2115, 2111b, 2112f–2114f plantar condylectomy in, 2111, 2113f return to play after, 2115, 2115b orthotic devices in, 2110, 2111f physical examination in, 2109 vs. wart, 2108f, 2109 Plantar nerves, 2044, 2044f, 2046f Plasmin, 372 Platelet(s) in coagulation, 370–371, 371f–372f in osteochondral fracture, 51 Platelet-derived growth factor, in fracture healing, 80 Platelet-rich fibrin matrix clot, in knee dislocation treatment, 1763, 1763f Playing cast, 1362 Playing surface, 2192–2197 for baseball, 2196–2197 compliant, 2199 frictional properties of, 2198, 2204, 2204f hardness of, 2197–2198, 2197f–2198f historical perspective on, 2193, 2196 for indoor sports, 2196 injury and, 2192–2204 clinical studies of, 2203–2204, 2203f–2204f, 2204t energy loss and, 2198–2199, 2199f experimental studies of, 2199–2203, 2200t, 2201f, 2202t, 2203f friction and, 2198, 2204, 2204f hardness in, 2197–2198, 2197f–2198f incidence in, 2196–2197 for playgrounds, 2197 for tennis, 2193–2196, 2194t–2195t, 2203, 2203f, 2204t for track, 2196, 2204, 2204f Plyoball exercises in core training, 287–288, 289f in knee rehabilitation, 294, 294f in shoulder rehabilitation, 296, 298f Pneumonia, 150 Pneumothorax, on-field, 525–526 Point estimate, 99 Polycystic ovarian syndrome, valproate and, 189 Polysomnography, 450 Polythiazide, 160t Popeye deformity, 1165, 1166f Popliteal artery, 1686, 1687f, 1748, 1838f aneurysm of, 1838, 1844 embryology of, 1836 entrapment of, 1836–1847 anatomy of, 1836, 1838f angiography in, 1840, 1842, 1843f–1844f ankle-brachial index in, 1839 biomechanics of, 1836 classification of, 1836–1837, 1837t clinical presentation of, 1837, 1838b computed tomographic angiography in, 1839–1840, 1840f gender and, 1837

Popliteal artery (Continued) historical perspective on, 1836 imaging in, 1839–1842, 1839f–1844f incidence of, 1836 magnetic resonance angiography in, 1840, 1842f magnetic resonance imaging in, 1840, 1841f–1842f patient history in, 1837 physical examination in, 1837–1839, 1838b treatment of, 1842, 1844–1847, 1845f, 1846b, 1846t complications of, 1846–1847 graft thrombosis after, 1847 medial approach to, 1844–1845, 1846t posterior approach to, 1844, 1845f, 1846t return to play after, 1847, 1847b ultrasonography in, 1839, 1839f traumatic injury to, 1750, 1751, 1753, 1753f Popliteal (Baker’s) cyst, 537–538, 538f Popliteal plexus, 1686 Popliteofibular ligament, 1685, 1687, 1719f, 1720–1721, 1721f, 1722f. See also Posterolateral corner Popliteus muscle-tendon complex, 1687–1688, 1720–1721, 1721f, 1731f Popliteus tendon anatomy of, 1719f, 1720–1721, 1721f, 1731f avulsion of, 541–542, 542f recess procedure for, 1732–1733, 1733f reconstruction of, 1736, 1736f stabilizing function of, 1585, 1588–1589 Population, statistical, 99 Positron emission tomography, 547 Post hoc power analysis, 111 Postconcussion syndrome, 659 Posterior circumflex humeral artery, 1071f, 1072 Posterior cruciate ligament (PCL). See also Posterior cruciate ligament (PCL) injury anatomy of, 1684–1688, 1684f–1686f, 1748 in children, 1714, 1714f anterolateral bundle of, 1684, 1685f–1686f, 1687, 1687t avulsion of, 1695, 1702 magnetic resonance imaging in, 569, 572f pediatric, 1716–1717, 1717f biomechanics of, 1687–1688, 1687t force measurements in, 1581–1582, 1585 observational studies of, 1581 stabilizing function in, 1584–1588 strain measurements in, 1582 in weight-bearing flexion, 1585 blood supply to, 1686, 1687f innervation of, 1686 ligament unloading exercises for, 222–224, 223t loading of, rehabilitative exercise effects on, 221–222, 222t posteromedial bundle of, 1684, 1685f–1686f, 1687, 1687t squat exercise effects on, 223, 223t, 224, 224f, 262 stabilizing function of, 1584–1588 stair climbing effects on, 223t, 224 stationary cycling effects on, 223, 223t Posterior cruciate ligament (PCL) injury, 1683–1712 acute vs. chronic, 1689 avulsion, 1695, 1702 magnetic resonance imaging in, 569, 572f pediatric, 1716–1717, 1717f chronic, 1689 treatment of, 1702–1703, 1702f


Posterior cruciate ligament (PCL) injury (Continued) classification of, 1689, 2216 clinical presentation of, 1688–1689, 1688f–1689f collateral ligamentous examination in, 1692 combined, 1689, 1700 treatment of, 1703–1704, 1706–1710, 1708f–1710f dial test in, 1691 gait evaluation in, 1692 grading of, 1689 incidence of, 1688 isolated natural history of, 1693, 1695, 1695f nonoperative treatment of, 1693–1695, 1694t, 1695f, 1701–1702, 1701f operative treatment of, 1701–1703, 1701f, 1705–1706, 1705f–1707f review of, 1695–1700, 1697t–1699t kinematic changes with, 1687–1688, 1687t limb alignment evaluation in, 1692 magnetic resonance imaging in, 1693 mechanisms of, 1688–1689, 1688f–1689f pediatric, 1713–1718, 1714f avulsion, 1716–1717, 1717f classification of, 1715 evaluation of, 1715–1716 magnetic resonance imaging in, 1716 mechanism of, 1714, 1715f multiligament, 1717 natural history of, 1716 radiography in, 1716 treatment of, 1716–1717, 1717f physical examination in, 1690f–1691f, 1691–1692 posterior drawer test in, 1690, 1690f, 2214 posterior sag test in, 1690, 1691f posterolateral corner injury and, 1732–1744, 1745f double-bundle reconstruction in, 1706–1710, 1708f–1710f proximal tibial osteotomy in, 1744–1747, 1746f posteromedial pivot test in, 1691 quadriceps active test in, 1691, 1691f radiography in, 1692–1693 radionuclide imaging in, 1693 reverse pivot shift test in, 1691f, 1692 thumb sign test in, 2214 treatment of, 1693–1710 nonoperative, 1693–1695, 1694t, 1695f, 1700, 1701f operative, 1695–1710, 1701f, 1702f. See also Posterior cruciate ligament (PCL) reconstruction complications of, 1712 outcomes of, 1711–1712 rehabilitation after, 1711 return to play after, 1712 valgus stress test in, 1692 varus stress test in, 1692 Posterior cruciate ligament (PCL) reconstruction in combined injury, 1700, 1706–1710, 1708f–1709f, 1710f complications of, 1712 double-bundle, 1705–1706, 1705f–1706f in combined injury, 1706–1710, 1708f–1710f evaluation of, 1696, 1699–1700, 1699t evaluation of, 1695–1700, 1697t–1698t fixation techniques in, 1700 in knee dislocation, 1755–1756, 1758, 1759f, 1762–1763, 1763f

Index Posterior cruciate ligament (PCL) reconstruction (Continued) outcomes of, 1711–1712 posterolateral corner injury and, 1706–1710, 1708f–1710f, 1743–1744 rehabilitation after, 222–224, 223t, 1711. See also Knee rehabilitation return to play after, 1712 single-bundle, 1688, 1705–1706, 1705f, 1707f evaluation of, 1696, 1699–1700, 1699t Posterior drawer test, in posterior cruciate ligament injury, 1690, 1690f, 2214 Posterior humeral circumflex artery, quadrilateral space compression of, 1142 Posterior interosseous nerve injury, in radial head fracture, 1261–1262 Posterior oblique ligament (POL), 1625, 1627f Posterior sag test, in posterior cruciate ligament injury, 1690, 1691f Posterior tibial tendon. See Tibial tendon, posterior Posterolateral corner (PLC). See also Posterolateral corner (PLC) injury anatomy of, 1685, 1718–1723, 1721f–1722f, 1748 biomechanics of, 1687–1688, 1687t, 1723–1725, 1723f dial test of, 1691 stabilizing function of, 1724–1725 Posterolateral corner (PLC) injury, 1718–1747 arthroscopy in, 1730–1731, 1732f biceps femoris in, 1722 in children, 1744 classification of, 1725, 1725t, 2216 clinical presentation of, 1725, 1725t, 1726b dial test in, 1727, 1728f dynamic shift test in, 1728 external rotation recurvatum test in, 1726, 1726f history in, 1725, 1726f incidence of, 1743 magnetic resonance imaging in, 1730, 1730f, 1731f mechanisms of, 1725, 1726f nonoperative treatment of, 1731–1732, 1744 operative treatment of, 1732–1741 biceps tenodesis in, 1733–1734, 1735f complications of, 1742, 1742f cruciate ligament reconstruction with, 1732, 1743 fibular collateral ligament reconstruction in, 1736–1737, 1737f intrasubstance repair in, 1733, 1734f PLC reconstruction in, 1737–1741, 1737t, 1738f–1740f popliteus tendon recession procedure in, 1732–1733, 1733f popliteus tendon reconstruction in, 1736, 1736f rehabilitation after, 1741–1742, 1741f, 1742t return to play after, 1742, 1742b two-tailed reconstruction in, 1734, 1736, 1736f varus correction and, 1744–1747, 1745f–1746f osteoarthritis and, 1725, 1743–1744 physical examination in, 1725–1728, 1726b, 1726f–1729f posterior cruciate ligament injury and, 1689, 1700, 1703–1704, 1744, 1745f double-bundle reconstruction in, 1706–1710, 1708f–1710f proximal tibial osteotomy in, 1744–1747, 1746f

Posterolateral corner (PLC) injury (Continued) posterior tibial translation in, 1728 posterolateral drawer test in, 1727, 1729f radiography in, 1728, 1730f reverse pivot shift test in, 1727–1728, 1729f treatment of, 1731–1741 varus stress test in, 1727, 1727f, 1727t Posterolateral corner (PLC) reconstruction, 1737–1741, 1741b biceps tenodesis for, 1733–1734, 1735f complications of, 1742, 1742f exposure for, 1737–1739, 1738f fixation technique for, 1739–1740, 1739f–1740f graft preparation for, 1739, 1739f in knee dislocation, 1758–1759, 1760f preparation for, 1737, 1737t rehabilitation after, 1741f, 1742t return to play after, 1742, 1742b two-tailed technique of, 1734, 1736, 1736f varus laxity after, 1742, 1742f Posterolateral drawer test, in posterolateral corner injury, 1727, 1729f Posteromedial corner, 1625, 1627f Posteromedial pivot test, 1691 Posterosuperior glenoid impingement. See Shoulder impingement, internal Postphlebitic syndrome, 376 Postural exercises, in trunk stabilization, 348–349 Potassium, caffeine effects on, 421 Power, statistical, 2218 Power analysis, 111–112, 116–117 Power nap, 453, 454b Prazosin in complex regional pain syndrome, 363t, 365 in hypertension, 160t Pre-experimental research, 103–104 Precision, measurement, 100 Predictive value, test, 108, 109f, 110t Pregabalin, in complex regional pain syndrome, 363t, 364 Pregnancy, exercise and, 481–483, 482b Preparticipation examination, 508–515, 512b abdominal examination in, 512 athlete history in, 509 cardiovascular examination in, 512 clearance for participation and, 513–515 frequency of, 508 genitourinary examination in, 512 logistics of, 508–509, 509t musculoskeletal examination in, 512–513 neurologic examination in, 513 objectives of, 508, 508t physical examination in, 509–513, 510f–511f, 514t–515t pulmonary examination in, 512 skin examination in, 513 station-based setup for, 508–509, 509t timing of, 508 visual examination in, 509 written health history in, 508–509 Press-up exercise, in shoulder rehabilitation, 241, 242f Pressure, compartment, 650–651, 1860, 1860t. See also Compartment syndrome Prevalence, 102, 102t, 103, 108, 109f, 110t, 2219 Priapism, androstenedione and, 418 Primary surgery, in on-field emergency, 517, 519–520, 520f, 520t, 521f Primidone, in epilepsy, 188 Profunda femoris artery, 1501 Progesterone, exercise effects on, 217t, 218


xxxix

Prolactin, exercise effects on, 217, 217t Pronator syndrome, 1317–1318 Pronator teres, hypertrophy of, 622 Prone exercises, in trunk stabilization, 342t, 345 Prone horizontal abduction exercise, in shoulder rehabilitation, 242–243, 243f Propionibacterium acnes infection, 415, 457 Propranolol in complex regional pain syndrome, 363t in hypertension, 160t Proprioceptive exercises ankle rehabilitation, 273, 275, 298, 340 in female athlete, 479–480 knee rehabilitation, 294–296, 1672, 1674 in ACL rehabilitation, 1674 cone ambulation, 295, 296f cone reaching, 296, 297f double-leg jumping, 296, 298f lunging, 296, 297f plyoball toss, 294, 294f side-to-side weight shifting, 294–295, 295f single-leg hopping, 296, 298f sports cord lunge, 296, 297f shoulder rehabilitation, 296, 298 MR Systems Cable Column, 298, 299f plyoball perturbations, 296, 298f plyoball Rebounder, 298, 299f wall bounce, 298, 298f Prostate cancer, anabolic-androgenic steroid effects on, 416 Protective equipment, in sudden death prevention, 170–171 Protein, dietary metabolism of, 211–212 for pediatric athlete, 467 powder, 409 requirements for, 404–405, 405t Protein C, 372, 373f deficiency of, 372, 374t Protein S, 372, 373f deficiency of, 372, 374t Proteoglycans articular cartilage, 41, 42, 43f, 44–45 loss of, 49, 49t bone, 67 ligament, 34 meniscal, 58 structure of, 43f tendon, 23–24 Prothrombin G20210A, 372, 374t Proximal first metatarsal osteotomy, in hallux valgus, 2070–2071, 2076b, 2077f, 2078–2079 Proximal row carpectomy, 1449–1450 Pseudoboutonnière deformity, 1389–1390 Pseudohypoparathyroidism, 74t, 77t Pseudoparalysis, in complex regional pain syndrome, 357–358 Psoriasis, 204–205, 204f Psychological factors/disorders in complex regional pain syndrome, 358 in pain dysfunction syndrome, 351, 352t team physician treatment of, 516 Psychological response, rehabilitation-related, 433–436 cognitive component of, 434–437 coping component of, 435–436 disruption and, 435 emotional nourishment and, 435 past coping and, 435–436 perceptual component of, 435 physiological component of, 434 Psychologist. See Sport psychologist Psychomotor vigilance task, 451, 452f

xl

Index

Psychotherapy, in complex regional pain syndrome, 365 Puberty. See also Children/adolescents flexibility at, 465 psychosocial aspects of, 466 Pubic rami, stress fracture of, 638, 638f Pubic symphysis, inflammation of, 1466, 1466f Pubis, anatomy of, 1452 Pubofemoral ligament, 1452, 1453f Pudendal artery, 1455f Pudendal nerve, 1454–1455 entrapment of, 1469 Pull-down exercise, in shoulder rehabilitation, 245, 247f Pulmonary contusion, on-field, 526 Pulmonary edema, high-altitude, 504 Pulmonary embolism, 370–385 age-related factors in, 375 evaluation of, 374, 376–378, 376t, 378f, 379f treatment of, 384–385, 384t Pump bump, 1963, 1998 Push-up exercise, in shoulder rehabilitation, 241, 241f, 245, 247f Pushing and pulling exercises, in core training, 287, 288f Pyelography, intravenous, in cervical spine anomalies, 712, 712f

Q Quadratus femoris, 1454t, 1455f Quadriceps active test, in posterior cruciate ligament injury, 1691, 1691f Quadriceps (Q) angle, 1553–1554, 1554f, 1595 Quadriceps muscle anatomy of, 1485, 1485f, 1550–1551, 1551f contraction of, for patellar evaluation, 1564 contusion of, 13, 1459, 1481–1484, 1482b in adolescents, 1484 biomechanics of, 1481 classification of, 1481–1482, 1481t clinical presentation of, 1482 complications of, 1483–1484, 1484b, 1484f imaging of, 1482 myositis ossificans with, 1483, 1484b, 1484f physical examination in, 1482 return to play after, 1484, 1484b treatment of, 1482–1484, 1482b, 1482f isometric strengthening of, in ACL-injured knee, 1586 myositis ossificans of, 1483, 1484b, 1484f, 1495–1496 neuromuscular activation exercise for, in knee rehabilitation, 256–257, 257f strain of, 1462, 1493–1497 in adolescents, 1497 clinical presentation of, 1493–1494, 1494f complications of, 1495–1496 grade of, 1494 imaging of, 1494–1495, 1494f–1495f physical examination of, 1494, 1494b, 1494f rehabilitation protocol for, 1496, 1496t return to play after, 1496, 1497b treatment of, 1495–1496, 1495b, 1496t strengthening of in ACL rehabilitation, 1671 in arthritis, 1774 Quadriceps tendon anatomy of, 1514 magnetic resonance imaging of, 560 repair of, 1524–1525, 1524f–1525f rupture of, 1521–1522, 1522t

Quadriceps tendon (Continued) complications of, 1525 evaluation of, 1522–1523, 1522f treatment of, 1523–1524, 1524f–1525f Quadrilateral space syndrome, 1142 Quadriplegia. See Cervical cord neurapraxia/ quadriplegia Quadruped progression exercise, 282–283 alternating arm and leg, 282–283, 283f drawing-in maneuver in, 282 hip extension, 282, 283f in trunk stabilization, 342t, 346 upper extremity lift, 282, 282f Qualification to play, 507. See also Preparticipation examination Qualitative research, 106–107 Quantitative sudomotor axon reflex test, 360–361 Quercetin, 409 Quinapril, 160t Quinine sulfate, in cramps, 12

R Raccoon eyes, 525 Radial artery, 1160f Radial collateral ligament anatomy of, 1301–1302, 1303f stabilizing effect of, 1193, 1195f, 1231, 1231f tear of, 576, 577f Radial head articular surface of, 1190, 1190f fracture of, 1258–1262 capitellar fracture with, 1259 classification of, 1260 coronoid process fracture with, 1259 evaluation of, 1258–1260, 1260f fragments in, 1260, 1260f magnetic resonance imaging in, 535f medial collateral ligament rupture with, 1259 nonunion of, 1278 operative treatment of, 1260–1262, 1275–1276 complications of, 1262 exposure in, 1260–1261, 1261f failure of, 1258, 1259f–1260f fixation in, 1261 prosthetic replacement in, 1261–1262 pediatric, 1286–1287 posterior dislocation and, 1259, 1261, 1263, 1264f, 1269 resection in, 1260, 1262 prosthetic, 1258, 1260f, 1261–1262 stabilizing effect of, 1192–1193, 1193f Radial neck, fracture of, 1280t, 1287–1288 Radial nerve anatomy of, 1159, 1161, 1161f injury to, 1315–1316. See also Radial tunnel syndrome in humeral shaft fracture, 1182 in lateral epicondylitis, 1199 vs. lateral epicondylitis, 618 in pediatric supracondylar fracture, 1282 Radial osteotomy, in Kienböck’s disease, 1377 Radial shortening, in Kienböck’s disease, 1377 Radial styloidectomy, 1449 Radial tunnel syndrome, 1315–1316 anatomy of, 1315–1316 etiology of, 1315 history in, 1316 nonoperative treatment of, 1316 operative treatment of, 1316 physical examination in, 1316


Radiation, heat loss by, 493, 499 Radiation exposure, in children, 588 Radiation therapy, in heterotopic ossification, 1277, 1294–1295, 1297 Radiocarpal ligaments, 1320 Radiofrequency ablation, in Wolff-ParkinsonWhite syndrome, 170 Radiofrequency sympathectomy, in complex regional pain syndrome, 366 Radiography, 533–534 in accessory navicular, 1963, 1963f in acetabular labral tears, 1470 in Achilles tendon injury, 1998, 2003, 2003f in acromioclavicular joint injury, 831b, 833f, 834f, 835–836, 836f–838f in acromion fracture, 861, 861f, 866, 866f–867f in ankle dislocation, 1945, 1946f in anterior cruciate ligament injury, 1650 in anterior glenohumeral joint instability, 934, 935f in anterior tibial stress fracture, 643, 644f in atlanto-occipital instability, 705, 705f in atlantoaxial instability, 705, 707f of atlas-dens interval, 694, 695f in atraumatic glenohumeral joint instability, 945 in avulsion fracture, 553, 556f in Bennett’s fracture, 1402, 1402f in bifurcate sprain, 1954, 1954f in bone cyst, 552, 553f in Buschke’s disease, 2166, 2166f in C1 posterior arch absence, 711, 711f in C3-C4 facet dislocation, 679, 679f in C3-C4 subluxation, 678–679, 679f in C5 fracture, 697, 697f in calcaneal apophysitis, 2162, 2162f in calcaneal stress fracture, 646, 647f in capitate fracture, 1348–1349 in capitellar osteochondritis dissecans, 623, 624f, 1241, 1242f–1245f in capsulorrhaphy arthropathy, 1106f in carpometacarpal joint dislocation, 533, 534f, 1387, 1387f in cervical fusion, 699, 699f, 700f in cervical spine compression fracture, 680–681, 680f, 681f–683f, 709, 709f in chondral defect, 1773 in complex regional pain syndrome, 358 in congenital lumbar stenosis, 747, 747f in coracoid fracture, 861, 862f, 878–879, 878f–879f, 880 in distal clavicular osteolysis, 855f in distal femoral stress fracture, 555f in distal fibular stress fracture, 644, 644f in distal humeral fracture, 1250 in distal radioulnar joint injury, 1374 in elbow heterotopic ossification, 1292–1293, 1292f, 1298f in elbow joint effusion, 534, 535f in extensor carpi ulnaris tendinopathy, 1354 in femoral neck stress fracture, 638, 640f–642f, 1465 in femoral shaft stress fracture, 1478t, 1479, 1479f–1480f in femoroacetabular impingement, 1471 in fifth metatarsal stress fracture, 648, 649f in fracture, 552–553 in Freiberg’s infraction, 1973, 1973f, 2166, 2167f in ganglion cyst, 1444 of glenohumeral joint, 947–949, 947b, 948f in glenohumeral joint instability, 915–916 in glenohumeral joint osteoarthritis, 1105f, 1108, 1108f

Index Radiography (Continued) in glenohumeral rheumatoid arthritis, 1106, 1107f in glenoid fracture, 861, 861f in glenoid rim fracture, 868f–870f in gymnast wrist, 1375 in hallux rigidus, 2182, 2182f in hallux valgus, 2069, 2069b, 2073f, 2075f in hamate fracture, 1346f in high (syndesmosis) ankle sprain, 1940–1942 in hip degenerative disease, 1503 in humeral cyst–related fracture, 552, 553f in humeral epicondyle fracture, 1286f in humeral head avascular necrosis, 1107, 1107f in humeral shaft fracture, 1178, 1179f–1181f in iliac spine avulsion fracture, 556f in ingrown toenail, 2098 in Iselin’s disease, 2167, 2168f–2169f in Jefferson fracture, 705, 706f in Jersey finger, 1425, 1425f in Kienböck’s disease, 1377, 1377b, 1378f in Klippel-Feil syndrome, 693, 693f, 711–712, 712f in knee arthritis, 1789–1790, 1790f in knee dislocation, 1753, 1752f–1753f in Köhler’s disease, 1973, 1973f, 2162, 2163f in lateral ankle sprain, 1918–1919, 1918f–1919f in lateral epicondylitis, 1199 in Lisfranc sprain, 1956–1957, 1957f, 2181f in lumbar degenerative spondylolisthesis, 748 in lumbar isthmic spondylolisthesis, 748, 749f of lumbar spine, 724–726, 725f in lumbar spine burst fracture, 735, 735f in lumbar spine stenosis, 746f in lunate fracture, 1353f in lunotriquetral ligament injury, 1331 in mallet finger, 1420f in medial ankle sprain, 1936, 1936f–1937f in medial collateral ligament injury, 1629, 1630f in medial malleolar stress fracture, 644–645, 645f in meniscal deficiency, 1619 in meniscal injury, 1602 in metacarpophalangeal joint dislocation, 1380, 1380f–1381f in metatarsal stress fracture, 648, 648f in myositis ossificans, 13, 14f in olecranon bursitis, 1210f, 1247, 1247f in olecranon fracture, 1271–1272 in olecranon stress fracture, 1225, 1225f in os acromiale, 859, 860f in os odontoideum, 692, 692f in Osgood-Schlatter disease, 1528 in osteitis pubis, 1466, 1490, 1491f in overhead throwing injury, 1217 in Panner’s disease, 623, 625f in pars interarticularis defects, 760, 760f in Parsonage-Turner syndrome, 1145 in patellar dislocation, 1538–1540, 1541f, 1558–1564, 1559f–1563f, 1560t–1561t, 1564t–1566t in patellar fracture, 1574, 1574f in patellar tendon rupture, 1523, 1523f in pectoralis major rupture, 1060 pediatric, 590 in ankle fracture, 1964 in avulsion fracture, 599 bone on, 591–592, 592f of cervical spine, 702, 703f of clavicle, 781f

Radiography (Continued) in clavicular fracture, 596, 596f in distal tibial epiphyseal fracture, 1641, 1642f, 1643f in elbow injury, 1229–1230, 1230f, 1279–1280 in Ewing’s sarcoma, 607, 609f, 610 in fibrous dysplasia, 606, 607f, 608f in fracture, 593–599, 594f–598f in hemangioma, 606 of hip, 587, 588f in inflammatory arthritis, 602–603, 602f in juvenile idiopathic arthritis, 602–603, 602f in Little Leaguer’s elbow, 1183, 1184f–1185f in Little Leaguer’s shoulder, 1173, 1174f in nonossifying fibroma, 605–606, 605f in osteochondroses, 599, 600f in osteomyelitis, 601, 602f in osteosarcoma, 606–607, 608f of physis, 591–592, 592f in posterior cruciate ligament injury, 1716 in proximal humeral physeal fracture, 1074–1075, 1075f–1076f in proximal humeral physeal stress fracture, 1092, 1093f of proximal humerus, 782, 782f in proximal tibial epiphyseal fracture, 1642, 1643f radiation dose in, 588 in slipped capital femoral epiphysis, 597, 598f, 1476, 1476f in supracondylar fracture, 596–597, 597f in thoracolumbar spine injury, 759–761, 760f in unfused os acromiale, 781, 781f in unicameral bone cyst, 606, 606f in Pellegrini-Stieda lesion, 1629, 1630f in perilunate dislocation, 1332 in peroneal tendinitis, 1989 in peroneal tendon subluxation, 1992 physics of, 533–534 in pisiform fracture, 1350, 1352f in plantar fasciitis, 2046–2047, 2047f in plantar keratoses, 2110, 2110f in posterior cruciate ligament injury, 1692–1693 in posterior glenohumeral joint instability, 937, 941–942 in posterior sternoclavicular joint dislocation, 799f in posterior tibial tendinitis, 1981 in posterior tibial tendon injury, 1979 in posterolateral corner injury, 1728, 1730f in proximal humeral fracture, 1037–1038, 1038b, 1039f–1042f in proximal metaphyseal humeral fracture, 1087 in proximal ulna fracture, 1271–1272 in quadriceps myositis ossificans, 1483, 1484f in quadriceps tendon rupture, 1523, 1523f in radial head fracture, 1259–1260, 1259f in radial osteomyelitis, 83f in recurrent patellar dislocation, 1558–1564, 1559f–1563f, 1560t–1561t, 1564t–1566t in recurrent posterior glenohumeral instability, 941–942 in retrocalcaneal bursitis, 2032–2034, 2032f, 2033f in rheumatoid arthritis of wrist, 1444 in rib fracture, 637, 637f, 894, 1187 in rotary atlantoaxial subluxation, 706–707, 708f in rotator cuff disorders, 615, 954–955, 955f, 998, 1000


xli

Radiography (Continued) in scaphoid fracture, 554f, 1333f, 1335f–1336f, 1336, 1365 in scapholunate ligament injury, 1325 in scapular fracture, 861, 861f–862f in scapular osteochondroma, 887, 888f in sesamoid dysfunction, 2090, 2091f–2092f in sesamoid osteochondrosis, 2169, 2170f in sesamoid stress fracture, 649, 649f in Sever’s disease, 1973, 1974f in shoulder impingement syndrome, 954–955, 955f in Sinding-Larsen-Johansson disease, 1529 in snapping hip syndrome, 1458 of soft tissues, 534, 535f in spear tackler’s spine, 694, 695f in spinal deformity, 737 in spinal lymphoma, 758f in spondylolysis, 635, 636f, 725, 726f, 762 in sternoclavicular joint injury, 798f, 802–805, 803f–804f in sternomanubrial dislocation, 898–899, 899f in stress fracture, 552–553, 633, 634t in subtalar dislocation, 1952–1953 in subtalar sprain, 1949–1950, 1949f in subungual exostosis, 2106, 2106f in supracondylar process fracture, 1186, 1186f in suprascapular nerve injury, 1121, 1122f in talar osteochondral lesions, 2144–2145, 2145t, 2147f in tarsal coalition, 1961, 1961f–1962f in tarsal navicular stress fracture, 646, 646f in thoracic compression fracture, 755f in thoracic outlet syndrome, 1133, 1133f of thoracic spine, 724, 724f in tibial fracture nonunion, 82f–83f in tibial stress fracture, 1852, 1852f, 2014, 2015f–2016f in trapezium fracture, 1347–1348, 1349f in triangular fibrocartilage complex tear, 1436 in triceps tendinitis, 1207 in triceps tendon rupture, 1170–1171, 1171f in triquetrum fracture, 1351f in turf toe, 2083–2084, 2084f, 2086f in ulnar collateral ligament injury, 1400, 1400f in ulnar neuropathy, 623 in ulnar styloid impaction syndrome, 1446, 1446f in ulnocarpal impaction syndrome, 1440 in valgus instability, 620 in varus malalignment, 1809–1814, 1812f, 1813f in vertebral body fracture, 698f in wrist injury, 1321, 1322, 1322f–1323f in wrist loose bodies, 1447 Radiolabeled leukocyte imaging, in osteomyelitis, 547 Radiolunate ligament, 1320 Radionuclide imaging, 543–547 in bone tumors, 547, 548f in cellulitis, 547 in complex regional pain syndrome, 359 in femoral neck stress fracture, 639, 641f, 642f in femoral shaft stress fracture, 1479, 1480f gamma camera for, 544 in high (syndesmosis) ankle sprain, 1942 in infection, 547 of lumbar spine, 726–727, 726f in metastatic disease, 547, 547f normal, 545f, 591f

xlii

Index

Radionuclide imaging (Continued) in occult fracture, 546, 552, 557 in osteitis pubis, 1466, 1466f in osteomyelitis, 547, 601, 602f in osteoporotic fracture, 546, 547f in pars interarticularis stress fracture, 726, 726f pediatric, 591, 591f in elbow injury, 1230 in osteomyelitis, 601, 602f in plantar fasciitis, 2046–2047, 2047f in posterior cruciate ligament injury, 1693 in pubic rami stress fracture, 638, 638f in quadriceps myositis ossificans, 1483 radiopharmaceuticals for, 544 in sacral stress fracture, 736, 736f in shin splints, 545, 545f in stress fracture, 552, 633, 634t in tarsal navicular stress fracture, 646, 646f in thoracic compression fracture, 734, 734f of thoracic spine, 726–727, 726f three-phase protocol for, 544 in tibial stress fracture, 545–546, 545f, 1852, 1853f, 2014–2015, 2015f in trauma, 545–546, 545f–547f in turf toe, 2084, 2084f whole-body, 544, 545f, 591, 591f in wrist injury, 1321 Radioscaphocapitate ligament, 1320, 1432, 1432f Radioscapholunate ligament, 1320, 1432, 1432f Radioulnar joint distal, injury to, in children, 1374–1375, 1374b proximal, heterotopic ossification at, 1297 Radius distal arthritis of, after scaphoid fracture, 1339–1340 physeal injury of, in gymnast, 1375–1376 vascular supply of, 1339 fracture of, in children, 594f, 595, 597 osteomyelitis of, 83f proximal. See also Radial head ossification of, 1228 Ramipril, 160t Randomized controlled trials, 101 Range of motion of acromioclavicular joint, 828, 828f in anterior cruciate ligament rehabilitation, 1670–1671 of hip, 1452t, 1503 of patella, 1557 after proximal humeral fracture, 1050, 1056 in rotator cuff disorders, 996, 998f of sternoclavicular joint, 794, 796f in thoracolumbar spine, 721, 759 in wrist injury, 1320 Rapid strep test, 150 Rasmussen’s syndrome, 190 Rate, 102, 102t false-negative/false-positive, 108, 109f Ratio method, in cervical spine stenosis evaluation, 683–686, 683f–685f Rebounder, in shoulder rehabilitation, 296, 299f Recreational drugs, 424–431. See also specific drugs Rectus femoris, 1454t, 1455f, 1481, 1550–1551. See also Quadriceps muscle Rectus sheath hematoma, 526 Red blood cells erythropoietin effects on, 420–421 high-altitude effects on, 503 Reduction-association of scapholunate (RASL) procedure, 1325, 1326f, 1327

Referred pain, to heel, 2047 Reflex(es) bulbocavernous, 675 in thoracolumbar spine injury, 722–723 Reflex sympathetic dystrophy. See Complex regional pain syndrome Regional intravenous sympathetic blockade, in complex regional pain syndrome, 360 Rehabilitation. See also at specific joints and disorders articular cartilage protection in, 225–228, 226f biofeedback in, 224–225, 233, 234f cryotherapy in, 234–235, 235f electrical currents in, 229–233 for functional restoration, 230–233, 231f–234f for pain modulation, 229–230, 230f for swelling, 230, 231f exercise prescription in, 238–293. See also Therapeutic exercise(s) iontophoresis in, 233–234, 235f in joint stiffness, 225, 225f laser in, 235–236, 236f in muscle atrophy, 224–225 psychological response in, 433–436 cognitive component of, 434–437 coping component of, 435–436 perceptual component of, 435 physiological component of, 434 sport psychologist in, 437–440 ultrasound in, 236–237 Rehabilitation cycle, 728, 728f Relative incidence rate, 102, 102t Relative motion, 89–90 Relative rate, 102, 102t Relative risk, 2218 Reliability measurement, 101f statistical, 100, 2217–2218 Relocation test in glenohumeral joint instability, 914, 915f, 939, 939f in glenohumeral joint osteoarthritis, 1108 in rotator cuff disorders, 996, 999f Renal osteodystrophy, 73t, 75t, 77t Repetitive trauma. See Overuse injury Research, 97–99, 98f. See also Statistics analytical, 107–108 clinical, 99–100 controls in, 101–102, 104–105 experimental, 103–106, 105f, 106f–107f hypothesis testing in, 110–112 philosophical, 108 pre-experimental, 103–104 qualitative, 106–107 question development for, 97 rate measures in, 102, 102t risk measurement in, 103 study design for, 99, 101–110, 101f–109f analytical, 107–108 blinding in, 104–105 control group in, 101–102, 104 experimental, 101f, 103–106, 105f matching in, 101 observational, 101–103, 101f, 103t, 106–107 power analysis in, 111 pre-experimental, 103–104 qualitative, 106–107 single-subject, 105–106, 105f–107f subjects for, 97 team for, 97 variables in, 97, 99


Reserpine in complex regional pain syndrome, 365 in hypertension, 160t Respiratory distress, 184–185, 184b. See also Bronchospasm Respiratory system cocaine effects on, 429 exercise effect on, 220 infection of, 149–150 marijuana effects on, 426 Resuscitation, in sudden death, 171–172, 171t Retinaculum patellar lateral, 1548, 1548f, 1551–1552 release of, 1545, 1567–1568 medial, 1548, 1548f, 1551–1552, 1551f release of, 1568 repair of, 1545–1546 peroneal inferior, 1987 superior, 1931, 1987 congenital absence of, 1991 disruption of, 1932 imbrication of, 1932–1933 reconstruction of, 1995 Retinoids, in acne, 205 Retrocalcaneal bursa, 2031, 2031f–2032f aspiration of, 2033 palpation of, 2032 Retrocalcaneal bursitis, 2030–2042 Achilles tendinosis with, 2030–2031, 2034, 2034f, 2036 anatomy of, 2031, 2032f biomechanics of, 2031 brisement therapy in, 2035 calcaneal exostosectomy in, 2037 endoscopic débridement in, 2037 evaluation of, 2032, 2032f, 2035f, 2036 Haglund’s deformity and, 2030, 2031f, 2038, 2038f nonoperative treatment of, 2035, 2037–2038, 2038f operative treatment of, 2035–2041, 2037f, 2038f–2040f orthotic devices in, 2035 os calcis in, 2031, 2031f–2032f parallel pitch line measurement in, 2036 radiography in, 2032–2034, 2033f–2034f return to play after, 2041 shock-wave therapy in, 2035 vs. soleus muscle anomaly, 2036 treatment of, 2035–2041 Retroclavicular Spurling’s test, 1132–1133, 1133f Reversal research design, 105, 105f Reverse pivot shift test in posterior cruciate ligament injury, 1692, 1692f in posterolateral corner injury, 1727–1728, 1729f in varus malalignment, 1807–1808 Reverse straight leg raising test, in thoracolumbar spine injury, 722 Rewarming therapy, 501, 528, 529 Rhabdomyolysis exertional, 496–497 magnetic resonance imaging in, 558 Rheumatoid arthritis glenohumeral joint, 1105t, 1106, 1107f arthroplasty in, 1114 arthroscopic treatment of, 1110–1111 wrist proximal row carpectomy in, 1449–1450 radial styloidectomy in, 1449 synovectomy in, 1443–1444

Index Rhomboid fossa, 793, 793f Rhomboid ligament, 793, 793f Rhomboids, anatomy of, 786, 786f, 859f, 886f Rhythmic stabilization training in core training, 286 in elbow rehabilitation, 255, 255f Rib(s) first, stress fracture of, 636–637, 637f floating, avulsion fracture of, 895–896, 896f fracture of, 893–896, 893t, 1187 avulsion, 895–896, 896f in children, 894 on-field, 525 return to play after, 894–895, 895f, 895t, 1187 stress, 895–896, 895t, 896f traumatic, 893–895, 895t middle, stress fracture of, 637 Riboflavin, requirements for, 406b Rickets, 72–73, 73t, 75t–77t, 79b Ring test, for CSF, 525 Ringworm, 198, 199f Risk, 102–103, 102t Roeder’s knot, 135, 135f Rolando fracture, 1403 Rolling side bridge exercise, in core training, 284, 284f Romanian deadlift exercise, 267–268, 269f single-leg, 268, 269f Roos’ test, in thoracic outlet syndrome, 1132, 1133f Rotary atlantoaxial subluxation, in children/ adolescents, 706–707, 708f Rotation training, in core training, 286–288, 288f–289f Rotator cuff, 986–1015. See also Infraspinatus; Subscapularis; Supraspinatus; Teres minor age-related changes in, 974–975, 975f anatomy of, 989–990, 989f–991f pediatric, 783, 784–785, 785f, 789–790, 789f arthrography of, 958 biomechanics of, 990–994, 992f–993f cyst of, 964–965, 965f, 980, 980t denervation of, 965, 965f, 975 disorders of. See Rotator cuff disorders; Rotator cuff tear(s) fatty atrophy of, 963, 963f, 965, 980 intramuscular cyst of, 964–965, 964f magnetic resonance imaging of, 564–566, 953, 953t, 958–965, 960f–964f, 960t pseudorupture of, 860 radiography of, 955f, 957 in shoulder rehabilitation, 241–243, 242f, 243f, 250t strengthening exercises for, 242–244, 242f, 243f, 244f, 1003–1006, 1004f–1007f, 1007 stretching exercises for, 1003, 1003f, 1007 ultrasonography of, 951–953, 952f, 953t vascular anatomy of, 989–990 Rotator cuff disorders. See also Rotator cuff tear(s) biomechanics of, 990–994, 992f denervation, 964–965, 965f, 975 disability with, 995, 1002 etiology of, 1001–1002 evaluation of, 994–1001 apprehension test in, 996, 999f arthrography in, 949–950, 949f, 958, 1000 arthroscopic, 1009–1010 chief complaint in, 994–995 Hawkins’ sign in, 997, 1000f impingement test in, 998 inspection in, 995, 996f

Rotator cuff disorders (Continued) load and shift test in, 996, 999f magnetic resonance imaging in, 958–965, 960f–965f, 1001, 1001f Neer’s sign in, 997, 1000f palpation in, 996, 997f patient history in, 995 physical examination in, 995–998, 996f–1000f radiography in, 955f, 957–958, 998, 1000 range of motion in, 996, 998f relocation test in, 996, 999f Speed’s test in, 997, 1000f ultrasonography in, 1000–1001 Yergason’s test in, 997, 1000f historical perspective on, 986, 986f nonoperative treatment of, 1006–1010, 1011 activity modification in, 1006 corticosteroid injection in, 1007 pharmacological, 1006–1007 strengthening exercises in, 242–244, 242f–244f, 1003–1006, 1004f–1006f, 1007, 1008f stretching exercises in, 1003, 1003f, 1007 ultrasound in, 1007 operative treatment of, 1008–1031. See also at Rotator cuff tear(s) arthroscopic, 1009–1010, 1012–1014, 1013f–1015f open, 1008–1009, 1014–1015 overuse-related, 612, 614–615, 615b, 1217–1219 peritendinous, 30 prevention of, 1003–1006, 1003f, 1004f–1006f severity of, 1002–1003 SLAP lesion and, 1024. See also SLAP (superior labrum, anterior to posterior) lesion Rotator cuff tear(s). See also Rotator cuff disorders aging and, 988 arthrography in, 949–950, 949f, 958 arthroscopic repair of, 1012–1014 arm positioning for, 1012 bursectomy with, 1013 care after, 1015 double-row technique for, 988, 988f, 1013, 1014f–1015f evaluation for, 1013 portals for, 1012–1013, 1013f subacromial decompression with, 1013, 1014f epidemiology of, 986–988 evaluation of. See Rotator cuff disorders, evaluation of fatty infiltration with, 770, 989, 989f full-thickness, 994 arthroscopic repair of, 1012–1014, 1013f–1015f magnetic resonance imaging in, 960–963, 960t, 961f–962f open repair of, 1014–1015 overhead throwing–related, 1218 postoperative care in, 1015 glenohumeral joint force in, 775 graft repair of, 989 historical perspective on, 986, 986f magnetic resonance arthrography in, 565–566, 567f natural history of, 988 in older patient, 974–975, 975f, 988 overhead throwing–related, 1218–1219 partial-thickness, 994 magnetic resonance imaging in, 960–961, 960t, 961f–962f


xliii

Rotator cuff tear(s) (Continued) overhead throwing–related, 1218–1219 treatment of, 1012 radiography of, 954–955, 955f, 957 recurrence of, 565–566, 567f, 988 treatment of, 615, 987–989, 988f, 1010–1015 nonoperative, 991, 1010 operative, 1011–1015, 1013f–1015f tendon transfer/graft in, 989 Rotator interval anatomy of, 773–774, 966, 966t, 990, 991f function of, 966, 966t magnetic resonance imaging of, 966, 966t, 967f tear of, 966, 967f Roux-Elmslie-Trillat procedure, 1595–1596 Rowing exercises on cable column, 240, 240f in core training, 286, 286f, 287, 288f with elastic resistance, 240, 240f prone, 240, 240f shoulder injury and, 249 in shoulder rehabilitation, 245, 247f in trapezius training, 240, 240f Running shoe. See Shoes Running Shoe Book, The (Cavanagh), 1875 Russian hamstring curl, 317f, 325

S Sacroiliac ligaments, sprain of, 1462 Sacrum anatomy of, 1451–1452 stress fracture of, 638, 736, 736f, 1465 Sagebrush bark sandal, 1873, 1874f Sagittal band bridge, 1390 Sagittal band rupture, 1390 SAID (specific adaptations to imposed demands) principle, 213–214 Sail sign, 706, 708f Salty sweater, 402 Sample/sampling, 99, 2218 consecutive, 99 convenience, 99 error and, 111 judgmental, 99 nonprobability, 99 nonrandom, 99 random, 99 Saphenous nerve, entrapment of, 1497–1499, 1497b, 1498f Saphenous vein graft, in popliteal artery entrapment, 1844–1845, 1845f, 1846b, 1846t, 1847 Sarcoidosis, 77t heel pain in, 2051 Sarcoma, radiation-induced, 1295 Sarcomere, 5, 207–208, 208f–209f Sarcoplasmic reticulum, 5, 7f Sartorius, 1454t, 1455f Satellite cell, 5 Scabies, 201, 201f Scalars, 86 Scalp in head injury, 658 pediculosis capitis of, 200–201, 201f Scaphoid. See also Scaphoid fracture anatomy of, 1319–1320, 1319f bipartite, 1366 humpback deformity of, 1340–1341 Scaphoid fracture adult, 1335–1340 classification of, 1335, 1335f, 1336t clinical manifestations of, 1335–1336 displaced, 1335, 1337, 1339

xliv

Index

Scaphoid fracture (Continued) magnetic resonance imaging in, 552, 554f nondisplaced, 1335, 1336–1337, 1338f nonunion of, 1339–1345, 1341f–1344f perilunate dislocation with, 1332, 1333f physical examination in, 1336 radiography in, 1336, 1336f return to play after, 1337, 1339 treatment of, 1336–1339 pediatric, 1364–1368 delayed union of, 1366, 1367f epidemiology of, 1364 evaluation of, 1364–1365 malunion of, 1368 nonunion of, 1367–1368 radial physeal injury with, 1365 stress-type, 1365–1366, 1366f treatment of, 1366 types of, 1365, 1365f Scaphoid graft, in scaphoid nonunion, 1341–1345, 1342f–1344f Scapholunate advanced collapse (SLAC) wrist, 1327–1330 stage I, 1328, 1328t stage II, 1328, 1328t, 1329f stage III, 1328–1329, 1328t, 1329f–1330f Scapholunate angle, 1322, 1322f Scapholunate dissociation, 1371 Scapholunate interosseous ligament, 1320 Scapholunate ligament, 1432–1433, 1432f injury to (Mayfield I), 1324–1330 acute, 1324, 1326 chronic, 1324, 1327 classification of, 1324 clinical manifestations of, 1324 magnetic resonance imaging in, 1325 pediatric, 1371–1374, 1374t physical examination in, 1324–1325, 1325f radiography in, 1323f, 1325 return to play after, 1326–1327 salvage procedures in, 1327–1330, 1328t, 1329f–1330f subacute, 1324 treatment of, 1325–1327, 1326f–1327f magnetic resonance imaging of, 575, 576f Scapula anatomy of, 858–859, 858f–859f pediatric, 781–782, 781f bursae about, 886, 887b, 887f dyskinesia of, 1007 fracture of. See Scapular fracture muscle attachments of, 858, 858f–859f, 885, 885b, 886f neck of, 782 neurovascular anatomy at, 858–859 osteochondroma of, 887, 888f in shoulder rehabilitation, 240 spine of, 782 strengthening exercises for, 1007, 1008f superomedial angle of, resection of, 888–889, 889f winging of, 616, 1124–1125, 1125f crepitus with, 888 differential diagnosis of, 1125 Scapular exercises protraction, 241, 241f, 250, 251t retraction, 245–246, 247f, 250, 251t strengthening, 1007, 1008f Scapular fracture. See also Acromion, fracture of; Coracoid, fracture of; Glenoid, fracture of of body, 863, 865–866 in children, 872, 875 classification of, 857, 858f evaluation of, 860–861 patient history in, 861

Scapular fracture (Continued) physical examination in, 860–861 radiography in, 861, 861f–862f incidence of, 857 malunion of, 865 mechanism of, 857, 865–866 nonunion of, 865 suprascapular nerve injury with, 1121 Scapular lag, 994, 1001 Scapular retraction test, 892 Scapulothoracic joint, 769, 885–893 anatomy of, 885–886, 885b, 886f pediatric, 784 biomechanics of, 776–777, 776f, 885–886 in children, 787–788, 788f bursitis of, 889–891, 891f crepitus of, 886–889, 887b, 888f–889f dissociation of, 1139 dyskinesia of, 891–892 endoscopy for, 890–891, 891f kinematics of, 776–777, 776f in shoulder impingement, 777 in shoulder rehabilitation, 239–240 Scapulothoracic rhythm, 776 Scheuermann’s disease, 737, 765, 766f Sciatic nerve, 1454, 1501, 1748–1749 entrapment of, 1468 vs. ischial bursitis, 1457 Scintigraphy. See Radionuclide imaging Scoliosis, 736–737 adult, 737 classification of, 737 degenerative, 737 idiopathic, 479, 757, 757f Scottie dogs, 725, 726f, 760, 760f Screening, 109–110 cardiovascular, 167–169, 168t Scrotum, on-field injury to, 527 Scrumpox, 197 Scurvy, 72–73, 73t Seasonal affective disorder, 444 bright light treatment of, 444–445, 445f Seasonal rhythms, 444 Second impact syndrome, 659 Secondary surgery, in on-field emergency, 520, 521f Segond’s fracture, 1650, 1722 Seizures. See also Epilepsy exercise effects on, 187–188 head injury and, 660–661 management of, 190 on-field, 522–523 terminology for, 186–187, 186b Semimembranosus, 1485, 1485f, 1625, 1625f–1627f. See also Hamstring muscles biomechanics of, 1626, 1628f Semitendinosus, 1485, 1485f. See also Hamstring muscles Semitendinosus tendon autograft, in ligament injury treatment, 37–38 Sensitivity, test, 108, 109f, 110, 110t, 2218 Sensory system in complex regional pain syndrome, 356 in thoracolumbar spine injury, 722, 722f Septal ablation, in hypertrophic cardiomyopathy, 170 Seronegative spondyloarthritis, heel pain in, 2033–2034, 2047 Serratia marcescens infection, 398, 398t Serratus anterior palsy of, 1130–1131, 1131f pediatric, 786 scapular attachment of, 858, 858f, 886f therapeutic exercise for, 240–241, 241f–242f


Sesamoid(s) anatomy of, 2087–2088, 2088f, 2169, 2170f arthritis of, 2089 bipartite, 2028, 2029f, 2088 dysfunction of, 2087–2096 classification of, 2088–2089 clinical presentation of, 2089 history in, 2089 imaging in, 2090, 2091f–2092f nonoperative treatment of, 2090, 2092b, 2093f operative treatment of, 2090–2095, 2092b, 2093b, 2094b, 2094f–2095f care after, 2096 complications of, 2096 return to play after, 2096, 2096b physical examination in, 2090, 2090b excision of, 2090–2095, 2093b–2094b, 2093f–2094f fracture of, 2088 nonunion of, 2093 function of, 2087f, 2088 keratosis beneath, 2114 nerve compression at, 2088–2089, 2089f osteochondritis of, 2089–2090, 2092f, 2169–2170, 2170f pain in, 2088–2089, 2088b shaving of, 2092–2095, 2094b, 2095f, 2096 stress fracture of, 648–650, 649f, 2016t, 2027–2028, 2030f vascular supply of, 2087–2088, 2088b Sesamoid ligaments, 2064–2065, 2065f, 2087–2088 Sesamoidectomy, 2090–2095, 2093b, 2093f, 2094b, 2094f care after, 2096 complications of, 2093–2094, 2096 Sesamoiditis, 2089 Sever’s disease, 1973–1974, 1974f, 2053–2054, 2143f, 2162, 2162f Shear force, 94f, 95 Shin splints, 15, 652, 652t, 1857. See also Chronic exertional compartment syndrome radionuclide imaging of, 545, 545f Shock-wave therapy in Achilles tendon injury, 1999 in lateral epicondylitis, 1200 in plantar fasciitis, 2049–2050, 2052 in retrocalcaneal bursitis, 2035 Shoes, 1873–1911 Achilles tendon protector of, 1889 advertising and, 1873, 1873f, 1875 air encapsulation in, 1892 alignment features of, 1900–1905, 1901f biomechanical aspects of, 1896–1906 alignment and control in, 1900–1905, 1901f, 1903f, 1904t–1905t energy return in, 1905–1906 friction and torque in, 1906 shock absorption and, 1897–1899, 1898t, 1899f, 2185–2187, 2185t, 2186f for cavus foot, 1900 cleats on, 2184, 2191–2192, 2195f–2196f collar of, 1889 components of, 1877–1878, 1878f, 1886–1887, 1887f, 1888f bottom, 1889–1890 glossary for, 1879–1886 upper, 1887–1889, 1888f–1889f copolymers for, 1895–1896, 1896t cork for, 1894 energy return from, 1905–1906 ethylene vinyl acetate for, 1892 eyelet stay of, 1888

Index Shoes (Continued) eyelets of, 1888, 1889f for female athlete, 490–491, 491b, 1886–1887 fit of, 1906–1911 flexibility test in, 1909–1910, 1910f guidelines for, 1910, 1910t individual variables in, 1908, 1908f, 1909 injury and, 2184–2185, 2184f kick test in, 1909 length in, 1909, 1909f manufacturing process and, 1908 measurements for, 1908, 1908f pinch test in, 1909, 1909f shape in, 1910 sizing for, 1906–1907, 1906t, 1907f flared heel for, 1902 flexibility of, 2188–2189, 2189f forefoot stabilizers of, 1889 gel encapsulation in, 1892 heel counter of, 1889, 1892 historical perspective on, 1873–1876, 1873f–1877f hyperpronation and, 2183 injury and, 2183–2192 cleats and, 2184, 2191–2192, 2195f–2196f control/support and, 2187–2189, 2187f–2189f cushioning and, 2185–2187, 2185t, 2186f historical perspective on, 2183–2184 incidence of, 2184 orthotics and, 2189–2190 outsole design and, 2190–2192, 2190t, 2191f, 2195f playing surface in, 2199–2203, 2200t, 2201f, 2202t, 2203f rear foot stability and, 2187–2189, 2187f, 2188f shoe fit and, 2184–2185, 2184f inlay of, 1893–1896, 1895t–1896t insert of, 1893–1896, 1895t–1896t insole board of, 1889, 1890t insole of, 1889 materials for, 1893–1896, 1895t–1896t shock absorption and, 1897–1899, 1898t, 1899f, 2185–2187, 2185t, 2186f last for, 1886–1887, 1887f–1888f leather for, 1892–1893, 1892f, 1894 lining of, 1889 materials for, 1890–1896 heel counter, 1892 inlay and insert, 1893–1896, 1895t–1896t insole, 1893–1896, 1895t– 1896t shock absorption of, 1897–1899, 1898t medial heel wedge for, 1872 midsole of, 1889–1890, 1890t midsole width for, 1902, 1903f neoprene for, 1894, 1895t nylon mesh for, 1893, 1893f nylon-weave uppers for, 1892–1893, 1893f orthotic devices for, 1872, 1893–1894, 1894f biomechanical aspects of, 1896–1906 injury and, 2189–2190 for pediatric athlete, 1974 rearfoot stability and, 1902–1904, 1903f shock absorption and, 1897–1899 outsole of, 1890 injury and, 2190–2192, 2190t, 2191f, 2195f pads for, 1893 for pediatric athlete, 1974 plantar pressure distribution of, 1899, 1899f plastics for, 1891–1892, 1891t, 1893, 1894–1895, 1895t–1896t playing surface interaction with. See Playing surface

Shoes (Continued) polyethylenes for, 1894–1895, 1895t polymers for, 1890, 1891t polyurethanes for, 1891–1892, 1895, 1895t polyvinyl chloride for, 1895 price of, 1911 pronation with, 1900–1905, 1901f quarter of, 1888 rearfoot control with, 1889, 1900–1905, 1901f injury and, 2187–2189, 2187f–2189f rubber for, 1891–1892, 1894 running injury and, 1904–1905, 1904t–1905t shock absorption of, 1897–1899, 1898t, 1899f, 2185–2187, 2185t, 2186f stress fracture and, 633, 1850 styrene-butadiene rubber for, 1894 toe box of, 1887 toe cap of, 1887 tongue of, 1889 torque testing of, 2200–2203, 2201f torsional flexibility of, 1902 turf toe and, 2082, 2082f, 2085 vamp of, 1888, 1888f viscoelastic materials for, 1895, 1895t Short arc quad exercise, in knee rehabilitation, 257 Short radiolunate ligament, 1320, 1433 Short stature anabolic-androgenic steroids and, 416 growth hormone in, 419 Shoulder. See also Glenohumeral joint; Rotator cuff arthroplasty of in fracture, 1046, 1048f in instability arthropathy, 1114 in osteoarthritis, 1113–1118, 1113f–1114f, 1116f–1118f, 1116t in rheumatoid arthritis, 1114 simulation of, 1151, 1153, 1153f–1155f arthroscopy of. See Arthroscopy, shoulder definitions for, 769–770 dislocation of. See Glenohumeral joint instability frozen. See Adhesive capsulitis hypermobility of, 616 infection of, 389–391, 390f, 391t, 392f instability of. See Glenohumeral joint instability intra-articular cartilage fragment in, 581, 583f laxity of, 769 ligaments of. See Glenohumeral ligament(s) Little Leaguer’s. See Little Leaguer’s shoulder magnetic resonance arthrography of, 535, 536, 536f, 565–566, 567f osteoarthritis of. See Glenohumeral joint osteoarthritis overuse injury to, 614–617, 615b pediatric, 779–786, 779f anatomy of, 780–786, 781f–785f biomechanics of, 786–790, 787f–789f development of, 780 kinesiology of, 790–791, 790f rehabilitation of. See Shoulder rehabilitation stiff, 1094, 1094b. See also Adhesive capsulitis stretching exercises for, 290f, 291, 1003, 1003f, 1007, 1011 subluxation of, 769 vascular anatomy of, 1137–1138, 1137f vascular injury of, 1137–1142 anatomy of, 1137–1138, 1137f axillary artery, 1140–1141 axillary vein, 1141–1142


xlv

Shoulder (Continued) clinical presentation of, 1138 dislocation-related, 1139–1140, 1140f, 1141f imaging of, 1139 physical examination in, 1138–1139, 1138f, 1139f scapulothoracic dissociation and, 1139 sternoclavicular dislocation and, 1140 subclavian artery, 1140–1141 trauma-related, 1139–1140, 1139f Shoulder impingement, 986–1015. See also Rotator cuff disorders; Rotator cuff tear(s); SLAP (superior labrum, anterior to posterior) lesion diagnosis of, 614–615, 954–955, 955f internal, 992–993, 1001–1002, 1002f, 1016, 1217, 1218 arthroscopic appearance of, 986, 987f evaluation of, 1216, 1216f glenohumeral internal rotation deficit disorder and, 979–980, 980f magnetic resonance imaging in, 978–979, 979f nonoperative treatment of, 1010 magnetic resonance imaging in, 955–956, 956f–959f, 959b osteophyte formation in, 956, 959f pathophysiology of, 954, 1016, 1016f radiography in, 954–955, 955f scapulothoracic joint in, 777 secondary, 1001, 1010, 1016 scapular lag and, 994, 1001 stages of, 614, 954, 1001 Shoulder rehabilitation, 231–232, 232f biofeedback in, 224–225, 233, 233f neuromuscular stimulation in, 231–232, 232f proprioceptive exercises for, 296, 298 MR Systems Cable Column, 298, 299f plyoball perturbations, 296, 298f plyoball Rebounder, 298, 299f wall bounce, 298, 298f therapeutic exercise for, 239–250 acute phase of, 249 after adhesive capsulitis release, 1102, 1103b advanced dynamic training in, 244–246, 245f–248f advanced phase of, 249 anterior capsule stresses in, 249 after arthroplasty, 1117–1118, 1117f–1118f behind-the-neck training in, 248–249 bench press in, 247–248, 248f gym training in, 247–249, 248f infraspinatus, 242–243, 242f–243f kinetic chain, 232, 232f latissimus dorsi, 241, 242f manual resistance training in, 246, 248f overhead press in, 248 pectoralis major, 241, 242f program design for, 249–250 after proximal humeral fracture, 1056–1057, 1057f–1058f return-to-activity phase of, 249–250, 250t–251t rotator cuff, 241–242 scapulothoracic joint, 239–240 serratus anterior, 240–241, 241f–242f after SLAP lesion repair, 1031, 1031f–1032f, 1031t subacute phase of, 249 subscapularis, 244 supraspinatus, 243–244, 243f–244f teres minor, 242–243, 242f–243f trapezius, 240, 240f–241f

xlvi

Index

Shoulder rehabilitation (Continued) upright rows in, 249 transcutaneous electrical nerve stimulation in, 229–230, 230f SI System, 85, 85t Sickle cell disease, 515t Sickle trait, exertional rhabdomyolysis and, 497 Side bridge exercise, in core training, 284, 284f Side-lying abduction exercise, in shoulder rehabilitation, 244, 244f Side-to-side weight shifting, in knee rehabilitation, 294–295, 295f Significance, statistical, 2218 Sinding-Larsen-Johansson disease, 599, 1526f, 1529–1530 Single heel rise test, 1979, 1979f Single-leg hopping exercise, in knee rehabilitation, 296, 298f, 315f, 329 Single-leg strength training in ankle rehabilitation, 273, 275f in core training, 286 in knee rehabilitation, 263–266, 264f–265f Single-leg toe raise test, in posterior tibial tendinitis, 1981 Single-photon emission computed tomography (SPECT), 544 in isthmic spondylolisthesis, 749, 749f in spondylolysis, 546, 546f, 635, 636f, 761, 761f in stress fracture, 633 Single-subject research design, 105–106, 105f–107f Sinus tarsi syndrome, 1951–1952, 1952t Sinusitis, 149 Sit-ups, partial, in trunk stabilization, 342t, 343 Skier’s thumb, 1399–1401, 1400f Skin abrasion of, 201–202 acne of, 205, 415 anatomy of, 193 chilblains of, 203 contact dermatitis of, 202, 203f eczema of, 204, 204f environmentally induced injury to, 202–203 erythrasma of, 194t, 195–196, 196f folliculitis of, 194–195, 194t, 195f–196f friction-induced injury to, 202, 202f–203f frostbite of, 203, 203f furunculosis of, 194–195, 194t herpes simplex virus infection of, 197, 197f human papillomavirus infection of, 197–198 impetigo of, 193–194, 193f–194f, 194t infection of, 193–200 bacterial, 193–196, 193f–194f, 194t fungal, 198–200, 198f–200f, 200t preparticipation examination of, 513, 515t return-to-play guidelines for, 195t viral, 196–198, 197f–198f inflammatory disorders of, 204–205, 204f–205f injury to, 201–204, 202f–203f laceration of, 201–202 larva migrans of, 201, 202f lesions of, 193–206 methicillin-resistant Staphylococcus aureus infection of, 395–397, 396b, 396f molluscum contagiosum of, 197, 198f necrosis of, after patellar fracture, 1576 parasitic infestations of, 200–201, 201f–202f pediculosis capitis of, 200–201, 201f pitted keratolysis of, 196, 196f preparticipation examination of, 513 psoriasis of, 204–205, 204f scabies of, 201, 201f sunburn of, 204

Skin (Continued) tinea infection of, 198–200, 198f–200f, 200t urticaria of, 205, 205f warfarin-related necrosis of, 381–382, 382f warts of, 197–198 SLAC (scapholunate advanced collapse) wrist, 1327–1330 stage I, 1328, 1328t stage II, 1328, 1328t, 1330f stage III, 1328–1329, 1328t, 1329f–1330f SLAP (superior labrum, anterior to posterior) lesion, 616, 1016, 1016f acromioclavicular joint resection failure and, 1024–1025 arthroscopic repair of, 1027–1031 complications of, 1032 débridement for, 1027–1028 knot-tying for, 1028, 1030–1031, 1030f–1031f outcomes of, 1031–1032 portals for, 1029–1030, 1029f postoperative prescription for, 1031, 1031t, 1031f–1032f return to play after, 1032 superior glenoid preparation for, 1027, 1027f suture anchors for, 1027–1028, 1030, 1030f, 1032 Bankart lesion in, 1021, 1023f biomechanics of, 1019–1021, 1019f–1021f classification of, 1021, 1022f, 2211, 2211f continuous detachment in, 1021, 1023f cord-like middle glenohumeral ligament with, 1021, 1023f evaluation of, 1021–1025, 1025t arthroscopic, 1025, 1027 flap-type, 1021, 1023f magnetic resonance arthrography in, 976, 977f, 978b magnetic resonance imaging in, 581, 583f, 1025, 1026f mechanisms of, 1020, 1020f–1021f, 1022–1024, 1024t, 1028 nonoperative treatment of, 1026 O’Brien active compression test in, 915, 1216, 1216f operative treatment of, 1026–1031, 1027f, 1029f–1030f evidence for, 1028–1029, 1029f physical examination in, 1024–1025, 1025t reciprocal cable model of, 1020, 1020f rotator cuff disorders and, 1024. See also Rotator cuff disorders torsional peel-back mechanism of, 1020, 1021f, 1024 type I, 976, 977f, 1021, 1022f type II, 976, 977f, 1021, 1022f, 1024f, 1026f, 1029f type III, 976, 977f, 1021, 1022f type IV, 976, 977f, 1021, 1022f, 1026f type V, 976, 1021 type VI, 976 type VII, 976 Sleep, 445–450, 446f–447f circadian process of, 445, 446f–447f in depression, 452 disorders of, 447–449 circadian impairment and, 453 homeostatic impairment and, 453 mood disorders and, 452–453 gates to, 453–454, 455f increased appetite for, 453 melatonin secretion and, 457 memory consolidation during, 449–450, 449f morningness-eveningness scale and, 456–457, 456f


Sleep (Continued) naps for, 453, 454b nocturnal window in, 454 nonpharmacologic promotion of, 447–448, 448b, 454b NREM, 446, 447f objective measurement of, 450–451, 451f–452f performance and, 454 postprandial, 453–454 refractory periods for, 454, 455f REM, 446, 447f stages of, 446–447, 447f subjective measurement of, 450, 450f Sleep apnea, 448–449 Sleep deprivation, 449–450 Sleep gates, 453–454, 455f Sleep inertia process, 445–446, 447f Sleep-wake cycle, 445, 446f Sleeper stretch, 290f, 291, 1003, 1003f Slide board leg curls, in knee rehabilitation, 266–267, 267f Slipped capital femoral epiphysis, 597, 598f, 1475–1476, 1476f, 1476t Small intestinal submucosa, in tendon healing, 28 Small intestine, on-field injury to, 527 Smokeless tobacco, 427–428 Snapping hip syndrome, 1458–1459 Snapping triceps tendon, 1226 Sneaker, 1876 Snowboarders, fracture in, 1183, 2155 Soccer, time of day and, 457 Sodium deficiency of, cramps and, 12 in hypertension, 159t loss of, 402 requirements for, 402 Soft tissue infection, 387–388, 387f, 388b, 389f, 389t classification of, 388 Soleus muscle anomaly of, vs. retrocalcaneal bursitis, 2036 stretching exercise for, 71, 71f Solvent abuse, 429–430 Soviet athletes, drug use by, 411–412 Spalding Company shoe, 1876, 1876f Spasm bronchial. See Bronchospasm muscle, delayed-onset soreness and, 12 Spear tackler’s spine, 694, 695f, 710 Spearman’s rank correlation, 113, 113f Specificity, test, 108, 109f, 110, 110t, 2218 Speed’s test in rotator cuff disorders, 997, 1000f in SLAP lesion, 1024–1025 Spencer shoe, 1875, 1875f Sperm, anabolic-androgenic steroid effects on, 416 Spinal accessory nerve anatomy of, 1125–1126 injury to, 1125–1126, 1126f Spinal bifida occulta, 693 Spinal blockade, in complex regional pain syndrome, 359, 366 Spinal canal:vertebral body ratio, in cervical spine, 694, 694f Spinal cord vs. cauda equina, 717–718 cervical decompression of, 675 injury to. See Spinal cord injury, cervical thoracic, 717–718 Spinal cord injury, cervical, 681–686 acute anterior, 674, 678 vs. burners/stingers, 524 in children/adolescents, 709–711

Index Spinal cord injury, cervical�� (Continued) grade of, 685–686 pathophysiology of, 690–691 prevention of, 686–690, 687f–690f recurrence of, 686, 686f spinal stenosis and, 683f–685f, 693–694, 710 squid axon injury model of, 690, 691f Spinal cord stimulation, in complex regional pain syndrome, 366–367 Spinal fusion in cervical spine injury, 699, 699f–700f in lumbar isthmic spondylolisthesis, 750, 750f, 764, 764f Spine. See also Cervical spine injury; Thoracolumbar spine injury computed tomography of, 539–541, 540f–541f core training for, 277–288, 277t, 289t abdominal bracing in, 280, 280f advanced functional training in, 288 AIR principles in, 279 bridging progression in, 281–282, 281f–282f curl-up progression in, 284–285, 285f gluteal training in, 285–286, 286f lateral flexion progression in, 283–284, 284f latissimus dorsi training in, 286 loading parameters in, 279–280 manual perturbation training in, 286, 287f program design for, 279 quadruped progression in, 282–283, 282f, 283f rhythmic stabilization training in, 286 rotation training in, 286–288, 288f–289f scapular training in, 286, 286f stress fracture of, 635–636, 636f–637f trunk stabilization program for, 341–349, 342t aerobic exercise in, 342t, 349 ball exercises in, 342t, 345 bridging exercise in, 342t, 344 dead bug exercise in, 342t, 343 partial sit-ups in, 342t, 343 postural exercises in, 348–349 prone exercises in, 342t, 345 quadruped exercises in, 342t, 346 stabilization exercises in, 343–348 wall slide exercises in, 342t, 347 water running in, 349 weight training in, 349 Spine board in cervical spine injury, 665, 666–667, 666f in thoracolumbar spine injury, 720, 734 Spinoglenoid ligament, 1120, 1120f Spinoglenoid notch, suprascapular nerve compression at, 1121, 1121f, 1123 Spirometry, in exercise-induced bronchospasm, 182 Spleen on-field injury to, 526–527 rupture of, infectious mononucleosis and, 151 size of, 151 Splenomegaly, clearance for participation and, 513, 515t Splint/splinting in Achilles tendon rupture, 2005 in boutonnière deformity, 1389, 1389f in elbow heterotopic ossification, 1295 in Jersey finger, 1426, 1427f, 1428 in mallet finger, 1388 in plantar fasciitis, 2049 in retrocalcaneal bursitis, 2035 in sagittal band rupture, 1390 in wrist disorders, 1361–1362, 1443

Splinter, ultrasonography of, 538, 539f Spondyloarthritis, seronegative, heel pain in, 2033–2034, 2047 Spondylolisthesis, 635, 637f cervical, traumatic, 678, 707–708 degenerative, 747–748, 748t, 752 isthmic, 748–750, 748t, 749f, 752 in children, 756, 756f, 763–764, 764f return to play after, 750 pediatric, 756, 756f, 762–764, 767, 767b surgery in, 763–764, 764f Spondylolysis, 635–636, 756, 756b, 762–763 computed tomography in, 546, 546f, 762, 763f radiography in, 635, 636f, 760, 760f radionuclide imaging in, 726, 726f return to play and, 767, 767b single-photon emission computed tomography in, 546, 546f, 635, 636f, 761, 761f Sport cord exercise, in knee rehabilitation, 271, 272f, 296, 297f Sport psychologist as clinician, 437–438 as consultant, 438–439 definition of, 439–440 as educator, 438 as facilitator, 438 Sport psychology, 437–440 Sports drinks, 401 Sports shoes. See Shoes Sprain ankle. See Ankle sprain bifurcate, 1953–1955, 1954f cervical, 673–674 Lisfranc, 1955–1960, 1956f–1957f, 1959f lumbar, 733 sternoclavicular joint. See Sternoclavicular joint injury subtalar, 1947–1952, 1947f–1949f, 1951f, 1952t thoracic, 732–733 wrist. See Scapholunate ligament, injury to Spring ligament, 1913f Spurling’s test in cervical spine injury, 672, 672f in thoracic outlet syndrome, 1132–1133, 1133f Squat and reach exercise, in knee rehabilitation, 270, 271f Squat exercise back, 262, 263f in core training, 286, 286f cruciate ligament effects with, 223, 223t, 224, 224f, 262–263 front, 262, 262f goblet, 261, 261f hex bar, 261–262, 262f in knee rehabilitation, 260–261, 261f multiplanar, 270, 270f patellar effects with, 226–227 patellofemoral joint stresses with, 262–263 quadriceps dominant, 258–263, 259f–260f, 261f–263f squat and reach, 270, 271f standing, 260–263, 261f–263f sumo, 309f, 329 wall, 260, 260f, 330 single-leg, 264, 265f Squat test, in meniscal injury, 1602 Squatting, patellofemoral joint reaction force with, 227, 1592–1593, 1592f Squeakers, 625 Squeeze test, in high (syndesmosis) ankle sprain, 1940, 1940f


xlvii

Squid axon injury, 690, 691f Stability ball bridges, in knee rehabilitation, 266, 267f Stability ball leg curl, in knee rehabilitation, 266–267, 267f Stability ball training, in shoulder rehabilitation, 245, 246f Stabilization exercises. See Trunk stabilization program Standard deviation, 112 Standing side bridge exercise, in core training, 284, 284f Stanford Sleepiness Scale, 450 Staphylococcus aureus infection, 395–397, 396b, 396f methicillin-resistant, 193, 194–195, 194t, 195f community-acquired, 194–195, 195f prevention of, 395–396, 396b Statistics, 97–119. See also Research accuracy in, 100 bias in, 100 causation in, 100–101 comparison of means, 112–113, 113f correlation in, 100–101 decision analysis in, 99 descriptive, 112–114, 113f error in, 100, 111, 118–119 hypothesis testing in, 99 inference in, 99 linear regression, 113, 113f logistic regression, 113–114, 114f P-value in, 110 population in, 99 power analysis in, 111–112, 116–117 precision in, 100 reliability in, 100 sample in, 99 sensitivity in, 110 specificity in, 110 study design in, 99, 101–110, 101f, 111 table analysis in, 114 terminology of, 2217–2218 two-by-two table analysis in, 108–109, 109f, 114 validity in, 100 variables in, 97, 99, 100–101, 112–114 Status epilepticus, 523 Stem cells, in knee cartilage lesions, 1776 Step-up exercises in ankle rehabilitation, 273, 275f in knee rehabilitation, 264, 264f Sterilization, allograft, 139 Sternoclavicular joint, 791–825. See also Sternoclavicular joint injury anatomy of, 769, 769f ligamentous, 792–794, 792f–795f pediatric, 783–784, 784f surgical, 792–794, 792f–795f vascular, 794, 797f arthritis of, 811–812, 820 computed tomography of, 804–805, 805f congenital disorders of, 799, 811 dislocation of. See Sternoclavicular joint injury, severe sprain (dislocation) hyperostosis of, 812 iatrogenic instability of, 824 injury to. See Sternoclavicular joint injury kinematics of, 775, 775f magnetic resonance imaging of, 804 pediatric anatomy of, 783–784, 784f biomechanics of, 786, 787f radiography of, 802–805, 803f–804f anteroposterior view for, 802

xlviii

Index

Sternoclavicular joint (Continued) Heinig view for, 803, 803f Hobbs view for, 803, 803f serendipity view for, 803–804, 804f range of motion of, 794, 796f spontaneous subluxation/dislocation of, 799, 801f, 811, 820 tomography of, 804, 805f Sternoclavicular joint injury, 792–825 atraumatic, 799, 801f, 811–812, 820–821 classification of, 798–799, 799f–800f anatomy-based, 798, 799f–800f cause-based, 798–799, 801f clavicular epiphysis in, 794, 796f complications of, 821–824, 821f–823f computed tomography in, 804–805, 805f historical perspective on, 791–792 hypotension with, 822, 823f iatrogenic instability after, 824 incidence of, 799, 801–802 K-wire migration with, 823 magnetic resonance imaging in, 804 mechanism of, 794–797, 798f direct force, 795 indirect force, 795–796, 798f mediastinal vessel compression with, 821, 822f mild sprain, 798, 802, 805, 812 moderate sprain (subluxation), 798, 802, 805–806, 806f, 812 physeal, 811 medial, 824–825, 824f anterior displacement, 811, 824–825 posterior displacement, 811, 825 treatment of, 819 return to sport after, 825 pin-related complications with, 823–824 radiography in, 802–805, 803f–804f anteroposterior view for, 802 Heinig view for, 803, 803f Hobbs view for, 803, 803f serendipity view for, 803–804, 804f range of motion in, 794, 796f severe sprain (dislocation), 806–810, 813–818 acute, 798 anterior, 798, 798f–799f, 802, 815–816 closed reduction for, 806, 812 incidence of, 799, 801 incidence of, 799, 801–802 mechanism of, 795–796, 798f nonoperative treatment of, 806–809, 812–814, 813f on-field, 526 operative treatment of, 809–810, 810f, 814–815, 814f–818f posterior, 798, 799f, 807–810, 816 abduction traction reduction for, 808, 808f adduction traction reduction for, 808, 808f closed reduction for, 798, 800f, 807–809, 808f, 812–813, 813f complications of, 821–823, 821f, 822f, 823f computed tomography of, 807, 807f evaluation of, 807 incidence of, 799, 801 operative complications of, 823–824 operative treatment of, 809–810, 810f, 814–816, 814f–818f postreduction care of, 809 signs and symptoms of, 802 ultrasonography of, 807f recurrent, 799, 809, 815 signs and symptoms of, 802

Sternoclavicular joint injury (Continued) unreduced, 799, 809, 814–816 vascular injury with, 1140 signs and symptoms of, 802 subcutaneous emphysema with, 821–822, 823f surgical anatomy in, 792–794, 792f–795f, 797f tomography of, 804, 804f tracheal displacement with, 821, 821f Sternomanubrial dislocation, 897, 898f–899f reduction of, 899, 899f Sternum anatomy of, 896–897, 897f fracture of, 896–900, 898f–899f mechanisms of, 897, 897f–898f return to play after, 899 treatment of, 899 Steroids. See Anabolic-androgenic steroids; Corticosteroid(s) Stiffness biomechanical, 93 elbow, 1293 joint, 225, 225f, 2176 meniscal, 60, 61f, 1600 muscle, 2177–2178 Stimson’s maneuver, 935, 936f Stimulants, 451–452, 452t Stinchfield test, in hip degenerative disease, 1503 Stingers clearance for participation and, 513 vs. spinal cord injury, 524 Straight leg raise, tibia translation with, 222 Straight leg raise exercise, in knee rehabilitation, 256–257, 257f, 267–268, 269f Straight leg raising test in hip degenerative disease, 1503 in lumbar disk herniation, 743 in thoracolumbar spine injury, 722, 723f Strain lumbar, 733 mechanical, 94 muscle. See Muscle(s), strain injury of and at specific muscles thoracic, 732–733 Strengthening exercise/training, 10. See also Core training; Therapeutic exercise(s) in ankle instability, 340 in children/adolescents, 465 in complex regional pain syndrome, 362 in female athlete, 479–480, 481 gastrosoleus, 273, 275f in hamstring strain prevention, 336–337, 337f in iliotibial band friction band syndrome, 628, 630f after proximal humeral fracture, 1057, 1058f quadriceps, 256–257, 257f, 258–263, 260f–263f rotator cuff, 242–244, 242f–244f, 1003–1007, 1004f–1007f scapula, 1007, 1008f serratus anterior, 240–241, 241f–242f shoulder, 246, 248f, 1003, 1004f–1006f, 1007, 1011 single-leg, 263–266, 264f–265f, 273, 275f, 286 total arm, 251–255, 251t, 252f–254f Streptococcus sanguis infection, 398, 398t Stress, seizures with, 187 Stress fracture, 631–650, 1851b acromial, 867 calcaneal, 556f, 646, 647f cuboid, 646


Stress fracture (Continued) cuneiform, 646 diagnosis of, 633 differential diagnosis of, 633 in endurance athlete, 632 in female, 483, 483b, 483f, 632–633, 1849–1850, 1851–1852, 1856, 2014 femoral neck, 554f, 638–640, 640f–644f femoral shaft, 641, 1477–1481. See also Femoral shaft, stress fracture of fibular, 644, 644f, 1849 fifth metatarsal, 648, 649f first proximal phalanx, 2028 foot and ankle, 2012–2030. See also Foot (feet), stress fracture of and at specific fractures great toe, 649–650, 649f humeral, 634–635, 635f, 1176–1177, 1178, 1179, 1180t, 1182 physeal, 1090–1093, 1093b, 1093f. See also Little Leaguer’s shoulder imaging of, 552–553, 554f–555f, 633, 634t incidence of, 632–633 leg-length inequality and, 632 lower extremity, 638–650, 1849–1856. See also Femoral shaft, stress fracture of; Tibia, stress fracture of magnetic resonance imaging in, 552–553, 554f–555f malleolar, 644–645, 645f, 2016t, 2018, 2020f metatarsal, 646–648, 648f–649f foot type and, 1904 metatarsal length and, 2182 shoewear and, 1898–1899 pars interarticularis (spondylolysis), 635–636, 756, 761, 761f, 762–763, 763f patellar, 641–643 pathogenesis of, 632–633 pelvic, 638 prevention of, 406, 634 proximal humeral physis, 1090–1093, 1093b, 1093f pubic rami, 638, 638f radionuclide imaging in, 545–546, 545f–547f, 552 recurrence of, 1856 rib, 636–637, 637f, 895–896, 895t, 896f sacral, 638 scaphoid, 1365–1366, 1366f sesamoid, 649–650, 649f shoe selection and, 633 spinal, 635–636, 636f–637f systemic factors in, 632 talar, 645 tarsal navicular, 645–646, 646f tibial, 643–644, 644f, 652, 652t, 1849–1856. See also Tibia, stress fracture of treatment of, 634 Stress-relaxation, 18, 19f, 95–96, 95f articular cartilage, 48 meniscal, 59 Stress-strain curve, 94, 94f Stretching animal model of, 19 in cramps, 12 plantar fascia, 2049 Stretching exercises, 288–293 biofeedback with, 292f, 293 gastrocnemius, 291, 291f hamstring, 289–290, 290f, 292f, 293 iliotibial band, 291–292, 291f knee, 292–293, 292f after proximal humeral fracture, 1056, 1057f shoulder, 290f, 291, 1003, 1003f, 1007, 1011 soleus, 71, 71f

Index Stroke volume, exercise effect on, 219, 219f, 220t Strychnine, 410 Stryker Intra-Compartmental Pressure Monitor, 1860 Student’s elbow. See Olecranon bursitis Study design, 101–110, 101f analytical, 107–108 blinding in, 104–105 control group in, 101–102, 104 experimental, 101f, 103–106, 105f matching in, 101 observational, 101–103, 101f, 102t–103t, 106–107 power analysis in, 111 pre-experimental, 103–104 qualitative, 106–107 single-subject, 105–106, 105f–107f Subacromial bursa, 990, 991f Subarachnoid hemorrhage, 661, 661f Subcalcaneal pain syndrome, 2042–2043. See also Plantar fasciitis Subchondral bone, 41f abrasion of, 52–63 Subclavian artery, injury to, 1140–1141 Subclavian vein, effort thrombosis of (Paget-Schroetter syndrome), 1129–1130, 1131f, 1134 Subclavius tendon, in sternoclavicular joint dislocation treatment, 810 Subdural hematoma, 660, 661f Sublabral foramen, 972, 972f Sublabral recess, 970f, 972 Subscapularis anatomy of, 770, 770f, 771, 910, 989, 989f, 1035f, 1035t, 1064–1065 fatty infiltration of, 989, 989f function of, 991 humeral attachment of, 1070–1071, 1071f pediatric, 785, 785f rupture of, 1064–1065 clinical evaluation of, 1065 treatment of, 1065 scapular attachment of, 858, 858f, 886f strengthening exercise for, 244 Subscapularis bursa, 771 Subscapularis tendon, 771. See also Rotator cuff; Rotator cuff disorders entrapment of, 957 tear of, 566, 963–964, 964f. See also Rotator cuff tear(s) Subtalar joint anatomy of, 1947–1948, 1947f–1948t biomechanics of, 1867–1869, 1868f–1870f, 1947–1948, 1948f dislocation of, 1952–1953, 1953f ligaments of, 1947–1948, 1947f, 1948t injury to. See Subtalar sprain motion of, 2178–2179, 2179f, 2179t muscle function at, 1868–1869, 1870f Subtalar sprain, 1947–1952 anatomy of, 1947–1948, 1947f, 1948t arthrography in, 1950 chronic, 1950–1951 computed tomography in, 1950 evaluation of, 1948–1949, 1949f grade I, 1948, 1950 grade II, 1948, 1950 grade III, 1948, 1950 history in, 1949 magnetic resonance imaging in, 1950 physical examination in, 1949, 1949f radiography in, 1949–1950, 1949f rehabilitation after, 1951 return to play after, 1952

Subtalar sprain (Continued) sinus tarsi syndrome and, 1951–1952, 1952t tarsal coalition and, 1933 treatment of, 1950–1951, 1951f Subtalar varus tilt test, 1949–1950 Subungual exostosis, 2105–2107 classification of, 2105, 2105t evaluation of, 2105–2106, 2106b, 2106f imaging in, 2106, 2106f nonoperative treatment of, 2106 operative treatment of, 2106–2107, 2107f care after, 2107 return to play after, 2107 Subungual hematoma, 2098 Subungual osteochondroma, 2105, 2105t Sudden death, 162–172 arrhythmogenic right ventricular cardiomyopathy and, 166, 167f causes of, 162–167, 163f, 163t commotio cordis and, 165, 165f coronary artery anomalies and, 165, 165f–166f definition of, 163 hypertrophic cardiomyopathy and, 164–165, 164f long QT syndrome and, 166–167, 167f myocarditis and, 165–166, 166f prevention of, 167–171 ablation procedures in, 170 β-adrenergic blockers in, 170 Bethesda Guidelines in, 169, 170t echocardiography in, 168 electrocardiography in, 168–169, 169t equipment in, 170–171 implantable defibrillators in, 169–170 preparticipation evaluation in, 167–168 screening for, 167–169, 168t, 509, 512, 512t resuscitation for, 171–172, 171t Sudeck’s atrophy, in complex regional pain syndrome, 358 Sudomotor function, in complex regional pain syndrome, 355 Sulcus angle in femoral trochlea dysplasia, 1563–1564, 1564t patellar, 1540 Sulcus sign, in glenohumeral joint instability, 914, 915f, 943, 943f Sunburn, 204 Sunscreen, 204 Superficial femoral artery, occlusion of, 1497–1499 Superficial peroneal nerve, 15f, 2062, 2063f entrapment of, 2062–2063, 2062f injury to, 1933 Superior peroneal retinaculum, 1931, 1987 congenital absence of, 1991 disruption of, 1932 imbrication of, 1932–1933 reconstruction of, 1995 Superior shoulder suspensory complex, 857, 863, 864f Supplement. See Dietary supplement(s) Suprachiasmatic nucleus, 443–444, 444f Supracondylar fracture, 596–597, 597f, 1186, 1186f, 1280t, 1281–1283, 1282f Suprascapular artery, 858 Suprascapular nerve anatomy of, 858–859, 1120–1121, 1120f, 1122f in coracoid fracture, 880, 882f–883f Suprascapular nerve injury, 616–617, 1120–1124 electromyography in, 1122, 1124 evaluation of, 1121–1123, 1122f ganglion cyst and, 1121, 1121f, 1123 magnetic resonance imaging in, 1121–1122 muscle atrophy with, 1121, 1122f


xlix

Suprascapular nerve injury (Continued) nerve conduction study in, 1122–1123 paralabral cyst and, 980, 980t radiography in, 1121, 1122f scapular fracture and, 1121 throwing-related, 1221 treatment of, 1123–1124 ultrasonography in, 1122 Suprascapular notch, suprascapular nerve compression at, 1120, 1120f, 1123 Supraspinatus anatomy of, 770, 770f, 910–911, 989, 989f, 1035t atrophy of, 770 fatty atrophy of, 963, 963f, 980 fatty infiltration of, 989, 989f humeral attachment of, 1070–1071, 1071f pediatric, 785, 785f scapular attachment of, 859f, 886f strengthening exercise for, 243–244, 243f–244f, 1003, 1006f Supraspinatus tendon, 770. See also Rotator cuff; Rotator cuff disorders calcification of, 566, 568f, 963, 963f tear of. See Rotator cuff tear(s) tendinopathy of, 30, 566, 568f, 960, 960f Sural nerve, 2060–2061, 2061f injury to, 2060–2061 Suture(s), 132–136 abrasion of, 133–134 biologic characteristics of, 132–133 deformation of, 134 demands on, 132 Duncan loop with, 135, 135f handling properties of, 136 knotting properties of, 135–136, 135f mechanical characteristics of, 133–134 Nicky’s knot with, 135, 135f Roeder’s knot with, 135, 135f selection of, 134, 136 strength of, 133–134 tensile load on, 134 Sweat, salt in, 402 Sweat glands, in children, 465 Sweating in complex regional pain syndrome, 355, 360–361 evaluation of, 360–361 Swimmer’s ear, vs. thoracic outlet syndrome, 1130 Swimming core body temperature in, 455f epilepsy and, 192 time of day and, 455f, 457 Syme amputation, of great toe, 2099, 2104f Sympathectomy, in complex regional pain syndrome, 366 Sympathetic ganglion blockade, in complex regional pain syndrome, 359, 365 Sympatholysis, in complex regional pain syndrome, 365 Synapse, in complex regional pain syndrome, 353–355, 354f Syncope, heat, 494, 529–530 Synephrine, 409 Synovectomy, of wrist, 1443–1444 Synovial cyst, glenohumeral, 617 Synovial disease, of hip, 1473

T t-test, 112–113, 113f, 116–117 Table lateral crunch exercise, 316f, 330 Taking-off-shoes test, in hamstring strain, 1486f, 1487

Index

Talalgia, 2034 Talar tilt, on stress radiography, 1918–1919, 1918f Talar tilt test in lateral ankle sprain, 1917–1918, 1917f in medial ankle sprain, 1936 in subtalar sprain, 1949 Talcum powder sclerosant, in olecranon bursitis, 1248 Talocalcaneal coalition, 1872, 1962 Talocalcaneal ligament, 1913f Talocrural joint. See Ankle Talofibular ligament anterior, 338, 1913–1914, 1913f–1915f biomechanics of, 1865–1866, 1866f injury to, 1866. See also Ankle sprain, lateral magnetic resonance imaging of, 573, 574f repair of, 1923–1924, 1923f, 1926–1928, 1926f, 1927f posterior, 338, 1913–1914, 1913f, 1914f injury to. See also Ankle sprain, lateral Talon noir, 202, 202f Talonavicular joint biomechanics of, 1869, 1870f impairment of, 1872 Talus eosinophilic granuloma of, 2161, 2161f fracture of, 2153–2156, 2154t–2155t, 2155f–2156f osteochondroses of. See Osteochondrosis (osteochondroses), talar pigmented villonodular synovitis of, 2161, 2161f stress fracture of, 645, 2016t, 2018–2019, 2021f Taping in ankle instability, 340, 1934 in lesser toe deformity, 2121, 2121f for plantar fasciitis, 2049–2050 for play, 1362 in sesamoid dysfunction, 2090, 2093f Tarsal coalition, 1933, 1960–1962, 1961f, 1962f, 2161, 2161f Tarsal joint, transverse biomechanics of, 1869, 1870f, 2179 impairment of, 1872 medial swivel syndrome of, 2179 Tarsal navicular osteochondrosis of, 599, 1972–1973, 1973f, 2162, 2163f stress fracture of, 645–646, 2016t, 2020–2022, 2023f Tarsal tunnel, 2057, 2057f release of, 2058–2059, 2059f Tarsal tunnel syndrome, 631–632, 2047, 2057–2059 anterior, 2061–2062, 2061f clinical features of, 2057, 2057f differential diagnosis of, 2058, 2058b electrodiagnostic studies in, 2058 etiology of, 2058 physical examination in, 2058 treatment of, 2058–2059, 2059f Tartan syndrome, 2198 Tazarotene, in acne, 205 Team physician, 507 emergency function of. See On-field emergency ethical responsibilities of, 530–531 examining function of. See Preparticipation examination institutional relationships of, 530 legal responsibilities of, 531 medicolegal responsibilities of, 531 minor care provision by, 531

Team physician (Continued) out-of-state practice by, 531 rewards of, 532 roles of, 507 supervisory function of, 516 support relationships of, 530 Teardrop fracture, 680–681, 681f Telmisartan, 160t Temperature, body clothing effects on, 499–500 disease effects on, 499 disorders of. See Cold injury; Heat illness/ injury; Hypothermia drug effects on, 499 Ten (10) test, in thoracic outlet syndrome, 1131 Tendinitis, 29–30, 1975, 1516 Achilles, 1997–2002. See also Achilles tendon, injury to flexor carpi radialis, 1356–1357 flexor carpi ulnaris, 1356–1357 flexor hallucis longus, 1983–1984, 1986, 1986f peroneal, 1988–1990 posterior tibial tendon, 1981–1983, 1982f triceps, 1207–1209 Tendinopathy, 29, 611–614, 612t, 613f. See also Overuse injury and at specific tendon disorders calcific, of supraspinatus, 566, 567f distal biceps, 566, 570f fluoroquinolone-related, 30 insertional, 30 magnetic resonance imaging in, 558 patellar, 560, 561f, 626–627, 626f, 1515–1518, 1517b, 1518t posterior tibial tendon, 563, 563f quadriceps, 560 rotator cuff, 565, 566, 566f, 567f, 770. See also Rotator cuff disorders; Rotator cuff tear(s) triceps tendon, 567 ultrasonography of, 538 Tendinosis, 611–612, 612t, 613f, 1975 Achilles, 30, 1975, 2030–2031, 2034, 2034f, 2036 patellar. See Patellar tendinosis wrist extensor, 617–619, 618f Tendodermodesis, in mallet finger, 1421–1422, 1421f Tendon(s), 20–31. See also specific tendons age-related changes in, 25, 30 biochemistry of, 22–24, 22f, 23f, 23t biomechanics of, 24–25, 25f, 26f blood supply of, 21 bone insertions of, 20–21 cells of, 20, 22, 24 interaction among, 24 collagen of, 20, 22–23, 22f, 23f, 23t adaptability of, 25–27 age-related changes in, 25 corticosteroid effects on, 26–27 exercise-related changes in, 25, 26f immobilization-related changes in, 25–26, 26f NSAID effects on, 27 synthesis of, 27–28 corticosteroid injection effects on, 26–27, 29, 31 degeneration of. See Tendinopathy and at specific tendon disorders elastin of, 23 exercise-related changes in, 25, 26f fibroblasts of, 20, 22, 24, 27 glycosaminoglycans of, 23–24 ground substance of, 23–24


Tendon(s) (Continued) healing of, 27–30 active mobilization in, 28 biomechanics of, 28 corticosteroid effects on, 29 inflammatory response in, 27–28 mechanical stress in, 28–29 nonsteroidal anti-inflammatory drug effects on, 29 passive mobilization in, 29 primary, 27–28 immobilization-related changes in, 25–26, 26f inflammation of. See Tenosynovitis injury to. See also at specific tendons diagnosis of, 30 exercise for, 31 healing after. See Tendon(s), healing of mechanisms of, 27 overuse, 29–30. See also Overuse injury trauma-induced, 30 treatment of, 30–31 innervation of, 22 load-deformation curve for, 25, 26f load-elongation curve for, 24–25, 25f magnetic resonance imaging of, 558, 560–569 at ankle, 560–563, 562f–566f at elbow, 566–567, 569f, 570f at hip, 567–568 at knee, 560, 561f, 562f at shoulder, 564–566, 566f, 567f, 568f at wrist, 568–569, 570f mechanical properties of, 24–25, 25f, 26f nonsteroidal anti-inflammatory drug effects on, 27, 29 proteoglycans of, 23–24 strength of, after injury, 28 stress relaxation of, 18, 19f stress-strain curve for, 25, 26f structure of, 20–22, 21f, 1515, 1517f syncytium of, 20 ultrasonography of, 538, 538f viscoelastic properties of, 24–25, 25f Tendon surface cells, 20, 24 Tendoscopy in flexor hallucis longus tendinitis, 1984 in peroneal tendinitis, 1990 in posterior tibial tendinitis, 1982–1983 Tennis elbow. See Epicondylitis, lateral Tennis racquet, 1199, 1200f Tennis shoulder, 1130 Tenosynovitis, 1975 de Quervain’s, 569, 570f, 624–625, 1355, 1356f magnetic resonance imaging in, 558 posterior tibial tendon, 538, 538f Tenosynovium, 20 Tenovagina, 20 Tensile loading testing, 93, 93f Tension pneumothorax, 525 Tensor fascia lata, 1454t, 1455f Terazosin in complex regional pain syndrome, 363t, 365 in hypertension, 160t Terbinafine, in dermatophyte infection, 200t Teres major, 771, 1034, 1035t scapular attachment of, 859f, 886f Teres major tendon, 771 Teres minor anatomy of, 770–771, 770f, 989, 989f, 1035t pediatric, 785, 785f function of, 991

Index Teres minor (Continued) humeral attachment of, 1070–1071, 1071f scapular attachment of, 859f, 886f strengthening exercises for, 242–243, 242f, 243f Teres minor tendon, 770. See also Rotator cuff tears of, 566 Terminology, 2207–2209, 2208t, 2209t epidemiological, 2218–2219, 2218t statistical, 2217–2218 Testis (testes) anabolic-androgenic steroid effects on, 416 disorders of, 515t on-field injury to, 527 Testosterone in endurance athlete, 633. See also Anabolic-androgenic steroids exercise effects on, 217t, 218 historical perspective on, 411–414 Tetanus, muscle, 7–8, 8f Thenar hammer syndrome, 1359 Therapeutic exercise(s), 238–293 in acromioclavicular joint injury, 838–840, 839f, 840f AIR acronym for, 238 ankle, 272–276 eccentric training in, 275–276, 276f gastrosoleus training in, 273, 275f neuromuscular control training in, 273, 275, 275f neuromuscular training in, 273, 274f proprioceptive training in, 273, 275, 275f single-leg training in, 273, 275f application concepts for, 238–239, 238t, 239t in atraumatic glenohumeral joint instability, 945, 945f after coracoid fracture, 884 core training in, 277–288, 277t, 289t abdominal bracing in, 280, 280f advanced functional training in, 288 AIR principles in, 279 bridging progression in, 281–282, 281f, 282f curl-up progression in, 284–285, 285f gluteal training in, 285–286, 286f lateral flexion progression in, 283–284, 284f latissimus dorsi training in, 286 loading parameters in, 279–280 manual perturbation training in, 286, 287f program design for, 279 quadruped progression in, 282–283, 282f, 283f rhythmic stabilization training in, 286 rotation training in, 286–288, 288f–289f scapular training in, 286, 286f elbow, 250–255 extensor training in, 253–254, 253f flexor training in, 251–253, 252f, 253f forearm muscle training in, 254–255, 254f, 255f rhythmic stabilization training in, 255, 255f total arm strengthening in, 251 glossary of, 324–330 knee, 255–272 ACL loading with, 221–222, 222t ACL strain measurements in, 1586–1588, 1586f, 1587t acute phase of, 255 advanced phase of, 255 gluteal muscle raise in, 267, 268f gluteal musculature, 257–258, 258f, 259f hamstring curls in, 266 hamstring raise in, 267, 268f

Therapeutic exercise(s) (Continued) hip extension in, 258, 258f, 267 hyperextension in, 267 leg press in, 259–260, 260f lunges in, 264–266, 265f, 266f manual perturbation training in, 270–271, 271f multiplanar squats in, 270, 270f neuromuscular activation, 256–258 neuromuscular control training in, 268–270, 269t, 270f PCL loading with, 221–222, 222t program design for, 256 proprioceptive training in, 268–270, 269t, 270f quadriceps, 256–257, 257f quadriceps dominant squatting, 258–263, 260f, 261f–263f return-to-activity phase of, 256 Romanian deadlift in, 267–268, 269f single-leg balance training in, 271 single-leg presses in, 263, 264f single-leg Romanian deadlift in, 268, 269f single-leg strength training in, 263–266, 264f, 265f single-leg wall squats in, 264, 265f slide board leg curls in, 266–267, 267f sport cord activities in, 271, 272f, 296, 297f squat and reach in, 270, 271f squats in, 260–263, 261f–263f stability ball bridges in, 266, 267f stability ball curls in, 266–267, 267f step-ups in, 264, 264f straight leg, 267–268 subacute phase of, 255 Total Gym in, 259–260, 260f unstable surface training in, 271, 272f wall squats in, 260, 260f loading parameters in, 277, 277t after proximal humerus fracture, 1057f–1058f shoulder, 239–250 acute phase of, 249 after adhesive capsulitis release, 1102, 1103b advanced dynamic training in, 244–246, 245f–248f advanced phase of, 249 anterior capsule stresses in, 249 after arthroplasty, 1117–1118, 1117f, 1118f behind-the-neck training in, 248–249 bench press in, 247–248, 248f gym training in, 247–249, 248f infraspinatus, 242–243, 242f–243f kinetic chain, 232, 232f latissimus dorsi, 241, 242f overhead press in, 248 pectoralis major, 241, 242f program design for, 249–250 after proximal humeral fracture, 1056–1066, 1057f, 1058f return-to-activity phase of, 249–250, 250t, 251t rotator cuff, 241–242 scapulothoracic joint, 239–240 serratus anterior, 240–241, 241f–242f after SLAP lesion repair, 1031, 1031t, 1031f–1032f subacute phase of, 249 subscapularis, 244 supraspinatus, 243–244, 243f–244f teres minor, 242–243, 242f–243f trapezius, 240, 240f, 241f upright rows in, 249 stretching, 288–293, 290f–292f warm-up for, 276


li

Thermogenesis, thermoregulatory, 498–499 Thermography, in complex regional pain syndrome, 360 Thermoregulation, 498–499 in children/adolescents, 465–466 Thiamin, requirements for, 406b Thigh pad with ring, 1482, 1482f Thomas test, in hip degenerative disease, 1503 Thompson-Terwilliger procedure, 2099, 2104f Thompson’s test, in Achilles tendon rupture, 2003 Thoracic outlet syndrome, 1127–1136, 1128b, 1142 Adson’s test in, 1131, 1132f anatomy of, 1127–1129, 1128f–1130f arteriography in, 1133 differential diagnosis of, 1128b fibrous muscular bands in, 1128, 1129f–1130f Halstead’s maneuver in, 1131, 1132f historical perspective on, 1127 lidocaine injection test in, 1133 magnetic resonance imaging in, 1133 neurologic symptoms in, 1129 nonoperative treatment of, 1134–1135, 1135f operative treatment of, 1134, 1135–1136, 1135f pain in, 1129 physical examination in, 1131 radiography in, 1133, 1133f retroclavicular Spurling’s test in, 1132–1133, 1133f return to play after, 1134 Roos’ test in, 1132, 1133f symptoms of, 1129–1131, 1130f–1131f ten (10) test in, 1131 Wright’s hyperabduction test in, 1132, 1132f Thoracic spine. See also Thoracolumbar spine injury anatomy of, 715–717, 715f–716f, 724, 724f, 754–755 blood supply of, 716, 716f computed tomography of, 541, 727 contusion of, 732–733 diskography of, 728 fracture of, 733–736, 733f, 734f in children/adolescents, 755, 755f compression, 546, 547f, 734–735, 734f, 755, 755f injury to. See Thoracolumbar spine injury innervation of, 716, 716f intervertebral disk of, 717, 717f herniation of, 738, 739f radiography of, 728 kyphosis of, 718, 736–737 ligaments of, 715 magnetic resonance imaging of, 727 muscles of, 715–716, 715f radiography of, 724, 724f, 728 radionuclide imaging of, 726, 726f sprain of, 732–733 stenosis of, 738–739, 739f strain of, 732–733 venous drainage of, 716–717 zygapophyseal joints of, 718, 719f Thoracolumbar spine. See also Thoracolumbar spine injury anatomy of, 715–717, 715f–717f biomechanics of, 718–719, 719f vs. cauda equina, 717–718 extension of, 718 flexion of, 718 lateral flexion of, 718 rotation of, 718 zygapophyseal joints of, 718, 719f

lii

Index

Thoracolumbar spine injury, 714–768 cold therapy for, 731 diagnostic blocks in, 731–732, 731t evaluation of, 719–728 diagnostic blocks in, 731–732, 731t diagnostic testing in, 723–728, 724f–727f imaging in, 723–728, 724f–727f inspection in, 721 neurologic examination in, 721–723, 722t, 722f–723f pain in, 719–720 palpation in, 721 patient history in, 719–720 physical examination in, 720–723, 722t, 722f–723f range of motion in, 721 straight leg raising test in, 722, 723f fracture, 733–736, 733f–�� 735f heat therapy for, 731 immobilization for, 720 lumbar spine stabilization for, 728–730, 730f medications for, 731 on-field, 524, 720 pediatric, 754–768 anatomy in, 754–755 classification of, 755–757, 755f, 755t, 756b, 756f–758f evaluation of, 757–762 Adam’s forward bend test in, 759 imaging in, 759–762, 760f, 761f neurologic examination in, 759 palpation in, 759 patient history in, 757–759, 759b physical examination in, 759, 759b range of motion in, 759 overuse syndrome and, 766 return to play after, 767–768, 767b treatment of, 762–766, 763b evidence for, 766–767 nonoperative, 762–763, 764–765, 765f operative, 763–764, 764f, 765–766 rehabilitation cycle in, 728, 728f return to play after, 750–752, 751f, 752t spine board for, 720, 734 sprain, 732–733 strain, 732–733 trigger point injections for, 732 Thorax, on-field injury to, 525–526 Thrombocytopenia, heparin-induced, 381 Thrombophilia, 372–374, 374f, 374t Thrombosis axillary artery, 1140–1141, 1141f effort axillary vein, 1141–1142 on-field, 527 subclavian vein, 1129, 1131f, 1134 throwing-related, 1226 venous. See also Deep venous thrombosis formation of, 370–374 endothelial damage in, 370–371, 371f, 372f hypercoagulability in, 371–372, 374f, 375f venous stasis in, 371 shoulder dislocation and, 1140, 1141f Throwing. See Overhead throwing Thumb, 1398–1403. See also Finger(s) Bennett’s fracture of, 1402–1403, 1402f–1403f, 1411–1412 carpometacarpal joint of dislocation of, 1398 subluxation of, 1398 dislocation of, 1398–1399 extensor tendon injury of, 1401–1402 fracture of, 1402–1403, 1402f pediatric, 1411, 1411f

Thumb (Continued) gamekeeper’s (skier’s), 1399–1401, 1400f, 1415 interphalangeal joint of, dislocation of, 1384, 1386 ligamentous injury of, 1398–1401, 1400f, 1401f, 1415 mallet, 1401–1402 metacarpophalangeal joint of collateral ligament injury at, 1399–1401, 1400f, 1401f, 1415 dislocation of, 1398–1399 radial collateral ligament injury at, 1401 ulnar collateral ligament injury at, 1399–1401, 1400f–1401f, 1415 Rolando fracture of, 1403 ulnar collateral ligament injury of, 1399–1401, 1400f pediatric, 1415 treatment of, 1400–1401, 1401f volar dislocation of, 1399 Thumb sign test, in posterior cruciate ligament injury, 2214 Thumb spica splint, in scaphoid fracture, 1337, 1338f Thyroid hormone, bone effects of, 72 Tiagabine, in epilepsy, 189, 191t Tibia anatomy of, patellar stability and, 1550 epiphyseal fracture of, 1642–1644, 1643f, 1643t, 1644b external rotation of, in posterior cruciate ligament injury, 1691 fracture of, in knee dislocation, 1752–1753, 1752f growth plate of, 1638 loading of, 1849 osteochondral lesions of, 2153, 2154f stress fracture of, 1849–1866 anatomic factors in, 1850 anterior, 643–644, 644f anterior knee pain with, 1855 biomechanics of, 1849 bone scan of, 1852, 1853f classification of, 1851, 1851t complications of, 1855–1856 computed tomography of, 1853 distal, 2017–2018, 2017f–2018f in children/adolescents, 1970, 1972f magnetic resonance imaging in, 2015, 2016f radiography in, 2014, 2015f–2016f radionuclide imaging in, 2014–2015, 2015f treatment of, 2016t dreaded black line in, 1852, 1852f evaluation of, 1851–1853, 1852f in female, 1849–1850, 1851–1852, 1856 magnetic resonance imaging of, 1852–1853, 1853f medial, 643, 652, 652t in military recruit, 1849, 1850, 1856 nonoperative treatment of, 1854 operative treatment of, 1854–1856 pain in, 1851 pathogenesis of, 1850–1851 physical examination in, 1852 radiography in, 1852, 1852f radionuclide imaging in, 545–546, 545f recurrence of, 1856 return to play after, 1856 risk factors in, 1849–1850 shoewear and, 1850, 1898–1899 sport-specific factors in, 1850 surface-related factors in, 1850


Tibia (Continued) training errors and, 1851 treatment of, 1854–1856 in untrained athlete, 1856 stress syndrome of (shin splints), 15, 652, 652t, 1857. See also Chronic exertional compartment syndrome radionuclide imaging of, 545, 545f translation of with non–weight-bearing knee extension, 222 in posterolateral corner injury, 1728 with straight leg raise, 222 Tibial artery injury, high tibial osteotomy and, 1832 Tibial eminence, fracture of, 1677–1679, 1678f, 1679f treatment of, 1677–1679 Tibial intercondylar artery, 1645 Tibial nerve entrapment of, 631–632, 2044, 2045f, 2047, 2057–2059. See also Tarsal tunnel syndrome injury to, 1752 posterior, 2043–2044 decompression of, 2058–2059, 2059f entrapment of, 2044, 2045f Tibial osteotomy high. See High tibial osteotomy in knee arthritis, 1792 in posterior cruciate ligament and posterolateral corner injury, 1744–1747, 1746f Tibial plateau anatomy of, 1748 fracture of computed tomography of, 542, 543f high tibial osteotomy and, 1832 in knee dislocation, 1752–1753 Tibial spine fracture, in children/adolescents, 469, 472f Tibial tendon anterior anatomy of, 1976 blood supply of, 1976 injury to, 1975–1977 evaluation of, 1976–1977 magnetic resonance imaging in, 560, 562f treatment of, 1977 longitudinal split tears in, 1977 posterior anatomy of, 1978–1979 blood supply of, 1978–1979 dysfunction of, 631–632 end-to-end repair of, 1980 injury to, 30, 1977–1981 end-to-end repair in, 1980 evaluation of, 1979, 1979f flexor digitorum longus transfer in, 1980 magnetic resonance imaging in, 562, 563f single heel rise test in, 1979, 1979f too-many-toes sign in, 1979, 1979f treatment of, 1980–1981 triple arthrodesis in, 1980 tendinitis of, 1981–1983, 1982f tenosynovitis of, 538, 538f Tibial tubercle osteochondrosis of (Osgood-Schlatter disease), 599, 1526f, 1527–1529 position of, 1555, 1555f, 1556f stress apophysitis of, 599 Tibiocalcaneal ligament, 1913f Tibiofemoral rotation test, in varus malalignment, 1806–1807, 1807f

Index Tibiofibular ligament anterior-inferior, 1913f, 1931, 1931f magnetic resonance imaging of, 573, 574f Tibiofibular syndesmosis, 1938–1940, 1939f injury to. See Ankle sprain, high (syndesmosis) Tibionavicular ligament, 1913f Tibiotalar ligament, 1913f Tillaux fracture, 597, 598f, 1965, 1966f, 1968–1969 Timolol, in complex regional pain syndrome, 363t Tinea capitis, 198, 198f, 199–200, 200t Tinea corporis, 198, 199, 199f, 200t Tinea cruris, 198, 199, 199f, 200t Tinea gladiatorum, 198 Tinea infection, 198–200, 198f–200f, 200t Tinea pedis, 198, 199f, 200t Tinel’s sign in cubital tunnel syndrome, 1312 in sesamoid dysfunction, 2090 Tissue Banking Project Team, 138 Tissue engineering, in ligament injury treatment, 39 Titin, 4–5 Tobacco use/abuse, 426–428, 428f Toe(s) fracture of pediatric, 1970, 1971f stress, 2028 great. See Hallux deviation of. See Hallux valgus; Hallux varus metatarsophalangeal joint injury to. See Turf toe sesamoids of. See Sesamoid(s) lesser, 2115–2132 anatomy of, 2115–2116 bunionettes of, 2132–2142 anatomy of, 2132, 2132b, 2133f classification of, 2133, 2134b evaluation of, 2133–2134, 2134b imaging in, 2134, 2134b nonoperative treatment of, 2134, 2134b operative treatment of, 2134–2141 care after, 2139–2141, 2140f, 2141f complications of, 2140–2141 diaphyseal metatarsal osteotomy in, 2135–2137, 2138b, 2139f, 2140f distal chevron osteotomy in, 1966f, 2135–2136, 2135b, 2137b distal metatarsal osteotomy in, 2135–2136, 2135b distal oblique osteotomy in, 2135– 2136, 2135b, 2136b, 2136f, 2137f lateral condylectomy in, 2134–2135, 2134b, 2135f, 2140, 2140f return to play after, 2141 physical examination in, 2134, 2134b corns of, 2116, 2117f treatment of, 2117f, 2124, 2129 deformity of, 2115–2132 capital oblique osteotomy for, 2114f, 2131, 2132f classification of, 2117–2119 claw, 2118, 2118t, 2119, 2120b, 2121–2125, 2122f, 2129 evaluation of, 2119–2121 flexor tendon transfer for, 2123, 2125f hammer, 2117, 2118t, 2119f, 2120b, 2121–2125, 2122f, 2123f, 2124b imaging in, 2121 mallet, 2118–2119, 2118t, 2119f, 2120b, 2121–2125, 2123f, 2124f, 2128–2129 metatarsal head arthroplasty for, 2124, 2130f

Toe(s) (Continued) metatarsal osteotomy for, 2124 nonoperative treatment of, 2121, 2121f, 2122f operative treatment of, 2121–2125, 2122f, 2123b, 2123f–2125f management after, 2130–2132, 2131b partial proximal phalangectomy for, 2124, 2129f physical examination in, 2120–2121, 2120b, 2120f, 2121f recurrence of, 2131 return to play after, 2132, 2132f interphalangeal joint motion in, 2181, 2182f medial deviation of, 2116, 2117f, 2119 treatment of, 2123–2124, 2128f metatarsophalangeal joint subluxation/dislocation of, 2116, 2119, 2120f, 2126f treatment of, 2123–2124, 2125b, 2126f–2130f molding of, 2131 taping of, 2121, 2122f turf. See Turf toe Toe cap, 2121, 2121f Toenail, 2096, 2096b, 2097f alcohol matrixectomy for, 2099–2100 complete avulsion procedures for, 2099, 2101f ingrown. See Ingrown toenail partial nail plate avulsion of, 2099, 2100f phenol matrixectomy for, 2099–2100, 2101, 2102, 2105f plastic nail wall reduction for, 2099, 2101f Thompson-Terwilliger procedure for, 2099–2100, 2104f Winograd procedure for, 2099, 2102f Zadik procedure for, 2099, 2103f Tomography, 534. See also Computed tomography (CT) in medial clavicular fracture, 804, 804f in sternoclavicular joint injury, 804 of thoracolumbar spine, 728 Too-many-toes sign, 1979, 1979f Tooth (teeth), on-field injury to, 525 Topiramate, in epilepsy, 189, 191t Total Gym, in knee rehabilitation, 259–260, 260f Trachea displacement of, sternoclavicular joint injury and, 821, 821f on-field injury to, 525 Traction in cervical spine fracture, 675 in proximal humeral physeal fracture, 1077 in rotary atlantoaxial subluxation, 707 Traction spurs, of elbow, 621–622 Training. See also Therapeutic exercise(s) altitude, physiological effects of, 220 endurance, physiological effects of, 215, 216t immune system effects of, 148, 148f resistance, physiological effects of, 214–215, 216t skeletal muscle response to, 213–214, 214t, 215f Tramadol, in complex regional pain syndrome, 364 Trandolapril, 160t Transcutaneous electrical nerve stimulation, in pain management, 229–230, 230f Transforming growth factor-β, in fracture healing, 79–80 Transforming growth factor-β1, in muscle injury, 16 Transverse process, lumbar, fracture of, 734


liii

Transverse scapular ligament, 1120, 1120f Trapezium anatomy of, 1319–1320, 1319f fracture of, 1345–1348, 1349f pediatric, 1370 Trapezius lower, therapeutic exercise for, 240, 240f–241f middle, therapeutic exercise for, 240, 240f pediatric, 785–786, 786f scapular attachment of, 859f, 886f strengthening exercise for, 240, 240f–241f, 1003, 1005f Trapezoid, anatomy of, 1319–1320, 1319f Trapezoid ligament, 827 Traveling, 531 jet lag with, 457–460, 458f adjustment avoidance and, 460 bright light exposure and, 458, 459f melatonin and, 459–460 performance and, 460 room light and, 458–459, 459t, 460t Trazodone, in complex regional pain syndrome, 363t Trendelenburg gait, 1555 Trephination, in meniscal injury, 1608 Tretinoin, in acne, 205 Triangular fibrocartilage complex (TFCC), 1433, 1433f, 1435, 1435f Triangular fibrocartilage complex (TFCC) tears, 575, 1435–1442 classification of, 1435–1436, 1436f history in, 1436 pediatric, 1374–1375, 1374b physical examination in, 1436 radiography in, 1436 return to play after, 1437, 1438, 1439, 1441 treatment of, 1436–1442 type 1A, 1435–1437, 1436f, 1437f type1B, 1435–1438, 1436f–1438f type1C, 1436, 1436f, 1438–1439, 1439f type 1D, 1436, 1436f, 1439 type 2, 1440–1441, 1441f Triceps dip exercise, shoulder injury and, 249 Triceps muscle anatomy of, 1158, 1160f, 1161f, 1170 rupture of, 1297 scapular attachment of, 858, 858f–859f, 886f Triceps tendinitis, 1207 diagnosis of, 1207 treatment of, 1207–1209 Triceps tendon magnetic resonance imaging of, 567 rupture of, 1170–1172, 1207–1209 complications of, 1172 diagnosis of, 1170–1171, 1171f, 1207 mechanism of, 1207 rehabilitation after, 1172, 1172t, 1208 treatment of, 1171–1172, 1171f, 1207–1209, 1208f, 1209f snapping, 1226 throwing-related injury to, 1221, 1226 Trigger, in pain dysfunction syndrome, 351 Trigger finger, 626 Trigger point injection, in low back pain, 732 Trimethoprim-sulfamethoxazole, in urinary tract infection, 153 Triplane fracture, 1966, 1967f, 1968–1969 Triquetrum anatomy of, 1319–1320, 1319f fracture of adult, 1349–1350, 1351f pediatric, 1368–1369, 1369f Trochanteric bursitis, 1455–1457, 1456f

liv

Index

Trochlea, femoral anatomy of, 1549–1550, 1550f, 1560, 1560f depth of, on radiograph, 1539, 1561, 1561f dysplasia of, 1550, 1560–1561, 1561f classification of, 1561, 1561f sulcus angle in, 1563–1564, 1564t treatment of, 1568–1569 Trochlear osteotomy, in trochlear dysplasia, 1568–1569 Trochleoplasty, in trochlear dysplasia, 1568–1569 Tropomyosin, 4, 5t Troponin, 4, 5, 5t Trunk stabilization program, 341–349, 342t aerobic exercise in, 342t, 349 ball exercises in, 342t, 345 bridging exercise in, 342t, 344 dead bug exercise in, 342t, 343 partial sit-ups in, 342t, 343 postural exercises in, 348–349 prone exercises in, 342t, 345 quadruped exercises in, 342t, 346 stabilization exercises in, 343–348 wall slide exercises in, 342t, 347 water running in, 349 weight training in, 349 TT-TG measurement, in patellofemoral disorders, 1565 Tubercle sulcus angle, 1555, 1556f Tuck jumps, 312, 312f, 330 Tumor bone, 74t, 77t, 547, 547f soft tissue, 558, 560f spinal, back pain and, 757, 758f Turf. See Playing surface Turf toe, 2081–2087 anatomy of, 2081–2082, 2082b, 2082f classification of, 2082, 2083b, 2083t complications of, 2087 evaluation of, 2083 flexibility/inflexibility and, 2182 footwear and, 2087 grade of, 2082, 2083b, 2083t, 2084 history in, 2083 imaging in, 2083–2084, 2084f, 2086f nonoperative treatment of, 2084–2085, 2085f, 2086b operative treatment of, 2085, 2086b physical examination in, 2083, 2083b playing surface and, 2198 return to play after, 2087, 2087b shoe design and, 2082, 2082f, 2087, 2188–2189 treatment of, 2083t Twitch, 7–8, 8f Two-by-two table analysis, 108–109, 109f

U Ulna fracture of, in children, 594f, 597 proximal articular surface of, 1189–1190, 1189f fracture of, 1271–1276 evaluation of, 1271–1273 nonunion of, 1278 operative treatment of, 1273–1276 arthrosis after, 1278 complications of, 1276, 1277–1278 infection after, 1278 instability after, 1277–1278 nonunion after, 1278 plate and screw fixation in, 1275 rehabilitation after, 1276–1277

Ulna (Continued) ulnar nerve injury after, 1277 wound problems after, 1278 Monteggia fracture of, 1259, 1260, 1260f, 1273, 1287 osteophyte of, 1223–1224, 1223f Ulnar artery, 1160f Ulnar collateral ligament (UCL) anatomy of, 1301, 1302f reconstruction of, 1222–1224, 1223f, 1237, 1238f, 1308, 1310, 1310f stabilizing effect of, 1193, 1194f, 1230–1231, 1231f Ulnar collateral ligament (UCL) injury, 619–620. See also Thumb, ulnar collateral ligament injury of magnetic resonance imaging in, 576, 577f pediatric, 1237, 1238f vs. tendinitis, 1221 throwing-related, 1221–1224, 1237 pediatric, 1237, 1238f Ulnar nerve anatomy of, 1159 injury to, 622–623, 1311–1315, 1361. See also Cubital tunnel syndrome in coronoid fracture fixation, 1271 in distal humeral fracture repair, 1256, 1277 after elbow trauma, 1277 in pediatric supracondylar fracture, 1282 throwing-related, 1226 Ulnar shortening, in gymnast, 1376, 1376f Ulnar styloid, fracture of, 468, 470f Ulnar styloid impaction syndrome, 1445–1447, 1446f return to play after, 1447 Ulnar styloid process index, 1446, 1446f Ulnar variance, in gymnast, 1376, 1376f Ulnocarpal impaction syndrome, 1440–1441 Ulnocarpal impingement, in gymnast, 1376 Ulnohumeral instability, after proximal ulnar fracture, 1276 Ulnolunate ligament, 1320 Ulnotriquetral ligament, 1320 Ultrasonography, 537–538 in Achilles tendon injury, 630, 1998, 2003–2004 in Baker’s cyst, 537, 538f in cyst aspiration, 585 in deep venous thrombosis, 376, 377f, 383 in elbow heterotopic ossification, 1293 in foreign body, 538, 539f of glenohumeral joint, 951–953, 952f in hamstring strain, 1487 in knee dislocation, 1751 in lateral epicondylitis, 1199 of neonatal hip, 590, 590f in Osgood-Schlatter disease, 1528 in patellar dislocation, 1541 of patellar tendon, 1519, 1519f pediatric, 590, 590f cartilage on, 592–593 soft tissues on, 593 in peroneal tendinitis, 1989 in popliteal artery entrapment, 1839, 1839f in quadriceps strain, 1494 of rotator cuff, 951–953, 952f, 953t, 1000–1001 in suprascapular nerve injury, 1122 in tibial tenosynovitis, 538, 538f transducer for, 537 in vascular injury, 1139 Ultrasound therapy in Achilles tendon injury, 1998 in fracture healing, 80 in lateral epicondylitis, 618


Ultrasound therapy (Continued) nonthermal, 237 in rehabilitation, 236–237 in rotator cuff disorders, 1007 thermal effects of, 237 in tibial stress fracture, 1854 Underage drinking, 424–425 United States Food and Drug Administration, 137, 138 Universal precautions, 153 Unstable surface training, in knee rehabilitation, 271, 272f Urethra, on-field injury to, 527 Urinary tract infection, 152–153 Urticaria, 205, 205f

V Vaccination, Lyme disease, 155–156 Vagal nerve simulator, in epilepsy, 189–190 Valacyclovir, in herpes gladiatorum, 197 Valgus extension overload, 621–622, 1224–1225. See also Overhead throwing injury Valgus instability, 619–620, 620f Validity, 100, 101f, 2217–2218 Valleix phenomenon, 2057 Valproate, in epilepsy, 188–189, 191t Valproic acid, in complex regional pain syndrome, 363t Valsartan, in hypertension, 160t Vancomycin, 387, 387t Variable, statistical, 2218 Variance, 112 analysis of, 112–113, 113f, 118 Varus malalignment, 1801–1803, 1802t, 1803f clinical presentation of, 1803–1804 correction wedge determination in, 1810–1811, 1812f, 1813f evaluation of, 1803–1814, 1805f, 1806t gait analysis in, 1808–1809, 1809f–1810f, 1811f gap angle in, 1812, 1813f imaging and calculations in, 1809–1814, 1811f–1814f, 1814t–�� 1815t open wedge angle measurement in, 1812–1814, 1813f–1814f, 1814t–1815t patellar height measurement in, 1811 physical examination in, 1804–1808, 1805f, 1806t, 1807f, 1808f treatment of, 1814–1835. See also High tibial osteotomy weight-bearing line ratio in, 1810, 1811f, 1812f Varus recurvatum test, in varus malalignment, 1807–1808 Varus stress test, in posterolateral corner injury, 1727, 1727f, 1727t Vascular injury in distal humeral fracture, 1282 in elbow dislocation, 1263, 1304 in knee dislocation, 1750, 1751, 1753, 1753f, 1764–1765 on-field, 527 shoulder, 1137–1142, 1138f, 1139f, 1140f in sternoclavicular joint sprain, 1140 ultrasonography in, 1139 Vasoconstriction, in complex regional pain syndrome, 355, 360 Vasodilation cold-induced, 500 in complex regional pain syndrome, 355, 360 Vastus medialis obliquus neuromuscular activation exercise for, in knee rehabilitation, 256–257, 257f in recurrent patellar dislocation, 1556

Index Vastus muscles, 1485, 1485f, 1550–1551, 1551f. See also Quadriceps muscle Vectors, 86 force, 86, 90f moment/torque, 86 Vegetarianism, iron deficiency and, 479 Vein. See also specific veins anatomy of, 370, 371f circulatory stasis in, 371. See also Thrombosis Venography, in deep venous thrombosis, 376, 377f Venous thromboembolism. See Deep venous thrombosis; Pulmonary embolism; Thrombosis Ventilation, high-altitude effects on, 503 Ventilation-perfusion scan, in pulmonary embolism, 378, 379f Ventricular fibrillation, 163, 164f. See also Sudden death Verapamil in complex regional pain syndrome, 363t in hypertension, 160t Verruca plantaris, 2107b, 2108f Vertebral injury. See Cervical spine injury; Thoracolumbar spine injury Vertebroplasty, 585 Viral infection, cutaneous, 196–198, 197f, 198f Virchow’s triad, 370–374, 371f, 375f Viscoelasticity, 95–96, 95f articular cartilage, 48 meniscus, 59–60, 60f skeletal muscle, 18, 19f tendon, 24–25, 25f Visual acuity on-field examination of, 525 preparticipation examination for, 509 Vitamin A, requirements for, 406b Vitamin B6, requirements for, 406b Vitamin B12, requirements for, 406b Vitamin C deficiency of, 72–73, 73t requirements for, 406b Vitamin D in bone metabolism, 71, 71t deficiency of, 72–73, 73t, 75t, 77t, 79b excess of, 74t, 77t requirements for, 406b Vitamin E, requirements for, 406b Vitamin K, requirements for, 406b Vitamin K antagonist prophylactic, in venous thromboembolism, 378–384, 381t in venous thromboembolism, 384–385, 384t Volar intercalary segmental instability (VISI), 1322, 1324f Volleyball players, nerve entrapment in, 616–617

W Wake maintenance zone, 450, 454–456, 455f Walking. See also Gait ankle joint motion in, 1866, 1867f vs. running, 1865, 1865f, 1866, 1866f subtalar joint motion in, 1868, 1869f transverse tarsal joint motion in, 1869, 1870f Wall slide exercises, in trunk stabilization, 342t, 347 Warfarin prophylactic, in venous thromboembolism, 378–384, 381t, 382f in venous thromboembolism, 384–385, 384t Warm-up exercise in exercise-induced bronchospasm, 184

Warm-up exercise (Continued) in injury prevention, 19 for therapeutic exercises, 276 Warming therapy, in frostbite, 203 Warts, 197–198, 2107b, 2108f Water. See also Fluid(s) cartilage, 41 intake of, 401 with creatine use, 418 requirements of, 401–402, 402t meniscal, 57, 57t Water intoxication, 529 Water running exercise, in trunk stabilization, 349 Watson-Jones procedure, 1924–1925, 1925f Watson’s maneuver, in scapholunate ligament injury, 1324–1325, 1325f Weakness in complex regional pain syndrome, 357 in rotator cuff disorders, 996 Weight gain of, 406, 408b loss of, 406, 407b, 409 in hypertension, 159t making, 406, 406b in preparticipation examination, 509 Weight-bearing, in ACL rehabilitation, 1671 Weight-bearing exercise in female athlete, 481 patellar effects of, 226–227, 226f, 227f Weight training. See also Strengthening exercise/training in trunk stabilization, 349 Wet bulb globe temperature, 528 White blood cells, exercise effects on, 147, 148t White coat hypertension, 157 Windlass mechanism, 2043 in gait, 1870, 1871f Winograd procedure, 2099, 2102f Wolff-Parkinson-White syndrome, 170 Women. See Female athlete World Anti-Doping Agency, 413 Wright’s hyperabduction test, in thoracic outlet syndrome, 1132, 1132f Wrisberg, ligament of, 1597–1598, 1598f, 1614, 1685, 1686f Wrist. See also Wrist injury Allen’s test of, 1320–1321, 1321f anatomy of, 1319–1320, 1319f, 1320f arthroscopy of. See Arthroscopy, wrist chondral lesions of, 1447–1449, 1448f chondromalacia of, 1447–1449 computed tomography of, 543, 544f development of, 1364, 1364t gymnast, 1366f, 1375–1376, 1376f Kienböck’s disease of, 1376–1377, 1377b, 1378f ligaments of, 1319–1320 injury to, 1321–1335. See also Wrist injury, ligament and at specific ligaments magnetic resonance imaging of, 575, 576f loose bodies of, 1447 magnetic resonance imaging arthrography of, 536 overuse injury of, 624–626 playing cast for, 1362 rheumatoid arthritis of proximal row carpectomy in, 1449–1450 radial styloidectomy in, 1449 synovectomy in, 1443–1444 splints for, 1361–1362 taping of, 1362 tendons of injury to, 1351, 1354–1357, 1355f, 1356f


lv

Wrist (Continued) magnetic resonance imaging of, 568–569, 570f vascular anatomy of, 1320, 1320f Wrist extensor tendinosis, 617–619, 618f Wrist injury adult, 1319–1362 fracture, 1335–1351. See also specific carpal bones ligament, 1321–1335. See also at specific ligaments capitolunate angle in, 1322, 1322f clinical manifestations of, 1322, 1324 Mayfield classification of, 1321–1322, 1323f radiography of, 1322, 1322f–1323f, 1324f scapholunate angle in, 1322, 1322f magnetic resonance imaging of, 1321 neural, 1359–1361 palpation in, 1320 physical examination of, 1320–1321, 1321f playing casts for, 1362 radiography of, 1321 range of motion in, 1320 rehabilitation for, 1362 splints for, 1361–1362 taping for, 1362 tendon, 1351, 1354–1357, 1355f–1356f vascular, 1357–1359, 1357f–1358f pediatric, 468, 470f, 1363–1377 epidemiology of, 1363 fracture, 1364–1371. See also specific carpal bones gender and, 1363 ligamentous, 1371–1377, 1372f, 1373f, 1376f overuse and, 1363–1364 physeal, 1364, 1365, 1375–1376 risk factors for, 1363–1364 sport type and, 1363 types of, 1364 Wrist roller training, in elbow rehabilitation, 254, 254f Wry neck, 706–707, 707f

X Xenograft, 38 Xeroradiography, in retrocalcaneal bursitis, 2033

Y Yergason’s test in rotator cuff disorders, 997, 1000f in SLAP lesion, 1024 Yohimbe, 409 Youth Risk Behavior Survey, 463, 466, 467 YoYo flywheel ergometer, in hamstring strain prevention, 337

Z Z band, 4f, 5, 6f, 13f Zadik procedure, 2099, 2101, 2102, 2103f Zeitgeber, 444 Ziegler, John, 411 Zinc, requirements for, 406b Zonisamide, in epilepsy, 191t Zygapophyseal joints, 718, 719f

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